Objective To investigate the effects of methylprednisolone(MP) on the expression of matrix metalloproteinase(MMP)-9 and airway inflammation in murine models of asthma. Methods Thirty female BALB/c mice were randomly divided into asthma group,MP group and control group(n=10).Murine models of acute asthma were established by ovalbumin(OVA) via peritoneal injection and intranasal instillation.The pathological changes of lung tissues were observed with HE staining,and cell quantitation was conducted in bronchalveolar lavage fluid(BALF).The expression of MMP-9 protein was determined by immunohistochemistry and gelatin zymogram,and the expression of MMP-9 mRNA was detected by RT-PCR. Results Compared with control group,there were more significant airway spasm and more infiltration of inflammatory cells in histologic examination,and there was higher eosinophil cell quantitation in BALF in asthma group(P

Adolescent ; Child ; Child, Preschool ; Clinical Trials as Topic ; Flow Cytometry ; Hematopoietic Stem Cell Transplantation ; Humans ; Immunophenotyping ; Leukemia, Myeloid, Acute ; diagnosis ; pathology ; therapy ; Neoplasm, Residual ; diagnosis ; pathology ; therapy ; Polymerase Chain Reaction ; Prognosis ; Recurrence ; Sensitivity and Specificity

Objective To analyze the clinical presentation and maternal-neonatal outcome of HELLP syndrome.Methods 32 cases with HELLP syndrome from January 2003 to January 2009 were analyzed retrospectively.Results The incidence of HELLP syndrome in preeclampsia was 3.7%.Complete HELLP were 17 cases,partial HELLP were 15 cases.Two pregnant women died(one case of intracranial hemorrhage,one case of acute left cardiac failure),the mortality was 6.3%.Five newborns died,the mortality was 15.6%.The main materal complications were DIC(8 cases),placental abruption(2 cases),intracranial hemorrhage(2 cases).The main perinatal complications were preterm labor(20 cases),newborn asphysia(17 cases),SGA(15 cases).Conclusion HELLP syndrome is one of the most serious obstetric complications,early diagnosis,early therapy,controlling hypertension and termination of pregnancy in time are most important for treatment.

Objective To investigate the protective effects of midazolam on noise-induced hearing loss in guinea pigs by testing reactive oxygen species (ROS) level in the cochlea and plasma SOD and MDA. Methods Totally forty male pigmented guinea pigs were randomly divided into four groups: control (C) , midazolam (M), normal saline (S) and noise-induced deafened (D) groups, with ten guinea pigs in each. Groups M, S and D were exposed to a continuous noise (4kHz , octave band, 100dB SPL) 3h every day for 3 consecutive days. Group M was treated with midazolam, which was administered intramuscularly (0.1mg/kg) 24h before noise exposure, and immediately upon and during noise exposure. Group S was exposed to noise and treated with the same volume of normal saline intramuscularly, the time of injection was the same as that of Group M. Group C was not exposed to noise, but was treated with midazolam intramuscularly, the time of injection and the dosage were the same as those of Group M. Group S was exposed to noise and treated with normal saline intramuscularly ,the time of injection was same with that of Group M.Group D was exposed to noise only. All animals received auditory brainstem response (ABR) threshold recording before and immediately after noise exposure. Blood was collected when the guinea pigs were killed after the last ABR threshold recording, and serum SOD activity and MDA content were detected. Both the cochleae were removed and prepared for ROS assay. Results After noise exposure, ABR threshold shift (1.6±1.5) and ROS content [(291.10±2.30)u/mL] in Group M were significantly lower than those in Groups S and D [41.7±3.3, 44.3±3.9; (348.52±3.60)u/mL, (315.56±6.70)u/mL, P<0.05]. Serum SOD activity and MDA content were significantly increased in Group M, but the amplitude was less than that in Groups S and D.Conclusion Midazolam can prevent noise-induced hearing loss by reducing the increased ROS level in the cochlea after noise exposure.

Objective To evaluate the effect of dexmedetomidine on noise-induced hearing loss in guinea pigs.Methods Twenty-four adult male guinea pigs,aged 3 months,weighing 400-500 g,were randomly divided into 3 groups (n =8 each) using a random number table:dexmedetomdine group (group D),noise-induced hearing loss group (group N) and dexmedetomidine + noise-induced hearing loss group (group DN).A loading dose of dexmedetomidine 5 μg/kg was infused over 5 min,followed by 135 min of infusion at a rate of 10 μg· kg-1 · h-1.The equal volume of normal saline was infused in group N.Groups N and DN were exposed to noise of 4 kHz center frequency and 118-122 dB SPL for 120 min starting from 20 min of administration.Mean arterial pressure (MAP) and cochlear blood flow (COBF) were recorded before administration and every 5 min during drug administration.The changing rate of COBF was calculated.Arterial blood samples were collected for determination of plasma concentration of noradrenaline (NE) by high performance liquid chromatography at 20 and 140 min of administration.Auditory brainstem response (ABR) threshold was recorded before administration and at 1 and 72 h and 10 days after the end of administration.Results Compared with group N,MAP was significantly decreased,the changing rate of COBF was increased at 5-10 min and 30-140 min of administration,ABR threshold was decreased at 1 and 72 h and 10 days after the end of administration,and the plasma concentration of NE was decreased at 140 min of administration in D + N group (P ＜ 0.05).Conclusion Dexmedetomidine can attenuate noise-induced hearing loss in guinea pigs possibly through inhibiting activation of sympathetic nerves and increasing COBF.

Airway Obstruction ; complications ; etiology ; physiopathology ; Asphyxia ; etiology ; physiopathology ; Fibroma ; complications ; pathology ; Humans ; Infant, Newborn ; Oropharyngeal Neoplasms ; complications ; pathology ; Rare Diseases

AIM: To investigate the influence of Astragalus Injection on morphology,cell cycle and oxidative stress of rat's glomerular mesangial cells(GMC) cultured with advanced glycation end products(AGEs). METHODS: GMC were incubated in culture medium containing AGEs in the presence of Astragalus Injection and aminoguanidin for 48 h.At the same time,the normal and control groups were established.Then the cultured GMC was stained by mixed fluorescence liquid and observed under fluorescence microscope.Cell cycle of GMC was analyzed using flowcytometry.The activity of SOD、MDA and GSH-PX in GMC supernatant were measured by test kit.The level of ROS was detected by flowcytometry. RESULTS: Morphology analysis showed that the morphology and structure of normal GMC were normal.The structure of most cells in AGEs was unclear,cell counts increased markedly and they grew intensively.Cell cycle analysis showed that cell percentage of S phase increased and G_0/G_1 reduced.The level of ROS,MDA remarkably increased,and SOD,GSHPX activity reduced.Whereas Astragalus Injection was added,cell morphology tended to be basically normal and cell counts decreased,the percentage of S phase also decreased.The level of ROS,MDA and the SOD,GSH-PX activity restored in comparison with the control groups. CONCLUSION: Astragalus Injection can prevent GMC from lesion caused by AGEs.Astragalus Injection may protect GMC from retarding the progression of diabetic nepropathy by partially inhibiting the occurrence of oxidative stress.

Objective To evaluate the effect of morphine on the proliferation and migration of human hepatocellular carcinoma (HCC) cells in an in vitro experiment.Methods The experiment was performed in 2 parts.Experiment Ⅰ Human HCC cells were inoculated in 6-well plates at a density of 2×105 cells/well (2 ml/well) and divided into 6 groups (n=12 each) using a random number table:control group (C group) and 10,25,50,100 and 200 ng/ml morphine groups (M1-M5 groups).Morphine at the final concentration of 10,25,50,100 and 200 ng/ml was added in M1-M5 groups,respectively.The equal volume of phosphate buffer solution was added in group C.The cells were cultured or incubated for 48 h.The expression of μ1-opioid receptor (MOR1) mRNA was measured by real-time polymerase chain reaction.The expression of MOR1 was detected by Western blot in C and M4 groups.Experiment Ⅱ Human HCC cells were inoculated in 96-well plates (1×103 cells/well) or in Transwell chambers(200 μl) and divided into 2 groups (n=9 each) using a random number table:control group (C group) and morphine group (M group).Morphine was added at the final concentration of 100 ng/ml in group M,and the equal volume of phosphate buffer solution (final volume 100 μl/well) was added in group C.The cells were cultured or incubated for 7 days.The cell proliferation was detected by methyl thiazolyl tetrazolium assay at 1-7 days of incubation or culture.The cell migration was determined by Transwell chamber assay at 30 h of incubation or culture.Results Experiment Ⅰ Compared with group C,the expression of MOR1 mRNA was significantly up-regulated in M1-M5 groups,and the expression of MOR1 was significantly up-regulated in group M4 (P<0.01).Compared with group M4,the expression of MOR1 mRNA was significantly down-regulated in M1-M3 and M5 groups (P<0.01).Experiment Ⅱ Compared with group C,the cell proliferation was significantly enhanced on 4th-7th days of incubation,and the number of cells passing through Transwell chambers was increased in group M (P<0.05 or 0.01).The cell proliferation was gradually enhanced on 4th-7th days of incubation in group M (P<0.05).Conclusion Morphine can promote the proliferation and migration of human HCC cells,and the mechanism is related to up-regulation of MOR1 expression in an in vitro experiment.

AIM: To study ethanol influence on gene mutations of HBV DNA and to offer testimony for clinical diagnosis and treatment of chronic hepatitis B.METHODS: 85 patients with chronic hepatitis B were divided into alcoholic group and non-alcoholic group.Gene chip technique was used to detect gene mutations located in Pre-C nt G1896A and nt A1814C,basal core promoter(BCP) nt A1762T and nt G1764A,P nt C528A and nt T552C.RESULTS: The mutation frequency on BCP nt A1762T and nt G1764A in alcoholic group was significantly higher than that in non-alcoholic group(P0.05).CONCLUSION: Ethanol stimulates HBV gene mutations on BCP nt A1762T and nt G1764A,enhances HBV DNA replication and gene expression,deteriorates the state of the illness.