Objective To investigate the expression of aquaporin-4 (AQP4) in cultured astrocytes after in vitro hypoxia induced by CoCl2. Methods After primary culture and subculture, the astrocytes were placed in a controlled atmosphere culture chamber. Both control group and hypoxia groups were established.These groups were further divided into seven sub-groups according to the different time intervals: 15, 30minutes and 1,2, 4, 6, 12 hours, respectively (6 apertures for each group). The shape of the astrocytes in each group was observed with light microscopy and transmission electron microscopy ( TEM ). All groups were examined using in situ hybridization, real time fluorescence quantitative reverse transcriptase polymerase chain reaction, immunocytochemistry and Western blot. The data was analyzed statistically with SPSS 13.0 software. Results There was significant consistency between the AQP4 mRNA and protein ( r =0. 85, P ＜0. 01 ). There was slight positive expression of AQP4 in a few astrocytes of the control groups. In the hypoxia groups, the expression of AQP4 increased within 15 minutes; the increase was most prominent between 1 and 4 hours( mRNA in hypoxia groups: 0. 26 ± 0. 04, 0. 31 ± 0. 02, 0. 36 ± 0. 04; control groups:0. 06 ±0. 01,0. 09 ±0. 01,0. 08 ±0. 01 )after hypoxia and became less between 6 and 12 hours; There was significant difference in the AQP4 expression between the hypoxia groups and control groups among different time points (t = 16. 51, 18.20, 15.26,all P＜0. 01 ). The corresponding pathological changes were cellular edema, which was most prominent between 1 and 4 hours. Under TEM, increase in size of the nucleolus and swelling of endoplasmic reticulum and mitochondria; these changes became more marked with time.Disruption of a few astrocytes was detected in the hypoxia groups at 12 hours. Conclusions The pathological change of astrocytes is cellular edema following hypoxia. There is a positive relationship between the presence and degree of cellular edema as well as the duration of hypoxia and the up-regulating of AQP4.These results imply that AQP4 expression is an important molecular mechanism of celluar edema of astrocytes.

Objective To investigate the significance of serum krebs Yon den lungen-6(KL-6), surfactant protein A(SP-A), surfactant protein D(SP-D )and matrix metalloprotease 7(MMP-7) in the diagnosis of idiopathic pul-monary fibrosis (IPF) and its relationship with pulmonary function .Methods Serum levels of KL-6, SP-D, SP-A and MMP-7 were detected by ELISA in 38 patients with IPF and serum from 38 patients with pneumonia and 38 normal controls.Serum levels of markers were further analyzed by operating characteristic curve receiver (ROC), from which the ideal level of each serum marker was obtained , and the follow-up of 6 months in patients with IPF . Explore the significance of the diagnosis of IPF and its correlation with pulmonary function .Results The expres-sion of MMP-7, SP-A, SP-D and KL-6 in serum of IPF patients was higher than that in the control group and healthy control group ( P<0.05) .The optimal cutoff value of KL-6 was 723.0 U/ml, SP-A was 67.2 ng/ml, SP-D was 98.1 ng/ml, and MMP-7 was 10.1 ng/ml.The sensitivity of KL-6 was 71.1% and 98.7%, SP-A was 81.6%and 97.4%, SP-D was 81.6%and 97.4%, MMP-7 was 68.4%and 98.7%.The sensitivity of combined KL-6, SP-A, SP-D and MMP-7 four serum markers was 100%, compared with a single serum index , the P value was less than 0.05, with statistical significance .IPF patients serum SP-A, MMP-7 and forced vital capacity within 6 months were significantly correlated(r1 =-0.574,P1 <0.001;r2 =-0.465,P2 =0.003).Conclusion KL-6, SP-A, SP-D and MMP-7 were highly expressed in serum of patients with IPF , and in the diagnosis of IPF , com-bined detection of 4 serum markers can improve the early diagnosis of IPF patients .Combined serum SP-A and MMP-7 levels can improve the accuracy of the IPF patients with pulmonary function changes , the prediction of dis-ease progression has a certain significance .

AlM:To investigate the features on prolonged central serous chorioretinopathy ( CSCR ) by optical coherent tomography ( OCT ) and to provide the basis of deciding the pathogenetic condition and prognosis. METHODS: Eighty - five patients who had been diagnosed with CSCR were grouped by suffering time as below: 32 patients suffered longer than 6mo as the prolonged and 53 patients with CSCR cured within that time. The imaging features of OCT were compared between the above groups.RESULTS:The incidence rate of neuroepithelial serous detachment extent above 500μm associated with pigmentary epithelial detachment in suffering eye and pigmentary epithelial damage in contralateral eye was significantly different between two groups. However, the incidence rate of neuroepithelial serous detachment extent above 4 000μm was not significant difference.CONCLUSlON:OCT could display clearly the change of every layer of retina with simplicity and visibility, which supplies us a new horizon to diagnose and trace CSCR. We could decide the pathogenetic condition and prognosis in accordance with the features of OCT, to provide references for the diagnosis and treatment of CSCR.

Background The pathogenesis of primary open angle glaucoma(POAG) and high myopia are very complex.To construct the regulatory network of virulence genes and relevant genes that involved in pathogenicity are helpful for reveal of the pathogenesis.Objective The aim of this study was to investigate myocilin(Myoc),a gene that contributes to POAG and high myopia in eyes of BXD Recombinant Inbred(BXD RI)mice and construct the regulatory network of Myoc.Methods The affymetrix microarray system was used to detect the differential expression of Myoc in the eyes of C57BL/6J(B6),DBA/2J(D2) and BXD RI mice.Expression quantitative trait loci (eQTL) mapping was performed to construct the regulatory network of Myoc gene.Results The average expression level of the Myoc gene in the BXD strains was 10.83,and the gene exhibited expression levels ranging from 8.39 in BXD55 mice tol 1.43 in B6 mice.The eQTL mapping for the Myoc gene showed a significant likelihood ratio statistic (LRS) of 21.78.The QTL was mapped in chromosome 2,and Myoc was located on chromosome 1,indicating that the Myoc gene was a trans-acting QTL.Olfml2a was identified to be a candidate upstream gene of Myoc by analysis of bioinformatics.Genetic regulatory network analysis demonstrated that a series of genes associated with Myoc probably played roles in the pathogenesis and development of POAG and high myopia.Conclusions The genetical genomics approach provides a powerful tool for constructing pathways that contribute to complex traits,such as POAG and high myopia.

Child ; Community-Acquired Infections ; epidemiology ; Humans ; Pneumonia ; epidemiology

Adult ; Cryptococcosis ; Cryptococcus neoformans ; Humans ; Lung Diseases, Fungal ; Male

Objective To investigate the expression of aquaporins 4 (AQP4) and histopathological changes in early phase of traumatic brain edema and the correlation between AQP4 expression and structural damage to blood-brain barrier (BBB).Methods A total of 120 healthy adult Wistar rats were divided into sham operation group and brain trauma group (which was subgrouped at hours 1,3,6,12 and 24 postinjury) according to random number table,with 20 rats per group.At each time point,brain water content was measured; brain edema and BBB structural changes were observed pathologically;IgG and AQP4 expressions in traumatic brain tissues were detected with immunohistochemical method and Western-blotting.Results In sham operation group,negatively stained IgG was observed and there were no abnormalities in brain tissue structure,brain water content as well as AQP4 expression.In brain trauma group,cerebral water content presented notable increase at 6 hours postinjury and peaked at 24hours; IgG expression showed significant increase at 1 hour postinjury,peaked at 6 hours postinjury and remained a high level at 24 hours.Pathologic observation revealed damage to BBB,blood red cells leaking out of the blood vessels,and tissue gap widening at 1 hour postinjury,which manifested as vasogenic brain edema.Further,those phenomena were gradually aggravated over time and became obvious at 6 hours postinjury.Intracellular edema occurred at 3 hours postinjury,with the presence of increased glial cell body,cytoplasm light staining or vacuolar degeneration,as well as mitochondria swelling and was also aggravated with time,particularly at 6 hours postinjury.Except that the previously mentioned two forms of edema coexisted at 12 hours postinjury,tissue necrosis,inflammatory cell infiltration and microglia proliferation were emerged and aggravated at 24 hours postinjury.AQP4 level decreased at 1 hour,minimized at 6 hours and regained at 12 hours,showing a V-shape curve.Conclusions Vasogenic edema characterized by BBB disruption is the primary histopathological change in early-phase of brain trauma,followed by the coexistence with intracellular edema and aggravation of the two forms of edema over time.AQP4 expression is down-regulated in the vasogenic edema phase but highly expressed at phase of the intracellular edema.

Objective To investigate the effect of intralesional lauromacrogol therapy on infantile hemangioma.Methods 30 cases all received intralesional injection of lauromacrogol.The changes of tumor size,texture and color were monitored and recorded.The adverse effects after medication were observed and managed accordingly.The adverse effects after medication were observed.The times of treatment were determined according to degree of reduction of tumor volume.To assess the efficacy,a 4 scales system was adopted.Results All patients had completed the treatment and followup.The overall response was scale Ⅰ in 2 cases (6.7 ％),scale Ⅱ efficacy in 4 patients (13.3 ％),scale Ⅲ efficacy in 5 cases (16.7 ％) and scale Ⅳ in 19 cases (63.3 ％).The smaller the tumor,the fewer the times of treatment,and the better the results.The effects of treatment were better if patient could be treated by intralesional lauromacrogol therapy in early stage.No severe adverse effects were observed during 6 months of follow-up.Conclusions Intralesional injection of lauromacrogol sclerotherapy is a safe and effective way to treat infantile hemangioma.

Histone deacetylases (HDACs) inhibition causes hyperacetylation of histones leading to growth arrest, differentiation and apoptosis of tumor cells, representing a new strategy in cancer therapy. Many of previously reported HDACs inhibitors are hydroxamic acid derivatives, which could chelate the zinc ion in the active site in a bidentate fashion. However, hydroxamic acids occasionally have produced problems such as poor pharmacokinetics, severe toxicity and low selectivity. Herein we describe the identification of a new series of non-hydroxamate HDACs inhibitors bearing diketo ester moieties as zinc binding group. HDACs inhibition assay and antiproliferation assays in vitro against multiple cancer cell lines were used for evaluation. These compounds displayed low antiproliferative activity against solid tumor cells, while good antiproliferative activity against human leukemic monocyte lymphoma cell line U937. Compound CPUYS707 is the best with GI50 value of 0.31 micromol x L(-1) against U937 cells, which is more potent than SAHA and MS-275. HDACs inhibition activity of these compounds is lower than that expected, further evaluation is needed.

Objective To investigate the effect of bifidobacteria on dextran sulphate sodium(DSS)- induced acute ulcerative colitis in mice.Methods Thirty BALB/C mice were randomly divided into nor- mal control group (n=10),0501 strain group (n=10) and c122 strain group (n=10).Fifty BALB/ C mice received 5% dextran sulphate sodium(DSS) for 7 days to induce ulcerative colitis.The mice were then divided to model group,negative control group(perfused with 0.9 NaCl solution ),positive control group(perfused with SASP of 20 mg/ml),DSS + 0501 strain group(perfused with 1?10~9 CFU/ml bifidobacteria 0501 strain solution and DSS + c122 strain group (perfused with 1?10~9 CFU/ml bifidobacteria c122 strain solution).All mice were sacrificed 9 days later.The colon specimens were measure by histoehemical staining with H-E.The expressions of interleukin-10 (IL-10) and its protein were detected by RT-PCR and immunohistochemistry respectively.Results The degree of colon inflam- mation in mice both in DSS+ 0501 strain and DSS+ c122 strain groups were aggravated and expressions of IL-10 mRNA and protein were reduced compared to model group.No colon inflammation was found in 0501 strain and c122 strain groups.Conclusion Some strain of bifidobaeteria may aggravate colon in- flammation in mice when mucosal harrier is destroyed.