Central nervous system(CNS)degenerative disorders refer to a spectrum of pathological alterations triggered by struc-tural damage to cerebral neural tissues,clinically manifested as diverse neurological dysfunction syndromes,including multiple sclerosis(MS),neurodegenerative diseases(NDs),and ische-mic stroke.The hallmark pathological features of these disorders involve irreversible neuronal damage and decompensation of functional neural networks,ultimately leading to progressive neurological deficits.Notably,with the accelerating global popu-lation aging,the incidence of these diseases has surged signifi-cantly.According to WHO statistics,they now rank among the top three global causes of disability and mortality.Current re-search has confirmed that the pathogenesis of CNS degenerative disorders exhibits high heterogeneity,encompassing multifaceted pathophysiological processes such as genetic predisposition,oxi-dative stress,protein misfolding,and metabolic dysregulation.This intricate pathogenic network not only complicates clinical differential diagnosis but also poses substantial challenges to the development of precision therapeutic strategies.Importantly,re-cent studies have revealed that mitochondrial homeostasis disrup-tion-induced inflammatory cascades(termed mitochondrial in-flammation)play a pivotal regulatory role in neurodegenerative progression.Key molecular mechanisms include impaired mito-phagy,aberrant mitochondrial DNA(mtDNA)release and NL-RP3 inflammasome activation.This review systematically deci-phers the molecular regulatory network of mitochondrial inflam-mation,with a focus on its biological effects in critical pathologi-cal events such as blood-brain barrier disruption,microglial hy-peractivation and neuronal apoptosis.The overarching aim is to provide a theoretical foundation for developing innovative thera-peutic strategies targeting mitochondrial homeostasis restoration.

Central nervous system(CNS)degenerative disorders refer to a spectrum of pathological alterations triggered by struc-tural damage to cerebral neural tissues,clinically manifested as diverse neurological dysfunction syndromes,including multiple sclerosis(MS),neurodegenerative diseases(NDs),and ische-mic stroke.The hallmark pathological features of these disorders involve irreversible neuronal damage and decompensation of functional neural networks,ultimately leading to progressive neurological deficits.Notably,with the accelerating global popu-lation aging,the incidence of these diseases has surged signifi-cantly.According to WHO statistics,they now rank among the top three global causes of disability and mortality.Current re-search has confirmed that the pathogenesis of CNS degenerative disorders exhibits high heterogeneity,encompassing multifaceted pathophysiological processes such as genetic predisposition,oxi-dative stress,protein misfolding,and metabolic dysregulation.This intricate pathogenic network not only complicates clinical differential diagnosis but also poses substantial challenges to the development of precision therapeutic strategies.Importantly,re-cent studies have revealed that mitochondrial homeostasis disrup-tion-induced inflammatory cascades(termed mitochondrial in-flammation)play a pivotal regulatory role in neurodegenerative progression.Key molecular mechanisms include impaired mito-phagy,aberrant mitochondrial DNA(mtDNA)release and NL-RP3 inflammasome activation.This review systematically deci-phers the molecular regulatory network of mitochondrial inflam-mation,with a focus on its biological effects in critical pathologi-cal events such as blood-brain barrier disruption,microglial hy-peractivation and neuronal apoptosis.The overarching aim is to provide a theoretical foundation for developing innovative thera-peutic strategies targeting mitochondrial homeostasis restoration.

Humans ; Lymphohistiocytosis, Hemophagocytic/complications* ; Neoplasms

Sjögren's syndrome(SS)is a chronic autoimmune disease that affects exocrine glands, especially salivary and lacrimal glands. The main clinical manifestations are dry mouth and dry eyes, but also multi-organ and multi-system can be involved. Cold agglutinin disease(CAD)is an autoimmune disease characterized by red blood cell agglutination in the blood vessels of extremities caused by cold agglutinin at low temperature, resulting in skin microcirculation disturbance, or hemolytic anemia. Cold agglutinin disease is divided into two categories, primary cold agglutinin disease and secondary cold agglutinin disease. Primary cold agglutinin disease is characterized with cold agglutinin titer of 1 ∶4 000 or more and positive Coomb's test. However, the Coomb's test is not necessarily positive and the cold agglutinin titer is between 1 ∶32 and 1 ∶4 000 in secondary cold agglutinin disease. Here, we reported an elderly patient admitted to hospital due to fever. He was diagnosed with respiratory infection, but he showed incompletely response to the anti-infection treatment. Further laboratory tests showed the patient with positive ANA and anti-SSA antibodies. Additionally, the patient complained that he had dry mouth and dry eyes for 1 year. Schirmer test and salivate gland imaging finally confirmed the diagnosis Sjogren's syndrome. During the hospital stay, the blood clots were found in the anticoagulant tubes. Hemolytic anemia was considered as the patient had anemia with elevated reticulocytes and indirect bilirubin. In addition, further examination showed positive cold agglutination test with a titer of 1 ∶1 024, and cold agglutinin disease was an important type of cold-resistant autoimmune hemolytic anemia. Furthermore, the patient developed cyanosis after ice incubating at the tip of the nose. Hence, the patient was diagnosed as CAD and he was successfully treated with glucocorticoids instead of anti-infection treatments. Hence, the patient was diagnosed with SS combined with secondary CAD. SS combined CAD are rarely reported, and they are both autoimmune diseases. The abnormal function of B lymphocytes and the production of autoantibodies might be the common pathogenesis of them. Cold agglutinin disease can lead to severe hemolytic anemia, even life-threatening. In clinical practice, timely recognizing and dealing with CAD might promote the prognosis of the patient.
Male ; Humans ; Aged ; Anemia, Hemolytic, Autoimmune/diagnosis* ; Sjogren's Syndrome/diagnosis* ; Anemia, Hemolytic/complications* ; Dry Eye Syndromes/complications* ; Autoantibodies

OBJECTIVE: To screen differentially expressed gene (DEG) related to myelodysplastic syndrome (MDS) based on Gene Expression Omnibus (GEO) database, and explore the core genes and pathogenesis of MDS by analyzing the biological functions and related signaling pathways of DEG. METHODS: The expression profiles of GSE4619, GSE19429, GSE58831 including MDS patients and normal controls were downloaded from GEO database. The gene expression analysis tool (GEO2R) of GEO database was used to screen DEG according to | log FC (fold change) |≥1 and P<0.01. David online database was used to annotate gene ontology function (GO). Metascape online database was used to enrich and analyze differential genes in Kyoto Encyclopedia of Genes and Genomes (KEGG). The protein-protein interaction network (PPI) was constructed by using STRING database. CytoHubba and Mcode plug-ins of Cytoscape were used to analyze the key gene clusters and hub genes. R language was used to diagnose hub genes and draw the ROC curve. GSEA enrichment analysis was performed on GSE19429 according to the expression of LEF1. RESULTS: A total of 74 co-DEG were identified, including 14 up-regulated genes and 60 down regulated genes. GO enrichment analysis indicated that BP of down regulated genes was mainly enriched in the transcription and regulation of RNA polymerase II promoter, negative regulation of cell proliferation, and immune response. CC of down regulated genes was mainly enriched in the nucleus, transcription factor complexes, and adhesion spots. MF was mainly enriched in protein binding, DNA binding, and β-catenin binding. KEGG pathway was enriched in primary immunodeficiency, Hippo signaling pathway, cAMP signaling pathway, transcriptional mis-regulation in cancer and hematopoietic cell lineage. BP of up-regulated genes was mainly enriched in type I interferon signaling pathway and viral response. CC was mainly enriched in cytoplasm. MF was mainly enriched in RNA binding. Ten hub genes and three important gene clusters were screened by STRING database and Cytoscape software. The functions of the three key gene clusters were closely related to immune regulation. ROC analysis showed that the hub genes had a good diagnostic significance for MDS. GSEA analysis indicated that LEF1 may affect the normal function of hematopoietic stem cells by regulating inflammatory reaction, which further revealed the pathogenesis of MDS. CONCLUSION Bioinformatics can effectively screen the core genes and key signaling pathways of MDS, which provides a new strategy for the diagnosis and treatment of MDS.
Computational Biology ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Gene Ontology ; Humans ; Myelodysplastic Syndromes/genetics*

Tibetan medicine is an essential part of Chinese medicine and has unique theoretical experience and therapeutic advantages. According to the development principle of inheriting the essence, sticking to the truth, and keeping innovative, the supervision department should give clear and reasonable guidance considering the characteristics of Tibetan medicine, establish a standard system for quality control, clinical verification and evaluation, and accelerate the research and commercialization of new drugs. In view of the needs of drug supply-side reform and the current situation of Tibetan medicine and new pharmaceutical research, we ponder and provide suggestions on the confusion faced by the current supervision of Tibetan drug registration, hoping to contribute to the supervision strategy of Tibetan drug registration and the high-quality development of Tibetan medicine industry.
Tibet ; Medicine, Tibetan Traditional ; Quality Control ; Pharmaceutical Research ; Drug Industry

Aim To investigate the effeet of Eehinaeo- side ( ECH ) regulating the expression of prohibitin (PHB) on MPP+ -induced apoptosis of SH-SY5Y eells and the underlying mechanism.Methods SH-SY5Y eells were seleeted and divided into control group, MPP+ group, MPP+ + ECH group, NC + MPP + group, NC + MPP+ + ECH group, PHB-RNAi + MPP + + ECH group.Cell survival rate was determined by CCK-8 assay.Cell morphology was observed using an inverted phase contrast mieroscope; the apoptotie eells were observed by Hoechst33342 fluorescence staining, whereas apoptotie rate, reactive oxygen speeies eon- tent, and mitochondrial membrane potential were ana¬lyzed by flow eytometry.The relative protein expres¬sions of PHB, Akt, p-Akt, Bel-2, Bax, and cleaved- easpase3 were determined by Western blot.Results Compared with eontrol group, the eell survival rate of MPP+ group signifieantly deereased.The growth state of the eells beeame significantly worse.Intracellular ROS content inereased, mitoehondrial membrane po tential decreased, apoptosis-related protein expression increased and the apoptotic rate increased.Compared with MPP+ group, MPP+ + ECH group significantly increased cell viability.The growth status of cells was significantly improved.Intracellular ROS content de¬creased, mitochondrial membrane potential increased, apoptosis-related protein expression decreased, and the apoptotic rate decreased significantly.The expression levels of PHB and p-Akt significantly increased.Com¬pared with NC + MPP+ + ECH group, p-Akt level de¬creased and the cell apoptotic rate increased in PHB- RNAi +MPP+ + ECH group.Conclusions Echino- side can reduce MPP + - induced apoptosis of SH-SY5Y cells, which may be realized by upregulating PHB ex¬pression and phosphorylation of Akt to protect mito¬chondrial function.

December of 2019 witnessed the outbreak of new coronavirus pneumonia in Wuhan city and a few localities. As a designated hospital, Tongji Hospital is designated as a hospital for the diagnosis and treatment of numerous patients of such a disease. Based on the medical cloud platform, the hospital has initiated a regional remote diagnosis center; based on its IT system, the hospital to operate its epidemic prevention and management mechanism, set up the self-service system for patients at the fever clinic, launched its online diagnosis and treatment services, and established a hospital epidemic supervision platform. By strengthening the informational support needed for epidemic prevention and control, the hospital has enhanced its efficiency of epidemic prevention and control, reducing the risk of cross-infection, and ensuring data security. Its experiences offer references for informationization support for other regions and hospitals in China.

As a designated hospital, Tongji Hospital shoulders the task of diagnosis and treatment of numerous patients of the disease. Based on the medical cloud platform, the hospital has initiated a regional remote diagnosis center; leveraging its IT system, the hospital initiates its epidemic prevention and management mechanism, sets up a self-service system for patients at the fever clinic, launches its online diagnosis and treatment services, and establishes a hospital epidemic supervision platform. By strengthening the informational support needed for epidemic prevention and control, the hospital has enhanced its efficiency of epidemic prevention and control, reducing the risk of cross-infection, and ensuring data security. Its experiences offer references for informationization support for other regions and hospitals in China.

AIM:To investigate the effects of baicalein on pulmonary arterial hypertension(PAH)induced by monocrotaline(MCT)in rats,and its molecular mechanism was further explored.METHODS: Male SD rats(n=28) were randomly divided into 4 groups: control group, MCT group, MCT+baicalein 50 mg/kg group and MCT +baicalein 100 mg/kg group.The PAH model was established by subcutaneous injection of MCT.After 2 weeks of modeling,the rats in baicalein treatment groups were gavaged baicalein 50 and 100 mg· kg -1· d-1for 14 d,the rats in control group were administered with saline.After 4 weeks of modeling,right ventricular systolic pressure(RVSP),right ventricular hypertro-phy index(RVHI)and right ventricular mass index(RVMI)were detected.Masson staining was used to detect the degree of lung fibrosis.The pathomorphological changes of the pulmonary vessels were observed by HE staining.Western blot was used to detect the expression of α-smooth muscle actin(α-SMA)in the lung tissue and the phosphorylation p 38,ERK and JNK in the artery.RESULTS:Compared with the control group,RVSP, RVHI and RVMI increased significantly in the MCT group(P<0.01).Pulmonary fibrosis and the thickening of pulmonary artery wall were observed.α-SMA was up-regulated and p38,ERK and JNK was activated significantly(P<0.01).Compared with the MCT group,baicalein(50 and 100 mg/kg)significantly decreased the RVSP,RVHI and RVMI(P<0.01).Lung fibrosis was reduced and the vas-cular wall thickening was decreased in baicalein-treated groups.Baicalein(50 and 100 mg/kg)inhibited the phosphoryla-tion of p38,ERK and JNK compared with the MCT group(P<0.01).CONCLUSION:Baicalein ameliorates MCT-in-duced PAH by the inhibition of pulmonary artery wall thickening at least partially via MAPK signaling pathway.