Boonebramsen5469

Alzheimer's disease (AD) is the most common cause of dementia and is characterized by the deposition of extracellular aggregates of amyloid-β (Aβ), the formation of intraneuronal tau neurofibrillary tangles and microglial activation-mediated neuroinflammation. One of the key molecules involved in microglial activation is galectin-3 (Gal-3). In recent years, extensive studies have dissected the mechanisms by which Gal-3 modulates microglial activation, impacting Aβ deposition, in both animal models and human studies. In this review article, we focus on the emerging role of Gal-3 in biology and pathobiology, including its origin, its functions in regulating microglial activation and neuroinflammation, and its emergence as a biomarker in AD and other neurodegenerative diseases. These aspects are important to elucidate the involvement of Gal-3 in AD pathogenesis and may provide novel insights into the use of Gal-3 for AD diagnosis and therapy.

Adolescent substance use continues to be a growing major public health concern in Africa. Recent studies infer an overall estimated prevalence of 42% among adolescents in sub-Saharan Africa. Unfortunately, this phenomenon is not adequately documented across many settings in the continent despite known negative health and social consequences on affected individuals and their communities. Little is known about the social context of substance use in Africa among this population. Our aim is to conduct a systematic review, exploring the determinants and associated factors that influence adolescent substance use in Africa.

We will search the following databases (from January 2000 onwards) PubMed, the Cochrane Library, African Journals Online (AJOL), Google Scholar, ScienceDirect and the World Health Organization (WHO) African Index Medicus. We will include population-based observational studies reporting on determinants and/or risk factors of substance use among adolescents (age 10-19 years) across Africa. Two reviewers will independently screen all citations, full-text articles and abstract data. Potential conflicts will be resolved through discussion. Study methodological quality (or bias) will be appraised using appropriate tools. If feasible, we will conduct a random-effects meta-analysis of data. We plan to conduct a meta-synthesis of qualitative studies where appropriate DISCUSSION This review will describe the range of determinants and associated factors found to significantly influence adolescent substance use in Africa over the last two decades. Documenting this evidence is important as it can potentially inform comprehensive interventions and treatment programmes that are targeted at adolescents and their parents in these settings.

PROSPERO CRD42020190158.

PROSPERO CRD42020190158.Chemical compounds can be identified through a graphical depiction, a suitable string representation, or a chemical name. A universally accepted naming scheme for chemistry was established by the International Union of Pure and Applied Chemistry (IUPAC) based on a set of rules. Due to the complexity of this ruleset a correct chemical name assignment remains challenging for human beings and there are only a few rule-based cheminformatics toolkits available that support this task in an automated manner. Here we present STOUT (SMILES-TO-IUPAC-name translator), a deep-learning neural machine translation approach to generate the IUPAC name for a given molecule from its SMILES string as well as the reverse translation, i.e. Chk2 Inhibitor II concentration predicting the SMILES string from the IUPAC name. In both cases, the system is able to predict with an average BLEU score of about 90% and a Tanimoto similarity index of more than 0.9. Also incorrect predictions show a remarkable similarity between true and predicted compounds.

Guizhi decoction (GZD), a classical Chinese herbal formula, has been widely used to treat hypertension, but its underlying mechanisms remain elusive. The present study aimed to explore the potential mechanisms and therapeuticeffects of GZD on hypertension by integrating network pharmacology and experimental validation.

The active ingredientsand corresponding targets were collected from the Traditional Chinese Medicine Systems Pharmacology database and Analysis Platform (TCMSP).The targets related to hypertension were identified from the CTD, GeneCards, OMIM and Drugbank databases. Multiple networks were constructed to identify the key compounds, hub targets, and main biological processes and pathways of GZD against hypertension. The Surflex-Dock software was used to validate the binding affinity between key targets and their corresponding active compounds. The Dahl salt-sensitive rat model was used to evaluate the therapeutic effects of GZD against hypertension.

A total of 112 active ingredients, 222 taammation and fibrosis.

The potential mechanisms and therapeutic effects of GZD on hypertension may be attributed to the regulation of cardiac inflammation and fibrosis.

Peritoneal fibrosis is one of the major complications induced by peritoneal dialysis (PD). Damaged integrity and function of peritoneum caused by peritoneal fibrosis not only limits the curative efficacy of PD and but affects the prognosis of patients. However, the detailed mechanisms underlying the process remain unclear and therapeutic strategy targeting TGF-β is deficient. Transforming growth factor-β (TGF-β) signaling participates in the progression of peritoneal fibrosis through enhancing mesothelial-mesenchymal transition of mesothelial cells.

The study aims to demonstrate the regulatory role of Sirtuin1 (SIRT1) to the TGF-β signaling mediated peritoneal fibrosis. SIRT1

mice were used to establish animal model. Masson's staining and peritoneal equilibration assay were performed to evaluate the degree of peritoneal fibrosis. QRT-PCR assays were used to estimate the RNA levels of Sirt1 and matrix genes related to peritoneal fibrosis, and their protein levels were examined by Western blot assays.

SIRT1 significantly decreased in vivo post PD treatment. SIRT1 knockout exacerbated peritoneal fibrosis both in vivo and vitro. Overexpression of SIRT1 efficiently inhibited peritoneal fibrosis by inhibiting the peritoneal inflammation and the activation of TGF-β signaling.

SIRT1 ameliorated peritoneal fibrosis both in vivo and in vitro through inhibiting the expression of protein matrix induced by TGF-β signaling.

SIRT1 ameliorated peritoneal fibrosis both in vivo and in vitro through inhibiting the expression of protein matrix induced by TGF-β signaling.