Burkholderia pseudomallei-absent soil bacterial community results in secondary metabolites that kill this pathogen.

Burkholderia pseudomallei is a Gram-negative bacterium found in soil and the causative agent of a severe disease in humans and animals known as melioidosis. It is intrinsically resistant to many antibiotics and has been reported resistant to the drugs of choice; ceftazidime. Microbial communities in soil in the presence and absence of B. pseudomallei were investigated using metagenomics approach. The variation in bacterial species diversity was significantly higher in soil samples without B. pseudomallei. Abundances of phyla Actinobacteria and Firmicutes were found significantly higher in B. pseudomallei-negative soils. Bacillus amyloliquefaciens KKU1 in phylum Firmicutes was discovered from negative soil and its secondary metabolites could inhibit clinical, environmental and drug resistant isolates of B. pseudomallei, together with some pathogenic Gram-negative but not Gram-positive bacteria. The antimicrobial activity from KKU 1 against B. pseudomallei was abolished when treated with proteinase K, stable in a wide range of pH and remained active after heating at 100 °C for 15 min. Precipitated proteins from KKU1 were demonstrated to cause lysis and corrugated surfaces of B. pseudomallei. The minimum inhibitory concentrations and minimum bactericidal concentrations of the precipitated proteins from KKU1 against B. pseudomallei were 0.97 μg/ml and 3.9 μg/ml. Interestingly, Native SDS-PAGE showed small active compounds of less than 6 kDa, along with other information collectively suggesting the properties of antimicrobial peptides. For the first time, culture-independent information in melioidosis endemic area could lead to a suspected source of metabolites that may help defense against B. pseudomallei and other pathogenic Gram-negative bacteria

Effect of Omega-3 Polyunsaturated Fatty Acid on the Prevention of Atrial Fibrillation after Off-Pump Coronary Artery Bypass Grafting

10.3329/uhj.v18i1.57878University Heart Journal18136-4

Admission Serum Uric Acid Levels and In-Hospital Outcomes in Patients with Acute Coronary Syndrome

Background: Uric acid is an independent risk factor for cardiovascular disease. Hospital admission for ischemic heart disease (IHD) is increasing rapidly in our country. Although studies were conducted abroad regarding association of serum uric acid with in-hospital outcomes in patients with acute coronary syndrome (ACS), no data is yet available to show the association in our country. Objective: The objective of this study was to assess the association of serum uric acid level on admission with in-hospital outcomes of the patients with ACS. Materials and Methods: This cross sectional comparative study was done in the Department of Cardiology, Dhaka Medical College Hospital (DMCH) from January to December 2012. After proper ethical consideration total 93 ACS patients were enrolled in the study by nonrandom sampling. Serum uric acid of all subjects was measured within 24 hours of admission. Then in-hospital outcomes were observed in all subjects. Results: The frequency of hyperuricemia among ACS patients was 24.7% (22.54% in male and 31.82% in female). Hyperuricemic patients significantly developed heart failure (30.4% vs 11.4%, p=0.032) and conduction defect (13.0% vs 1.4%, p=0.017) than normouricemic subjects. The mean ejection fraction was significantly lower in hyperuricemic patients than patients with normal uric acid level (50.87 ± 10.27% vs 55.94 ± 6.66%). The mean ± SD duration of hospital stay of hyperuricemic group was significantly longer in patients with ACS (8.26 ± 1.18 vs 7.51±1.18 days, p=0.010). Conclusion: The measurement of serum uric acid level, an easily available and inexpensive biochemical tool, might turn out as a valuable risk marker for prediction of in-hospital outcomes in patients with ACS

Gut microbiota signatures are associated with toxicity to combined CTLA-4 and PD-1 blockade

International audienceTreatment with combined immune checkpoint blockade (CICB) targeting CTLA-4 and PD-1 is associated with clinical benefit across tumor types, but also a high rate of immune-related adverse events. Insights into biomarkers and mechanisms of response and toxicity to CICB are needed. To address this, we profiled the blood, tumor and gut microbiome of 77 patients with advanced melanoma treated with CICB, with a high rate of any ≥grade 3 immune-related adverse events (49%) with parallel studies in pre-clinical models. Tumor-associated immune and genomic biomarkers of response to CICB were similar to those identified for ICB monotherapy, and toxicity from CICB was associated with a more diverse peripheral T-cell repertoire. Profiling of gut microbiota demonstrated a significantly higher abundance of Bacteroides intestinalis in patients with toxicity, with upregulation of mucosal IL-1β in patient samples of colitis and in pre-clinical models. Together, these data offer potential new therapeutic angles for targeting toxicity to CICB