Synthesis, quantum chemical calculations, in silico and in vitro bioactivity of a sulfonamide-Schiff base derivative.

The sulfonamide Schiff base compound (E)-4-((4-(dimethylamino)benzylidene)amino)-N-(5-methylisoxazol-3-yl)benzenesulfonamide was successfully prepared and fully characterized. The foremost objective of this study was to explore the molecular geometry of the aforementioned compound and determine its drug likeness characteristics, docking ability as an insulysin inhibitor, anticancer and antioxidant activities. The molecular structure of this compound was optimized using the B3LYP/6-311G+(d,p) level of theory. The compound was completely characterized utilizing both experimental and DFT approaches. Molecular electrostatic potential, frontier molecular orbitals, Fukui function, drug likeness, and in silico molecular docking analyses of this compound were performed. Wave functional properties such as localized orbital locator, electron localization function and non-covalent interactions were also simulated. The compound was screened for anticancer and antioxidant activities using in vitro technique. The observed FT-IR, UV-Vis, and 1H NMR results compared with simulated data and both results were fairly consistent. The experimental and computational spectral findings confirm the formation of the Schiff base compound. Both π-π* and n-π* transitions were observed in both experimental and computational UV-Vis spectra. The examined compound followed to Pfizer, Golden Triangle, GSK, and Lipinski's rules. Consequently, it possesses a more favorable absorption, distribution, metabolism, excretion, and toxicity (ADMET) profile, making it a suitable candidate for non-toxic oral drug use. Moreover, the compound exhibited promising insulysin inhibition activity in an in silico molecular docking. The compound showed in vitro anticancer activity against A549 cancer cells with an IC50 value of 40.89 µg/mL and moderate antioxidant activity.

Lumpy skin disease outbreak in cattle population of Chattogram, Bangladesh.

BACKGROUND: Lumpy skin disease (LSD) is an important viral disease causing significant economic losses in commercial livestock production. In mid-2019, an outbreak of LSD has been reported in cattle population from different parts of Bangladesh including Chattogram division. A cross-sectional surveillance study was undertaken from August 2019 to December 2019 to investigate the prevalence and associated risk factors of LSD in cattle in Chattogram district. METHODS: A total of 3,327 cattle from 19 commercial farms were examined for the LSD specific skin lesions and associated risk factors. A total of 120 skin biopsies were collected from the suspected animal for the confirmation of the disease using molecular detection and histopathological examination. Partial genome sequencing and phylogenetic analyses were performed on selected viral isolates. RESULTS: The overall clinical prevalence of LSD in the study population was 10% (95% confidence interval [CI]: 9.4%-11%) where the highest farm level outbreak frequency was 63.33% (95% CI: 45.51%-78.13%) and the lowest 4.22% (95% CI: 3.39%-5.25%). Crossbred and female cattle showed a significantly higher prevalence of the disease compared to their counterparts. Introduction of new animals in farms was found to be one of the most significant risk factors in the transmission of the disease. All suspected skin biopsies were positive for LSD virus (LSDV) infection with granulomatous and pyogranulomatous dermatitis was revealed on histopathology. Phylogenetic analysis based on the inverted terminal repeat region of the LSDV gene suggested that the locally circulating strain was closely related to the strains isolated from the Middle East and North African countries. CONCLUSIONS: The data generated in this study would be beneficial to the field veterinarians and animal health decision makers in the country as well as it will aid in taking appropriate measures to prevent further relapse or outbreak of this disease in future.

Increased susceptibility to Mycobacterium tuberculosis infection in a diet-induced murine model of type 2 diabetes.

Tuberculosis (TB)-type 2 diabetes mellitus (T2D) comorbidity is re-emerging as a global public health problem. T2D is a major risk factor for increased susceptibility to TB infection and reactivation leading to higher morbidity and mortality. The pathophysiological mechanisms of T2D contributing to TB susceptibility are not fully understood, but likely involve dysregulated immune responses. In this study, a diet-induced murine model that reflects the cardinal features of human T2D was used to assess the immune responses following an intravenous Mycobacterium tuberculosis (Mtb) infection. In this study, T2D significantly increased mortality, organ bacillary burden and inflammatory lesions compared to non-diabetic controls. Organ-specific pro-inflammatory cytokine responses were dysregulated as early as one day post-infection in T2D mice. Macrophages derived from T2D mice showed reduced bacterial internalization and killing capacity. An early impairment of antimycobacterial functions of macrophages in diabetes is a key mechanism that leads to increased susceptibility of T2D.