OBJECTIVE To investigate the pathogenic causes of community-acquired pneumonia(CAP) in adult patients in Tongling.METHODS A prospective study was performed on 260 consecutive adult patients with CAP in Tongling city during last three years.Bacteria culture of sputum and serological tests in paired serum samples were detected.RESULTS Of 260 patients with etiological evaluation,128(49.2%) patients had an identifiable etiology,63(24.2%) had positive outcome from sputum cultured,atypical pathogens were detected from 75(28.8%)patients.Pathogens identified in 128 patients were:Mycoplasma pneumoniae(35.4%),Chlamydia pneumoniae(17.7%) and Streptococcus pneumoniae(13.6%).6.5% All patients had mixed infection.The resistance rate of S.pneumoniae to penicillin and erythromycin was 5 and 50%,respectively.CONCLUSIONS Atypical pathogens have important role in CAP,of which M.pneumoniae is the most common pathogen.S.pneumoniae and K.pneumoniae are the commonly encountered bacteria for CAP in Tongling.

Aim To observe the expression of migration inhibitory factor (MIF) in the enteric neurons,and to explore the nervous regulation on MIF activity in experimental colitis.Methods Colitis was induced in sensitized rat and mouse by 2,4-dinitrochlorobenzene(DNCB)enema.MIF activity was measured both in the mesentery lymphocyte(by MTT)and in the enteric neurons(by immunofluorescence double staining).6-OHDA was intraperitonealy (ip) administered to mouse before DNCB treatment.Norepinephrine(NE) was added to lymphocyte culture in vitro during MIF preparation.Results The expression of MIF protein in enteric neuron was increased in DNCB-induced colitis in rat.ip 6-OHDA in colitis mouse(38～150 mg?kg-1) resulted in a further increase of MIF activity than ip vehicle in colitis mouse (P

Objective To structure the model of acute carbon monoxid poisoning(ACOP)in rats. Evaluate the effectiveness of the poisoning on the pulmonary function and the significance of carbon monoxide hemoglobin(HbCO)and oxygenation index in diagnosis of acute lung injury(ALI)/acute respiratory distress syndrome(ARDS).Method Eighty healthy adult male Wistar rats were randomized into 4 groups.According to the concentration of CO,poisoning group was randomized into three groups(each group=20),group A,group B,group C.After poisoned,arterial blood was collected rapidly for arterial blood gas analysis.According to the pathological changes,the models were divided into ALI/ARDS group and non-ALI/ARDS group.Results Compared with control group,the incident rate of ALI/ARDS in group B(25%)and group C(55%)were significantly higher(P

OBJECTIVETo explore activity laws of mitochondrial complex II in patients of deficiency-cold syndrome (DCS) and deficiency-heat syndrome (DHS) under various ambient temperatures.

METHODSSubjects were recruited by questionnaire and expert diagnosis from grade 1 - 3 undergraduates at Henan College of Traditional Chinese Medicine in November 2012, and assigned to a normal control group, the DCS group, and the DHS group, 20 in each group. Their venous blood samples were collected at two different temperature conditions. Activities of mitochondrial complex II were measured by spectrophotometry.

RESULTS(1) Comparison of mitochondrial complex It under various ambient temperatures: Compared with room temperature in the same group, activity values were all increased in the normal control group at cold temperature with significant difference (P <0.05), but there was no significant difference in the DCS group and the DHS group (P >0. 05). Compared with the normal control group, activity values of complex H were reduced in the DCS group at cold and room temperatures with significant difference (P <0.05). Compared with the DCS group, activity values of complex It were increased in the DHS group with significant difference (P <0. 05). (2) Changes of adjustment rates: Compared with room temperature, the adjustment rate all rose at cold temperature in the normal control group and the DHS group with significant difference (P <0.05), but with no significant difference found in the DCS group (P >0. 05). Compared with the normal control group at the same temperature, the adjustment rate in the DHS group and the DCS group was all reduced at cold and room temperatures with significant difference (P <0. 05). There were no significant difference in the adjustment rate between the DHS group and the DCS group (P > 0. 05).

CONCLUSIONSEnvironment temperature can affect the activity of mitochondrial complex II with different influence degrees on different syndrome types of people, but its change trend are basically identical.

Objective To detect the differentially expressed microRNAs (miRNAs) in bladder cancer tissue and normal bladder tissue. Methods Total RNA was extracted from bladder cancer tissue and normal bladder tissue by Trizol, and then miRNAs were isolated and enriched from the total RNA. Mammalian miRNA microarrays were used to analyze the differentially expressed miRNAs between the bladder cancer tissue and normal tissue. Data analysis was performed by software of LuxS-can3. 0 and SAM version 2. 1. Choose let-7 gene which was interesting to us, and validation of mi-croarray results was carried out by northern blotting. Results Compared with normal bladder tissues, there were 71 differentially expressed miRNAs in bladder cancer tissue, of which there were 38 down-regulated ones and 33 up-regulated ones. Among these miRNAs, 26 miRNAs were the most significant with 12 up-regulated and 14 down-regulated. The expression of let-7 gene in bladder cancer was down-regulated to normal bladder tissue by northern blotting, which was in agreement with the results of the miRNA microarrays. Conclusion There are differentially expressed miRNAs between bladder cancer tissue and normal bladder tissue, and let-7 gene is probably as a tumor suppressor in bladder cancer.

Objective To investigate the apoptosis inducing effects of oridonin on leukemic THP-1 cells and its mechanisms of action. Methods THP-1 cells in culture medium in vitro were given different concentrations of oridonin (16～56 μmol/L) for 24, 48 and 72 h. The inhibitory rate of the cells were measured by MTT assay, apoptotic morphology was observed by Hoechst 33258 staining, and Annexin V/PI staining was used to detect cell apoptosis by flow cytometry (FCM). Caspase-3 and poly (ADP-ribose) polymerase (PARP) expression were detected by Western blotting. Results Oridonin (over 32 μmol/L) could inhibit the growth of THP-1 cells and cause apoptosis remarkably, the suppression was both in time-and dose-dependentmanner. Marked morphological changes of cell apoptosis such as condensation of chromatin was clearly observed by Hoechst 33258 staining, and Annexin V/PI staining showed that apoptotic cells gradually increased after the cells treated with oridinon. Western blotting showed cleavage of the caspase-3 zymogen protein (32×103), with the appearance of its 20×103 subunit, and a cleaved 89×103 fragment of 116×103 PARP was also found. Conclusion Oridonin can inhibit cell growth and induce apoptosis in THP-1 cells via activation of caspase-3. The results indicated that oridonin might be an important potential anti-leukemia reagent.

Objective To test reliability and validity of a verbal behavior assessment scale (VerBAS). Methods The VerBAS was used to evaluate 20 patients with speech disorder repeatedly by the same investigator with a two week interval to assess its reliability. The construct validity of the VerBAS was evaluated by using it to evaluate 235 patients with speech disorder. Results The test-retest correlation coefficient γ was 0.723,which was significant at the 5% confidence level. Cronbach'a a=0.819. Three distinct factors were identified: receptive speech,communicative speech and delineative speech;and their accumulated variance contribution was 83%. Conclusion The Verbal Behavior Assessment Scale had satisfactory reliability and validity, It can be used to evaluate the patients with speech disorder and could provide a reference for speech rehabilitation training.

Objective To investigate the apoptosis inducing effect of peroxisome proliferator-activated receptor r(PPARr)agomst on leukemic K562 cells and its mechanisms of action.Methods K562 cells in culture medium in vitro were given different concentrations of PPARragonist rosiglitazone(RGZ)(20-80 umol/L)for O,24,48 and 72h The inhibitory rate of the cells were measured by MTT assay,cell apoptosis was detected by Annexin V/PI staining,and the expression of P53 protein as well as the activity of caspase-3 were also detected.Results RGZ(over 40umoL/L)could inhibit the growth of K562 cells and cause apopto-sis remarkably,the suppression Was both in time-and dose-dependent manner.The expression of P53 pmtein was upregulated and the activity of caspase-3 Was increased concomitantly after the cells werle treated by RGZ.Conclusion PPARr agonist RGZ(over 40 umol/L)can induce apoptosis on K562 cells signifieantly,upregu-lation the expression of P53 protein as well as increasing caspase-3 activity may be one of its most important mechamisms.

Relatively uniform-sized nanoparticles made of poly (lactic-co-glycolic acid) (PLGA) were prepared by premix membrane emulsification method. After the drug loading property was completed, the dynamic tissue distribution of nanoparticles was recorded. With the average particle size and span as indexes, membrane pore size, number of passing membrane times, membrane pressure, volume ratio of oil-water phase and the concentration of poly(vinyl alcohol) (PVA) in external water phase were investigated by single factor test, the optimum preparation technology of blank PLGA nanlparticles was as following: pore size of SPG membrane was 1 μm, membrane pressure was 1. 15 MPa, the number of passing membrane time was 3, the mass fraction of PVA of 2%, volume ratio of oil-water phase of 1 : 5. Prepared nanoparticles were round with smooth surface, the mean diameter was 332.6 nm, span was 0.010, the confocal laser scanning microscope (CLSM) concluded that fluorescent substance is uniform composizion in PLGA nanoparticle, and the in vivo imaging technology in mice include that the nanoparticles show good liver and spleen targeting property.
Animals ; Drug Carriers ; chemistry ; Drug Delivery Systems ; instrumentation ; Emulsions ; chemistry ; Fluorescent Dyes ; chemistry ; Lactic Acid ; chemistry ; Mice ; Mice, Nude ; Nanoparticles ; chemistry ; Particle Size ; Polyglycolic Acid ; chemistry

The role of methyl-CpG binding domain protein 2 (MBD2) in an ApoE-deficient mouse model of age-related macular degeneration (AMD) was investigated. Eight-week-old Mbd2/ApoE double deficient (Mbd2(-/-) ApoE(-/-)) mice (n=12, 24 eyes, experimental group) and MBD2 (wt) ApoE(-/-) mice (n=12, 24 eyes, control group) were fed on Western-type diet for 4 months. The mice were sacrificed, and total serum cholesterol levels were analyzed and Bruch's membrane (BM) of the eyes was removed for ultrastructural observation by transmission electron microscopy. Moreover, intercellular adhesion molecule 1 (ICAM-1) immunoreactivities were evaluated by fluorescence microscopy in sections of the eyes in both groups for further understanding the function mechanism of MBD2. There was no significant difference in the total serum cholesterol levels between control group and experimental group (P>0.05). Transmission electron microscopy revealed that AMD-like lesions, various vacuoles accumulated on BM, notable outer collagenous layer deposits and dilated basal infoldings of retinal pigment epithelium (RPE) were seen in both groups, and the BM in control group was significantly thickened as compared with experimental group (P<0.05). Fluorescence micrographs exhibited the expression of ICAM-1 in choroid was higher in control group than in experimental group. We are led to conclude that MBD2 gene knockout may lead to accumulation of more deposits on the BM and influence the pathogenesis of AMD via triggering endothelial activation and inflammatory response in choroid, improving microcirculation, and reducing lipid deposition so as to inhibit the development of AMD-like lesions. Our study helps to provide a new therapeutic approach for the clinical treatment of AMD.