Bisphosphonate rescue post-traumatic osteoarthritis by promoting the calcium signaling in chondrocytes

Introduction Post-traumatic osteoarthritis(PTOA)is a long-term adverse consequence of joint trauma,e.g.,meniscus or ligament tears,which are among the most common injuries for young adults with excessive physical activities,such as athletes and military employees.Currently,few preventive treatments exist for PTOA,with typical outcomes being gradual cartilage degeneration and eventual loss of joint function.Apoptosis and altered etabolism of chondrocytes,the sole cell type in cartilage,may be responsible for the development of PTOA in a subset of patients without traumatic cartilage destruction but with persistent altered joint loading post-trauma,which is the focus of this study.

LKB1 depletion-mediated epithelial-mesenchymal transition induces fibroblast activation in lung fibrosis

The factors that determine fibrosis progression or normal tissue repair are largely unknown.We previously demonstrated that autophagy inhibition-mediated epithelial-mesenchymal transition(EMT)in human alveolar epithelial type Il(ATIl)cells augments local myofibroblast differentiation in pulmonary fibrosis by paracrine signaling.Here,we report that liver kinase B1(LKB1)inactivation in ATIl cells inhibits autophagy and induces EMT as a conse-quence.In IPF lungs,this is caused by the down-regulation of CAB39L,a key subunit within the LKB1 complex.3D co-cultures of ATIl cells and MRC5 lung fibroblasts coupled with RNA sequencing(RNA-seq)confirmed that paracrine signaling between LKB1-depleted ATIl cells and fibroblasts augmented myofibroblast differentiation.Together,these data suggest that reduced autophagy caused by LKB1 inhibition can induce EMT in ATIl cells and contribute to fibrosis via aberrant epithelial-fibroblast crosstalk.

Integrated analysis reveals the protective mechanism and therapeutic potential of hyperbaric oxygen against pulmonary fibrosis

Idiopathic pulmonary fibrosis (IPF) is a dreadful, chronic, and irreversibly progressive disease leading to death with a few effective treatments. Our previous study suggested that repetitive hyperbaric oxygen (HBO) treatment alleviates bleomycin-induced pulmonary fibrosis in mice. Here, we investigated the protective mechanism of HBO treatment against pulmonary fibrosis using an integrated approach. Analyzing publicly available expression data from the mouse model of bleomycin-induced pulmonary fibrosis as well as IPF patients, several potential mechanisms of relevance to IPF pathology were identified, including increased epithelial-to-mesenchymal transition (EMT) and glycolysis. High EMT or glycolysis scores in bronchoalveolar lavage were strong independent predictors of mortality in multivariate analysis. These processes were potentially driven by hypoxia and blocked by HBO treatment. Together, these data support HBO treatment as a viable strategy against pulmonary fibrosis.

Different Laboratory Abnormalities in COVID-19 Patients with Hypertension or Diabetes

Dear Editor,The pandemic of COVID-19,a disease caused by severe acute respiratory syndrome coronavirus 2(SARS-Co V-2;previously known as 2019-n Co V),has placed an enormous burden on health authorities in 213 countries and territories.At the time of writing,over 26 million cases have been recorded across the world,with more than 870 k associated deaths(www.worldometers.info/coronavirus/).World Bank warns COVID-19 pandemic risks dramatic rise in poverty,with the majority of economies expecting to suffer from falling levels of GDP in 2020.