A novel long noncoding RNA ENST00000597482 serves as a potential biomarker for disease activity and diagnosis of systemic lupus erythematosus.

Objectives: Emerging evidence indicate that long noncoding RNAs (lncRNAs) may play an important role in the pathogenesis of systemic lupus erythematosus (SLE) however, the contribution of lncRNAs to SLE remains largely unclear. Our study aimed to explore the lncRNA expression profiles in peripheral blood mononuclear cells (PBMCs) from SLE patients.

Methods: LncRNA sequencing was used to detect differentially expressed genes in PBMCs from 5 SLE-MIX samples and 3 healthy controls (HC)-MIX samples, and the expression of selected lncRNAs was further verified by real-time quantitative polymerase chain reaction (RT‒qPCR).

Rosmarinic acid ameliorated oxidative stress, neuronal injuries, and mitochondrial dysfunctions mediated by polyglutamine and ɑ-synuclein in Caenorhabditis elegans models.

Numerous natural antioxidants have been developed into agents for neurodegenerative diseases (NDs) treatment. Rosmarinic acid (RA), an excellent antioxidant, exhibits neuroprotective activity, but its anti-NDs efficacy remains puzzling. Here, Caenorhabditis elegans models were employed to systematically reveal RA-mediated mechanisms in delaying NDs from diverse facets, including oxidative stress, the homeostasis of neural and protein, and mitochondrial disorders.

Aberrant phenotypes of circulating γδ-T cells may be involved in the onset of systemic lupus erythematosus.

Objective: Human gamma-delta T cells (γδ-T cells) play crucial roles in both innate and adaptive immune responses. However, much less is known about the immune status of γδT cells in systemic lupus erythematosus (SLE) patients. The objective of this study was to explore potential relationships between the frequency of γδ-T-cell subpopulations and disease activity, autoantibody titres and renal involvement in patients with SLE.

Using fs/QCA to explore the influencing factors of urban green infrastructure development and its combinational drivers: the case of the Yangtze River Delta region of China.

High levels of urban green infrastructure (UGI) development can help mitigate the climate, biodiversity, and habitat crises faced by cities and support the achievement of sustainable urban development. Based on the relevant data of 41 cities in the Yangtze River Delta region obtained from 2011 to 2020, this study measured the development level of natural and geographic conditions, economic development, urban construction, social and cultural development, and eco-environment quality and urban green infrastructure (UGI); evaluated the development trend of UGI in the region during the 12th Five-Year Plan and 13th Five-Year Plan by using entropy TOPSIS; and used fs/QCA to explain the high-level development path of each city toward the achievement of a green infrastructure. The results showed that (1) the development level of UGI in the Yangtze River Delta region decreases from southeast to northwest, and gradually decreases from Shanghai, Hangzhou, and other central cities.

Acetyl-CoA carboxylase 1 depletion suppresses de novo fatty acid synthesis and mitochondrial β-oxidation in castration-resistant prostate cancer cells.

Cancer cells, including those of prostate cancer (PCa), often hijack intrinsic cell signaling to reprogram their metabolism. Part of this reprogramming includes the activation of de novo synthesis of fatty acids that not only serve as building blocks for membrane synthesis but also as energy sources for cell proliferation. However, how de novo fatty acid synthesis contributes to PCa progression is still poorly understood.

Phenotypical changes and clinical significance of CD4/CD8 T cells in SLE.

Objective: T cells display significant phenotypical changes and play multiple roles in promoting the immune response in SLE. The frequencies of T cell subpopulations in SLE are still not well understood. To better understanding the phenotypic abnormalities of T cells in SLE will help us to clarify disease immunopathology and to find promising biomarkers for disease monitoring and control.

New Trends in Pharmacological Treatments for Osteoarthritis.

Osteoarthritis (OA) is the leading cause of function loss and disability among the elderly, with significant burden on the individual and society. It is a severe disease for its high disability rates, morbidity, costs, and increased mortality. Multifactorial etiologies contribute to the occurrence and development of OA.

Efficient Generation of Pathogenic A-to-G Mutations in Human Tripronuclear Embryos via ABE-Mediated Base Editing.

Base editing systems show their power in modeling and correcting the pathogenic mutations of genetic diseases. Previous studies have already demonstrated the editing efficiency of BE3-mediated C-to-T conversion in human embryos. However, the precision and efficiency of a recently developed adenine base editor (ABE), which converts A-to-G editing in human embryos, remain to be addressed.

Correction of the Marfan Syndrome Pathogenic FBN1 Mutation by Base Editing in Human Cells and Heterozygous Embryos.

There are urgent demands for efficient treatment of heritable genetic diseases. The base editing technology has displayed its efficiency and precision in base substitution in human embryos, providing a potential early-stage treatment for genetic diseases. Taking advantage of this technology, we corrected a Marfan syndrome pathogenic mutation, FBN1.

CRISPR/Cas9-mediated gene editing in human zygotes using Cas9 protein.

Previous works using human tripronuclear zygotes suggested that the clustered regularly interspaced short palindromic repeat (CRISPR)/Cas9 system could be a tool in correcting disease-causing mutations. However, whether this system was applicable in normal human (dual pronuclear, 2PN) zygotes was unclear. Here we demonstrate that CRISPR/Cas9 is also effective as a gene-editing tool in human 2PN zygotes.

A subpathway-based method of drug reposition for polycystic ovary syndrome.

The need for development of new therapeutic agents for polycystic ovary syndrome (PCOS) is urgent due to general lack of efficient and specialized drugs currently available. We aimed to explore the metabolic mechanism of PCOS and inferred drug reposition for PCOS by a subpathway-based method. Using the GSE34526 microarray data from the Gene Expression Omnibus database, we first identified the differentially expressed genes (DEGs) between PCOS and normal samples.