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1.
Int Clin Psychopharmacol ; 39(3): 195-200, 2024 May 01.
Artículo en Inglés | MEDLINE | ID: mdl-37781786

RESUMEN

Hepatocyte injury is assessed by serum aspartate transaminase and alanine transaminase estimation. In psychiatric populations, antipsychotic drugs (AD) are culprit in hepatic dysfunction. To assess transaminitis among psychiatric patients treated by AD. This cross-sectional study was conducted in Zagazig University Hospitals in Egypt, from December 2022 to February 2023. A total of 135 adult patients aged ≥ 18 years, were diagnosed with psychiatric disorders after exclusion of patients receiving any hepatotoxic drugs, viral hepatitis, having chronic liver or kidney diseases, diabetes mellitus, mental retardation, and pregnant females. Among the 135 patients, 104 (77.0%) were males. Their age was 32 ±â€…9, The most popular used class of AD was atypical AD 84 (62.2%). The overall incidence of transaminitis among patients receiving AD was 23/135 (17.04%) of patients; 13 (56.5%) were on atypical AD compared to 10 (43.5%) patients receiving combined AD, without any statistically significant difference. The use of AD in patients with psychiatric disorders is potentially safe with minimal transaminitis (

Asunto(s)
Hígado , Trastornos Mentales , Adulto , Masculino , Femenino , Humanos , Estudios Transversales , Alanina Transaminasa/uso terapéutico , Aspartato Aminotransferasas/uso terapéutico , Trastornos Mentales/tratamiento farmacológico , Trastornos Mentales/epidemiología
2.
Biomedicines ; 11(12)2023 Dec 08.
Artículo en Inglés | MEDLINE | ID: mdl-38137476

RESUMEN

BACKGROUND: The harmful consequences of non-alcoholic fatty liver disease (NAFLD) are posing an increasing threat to public health as the incidence of diabetes and obesity increases globally. A non-invasive treatment with a range of autonomic and metabolic benefits is transcutaneous vagus nerve stimulation (tVNS). AIM OF THE STUDY: To investigate the possible preventive impacts of VNS against adult rats' NAFLD caused by a high-fat diet (HFD) and to clarify the underlying mechanisms. METHODS: A total of thirty-two adult male rats were split into two groups: the HFD-induced NAFLD group (n = 24) and the control normal group (n = 8). The obesogenic diet was maintained for 12 weeks to induce hepatic steatosis. The HFD-induced NAFLD group (n = 24) was separated into three groups: the group without treatment (n = 8), the group with sham stimulation (n = 8), and the group with VNS treatment (n = 8). VNS was delivered for 30 min per day for 6 weeks after the establishment of NAFLD using a digital TENS device. The subsequent assessments included hepatic triglyceride, cholesterol content, serum lipid profile, and liver function testing. In this context, inflammatory biomarkers (TNF-α, IL-6) and hepatic oxidative stress (MDA, SOD, and GPx) were also assessed. To clarify the possible mechanisms behind the protective benefits of VNS, additional histological inspection and immunohistochemistry analysis of TNF-α and Caspase-3 were performed. RESULTS: In the NAFLD-affected obese rats, VNS markedly decreased the rats' body mass index (BMI) and abdominal circumference (AC). Liver function markers (albumin, ALT, and AST) and the serum lipid profile-which included a notable decrease in the amounts of hepatic triglycerides and cholesterol-were both markedly improved. Additionally, oxidative stress and inflammatory indicators showed a considerable decline with VNS. Notably, the liver tissues examined by histopathologists revealed that there is evidence of the protective impact of VNS on the oxidative and inflammatory states linked to HFD-induced NAFLD while maintaining the architectural and functional condition of the liver. CONCLUSIONS: Our findings suggest that VNS may represent a promising therapeutic candidate for managing NAFLD induced by obesity. It can be considered to be an effective adjuvant physiological intervention for the obese population with NAFLD to spare the liver against obesity-induced deleterious injury.

3.
J Cardiovasc Pharmacol ; 81(5): 381-388, 2023 05 01.
Artículo en Inglés | MEDLINE | ID: mdl-36857749

RESUMEN

ABSTRACT: Myocardial infarction is among the leading causes of mortality. Menaquinone-4 (MK-4), a vitamin K2 analog, might play a role in rescuing cardiac ischemia/reperfusion (I/R) injury. This work aimed to discover the potential cardioprotective role of MK-4 against myocardial I/R injury in rats. Thirty-two rats were categorized into 3 groups: (I/R) control group: subjected to I/R protocol (received vehicle), MK-4 preconditioning group: MK-4 infusion for 20 minutes before the I/R protocol, and MK-4 postconditioning group: MK-4 infusion for 20 minutes at the start of the reperfusion phase. The hearts were placed in the Langendorff apparatus, and the left ventricular developed pressure (LVDP), heart rate (HR), + (LV dP/dt) max, - (LV dP/dt) max, and Tau were calculated. The necrotic mass was determined by staining it with nitro blue tetrazolium. Creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and C- reactive protein (CRP), as well as cardiac superoxide dismutase (SOD), nitric oxide (NOx), malondialdehyde (MDA), and glutathione (GSH) levels were all evaluated. MK-4 postconditioning significantly reduced myocardial infarct size; increased LVDP, + (LV dp/dt) max, - (LV dp/dt) max, and HR; reduced Tau, CK-MB, LDH, CRP, IL-6, TNF-α, MDA, and NOx levels; and increased SOD activity, whereas no significant difference in the GSH level was detected. In conclusion, these data imply that MK-4 may protect the heart from the consequences of I/R.


Asunto(s)
Daño por Reperfusión Miocárdica , Factor de Necrosis Tumoral alfa , Ratas , Animales , Vitamina K 2/farmacología , Vitamina K 2/metabolismo , Ratas Sprague-Dawley , Factor de Necrosis Tumoral alfa/metabolismo , Interleucina-6/metabolismo , Estrés Oxidativo , Daño por Reperfusión Miocárdica/patología , Superóxido Dismutasa/metabolismo , Glutatión , Miocardio/patología
4.
J Clin Aesthet Dermatol ; 15(8): 22-26, 2022 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-36061485

RESUMEN

Background: Psoriasis vulgaris is a chronic, relapsing, inflammatory disorder marked by an intensified immune response. The role of immunogenetics in psoriasis is still poorly understood; however, experts agree that its expression depends on proinflammatory cytokines.Forkhead box class O3A (FOXO3a), a transcription factor, plays a crucial role in intercellular regulation, oxidative stress, deoxyribonucleic acid (DNA) repair, and cell death. Objective: The objective of this study was to investigate the role of FOXO3a genetic polymorphism as a risk factor for psoriasis vulgaris and assess its possible relationship with disease severity. Methods: A comparative case-control study included 53 patients with psoriasis and 41 matched healthy controls. We measured serum FOXO3a levels and used the PCR-RFLEP technique to detect FOXO3a genetic polymorphism (rs13217795) in both groups. Results: Our results revealed significantly higher serum FOXO3a levels in the psoriasis group compared to the control group (p≤0.001). Serum FOXO3a levels were significantly higher in patients with severe psoriasis than in those with mild-to-moderate disease. FOXO3a genotypes found homozygous mutant genotype (TT) was substantially more frequent in the psoriasis group than in the control group. Furthermore, the T allele was more frequent in the psoriasis group than in the control group. Conclusion: The study indicates that rs13217795 polymorphism of the FOXO3a gene is strongly associated with susceptibility to psoriasis. Also, the serum level of FOXO3a is significantly higher in patients with severe psoriasis, compared to patients with mild-to-moderate psoriasis. This finding could be an area of future targeted therapy.

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