An LIR motif in the Rift Valley fever virus NSs protein is critical for the interaction with LC3 family members and inhibition of autophagy.

Rift Valley fever virus (RVFV) is a viral zoonosis that causes severe disease in ruminants and humans. The nonstructural small (NSs) protein is the primary virulence factor of RVFV that suppresses the host's antiviral innate immune response. Bioinformatic analysis and AlphaFold structural modeling identified four putative LC3-interacting regions (LIR) motifs (NSs 1-4) in the RVFV NSs protein, which suggest that NSs interacts with the host LC3-family proteins. Using, isothermal titration calorimetry, X-ray crystallography, co-immunoprecipitation, and co-localization experiments, the C-terminal LIR motif (NSs4) was confirmed to interact with all six human LC3 proteins. Phenylalanine at position 261 (F261) within NSs4 was found to be critical for the interaction of NSs with LC3, retention of LC3 in the nucleus, as well as the inhibition of autophagy in RVFV infected cells. These results provide mechanistic insights into the ability of RVFV to overcome antiviral autophagy through the interaction of NSs with LC3 proteins.

Radical cystectomy: minimizing operative blood loss with a "stapling technique".

We describe our experience with a surgical technique using the multiple fire Endo-GIA-30-3.5 stapler to control the vascular pedicles during radical cystectomy. This technique was performed in 16 radical cystectomies, including three pelvic anterior exenterations for female invasive bladder carcinoma, and compared with 23 cases treated with the conventional method. It was associated with a significant decrease in the intraoperative and postoperative blood loss and a shorter operative time.

The role of selenium deficiency in dilated cardiomyopathy in Saudi Arabia.

BACKGROUND: Selenium deficiency is implicated in the etiology of endemic juvenile dilated cardiomyopathy in China, and in sporadic cases in other countries. The aim of this study was to evaluate the role of selenium deficiency in the pathophysiology of dilated cardiomyopathy in the Saudi Arabian population. PATIENTS AND METHODS: Plasma and urine selenium concentrations from 72 Saudi patients with confirmed dilated cardiomyopathy were compared with corresponding values from 70 control subjects of the same national origin who had normal ventricular function. RESULTS: Plasma and urine selenium concentrations (mean+/-SD) were 1.347plusmn;0.45 and 0.49+/-0.37 micromol/L, respectively, for the patient group, and 1.32+/-0.41 and 0.60+/-0.41 micromol/L, respectively, for the control group. The differences in the values between the two groups were statistically insignificant. CONCLUSION: In the Saudi population, dilated cardiomyopathy is not caused by selenium deficiency.