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Students entering university are expected to be active, collaborative, self-regulated and self-directed in their learning. However, this expectation upon entry level is beyond their capacity due to the complex nature of tertiary education compared to that of secondary-level education. A novel hybrid pedagogical model integrating Team-based and case-based learning was employed to assist students to develop such skills. To explore the impact of the hybrid pedagogy, a mixed-methods research design was implemented examining students' academic performances and responses to a motivation and self-regulation of Learning questionnaire. Results revealed enhanced academic performance and high mean scores on questionnaire items, post intervention. Forty-four percent of total respondents provided some insight highlighting that curriculum contextualisation, relevance and positive social interdependence led to a positive student experience. In addition, student feedback also suggested that this model could be a useful analytical tool to personalise data-driven student feedback, identify students' gaps in knowledge and correct misconceptions. Overall, students' interactions with the learning material, their interactions with their instructors and their interactions among their peers are all enhanced, translating into increased academic performance in both summative and formative assessments. The success of implementing this hybrid pedagogical model may prove useful for different stakeholders such as curriculum designers, course coordinators and instructors in science units. [Author abstract]

Parkinson’s disease (PD) is a progressive neurodegenerative disorder affecting the substantia nigra where functions controlling body movement take place. Manganese (Mn) overexposure is linked to a neurologic syndrome resembling PD. Sesamol, thymol, wheat grass (WG), and coenzyme Q10 (CoQ10) are potent antioxidants, anti-inflammatory, and anti-apoptotic nutraceuticals. We investigated the potential protective effects of these nutraceuticals alone or in combinations against MnCl2-induced PD in rats. Seven groups of adult male Sprague Dawley rats were categorized as follows: group (I) was the control, while groups 2–7 received MnCl2 either alone (Group II) or in conjunction with oral doses of sesamol (Group III), thymol (Group IV), CoQ10 (Group V), WG (Group VI), or their combination (Group VII). All rats were subjected to four behavioral tests (open-field, swimming, Y-maze, and catalepsy tests). Biochemical changes in brain levels of monoamines, ACHE, BDNF, GSK-3β, GABA/glutamate, as well as oxidative stress, and apoptotic and neuroinflammatory biomarkers were evaluated, together with histopathological examinations of different brain regions. Mn increased catalepsy scores, while decreasing neuromuscular co-ordination, and locomotor and exploratory activity. It also impaired vigilance, spatial memory, and decision making. Most behavioral impairments induced by Mn were improved by sesamol, thymol, WG, or CoQ10, with prominent effect by sesamol and thymol. Notably, the combination group showed more pronounced improvements, which were confirmed by biochemical, molecular, as well as histopathological findings. Sesamol or thymol showed better protection against neuronal degeneration and some behavioral impairments induced by Mn than WG or CoQ10, partly via interplay between Nrf2/HO-1, TLR4/NLRP3/NF-κB, GSK-3β and Bax/Bcl2 pathways.

Background Manganism, a central nervous system dysfunction correlated with neurological deficits such as Parkinsonism, is caused by the substantial collection of manganese chloride (MnCl2) in the brain. Objectives To explore the neuroprotective effects of natural compounds, namely, micronized zeolite clinoptilolite (ZC) and punicalagin (PUN), either individually or in combination, against MnCl2‐induced Parkinson's disease (PD). Methods Fifty male albino rats were divided into 5 groups (Gps). Gp I was used as the control group, and the remaining animals received MnCl2 (Gp II–Gp V). Rats in Gps III and IV were treated with ZC and PUN, respectively. Gp V received both ZC and PUN as previously reported for the solo‐treated plants. Results ZC and/or PUN reversed the depletion of monoamines in the brain and decreased acetyl choline esterase activity, which primarily adjusted the animals' behavior and motor coordination. ZC and PUN restored the balance between glutamate/γ‐amino butyric acid content and markedly improved the brain levels of brain‐derived neurotrophic factor and nuclear factor erythroid 2‐related factor 2/heme oxygenase‐1 and decreased glycogen synthase kinase‐3 beta activity. ZC and PUN also inhibited inflammatory and oxidative markers, including nuclear factor kappa‐light‐chain‐enhancer of activated B cells, Toll‐like receptor 4, nucleotide‐binding domain, leucine‐rich‐containing family, pyrin domain‐containing‐3 and caspase‐1. Bcl‐2‐associated X‐protein and B‐cell leukemia/lymphoma 2 protein (Bcl‐2) can significantly modify caspase‐3 expression. ZC and/or PUN ameliorated PD in rats by decreasing the levels of endoplasmic reticulum (ER) stress markers (p‐protein kinase‐like ER kinase (PERK), glucose‐regulated protein 78, and C/EBP homologous protein (CHOP)) and enhancing the levels of an autophagy marker (Beclin‐1). Discussion and Conclusion ZC and/or PUN mitigated the progression of PD through their potential neurotrophic, neurogenic, anti‐inflammatory, antioxidant, and anti‐apoptotic activities and by controlling ER stress through modulation of the PERK/CHOP/Bcl‐2 pathway. ZC: zeolite clinoptilolite, PUN: punicalagin, PD: parkinsonism disease, Mn: manganese, ACHE: acetyl choline esterase, MDA: Malondialdehyde, SOD: Superoxide dismutase, TAC: total antioxidant capacity, DA: Dopamine, NE: norepinephrine, 5HT: serotonin, PCR: polymerase chain reaction, BAX: Bcl‐2‐associated X‐protein, Bcl2: B‐cell leukemia/lymphoma 2 protein, ELISA: Enzyme‐linked Immunosorbent Assay, Enzyme BDNF: Brain‐derived neurotrophic factor, GSK‐3β: Glycogen synthase kinase‐3 beta, glu: glutamate, PGE‐2: Prostaglandin E2, GABA: Gamma‐aminobutyric acid, CHOP: C/EBP Homologous Protein, GRP78: Glucose‐Regulated Protein 78, PERK: protein kinase‐like endoplasmic reticulum kinase, iNOS: Inducible nitric oxide synthase, IL‐1β: Interleukin ‐1β, NF‐kB: nuclear factor kappa‐light‐chain‐enhancer of activated B cells, TLR4: Toll like receptor 4, NLRP3: nucleotide‐binding domain, leucine‐rich–containing family, pyrin domain–containing‐3, COX‐2: Cyclooxygenase 2, TNF‐α: Tumor necrosis factor alpha, Nrf2: nuclear factor erythroid 2‐related factor 2, HO‐1: Heme oxygenase‐1, I.P: Intraperitoneal, P.O: oral.

Background. Deregulation of the Wnt signaling pathway had a role in haematological malignancies. Previous studies reported that lymphoid enhancer factor 1 (LEF1) expression and serum Galectin-3 level could affect clinical parameters and outcome in acute myeloid leukemia patients, but as far as we know, no study has addressed their combined effect on AML patients. Aim. We studied the expression of LEF1 by real-time qPCR and measured serum level of Gal.3 by ELISA technique in peripheral blood of 69 AML patients and correlated it with different clinicopathological criteria of patients, response, PFS and OS. Results. We found high expression (LEF1high) was associated with better OS (p=0.02) and EFS (p=0.019) compared to LEF1low, low serum Gal.3 level had better OS (p=0.014) and EFS (p=0.02) compared to high serum Gal.3 level. LEF1high less likely to carry a FLT3-ITD (p=0.047) compared to LEF1low patient, also LEF1high characterized by favorable risk (p=0.02) than LEF1low patients. While patients with higher Gal-3 levels characterized by poor risk (p=0.02) than lower Gal.3 lels, also more likely to carry a FLT3-ITD with borderline significance (p=0.054). Combined LEF1high/Gal.3 low patients had lower baseline blast percentages (p=0.02), favorable risk (p=0.01), less likely to carry FLT3-ITD (p=0.02), higher CR rate (p=0.055), shorter time to CR (0.001) than other groups. Among high Gal.3 level group, LEF1high expression improved OS and EFS (20 and 15 months respectively) vs LEF1low expression (13 and 8 months respectively). Conclusion. We conclude that high LEF1 expression was a favorable prognostic marker which can define AML patient risk and outcome independent from assessing the serum galectin.3 level.

Scar is defined as “the fibrous tissue that restores normal tissue damaged by trauma or disease”. Naturally, Scar tissue is a protection mechanism due to tissue injury. Acne vulgaris (acne) is a chronic inflammatory skin condition strongly related with excessive production of sebum, aberrant keratinization, and bacterial colonization inflammatory reactions. Every year there are more than 100 million patients who develop scar formation produced by several factors, such as post-inflammatory acne and trauma. Scars usually take place during certain phases of wound healing: inflammation, granulation, and reshaping. In the third phase (matrix remodeling phase) fibroblasts and keratinocytes produce enzymes which determine the architecture of the extracellular matrix which are matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMP). Matrix metalloproteinases damage extracellular matrix (ECM) and interact and form a lytic cascade for ECM remodeling. Consequently, an imbalance in the ratio of MMPs to tissue inhibitors of MMPs results in the development of atrophic or hypertrophic scars. Insufficient response leading to reduced deposition of collagen factors and formation of an atrophic scar while, if the healing response is too exuberant, a raised nodule of fibrotic tissue forms hypertrophic scars