Prospective insight into the role of benzyl propylene glycoside as a modulator of the cGAS-STING signaling pathway in the management of nonalcoholic fatty pancreas animal model

BACKGROUND: Nonalcoholic fatty pancreatitis (NAFP) is one of the metabolic syndrome manifestations that need further studies to determine its molecular determinants and find effective medications. We aimed to investigate the potential effect of benzyl propylene glycoside on NAFP management via targeting the pancreatic cGAS-STING pathway-related genes (DDX58, NFκB1 & CHUK) and their upstream regulator miRNA (miR-1976) that were retrieved from bioinformatics analysis. METHODS: The rats were fed either normal chow or a high-fat high-sucrose diet (HFHS), as a nutritional model for NAFP. After 8 weeks, the HFHS-fed rats were subdivided randomly into 4 groups; untreated HFHS group (NAFP model group) and three treated groups which received 3 doses of benzyl propylene glycoside (10, 20, and 30 mg/kg) daily for 4 weeks, parallel with HFHS feeding. RESULTS: The molecular analysis revealed that benzyl propylene glycoside could modulate the expression of the pancreatic cGAS-STING pathway-related through the downregulation of the expression of DDX58, NFκB1, and CHUK mRNAs and upregulation of miR-1976 expression. Moreover, the applied treatment reversed insulin resistance, inflammation, and fibrosis observed in the untreated NAFP group, as evidenced by improved lipid panel, decreased body weight and the serum level of lipase and amylase, reduced protein levels of NFκB1 and caspase-3 with a significant reduction in area % of collagen fibers in the pancreatic sections of treated animals. CONCLUSION: benzyl propylene glycoside showed a potential ability to attenuate NAFP development, inhibit pancreatic inflammation and fibrosis and reduce the pathological and metabolic disturbances monitored in the applied NAFP animal model. The detected effect was correlated with modulation of the expression of pancreatic (DDX58, NFκB1, and CHUK mRNAs and miR-1976) panel.

Aetiological factors of profound sensorineural deafness in Sudanese children

This is a preliminary study to determine the aetiological factors associated with profound sensorineural deafness in Sudanese children. Patients and A retrospective study of 264 Sudanese children suffering from profound sensorineural deafness with poor or no speech development. A detailed history questionnaire was obtained for all cases. General medical and local E.N.T. examination for all children was carried out by the authors. The audiometric investigations includcd play- free field and pure tone audiometry according to the child age. Haematological, biochemical and radiological investigations were performed where indicated. Ages ranged from 14 months to 14 years with a mean age of 5.5 years. The male to female ratio was 1.1:1.0. One hundred flinty eight cases were born as a result of consanguineous marriages and 120 cases had a positive family history of deafness. One hundred and fifty four children were exposed to quinine therapy. Fourteen children had received gentamicin therapy as neonates. Thirty children developed deafness following mumps. Eighteen children acquired deafness after meningococcal meningitis. Syndromic types of deafness accounted for 12 cases. The most common factors associated with the aetiology of profound sensori-neural deafness in Sudanese children were consanguinity, infectious diseases and ototoxic drugs. Measures such as genetic counseling, control of infectious diseases, vaccination, careful use and monitoring of ototoxic drugs should play an important role in the prevention and reduction of the incidence of profound sensorineural deafness in the community