Objective: To analyze the situation of new occupational diseases in Hengyang City from 2006 to 2017, and put forward prevention and control strategies. Methods: The data of the new occupational disease report of Hengyang city in the Occupational Disease and Occupational Health Information Monitoring System from January 1, 2006 to December 31, 2017 was collected, and the age, working years, and the region and industry of the new occupational disease patients were analyzed. Results: From 2006 to 2017, there were 7 categories, 30 kinds and 2 110 cases of new occupational diseases in Hengyang City, including 1 117 cases of pneumoconiosis, 951 cases of chronic occupational poisoning, 15 cases of acute occupational poisoning, 12 cases of occupational otolaryngological and stomatological diseases, 7 cases of occupational skin diseases, 6 cases of occupational diseases caused by physical factors, and 1 case of occupational eye diseases(cataracts), 1 case of occupational tumor (lung cancer and skin cancer caused by arsenic and its compounds). New occupational diseases were mainly concentrated in Changning and Leiyang County-level city (87.82%, 1 853/2110), among which occupational poisoning had the most incidence in Changning County-level city (97.83%, 945/966), and pneumoconiosis had the most incidence in Leiyang County-level city (67.05%, 749/1 117). New occupational diseases were mainly concentrated in the manufacturing and mining industries (95.59%, 2 017/2 110). Pneumoconiosis (63.74%, 712/1 117) and acute occupational poisoning (60.00%, 9/15) were mainly caused by small businesses. Chronic occupational poisoning (61.62%, 586/951) and occupational otolaryngological and stomatological diseases (75.00%, 9/12) were mainly caused by large enterprises. Conclusion The new occupational diseases in Hengyang city are mostly pneumoconiosis and chronic occupational poisoning, and we should focus on strengthening the prevention and control of occupational diseases in the mining industry and manufacturing industry.

Depression is a kind of complex mental illness， which is mainly treated by western medicine at present， but the effect of western antidepressant drugs is not good due to the combined influence of side effects and individual differences of patients. Depression is a "stagnation syndrome" in traditional Chinese medicine， and its treatment principle is to disperse stagnated liver Qi for relieving Qi stagnation. The classic traditional Chinese medicine formula Chaihu Shugansan （CHSGS） has a long history of treating depression and demonstrates significant therapeutic efficacy. Clinically， the addition and subtraction of CHSGS is flexible， but the properties of the active ingredients are vague， and the mechanism and function are unclear. In order to elucidate the pharmacodynamic basis and antidepressant mechanism of CHSGS， this article reviews the pharmacodynamic material basis of CHSGS， clinical research and antidepressant mechanism research progress. Clinically， CHSGS can treat various types of depression such as primary depression， post-stroke depression， and postpartum depression. This article summarizes 32 main ingredients of CHSGS， among which albiflorin， ferulic acid， naringin， hesperidin， saikosaponin a， glycyrrhetinic acid， tangeretin， meranzin hydrate， nobiletin and glycyrrhizic acid are the quality markers （Q-markers） for the antidepressant effect of CHSGS. The antidepressant mechanism of CHSGS is complex， including regulating monoamine neurotransmitters， hypothalamic-pituitary-adrenal （HPA） axis， neurotrophic factors， inflammatory response， cell damage-related pathways， oxidative stress， etc. This article helps to deeply understand the pharmacodynamic basis and mechanism of CHSGS in treating depression， and provides a theoretical basis for the clinical application of CHSGS in treating depression and the development of antidepressant drugs.

Objective : The purpose of this study was to investigate the effects of OTU deubiquitinase,ubiquitin aldehyde binding 2(OTUB2)on the activity of DEAD-box helicase 54(DDX54)and its influence on the formation of neutrophil extracellular traps(NETs)and the vitality and invasion ofcolorectal cancer(CRC)cells. Methods: Peripheral blood neutrophils were isolated from CRC patients and healthy controls,then stimulated with phorbol-12- myristate-13-acetate(PMA)or DNase I for 4 hours.Westem blot analysis was performed to detect the expression of NETs markers,myeloperoxidase(MPO),and citrullinated histone H3(Cit-H3).The expression of OTUB2 or DDX54 was manipulated in SW480 cells,and they were co-cultured with neutrophils.The cells were divided into the following groups:Control group(without any treatment),NETs group,vector group,OTUB2 group,NETs+ si-OTUB2 group(SW480 cells,SW480 cells transfected with vector,OTUB2 overexpression plasmid and si- OTUB2 were co-cultured with PMA-treated neutrophils,respectively),OTUB2+DNase I group(SW480 cells transfected with OTUB2 overexpression plasmid co-cultured with neutrophils treated with DNase I),si- OTUB2group,OTUB2+si-NCgroup,OTUB2+si-DDX54group(SW480 cells transfected with si-0TUB2,OTUB2 overexpressing plasmid and si-NC,OTUB2 overexpressing plasmid and si-DDX54 were co-cultured with neutro- phils,respectively).ELISA was used to measure the relative expression of MPO-DNA complexes and the concen- tration of Cit-H3 in the supernatant of SW480 cells.MTT and Transwell assays were performed to evaluate cell via- bility and invasive ability.RNA sequencing was conducted to screen downstream genes regulated by OTUB2.The interaction between DDX54 and OTUB2 was validated using quantitative real-time polymerase chain reaction(qRT- PCR),co-immunoprecipitation(Co-IP),Clutathione S-Transferase(CST)pull-down,and His-tag pull-down experiments. Results : Compared to healthy individuals,there was an increased formation of NETs in the peripheral blood of CRC patients.The CRC cells in the NETs group exhibited increased cell viability and invasion compared to the control group(P<0.05).In comparison to the vector group,the OTUB2 group showed increased relative ex- pression of MPO-DNA complexes and Cit-H3,as well as increased cell viability and invasion(P<0.05).Howev- er,when compared to the OTUB2 group,the OTUB2+DNase I group exhibited decreased relative expression of MPO-DNA complexes and Cit-H3,as well as decreased cell viability and invasion(P<0.05).Co-IP,GST pull- down,and His-tag pull-down experiments demonstrated the interaction between OTUB2 and DDX54.In comparison to the OTUB2 +si-NC group,the OTUB2 +si-DDX54 group showed decreased relative expression of MPO-DNA complexes and Cit-H3,as well as decreased cell viability and invasion(P<0.05). Conclusion deubiquitinating enzyme OTUB2 can increase the formation of NETs and promote CRC cell viability and invasion by up-regulating DDX54.

Animals ; Bleomycin ; Epithelial-Mesenchymal Transition ; Lung ; Male ; Pulmonary Fibrosis/drug therapy* ; Rats ; Rats, Sprague-Dawley ; Simvastatin/pharmacology*

In recent years， the field of network pharmacology （NP） has developed rapidly， but the flawed and routine workflow has seriously affected the scientificity and reliability of NP analysis results. For complex diseases caused by environmental and genetic factors， symptomatic treatment or drugs targeting a single pathophysiological process cannot prevent or delay the progression of the disease， so the drug development fails or withdraws from the market. Therefore， there is an urgent need to develop new ideas for NP analysis that combines multiple pathophysiological processes. The key pathophysiological process is an important and complete set of pathological changes in the process of the occurrence， development， and outcome of the disease， which represents the current comprehensive and profound understanding of the nature of the disease. In order to improve the quality of NP research and promote the healthy development of the NP field， this paper proposes a new idea of NP analysis based on key pathophysiological processes. Based on the long-term clinical practice of traditional Chinese medicine and the key pathophysiological process of the disease， the method comprehensively analyzes the pharmacological mechanism and active ingredients of traditional Chinese medicine compound from the perspective of key pathophysiological process， which increases the scientifically， reliability， and repeatability of the analysis results. This paper takes Alzheimer's disease （AD） as an example to illustrate the necessity， feasibility， main workflow， advantages， and disadvantages of this method， and it is expected to screen disease-modifying drugs that prevent or reverse the course of the disease and promote the clinical transformation of research results.

The purpose of this study was to explore the effect and mechanism of dihydromyricetin (DHM) on Parkinson's disease (PD)-like lesions in type 2 diabetes mellitus (T2DM) rats. The T2DM model was established by feeding Sprague Dawley (SD) rats with high-fat diet and intraperitoneal injection of streptozocin (STZ). The rats were intragastrically administered with DHM (125 or 250 mg/kg per day) for 24 weeks. The motor ability of the rats was measured by balance beam experiment, the changes of dopaminergic (DA) neurons and the expression of autophagy initiation related protein ULK1 in the midbrains of the rats were detected by immunohistochemistry, and the protein expression levels of α-synuclein (α-syn), tyrosine hydroxylase (TH), as well as AMPK activation level, in the midbrains of the rats were detected by Western blot. The results showed that, compared with normal control, the rats with long-term T2DM exhibited motor dysfunction, increased α-syn aggregation, down-regulated TH protein expression, decreased number of DA neurons, declined activation level of AMPK, and significantly down-regulated ULK1 expression in the midbrain. DHM (250 mg/kg per day) treatment for 24 weeks significantly improved the above PD-like lesions, increased AMPK activity, and up-regulated ULK1 protein expression in T2DM rats. These results suggest that DHM may improve PD-like lesions in T2DM rats by activating AMPK/ULK1 pathway.
Rats ; Animals ; Parkinson Disease ; Rats, Sprague-Dawley ; AMP-Activated Protein Kinases ; Diabetes Mellitus, Type 2 ; Autophagy-Related Protein-1 Homolog

Biodegradable vascular stents have better biocompatibility than drug-eluting stents. The blood vessels are rebuilt and degraded after normal physiological functions are restored. Due to it will not stay in the body for a long time and the patients don't need taking anti-rejection drugs all the time, it becomes the focus of attention in the treatment of coronary heart disease. This article introduced the development history of biodegradable stents and reviewed the research status of several different materials of vascular stents (animals or humans)
Absorbable Implants ; Animals ; Drug-Eluting Stents ; Humans ; Stents

Chloroquine is a quinine derivative which is synthesized by German scholars in 1934. In addition to its anti-malaria, treatment of systemic lupus erythematosus and immunomodulatory effects, chloroquine is also found valuable in broad-spectrum antiviral treatment. Clinical trials have confirmed that chloroquine has a good effect on acquired immunodeficiency syndrome. In 2019, there were many patients infected with novel coronavirus (severe acute respiratory syndrome coronavirus 2, SARS-CoV-2). Preliminary clinical trials showed that chloroquine had obvious curative effect on patients with SARS-CoV-2. We summarize the effects of chloroquine to different viruses, explain its mechanism, and compare the results of its experiments in vitro and in vivo. The antiviral effect of chloroquine in vivo and in vitro are not consistent, which may be related to the model of animal, dosage and distribution of chloroquine in vivo, and the design of clinical research.

自噬是细胞内一种高度保守的生理过程，可通过溶酶体系统降解过量或受损的细胞器、有毒的蛋白聚集体和病原体等。最新研究表明，海马钙素样1（HPCAL1）可作为特异性自噬受体和铁死亡的正调节因子。HPCAL1可选择性降解钙粘素2（CDH2），加速脂质过氧化，促进癌细胞铁死亡。iHPCAL1是抑制HPCAL1的小分子化合物，可抑制Erastin诱导的肿瘤细胞铁死亡。此外，它还可以抑制铁死亡诱导的急性胰腺炎。本文通过对HPCAL1在铁死亡中的具体作用机制进行概述，为HPCAL1作为铁死亡相关疾病的潜在治疗靶点提供新思路和理论依据。
Ferroptosis ; Cell Line, Tumor ; Autophagy

Objective We detected the level of serum calmodulin，γ-aminobutyric acid（GABA），glutamic acid（Glu） and GABA/Glu in insomnia patients，explored their association with insomnia.Methods The casecontrol study was used. This study comprised 119 insomnia patients and 122 healthy control subjects. Enzyme linked immunosorbent assay（ELISA） was utilized to measure the level of serum CaM，GABA，Glu and GABA/Glu. The correlation between the level of serum CaM and GABA/Glu was performed by correlation analyze. Results Our results suggested the level of serum CaM,GABA,GABA/Glu were significantly lower，and the level of serum Glu was significantly higher in patients with insomnia compared to the control group（P<0.05）.The level of serum CaM was positively correlated with GABA/Glu in insomnia patients（r=0.475，P<0.05）.Conclusion CaM downregulation increases the risk of insomnia，and the mechanism may be related to the downregulation of GABA/Glu level.