[2012.10.25]

How to Stop Winter from Weathering Your Skin: Top Ten Tips for Preventing 'Winter Itch'

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ScienceDaily (Oct. 24, 2012) — All winter flakes are not made of snow. Cold weather, with its low relative humidity, wreaks havoc on our skin, making it dry and flaky. Skin dries out if it's deprived of moisture and this dryness often aggravates itchiness, resulting in a condition commonly referred to as "winter itch."

==resources==NewYork-Presbyterian Hospital/Columbia University Medical Center and NewYork-Presbyterian Hospital (2012, October 24). How to stop winter from weathering your skin: Top ten tips for preventing 'winter itch'. ScienceDaily. Retrieved October 25, 2012, from 

• http://www.sciencedaily.com­/releases/2012/10/121024164617.htm?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+sciencedaily+%28ScienceDaily%3A+Latest+Science+News%29

Infants Exposed to Specific Molds Have Higher Asthma Risk

ScienceDaily (Aug. 2, 2012) — In the United States, one in 10 children suffers from asthma but the potential environmental factors contributing to the disease are not well known. Cincinnati-based researchers now report new evidence that exposure to three types of mold during infancy may have a direct link to asthma development during childhood.

Journal Reference:

1. Tiina Reponen, James Lockey, David I. Bernstein, Stephen J. Vesper, Linda Levin, Gurjit K. Khurana Hershey, Shu Zheng, Patrick Ryan, Sergey A. Grinshpun, Manuel Villareal, Grace LeMasters. Infant origins of childhood asthma associated with specific molds. Journal of Allergy and Clinical Immunology, 2012; DOI:10.1016/j.jaci.2012.05.030

HIV-Infected T Cells Help Transport the Virus Throughout the Body

ScienceDaily (Aug. 1, 2012) — A new study has discovered one more way the human immunodeficiency virus (HIV) exploits the immune system. Not only does HIV infect and destroy CD4-positive helper T cells -- which normally direct and support the infection-fighting activities of other immune cells -- the virus also appears to use those cells to travel through the body and infect other CD4 T cells. The study from Massachusetts General Hospital (MGH) investigators, which will appear in the journal Nature and has received advance online release, is the first to visualize the behavior of HIV-infected human T cells within a lymph node of a live animal, using a recently developed "humanized" mouse model of HIV infection.

• HIV disseminates in the body of an infected individual by 'hitching a ride' on the T cells it infects: Infected T cells continue doing what they usually do, migrating within and between tissues such as lymph nodes, and in doing so they carry HIV to remote locations that free virus could not reach as easily. 
• When HIV is introduced into blood or tissues, the virus binds to CD4 molecules on the surface of helper T cells, injecting its contents into cells and setting off a process that leads to the assembly and release of new virus particles.早期以為是病毒隨體液/血液傳播
• lymph nodes -- known to be important sites of HIV replication 
• the researchers injected the animals with HIV engineered to express green fluorescent protein (GFP), allowing them to track the movement of infected cells within living animals using a method called intravital microscopy. 

T cell

T cells or T lymphocytes belong to a group of white blood cells known aslymphocytes, and play a central role in cell-mediated immunity. 
T helper cell (T_H cells) assist other white blood cells in immunologic processes, including maturation of B cells into plasma cellsand memory B cells, and activation of cytotoxic T cells and macrophages. These cells are also known as CD4⁺ T cells because they express the CD4 protein on their surface.

Journal Reference:

1. Thomas T. Murooka, Maud Deruaz, Francesco Marangoni, Vladimir D. Vrbanac, Edward Seung, Ulrich H. von Andrian, Andrew M. Tager, Andrew D. Luster, Thorsten R. Mempel.HIV-infected T cells are migratory vehicles for viral dissemination. Nature, 2012; DOI: 10.1038/nature11398

Peptide Controls Blood Sugar in People With Congenital Hyperinsulinism, Pilot Study Suggests

ScienceDaily (Aug. 1, 2012) — A pilot study in adolescents and adults has found that an investigational drug shows promise as the first potential medical treatment for children with the severest type of congenital hyperinsulinism, a rare but potentially devastating disease in which gene mutations cause insulin levels to become dangerously high.




congenital hyperinsulinism

• There is currently no effective medicine for children with the most common and most severe form of hyperinsulinism, 
• this investigational drug, a peptide called exendin-(9-39), controls blood sugar levels in people, a very promising result. 

Journal Reference:

1. Diva D. De Leon. The GLP-1 Receptor Antagonist Exendin-(9-39) Elevates Blood Fasting Glucose Levels in Congenital Hyperinsulinism due to Inactivating Mutations in the ATP-sensitive Potassium Channel.Diabetes, October 2012 DOI: 10.2337/db12-0166

Coffee May Help Some Parkinson's Disease Movement Symptoms, Research Suggests

ScienceDaily (Aug. 1, 2012) — While drinking coffee with caffeine each day does not appear to reduce sleepiness among people with Parkinson's disease, it may have a benefit in controlling movement, according to new research published in the August 1, 2012, online issue of Neurology®, the medical journal of the American Academy of Neurology.

• For the study, 61 people with Parkinson's disease who showed symptoms of daytime sleepiness and some motor symptoms were given either a placebo pill or a pill with 100 milligrams of caffeine two times a day for three weeks, then 200 milligrams twice a day for three weeks, which was the equivalent of between two and four cups of coffee per day. 
• After six weeks, the half that took the caffeine supplements averaged a five-point improvement in Parkinson's severity ratings compared to those who didn't consume caffeine. 
• The study authors noted that the length of the study was short and that the effects of caffeine may lessen over time

帕金森氏症（英语：Parkinson's Disease），或譯巴金森氏病，中国大陆譯作帕金森病，台湾譯作帕金森氏症， 港澳譯作柏金遜症，是一種慢性的中樞神經系統退化性失調，它會損害患者的动作技能、語言能力以及其他功能。它的病因目前仍不明，推測和大腦底部基底核（basal ganglia）以及黑質（substantial nigra）腦細胞快速退化，無法製造足夠的神經引導物質多巴胺（Dopamine）和膽鹼作用增強有關。腦內需要多巴胺來指揮肌肉的活動；缺乏足夠的多巴胺就產生各種活動障礙。 

Story Source:

The above story is reprinted from materials provided byAmerican Academy of Neurology (AAN).

Artificial Butter Flavoring Ingredient Linked to Key Alzheimer's Disease Process

ScienceDaily (Aug. 1, 2012) — A new study raises concern about chronic exposure of workers in industry to a food flavoring ingredient used to produce the distinctive buttery flavor and aroma of microwave popcorn, margarines, snack foods, candy, baked goods, pet foods and other products. It found evidence that the ingredient, diacetyl (DA), intensifies the damaging effects of an abnormal brain protein linked to Alzheimer's disease.

• DA gives microwave popcorn its distinctive buttery taste and aroma. DA also forms naturally in fermented beverages such as beer, and gives some chardonnay wines a buttery taste. 
• DA has an architecture similar to a substance that makes beta-amyloid proteins clump together in the brain -- clumping being a hallmark of Alzheimer's disease. 
• DA did increase the level of beta-amyloid clumping. 

維基百科/阿兹海默病：

阿茲海默病（英语：Alzheimer's disease，簡稱AD），或稱腦退化症（舊譯為阿尔茨海默病、老人失智症／老年痴呆症，英语：Senile Dementia of the Alzheimer Type，簡稱SDAT），是一种持续性神经功能障碍，也是失智症中最普遍的成因。

Journal Reference:

1. Swati S. More, Ashish P. Vartak, Robert Vince. The Butter Flavorant, Diacetyl, Exacerbates β-Amyloid Cytotoxicity. Chemical Research in Toxicology, 2012; : 120706140246003 DOI: 10.1021/tx3001016

Molecular Switch Identified That Controls Key Cellular Process: Gives Insight Into Cancer

ScienceDaily (Aug. 1, 2012) — The body has a built-in system known as autophagy, or 'self-eating,' that controls how cells live or die. Deregulation of autophagy is linked to the development of human diseases, including neural degeneration and cancer.

• 研究團隊discovered a critical molecular switch that regulates autophagy. They also studied the links between autophagy and a cellular process called senescence that stops cell growth permanently. 
• ASPP2, a tumor suppressor, as a molecular switch that can dictate the ability of a common cancer gene, known as the RAS oncogene, to either stop or promote senescence. 
• We found that in the presence of the common cancer-causing RAS oncogene, ASPP2 interacted with a protein complex that is responsible for deciding cell fate via autophagy. [oncogene: A gene that in certain circumstances can transform a cell into a tumor cell]
• Some of the recently developed anti-cancer drugs are potent inducers of autophagy. The new findings may also offer an explanation as to why patient response to these drugs can vary dramatically. 

Journal Reference:

1. Y. Wang, X. D. Wang, E. Lapi, A. Sullivan, W. Jia, Y.-W. He, I. Ratnayaka, S. Zhong, R. D. Goldin, C. G. Goemans, A. M. Tolkovsky, X. Lu. Autophagic activity dictates the cellular response to oncogenic RAS. Proceedings of the National Academy of Sciences, 2012; DOI:10.1073/pnas.1120193109