Spondyloarthritis (SpA) is a group of chronic inflammatory diseases which predominantly involve spine and/or peripheral joints. SpA can be disabling and seriously affect the quality of life and function of patients. With the increasing clinical use of targeted drug therapy, precise and standardized use becomes the focus. China's first Consensus on Targeted Drug Therapy for Spondyloarthritis was developed by National Clinical Research Center for Dermatologic and Immunologic Diseases using international norms for consensus development. The consensus addresses 13 important clinical questions, ranging from principles, patient eligibility, pre-treatment screening, treatment initiation, drug selection and switch, co-medication, to adverse event monitoring of targeted drug therapy in SpA, and recommends treatment for specific patients, playing a key role in guiding clinical practices.

Objective:To investigate the effects and possible mechanisms of caffeic acid phenethyl ester (CAPE) on the replication, amplification, and fibre formation of prions (PrP Sc). Methods:The CCK8 assay was used to detect the cell viability of the prion-infected cell model SMB-S15 after CAPE treatment for 3 days and 7 days and the maximum safe concentration of CAPE for SMB-S15 was obtained. The cells were treated with a concentration within a safe range, and the content of PrP Sc in the cells before and after CAPE treatment was analyzed by western blot. Protein misfolding cycle amplification (PMCA) and western blot were used to assess changes in PrP Sc level in amplification products following CAPE treatment. Real-time-quaking induced conversion assay (RT-QuIC) technology was employed to explore the changes in fibril formation before and after CAPE treatment. The binding affinity between CAPE and murine recombinant full-length prion protein was determined using a molecular interaction assay. Results:CCK8 cell viability assay results demonstrated that treatment with 1 μmol/L CAPE for 3 and 7 days did not exhibit statistically significant differences in cell viability compared to the control group (all P<0.05). However, when the concentration of CAPE exceeded 1 μmol/L, a significant reduction in cell viability was observed in cells treated with CAPE for 3 and 7 days, compared to the control group (all P<0.05). Thus, 1 μmol/L was determined as the maximum safe concentration of CAPE treatment for SMB-S15 cells. The western blot results revealed that treatment with CAPE for both 3 and 7 days led to a detectable reduction in the levels of PrP Sc in SMB-S15 cells (all P<0.05). The products of PMCA experiments were assessed using western blot. The findings revealed a significant decrease in the levels of PrP Sc (relative grey value) in the PMCA amplification products of adapted-strains SMB-S15, 139A, and ME7 following treatment with CAPE, as compared to the control group (all P<0.05). The RT-QuIC experimental results demonstrated a reduction in fibril formation (as indicated by ThT peak values) in CAPE-treated mouse-adapted strains 139A, ME7, and SMB-S15, as well as in SMB-S15 cells infected with prions. Furthermore, CAPE exhibited varying degrees of inhibition towards different seed fibrils formation, with statistically significant differences observed (all P<0.05). Notably, CAPE exhibited a more pronounced inhibitory effect on ME7 seed fibrils. Molecular interaction analyses demonstrated significant binding between CAPE and murine recombinant prion protein, and the association constant was (2.92±0.41)×10 -6 mol/L. Conclusions:CAPE inhibits PrP Sc replication, amplification, and fibril formation in vitro possibly due to specific interactions with the prion protein at the molecular level.

Objective:To investigate the effects and possible mechanisms of caffeic acid phenethyl ester (CAPE) on the replication, amplification, and fibre formation of prions (PrP Sc). Methods:The CCK8 assay was used to detect the cell viability of the prion-infected cell model SMB-S15 after CAPE treatment for 3 days and 7 days and the maximum safe concentration of CAPE for SMB-S15 was obtained. The cells were treated with a concentration within a safe range, and the content of PrP Sc in the cells before and after CAPE treatment was analyzed by western blot. Protein misfolding cycle amplification (PMCA) and western blot were used to assess changes in PrP Sc level in amplification products following CAPE treatment. Real-time-quaking induced conversion assay (RT-QuIC) technology was employed to explore the changes in fibril formation before and after CAPE treatment. The binding affinity between CAPE and murine recombinant full-length prion protein was determined using a molecular interaction assay. Results:CCK8 cell viability assay results demonstrated that treatment with 1 μmol/L CAPE for 3 and 7 days did not exhibit statistically significant differences in cell viability compared to the control group (all P<0.05). However, when the concentration of CAPE exceeded 1 μmol/L, a significant reduction in cell viability was observed in cells treated with CAPE for 3 and 7 days, compared to the control group (all P<0.05). Thus, 1 μmol/L was determined as the maximum safe concentration of CAPE treatment for SMB-S15 cells. The western blot results revealed that treatment with CAPE for both 3 and 7 days led to a detectable reduction in the levels of PrP Sc in SMB-S15 cells (all P<0.05). The products of PMCA experiments were assessed using western blot. The findings revealed a significant decrease in the levels of PrP Sc (relative grey value) in the PMCA amplification products of adapted-strains SMB-S15, 139A, and ME7 following treatment with CAPE, as compared to the control group (all P<0.05). The RT-QuIC experimental results demonstrated a reduction in fibril formation (as indicated by ThT peak values) in CAPE-treated mouse-adapted strains 139A, ME7, and SMB-S15, as well as in SMB-S15 cells infected with prions. Furthermore, CAPE exhibited varying degrees of inhibition towards different seed fibrils formation, with statistically significant differences observed (all P<0.05). Notably, CAPE exhibited a more pronounced inhibitory effect on ME7 seed fibrils. Molecular interaction analyses demonstrated significant binding between CAPE and murine recombinant prion protein, and the association constant was (2.92±0.41)×10 -6 mol/L. Conclusions:CAPE inhibits PrP Sc replication, amplification, and fibril formation in vitro possibly due to specific interactions with the prion protein at the molecular level.

A 63-year-old maintenance hemodialysis patient with diabetic nephropathy was reported. The patient was incapacitated, with systemic edema, heart failure, severe anemia, malnutrition, gastrointestinal bleeding, and intractable hypertension. We adopted integrated management methods such as "multidisciplinary collaboration" and "doctor-patient collaboration": by accurately controlling the volume load to protect the residual renal function, taking into account the treatment of underlying diseases and complications, integrating the clinical parameters of dialysis and the interdialysis period, and combining the subjective clinical symptom score with the objective index analysis, the objectives of effectively controlling the dry weight of patients, alleviating complications, improving nutrition and protecting the residual renal function were finally achieved. The quality of life of the patient had been significantly improved.

Diabetic kidney disease (DKD) is a primary cause of chronic kidney disease and end-stage renal disease, as well as one of the most common microvascular consequences of diabetes mellitus. Obesity, as a metabolic disease, has a substantial impact on the onset and progression of DKD. Epidemiological studies have revealed obesity is a risk factor of DKD and end-stage renal disease, which can promote the occurrence and progression of DKD through various mechanisms, including alterations in hemodynamics, metabolic regulation, and chronic inflammation. Clinical researches also have demonstrated the importance of various weight loss interventions in the prevention and management of DKD. Therefore, gaining a deeper understanding of the correlation between obesity and DKD will contribute to improving the prognosis and quality of life of individuals with diabetes mellitus. The paper reviews the relationship between obesity and DKD on the epidemiological characteristics of obesity and DKD, the potential mechanism of obesity affecting DKD and the influence of obesity intervention on DKD.

Asians ; China/epidemiology* ; Humans ; Patient Discharge ; Patient Readmission

Background::The risk for chronic kidney disease (CKD) is influenced by genetic predisposition, sex, and lifestyle. Previous research indicates that coffee is a potentially protective factor in CKD. The current study aims to investigate whether sex disparity exists in the coffee–CKD association, and whether genetic risk of CKD or genetic polymorphisms of caffeine metabolism affect this association.Methods::A total of 359,906 participants from the UK Biobank who were enrolled between 2006 and 2010 were included in this prospective cohort study, which aimed to estimate the hazard ratios for coffee intake and incident CKD using a Cox proportional hazard model. Allele scores of CKD and caffeine metabolism were additionally adjusted for in a subsample with qualified genetic data ( n = 255,343). Analyses stratified by genetic predisposition, comorbidities, and sex hormones were performed. Tests based on Bayesian model averaging were conducted to ascertain the robustness of the results. Results::Coffee was inversely associated with CKD in a dose-dependent manner. The effects of coffee did not differ across different strata of genetic risk for CKD, but were more evident among slower genetically predicted caffeine metabolizers. Significant sex disparity was observed ( P value for interaction = 0.013), in that coffee drinking was only associated with the risk reduction of CKD in females. Subgroup analysis revealed that testosterone and sex hormone-binding globulin (SHBG), but not estradiol, modified the coffee–CKD association. Conclusions::In addition to the overall inverse coffee–CKD association that was observed in the general population, we could also establish that a sex disparity existed, in that females were more likely to experience the benefit of the association. Testosterone and SHBG may partly account for the sex disparity.

Objective:To study clinical characteristics and pregnancy outcomes under anti-coagulation therapy of non-criteria obstetric antiphospholipid syndrome.Methods:Patients suspected of obstetric antiphospholipid syndrome(OAPS) were recruited through Chinese Rheumatism Data Center from 2015 to 2019 consecutively. Patients fulfilling 2006 Sydney revised antiphospholipid syndrome criteria were classified as OAPS. Patients fulfilling definition of non-criteria OAPS(NCOAPS) by expert consensus on diagnosis and management of obstetric antiphospholipid syndrome of China were classified as NCOAPS. Clinical characteristics and laboratory results of two groups were compared. Live birth rates and pregnancy outcomes under anti-coagulation therapy were studied.Results:A total of 88 patients were enrolled, including 56 patients (63.6%) as OAPS, 32(36.4%) as NCOAPS. Live births were only reached in 16.1% (9/56) in OAPS patients and 12.5%(4/32) in NCOAPS. Fetal losses after 10 weeks of gestation and pre-eclampsia before 34 weeks were more common in OAPS group compared to NCOAPS group [78.6%(44/56) vs. 18.8%(6/32), P<0.001; 25.0%(14/56) vs. 3.1%(1/32), P=0.020, respectively]. After enrollment, 15 pregnancies were recorded in OAPS, 10 in NCOAPS, all of whom were treated with low-dose aspirin (LDA) combined with low-molecular weight heparin (LMWH). Live birth rates saw dramatic improvements compared to baseline levels in OAPS [16.1% (9/56) vs. 11/15] along with NCOAPS [12.5% (4/32) vs. 7/10]. Conclusion:Though NCOAPS and OAPS patients differ in antiphospholipid antibody spectrum and pattern of pregnancy morbidities, both groups benefit from LDA combined with LWMH treatment, as live birth rates improve. Non-criteria OAPS patients are recommended to receive anti-coagulation therapy during pregnancy.

Autophagy is a critical cellular homeostatic mechanism, and its dysfunction is linked to invasive breast carcinoma (BRCA). Recently, several omics methods have been applied to explore autophagic regulators in BRCA; however, more reliable and robust approaches for identifying crucial regulators and druggable targets remain to be discovered. Thus, we report here the results of multi-omics approaches to identify potential autophagic regulators in BRCA, including gene expression (EXP), DNA methylation (MET) and copy number alterations (CNAs) from The Cancer Genome Atlas (TCGA). Newly identified candidate genes, such as

Distal junctional problem (DJP) is one of the severe complications after spinal correction, fixation and fusion. As the number of patients receiving spinal surgery increased recently, the incidence of DJP also increased dramatically. Compared with proximal junctional problem, the incidence of DJP is low. However, the clinical symptoms are severe, and the rate of surgical revision is high in patients with distal junctional problems. DJP include distal junctional kyphosis (DJK) and distal junctional failure(DJF). The definition of DJK is confusing, however, and the most commonly used was that the distal junction Angle at the last follow-up was greater than 10° and increased by 10° compared with that before surgery. There are 6 DJF modes: progressive loss of lumbar lordosis,acute wedging in the disc below the instrumentation, fracture of LIV, osteoporotic fracture below the long rigid fixation, failure of the instrumentation at LIV, spinal stenosis and or segmental instability underneath the instrumentation. Possible risk factors for DJP include weight, age, type of spinal deformity, osteoporosis, choice of LIV, hip disease, deformity location, surgical approach, surgical procedure, fusion segments, fixation devices, LIV at L5, fixed to S1 with no iliac screws, poor restoration of spinal alignment, et al. Currently, there are some controversies in DJP, mainly including the incidence, risk factors whether needs to and how to revise. The review intends to conduct a simple literature review of the current DJP diagnostic criteria, incidence, risk factors, and other research progress, in order to improve the understanding of the distal junction problem.