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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.

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.

Homing and tumor attenuation potential of BM-MSCs labelled with superparamagnetic iron-oxide nanoparticles (SPIONs) in a rat model of hepatic cirrhosis was evaluated. Rat BM-MSCs were derived, characterized and labelled with SPIONs (200 nm; 25 mg Fe/ml). Hepatic cirrhosis was induced in Wistar rats (n=30; 10/group) with carbon tetrachloride (CCl4; 0.3 mL/kg body weight) injected twice a week for 12 weeks. Group-I was administered vehicle (castor-oil) alone; Group-II received two doses of unlabelled BM-MSCs (3x106 cells) and Group-III received two doses of SPIONs labelled BM-MSCs (3x106 cells) via tail vein injection (0.5 ml) at weekly intervals. All animals were sacrificed after two weeks for histological, radiological and biochemical analysis. Derived BM-MSCs demonstrated MSCs related CD markers. Histology confirmed induction of hepatic cirrhosis with CCL4. Levels of alanine-aminotransferase, aspartate-aminotransferase,alkaline-phosphatase and gamma glutamyl-transferase returned to normal levels following treatment with BM-MSCs. Uptake and homing of SPIONs labelled BM-MSCs, and reduction in the size of cirrhotic nodules were confirmed using transmission electron microscopy and magnetic resonance imaging respectively. BM-MSCs reduced the pathological effects of CCL4 induced hepatic cirrhosis and labelling BMMSCs with SPIONs were non-toxic and enabled efficient tracking using non-invasive methods.

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.

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.

Cardiac Arrhythmias (CA) are responsible for syncope and sudden cardiac death (SCD) in several million cases worldwide. The molecular basis of CA pathogenesis is known, but the underlying mechanisms connecting genotype to phenotype changes in the proteins are not yet fully explored. Hence, in this study, three LQT2-linked missense mutations (Thr613Met, Ser641Phe and Gly648Ser) located in exon-7 region of KCNH2 gene identified in CA patients was assessed for their deleteriousness using diverse computational algorithms. The SIFT and PolyPhen-2 methods, which depends on sequence conservation across species, and protein structure-based information have attributed pathogenicity to these variants. Protein behavior studies at 3D level have identified that these three missense mutations induce biochemically severe amino acid changes that may alters the structure and function of KCNH2. Our molecular docking suggested that mutant KCNH2 protein shows a similar binding interactions to KB-R7943 as compared to the wild type model. These findings could be useful in resorting to alternate therapies for subset of CA patients who show limited therapeutic response to KB-R7943. This study supports that in silico approaches could act as a first-line filters to screen the potential impact of CA linked KCNH2 mutations depending upon the perspective of molecular evolution and phenotype of proteins.

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: Vitamin D deficiency has been associated with adverse health outcomes. We examined genetic and environmental determinants of serum 25(OH)D3 and 1,25(OH)2D3 in childhood. Methods: The study sample consisted of 322 healthy Australian children (predominantly Caucasians) who provided a venous blood sample. A parental interview was conducted and skin phototype and anthropometry measures were assessed. Concentrations of 25(OH)D3 and 1,25(OH)2D3 were measured by selective solid-phase extraction-capillary liquid chromatography-tandem mass spectrometry. These concentrations were deseasonalised where relevant to remove the effect of month of sampling. Results: Deseasonalised log 25(OH)D3 and 1,25(OH)2D3 concentrations were only moderately correlated (r=0.42, pConclusions: Environmental factors and genetic factors contributed to both vitamin D metabolite concentrations. The intriguing finding that the higher ambient UVR contributed to higher 1,25(OH)2D3 after accounting for 25(OH)D3 concentrations requires further evaluation.

This article was migrated. The article was not marked as recommended. Clinical biochemistry is one of the foundational sciences essential for preparing medical students to achieve the optimal benefit of their clinical experience. In the Faculty of Medicine of King Abdulaziz University (FOM-KAU), clinical biochemistry is taught as a core course and system-based modules in 2nd, 3rd and 4th year. The teaching strategy is mainly teacher-centered, with lecture comprising the highest percentage among teaching methods, while self-directed learning (SDL) receiving the lowest percentage.The aim of this study was to evaluate the current teaching methods of clinical biochemistry at the FOM-KAU, while concurrently assessing the need for introducing a new student-centred teaching method. This was done through evaluating the level of knowledge, interest, and attitude of medical students and teaching faculty in Team Based Learning (TBL) in clinical biochemistry courses.The results of this study revealed that almost half of the second year medical students did not enjoy attending clinical biochemistry lectures. In addition, approximately half of them recall only 30% of the information they have learned one year after the exam. On the other hand, more than 50% of them enjoyed solving problems /cases, and doing activities during the session. At the same time students and academic staff members had some concerns regarding introducing TBL as a new teaching method. In conclusion, the current teaching methods of clinical biochemistry at the FOM-KAU needs to be modified, with introducing more student-centered teaching methods, like TBL. However, students' concerns such as team work, and faculty concerns regarding student preparation need to be addressed carefully with the participation of all stakeholders. Workshops to teach both students and faculty the elements of TBL would be of great benefit to address any concerns.

Familial hypercholesterolaemia (FH) is a common genetic disorder characterized by high plasma low-density lipoprotein (LDL)-cholesterol and premature coronary artery disease. Many factors, such as illness, high-dose statin therapy or a strict vegan diet can cause hypobetalipoproteinaemia (HBL). The more common secondary causes of HBL in the hospital setting include cachexia, intestinal malabsorption, malnutrition, severe liver disease and hyperthyroidism. We report a case of HBL in a 43-year-old man with previously demonstrated marked hypercholesterolaemia who attended a lipid disorders clinic for FH cascade screening. Surprisingly, a lipid profile taken at that time showed low plasma LDL-cholesterol and apolipoprotein B concentrations of 1.6 mmol/L and 0.61 g/L, respectively. He was not on lipid-lowering therapy. DNA sequencing showed that he was heterozygous for the LDLR gene mutation (C677R) present in other affected family members. Of interest, his serum transaminases were increased by ∼3-fold and hepatitis serology and genotyping confirmed a diagnosis of hepatitis C virus (HCV) infection. In summary, we describe a case of HBL secondary to chronic HCV infection in a patient with FH, confirmed by mutational analysis.

Aims Vitamin B12 deficiency is usually due to dietary factors, however clinicians always consider the possibility of autoimmune pernicious anaemia. The Schillings test is no longer routinely available and therefore diagnosis often includes the specific intrinsic factor auto-antibodies (IFAb) +/– parietal cell auto-antibodies (PCAb). Holo-transcobalamin (HoloTC), also known as active B12, has proved to be a more reliable indicator of B12 deficiency than measuring total B12 (TB12). We therefore reviewed our experience with this test to see if HoloTC was more closely associated with pernicious anaemia testing. Methods We reviewed 1359 patients where HoloTC +/– TB12 was measured as well as one or more of IFAb and PCAb. We used each patient’s first B12 result(s) for the analysis. HoloTC was measured by Abbott AxSym and total B12 was measured by Abbott Architect. PCAb antibodies are detected by immunofluor-escence whereas IFAb are measured by Alegria automated ELISA. Results When HoloTC was very low ( Conclusions PCAb were more likely to be positive at any B12 level consistent with its known poor specificity. The more specific IFAb positivity is more likely to be associated with low HoloTC levels than low TB12 levels.