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Postuar nga NS-6 datë 08 Shkurt 2006 - 00:14:

Adult stem cells from knee fat turned into cartilage, bone, fat cells

Cod. A08022006

Adult stem cells from knee fat turned into cartilage, bone, fat cells
1.DALLAS-Duke University Medical Center researchers have "reprogrammed" adult stem cells taken from a small deposit of fat behind the kneecap into functioning cartilage, bone or fat cells that could potentially be grown into replacement tissues.

2.The research team, which reported last year that they were able to turn fat cells taken from liposuction procedures into functional cartilage cells, provides further evidence that stem cells taken from different adult sources have the potential to be transformed into multiple specialized cell types.

3."In scientific terms, we have found a new source of adult stem cells that can be changed into different cells and tissues," said M. Quinn Wickham, who presented the results of the Duke research today (Feb. 10) at the annual meeting of the Orthopedic Research Society. Wickham is a fourth-year medical student working in the laboratory of Farshid Guilak, director of orthopedic research at Duke and senior member of the research team.

4."On the clinical side, for example, it would be relatively easy for a knee surgeon to obtain some of these fat cells using a minimally invasive approach," Wickham continued. "We could then grow cartilage custom-made for the individual to repair an injury in the knee with the patient's own tissue."

5.The fat pad is a dense structure behind the patella, or kneecap, that is unlike typical fat tissue found throughout the body, the researchers said. While its function is not well understood, researchers do know that it is metabolized much more slowly than subcutaneous fat.

6."This is another demonstration that adult stem cells are not necessarily locked into their current fate, and furthermore, we can reprogram them into becoming other cell types," Guilak said. "It is unlikely that one source of stem cells can be used to treat the wide variety of medical problems and diseases, but different clinical problems could be addressed by using adult cells taken from different spots throughout the body, without the same ethical concerns associated with embryonic stem cells."

7.In the current study, the researchers took the fat pads from patients whose knee joints were removed during total joint replacement surgery. The researchers focused on specific cells within the samples known as adipose-derived stromal cells, which under normal situations would receive environmental cues to transform themselves into fat pad cells. After the samples were treated with a series of enzymes and centrifuged, the separated stromal cells were treated with a biochemical cocktail of different steroids and growth factors.

8."By treating these stromal cells with different agents, we were able to induce them to commit to multiple lineages," Wickham said. "These findings suggest that the fat pad, given its location and accessibility, may prove to be an excellent source of progenitor cells for tissue engineering or other cell-based therapies."

9.In addition to controlling their biochemical environment, the researchers were able to grow different cell types from the adult stem cells by controlling their shape in a three-dimensional matrix, a crucial advance for using resulting tissues as human therapies. To grow cartilage, groups of cells were infused into a matrix made of a substance known as alginate, a complex carbohydrate that is often used as the basis of bioabsorbable dressings.
The therapeutic potential for tissues grown from these adult stem cells is large and varied, Wickham said.

10."For example, fat tissue could be custom grown for use in reconstructive or cosmetic cases performed by plastic surgeons," Wickham said. "The bone tissue could be used to repair bone defects caused by disease or trauma." Since cartilage is a tissue type that is poorly supplied by blood vessels, nerves and the lymphatic system, it has a very limited capacity for repair when damaged. The researchers believe that this would be one of the earliest therapeutic uses of such tissue engineering techniques.

11."For patients with tissue damage, we envision being able to remove a small piece of fat, and then growing customized, three-dimensional pieces of tissue which would then be surgically implanted where needed," Guilak continued. "One of the beauties of this system is that since the cells are from the same patients, there are no worries of adverse immune responses or disease transmission. However, we would still like to test whether cells from a person's fat tissue could be used to treat another patient without being rejected."

12.Guilak estimated that it might be more than five years before this approach becomes a clinical reality. However, based on the results of numerous prior animal studies, and the results of the current experiments, the researchers are confident that this strategy has potential. Collaborating with the Duke team was Dr. Jeff Gimble of Durham, N.C.-based Artecel Sciences, who holds the patent for the process of isolating these cells from fat. Guilak is a consultant for Artecel Sciences.


Postuar nga NS-6 datë 08 Shkurt 2006 - 00:19:

Oxygen Key Switch In Transforming Adult Stem Cells From Fat Into Cartilage

Cod. B08022006

Oxygen Key Switch In Transforming Adult Stem Cells From Fat Into Cartilage

1.NEW ORLEANS -- In their ongoing research on turning adult stem cells isolated from fat into cartilage, Duke University Medical Center researchers have demonstrated that the level of oxygen present during the transformation process is a key switch in stimulating the stem cells to change.
Their findings were presented today (Feb. 2, 2003) at the annual meeting of the Orthopedic Research Society.

2.Using a biochemical cocktail of steroids and growth factors, the researchers have "retrained" specific adult stem cells that would normally form the structure of fat into another type of cell known as a chondrocyte, or cartilage cell. During this process, if the cells were grown in the presence of "room air," which is about 20 percent oxygen, the stem cells tended to proliferate; however, if the level of oxygen was reduced to 5 percent, the stem cells transformed into chondrocytes.

3.This finding is important, the researchers say, because this low oxygen level more closely simulates the natural conditions of cartilage, a type of connective tissue that cushions many joints throughout the body. However, since it is a tissue type poorly supplied by blood vessels, nerves and the lymphatic system, cartilage has a very limited capacity for repair when damaged. For this reason, the Duke investigators are searching for a bioengineering approach to correct cartilage injury.

4."Our findings suggest that oxygen is a key determinant between proliferation and differentiation, and that hypoxia, or low oxygen levels, is an important switch that tells cells to stop proliferating and start differentiating,' said David Wang, a fourth-year medical student at Duke, who presented the results of the Duke research.

5.Farshid Guilak, Ph.D., director of orthopedic research and senior member of the Duke team, said that the combination of growth factors sets the adult stem cells on the right path, while controlling oxygen levels inspires the cells to more readily transform into chondrocytes. Without the growth factors, he said, changing oxygen levels has no effect on the cells.

6."For us, the ultimate goal is the development of a bioreactor where we can very carefully control the physical and chemical environment of these cells as they transform," Guilak said. "The results of these experiments which demonstrated the role of oxygen levels in the process represent another important step in achieving this goal."

7.Two years ago at the Orthopedic Research Society meeting, the Duke team for the first time reported that cartilage cells can be created from fat removed during liposuction procedures. Not only were the researchers able to make cells change from one type into another, they grew the new chondrocytes in a three-dimensional matrix, a crucial advance for success in treating humans with cartilage damage.

8.In their latest experiments, the team used the materials collected from liposuction procedures performed on multiple human donors. These materials were then treated with enzymes and centrifuged until cells known as adipose-derived stromal cells remained. These isolated cells were infused into three-dimensional beads made up of a substance known as alginate, a complex carbohydrate that is often used as the basis of bioabsorbable dressings, and then treated with the biochemical cocktail.

9.Those cells grown in hypoxic conditions saw growth inhibited by as much as 44 percent, but saw as much as an 80 percent increase in chondrocyte differentiation.

"No one has looked at the role of hypoxia in the creation of chondrocytes, but it made sense since cartilage normally exists in an hypoxic environment," Wang said. "While we know oxygen plays a role, we don't know the mechanism. The next questions to answer are how the cells sense the level of oxygen around them and then turn that into a metabolic change."

10.The researchers anticipate that the first patients to benefit from this research would be those who have suffered some sort of cartilage damage due to injury or trauma. Farther down the line, they foresee a time when entire joints ravaged by osteoarthritis can be relined with bioengineered cartilage.

11."We don't currently have a satisfactory remedy for people who suffer a cartilage-damaging injury," Guilak said. "There is a real need for a new approach to treating these injuries. We envision being able to remove a little bit of fat, and then grow customized, three-dimensional pieces of cartilage that would then be surgically implanted in the joint. One of the beauties of this system is that since the cells are from the same patients, there are no worries of adverse immune responses or disease transmission."

The Duke researchers have developed several animal protocols to test how this cartilage fares in a living system.

p.s: maybe the news is a bit old but the information given seems interesting,so i brought it here...


Postuar nga NS-6 datë 12 Shkurt 2006 - 01:00:

Max Planck Researchers Discover A Protein Which Is Deadly For Anthrax Bacteria

Cod. C12022006

Source: Max Planck Society
Date: 2005-11-12

Max Planck Researchers Discover A Protein Which Is Deadly For Anthrax Bacteria
1.Scientists from the Max Planck Institute for Infection Biology in Berlin discovered why lung, but not skin, anthrax infections are lethal. As reported in the newest issue of PloS Pathogen (November 2005) Neutrophils, a form of white blood cells, play a key role in anthrax infections.

2.They can kill Bacillus anthracis by producing a protein called alpha-defensin. This discovery might now pave the way towards the development of new therapiesfor the fatal lung form of anthrax.

3.Bacillus anthracis is the causative agent of anthrax. What makes Bacillus anthracis especially dangerous is that these bacteria can form spores. The spores are extremely resistant against environmental stress and can survive for years.Infection with Bacillus anthracis can take place either via the lung or through the skin. Interestingly, the lung form of anthrax is almost always fatal, whereas skin infections remain localized and are rarely lethal. In contrast to the lung form, the skin form of anthrax can be treated without problems and most patients recover. During the past few years, Bacillus anthracis has also been used as a weapon for bioterrorism. Anthrax spores were sent in envelopes and inhaled and resulted in the death of 5 people in the USA.

4.The findings of the lab of Arturo Zychlinsky now help clarifying why the skin form is harmless in contrast to the lung form. After a skin infection with Bacillus anthracis, neutrophils are recruited to the site of infection. Neutrophils are white blood cells that can identify and kill microbes. In the skin, neutrophils take up the spores, which germinate inside the neutrophil to a vegetative ("growing") bacterium. This vegetative bacterium is then attacked and killed within the neutrophil. The scientists succeeded in identifying the substance responsible for the killing of the bacteria. After fractionation of neutrophil components only one protein remained which is sufficient for killing Bacillus anthracis: alpha-defensin

5.This mechanism is not effective in the lung form of anthrax. Here, the number of neutrophils recruited to the site of infection is known to be low, and insufficient to kill bacteria. Thus, inhaled spores can germinate and spread through the organism. The scientists in Berlin now hope that their discovery will help to develop new drugs against the lung form of anthrax. There might be the possibility that the inhalation of alphadefensin might kill vegetative bacteria in the lung and prevent dissemination.


Postuar nga NS-6 datë 13 Mars 2006 - 22:38:

New method to increase the efficiency of contrast radiology

Cod. A13032006

1.A new method to increase the efficiency of contrast radiology may open the way to earlier and more reliable diagnosis of, for example, breast cancer. With new integrated electronics and signal processing, the image quality can be improved sharply.
This was demonstrated by Hans Bornefalk at the Royal Institute of Technology as he presented his doctoral thesis about the technology on March 10.

2.To date, the new technology has only been tested in a test rig, but in principle it can open the way for earlier and more reliable diagnosis of, for example, breast cancer. In a long-term perspective, there are a number of other radiological applications in which contrast substances are used today.

3.To grow, a cancer needs to form its own blood vessels, which are often of poor quality and can leak. In contrast radiology, a contrast substance such as iodine is injected into the blood stream so that the blood vessels can be seen on the radiology images. Indirectly, then the cancer is also seen through the leakage in these blood vessels. Normally, a series of images is required to secure the contrast image.

4.With Hans Bornefalk's new method, one radiology image is sufficient to benefit from the contrast information. In addition, the image quality can be sharply improved or the ray dosage reduced. This is possible by being able to trace and register each X-ray separately. Since the X-rays can also be separated into two categories, in which one has higher and the other lower energy than the contrast substance's threshold value for maximum absorption energy, totally new possibilities emerge.

5."With the proper electronics, you can precisely separate the X-rays that are above and below this threshold value and highlight the differences between the blood vessels and surrounding tissue in a totally different manner," relates Hans Bornefalk. " Radiology examinations can be carried out quicker and more reliably and the risk for blurredness due to movement between images is eliminated."

6.Clinical tests are required to verify the new technology and maximize the clinical benefits. Sectra, a company that develops and manufactures equipment for radiology examinations, has plans to integrate the new technology into its future products.

7."This fits well into our mammography operations and will reinforce the world-leading position of Swedish industry in this area," says Jesper Söderqvist, President of Sectra Mamea in Kista.

In intense competition, Hans Bornefalk's work was recognized a few weeks ago as the "Best Student Contribution" at a major conference for medical radiology technology in San Diego, California, in the US.

p.s: numrat behen ne menyre qe kur ta lexoni te arrini nje perqendrim me i mire duke qene se artikujt e gjate mund te cojne edhe ne ngaterrese gjate leximit.


Postuar nga NS-6 datë 15 Mars 2006 - 22:57:

Statin drug reverses heart disease

Cod. B15032006

Published: Wednesday, 15-Mar-2006

1.Researchers say a high dose of a cholesterol-lowering statin drug can reverse the build-up of plaque in coronary arteries.
Such a build up can lead to a heart attack or stroke, and the researchers say this is the first time statins have been shown to have such an effect.

They say the changes in cholesterol levels seen in the study were the largest ever seen in a major trial of statin drugs.

2.A study of more than 500 patients found that after two years of treatment with a high dose of the cholesterol-lowering statin drug, Crestor, plaque volume was reduced by 7 to 9 percent.

The drug was also found to lower levels of LDL "bad" cholesterol by more than 53 percent to 60.8 and raised levels of HDL, or "good" cholesterol by nearly 15 percent to an average of 49.

3.Although Crestor is considered to be one of the most powerful statin drugs, concerns about the potential side effects such as muscle damage and kidney damage, especially among Asians,have somewhat tarnished it's reputation.

Just last year the U.S. Food and Drug Administration dismissed a petition by the consumer group Public Citizen to have Crestor banned.

The changes in cholesterol levels seen in the study were the largest ever seen in a major trial of statin drugs, say the researchers.

4.According to Dr. Steve Nissen, interim director of the department of cardiovascular medicine at the Cleveland Clinic and the study's lead author, "the results were shockingly positive".

5.The trial does however leave unanswered the question of whether less plaque means fewer heart attacks and strokes; Nissen says the study does indicate very low LDL levels along with raised HDL, can partially reverse heart disease.

Apparently the patients in the trial had not been treated previously with statins.

Other statin drugs such as Lipitor, Zocor and Vytorin, might also lead to similar plaque regression, says Nissen.

6.Atherosclerosis results when a build-up of cholesterol, inflammatory cells and fibrous tissue form areas in the artery wall called plaques.

If these plaques rupture, they can block blood flow to critical organs, such as the heart or brain, and can lead to heart attack or stroke.

7.Nissen said he doubted that a statin drug could reduce plaque by much more than the levels seen in the Crestor trial, which used the highest approved dose for the drug.

But some experts are cautious about the findings and say more study is needed.

Many regard lifestyle changes, such as eating a better diet, and exercising regularly as the key to managing cardiovascular disease.

8.Crestor is produced by drug company AstraZeneca who sponsored the trial.

The results were presented at a meeting of the American College of Cardiology in Atlanta.

The study will be published in the April edition of the Journal of the American Medical Association.


Postuar nga darke datë 21 Mars 2006 - 10:07:

Question Prolactina

Hello doctor!

How is going with your section? I see it is growing and growing. I have a question for you; it's about an hormon called PROLACTINA ("prolactina" is in Spanish, and I beg you pardom cause I don't know how it is written in English; maybe they both are seemed). So the question is: how does the prolactina affect to the body? and what happen when the level of this hormon is very high? what would be your diagnosis? :p

Ciao ciao. See you!

Kisses...


Postuar nga NS-6 datë 21 Mars 2006 - 22:09:

prolactina and its hyperproduction

Cod. B21032006

Hi there darkeeeee!!!Where have u been? How's the new generation going? Do they respect the teacher?...my section is growing every day...and i like that a lot

Now ur question:
Prolactina is a hormone produced by the pituitary gland and its major effect is seen in the women...mainly on the mammary gland. It stimulates the milk production... In fact when the baby sucks the mammary gland,there begins a response to this by producing prolactina that increases the milk production and release.

When the level of prolactina is high u have to consider the cause of this:
It may be physiological as in case of pregnancy when the level increases or it may be due to stress or physical activity.However except the first case which may be the most common as a physiological cause,mostly it is due to a pituitary adenoma.In fact prolactinoma is in first rank in the pituitary adenomas cases.The symptoms are menstruation cycle problems such as amenorrhea(no menstruation cycle) and also galactorrea (milk comes out from the nipples spontaneously or after a small pressure on it).these are the primary peripheral symptoms even why there might be other symptoms but they might be misunderstood because not very specific.there are also other symptoms due to the mass of the adenoma which varies from problems on the ocular nerve to the destruction of the remaining part of the pituitary gland due to the pressure on that part.
Diagnosis is based on symptoms like vision problems,cefalea or presence of amenorrhea or galatorrea (even why for these there are other test that will be done to verify other hypothesis). Prolactine concentration in plasma will be over the limits...i don't remember if there is another exam to measure the concentration of prolactina (i think there is smth with the thyroglobulin but i don't remember it very well)...if there is the suspect of an adenoma, MRN is the best to identify the location and the dimensions.

iIcant say u anything about the therapy becouse i dont know it ...i havent studied it...i may give u any information more if i search the book!
Up to then have a nice day...
And sorry for my english...as always it sucks...and it getS no milk from that

p.s: If any of u knows anything more,I'd invite em to write it down!


Postuar nga darke datë 22 Mars 2006 - 10:36:

Lightbulb Re: prolactina and its hyperproduction

miredita zoti ns-6!
si je? I've been very well and working hard. Well, about the new generation... I could say it's very predictable . At the begining they see you and they observe you with shyness but soon they start to have confidence, and here it's when darke has to show her eyeteeth Let me tell you what happened once... During some days everything was ok. I always have tried that the alumns enjoy in my class, but as I told u before sometimes they take too much confidence. Once I came to the class as every morning and everybody was talking. I gave them 5 minutes to be ready while I was taking note about the absents. I finished and they continued talking and talking. I said, ok, today we will study "Parelelism". They just stopped for two seconds to watch me, and then they continued talking. I started explaining the lesson anyway (I was on foot, writting and talking in the blackboard) but everybody continued talking and talking. As I saw that anyone was paying attention to my explanation, I said in low voice: "ok, I see you are not interested to hear me today so Bye Bye. See you tomorrow". And I started to take my stuffs and my bag. The classroom became suddenly in silence and everybody was like this Some alumns started to beg me pardom and to say Please, don't go professor, forgive us, don't go please. But I didn't say anything and in a very calm way I went from the class The next days never never never they started to talk again when i'm explaining:p
I have enjoyed a lot my throat has been the one who has suffered most

Hej, your explanation has been very helpful. Let's try a diagnosis:
The data would be this one: a woman, no pregnant, the whole blood analysis is ok except the level of prolactina that is very high. Some menstruations alterations (like two menstruations in a month). what would you do?


Postuar nga NS-6 datë 22 Mars 2006 - 14:53:

some info more

hahahahaha,i knew u were e good teacher...however remember the albanian methods i have told u...they have never failed in their whole history

ok,let's get back to the diagnosis:
did she measure the gonadotrophin releasing hormone(GnRH),follicle stimulating hormone(FSH) and the luteinising hormone(LH)?
prolactina is inhibitory for GnRH and so there will be a LH anomaly in concentration...this is seen in already 70% of the women with hyperprolactinoma.

also there is a dynamic test with TRH (thyreotropina) that shows whether it is an adenoma or a functional hyperprolactina (info based on the endocrinology manual of Andreoli)

MNR and CT are gold standart as it is used in medicine (the best,it means) to analyse any pituitary problem...

these are used in order to discover the primary causes of hyperproduction...there are some other causes that are rare but they need a more specialistic approach which i dont know by now...


Postuar nga amor alucius datë 22 Mars 2006 - 17:58:

Re: Re: prolactina and its hyperproduction

Citim:
Po citoj ato që tha darke
. Once I came to the class as every morning and everybody was talking. I gave them 5 minutes to be ready while I was taking note about the absents. I finished and they continued talking and talking. I said, ok, today we will study "Parelelism". They just stopped for two seconds to watch me, and then they continued talking. I started explaining the lesson anyway (I was on foot, writting and talking in the blackboard) but everybody continued talking and talking. As I saw that anyone was paying attention to my explanation, I said in low voice: "ok, I see you are not interested to hear me today so Bye Bye. See you tomorrow". And I started to take my stuffs and my bag. The classroom became suddenly in silence and everybody was like this Some alumns started to beg me pardom and to say Please, don't go professor, forgive us, don't go please. But I didn't say anything and in a very calm way I went from the class The next days never never never they started to talk again when i'm explaining:p
I have enjoyed a lot my throat has been the one who has suffered most



NS-6,te lutem,mos e leviz kete postimin pa u lexuar nga marresi.Flm

Darke,can you bear some constructive critics?Please,accept my apologies if you think any of the following words is untrue.I'm not a teacher but I've a proff.home,I've asisted a lot of his lessons...and I'm a student myself(once I've been a pupil too),so I know more or less what must happen in order to have a successful lesson.


Where is your LEAD-IN?
Where is your PRESENTATION?
Are your pupils CENTRAL in this didactical method?
Is this INDUCTIVE learning?
And what about the TRANSLATION of the elements of some image you've brought with you to present your new topic?What about the next fase in your didactical method: INTERPRETATION?
ONLY when you've finished the above-mentioned steps you can say what your topic is about.
It's a very common mistake but it's a CAPITAL one,you saw the consequences.If I had been in their places,although I'm older and I can concetrate me longer than them,I would have acted the same.

A teacher NEVER opens his mouth to tell something about the lesson if they're not quiet,your first 2 minutes determinate ALL your lesson.
A teacher NEVER tells the topic immediately,but first brings something that connects with their world f.e. a picture with the elements you'are going to use later.Then you ask them to READ it,fi(f.e.-a building-a square object),then they interprate it(This is a building,miss).Then you write some of it's elements THENNNN you tell ur topic.
U can ask why is your lead-in that important?It's simple,if it's a good one,you get their ATTENTION immediately.
It's said that in teaching the importance of your content is 40%,the importance of your didactical method is 60%.


Postuar nga darke datë 22 Mars 2006 - 20:04:

Thumbs up Re: Re: Re: prolactina and its hyperproduction

NS-6: Uhhh thank you for your answers. Hmmm but I don't know what you ask me. I will give you any new info that i get

amor alucius: Hey... of course I bear constructive critics; actually they are the ones that I only accept. I thank you very much your message, even I have to say that I’ve enjoyed reading you.
I know perfectly that what I did sounds and is kinda impulsive, but in that moment is what I resolved to do, because my patience has a very near limit when unpoliteness is on the table. And I’m sorry for this, but I am like this, bad or good teacher I don’t allow that someone don’t respect me.
About the didactical method, nothing else to say about the “building knowledge”, because that is the right way to teach. But you can’t teach anything if the students are not dispossed to listen to you, to see what you have to bring them. And this yes is a problem. Please, could you ask to your prof.home about technics to improve motivation in the alumns?:p. I would be very grateful to know about this; I yes am very interested on this matter. And this is what I most missed in my experience as a teacher when I arrived to that school.
So this is the main point where I concentrated my energy: motivation. And first of all “respect” to the people, and above all when someone is talking to you. Then to stimulate them, to make them to have curiosity about my subject.
Well, I don’t know if they learned too much about Technical Drawing, but I tell you that they improved their creativity and their way to behave with people as “people”, at least with me
I’m sure that “education” is a word that means something further than knowledge, and in the real world you have to teach to the students more than your subject, you have to teach them to be persons.


Postuar nga NS-6 datë 22 Mars 2006 - 21:55:

its nice to see a teacher getting instructed ...darke,ur gonna give me some free lessons about art, o.k?:p...or better,some lessons in spanish.do u remember,i was goin well with my spanish

amor,shkrimet nuk do levizet osefshihet sepse fundja kjo teme ka qene hap posacerisht per darken dhe normalisht pervec mjeksise mund te kete edhe muhabet te lire...qe te mos behen gjerat monotone


Postuar nga NS-6 datë 23 Mars 2006 - 00:00:

The birth of words: Ten-month-olds learn words through perceptual salience

Cod. A23032006

Medical Studies/Trials
Published: Wednesday, 22-Mar-2006

Infants are listening and learning their first words as young as 10 months, but they are only learning the words for objects that are of interest to them, not for objects of interest to the speaker, according to researchers at Temple University, University of Delaware and University of Evansville.
Their findings are reported in a new study, "The birth of words: Ten-month-olds learn words through perceptual salience," being published in the March/April issue of the journal Child Development (Vol. 77, Issue 2).

In their study, the researchers showed infants two separate objects--one "interesting" and one "boring" in order to teach infants new words. The researchers examined whether 10-month-olds are guided by how much they like an object (i.e., perceptual cues) as well as which object the speaker with them is naming (i.e., social cues) to learn a new word.

At 10 months, before they say much of anything, the researchers discovered that the infants were truly capable of learning two new words in a single session. Using a measure of word comprehension (rather than expecting babies to say the word), they found that infants paired a new word to the object they liked best, regardless of which object the speaker named.

"We found that you could look at one of the objects, pick that object up and even move it, but the baby naturally assumes that the word you're speaking goes with the object that they think is interesting, not the object that you show an interest in," says Kathy Hirsh-Pasek, the Lefkowitz Professor of Psychology and director of the Temple University Infant Lab, and one of the study's co-investigators.

"Ten-month-olds simply 'glue' a label onto the most interesting object they see," adds Shannon Pruden, a doctoral student in psychology at Temple and the study's lead author. "Perhaps this is why children learn words faster when parents look at and name the objects that infants already find interesting."

According to the researchers, these results have huge implications for parents and caregivers. They suggest that babies are listening into our conversations and trying to learn words well before they can say them. The findings also suggest that when we speak to our infants, we should talk about things that they like, not what we like.

As parents and caregivers, we must be sensitive and responsive to infants' interests as they don't have the flexibility to adopt our interests, says Hirsh-Pasek.

"Little babies are learning words fast, even at 10 months when they aren't saying much at all and that's huge," says co-investigator Roberta Michnick Golinkoff, the H. Rodney Sharp Professor of Education at Delaware. "So, parents should talk to their babies from early on because that's the only way that infants can learn language. They should also talk about what the baby is interested in."

The researchers added that around 18 months of age, a child's focus changes and they begin to learn words differently, using the speaker's interest as a guide.

"The 18-month-old is a social sophisticate who can tap into the speaker's mind and the vast mental dictionary that the adult has to offer," says Hirsh-Pasek. "At 10 months they just cannot take the speaker's perspective into consideration."


Postuar nga amor alucius datë 23 Mars 2006 - 18:37:

Darke!

I wanna tell u a story that happened sometimes ago:
I was asisting to the lessons of my"home-prof",with my bf,and in a aula of 600 students came in a boy with a Stella Artois in his hand.He sat down,opened his beer and began drinking,laughing and talking to his neighbours.The proff.saw that,afterwards he told me he couldn't believe his eyes,he went to the guy with a nice smile on his face and said calmly:"the catheder is empty,go and finish your beer there".The boy blushed,the proff said again"I'm not joking,go there and finish it meanwhile we enjoy the view".He HAD to go there while 1200 eyes were staring at him,the two assistents couldn't contain them self from laughing,once he was there he couldn't drink his beer from the embarrassment.Only after the proff had finished his lesson he could go From then on he was known as"the guy with the Stella"

I told the story to make clear that sometimes you need to pick out the main troublemaker,to punish him in a"funny"way in order to regain the peace in the group.Ofcourse,after you've practised a didactical correct method in ur lesson(changing of working method every 10 min.,enough images,enough interaction with your pupils...)


P.s.How can I learn drawing ?


Postuar nga darke datë 26 Mars 2006 - 12:41:

Thumbs up Re: Darke!

Citim:
Po citoj ato që tha amor alucius

P.s.How can I learn drawing ?


just drawing, drawing and drawing


Postuar nga NS-6 datë 31 Mars 2006 - 22:23:

Malaria, mosquitoes and man - breaking a deadly cycle (1)

Cod. B01042006

Disease/Infection News
Published: Friday, 31-Mar-2006

Malaria kills a child every thirty seconds in Sub-Saharan Africa, according to recent estimates. It is a huge problem currently threatening over 40% of the world's population and still on the increase. The infection causes more than 300 million acute illnesses and at least a million deaths annually, and is recognised as a major factor impeding the development of some of the poorest nations.
Past strategies to kill off mosquitoes with insecticides failed as they developed resistance, just as malaria itself has developed resistance to some of the drugs used to control the disease.

Researchers at the Institute for Science and Technology in Medicine at Keele University, in the West Midlands region of the UK, are focusing their efforts on trying to break the transmission cycle through which the disease is passed on, by studying the complex relationship between the parasite and the mosquito itself.

Paul Eggleston, Professor of Molecular Entomology, School of Life Sciences, Keele University, said: "We have growing problems with insecticide resistance - we now have mosquitoes which are resistant to every class of insecticidal compound that we can throw at them, the parasites themselves are becoming resistant to all of the drugs we can use to try and tackle the disease. So we're starting to think about this complex set of interactions that take place between the mosquito and the parasite and whether there are ways within that set of interactions that we can tackle the transmission cycle itself."

Hilary Hurd, Professor of Parasitology, School of Life Sciences, Keele University, said: "I think one of the surprising things is that it takes so long for the malaria parasite to develop in the mosquito. It takes around 15 days and the mosquito in the wild often only lives that long. So it's very much a tight rope that the parasite's walking, it must keep it's mosquito alive long enough for it to survive to transmit it once it's infective, back into the next person. So that time period is the key aspect of the life cycle."

One discovery of particular interest is that many of the parasites contained in the blood cells a mosquito absorbs during a blood meal, are killed off within the mosquito's gut within the first twenty-four hours.

At Keele they think one method by which this is done is a means known as "programmed cell death", so they are investigating how this is triggered, and whether that action could be enhanced.

Another area of weakness they have discovered in this complex parasitic relationship is that the infected female mosquito produces fewer eggs. The likelihood is that this is a resource management strategy so the mosquito lives longer allowing the parasite to mature to an infective stage. If the mosquito was made to lay more eggs, it would die too early for the parasite to mature, again breaking the transmission cycle.

Professor Hilary Hurd: "If we can understand more about the biology and particularly the molecules involved and that are critical to maintaining the cycle then we can try to interfere with those molecules perhaps by manipulating the mosquito genetically so that a key molecule is produced in more abundance or is not produced at all and upset this delicate balance between infection and survival."
continues....


Postuar nga NS-6 datë 31 Mars 2006 - 22:24:

Malaria, mosquitoes and man - breaking a deadly cycle (2)

Cod. C01042006

While some researchers in Keele University's Centre for Applied Entomology and Parasitology, are studying the biology of the mosquito, others are working on this genetic engineering approach, to see if they can inhibit the mosquito from passing on the parasite.

By injecting mosquito embryos with different genes with fluorescent markers that show up under ultraviolet light, they can track the genetically modified mosquitoes as they grow, and also see where the genes go. While they can introduce new genes, its not a precise process, and they can't yet predict where they might end up in a chromosome, or whether they could damage existing genes.

Professor Paul Eggleston said: "The main limitation is simply one of efficiency. This is a very inefficient and technically demanding procedure, so at Keele we've been trying to think up new ways to get round these limitations and inefficiencies. One way is to introduce a docking site into the mosquito chromosome. This is simply a target into which we can integrate any new gene of our choice and we know that if the genes go into this target site they are going to be reliably expressed and we also know that they are not going to have a negative impact on any of the normal genes within the mosquito."

The aim is to engineer a mosquito which is simply incapable of transmitting malaria.

Professor Paul Eggleston added: "What I would like to do with our new technology is to introduce a whole suite of transgenes, novel genes into the mosquito so we can have what I think of as a multi-hit approach. We want to be able to tackle the parasite at several different places within the insect all at the same time to make sure that no parasites survive and therefore we've effectively broken the transmission cycle."

The ultimate vision is to replace natural populations of malaria carrying mosquitoes in disease endemic areas, with a "genetically modified mosquito" incapable of carrying the malaria parasite, and freeing large sections of the world's population from the daily tragedy of young lives lost to this deadly disease.


Postuar nga NS-6 datë 05 Prill 2006 - 00:31:

Adult stem cells can be used to make new tendon or ligament tissue

Cod. B05042006

Medical Research News
Published: Tuesday, 4-Apr-2006

Weekend athletes who overexert themselves running or playing basketball may one day reap the benefits of research at the Hebrew University of Jerusalem that shows that adult stem cells can be used to make new tendon or ligament tissue.
Tendon and ligament injuries present a major clinical challenge to orthopedic medicine. In the United States, at least 200,000 patients undergo tendon or ligament repair each year. Moreover, the intervertebral disc, which is composed in part of tendon-like tissue, tends to degenerate with age, leading to the very common phenomenon of low-back pain affecting a major part of the population.

Until the present time, therapeutic options used to repair torn ligaments and tendons have consisted of tissue grafting and synthetic prostheses, but as yet, none of these alternatives has provided a successful long-term solution.

A novel approach for tendon regeneration is reported in the April issue of the Journal of Clinical Investigation. Researchers Prof. Dan Gazit and colleagues at the Skeletal Biotechnology Laboratory at the Hebrew University Faculty of Dental Medicine engineered mesenchymal stem cells (MSCs), which reside in the bone marrow and fat tissues, to express a protein called Smad8 and another called BMP2.

When the researchers implanted these cells into torn Achilles tendons of rats they found that the cells not only survived the implantation process, but also were recruited to the site of the injury and were able to repair the tendon. The cells changed their appearance to look more like tendon cells (tenocytes), and significantly increased production of collagen, a protein critical for creating strong yet flexible tendons and ligaments.

Tendon tissue repair was detected using a special type of imaging known as proton DQF MRI, developed by Prof. Gil Navon at Tel Aviv University, which recognizes differences among collagen-containing tissue such as tendon, bone, skin, and muscle. The authors note that BMP and Smad proteins are involved in other tissues such as nerve and liver, suggesting that this type of delivery technology may be helpful for other degenerative diseases.

In an accompanying commentary in the Journal of Clinical Investigation, Dwight A. Towler and Richard Gelberman from the Washington University School of Medicine in St. Louis, Missouri, state, "Given our limited understanding of how MSCs become tenocytes, the recent progress demonstrated in these studies is quite remarkable and may be potentially useful in cell-based therapeutic approaches to musculoskeletal injuries."


Postuar nga NS-6 datë 07 Prill 2006 - 23:56:

Type 2 diabetics' urine acidity increases risk for kidney stones

Cod. A08042006

Medical Studies/Trials
Published: Friday, 7-Apr-2006

People with type 2 diabetes have highly acidic urine, a metabolic feature that explains their greater risk for developing uric-acid kidney stones, researchers at UT Southwestern Medical Center have found.
The study - the first to compare the urinary biochemical characteristics of type 2 diabetics with those of normal volunteers - is available online and will be published in the May issue of the Journal of the American Society of Nephrology.

Individuals with type 2 diabetes (non-insulin dependent diabetes mellitus) are at increased risk for developing kidney stones in general, and have a particular risk for uric-acid stones. The mechanisms for this greater risk were previously not entirely understood. This new study demonstrates that the propensity for type 2 diabetics to develop uric-acid stones is elevated because their urine is highly acidic.

"Our next step is to find out what causes type 2 diabetics to have an abnormally acidic urine, and what other urinary factors protect some diabetics who do not form uric-acid stones," said Dr. Mary Ann Cameron, the paper's lead author and a postdoctoral trainee in internal medicine.

Obesity and a diet rich in animal protein are associated with abnormally acidic urine. In earlier studies, UT Southwestern researchers also concluded that uric-acid stones are associated with insulin resistance and type 2 diabetes.

But when researchers in this latest study accounted for these components, type 2 diabetics continued to have more acidic urine levels when compared to nondiabetics. These findings suggest that other factors associated with type 2 diabetes or insulin resistance account for the overly acidic urine in this population.

"Diet intake and obesity, those two factors alone, don't explain the whole picture," said Dr. Naim Maalouf, an author and assistant professor of internal medicine. "So, other unrecognized factors may play a role."

Dr. Khashayar Sakhaee, senior author of the study and chief of mineral metabolism, said: "Our group at UT Southwestern was the first to determine that the more overweight a person is the more likely he or she is to form uric-acid kidney stones."

More than 18 million people in the United States live with diabetes, a chronic disease that affects the body's ability to produce or respond to insulin and that can lead to life-threatening illness, including heart disease and stroke.

Kidney stones are solid deposits that form in the kidneys from substances excreted in urine. When waste materials in urine do not dissolve completely, microscopic particles begin to form and, over time, grow into stones. These solid deposits can remain in the kidney or they can break loose and travel down the urinary tract. Small stones can pass out of the body naturally, but larger stones can get stuck in a ureter, the bladder or the urethra, possibly blocking the flow of urine and often causing intense pain.

Uric acid stones are more difficult to diagnose than other types of stones because they don't show up on regular abdominal X-rays, often delaying the diagnosis and leading to the continued growth of the stone.


Postuar nga NS-6 datë 12 Prill 2006 - 00:52:

Scientists find that growth hormone is produced in the brain

Cod. B12042006

Medical Research News
Published: Tuesday, 11-Apr-2006
1.Scientists have found that growth hormone, a substance that is used for body growth, is produced in the brain, according to an article published in the Proceedings of the National Academy of Sciences.
The researchers -- from three institutions -- found that growth hormone is produced within the hippocampus, a structure deep inside the brain that is involved in memory and emotion.

2.The scientists also found that more growth hormone is produced in females than in males, and more in adults. More growth hormone was also produced in response to estrogen. The study has implications for menopausal women using estrogen replacement therapy and for athletes taking growth hormone and anabolic steroids to increase muscle mass.

The scientists suspect that reasoning and mood may also be affected by these differences in the amount of growth hormone in the brain.

3."Growth hormone has been associated with growth of muscles and bones, and the production of it was believed to lie mainly in the pituitary gland," said co-author Ken S. Kosik, co-director of the Neuroscience Research Center at the University of California, Santa Barbara. "No one had thought too much about what growth hormone might be doing in the brain. Hormones in the brain may not be obvious compared to what they are doing in the rest of the body."

4.The authors previously found that hippocampal growth hormone increases with learning. The current study shows that the hormone is very different in males versus females.

"Males and females look different, we act different, so of course our brains are different," said Tracey J. Shors, co-author and a professor of psychology at the Center for Collaborative Neuroscience at Rutgers: the State University of New Jersey. "There are remarkable differences. People used to think of females as a male with hormones. That's just not the case."

5.The authors found that growth hormone in the brain is increased with stress, especially in males. The effect in females depended on how much estrogen they had at the time. "One interesting interpretation of these results is that exposure to a stressful event increases growth hormone expression in males -- but the increase in females may be dependent on their levels of estrogen at the time," said first author Christine P. Donahue. Donahue, formerly a postdoctoral fellow of Ken Kosik, is an instructor in the Department of Neurology at Harvard Medical School.

6.The authors suggest that because growth hormone in the body is associated with growth of the body, it may also cause growth in the brain. Females have more dendritic spines (parts of neurons) in the hippocampus than do males. This is especially true when estrogen levels are high and when growth hormone levels are high. They also produce more new neurons in the hippocampus during this time.

7."Sex differences in the brain is an area of research that has exploded in recent years," said Shors. "Sex hormones, like estrogen, have a tremendous effect on the growth and architecture of the brain. Several studies in our lab and in others have shown that males learn differently than females. It is possible that sex differences in these hormones are somehow involved."


Postuar nga NS-6 datë 16 Prill 2006 - 22:44:

Passive smoking increases diabetes risk

Cod. A16042006

Published: Tuesday, 11-Apr-2006

1.A study published on the British Medical Journal website shows for the first time that breathing other people's smoke raises the risk of developing glucose intolerance, the precursor to diabetes.
The US research also shows that overall, white Americans are more susceptible to this effect than African-Americans.

2.Researchers examined 4572 men and women in four US cities, dividing them into four categories of smoking status: ranging from those who smoked, to those who had neither smoked nor breathed in other people's smoke. The study focussed only on those who were white or African-American.

3.The authors then tracked how many participants developed glucose intolerance - where the body can no longer produce enough insulin to regulate blood sugar - over 15 years of follow-up.

The study found that smokers had the highest risk, with 22% of them getting the disease over the study period. Non-smokers who had no exposure to second-hand smoke had the lowest risk, with less than 12% developing the condition.

But 17% of those who had never smoked themselves but were subject to second-hand smoke also developed glucose intolerance - higher than the 14% risk rate in the group who had previously smoked and given up.

4.Those breathing second-hand smoke are exposed to many toxins, say the authors. And the chemical reactions which produce second-hand smoke mean that some of those toxins may be at even higher concentrations than the levels breathed in directly by smokers. If one of these toxins particularly affects the pancreas - the organ which produces insulin - this may explain the findings, they suggest.

Until now, it had not been known that those breathing second-hand smoke faced an increased risk of diabetes, say the researchers. More studies are now needed, they conclude.

original source site:
http://www.bmj.com


Postuar nga NS-6 datë 17 Prill 2006 - 23:20:

First gene therapy human trial in the United States for a form of muscular dystrophy

Cod. A18042006

First gene therapy human trial in the United States for a form of muscular dystrophy under way (PART 1)
Published: Sunday, 16-Apr-2006

1.The clinical trial for Duchenne muscular dystrophy (DMD) tests the safety and effectiveness of a therapy that was developed over two decades by scientists at the University of North Carolina Chapel Hill's School of Medicine and the University of Pittsburgh.
The trial was launched March 28, at Columbus Children's Hospital in Ohio, an affiliate of Ohio State University's School of Medicine. In the trial, six boys with DMD will receive replacement genes for an essential muscle protein.

2.Each of the boys will receive replacement genes via injection into a bicep of one arm and a placebo in the other arm. Neither the investigators nor the participants will know which muscle got the genes. After several weeks, an analysis of the injected muscle tissue's microscopic appearance, as well as extensive testing of the health and strength of the trial participants, will reveal whether gene therapy for DMD is likely to be safe and whether it's likely to result in persistent production of the essential protein in muscle cells.

3.Muscular dystrophies are genetic disorders characterized by progressive muscle wasting and weakness that begin with microscopic changes in the muscle. As muscles degenerate over time, the person's muscle strength declines.

Duchenne muscular dystrophy is a genetic disease that begins in early childhood, causes progressive loss of muscle strength and bulk, and usually leads to death in the 20s from respiratory or cardiac muscle failure. DMD occurs when a gene on the X chromosome fails to make the essential muscle protein dystrophin. One of nine types of muscular dystrophy, DMD primarily affects boys.

4.Currently, the best medical therapy can only slow the progressive muscle weakness of DMD.

5.The gene for dystrophin is one of the largest genes in the human body, and miniaturizing it, while retaining the crucial elements of its set of DNA instructions, has been among the greatest challenges to the gene therapy field.

6.The new Biostrophin therapy uses a novel combination of advanced technologies, including a miniaturized replacement dystrophin gene and nano delivery technology called biological nanoparticles. Developed from a virus known as adeno-associated virus (AAV), the nanoparticles are engineered specifically to target and carry the "minidystrophin" gene to muscle cells.

The therapy was made possible by the pioneering research in AAV by Dr. Richard Jude Samulski, professor of pharmacology and director of the Gene Therapy Center at UNC, and Dr. Xiao Xiao, a former UNC postdoctoral researcher in Samulski's laboratory now with the University of Pittsburgh Human Gene Therapy Center and associate professor of orthopedic surgery.

7.Samulski has long pioneered methodologies for making viruses deliver genes. As a graduate student at the University of Florida in the early 1980s, his thesis project was developing the AAV as a vector for therapeutic genes. This work eventually led to isolation of type-2 AAV, which has been used for gene therapy trials in cystic fibrosis and in several other settings, Samulski said.

"It's what we would call the parent virus that everybody started with."

Samulski moved to the University of Pittsburgh in 1986, joining the biology department as an assistant professor with his own laboratory. His first graduate student was Xiao, who had just come from China. Xiao focused on the lab's AAV vector project. "We've continued to have productive collaborations ever since he graduated from my lab," Samulski said.


Postuar nga NS-6 datë 17 Prill 2006 - 23:28:

First gene therapy human trial in the United States...(PART 2)

First gene therapy human trial in the United States for a form of muscular dystrophy under way (PART 2)

8.In 1993, Samulski moved to the University of North Carolina at Chapel Hill, becoming director of UNC's new Gene Therapy Center. Xiao moved first into industry, then to UNC as a postdoctoral researcher in Samulski's gene therapy center. In 1996, the team published a report of the first muscle gene delivery involving an AAV vector.

Xiao then returned to Pittsburgh in 1998, where he worked on muscle biology with an eye toward gene transfer, while Samulski remained focused on the vector aspects of AAV, the delivery system.

At Pittsburgh, Xiao had developed a miniaturized version of the gene for dystrophin, the muscle protein needed by people with DMD. Eager to test it in a vector, he contacted his former mentor.

9."The dystrophy gene is like a long picket fence. It's the largest gene in the human body, occupying 1 percent of the X chromosome," Samulski said. "Xiao Xiao began removing pegs, or pickets, from the fence, making it smaller and smaller but kept testing to see if it would still perform its function," Samulski said.

10.Xiao then began looking for a way he might move his minidystrophin gene forward clinically.

"We had just finished demonstrating that we could make clinical-grade virus for another genetic disorder called Canavan's disease, an enzyme deficiency disorder," Samulski said. "We were the first academic institution to ever make FDA-certified AAV vectors to go into the brains of children with Canavan's disease. So we had cut our teeth and had a bit of a track record by 2002, and that's when Xiao approached me."

11.Xiao told Samulski he wanted to put his new minidystrophin gene into an AAV vector and test it.

"He wanted to know if UNC could make the virus, and that's when I told him that we were using this virus for Canavan's disease and for other efforts. We had started improving the vectors, and we had developed some new ones that we thought were better for muscle."

12.Xiao and Samulski put their projects together and formed Asklepios BioPharmaceutical Inc. (AskBio) in 2003. Along with the rights granted by UNC to Samulski's vector technology, AskBio acquired the intellectual property rights to Xiao's uniquely miniaturized dystrophin gene.

In July 2004, the Muscular Dystrophy Association (MDA) awarded $1.6 million to AskBio to develop gene therapy strategies for DMD.

Rounding out the AskBio team clinically is neurologist Dr. Jerry R. Mendell, co-director of the MDA clinic at Columbus Children's Hospital; professor of pediatrics, neurology and pathology at Ohio State University's School of Medicine; and head of the neuromuscular research program and Center for Gene Therapy at Columbus Children's Research Institute. In the clinical trial at the Columbus Children's Hospital's MDA clinic, Mendell will administer the injections.

13.Following extensive laboratory toxicity experiments required by the U.S. Food and Drug Administration demonstrating that minidystrophin gene transfer was unlikely to harm and could ultimately benefit muscles affected by DMD, approval was granted March 3, 2006, to proceed with the human trial.

"After years of encouraging pre-clinical results, I'm excited that AskBio will help bring this promising new therapy into the clinic, and look forward with a great deal of optimism to offering this initial step toward hope for the DMD community," Samulski said.

http://www.unc.edu


Postuar nga NS-6 datë 24 Prill 2006 - 00:51:

Emphysema patients benefit from one-sided lung reduction (1)

Cod. A24042006

By Gwen Ericson


April 4, 2006 -- In many cases of advanced emphysema — a chronic, progressive lung condition that interferes with breathing — reducing the size of the lungs by surgically removing lobes from both sides has been shown to improve both survival and quality of life. But some emphysema patients can't tolerate this bilateral operation.


1.Lung volume reduction surgery showing the stapler and the typical location of resection of the lung
Now a study conducted by researchers at Washington University School of Medicine in St. Louis and the University of Pennsylvania Health System has shown that unilateral, or one-sided, lung volume reduction surgery has significant benefits for some emphysema patients, offering help to those who are not candidates for the bilateral surgery.

2.The researchers described their work in January at the 42nd annual meeting of the Society of Thoracic Surgeons, a not-for-profit educational organization representing more than 4,800 chest surgeons worldwide.

"A certain subset of emphysema patients are poor candidates for bilateral surgery," says Bryan Meyers, M.D., associate professor of surgery. "Patients who have scarring on one side of their chest from past surgery, patients with coexisting heart conditions and the small segment of patients whose emphysema affects only one side of their lungs — these are all candidates for a unilateral lung volume reduction procedure."

3.The presentation at the annual meeting discussed outcomes for 49 emphysema patients who underwent unilateral lung volume reduction surgery at the School of Medicine and Barnes-Jewish Hospital. After the procedure, the patients on average had over 30 percent increased lung function as measured by how much air they could blow out with a vigorous breath in one second. Although the improvement in function gradually decreased, as expected with this incurable and progressive disease, the benefits lasted at least three years for the average patient.

4.Tests also showed that the unilateral surgery patients had lower amounts of air left in the lung after exhalation, indicating they could exhale more thoroughly. This improvement also gradually decreased but lasted at least five years for the average patient.

In addition, requirements for supplemental oxygen declined substantially after the operation....continues


Postuar nga NS-6 datë 24 Prill 2006 - 00:54:

Emphysema patients benefit from one-sided lung reduction (2)

5.Bryan Meyers
"We saw not only a functional benefit but also a survival benefit from the unilateral surgery," Meyers says. "After three years, 83 percent of the patients who had the unilateral procedure were still alive and after five years, 55 percent had survived. That's a significant increase in survival rate compared to emphysema patients who don't have surgery."

6.Survival for patients who had the unilateral procedure was the same as for a similar group of patients who had the bilateral procedure, and a national trial of lung volume reduction surgery clearly demonstrated that the bilateral procedure increases survival.

7.The current bilateral lung volume reduction procedure was pioneered at the School of Medicine in 1993 to treat end-stage emphysema. Removal of 20 percent to 30 percent of the lung on each side allows the remaining, less-diseased portion of the lung to function better, giving patients an improved quality of life.

8."Try taking a deep breath and then another breath without exhaling the first, and you'll get a feel for what happens in emphysema," Meyers says. "The lungs of emphysema patients are maximally expanded because the lung's air sacs have lost their elasticity and can't push air out. With the expansion of the lungs and chest, the patients don't have much ability to move air back and forth. But we found if we remove part of the lungs, we make it possible for the ribs and diaphragm to return to a more normal position, and it becomes easier for the patients to breathe."

Early reported successes led to the lung volume reduction procedure's rapid spread, but concerns about the safety and effectiveness led to a systematic evaluation of patient selection criteria and long-term outcomes in the National Emphysema Treatment Trial (NETT), which ran from 1996 to 2002.

9.Excluding patients at high risk of dying after surgery or with little chance of functional benefit, NETT researchers found that on average, patients with severe emphysema who undergo lung volume reduction are more likely to function better and don't face an increased risk of death compared to those who receive only medical therapy. Overall, patients who had the surgery were more likely than those who were treated only medically to improve in function, symptoms and quality of life.

"As the result of NETT, Medicare now pays for bilateral lung volume reduction surgery for qualified emphysema patients," Meyers says. "But they need more data on the efficacy of the unilateral procedure before they will approve coverage, and we believe this study helps provide that."

Sultan PK, Meyers BF, Guthrie TJ, Davis GE, Yusen RD, Lefrak SS, Patterson GA, Cooper JD. Unilateral lung volume reduction: Long-term outcome in 49 emphysema patients. Presented at the 42nd annual meeting of the Society of Thoracic Surgeons. January 2006.

Funding from the National Institutes of Health supported this research.

article taken from the Washington University School website...


Postuar nga NS-6 datë 02 Maj 2006 - 00:05:

New treatment against persistent ulcer-inducing bacteria successful

Cod. A02052006

Published: Monday, 1-May-2006
For those who suffer from stomach ulcers, the daily routine of breakfast, lunch and dinner can be painful. A common cause of these ulcers, as well as other gastric malignancies, is a bacterium called Helicobacter pylori . For some, this infection can be persistent and difficult to treat.

Many approaches have been taken in an attempt to clear such infections, but with limited or unsuccessful outcomes. In a recent meta-analysis of therapies published in the April issue of The American Journal of Gastroenterology, Levofloxacin-based triple therapy was found to be better tolerated and more effective than bismuth-based quadruple therapy for patients with persistent H. pylori despite previous treatment attempts. Levofloxacin is commonly prescribed to treat such infections as pneumonia, bronchitis and urinary tract infections.

According to author William D. Chey, "Helicobacter pylori is a highly prevalent chronic infection with a worldwide prevalence of nearly 50% and U.S. prevalence of 20-40%." This bacterial infection is particularly difficult to treat because of its ability to adapt to the harsh environment in the stomach. The bacterium guards itself in the lining of the stomach, which prevents the body's natural defenses (Killer T Cells) from attacking it.

Levofloxacin-based triple therapy may offer an effective and safe treatment option for patients with persistent H. pylori infection, according to researchers. With so many people living with this infection, it has become increasingly important to achieve effective methods of treatment. Levofloxacin-based therapy may prove to be this method.


Postuar nga NS-6 datë 02 Maj 2006 - 23:19:

Kidney patients warned away from potassium

Cod. B03052006

Published: Tuesday, 2-May-2006
Many kidney failure patients are increasing their chance of nerve damage in their legs and feet by simply having too much potassium in their diet, according to research carried out by the University of New South Wales (UNSW), the Prince of Wales Medical Research Institute (POWMRI) and the Prince of Wales Hospital.
The researchers found that high levels of potassium, which is found in foods such as bananas and peanuts, is responsible for causing nerve damage in these patients, which in extreme cases can lead to people being forced to use a wheelchair.

One in three Australian adults have an increased risk of developing kidney disease, which is commonly caused by diabetes. In end stage kidney disease, the kidneys function at less than ten percent of normal capacity and cannot sustain life of the patient without dialysis or a kidney transplant. 52,000 Australians have severe kidney function impairment or kidney failure (Kidney Health Australia).

"The majority of people with end-stage renal failure have nerve damage, in their legs and arms. This can mean they have difficulty walking or in feeling their feet," said Dr Arun Krishnan, a Neurologist and PhD candidate in the Faculty of Medicine at UNSW. "Once nerve damage develops, it cannot be reversed unless the patient undergoes renal transplantation. But our research indicates that patients do have some control over their situation.

"We found that higher levels of potassium in renal failure patients cause that nerve damage," said Dr Krishnan. "The clear health message is that anyone with kidney failure or chronic kidney problems should regulate their intake of potassium in an attempt to preserve nerve function."

Potassium is found in foods such as bananas, peanuts, soybeans, apricots and sultanas.

The research Sensory nerve excitability and neuropathy in end stage kidney disease has just been published in the Journal of Neurology, Neurosurgery and Psychiatry.

"Scientists have known for a long time that potassium was an important substance in terms of regulating nerve function, but until now no-one has made the connection between kidney function and nerve function," said co-author UNSW Associate Professor Matthew Kiernan, a neurologist based at the Prince of Wales Hospital.

"Until now, kidney specialists have been less concerned about higher levels of potassium amongst these patients, unless they were affecting the heart," said Professor Kiernan. "The clear message is that potassium levels need to be monitored in terms of nerve function too."

The other authors are R K S Phoon, B Pussell and J Charlesworth, all from the Department of Nephrology at the Prince of Wales Hospital.

The research was supported by the Australian Association of Neurologists Research Fellowship and the NHMRC. Grant support from the Brain Foundation, the Sylvia and Charles Viertel Charitable Foundation and the Ramaciotti Foundation.


Postuar nga NS-6 datë 19 Maj 2006 - 00:47:

Genetic testing can improve newborn screening tests for hearing defects

Cod. B19052006

Published: Wednesday, 17-May-2006
1.Researchers have identified several changes that could be made to existing newborn screening tests for hearing defects that could advance the standard of care in detecting deaf infants, according to an article in the New England Journal of Medicine.
Walter E. Nance, M.D., Ph.D., professor of human genetics in Virginia Commonwealth University's School of Medicine, and Cynthia C. Morton, Ph.D., a professor of human genetics at the Harvard Medical School, have summarized four important criteria to be considered for screening programs throughout the country for newborn hearing defects. These include the prompt confirmation of abnormal results from screening tests; adoption of an etiologic focus to determine the cause of the deafness; initiation of molecular genetic testing for all newborns; and better recognition of infants at risk for late-onset hearing loss occurring prior to speech and language development.

2.Molecular genetic testing of blood spots from all newborn infants for the presence of the CMV virus, connexin deafness, Pendred syndrome and mitochondrial mutations in the 12S rRNA gene would allow the immediate diagnosis of the commonest forms of genetic and environmental deafness that are expressed at birth, according to the article, published in the May 18 issue of the New England Journal of Medicine. In addition, these tests would allow for the identification of infants at risk for the commonest genetic, environmental and preventable causes of delayed onset prelingual deafness.

3."If hearing loss is detected at birth and appropriate intervention is promptly initiated the educational outcome for deaf infants can be dramatically improved," said Nance, who is the corresponding author of the article. "Although newborn hearing screening programs have improved the lives of infants throughout the world, our report suggests several specific ways in which these programs can be improved, including the screening of all newborns for a limited number of the major genetic and environmental causes of hearing loss."

According to Nance, who has been studying genetic deafness for more than 30 years, identifying the actual cause of the deafness can be just as important as detecting the hearing loss. He said that data from genetic testing would provide a powerful supplement to audiologic testing that could greatly improve the overall effectiveness of these programs.

4.In 1964, Marion Downes, a distinguished audiologist, first showed that profound deafness could be recognized in newborn infants by painstaking observations of their response to sounds. Since that time, advances in technology now allow the automated screening of infants by trained technicians. At the same time, dramatic advances have been made in understanding the causes of deafness.

5.In addition to many environmental causes of deafness, researchers have identified more than 100 genes that are linked to deafness. Nance said that approximately 50 percent to 60 percent of childhood hearing loss in developed countries is due to genetic factors.

6.Hearing is essential for the normal acquisition of speech. According to Nance, if oral or sign language is not acquired during a critical developmental stage, deaf children may never achieve their full developmental potential. Other studies have indicated that early detection of hearing loss and intervention can improve the educational and social outcomes of these newborns.

original site of the article:
http://www.vcu.edu


Postuar nga Cindi datë 24 Maj 2006 - 16:23:

Mood swings and irritability — no fun for anyone!

Cod. A24052006

From women to women.


Mood swings and irritability are closely related. We use “mood swing” to describe a reaction that isn’t appropriate to what triggered it. “Irritability” to most of us means an angry or impatient reaction to something that happens.

What causes mood swings and irritability? In both cases, the physiology is based on hormonal imbalance. The underlying cause may be fatigue — and if you’re having hot flashes or insomnia, you are very fatigued! But it can also be the sudden shifts in hormonal balance so characteristic of perimenopause, especially when your body doesn't have enough support to maintain its natural balance.

Mood swings and irritability have an emotional aspect as well. Perimenopause is a time when many women find their true voices. That’s a good and natural process. You may note the resurfacing of old emotional issues that remain unresolved. This work is important, not just to relieve your mood swings, but for your very health.

Women often come to us saying, “I thought I was losing my mind!” because they’re shocked by their mood swings and irritability. For them it’s a relief to know that their moods have a physical basis and can be relieved. There’s usually nothing wrong with you that you can’t fix by taking better care of yourself.

We’ve been very successful in our Personal Program in helping women find relief from their mood swings and irritability. Even severe mood swings can be alleviated by providing your body with the support it needs to achieve hormonal balance. So here’s what we recommend you do next:

If you’d like to get started, the first step is to take our on-line Hormonal Balance Profile. It’s easy, informative, and free.

If you’d like to learn more about the biology behind the Personal Program, go to How It Works.

If you have questions about whether the Program will work for you, call us toll-free at 1-800-254-1734 . We’re here to listen and help.


Postuar nga Cindi datë 24 Maj 2006 - 17:08:

Explaining food cravings

Cod. B24052006

An enormous percentage of women crave sugar, carbohydrates, or alcohol. In most cases, these food cravings are not true eating disorders, but instead are signs of hormonal imbalance caused by a lack of healthy nutrition.

Your personal issue may be the afternoon snack (often chocolate or candy or a food that’s also heavy in carbohydrates), too many potato chips, the extra glass of wine at night, or a hundred other variations. But the underlying mechanism, and the way to curb cravings, is the same. And it has nothing to do with willpower, or your lack thereof!

What food cravings mean
Food cravings mean that the body has its signals mixed up. When we are exhausted or blue, we have low blood sugar and/or low serotonin, and the body signals the brain that it needs a pick-me-up. This signal causes a sugar craving or carbohydrate craving.

Serotonin is our basic feel-good hormone. If serotonin is low, we feel sad or depressed. And hormonal imbalance or weak digestion can lead to low serotonin. Unfortunately, sugars and simple carbohydrates release a short burst of serotonin — we feel good for a moment, but soon return to our low-serotonin state — then crave more sugar and simple carbohydrates. It’s a downward spiral.

If you eat a low-fat diet in the hope of losing weight, you unintentionally make the problem worse. If, like millions of women, you have eaten a low-fat, high-carbohydrate diet for many years, or followed fad diets, the odds are good that you have become at least partially insulin resistant.

Insulin is responsible for maintaining stable blood sugar levels by telling the body’s cells when to absorb glucose from the bloodstream. Being insulin resistant means your body stops responding to insulin, and instead grabs every calorie it can and deposits it as fat. So no matter how little you eat, you will gradually gain weight.

At the same time, your cells cannot absorb the glucose they need, so they signal your brain that you need more carbohydrates or sugars. The result is persistent food cravings.

Even worse, insulin resistance leads directly to obesity, diabetes, and heart disease. Many experts believe it is the root cause of the epidemic of those diseases in America today. And a low-fat diet makes it far more likely you will suffer from this condition.

Millions of American women are now trying the Atkins Diet or the South Beach Diet. While these diets are an improvement over the conventional low-fat, high-carbohydrate diet, they can worsen your metabolic problems, because dieting itself is stressful to the body. So many women need to heal their metabolism first before even considering weight loss.

Another cause of food cravings is adrenal fatigue. If you are under a great deal of stress, or suffer from insomnia or sleep deprivation, you are probably exhausted much of the time. This leads to adrenal fatigue or outright adrenal exhaustion, which in turn signals the body it needs a pick-me-up. You may resort to sugar or carbohydrate snacks or coffee during the day and carbohydrates or alcohol at night, all of which exacerbate the problem.

How to curb cravings
Women who blame themselves for their food cravings only worsen their mood and increase their need for serotonin. That’s when a pattern of emotional eating can develop. Remember, there are biological causes of sugar cravings, and your carbohydrate craving is rarely just a behavioral problem. The root problem is more likely inadequate nutrition.

How to break this vicious cycle? To reduce food cravings, the body needs real support — and lots of it. We have seen over and over that eating healthy foods, adding pharmaceutical–grade nutritional supplements and moderate exercise can almost miraculously curb cravings. Your metabolism will heal itself when provided with the necessary nutritional support. If it has been damaged, the process can take some time, but it will happen. The good news is — you don’t have to give up chocolate!

We’ve been very successful in our Personal Program in resolving cravings of all kinds. So here’s what we recommend you do next:

If you’re ready to get started, consider joining the Personal Program. The first step is to complete our on-line Hormonal Balance Profile. It’s easy and informative.

If you’d like to learn more about the biology behind the Program, go to How It Works.

If you have questions about whether the Program will work for you, call us toll-free at 1-800-254-1734 . We’re here to listen and help.


If you’re under a lot of stress and feel exhausted much of the time, be sure to read our article on adrenal fatigue.

Click here to return to Symptoms.


Postuar nga NS-6 datë 26 Maj 2006 - 00:20:

AIDS Origin Traced to Chimp Group in Cameroon

Cod. A26052006

darke,look what i got here:
 
AIDS Origin Traced to Chimp Group in Cameroon
James Owen
for National Geographic News

 
May 25, 2006
Chimpanzees living in dense jungles in Africa have been confirmed as the probable source of the HIV virus which caused the human AIDS pandemic.

Researchers have identified simian immunodeficiency virus (SIV) in wild apes for the first time. The virus, which at some point jumped to humans as human immunodeficiency virus (HIV), has been found in chimpanzees in Cameroon, west-central Africa. (Cameroon map and profile)
 
Scientists have long suspected that HIV had its in origins in wild chimp populations. But previously SIV had been found only in some captive chimps.
The discovery in wild chimps was made by an international research team, which detected SIV antibodies in chimpanzee feces gathered from forests.
The virus was found in chimpanzees in southeastern Cameroon, where SIV infection rates were as high as 35 percent in some chimp populations.
 
Further genetic analysis linked these chimps to the source of the main strain of HIV-1, the most prevalent form of HIV. The team's findings are to be published tomorrow in the journal Science.
The Cameroonian chimps showed a diversity of SIV strains, with some twice as similar to human HIV strains as any found in captive apes, says study team member Beatrice Hahn, a professor of medicine at the University of Alabama at Birmingham.
 
"Two clusters [of SIV strains] were very closely related to human strains," she added.
 
These human strains belong to the M group of HIV-1, the group which has spread among humans worldwide.
The SIV clusters were restricted to communities of the chimpanzee subspecies Pan troglodytes troglodytes.
 
Origins of AIDS
 
The team says the findings provide the clearest picture yet of the 70-year-old origins of the current human AIDS pandemic.

"We think it's likely that the cross-species transmission took place locally" in the Cameroon region, Hahn said.
Hunters in the region who caught and ate chimps were probably the first to contract HIV, she adds.
"Based on what we know about the biology of these viruses, you need to be exposed to infectious blood or body fluids," she said. "You don't get it by petting a chimp."
From southeastern Cameroon the virus appears then to have spread south via the Sangha and Congo Rivers.
 
"Eventually the virus ended up in a major metropolitan area, which would either be Kinshasa [Democratic Republic of the Congo]or Brazzaville [Republic of the Congo]," Hahn added. "That's where we believe the AIDS pandemic really started."
 
Chimps in turn are thought to have picked up SIV by eating infected monkeys.
 
A study published in 2003 in Science suggested a chimp strain of SIV arose through repeated transmissions and recombination of similar viruses found in red-capped mangabeys and greater spot-nosed monkeys. (Read a story about this study.)
This previous research was led by Paul Sharp of the Institute of Genetics at the University of Nottingham in England.
 
"We now know there are more than 30 species of monkeys across Africa which have their own forms of SIVs," said Sharp, who was also involved with the new study
 
Ape Infection
Chimps, however, are the only apes known to be infected.
 
"The chimp virus is a mosaic of viruses that infect prey monkeys," the University of Alabama's Hahn said. "Chimps had to eat these monkeys first but they have certainly had their infection a lot longer than humans."
 
She says the diversity of new SIV strains detected in Cameroon chimps raises the possibility that the animals could pass on new types of HIV infection to humans.
This, says Hahn, could hinder the global fight against AIDS.
 
"Cross-species transmissions could have already occurred and may have gone unrecognized," she added.
 
Hahn says it's unlikely that further, recently acquired chimp infections have led to AIDS epidemics in humans. But such transmissions could undermine the effectiveness of AIDS vaccines currently under development.
 
"If we ever had a vaccine that worked and you then bring in a new virus that's 30 or 40 percent different, that's probably not a good thing," she said.
 
"It might be much more difficult to detect one of these other chimp viruses if it jumped into humans," the University of Nottingham's Sharp added.
 
On the other hand, further studies of wild chimp populations could help in finding new treatments for AIDS sufferers, Sharp says.
 
"As far as we know, the chimps don't get any type of AIDS-like disease," he said. "That's part of the reason for being very interested in the infection of chimps, because chimps and humans are very similar genetically."
 
source: www.nationalgeographic.com

 

also,take a look at:
-AIDS origins (Cod. A 27112005)


Postuar nga NS-6 datë 10 Qershor 2006 - 01:15:

ACE inhibitors may pose more birth defect risks

Cod. B10062006

June 9, 2006
by Carole Bartoo
The Food and Drug Administration is looking at evidence examined by researchers at the Monroe Carell Jr. Children's Hospital at Vanderbilt to determine if new warnings need to be put on common blood pressure medications regarding an increased risk of birth defects for babies whose mothers take the medications during the first trimester of pregnancy.

William Cooper, M.D., M.P.H., associate professor of Pediatrics, was first author of a study in the New England Journal of Medicine, along with colleagues from the departments of Pediatrics, Preventive Medicine and Biostatistics. Cooper and co-authors found that infants born to mothers who took angiotensin converting enzyme inhibitors (ACE inhibitors) during the first trimester of pregnancy had an increased risk of major birth defects compared with infants whose mothers did not take these medications.

“We knew ACE inhibitors were a possible cause of adverse fetal outcomes when exposure occurred later in pregnancy, but it has not been well studied in the first trimester,” Cooper said.

“We were very surprised that even after controlling for other risk factors, the TennCare records we examined showed a clear increase in a broad range of birth defects following first trimester-only exposures.”

This research is important because the number of women of childbearing age who develop high blood pressure and are prescribed ACE inhibitors is increasing in this country, according to other data included in the study.

ACE inhibitors already carry a warning stating that they can cause injury and even death to the developing fetus when used during the second and third trimesters of pregnancy.

The warning states that use of ACE inhibitors should be discontinued as soon as possible when pregnancy is detected.

Cooper and his co-authors performed the research within the Child and Adolescent Health Research Unit at Children's Hospital.

The study was jointly funded by the FDA and Vanderbilt's Center for Education and Research on Therapeutics, which is funded through the Department of Health and Human Services' Agency for Healthcare Research and Quality. Results were published in the June 8 issue of the New England Journal of Medicine.


Postuar nga NS-6 datë 11 Qershor 2006 - 01:08:

Scientists Unlock More Secrets Of HIV And SARS

Cod. D11062006

Source: Biotechnology and Biological Sciences Research Council
10 may 2006
UK scientists have cracked one of the key biological processes used by viruses such as HIV and SARS when they replicate according to a paper published in the journal Nature tomorrow (11 May). Viruses are able to interfere with the host cell processes that our bodies use to replicate cells, and protein synthesis is often one of their targets. For the first time, researchers at the Universities of Cambridge and Oxford have witnessed virus-induced "frameshifting" in action and have been able to identify the crucial role of particular elements. The research, funded by the Biotechnology and Biological Sciences Research Council (BBSRC), the Medical Research Council (MRC), The Royal Society and The Wellcome Trust, brings us another step closer to understanding the fundamental workings of these devastating viruses.

The scientists have revealed the workings of the process known as 'ribosomal frameshifting' that forces a mis-reading of the genetic code during protein synthesis. The correct expression of most genes depends upon accurate translation of the 'frame' of the genetic code, which has a three nucleotide periodicity. Viruses such as HIV and SARS bring into the cell a special signal that forces the ribosome to back up by one nucleotide, pushing it into another 'frame' and allowing synthesis of different viral proteins. These are exploited by viruses and help them to survive and multiply.

The British researchers successfully imaged frameshifting in action and for the first time observed how a virus encoded element called an RNA pseudoknot interferes with the translation of the genetic code to allow viruses like HIV and SARS to express their own enzymes of replication.

Dr Ian Brierley, the project leader at the University of Cambridge, said: "This collaborative project was set up with Dr Robert Gilbert's team in Oxford to investigate the structure of a frameshifting ribosome using electron microscopy. The images we obtained give us an insight into how a virus-encoded RNA pseudoknot can induce frameshifting and may be useful in designing new ways to combat virus pathogens that use this process."

Professor Julia Goodfellow, Chief Executive of the Biotechnology and Biological Sciences Research Council, which was one of the main funders, said: "This is exciting and valuable research and demonstrates clearly why investment in fundamental science is so important. The treatments and therapies that we now take for granted are based on decades of work by scientists furthering our understanding of natural processes. The work to explore fundamental biology today is laying the foundation for potential medical applications over the next twenty years."

 

original source: http://www.sciencedaily.com/release...60510191609.htm


Postuar nga NS-6 datë 27 Qershor 2006 - 23:14:

Use Embryonic Stem Cells To Awaken Latent Motor Nerve Repair (1)

Cod. A28062006

Source: Johns Hopkins Medical Institutions
 
Posted: June 26, 2006
 

Hopkins Scientists Use Embryonic Stem Cells, New Cues To Awaken Latent Motor Nerve Repair
In a dramatic display of stem cells’ potential for healing, a team of Johns Hopkins scientists reports that they’ve engineered new, completed, fully-working motor neuron circuits -- neurons stretching from spinal cord to target muscles -- in paralyzed adult animals.
 

The research, in which mouse embryonic stem (ES) cells were injected into rats whose virus-damaged spinal cords model nerve disease, shows that such cells can be made to re-trace complex pathways of nerve development long shut off in adult mammals, the researchers say.
 
“This is proof of the principle that we can recapture what happens in early stages of motor neuron development and use that to repair damaged nervous systems,” says Douglas Kerr, M.D., Ph.D., a neurologist who led the Hopkins team.
 
“It’s a remarkable advance that can help us understand how stem cells can begin to fulfill their great promise,” says Elias A. Zerhouni, director of the National Institutes of Health. “Demonstrating restoration of function is an important step forward, though we still have a great distance to go.”
 
The researchers created what amounts to a cookbook recipe to restore lost nerve function, Kerr explains. The approach could one day repair damage from such diseases as ALS (Lou Gehrig’s disease), multiple sclerosis or transverse myelitis or from traumatic spinal cord injury, the researchers say. “With small adjustments keyed to differences in nervous system targets,” Kerr says, “the approach may also apply to patients with Parkinson's or Huntington’s disease.”
 
In a report on the study, to be released online June 26 in the Annals of Neurology, the Hopkins team says 11 of the 15 treated rats gained significant, though partial, recovery from paralysis after losing motor neurons to an aggressive infection with Sindbis virus -- one that, in rodents, specifically targets motor neurons and kills them. The animals recovered enough muscle strength to bear weight and step with the previously paralyzed hind leg.
 
Kerr likens the approach to electrical repair. “Paralysis is like turning on a light switch and the light doesn’t go on. The connectivity is messed up but you don’t know where. We’ve asked stem cells to go where needed to fix the circuit.”
 
For a brief period after a nerve dies, it leaves behind what’s essentially an empty shell, with some scaffolding and non-nerve substances remaining. But with ES injections at the right time and place, and by adding the right cues, we’ve learned to restore the biological ‘memory’ for growing neurons, which is clearly still in place,” he added.
 
The motor circuit engineering combines recent discoveries on stem cell differentiation, a growing understanding of early development of the nervous system, and insights into behavior of the nervous system in traumatic injury, Kerr notes.
 
“As adults, our cells no longer respond to early developmental cues because those cues are usually gone,” says Kerr. “That’s why we don’t recover well from severe injuries. But that’s what we believe we have changed. We asked what was there when motor neurons were born, and specifically what let motor neurons extend outward. Then we tried to bring that environment back, in the presence of adaptable, receptive stem cells.”
 
In the study, Kerr’s team first pre-treated cultures of mouse embryonic stem cells with growth factors that both increase survival and prompt specialization into motor neurons. Adding retinoic acid and sonic hedgehog protein -- agents that direct cells in the first weeks of life to assume the proper places in the spinal cord -- readied the conditioned ES cells for the motor neuron circuit that starts in the spinal cord. Then, stem cells were fed into the paralyzed rats’ spinal cords.

continues...


Postuar nga NS-6 datë 27 Qershor 2006 - 23:16:

Use Embryonic Stem Cells To Awaken Latent Motor Nerve Repair (2)

Extending new motor neurons in an adult nervous system, however, meant overcoming hurdles. One involved myelin, the fatty material that insulates mature motor neurons. Like the coating on electrical wire, myelin prevents weakening of the traveling electrical impulse and lets it continue long distances. In humans, the myelinated sciatic nerve, for example, exits the spinal cord and extends to the leg muscles it activates, carrying impulses several feet.
 
Once laid down, however, myelin inhibits further nerve growth -- nature’s way to discourage excessive wiring in the nervous system. “We had to overcome inhibition from myelin lingering in the dead nerve pathways,” Kerr explains. Two recently-developed agents, rolipram and dbcAMP enabled that.
 
The assorted treatments let the new motor neurons survive, grow through the spinal cord and extend slightly into the outlying nervous system. A second hurdle remained in getting the neurons to skeletal muscle targets.
 
As suggested by earlier work by team member Ahmet Hoke on repair in the outlying, peripheral nervous system, the researchers applied GDNF, a powerful stimulator of neuron growth, to the remains of the newly-dead sciatic nerve at a point near its former leg muscle contacts. GDNF attracted the extending motor neurons, “luring” them to the muscles. To ensure a continuous supply of GDNF, the researchers relied on injected fetal mouse neural stem cells, a known source of the molecule.
 
Of some 4,100 new motor neurons created in the spinal cord, roughly 200 exited the cord and 120 reached skeletal muscle, forming typical nerve-muscle junctions, with appropriate, typical chemical markers. Microscopically, the neurons and their muscle associations appear identical to natural ones in healthy animals.
 
Fifty of the new neurons were found to carry electrical impulses. (Because such testing is time and labor intensive, only a small area of leg muscle was assayed. The improved ability of treated rats, however, suggests more functional neurons are likely.) The rats gained weight, were more mobile in their cages and measures of muscle strength increased.
 
Animals treated without even one component of the “cocktail” experienced no such recovery. Novel ways of tracing the neurons back to their source assured the scientists that they indeed had come from the injected stem cells, not from lingering host neurons.
 
Research begins this summer to see how well the technique applies to human nerve recovery, using federally-approved human ES cells in larger mammals like pigs, Kerr says. Each of six academic institutions in a new collaboration will tackle a different major question of safety and effectiveness. Questions of tumor-formation, often a concern with ES cells, of the safety of surgery and of the ES cells’ ability to form healthy motor circuits are major questions to answer. Several years of testing and thorough data evaluation would occur before applying to the FDA to approve human clinical trials. The study was supported by Families of SMA, Andrew’s Buddies/Fight SMA, the ALS Association and The Robert Packard Center for ALS Research at Johns Hopkins, the Muscular Dystrophy Association, Wings Over Wall Street, and a grant from the NIH.
 
Kerr is a grantee of The Packard Center for ALS Research at Johns Hopkins. He also directs Project RESTORE, a Hopkins-based undertaking to advance therapies for transverse myelitis and multiple sclerosis.
 
source: www.sciencedaily.com


Postuar nga NS-6 datë 13 Korrik 2006 - 00:29:

Avoiding Punishment Is Its Own Reward

Cod. A13072006

12 july 2006
To give your child an incentive to take out the garbage, you might offer to buy her a treat, or you might threaten to withhold her regular allowance. Does the child respond the same way to reward as it does to avoiding punishment? Psychologists have evidence from certain kinds of behavioral experiments to believe that avoiding punishment is itself a reward.

In a new study published online in the open-access journal PLoS Biology , Hackjin Kim, Shinsuke Shimojo, and John O'Doherty investigated this question by scanning the brains of humans performing a simple instrumental conditioning task. A brain area called the medial orbitofrontal cortex (OFC) has been linked to reward-related stimuli, particularly when the reward involves money. The researchers found that the OFC is also activated for avoidance learning, supporting the hypothesis that these cognitive processes share neural mechanisms.

Sixteen people participated in the study, during which they could either lose or win one dollar in an instrumental choice task. During the experimental trials, participants selected one of two fractal images presented on a screen. After a fractal was chosen, it became brighter, and four seconds later the participant got one of four types of feedback: reward (a picture of a dollar bill and the message, You win!), negative outcome (same image, with the text, You lost!), neutral (a scrambled bill with the text, No change), or nothing (a blank screen). During reward trials, the choice led to a high or low probability of reward (earning a dollar); during avoidance trials, the choice led to a high or low probability of avoiding a negative outcome (losing a dollar).

Over time, participants learned to choose fractals associated with a greater probability of reward and a lower probability of a negative outcome. And, as predicted, the medial OFC showed a higher response when participants chose an option that resulted in not losing the dollar or in winning it. Conversely, when participants' choices resulted in negative outcomes and when there was no reward offered OFC activity declined. Compared to neutral trials, reward and avoidance events produced significantly greater brain activity, while negative outcomes and neutral events linked to no chance of reward resulted in significantly decreased activity. Kim et al. argue that these functional magnetic resonance imaging (fMRI) results provide direct evidence that avoiding bad outcomes and receiving a reward provoke a similar response in the medial OFC.

Avoiding negative outcomes and receiving rewards amount to the same thing for the brain: achieving a goal. Reward serves as an external signal that reinforces behavior associated with a positive outcome, Kim et al. explain, and punishment amounts to an intrinsic reward signal that reinforces actions linked to avoiding bad outcomes. With fMRI evidence connecting avoidance and reward circuits, researchers can now determine which neuron populations within the OFC contribute to the avoidance "reward response"and perhaps shed light on the neurobiological roots of pathological risk-seeking behavior.

source: www.sciencedaily.com


Postuar nga Izolda datë 13 Korrik 2006 - 17:40:

Interesante...


Postuar nga NS-6 datë 14 Korrik 2006 - 00:26:

Thumbs up Morning sickness - a form of protection for mother and baby

Cod. A14072006

Published: Wednesday, 12-Jul-2006

As many as 90% of mothers experience nausea during pregnancy, and about half that number vomit.

Although it is more common in the first three months some women are nauseous throughout their pregnancy.

The name "morning sickness" is misleading because nausea can occur at any time of day and in the most serious cases it can become hyperemesis gravidarum, or excess vomiting, which can be fatal.

In research by Liverpool University, where an analysis of 56 previous studies in 21 countries was carried out, the prevalence of nausea and sickness in pregnant women was examined.

Researchers Dr. Gillian Pepper and Dr. Craig Roberts linked these figures to the typical diet in each country and suggest there is a link between nausea and diet.

They say morning sickness might have evolved to ensure pregnant women do not digest too much unhealthy food.

They found evidence that nausea and vomiting in pregnancy is associated with high intake of sugar, alcohol, oils and meat.

For some women even the common smells, particularly fat and fried food, and the sight of food cooking is enough to bring on a wave of nausea.

Another study found that 50% of women developed an aversion to alcohol in their first three months and there appears to be mounting evidence that morning sickness is the body protecting itself against harmful substances in food.

It seems countries with a high intake of sugars, sweeteners, stimulants such as caffeine, vegetables, meats, milk and eggs had more sick pregnant women, and those with high intake of cereals and pulses had lower levels.

The researchers believe that the pregnant human body may have evolved an aversion to foods containing high levels of toxins, and that this may have carried over into modern living.

They suggest that the body might reject meat because of the relatively high risk that it might harbour disease-causing agents while the low level of plant toxins in cereals may make them particularly unlikely to trigger nausea.

But the body's rejection of sugars and oils is less easy to explain.

Lead researcher Dr. Roberts says womens' bodies may be pre-programmed by evolution to avoid particular foodstuffs in the first trimester and the nausea could be nature's way of avoiding problems in pregnancy for both mother and foetus.

Experts say the theory makes sense as morning sickness is always worst in the first three months, which is when the most important part of a foetus's development is happening.

They say it is sensible for a woman to eat healthily in pregnancy, but more important she avoid alcohol, smoking or drugs.


Postuar nga Izolda datë 14 Korrik 2006 - 10:08:

Ne muajin e pare te shtatzanise kam zhvilluar neveri per disa lloj ushqimesh, por kryesisht vezet dhe nje lloj embelsire. Kam vrare shume mendjen ne lidhje me rolin e GCH-se ne kete proces por nuk shihja logjike. Sepse ne mjekesi gjithcka e ka nje arsye madhore, sado qe ne veshtrim te pare duket rastesi ose rrjedhoje e evolucionit (ne te cilin nuk besoj aspak). Tani ky lajm ploteson ne menyre te perkryer mozaikun e kesaj enigme. Faleminderit NS-6.


Postuar nga NS-6 datë 14 Korrik 2006 - 20:30:

me vjen mire qe artikulli te paska qene ne ndihme...sic e the,cdo gje e ka nje shpjegim ne mjeksi,dhe keto gjera nuk i lene shume vend rastesise sic thote teorija e evolucionit (qe nuk i besoj fare)...ndoshta ne te ardhmen do ti bej nje analize kesaj teorie tek tema e gjenetikes

ne kete teme,jam duke vendos artikujt qe me duken me interesante nder ato qe me qellon te lexoj here pas here!jane ne pergjithsi lajme te fresketa te marre nga sitet kryesore te lajmeve mjeksore

p.s: darke,sorry about the albanian language here ...Izolda,shkaku i kesaj teme ka qene darke,qe eshte spanjolle dhe nuk ka mundesi qe te kuptoje ato gjera qe ishin ne shqip...kshu qe ketu mund te shohe artikuj ne anglisht


Postuar nga Izolda datë 14 Korrik 2006 - 22:21:

Wink

OK, english is fine with me. I'll try myself to provide you with some news from medicine.


Postuar nga NS-6 datë 14 Korrik 2006 - 23:36:

Smile

that would be great...thanks


Postuar nga darke datë 15 Korrik 2006 - 10:29:

Thumbs up

very interesting the two last articles!. Thank you Mr. doctor NS-6


Postuar nga Izolda datë 16 Korrik 2006 - 00:47:

Measuring Proteins In Spinal Fluid for the Alzheimer Disease

Cod. A16072006

Measuring Proteins In Spinal Fluid May Provide Early Clue To Alzheimer's Disease

Early signs of the development of Alzheimer's disease can be seen in the cerebrospinal fluid of middle-aged adults who are genetically predisposed to the neurologic condition.

The two strongest risk factors for Alzheimer's disease are aging and the presence of an allele (type of gene) known as apolipoprotein E*4 (APOE*4), according to background information in the article. Those with the APOE*4 allele develop clinical dementia about 10 to 15 years earlier than those who do not have the APOE*4 allele. Previous studies have shown that the plaques that form in the brain during Alzheimer's disease, which are made of proteins known as â-amyloids, begin forming years before affected individuals experience any symptoms of the disease. As â-amyloid proteins, predominately of a type known as Aâ42, clump together, fewer are available to circulate through the nervous system. Therefore, lower levels of the Aâ42 in the cerebrospinal fluid surrounding the brain and spinal cord serve as biomarkers or chemical indicators of the development of Alzheimer's disease.
Scientists estimated the combined effect of aging and the APOE*4 allele on levels of Aâ42 and another â-amyloid, Aâ40, in 184 adults (94 men and 90 women, average age 50 years). The participants underwent clinical and laboratory screening and were found to be cognitively normal-that is, they had no difficulties with thinking, learning or memory. Researchers took samples of cerebrospinal fluid in the morning after an overnight fast and measured participants' Aâ42 and Aâ40 levels in addition to determining whether each individual had the APOE*4 allele.
Those who were older and who had the APOE*4 allele were more likely to have lower levels of Aâ42. For those who did not have the APOE*4 allele, Aâ42 levels rose slightly until about age 50 years then begin to decline slowly. On the other hand, those with the APOE*4 allele experienced a slight decline in Aâ42 in their younger years and then a dramatic drop between ages 50 and 60 years. Levels of Aâ42 were not associated with scores on any cognitive or memory tests. "In persons with the APOE*4 allele, decline in cerebrospinal fluid Aâ42 concentration possibly begins in young adulthood, followed by marked acceleration of this decline beginning in midlife-decades before clinical manifestations of Alzheimer's disease," the authors write. The same relationship did not hold true for Aâ40, which, although it is also found in amyloid plaques, is less prevalent there than Aâ42; levels of Aâ40 did not change with age in those with the APOE*4 allele and decreased with age in those without the APOE*4 allele.
These findings have implications for the preclinical diagnosis of Alzheimer's disease, as well as for treatment. Therapeutic strategies aimed at prevention of Alzheimer's disease may need to be applied in early midlife or even younger ages to have maximal effect on amyloid deposition. Primary prevention trials for Alzheimer's disease targeting elderly persons may be too late to affect the early stages of disease pathology.


Postuar nga NS-6 datë 20 Korrik 2006 - 13:51:

Scientists Discover Why Cornea Is Transparent And Free Of Blood Vessels...

Cod. A20072006

Scientists Discover Why Cornea Is Transparent And Free Of Blood Vessels, Allowing Vision

Source: Schepens Eye Research Institute
Posted: July 18, 2006

Scientists at the Harvard Department of Ophthalmology's Schepens Eye Research Institute and Massachusetts Eye and Ear Infirmary (MEEI) are the first to learn why the cornea, the clear window of the eye, is free of blood vessels--a unique phenomenon that makes vision possible. The key, say the researchers, is the unexpected presence of large amounts of the protein VEGFR-3 (vascular endothelial growth factor receptor-3) on the top epitelial layer of normal healthy corneas.

According to their findings, VEGFR-3 halts angiogenesis (blood vessel growth) by acting as a "sink" to bind or neutralize the growth factors sent by the body to stimulate the growth of blood vessels. The cornea has long been known to have the remarkable and unusual property of not having blood vessels, but the exact reasons for this had remained unknown.

These results, published in the July 25, 2006 issue of the Proceedings of the National Academy of Sciences and in the July 17 online edition, not only solve a profound scientific mystery, but also hold great promise for preventing and curing blinding eye disease and illnesses such as cancer, in which blood vessels grow abnormally and uncontrollably, since this phenomenon, present in the cornea normally, can be used therapeutically in other tissues.

"This is a very significant discovery," says Dr. Reza Dana, Senior Scientist at the Schepens Eye Research Institute, head of the Cornea Service at the Massachusetts Eye and Ear Infirmary, and an associate professor at Harvard Medical School, and the senior author and principal investigator of the study. "A clear cornea is essential for vision. Without the ability to maintain a blood-vessel-free cornea, our vision would be significantly impaired," he says, adding that clear, vessel-free corneas are vital to any animal that needs a high level of visual acuity to survive.

The cornea, one of only a few tissues in the body that actively keep themselves vessel-free (the other is cartilage), is the thin transparent tissue that covers the front of the eye. It is the clarity of the cornea that allows light to pass onto the retina and from there to the brain for interpretation. When the cornea is clouded by injury, infection or abnormal blood vessel growth, vision is severely impaired, if not destroyed.

Scientists have been wrestling with the "clarity" puzzle for many decades. And, while some previous studies have revealed small clues, none have pointed to one major mechanism, until this study.

In most other tissues of the body, blood vessel growth or angiogenesis occurs in response to a need for increased blood flow to heal an injured or infected area. The immune system sends in growth factors such as vascular endothelial growth factor (VEGF) to bind with a protein receptor called VEGFR-2 on blood vessels to trigger vessel growth. Three forms of VEGF--A, C, and D--bind with this receptor. Two of them, C and D also bind with VEGFR-3, which is usually found on cells lining lymphatic vessels, to stimulate the growth of lymphatic vessels.

Dana's team began to suspect the involvement of VEGFR-3 in stopping blood growth in corneas when they noticed unexpectedly that large amounts of the protein seemed to exist naturally on healthy corneal epitelium, a previously unknown location for the receptor. Dana and his team were already aware from clinical experience that the epiteelium most likely played a role in suppressing blood vessel growth on the cornea, having witnessed blood vessels develop on corneas stripped of their epitelial layers.

They began to theorize that the large amounts of VEGFR-3, in this new, non-vascular location, might be attracting and sucking up all the C and D VEGF growth factors, thereby blocking them from binding with VEGFR-2. And, because this binding took place in a non-vascular setting, the growth factors were neutralized.

To test their theory, the team conducted a series of experiments.

Using corneal tissue from mice, the team did the following.

They conducted chemical analyses that demonstrated that VEFGR-3 and the gene that expressed it were indeed present on the corneal epitelium. Next, in two separate experiments, they compared corneas with and without epitelial layers that were injured. They found that only the corneas without epitelial layers developed blood vessels, implicating the role of the epitelium in suppressing blood vessel growth To further prove their theory, they added a VEGFR-3 substitute to corneas stripped of their epitelial layers and found that vessel growth continued to be suppressed, replacing the normal anti-angiogenic role of the epitelium. Finally they exposed intact corneas to an agent that blocked VEGFR-3 and found that blood vessels began to grow, formally demonstrating that the corneal epitelium is key to suppression of blood vessels and that the key mechanism is expression of VEGFR-3.

"The results from this series of tests, confirmed our belief that the presence of VEGFR-3 is the major factor in preventing blood vessel formation in the cornea," says Dana, who says that the discovery will have a far reaching impact on the development of new therapies for eye and other diseases.

"Drugs designed to manipulate the levels of this protein could heal corneas that have undergone severe trauma or help shrink tumors fed by rapidly growing abnormal blood vessels," he says. "In fact, the next step in our work is exactly this."


Postuar nga Cindi datë 17 Nëntor 2006 - 16:43:

Acid blues: the truth behind the buzz about pH balance

Cod. B17112006

NS_6 dikur kemi diskutuar per ambjentin acid dhe bazik ne trupin e njeriut dhe e konsiderova si nje artikull te rendesishem per shendetin. Sorry eshte ne anglisht. Mund ta spostosh ne temen qe ti e quan te pershtatshme.

Flm-football



by Marcelle Pick, OB/GYN NP

Think fast: What’s your pH?

If you are like a lot of my patients, you might be familiar with the term “pH” from biology class or a skin cleanser commercial. But the idea of balancing your inner pH has become a hot trend these days, making headlines, spawning an assortment of products in many health food stores, and collecting a fair share of serious devotees — many of whom are adopting a strict dietary regime and ingesting a lot of supplements to “alkalize” their bodies in reaction to the overly acidic diet of most modern Americans.

The pH scale is shorthand for the ratio of acid to alkaline (base) activity. When it comes to your health, what role does pH play? Proponents would have you believe that balancing your pH will cure all health woes. While pH is one of many factors I look at when considering a woman’s health, I would never consider it to the exclusion of everything else. That’s far too simplistic and doesn’t take into account the complicated role pH plays in our physiology.

The underlying truth to the pH equation is that different areas of your body have corresponding “normal” pH ranges. The key to balance is having the right pH in the right place. Testing your pH can be a valuable tool when you are learning about your body, but it needs to be understood within a wider context. To make sense of this, and help you answer my initial question, let’s discuss what pH is and what proactive steps you can take to keep it working in your favor.

The basics — and the acids

The concept of pH — a measure of the acidity of a solution in terms of its hydrogen ion activity — was introduced in the early 1900’s. Some believe the abbreviation “pH” is a contraction of the Latin pondus hydrogenii, meaning weight of hydrogen or potential hydrogen. Others trace the abbreviation to the French pouvoir hydrogène, or hydrogen power. Whatever its roots, pH is the scale that represents whether something is acidic (more hydrogen activity) or alkaline (less hydrogen activity).

Pure water has a pH of 7.0, directly in the middle of the pH scale, which is considered neutral. Readings below 7.0 are considered acidic, and numbers above 7.0 are considered basic, or alkaline. Various substances in our lives can fall on widely varying sides of that neutral point. Coffee has a pH of 5.0 (on the acidic side of neutral), and the aptly named acid rain we hear about measures way below neutral, at about –5.0. On the other side are things like household lye, which has a strongly alkaline pH of 12.5.

But how does this relate to pH in our bodies, and how do we know when things aren’t right?

Body pH balance
In terms of body pH balance, there is no one “correct” reading for the entire body. For instance, healthy human skin has a proper pH of 5.5 (slightly acidic). Saliva, on the other hand, has a pH of around 6.5–7.4 (teetering on either side of neutral). Similarly, when the body is in good working order, human blood reveals a pH of about 7.3–7.4 (slightly alkaline). Other parts of a healthy, well-functioning body will show still different pH readings.

Why is this? It’s all part of the same body, so why wouldn’t a person’s acid/alkaline balance be the same all over? Because different parts of our bodies serve different purposes. Each of those purposes and the related processes requires a different acid/alkaline environment for optimum function.

Skin needs to be slightly acidic in order to deal with environmental factors like bacteria and other toxins. Likewise, the vagina maintains an acidic environment to protect itself, and when the pH is changed, infections like bacterial vaginosis and yeast infections can result. The stomach and other parts of the digestive system are highly acidic out of biological necessity. The digestive acids are part of how we process and use the foods we eat as fuel. They are part of our internal combustion for nutrition.

Part of the confusion over body pH arises from the relatively neutral pH balance of our blood, saliva, and urine — what we can easily test for. This has led to the misapprehension that pH levels are static throughout the body when in fact they are not. Eating more of certain alkalizing foods (particularly leafy greens) can help balance the pH level of your GI tract over time and ultimately promote better well-being, but this doesn’t happen in a vacuum. It takes time and commitment to certain lifestyle changes, including exercise and regular detoxification. It also takes knowing whether or not your pH is truly off balance.

Enthusiasts of the “pH miracle” say that simply living in the modern world — with its reliance on refined sugars, grain-fed beef, and unhealthy fats — means we are all overly acidic. I agree with this to an extent, but would not go so far as to apply this notion universally. And I certainly think that before anyone begins megadosing on supplements or downing gallons of “green” water, they need to define their individual needs. (Remember, the key to pH is balance!) The best way to do this? Test your pH.

Testing your pH
Physicians use esophageal and gastric pH meters to help identify the causes of heartburn and gastroesophageal reflux disorder (GERD). Such tests determine the amount of acid in the environment being tested. Similarly, you can test the pH of your saliva and/or your urine with simple litmus strips, which are available in most pharmacies. Keep in mind that in order to get the full picture of your body’s pH, you’ll need to carry out the test several times throughout the day.

Tracking your urine or salivary pH over the course of a few days will provide a window into what is going on in your internal world. A diet that lacks essential vitamins and nutrients and is high in acid–forming foods will show up in acidic urine. This is a good indicator that your body is struggling to maintain an optimal digestive environment (also affected by your intestinal flora and immune system), which could be contributing to systemic inflammation — that ubiquitous bugaboo at the root of so many chronic health concerns, including heart disease, high blood pressure, and obesity. Over time this struggle may be mirrored by a steady rise of the pro-inflammatory blood acid homocysteine in your blood.

And of course, you are what you eat.

pH and the diet
Advocates of what is called an alkalinizing diet can be very adamant in their opinions. Scientific studies of these theories are greatly lacking, and many practitioners of conventional medicine look askance at correlations between pH in the diet and pH in the body. But I find that much of what the pH–diet proponents are saying is useful, if taken in the broader context of a woman’s whole health picture.

Many of the theories are based on the assumption that the pH of the diet should support and reflect what we know to be the properly balanced pH of human blood, which is normally 7.35–7.45. Or that what we eat, averaged out, should have a neutral pH. They believe that when the diet does not support the body’s natural pH balance, all systems suffer, and disease and illness can result.

The digestive system is acidic; it has to be in order to function. Short of consuming so much of something that it would amount to poisoning, a human being simply can’t consume enough of any alkaline substance to ultimately change what’s happening in the stomach for more than a few minutes. The stomach — and the body — will go to its internal stores to regain its own pH balance.

Blood, too, maintains its own pH balance. There is a dangerous and relatively unique condition known as acidosis, present when blood acidity falls below 7.35. This can be caused by significant lung or liver problems, or other situations which allow carbon dioxide to build up in the bloodstream. But for most people, in most situations, the body balances the blood’s pH as a matter of course.

Our bodies know what the balance is, and they find it — if we let them and if we give them what they need through diet and nutritional supplements to maintain it on their own. Most importantly, you can’t just add lots and lots of alkaline foods and supplements to your diet and presume these will offset any amount of acid you consume or create. The idea is to remove the overproductive acid sources first because in most situations, no amount of alkalizing can balance a toxically acidic environment. And to cap it off, detoxification is slower in an overly acidic environment.

You may think it’s acid — but it’s not

Considering whether a food is acidic or alkaline in the diet can require some mind-bending because it’s easy to think of acids as things that dissolve and corrode. That comes from our common use of the word. But think of the corrosive nature of raw lye (very alkaline), and it’s easy to see that we have to think of the words differently when it comes to pH in the diet.

Some foods that we think of as “acidic” are, in fact, alkaline in the diet. This is because what is being measured is whether the food is acid–forming or alkaline–forming, not where the food itself falls on the pH scale. So, things like lemons and tangerines are alkalizing, even though we think of citrus as sharp and sour, and it does contain several acids. Similarly, foods we might normally think of as absorbent and noncorrosive in nature are effectively acid-forming when ingested. Oatmeal and soybeans are two examples. What’s important is not the pH of the food as it goes into our bodies, but the resultant pH as our digestive systems burn the food, and what sorts of residue the burned-through nutrients leave behind. In Traditional Chinese Medicine, the concept of balance is described as “warming”/yang or “cooling”/yin foods.

This isn’t the sort of association most of us can make instantly, so we have compiled a basic list of common acidic and alkalizing foods to guide you. But why is it important to have the proper acid–alkaline balance in our diets? The answer has to do with the dance that occurs between acid and alkaline elements in our digestion.

pH and digestion

In our goal to obtain all the nutrients our bodies need from our food, pH plays an essential role, both in the breakdown of food and in providing an optimal environment for the microbes that colonize the gut. The process begins in the mouth, where the enzyme amylase is present. Amylase, responsible for breaking down starch, works in a fairly neutral environment, so when the pH falls below 6.5 it is no longer active.

As food makes its way from your mouth to your stomach, the pH along the passageway begins to fall. Your stomach pH can range from 1.5 to 7.0, depending on the stage of digestion it’s in. Pepsin, the enzyme responsible for protein breakdown, needs an acidic environment and therefore gets released into the stomach when pH is low. The stomach pH continues to fall, and at about 2.0, fat collects into globules and the “bolus” of food makes its way to the small intestine.

Your small intestine is where most of the nutrients in your food get absorbed, and where the pH increases from 2.0 to 6.5 as the food passes from the stomach to the small and large intestines.

The acidic environment of the stomach is not only necessary for processing food, but it also helps to protect your body from pathogenic organisms or food antigens that shouldn’t be there. Interestingly, in my experience, many people with acid reflux and heartburn — a condition conventional medicine blames on an overly acidic diet—actually have too little acid in their stomachs — a problem that’s compounded by all those peptic reuptake pills like Pepcid and TUMS that increase the alkaline quota in the stomach. I find that many of my patients get rid of their heartburn and acid reflux by adding more acid to their diets. For more on this, please see our article on IBS.

Protein — particularly in the form of red meats — requires huge amounts of alkaline minerals for complete digestive processing. When the system goes looking for this alkalinity needed to offset the acids, it looks first to the foods in the digestive system. This is where the good greens and essential vitamins and minerals come in. If it fails to find alkaline nourishment there, one of the first places it goes searching is to the calcium (as well as magnesium, phosphorus and potassium) stored in our bones.

pH and bone loss
The relationship between bone loss and blood acidity is an emerging area of study. It’s been known for a while that vegetarians and women eating a low–protein diet have a lower rate of bone loss over time. (In one recent study of over a thousand postmenopausal women, a diet rich in vegetable sources of protein versus animal proteins was associated with lower rates of bone loss and risk of fracture.)

This may be because as the body is digesting acid–producing foods, such as the red meat, poultry and eggs non-vegetarians eat, the net dietary acid load increases as pH drops, and the body looks for a way to bring the balance back. Calcium and other elements in short supply can be borrowed from the bone to achieve this balance. The result is loss in bone density. Vegetarians not only have less acid produced during digestion, but vegetables and fruits additionally metabolize into potassium bicarbonate (think Alka–Seltzer), which helps to offset imbalance.

But don’t forget that bone loss is a natural, in fact vital process. Only bone loss (called resorption) can initiate healthy new bone formation (called deposition or formation). As with all things in nature, good bone health relies on a balance between this action and counteraction, like breathing out and breathing in. However, when the body has to drain the stores to offset acid overload in the digestive track, the net result can be loss of bone density, which can lead to osteopenia and ultimately osteoporosis.

New studies are showing that high levels of homocysteine in the blood double the risk of osteoporosis–related fractures, along with other inflammatory conditions like heart attack, stroke, fuzzy thinking, and Alzheimer’s disease. A recent report published in the New England Journal of Medicine asserted that elevated homocysteine levels inhibit new bone formation by interrupting the cross-linking of collagen fibers in bone tissue.

It’s also possible, as I mentioned above, that the body tries to neutralize acidic blood serum (i.e., low pH) by releasing more bone calcium. Homocysteine levels can also be stabilized by eating foods and taking a vitamin supplement rich in folic acid, B12, and B6. Some researchers also describe a beneficial synergistic effect on homocysteine levels between omega–3 fatty acids and the metabolism of these vitamins.

Be aware that a minority of the population cannot convert folic acid due to certain enzyme deficiencies. If your homocysteine levels remain high even after a few weeks of B supplementation, you may want to ask your practitioner about adding a more bioavailable form of folate called 5-methyl-tetrahydrofolate (MTHFT) to your diet.

Relative to both pH and digestion and pH and bone loss, get this: Just by eating foods such as slow-roasted sweet potatoes, onions, and leeks, which are high in inulin, you can optimize your body’s ability to fully absorb the calcium present in your food and thereby decrease your risk for osteoporosis. Inulin is a type of prebiotic — it is believed to serve as a welcoming “fuel” for friendly gut flora, paving the way for beneficial bacteria to thrive further down into the colon, where it lowers the pH and improves the solubility and absorption of calcium by the body.

Naturally improving your pH balance

The most important aspect of this is to understand that you must make the proper nutrients, vitamins and minerals available to your body when it needs them. At Women to Women, we call this optimal nutrition, and in this day and age you need to work a little to get it. Here are some ideas on how to balance your diet and support healthy digestive pH levels.

Take a high-quality daily multivitamin like the one we offer through our Personal Program. This will offset any nutritional gaps and insure that your body has the reserves it needs. The right supplement should contain essential vitamins and minerals, including calcium and magnesium. In addition, I recommend an essential fatty acid supplement, and a good quality probiotic can help the body absorb the minerals that are all-important to your bones.
Fill your plate with fresh vegetables, particularly the dark green leafy kind. Add fresh lemon or lime to foods and beverages as a flavor accent. Enjoy plenty of fruit between meals. Again, foods which are fresh, organic, and deeply pigmented or brightly colored are the kinds that benefit you the most!
Consider boosting your diet with “green foods” or “green drinks,” which contain the pigment chlorophyll in abundance. The plant world’s equivalent of the hemoglobin in our blood, we can thank chlorophyll for generating all our food (except perhaps fungi!). It works in the body as a strong detoxifier and immunity–building agent. Foods that contain high levels of chlorophyll include the algae Spirulina and Chlorella and the juice of wheat grass and other sprouted grains. These foods offer high levels of other micronutrients as well, and their neat packaging can be especially helpful for those who lack time to prepare whole balanced meals or people recovering from illness.
Watch your red meat intake, and keep your servings of the acidifying proteins down to 4 oz per meal (the size of a deck of cards).
Avoid refined carbohydrates whenever you can, including sugar, and emphasize the “whole” in whole grains. Eliminate all processed foods, particularly those that contain partially hydrogenated oils (trans fats).
Clear the digestive slate with a gentle detox plan, like our Quick Cleanse, to get a better reading on how your diet — and pH — are affecting your sense of well-being. You may be surprised at how well you feel!
If you suffer from IBS, acid reflux, or regular heartburn, consider testing your pH. Remember that you may have too little acid in your stomach, not too much. Don’t just assume that an acid stomach means you’re too acidic.
Chew your food slowly and thoroughly. Enjoy every bite!
The beauty of balance

The subject of body pH may be having its 15 minutes of fame — and if it helps you to tune in to what’s going on in your body and eat a healthier diet, I’m all for that. Indeed, there are some people who are extremely sensitive to fluctuating pH levels and need to take serious action — but you won’t know until you find a good healthcare practitioner to guide you. And even then, pH is only one piece of the puzzle. To my mind, pH is a helpful indicator of overall balance in the body. But it’s just the tip of the iceberg, and no amount of trendy drinks or diet plans will make it more than that.

That being said, paying attention to your pH is one place you can begin to make a positive change. If it feels like a good place for you to start taking better care of yourself, I encourage you to do so. From there, it’s my hope that you will continue to listen to your body and help it find balance on all fronts, including your hormones, your emotions, and your lifestyle.


Postuar nga Pashai_1987 datë 21 Dhjetor 2006 - 21:27:

a ka ndonje qe di kete

mirmbrema
nuk e di nese ju ketu jeni doktorra apo thjesht te apasionuar pas mjeksis por kisha nje pyuetje:
pasi kam ber disa rezonanca magnetike nuk e di si quhen ne shqip/anglish por esht nje lloj scaneri modern ne tru ,ne foto kan gjtur disa(shum) njolla te bardha dhe nuk mund te shpjegojn dot neurologet nga vijen dhimbja ime e kokes
tani ato me kerkojn te bej nje"ponksion lamber" esht nje lloj gjilpere ne shtyllen kurrizore per te hequr lengun qe ndodhe aty dhe te bejn analizat e ketij lengu ose te me bejn nje gilper ne kok dhe te heqin nga lengu qe rrethon trurin por kete un nuk kam per ta pranuar kurr!!
tani mund te me thoni ju a eshte e rreziksheme kjo "poncion lomber" dhe a ka pasoja sepse te gjith mjeket ketu ne Belgjik me thon "oh ska asnj gje esht shum e leht dhe nuk ka asnje pasoj por duhet te rrish shtri 10 or pas asaj gjilperes"
un kam sh frik dhe nuk dua ta bej kete gjiilper
flm


Postuar nga NS-6 datë 21 Dhjetor 2006 - 22:21:

pasha,atehere ajo qe thua ti,nese e kam kuptuar mire eshte nje rakicentesi ose e thene me fjale me te thjeshta marrje e lengut qe ndodhet perreth palces kurrizore...analiza behet ne shtyllen kurrizore dhe jo ne tru. per sa i perket rreziqe,nese do kishte, atehere mjeket do ti merrnin parasysh kshu qe nuk ka pse te shqetesohesh per kete gje perderisa kane vendos per te te bere ate analize!eshte nje analize qe normalisht e kryejne persona te kualifikuar per ate pune dhe ne disa raste eshte e vetmja menyre per te arritur nje diagnoze te sakte!gjithsesi,nese ke ndonje dyshim per pasojat qe mund te kete,fare thjeshte mund te pyesesh mjeket qe jane te detyruar per te te njoftuar nese procedura do te kishte ndonje pasoje demtuese...une per vehte,nuk di te te them gje per faktin se pasojat vleresohen bazuar ne gjendjen e pacientit dhe nuk eshte qe mund te thuash qe filani do kete pasoje sepse jane keto te perqindje te gjetura nga filan studim,etj etj...pra,berja e analizes vendoset nga mjeku nese eshte e nevojshme apo jo!
ti ke frike?beh,kushdo qe semuret eshte i frikesuar per semundjen qe ka!nese ke frike,ke gjithmone alternativen te mos pranosh dhe te kthehesh ne shtepi me problemin qe ke....ose ose mund ta besh ate analize me shpresen qe te gjejne shkakun dhe te te japin nje terapi te sakte...gjithsesi,fjala e fundit te takon ty!por per analizen,mjeket qe po te kurojne e dijne me mire gjendjen qe je (besoj te kane bere analiza te tjera para se te te detyrojne te besh kete gje) dhe mund te te sqarojne me mire

kete pergjigje mund te te jap une!


Postuar nga Pashai_1987 datë 21 Dhjetor 2006 - 22:28:

Citim:
Po citoj ato që tha NS-6
pasha,atehere ajo qe thua ti,nese e kam kuptuar mire eshte nje rakicentesi ose e thene me fjale me te thjeshta marrje e lengut qe ndodhet perreth palces kurrizore...analiza behet ne shtyllen kurrizore dhe jo ne tru. per sa i perket rreziqe,nese do kishte, atehere mjeket do ti merrnin parasysh kshu qe nuk ka pse te shqetesohesh per kete gje perderisa kane vendos per te te bere ate analize!eshte nje analize qe normalisht e kryejne persona te kualifikuar per ate pune dhe ne disa raste eshte e vetmja menyre per te arritur nje diagnoze te sakte!gjithsesi,nese ke ndonje dyshim per pasojat qe mund te kete,fare thjeshte mund te pyesesh mjeket qe jane te detyruar per te te njoftuar nese procedura do te kishte ndonje pasoje demtuese...une per vehte,nuk di te te them gje per faktin se pasojat vleresohen bazuar ne gjendjen e pacientit dhe nuk eshte qe mund te thuash qe filani do kete pasoje sepse jane keto te perqindje te gjetura nga filan studim,etj etj...pra,berja e analizes vendoset nga mjeku nese eshte e nevojshme apo jo!
ti ke frike?beh,kushdo qe semuret eshte i frikesuar per semundjen qe ka!nese ke frike,ke gjithmone alternativen te mos pranosh dhe te kthehesh ne shtepi me problemin qe ke....ose ose mund ta besh ate analize me shpresen qe te gjejne shkakun dhe te te japin nje terapi te sakte...gjithsesi,fjala e fundit te takon ty!por per analizen,mjeket qe po te kurojne e dijne me mire gjendjen qe je (besoj te kane bere analiza te tjera para se te te detyrojne te besh kete gje) dhe mund te te sqarojne me mire

kete pergjigje mund te te jap une!



flm shum
por un thjesht nuk kam besim tek mjekt ato gjithmon thon nuk ka gje eshte shum e leht ect ect ato me kan ber analizat e gjakut per te par nese ka ndonje semundje pathlogjike por fatmirsisht nuk kam asnj semundje dhe dhimbje koke nuk kam patur kurr ne jet por ka nja 2 vjet qe po shtohen ca per me teper un jam vetem 30 vjeç dhe nuk esht aspak normale keto dhimbjet e kokes
nejse un te falenderoj per komentin


Postuar nga NS-6 datë 21 Dhjetor 2006 - 22:51:


beh,konsidero faktin qe ato qe do te te bejne analizen nuk eshte qe e bejne per here te pare ate gje keshtu qe atyre u duket e lehte per ta bere ...pastaj mendo nese do te ta benin gogol ate analize personave qe duhet ta bejne...do ta kishte bere kush deri me sot?thjesht merre si procedure te nevojshme qe mjeku e ka konsideru qe mund te te jape nje pergjigje per dhimbjen e kokes qe ke!gjithsesi,per cdo dyshim,mjeku qe po te kuron mund te te sqaroje shume me mire!
ishallah analiza te tregon se cfare ke,keshtu qe te fillosh nje kure sa me te sakte
te uroj nje sherim te shpejte nga ajo dhimbje koke!


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