Outcome of COVID-19 in patients with idiopathic inflammatory myopathy during the Omicron wave in China: A longitudinal observational study.

Objective: The coronavirus disease pandemic brought unknown challenges to patients with idiopathic inflammatory myopathy, who are often heavily immunosuppressed and have comorbidities. We aimed to investigate the outcomes and risk factors of coronavirus disease in Chinese patients with idiopathic inflammatory myopathy during the Omicron wave.

Methods: This observational study included patients with idiopathic inflammatory myopathy who visited the China-Japan Friendship Hospital.

Leveraging the sugarcane CRISPR/Cas9 technique for genetic improvement of non-cultivated grasses.

Under changing climatic scenarios, grassland conservation and development have become imperative to impart functional sustainability to their ecosystem services. These goals could be effectively and efficiently achieved with targeted genetic improvement of native grass species. To the best of our literature search, very scant research findings are available pertaining to gene editing of non-cultivated grass species (switch grass, wild sugarcane, Prairie cordgrass, Bermuda grass, Chinese silver grass, etc.

Interstitial Lung Disease Is a Major Characteristic of Patients Who Test Positive for Anti-PM/Scl Antibody.

Objective: This study aimed to analyze the clinical features of anti-PM/Scl antibodies in Chinese patients.

Method: We reviewed the clinical data of anti-PM/Scl antibody-positive patients, including their long-term follow-up.

Results: A total of 30 patients carried anti-PM/Scl antibodies, 21 (70%) were females, and the mean age was 55.

Aberrant mTOR/autophagy/Nurr1 signaling is critical for TSC-associated tumor development.

Tuberous sclerosis complex (TSC), an inherited neurocutaneous disease, is caused by mutations in either the TSC1 or TSC2 gene. This genetic disorder is characterized by the growth of benign tumors in the brain, kidneys, and other organs. As a member of the orphan nuclear receptor family, nuclear receptor related 1 (Nurr1) plays a vital role in some neuropathological diseases and several types of benign or malignant tumors.

SLC7A11/xCT Prevents Cardiac Hypertrophy by Inhibiting Ferroptosis.

Purpose: Systemic hypertension may induce adverse hypertrophy of the left cardiac ventricle. Pathological cardiac hypertrophy is a common cause of heart failure. We investigated the significance of ferroptosis repressor xCT in hypertrophic cardiomyopathy.

αB-crystallin/HSPB2 is critical for hyperactive mTOR-induced cardiomyopathy.

Even though aberrant mechanistic target of rapamycin (mTOR) signaling is known to cause cardiomyopathy, its underlying mechanism remains poorly understood. Because augmentation of αB-crystallin and hspB2 was presented in the cortical tubers and lymphangioleiomyomatosis of tuberous sclerosis complex patients, we deciphered the role of αB-crystallin and its adjacent duplicate gene, hspB2, in hyperactive mTOR-induced cardiomyopathy. Cardiac Tsc1 deletion (T1-hKO) caused mouse mTOR activation and cardiomyopathy.

The effects of infliximab in treating idiopathic inflammatory myopathies: A review article.

Anti-TNF treatment may be useful for patients with idiopathic inflammatory myopathies (IIMs). The purpose of this study is to assess the efficacy of infliximab (IFX) in the management of IIMs. Two databases (ie, PubMed and China National Knowledge Infrastructure) were searched up to Nov 2020 for studies investigating skin lesions and muscular weakness in patients with IIMs treated with IFX.

Pituitary dysfunction in patients with ANCA associated vasculitis: prevalence, presentation, and outcomes.

Background: The antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) are rare multisystem autoimmune diseases characterized by inflammatory cell infiltration causing necrosis of small blood vessels. Pituitary involvement in AAV is poorly described. This study aimed to describe the prevalence, clinical characteristics, and outcomes of pituitary involvement in patients with AAV.

mTOR-dependent upregulation of xCT blocks melanin synthesis and promotes tumorigenesis.

Loss of either TSC1 or TSC2 causes tuberous sclerosis complex (TSC) via activation of mTOR signaling pathway. The two prominent features of TSC are skin lesions including hypomelanic macules and benign tumors in multiple organs, whose molecular alterations are largely unknown. We report here that X cystine/glutamate antiporter (xCT) was elevated in Tsc2 or Pten cells, Tsc1 knockout mouse tissues and TSC2-deficient human kidney tumor.

Phosphoglyceric acid mutase-1 contributes to oncogenic mTOR-mediated tumor growth and confers non-small cell lung cancer patients with poor prognosis.

As a hallmark of cancer, the Warburg effect (aerobic glycolysis) confers a selective advantage for the survival and proliferation of cancer cells. Due to frequent aberration of upstream proto-oncogenes and tumor suppressors, hyperactive mammalian/mechanistic target of rapamycin (mTOR) is a potent inducer of the Warburg effect. Here, we report that overexpression of a glycolytic enzyme, phosphoglyceric acid mutase-1 (PGAM1), is critical to oncogenic mTOR-mediated Warburg effect.

Genotypic variation in transpiration efficiency due to differences in photosynthetic capacity among sugarcane-related clones.

Sugarcane, derived from the hybridization of Saccharum officinarum×Saccharum spontaneum, is a vegetative crop in which the final yield is highly driven by culm biomass production. Cane yield under irrigated or rain-fed conditions could be improved by developing genotypes with leaves that have high intrinsic transpiration efficiency, TEi (CO2 assimilation/stomatal conductance), provided this is not offset by negative impacts from reduced conductance and growth rates. This study was conducted to partition genotypic variation in TEi among a sample of diverse clones from the Chinese collection of sugarcane-related germplasm into that due to variation in stomatal conductance versus that due to variation in photosynthetic capacity.

Deficient TSC1/TSC2-complex suppression of SOX9-osteopontin-AKT signalling cascade constrains tumour growth in tuberous sclerosis complex.

Tuberous sclerosis complex (TSC) is an autosomal dominant genetic disorder featured with multi-organ benign tumours. Disruption of TSC1/TSC2 complex suppression on mammalian/mechanistic target of rapamycin (mTOR) signalling causes TSC. Hyperactive mTOR-mediated negative feedback regulation of AKT partially contributes to the benign nature of TSC-associated tumours.

Homozygous ALOXE3 Nonsense Variant Identified in a Patient with Non-Bullous Congenital Ichthyosiform Erythroderma Complicated by Superimposed Bullous Majocchi's Granuloma: The Consequences of Skin Barrier Dysfunction.

Non-bullous congenital ichthyosiform erythroderma (NBCIE) is a hereditary disorder of keratinization caused by pathogenic variants in genes encoding enzymes important to lipid processing and terminal keratinocyte differentiation. Impaired function of these enzymes can cause pathologic epidermal scaling, significantly reduced skin barrier function. In this study, we have performed a focused, genetic analysis of a probrand affected by NBCIE and extended this to his consanguineous parents.

Brain-expressed X-linked 2 Is Pivotal for Hyperactive Mechanistic Target of Rapamycin (mTOR)-mediated Tumorigenesis.

Frequent alteration of upstream proto-oncogenes and tumor suppressor genes activates mechanistic target of rapamycin (mTOR) and causes cancer. However, the downstream effectors of mTOR remain largely elusive. Here we report that brain-expressed X-linked 2 (BEX2) is a novel downstream effector of mTOR.

NFκB up-regulation of glucose transporter 3 is essential for hyperactive mammalian target of rapamycin-induced aerobic glycolysis and tumor growth.

Accumulating evidence indicates that mammalian target of rapamycin (mTOR) exerts a crucial role in aerobic glycolysis and tumorigenesis, but the underlying mechanisms remain largely obscure. Results from Tsc1- or Tsc2-null mouse embryonic fibroblasts (MEFs) and human cancer cell lines consistently indicate that the expression of glucose transporter 3 (Glut3) is dramatically up-regulated by mTOR. The rapamycin-sensitive mTOR complex 1 (mTORC1), but not the rapamycin-insensitive mTOR complex 2 (mTORC2), was involved in the regulation of Glut3 expression.