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Aluminum, the third most plentiful metal in the Earth’s crust, has potential for human exposure and harm. Oxidative stress plays an essential role in producing male infertility by inducing defects in sperm functions. We aimed to investigate the role of endoplasmic reticulum (ER) stress and mitochondrial injury in the pathogenesis of aluminum chloride (AlCl3)-induced testicular and epididymal damage at the histological, biochemical, and molecular levels, and to assess the potential protective role of taurine. Forty-eight adult male albino rats were separated into four groups (12 in each): negative control, positive control, AlCl3, and AlCl3 plus taurine groups. Testes and epididymis were dissected. Histological and immunohistochemical (Bax and vimentin) studies were carried out. Gene expression of vimentin, PCNA, CHOP, Bcl-2, Bax, and XBP1 were investigated via quantitative real-time polymerase chain reaction (qRT-PCR), besides estimation of malondialdehyde (MDA) and total antioxidant capacity (TAC). Light and electron microscopic examinations of the testes and epididymis revealed pathological changes emphasizing both mitochondrial injury and ER stress in the AlCl3 group. Taurine-treated rats showed a noticeable improvement in the testicular and epididymal ultrastructure. Moreover, they exhibited increased gene expression of vimentin, Bcl-2, and PNCA accompanied by decreased CHOP, Bax, and XBP1 gene expression. In conclusion, male reproductive impairment is a significant hazard associated with AlCl3 exposure. Both ER stress and mitochondrial impairment are critical mechanisms of the deterioration in the testes and epididymis induced by AlCl3, but taurine can amend this.

Abstract: The incidence of metabolic syndrome and diabetes mellitus is increasing globally. A diet rich in carbohydrates increases the hyperglycemic state. While considering the lifestyle changes to combat life-threatening diseases, there is an effort to decrease the daily intake of carbohydrates. A low-carbohydrate diet also makes the body rely more on fat for energy, so there is less fat accumulation. A diet is considered to be low-carbohydrate ketogenic if the intake is ≤ 50 g per day. The ‘low -carbohydrate ketogenic diet’ (LCKD) produces ketosis. LCKD contains high-fat, moderateprotein, and low-carbohydrate components. The main objectives of the present review are to discuss insulin resistance in different viscera of the body, describe the role of adipokines in insulin resistance, understand the mechanism of ketogenesis, and determine the impact of LCKD in overcoming insulin resistance in the body. In the present review, we also highlight the beneficial effects of LCKD in metabolic, neurodegenerative, cardiovascular, and lipid disorders and discuss the effect on longevity and aging. LCKD may help in combating the morbidity and mortality arising from the above-mentioned diseases and also help in leading a better quality of life.

This current study aims to analyse students’ perceptions regarding implementing project-based learning (PjBL) in teaching a molecular biology course to second-year pharmacy students at King Abdulaziz University as a sort of active student-centred learning method. Sixty-five male and 90 female students were enrolled in this study. This research used survey instruments to assess learners’ perceptions. The survey was divided into four sections that consisted of closedended questions to evaluate students’ overall perceptions of PjBL, communication skills, project management and teamwork activity during their project management process. A 5-point Likert scale was used. Regarding overall learning and students’ satisfaction with the PjBL experience, the percentage was 72.73%, with a score of 21.82 over 30. The percentage of students’ perceptions towards the improvement of their communication skills was 60.98%, with a score of 15.25 over 25. The percentage of students’ perceptions of project management skills was 64.97%, with a score of 12.99 over 20. Finally, regarding teamwork, the survey revealed a percentage of 71.81%, with a score of 43.08 over 60. There was a positive correlation between students’ perceptions of the questionnaire’s four parts and their grade point average (GPA) in the molecular biology course. It can be concluded that PjBL is an effective tool in the active-learning process. PjBL can improve students’ communication and management skills. Also, it encourages teamwork activities between students.

Autophagy is a cellular process that eliminates unnecessary cytoplasmic materials, such as long-age proteins, destroyed organelles, and foreign microorganisms. Macroautophagy (MaA), chaperone-mediated autophagy, and microautophagy are the three main types of autophagy. It is regulated by the integration of signaling from the AMPK and mTOR-ULK1 pathways. Autophagy plays a physiological role in health, and its dysregulation could be a pathophysiologic mechanism in different disease conditions. In the current study, we reviewed papers of Google Scholar database, PubMed, PubMed Central, Cochrane Database of Systematic Reviews, MEDLINE, and MedlinePlus with no time limitation and a recent World Health Organization report. In the current review, it could be concluded that autophagy plays many physiological functions, including immune system modulation, and regulates different cellular processes such as metabolism, protein synthesis, and cellular transportation. Dysregulation of autophagy is implicated in tumorigenesis, aging, age-related neurodegeneration, and endothelial dysfunctions. Autophagy dysregulation is also implicated in the newly discovered CoV-COVID-19 pathogenesis.

Obesity is associated with the quantitative changes in miRNAs and their target genes. However, the molecular basis of their dysregulation and expression status correlations is incompletely understood. Therefore, this study aims to examine the shared differentially expressed miRNAs and their target genes between blood and adipose tissues of obese individuals to identify potential blood-based biomarkers.In this study, 3 gene expression datasets (two mRNA and one miRNA), generated from blood and adipose tissues of 68 obese and 39 lean individuals, were analyzed by a series of robust computational concepts, like protein interactome mapping, functional enrichment of biological pathways and construction of miRNA-mRNA and transcription factor gene networks.The comparison of blood versus tissue datasets has revealed the shared differential expression of 210 genes (59.5% upregulated) involved in lipid metabolism and inflammatory reactions. The blood miRNA (GSE25470) analysis has identified 79 differentially expressed miRNAs (71% downregulated). The miRNA-target gene scan identified regulation of 30 shared genes by 22miRNAs. The gene network analysis has identified the inverse expression correlation between 8 target genes (TP53, DYSF, GAB2, GFRA2, NACC2, FAM53C, JNK and GAB2) and 3 key miRNAs (hsa-mir-940, hsa-mir-765, hsa-mir-612), which are further regulated by 24 key transcription factors.This study identifies potential obesity related blood biomarkers from large-scale gene expression data by computational miRNA-target gene interactome and transcription factor network construction methods.

This work aimed to measure serum vascular endothelial growth factor (VEGF) levels before and after Conventional transarterial chemoembolization (cTACE) versus drug-eluting beads (DEB)-TACE and evaluate its efficacy in predicting response to therapy and tumor recurrence.114 patients with unresectable hepatocellular carcinoma complicating hepatitis C virus-related cirrhosis were included. They underwent cTACE (58) or DEB-TACE (56). VEGF serum levels were measured before and on days 1 and 30 after TACE. Patients with complete response (CR) after TACE were followed-up for one year. Statistical analysis was done.VEGF level was higher than baseline after cTACE (VEGF serum levels may predict response to therapy in patients treated by DEB-TACE or cTACE but it has no relation to tumor recurrence.

The current study aimed to investigate the diagnostic value of glycated albumin (GA), glycated hemoglobin (HbA1c), and a number of routine biomarkers as noninvasive indicators of liver fibrosis in patients with chronic hepatitis C (CHC). One hundred patients with CHC were subjected to full medical history and examination, in addition to ultrasound-guided liver biopsy and histopathological examination for assessment of liver fibrosis stage. GA and HbA1c values, GA/HbA1c ratio, liver function tests, complete blood count, and alpha fetoprotein (AFP) were determined. A novel noninvasive index, dubbed Fibrosis Prediction Score (FPS), was selected for predicting significant liver fibrosis based on total bilirubin, glycated albumin, platelet count, age, and AFP. A validation study for FPS was applied on archival data which include 66 diabetics' patients. The FPS had area under the curve (AUC) of 0.92 for classification of patients with significant fibrosis with 81% sensitivity and 95% specificity. The AUCs of FPS in predicting advanced fibrosis and cirrhosis were 0.86 and 0.82, respectively. Comparison of AST-to-platelet ratio index (APRI) and FIB-4 with FPS indicated increased sensitivity and specificity of FPS over APRI and FIB4 in both significant and advanced fibrosis. FPS has a good sensitivity and specificity for prediction of significant and advanced liver fibrosis in patients with CHC.

Background and Aim: Alzheimer’s disease (AD) is the most common cause of dementia. 80% of all dementia is due to AD. Diagnosis of AD is a difficult task, as the accurate diagnosis requires post-mortem examination of brain autopsy samples. Diagnosis of AD in living individuals can be aided by the establishment of the clinical criteria, positron emission tomography (PET) examination, and biomarkers. The study of biomarkers for diagnosis of AD could help clinicians to evaluate individuals at risk, and confirm the occurrence as well as the progression of AD in a non-invasive manner. High sensitivity and high specificity of the used markers are mandatory criteria for these biomarkers to trusted for AD diagnosis and prognosis. So, this review article aims to focus on the potential use of body fluids as a source of the biomarkers that are used for investigating patients with AD. Methodology: In the current study, we reviewed scientific articles that discuss AD pathogenesis and diagnosis of Google Scholar database, Pubmed, Pubmed Central, Cochrane Database of Systematic Reviews (CDSR), MEDLINE, and MedlinePlus with no time limitation. Moreover, we discussed the use of recently discovered biomarkers that are detected in blood, CSF, saliva, and urine. Conclusion: In the current review, it could be concluded that in addition to the blood and cerebrospinal fluid as common biological samples for the diagnosis of AD, saliva and urine are useful potential biological samples. Moreover, both are noninvasive samples that give them priority to be used.

Endoplasmic reticulum (ER) stress could participate in high-fat diet (HFD)-induced hepatic steatosis. The current study aims to investigate the role of ER stress as well as inflammation as possible pathophysiologic mechanisms of HFD-induced hepatic steatosis at ultrastructure and molecular levels. Fifteen control rats on ordinary diet and 30 HFD-fed rats were enrolled in the study. Histological and EM examinations of rats' liver were carried out. Molecular study of TNF-α, CRP, and HNF4α by RT qPCR as well as biochemical investigation of liver function and lipids profile were done. Hepatic steatosis was induced with lipid droplets accumulation at histological level and mega-mitochondria with reduced ER-mitochondrial distance at EM level. Increased gene expression of TNF-α and CRP was significantly correlated with the reduced HNF4α expression and with other ER stress markers. In conclusion, endoplasmic reticulum stress, confirmed at ultrastructure level, plays an important role in pathogenesis of HFD-induced hepatic steatosis. HNF4α downregulation as well as increased expression of hs-CRP and TNF-α enforce the concept of interplay between ER stress, hepatic subclinical inflammation, and disturbed gene expression regulation in the pathogenesis of HFD-induced hepatic steatosis.

This scoping review aims to clarify the interplay between obesity, vitamin D deficiency, cellular senescence, and obesity-related metabolic consequences, mainly subclinical atherosclerosis, and non-alcoholic fatty liver disease (NAFLD). Obesity is a significant global health problem that involves cellular, environmental, behavioral, and genetic elements. The fundamental cause of obesity throughout all life stages is an energy imbalance, and its consequences are countless and, foremost, very common. Obesity has been comprehensively studied in the literature given its association with low serum vitamin D, with many proposed mechanisms linking the two conditions. Moreover, markers of exaggerated cellular senescence have been proven to accumulate in obese individuals. Subclinical atherosclerosis initiates an early stage that ends in serious cardiac events, and obesity, low vitamin D, and senescent cells largely contribute to its associated chronic low-grade inflammation. Furthermore, NAFLD signifies the hepatic manifestation of metabolic syndrome, and studies have highlighted the important role of obesity, vitamin D deficiency, and cellular senescence in its development. Therefore, we outlined the most important mechanisms tying these conditions to one another.

The RECK gene, a tumor suppressor gene, inhibits angiogenesis, invasion, and tumor metastasis. Epigenetic regulation of the RECK gene constitutes a potent approach to the molecular basis of liver malignancy. This study aims to evaluate the promoter methylation status of the RECK gene and its serum level in patients with hepatitis C virus (HCV)-related hepatocellular carcinoma (HCC) and the potential association of RECK gene methylation with clinical criteria of HCC. One hundred and fifty-five subjects were included (healthy control [55], chronic HCV patients [55], HCV-related HCC patients [45]). The methylation status of the RECK gene promoter and serum RECK level were investigated by methylation-specific PCR and enzyme-linked immunosorbent assay techniques, respectively. RECK gene promoter hypermethylation was recorded in 46.7% of HCC patients, and 10.9% of HCV patients, but not in control subjects (0%). It was related to RECK protein level, varices, edema, ascites, lymph node metastasis, vascular invasion, and the largest diameter of focal lesions. Meanwhile, it was not associated with focal lesion number nor distant metastasis of HCC. In conclusion, RECK gene promoter hypermethylation is linked to HCV genotype-4-related HCC. Moreover, different degrees of RECK gene promoter methylation are associated with serum RECK level, lymph node metastasis, and vascular invasion, which could prove its pathogenic role in hepatocarcinogenesis in chronic HCV-infected patients.

Systemic Lupus Erythematosus (SLE) and systemic sclerosis (SSc) are systemic inflammatory autoimmune disorders characterized by a large spectrum of clinical and laboratory features. The aim of the present study was to investigate the possible use of serum level of soluble intercellular adhesion molecule-1(sICAM-1) and soluble interleukin-2 receptor (sIL-2Ra) as biomarkers for monitoring of SLE and SSc disease activity. Moreover, it aimed to compare the specificity and sensitivity as well as cut-off value of both biomarkers in a sample of Egyptian patients. 50 SLE patients, 30 SSc patients and 60 age and sex matched healthy controls were enrolled in our study. sICAM-1and sIL-2Ra were measured in serum samples obtained from all participants. In addition to Erythosedimentation rate (ESR), complete blood count (CBC), Antineuclearantibodies (ANA) estimation, disease activity of both diseases were also assessed. sICAM-1and sIL-2Ra levels were higher in SLE and SSc patients versus control. Both parameters are correlated with each other as well as the activity parameters. A cut-off levels of 455.59 (ng/ml) &2525935 (pg/ml) in both SLE & SSs respectively was observed with the highest specificity and sensitivity. It could be concluded that sICAM-1 and sIL-2Ra are noninvasive biomarkers for SLE and SSc that could play a pathophysiologic role in development and progression of both diseases. Moreover, sICAM-1 and sIL-2Ra are correlated with the disease activity at cut-off values of 455.59 (ng/ml) & 2525935(pg/ml) respectively.

Hepatitis C virus (HCV) related liver cirrhosis occurs in about 20% of chronically infected patients over a duration of 10-20 years, and within 5 years approximately 10-20% of these cirrhotic patients will develop hepatocellular carcinoma (HCC). Previous studies report that the X-ray repair cross-complementing group1 gene (XRCC1) is important in the risk of HCC development; however, results obtained from these studies are conflicting rather than conclusive. We hypothesised an association between single nucleotide polymorphisms (SNPs) in XRCC1 with the HCC risk on a background of chronic hepatitis C.We recruited 210 subjects, 70 with HCC, 70 with cirrhosis and 70 healthy controls. Two SNPs [c.1254CT(rs2293035) and c.1517GC(rs139599857)] in XRCC1 were genotyped using created restriction site-polymerase chain reaction (CRS-PCR) and PCR-restriction fragment length polymorphism (PCR-RFLP) methods.The TT genotype, CT genotype and T-allele in c.1254CT (rs2293035) were linked to risk of HCC compared to the CC genotype: OR 3.58 [confidence interval (CI) 95%: 1.19-10.7] p = 0.019; OR 2.16 (CI 95%: 1.04-4.47) p = 0.037 and OR 2.10 (CI 95%: 1.2-3.3) p = 0.006, respectively. Regarding c.1517GC (rs139599857), the CC genotype, GC genotype and C-allele were linked with higher risk of developing HCC compared to GG genotype: OR 4.77 (CI 95%: 1.3-16.9), p = 0.016; OR 3.02 (CI 95%: 1.46-6.2), p = 0.002 and OR 2.4 (CI 95%: 1.4-4.0), p = 0.001, respectively.We conclude that the T-allele of c.1254CT (rs2293035) and the C allele of c.1517GC (rs139599857) genetic variants may be associated with increased HCC risk among chronic hepatitis C patients.

The exact link between obesity, vitamin D deficiency, and their relation to cellular senescence in the pathogenesis of subclinical atherosclerosis is still under debate. Therefore, the current study aims to verify the possible role of vitamin D deficiency and cellular senescence in the pathogenesis of obesity-related subclinical atherosclerosis. Moreover, it aims to investigate the possible protective role of vitamin D supplementation. Fifty-seven male albino rats were enrolled in the study and classified into four groups: negative (10) and positive control groups (10), an obese model group (24), and a vitamin-D-supplemented obese group (13). Aortic tissue samples and fasting blood samples were collected. The following biochemical investigations were performed: serum cholesterol, triglycerides, HDL-C, LDL-C, ALT, AST, CPK, CK-MB, and hs-cTnt. HOMA-IR was calculated. Moreover, serum SMP-30, 25 (OH)Vitamin D3, and eNOS were determined by the ELISA technique. Aortic gene expression of eNOS, SMP-30, and P53 was estimated by real-time qRT-PCR. Serum 25(OH) D3 and SMP-30 were lower in the obese group. In addition, the obese group showed higher serum lipid profile, HOMA-IR, eNOS, ALT, AST, CPK, CK-MB, and hs-cTnt than the control groups, while decreased levels were found in the vitamin-D-treated obese group. Gene expression of eNOS and SMP-30 were in accordance with their serum levels. A positive correlation was found between vitamin D level and SMP-30. In conclusion, obesity is associated with vitamin D deficiency and enhanced cellular senescence. They could play a role in the pathogenesis of obesity-associated subclinical atherosclerosis and endothelial dysfunction. Vitamin D supplements could play a protective role against such obesity-related comorbidity.

BackgroundAt King Abdulaziz University, medical and health science schools depend on admission exams (aptitude and achievement) and preparatory year scores in their students’ selection. However, with the growing number of applicants and the drastic changes in teaching and assessment in these colleges, continuous assessment and development of admission criteria are needed. In this study, we aimed to evaluate the correlation of admission exam scores, in addition to the preparatory year Grade Point Average (GPA), with academic performance in the basic science subjects such as Clinical Biochemistry and Clinical Pharmacology in health science colleges.MethodsThe study was conducted on four cohort studies, two faculty of nursing cohorts; nursing students (2017-2018,n=146) nursing students (2018-2019,n=81), and two faculty of applied medical sciences cohorts, clinical nutrition students (2017-2018,n=33), and clinical nutrition students (2018-2019,n=28). The students’ scores of General Aptitude Test (GAT), Scholastic Achievement Admission Test (SAAT), and preparatory year GPA were all recorded at the beginning of each semester before the beginning of courses. Clinical Biochemistry and Clinical Pharmacology exam results were recorded at the end of the semester. Correlation was done for each cohort and all cohorts pooled.ResultsResults showed only a weak correlation detected between SAAT and the overall achievement in Clinical Biochemistry (r= 0.192,P= 0.042) in nursing students (2017-2018), but no correlation was seen with SAAT or preparatory year scores. There was also no significant correlation between admission exams scores and the students’ academic achievement in Clinical Biochemistry or Clinical Pharmacology. On the other hand Clinical Pharmacology exam results showed a significant positive correlation with Clinical Biochemistry results (r=0.688,P=0.000).ConclusionOur results could indicate the need to revisit the admission criteria for these colleges. Furthermore, specific preparatory year tracks for health science colleges can ensure that students improve the specific skills and knowledge required for their future college years3

Background. Oral mucositis is the most debilitating and troublesome adverse effect of irinotecan (CPT-11) treatment. It adversely affects the patient quality of life. The aim of this work was to study the histological, immunohistochemical, and molecular changes in the oral mucosa by CPT-11 and the possible alleviated role of atorvastatin. Methods. Rats were randomly divided into control, CPT-11-treated group, and CPT-11+ atorvastatin-treated group. At the end of the experiment, the anterior two-thirds of the tongue was dissected out and divided into two parts: one part for light microscopic examination and the second for molecular study. Results. CPT-11-treated group revealed loss of normal mucosal organization, areas of ulceration and inflammation, and loss of architecture of lingual papillae. A significant decrease in immunohistochemical and molecular gene expression of Ki-67 and antiapoptotic Bcl-2 levels was observed. A significant increase in NF-κB immunohistochemical and mRNA gene expression level and a nonsignificant increase in Nrf2 gene expression were detected. Coadministration of atorvastatin showed remarkable improvement in the histopathological picture with a significant increase in Ki-67 and Bcl-2, a significant decrease in NF-κB protein and gene expression, and a significant increase in Nrf2 gene expression. Conclusion. Atorvastatin substantially attenuates CPT-11-induced oral mucositis through the initiation of the antiapoptotic gene, modulation of the inflammatory, and antioxidant gene expression.

Background: In King Abdulaziz University, medical and health science schools depend on admission exams (Aptitude and Achievement) and Preparatory year scores in their students’ selection. However, with the growing number of applicants and the drastic changes in teaching and assessment in these colleges continuous assessment and development of admission criteria are needed. In this study, we aimed to evaluate the correlation of admission exam scores, in addition to the Preparatory year GPA, with academic performance in the basic science subjects such as Clinical Biochemistry and Clinical Pharmacology in health science colleges.Methods: The study was conducted on four cohort studies, two faculty of nursing cohorts; Nursing students (2017-2018,n=146) Nursing students (2018-2019,n=81), and two faculty of applied medical sciences cohorts, C.Nutrition students (2017-2018,n=33), C.Nutrition students (2018-2019,n=28) .The students’ scores of GAT, SAAT, and preparatory year GPA were all recorded at the beginning of each semester before the beginning of courses. Clinical Biochemistry and Clinical Pharmacology exam results were recorded at the end of the semester. Correlation was done for each cohort and all cohorts pooled. Results: Results showed that there was no significant correlation between admission exams scores and the students ‘academic achievement in Clinical Pharmacology, and with only a weak correlation detected between SAAT and the overall achievement in Clinical Biochemistry ( r= 0.192*, P= 0.042) in Nursing students (2017-2018). On the other hand Clinical Pharmacology exam results showed a significant positive correlation with Clinical Biochemistry results (r=0.688, P=0.000). Conclusion: Our results could indicate the need to revisit the admission criteria for these colleges. Furthermore, specific preparatory year tracks for health science colleges can ensure that students improve the specific skills and knowledge required for their future college years.

Background Nonalcoholic fatty liver disease (NAFLD) is a pathological process characterized by excessive hepatic fatty deposition with possible involvement of vitamin D deficiency and cellular senescence. The aim of this study is to investigate the pathophysiologic role of vitamin D deficiency and cellular senescence in NAFLD development. Moreover, it aims to investigate the potential protective role of vitamin D supplementation. Methods This is an experimental Case/Control study. Forty-five male albino rats were enrolled in this study. Animals were divided into four groups: negative and positive control groups (10 for each group), a model of NAFLD (11) and vitamin D–treated NAFLD groups (14). At the end of the experiment, all rats were subjected to the following investigation; biochemical estimation of serum 25 hydroxycholecalciferol, senescence marker protein–30 (SMP-30), lipid profile and calculation of homeostatic model of insulin resistance (HOMA-IR). Results NAFLD group shows a significant increase in glucose, insulin levels, and HOMA- IR compared with both normal controls. This finding indicates the intimate association between insulin resistance and NAFLD pathogenesis. Moreover, it was found that NAFLD group shows a significant decrease in SMP-30 level compared with normal controls. While vitamin D–treated NAFLD group shows significant increased SMP-30 and decrease in HOMA-IR in comparison with nontreated NAFLD group. Conclusion Vitamin D deficiency and increased cellular senescence are key features of NAFLD. Vitamin D supplementation could play a protective role, which needs further investigation including clinical human study.

Background Androgenetic alopecia (AGA) is associated with a risk of coronary heart disease (CHD), although the causes underlying this association are not clear. Serum homocysteine (SH) is a known risk factor for CHD, and methylene tetrahydrofolate reductase enzyme (MTHFR) plays a crucial role in the remethylation of homocysteine to methionine. The polymorphism C677T that affects the catalytic domain of the MTHFR protein leads to a high levels of SH. Our hypothesis was that this polymorphism and SH level are risk factors for CHD in patients with AGA. Materials and methods A total of 106 patients with AGA and 100 well-matched healthy controls were enrolled in the study. SH levels were estimated. DNA was extracted and polymerase chain reaction amplification, followed by restriction enzyme digestion for MTHFR (C677T) gene, was conducted. Results SH levels were significantly higher in the patient group and highest in those with the TT genotype. The mutant T allele was associated with hyperhomocysteinemia and an increased risk of CHD in patients with AGA. Conclusions AGA is associated with a higher risk of developing CHD due to the associated higher level of SH that, in turn, depends on and is correlated with mutant MTHFR genotypes. Cardiac evaluation and follow-up of patients with AGA is recommended for early detection and treatment of CHD to avoid an overall detrimental course.

Non-alcoholic fatty liver disease (NAFLD) is a public health burden associated with significant liver-related and unrelated morbidity and mortality [1]. Results of epidemiological studies suggest t...

Introduction: Male factor is responsible for about half of infertility problems. However, the reasons for the decrease in male fertility are still broadly unclear. The mechanisms of how smoking may impact male fertility have not been established. However, with its influence on different semen parameters, it is regarded as a risk factor for infertility.Aim: To investigate the effect of chronic smoking on spermatozoa NRF2 expression and DNA fragmentation in infertile men with apparently normal seminogram and to determine if NRF2 expression and DNA fragmentation markers could be possible predictors of the impact of chronic cigarette smoking on male fertility.Methods: Semen samples were collected from 170 subjects; 65 nonsmokers (40 fertile and 25 infertile) and 105 smokers (25 fertile and 80 infertile). NRF2 gene expression, 8-OHdG and DNA fragmentation were assayed.Results: There were significant increases in 8-OHdG and %DNA fragmentation with a significant decrease in NRF2 gene expression in infertile smokers. ROC curve analysis of spermatozoa NRF2 gene expression showed 95% sensitivity 93.3% specificity at cutoff value ≤0. 931 (p 19.33 pg/ml predicting the detrimental effect of smoking on spermatozoa DNA.Conclusion: Chronic cigarette smoking may be a hidden causative mechanism of delayed fertility. Spermatozoa NRF2 gene expression and seminal 8-OHdG levels may serve as sensitive diagnostic indicators predicting smoking induced infertility. So, the presence of normal seminal parameters could not be an exclusion of potential effect of chronic smoking on male fertility.

With emerge of the COVID-19 pandemic, video-based lectures (VBLs) was widely used as an effective online faculty development tool. VBLs varies from short videos (5-minute) to the long one (1-2 hours). So, the current study aims to evaluate the effectiveness of long VBLs versus short VBLs. A total of 21 short (9) and long (12) VBLs were produced, in 2020, by the authors. The metadata for all of VBLs was downloaded from YouTube [VBLs overview data, audiences’ engagement data, and audience retention (AR) report]. The viewership data included the number of views (4800), watch time by hours (173.6), males to females’ ratio (79/21), the number of the subscribers (157), the video length (2.9±1.2 minutes), number of viewers (241.1±157.8), and the watch time (5.1±3.3 hours). The audience retention is presented as average view duration (1.1±0.4 hours) and average percentage view (42.8±7.9%). Lastly, audience engagement is represented by the number of subscribers (6.4±7.4), likes (9.7±8.0), and dislikes (0.3±0.7). The comparison of the mean audience retention and engagement between short and long VBLs showed that short VBLs had significantly higher number of subscribers and likes as well as the average percentage views in comparison to long VBLs. We could conclude that short VBLs are more effective and efficient as a regard audience retention and engagement. Moreover, the more use of advanced technology for video development makes it more engaging.

Background. Fractalkine is produced in seminal plasma in small amounts and correlates with sperm motility. Purpose. To investigate the possible effect of low-level leucospermia on spermatozoa oxidative stress and sDNA fragmentation in patients with subclinical varicocele and apparently normal seminogram, and also to study the role of spermatozoal fractalkine and its receptor (CX3CR1) gene expression as a marker of spermatozoa inflammatory response. Methods. This study included 80 patients with subclinical varicocele (45 fertile and 35 infertile) and 45 age-matched fertile volunteers. In semen samples, fractalkine and CX3CR1 gene expression were investigated by qRT-PCR. Moreover, seminal plasma malondialdehyde (MDA) and total antioxidant capacity (TAC) were measured. Results. There are significant decrease in semen quality and significant increase in seminal leucocytes count in subclinical varicocele. Our results show a significant increase in MDA and TAC levels, DNA fragmentation, and expression levels of fractalkine and its receptor (CX3CR1) in subclinical varicocele groups. Conclusion. Subclinical varicocele induces seminal and spermatozoal subclinical inflammatory response in the form of low-level leucospermia and increased mRNA expression of the fractalkine signaling pathway, leading to increased spermatozoal ROS production, oxidative stress, and DNA fragmentation. These could cooperate in the pathogenesis of delayed fertility in males with subclinical varicocele.

Background and aim of the work The current study postulated that cyclosporine A (CSA) could induce gender-specific renal damage. Hence, the current study aims to investigate the nephrotoxic effect of perinatal exposure of male and female rat progeny to CSA. Moreover, it aims to evaluate the oxidative stress and inflammation as a possible pathophysiologic mechanism. Materials and methods Female rats were randomly allocated to two groups of four and assigned to undergo either CSA (15 mg/kg/day; the 6th day after conception and continuing until the progeny were weaned) or vehicle treatment as control groups. At the age of 6 weeks, the progeny were divided into the following four groups: male progeny of control-group mothers (M-vehicle, 7); male progeny of CSA-treated mothers (M-CSA, 9); female progeny of control-group mothers (F-vehicle, 7); and female progeny of CSA-treated mothers (F-CSA, 6). Serum adiponectin, tumor necrosis factor-α (TNF-α) and creatinine, creatinine clearance, and urinary 8-isoprostane were measured. Histopathological examination by hematoxylin and eosin stain of Kidney was carried out. Results Proteinuria and decreased creatinine clearance are significant in M-CSA than M-vehicle and F-CSA. 8-isoprostane is lower in F-CSA than F-vehicle. Increased TNF-α and decreased adiponectin levels in M-CSA than M-vehicle were observed. No significant differences were found in female rat groups. Conclusion From the current study, it could be concluded that CSA could induce renal inflammation as well as oxidative stress that may explain the impaired renal function. The sex difference was a prominent finding in their vulnerability to CSA effects.

Background: Sodium valproate (VPA) is an antiepileptic drug (AED) licensed for epilepsy and used during pregnancy in various indications. Alpha-lipoic acid (ALA) is a natural compound inducing endogenous antioxidant production. Our study aimed to investigate the effect of prenatal administration of VPA on the pancreas of rat offspring and assess the potential protective role of ALA co-administration during pregnancy. Methods: Twenty-eight pregnant female albino rats were divided into four groups: group I (negative control), group II (positive control, ALA treated), group III (VPA-treated), and group IV (VPA-ALA-treated). The pancreases of the rat offspring were removed at the fourth week postpartum and prepared for histological, immune-histochemical, morphometric, molecular, and oxidative stress marker studies. Results: In group III, there were pyknotic nuclei, vacuolated cytoplasm with ballooning of acinar, &alpha, and &beta, cells of the pancreas. Ultrastructural degeneration of cytoplasmic organelles was detected. Additionally, there was a significant increase in oxidative stress, a decrease in insulin-positive cell percentage, and an increase in glucagon positive cells in comparison to control groups. Moreover, VPA increased the gene expression of an apoptotic marker, caspase-3, with a decrease in anti-apoptotic Bcl2 and nuclear factor erythroid 2-related factor 2 (Nrf2) transcriptional factor. Conversely, ALA improved oxidative stress and apoptosis in group VI, and a consequent improvement of the histological and ultrastructure picture was detected. Conclusion: ALA co-administration with VPA significantly improved the oxidative stress condition, histological and morphometric picture of the pancreas, and restored normal expression of related genes, including Nrf2, caspase-3, and Bcl-2. Administration of &alpha, lipoic acid has a protective effect against VPA-induced pancreatic oxidative damage via its cytoprotective antioxidant effect.

This article was migrated. The article was marked as recommended. Background and aim of the study: Proper online students'/teacher communication and awareness of the use of Blackboard as an online learning community could result in the improvement of student academic achievement. So, the aim of the current project was directed to encourage students and faculty for using Blackboard as an online learning community tool. Moreover, it aimed to measures their perceptions. Subjects and Methods: The study was directed to the second year Medical students during teaching of Clinical Biochemistry. We started by pre-implementation survey, followed by orientation workshop, engaging students for Blackboard implementation then ended in post-implementation survey to evaluate how come students are engaged and satisfied. Results: The first questionnaire group indicated the students' perceptions of Blackboard use and usefulness as an online learning community tool. The second questionnaire group was related to the Interest & Enjoyment of using Backboard. While Blackboard Tools are presented in the third questionnaire questions group. The comparison regarding the total perception of the three groups of the questionnaire between pre-implementation versus post-implementation survey results showed significant improvement of students' perception in the post-implementation phase. By correlating grades in Clinical Biochemistry and total GPA to the questionnaire groups, total perceptions showed a non-significant correlation between all studied parameters in the pre-implementation phase while significant positive correlations were detected in the post-implementation phase. Conclusion: Based on the presented second-year medical students' perception and satisfaction, we could confirm that the Blackboard online platform is a very successful online line learning community tool. Blackboard together with face to face classroom-based learning methods helps students for better learning achievement. Moreover, the online learning community is considered a complementary tool to that of classroom-based learning as it facilitates students/students and students'/faculty communication and minimizes the time required for physical contacts.

Background: The 2019-2020 coronavirus pandemic has affected educational systems worldwide, leading to widespread closures of schools and universities and social distancing Hence, the shift to an online tool was required Aims and Objectives: The main problem postulated is the lack of student-teacher interaction that occurs with online learning Methods: The Blackboard Collaborate Ultra platform was used to deliver lectures on clinical biochemistry and the reproductive module to our students Our main goal was to achieve students' engagement and interaction Results: There were 189 male students enrolled in the reproductive module The attendance rate was 93%-95% The download of the recording was 100% The active participation rate was up to 87% Hence, Blackboard Collaborate Ultra's virtual classrooms are very useful tools for online interactive lecturing Conclusion: Based on this experience gained, we could conclude that interactive virtual classroom lecturing can be used in addition to or instead of traditional lectures during ordinary situations as a successful online learning community tool © MEDKNOW 2020 All rights reserved

BACKGROUND The first-line treatment option for intermediate-stage hepatocellular carcinoma is trans-arterial chemoembolization (TACE). Blood indices, such as lymphocyte/monocyte ratio (LMR), lymphocyte count, neutrophil/lymphocyte ratio (NLR), platelet/lymphocyte ratio (PLR), monocyte-granulocyte/lymphocyte ratio (MGLR) and red blood cell distribution width (RDW), are prognostic biomarkers in certain diseases. The model for end-stage liver disease (MELD) and Child-Turcotte-Pugh (CTP) scores have been designed for patients with cirrhosis waiting for liver transplantation and in patients with hepatocellular carcinoma. We hypothesized possible roles for these blood indices, and the MELD and CTP scores as predictors for early recurrence of hepatocellular carcinoma after TACE. METHODS Routine laboratory indices determined the NLR, LMR, MGLR, RDW, PLR, as well as MELD and CTP scores in 147 patients. Sensitivity and specificity of the indices for hepatocellular carcinoma recurrence 36 months after TACE were estimated by receiver operator characteristic curve. RESULTS In multivariate regression analysis, only male sex, the lymphocyte count, CTP, the MGLR and the MELD score significantly (P

Background Many oral presentations of osteoporosis-a bone metabolic disease-were recorded. Thus, we aimed to assess panoramic radiomorphometric indices with bone mineral density (BMD) values among Saudi postmenopausal women and its importance in the prediction of osteoporosis. Methods A total of 431 Saudi women were enrolled in this study. Panoramic radiographs were obtained at the time of BMD measurement. Subjects were fatherly classified into; normal BMD, osteopenia, and osteoporosis groups. Serum follicle-stimulating hormone, luteinizing hormone (LH), estradiol (E2), 25-hydroxy-vitamin D (25[OH]D) and intact-parathyroid hormone were measured. Moreover, serum creatinine, calcium, and phosphate, together with serum osteocalcin (s-OC), procollagen type I N-terminal propeptide (s-PINP) and cross-linked C-terminal telopeptide of type 1 collagen (s-CTX) were measured. Receiver-operator curve (ROC) curve analysis for use of mandibular cortical width (MCW), panoramic mandibular index (PMI), and maxillary-mandibular ratio (M/M ratio) to differentiate women with osteoporosis or osteopenia from normal subjects was calculated. Cut off values of 4.6 at T score

BackgroundSystemic sclerosis (SSc) is an autoimmune disorder of unknown origin, characterized by excess accumulation of the extracellular matrix in the skin and other internal organs.Aim of the workThe current study was designed to establish an animal model of SSc in order to analyze the histologica

Prostate cancer is one of the most common cancers and the second cause of cancer-related deaths among men. Metals are recognized as chemical carcinogens where chronic exposures to such metals are implicated in the development of cancer, including prostate cancer. This in vitro study demonstrates the relative death sensitivity of prostatic (RWPE-1) cells to arsenic (As), cadmium (Cd), and chromium (Cr) as environmental pollutants through its apoptotic effects and the effect of these chemicals on prostate-specific antigen (PSA) gene expression as a marker for their carcinogecity. RWPE-1 cells were divided into three groups that were treated with As, Cd, and Cr in three replicates, at three different concentrations for each metal for 48 h. A control group consisted of untreated RWPE1 cells was used. Apoptosis was assessed using comet assay and caspase 3 gene expression; meanwhile, PSA gene expression was evaluated by semiqualitative real-time PCR (RT-PCR). One of the novel findings of this study is that arsenic and cadmium at low concentrations decreased apoptosis of RWPE-1 cells in a concentration-dependent manner while chromium induced significant concentration-dependent increase in apoptosis. Yet, at the highest concentrations, apoptosis was relatively more induced by all chemicals. Arsenic was the most chemical inhibiting apoptosis in RWPE-1 cells at low concentration. While at the moderate and highest concentrations, cadmium was the most inhibiting chemical of RWPE-1 cells' apoptosis. No distinct differences between treated and untreated cells for PSA gene expression were observed. It can be concluded that As and Cd, at low concentrations, can reduce apoptosis of prostatic cells in a concentration-dependent manner while chromium induced it; however, all metal salts used in this study did not induce PSA gene expression.

Background: Academic staff members, who are responsible for teaching and training, should be aware of the principle of online course design, development, and implementation. The aim of this study is to evaluate instructors’ skills and needs for conducting distance learning healthcare courses, including the level of assistance they need to implement and use online and software tools in online courses.Methods: The current study applied online faculty survey used by the Center for Teaching Excellence, University of South Carolina to assess the faculty’s instructional technology needs for training and support. The survey asked faculty staff about a broad number of classroom and online technologies, with a helpful response scale that reveals not only what the faculty is already using, but also what the instructors want to use and what they need help with.Results: The results of this study revealed a significant need of faculty staff members for the training and development of their skills in almost all tools used for conducting online courses. The female responder was higher than males. Regarding the use of software, although the majority of participating staff members in this study use almost all software tools required for conducting online healthcare courses, they expressed a need for help in developing new ideas to use the software effectively.Conclusions: From this study, it could be concluded that it is essential to organize comprehensive faculty development training courses for staff members to help them in conducting their online courses or converting their face-to-face courses to blended courses effectively.

To evaluate the effect of immediate postpartum curettage on rapid resolution of clinical and laboratory indices in pre-eclampsia and eclampsia women. A randomized controlled study, comprised of 420 pre-eclamptic or eclamptic women with singleton pregnancy 24 weeks gestation and more. Patients were divided into two groups: 220 patients underwent immediate postpartum curettage and 200 patients as a control group. The clinical and laboratory prenatal parameters showed no statistical significant differences between both groups. The follow-up for the postnatal clinical and laboratory data showed significant improvement for the mean arterial blood pressure in the curettage group over 6, 12, and 24 h after delivery and significant improvement in the platelet count as well. The average time required for MAP to reach 105 mmHg or less was significantly shorter (P

Background and aim: Loss of p53 function has been suggested to be a critical step inmultistage hepatocarcinogenesis. So, we aimed to investigate the frequency of P53codon 72 gene polymorphism and its relation to plasma P53 levels in Egyptianpatients with hepatocellular carcinoma (HCC) on top of viral and nonviral etiologies.Methods: This is a hospital-based case-control study which included 159 HCCpatients in addition to 83 healthy volunteers as controls. Patients were classified into:63 patients with HCC complicating cirrhosis due to HCV; 55 patients with HCCcomplicating cirrhosis due to HBV and 41 patients with HCC complicating cirrhosisdue to nonviral causes. Quantitative determination of plasma P53 levels wasperformed by ELISA. P53 Arg 72 Pro gene polymorphism was carried out byconventional PCR followed by restriction enzyme digestion (PCR-RFLP). Results:There were significant increases in α.fetoprotein and plasma P53 levels in all studiedgroups in relation to the control group. AA genotype and A allele were more in thecontrol group, PP genotype and P allele were more frequent in HCV related HCCgroup & HCC with non viral causes. AP genotype and P allele were more frequent inHBV related HCC group. P 53 plasma level showed significant increase in all groupsin relation to the control group in AA genotype, AP genotype and PP genotype. Therewere significant increases in AP and PP genotype in all studied groups in comparisonto AA genotype. Plasma P53 level showed significant increase in all groups in bothallele A and allele P when compared with the control group. Also, it showedsignificant increase in their levels in P allele when compared with that of A allele inall studied groups. Conclusion: plasma p53 protein level could be considered as anadditional tumor marker to AFP to increase the diagnostic potential of AFP in HCCpatients. Therefore, P53codon 72 gene polymorphism could be used as an indicatorof the genetic susceptibility for future development of HCC in Egyptian cirrhoticpatients.

To build a diagnostic non-invasive model for screening of large varices in cirrhotic hepatitis C virus (HCV) patients.This study was conducted on 124 post-HCV cirrhotic patients presenting to the clinics of the Endemic Medicine Department at Mansoura University Hospital for evaluation before HCV antiviral therapy: 78 were Child A and 46 were Child B (score ≤ 8). Inclusion criteria for patients enrolled in this study was presence of cirrhotic HCV (diagnosed by either biopsy or fulfillment of clinical basis). Exclusion criteria consisted of patients with other etiologies of liver cirrhosis, e.g., hepatitis B virus and patients with high MELD score on transplant list. All patients were subjected to full medical record, full basic investigations, endoscopy, and computed tomography (CT), and then divided into groups with no varices, small varices, or large risky varices. In addition, values of Fibrosis-4 score (FIB-4), aminotransferase-to-platelet ratio index (APRI), and platelet count/splenic diameter ratio (PC/SD) were also calculated.Detection of large varies is a multi-factorial process, affected by many variables. Choosing binary logistic regression, dependent factors were either large or small varices while independent factors included CT variables such coronary vein diameter, portal vein (PV) diameter, lieno-renal shunt and other laboratory non-invasive variables namely FIB-4, APRI, and platelet count/splenic diameter. Receiver operating characteristic (ROC) curve was plotted to determine the accuracy of non-invasive parameters for predicting the presence of large esophageal varices and the area under the ROC curve for each one of these parameters was obtained. A model was established and the best model for prediction of large risky esophageal varices used both PC/SD and PV diameter (75% accuracy), while the logistic model equation was shown to be (PV diameter × -0.256) plus (PC/SD × -0.006) plus (8.155). Values nearing 2 or more denote large varices.This model equation has 86.9% sensitivity and 57.1% specificity, and would be of clinical applicability with 75% accuracy.

The clinical application of doxorubicin is limited by its cardiotoxicity. The present study investigated the effect of valsartan on doxorubicin-induced cardiotoxicity in rats. Rats were divided into 6 groups: control, control + valsartan (10 mg/kg, for 14 days, orally), doxorubicin-treated (2.5 mg/kg, 3 times/week for 2 weeks, intraperitoneally), valsartan then doxorubicin, valsartan + doxorubicin, and doxorubicin then valsartan. ECG, isolated heart, lipid peroxidation (thiobaribituric acid reactive substances (TBARS)), total antioxidant capacity (TAC), and Bax, Bcl-2, and senescence marker protein 30 (SMP30) gene expression were measured in cardiac tissue. Blood samples were collected to measure lactate dehydrogenase (LDH) and creatine kinase MB (CK-MB). Doxorubicin significantly increased LDH, CK-MB, TBARS, heart rate (HR), Bax gene expression, and −dP/dtmax and decreased TAC, Bcl-2 and SMP30 gene expression, left ventricular developed pressure (LVDP), and +dP/dtmax. Also, doxorubicin lengthened ST, QT, and QTc intervals. Concurrent or post- but not pre-treatment of doxorubicin-treated rats with valsartan reduced LDH, CK-MB, TBARS, HR, Bax gene expression, −dP/dtmax, and ST, QT, and QTc intervals and increased TAC, Bcl-2 and SMP30 gene expression, LVDP, and +dP/dtmax. Therefore, we conclude that concurrent or post- but not pre-treatment of doxorubicin-induced rats with valsartan attenuated doxorubicin-induced cardiotoxicity through inhibiting oxidative stress, apoptosis, and senescence.

The objective of this study was to investigate the modulation of metabolic dysfunctions, adiponectin levels, and cardiac dysfunctions of type 2 diabetes mellitus (T2DM) by a combination of the insulin sensitizer rosiglitazone and angiotensin receptor blocker telmisartan in an experimental rat model. Fifty male adult Sprague–Dawley rats were divided equally into 5 groups. Group I: fed normal chow; served as normal control group. Groups II–V: fed a high-fat diet (HFD) for 2 weeks, followed by injection of streptozotocin (STZ; 35 mg/kg) to create a model of T2DM. Group II: treated with vehicle. Group III: treated with rosiglitazone (4 mg/kg). Group IV: treated with telmisartan (5 mg/kg). Group V: treated with both agents. Untreated HFD-STZ rats showed elevated fasting blood glucose, insulin, homeostasis model assessment (HOMA) index, triglycerides (TGs), low-density lipoprotein cholesterol (LDL), and total serum cholesterol (TC), with a decrease in high-density lipoprotein cholesterol (HDL) and adiponectin levels (p < 0.001). Rosiglitazone exerted more improvement in all parameters than telmisartan did, and a combination of both did not augment the improvement further, except for TGs and adiponectin. For the isolated atrial study, a combination of rosiglitazone and telmisartan corrected the responses of the atria of HFD-STZ rats to the negative inotropic effect induced by adenosine better than either one did alone, whereas this combination, surprisingly, significantly attenuated the positive inotropic response to β-adrenoreceptor and α-adrenoreceptor agonists. In conclusion, rosiglitazone significantly improved the metabolic and cardiac dysfunctions in T2DM. Moreover, a combination of rosiglitazone and telmisartan offered more improvement in serum TGs and adiponectin, and restored the atrial inotropic response to adenosine. Surprisingly, this combination significantly attenuates the positive inotropic response to α1-adrenoreceptor and β-adrenoreceptor agonists.