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Your search keyword '"El-Yazbi, Ahmed F."' showing total 365 results
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365 results on '"El-Yazbi, Ahmed F."'

18. Evaluation of a structured pharmacist-led intervention on glycemic control in underprivileged diabetic patients: a randomized open-label trial.

Author

Abdul-Latif, Maha, Nagib, Reem, Amin, Mohamed, and El-Yazbi, Ahmed F

Subjects
GLYCEMIC control, INSULIN therapy, DIABETES, EXPERIMENTAL design, PEOPLE with diabetes
Abstract

Objective This study assesses the impact of a structured clinical pharmacist intervention on glycemic control in diabetic patients maintained on intensive insulin therapy attending the internal medicine clinic in a hospital with limited financial resources. Methods A randomized parallel open-label clinical trial design was employed. Ethical approval was obtained from the Egyptian Ministry of Health (MOH) ethics committee. Adult diabetic patients, on intensive insulin therapy, were recruited from an internal medicine clinic at an MOH hospital. Patients were randomly allocated into two groups; control, on premixed insulin twice daily, and intervention, receiving a structured pharmacist intervention including the addition of regular insulin doses as needed. Patients were followed up for three months. A 1% reduction of HbA1c level at the conclusion was considered the primary outcome. Key findings One hundred and twenty-five patients (62 control and 63 intervention) consented to participate in the study, of whom 98 (46 control and 52 intervention) completed the follow-up period. At three months, the odds ratio for HbA1c reduction by at least by 1% in the intervention group was 3.2 (95% CI 1.45–7.08). Very few cases of hypoglycemia were reported in either group. The HbA1c reduction was not affected by age, weight, or literacy status of the patients. Conclusions Clinical pharmacist interventions, even in environments with scarce resources and socioeconomic challenges, remain effective in achieving better glycemic control. This trial has been registered in the Pan-African Clinical Trial Registry (PACTR201610001812290, https://pactr.samrc.ac.za/). [ABSTRACT FROM AUTHOR]

Published
2024
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19. Integrated Biomarker Response Emphasizing Neuronal Oxidative Stress and Genotoxicity Induced by Oxamyl in Sprague Dawley Rats: Ameliorative Effect of Ginseng as a Neuroprotective Agent.

Author

Abdallah, Salwa M., Muhammed, Reham E., Mohamed, Reda E., Khalil, Wagdy K. B., Taha, Dalia A., Shalaby, Mohamed B., Elgohary, Islam, Abdallah, Amr A., Habib, Hosam M., and El-Yazbi, Ahmed F.

Subjects
SPRAGUE Dawley rats, AGRICULTURE, OXIDATIVE stress, BONE marrow, GINSENG, GENETIC toxicology
Abstract

Climate change has led to increased and varying pest infestation patterns, triggering a rise in pesticide usage and exposure. The effects of oxamyl, a widely used nematicide in Egypt, encompasses typical signs of carbamate intoxication; nevertheless, long-term effects of oxamyl exposure, particularly on the nervous system, require further elucidation. This study systematically investigated the mechanism and manifestations of repeated subacute exposure to sublethal doses of oxamyl in male SD rats. Data showed a dose-dependent genotoxic effect, manifested as increased bone marrow micronuclei and decreased brain expression of key genes involved in neurogenesis and neuronal development. Coincidently, brain histopathology showed dose-dependent neurodegeneration in various regions, associated with a significant increase in GFAP immunoreactivity, indicative of neuroinflammation. Biochemical examination revealed a typical pattern of cholinesterase inhibition by carbamates in serum and brain tissue, as well as increased oxidative stress markers in the brain such as SOD activity reduction, alongside an increase in NO and MDA. The ability of Ginseng at a 100 mg/Kg dose to ameliorate the effects of oxamyl exposure was investigated. Ginseng use, either as a protective or therapeutic regimen, attenuated the observed genotoxic, neuroinflammatory, and biochemical alterations. Our results indicate that repeated exposure to oxamyl triggers an integrative neurotoxic response, driven by genotoxicity, oxidative stress, and neuroinflammation, that could trigger an increase in neurological and cognitive disorders. These findings emphasize the urgent need for confirmatory translational studies in human subjects to assess these changes and inform policy decisions regarding safe levels of usage and appropriate agricultural and public health practices. [ABSTRACT FROM AUTHOR]

Published
2024
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28. Tackling neuroinflammation and cholinergic deficit in Alzheimer's disease: Multi-target inhibitors of cholinesterases, cyclooxygenase-2 and 15-lipoxygenase

Author

AlFadly, Ehab D., Elzahhar, Perihan A., Tramarin, Anna, Elkazaz, Salwa, Shaltout, Hossam, Abu-Serie, Marwa M., Janockova, Jana, Soukup, Ondrej, Ghareeb, Doaa A., El-Yazbi, Ahmed F., Rafeh, Rim W., Bakkar, Nour-Mounira Z., Kobeissy, Firas, Iriepa, Isabel, Moraleda, Ignacio, Saudi, Manal N.S., Bartolini, Manuela, and Belal, Ahmed S.F.

Published
2019
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43. Inclusion of Nitrofurantoin into the Realm of Cancer Chemotherapy via Biology-Oriented Synthesis and Drug Repurposing

Author

Elzahhar, Perihan A., primary, Nematalla, Hisham A., additional, Al-Koussa, Houssam, additional, Abrahamian, Carla, additional, El-Yazbi, Amira F., additional, Bodgi, Larry, additional, Bou-Gharios, Jolie, additional, Azzi, Joyce, additional, Al Choboq, Joelle, additional, Labib, Hala F., additional, Kheir, Wassim Abou, additional, Abu-Serie, Marwa M., additional, Elrewiny, Mohamed A., additional, El-Yazbi, Ahmed F., additional, and Belal, Ahmed S. F., additional

Published
2023
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47. Adipose tissue mitochondrial dysfunction and cardiometabolic diseases:On the search for novel molecular targets

Author

Ibrahim, AlZaim, Eid, Ali H., Abd-Elrahman, Khaled S., and El-Yazbi, Ahmed F.

Subjects
Pharmacology, UCP1, Diabetes Mellitus, Type 2, Adipose Tissue, Cardiovascular Diseases, Adipose, Humans, Metabolic disease, Obesity, Cardiovascular disease, Biochemistry, Mitochondria
Abstract

Cardiometabolic diseases present an escalating global health and economic burden. Such a surge is driven by epidemic prevalence rates of metabolic disorders, such as obesity and type 2 diabetes, and their associated cardiovascular complications, majorly contributing to morbidity and mortality. A fundamental challenge impeding the effective management and therapy of these complications is a lack of clear understanding of the molecular mechanisms underpinning disease initiation and progression. Over the past decade, a role for metabolic disease-associated adipose tissue dysfunction and inflammation in evoking cardiovascular and renal deterioration emerged, together with a growing recognition of the positive impact of pharmacological tools modulating adipose tissue function. Adipose tissue is a plastic endocrine organ whose homeostasis is essentially dependent on the intercellular communication of its comprising cellular components. Yet, despite being a principal regulator of adipose tissue metabolic activity, changes in aspects of adipose tissue mitochondrial biogenesis, dynamics, and bioenergetics in the context of cardiometabolic disorders have not garnered the necessary attention. Here, we gather the available evidence on the contribution of mitochondrial dysfunction to that of the adipose tissue in metabolic diseases, and to the ensuing cardiovascular deterioration. The involved molecular pathways are highlighted together with potential targets for intervention. The effects of several drug classes with known beneficial impact on adipose tissue remodeling and mitochondrial dysfunction in such a context are discussed. Finally, future research aspects in this domain are explored. This work is supported by a grant #45912 from the Science, Technology, and Innovation Funding Authority in Egypt to AFE.

Published
2022
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