OBJECTIVETo evaluate the influence of major histocompatibility complex class I chain-related gene A (MICA) antibodies on acute rejection (AR) and renal function in early stage after renal transplantation.

METHODSA total of 197 renal transplant candidates admitted in Nanfang Hospital in 2009-2010 were enrolled in this study. MICA antibodies and their specificity were detected in all the patients, and 139 patients were followed up for early acute rejection (AR) and graft function after transplantation.

RESULTSMICA antibodies were positive before transplantation in 45 candidates (22.84%). Eleven specific MICA antibodies were identified, among which the frequency of MICA019 antibody (65.7%) was significantly higher than that of MICA015 (8.6%) and MICA017 (8.6%) (P<0.01). Eighteen patients with positive MICA antibodies were single-specific and 17 were polyspecific (51.4% vs 48.6% ). Of the 139 patients undergoing renal transplantation, 39 developed early AR (28.1%). Of the 45 candidates positive for MICA antibodies, 38 received renal transplantation and early AR occurred in 14 of them (36.8%); 101 of 152 candidates negative for MICA antibodies underwent renal transplantation, and 25 experienced early AR (24.8%).

CONCLUSIONMICA019 antibody is a frequent MICA antibody possibly due to the high frequency MICA019 gene in Chinese population.

Adult ; Antibodies ; immunology ; Antibody Specificity ; Female ; Graft Rejection ; immunology ; Graft Survival ; immunology ; Histocompatibility Antigens Class I ; genetics ; immunology ; Humans ; Kidney Transplantation ; Male ; Middle Aged

Objective:To investigate the clinical characteristics, long-term prognosis and changes of pulmonary function in children with idiopathic pulmonary fibrosis (IPF).Methods:The clinical data, long-term prognosis and changes of pulmonary function of children with IPF admitted to the Department of Pediatric Respiratory Center in Children′s Hospital of Chongqing Medical University from January 2008 to December 2018 were retrospectively analyzed.Results:A total of 28 cases were included, with the median age of 3.9 years (range: 0.5 to 15.7 years). Cough (28 cases, 100.0%), tachypnea (25 cases, 89.3%), cyanosis (19 cases, 67.9%), dyspnea (11 cases, 39.3%), Velcho rales (12 cases, 42.9%), inspiratory three concave sign (11 cases, 39.3%), clubbed fingers and toes (6 cases, 21.4%) and diminished breath sounds (5 cases, 17.9%) were main clinical manifestations.Chest high-resolution computed tomography (HRCT) mainly displayed grid shadow, irregular sac-like light-transparent shadow with ho-neycomb changes and dense shadow, partial (7 cases) pulmonary interstitial emphysema/emphysema/pneumomediastinum.Three cases of lung biopsy showed hyperplasia and consolidation of alveolar space and alveolar septal fibrosis, thickening of alveolar wall and coexistence of new and old lesions.In this group, 4 cases did not receive drug therapy due to other reasons (3 cases abandoned therapy, and 1case died of respiratory and circulatory failure during hospitalization). Twenty-four cases were treated with single or combination of oral Prednisone, N-acetylcysteine and Azithromycin.Eleven cases had improved symptoms when discharged, and 13 cases showed no improvement.Twenty-four cases continued to receive oral medication therapy according to the original protocol.Eight cases were followed up for chest HRCT for 3 months to 4 years, the chest HRCT lesions of 7 cases were similar to before, and those of 1 case increased than before.All cases received telephone follow-up for 2 to 7 years; the maximum duration of medication was 4 years.Twelve cases were lost to follow-up, 7 cases had motion limitation, 3 cases died, and 2 cases had no clinical symptom.Three cases were followed up for pulmonary function for 2 to 3 years, among which 2 cases had pulmonary function decreased than before; 1 case had improvements in forced vital capacity as a percentage of the predicted value and peak expiratory flow as a percentage of the predicted value, but decline in forced expiratory volume in the first se-cond as a percentage of the predicted value.Conclusions:The clinical manifestations of children with IPF are lack of specificity.Chest HRCT is of great value in the diagnosis of IPF and preliminary monitoring of the activity of lesion.In the long-term follow-up, some of cases have improvements in symptoms; pulmonary function mostly decreases, but part of indexes can be improved.

Objective:To explore the clinical characteristics and the therapeutic approach in children with pulmonary embolism(PE).Methods:The clinical data of 8 patients with PE who hospitalized at the Children′s Hospital of Chongqing Medical University from March 2001 to October 2018 were retrospectively analyzed.Results:Among the 8 cases with PE, 3 cases were male and 5 cases were female, the age of subjects ranged from 0.6 to 11.7 years old, the median age was 7.96 years old.All of them had underlying diseases, among them, congenital heart disease with infective endocarditis accounted for 37.5%(3 case). Among the 8 cases, 4 cases presented with symptoms of respiratory tract infection, 7 cases had shortness of breath, 5 cases had cough, 3 cases had chest pain, 2 cases had hemoptysis, and 1 case had typical triad of PE with chest pain, dyspnea and hemoptysis.Among the 8 cases, 7 cases did the arterial blood gas analysis and showed hypoxemia; 6 cases did the D-dimer and the value>500 μg/L; 5 cases did the electroca-rdiogram and 4 cases(80.0%) showed sinus tachycardia, and 2 cases(40.0%) had ST-T changes, all of them did echocardiography and 3 cases(37.5%) of which indicated pulmonary artery excrescence, 7 cases of which did spiral CT pulmonary angiography and 5 cases(71.4%) of them prompted pulmonary vascular filling defects, 6 cases(75.0%) of which were embolized in the lower lobe of the lung.Three cases received anticoagulant therapy, and 1 of them was treated with combined thrombectorny, 1 case of them died.Two cases received thrombectomy, 1 case of them died.Three cases were not treated with thrombectomy and anticoagulation therapy, 2 cases of them died.Conclusions:The mortality of PE in children is high.The clinical manifestations of PE in children are not typical and difficult to distinguish from respiratory infections.For children with high risk factors of PE, once clinical symptoms related to PE occur, D-dimer, echocardiography, and spiral CT pulmonary angiography should be done soon for early diagnosis and treatment.

Objective:To explore clinical features, etiology and mechanism of pulmonary bullae in children.Methods:The clinical data of children with diagnosis or suspected diagnosis of pulmonary bullae, including the general situation, etiology, pathogen composition, number and location, prognosis and so on, in the Inpatient Department of Children′s Hospital of Chongqing Medical University from March 1993 to August 2019 were retrospectively analyzed.Results:Among the 163 patients, there were 130 cases of respiratory tract infection, and 11 cases of pneumothorax alone.Totally, 22 cases were found pulmonary bullae in the chest CT examination without typical symptoms.Etiology: viruses accounted for 19.02%(31/163 cases), with mainly respiratory syncytial virus (9.20%, 15/163 cases); bacterial infection took up 28.83%(47/163 cases), mostly Haemophilus influenzae (13/163 cases, 7.98%) and Staphylococcus aureus (10/163 cases, 6.13%). Pulmonary bullae was more common in the right lung (82 cases). It took 7 days to 9 months for bullae to reduce, shrink or disappear.In some cases, there was no significant change in bullae even after 19 months. Conclusion:Pulmonary bullae can be seen in infection, tumor, auto-immune diseases and so on, most of which are bacterial infections.Bullae may exist for a long time.The mechanism of pulmonary bullae may include the narrowing of lumen, followed by the thickening of bronchial wall, ischemic necrosis and alveolar expansion due to the clogging of distal small vessels or capillaries, the degradation of connective tissue and dissociation of elastic tissue, the destruction of the bronchiolar wall, disturbing ion channels and mitochondria metabolism and destroying the connection of epithelial cells.

At present， major depressive disorder （MDD） is highly prevalent with advanced neurological disorders as the main pathological manifestations. As the physiological function bearer of higher neural activity， gray matter has become the focus of MDD treatment. However， recent research has shown that white matter and gray matter are independent of each other in the central nervous system （CNS）， and their functions are integrated and linked. In addition to gray matter damage， white matter damage is also the core driving event of disease progression and determines the outcome of MDD. At the treatment level， the current drug treatment of MDD mainly focuses on gray matter repair， while ignoring the importance of white matter integrity for the treatment of the disease， which has become the weakness of the current treatment of MDD. Traditional Chinese medicine （TCM） has good application potential in white matter repair. This paper elaborated on the following three aspects. ① The roles of white matter damage in the occurrence and development of MDD were summarized. ② The key link of white matter repair in MDD was elaborated with microglia microenvironment regulation as the entry point. ③ The application value of TCM in white matter repair in MDD was analyzed. This review aims to highlight the importance of white matter integrity in the treatment of MDD and is expected to expand the understanding dimension of the activity of related Chinese medicines in MDD from the perspective of white matter repair and analyze its potential application value.

Tumor metastasis is the major cause of death for tumor patients and the key bottleneck of clinical treatment. In recent years， basic and clinical studies have recognized that tumor microenvironment （TME） is highly correlated with tumor metastasis， which provides hope for anti-metastatic drug development and clinical treatment. At present， the mainstream studies on TME represented by immune checkpoint inhibitors （ICIs） mainly focus on the rectification of immune function of T cells and B cells. However， a large number of studies have shown that the significance of other members of TME for tumor metastasis cannot be ignored， which greatly reflects the progress of anti-metastatic research based on TME regulation. This review focused on tumor metastasis， summarized the mechanism of action of non-T and non-B immune cells ［tumor-associated macrophages （TAMs） and tumor-associated neutrophils （TANs）］ and non-immune members ［vascular endothelial cells （ECs）， tumor-associated fibroblasts （CAFs）， and blood platelet］ in the process of tumor metastasis in TME based on the literature over the recent five years， and explored their key value in the treatment of metastasis. At the treatment level， this review focused on the perspective of the integration of frontier and traditional methods and took the functional homeostasis remodeling of TME as the entry point to summarize the activity and mechanism of traditional Chinese medicine （TCM） regulation of non-T and non-B immune cells and non-immune members and highlight its advantages and characteristics in clinical intervention of metastasis. This review helps to break through the limitations of over-reliance on T and B immune cells in anti-metastatic research， make the research rely on a wider range of cell groups， explore the potential value of TME in anti-metastatic drug intervention， and enrich the idea and strategy of understanding the anti-metastatic pharmacological activity. The review is also expected to provide a broader vision for the research and development of new anti-metastatic drugs.

Demyelination of the central nervous system often occurs in neurodegenerative diseases， such as multiple sclerosis （MS）. The myelin sheath， a layer of myelin membrane wrapping the axon， plays a role in the rapid conduction and metabolic coupling of impulses for neurons. The exposure of the axon will lead to axonal degeneratio， and further neuronal degeneration， which is the main cause of dysfunction and even disability in patients with demyelinating neurodegenerative diseases. In addition to the demyelination of mature myelin sheath， remyelination disorder is also one of the major reasons leading to the development of the diseases. The myelin sheath is composed of oligodendrocytes （OLs） derived from oligodendrocyte progenitor cells （OPCs） which are differentiated from neural stem cells （NSCs）. The process of myelin regeneration， i.e.， remyelination， is the differentiation of NSCs into OLs. Recent studies have shown that this process is regulated by a variety of genes. MicroRNAs， as important regulators of neurodegenerative diseases， form a complex regulatory network in the process of myelin regeneration. This review summarizes the main molecular pathways of myelin regeneration and microRNAs involved in this process and classifies the mechanisms and targets. This review is expected to provide a theoretical reference for the future research on the treatment of demyelinating diseases by targeting the regulation of microRNAs.