The wound healing process is an intricate biological phenomenon that requires various crucial components, including repair cells, proteins, and biological factors. The process of wound healing can be categorized into three interrelated stages: the stage of inflammation, proliferation, and remodeling. Any interruptions during this process can lead to wound healing that deviates from the typical progression. It is crucial to highlight that growth factors have a profoundly influential effect in this particular situation. This study conducts a thorough and analytical literature review to investigate the essential role of growth factors (TGF-β, PDGF, KGF, FGF, Pro Collagen, and VEGF) in wound healing. This study examines the biochemical and molecular mechanisms via which these growth factors impact the wound healing process, including the inflammation, proliferation, and remodeling phases, by analyzing current and authoritative scientific literature. This paper precisely outlines the role of these variables, including the role of the stem cell secretome enriched with growth factors such as TGF-β, PDGF, KGF, FGF, Pro Collagen, VEGF, and exogenous factors, as previously discussed. It explores their impact on tissue regeneration, angiogenesis, and extracellular matrix formation, essential components of the wound healing process. The main objective of this study is to provide a comprehensive summary of the latest research findings, which includes an in-depth analysis of the contributions of stem cell secretomes to wound healing. The findings provide useful insights into potential growth factor-based treatment approaches, highlighting how the components of the stem cell secretome can be leveraged to enhance the wound healing process.

The aging population poses a serious challenge concerning an increased prevalence of Alzheimer’s disease (AD) and its impact on global burden, morbidity, and mortality. Oxidative stress, as a molecular hallmark that causes susceptibility in AD, interplays to other AD-related neuropathology cascades and decreases the expression of central and circulation brain-derived neurotrophic factor (BDNF), an essential neurotrophin that serves as nerve development and survival, and synaptic plasticity in AD. By its significant correlation with the molecular and clinical progression of AD, BDNF can potentially be used as an objectively accurate biomarker for AD diagnosis and progressivity follow-up in future clinical practice. This comprehensive review highlights the oxidative stress interplay with BDNF in AD neuropathology and its potential use as an AD biomarker.

BACKGROUND: Secretome production by stem cells depends on their culture conditions such as oxygen concentration and the composition of the culture media. In this study, we investigated the secretion of neurotrophic growth factors of human umbilical cord mesenchymal stem cells (hUC-MSCs) in amino acid-rich culture medium and under hypoxic condition.METHODS: hUC-MSCs were cultured in normoxic and various hypoxic (1%, 5%, 10%) conditions in an amino acid-rich culture medium. The end-point parameters (cell proliferation and survival, cell morphology and growth factor secretion) were measured at 3 time-points (48 hours, 72 hours and 96 hours). ELISA-based methods were used for neurotrophic factors detection, including neurotrophic growth factor (NGF), vascular endothelial factor (VEGF), and brain-derived neurotrophic factor (BDNF).RESULTS: NGF secretion was not detectable at any time points both in normoxia and hypoxia. BDNF secretion under normoxia was induced at 48 h time point and reached the highest level at an average of 181.9±13.01 pg/mL at 96 hours, whereas hypoxia exposure to hUC-MSCs only induced the BDNF secretion at low level. VEGF secretion was barely detectable in normoxic condition. However, VEGF secretion reached the highest level at an average of 7707.55±2110.85 pg/mL in 5% hypoxia at 96 hours.CONCLUSION: Combination of amino acid-rich culture medium and hypoxia condition dramatically induced high VEGF secretion by hUC-MSCs, especially at 5% hypoxia, induced mild BDNF secretion and had no effect toward NGF secretion.KEYWORDS: human umbilical cord mesenchymal stem cells, neurotrophic growth factor, amino acid-rich, hypoxia

Parkinson’s disease (PD) is the second most common progressive neurodegenerative disease, characterized by apoptosis of dopaminergic neurons in substansia nigra pars compacta (SNpc) caused by ⍺-synuclein aggregation. The use of secretomes released by medicinal signaling cells (MSCs) is one the promising preventive approaches that target several mechanisms in the neuropathology of PD. Its components target the lack of neurotrophin factors, proteasome dysfunction, oxidative stress, mitochondrial dysfunction, and at last neuroinflammation via several pathways. The complex and obscure pathology of PD induce the difficulty of the search of potential preventive approach for this disease. We described the potential of secretome of MSC as the novel preventive approach for PD, especially by targeting the said major pathogenesis of PD.

During the COVID-19 pandemic, medical students might be vulnerable to excessive screen time exposure to cope with distance learning-induced distress. This study aimed to evaluate the distress and screen time before and after distance learning was initiated. Data were collected from 215 subjects. Statistical significance was accepted at P<0.05. The prevalence of distress among medical students was 25.61% and 27.06% before and after distance learning was executed, respectively. Academic-related stressor (ARS) was reported by 49.28% and 63.29% of students during the first and second surveys. The proportion of students with daily screen time ≥7 hours was 51.21% and 63.77% for the first and second surveys, respectively. ARS, interpersonal and intrapersonal-related stressor (IRS), social-related stressor (SRS), and average daily screen time significantly rose in 3-month-time (P<0.0001, P=0.0014, P=0.0261, P=0.0022). There was a significant association between distress and screen time (P=0.0313). ARS was the leading cause of distress. The majority of respondents had a daily screen time ≥7 hours. Both distress and screen time levels significantly increased as distance learning kept progressing. Keywords: COVID-19; distance learning; mental distress; medical students;                        screen time.

Background Many studies have reported the presence of Positive Regulatory/Su(var)3-9, Enhancer-of-zeste and Trithorax Domain 2 (PRDM2) downregulation in cancer. However, its potential as a diagnostic biomarker is still unclear. Hence, a systematic review and meta-analysis were conducted to address this issue. Introduction As of 2018, cancer has become the second leading cause of death worldwide. Thus, cancer control is exceptionally vital in reducing mortality. One such example is through early diagnosis of cancer using tumor biomarkers. Having a function as a tumor suppressor gene (TSG), PRDM2 has been linked with carcinogenesis in several solid tumor. This study aims to assess the relationship between PRDM2 downregulation and solid tumor, its relationship with clinicopathological data, and its potential as a diagnostic biomarker. This study also aims to evaluate the quality of the studies, data reliability and confidence in cumulative evidence. Materials & Methods A protocol of this study is registered at the International Prospective Register of Systematic Reviews (PROSPERO) with the following registration number: CRD42019132156. PRISMA was used as a guideline to conduct this review. A comprehensive electronic search was performed from inception to June 2019 in Pubmed, Cochrane Library, ProQuest, EBSCO and ScienceDirect. Studies were screened and included studies were identified based on the criteria made. Finally, data synthesis and quality assessment were conducted. Results There is a significant relationship between PRDM2 downregulation with solid tumor (RR 4.29, 95% CI [2.58–7.13], P < 0.00001). The overall sensitivity and specificity of PRDM2 downregulation in solid tumors is 84% (95% CI [39–98%]) and 86% (95% CI [71–94%]), respectively. There is a low risk of bias for the studies used. TSA results suggested the presence of marked imprecision. The overall quality of evidence for this study is very low. Discussion We present the first meta-analysis that investigated the potential of PRDM2 downregulation as a diagnostic biomarker in solid tumor. In line with previous studies, our results demonstrated that PRDM2 downregulation occurs in solid tumor. A major source of limitation in this study is the small number of studies. Conclusions Our review suggested that PRDM2 is downregulated in solid tumor. The relationship between PRDM2 downregulation and clinicopathological data is still inconclusive. Although the sensitivity and specificity of PRDM2 downregulation are imprecise, its high values, in addition to the evidence that suggested PRDM2 downregulation in solid tumor, hinted that it might still have a potential to be used as a diagnostic biomarker. In order to further strengthen these findings, more research regarding PRDM2 in solid tumors are encouraged.