[The role of mother-child relationship in the association between maternal parenting stress and emotional and behavioral problems in preschool children]. / æ¯å­å ³ç³»åœ¨æ¯äº²å »è‚²åŽ‹åŠ›ä¸Žå­¦é¾„å‰å„¿ç«¥æƒ ç»ªè¡Œä¸ºé—®é¢˜å ³è”ä¸­çš„ä½œç”¨.

OBJECTIVES: To study the moderating effect of mother-child relationship in the association between maternal parenting stress and emotional and behavioral problems in preschool children, and to provide reference for the prevention and control of emotional and behavioral problems in preschool children. METHODS: Using a stratified cluster sampling method, 2 049 preschool children were surveyed from November to December 2021, who sampled from 12 kindergartens in Wuhu City, Anhui Province. The emotional and behavioral problems of preschool children were assessed with the Strength and Difficulties Questionnaire. Pearson correlation analysis was used to evaluate the relationship of maternal parenting stress and mother-child relationship with children's emotional and behavioral problems. The PROCESS Macro was used to analyze the moderating effect of conflicted and dependent mother-child relationships in the association between maternal parenting stress and emotional and behavioral problems in these preschool children. RESULTS: Among these preschool children, maternal parenting stress was positively correlated with the scores of emotional symptoms, conduct problems, hyperactivity, and peer problems subscales and total difficulty scores (P<0.001); intimate mother-child relationships were negatively correlated with the scores of conduct problems, hyperactivity, and peer problems subscales and total difficulty scores (P<0.001); conflicted and dependent mother-child relationships were positively correlated with the scores of emotional symptoms, conduct problems, hyperactivity, and peer problems subscales and total difficulty scores (P<0.001). After controlling for relevant confounding factors, conflicted mother-child relationship (ß=0.05, P=0.001) and dependent mother-child relationship (ß=0.04, P=0.012) were found to have a moderating effect on the association between maternal parenting stress and total difficulty scores in these preschool children. CONCLUSIONS: Negative mother-child relationships play a moderating role in the association between maternal parenting stress and emotional and behavioral problems in preschool children. Prevention of emotional and behavioral problems in preschool children should focus on reducing maternal parenting stress and improving negative mother-child relationships.

Case report: A double pathogenic mutation in a patient with late-onset MELAS/PEO overlap syndrome.

Mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) and progressive external ophthalmoplegia (PEO) are established phenotypes of mitochondrial disorders. They are maternally-inherited, multisystem disorder that is characterized by variable clinical, biochemical, and imaging features. We described the clinical and genetic features of a Chinese patient with late-onset MELAS/PEO overlap syndrome, which has rarely been reported. The patient was a 48-year-old woman who presented with recurrent ischemic strokes associated with characteristic brain imaging and bilateral ptosis. We assessed her clinical characteristics and performed mutation analyses. The main manifestations of the patient were stroke-like episodes and seizures. A laboratory examination revealed an increased level of plasma lactic acid and a brain MRI showed multiple lesions in the cortex. A muscle biopsy demonstrated ragged red fibers. Genetic analysis from a muscle sample identified two mutations: TL1 m.3243A>G and POLG c.3560C>T, with mutation loads of 83 and 43%, respectively. This suggested that mitochondrial disorders are associated with various clinical presentations and an overlap between the syndromes and whole exome sequencing is important, as patients may carry multiple mutations.

Efficacy of Spleen-invigorating Chinese Medicinals in Repairing Intestinal Mucosal Barrier Injury： A Review / 中国实验方剂学杂志

As the first line of defense between the intestinal environment and the outside world， the intestinal mucosal barrier is essential for maintaining the intestinal homeostasis. The intestinal mucosal barrier injury will change the intestinal permeability and allow bacterial translocation and the entry of endotoxins into blood， thus triggering a series of inflammatory responses， followed by the injury of related tissues and the aggravation of primary diseases. The spleen， the acquired foundation， is responsible for maintaining the internal and external balance of the body and resisting external evils. Its physiological function is similar to that of the intestinal mucosal barrier. Spleen deficiency easily leads to intestinal mucosal barrier dysfunction. Therefore， replenishing Qi， invigorating spleen， and restoring the efficacy of spleen and stomach qi in defensing and governing transportation and transformation are the keys to prevent and treat intestinal mucosal barrier injury. In recent years， studies have shown that the spleen-invigorating Chinese medicinals repair the intestinal mucosal injury by promoting the expression of intestinal epithelial tight junction proteins， regulating the intestinal immune function， microbial flora， and metabolites， and supplementing the intestinal nutrition， enabling them to gradually become a research hotspot. After reviewing the relevant articles published in China and abroad， this paper expounded the common syndrome types of traditional Chinese medicine （TCM）， the changes in intestinal mucosal barrier induced by spleen deficiency， the repairing effects of spleen-invigorating Chinese medicinals on intestinal mucosal barrier injury， in order to provide some clues for the research on the treatment of intestinal mucosal barrier dysfunction-related diseases with spleen-invigorating Chinese medicinals.

The main active components of Curcuma zedoaria reduces collagen deposition in human lung fibroblast via autophagy.

Disordered collagen production by fibroblasts in response to tissue injury contributes to pulmonary fibrosis (PF). Therefore, elimination of collagen deposition has becoming a potential target in PF treatment which despite standard anti-fibrosis regiment still remains challenge. Curcumin and curcumol are regarded as the main active components extraction from the rhizomes of Curcuma zedoaria, which is widely used for inhibition the proliferation of multiple cells. However, the molecular basis for the function of curcumin and curcumol in limiting fibrogenesis still unknown. In this study, we have investigated the effects of curcumin and curcumol in the fibroblast overproliferation model human lung fibroblast (HLF) inducing by TGF-ß1. The growth-inhibitory effects of the components wasn't observed from 8 to 64 µg/ml. Administration of curcumin or curcumol significantly diminished the level of hydroxyproline hydroxyproline and α-smooth muscle actin (α-SMA), also the collagen Ⅰ (Col-Ⅰ) and collagen Ⅲ (Col-Ⅲ) deposition were reduced in the HLF. Furthermore, related to the collagen synthesis proteins including N-terminal pro-peptide for Type Ⅰ collagen (PⅠNP), N-terminal pro-peptide for Type Ⅲ collagen (PⅢNP) and prolyl-hydroxylase (PHD) were degraded gracefully at dose-dependent manner. Autophagy as the scavenger was crippled in TGF-ß1-fibroblast overproliferation HLF, conversely the increased autophagosomes have been spotted in cytoplasm under transmission electron microscope which is consistent with up-regulation of Beclin1 and ATG7 after treatment with curcumin or curcumol in this study. Additionally, blocking autophagy by inhibitor chloroquine (CQ) caused collagen deposition, providing further evidence regard to autophagy activation capacity of curcumin and curcumol. Our findings provide a detailed understanding that the function of curcumin and curcumol on decreasing collagen deposition mediating by autophagy mechanism, which may also inspire the further research on PF at different perspectives.

Research Progress of Butyrate-producing Bacteria in Regulating Intestinal Microecology and Interventional Effect of Chinese Herbal Medicine / 中国实验方剂学杂志

Butyrate-producing bacteria are specific intestinal bacteria with butyrate as the main metabolite, and most of them are Firmicutes.Butyrate-producing bacteria can synthesize butyrate with non-digestible carbohydrates in the diet, and then regulate intestinal microecology and microenvironment, thereby supplying energy to intestinal epithelial cells, affecting intestinal mucosal barrier, adjusting intestinal flora structure and regulating host immunity, so as to alleviate obesity, hypertension and other diseases.Therefore, the targeted regulation of butyrate-producing bacteria and butyrate has become a potential vital method for the prevention and treatment of many diseases.After oral administration, Chinese herbal medicine (CHM) enters the body, and first contacts gastrointestinal tract, so the interaction between CHM and microbiota existing in the intestine is an inevitable important process.It has been confirmed that CHM could regulate intestinal flora; and due to its complex composition and numerous components, CHM can exert interventional effects at multiple levels, in multiple pathways and on multiple targets.Its effect on the butyrate-producing bacteria is as follows.In the intestinal tract, CHM can play a " prebiotic" role, and enrich the beneficial butyrate-producing bacteria, and polysaccharides in CHM can be used as a fermentation substrate to promote the synthesis of butyrate, so as to achieve the effective regulation of butyrate-producing bacteria and butyrate.Based on that, this paper explored the relationship among butyrate-producing bacteria, butyrate and intestinal microecology, and reviewed relevant researches about the intervention of CHM on butyrate-producing bacteria to regulate intestinal microecology in recent years, in order to provide new research ideas for the application of CHM to prevent and treat diseases, as well as drug development.

Increased Macroautophagy in Interferon-Gamma-Producing T Cells from Patients with Newly Diagnosed Systemic Lupus Erythematosus / 中华医学杂志(英文版)

<p><b>Background</b>Imbalance of interferon-gamma (IFN-γ), interleukin (IL)-4, and IL-17 producing by T cells is confirmed to contribute to the pathogenesis of systemic lupus erythematosus (SLE). Autophagy is now emerging as a core player in the development and the function of the immune system. Therefore, we investigated the autophagic behavior in IFN-γ-, IL-4-, and IL-17-producing T cells from patients with SLE.</p><p><b>Methods</b>Thirty patients with SLE and 25 healthy controls matched for gender and age were recruited between September 2016 and May 2017. The autophagic levels in IFN-γ T cells, IL-4 T cells, and IL-17 T cells from patients with newly diagnosed SLE and healthy controls were measured using flow cytometry. The plasma levels of IFN-γ were determined by enzyme-linked immunosorbent assay in SLE patients and healthy controls. Unpaired t-tests and the nonparametric Mann-Whitney U-test were used to compare data from patients with SLE and controls. Spearman's rank correlation coefficient was applied for calculation of the correlation between parallel variables in single samples.</p><p><b>Results</b>Our results showed increased percentage of autophagy in IFN-γ T cells from patients with SLE and healthy controls ([8.07 ± 2.72]% vs. [3.76 ± 1.67]%, t = 5.184, P < 0.001), but not in IL-4 T cells or IL-17 T cells (P > 0.05) as compared to healthy donors. Moreover, the plasma levels of IFN-γ in SLE patients were significantly higher than those in healthy controls ([68.9 ± 29.1] pg/ml vs. [24.7 ± 17.6] pg/ml, t = 5.430, P < 0.001). Moreover, in SLE patients, the percentage of autophagy in IFN-γ T cells was positively correlated with the plasma levels of IFN-γ (r = 0.344, P = 0.046), as well as the disease activity of patients with SLE (r = 0.379, P = 0.039).</p><p><b>Conclusion</b>The results indicate that autophagy in IFN-γ T cells from SLE patients is activated, which might contribute to the persistence of T cells producing IFN-γ, such as Th1 cells, and consequently result in the high plasma levels of IFN-γ, and then enhance the disease activity of SLE.</p>