Effects of a DASH-like diet containing lean beef on vascular health.

A DASH (dietary approaches to stop hypertension) dietary pattern rich in fruits and vegetables and low-fat dairy products with increased dietary protein provided primarily from plant protein sources decreases blood pressure. No studies, however, have evaluated the effects of a DASH-like diet with increased dietary protein from lean beef on blood pressure and vascular health. The aim of this study was to study the effect of DASH-like diets that provided different amounts of protein from lean beef (DASH 28 g beef per day; beef in an optimal lean diet (BOLD) 113 g beef per day; beef in an optimal lean diet plus additional protein (BOLD+) 153 g beef per day) on blood pressure, endothelial function and vascular reactivity versus a healthy American diet (HAD). Using a randomized, crossover study design, 36 normotensive participants (systolic blood pressure (SBP), 116 ± 3.6 mm Hg) were fed four isocaloric diets,: HAD (33% total fat, 12% saturated fatty acids (SFA), 17% protein (PRO), 20 g beef per day), DASH (27% total fat, 6% SFA, 18% PRO, 28 g beef per day), BOLD (28% total fat, 6% SFA, 19% PRO, 113 g beef per day) and BOLD+ (28% total fat, 6% SFA, 27% PRO, 153 g beef per day), for 5 weeks. SBP decreased (P<0.05) in subjects on the BOLD+ diet (111.4 ± 1.9 mm Hg) versus HAD (115.7 ± 1.9). There were no significant effects of the DASH and BOLD diets on SBP. Augmentation index (AI) was significantly reduced in participants on the BOLD diet (-4.1%). There were no significant effects of the dietary treatments on diastolic blood pressure or endothelial function (as measured by peripheral arterial tonometry). A moderate protein DASH-like diet including lean beef decreased SBP in normotensive individuals. The inclusion of lean beef in a heart healthy diet also reduced peripheral vascular constriction.

Importance of hand germ contamination in health-care workers as possible carriers of nosocomial infections.

The importance of hands in the transmission of nosocomial infection has been world wide admitted. However, it is difficult to induce this behavior in health-care workers. The aim of the present work was to point out the importance of hand bacteria colonization, the influence of hand washing and of patient physical examination. One hundred health-care workers were randomly divided in two groups: Group A without hand washing previous to patient physical examination or handling (PPE); group B with hand washing previous to PPE. Direct fingerprint samples in Columbia agar before and after PPE were obtained. The colonies were counted and identified by conventional techniques, and antibiograms according to NCCLS were performed. Before PPE group A participants showed a high number of bacteria regarding group B participants (73.9 Vs 20.7; p < 0.001); 44 out of 50 participants were carriers of potentially pathogen bacteria. No group B participants were carriers of potential pathogen bacteria before PPE. The latter group showed an increase in number of bacteria after PPE (20.7 CFU (before) Vs 115.9 CFU (after); p < 0.001). Sixteen group B participants were contaminated after PPE with potential pathogens such as S. aureus (50% of them methicillin resistant); Escherichia coli, Pseudomonas aeruginosa and Enterococcus faecalis, half of them multiresistant. We can conclude on the importance of these results to implement educational programs and to provide the health-care workers with the proper commodities to fulfill this practice.

The t(12;21) translocation converts AML-1B from an activator to a repressor of transcription.

The t(12;21) translocation is present in up to 30% of childhood B-cell acute lymphoblastic and fuses a potential dimerization motif from the ets-related factor TEL to the N terminus of AML1. The t(12;21) translocation encodes a 93-kDa fusion protein that localizes to a high-salt- and detergent-resistant nuclear compartment. This protein binds the enhancer core motif, TGTGGT, and interacts with the AML-1-binding protein, core-binding factor beta. Although TEL/AML-1B retains the C-terminal domain of AML-1B that is required for transactivation of the T-cell receptor beta enhancer, it fails to activate transcription but rather inhibits the basal activity of this enhancer. TEL/AML-1B efficiently interferes with AML-1B dependent transactivation of the T-cell receptor beta enhancer, and coexpression of wild-type TEL does not reverse this inhibition. The N-terminal TEL helix-loop-helix domain is essential for TEL/AML-1B-mediated repression. Thus, the t(12;21) fusion protein dominantly interferes with AML-1B-dependent transcription, suggesting that the inhibition of expression of AML-1 genes is critical for B-cell leukemogenesis.