Objective Platelet aggregation, activation induced by bubbles is the main cause of decompression sick-ness.Clopidogrel(Clo) can decrease platelet aggregation through inhibiting the bind of fibrinogen and ADP .This study is designed to find if Clopidogrel can paly a protective role in decompression sickness and explore the intervention mechanism . Methods Totally 111 male SD rats divided into 3 groups:normal control group (n=20), decompression sickness(DCS) group(n=46), and DCS+Clo(Clopidogrel)treated decompression sickness (DCS+Clo)group(n=45).The rats in DCS and DCS+Clo group were placed in chamber and compressed to 1.5 MPa at speed of 2t/4 , the time of compression and res-idence was 4.5 min totally, then decompressed to surface at a speed of 3 m/s.The mortality and behavioral of rats were ob-served within 30 min post decompression .The pathology and the wet/dry ratio of lung , WBC and platelet counts in periph-eral blood, the expression of activated platelets , and immunohistochemical detection of lung tissue CD 41 expression were also been tested .Results We found Clo reduces the DCS mortality risk ( mortality rate:11/45 in DCS+Clo group vs 28/46 in DCS group, P<0.01).Clo reduced the lung injury, the wet/dry ratio of lung, the accumulation of platelet and leu-kocyte in lung , the WBC counts and activated platelets in peripheral blood .Conclusion Clo can play a protective role in decompression sickness through reducing post-decompression platelet consumption and activation , decreasing the activation of leukocytes .

Objective To explore the relationship between the expression of LIGHT/HVEM in patients after allo-HSCT and the development of GVHD. Methods The expression of LIGHT and HVEM in T lymphocytes was detected by FACS Calibur. Results All patients achieved engraftment and hematopoiesis reconstitution, aGVHD occurred in 9 of 26 patients (34.6%) with grade Ⅲ-Ⅳ aGVHD in 3 cases. Seven cases developed cGVHD (26.9%). LIGHT was not expressed in T lymphocytes from healthy donors and patients without GVHD, while constitutive expression of HVEM was detected. When aGVHD occurred, the expression levels of LIGHT in T lymphocytes were significantly increased, while those of HVEM decreased. After GVHD was controlled, the expression levels of those co-stimulators went back to normal On the day 15 after transplantation, the expression of LIGHT in T lymphocytes of patients with aGVHD later was significantly higher, while that of HVEM lower than in those without aGVHD. The patients with aGVHD of grades Ⅲ-Ⅳ demonstrated higher LIGHT expression than in those with aGVHD of grades Ⅰ-Ⅱ. Conclusion The expression of LIGHT and HVEM might be involved in the development of GVHD after allo-HSCT and could be used as one of the useful indicators in predicting aGVHD.

Objective To explore the relation between vitamin D deficiency and susceptibility to spinal tuberculosis. Methods A total of 163 hospitalized patients with untreated spinal tuberculosis in Tianjin Haihe hospital were enrolled in this study from June 2013 to May 2016. A total of 170 individuals participated in health examination program at the same period were enrolled as the control group. The serum level of 25-hydroxyvitamin D [25(OH)D] was measured by enzyme linked immunosorbent assay. The 25(OH)D grading included serious deficiency group (<25 nmol/L), deficiency group (≥25 nmol/L and <50 nmol/L), insufficiency group (≥50 nmol/L and <75 nmol/L) and sufficiency group (≥75 nmol/L). Histopathological classification was confirmed by intraoperative findings. Results The serum level of 25(OH)D was significantly lower in patient group [23.99(20.55,29.54)nmol/L] than that of control group [42.94(35.68,51.04) nmol/L] (P<0.01), and which was also significantly lower in four seasons than that of controls (P<0.05). The serum levels of 25(OH)D were significantly higher in summer group than those of winter group in both patient and control groups (P<0.008 3). The proportion of patients with serious deficiency of 25(OH)D was significantly higher in spring and winter groups in patient group, which was significantly lower in summer group (P<0.01). There was no significant difference in patients with serious deficiency of 25(OH)D between four seasons (P<0.01). For control group, there was a higher proportion of cases with deficiency of 25(OH)D in four seasons, and there was no significant difference in the distribution of seasons (P>0.05). In patient group, there were 107 cases of caseous necrosis type, 56 cases of hyperplasia type, and the proportion of caseous necrosis type was significantly higher in the severe deficiency group (79.17%, 76/96) than that of deficiency group (46.27%, 31/67, P<0.01). Conclusion Excluding the effect of season, vitamin D deficiency is associated with susceptibility to spinal tuberculosis and histopathologic classification.

Objective To investigate the effect of N-acetylcysteine ( NAC) on lung and heart injury of rats with a fast floating escape induced decompression sickness .Methods Eighty male Sprague-Dawley rats were randomly and evenly divided into four groups:control group and three NAC prevention groups .The NAC groups were treated with different doses of NAC(250, 500 or 1000 mg/kg)by intraperitoneal injection 1 h before entrance.In the control group, rats were given an equal volume of saline1h before entrance.The air was pressurized at the 2t/7 exponential rate to 1.5 MPa which was maintained for 4 min and then uniformly decompressed to atmospheric pressure .The extravehicular survival and pathological changes in the lung and heart tissue were detected 0.5 h after rat egress.Results The survival rate of rats treated with NAC 500 mg/kg(90%) was significantly higher than that of those treated with saline (65%)alone (P<0.05).There was large break and fusion in the structure of pulmonary alveolus of control group besides obvious erythrocyte exudation , cardiac muscle fibers edema ,and obvious denaturation and break .Conclusion NAC can play a protective role in rats with a fast floating escape induced decompression sickness by mitigating the injury to and inflammation of lung and heart tissue .

Objective To investigate the intervention of chemokine receptor 4(CXCR4) antagonist AMD3100 in lung tissues of rats during pulmonary oxygen intoxication.Methods Forty SD rats were randomly divided into 4 groups:normal pressure air PBS group, normal pressure air antagonist group , oxygen exposure PBS group and oxygen exposure antagonist group, each consisting of 10 animals.The last two groups were compressed to 0.23 MPa at an exponential rate of 0.1 MPa/min by pure oxygen.Pathological changes of lung tissues were observed by hematoxylin eosin stain.Changes in TNF-αand IL-1βexpression levels in the lung tissues of rats were detected by ELISA.Changes in CXCR4 expression levels were ob-served by Western blotting.Results Pathological examination indicated that edema and hemorrhage in the alveolar and pulmonary interstitial tissue of oxygen exposure antagonist group were lighter than in oxygen exposure PBS group.The levels of TNF-α, IL-1βand cleaved-caspase-3 in the lung tissues of the oxygen exposure antagonist group were lower than in oxy-gen exposure PBS group.Conclusion Blocking CXCR4 with AMD3100 can effectively alleviate lung injury during pulmo-nary oxygen intoxication.

Objective To study the expression levels of microRNA (miR)-16 and miR-146a in rat lungs of decompres-sion sickness (DCS) caused by fast buoyancy ascent escape or diving .Methods At 0.5 h after fast buoyancy ascent es-cape or diving, the pathological changes in rat lungs and expression levels of miR-16,and miR-146a were detected by re-verse transcription-quantitive polymerase chain reaction and compared with normal control group .Results The pathological characteristics of lungs in two DCS groups were tissue damage .At 0.5 h after DCS caused by fast buoyancy ascent escape , the lung tissue expression levels of miR-16 and miR-146a did not significantly change compared with normal control and diving DCS groups ,but the rat lung tissue expression level of miR-146 a in diving DCS group was obviously increased , com-pared with normal control group .Conclusion miR-146a may play a role in post-transcriptional regulation in the process of diving DCS .

Objective To study the pathological changes of lung tissues during fast floating escape-induced decompres-sion sickness.Methods Eighty male SD rats were randomly divided into 2 groups, 60 in fast floating escape group (escape group) , and 20 in control group .Rats in the control group were only put in a cabin under the same atmospheric pressure (ATM).Rats in escape group were pressurized to 1.5 MPa by pressure air at the 2t/7 exponential rate and stayed for 4 min till decompression.Then the rats′survival rate was observed after 0.5 h, lung tissue specimens were collected from each rat, the pathological score was taken , according to the degree of lung injury and the R language was used for statistical analysis.Results The mortality rate was 50%.Lung tissues of these rats were pathologically characterized by stromal lung thickening, edema, and hyperemia.Kruskal non-parametric test analysis found a significant difference (P=0.0016) between the two groups .Nemenyi test was used in pairwise comparison .The death and survival animals in escape group compared with the control group, the scores were significantly different (P<0.05).The scores had no significant difference between the deach and survival animal in escape group .Conclusion Decompression sickness caused by fast floating es-cape can significantly damage the blood-lung barrier to cause pulmonary edema .

Objective To study the effect of nicardipine on fast floating escape induced lung injury in animal models with decompression sickness .Methods Sixty male SD rats were randomly and evenly divided into three groups:blank control, control and nicardipine groups .The nicardipine group was given nicardipine 50 mg/kg orally 0.5 h before entrance.In the control group, rats were given an equal volume of saline 0.5 h before entrance.The blank control group only stayed in the vehicle without any pressurized procedure .The air was pressurized at the 2t/7 exponential rate to 1.5 Mpa which was maintained for 4 min, and then uniformly decompressed to atmospheric pressure .The extravehicular survival and lung pathology were observed in rats after 0.5 h, IL1-βand TNF-αexpression levels were detected by ELISA , and the Caspase 3 expression in lung tissue was detected by Western blot .Results The incidence and mortality rate were 80%and 50%respectively in control group ,and 100%and 80%in the experimental group .The surviving animals in the two groups suffered from alveolar and interstitial lung hemorrhage , with widened interstitial lung .IL1-βin the experimental group was significantly higher than in the normal control group , while TNF-αhad no significant change .After nicardipine treatment pro-caspase 3 did not change significantly , but cleaved-caspase 3 increased significantly .Conclusion Nicardipine can aggravate lung injury caused by fast floating escape-induced decompression sickness if used before decompression.

Objective To investigate the effect of PPAR-δ on the lung injury of rats induced by hyperbaric oxygen (HBO2) exposure.Methods Sixty male Sprague-Dawley rats were randomly divided into six groups:air+vehicle, air+GW0742, and air+GSK0660, HBO2 +vehicle, HBO2 +GW0742, HBO2 +GSK0660.Lung injury was induced in rats by HBO2exposure (2.3 ATA, 100%O2, 8 h).Rats were injected with vehicle[10%DMSO in 0.3 ml NaCl 0.9%(v/v)] or GW0742 (0.3 mg/kg, ip) or GSK0660 (1 mg/kg, ip) at 1, 6 and 12 hours before either air or oxygen exposure .Protein levels in the bronchoalveolar lavage fluid ( BALF) , wet/dry ratio of the lung and the pathological changes in the lung tissue were detected 30 min after rats′egress.Results and Conclusion For the HBO2 +GW0742 group, the protein levels in BALF, the wet/dry ratio of the lung and the pathological changes in lung tissues all significantly decreased compared with those of the air group .These changes in HBO 2 +GSK0660 group tended to increase the level of lung injury .PPAR-δhas a protective effect on pulmonary oxygen toxicity induced by HBO 2 .

OBJECTIVETo study the severe acute respiratory syndrome (SARS)-associated coronavirus genotype and its characteristics.

METHODSA SARS-associated coronavirus isolate named ZJ01 was obtained from throat swab samples taken from a patient in Hangzhou, Zhejing province. The complete genome sequence of ZJ01 consisted of 29,715 bp (GenBank accession: AY297028, version: gi: 30910859). Seventeen SARS-associated coronavirus genome sequences in GenBank were compared to analyze the common sequence variations and the probability of co-occurrence of multiple polymorphisms or mutations. Phylogenetic analysis of those sequences was done.

RESULTSBy bioinformatics processing and analysis, the 5 loci nucleotides at ZJ01 genome were found being T, T, G, T and T, respectively. Compared with other SARS-associated coronavirus genomes in the GenBank database, an A/G mutation was detected besides the other 4 mutation loci (C:G:C:C/T:T:T:T) involved in this genetic signature. Therefore a new definition was put forward according to the 5 mutation loci. SARS-associated coronavirus strains would be grouped into two genotypes (C:G:A:C:C/T:T:G:T:T), and abbreviated as SARS coronavirus C genotype and T genotype. On the basis of this new definition, the ZJ01 isolate belongs to SARS-associated coronavirus T genotype, first discovered and reported in mainland China. Phylogenetic analysis of the spike protein gene fragments of these SARS-associated coronavirus strains showed that the GZ01 isolate was phylogenetically distinct from other isolates, and compared with groups F1 and F2 of the T genotype, the isolates of BJ01 and CUHK-W1 were more closely related to the GZ01 isolate. It was interesting to find that two (A/G and C/T) of the five mutation loci occurred in the spike protein gene, which caused changes of Asp to Gly and Thr to Ile in the protein, respectively.

CONCLUSIONAttention should be paid to whether these genotype and mutation patterns are related to the virus's biological activities,epidemic characteristics and host clinical symptoms.