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Objective To compare the efficacy of dexmedetomidine and fentanyl to reduce hemodynamic and biochemical stress markers associated with endotracheal intubation under general anesthesia. Methods We performed a prospective randomized controlled study of 80 patients and 20 healthy controls at Assiut University from January to June 2024. The patients were allocated to two groups: Group D received dexmedetomidine and Group F received fentanyl. Blood samples were collected at four time points: T0 (baseline), T1 (2 minutes after induction of anesthesia), T2 (1 minute after intubation), and T3 (10 minutes post-intubation), for stress marker analysis. Results Intubation significantly increased stress markers in both groups compared to baseline. Group D showed significantly lower cortisol, norepinephrine, and lactate concentrations at T1, T2, and T3; and hemodynamic parameters at T2; whereas Group F demonstrated earlier post-operative recovery. Conclusions Both drugs increased stress markers, but dexmedetomidine more effectively reduced biochemical marker concentrations, suggesting better stress control, whereas fentanyl use led to quicker recovery. Dexmedetomidine is more effective at reducing intubation-induced stress, whereas fentanyl facilitates faster post-operative recovery.

Background This study tested the association between serum levels of microRNA-486, −146b and -15b and betatrophin in normal and obese children with/without type 2 diabetes mellitus (T2DM). Methods the study included 120 children; divided into three groups: G1 (50 healthy), G2 (35 obese) and G3 (35 obese with T2DM). The levels of microRNA-486, 146b and 15b and serum betatrophin were measured by their corresponding methods. Results serum microRNA-486, −146b, −15b and betatrophin levels were significantly high in G3 followed by G2 then G1 ( p  = 0.002, > 0.001, > 0.001, and > 0.001, respectively). Especially in G3, these levels correlated positively with the BMI percentile (r = 0.44, 0.58, 0.38, and 0.46, p  = 0.007, > 0.001, 0.021, and 0.005, respectively), serum glucose (r = 0.56, 0.49, 0.82, 0.60, and 0.42, p  > 0.001, 0.003, > 0.001, and > 0.001, respectively) and HbA1c% (r = 0.56, 0.39, 0.66, and 0.42, p  > 0.001, 0.019, > 0.001, and 0.032, respectively) while, showed negative correlations with correlated with serum insulin levels (r = − 0.37, − 0.42, − 0.58, and − 0.41, p  = 0.021, 0.012, > 0.001 and 0.013, respectively) and with serum C-peptide levels (r = − 0.76, − 0.50, − 0.35 and − 0.42, p  > 0.001, 0.002, 0.036 and 0.011, respectively). Serum betatrophin levels correlated positively with microRNA-486, −146b and -15b levels in G2 (r = 0.35, 0.80, and 0.67, p  = 0.036, > 0.001, and,> 0.001, respectively), and in G3 (r = 0.57, 0.36, and 0.38, p  > 0.001, 0.029 and, 0.023, respectively). Conclusions Circulating microRNA-486, 146b and 15b increase significantly in obese children with T2DM and these levels correlate positively with serum betatrophin levels. Further studies are required to test the role of targeting of these microRNAs and betatrophin in the timely management of obesity and/or T2DM in children.

Background Previous studies have reported conflicting results about the association of vitamin D (VD) level with coronary artery disease (CAD). We aimed to study the association of VD with atherosclerotic CAD in Egyptian individuals. Results We prospectively enrolled 188 consecutive CAD patients with a median age of 55(50–62) years; 151(80.3%) were male. All patients were diagnosed by cardiac catheterization and were compared with 131 healthy controls. VD levels were measured in serum samples of all participants. Compared to controls, CAD patients had a significantly lower median VD level, 14.65 (9.25–21.45) versus 42.0 (32.0–53.0) ng/mL, p  < 0.001. VD was correlated with the number of diseased coronary arteries and lipid profile (total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and triglycerides, p  < 0.001 for each). By multivariate analyses, VD was an independent predictor of CAD [OR 1.22 (95% CI 1.07–1.4), p  = 0.003, optimal cut-off value 30 ng/mL (AUC 0.92, sensitivity 81% and specificity 81.4%), p  < 0.001], and the number of diseased coronary arteries, p  < 0.001, especially three-vessel disease [OR 0.83 (95% CI 0.72–0.95), p  = 0.008]. Conclusions We have shown that low VD should be considered a non-traditional risk factor for CAD in Egyptian individuals. Low VD was correlated with coronary atherosclerosis, especially in patients with multivessel effects.

Schizophrenia is a typical -methyl-d-aspartate receptor (NMDA-R) hypofunction disorder. Decreased d-serine (d-Ser) levels in the periphery occur in schizophrenia and may reflect decreased availability of d-Ser to activate NMDA-R in the brain. The objective of this study was to investigate the role of d-Ser metabolism in the pathogenesis of schizophrenia via biochemical assays and correlates, the serum level of d-Ser, d-serine racemase (SR) (responsible for its formation from l-serine [l-Ser]) and d-amino acid oxidase (DAAO) (responsible for its catabolism), among different clinical types of schizophrenia patients. This cross-sectional case-control study was carried out on 100 patients and 50 controls. They were recruited from the outpatients' psychiatric unit of the Neuropsychiatric Department of Assiut University Hospital, Upper Egypt. The type of schizophrenia was determined according to the ( ), while the severity of schizophrenia was determined according to the ( ). Serum d-Ser levels were estimated using high-performance liquid chromatography (HPLC), while serum SR and DAAO were measured using commercially available enzyme-linked immunosorbent assay kits. There were significantly lower mean serum levels of d-Ser and SR and significantly higher mean serum levels of DAAO ( -value <0.01 for each) among schizophrenia patients when compared with the control group. Paranoid schizophrenia had the highest frequency, with a significantly lower serum levels of d-Ser and SR in the residual type and significantly higher serum levels of DAAO in undifferentiated and catatonic types. Combined receiver-operating characteristic curve for serum d-Ser, SR and DAAO indicated that the best serum level cutoff points at which schizophrenia manifestations started to appear were ≤ 61.4 mg/L for d-Ser, ≤ 15.5 pg/mL for SR and >35.6 pg/mL for DAAO. The present study confirms that disturbed d-Ser metabolism could be implicated in the pathogenesis of schizophrenia.

Background and Aims. Both paracetamol (PA) and phenacetin (PH) are analgesic and antipyretic agents. Part of phenacetin therapeutic activity is attributed to its metabolism into paracetamol. Paracetamol causes direct hepatic oxidative stress damage. The present study aimed to investigate the possible damaging effects of both PA and PH, when used in therapeutic doses, on rat liver and to compare the antioxidant and hepatoprotective effects of N-acetylcysteine (NAC), N-acetyl-methionine (NAM), and N-acetylglucosamine (NAG) against PA- or PH-induced hepatic damage. Methods. 90 male Wistar albino rats (120-140 gm) were undertaken, categorized randomly into 9 groups of 10 rats each, and administered by gavage for 2 weeks with DMSO 1% (controls), PA, PA+NAC, PA+NAM, PA+NAG, PH, PH+NAC, PH+NAM, and PH+NAG. Biochemical assays of malondialdehyde (MDA), nitric oxide (NO), reduced glutathione (GSH), total thiols, and alpha-fetoprotein (AFP) in liver homogenates and serum assays of ALT, AST, 8-hydroxy guanine (8-OH-Gua), and AFP were done. Also histopathological examinations of liver tissues in various groups were done. Results. PA and PH cause significant increase in hepatic levels of MDA, NO, and AFP and serum ALT, AST, and 8-OH-Gua levels, with significant decrease in hepatic GSH and total thiols. NAG and NAC significantly improve the PA- and PH-induced hepatic and blood, biochemical, and histopathological disturbances, respectively. Conclusions. Both PA and PH induce oxidative stress in rat liver within their therapeutic doses. NAG and NAC in pharmacological doses can antagonize the oxidative damaging effect of both PA and PH.

BackgroundParkinson’s disease is one of the neurodegenerative disorders that is caused by genetic and environmental factors or interaction between them. Solute carrier family 41 member 1 within the PARK16 locus has been reported to be associated with Parkinson’s disease. Cognitive impairment is one of the non-motor symptoms that is considered a challenge in Parkinson’s disease patients. This study aimed to investigate the association of rs11240569 polymorphism; a synonymous coding variant in SLC41A1 in Parkinson’s disease patients in addition to the assessment of cognitive impairment in those patients.ResultsIn a case -control study, rs11240569 single nucleotide polymorphisms in SLC41A1, genes were genotyped in 48 Parkinson’s disease patients and 48 controls. Motor and non-motor performance in Parkinson's disease patients were assessed by using the Movement Disorder Society-Sponsored Revision of the Unified Parkinson’s Disease Rating Scale (MDS-UPDRS). The genotype and allele frequencies were compared between the two groups and revealed no significant differences between case and control groups for rs11240569 in SLC41A1 gene with P value .523 and .54, respectively. Cognition was evaluated and showed the mean ± standard deviation (SD) of WAIS score of PD patients 80.4 ± 9.13 and the range was from 61 to 105, in addition to MMSE that showed mean ± SD 21.96 ± 3.8.ConclusionGenetic testing of the present study showed that rs11240569 polymorphism of SLC41A1 gene has no significant differences in distributions of alleles and genotypes between cases and control group, in addition to cognitive impairment that is present in a large proportion of PD patients and in addition to the strong correlation between cognitive impairment and motor and non-motor symptoms progression.

Background The prevalence of breast cancer (BC) is high among cancers in Egypt, ranking it the most common cause of cancer mortality in women. BRCA1 and BRCA2 tumor suppressors proteins have a specific relationship with BC. Plasma free amino acids levels (PFAAs) have been reported to exhibit altered profiles among cancer patients. Thus, the present study aims to examine the alteration of the PFAAs profiles and investigate their association with BRCA1 and 2 circulating levels in Egyptian females diagnosed with BC and in females with family history of BC to establish potential early detection strategies for BC. Methods and results This study included 26 BC patients, 22 females with family history of BC (relatives) in addition to 38 healthy females as control group. Quantitative measurement of PFAAs was determined by the ion exchange separation method through high performance liquid chromatography. BRCA1 and BRCA2 concentrations were determined using ELISA. Our results showed PFAAs profiles in BC patients and in females with BC family history with significant upregulation in mean plasma levels of Alanine, Phenylalanine, Glutamate and Cysteine and downregulation of Taurine, Threonine, Serine, Glycine, Valine, Methionine and Histidine levels compared to controls. Also, a significant positive correlation was observed between plasma BRCA1 and Valine levels while a significant negative correlation was observed between BRCA2 and Lysine plasma levels. Conclusion PFAAs profile can potentially be used in early screening for BC patients and for susceptible females.

Background Lung cancer (LC) is the most common form of cancer in the world. Of the proteins involved in cell differentiation and proliferation, the epidermal growth factor receptor (EGFR) is among the most significant. Amino acids play a crucial role in cell physiology as metabolic regulators. The benefits of liquid biopsies are their non-invasive nature, ease of collection, and ability to depict the entire tumor’s status. The present study is designed to detect the relation between the EGFR exon 19 747–750 deletion mutation and lung cancer and investigate the patterns of alterations of plasma-free amino acids (PFAA) in lung cancer patients of different histopathological types and stages as biomarkers for early detection of lung cancer. Methods The study sample comprised 60 lung cancer patients and 60 age- and sex-matched healthy individuals as the control group. Polymerase chain reaction and restriction fragment length polymorphism (PCR–RFLP) were used to examine the EGFR exon 19 747–750 deletion mutation, and an AA analyzer was used to quantify the plasma free amino acid (PFAA) profile. Results Compared with controls, LC patients had significantly higher levels of three AAs and significantly lower levels of fifteen AAs. Thirteen AAs varied significantly between stages I and II. In the lung cancer group, the percentage of cases of mutant EGFR exon-19 deletion increased to 30% from 13.3% in the control group. The histological forms of lung cancer did not significantly differ in this rise. Valine and citrulline plasma levels were substantially greater in the mutant than in the wild-type. Lysine, histidine, and methionine were the independent predictors of the LC group in multivariate analysis. Conclusion Lung cancer development is influenced by the EGFR exon 19 747–750 deletion mutation, and the prognosis and early prediction of lung cancer are greatly affected by the amino acid profile concentrations.

Cardiovascular diseases have become a leading global health burden, with rising mortality worldwide. WNT and JAK/STAT have been highlighted as emerging biomarkers in cardiovascular disease pathogenesis. This study assessed the Wnt/JAK-STAT signaling pathway in relation to SFRP5 and genetic polymorphisms in cardiac patients. This prospective case-control study included 100 patients with various cardiac diseases (IHD, valvular heart disease, HF, cardiomyopathy, and arrhythmia) and 50 matched healthy controls. Clinical and echocardiographic assessments were performed. Plasma SFRP5, Wnt5a, and JAK levels were measured using ELISA; STAT5A expression by flow cytometry; and SFRP5 (rs780369540) gene polymorphism by TaqMan real-time PCR were also performed in all participants. Cardiac patients showed significantly higher median BMI (33 vs. 28.5 kg/m , = 0.001) and markedly increased median value of each Wnt5a (16.85 vs. 5.6 pg/mL, < 0.001), median JAK (9.45 vs. 2.4 pg/mL, < 0.001), and STAT5A expression (87.55% vs. 33%, < 0.001), with lower SFRP5 levels (4 vs. 6.7 ng/L, < 0.001) compared to control. The SFRP5 (rs780369540) T allele was more frequent in patients (51.5% vs. 32%, = 0.001), and dominant TT + TC genotypes were higher (66% vs. 42%, = 0.005) compared to the control group. TT carriers showed higher median Wnt5a, lower median SFRP5, and reduced ejection fraction compared to other genotypes (TC, CC) carriers. Multivariate analysis identified elevated Wnt5a, JAK, and decreased SFRP5 as independent predictors of cardiovascular disease ( < 0.05). Cardiac patients showed altered WNT5a, JAK, and SFRP5 levels. SFRP5 polymorphism predicted cardiovascular risk independently.

The role of the male factors in the couple’s infertility has been significantly increased in recent years due to a sententious assessment of male reproductive functions and enhanced diagnostic tools. We investigated the correlations among the seminal plasma (SP) levels of each of zinc, testis-expressed sequence 101 (TEX101), and free amino acids levels with reproductive hormones in adult fertile and infertile men. The study included 100 infertile men categorized into 50 non-obstructive azoospermic patients and 50 patients with idiopathic oligoasthenoteratozoospermia (iOAT), in addition to 50 fertile controls. Semen analyses, serum ELISA assays for male reproductive hormones (follicle-stimulating hormone (FSH), luteinizing hormone (LH), total testosterone, and prolactin), colorimetric assays of SP zinc and total proteins, SP free amino acids using high-performance liquid chromatography (HPLC), and ELISA assays of SP TEX101 were performed for all subjects. Infertile men with azoospermia had significantly lower SP median levels of zinc, TEX101, and many SP free amino acids compared to both men with iOAT and fertile controls (P ˂ 0.05 for all). There were lower SP levels of zinc and some free amino acids among men with iOAT compared to the fertile controls (P ˂ 0.05 for all) with non-significant difference regarding to SP TEX101 (P ˃ 0.05). Azoospermic men exhibited negative correlations between FSH, LH, and prolactin with some SP free amino acids (P ˂ 0.05 for all), and a positive correlation between glycine with total testosterone (P ˂ 0.05). Among iOAT patients, LH and FSH were positively correlated with SP zinc, TEX101, and some measured free amino acids (P ˂ 0.05 for all). Total testosterone was positively correlated with some amino acids, while prolactin was negatively correlated with glycine (P ˂ 0.05 for all). iOAT and azoospermic men exhibited low SP zinc and some free amino acids levels that were more pronounced in azoospermic men and were significantly associated with the reproductive hormones. TEX101 could be a helpful confirmatory test for azoospermia.