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.
Dr. Firas Bazzari (MSc., Ph.D.) is a Clinical/Molecular Pharmacologist specializing in the field of Neuropsychopharmacology, Neurodegenerative and Metabolic Disorders. Dr. Bazzari is also an active member of multiple national and international associations/societies including British Pharmacological Society (BPS), American Society of Pharmacology and Experimental Therapeutics (ASPET), American Psychological Association (APA) and International Pharmaceutical Federation (FIP)
Ph.D. in Pharmacology & Toxicology
MSc. in Clinical Pharmacology
BSc. in Pharmacy
There is an increasing interest in the therapeutic use of cannabis worldwide, with a number of cannabinoid-derived drugs currently approved by the Food and Drug Administration (FDA) for certain indications. This study was conducted via a printed questionnaire and aimed to explore the attitudes and knowledge regarding the therapeutic use of cannabis and cannabinoids among community pharmacists residing in Amman, Jordan. The results revealed a neutral to low agreement level regarding the medical usefulness of cannabis; however, a higher agreement level was observed for FDA-approved cannabinoid-derived drugs. The majority of the participants reported that they did not learn enough regarding cannabinoids, do not adequately remember what they have learned, and do not actively look for information after graduation. The average percentages of correct identification of cannabis/cannabinoid FDA-approved drug indications, common adverse effects, interacting drugs, and cautions/contraindications were 40.6%, 53%, 49.4%, and 57.3%, respectively, with an overall correct identification rate of 51.1% of the participants. In conclusion, the results indicate an inadequate level of knowledge with a significant room for improvement regarding the various aspects of cannabinoid pharmacology.
Alzheimer’s disease (AD) is the most prevalent neurodegenerative disorder and the most common cause of dementia in the elderly. The complexity of AD has hindered the development of either a cure or a disease-modifying therapy to halt the disease progression. Numerous hypotheses were presented in order to explain the mechanisms underlying the pathogenesis of AD. Introduced in 1992, the “Amyloid Cascade Hypothesis” had a huge impact on the field and inspired the rise of various drug candidates, especially amyloid-beta (Aβ)-directed drugs; including beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) inhibitors. Adopted by a number of pharmaceutical companies, the development of BACE1 inhibitors has gained momentum in the past decade with promising results from experimental and early clinical-phase studies. Nevertheless, nearly all BACE1 inhibitors failed in later phases of clinical trials, due to safety and/or efficacy issues, and others were discontinued early in favor of second-generation small-molecule candidates. This paper aims to provide a comprehensive review of all BACE1 inhibitors to ever reach clinical trials, and we discuss the challenges and different perspectives on whether BACE1 inhibitors are to be reconsidered or revitalized in the future.
Maladaptation in sensory neural plasticity of nociceptive pathways is associated with various types of chronic pain through central sensitization and remodeling of brain connectivity. Within this context, extensive research has been conducted to evaluate the mechanisms and efficacy of certain non-pharmacological pain treatment modalities. These include neurostimulation, virtual reality, cognitive therapy and rehabilitation. Here, we summarize the involved mechanisms and review novel findings in relation to nociceptive desensitization and modulation of plasticity for the management of intractable chronic pain and prevention of acute-to-chronic pain transition.
Lucid dreaming is a phenomenon in which the dreamer is aware that he/she is dreaming while the dream is still going on. Many studies investigated the prevalence of lucid dreaming in various populations; however, no study has been conducted in the Arab Middle East region. As age and cultural differences in attitudes towards dreams may influence lucid dreaming, we aimed to investigate lucid dreaming and associated sleep characteristics among university students in West Bank Palestine. This cross-sectional study was conducted through an online questionnaire and a total of 390 students participated. The results revealed a prevalence of 71% and frequency of 0.77 (SD=1.85) lucid dreams/month. The awareness level of lucid dreaming was 38.5% and significantly associated with lucid dreaming incidence. Participant demographics and certain sleep factors such as sleep time, latency, duration and perceived quality did not influence lucid dreaming. However, nocturnal awakening significantly associated with the occurrence of lucid dreams. Dream characteristics including dream frequency, dream recall, day-dreaming and perceived meaningfulness of dreams were all associated with lucid dreaming and positively correlated with its frequency. The results show comparable lucid dreaming patterns to other populations and indicate its dependence on many dream characteristics.
Brain-derived neurotrophic factor (BDNF) is the most abundant neurotrophin in the adult brain and functions as both a primary neurotrophic signal and a neuromodulator. It serves essential roles in neuronal development, maintenance, transmission, and plasticity, thereby influencing aging, cognition, and behavior. Accumulating evidence associates reduced central and peripheral BDNF levels with various neuropsychiatric disorders, supporting its potential utilization as a biomarker of central pathologies. Subsequently, extensive research has been conducted to evaluate restoring, or otherwise augmenting, BDNF transmission as a potential therapeutic approach. Promising results were indeed observed for genetic BDNF upregulation or exogenous administration using a multitude of murine models of neurological and psychiatric diseases. However, varying mechanisms have been proposed to underlie the observed therapeutic effects, and many findings indicate the engagement of disease-specific and other non-specific mechanisms. This is because BDNF essentially affects all aspects of neuronal cellular function through tropomyosin receptor kinase B (TrkB) receptor signaling, the disruptions of which vary between brain regions across different pathologies leading to diversified consequences on cognition and behavior. Herein, we review the neurophysiology of BDNF transmission and signaling and classify the converging and diverging molecular mechanisms underlying its therapeutic potentials in neuropsychiatric disorders. These include neuroprotection, synaptic maintenance, immunomodulation, plasticity facilitation, secondary neuromodulation, and preservation of neurovascular unit integrity and cellular viability. Lastly, we discuss several findings suggesting BDNF as a common mediator of the therapeutic actions of centrally acting pharmacological agents used in the treatment of neurological and psychiatric illness.
Insulin resistance is a major risk factor for Alzheimer’s disease (AD). Chenodeoxycholic acid (CDCA) and synthetic Farnesoid X receptor (FXR) ligands have shown promising outcomes in ameliorating insulin resistance associated with various medical conditions. This study aimed to investigate whether CDCA treatment has any potential in AD management through improving insulin signaling. Adult male Wistar rats were randomly allocated into three groups and treated for six consecutive weeks; control (vehicle), AD-model (AlCl3 50 mg/kg/day i.p) and CDCA-treated group (AlCl3 + CDCA 90 mg/kg/day p.o from day 15). CDCA improved cognition as assessed by Morris Water Maze and Y-maze tests and preserved normal histological features. Moreover, CDCA lowered hippocampal beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) and amyloid-beta 42 (Aβ42). Although no significant difference was observed in hippocampal insulin level, CDCA reduced insulin receptor substrate-1 phosphorylation at serine-307 (pSer307-IRS1), while increased protein kinase B (Akt) activation, glucose transporter type 4 (GLUT4), peroxisome proliferator-activated receptor gamma (PPARγ) and glucagon-like peptide-1 (GLP-1). Additionally, CDCA activated cAMP response element-binding protein (CREB) and enhanced brain-derived neurotrophic factor (BDNF). Ultimately, CDCA was able to improve insulin sensitivity in the hippocampi of AlCl3-treated rats, which highlights its potential in AD management.
The phenomenon of lucid dreaming, in which an individual has the ability to be conscious and in control of his dreams, has attracted the public attention, especially in the era of internet and social media platforms. With its huge popularity, lucid dreaming triggered passionate individuals, particularly lucid dreamers, to spread their thoughts and experiences in lucid dreaming, and provide a number of tips and techniques to induce lucidity in dreams. Scientific research in the field of sleep and dreams has verified the phenomenon of lucid dreaming for decades. Nevertheless, various aspects regarding lucid dreaming are not fully understood. Many hypotheses and claims about lucid dreaming induction are yet to be validated, and at present lucid dreaming still lacks efficient and reliable induction methods. Understanding the molecular basis, brain physiology, and underlying mechanisms involved in lucid dreaming can aid in developing novel and more target-specific induction methods. This review will focus on the currently available scientific findings regarding neurotransmitters’ behavior in sleep, drugs observed to affect dreams, and proposed supplements for lucid dreaming, in order to discuss the possibility of inducing lucid dreams from a pharmacological point of view.
All Rights Reseved © 2023 - Developed by: Prof. Mohammed M. Abu Shquier Editor: Ali Mayyas
