OBJECTIVE:To study the protective effect of tanshinoneⅡA(TSⅡA)sulfonate injection against vancomycin(VAN)-induced renal injury model rats and its mechanism. METHODS:72 rats were randomly divided into blank group,model group, positive control group(amifostine,1 mg/kg)and TSⅡA sulfonate injection low-dose,medium-dose and high-dose groups(15,30, 60 μg/kg),with 12 rats in each group. Except for blank group,those groups were given VAN(200 mg/kg)intravenously via tail vein to induce renal injury rat model;after modeling,each drug group was given relevant medicine intraperitoneally once a day, and blank group and model group were given normal saline intragastrically for consecutive 10 days. The levels of 24 h protein, NAG and KIM-1 in urine were determined,and those of Cys C,Scr and BUN in serum and those of SOD,MDA,GSH-Px and NO in renal homogenate were also determined;the pathological change of renal tissue was observed. RESULTS:Compared with blank group,the levels of Cys C,Scr and BUN in serum,those of 24 h protein,NAG and KIM-1 in urine and those of MDA and NO in renal tissue increased significantly in model group,while the levels of SOD and GSH-Px decreased significantly(P<0.01);the pathological slice indicated that model group suffered from renal injury such as kidney tubules albuminoid degeneration,brush border abscission,renal tubular epithelial cell disintegration and abscission. Compared with model group,the levels of Cys C,Scr and BUN in serum,those of 24 h protein,NAG and KIM-1 in urine and those of MDA and NO in renal tissue decreased signifi-cantly in treatment groups,while the levels of SOD and GSH-Px in renal tissue increased significantly(P<0.05 or P<0.01);path-ological changes of renal tissue were relieved significantly. CONCLUSIONS:TSⅡ A sulfonate injection can effectively relieve VAN-induced renal injury in rats,and its mechanism may be associated with inhibiting the oxidative reaction of rats in vivo.

OBJECTIVE:To identify the influence of twisting or untwisting Taixi(K13) on the brain function by observing functional mag-netic resonance imaging.METHODS:Twelve healthy young cases were enrolled in this research.A block design including three blocks which baseline and stimulation appear alternately was adapted.In stimulation phase,the needle was twisted manually,or not twisted.Scanned images were analyzed using SPM2.RESULTS:The right superior temporal gyrus(BA22),left medial frontal gyrus(BA46),followed by right and left postcentral gyrus of parietal lobe(BA2,BA3),left inferior frontal gyrus(BA45) and left inferior parietal lobule(BA40) were evoked by acu-puncture at Taixi,but there was no activeation area after untwisting acupoint.CONCLUSION:The different areas evoked by twisting or untwisting Taixi acupoint are closely related with the internal organs as well as the course of the channels and collaterals.

OBJECTIVE To investigate the genes of disinfectant-sulfadiazine and antibiotic resistance of Escherichia coli strains in elderly wards.METHODS Polymerase chain reaction and dilution test were used to detect and analyze the disinfectant-sulfadizane drug resistance gene and drug resistance of the E.coli.RESULTS From 30 E.coli strains isolated from elderly patients,21 were detected carrying disinfectant-sulfadizine drug resistance genes,and the positive rate of qacE△1-sulⅠ was 70.0%.CONCLUSIONS The detection rate of disinfectant-sulfadiazine drug resistance gene from E.coli strains isolated from elderly patients,the bacteria detection rates are relatively high.Most of the isolates were resistant to commonly used antibiotics.It suggests that clinical drug-resistant strains may be resistant to disinfectants.This condition should be paid much attention by disinfection wotkers of our country.

Objective To study the clinical characteristics of healthcare-associated pneumonia (HCAP).Methods A retrospective cohort study was conducted on consecutive hospitalized pneumonia cases from January 2007 through April 2008.Results HCAP group of 75 patients was compared with 133 patients of community-acquired pneumonia (CAP) and 76 patients of hospital-acquired pneumonia (HAP). Most of HCAP patients had a history of recent hospitalization (47 cases), clinical IV infusion (27 cases), and prior chemotherapy or antibiotic therapy (27 cases). Underlying diseases were identified in 71 (94.7%) of HCAP patients, significantly higher than that in CAP group (37.6%, P<0.01). Positive sputum culture in CAP, HCAP and HAP was 22.6%, 56.9%, 77.6% respectively. Antibiotic resistance of bacteria in HCAP (71.43%) and HAP (80%) was comparable (P>0.05). Initial antibiotic therapy was effective in 47 (62.6%) cases of HCAP. Only 52.9% of the identified pathogens were sensitive to initial antibiotic therapies. The mortality of HCAP (12%) was similar to HAP (23%, P>0.05), but significantly higher than CAP (3%, P<0.05).Conclusions HCAP is a common type of pneumonia, which is characterized by more resistant pathogens, higher mortality, more comorbidities and poor outcomes. Antibiotic therapy should cover the hospital acquired bacterial pathogens.

Objective To investigate the effects of angiotensinⅡ(AngⅡ), Benazepril(Bena) and Losartan on proliferation and collagen synthesis of cultured rat cardiac fibroblasts(CFb) derived from SHR (CFbSHR) and WKY (CFbWKY). Methods CFb derived from 12-week-old SHR and WKY was cultured by outgrowth of tissue block. Cell proliferation of CFb was determined by direct cell counting .3H-Proline incorporation of CFb was measured after incubation with AngⅡ,Bena and Losartan. Results In serum free(0.4%FCS) medium, cell number of CFb derived from SHR and WKY were not influenced by AngⅡ(10-10mol～10-6mol)and Bena(10-9mol～10-5mol). Increased 3H-proline incorporation wa s induced by AngⅡ in a concentration dependent manner. Benazepril caused an decrease in 3H-Proline incorporation in CFb derived from SHR and WKY. The increased collagen synthesis induced by AngⅡ(10-7mol) was inhibited by Losartan((10-10mol～10-6mol） i n a concentration dependent manner. Conclusion Proliferation of CFb were not influenced by AngⅡ and Bena. Collagen synthesis of CFb was promoted by AngⅡ and inhibited by Bena. Collagen synthesis of CFb in duced by AngⅡ was inhibited by losartan.

Objective To explore the related risk factors of severe mycoplasma pneumonia in children.Methods 86 children with mycoplasma pneumonia were selected as the observation group.At the same time,30 normal children were selected as the control group.The observation group included 33 cases of mild mycoplasma pneumo nia(A group) and 53 cases of severe mycoplasma pneumonia(B group).The clinical data of the three groups were ret rospectively analyzed,and the related risk factors of severe mycoplasma pneumonia in children were analyzed.Results The risk factors of severe mycoplasma pneumonia in children were age ＞ 5 years (x2 =28.776,P ＜ 0.05),immunoglobulin IgG(x2 =3.004,P ＜ 0.05),immunoglobulin IgM (x2 =2.147,P ＜ 0.05),immunoglobulin IgA (x2 =2.036,P ＜ 0.05),WBC (x2 =6.119,P ＜ 0.05),neutrophil percentage (x2 =8.374,P ＜ 0.05),the positive rate of CD8(x2 =11.665,P＜0.05),the positive rate of CD4(x2 =12.901,P＜0.05).Conclusion For children with risk factors of severe mycoplasma pneumonia should be early diagnosed,prevented and treated,thereby reducing the burden on patients.

AIM: To investigate the effects of fibronectin (FN) on the proliferation and collagen synthesis in cultured rat cardiac fibroblasts (CFb) derived from SHR (CFb SHR ) and WKY (CFb WKY ). METHODS: CFb derived from 12-week-old spontaneously hypertensive rat (SHR) and WKY was cultured by outgrowth of tissue block. Cell proliferation of CFb was measured by cell number counting and [ 3H]-TdR incorporation using 24-well plates pre-coated with 5 ?g/cm 2 of FN. Collagen synthesis was determined by [ 3H]-proline incorporation. RESULTS: As compared with control, the cell number of fibroblasts derived from SHR and WKY were significantly increased to 163.75% and 170.42% respectively after 72 h incubation with FN in the presence of 0.4% FCS from a intial cell density of 1?10 4 cells/mL. DNA synthesis of CFb was markedly promoted by FN [CFb SHR : ( 44?734 ? 8?981 )counts/min vs ( 29?233 ? 6?746 ) counts/min, P

Objective:To study the effects of panax notoginsenosides on the proliferation and oxidation indices of cisplatin-induced nephroxicity in HK-2 cells. Methods:HK-2 cells were cultured in vitro till the number was up to 1 × 106/ml. The cells were inoculated in 96-well culture plate and randomly divided into six groups:normal saline ( NS) group,the model group, the positive control group and the high dose group , medium dose group and low dose group of panax notoginsenosides ( PNS) . The nephroxicity model was dupli-cated with the addition of cisplatin (the final concentration was 6. 25μg·L-1). The model group, positive control group and the three panax notoginsenosides groups was treated with saline solutions, amifostine, panax notoginsenosides at the dose of 100,50 and 25 mg· L-1 , respectively. The cell viability was detected with an MTT method, the content of MDA and the activity of SOD, GSH-PX and LDH were measured and the cell structure was observed. DCFH-DA was used as the fluorescence probe to detect the level of ROS by a fluorescence microplate reader. Results:Compared with those in the model group, the cell viability and the activity of SOD and GSH-PX in the three PNS groups and the positive control group significantly increased (P<0. 05);the content of MDA, the level of ROS and the activity of LDH significantly decreased (P<0. 05); the cell structure was significantly improved. Conclusion: PNS can pro-mote the proliferation of HK-2 cells in vitro, and improve the biochemical parameters and enzyme levels. The results suggest that PNS has a protective effect on HK-2 cell,and the protective mechanisms may be related with its antioxidant effect.

Objective To investigate the effects of microRNA-21-5p (miR-21-5p) on hyperoxic acute lung injury (HALI) in rats and provide a theoretical basis for HALI gene therapy. Methods One hundred and sixty Sprague-Dawley (SD) rats were randomly divided into four groups with number table:hyperoxia control group, phosphate buffer saline (PBS) group, blank virus group and miRNA-21-5p group (each, n = 40). The rats in hyperoxia control group were fed directly in the hyperoxia box (oxygen concentration > 90%); in the other three groups, 200 μL PBS, 200μL slow virus and 200μL miRNA-21-5p slow virus were dropped into the nose respectively, and then they were fed in the hyperoxia box. The rats were exposed to hyperoxia in the boxes for 0, 24, 48 and 72 hours in all the groups, and at each time point, 10 rats were taken randomly from each group to perform arterial blood-gas analysis, calculate oxygenation index (OI) and respiratory index (RI). Afterwards the rats were sacrificed by blood-letting from carotid artery under intra-peritoneal anesthesia, and the lung tissues were obtained to measure the left lung wet/dry weight (W/D) ratio, hemotoxylin-eosin (HE) staining was made and the pathological changes of the right lung were observed under light microscope and the pathological score was measured. Results At 0 hour, the OI, RI, lung W/D ratio and the lung tissue pathology score in rats with hyperoxic injury had no statistically significant differences among the four groups (all P>0.05). With the extension of time, the level of OI was gradually reduced, and the levels of RI, pathologic score and W/D ratio of lung tissues were gradually increased. Compared with the hyperoxia control group, in miRNA-21-5p group, the levels of OI were increased significantly at 24, 48 and 72 hours after the exposure to hyperoxia [mmHg (1 mmHg = 0.133 kPa): 24 hours 358.10±29.25 vs. 306.19±37.23, 48 hours 336.67±29.27 vs. 269.70±29.00, 72 hours 323.81±19.05 vs. 203.81±43.40, all P < 0.05], whereas the levels of RI were decreased significantly (24 hours 0.23±0.05 vs. 0.31±0.06, 48 hours 0.28±0.07 vs. 0.38±0.06, 72 hours 0.30±0.04 vs. 0.46±0.07, all P <0.05), the pathologic scores were decreased significantly (24 hours 0.60±0.52 vs. 0.90±0.74, 48 hours 1.30±0.95 vs.2.90±1.20, 72 hours 1.90±0.88 vs. 4.70±1.57, all P < 0.05) and the levels of W/D ratio were decreased obviously (24 hours 3.77±0.38 vs. 4.14±0.46, 48 hours 3.83±0.31 vs. 4.56±0.34, 72 hours 3.89±0.31 vs. 5.32±0.27, all P<0.05). Compared with the hyperoxia control group, the index results of the PBS group and the blank virus group after staying in the box had no statistical significant differences at each time point (all P>0.05). Under the optical microscope, along with the prolongation of exposure to hyperoxia, the structure of alveoli was gradually disturbed, their walls fractured and damaged, alveolar septa widened, edematous, infiltrated with inflammatory cells and in part of the rats a small amount of red blood cell exudates could be seen, but the degree of lung pathological injury in miRNA-21-5p group was much milder than that of the other groups. Conclusion The rat persistently exposed to hyperoxia for 24 hours can establish the rat model of HALI successfully, and the miRNA-21-5p can protect the lung tissue from the damage to some degrees in HALI rats.

ObjectiveTo evaluate the significance of the detection of serum C-reactive protein (CRP) in elderly patients with diabetes mellitus and cerebral infarction.MethodsSeventy-two patients with diabetes mellitus and cerebral infarction (diabetic cerebral infarction group),66 patients with cerebral infarction and without diabetes mellitus (non-diabetic cerebral infarction group) and 60 healthy persons (control group) from October 2008 to January 2011 were selected.The level of serum CRP was detceted.ResultsThe level of CRP was ( 3.81 ± 2.23 ) mg/L in diabetic cerebral infarction group,( 2.48 ± 2.24 ) mg/L in non-diabetic cerebral infarction group and (0.68±0.16) mg/L in control group.The levels of CRP in diabetic cerebral infarction group and non-diabetic cerebral infarction group were significantly higher than that in control group (P ＜ 0.05).The level of CRP in diabetic cerebral infarction group was obviously higher than that in non-diabetic cerebral infarction group(P ＜0.05).CRP abnormal rate was 70.8％(51/72) in diabetic cerebral infarction group and 43.9％ (29/66) in non-diabetic cerebral infarction group,which had statistical significance (P ＜ 0.05).ConcluslonCRP has important predictive value to the occurrence and development of diabetic cerebral infarction.