Age-related decline in skeletal muscle mass and function among elderly men and women in Shanghai, China: a cross sectional study.

OBJECTIVE: To investigate the relationship of muscle mass and muscle function with age. METHODS AND STUDY DESIGN: The study including 415 participants (aged 60-99 years). Upper (UMM) and lower (LMM) limbs muscle mass and whole body fat free mass (FFM) were measured by bioelectrical impedance analysis. The appendicular skeletal muscle mass (ASM) index (ASM/height2) was calculated. Muscle function was assessed by measuring hand grip strength (HGS) and gait speed. RESULTS: Using ASM index cutoff values we found that higher prevalence of sarcopenia in women than in men (33.5% vs 23.6%, p=0.025). In the upper limb, HGS (ß=-0.809) declined more rapidly with age than did UMM (ß=-0.592) in men, but not in women (ß=-0.389 and ß=-0.486 respectively). In the lower limb, gait speed declined more rapidly than LMM in both men (ß=-0.683 vs ß=-0.442) and women (ß=-1.00 vs ß=-0.461). The variance of UMM explained 28-29% of the variance of HGS, and LMM explained 7-8% of the variance of gait speed in women and men respectively. In addition to the common predictors (BMI and age), the specific predictors were smoking, exercise and education for FFM and ASM, and smoking, drinking and exercise for HGS (p<0.05). CONCLUSIONS: Loss of muscle function is greater than the decline of muscle mass particularly in the upper limbs in men. However, women are more prone to have low muscle mass than the men. Exercise programs need to be designed gender specifically.

[The relationship between the polymorphism of immunity genes and both aging and age-related diseases].

Aging is acommon, progressive and irreversible state of multi-cell dysfunction. Immune aging mainly includes the declines of regenerative capacity and lymphoid lineage differentiation potential, the hyporesponsive to infection and vaccination, the hyperresponsive in the context of inflammatory pathology, and the increased risk of autoimmunity. The dysfunction of aged immune system accelerates the occurrence of aging and age-related diseases. The mutation of immunity genes that affect immune responses accelerates or slows aging process and age-related diseases. The frequencies of acquired immunity genes, such as immune protective HLA II DRB1*11 and DRB*16-associated haplotype, are increased in the longevity populations. The increased susceptibility of immune inflammatory response, morbidity and mortality in the elderly is often associated with decreased frequencies of anti-inflammatory factor IL-10 -1082G allele, TNF-ß1 haplotype cnd10T/C, cnd25G/G, -988C/C, -800G/A, low proinflammatory fator TNFa level related extended TNF-A genotype -1031C/C, -863C/A, -857C/C, IL-6-174 CC and IFN-γ+874 T allele as well. The innate immunity genes, such as highly expressed anti-inflammatory +896 G KIR4 allele, CCR5Δ32 variant, -765 C Cox-2 allele, -1708 G and 21 C 5-Lox alleles are detected in centenarians. In age-related diseases, a higher CMV-specific IgG antibody level in elderly individuals is associated with a decreased frequency of KIR haplotypes KIR2DS5 and A1B10 and an increased frequency of MBL2 haplotypes LYPB, LYQC and HYPD that result in the absence of MBL2 protein. The increased frequencies of CRP ATG haplotypes and CFH 402 His allele indicate high mortality in the elderly. In the present study, we review the advances in the polymorphism and haplotype of innate and adoptive immunity genes, and their association with both aging and age-related diseases. To strengthen the analysis of extended haplotypes, epigenetic studies of immunity genes and genetic study of hematopoietic stem cell senescence will be helpful to understand the accurate basis of aging-related immune genetics better.

[Oxi-inflamm-aging and its association with the polymorphism of ApoE genes].

The lifelong exposure of antigens and stressors results in chronic oxidative stress situation in the organism. The free radicals and reactive oxygen species (ROS) with high reactivity produced by our cells under oxidative stress will cause oxidative damage in biomolecules. The oxidative damage leads to the releases of both damage-associated-molecular patterns (DAMPs) and intracellular cytokines. DAMPs activate pathogen recognition receptors (PRRs) and non-PRRs. Intracellular cytokines activate signalling pathways downstream of PRRs. Activation of these receptors results in the upregulation of cytokines and chemokines, which are released to recruit and activate additional inflammatory cells and cause the systemic and chronic sterile inflammation. The regulatory system, especially immune systems play an important role in homeostasis maintenance in the organism. The cells of immune systems are very vulnerable to oxidative damage. Once the homeostasis is destroyed, an imbalance between inflammatory and anti-inflammatory networks will occur. Genetic factor also is an important factor of oxi-inflamm-aging and age-related diseases. Many genes are involved in oxidative stress, inflammation process, and the genomic variations within most of these genes might produce different effects on oxi-inflamm-aging. The polymorphism of ApoE genes can affect the antioxidant and immunomodulatory/anti-inflammatory properties of the organism. ApoE genotype-phenotype is associated with the progress and prognosis of oxi-inflamm-aging, age-related diseases as well. Anti-inflammation together with regulation of the expression of ApoE might be an efficient method against oxi-inflamm-aging. Based on our previous studies, the progresses in these areas are reviewed.

[Aging and aging intervention by coloric restriction in nonhuman primate rhesus monkeys].

Nonhuman primate rhesus monkey is a ideal model for human aging and aging intervention. Same with human aging, rehesus monkey demonstrates age-related aging and diseases in endocrine, neural, immune and cardiovascular system. Coloric restriction can slow down the primary and secondry aging efficently. The mechanism may be to suppress the oxidative stress-inflammaging-DNA damage by mediating the nutrient sensitive metablic signal pathways, and activate damaged DNA repair. However, the differeces of study design, husbandry and diet composition may differently affect CR against the the primary and secondry effects in a long-lived nonhuman primate. Optimization in protocol design, control of the experimetal variables, and shortening the experimental period will be advantageous to understand the mechanistic questions about the anti-aging effects of CR.

A meta-analysis of core stability exercise versus general exercise for chronic low back pain.

OBJECTIVE: To review the effects of core stability exercise or general exercise for patients with chronic low back pain (LBP). SUMMARY OF BACKGROUND DATA: Exercise therapy appears to be effective at decreasing pain and improving function for patients with chronic LBP in practice guidelines. Core stability exercise is becoming increasingly popular for LBP. However, it is currently unknown whether core stability exercise produces more beneficial effects than general exercise in patients with chronic LBP. METHODS: Published articles from 1970 to October 2011 were identified using electronic searches. For this meta-analysis, two reviewers independently selected relevant randomized controlled trials (RCTs) investigating core stability exercise versus general exercise for the treatment of patients with chronic LBP. Data were extracted independently by the same two individuals who selected the studies. RESULTS: From the 28 potentially relevant trials, a total of 5 trials involving 414 participants were included in the current analysis. The pooling revealed that core stability exercise was better than general exercise for reducing pain [mean difference (-1.29); 95% confidence interval (-2.47, -0.11); P = 0.003] and disability [mean difference (-7.14); 95% confidence interval (-11.64, -2.65); P = 0.002] at the time of the short-term follow-up. However, no significant differences were observed between core stability exercise and general exercise in reducing pain at 6 months [mean difference (-0.50); 95% confidence interval (-1.36, 0.36); P = 0.26] and 12 months [mean difference (-0.32); 95% confidence interval (-0.87, 0.23); P = 0.25]. CONCLUSIONS: Compared to general exercise, core stability exercise is more effective in decreasing pain and may improve physical function in patients with chronic LBP in the short term. However, no significant long-term differences in pain severity were observed between patients who engaged in core stability exercise versus those who engaged in general exercise. SYSTEMATIC REVIEW REGISTRATION: http://www.crd.york.ac.uk/PROSPERO PROSPERO registration number: CRD42011001717.

Hyperlipidemic versus healthy pancreases: a proteomic analysis using an animal model.

Hyperlipidemia is associated with a variety of pancreatic diseases; however, the underlying pathophysiology and molecular mechanisms remain undefined. Here, we performed a comparative proteomic analysis of pancreatic tissue obtained from hyperlipidemic rats to identify proteins that may be involved in mediating hyperlipidemia-associated pancreatic injury. Rats were fed a high-fat diet to induce hyperlipidemia. Control rats were fed a diet with normal fat content. Pancreatic tissue samples were obtained after 6 or 12 weeks and comparative proteomic analysis, using gel electrophoresis and mass spectrometry, was conducted to identify proteins, the expression of which were altered in pancreases from hyperlipidemic compared with control rat pancreases. The expression levels of 3 of 13 proteins were significantly altered in pancreatic samples from hyperlipidemic rats. Alpha-amylase and arginase II were dysregulated by more than twofold. These modulations persisted in pancreatic tissue obtained from late-stage hyperlipidemic rats. The levels of alpha-amylase and arginase II were significantly altered in pancreases obtained from rats with hyperlipidemia. These enzymes may be putative biomarkers of hyperlipidemia-mediated pancreatic injury.