The study aims to investigate: (1) the prevalence of cannabis among epileptic patients seen at Mansoura University Hospital, (2) serum levels and gene expression of cytokines in epilepsy patients and the controls. and (3) the possibility that cannabis use affects the cytokine levels in epilepsy patients, triggering its future use in treatment. We recruited 440 epilepsy patients and 200 controls matched for age, gender, and ethnicity. Of the epileptic patients, 37.5% demonstrated lifetime cannabis use with a mean duration of 15 ± 73 years. Serum levels of interleukin IL-1α, IL-1β, IL-2, IL-4, IL-6, IL-8, IL-10, and tumor necrosis factor-α (TNF-α), were analyzed and gene expression analysis was conducted only for those cytokines that were different between groups in the serum analysis. The “Epilepsy-only” patients had significantly higher serum and mRNA levels of IL-1α, β, IL-2,6,8, and TNF-α compared to the controls and the “Cannabis+Epilepsy” group (p = 0.0001). IL-10 showed significantly lower levels in the “Epilepsy-only” patients compared to the controls and “Cannabis+Epilepsy” (p = 0.0001). Cannabis use is prevalent among epilepsy patients. Epilepsy is characterized by a pro-inflammatory state supported by high serum and gene expression levels. Cannabis users demonstrated significantly lower levels of inflammatory cytokines compared to epilepsy non-cannabis users which might contribute to its use in the treatment of resistant epilepsy.

The aim of this study was to compare the in vitro cytotoxic effect of tramadol and M1 metabolite in HepG2 cell line, the underlying mechanism, and PI3K/AKT/mTOR as potential target. Concentrations representing therapeutic level for tramadol (2 µM) and M1 metabolite (0.5 µM) were used. In additions other increasing concentrations representing higher toxic levels were used (6, 10 µM for tramadol and 1.5, 2.5 µM for M1 metabolites). Cytotoxicity was assessed at 24, 48 and 72 hours. Both tramadol and M1 metabolites were able to produce cytotoxicity in dose and time dependent manner. Insignificant difference was detected between cells exposed to tramadol and M1 metabolite at therapeutic concentrations. Tramadol induced apoptotic and autophagic cell death while M1 metabolite induced apoptosis only. For PI3K/AKT/mTOR pathway, therapeutic concentration of tramadol was only able to increase phosphorylation of AKT while higher toxic concentrations were able to increase phosphorylation of whole pathway; Meanwhile, M1 metabolite was able to increase the phosphorylation of the whole pathway significantly in therapeutic and toxic concentrations. In conclusion, both tramadol and M1 are equally cytotoxic. Apoptosis and autophagy both mediate hepatic cell death. PI3K/AKT pathway is involved apoptosis induction while autophagy is regulated through mTOR independent pathway.

Organochlorines (OCs) are groups of highly toxic pesticides with known immunotoxicity. The present work aimed to study the potential association between serum residues of OCs and the risk of developing systemic lupus erythematosus (SLE) as well as correlating to the clinical-laboratory manifestations in a sample of Egyptian SLE patients. A cross-sectional study was conducted on 132 patients environmentally exposed to OCs. Patients were diagnosed as SLE based on the American College of Rheumatology (ACR) revised criteria. Systemic Lupus Erythematosus Disease Activity Index-2000 (SLEDAI-2K) score was calculated to stratify the disease severity. Blood and urine samples were collected to measure the levels of OCs, serological markers, and urinary protein. The most frequently detected OCs were p,p’-DDE; lindane; and hexachlorobenzene (HCB). The risk of developing SLE was significantly associated with detected p,p’-DDE and HCB (B value 7.704 and 14.33, respectively). Hexachlorobenzene, in addition, was significantly associated with increased SLEDAI-2K score and polycythemia. Lindane was significantly associated with hypocomplementemia, cardiac manifestations of SLE, anemia, and leucopenia. In conclusion, the detected OCs p,p’-DDE and HCB are associated with increased risk of SLE in Egyptian patients and correlates to the manifestations of disease severity.

The aim of the study was to evaluate the effect of intravenous lipid emulsion (ILE) as a putative antidote on the survival time of ALP intoxicated patients and whether it ameliorates the clinical outcome or not. The present clinical study was conducted in Mansoura Emergency Hospital, and it involves patients presented with acute aluminum phosphide poisoning (ALP). Sociodemographic and full clinical examination were documented. Patients received either the standard therapy or standard therapy plus ILE. Over a period of five years, a total of 87 acutely intoxicated patients were analyzed in which (56 were females (64.4%), and 31 were males (35.6%). The mean age was 28.23±9.69 years. The mortality rate for ALP poisoning was 67.8%. Despite the poor outcome of cardiopulmonary resuscitation (CPR) following ALP toxicity, the survival time among patients received ILE was significantly longer compared to the group of patients received only standard therapy, in which 7.3% versus 30.4% survived 6-24 hours, 34.1% versus 21.7% survived 25-48 hours while 36.6% versus 6.5% survived between 49–72 hours respectively with p-value=<0.001. From previous data, it can be concluded that the use of ILE as an antidote during resuscitative measure following ALP toxicity showed a slight improvement in the term of survival time, however, it doesn’t decrease the mortality rate. Further studies are imperative to prove the effectiveness of ILE as an antidote for ALP toxicity and whether it could be considered in the CPR measures of poisoning cases.

Bisphenol-A (BPA) is one of the commonest chemicals used in the manufacturing of plastics. Childhood obesity is one of the most serious public health challenges of the 21st century that affects many low- and middle-income countries, including Egypt. This study was conducted to correlate between BPA exposure and risk of obesity in a sample of Egyptian children and to find out whether adiponectin (ADP) can be utilized as an exposure biomarker or not. This study was conducted on 80 children. They were divided into two groups according to their body mass index (BMI): Study group included 40 obese children (BMI ≥ 95th percentile), and control group included 40 normal-weight children (BMI 5th - 85thpercentile). Levels of urinary BPA and serum ADP were estimated using HPLC and ELISA respectively. The study revealed that statistically significant increase in mean adjusted urinary BPA levels (P < 0.001) and serum ADP levels (P < 0.001) between study and control groups. Within the study group, a statistically significant positive correlation was found between urinary BPA levels and BMI (r = 0.956), meanwhile, statistically significant negative correlations were found between urinary BPA levels and serum ADP levels, as well, serum ADP levels and BMI (r= - 0.947, - 0.984 respectively). Binary logistic regression analysis showed that odds ratio for serum ADP level was 0.146 with 95% CI: 0.003-0.66, P=0.012. Significant increased risk for obesity among BPA exposed children was found and ADP can be used as a predictor biological marker for BPA-induced obesity.