Background: Acetaminophen (N-acetyl-para-aminophenol, or APAP) poisoning, whether intentional or accidental, is a major general health problem, with its toxicity prevalence significantly increasing in many countries. Currently, acetaminophen is considered one of the main causes of acute liver failure globally.

Aim: The aim of this study was to evaluate the possible hepatoprotective effect of Omega-3,6,9 against acetaminophen-induced hepatotoxicity in albino male mice.

Methods: Thirty-five albino male mice were randomly divided into five groups: Group 1 (the negative control) received liquid paraffin orally at a dose of 10 ml/kg for t

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A many risk challenge in (settings hospital) are multi- bacteria are antibiotic-resistant. Some type strains that ability adhesion surface-attached bio-film census. Fifteen MRSA isolates were considered as high biofilm producers Moreover all MRSA isolates; M3, M5, M7 and M11 produced biofilms but the thickest biofilm seen M7strain. The MIC values of N. sativa oil against clinical isolates of MRSA were between (0.25, 0.5, 0.75, 1.0) μg/ml While MRSAcin (50, 75, 100, 125) µg\ ml. All biofilms treated with MRSAcin and Nigella sativa developed a presence of live cells after cultured on plate agar with inhibition zone between MIC (18 – 15) and (14- 11)mm respectively.Yet, results showed that MRSA supernatant developed a inhibitory ef

The rapid spread of the COVID-19 coronavirus in 2019 infected many people, primarily affecting the respiratory system. Both COVID-19 and type 2 diabetes have been associated with numerous risks that have become life-threatening. The study studied the link between galectin levels and some clinical characteristics in Iraqis with type 2 diabetes and COVID-19 against those without diabetes. The study included 120 patients and healthy men. Three groups were formed for this study depending on the initial mutant cell line: 80 samples of individuals with type 2 diabetes, aged 40–60 years, with and without COVID-19, were included in each of the first and second groups. The control group consisted of 40 research participants who were matched for ag

Irinotecan induced-mucositis is an inflammatory event of intestine caused by an increase in concentration of active metabolite 7­ethyl­10-hydroxycamptothecin (SN­38) in the intestine. Irinotecan must first be converted by a carboxylesterase (CES) to the active metabolite (SN­38), which is subsequently glucuronidated by the hepatic enzyme to SN38G. The SN-38G is deconjugated in the intestine to SN-38 via ?-glucuronidase produced by the intestinal bacterial flora, which accounts for SN-38 delayed intestinal mucositis of irinotecan. To study the protective effect of mentha in irinotecan-induced mucositis, intestinal mucositis induced by I.P injection of irinotecan (75mg/Kg/day) for 4 days. Mentha ethanolic extract orally administered to