: Background: Aflatoxin (AF), a metabolite of Aspergillus flavus, is injurious to vital body organs. The bacterial defense against such mycotoxins has attracted significant attention. Lactic acid bacteria (LAB) are known to ameliorate AF toxicity. Methods: Thirty adult male rats were divided into six groups (five each) to perform the experiments. The control (Co) group was fed a basal diet and water. Each of the following periods lasted 21 days: the milk (MK) group orally received milk (500 µL); LAB suspension (500 µL) containing 107 cfu/mL was orally provided to the LAB group; AF (0.5 mg/kg) was orally given to the AF group; and a combination of AF and LAB was administered to the AF + LAB group. The AF/LAB group was initially given AF for 21 days, followed by LAB for the same period. Finally, the rats were dissected to retrieve blood and tissue samples for hematological, biochemical, and histological studies. Results: The results revealed a significant decrease in RBCs, lymphocytes, total proteins, eosinophil count, albumin, and uric acid, whereas the levels of WBCs, monocytes, neutrophils, creatinine, urea, aspartate aminotransferase, alkaline phosphatase, alanine aminotransferase, lactate dehydrogenase, and creatinine kinase significantly increased in the AF group in comparison to the control group. The histological examination of the AF group revealed necrosis and apoptosis of the kidney’s glomeruli and renal tubules, nuclei vacuolization and apoptosis of hepatocytes, congestion of the liver’s dilated portal vein, lymphoid depletion in the white pulp, localized hemorrhages, hemosiderin pigment deposition in the spleen, and vacuolization of seminiferous tubules with a complete loss of testis spermatogenic cells. Meanwhile, protective and therapeutic LAB administration in AF-treated rats improved the hematological, biochemical, and histological changes. Conclusions: The study revealed LAB-based amelioration to AFB1-induced disruptions of the kidney, liver, spleen, and testis by inhibiting tissue damage. The therapeutic effects of LAB were comparatively more pronounced than the protective effects.

Acute kidney injury (AKI) is an independent risk factor for neonatal death. Since neonatal early renal injury usually has no specific clinical symptoms, many AKI cases are often missed the best time of early intervention if there is no relevant examination. Perinatal asphyxia (PA) can lead to AKI. The study aimed to assess efficacy of serum cystatin C (CystC) in early prediction of AKI in full-term neonates with PA. The study was conducted at the neonatal intensive care unit, Assiut University Children Hospital from January 2019 to January 2021. Seventy full-term neonates with documented PA were enrolled in the study. Baseline laboratory data and serum CystC levels were assessed. Out of those 70 neonates with PA, 21 (30%) developed AKI, while 49 (70%) neonates did not develop AKI. Majority of non-AKI group had stage-I hypoxic-ischemic encephalopathy (HIE) (61.2%), while majority of AKI had stage-III HIE (61.9%). A significantly higher serum CystC level was found among AKI group than those without AKI (1.50
0.12 vs. 0.90
0.14, p < 0.001). The predictors for AKI among neonates with PA were low birth weight, serum CystC levels, hypotension, and stage-III HIE. Serum CystC has 94.3% overall accuracy for prediction of AKI. In conclusion, AKI in neonates with PA is common. CystC is a promising biomarker in early prediction of AKI in such cases. Future studies are warranted to confirm these findings.

Traumatic brain injury (TBI) is a quite common health problem. A lot of delayed complications are related to inflammatory responses that occurred within the brain itself. Atorvastatin is related to lipid lowering drugs carrying some anti-inflammatory properties and upon this fact this study hypothesis was built.

Methods

Twenty adult patients with TBI, Glasgow coma scale (GCS) 9–11. Patients were equally and randomly allocated into two groups (group C as control group and group S received atorvastatin 40 mg once daily for 48 h). After 48 h, participants have undergone magnetic resonance imaging brain spectroscopy examination (MRS). The spectral peaks of N-Acetyl aspartate (NAA), Choline, and Creatinine (Cr) were assessed in brain tissue. The primary outcome was presented as ratios of NAA/Cr), Cho/Cr, and NAA/Cho. Other outcomes included GCS and ICU stay

Introduction: ARID1A (AT-rich interacting domain 1A) gene, a subunit of the SWI/SNF (switch/sucrose non-fermentable) complex, is a tumor suppressor gene. Mutations of this gene with loss of the corresponding protein were detected in different types of cancer. Here, we investigated ARID1A protein expression in endometrioid endometrial carcinoma (EEC), and assessed the correlation between its expression values and the pathological features of EEC.

Materials and methods: The study included 26 cases of EEC and five cases of proliferative endometrium (PE, control group). Immunostaining was done using streptavidin staining methods and ARID1A rabbit monoclonal antibody. Slides were examined and scored for ARID1A nuclear positivity.

Results: Nuclear ARID1A protein expression was observed in all cases of PE, and in 54% of EEC cases. We found significant down-regulation of ARID1A protein expression in EEC (Immunoreactivity score [IRS] = 2.69 ± 2.42) as compared to PE (IRS = 7.4 ± 2.3). Also, there was a significant inverse correlation between ARID1A protein expression value and pathological stage of EEC (r = -0.43, p = 0.040).

Conclusions: Alterations of ARID1A protein expression seem to play a role in the pathogenesis of EEC. The diagnostic and prognostic ramifications of these alterations are open for future studies.