DELAY AGEING LONG LIFE HEALTH INFORMATION
ARE YOU WORRIED ABOUT TENSION?
ARE YOU DISGUSTED WITH LIFE?
ARE YOU DEPRESSED?
DO YOU WANT HAPPINESS?
DO NOT WORRY .FOLLOW THIS BLOG.
MOST IMPORTANT REQUIREMENT IS TO BE FAITHFUL TO YOUR RELIGION .
OBEY COMMANDMENTS.
REGULARLY ATTEND CHURCH/TEMPLE/MOSQUE.
PRACTISE YOUR RELIGION.
STAY YOUNG BLOG
HOW TO DELAY AGEING PROCESS.STAY YOUNG AT 65
GOOD LOOKS AT 65
STRONG & HEALTHY AT65
LOOK YOUNG & HAPPY
INDEX
1.Good Religeous Life
Good Family Life
2..Aerobic Exercises
Walking -30 min
Jogging
Exercise Machines
3..Healthy food
Cholesterol Free
Vegitarian Diet
Less Red Meat
4..Keep Cool
Do not get irritable
5..Meditation
6..Rest & Relaxation
7..Yoga
8..Vitamins & Minerals
VitA
Vit B
Vit C
VitE-Natural better
Selenium
Zinc
9..Ginsen Products
10..Pure,Healthy Environment
Low-CO,SO2,
11. Sex
Safe Sex to be continued
Single cell 'can store memories'Just one brain cell is capable of holding fleeting memories vital for our everyday life, according to US scientists.A study of mouse brain cells revealed how they could keep information stored for as long as a minute.A UK specialist said that understanding these short-term memories might help unlock the secrets of Alzheimer's Disease. To perform normal functions, we need the ability to store, quickly and reliably, large amounts of data, but only a small amount of this needs to be retained in the longer term.
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AGEs, oxidant stress, and inflammation: round and round we goTopAbstractIntroductionAGEs: diabetes, RAGE, and...AGEs, oxidant stress, and...AGE and AGEing: an...Hypotheses and perspectivesHow do we break...Blocking AGEing—to a...AcknowledgmentsReferences
RAGE and implications for the pathogenesis of type 1 diabetes: nearly full circleBased on the findings that RAGE appeared to play key roles in euglycemic inflammation, we hypothesized that RAGE might play a role in autoimmune disease, such as that observed in type 1 diabetes. To test this premise, we studied the role of RAGE in a model of adoptive transfer of diabetogenic spleen cells into NOD/SCID mice (Chen et al., 2004 ). Both RAGE and S100 were expressed on islet cells with an inflammatory infiltrate in sections of pancreata from diabetic NOD/SCID mice that had received a transfer of splenocytes, but not from control NOD/SCID mice. In addition to RAGE expression in endocrine cells, other studies demonstrated that RAGE was also expressed at least in a population of T cells (CD4+ and CD8+) and B cells (Chen et al., 2004 ).To test the potential role of RAGE in mediating autoimmune diabetes in this model, we transferred splenocytes from a diabetic NOD donor into NOD/SCID mice; NOD/SCID mice were treated with either sRAGE or mouse serum albumin. Treatment with sRAGE significantly reduced the rate of transfer of diabetes. By day 36 after transfer, 22 of 24 (92%) control animals but only 2 of 25 (10%) mice treated with sRAGE were diabetic. In parallel, the expression of key cytokines, IL-1beta and TNF-alpha, was significantly reduced in the sRAGE-treated islets compared with vehicle-treated animals. The expression of IL-10 was strikingly increased in sRAGE-treated mice islets, along with increased transforming growth factor (TGF)-beta, compared to vehicle-treated animals (Chen et al., 2004 ).Further, in the context of our proposed model of AGEs and RAGE triggering a vicious cycle of injury with multiple points of amplification, glucose, AGEs, and oxidative stress augment injury to islets and beta cells (El-Assaad et al., 2003 ; Robertson, 2004 ; Wu et al., 2004 ). Certainly, in the context of islet transplantation, stopping the cycle of AGE generation and oxidative stress, in part via RAGE, may diminish injury to newly transplanted islets.Interestingly, when preactivated diabetogenic BDC2.5 cells were injected into mice, sRAGE had no effect on preventing diabetes. Such observations require that we "re-open" the issue of potential roles for RAGE in the adaptive immune response. Studies to rigorously address this hypothesis are underway at this time.Taken together, these findings suggest that it will be critical to dissect each potential component of RAGE-dependent mechanisms in autoimmunity. Specifically, do roles exist for RAGE in both the adaptive immune response and/or the amplification of immune/inflammatory injury in autoimmunity targets such as islets? Will there be beneficial roles for RAGE blockade in attenuating rejection after allogeneic islet transplantation? These concepts must be addressed by instituting RAGE blockade at distinct time points either alone or in combination with classical immunosuppressive agents in experimental models of allogenic islet transplantation. Such studies are underway at this time.Indeed, AGEs, too may be found on aging lymphocytes
EXTRA DATA:-GLYCOBILOGY JOURNAL
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