In 5 out of 50 subjects from risperidone group (10%) and in 1 from olanzapine

group (2.6%) testosterone levels were below the tower limit (<241 ng/ml), which reflected Leydig’s cell impairment. In one patient receiving risperidone and in three receiving olanzapine, inhibin B level was below 80 pg/ml, indicating Sertoli’s cell dysfunction. At the final evaluation the mean serum prolactin level was markedly higher in patients taking risperidone, whereas their FSH levels were lower than in patients receiving olanzapine. In all investigated groups, except for the risperidone-hyperprolactinemic group inhibin B levels were negatively correlated with serum FSH. The mean LH, FSH, testosterone and estradiol levels were selleck chemicals llc within the normal reference range at initial and final evaluation. The non-adherence to medications and ASEX scores were significantly

higher in risperidone groups. Sexual dysfunction and medication non-adherence was not related OSI-027 molecular weight to protactin or gonadal hormone levels.

Conclusions: Risperidone elicited higher PRL elevation than olanzapine. Treatment with this gonadotropins (FSH). The cause of olanzapine-elicited reduction of inhibin B level and the tack of negative correlation between FSH and inhibin B in patients with risperidone-induced hyperprolactinemia require further investigation. Patients receiving risperidone showed higher level of sexual dysfunction and treatment non-adherence than those treated with olanzapine. (C) 2008 Elsevier Ltd. All rights reserved.”
“Objectives: This study tested the hypothesis that monocyte chemotactic protein 1 (MCP1) is required for abdominal aortic aneurysm(AAA) and smooth muscle phenotypic modulation in amouse elastase perfusion model.

Methods:

Infrarenal aortas of C57BL/6 (wild type [WT]) and MCP1 knockout (KO) mice were analyzed at 14 days after perfusion. Key cellular sources of MCP1 were identified using bone marrow transplantation. Cultured aortic smooth muscle cells find more (SMCs) were treated with MCP1 to assess its potential to directly regulate SMC contractile protein expression and matrix metalloproteinases (MMPs).

Results: Elastase perfused WT aortas had a mean dilation of 102% (n = 9) versus 53.7% for MCP1KO aortas (n = 9, P < .0001) and 56.3% for WT saline-perfused controls (n = 8). Cells positive for MMP9 and Mac-2 were nearly absent in the KO aortas. Complimentarily, the media of the KO vessels had abundant differentiated smooth muscle and intact elastic fibers and markedly less MMP2. Experiments in cultured SMCs showed MCP1 can directly repress smooth muscle markers and induce MMP2 and MMP9. Bone marrow transplantation studies showed that KO of MCP1 in bone marrow-derived cells protects from AAA formation. Moreover, KO in the bone was significantly more protective than global KO, suggesting an unexpected benefit to selectively depleting MCP1 in bone marrow-derived cells.