كتابة النص: الأستاذ الدكتور يوسف أبو العدوس - جامعة جرش قراءة النص: الدكتور أحمد أبو دلو - جامعة اليرموك مونتاج وإخراج : الدكتور محمد أبوشقير، حمزة الناطور، علي ميّاس تصوير : الأستاذ أحمد الصمادي الإشراف العام: الأستاذ الدكتور يوسف أبو العدوس
فيديو بمناسبة الإسراء والمعراج - إحتفال كلية الشريعة بجامعة جرش 2019 - 1440
فيديو بمناسبة ذكرى المولد النبوي الشريف- مونتاج وإخراج الدكتور محمد أبوشقير- كلية تكنولوجيا المعلومات
التميز في مجالات التعليم والبحث العلمي، وخدمة المجتمع، والارتقاء لمصاف الجامعات المرموقة محليا واقليميا وعالميا.
المساهمة في بناء مجتمع المعرفة وتطوره من خلال إيجاد بيئة جامعية، وشراكة مجتمعية محفزة للابداع، وحرية الفكر والتعبير، ومواكبة التطورات التقنية في مجال التعليم، ومن ثم رفد المجتمع بما يحتاجه من موارد بشرية مؤهلة وملائمة لاحتياجات سوق العمل.
تلتزم الجامعة بترسيخ القيم الجوهرية التالية: الإلتزام الإجتماعي والأخلاقي، الإنتماء،العدالة والمساواة، الإبداع، الجودة والتميّز، الشفافية والمحاسبة، الحرية المنظبطة والمستقبلية.
دكتور استاذ
Glycogen synthase kinase 3 (GSK3) encodes a serine/threonine protein kinase. We investigated the effects of Subcutaneous (SC) glucose administration on the expression of glycogen synthase kinase 3 (GKS-3) isomers ( and) genes in the cerebral cortex of mice with the aim of determining the possible mechanism(s) involved in mitochondrial dysfunction induced by hyperglycemia. Adult male BALB/c mice were treated with 12 gm/kg glucose solution SC once daily for 3 days. Ultrastructure study, histopathological analysis, and Real-time PCR investigations were carried out on the cerebral cortex from glucose treated mice and from vehicle-treated control animals. We observed signi????icant ultrastructural damage of mitochondria in the cerebral cortex of mice received high doses of glucose. Histopathological alterations in the cortex of these animals were also detected. A signi????icant increased of GSK-3 gene expression and decreased expressions of GKS-3 gene in high glucose treated animals were noticed. The hyperglycemia-induced ultrastructural changes may occur via modulation of gene expression of GSK-3 isomers, and we hypothesize this as an early etiopathological factor in hyperglycemiarelated neurodegenerative diseases (NDD).
Renal failure is a serious disease and pandemic health challenge, and its development to end-stage renal failure can be delayed or prevent by early diagnosis. Serum markers for detecting early renal impairment include creatinine, cystatin C, β-microglobulin and others. To assess the potential role of serum markers for early detection of renal impairment (RI) in Hail population, Saudi Arabia. Serum levels of cystatin C, creatinine and other factors were measured in 135 renal failure patients and 150 controls. Receiver operating characteristic (ROC) curve analysis was performed to assess the utility of biomarkers for early diagnosing renal impairment (RI).The area under the ROC curve (AUC) for serum cystatin C (Cys C) (0.946) was significantly higher than that of creatinine (0.907, p = 0.048),which indicates Cys C to be a better biomarker for early detection of RI compared to the commonly used serum creatinine. However, serum creatinine was found to be superior to urea (AUC = 0.727, p < 0.01) and uric acid (AUC = 0.619, p < 0.01).When serum Cys C and serum creatinine were simultaneously considered i.e. each marker was positive, the sensitivities were 98.4%, 98.6% and 98.5% for males, females and total patient group, respectively. The specificity and positive predictive value increased to 100% for all mentioned situations. Taking together, the study demonstrated that serum cystatin C is a valuable marker for early detection of renal impairment in males, nevertheless it is more valuable when analyzed with serum creatinine.
Cancer chemoprevention is a novel and recognized approach to inhibit, delay or reverse the process of cancer development by using natural products. Our aim of this study was to examine the chemopreventive potential of fish oil on 7, 12-Dimethylbenz (a) Anthracene (DMBA)-initiated and croton oil-promoted skin papillomagenesis model in mice. Oral treatment of fish oil at a dose of 25 µl per animal resulted in significant reduction of tumor incidence, tumor burden, tumor yield, and the cumulative number of papillomas in DMBA+croton oil+fish oil treated group compared to only DMBA +croton oil administered positive control group. Pre-treatment of fish oil also increased the latency period of tumor development and a significant reduction in the weight and size of the skin papillomas. Furthermore, biochemical assays revealed a significant increase in the hepatic enzymatic and nonenzymatic antioxidants like glutathione-S-transferase, superoxide dismutase, catalase, and reduced glutathione whereas lipid peroxidation was found to be significantly reduced as a result of fish oil treatment. Thus, the results of the present study clearly indicate that fish oil has potent chemopreventive efficacy against two-stage skin carcinogenesis which can be partially attributed to its anti-oxidative and anti-peroxidative effect.
In this study, the effect of royal jelly on the nephrotoxicity of Gentamicin in the kidneys of female rats wasinvestigated by evaluation of serum indices and histopathological analyses. Thirty female Wistar albino rats were randomly divided into five groups; Group (1) negative control (NC) inoculated intraperitoneally IP with NS for 10 days; Group (2) Royal Jelly (RJ) 50 mg/kg body weight was given orally for 10 days; Group (3) Gentamicin (Gen) 100 mg/ kg inoculated IP for 10 days served as positive control; Group (4) RJ + Gen was given royal jelly orally at a dose of 50 mg/ kg body weight for 10 days and thereafter, 100 mg/ kg Gen was administered IP for 10 days; and Group (5) Gen + RJ was inoculated IP with Gen for 10 days as a dosage of 100 mg/ kg and thereafter, was given RJ orally as a dose of 50 mg/ kg body weight. Gentamicin has a significant effect on serum urea and creatinine where urea in positive control (Gen) group found to be significantly higher (242±53.5) in comparison to negative control (NC) group (58±4.0). The effect of gentamicin on serum urea was almost nullified when royal jelly was given after gentamycin (43±4.0) while royal jelly given before gentamicin slightly lowers urea but the effect is not statistically significant (209±41.7). Royal jelly alone has no significant effect on serum urea (35±4.4). Almost the same was observed regarding the creatinine in positive control (Gen) group was found to be significantly higher (2.41±0.455) in comparison to negative control (NC) group (0.47±0.005). The effect of gentamicin on serum creatinine was almost nullified when royal jelly was given after gentamicin (0.61±0.053) while royal jelly given before gentamicin slightly lowers creatinine but the effect is not statistically significant (1.67±0.238). Royal jelly alone has no significant effect on serum creatinine (0.47±0.005). Histopathological sections revealed gentamicin group 3 to exert massive degeneration of the tubular epithelium with presence of eosinophilic hyaline cast in the lumen plus dilatation of the renal tubules. In addition there was thickening of the basement membrane of the glomeruli and congestion of the glomerular tuft with sometimes detachment and disappearance of the tubular epithelium of the glomerular membrane. Regarding the groups of royal jelly given before or after gentamicin; there was dilatation of the renal tubules showed some of the tubules to be filled with eosinophilic hyaline material plus thickening of the basement membrane of the glomeruli, vacuolation of the glomerular epithelium, capillary congestion, degeneration of the tubular epithelium when gentamicin was given after royal jelly, this is nearly similar to NC group. The picture was seemed to be better when royal jelly has been given after gentamicin where it was showed no significant pathological changes in glomeruli and tubular epithelium compared to NC group. Royal jelly alone showed wide spread of dilation of renal tubules withoutsignificant c pathological changes of tubules. No significant effect in the serum indices for uric acid, total protein and albumin in all groups.
Aim: The main objectives of this work were to prove that subcutaneous injection of high doses of glucose can lead to occurrence of glycogen granules inside ultrastructurally changed mitochondria of mouse cerebral cortex and to check whether blocking of mitochondrial permeability transition pore (MPTP) by cyclosporine A would diminish occurrence of these granules inside some mitochondria. By this, we aimed to explore if hyperglycemia-induced intramitochondrial glycogen granules (HIMG) may represent a molecular pathway through which hyperglycemia may lead to dysfunction of brain mitochondria. Materials and Methods: Electron microscopic studies and histopathological investigations have been carried out. We then incubated samples of brain cortex of mouse injected with high doses of glucose in alpha-amylase solvent or disolvent alone before being subjected to microscopic examination. Results: Electron microscopy experiments established that the observed granules are built of glycogen. It has been also demonstrated that blocking of MPTP by cyclosporine A diminished occurrence of glycogen inside some mitochondria in cerebral cortex, thus inhibiting hyperglycemia-induced apoptotic signaling that results from increased vulnerability of mouse brain mitochondria. Concurrently, cyclosporine A partially suppressed the histopathological changes of brain cortex of these animals. Conclusions: Taken together, this study indicates that cytotoxicity of hyperglycemia might occur through HIMG and we postulate this as a key molecular pathway through which hyperglycemia may lead to dysfunction of brain mitochondria. This is the first report showing HIMG as a cytotoxic molecular mechanism in mouse model.
Obesity is a known risk factor for several diseases and also negatively affects physical functioning. It isidentified that obesity is an independent risk factor for cardiovascular (CV) disease. However, only few studies haveinvestigated the association of different anthropometric measures with carotid plaque. We in this study aimed to investigate, compare and find the correlation between four measures in normal and obese adults: Anthropometric, Blood Analysis.Smoking habit and presence of Carotid Arterial Plaque. We included 44 healthy young collegiate students aged 20-25 years and were divided into two based on their body mass index: normal weight (n=15) and obese (n=29). Anthropometric measurements such as body weight, body mass index (BMI), waist / hip ratio (WHR), body fat percentage (BFP) and visceral fat area (VFA) and from the collected venous blood, total cholesterol, triglycerides, HDL cholesterol, LDL cholesterol and glucose were measured. Presence of carotid arterial plaque [CAP] was identified by ultrasonography. Plaque presence was defined as e”1 plaque in any of the carotid arteries. Data were analyzed using independent t-test.Pearson’s correlation coefficient was used to find the correlations between the measured parameters. After adjustment for age and sex between the groups, there was strong evidence of significant difference between groups for anthropometric measures [Weight, BMI, WHR, BFP and VFA] and also for serum HDL, LDL and triglycerides levels (p < 0.01). But there was no difference for serum total cholesterol and glucose concentrations (p > 0.05). CAP was found in 69% of obese subjects and a strong correlation was found between smoking and presence of carotid plaque. A smoker is 1.84 times subjected to plaque occurrence than non-smoker among obese participants. In this study we found high prevalence of CAP among the obese adults. Occurrence of CAP was significantly increased among the smokers’ ones. Thus, evaluation of obese patients with this anthropometric, lipid profile and cigarette smoking could help the individuals to identify the risk of higher residual cardiovascular incidence.
Citropin 1.1 is an amphipathic alpha-helical cationic peptide that exhibits potent anticancer activity in vitro. Citropin 1.1 was found to be active against 60 cancer cell lines, and this activity was mainly attributed to its ability to bind and lyse membranes of cancer cells. One of the major drawbacks of developing Citropin 1.1 as an anticancer agent is its lack of apparent selectivity toward cancer cells and its ability to cause signiϐicant lysis of normal human erythrocytes and mammalian cells at high concentrations. This low selectivity index places severe restraints on the development of Citropin 1.1 as a novel anticancer agent. In this study, we have designed a Citropin 1.1 analog named Citropin A that retained the biological activity of the parent peptide. Citropin A was fused to an anionic fragment in order to neutralize the positive charge carried on the parent peptide rendering it inactive. The resultant hybrid peptide named Citropin-MMP was designed to contain a Matrix metalloproteinase (MMP) cleavable consensus sequence that would be cleaved to release the active Citropin A once it encounters highly metastatic MMP producing cancer cells. Citropin-MMP was found to be completely inactive against non-MMP producing cancer cells and normal mammalian cells. However, when CitropinMMP was administered to MMP producing cells, its antiproliferative activity was regained, and the peptide displayed exclusive activity against MMP producing cancer cell lines. The data of our study indicate that this enzyme-based cleavage strategy could prove to be successful for the development of CitropinMMP as a novel therapeutic agent for the purpose of inhibiting the proliferation and invasion of highly metastatic invasive cancer cells
Citropin 1.1 is an amphipathic alpha-helical cationic peptide that exhibits potent anticancer activity in vitro. Citropin 1.1 was found to be active against 60 cancer cell lines, and this activity was mainly attributed to its ability to bind and lyse membranes of cancer cells. One of the major drawbacks of developing Citropin 1.1 as an anticancer agent is its lack of apparent selectivity toward cancer cells and its ability to cause signiϐicant lysis of normal human erythrocytes and mammalian cells at high concentrations. This low selectivity index places severe restraints on the development of Citropin 1.1 as a novel anticancer agent. In this study, we have designed a Citropin 1.1 analog named Citropin A that retained the biological activity of the parent peptide. Citropin A was fused to an anionic fragment in order to neutralize the positive charge carried on the parent peptide rendering it inactive. The resultant hybrid peptide named Citropin-MMP was designed to contain a Matrix metalloproteinase (MMP) cleavable consensus sequence that would be cleaved to release the active Citropin A once it encounters highly metastatic MMP producing cancer cells. Citropin-MMP was found to be completely inactive against non-MMP producing cancer cells and normal mammalian cells. However, when CitropinMMP was administered to MMP producing cells, its antiproliferative activity was regained, and the peptide displayed exclusive activity against MMP producing cancer cell lines. The data of our study indicate that this enzyme-based cleavage strategy could prove to be successful for the development of CitropinMMP as a novel therapeutic agent for the purpose of inhibiting the proliferation and invasion of highly metastatic invasive cancer cells.
Preventive vaccines work to protect an individual from infection or disease by introducing a small component or a nonharmful form of the pathogen (called the foreign antigen) into the body. The body produces an immune response to the pathogen by generating antibodies (via the humoral response), killer cells (via the cell mediated response), or both and development of immunologic memory. We reviewed the recent literature on types of vaccines and older studies were included selectively if historically relevant but none of these vaccines is ideal and can be recommended unrestrictedly therefore, the use of biotechnology could allow cheap production of valuable vaccines, while providing enhanced safety by avoidance of both human and animal viruses or other contaminants. Vaccine have been studied extensively to help eradication the infectious disease and thereby decrease the need for drugs
Glycogen synthase kinase 3 (GSK3) encodes a serine/threonine protein kinase. We investigated the effects of Subcutaneous (SC) glucose administration on the expression of glycogen synthase kinase 3 (GKS-3) isomers (α and β) genes in the cerebral cortex of mice with the aim of determining the possible mechanism(s) involved in mitochondrial dysfunction induced by hyperglycemia. Adult male BALB/c mice were treated with 12 gm/kg glucose solution SC once daily for 3 days. Ultrastructure study, histopathological analysis, and Real-time PCR investigations were carried out on the cerebral cortex from glucose treated mice and from vehicle-treated control animals. We observed signiϐicant ultrastructural damage of mitochondria in the cerebral cortex of mice received high doses of glucose. Histopathological alterations in the cortex of these animals were also detected. A signiϐicant increased of GSK-3α gene expression and decreased expressions of GKS-3β gene in high glucose treated animals were noticed. The hyperglycemia-induced ultrastructural changes may occur via modulation of gene expression of GSK-3 isomers, and we hypothesize this as an early etiopathological factor in hyperglycemiarelated neurodegenerative diseases (NDD)
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