Caspase-2 promotes obesity, the metabolic syndrome and nonalcoholic fatty liver disease.

Obesity and its resulting metabolic disturbances are major health threats. In response to energy surplus, overtaxed adipocytes release fatty acids and pro-inflammatory factors into the circulation, promoting organ fat accumulation (including nonalcoholic fatty liver disease), insulin resistance and the metabolic syndrome. Recently, caspase-2 was linked to lipoapoptosis, so we hypothesized that caspase-2 might be a critical determinant of metabolic syndrome pathogenesis. Caspase-2-deficient and wild-type mice were fed a Western diet (high-fat diet, enriched with saturated fatty acids and 0.2% cholesterol, supplemented with fructose and glucose in the drinking water) for 16 weeks. Metabolic and hepatic outcomes were evaluated. In vitro studies assessed the role of caspase-2 in adipose tissue proliferative properties and susceptibility for lipoapoptosis. Caspase-2-deficient mice fed a Western diet were protected from abdominal fat deposition, diabetes mellitus, dyslipidemia and hepatic steatosis. Adipose tissue in caspase-2-deficient mice was more proliferative, upregulated mitochondrial uncoupling proteins consistent with browning, and was resistant to cell hypertrophy and cell death. The liver was protected from steatohepatitis through a decrease in circulating fatty acids and more efficient hepatic fat metabolism, and from fibrosis as a consequence of reduced fibrogenic stimuli from fewer lipotoxic hepatocytes. Caspase-2 deficiency protected mice from diet-induced obesity, metabolic syndrome and nonalcoholic fatty liver disease. Further studies are necessary to assess caspase-2 as a therapeutic target for those conditions.

Prevention of deep vein thrombosis in aesthetic surgery patients.

Like other surgical patients, those undergoing elective aesthetic surgery are at risk for deep vein thrombosis. The author discusses ways to reduce this risk, such as limiting the number of procedures performed in the same operative session, using mechanical devices and pharmacologic agents, and doing careful postoperative assessment.

Patients with cutaneous lupus erythematosus who smoke are less responsive to antimalarial treatment.

BACKGROUND: Reports suggest that cigarette smoking might interfere with the effectiveness of antimalarial therapy as first-line treatment for cutaneous lupus erythematosus. Patients refractory to this treatment often must be treated with potentially more toxic regimens. OBJECTIVE: Our purpose was to examine the effects of cigarette smoking on the therapeutic response to antimalarial agents in patients with discoid lupus erythematosus (DLE) and subacute cutaneous lupus erythematosus (SCLE). METHODS: A total of 61 patients (47 DLE, 14 SCLE) were selected on the basis of the following criteria: (1) skin biopsy was consistent with cutaneous LE, (2) a smoking history was available, and (3) an adequate trial of antimalarial therapy was completed. Patients were classified as antimalarial responders or nonresponders on the basis of descriptions in their medical records. Two-by-two table analysis was performed comparing response rates in smokers versus nonsmokers. RESULTS: A significant difference (P<.0002) in the antimalarial response rate was observed for smokers (40%) versus nonsmokers (90%). CONCLUSION: These results indicate that patients with cutaneous LE who smoke are significantly less likely to respond to antimalarial therapy.

An assessment guide for community health nurses.

An assessment tool based on the Omaha Classification System broadens the focus of nursing diagnosis to encompass the cultural and sociological aspects of each area of patient assessment.