In total, 11 patients were included in the study. Seven patients completed benzodiazepine withdrawal.

We found that BDNF plasma levels were significantly selleck chemical increased in the benzodiazepine-dependent patients (p = 0.011) compared to a healthy control group (14 age- and sex-matched persons) and decreased significantly (p = 0.029) due to benzodiazepine withdrawal, whereas GDNF plasma levels did not differ (p = 0.886) and change (p = 0.180)

significantly.

In conclusion, we assume that benzodiazepines may partly act by similar neurobiological mechanisms like antidepressant medication, which may explain the high frequency of benzodiazepine dependence in affective disorders.”
“Background and purpose: Previous imaging studies have described gray and white matter alterations in the cerebellum, the posterior aspects of the visual system and in the corpus callosum in patients with schizophrenia.

Here, we investigated these regions in more detail using tract-based spatial statistics (TBSS). Additionally, we evaluated potential changes in lateralization of the optic radiation

and the superior cerebellar peduncle.

Material and methods: We studied 12 patients with first-admission schizophrenia and a group of age-matched healthy controls. The diffusion tensor imaging data were preprocessed using tract-based spatial statistics and the obtained white matter skeleton was used to perform a regional analysis of fractional anisotropy in the corpus callosum, the optic radiation, and the SB202190 research buy superior and middle cerebellar peduncles.

Results:

Using TBSS, a significant reduction of fractional anisotropy in the whole corpus callosum and the optic radiation but not in the middle and superior cerebellar peduncles was found. Furthermore, a significantly decreased lateralization of the optic radiation and the superior cerebellar peduncles in patients was observed.

Conclusion: Our findings substantiate the concept that schizophrenia is a neurodevelopmental disorder and indicate that changes in lateralization may play a key role in the pathogenesis of this disease. (c) 2013 Elsevier Ireland Ltd. All rights reserved.”
“To test the hypothesis that metformin protects against fructose-induced FAD steatosis, and if so, to elucidate underlying mechanisms, C57BL/6J mice were either fed 30% fructose solution or plain water for 8 weeks. Some of the animals were concomitantly treated with metformin (300 mg/kg body weight/day) in the drinking solution. While chronic consumption of 30% fructose solution caused a significant increase in hepatic triglyceride accumulation and plasma alanine-aminotransferase levels, this effect of fructose was markedly attenuated in fructose-fed mice concomitantly treatment with metformin.