Objective To understand the prevalence situation of common respiratory tract pathogens in Shihezi area to provide reliable basis for clinical diagnosis and treatment Methods The serum samples from the inpatients with acute respiratory tract in‐fection in the First Affiliated Hospital of Medical College of Shihezi University from January to June 2014 were collected and detec‐ted 9 kinds of common pathogens by using the indirect immuno‐fluorescence assay .Results Among 810 serum samples ,the IgM antibody positive detection rate was 32 .35% ,the detection rates of various pathogens from high to low were Mycoplasma pneumon‐iae(MP ,21 .48% ) ,Q fever rickettsia (COX ,8 .8% ) ,legionella pneumophila(LP1 ,5 .18% ) ,Chlamydia pneumoniae(CP ,4 .2% ) ,in‐fluenzaBvirus(INFB,2.22% ),parainfluenzavirus(PIVs,1.24% )andrespiratorysyncytialvirus(RSV,0.50% ).MPinfectionwas dominated by young children ,the detection rate in females was higher than that in males (P<0 .05);majority of COX infection were young adults ,the detection rate in males was higher than that in females (P<0 .05) .Conclusion MP is the main respiratory tract infection pathogen in children and COX is the main respiratory tract infection pathogen among young adults in Shihezi area .

Objective To investigate the effects of recombinant human growth hormone (rhGH) on tumor growth and vascular endothelial growth factor (VEGF) expression of human gastric carcinoma xenografts in nude mice with different expressions of growth hormone receptor (GHR). Methods Immunocytochemical method was used to pick out one GHR-positive and one GHR-negative cell line. Then the cells were subcutaneously injected into 24 nude mice separately. The nude mice bearing two different kinds of human gastric caicinoma were equalges of body weight and tumor volume of nude mice were recorded. Serum concentrations of VEGF in peripheral blood were analyzed by ELISA. VEGF protein and mRNA expression in tumor tissue were detected by immunohistochemistry and RT-PCR, respectively. Results We chose SGC-7901 as GHR positive group, and MKN-45 as the negative one. For nude mice bearing GHR + SGC-7901 xenografts, the tumor volumes were significantly larger in rhGH groups than in control group (P ＜ 0.05), and the high-dose rhGH group revealed greater effect (P ＜ 0. 05).Body weights were not significantly different among three groups (P ＞ 0. 05). Serum VEGF concentration was (252.94 ± 15.32) ng/L in the high-dose rhGH group, which was significantly higher than that in control group [(49.94 ± 5.73) ng/L] and low-dose rhGH group [(167.60 ± 9.54) ng/L] (P ＜ 0.05). Moderate positive staining with VEGF was observed in the control group, while VEGF staining was strong in rhGH administration groups. The relative expression of VEGF mRNA for the high-dose rhGH group was 0. 6470 ± 0. 0447, which was significantly higher than that in control group (0. 3230 ± 0. 0258)and low-dose rhGH group (0. 412 ± 0. 0351)(P ＜ 0.05). While for nude mice bearing GHR-MKN-45 xenografts, the body weights of the rhGH-administrated groups were significantly higher than that of control group (P ＜ 0.05), while tumor growth, serum VEGF concentration, and the expressions of VEGF mRNA and protein in tumor tissue were not significantly different (P ＞ 0.05).Conclusions rhGH can promote tumor growth and increase the expression of VEGF in the GHR-highly-expressed SGC-7901 xenograft tumor model. However, such effects do not exist in GHR-negatively-expressed MKN-45 xenograft tumor model. The existence of GHR may be a key target where rhGH influences the secretion of VEGF.

Objective: To investigate the alterations of bcl-2 gene family in the rat brain and the molecular mechanism of neuronal apoptosis follow ing traumatic brain injury (TBI). Methods: Male Sprague-Dawley rats were subjected to lateral fluid percussion brain injury(FPBI) of moderate severity. bax and bcl-xL mRNA and protein expression was detected by RT-PCR an d immunohistochemistry. In addition to morphological evidence of apoptosis, TUNE L histochemistry was used to identify DNA fragmentation in situ under both l ight and electron microscope, whereas characteristic internucleosomal DN A fragm entation of apoptosis was demonstrated by DNA gel electrophoresis. Resul ts: bcl-xL mRNA and protein decreased in the ipsilateral hemisphere t o the impact site as early as 6 h post-injury［(67.42±7.54)% and (85.85±5.72)% r espectively］. The decrease in bcl-xL mRNA and protein preceded apoptosis was observed 12 h post-injury. And this was the main cause of up-regulation of the ratio of bax to bcl-xL in the acute period(minutes-hours) followin g FPBI. bax mRNA and protein were observed to rise slowly, doubled 3 d post- injury, returned to sham level slowly. The delayed cell death (days-weeks) migh t associated with the up-regulation of pro-apoptotic gene bax. Conclusio n: The expression of bcl-xL and bax coincide with apoptosis following TBI. The reg ulation of bax and bcl-xL by TBI occur before transcription. The balance of bax/bcl-xL ratio determines the neurocytes to survive or die following FPBI.

Objective: To investigate the alteration of bcl- 2 gene family in the rat brain and the molecular mechanism of neuronal apoptosis following traumatic brain injury. Methods: Male Sprague -Dawley rats were subjected to lateral fluid percussion brain injury(FPI) of mo derate severity. Bcl-2, Bcl-x and Bax protein expression was detected by immun ohistochemistry. Results: (1) The immunoreactivity of Bcl-2 and Bcl-x protein decreased in the hippocampus ipsilateral impact site as early as 6 h post-injury, and this was the main cause of down-regulation of the ratio of Bcl-2+Bcl-x to Bax. (2) During 1-3 d after injury, the Bax protein express i on increased significantly, while the Bcl-2 and Bcl-x protein expression decre ased relatively slow. The decreased ratio of Bcl-2+Bcl-x to Bax was mainly due to the Bax up-regulation. Conclusion: The bcl-2 gene family is involved in neuronal apoptosis after FBI, and the protein expression alteration of the family members leads the neuronal cell to apoptosis.

Object To study the effects of Helicobacter pylori(H.pylori) infection on gastric mucosa.Methods The 63 patients who was H.pylori positive for 10 years were examined by endoscopy and pathology.Results① Ten years later 16/63(25.4％ ) patients were H.pylori negative and 47/63(74.6％ ) patients persistent H.pylori positive.② At 10－ year follow up the H.pylori persistent positive and negative patients have the incidence of peptic ulcer naising from 29.78％ to 53.19％ (P0.05)respectively.④ The initial and 10－ year follow－ up data were that the incidences of erosion of gastric mucosa were 17.02％ and 38.29％ (P

Objective: To investigate the effects of adenosine A 1 receptor agonist N 6 cyclohexyladenosine(CHA) on neurofunction after fluid percussion injury in rats. Methods: The effects of CHA intra cerebroventricular injection 10 min before brain trauma on rats neurofunction and neuropathological changes were evaluated. Results: Compared with the control group, CHA could ameliorate the behavior deficits and improve pathological change. Conclusion: Adenosine A 1 receptor plays an important neuroprotective role in rat secondary injuries following brain trauma.

Humans ; Influenza A virus ; Influenza Vaccines ; Influenza, Human ; epidemiology ; prevention & control ; virology

Objective: To investigate the alteration of bcl 2 gene family in the rat brain and the molecular mechanism of neuronal apoptosis following traumatic brain injury. Methods: Male Sprague Dawley rats were subjected to lateral fluid percussion brain injury(FPI) of moderate severity. Bcl 2, Bcl x and Bax protein expression was detected by immunohistochemistry. Results: (1) The immunoreactivity of Bcl 2 and Bcl x protein decreased in the hippocampus ipsilateral impact site as early as 6 h post injury, and this was the main cause of down regulation of the ratio of Bcl 2+Bcl x to Bax. (2) During 1 3 d after injury, the Bax protein expression increased significantly, while the Bcl 2 and Bcl x protein expression decreased relatively slow. The decreased ratio of Bcl 2+Bcl x to Bax was mainly due to the Bax up regulation. Conclusion: The bcl 2 gene family is involved in neuronal apoptosis after FBI, and the protein expression alteration of the family members leads the neuronal cell to apoptosis.

Objective: To investigate the alteration of bcl- 2 gene family in the rat brain and the molecular mechanism of neuronal apoptosis following traumatic brain injury. Methods: Male Sprague -Dawley rats were subjected to lateral fluid percussion brain injury(FPI) of mo derate severity. Bcl-2, Bcl-x and Bax protein expression was detected by immun ohistochemistry. Results: (1) The immunoreactivity of Bcl-2 and Bcl-x protein decreased in the hippocampus ipsilateral impact site as early as 6 h post-injury, and this was the main cause of down-regulation of the ratio of Bcl-2+Bcl-x to Bax. (2) During 1-3 d after injury, the Bax protein express i on increased significantly, while the Bcl-2 and Bcl-x protein expression decre ased relatively slow. The decreased ratio of Bcl-2+Bcl-x to Bax was mainly due to the Bax up-regulation. Conclusion: The bcl-2 gene family is involved in neuronal apoptosis after FBI, and the protein expression alteration of the family members leads the neuronal cell to apoptosis.