Objective: To study the prevalence and antimicrobial susceptibility of Ureaplasma urealyticum (Uu) and Mycoplasma hominis (Mh) in Changsha, and provide laboratory evidence for clinical drug use. Methods: A retrospective study was conducted to analyze 53 006 specimens of suspected genital mycoplasma infection in Xiangya Second Hospital of Changsha District and Hunan Wangwang Hospital from 2010 to 2017, and to analyze the infection rate and drug resistance rate of Uu and Mh. Results: From 2010 to 2017, a total of 53 006 specimens were detected, where there were 16 830 cases of Uu infection, the infection rate was 31.75%; 2 471 cases of Mh infection, the infection rate was 4.66%; and 1 071 cases of Uu and Mh mixed infection, the infection rate was 2.02%. Male Uu infection rate was 19.48%(5 989/30 749), which was lower than the female infection rate 48.71%(10 841/22 257) (χ²=5 091, P<0.001); male Mh infection rate was 3.16%(973/30 749), lower than female infection rate 6.73%(1 498/22 257) (χ²=369,P<0.001). The population of genital mycoplasma infection is concentrated between 20 and 40 years old, accounting for 71.76% (12 077/16 830). The drug resistance rates of Uu and Mh to doxycycline and minocycline were less than 2%, while the drug resistance rate to quinolones was higher; The resistance rate of Uu to macrolide antibiotics such as erythromycin, josamycin and clarithromycin were less than 2%, while the resistance rate to azithromycin, erythromycin and roxithromycin were higher, 29.74%(5 006/16 830) and 53.74%(9 045/16 830), respectively, and the resistance rate of Mh to macrolide antibiotics (except josamycin) was higher than 90%.Between 2010 and 2017, a gradually increasing resistance of ureaplasmas to azithromycin, from 3.81% (46/1 206) in 2010 to 53.15% (1 503/2 828) in 2017, and decreasing resistance to gatifloxacin and thiamphenicol were observed, from 76.78% (926/1 206) and 60.28% (727/1 206) in 2010 decreased to 34.23% (968/2 828) and 37.87% (1 071/2 828) in 2017, respectively. The resistance rate of Mh to gatifloxacin and thiamphenicol were decreased, from 68.93% (122/177) and 41.81% (74/177) in 2010 to 53.54% (159/297) and 21.21% (63/297) in 2017, respectively. Conclusions Doxycycline, minocyclinum and josamycin are good treatment options for genital mycoplasma in Changsha. The resistance rate of Uu to azithromycin is increasing, suggesting that the abuse of azithromycin is present in Changsha, and indicating that better management of antibiotics is necessary.

Objectives To analyze the changes of serum complement C1q level in patients with metabolic syndrome (MS) and investigate whether it is associated with lipid metabolism and glycometabolism. Methods In a cross-sectional study, the subjects were selected as the patients and healthy people who went to the second xiangya hospital of central south university from July 2017 to June 2018. A total of 152 MS patients were enrolled and another 90 healthy subjects were enrolled as control group. Anthropometry parameters such as body mass index (BMI), systolic blood pressure (SBP), diastolic blood pressure (DBP) were measured. Serum concentrations of C1q and other biochemical indexes including blood glucose (GLU), triglycerides (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C) were measured in all groups. The correlations between C1q and these parameters were analyzed by spearman's rho test and the clinical value of C1q in predicting MS was further evaluated by stepwise multiple linear regression analysis. Results MS group had higher serum C1q levels (244.34±62.66) mg/L compared with the control group (202.37±35.92) mg/L (t=-6.250, P=0.000). C1q levels (244.34±62.66) mg/L were positively associated with TG levels [2.34(1.89, 3.62)] mmol/L (r=0.245, P=0.001), TC levels (4.91±1.26) mmol/L (r=0.398, P=0.000), LDL-C levels (3.23±1.03) mmol/L (r=0.325, P=0.000) in MS group, While C1q levels (258.92±69.59)mg/L were positively associated with SBP (144.76 ± 22.94) mmHg (r=0.388, P=0.018), TG levels [2.65(1.87, 3.82)] mmol / L (r=0.482, P=0.003), TC levels (5.18±1.31) mmol/L (r=0.529,P=0.001) in MS patients with obesity. The stepwise multiple regression analysis showed that TG levels were independently correlated with serum C1q levels both in MS patients (β=0.302, P=0.000) and in MS patients with obesity (β=0.653, P=0.000) after adjusting for age, gender and other biochemical markers. Conclusions MS patients had higher C1q levels than healthy subjects and serum C1q levels were closely positive related to harmful lipid profiles. Serum TG level was an independent influencing factor of serum C1q in MS patients.

ObjectiveTo investigate the molecular mechanism of the anti-inflammatory effect of Erchentang in the lung tissue of the rat model of chronic obstructive pulmonary disease （COPD） via the heparin-binding factor （Midkine）/transmembrane receptor protein （Notch2）/Hey1 signaling pathway. MethodSixty SD rats were randomized into normal group， model group， modified Erchentang （5， 10， 20 g·kg^-1·d^-1） groups， and Notch1 pathway inhibitor （γ-secretase inhibitor， DAPT， 0.02 g·kg^-1） group， with 10 rats in each group. The rat model of COPD was established by cigarette smoke combined with lipopolysaccharide （LPS）. After the modeling， the rats were administrated with corresponding drugs by gavage， and those in the normal and model groups were administrated with normal saline by gavage for 21 days. The levels of Midkine， cytokine-induced neutrophil chemoattractant-1 （CINC-1）， macrophage-derived chemokine （MDC）， chemokine ligand 5 （CXCL5）， neutrophil elastase （NE）， and nuclear factor-kappa B （NF-κB） p65 in bronchoalveolar lavage fluid （BALF） were determined by enzyme-linked immunosorbent assay （ELISA）. Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） and immunohistochemistry were respectively employed to determine the mRNA and protein levels of Midkine， Notch2， and Hey1 in the lung tissue. ResultCompared with the normal group， the modeling increased the levels of Midkine， CINC-1， MDC， CXCL5， NE， and NF-κB p65 in BALF （P<0.01） and up-regulated the mRNA and protein levels of Midkine， Notch2， and Hey1 in the lung tissue （P<0.01）. Compared with the model group， medium- and high-dose modified Erchentang and DAPT lowered the levels of Midkine， CINC-1， MDC， CXCL5， and NF-κB p65 in BALF （P<0.01） and down-regulated the mRNA levels of Midkine， Notch2， and Hey1 （P<0.01）. ConclusionModified Erchentang may inhibit the inflammation in COPD rats by down-regulating the expression of Midkine， Notch2， and Hey1 and reducing the content of Midkine， CINC-1， MDC， and CXCL5.

ObjectiveTo study the effect of modified Erchentang on the expression of key molecules in the high mobility group Box 1 protein （HMGB1）/receptor for advanced glycation endproduct （RAGE）/nuclear factor-κB （NF-κB） signaling pathway in bronchioles of rats with chronic obstructive pulmonary disease （COPD）， to explore the mechanism of modified Erchentang against bronchiolar inflammation of COPD rats via HMGB1/RAGE/NF-κB signaling pathway. MethodSixty SD rats were randomly divided into normal group， model group， modified Erchentang low-， medium- and high-dose groups （5， 10， 20 g·kg^-1·d^-1） and ethyl pyruvate （HMGB1 inhibitor） group， with 10 in each group. The COPD rat model was prepared by cigarette smoke combined with tracheal injection of lipopolysaccharide （LPS）. After modeling， the modified Erchentang groups were given corresponding drugs （ig） and Ringer's solution （4 mL， ip）， while the EP group was treated with equal volume of normal saline （ig） and EP （0.04 g·kg^-1·d^-1， ip）. The normal group and the model group received equal volume of normal saline （ig） and Ringer's solution （ip） for 21 consecutive days. The contents of HMGB1， chemokine （C-X-C motif） ligand 1 （CXCL1）， CXCL2 and monocyte chemotactic protein-1 （MCP-1） in bronchoalveolar lavage fluid （BALF） were detected by enzyme-linked immunosorbent assay （ELISA）. The mRNA expressions of HMGB1， RAGE and NF-κB p65 were determined by Real-time polymerase chain reaction （Real-time PCR）， and the protein expressions of HMGB1， RAGE， p-NF-κB p65， and alpha-smooth muscle actin （α-SMA） in bronchioles tissue of rats were determined by immunohistochemistry （IHC）. ResultCompared with the conditions in the normal group， the forced vital capacity （FVC）， forced expiratory volume in the first second （FEV1） and FEV1/FVC in the model group were decreased （P<0.01） while the contents of HMGB1， CXCL1， CXCL2 and MCP-1 in BALF were increased （P<0.01）. And the model group presented higher mRNA expressions of HMGB1， RAGE and NF-κB p65 （P<0.01） and protein expressions of HMGB1， RAGE， p-NF-κB p65 and α-SMA （P<0.05， P<0.01） than the normal group. Compared with the model group， the modified Erchentang medium- and high-dose groups had increased FEV1/FVC （P<0.05， P<0.01）， lowered contents of HMGB1， CXCL1， CXCL2 and MCP-1 in BALF （P<0.05， P<0.05）， and reduced mRNA expressions of HMGB1， RAGE and NF-κB p65 （P<0.05， P<0.01） and protein expressions of HMGB1， RAGE， p-NF-κB p65 and α-SMA （P<0.05， P<0.01）. ConclusionModified Erchentang can resist bronchiolar inflammation of COPD rats. The mechanism may be related to down-regulating the mRNA expressiona of HMGB1 and RAGE， inhibiting the activity of NF-κB， and reducing the release of HMGB1， CXCL1， CXCL2 and MCP-1， thus suppressing the inflammatory injury and abnormal repair of bronchioles.

Systemic lupus erythematosus (SLE) is an autoimmune disease with multiple organ involvement. There are still many limitations and individual differences in the treatment based on glucocorticoids and immunosuppressants. In recent years, more and more studies have shown that the combination of traditional Chinese medicine in the treatment of SLE has the advantages of good efficacy, low adverse reactions, and high safety. However, the exact regulatory mechanism and combined traditional Chinese medicine in the treatment of SLE are still unclear. This paper reviews the research on the mechanism of traditional Chinese medicine in the treatment of SLE from metabonomic, immune cells, lymphocyte factors and apoptosis, etc, provides ideas for exploring the mechanism of traditional Chinese medicine in the treatment of SLE with modern methods.

ObjectiveTo observe the effect of modified Erchentang on the expression of key molecules in the Jagged1/Notch1/Hes1 signaling pathway in lung tissues of rats with chronic obstructive pulmonary disease （COPD） and explore its anti-inflammatory effect and molecular mechanism on COPD through the Jagged1/Notch1/Hes1 signaling pathway. MethodSixty SD rats were randomly divided into normal group， model group， low-， medium-， and high-dose modified Erchentang groups （5， 10， 20 g·kg^-1）， and γ-secretase inhibitor DAPT group （0.02 g·kg^-1）， with 10 rats in each group. The COPD model was induced in rats by cigarette smoking combined with intratracheal instillation of lipopolysaccharide （LPS）. Rats were treated with corresponding drugs by gavage， while those in the normal group and the model group were treated with the same amount of normal saline by gavage. The serum levels of Notch1， soluble intercellular adhesion molecule-1 （sICAM-1）， activated leukocyte cell adhesion molecule （ALCAM）， and soluble vascular adhesion molecule-1 （sVCAM-1） were detected by enzyme-linked immunosorbent assay （ELISA）. The mRNA expression of Jagged1， Notch1， and Hes1 was detected by Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR）. The protein expression of Jagged1， Notch1， Notch1 intracellular domain （NICD1）， and Hes1 in lung tissues of rats was detected by immunohistochemistry （IHC）. ResultCompared with the normal group， the model group showed increased serum content of Notch1， sICAM-1， ALCAM， and sVCAM-1 （P<0.01）， increased mRNA expression of Jagged1， Notch1， and Hes1 in lung tissues （P<0.01）， and increased protein expression of Jagged1， Notch1， NICD1， and Hes1 （P<0.01）. Compared with the model group， the medium- and high-dose modified Erchentang groups and the DAPT group showed decreased serum content of Notch1， sICAM-1， ALCAM， and sVCAM-1 （P<0.05， P<0.05）， down-regulated mRNA expression of Jagged1， Notch1， and Hes1 （P<0.05， P<0.01）， and reduced protein expression of Jagged1， Notch1， NICD1， and Hes1（P<0.05， P<0.01）. ConclusionModified Erchentang may inhibit the inflammatory response in the lung of COPD rats， and its mechanism may be related to the resistance of inflammatory injury in the lung by decreasing the mRNA expression of Jagged1， Notch1， and Hes1 and inhibiting the release of Notch1， sICAM-1， ALCAM， and sVCAM-1.

Background Coal workers' pneumoconiosis (CWP) is a serious occupational disease. Whether ferroptosis, a form of necrotic regulated cell death, is involved in coal dust induced mouse models of CWP needs further survey. Objective This experiment is designed to elucidate the role of ferroptosis in the formation of CWP induced by coal dust in mice. Methods C57BL/6J mice were randomly assigned to a saline group or a CWP group, with eight mice in each group. The mice were treated with 0.1 mL normal saline or 0.1 mL coal dust suspensions (50g·L^-1) via intra-tracheal instillation. HE staining and Masson staining were used to show lung injury and lung fibrosis. Iron concentration in mouse lung tissues was measured using iron assay kit. Lipid peroxidation was estimated in lung tissues by malondialdehyde (MDA) concentration and immunofluorescence intensity, and the ratio of glutathione (GSH) to L-glutathione oxidized (GSSG). Western blotting and real-time fluorescence-based quantitative PCR were used to test protein and mRNA expression levels of glutathione peroxidase 4 (GPX₄) and ferritin in mice. Results Coal dust injured pulmonary structure, thickened alveolar wall, and caused collagen deposition and infiltration of inflammatory cells in the CWP group. The iron concentration in the CWP group [(10.75 ± 5.42) mg·L⁻¹] was higher than that in the saline group [(1.14 ± 0.37) mg·L⁻¹] (P < 0.01). The MDA concentration in the CWP group [(37.32 ± 12.18) μmol·L⁻¹] was higher than that in the saline group [(18.70 ± 8.22) μmol·L⁻¹] (P <0.01). The immunofluorescence intensity of MDA in the CWP group was stronger than that in the saline group. The GSH/GSSG ratio decreased in CWP treated mice (1.50 ± 1.70) compared with the normal saline treated ones (4.95 ± 2.86) (P < 0.01). Compared with the saline group (38.84 ± 15.61 for GPX₄, 225.90 ± 54.34 for ferritin), the relative expression levels of GPX₄ and ferritin mRNA in the CWP group were downregulated (14.29 ± 7.21 for GPX₄, 106.70 ± 36.70 for ferritin) (P < 0.01). Compared with the saline group (1.47 ± 0.54 for GPX₄, 1.73 ± 0.34 for ferritin), the relative expression levels of GPX₄ and ferritin protein in the CWP group were also downregulated (0.92 ± 0.22 for GPX₄, 0.97 ± 0.09 for ferritin) (P < 0.05). Conclusion Ferroptosis may be involved in the formation of coal workers' pneumoconiosis induced by coal dust in mice.