摘要：
Atherosclerosis is a chronic inflammatory response that increases the risk of cardiovascular diseases. An in-depth study of the pathogenesis of atherosclerosis is critical for the treatment of atherosclerotic cardiovascular disease. The development of atherosclerosis involves many cells, such as endothelial cells, vascular smooth muscle cells, macrophages, and others. The considerable effects of macrophages in atherosclerosis are inextricably linked to macrophage polarization and the resulting phenotype. Moreover, the significant impact of macrophages on atherosclerosis depend not only on the function of the different macrophage phenotypes but also on the relative ratio of different phenotypes in the plaque. Research on atherosclerosis therapy indicates that the reduced plaque size and enhanced stability are partly due to modulating macrophage polarization. Therefore, regulating macrophage polarization and changing the proportion of macrophage phenotypes in plaques is a new therapeutic approach for atherosclerosis. This review provides a new perspective for atherosclerosis therapy by summarizing the relationship between macrophage polarization and atherosclerosis, as well as treatment targeting macrophage polarization.
关键词：
cancer stem cells;signalling pathway inhibitors;targeted therapy;small-molecule chemicals;tumour microenvironment
摘要：
The poor survival and prognosis of individuals with cancer are often attributed to tumour relapse and metastasis, which may be due to the presence of cancer stem cells (CSCs). CSCs have the characteristics of self-renewal, differentiation potential, high carcinogenicity, and drug resistance. In addition, CSCs exhibit many characteristics similar to those of embryonic or tissue stem cells while displaying persistent abnormal activation of self-renewal pathways associated with development and tissue homeostasis, including the Wnt, Notch, Hedgehog (Hh), TGF-beta, JAK/STAT3, and NF-kappa B pathways. Therefore, we can eliminate CSCs by targeting these self-renewal pathways to constrain stem cell replication, survival and differentiation. At the same time, we cannot neglect the ping-pong effect of the tumour microenvironment, which releases cytokines and promotes self-renewal pathways in CSCs. Recently, meaningful progress has been made in the study of inhibitors of self-renewal pathways in tumours. This review primarily summarizes several representative and novel agents targeting these self-renewal signalling pathways and the tumour microenvironment and that represent a promising strategy for treating refractory and recurrent cancer.
摘要：
Chronic systolic heart failure (CSHF) was a complex syndrome. Recently, vagus nerve stimulation (VNS), a novel treatment method, has emerged for the treatment of CSHF. therefore the aim of this study was to explore the possible mechanism of VNS treatment alleviating CSHF in rats. Firstly, we found after VNS treatment for 72 h, the level of B-type natriuretic peptide in VNS group was lower than that in CSHF group. In addition, VNS treatment induced the elevated left ventricular ejection fraction level, reduced left ventricular end diastolic volume and left ventricular end systolic volume level in VNS group, suggesting a mitigation of CSHF by VNS. Then we found the level of miR-183-3p in CSHF group was much lower than that in VNS group by High-throughput sequencing. The further results indicated that Bcl-2 interacting protein 3 like (BNIP3L) was identified as the target gene of miR-183-3p, and the expression of BNIP3L was notably reduced in rats of VNS group compared with CSHF group. Moreover, the down-regulated expression of miR-183-3p increased BNIP3L-mediated autophagy in rats of CSHF group compared with VNS group. Further mechanism findings demonstrated that up-regulation of miR-183-3p reduced the expression of BNIP3L, while down-regulation of miR-183-3p facilitated the expression of BNIP3L in H9c2 cells. miR-183-3p could also regulate autophagy by targeting BNIP3L in vitro, which was manifested by overexpression of miR-183-3p to inhibit BNIP3L-mediated autophagy. Our data demonstrated that VNS treatment benefited CSHF via the up-regulation of miRNA-183-3p, which reduced the BNIP3L-mediated autophagy, providing a new therapeutic direction for CSHF.
摘要：
Aims & ScopeFoundations of Chemistry is an international journal which seeks to provide an interdisciplinary forum where chemists, biochemists, philosophers, historians, educators and sociologists with an interest in foundational issues can discuss conceptual and fundamental issues which relate to the `central science' of chemistry. Such issues include the autonomous role of chemistry between physics and biology and the question of the reduction of chemistry to quantum mechanics. The journal will publish peer-reviewed academic articles on a wide range of subdisciplines, among others: chemical models, chemical language, metaphors, and theoretical terms; chemical evolution and artificial self-replication; industrial application, environmental concern, and the social and ethical aspects of chemistry's professionalism; the nature of modeling and the role of instrumentation in chemistry; institutional studies and the nature of explanation in the chemical sciences; theoretical chemistry, molecular structure and chaos; the issue of realism; molecular biology, bio-inorganic chemistry; historical studies on ancient chemistry, medieval chemistry and alchemy; philosophical and historical articles; and material of a didactic nature relating to all topics in the chemical sciences. Foundations of Chemistry plans to feature special issues devoted to particular themes, and will contain book reviews and discussion notes. Audience: chemists, biochemists, philosophers, historians, chemical educators, sociologists, and other scientists with an interest in the foundational issues of science.Coverage in the Journals@Ovid database begins with the March 1999 issue.
作者机构：
[Zhao, Tie] Univ South China, Inst Pathogen Biol, Collaborat Innovat Ctr New Mol Drug Res, Hengyang, Peoples R China.;[Zhao, Tie] Univ South China, Key Lab Special Pathogen Prevent & Control Hunan, Collaborat Innovat Ctr New Mol Drug Res, Hengyang, Peoples R China.;[Zhao, Tie] Univ South China, Hengyang Med Coll, Inst Pathogen Biol, 28 West Changsheng Rd, Hengyang 421001, Hunan, Peoples R China.;[Zhao, Tie] Univ South China, Hengyang Med Coll, Key Lab Special Pathogen Prevent & Control Hunan, 28 West Changsheng Rd, Hengyang 421001, Hunan, Peoples R China.
通讯机构：
[Zhao, Tie] U;Univ South China, Hengyang Med Coll, Inst Pathogen Biol, 28 West Changsheng Rd, Hengyang 421001, Hunan, Peoples R China.;Univ South China, Hengyang Med Coll, Key Lab Special Pathogen Prevent & Control Hunan, 28 West Changsheng Rd, Hengyang 421001, Hunan, Peoples R China.
摘要：
Ain-Shams Journal of Anesthesiology is the official journal issued by the Department of Anesthesiology, Intensive Care, and Pain Management, Faculty of Medicine, Ain-Shams University, Cairo, Egypt. It publishes original articles, reviews, case reports, editorials, and comments on all aspects anesthesiology, critical care, trauma, pain manamgement, resuscitation, and anesthesia education. Its main aim is to help raise the standard of scientific research locally and regionally through connection with the advanced world abroad.
作者机构：
[Yang, Mingxiu; Huang, Weiguo] Univ South China, Hengyang Med Coll, Canc Res Inst, Hunan Prov Key Lab Tumor Cellular & Mol Pathol 20, Hengyang, Hunan, Peoples R China.;[Huang, Weiguo] Univ South China, Hengyang Med Coll, Canc Res Inst, 28 West Changsheng Rd, Hengyang City, Hunan, Peoples R China.
通讯机构：
[Huang, Weiguo] U;Univ South China, Hengyang Med Coll, Canc Res Inst, 28 West Changsheng Rd, Hengyang City, Hunan, Peoples R China.
摘要：
Texture analysis is an emerging field that allows mathematical detection of changes in MRI signals that are not visible among image pixels. Alzheimer's disease, a progressive neurodegenerative disease, is the most common cause of dementia. Recently, multiple texture analysis studies in patients with Alzheimer's disease have been performed. This review summarizes the main contributors to Alzheimer's disease-associated cognitive decline, presents a brief overview of texture analysis, followed by review of various MR imaging texture analysis applications in Alzheimer's disease. We also discuss the current challenges for widespread clinical utilization. MR texture analysis could potentially be applied to develop neuroimaging biomarkers for use in Alzheimer's disease clinical trials and diagnosis.
期刊：
ONCOTARGETS AND THERAPY,2020年13:2551-2562 ISSN：1178-6930
通讯作者：
Tang, Yunlian
作者机构：
[Yang, Ping; Liu, Bingxue; Tang, Yunlian; Wu, Chu] Univ South China, Med Coll Hengyang, Key Lab Tumor Cellular & Mol Pathol, Canc Res Inst, Hengyang 421001, Hunan, Peoples R China.
通讯机构：
[Tang, Yunlian] U;Univ South China, Med Coll Hengyang, Key Lab Tumor Cellular & Mol Pathol, Canc Res Inst, Hengyang 421001, Hunan, Peoples R China.
关键词：
PDAC;CDKN2A;cell cycle;genes;biomarkers
摘要：
Pancreatic cancer has a high mortality rate and its incidence has risen rapidly in recent years. Meanwhile, the diagnosis and treatment of this cancer remain challenging. Pancreatic ductal adenocarcinoma (PDAC) is the most common type of pancreatic cancer, but, currently, no sufficiently effective modalities for its treatment exist. The early diagnosis rate of pancreatic cancer is low and most patients have reached an advanced stage at the time of diagnosis. PDAC evolves from precancerous lesions and is highly aggressive and metastatic. It is essential to understand how the disease progresses and metastasizes. CDKN2A mutations are very common in PDAC. Therefore, here, we have performed a literature review and discuss the role of CDKN2A and some related genes in the development of PDAC, as well as the basis of gene targeting with a correlation coefficient of CDKN2A above 0.9 on the STRING website. It is noteworthy that the interaction of CDKN2A with each gene has been reported in the literature. The role of these genes and CDKN2A in PDAC may provide new directions that will advance the current knowledge base and treatment options since cancer progression is realized through interactions among cells. Our findings provide new insights into the treatment of PADC that can, to some extent, improve the diagnosis rate and quality of life of patients.
摘要：
Objective: To investigate whether hydrogen sulfide (H2S) counteracts formaldehyde (FA)-induced cognitive defects and whether the underlying mechanism is involved in the upregulation of hippocampal brain-derived neurotrophic factor (BDNF) expression. Methods: The cognitive function of rats was evaluated by the Morris water maze (MWM) test and the novel object recognition test. The content of superoxide dismutase (SOD) and malondialdehyde (MDA) in the hippocampus were detected by enzyme-linked immunosorbent assay (ELISA). The neuronal apoptosis in the hippocampal CA1 region was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick-end (TUNEL) staining. The expression of the BDNF protein was detected by Western blot and immunohistochemistry. Results: We found that sodium hydrosulfide (NaHS, a donor of H2S) significantly reversed the impairment in the function of learning and memory in the MWM test and the novel objective recognition task induced by intracerebroventricular injection of FA. We also showed that NaHS significantly reduced the level of MDA, elevated the level of SOD, and decreased the amount of TUNEL-positive neurons in the hippocampus of FA-exposed rats. Moreover, NaHS markedly increased the expression of hippocampal BDNF in FA-exposed rats. Conclusions: H2S attenuates FA-induced dysfunction of cognition and the underlying mechanism is involved in the reduction of hippocampal oxidative damage and apoptosis as well as upregulation of hippocampal BDNF.
摘要：
As a major type of immune cells with heterogeneity and plasticity, macrophages are classically divided into inflammatory (M1) and alternative/anti-inflammatory (M2) types and play a crucial role in the progress of the inflammatory diseases. Recent studies have shown that metabolism is an important determinant of macrophage phenotype. Mitochondria, one of the most important compartments involving cell metabolism, are closely associated with the regulation of cell functions. In most types of cell, mitochondrial oxidative phosphorylation (OXPHOS) is the primary mode of cellular energy production. However, mitochondrial OXPHOS is inhibited in activated M1 macrophages, rendering them unable to be converted into M2 phenotype. Thus, mitochondrial metabolism is a crucial regulator in macrophage functions. This review summarizes the roles of mitochondria in macrophage polarization and analyzes the molecular mechanisms underlying mitochondrial metabolism and function, which may provide new approaches for the treatment of metabolic inflammatory diseases.
摘要：
The therapeutic effect of metformin (Met) on atherosclerosis was studied here. Effects of methionine and Met on the induction of inflammatory response and H2S expression in peritoneal macrophages were evaluated. Enzyme-linked immunosorbent assay, immunohistochemistry assay, western blot, and quantitative reverse transcription polymerase chain reaction were conducted to observe the levels of cystathionine gamma-lyase (CSE), DNA methyltransferases 1 (DNMT1), DNMT3a, DNMT3b, tumor necrosis factor (TNF- alpha), interleukin 1b (IL-1 beta), and hydrogen sulfide (H2S). Luciferase and bisulfite sequencing assays were also utilized to evaluate the CSE promoter activity as well as the methylation status of CSE in transfected cells. Methionine significantly elevated Hcy, TNF-a, H2S, and IL-1 beta expression while decreasing the level of CSE in C57BL/6 mice. In contrary, co-treatment with Methionine and Met reduced the detrimental effect of Methionine. Homocysteine (Hcy) decreased H2S expression while promoting the synthesis of IL-1 beta and TNF-alpha in THP-1 and raw264.7 cells. Treatment of THP-1 and raw264.7 cells with methionine and Met reduced the activity of methionine in dose dependently. Moreover, Hcy increased the expression of DNMT and elevated the level of methylation in the CSE promoter, whereas the co-treatment with methionine and Met attenuated the effects of Hcy. Methionine significantly decreased plasma level of CSE while increasing the severity of inflammatory responses and plasma level of Hcy, which in turn suppressed H2S synthesis and enhanced DNA hypermethylation of CSE promoter to promote the pathogenesis of atherosclerosis. In contrary, co-treatment with methionine and Met reduced the detrimental effect of methionine.
