Liaoning University of Traditional Chinese Medicine

About: Liaoning University of Traditional Chinese Medicine is a education organization based out in Shenyang, China. It is known for research contribution in the topics: Randomized controlled trial & Acupuncture. The organization has 2040 authors who have published 1326 publications receiving 14664 citations.

Diagnosis, treatment, and prevention of 2019 novel coronavirus infection in children: experts' consensus statement.

Abstract: Since the outbreak of 2019 novel coronavirus infection (2019-nCoV) in Wuhan City, China, by January 30, 2020, a total of 9692 confirmed cases and 15,238 suspected cases have been reported around 31 provinces or cities in China. Among the confirmed cases, 1527 were severe cases, 171 had recovered and been discharged at home, and 213 died. And among these cases, a total of 28 children aged from 1 month to 17 years have been reported in China. For standardizing prevention and management of 2019-nCoV infections in children, we called up an experts’ committee to formulate this experts’ consensus statement. This statement is based on the Novel Coronavirus Infection Pneumonia Diagnosis and Treatment Standards (the fourth edition) (National Health Committee) and other previous diagnosis and treatment strategies for pediatric virus infections. The present consensus statement summarizes current strategies on diagnosis, treatment, and prevention of 2019-nCoV infection in children.

MMP13 is a critical target gene during the progression of osteoarthritis

Abstract: Osteoarthritis (OA) is a degenerative joint disease affecting a large population of people. The mechanism of this highly prevalent disease is not fully understood. Currently there is no effective disease-modifying treatment for OA. The purpose of this study was two-fold: 1) to investigate the role of MMP13 in the development of OA; and 2) to evaluate the efficacy of the MMP13 inhibitor CL82198 as a pharmacologic treatment for preventing OA progression. To investigate the role of the endogenous Mmp13 gene in OA development, tamoxifen was administered to two-week-old Col2CreER;Mmp13 fx/fx (Mmp13 Col2ER ) and Cre-negative control mice for five days. OA was induced by meniscal-ligamentous injury (MLI) when the mice were 10 weeks old and MLI or sham-operated joints were harvested 4, 8, 12, or 16 weeks after surgery. To evaluate the efficacy of CL82198, MLI surgery was performed on 10-week-old wild type mice. CL82198 or saline was administered to the mice daily beginning immediately after the surgery for up to 16 weeks. The joint tissues collected from both experiments were evaluated by cartilage grading, histology/histomorphometry, immunohistochemistry (IHC), and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining. The ability of CL82198 to inhibit MMP13 activity in vitro was confirmed by ELISA. The OA progression was decelerated in Mmp13 Col2ER mice 8, 12, and 16 weeks post-surgery. Cartilage grading by blinded observers confirmed decreased articular cartilage degeneration in Mmp13 Col2ER mice at 8, 12 and 16 weeks compared to Cre-negative mice. Histomorphometric analysis demonstrated that Mmp13 Col2ER mice had a higher articular cartilage area and thickness at 12 and 16 weeks post-surgery compared to the control mice. Results of IHC revealed greater type II collagen and proteoglycan expression in Mmp13 Col2ER mice. Chondrocyte apoptosis, as determined by TUNEL staining, was higher in control mice compared to Mmp13 Col2ER mice. CL82198 inhibited MMP13 activity in conditioned media from vehicle (> 85%) or bone morphogenetic protein 2 (BMP2)-treated (> 90%) primary murine sternal chondrocytes. Intraperitoneal injection of CL82198 decelerated MLI-induced OA progression, increased type II collagen and proteoglycan levels, and inhibited chondrocyte apoptosis compared to saline treatment as determined by OA grading, histology, histomorphometry, IHC, and TUNEL staining, respectively. Mmp13 is critical for OA progression and pharmacologic inhibition of MMP13 is an effective strategy to decelerate articular cartilage loss in a murine model of injury-induced knee OA.

Prevalence of gestational diabetes mellitus in mainland China: A systematic review and meta-analysis

Abstract: Aims/introduction Pregnant women with gestational diabetes mellitus (GDM) are at a higher risk of adverse pregnancy outcomes. The aim of the present study was to estimate the pooled prevalence of GDM in mainland China according to International Association of Diabetes and Pregnancy Study Groups criteria. Materials and methods We carried out a systematic review by searching both English and Chinese literature databases. Random effects models were used to summarize the prevalence of GDM in mainland China. Subgroup and sensitivity analyses were carried out to address heterogeneity. Publication bias was evaluated using Egger's test. Results A total of 25 papers were included in the meta-analysis, involving 79,064 Chinese participants. The total incidence of GDM in mainland China was 14.8% (95% confidence interval 12.8-16.7%). Subgroup analysis showed that the age, bodyweight and family history of diabetes mellitus could significantly increase the incidence of GDM. Conclusions To the best of our knowledge, this systematic review is the first to estimate the pooled prevalence of GDM among women in mainland China according to International Association of Diabetes and Pregnancy Study Groups criteria. The results of our systematic review suggest a high prevalence of GDM in mainland China, indicating that this country might have the largest number of GDM patients worldwide.

Deletion of the transforming growth factor β receptor type II gene in articular chondrocytes leads to a progressive osteoarthritis-like phenotype in mice.

Abstract: Osteoarthritis (OA) is the most common degenerative joint disease, affecting >25% of the US population age >18 years. The major pathologic changes of OA include abnormal articular chondrocyte maturation, progressive loss and destruction of articular cartilage, osteophyte formation, and subchondral sclerosis. The etiology of OA is multifactorial, including joint injury, obesity, aging, and heredity (1–3). There are currently no interventions to restore degraded cartilage or decelerate the progression of OA, as the precise signaling pathways involved in initiation and progression of OA are still poorly understood. Ex vivo studies with tissues obtained from OA patients and in vivo studies with mutant mouse models suggest that the factors involved in development of OA include growth factors, such as transforming growth factor β(TGFβ) and Indian hedgehog (IHH), and signaling molecules, such as Smads, β-catenin, and hypoxia-inducible factor 2α (HIF-2α) (4–8). TGFβ signaling strongly inhibits chondrocyte hypertrophy and maturation. In canonical TGFβ signaling, the TGFβ ligand binds to TGFβ receptor type II (TGFβRII), which then phosphorylates the type I transmembrane serine/threonine kinase receptor. The activated kinase subsequently phosphorylates Smad2 or Smad3 (receptor-activated Smad), which then forms a heteromeric complex with Smad4 (common-mediator Smad), translocates into the nucleus, and interacts with other DNA binding proteins to regulate target gene transcription (9). Recent genetic manipulations suggest that dys-regulation of TGFβ signaling induces development of OA via the TGFβ/Smad3 signaling pathway in chondrocytes (4,10). Transgenic mice overexpressing a dominant-negative form of TGFβRII (dn-TGFβRII) in skeletal tissue were found to exhibit cartilage disorganization and progressive cartilage degradation resembling the features of OA in humans (10). Similar to the dn-TGFβRII–transgenic mice, Smad3-knockout (KO) mice were also found to display progressive articular cartilage degradation and osteophyte formation (4). A recent study showed that a single-nucleotide polymorphism in the Smad3 gene was correlated with the incidence of hip and knee OA in a cohort of 527 patients (11). More recently, different types of Smad3 mutations were identified in patients with a syndromic form of aortic aneurysms and early-onset OA (12,13). These observations strongly support the notion that the TGFβ/Smad3 signaling pathway in chondrocytes plays an essential role in the development of OA. However, the critical downstream target genes of TGFβ signaling involved in the development of OA remain unknown. The progressive loss of articular cartilage is a fundamental feature of OA. Articular cartilage consists of a dense meshwork of interconnected collagen fibrils within which is embedded a rich matrix of negatively charged proteoglycans. The negative charge attracts ions and provides the tissue with a high osmotic pressure that resists compressive force and provides boundary lubrication (14). Human clinical and animal studies have shown that matrix metalloproteinase 13 (MMP-13) plays a pivotal role during cartilage degradation. MMP-13 is a primary collagenase that preferentially cleaves type II collagen in articular cartilage (15). Clinical investigations have revealed that MMP-13 expression is elevated in articular cartilage of OA patients (16). Expression of the constitutively active Mmp13 gene leads to an OA-like phenotype in mice (17). In addition to MMP-13, ADAMTS-5, the principal enzyme responsible for degradation of aggrecan in articular cartilage, plays a critical role during OA development. Studies have shown that expression levels of Adamts5 are significantly increased during OA development (18). Deletion of the Adamts5 gene prevented articular cartilage degradation in mouse models of surgically or chemically induced OA (19–21). To determine the mechanism of inhibition of TGFβ signaling in the development of OA, we generated chondrocyte-specific Tgfbr2Col2ER mice by breeding Col2-CreER–transgenic mice (22,23) with Tgfbr2flox/flox mice. Gene deletion was induced by injection of tamox-ifen into 2-week-old mice, and alterations in the articular cartilage were analyzed at ages 3 and 6 months. Our studies demonstrated that deletion of the Tgfbr2 gene at the postnatal/adult stage led to a severe OA-like phenotype. Our in vitro studies demonstrated that inhibition of TGFβ signaling up-regulated Mmp13 and Adamts5 expression in articular cartilage tissue. MMP-13 is a collagenase that mainly degrades type II collagen. ADAMTS-5 is an aggrecanase that degrades aggrecan. Type II collagen and aggrecan are the principal matrix components present in articular cartilage. Because both MMP-13 and ADAMTS-5 play critical roles in the development of OA (12,21,24), we reasoned that Mmp13 and Adamts5 might be the key downstream target genes of TGFβ signaling in articular chondrocytes during OA development. In this study, we demonstrated that deletion of the Mmp13 or Adamts5 gene in mice of the Tgfbr2Col2ER background significantly prevented the OA-like phenotype observed in Tgfbr2Col2ER mice, which suggests that MMP-13 and ADAMTS-5 are critical downstream targets of TGFβ signaling during OA development.