ช็อกโกแลตไปยุให้สิวพุ

thairath130502_003ศูนย์แพทย์มหาวิทยาลัยในเนเธอร์แลนด์ค้นคว้าพบว่า การกินช็อกโกแลตเป็นของแสลง อาจก่อให้เกิดการอักเสบ ทำให้สิวขึ้นง่าย

นักวิจัยได้พบว่า ผู้ที่แข็งแรงปกติดี เมื่อให้กินช็อกโกแลตวันละ 48.6 กรัม 4 วันติดกัน แล้วนำตัวอย่างเซลล์โลหิตของเขาไปสัมผัสเชื้อแบคทีเรียที่ส่งเสริมให้เป็นสิว ปรากฏอาการของระบบภูมิคุ้มโรคอักเสบขึ้น ซึ่งแสดงว่าช็อกโกแลตมีส่วนส่งเสริมให้เกิดสิว

อย่างไรก็ตาม นักวิจัยกล่าวว่า ผลที่ปรากฏยังเป็นเพียงขั้นต้นเท่านั้น ควรจะต้องมีการศึกษาเพิ่มเติมอีก เพื่อจะให้รู้ว่าส่วนประกอบต่างๆ ของช็อกโกแลต ตั้งแต่ไขมันและน้ำตาล อย่างไหนเป็นตัวการ.

ที่มา : ไทยรัฐ 2 พฤษภาคม 2556

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huffingtonpost130423_001

Chocolate May Trigger Acne By Changing Immune System, Study Suggests

By: Rachael Rettner, MyHealthNewsDaily Senior Writer
Published: 04/23/2013 12:21 PM EDT on MyHealthNewsDaily

Eating chocolate may change the immune system in ways that aggravate acne, a small new study from the Netherlands suggests.

In the study, researchers collected blood from seven healthy people before and after they ate 1.7 ounces of chocolate, each day for four days. (The chocolate contained about 30 percent cocoa.)

The researchers then exposed the blood cells to bacteria called Propionibacterium acnes, which contribute to acne when they grow inside clogged pores and cause pores to become inflamed, and to Staphylococcus aureus, another skin bacteria that can aggravate acne.

After eating chocolate, the participants’ blood cells produced more interleukin-1b, a marker of immune system inflammation, when exposed to Propionibacterium acnes. This suggests chocolate consumption could increase the inflammation that contributes to acne, the researchers said.

In addition, eating chocolate increased production of another immune system factor called interleukin 10 after exposure to Staphylococcus aureus. Interleukin 10 is thought to lower our bodies’ defenses against microorganisms, and thus, higher levels of interleukin 10 could create conditions that allow bacteria to infect pimples, and worsen them, the researchers said.

However, the results are preliminary, and the jury is still out on whether indulging in the sweet treat can really prompt a breakout.

Future studies should look into which components of chocolate (fats, sugars, etc.) might be responsible for the effects, and whether fat-free chocolate would have a different effect, the researchers said.

A 2011 study also found that chocolate consumption worsened acne, but the study involved only 10 men who consumed pure chocolate.

Although there’s a lot of talk about chocolate and other foods playing a role in acne, there’s very little evidence to show they do, said Dr. Kanade Shinkai, a dermatologist at the University of California, San Francisco School of Medicine, who specializes in acne treatments.

“I think there’s 10 times more discussion about it than there is data,” Shinkai said.

There is some evidence that so-called high glycemic foods, such as white bread, which release sugar very quickly into the bloodstream, may be linked to acne, Shinkai said. For instance, one study found that a population in Papua New Guinea with a low glycemic diet had no cases of acne across all ages, while in the United States more than 80 percent of teenagers have acne. Other studies looking at a possible link between diary products and acne have had conflicting results, Shinkai said.

While there may be a subset of people whose acne is influenced by diet, this is probably not true for everyone, Shinkai said. Multiple factors contribute to acne, including genetics, hormones and certain medications.

Shinkai said most dermatologists do not recommend dietary changes to help with acne, unless a patient is certain that a particular food is linked with his or her acne. Shinkai cautioned against broad dietary restrictions, such as avoiding diary, because diary products are important sources of calcium and vitamin D for many people, and the nutritional benefits of the products outweigh the impact of acne, she said.

Eating small amounts of chocolate has been linked with health benefits, such as a reduced risk of heart attack and stroke.

The new study, conducted by researchers at the Radboud University Nijmegen Medical Center in the Netherlands, was published online March 1 in the journal Cytokine.

SOURCE : www.huffingtonpost.com

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พบวิธีเผด็จศึก โรคมะเร็งทั้งฝูง

thairath130404_001วารสาร “วิทยาศาสตร์” ของสหรัฐฯ รายงานว่า นักวิจัยมหาวิทยาลัยสแตนฟอร์ดค้นพบยาที่สามารถรักษามะเร็งเต้านม มะเร็งมดลูก ลำไส้ กระเพาะปัสสาวะ สมอง ตับและต่อมลูกหมาก ให้หาย หรือทำให้หดเล็กลงได้

นักวิทยาศาสตร์ของโรงเรียนแพทย์คนหนึ่งจาระไนให้ฟังว่า “เราได้พบในการศึกษาว่าเมื่อมะเร็งเข้าตัวเราได้แล้ว แม้แต่ภูมิคุ้มโรคก็ไม่อาจทำอะไรได้ ไม่ว่าจะขัดขวางไม่ให้เติบโต และป้องกันไม่ให้ลุกลามออกไปได้” แต่ได้พบหนทางใหม่ที่จะจัดการกับมัน และยังพบว่าสารเคมีใหม่นี้สามารถรับมือกับโรคมะเร็งทั้งฝูงได้

เขาเปิดเผยต่อไปว่า เหตุที่ร่างกายไม่อาจจะต่อต้านเซลล์มะเร็งได้ ก็เพราะมันมีวิธีปกป้องตัวเองจากระบบภูมิคุ้มโรค โดยการชูธงหรือเครื่องหมายบอกว่า “เราเป็นมิตร อย่าทำอะไรเรา” ซึ่งวิธีแบบนี้เซลล์สำคัญอื่นๆในตัวเรา อย่างเซลล์โลหิตก็มีใช้อยู่แล้ว

นักวิจัยมหาวิทยาลัยสแตนฟอร์ดได้พบวิธีที่จะสกัดมันไม่ให้ส่งสารนี้ได้ โดยส่งภูมิต้านทานเฉพาะไปรับหน้าแทน ซึ่งจะเข้าทำลายมันลง ในการทดลองครั้งหลัง ยังได้พบว่าวิธีนี้จะสามารถปราบมะเร็งได้หลายชนิด แต่ยังจะต้องใช้เวลาอีกสักพักกว่าจะนำมาใช้กับมนุษย์ได้.

ที่มา : ไทยรัฐ 4 เมษายน 2556

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Cancer (middle green) scene from a microscope in breast tissue from a mouse at Stanford University in Palo Alto, Calif., on Tuesday, March 27, 2012. In identifying the protein in cancer, scientists are discovering how to block the protein to get the immune system to eliminate the cancer cells. Photo: Liz Hafalia, The Chronicle

Cancer (middle green) scene from a microscope in breast tissue from a mouse at Stanford University in Palo Alto, Calif., on Tuesday, March 27, 2012. In identifying the protein in cancer, scientists are discovering how to block the protein to get the immune system to eliminate the cancer cells. Photo: Liz Hafalia, The Chronicle

Stanford: Antibody offers hope against cancers

MEDICINE
Victoria Colliver
Saturday, March 31, 2012

In a potential breakthrough for cancer research, Stanford immunologists discovered they can shrink or even get rid of a wide range of human cancers by treating them with a single antibody.

The experiments were done on cancerous tumors transplanted into mice, but the researchers hope to move to human clinical trials within the next couple of years.

“We have made what we think is a big advancement … and we’re going to push as hard as we can and as fast we can,” said Dr. Irving Weissman, pathology professor at the Stanford University School of Medicine and director of Stanford’s Institute of Stem Cell Biology and Regenerative Medicine.

The researchers focused on blocking a protein, which they refer to as the “don’t eat me” molecule because it sits on tumor cells signaling the body’s immune system not to attack it. By introducing the antibody, the scientists were able to block the protective signal, otherwise known as CD47, allowing the immune system to go after the cancer cells.

Broad range of cancers

Researchers say CD47 is the only target found so far on the surface of all cancer cells. That means the antibody offers hope as a weapon against a broad range of cancers – breast, ovarian, colon, bladder, brain, liver and prostate.

Cancerous breast tissue from mice is seen at Stanford University in Palo Alto, Calif., on Tuesday, March 27, 2012. In identifying the protein in cancer, scientists are discovering how to block the protein to get the immune system to eliminate the cancer cells. Photo: Liz Hafalia, The Chronicle

Cancerous breast tissue from mice is seen at Stanford University in Palo Alto, Calif., on Tuesday, March 27, 2012. In identifying the protein in cancer, scientists are discovering how to block the protein to get the immune system to eliminate the cancer cells. Photo: Liz Hafalia, The Chronicle

The research involved taking cells from Stanford cancer patients, planting them into matching locations in the bodies of mice, and then administering the antibody. The antibody completely destroyed the tumor in some cases but also prevented the cancer from spreading.

“The most common result was the tumor growth was inhibited – not fully cured – but in a few weeks dramatically decreased,” said Stephen Willingham, postdoctoral researcher and co-lead author of the study.

The study, published online this week in the journal Proceedings of the National Academy of Sciences, has drawn praise from other researchers.

“The data is indeed exciting, and the effects are significant,” said Tyler Jacks, director of the Koch Institute for Integrative Cancer Research at the Massachusetts Institute of Technology, who was not involved in the study.

Research on mice

But Jacks noted that the research has been limited to mice, and disease in humans tends to be much more complex.

“That’s a commonly used preclinical model, but there are other examples when therapeutic effectiveness in such models has not translated well in real disease,” Jacks said. “We need to see what happens when the treatments are (used) in patients.”

The Stanford team said the “don’t eat me” CD47 signal has long been identified and is associated, in particular, with the treatment of leukemia. CD47 is found in healthy cells but tends to be expressed in higher levels in cancerous cells.

Lead authors Jens Volkmer, M.D. and Stephen Willingham, Ph.D, (right) look at samples of breast cancer tumors from mice under a microscope at Stanford University in Palo Alto, Calif., on Tuesday, March 27, 2012. They have been identifying the protein in cancer and discovering how to block the protein to get the immune system to eliminate the cancer cells. Photo: Liz Hafalia, The Chronicle

Lead authors Jens Volkmer, M.D. and Stephen Willingham, Ph.D, (right) look at samples of breast cancer tumors from mice under a microscope at Stanford University in Palo Alto, Calif., on Tuesday, March 27, 2012. They have been identifying the protein in cancer and discovering how to block the protein to get the immune system to eliminate the cancer cells. Photo: Liz Hafalia, The Chronicle

Limited side effects

The researchers were concerned that any treatment would single out normal cells as well as malignant ones. They discovered, however, that the antibody selected older, red blood cells, causing mild but temporary anemia and no other adverse side effects.

“That was the best moment. We found a way to utilize this antibody to treat (the cancer) without having major toxicity,” said Dr. Jens-Peter Volkmer, the study’s other lead author.

The Stanford team’s continuing research is being funded by a grant from the California Institute for Regenerative Medicine. The organization was created by Proposition 71, passed by voters in 2004 to support stem cell research.

SOURCE: www.sfgate.com

โดนเห็บกัดอาจเปลี่ยนคุณเป็นมังสวิรัติ เนื่องจากมันฉีด ‘พิษ’ ที่ก่อให้เกิดอาการแพ้เนื้อสัตว์

สารประกอบคาร์โบไฮเดรตที่เข้าไปในกระแสเลือดโดยการกัด มีอยู่ในเนื้อสัตว์

มีผู้ที่ถูกเห็บกัดจำนวนหนึ่งที่ถูกกระตุ้นให้แพ้อาหาร และถามหาเมนูอาหารที่ปราศจากเนื้อสัตว์

นักวิจัยกล่าวว่า คุณจะไม่รู้สึกอยากกินสเต็กอีกต่อไปภายหลังจากถูกเห็บกัด

จากการศึกษา เมื่อถูกแมลงคล้ายแมงมุมกัดจะกระตุ้นให้เกิดอาการแพ้เนื้อสัตว์ได้

ในสหรัฐอเมริกา มีสามกรณีของการเกิดปฏิกิริยาแปลก ๆ ผู้ป่วยทรมาณอย่างรุนแรงเป็นเวลาหลายชั่วโมงหลังจากกินเนื้อแดง

ผู้เชี่ยวชาญตรวจสอบการตอบสนองล่าช้าต่อการแพ้ จากเห็บกัด – โดยเฉพาะเห็บโลนสตาร์

สารประกอบคาร์โบไฮเดรตฉีดเข้าไปในกระแสเลือดโดยการกัด มีอยู่ในส่วนประกอบเนื้อสัตว์  กัดแรกจะไปกระตุ้นระบบภูมิคุ้มกันของร่างกายในจดจำและมีการตอบสนองครั้งต่อไปเมื่อเจอสารตัวนี้อีกครั้ง

ผลคือเมื่อเหยื่อผู้ที่ไม่สงสัยว่าถูกกัดพยายามกินสเต็ก ลมพิษก็ลุกลาม และแพ้แบบรุนแรงขนาดเสียชีวิต

ดร. ซูซาน วูลเวอร์ จาก มหาวิทยาลัย เวอร์จิเนีย คอมมอนเวล์ธ และเพื่อนร่วมวิจัยอธิบายไว้ในวารสารการแพทย์

ที่ไหนมีเห็บเฉพาะถิ่นเช่นในทางตะวันออกเฉียงใต้ ของสหรัฐ, แพทย์ควรตระหนักถึงโรคใหม่นี้แสดงถึงการแพ้แบบรุนแรง

คำแนะนำปัจจุบันคือการให้คำปรึกษาผู้ป่วยที่จะหลีกเลี่ยงเนื้อสัตว์เลี้ยงลูกด้วยนมทั้งหมด เช่น เนื้อวัว, เนื้อหมู, เนื้อแกะและเนื้อกวาง

เห็บโลนสตาร์ (Lone Star) อาจจะกระตุ้นระบบภูมิคุ้มกันของร่างกายให้ต่อต้านสารประกอบที่พบในเนื้อสัตว์

ขอแนะนำให้อาบน้ำทันทีที่กลับมาจากการสำรวจหรือทำงานนอกบ้านและให้ตรวจร่างกายหาเห็บอย่างละเอียด

ใช้แหนบคีบเห็บให้ใกล้ผิวหนังที่สุดและดึงออกไปทิ้งให้ไกล

เห็บยังสามารถแพร่กระจายการติดเชื้อแบคทีเรีย โรคอาการแรกที่พบมากที่สุดคือผื่นแดงเป็นวงกลมรอบ ๆ รอยกัด หากทิ้งไว้ไม่ทำการรักษา พัฒนาอาการขึ้นไปอีกเป็นปี คือมีอาการปวดกล้ามเนื้อ, บวมตามข้อต่อและใบหน้าอัมพาตชั่วคราว

สถาบันคุ้มครองสุขภาพ (HPA) ประมาณการณ์ว่าในแต่ละปี มีผู้ป่วยจากโรค Lyme  2,000 ถึง 3,000 ในอังกฤษและเวลส์

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โรคทูลาริเมีย (Tularemia

โรคลัยม์ (Lyme Disease)

 

How a tick bite can turn you vegetarian: They inject a ‘venom’ that triggers meat allergy

  • A carbohydrate compound injected into the bloodstream by the bite is also present in meat

By DAILY MAIL REPORTER

PUBLISHED: 14:04 GMT, 25 July 2012 | UPDATED: 06:56 GMT, 26 July 2012

A carbohydrate compound injected into the bloodstream by the bite is also present in meat

Meat-free menu? A handful of tick-bite cases in the U.S have triggered food allergies

A steak may never seem as appetising again after a tick bite, warn researchers.

Being bitten by one of the spider-like bugs can trigger a severe allergy to meat, scientists have learned.
Three cases of the strange reaction were identified in the US. The patients suffered severe symptoms several hours after eating red meat.

Experts traced the delayed allergic response to bites from a tick – specifically the Lone Star tick.
A carbohydrate compound injected into the bloodstream by the bite is also present in meat. The initial bite is thought to prime the immune system to react next time it encounters the substance.
The result when the unsuspecting victim tries tucking into a steak can be an outbreak of hives, or even life-threatening anaphylactic shock.

Dr Susan Wolver, from Virginia Commonwealth University, and colleagues described the research in the Journal of Internal Medicine.

They wrote: ‘Where ticks are endemic, for example in the south-eastern United States, clinicians should be aware of this new syndrome when presented with a case of anaphylaxis.
‘Current guidance is to counsel patients to avoid all mammalian meat – beef, pork, lamb and venison.’

Lone star ticks may prime the immune system against a compound found in meat

It is recommended to shower as soon as returning inside after exploring or working outdoors and also to perform a full body inspection for any ticks.
Remove the tick with tweezers by gently gripping it as close to the skin as possible and pulling it away from the skin.

The insects can also spread the bacterial infection Lyme disease. The most common early symptom is a red circular rash that develops around the bite. If left untreated you can develop symptoms up to years later including muscle pain, swelling of the joints and temporary facial paralysis.
The Health Protection Agency (HPA) estimates that there are 2,000 to 3,000 cases of Lyme disease in England and Wales each year.

Data From: dailymail.co.uk

เลี้ยงสัตว์ช่วงอุ้มท้อง ลดปัญหาภูมิแพ้ลูกได้

งานวิจัยใหม่ชี้ว่า แม่ที่เลี้ยงสัตว์ในเวลาตั้งครรภ์ จะช่วยลดโอกาสที่ลูกจะเป็นโรคภูมิแพ้และหืดหอบได้ อย่างไรก็ตามงานวิจัยชี้ว่า เชื้อชาติ และวิธีการคลอดบุตรก็มีส่วนเกี่ยวข้องเช่นกัน

งานวิจัยชิ้นนี้จัดทำโดยโรงพยาบาลเฮนรีฟอร์ด เมืองดีทรอยต์ โดยเก็บตัวอย่างจากการทำคลอดบุตรในโรงพยาบาลทั้งหมด 1,187 คน ตั้งแต่ปี 2546 ถึงปี 2550 แบ่งเป็นการทำคลอดด้วยวิธีธรรมชาติ 751 ราย และการทำคลอดด้วยการผ่าตัด 436 ราย ส่วนครอบครัวที่มีสัตว์เลี้ยงขณะตั้งครรภ์มีทั้งหมด 420 ครอบครัว และแบ่งการเก็บตัวอย่างเลือดทารกออกเป็น วัยแรกเกิด วัย 6 เดือน วัย 1 ขวบ และวัย 2 ขวบ

นักวิจัยประจำโรงพยาบาลเฮนรีฟอร์ดพบว่า ทารกในช่วงแรกเกิดไปจนถึง 2 ขวบ ที่อาศัยร่วมกับสัตว์เลี้ยงภายในบ้าน จะมีระดับสารแอนติบอดี อิมมูโนโกลบูลินอี (ไอจีอี) โดยเฉลี่ยน้อยกว่าปกติ 28% ซึ่งสารตัวนี้มีส่วนก่อให้เกิดโรคภูมิแพ้และหืดหอบได้

อย่างไรก็ตาม ทารกชาวตะวันตก เอเชีย และตะวันออกกลาง ของครอบครัวที่เลี้ยงสัตว์ภายในบ้าน จะมีระดับไอจีอีโดยเฉลี่ยต่ำกว่าปกติ 33% ในระหว่างที่ทารกชาวผิวดำที่มีสัตว์เลี้ยงภายในบ้านจะมีระดับไอจีอีต่ำกว่าปกติ 23%

นอกจากนี้ ทารกที่คลอดด้วยวิธีตามธรรมชาติ ยังช่วยลดระดับสารไอจีอีลงได้อีกเช่นกัน เมื่อเปรียบเทียบกับทารกที่คลอดด้วยวิธีการผ่าตัด

ดร.คริสติน โคล จอห์นสัน ผู้อำนวยการแผนกวิทยศาสตร์สาธารณสุข โรงพยาบาลเฮนรีฟอร์ด และผู้นำการวิจัย กล่าวว่า การได้สัมผัสไมโครแบคทีเรียตั้งแต่ช่วงเวลาแรกเกิด มีผลกระทบต่อการพัฒนาภูมิต้านทานของทารก

ดร.จอห์นสันกล่าวว่า ข้อค้นพบนี้สนับสนุนทฤษฎีพัฒนาการโรคภูมิแพ้ ซึ่งเป็นทฤษฎีที่ตั้งสมมติฐานว่า การได้สัมผัสแบคทีเรียหรือสารกระตุ้นตั้งแต่วัยเยาว์ จะช่วยพัฒนาภูมิคุ้มกันต่อการเป็นโรคภูมิแพ้และหืดหอบได้

เธออธิบายว่า การคลอดลูกตามวิธีธรรมชาติช่วยลดอาการภูมิแพ้ เพราะเมื่อทารกเคลื่อนตัวผ่านช่องคลอด แบคทีเรียที่อยู่ในบริเวณนั้นจะช่วยกระตุ้นระบบภูมิคุ้มกันของทารก และลดความเสี่ยงในการเป็นโรคภูมิแพ้ในอนาคต

อย่างไรก็ตาม ดร.จอห์นสันกล่าวว่า พันธุกรรมก็มีผลต่อระดับสารไอจีอีในร่างกาย โดยเฉพาะชาวแอฟริกัน และแอฟริกัน-อเมริกัน.

 

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Want an asthma-free child? Get a pet while you are pregnant

By LAUREN PAXMAN

Last updated at 3:13 PM on 17th February 2012

Mothers who spend time with pets during their pregnancy are less likely to have children with allergies and asthma, a study has revealed.

But the race of the child – and how they were delivered – also plays a part.

Researchers at the Henry Ford Hospital in Detroit found that babies who have indoor prenatal pet exposure have a pattern of lower levels of the antibody Immunoglobulin E, or IgE, between birth and their second birthday.

IgE is linked to the development of allergies and asthma.

Levels of the antibody were, on average, 28 per cent lower during infancy in babies who had indoor prenatal pet exposure compared to babies from pet-free homes.

However IgE levels were 33 per cent lower in those babies from European, Asian or Middle Eastern descent compared to 23 per cent in kids who were African-American.

And the levels were also lower in infants who had indoor prenatal pet exposure and were born vaginally, compared to those born by caesarean section.

Dr Christine Cole Johnson, chair of Henry Ford’s Department of Public Health Sciences and senior author of the study said: ‘We believe having a broad, diverse exposure to a wide array of microbacteria at home and during the birthing process influences the development of a child’s immune system.’

Dr Johnson added that the findings support the so-called hygiene hypothesis.

This is the theory that early childhood exposure to infectious agents affects the immune system’s development and onset of allergies and asthma.

Dr Johnson theorised that babies born through the birth canal are exposed to a higher and more diverse burden of bacteria, further boosting the immune system’s protection against allergies.

She said that ‘genetic variants’ could explain the higher levels of IgE levels in African American newborns.

She added: ‘Our findings may provide insight into the biological mechanisms that increase the risk for allergic disorders.’

Henry Ford researchers followed 1,187 newborns August 2003 and November 2007 and collected blood samples for measuring IgE levels at birth, six months, one year and two years.

Of the birth mothers, 62 percent were African American and 33 percent were European Americans.

Of the babies born, 751 were delivered vaginally and 436 were delivered cesarean.

There was at least one indoor pet in the homes of 420 mothers.

The findings are published online at the Journal of Allergy and Clinical Immunology.

Why bad immunity genes survive: Study implicates arms race between genes and germs

University of Utah biologists found new evidence why mice, people and other vertebrate animals carry thousands of varieties of genes to make immune-system proteins named MHCs – even though some of those genes make us susceptible to infections and to autoimmune diseases.

นักชีววิทยาของมหาวิทยาลัยยูทาห์ พบหลักฐานใหม่ที่ว่าทำไมหนูคนและสัตว์มีกระดูกสันหลังอื่น ๆ จึงมียีนหลายพันสายพันธุ์ที่สร้างโปรตีนระบบภูมิคุ้มกันของร่างกายที่ชื่อ MHCs – แม้ว่าบางส่วนของยีนเหล่านั้นทำให้เราไวต่อการติดเชื้อโรคและไวต่อการเกิดโรคภูมิคุ้มกันผิดปกติ

This electron microscope image shows yellow particles of a mouse leukemia virus named Friend virus emerging or “budding” out of an infected white blood cell known as a T-cell. By allowing the Friend virus to mutate and evolve in mice, University of Utah researchers produced new evidence that an arms race between microbes and immune-system MHC genes is responsible for maintaining an amazing diversity of those genes, even though some of them are responsible for autoimmune and infectious diseases that make us sick. Credit: Elizabeth Fischer and Kim Hasenkrug, NIH

Major histocompatibility complex” (MHC) proteins are found on the surface of most cells in vertebrate animals. They distinguish self from foreign, and trigger an immune response against foreign invaders. MHCs recognize invading germs, reject or accept transplanted organs and play a role in helping us smell compatible mates.

“This study explains why there are so many versions of the MHC genes, and why the ones that cause susceptibility to diseases are being maintained and not eliminated,” says biology Professor Wayne Potts. “They are involved in a never-ending arms race that causes them, at any point in time, to be good against some infections but bad against other infections and autoimmune diseases.”

By allowing a disease virus to evolve rapidly in mice, the study produced new experimental evidence for the arms race between genes and germs – known technically as “antagonistic coevolution.” The findings will be published online the week of Feb. 6, 2012, in the journal Proceedings of the National Academy of Sciences.

Potts, the senior author, ran the study with first author and former doctoral student Jason Kubinak, now a postdoctoral fellow in pathology. Other co-authors were biology doctoral student James Ruff, biology undergraduate C. Whitney Hyzer and Patricia Slev, a clinical assistant professor of pathology. The research was funded by the National Science Foundation and the National Institute of Allergy and Infectious Diseases.

 

Theories for the Diversity of Immune-System MHC Genes

Most genes in humans and other vertebrate have only one or two “alleles,” which are varieties or variants of a single gene. Although any given person carries no more than 12 varieties of the six human MHC genes, the human population has anywhere from hundreds to 2,300 varieties of each of the six human genes that produce MHC proteins.

“The mystery is why there are so many different versions of the same [MHC] genes in the human population,” Kubinak says, especially because many people carry MHCs that make them susceptible to many pathogens (including the AIDS virus, malaria and hepatitis B and C) and autoimmune diseases (including type I diabetes, rheumatoid arthritis, lupus, multiple sclerosis, irritable bowel disease and ankylosing spondylitis).

Scientists conducted experiments that allowed a disease virus to evolve rapidly in mice. Credit: Wayne Potts, University of Utah

 

Scientists have proposed three theories for why so many MHC gene variants exist in vertebrate animal populations (invertebrates don’t have MHCs), and say all three likely are involved in maintaining the tremendous diversity of MHCs:

— An organism with more MHC varieties has a better immune response than organisms with fewer varieties, so over time, organisms with more MHCs are more likely to survive. However, this theory cannot explain the full extent of MHC diversity.

— Previous research indicates people and other animals are attracted to the smell of potential mates with MHCs that are “foreign” rather than “self.” Parents with different MHC variants produce children with more MHCs and thus stronger immune systems.

— Antagonistic coevolution between an organism and its pathogens. Kubinak says: “We have an organism and the microbes that infect it. Microbes evolve to better exploit the organism, and the organism evolves better defenses to fight off the infection. One theory to explain this great diversity in MHC genes is that those competing interests over time favor retaining more diversity.”

 

The Arms Race between Germs and MHC Genes

“You naturally keep genes that fight disease,” Kubinak says. “They help you survive, so those MHC genes become more common in the population over time because the people who carry them live to have offspring.”

Pathogens – disease-causing viruses, bacteria or parasites – infect animals, which defend themselves with MHCs that recognize the invader and trigger an immune response to destroy the invading pathogen.

But over time, some pathogens mutate and evolve to become less recognizable by the MHCs and thus evade an immune response. As a result, the pathogens thrive. MHCs that lose the battle to germs become less common because they now predispose people who carry them to get sick and maybe die. It was thought such disease-susceptibility MHC genes eventually should vanish from the population, but they usually don’t.

Why? While some of those MHCs do go extinct, others can persist, for two reasons. First, some of the now-rare MHCs gain an advantage because they no longer are targeted by evolving microbes, so they regain an ability to detect and fight the same germ that earlier defeated them – after that germ mutates yet again. Second, some of the rare MHCs can mount an effective immune response against completely different microbes.

 

How the Study was Performed; Implications of the Findings

The researchers studied 60 mice that were genetically identical, except the mice were divided into three groups, each with a different variety of MHC genes known as b, d and k, respectively.

A mouse leukemia virus named the Friend virus was grown in tissue culture and used to infect two mice from each of the three MHC types. The fast-evolving retrovirus grew within the mice for 12 days, attacking, enlarging and replicating within the spleen and liver. Virus particles in the spleen were collected, and the severity of illness was measured by weighing the enlarged spleen.

 

Many people carry MHCs that make them susceptible to pathogens like the AIDS virus. Credit: NIH

Then, virus taken from each of the first three pairs of mice (b, d and k) was used to infect another three pair of mice with the same MHC types. The process was repeated until 10 pairs of mice in each MHC type were infected, allowing the virus time to mutate.

In this first experiment, the biologists showed they could get the Friend virus to adapt to and thus evade the MHC variants (b, d or k) in the mouse cells it attacked.

Next, the researchers showed that the virus adapted only to specific MHC proteins. For example, viruses that adapted to and sickened mice with the MHC type b protein still were attacked effectively in mice that had the type d and k MHCs.

In the third experiment, the researchers showed that pathogen fitness (measured by the number of virus particles in the spleen) correlated with pathogen virulence (as measured by spleen enlargement and thus weight). So the virus that evaded MHC type b made mice with that MHC sicker.

Together, the experiments demonstrate “the first step in the antagonistic coevolutionary dance” between a virus and MHC genes, Potts says.

Potts says the findings have some important implications:

— The use of antibiotics to boost productivity in dairy herds and other livestock is a major reason human diseases increasingly resist antibiotics. Selective breeding for more milk and beef has reduced genetic diversity in livestock, including their MHCs. So breeding more MHCs back into herds could enhance their resistance to disease and thus reduce the need for antibiotics.

— Because their populations are diminished, endangered species have less genetic diversity, making them an easier target for germs. Potts says it would be desirable to breed protective MHCs back into endangered species to bolster their disease defenses.

— Genetic variation of MHCs in people and other organisms is important for limiting the evolution and spread of emerging diseases. In effect, Potts and colleagues created emerging diseases by making a virus evolve in mice. “It’s a model to identify what things change in viruses to make them more virulent and thus an emerging disease.”

 

Data from: medicalxpress , February 6, 2012

The ‘growing pains’ that could cripple you for life

The ‘growing pains’ that could cripple you for life
By ISLA WHITCROFT
UPDATED: 00:14 GMT, 30 November 2010

Paul Curry’s teenage years were blighted by what doctors insisted were growing pains. Not just the odd sharp stab or ache that many youngsters suffer, but attacks that were so severe he was often bedridden for days.
‘The pain was dull, gnawing deep inside both hips,’ says Paul, 28, from Durham. ‘It was excruciating.

‘The first time it happened I was 13 and mad about sport, particularly rugby. I assumed — as did my parents — it was growing pains or a sporting injury and so would go away.’

At risk: Young males are most likely to suffer from Ankylosing Spondylitis(AS), a progressive rheumatic disease that causes inflammation around joints

Unfortunately, over the next few years not only did the pain worsen, but the attacks became more frequent and lasted longer.

‘Sometimes I could cope by taking painkillers, but other times I’d be in bed for days, screaming with pain,’ says Paul.

Over the next few years, his parents took him to see his GP several times. He diagnosed growing pains and said it was ‘something Paul would grow out of’.

A consultant orthopaedic ­surgeon, to whom Paul was referred privately at the age of 16, then pronounced he was suffering from Sherman’s disease, a mild condition that causes a slight curvature of the upper spine.

‘He said that by the time I was 21 I’d have grown out of it. In the meantime, I was to keep taking painkillers,’ he says.

Sadly, Paul, from Durham, didn’t have Sherman’s disease, but Ankylosing Spondylitis (AS), a progressive rheumatic disease that causes inflammation around bone joints and ligaments.

Left untreated, this causes bone erosion, which stimulates the immune system into a healing process. This, in turn, produces an overgrowth of bone, which leads to the fusion of bones such as the spine and hips and eventually immobility. The damage is irreversible.

Some 400,000 Britons are affected by AS, with symptoms usually appearing between the ages of 25 and 34 — though ­teenagers and older people can be affected.

Unfortunately, like Paul, many sufferers are mis-diagnosed — with devastating consequences.

Today, at 28, Paul is racked with constant pain. The discs in the lower half of his spine have fused, as have his hip and pelvic joints.

Three vertebrae at the top of his neck are also affected and this once super-fit teenager counts himself lucky if he walks without using a stick.
At night, his joints stiffen and spasm and he is dependent on a daily dose of morphine.

Late diagnosis: Paul Curry’s crippling condition was not spotted until his 20s

Not surprisingly, in the past, the condition has left Paul feeling depressed.

‘I still get distressed about what might have been had I been properly diagnosed early on,’ says Paul who, after getting a degree in business management, had to move back in with his parents because he is often confined to bed for days at a time.

Despite spending thousands of pounds on specialists over the years, Paul wasn’t diagnosed until he was 26, when an astute physiotherapist recognised his symptoms and advised him to see a rheumatologist.

‘She examined me and said she was almost certain I had AS,’ says Paul.

‘Blood tests and an MRI scan confirmed this. It was a scary diagnosis, but an utter relief that at last I knew what I was dealing with.’

Shockingly, the average delay in diagnosing the condition is ten years, according to a survey for the National Ankylosing Spondylitis Society (NASS).

‘There is a lack of awareness of the condition and how to distinguish the symptoms from other causes such as back pain,’ says Dr Andrew Keat, consultant rheumatologist at Northwick Park Hospital, Harrow, Middlesex, and a specialist in AS.

‘Unfortunately, the very people who suffer most from the ­condition — young males — are also the ones who tend to be the most active,’ he says.

‘Therefore, it’s easy to write off their symptoms as being a sporting injury or even just growing pains.’

The main distinguishing ­symptom is inflammatory joint pain, which comes on slowly and usually occurs in the lower back or hips. Crucially, it improves with exercise and worsens with inactivity, meaning it’s often severe at night.

‘These symptoms should be a red light to your GP that ­inflammation is occurring,’ says Dr Keat. ‘If anti-inflammatories don’t help after a few weeks, the symptoms need further investigation by a rheumatologist.’
There is no one simple test, says Dr Keat.

‘We look at family history, symptoms, make a physical examination and take blood tests for signs of inflammation. X-rays rarely show the condition so an MRI scan is essential,’ he says.

Ironically, once the condition is diagnosed, treatment is ­usually effective — with anti-inflammatories such as ibuprofen and exercise, as movement discourages the fusion process.

Exercise can make a significant difference, as Liz Ledger proves. Now 28, she had severe hip pains from the age of 17; these were also blamed on growing pains.

‘I lost count of how many health professionals I saw,’ says Liz, a sales and marketing ­manager from Bristol.

However, she worked out that the pain receded when she ­exercised and over the years she has devised a routine that kept it manageable.

But by her mid-20s the pain was increasingly severe. Finally, in October 2007, she suffered a flare-up that left her bed-bound.

‘I dragged myself to the GP and insisted that I wasn’t ­leaving without a referral to a rheumatologist.’

An MRI scan and blood test confirmed AS; her first four ­vertebrae had fused and there were signs of fusion in the hips and pelvic joints.

Her condition is being managed by anti-inflammatories and pain-killers. She does cycle classes, body conditioning and gentle running six days a week.
‘It’s a commitment, but it means the difference between mobility and immobility,’ she says.

‘AS can be a devastating ­condition, but one positive thing is that the sufferer can actually help themselves,’ says Jane Skerrett of the NASS.

‘The earlier a patient gets on to a suitable exercise regimen the better.’
The charity has launched an exercise guide, developed by a rheumatologist and physiotherapists, that contains a full ­fitness programme as well as advice.

Despite his pain, Paul makes sure he always does gentle stretching and walking. And ­having recently married, he remains optimistic and is keen to start a family.

Liz, who was diagnosed earlier in the disease cycle, is also upbeat. ‘I recently completed a half-marathon,’ she says.

‘Now I’m back at work and have a social life. Exercise has given me control of this disease.’

Data from: dailymail.co.uk