3 +/- 9.5 years, 72.8% male). None were taking a beta-blocker at presentation, but all had started by 4 LOXO-101 purchase months’ follow-up. The patients were reweighed after 1 year. There was an increase in weight (0.9 +/- 7.0 kg; P = .03) and

body mass index (0.2 +/- 2.4 kg/m(2); P = .02). Patients in New York Heart Association (NYHA) functional class III or IV had no significant weight change, whereas those in class I or II had an increase of 1.62 kg (P < .0001). In patients who had no peripheral edema at baseline or I year, there was a greater increase in weight (1.3 +/- 6.9 kg; P = .01).

Conclusions: Beta-blocker use and intensification of heart failure treatment is associated with weight gain in CHF. The increase is greater in those who are nonedematous and tends to occur in patients with NYHA functional class I and II symptoms. (J Cardiac Fail 2012;18:233-237)”
“In AZD8186 mouse vitro experiments confirmed that a 10-mer peptide derived from human mammary-associated serum amyloid A3 (M-SAA3) protected intestinal epithelial cells from enteropathogenic

Escherichia coli (EPEC) adherence. The entire 42-mer human M-SAA3 protein was even more effective, reducing EPEC binding by 72% relative to untreated cells (P < 0.05), compared with 25% and 57% reductions for the human 10-mer and Lactobacillus GG, respectively. However, none of the M-SAA3 peptides reduced Salmonella invasion in vitro (P > 0.05). Each of the M-SAA3 10-mer peptides and the 42-mer was then administered orally to mice at 500 mu g day(-1) for 4 days before deliberate infection with either Citrobacter rodentium (mouse model of EPEC) or Salmonella Typhimurium. None of the peptides protected against Salmonella infection and the 42-mer may even increase infection, as

there was a trend VX-680 towards increased Salmonella counts in the liver and small intestine in 42-mer-treated mice compared with those in sodium acetate-treated control mice. Citrobacter counts were reduced in the caecum of mice administered the 42-mer relative to a scrambled 10-mer (P < 0.05), but not compared with the sodium acetate control and no reductions were observed in the faeces or colon. Overall, although promising anti-infective activity was demonstrated in vitro, neither the 42-mer M-SAA3 protein nor a 10-mer peptide derivative prevented enteric infection in the animal models tested.”
“Background: The goal of the present study was the characterization of Plasmodium falciparum genes associated to malaria drug resistance (pfcrt, pfdhfr and pfdhps), in samples from two Brazilian localities.

Methods: Parasites from 65 P. falciparum samples were genotyped using nested-PCR and direct DNA sequencing.

Results: Six resistant sulphadoxine-pyrimethamine (SP) pfdhfr genotypes and one haplotype associated to SP sensitivity were detected.