The common complication of ischemic brain injury was ischemic brain edema,which was closely related to the function of the blood-brain barrier (BBB).In vitro studies,which have shown that vascular endothelial growth factor (VEGF) could bind to the receptor to activate a variety of cell signaling pathways,by inhibiting cell apoptosis,reduce oxidative stress and play a protective role in the brain.Fulong Antithrombotic Pill,Shenfu Injection,Naotaitong Granule and others traditional Chinese medicine can regulate the treatment of BBB injury by VEGF regulation.This article reviewde the study progress of VEGF and its related pathways in ischemic brain injury,and the treatment of BBB injury by Chinese medicine by interventional VEGF and its related pathways,which provide a theoretical basis for the clinical treatment of cerebral ischemic abnormalities and the development of new drugs.

OBJECTIVE: To investigate the epidemiological features in patients with allergic rhinitis (AR) in Yichang city, and put forward effective prevention and control measures. METHOD: Collecting the data of allergic rhinitis in city proper from 2010 to 2013, input the data into the database and used statistical analysis. RESULT: In recent years, the AR patients in this area increased year by year. The spring and the winter were the peak season of onset. The patients was constituted by young men. There was statistically significant difference between the age, the area,and the gender (P < 0.01). The history of allergy and the diseases related to the gender composition had statistical significance difference (P < 0.05). The allergens and the positive degree in gender, age structure had statistically significant difference (P < 0.01). CONCLUSION Need to conduct the healthy propaganda and education, optimizing the environment, change the bad habits, timely medical treatment, standard treatment.
Allergens ; China ; epidemiology ; Female ; Humans ; Male ; Rhinitis, Allergic ; epidemiology ; Seasons

This paper analyzed and concluded successful experience and mechanisms of regional global per capita budget implemented since 2015 in Anhui province,including the formation of mutual incentive and restraint mechanism, the mechanism of controlling expenses spontaneously and resource allocation efficiently.After the reform, flow of hospitalized patients was more rational, and the financial burden of patients was alleviated, while the capacity of medical institutions was improved notably in pilot counties.The successful experience of Anhui province can put forward corresponding suggestions to guide the future work in other areas.

Objective To evaluate the effects of quantifying food thickness on reducing aspiration in stroke patients with dysphagia.Methods A total of 76 stroke patients with grade 2 to grade 3 dysphagia hospitalized in department of neurology from March to August,2017,screened by Kubota's drinking water test was recruited and divided randomly into the experimental group(n=38) and the control group(n=38).The patients in the experimental group were treated with conventional dietary nursing and dietary guidance according to the results of quantifying food thickness via thickening agent.The patients in the control group were treated with conventional dietary nursing.Results There were 8 cases (21.05％) occurring aspiration in the experimental group,and there were 28 cases (73.68％) in the control group,and the difference was statistically significant (P＜0.01).Conclusion Quantification of food thickness using thickening agent can effectively reduce the rates of aspiration in stroke patients with dysphagia.

Objective: To evaluate the effect of dexmedetomidine on mitochondrial dynamics in mice with endotoxin-induced acute lung injury (ALI). Methods: Thirty clean-grade healthy adult male C57BL/6 mice, weighing 20-25 g, aged 2 months, were divided into 3 groups (n=10 each) using a random number table method: control group (group C), endotoxin-induced ALI group (group LPS) and endotoxin-induced ALI plus dexmedetomidine group (group LPS+ DEX). In LPS and LPS+ DEX groups, lipopolysaccharide (LPS) 10 mg/kg was injected via the caudal vein to establish the model of endotoxin-induced ALI.In group LPS+ DEX, dexmedetomidine 50 μg/kg was intraperitoneally injected at 30 min before injection of LPS, while the equal volume of normal saline was given instead in C and LPS groups.The mice were sacrificed at 6 h after LPS administration, and lung tissues were obtained for examination of the pathological changes (with a light microscope) which were scored and for determination of the level of reactive oxygen species (ROS) and expression of mitochondrial fusion proteins mitofusin 1 (Mfn1), Mfn2, optic atrophy 1 (OPA1), dynamin-related protein 1 (Drp1) and fission protein 1 (Fis1)(using Western blot). Results: Compared with group C, the lung injury scores and ROS level in lung tissues were significantly increased, the expression of Mfn1, Mfn2 and OPA1 was down-regulated, and the expression of Drp1 and Fis1 was up-regulated in LPS and LPS+ DEX groups (P<0.05). Compared with group LPS, the lung injury scores and ROS level in lung tissues were significantly decreased, the expression of Mfn1, Mfn2 and OPA1 was up-regulated, and the expression of Drp1 and Fis1 was down-regulated in group LPS+ DEX (P<0.05). Conclusion Dexmedetomidine can reduce endotoxin-induced ALI through maintaining the mitochondrial fusion-fission balance in mice.

Objective:The degree of involvement of extraocular muscles varies across different regions of retrobulbar tissue in patients with thyroid eye disease, but the mechanism is unclear. This study aims to explore the relationship between differential expression of thyroid-stimulating hormone receptor(TSHR) in different parts of the extraocular muscles and the varying degrees of muscle involvement.Methods:The medial, lateral, superior, and inferior rectus muscle were separated from the retrobulbar tissue of rats, and the expression level of TSHR in four extraocular muscles was detected by immunofluorescence and qPCR. Extraocular muscle tissue of patients with strabismus was collected to detect the expression of TSHR and the cell types expressed by fluorescence.Results:The results of qPCR showed that the expression of TSHR in the medial rectus muscle was significantly higher than that in the lateral, superior, and inferior rectus muscle(medial rectus vs lateral rectus, P=0.012; medial rectus vs superior rectus, P=0.015; medial rectus vs inferior rectus, P=0.013), but there was no difference in insulin-like growth factor 1(IGF-1R) expression. Immunofluorescence showed that TSHR was co-expressed with PAX7, a molecular marker of muscle satellite cells, and the expression level in the medial rectus muscle of rats and humans was significantly higher than those in the other three extraocular muscles. Conclusion:The high specific expression of TSHR in the satellite cells of the medial rectus muscle may be the reason why the medial rectus muscle is most susceptible to involvement in thyroid eye disease.

Objective To screen out the cytokines relating to cardiac insufficiency caused by au-toantibodies against the second extracellular loop of the β1-adrenoceptor(β1-AA) using cytokine chip tech-nique, and to analyze the changes in signaling pathways. Methods Blood samples were collected from 67 patients with coronary artery disease(CAD) and 42 healthy subjects. ELISA was performed to detect β1-AA in plasma. BALB/c mice were passively immunized with the monoclonal antibodies against β1-AA (β1-AA mAb). Dynamic changes in mouse cardiac structure and functions were detected by heart ultrasound. Hema-toxylin and eosin (HE) and Masson staining were used to observe morphological changes in heart tissues.Cytokine chip technique was used to screen out the cytokines causing myocardial injury. Gene Ontology (GO) and KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway enrichment analysis were used to classify the differentially expressed cytokines. Results Patients with CAD showed increased titer and posi-tive rate of β1-AA as compared with healthy subjects(P<0.001). The mouse model of heart injury was in-duced by β1-AA at the 8th week after immunization. A total of 37 differentially expressed cytokines were found in the model group,of which 11 cytokines were up-regulated and 26 cytokines were down-regulate as compared with those in the mouse control group. The level of CXCL16 was significantly increased in β1-AA-positive mice. GO analysis showed that CXCL16 was mainly involved in life processes including the positive regulation of cell death, migration, locomotion and cellular component movement. KEGG pathway enrich-ment analysis showed CXCL16 was significantly enriched in the pathway of cytokine-cytokine receptor inter-action and chemokine signaling pathway. ELISA showed that compared with β1-AA-negative patients, CXCL16 level was significantly increased in β1-AA-positive patients (P<0.01). A positive correlation was found between β1-AA and CXCL16 (P<0.01,r=0.43). Conclusion CXCL16 may play a critical role in the development of cardiac insufficiency induced by β1-AA.

Objective To evaluate the role of endogenous heme oxygenase-1/carbon monoxide ( HO-1/CO) signaling pathway in endoplasmic reticulum stress during endotoxin-induced acute lung injury ( ALI) in rats. Methods Forty healthy clean-grade male Sprague-Dawley rats, aged 8 weeks, weighing 190-210 g, were divided into 4 groups ( n=10 each) using a random number table method: control group (group C), ALI group, ALI plus ZnPP-IX group (group AZ), and ALI plus vehicle sodium bicarbonate group ( group AV) . ALI was induced by intravenously injecting lipopolysaccharide 5 mg/kg in anesthetized rats. At 30 min before establishing the model, ZnPP-IX 10μmol/kg (diluted to 1 ml in 50 mmol/L sodium bicarbonate) was intraperitoneally injected in group AZ, and 50 mmol/L sodium bicarbonate 1 ml was intra-peritoneally injected in group AV. After injecting lipopolysaccharide for 6 h, blood samples were collected from the common carotid artery for determination of plasma CO concentration, the rats were then sacrificed, and lungs were removed for microscopic examination of the pathological changes which were scored and for determination of CO level, wet to dry weight ratio ( W/D ratio) , cell apoptosis ( by TUNEL) , and expres-sion of heme oxygenase-1 ( HO-1) , glucose-regulated protein 78 ( GRP78) , phosphorylated protein kinase R-like endoplasmie reticulum kinase (p-PERK), phosphorylated eukaryotic translation initiation factor 2 alpha ( p-elF2 ) , CCAAT/enhancer-binding protein homologous protein ( CHOP ) and caspase-12 in lung tissues ( by Western blot) . Apoptosis index ( AI) was calculated. Results Compared with group C, the lung injury scores, W/D ratio, AI and CO levels in plasma and lung tissues were significantly increased, and the expression of HO-1, GRP78, p-PERK, p-elF2, CHOP and caspase-12 was up-regulated in the other three groups ( P＜0. 05) . Compared with group ALI, lung injury scores, W/D ratio and AI were sig-nificantly increased, CO levels in plasma and lung tissues were decreased, the expression of HO-1 was down-regulated, and the expression of GRP78, p-PERK, p-elF2, CHOP and caspase-12 was up-regula-ted in group AZ (P＜0. 05), and no significant change was found in the parameters mentioned above in group AV ( P＞0. 05) . Conclusion HO-1/CO signaling pathway produces endogenous protection possibly through inhibiting endoplasmic reticulum stress during endotoxin-induced ALI in rats.

Objective To evaluate the endotoxin-induced endogenous protective mechanism of alveolar type Ⅱ epithelial cells of rats and the relationship with p38 mitogen-activated protein kinase (p38MAPK)-HO-1-mitochondrial fusion signaling pathway.Methods Rat alveolar type Ⅱ epithelial cells were seeded in 6-well plates at a density of 2× 105 cells/ml and divided into 5 groups (n =15 each) using a random number table method:control group (group C),lipopolysaccharide (LPS) group (group L),LPS plus p38MAPK inhibitor SB203580 group (group LS),LPS plus dimethyl sulfoxide group (group LD),and SB203580 group (group S).Cells were conventionally cultured in group C.The model of endotoxin-challenged alveolar type Ⅱ epithelial cells was established by giving LPS 10 μg/ml in L,LS and LD groups.SB203580 10 μmol and 0.1％ dimethyl sulfoxide 100 μμmol were added at 1 h before giving LPS in group LS and group LD,respectively.SB203580 10 μ mol was added to the culture medium in group S.All the cells were incubated for 24 h.The malonaldehyde (MDA) content and superoxide dismutase (SOD) activity in the culture medium were determined by thiobarbituric acid assay and xanthine oxidase method,respectively.The expression of p38MAPK,phosphorylated p38MAPK (p-p38MAPK),hemeoxygenase-1 (HO-1),mitofusin 1 (Mfn1),Mfn2,and optical atrophy-1 (OPA1) was measured by Western blot.Results Compared with group C,the MDA content was significantly increased,the SOD activity was decreased,and the expression of p-p38MAPK and HO-1 was up-regulated,and the expression of Mfn1,Mfn2 and OPA1 was down-regulated in L,LS and LD groups (P＜0.05).Compared with group L,the MDA content was significantly increased,the SOD activity was decreased,and the expression of pp38MAPK,HO-1,Mfn1,Mfn2 and OPA1 was down-regulated in group LS (P＜0.05),and no significant change was found in the indices mentioned above in group LD (P＞0.05).Conclusion The endotoxin-induced endogenous protective mechanism of alveolar type Ⅱ epithelial cells is related to p38MAPK-HO-1-mitochondrial fusion signaling pathway in rats.

Myeloid sarcoma (MS) is a tumor mass formed by the proliferation of one or more myeloid primitive cells outside the marrow, which is mostly related to acute myeloid leukemia (AML). It is reported that 2.5% to 9.1% of AML patients have MS, and AML with spinal canal MS is very rare. Spinal canal MS often has an acute onset and is difficult to diagnose. It is easy to cause missed diagnosis and misdiagnosis, which will lead to a delay in accurate diagnosis seriously affecting the treatment and quality of life among these patients. The clinical data, diagnosis and treatment process of a case of MS with multiple space occupying lesions in the spinal canal diagnosed and treated by the Department of Hematology of Peking Union Medical College Hospital are reported, in order to provide reference for clinical workers.