Notes

Pre-natal Assessments: Any Prologue for you to Postnatal Pathology Understandings.
Epigenetic mechanisms, such as acetylation, methylation, and succinylation, play pivotal roles in the regulation of multiple normal biological processes, including neuron regulation, hematopoiesis, bone cell maturation, and metabolism. In addition, epigenetic mechanisms are closely associated with the pathological processes of various diseases, such as metabolic diseases, autoimmune diseases and cancers. Epigenetic changes may precede genetic mutation, so research on epigenetic changes and regulation may be important for the early detection and diagnosis of disease. Histone deacetylase11 (HDAC11) is the newest member of the histone deacetylase (HDAC) family and the only class IV histone deacetylase. HDAC11 has different expression levels and biological functions in different systems of the human body and is among the top 1 to 4% of genes overexpressed in cancers, such as breast cancer, hepatocellular carcinoma and renal pelvis urothelial carcinoma. This article analyzes the role and mechanism of HDAC11 in disease, especially in tumorigenesis, in an attempt to provide new ideas for clinical and basic research.In current aging societies, diabetes mellitus and neurodegenerative diseases represented by Alzheimer's disease are highly prevalent among adults, especially the elderly all over the world. It is worth noting that a substantial body of evidence suggests diabetes contributes to accelerated neurodegenerative processes and the decline of cognition. Over the last few years, some studies have indicated neurovascular uncoupling and disrupted functional connectivity in the early stages of many neurodegenerative diseases, and the concept of the neurovascular unit (NVU) has been highlighted to understand the initiation and progression of neurodegenerative diseases recently. Considering that some components of the NVU are also demonstrated to have abnormal morphology and function under the condition of diabetes, we propose the hypothesis that diabetes may promote the onset and development of neurodegenerative diseases by impairing the integrity of the NVU, named Diabetes-NVU-Neurodegeneration Hypothesis. The existing body of literature supporting the hypothesis and elucidating the underlying mechanisms will be summarized in this review.Methotrexate (MTX) is a chemotherapeutic drug commonly used to treat cancers that has an adverse effect on patients' cognition. Metformin is a primary treatment for type 2 diabetes mellitus that can pass through the blood-brain barrier. Metformin has neuroprotective actions, which can improve memory. In the present study, we examined the ability of metformin in MTX chemotherapy-generated cognitive and hippocampal neurogenesis alterations. Male Sprague-Dawley rats were allocated into control, MTX, metformin, preventive, and throughout groups. MTX (75 mg/kg/day) was given intravenously on days 7 and 14 of the study. Metformin (200 mg/kg/day) was injected intraperitoneally for 14 days. Some of the MTX-treated rats received co-treatment with metformin once a day for either 14 (preventive) or 28 days (throughout). After treatment, memory ability was evaluated using novel object location and novel object recognition tests. Ki67 (proliferating cells), BrdU (survival cells), and doublecortin (immature neurons, DCX) positive cells in the subgranular zone (SGZ) of the hippocampal dentate gyrus were quantified. We found that reductions of cognition, the number of proliferating and survival cells and immature neurons in the SGZ were ameliorated in the co-treatment groups, which suggests that metformin can prevent memory and hippocampal neurogenesis impairments induced by MTX in adult rats.Epilepsies are a diverse group of neurological disorders, which are characterized by spontaneous recurrent seizures. Although a wide range of pathogenic mechanisms such as alterations in ion channels, inflammation and neuronal loss have been reported to be implicated in the epileptogenesis, the underlying pathogenesis of epilepsy remains unclear currently. Endoplasmic reticulum (ER) stress is regarded as a condition that unfolded or misfolded proteins accumulate in the ER lumen. Excessive or prolonged ER stress causes the activation of the unfolded protein response (UPR) to buffer ER stress and restore ER homeostasis. Increasing evidence has indicated dysregulated ER stress during epileptogenesis, which may participate in various pathological processes associated with epilepsy. In this present review, we summarized recent advances in the involvement of ER stress in the pathogenesis of epilepsy. Additionally, the antiepileptic and neuroprotective effects of interventions targeting ER stress were also discussed.Mesenchymal stromal cells (MSCs) have been used for the treatment of neuronal injury and neurodegenerative diseases. Their underlying mechanism may involve increased secretion of paracrine factors, which promotes tissue repair. Presently, exosomes have been regarded as important components of paracrine secretion and paracrine factors. MSC exosomes represent a promising opportunity to develop novel cell-free therapy approaches. In this study, exosomes from nasal olfactory mucosa MSCs (OM-MSCs) were extracted and purified using ultracentrifugation, resulting in exosome diameters of 40-130 nm. Similar to other exosomes, OM-MSC exosomes were CD63- and CD81-positive and calnexin-negative. Functionally, OM-MSC exosomes promoted human brain microvascular endothelial cell (HBMEC) proliferation and migration. The present study analyzed the OM-MSC exosome paracrine proteome. A total of 304 exosome-associated proteins were identified by LC-MS/MS, including plasminogen activator inhibitor 1 (SERPINE 1), insulin-like growth factor binding protein family members (IGFBP 4 and 5), epidermal growth factor receptor (EGFR), neurogenic locus notch homolog protein 2 (NOTCH 2), apolipoprotein E (APOE), and heat shock protein HSP90-beta (HSP90AB1). These molecules are known to be important in neurotrophic, angiogenesis, cell growth, differentiation, apoptosis, and inflammation and are highly correlated with the mechanism of tissue repair and neural restoration. Nuciferine datasheet These observations may provide a basis for further evaluation of OM-MSC exosome potential as a novel therapeutic modality.
Website: https://www.selleckchem.com/products/nuciferine.html