Objective:To summarize the clinical characteristics and factors that may affect the flare of patients with systemic lupus erythematosus (SLE).Methods:A total of 300 patients with SLE who were treated with standard treatment in the outpatient clinic of the department of rheumatology and immunology of the Second Affiliated Hospital of Air Force Military Medical University of PLA, were enrolled, and the patients were divided into 24 patients in the complete response group, 40 cases in the no response group, 192 cases in the treatment response group, and 44 cases in the low disease activity group according to the response to treatment. The differences in clinical characteristics and survival rates between the groups were compared and analyzed. Comparisons of count data were made using analysis of variance (ANOVA), comparisons of measurement data were made using the chi-square test or the Fisher′s ecact test, and survival rates were expressed as Kaplan-Meier curves. Cox regression analysis was adapted to explore risk factors for flare in these patients.Results:A total of 300 patients were followed. With a median follow-up time of 18 (1, 36) months, a total of 42 patients experienced flare. The clinical characteristics of the four groups were compared, and there were significant differences in age ( F=4.39, P=0.005), the presence of lupus nephritis ( χ2=12.66, P=0.005), hemoglobin level ( F=2.73, P=0.044), NLR level( F=3.88, P=0.010), cystatin C level( F=3.11, P=0.027), anti-RNP antibody ( χ2=12.04, P=0.007), anti-Sm antibody ( χ2=8.33, P=0.040), anti-SSB antibody ( P=0.014), anti-nucleosome antibody ( P=0.014), and anti-ribosomal P protein antibody ( χ2=11.83, P=0.008). There was no significant difference in survival between the four groups. Cox analysis showed that the combination of other autoimmune diseases [ HR(95%CI)=3.23(1.58, 6.57), P=0.001], anti-Sm antibody [ HR(95%CI)=2.15(1.04, 4.43), P=0.038], and anti-RNP antibody [ HR(95%CI)=2.54(1.13, 5.68), P=0.023] were risk factors for flare in patients with SLE who could reach the treatment target. Conclusion:Patients with SLE with different treatment responses have different clinical features, and all treatment can significantly improve the recurrence rate no matter what level of response to treatment. Patients concurrent with other autoimmune diseases, positive anti-Sm antibodies, and positive anti-RNP antibodies are at highrisk of flare.

Peripheral pulmonary lesions(PPL),including peripheral pulmonary nodules,are common lung problems.As the increase of patients with lung nodules,the demand for tissue sampling also increases.Safe and accurate biopsy techniques are very important for patients to identify benign and malignant lesions.Electronic bronchoscopy is one of the biopsy techniques for the diagnosis of PPL in recent decades.Various guiding techniques,such as radial probe endobronchial ultrasound and virtual navigation bronchoscope,have been proved to improve the performance of conventional bronchoscopy.This paper aims to provide an review of the available data on advanced bronchoscopic techniques and explore their application in diagnosing PPL.

Objective:To analyze the Risk factors for rapid progression of inpatients with anti-melanoma differentiation associated gene5 (MDA5) antibody-positive dermamyositis (DM) complicated with interstitial lung disease (ILD), and construct a clinical predictive model.Methods:A total of 63 hospitalized patients with anti MDA5 positive DM combined with ILD (MDA5+ DM-ILD) from January 1, 2016 to May 30, 2022 at the Second Affiliated Hospital of the Air Force Military Medical University were included in the study. They were divided into a control group (DM-ILD) and an observation group (DM-RPPILD) based on whether they had rapidly progressing interstitial lung disease (RPILD). Retrospective collection and organization of clinical case data from patients were conducted, and binary logistic regression was used to summarize the risk factors of DM-RPILD. R software was used to construct a clinical prediction model for RPILD occurrence using training set data, and validation set data was used to verify the predictive ability of the model.Results:The proportion of patients with SpO 2<90% at the initial diagnosis of ILD, the titers of anti MDA5 antibodies, immunoglobulin M (IgM), serum ferritin (FER) levels, and positive rates of anti Ro52 antibodies in the observation group were higher than those in the control group, the lymphocyte (LYM) count level was lower than that of the control group (all P<0.05). Binary logistic regression analysis showed SpO 2<90% at the initial diagnosis of ILD, FER level, LYM count, and anti Ro52 antibody were the influencing factors for the occurrence of RPILD (all P<0.05). The area under the curve (AUC) of the training set prediction model for predicting resistance to MDA5+ DM-RPILD was 0.922(95% CI: 0.887-0.957), with a sensitivity of 95.7% and a specificity of 72.5%; In the validation set, the prediction model predicted an AUC of 0.939(95% CI: 0.904-0.974) for resistance to MDA5+ DM-RPILD, with a sensitivity of 90.0% and a specificity of 88.9%; The calibration curves of the training and validation sets indicated that the predictive model had good calibration ability. Conclusions:SpO 2<90% at the initial diagnosis of ILD, FER levels increase, LYM count levels decrease, and anti Ro52 antibody positivity are risk factors for RPILD. The constructed clinical model has good predictive ability and has certain guiding significance for clinical work.

Primary biliary cholangitis is a chronic autoimmune cholestatic disease with a progressive course. This disease is not rare in China, but standardized diagnosis and treatment for primary biliary cholangitis are insufficient. Based on the evidence and guidelines from China and other countries, Rheumatology Branch of Chinese Medical Association developed the recommendations of diagnosis and treatment for primary biliary cholangitis in China. The aim is to help clinicians recognize clinical characters, therapeutic selection and prognosis judgement of primary biliary cholangitis, which will contribute to make diagnosis in time, to select treatment properly and to manage follow-up scientifically.

Objective:To investigate the correlation between total MRI burden and serum uric acid level in patients with cerebral small vessel disease(CSVD) and its gender differences.Methods:A total of 217 patients with CSVD were retrospectively included as the research objects, and the clinical data such as serum uric acid value were collected.The imaging findings of patients with CSVD were evaluated by MRI, and the total MRI burden score of CSVD was calculated.According to the total MRI burden score of CSVD, patients with CSVD were divided into mild-to-moderate burden group ( n=133) and severe burden group ( n=84). SPSS 20.0 software was used for data analysis and processing.Logistic regression was used to analyze the relationship between uric acid and the total MRI burden score of CSVD. Results:The serum uric acid of severe burden group was higher than that of mild-to-moderate burden group((326.94±70.95)μmol/L, (293.42±80.52)μmol/L, P=0.002). The multivariate logistic regression analysis showed that the elevated level of serum uric acid was an independent risk factors for total MRI burden of CSVD ( β=0.005, OR=1.005, 95% CI=1.001-1.009, P=0.019). The patients with CSVD were equally divided into four group based on the serum uric acid concentration.After controlling the confounding factors, with the increase of uric acid level, the risk of aggravating total MRI burden score of CSVD increased, and the difference was statistically significant( P=0.001). Serum uric acid(for each quartile increase)was an independent risk factor for total MRI burden in male patients with CSVD( β=0.482, OR=1.619, 95% CI=1.125-2.330, P=0.010), while there was no significant difference in female patients( P=0.070). Conclusion:Serum uric acid level is a risk factor for increasing the total MRI burden in male patients with CSVD, but this effect is not found in female patients with CSVD.

Coronaviruses (CoVs), a family of enveloped positive-sense RNA viruses, are characterized by club-like spikes that project from their surface, unusually large RNA genome, and unique replication capability. CoVs are known to cause various potentially lethal human respiratory infectious diseases, such as severe acute respiratory syndrome (SARS), Middle East respiratory syndrome (MERS), and the very recent coronavirus disease 2019 (COVID-19) outbreak. Unfortunately, neither drug nor vaccine has yet been approved to date to prevent and treat these diseases caused by CoVs. Therefore, effective prevention and treatment medications against human coronavirus are in urgent need. In the past decades, many natural compounds have been reported to possess multiple biological activities, including antiviral properties. In this article, we provided a comprehensive review on the natural compounds that interfere with the life cycles of SARS and MERS, and discussed their potential use for the treatment of COVID-19.

Objective To study the expression of long non-coding RNA (LncRNA) stomach cancer-associated transcript 16 (STCAT16) in gastric cancer tissues and its effects on the proliferation, migration and invasion of gastric cancer cells.Methods The different expression of STCAT16 in 32 cases of gastric carcinoma and corresponding adjacent tissues was detected by real-time fluorescence quantitative polymerase chain reaction (PCR).The STCAT16 overexpression plasmid and empty vector was separately transfected gastric cancer cell line AGS with low expression of STCAT16.The cell proliferation of empty vector group, non-transfection group and STCAT16 analogue transfection group was evaluated by cell counting kit-8 (CCK-8) assay at 0, 24, 48, 72 and 96 hours after transfection.The colony forming ability was tested by colony formation assay.The cell invasion ability was measured by Transwell chamber assay and migration ability was tested by scratch-wound assay.The effects of STCAT16 on tumorigenicity in vivo were verified by tumorigenicity experiments in nude mice.T-test and one-way analysis of variance were performed for data analysis.Repeated measures analysis of variance was used to compare the repeated measured data among groups.Chi square test and Fisher exact probability method were used for comparison of counting data.Results The expression of STCAT16 in gastric cancer tissues was low (0.87±0.19), while it was high in corresponding adjacent tissues (2.32±0.37), and the difference was statistically significant (t=-20.859, P<0.05).The expression of STCAT16 of STCAT16 analogue transfection group was higher than that of empty vector group (3.43±0.25 vs 1.00±0.06), and the difference was statistically significant (t=-16.795,P<0.05).Compared to empty vector group and non-transfection group, the cell proliferation decreased in STCAT16 analogue transfection group at 72 and 96 hours after transfection (1.41±0.07, 1.42±0.08, 1.03±0.09, and 1.72±0.11, 1.78±0.14, 1.24±0.08, respectively), and the differences were statistically significant (t=15.043,5.358, 12.193 and 8.109, all P<0.05).The results of colony formation assay indicated that the colony forming ability of gastric cells in STCAT16 analogue transfection group was lower than that in empty vector group (97.3±9.1 vs 185.0±20.1) and non-transfection group (97.3±9.1 vs 138.0±11.1), and the differences were statistically significant (t=11.634 and 4.417,both P<0.05).The results of Transwell assay showed that the number of AGS cells passing through the membrane of STCAT16 analogue transfection group was significantly less than those of empty vector group and non-transfection group (151.0±28.1 vs 228.0±38.2 and 151.0±28.1 vs 199.3±17.9), and the differences were statistically significant (t=4.823 and 4.747,both P<0.05).After transfection for 48 hours and 72 hours, the scratch-wound repair rate of STCAT16 analogue transfection group decreased, compared with those of empty vector group and non-transfection group ((52.67±6.11)%, (53.33±5.51)%, (42.67±4.72)%, and (90.67±2.51)%, (90.60±5.41)%, (69.67±1.52)%, respectively), and the differences were statistically significant (t=5.773, 5.955, 21.000 and 5.881, all P<0.05).The results of tumorigenicity in nude mice showed that compared with those of empty vector group, the tumor size of STCAT16 analogue transfection group was smaller at one-, two-, three-and four-week ((0.42±0.10) cm3 vs (0.16±0.05) cm3, (0.66±0.13) cm3 vs (0.34±0.05) cm3, (1.25±0.22) cm3 vs (0.54±0.13) cm3, (2.54±0.46) cm3 vs (0.78±0.41) cm3)), and the differences were statistically significant (t=3.175, 4.190, 7.996 and 9.705, all P<0.05).Conclusions STCAT16 is lowly expressed in gastric cancer tissues.The proliferation, migration, invasion ability and tumorigenicity in nude mice of gastric cancer cell is inhibited after upregulating the expression of STCAT16.

Background:Recurrent acute pancreatitis(RAP)is a special type of acute pancreatitis(AP). Finding the cause is the key to avoid the recurrence of RAP. Aims:To investigate the risk factors of RAP. Methods:The clinical data of 43 patients with RAP and 130 patients with only one time AP(control group)were retrospectively analyzed. Risk factors of recurrence of RAP were analyzed. Results:Univariate analysis showed that no significant differences in etiology,severity, serum levels of cholesterol,calcium,white blood cell count,amylase,ALT,AST,total bilirubin,direct bilirubin and C-reactive protein were found between RAP group and control group(P > 0. 05). Serum triglyceride level,blood glucose level and CT score in RAP group were significantly higher than those in control group(t = 3. 260,P < 0. 05;t = 2. 720, P < 0. 05;t = 2. 162,P < 0. 05). Logistic regression analysis demonstrated that serum triglyceride level,blood glucose level and CT score were risk factors of RAP(oR = 1. 86,95% CI:1. 05-3. 68,P = 0. 03;oR = 1. 23,95% CI:1. 01-1. 50,P = 0. 04;oR = 2. 46,95% CI:1. 00-6. 03,P = 0. 04). Conclusions:The recurrence of RAP is related with serum triglyceride level,blood glucose level and CT score.

Objective To evaluate the frequency of mutations that occur in PHEX,FGF - 23 and DMP - I genes associated with familial hypophosphatemic vitamin D resistant rickets among 6 patients from 4 families in China. Methods The peripheral blood samples from 4 families were collected and other 10 persons from different families were selected as normal controls,and then the total gene DNA was extracted from the whole blood. Using polymerase chain reaction(PCR)amplication,sequences of the exons and flanking zones in PHEX,FGF - 23 and DMP - I genes were sequenced by direct DNA sequencing and TA cloning,and then the mutations found were analyzed. Results In exon 6 of DMP - I gene,c1218 C ﹥ T and c1230 G ﹥ A mutations were detected in lineage 1,as same sense mutation (propositus and its sister:homozygous mutation;mother:heterozygous mutation);c1333 - 1334 GC ﹥ TT mutation,as missense mutation,was found in exon 12 of PHEX gene on the propositus of lineage 2,determined as heterozygous muta-tion,but the same mutation was not found from their parents. In exon 3 of FGF - 23 gene,c716 C ﹥ T,p. T239M hetero-zygous mutation was found on the propositus and its mother. In exon 6 of the DMP - I gene,c205 A ﹥ T homozygous mutation was detected in lineage 3. In lineage 3,c716 C ﹥ T mutation of the FGF - 23 gene was detected,and the pro-positus and their father had the same mutation. No disease causing mutations of the PHEX,FGF - 23 and DMP - I genes were detected in the family members of lineage 1,3 and 4. Conclusions The mutation c1333 - 1334 GC ﹥ TT detected in exon 12 of PHEX gene might be the cause of disease for the propositus of lineage 2,as missense mutation, which needs further verification;c716 C ﹥ T,p. T239M mutation of the FGF - 23 gene detected in lineage 2 and 3 might not be the causes of the hypophosphatemic rickets and abnormal phenotype.

Objectives To study the molecular genetics of Niemann-Pick's disease (NPD), and its implication in the diagnosis of NPD. Methods The clinical data and blood samples of three unrelated families were collected. The genomic DNA was extracted from peripheral blood. The six coding exons and their lfanking intronic sequences of SMPD1 gene in all members of three pedigrees were ampliifed by polymerase chain reaction (PCR). The SMPD1 gene sequencing results were compared with the normal sequence from Genbank to identify possible causative mutations. The ampliifcation products of exons where mutations were located were cloned into TA vector for further conifrmation. Results Family 1 proband had homozygous T107C mutation and the parents had heterozygous T107C mutation. The homozygous delete mutation (c.108-113delGCTGGC) was detected and conifrmed by TA cloning in all members of family 2 and 3. The 20 normal control members did not have this delete mutation. Conclusions The genetic basis of NPD in the proband of family 1 is the homozygous T107C mutation in SMPD1 gene, while parents in family 1 are carriers of recessive T107C mutation. The homozygous mutation c.108-113delGCTGGC exists in SMPD1 gene in all members of the family 2 and 3. This delete mutation is considered to be genetic polymorphism.