National Health and Family Planning Commission

About: National Health and Family Planning Commission is a government organization based out in Beijing, China. It is known for research contribution in the topics: Population & Kashin–Beck disease. The organization has 2379 authors who have published 1440 publications receiving 20078 citations. The organization is also known as: Ministry of Health of the People's Republic of China.

A multicenter, double-blind, randomized, comparison study of the efficacy and safety of tigecycline to imipenem/cilastatin to treat complicated intra-abdominal infections in hospitalized subjects in China

Abstract: Purpose To assess the efficacy and safety of tigecycline in treating complicated intra-abdominal infections (cIAIs) in hospitalized patients in China. Patients and methods A Phase IV, multicenter, randomized, double-blinded, active-controlled, non-inferiority study was conducted. Hospitalized cIAI patients ≥18 years of age were randomized (1:1) to receive intravenous tigecycline (initial dose 100 mg, then 50 mg q12h) or imipenem/cilastatin (500 mg/500 mg or adjusted for renal dysfunction, q6h) for 5-14 days. The primary end point was clinical response for clinically evaluable (CE) subjects at test-of-cure (TOC) assessment. Results Four hundred and seventy subjects were randomized; 232 in the tigecycline and 231 in the imipenem/cilastatin group were treated. Tigecycline was non-inferior to imipenem/cilastatin with respect to clinical response at TOC for all CE subjects, ie, the lower bound of the two-sided 95% CI (-12.0%, -1.4%) for the treatment difference in cure rate, tigecycline (89.9%) minus imipenem/cilastatin (96.6%), was >-15%. As non-inferiority was concluded in the CE population, superiority of tigecycline over imipenem/cilastatin and superiority of imipenem/cilastatin over tigecycline were tested on the CE and the modified intent-to-treat (mITT) populations according to pre-specified statistical criteria, and neither could be demonstrated (the cure rate was 82.8% vs 88.7%, difference -6.0% [-12.8%, 0.8%], for the mITT population). The subject-level microbiological response rate at TOC for the microbiologically evaluable population was 88.0% (110/125) vs 95.3% (102/107, difference -7.3% [-15.2%, 0.5%]). Nausea, drug ineffectiveness, postoperative wound infection, vomiting, and pyrexia were the most common adverse events in tigecycline-treated subjects; pyrexia, nausea, vomiting, and increased alanine aminotransferase and aspartate aminotransferase levels were most common in imipenem/cilastatin-treated subjects; none were unanticipated. Conclusion Tigecycline was non-inferior to imipenem/cilastatin in treating hospitalized adult patients with cIAI. Superiority of tigecycline over imipenem/cilastatin or imipenem/cilastatin over tigecycline could not be demonstrated. Safety was consistent with the known profile for tigecycline. Clinicaltrialsgov identifier NCT01721408.

Integrating transcriptome-wide study and mRNA expression profiles yields novel insights into the biological mechanism of chondropathies

Abstract: Chondropathies are a group of cartilage diseases, which share some common pathogenetic features. The etiology of chondropathies is still largely obscure now. A transcriptome-wide association study (TWAS) was performed using the UK Biobank genome-wide association study (GWAS) data of chondropathies (including 1314 chondropathy patients and 450,950 controls) with gene expression references of muscle skeleton (MS) and peripheral blood (YBL). The candidate genes identified by TWAS were further compared with three gene expression profiles of osteoarthritis (OA), cartilage tumor (CT), and spinal disc herniation (SDH), to confirm the functional relevance between the chondropathies and the candidate genes identified by TWAS. Functional mapping and annotation (FUMA) was used for the gene ontology enrichment analyses. Immunohistochemistry (IHC) was conducted to validate the accuracy of integrative analysis results. Integrating TWAS and mRNA expression profiles detected 84 candidate genes for knee OA, such as DDX20 (PTWAS YBL = 1.79 × 10− 3, fold change (FC) = 2.69), 10 candidate genes for CT, such as SRGN (PTWAS YBL = 1.46 × 10− 3, FC = 3.36), and 4 candidate genes for SDH, such as SUPV3L1 (PTWAS YBL = 3.59 × 10− 3, FC = 3.22). Gene set enrichment analysis detected 73 GO terms for knee OA, 3 GO terms for CT, and 1 GO term for SDH, such as mitochondrial protein complex (P = 7.31 × 10− 5) for knee OA, cytokine for CT (P = 1.13 × 10− 4), and ion binding for SDH (P = 3.55 × 10− 4). IHC confirmed that the protein expression level of DDX20 was significantly different between knee OA cartilage and healthy control cartilage (P = 0.0358). Multiple candidate genes and GO terms were detected for chondropathies. Our findings may provide a novel insight in the molecular mechanisms of chondropathies.

Dietary exosome-miR-23b may be a novel therapeutic measure for preventing Kashin-Beck disease (Review)

Abstract: Previous studies have identified a close association between diet and the prevalence of Kashin-Beck disease (KBD); however, the mechanisms via which the diet protects against KBD-associated cartilage injury has remained elusive. Recent international research studies have revealed a therapeutic role of dietary exosome micro (mi)RNAs in repairing chondrocyte lesions by regulating genes and proteins associated with cellular apoptosis and extracellular matrix. Vital molecules affecting bio-functions of chondrocytes, including miR-23b and protein kinase cyclic AMP-activated catalytic subunit β, were preliminarily identified to be dysregulated in cells and cartilage tissue of KBD patients. The function of dietary exosome in the repair of chondrocyte lesions in KBD is a novel topic in this field. It is worth exploring the protective role of dietary exosome-miR-23b against chondrocyte damage through the regulation of the protein kinase A (PKA) signaling pathway. The following aims are significant in future studies: i) To verify the association between exosome and cartilage damage in KBD patients; ii) to identify whether the protective mechanism of miR-23b in cartilage damage proceeds through regulating the PKA pathway; and iii) to explore the therapeutic role of dietary exosome-miR-23b in repairing chondrocyte lesions induced by environmental risk factors. These ideas may help establish the therapeutic role and mechanisms of dietary exosome-miR-23b in repairing chondrocyte lesions at the molecular, cellular and organismal level. These studies may simultaneously elucidate the disease pathogenesis and provide evidence for novel biomarkers and therapeutic methods for KBD.

A bivariate genome-wide association study identifies ADAM12 as a novel susceptibility gene for Kashin-Beck disease

Abstract: Kashin-Beck disease (KBD) is a chronic osteoarthropathy, which manifests as joint deformities and growth retardation. Only a few genetic studies of growth retardation associated with the KBD have been carried out by now. In this study, we conducted a two-stage bivariate genome-wide association study (BGWAS) of the KBD using joint deformities and body height as study phenotypes, totally involving 2,417 study subjects. Articular cartilage specimens from 8 subjects were collected for immunohistochemistry. In the BGWAS, ADAM12 gene achieved the most significant association (rs1278300 p-value = 9.25 × 10−9) with the KBD. Replication study observed significant association signal at rs1278300 (p-value = 0.007) and rs1710287 (p-value = 0.002) of ADAM12 after Bonferroni correction. Immunohistochemistry revealed significantly decreased expression level of ADAM12 protein in the KBD articular cartilage (average positive chondrocyte rate = 47.59 ± 7.79%) compared to healthy articular cartilage (average positive chondrocyte rate = 64.73 ± 5.05%). Our results suggest that ADAM12 gene is a novel susceptibility gene underlying both joint destruction and growth retardation of the KBD.