Category Health/Medical

Researchers find Mechanism for precise Targeting of the Immune Response

A space-filling model of the solved protein complex responsible for the selection of antigens. Credit: AG Tampé

A space-filling model of the solved protein complex responsible for the selection of antigens. Credit: AG Tampé

The immune system checks the health of cells by examining a kind of molecular passport. Sometimes, cells present the wrong passport, which can lead to autoimmune diseases, chronic inflammations or cancer. Scientists of the Goethe University Frankfurt explain the process how this happens in the new issue of the journal Science.

Most cells provide the T cells of the adaptive immune system with information about their condition by presenting selected components of their interior (called antigens) on their surface. If these components include fragments of viruses or altered cell components, the affected cell is eliminated. The selection of the antigens is essential in this process...

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A Dietary Supplement Dampens the Brain Hyperexcitability seen in Seizures or Epilepsy

This is Lori McMahon and Luke Stewart. Credit: UAB

This is Lori McMahon and Luke Stewart. Credit: UAB

These results in animal models, represent a potentially novel therapeutic target for the treatment of seizure disorders. University of Alabama at Birmingham researchers have found that inducing a biochemical alteration in brain proteins via the dietary supplement glucosamine was able to rapidly dampen that pathological hyperexcitability in rat and mouse models. These results represent a potentially novel therapeutic target for the treatment of seizure disorders, and they show the need to better understand the physiology underlying these neural and brain circuit changes.

Proteins are the workhorses of living cells, and their activities are tightly and rapidly regulated in responses to changing conditions...

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Learning and Staying in Shape key to Longer Lifespan, study finds

Age-specific and sex-specific effects of the 4 GWS associations in LifeGen and the validated candidate loci. The four GWS and three suggestive replicated loci were analysed for age-specific and sex-specific effects on lifespan. a The variants at APOE and CHRNA3/5 exhibit sexually dimorphic effects on parental mortality, while all other variants exhibit more modest often non-significant sex-specific differences. b The effects of each gene on male and female lifespan were meta-analysed and studied in the cases that died aged between 40 and 75 or after 75. APOE exerts a much greater effect in the older age group, while most of the other genes exhibit the opposite effect. FOXO3 appears neutral, if not positive, in the earlier age group. c Effects on mortality were studied in both age groups for both sexes. APOE has the strongest effect on females aged 75+, CHRNA3/5 acts on males aged 40−75 and all other genes display more ambiguous trends

Age-specific and sex-specific effects of the 4 GWS associations in LifeGen and the validated candidate loci. The four GWS and three suggestive replicated loci were analysed for age-specific and sex-specific effects on lifespan. a The variants at APOE and CHRNA3/5 exhibit sexually dimorphic effects on parental mortality, while all other variants exhibit more modest often non-significant sex-specific differences. b The effects of each gene on male and female lifespan were meta-analysed and studied in the cases that died aged between 40 and 75 or after 75. APOE exerts a much greater effect in the older age group, while most of the other genes exhibit the opposite effect. FOXO3 appears neutral, if not positive, in the earlier age group...

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KLF-mediated lifespan extension is dependent on autophagy. Klf-3 transcript levels in wild-type animals subjected to 2 days of chronic dietary restriction (sDR, OP50 diluted to 108 cfu/ml) (a) or inhibition of TOR signaling by RNAi against let-363 (b) starting from day 1 of adulthood. All lines were raised and maintained at 20 °C. *P-value < 0.05 by Student’s T-test, N = 3 biological replicates. c qPCR analysis of a panel of autophagy-related genes in day 1 klf-3 o/e and loss of function of both klf-3 and klf-1 animals compared to wild type. Double loss of function of klf-3 and klf-1 was performed as described previously utilizing the klf-3(ok175) mutant and simultaneous RNAi feeding targeting klf-1. All lines were raised and maintained at 20 °C. *P-value < 0.05 by Student’s T-test, N = 3 biological replicates (d, representative picture). e Autophagy in klf-3 o/e animals as determined by numbers of GFP::LGG-1 punctae in seam cells (red arrow denotes GFP-positive puncta) with knockdown of bec-1 in both wild-type and klf-3 o/e animals. *P-value < 0.05, # P-value ≤ 0.1 after one-way analysis of variance followed by the Tukey’s post hoc test. N = 10–20 animals counted. (f, wild-type representative image, g, klf-3 o/e representative image) Electron microscopy images of klf-3 o/e and wild-type animals in animals aged 9 days. Arrowheads indicate sizeable (≥500 nm) autolysosomes as recognized by single-membrane limited vacuolar structures with visible mixed cytoplasmic contents. Full images reproduced in Supplementary Fig. 11, with additional images. h Lifespan analysis of wild-type and klf-3 o/e animals fed RNAi bacteria targeting bec-1 from day 1 of adulthood. All lines were raised and maintained at 20 °C. P-value < 0.05 by Mantel–Cox log-rank tests. See also Supplementary Table 6 for details of lifespan analyses and replicate experiments. All error bars represent standard error of the mean (SEM)

KLF-mediated lifespan extension is dependent on autophagy. Klf-3 transcript levels in wild-type animals subjected to 2 days of chronic dietary restriction (sDR, OP50 diluted to 108 cfu/ml) (a) or inhibition of TOR signaling by RNAi against let-363 (b) starting from day 1 of adulthood. All lines were raised and maintained at 20 °C. *P-value < 0.05 by Student’s T-test, N = 3 biological replicates. c qPCR analysis of a panel of autophagy-related genes in day 1 klf-3 o/e and loss of function of both klf-3 and klf-1 animals compared to wild type. Double loss of function of klf-3 and klf-1 was performed as described previously utilizing the klf-3(ok175) mutant and simultaneous RNAi feeding targeting klf-1. All lines were raised and maintained at 20 °C. *P-value < 0...

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