Based on comorbidities and healthcare resources used, patients with TRD appeared to represent a clinically complex subgroup of individuals with MDD. TRD was associated with significant cost burden.

Liver damage is a serious clinical complication of ␥-irradiation. We therefore exposed rats to singledose ␥-irradiation (25 Gy) that was focused on the liver. Three to six hours after irradiation, an increased number of neutrophils (but not mononuclear phagocytes) was observed by immunohistochemistry to be attached to portal vessels between and around the portal (myo)fibroblasts (smooth muscle actin and Thy-1 ؉ cells). MCP-1/CCL2 staining was also detected in the portal vessel walls , including some cells of the portal area. CC-chemokine (MCP-1/CCL2 and MCP-3/CCL7) and CXC-chemokine (KC/CXCL1, MIP-2/CXCL2, and LIX/CXCL5) gene expression was significantly induced in total RNA from irradiated livers. In laser capture microdissected samples, an early (1 to 3 hours) up-regulation of CCL2, CXCL1, CXCL8, and CXCR2 gene expression was detected in the portal area but not in the parenchyma; with the exception of CXCL1 gene expression. In addition, treatment with an antibody against MCP-1/CCL2 before irradiation led to an increase in gene expression of interferon-␥ and IP-10/CXCL10 in liver tissue without influencing the recruitment of granulocytes. Indeed, the CCL2, CXCL1, CXCL2, and CXCL5 genes were strongly expressed and further up-regulated in liver (myo)fibroblasts after irradiation (8 Gy). Taken together, these results suggest that ␥-irradiation of the liver induces a transient accumulation of granulocytes within the portal area and that (myo)fibroblasts of the portal vessels may be one of the major sources of the chemokines involved in neutrophil recruitment. Moreover, inhibition of more than one chemokine (eg, CXCL1 and CXCL8) may be necessary to reduce leukocytes recruitment.

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Investigations into the genetic basis of attention-deficit/hyperactivity disorder (ADHD) continue to yield compelling results as candidate gene studies reveal more information about this elusive disorder. Family, twin, and adoption studies further the notion that ADHD is a highly heritable disorder with direct genetic and environmental influence. The year 2005 saw many ADHD candidate gene studies, with most focused on the catecholaminergic candidates. Although many genes were studied in 2005, a large portion of findings has been supportive of the roles of dopaminergic genes' relationship to clinical phenotypes and drug response. These studies often require replication. Clinical implications continue to be speculative, as larger sample sizes are needed to validate findings to the general population. Further understanding of endophenotypes and the impact of comorbidities also is necessary for proper clinical intervention. Forthwith, we provide a summary of ADHD genetic studies published in 2005.

To describe a simplified method of malar fat pad elevation to rejuvenate the midface, nasolabial folds, labiomental folds, infraorbital hollows, and jowls via a percutaneous approach.Patients and Design: One hundred eighteen patients were evaluated over a 12-month period in a prospective fashion by the operating surgeon. Preoperative and postoperative photographs were used for comparison.Setting: Private practice.Main Outcome Measures: Elevation of the malar fat pad by a measured amount.Results: At 3 months, all patients had a significant elevation of the malar fat pad (3-7 mm), with the exception of 2 early patients who underwent revision surgery, with satisfactory results.Conclusions: A simplified method of malar fat pad elevation is described. This method allows for elevation of the malar fat pad without extensive dissection. Excellent results are obtained with very little morbidity.