The personality construct of alexithymia refers to difficulties i

The personality construct of alexithymia refers to difficulties in emotional self-regulation and contributes as a risk factor to several mental disorders. Alexithymic individuals show an impoverished selleckchem conscious experience of emotions but an intact autonomic emotional response. Persons with high alexithymia scores reportedly show a reduced activation of the anterior cingulate cortex (ACC) during the processing of emotional stimuli. An interaction between two polymorphisms on the BDNF and DRD2/ANKK1 gene has been recently associated with reduced gray matter volume in the ACC and higher trait anxiety.

Methods: We conducted a genetic association study. A total of 664 healthy participants completed the Toronto Alexithymia Scale questionnaire and were genotyped for the BDNF Val66Met (rs6265) and the DRD2/ANKK1 Taq IA (rs1800497) polymorphisms. Results: Carriers of at least one BDNF 66Met and one DRD2/ANKK1 A1 allele

showed the highest scores in the total Toronto Alexithymia Scale and in the subscale “”Difficulties Identifying Feelings.”" Conclusion: In line with recent studies investigating the role of BDNF Val66Met and DRD2/ANKK1 Taq IA polymorphisms on anxiety and gray matter volume in the ACC, our findings provide the first evidence for a genetic contribution to alexithymia.”
“The glial cell-line derived neurotrophic factor (GDNF) is crucial for ureteric bud morphogenesis, spermatogenesis, and development of the enteric nervous system and is a potent Selleck Forskolin survival factor for various neuronal this website populations. However, the impact of GDNF, at least on cell survival, was found to depend strongly on the presence of transforming growth factor (TGF-). In this study, we investigate the role of TGF- in GDNF-induced neuronal differentiation. In a cell culture paradigm of N2aGT cells (neuroblastoma cell line), we show that TGF- signaling localizes the GDNF ligand-binding

receptor GFRa1 to the cell surface, which is a known mechanism by which TGF- is able to facilitate GDNF signaling. TGF–mediated GDNF signaling slightly elevated the phosphorylation state of Ret, the canonical coreceptor for the GPI-linked (glycosyl-phosphatidylinositol) GFRa1. On the basis of morphological as well as immunocytological data, we finally show that GDNF-mediated neuronal differentiation is intensified when GDNF and TGF- act in concert.”
“Bacterial meningitis kills or maims about a fifth of people with the disease. Early antibiotic treatment improves outcomes, but the effectiveness of widely available antibiotics is threatened by global emergence of multidrug-resistant bacteria. New antibiotics, such as fluoroquinolones, could have a role in these circumstances, but clinical data to support this notion are scarce.

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