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A new mechanism for extending lifespan by “diet restrictions”

Posted by star on 2019-04-17 19:10:33
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    Dietary restriction (DR), the reduction in food intake without causing malnutrition, is an effective way to promote longevity in a wide range of species. Similar to many other mediators of longevity, DR not only extends an organism’s lifespan but also decreases the incidence of age-related diseases and promotes health span as well. However, the relevant regulatory mechanisms are still unclear.
    The Chinese researcher revealed the temporal regulation of microRNAs in the reproductive signal-mediated longevity model. MicroRNAs are a class of small-molecule non-coding RNAs that regulate gene expression primarily through base pairing and play an important role in many biological processes.
    The latest research shows that DR does not open the mir-235 molecular switch during the development of the nematode. In the adult stage, the “diet restriction” quickly turns on the mir-235 molecular switch and inhibits cwn-1/WNT4, thereby increasing the level of autophagy and prolonging the lifespan of nematodes.
    The study first showed that signaling pathways are important in life regulation and in further understanding of aging. Secondly, this time-series regulation prolongs lifespan while ensuring normal development, revealing a subtle regulation of the body. And it suggests that the same intervention produces different effects at different developmental stages or ages of the animal. It has important guiding significance for anti-aging research.



Exercise-Induced Activated Platelets Promote Neuronal Differentiation

Posted by star on 2019-04-16 23:25:11
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    When we exercise, the stem cells in the hippocampus divide and transform into new neurons, which improves memory. But it’s not clear why stem cells begin to divide and form new neurons after exercise. In other words, how does exercise change our brains?
    Researchers from University of Queensland and Dresden University of Technology identified the causes of brain function enhancement triggered by exercise.
    The study showed that many of the changes in the blood after exercise were related to platelets. Platelets cause neural stem cells to multiply and develop into neurons, and other types of cells are formed. Platelets are activated after acute periods of running, and that activated platelets promote neurogenesis, an effect that may be mediated by platelet factor 4. EX vivo, the beneficial effects of activated platelets and platelet factor 4 on neural precursor cells were dentate gyrus specific and not observed in the subventricular zone.
    Furthermore, the consumption of circulating platelets in mice eliminates the increase in precursor cell proliferation in the dentate gyrus following exercise. These findings suggest that platelets and their released factors can modulate adult neural precursor cells under physiological conditions and provide an interesting link between exercise-induced platelet activation and post-exercise regulation of neurogenesis.



Healthy infant intestinal bacteria protect against food allergy

Posted by star on 2019-04-15 22:56:59
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    Life-threatening food allergies strikingly increase around the world especially in Westernized societies. One hypothesis to explain this rising prevalence is that lifestyle practices in the twenty-first century, including misuse of antibiotics, dietary changes, and higher rates of Caesarean birth and formula feeding have altered intestinal bacterial communities; early-life alterations may be particularly detrimental.
    Latest study found that intestinal bacteria are critical for regulating allergic responses to dietary antigens and suggest that interventions that modulate bacterial communities may be therapeutically relevant for food allergy.
    The researchers in the United States colonized germ-free mice with feces from healthy or cow's milk allergic (CMA) infants. They found that germ-free mice colonized with bacteria from healthy, but not CMA, infants were protected against anaphylactic responses to a cow's milk allergen. Differences in bacterial composition separated the healthy and CMA populations in both the human donors and the colonized mice. Healthy and CMA colonized mice also exhibited unique transcriptome signatures in the ileal epithelium. Correlation of ileal bacteria with genes upregulated in the ileum of healthy or CMA colonized mice identified a clostridial species, Anaerostipes caccae, which protected against an allergic response to food.



Peptidyl transferase activity resides in the 23S rRNA

Posted by star on 2019-04-15 01:46:56
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    Once the aminoacyl-tRNA is bound to the A-site, the ribosome is ready for peptide bond formation, which is catalyzed by the peptidyl transferase activity of the 50S ribosomal subunit. This reaction begins with the nucleophilic attack of the amino group of the A-site tRNA on the partially positively charged carbonyl carbon atom in the ester bond that links the peptidyl (or fMet) group. To the P-site tRNA. The resulting tetrahedral transition state rearranges to produce an uncharged tRNA at the P-site and. apeptidyl-tRNA at the A-site with one more amino acid than the original peptidyl-tRNA.
    The initial method for assaying peptidyl transferase activity required an intact ribosome, mRNA, a P-site peptidyl-RNA and an A-site aminoacyl-tRNA, making it difficult to determine whether peptidyl transferase or some other factor required for peptide bond formation was being monitored. A more direct assay for peptidyl transferase activity was required. The antibiotic puromycin, which is produced by the gram-positive bacteria Streptomyces alboniger, helped to solve the problem. Puromycin is remarkably similar in structure to the tyrosyladenosine group at the 3’-end of Tyr-tRAN. Because of this close resemblance, peptidyl transferase can use puromycin as a substrate in place of aminoacyl-tRNA at the A-site. As a consequence of this relaxed substrate recognition, the peptidyl transferase transfers a peptidyl group from a peptidyl-tRNA at the P-site to puromycin, causing premature polypeptide chain termination and peptidyl-puromycin release. Thus puromycin can serve as a model substrate for the peptide bond-forming reaction and is well-suited for the study of this reaction.
    In the mid-1960s, Robin Monro and coworkers used their knowledge of puromycin’s mechanism of action to devise a direct method to measure peptidyl transferase activity, called the fragment assay. This assay measures fMet-puromycin fo......

Glucocorticoids promote breast cancer metastasis

Posted by star on 2019-04-14 23:26:57
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    Metastasis is the fatal hallmark of cancer. Diversity within or between tumours and metastases that develops during disease progression is a serious hurdle for therapy. So it is crucial for the success of personalized cancer therapy to understand the cellular and molecular processes that underlie both intra-patient tumour heterogeneity and metastasis.
    Researchers in Switzerland used transcriptional profiling of tumours and matched metastases in patient-derived xenograft models in mice, the result showed cancer-site-specific phenotypes and increased glucocorticoid receptor activity in distant metastases. The glucocorticoid receptor mediates the effects of stress hormones, and of synthetic derivatives of these hormones that are used widely in the clinic as anti-inflammatory and immunosuppressive agents. The study shows that the increase in stress hormones during breast cancer progression results in the activation of the glucocorticoid receptor at distant metastatic sites, increased colonization and reduced survival.
    Proteomics and phospho-proteomics studies implicate the glucocorticoid receptor in the activation of multiple processes in metastasis and in the increased expression of kinase ROR1, both of which correlate with reduced survival. The ablation of ROR1 reduced metastatic outgrowth and prolonged survival in preclinical models.
    Results indicate that the activation of the glucocorticoid receptor increases heterogeneity and metastasis, which suggests that caution, is needed when using glucocorticoids to treat patients with breast cancer who have developed cancer-related complications.



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