Social well-being may be a major determinant of overall QOL for p

Social well-being may be a major determinant of overall QOL for patients with colon cancer. (C) 2011 Elsevier Ltd. All rights reserved.”
“Monocyte accumulation in renal allografts is associated with allograft dysfunction. As monocyte influx occurs acutely following reperfusion, we investigated the effect of ischemia-reperfusion injury (IRI) on monocyte colony stimulating factor (m-CSF), a key ACY-738 cost cytokine in monocyte recruitment. We hypothesized that renal tubule epithelial cells (RTECs) could produce m-CSF in response to IRI, which could in turn promote monocyte

activation. Real time PCR was used to measure levels of intragraft m-CSF transcripts in patients during IRI and clinical rejection. Also, m-CSF production by RTECs following IRI simulation in vitro was measured using ELISA. Monocyte STI571 expression of CD40 and CD80 was then analyzed using flow cytometry following co-culture with supernatants of RTECs after IRI. Monocyte expression of CD40, CD80 and HLA-DR was then examined following treatment with rh-m-CSF (10, 36, and 100 ng/ml), as was monocyte size and granularity. We found that intragraft m-CSF transcription was significantly increased postreperfusion (P = 0.002) and during clinical rejection (P = 0.002). We also found that RTECs produced m-CSF in response to IRI in vitro (P = 0.036). Monocytes co-cultured with the supernatants

of postischemic RTECs became activated as evidenced by increased expression of CD40 and CD80. Also, monocytes treated with recombinant m-CSF assumed an activated phenotype exhibiting increased size, granularity and expression of CD40, CD80, CD86, and HLA-DR, and demonstrating enhanced see more phagocytic activity. Taken together, we suggest that renal tubular cell derived m-CSF is a stimulus for monocyte activation and may be an important target for control of IRI-associated immune activation.”
“Objective: This study examined

the genetic association between variation in the cannabinoid receptor 1 (CNR1) gene and cannabis dependence symptoms.

Method: Adolescent and young adult subjects were recruited from three settings: a treatment program for youth with substance use disorders, the criminal justice system, and the community. A case-control sample consisted of 224 cases who endorsed at least one dependence symptom and 108 controls who tried cannabis but endorsed no symptoms. A family-based sample of 219 families was also analyzed.

Results: Case-control analysis identified a nominal association between SNP rs1049353 and having one or more cannabis dependence symptoms (p = .029), but the association did not hold up in a combined sample. Family-based analysis found a trend for the same SNP (p = .07). We did not replicate a previous report that SNP rs806380 was associated with the development or cannabis dependence.

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