Fipronil (FIP) is an insecticide commonly used in many fields, such as agriculture, veterinary medicine, and public health, and recently it has been proposed as a potential endocrine disrupter. The purpose of this study was to inspect the reproductive impacts of FIP and the possible protective effects of cerium nanoparticles (CeNPs) on male albino rats. Rats received FIP (5 mg/kg bwt; 1/20 LD₅₀), CeNPs (35 mg/kg bwt) and FIP+CeNPs per os daily for 28 days. Serum testosterone levels, testicular oxidative damage, histopathological and immunohistochemical changes were evaluated. FIP provoked testicular oxidative damage as indicated by decreased serum testosterone (≈60%) and superoxide dismutase (≈50%), glutathione peroxidase activity (≈46.67%) and increased malondialdehyde (≈116.67%) and nitric oxide (≈87.5%) levels in testicular tissues. Furthermore, FIP induced edematous changes and degeneration within the seminiferous tubules, hyperplasia, vacuolations, and apoptosis in the epididymides. In addition, FIP exposure upregulated interleukin-1β (IL-1β), nitric oxide synthase 2 (NOS), caspase-3 (Casp3) and downregulated the Burkitt-cell lymphomas (BCL-2), inhibin B proteins (IBP), and androgen receptor (Ar) mRNA expressions Casp3, nitric oxide synthase (iNOS), ionized calcium-binding adapter molecule 1(IBA1), and IL-1β immunoreactions were increased. Also, reduction of proliferating cell nuclear antigen (PCNA), mouse vasa homologue (MVH), and SOX9 protein reactions were reported. Interestingly, CeNPs diminished the harmful impacts of FIP on testicular tissue by decreasing lipid peroxidation, apoptosis and inflammation and increasing the antioxidant activities. The findings reported herein showed that the CeNPs might serve as a supposedly new and efficient protective agent toward reproductive toxicity caused by the FIP insecticide in white male rats.

Background: Studies regarding treatment of acute toxicity with diclofenac (ATD) are quite few. Diclofenac is commonly prescribed in neurology, psychiatry, and general medicine practice. This study investigated possible colon-protective effects exerted by Ajwa date fruit extract (ADFE), a prophetic medicine remedy native to Al-Madinah, Saudi Arabia against ATD. Phytochemicals in ADFE as gallic acid and quercetin have reported protective effects against ATD. Methods: Total phenols and flavonoids in ADFE were estimated as equivalents to gallic acid and quercetin. Four experimental groups were allocated each of six rats: control group, ATD group received a single dose of 150 mg diclofenac intraperitoneally, toxicity prevention group received a single dose of ADFE orally followed 4 hours later by diclofenac injection, and toxicity treatment group received a similar diclofenac dose followed 4 hours later by a single dose of ADFE. Four days later, animals were sacrificed. Histological and biochemical examinations were done. Results: ADFE has a total phenolic content of 331.7 gallic acid equivalent/gram extract and a total flavonoid content of 70.23 quercetin equivalent/gram. ATD significantly increased oxidative stress markers as serum malondialdehyde (MDA) and hydrogen peroxide (H₂O₂). Serum MDA and H₂O₂ were significantly scavenged by ADFE. ATD significantly (p< 0.001) decreased antioxidant power as serum total antioxidant capacity and catalase activity. That was reversed by ADFE in both prevention and treatment groups. Histologically, ATD caused complete destruction of colonic crypts architecture, patchy loss of the crypts, loss of the surface epithelium, absent goblet cells and submucosal exudate, heavy infiltration of the lamina propria and submucosa with inflammatory cells, mainly lymphocytes and eosinophils. There were mucosal haemorrhages and submucosal dilated congested blood vessels. All that was prevented and treated using ADFE. Conclusion: ADFE is rich in quercetin and gallic acid equivalents that exert potent antitoxic effects. ADFE is strongly recommended for preventive and therapeutic colon effects against ATD.

Background: Adequate sleep is crucial for maintaining memory, emotional regulation, mental sharpness, and general health. Students pursuing medical degrees frequently experience interrupted sleep patterns because of rigorous academic workloads and hospital duties, potentially harming both their wellness and educational outcomes. Aim: This study aims to examine how sleep quality influences academic performance in medical and health sciences undergraduates at Batterjee Medical College, Saudi Arabia, in the 2024-2025 academic year. Methods: A cross-sectional study involving 175 medical students was carried out using standardized questionnaires, such as the Epworth Sleepiness Scale and the Pittsburgh Sleep Quality Index (PSQI), to assess sleep quality. The students' academic performance was assessed according to their cumulative grade point average (GPA). Results: A total of 175 medical students participated in the study, of whom 118 (67.4%) were male. Regarding age distribution, 95 (54.3%) were aged 18-22, and 41 (23.4%) were aged 23-27. The participants came from various specialties, including pharmacy, dentistry, medicine, physical therapy, and nursing, with educational levels ranging from preparatory year to postgraduate. Among the 175 responses received, 93 (53.1%) had an outstanding GPA, 13 (7.4%) had a good GPA, and two (1.1%) had a below-average GPA. The average PSQI score was 6.7 (±3.5). Poor sleep quality was reported by 129 (73.7%) of participants, while 46 (26.3%) reported good sleep quality. Key factors influencing sleep quality included caffeine consumption (157, 89.7%), family history of sleep disorders (38, 21.7%), psychiatric illness (25, 14.3%), and chronic diseases (10, 5.7%). Conclusion: Poor sleep quality is a common issue among medical students, negatively impacting both their academic success and overall well-being. Implementing effective sleep habits and better time management strategies is crucial for improvement.

Background: Medical and health sciences students face significant academic, clinical, and social pressures that increase their risk of psychological distress. Prior studies report elevated levels of depression, anxiety, and stress in this group. Barriers to accessing mental health services such as stigma, confidentiality concerns, limited awareness, and fear of negative consequences further compound this risk. Understanding the prevalence, determinants, and service barriers is essential for developing effective support systems. Aim: To determine the prevalence and determinants of depression, anxiety, and stress among medical and health sciences students at Batterjee Medical College, Saudi Arabia, and to identify barriers limiting their access to mental health services. Methods: A cross-sectional study was conducted among 384 students using a self-administered online survey. The Depression Anxiety Stress Scales-21 (DASS-21) assessed psychological distress, while the Barriers to Mental Health Services Scale-Revised (BMHSS-R) measured perceived obstacles to seeking help. Data were analyzed to identify prevalence, associated demographic and academic factors, and barriers to mental health service utilization. Results: Depression, anxiety, and stress (DAS) were evaluated using validated DASS-21 subscales demonstrating excellent internal consistency ( α > 0.88). The total BMHSS score showed significant associations with academic factors, including major, year of study, and GPA ( p ≤ 0.01). Gender was a strong predictor of psychological distress, with female students reporting significantly higher mean scores across all DAS domains ( p ≤ 0.000439). Age was significantly associated with anxiety and stress ( p ≤ 0.024). Students residing in urban areas reported higher anxiety scores than those in rural regions ( p = 0.029). These findings identify gender, age, and residence as key demographic risk factors requiring targeted interventions. Conclusion: The study found a high prevalence of depression, anxiety, and stress among medical and health sciences students, with demographic and academic characteristics emerging as significant correlates. Intrinsic barriers, such as stigma and self-reliance, and extrinsic barriers, including accessibility and cost, further limited help-seeking and compounded psychological distress. These findings emphasize the need for comprehensive institutional mental health strategies and longitudinal research to enhance student wellbeing.

Background: Prophylactic probiotics and intermittent fasting (IF) substantially modulate the neuropsychological functions and exercise capacity in rats subjected to sleep deprivation (SD). A comparative study was conducted to analyze the effects of probiotics and IF on SD-induced neuropsychological disturbances and compromised muscle endurance. Methods: Forty albino Wistar rats were randomly assigned to four groups. The NSD group was maintained on a standard chow diet for 12 weeks. The SD group followed an SD regimen for 72 h per week over 8 weeks, starting from the fifth week. The SDP group received probiotics at a dose of colony-forming units (CFUs)/100 g/day for 4 weeks prior to SD, followed by 8 weeks of concurrent probiotic administration with SD. The SDIF group underwent an alternate-day fasting regimen for 4 weeks before SD, followed by 8 weeks of simultaneous SD combined with IF. Neuropsychological functions and exercise capacity were tested, and then the brains were carefully dissected, sectioned, and processed for hematoxylin and eosin, cresyl violet, and immunohistochemical staining. Results: Inflammatory markers, including interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and hippocampal expression of the circadian locomotor output cycles kaput ( CLOCK ) gene, were significantly elevated in the SD group. Conversely, it showed significant decreases in endurance, exploratory behavior, hippocampal superoxide dismutase (SOD) activity, and fecal short-chain fatty acids (SCFAs). Histological analysis also revealed hippocampal gliosis, apoptosis, CA1 pyramidal cell degeneration, layer disorganization, and upregulation of glial fibrillary acidic protein (GFAP), NF-κB, and cleaved caspase-3. Nevertheless, both probiotics and IF markedly reduced serum MDA, hippocampal CLOCK gene expression, gliosis, and apoptosis and enhanced memory performance. In addition, they significantly increased hippocampal SOD activity and SCFAs. Conclusion: These findings indicate that prophylactic probiotics decrease cognitive disruption and impaired muscle endurance caused by SD through CLOCK gene regulation compared to that with IF. This highlights the need for further research to elucidate these mechanisms. Histological findings also supported these results, showing improved neuronal structure in the hippocampus following probiotic treatment.