Organophosphorus pesticides (OPPs) are widely used and have recently been linked to metabolic syndrome (MS). This study aimed to investigate the probable association between chronic OPP exposure and MS among farm workers in Sharkia Governorate, Egypt, and to assess the potential role of peroxisome proliferator-activated receptor gamma (PPARγ). This comparative cross-sectional study included 140 participants, equally divided into OPP-exposed farm workers and non-exposed subjects. OPP exposure was confirmed by detecting plasma residues and cholinesterase activity. MS was diagnosed by assessing body mass index (BMI), waist circumference (WC), blood pressure, plasma glucose, serum insulin, and lipid parameters. Oxidative and inflammatory markers, including malondialdehyde (MDA), gamma-glutamyl transferase (GGT), ferritin, superoxide dismutase (SOD), tumor necrosis factor-alpha (TNF-α), and high-sensitivity C-reactive protein (hs-CRP), were measured. The mRNA expression of the PPARγ and paraoxonase 1 (PON1) genes was also investigated. In total, 60% of farm workers demonstrated MS, compared with 10% of non-exposed participants. Workers exhibited elevated oxidative and inflammatory indices and reduced PPARγ and PON1 expression. PPARγ positively correlated with high-density lipoprotein (HDL), SOD, and PON1, while negatively correlating with glucose, insulin resistance (IR), low-density lipoprotein (LDL), triglycerides (TGs), MDA, GGT, ferritin, TNF-α, and hs-CRP. The study concluded that chronic OPP exposure was associated with increased oxidative stress and inflammation, reduced PPARγ and PON1 expression, disturbed glucose and lipid metabolism, and increased IR. The observed associations between PPARγ downregulation, metabolic disturbances, and oxidative and inflammatory markers suggest that PPARγ dysregulation may represent a potential mechanistic link between chronic OPP exposure and MS. However, this proposed mechanism requires further validation.
Samar Sakr, M. El-Daly, R. Elshamy et al.· Toxics· 0 citations
Respiratory viral infections caused by seasonal influenza, respiratory syncytial virus (RSV), and pandemic-potential coronaviruses are responsible for several million hospitalisations and an estimated several hundred thousand deaths each year, a burden underscored by the severe 2024–2025 influenza season and the continued emergence of zoonotic threats such as clade 2.3.4.4b H5N1. This review critically examines the pharmacological basis for targeting host cell-surface receptors as a strategy for the treatment and prophylaxis of respiratory viral infections, evaluates the current evidence for each major receptor axis, and identifies the key translational gaps that must be addressed. Respiratory viruses, including influenza, RSV, SARS-CoV-2, and MERS-CoV, collectively cause millions of hospitalisations annually, and the persistent challenges of antigenic drift, zoonotic emergence, and antiviral resistance highlight the need for mechanistically distinct strategies. Host-directed therapies (HDTs) targeting conserved receptors (ACE2, DPP4, sialic acids, TMPRSS2) exploit genetically stable host factors required for viral entry. Across the receptor axes reviewed here, we appraise more than a dozen candidate agents spanning preclinical development through Phase III evaluation, including TMPRSS2 inhibitors, soluble ACE2 decoys, anti-CD147 and receptor-blocking monoclonal antibodies, the sialidase fusion protein DAS181, and avian IgY preparations. This evidence reveals a consistent gap between robust preclinical activity and as-yet-limited clinical efficacy. We conclude that host receptor targeting is a mechanistically rational but still clinically unproven component of the respiratory antiviral landscape; its value is most plausibly realised in defined niches—prophylaxis, early outpatient treatment, and combination with direct-acting antivirals—and within pandemic preparedness frameworks, provided that the safety, delivery, and trial-design challenges identified here are resolved.
Sherif A. El-Kafrawy, Norah A. Othman, M. Zeyadi et al.· Frontiers in Cellular and In...· 0 citations
Clopidogrel is widely used for secondary prevention of ischemic stroke (IS). Its effectiveness is significantly affected by genetic variations in the CYP2C19 gene. The occurrence and clinical implications of loss-of-function alleles (LoFA) within Egyptian populations remain underassessed. This study aimed to assess the prevalence of CYP2C19 LoFA in Egyptian IS patients, and their influence on clopidogrel effectiveness and the likelihood of recurrent IS. This prospective cohort study conducted in a tertiary stroke center included 182 consecutive acute IS patients. CYP2C19 genotypes were determined using TaqMan real-time PCR primers and probes. A total of 220 patients were enrolled; 182 completed follow-up. CYP2C19 *2 and *3 GA/AA genotypes were significantly associated with recurrent IS (OR 7.5; 95% CI 3.41–16.64 and OR 5.7;95% CI 2.49–13.17, respectively). In multivariable analysis adjusted for vascular risk factors, CYP2C19 LoFA remained independent predictors of recurrence (adjusted OR 5.62; 95% CI 1.85–27.40 and adjusted OR 4.08; 95% CI 1.41–21.59 for CYP2C19*2 and *3, respectively). CYP2C19 LoFA are highly prevalent in Egyptian IS patients and were independently associated with clopidogrel non-response and recurrent stroke. Further large, multi-center studies should evaluate cost-effectiveness and long-term outcomes of personalized antiplatelet strategies in this population.
Sara F. Saadawy, Noha T. Sarhan, M. El-Daly· The Egyptian Journal of Neur...· 0 citations
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