Relationship between time to clinical remission and relapse in adults with steroid-sensitive minimal change disease: a retrospective cohort study.

OBJECTIVE: Minimal change disease (MCD) is a common nephrotic syndrome that is usually steroid-sensitive and has high relapse rate. The aim of this study was to investigate the relationship between time to clinical remission and recurrence after the initial steroid therapy. METHODS: Among 305 adult patients diagnosed with MCD via light and electron microscopy, sensitive to steroids, and hospitalized for nephrotic syndrome in the Department of Nephrology of the Affiliated Hospital of Guangdong Medical University in China, 88 were included in this retrospective cohort study. Cox regression analysis was performed with time to clinical remission and 24-hour urine protein quantification (24 hUTP), absolute basophil (BA) and basophil percentage (BA%) as independent variables. Independent variables with significant differences and the time to remission were used to construct a Cox regression model to exclude the influence of confounding factors. The receiver operating characteristic (ROC) curve was plotted according to the independent variable of time to clinical remission. RESULTS: No significant differences were found between the relapse and non-relapse groups in terms of sex, age at onset, or prevalent hypertension. There were significant differences in time to clinical remission, 24 hUTP, BA and BA% between the relapse and non-relapse groups. The risk of recurrence was significantly higher in patients with clinical remission of 15-21, 22-28 and 29-56 days than in those who had clinical remission of 1-7 days. In addition, patients with clinical remission of >26.5 days had a significantly higher risk of recurrence than those in the other groups. CONCLUSIONS: Overall, the time of clinical remission is a potential factor for predicting the recurrence of steroid-sensitive MCD in adults.

The development and improvement of immunodeficient mice and humanized immune system mouse models.

Animal models play an indispensable role in the study of human diseases. However, animal models of different diseases do not fully mimic the complex internal environment of humans. Immunodeficient mice are deficient in certain genes and do not express these or show reduced expression in some of their cells, facilitating the establishment of humanized mice and simulation of the human environment in vivo. Here, we summarize the developments in immunodeficient mice, from the initial nude mice lacking T lymphocytes to NOD/SCID rgnull mice lacking T, B, and NK cell populations. We describe existing humanized immune system mouse models based on immunodeficient mice in which human cells or tissues have been transplanted to establish a human immune system, including humanized-peripheral blood mononuclear cells (Hu-PBMCs), humanized hematopoietic stem cells (Hu-HSCs), and humanized bone marrow, liver, thymus (Hu-BLT) mouse models. The different methods for their development involve varying levels of complexity and humanization. Humanized mice are widely used in the study of various diseases to provide a transitional stage for clinical research. However, several challenges persist, including improving the efficiency of reconstructing the human B cell immune response, extending lifespan, improving the survival rate of mice to extend the observation period, and improving the development of standardized commercialized models and as well as their use. Overall, there are many opportunities and challenges in the development of humanized immune system mouse models which can provide novel strategies for understanding the mechanisms and treatments of human disease.

LncRNA Expression Profiles in Systemic Lupus Erythematosus and Rheumatoid Arthritis: Emerging Biomarkers and Therapeutic Targets.

Systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) are two common multisystem autoimmune diseases that share, among others, many clinical manifestations and serological features. The role of long non-coding RNAs (lncRNAs) has been of particular interest in the pathogenesis of autoimmune diseases. Here, we aimed to summarize the roles of lncRNAs as emerging novel biomarkers and therapeutic targets in SLE and RA. We conducted a narrative review summarizing original articles on lncRNAs associated with SLE and RA, published until November 1, 2021. Based on the studies on lncRNA expression profiles in samples (including PBMCs, serum, and exosomes), it was noted that most of the current research is focused on investigating the regulatory mechanisms of these lncRNAs in SLE and/or RA. Several lncRNAs have been hypothesized to play key roles in these diseases. In SLE, lncRNAs such as GAS5, NEAT1, TUG1, linc0949, and linc0597 are dysregulated and may serve as emerging novel biomarkers and therapeutic targets. In RA, many validated lncRNAs, such as HOTAIR, GAS5, and HIX003209, have been identified as promising novel biomarkers for both diagnosis and treatment. The shared lncRNAs, for example, GAS5, may participate in SLE pathogenesis through the mitogen-activated protein kinase pathway and trigger the AMP-activated protein kinase pathway in RA. Here, we summarize the data on key lncRNAs that may drive the pathogenesis of SLE and RA and could potentially serve as emerging novel biomarkers and therapeutic targets in the coming future.