Background: PASS is a peer-led structured academic mentoring program designed to provide academic assistance for new students in their transition from college to university studies and also for students struggling in certain units. This study aims to establish acquired skills by peer leaders associated with peer-led mentoring via the PASS program, and to explore the role played by these acquired skills in their journey to become a successful doctor.Methods: Study participants were forty selected second-year undergraduate medical students at Monash University Malaysia with commendable examination results. Validated pre-test and post-test questionnaires were administered to explore changes in the level of communication, leadership, professional, and pedagogical skills before and after participation in peer mentoring program. Qualitative analysis of focused group interviews was performed by an independent investigator to identify how the skills developed as a peer mentor may help with becoming a good doctor. Major themes were identified with the thematic-analysis approach.Results: Thirty-eight students completed the pre-test and post-test questionnaires. Peer leaders reported improvement in oral and written skills for teaching; increased confidence to give constructive feedback; better stress management; efficient time management; improved interpersonal skills; and enhanced problem-solving and critical thinking capabilities. Eight major themes were identified from the interview and peer leaders reported positive experience of working in diverse environments and shouldering of responsibilities.Conclusions: Peer-led mentoring provides a good opportunity for medical students to shoulder responsibilities as a leader and offers an experience of managing a team of their peers and juniors which in turn may enhance their communication, interpersonal, and leadership skills.

Type 2 diabetes (T2D) with depression causes severe cognitive impairments. The devastating conditions will further compromise the overall quality of life. The overconsumption of high-fat and high-sucrose (HFS) diet is one of the modifiable risk factors for T2D, depression, and cognitive impairments. Thus, it is essential to identify effective therapeutic strategies to overcome the cognitive impairments in T2D with depression. We proposed environmental enrichment (EE) which encompasses social, cognitive, and physical components as the alternative treatment for such impairments. We also investigated the potential neuroprotective properties of the antidiabetic drug metformin. This study aimed to investigate the effects of EE and metformin interventions on hippocampal neuronal death, and hippocampal-dependent memory impairment in T2D rats under stress. Thirty-two male rats (200-250 g) were divided into four groups: C group (standard diet + conventional cage), DS group [HFS-induced T2D + restraint stress (RS)], DSE group [HFS-induced T2D + RS + EE] and DSEM group [HFS + RS + EE + metformin]. Serum corticosterone (CORT) was measured to evaluate stress levels. The serum Free Oxygen Radicals Testing (FORT) and Free Oxygen Radicals Defence Test (FORD) were measured to evaluate the systemic oxidative status (OS). Serum brain-derived neurotrophic factor (BDNF) and T-maze tasks were performed to evaluate cognitive functions. Rats were humanely sacrificed to collect brains for histological, morphometric, and hippocampal gene expression studies. The CORT and the serum FORT levels in the DSE and DSEM groups were lower than in the DS group. Meanwhile, the serum BDNF, T-maze scores, histological, and morphometric analysis were improved in the DSE and DSEM groups than in the DS group. These findings supported that EE and the combined interventions of EE and metformin had neuroprotective properties. The hippocampal gene expression analysis revealed that the DSE and DSEM groups showed improved regulation of BDNF-TrkB signalling pathways, including the BDNF/TrkB binding, PI3K - Akt pathway, Ras-MAPK pathway, PLCγ-Ca2+ pathway, and CREB transcription. EE and the combined interventions of EE and metformin improved hippocampal neuron survival and hippocampal-dependent memory in T2D rats under stress by enhancing gene expression regulation of neurogenesis and synaptic plasticity.

An environmental enrichment (EE) cage consisting of a broad living area and various stimulators triggers social, cognitive, and physical activities. EE has been utilized in a wide range of neurological and non‐neurological studies. However, the details of the environmental enrichment protocol were not well described in these studies. This has resulted in uncertainty and inconsistency in methodology, which may thus fail to replicate environmental enrichment effects, influencing the study outcome. Here we describe the basic guidelines and present an easy‐to‐follow protocol for environmental enrichment in rat models. © 2021 Wiley Periodicals LLC.Basic Protocol: Environmental enrichment housing

Recently, there have been investigations on metformin (Met) as a potential treatment for bone diseases such as osteoporosis, as researchers have outlined that type 2 diabetes mellitus (T2DM) poses an increased risk of fractures. Hence, this systematic review was conducted according to the 2020 PRISMA guidelines to evaluate the evidence that supports the bone-protective effects of metformin on male animal models with T2DM. Five databases—Google Scholar, PubMed, Wiley Online Library, SCOPUS, and ScienceDirect—were used to search for original randomized controlled trials published in English with relevant keywords. The search identified 18 articles that matched the inclusion criteria and illustrated the effects of Met on bone. This study demonstrates that Met improved bone density and reduced the effects of T2DM on adiposity formation in the animal models. Further research is needed to pinpoint the optimal dosage of Met required to exhibit these therapeutic effects.

Effect of streptozotocin induced diabetes on rat hippocampus

Background: The Western-style diet-induced type 2 diabetes mellitus (T2D) may eventually trigger neurodegeneration and memory impairment. Thus, it is essential to identify effective therapeutic strategies to overcome T2D complications. This study aimed to investigate the effects of environmental enrichment (EE) and metformin interventions on metabolic dysfunctions, hippocampal neuronal death, and hippocampal-dependent memory impairments in high-fat/high-sucrose (HFS) diet-induced T2D rats. Methods: Thirty-two male rats (200–250 g) were divided into four groups: C group (standard diet + conventional cage); D group (HFS diet + conventional cage); DE group (HFS diet + EE cage/6hr daily); and DM group (HFS diet + metformin + conventional cage). Body weight was measured every week. T-maze tasks, anthropometric, biochemical, histological, and morphometric parameters were measured. The expression changes of hippocampal genes were also analyzed. Results: The anthropometric and biochemical parameters were improved in DE and DM groups compared with the D group. DE and DM groups had significantly higher T-maze percentages than the D group. These groups also had better histological and morphometric parameters than the D group. The interventions of EE and metformin enhanced the expression of hippocampal genes related to neurogenesis and synaptic plasticity (BDNF/TrkB binding, PI3K-Akt, Ras–MAPK, PLCγ–Ca²⁺, and LTP). Conclusion: Environmental enrichment (EE) and metformin improved metabolic functions, hippocampal neuron survival, and hippocampal-dependent memory in HFS diet-induced T2D rats. The underlying mechanisms of these interventions involved the expression of genes that regulate neurogenesis and synaptic plasticity.