Optimal glycemic control is associated with a lower rate of target vessel revascularization in treated type II diabetic patients undergoing elective percutaneous coronary intervention

OBJECTIVES: We examined the association between glycemic control determined by preprocedural hemoglobin A1c (A1c) and the incidence of target vessel revascularization (TVR) in diabetic patients undergoing elective percutaneous coronary intervention (PCI). BACKGROUND: Patients with diabetes mellitus (DM) have increased rates of restenosis and a worse clinical outcome after PCI than patients without DM. METHODS: A total of 239 patients (60 without DM and 179 with DM) were enrolled in this study. Optimal glycemic control was defined as A1c < or =7%, and suboptimal control was defined as A1c >7%. Follow-up was performed at six and 12 months after the index intervention. RESULTS: Diabetic patients with optimal glycemic control had a rate of 12-month TVR similar to that of nondiabetic patients (15% vs. 18%, p = NS). Diabetic patients with A1c >7% had a significantly higher rate of TVR than those with A1c <7% (34% vs. 15%, p = 0.02). In a multiple logistic regression analysis, A1c >7% was a significant independent predictor of TVR (odds ratio 2.87, 95% confidence interval 1.13 to 7.24; p = 0.03). Optimal glycemic control was associated with a lower rate of cardiac rehospitalization (15% vs. 31%, p = 0.03) and recurrent angina (13% vs. 37%, p = 0.002) at 12-month follow-up. CONCLUSIONS: In diabetic patients undergoing elective PCI, optimal glycemic control (A1c < or =7%) is associated with a lower rate of TVR, cardiac rehospitalization, and recurrent angina. These data suggest that aggressive treatment of DM to achieve A1c < or =7% is beneficial in improving the clinical outcome after PCI.     

Developmental origins of murine γδ T-cell subsets

Murine γδ T cells display diverse responses to pathogens and tumours through early provision of pro-inflammatory cytokines such as interleukin-17A (IL-17) and interferon-γ (IFN-γ). Although it is now clear that acquisition of these cytokine-secreting effector fates is to a great extent developmentally pre-programmed in the thymus, the stages through which γδ progenitor cells transition, and the underlying mechanistic processes that govern these commitment events, are still largely unclear. Here, we review recent progress in the field, with particular consideration of how TCR-γδ signalling impacts on developmental programmes initiated before TCR-γδ expression.     

Cutaneous immunosurveillance by self-renewing dermal gammadelta T cells

The presence of γδ T cell receptor (TCR)-expressing cells in the epidermis of mice, termed dendritic epidermal T cells (DETCs), is well established. Because of their strict epidermal localization, it is likely that DETCs primarily respond to epithelial stress, such as infections or the presence of transformed cells, whereas they may not participate directly in dermal immune responses. In this study, we describe a prominent population of resident dermal γδ T cells, which differ from DETCs in TCR usage, phenotype, and migratory behavior. Dermal γδ T cells are radioresistant, cycle in situ, and are partially depend on interleukin (IL)-7, but not IL-15, for their development and survival. During mycobacterial infection, dermal γδ T cells are the predominant dermal cells that produce IL-17. Absence of dermal γδ T cells is associated with decreased expansion in skin draining lymph nodes of CD4(+) T cells specific for an immunodominant Mycobacterium tuberculosis epitope. Decreased CD4(+) T cell expansion is related to a reduction in neutrophil recruitment to the skin and decreased BCG shuttling to draining lymph nodes. Thus, dermal γδ T cells are an important part of the resident cutaneous immunosurveillance program. Our data demonstrate functional specialization of T cells in distinct microcompartments of the skin.     

A complex phenotype of peripheral neuropathy, myopathy, hoarseness, and hearing loss is linked to an autosomal dominant mutation in MYH14

Both peripheral neuropathy and distal myopathy are well-established inherited neuromuscular disorders characterized by progressive weakness and atrophy of the distal limb muscles. A complex phenotype of peripheral neuropathy, myopathy, hoarseness, and hearing loss was diagnosed in a large autosomal dominant Korean family. A high density single nucleotide polymorphism (SNP)-based linkage study mapped the underlying gene to a region on chromosome 19q13.3. The maximum multipoint LOD score was 3.794. Sequencing of 34 positional candidate genes in the segregating haplotype revealed a novel c.2822G>T (p.Arg941Leu) mutation in the gene MYH14, which encodes the nonmuscle myosin heavy chain 14. Clinically we observed a sequential pattern of the onset of muscle weakness starting from the anterior to the posterior leg muscle compartments followed by involvement of intrinsic hand and proximal muscles. The hearing loss and hoarseness followed the onset of distal muscle weakness. Histopathologic and electrodiagnostic studies revealed both chronic neuropathic and myopathic features in the affected patients. Although mutations in MYH14 have been shown to cause nonsyndromic autosomal dominant hearing loss (DFNA4), the peripheral neuropathy, myopathy, and hoarseness have not been associated with MYH14. Therefore, we suggest that the identified mutation in MYH14 significantly expands the phenotypic spectrum of this gene.     

Mass flea outbreak at a child care facility: case report.

Cat fleas, Ctenocephalides felis Bouchet, were collected at a Mississippi child care facility after reports of large numbers of adult fleas occurring on children and personnel. One building yielded 161 (99 percent) of the fleas collected. Urticarial lesions due to flea bites occurred on the legs of six children. Flea presence was due to cats occupying the crawl space. Fleas were eradicated by eliminating entry of cats and using residual insecticides throughout the facility.     

Quantitative real-time PCR identifies a critical region of deletion on 22q13 related to prognosis in oral cancer

Quantitative real time PCR was performed on genomic DNA from 40 primary oral carcinomas and the normal adjacent tissues. The target genes ECGFB, DIA1, BIK, and PDGFB and the microsatellite markers D22S274 and D22S277, mapped on 22q13, were selected according to our previous loss of heterozygosity findings in head and neck tumors. Quantitative PCR relies on the comparison of the amount of product generated from a target gene and that generated from a disomic reference gene (GAPDH-housekeeping gene). Reactions have been performed with normal control in triplicates, using the 7700 Sequence Detection System (PE Applied Biosystems). Losses in the sequences D22S274 (22q13.31) and in the DIA1 (22q13.2-13.31) gene were detected in 10 out of 40 cases (25%) each. Statistically significant correlations were observed for patients with relative copy number loss of the marker D22S274 and stages T3-T4 of disease (P=0.025), family history of cancer (P=0.001), and death (P=0.021). Relative copy number loss involving the DIA1 gene was correlated to family history of cancer (P<0.001), death (P=0.002), and consumption of alcohol (P=0.026). Log-rank test revealed a significant decrease in survival (P=0.0018) for patients with DIA1 gene loss. Relative copy number losses detected in these sequences may be related to disease progression and a worse prognosis in patients with oral cancer.