OBJECTIVE To investigate the profile of pathogen of infection in kidney disease patients. METHODS Pathogen of infection in kidney disease patients in our hospital from Jan 2004 to Feb 2006 was retrospectively investigated. RESULTS A total of 240 pathogen strains were isolated from 223 cases.Of the 240 isolated strains the rate of strains of Gram-negative bacilli was 55.4%,that of the Gram-positive cocci was 26.3%,the rate of fungi was 10.0% and that of the Gram-positive bacilli was 8.3%.The positive rate of Escherichia coli was the highest followed by Haemophilus influenzae.54.2% Of isolates were from urine,21.3% from sputum.The isolated pathogens resisted at different degrees to antibiotics which were used frequently in clinic.The rate of polyinfection was not high. CONCLUSIONS Pathogen of infection in kidney disease patients is mainly Enterobacteriaceae.The isolates mainly are E.coli which is multi-resistant.It mainly causes the urinary infections.

OBJECTIVE To analyze the risk factors and the drug-resistance of nosocomial acquired lung infection by Chryseobacterium meningosepticum.METHODS A retrospective investigation of the clinical correlative data and the drug sensitivity results of 60 cases with nosocomial acquired lung infection by C.meningosepticum from Jan 2004 to Jan 2006 was conducted in local hospital.RESULTS The patients were mainly distributed at ICU,respiration and neurosurgery wards.They had severe underlying diseases(100.0%),tracheal intubation(56.7%),central venous catheter(25.0%) and urine catheter(16.7%) treatments and applications of more than three antibiotics(68.3%).The drug-resistance of C.meningosepticum was serious.The antibiotic drugs which had higher susceptibility ratio were cefoperazone/sulbactam,fluoroquinolones,et al.CONCLUSIONS The main risk factors of nosocomial acquired lung infection by C.meningosepticum are severe underlying diseases,various invasive treatments,long-term hospitalization and inappropriate use of broad spectrum antibiotics.Clinical isolates are multi-drug resistant to many kinds of antibiotics.

Objective To explore the method of target volume determination of postoperative 125I seeds interstitial brachytherapy in parotid gland carcinoma.Methods A total of 31 cases( 14 males and 17 famales) with primary parotid carcinoma who were treated in Peking University Hospital of Stomatology from Oct 2002 to Nov 2006.The patients' average age was 38.2 years.All patients underwent tumor resection and postoperative 125I seeds interstitial brachytherapy with 60 Gy matched peripheral dose.The spiral CT was performed for treatment plan and quality verification before and after the brachytherapy.The bone and muscle landmarks surrounding parotid were selected as reference for target volume determination.D90 of target volume and dose of organs at risk were calculated,while the target volume and D90 of target volume of verification were compared with that of treatment plan through quality verification.Results The target volume or D90 of target volume before and after treatment was not statistically different.D90 of target volume was more than 60 Gy.During 3 -7 years of follow-up,all patients had no recurrence.ConclusionsAccording to the follow-up results,the method used for target volume determination in this paper might be satisfied.

Objective To observe the fixity of 125I seed after implantation in parotid region. Methods Ten patients treated with 125I seed interstitial brachytherapy in parotid were randomly selected. Within one week after the treatment, two plane radiographs were taken by radiotherapy simulator and 125I seed was counted. All plane dosimetry analysis were performed by treatment planning system. The areas surrounded by 50%, 100% and 150% of prescription dose curve and dose equality index were calculated. Two months after the treatment, the same examination were repeated and were compared with t test. Results The number of seeds was equal in two examination. There were no signifieant differences in two examinations either for the areas surrounded by 50%, 100% and 150% of prescription dose curve or for the dose equality index. Conclusions The position of 125I seed after implantation in parotid region is quite fixable, which can ensure the curative effect.

Objective To study the influence of 125I seed interstitial brachytherapy in parotid region on the recovery of facial nerve function. Methods A total of the data of 21 patients with primary parotid carcinoma were treated with resection and 125I interstitial brachytherapy. All the patients had no facial palsy before operation and the prescribed dose was 60 Gy. During 4 years of follow-up, the HouseBrackmann grading scales and ENoG were used to evaluate the function of facial nerve. According to the modified regional House-Brackmann grading scales, the facial nerve branches of patients in affected side were divided into normal and abnormal groups, and were compared with those in contra-lateral side.Results Post-operation facial palsy occurred in all the patients, but the facial palsy recovered within 6 months. The latency time differences between affected side and contralateral side were statistically significant in abnormal group from 1 week to 6 months after treatment ( t = 2.362, P = 0.028 ), and were also different in normal group 1 week after treatment ( t = 2.522, P = 0.027 ). Conclusions 125I interstitial brachytherapy has no influence on recovery of facial nerve function after tumor resection and no delayed facial nerve damage.

Objective To evaluate the effect of dexmedetomidine on acute lung injury induced by scalds in rats.Methods Seventy-five male Sprague-Dawley rats,weighing 200-220 g,were randomly divided into 5 groups (n =15 each) using a random number table:control group (group C),scald group (group S),dexmedetomidine group (group D),α-bungarotoxin (α-BGT) group,and dexmedetomidine+ α-BGT group (group D+α-BGT).About 30％ of the total body surface was shaved and then exposed to 98 ℃ water for 12 s in S,D,α-BGT and D+α-BGT groups.The back of rats was exposed to 37 ℃ water for 12 s in group C.Rats were resuscitated with lactated Ringer's solution injected intraperitoneally according to Parkland formula within 24 h after establishment of the model.In D,α-BGT,and D+α-BGT groups,dexrnedetomidine 40 μg/kg,α7 nicotinic acetylcholine receptor antagonist α-BGT 1 μg/kg,and α-BGT 1 μg/kg plus dexmedetomidine 40 μg/kg were injected intraperitoneally,respectively,at 15 min before establishnent of the model.At 24 h after establishment of the model,the rats were sacrificed,and lungs were removed for examination of the pathological changes and for determination of myeloperoxidase (MPO) activity,in terleukin-1beta (IL-1β),tumor necrosis factor-alpha (TNF-α),and IL-6 contents (by enzyme-linked immunosorbent assay),and nucleoprotein factor kappa B (NF-κB) (by Western blot).The lung water content [(wet weight-dry weight)÷wet weight× 100％] was calculated.Results Compared with group C,the lung water content,MPO activities,and contents of IL-1β,TNF-α and IL-6 were significantly increased,and the expression of NF-κB was up-regulated in S,α-BGT and D groups (P＜0.05).Compared with group S,the lung water content,MPO activities,and contents of IL-1β,TNF-α and IL-6 were significantly decreased,and the expression of NF-κB was down-regulated in D and D+α-BGT groups (P＜0.05),and no significant change was found in the parameters mentioned above (P＞0.05),and the pathological changes were significantly attenuated in group α-BGT.Compared with group D,the lung water content,MPO activities,and contents of IL-1β,TNF-α and IL-6 were significantly increased,the expression of NF-κB was up-regulated (P＜0.05),and the pathological changes were aggravated in group D + α-BGT.Conclusion Dexmedetomidine can mitigate scalds-induced acute lung injury in rats.

Objective To evaluate the role of α7 nicotinic acetylcholine receptor (α7nAChR) in reduction of endotoxin-induced acute lung injury (ALI) by limb ischemic preconditioning in mice.Methods Eighty healthy male C57BL/6 mice,aged 8-10 weeks,weighing 22-26 g,were randomly divided into 5 groups (n =16 each) using a random number table:control group (group C),ALI group,limb ischemic preconditioning group (group P),α-bungarotoxin (α-BGT) group,and limb ischemic preconditioning +α-BGT group (group P+α-BGT).Normal saline 100 μl was intratracheally instilled in group C.In group ALI,lipopolysaccharide 5 mg/kg was intratracheally instilled (in normal saline) to establish the model of endotoxin-induced ALI.In group P,the mice were subjected to 6 cycles of 5-min ischemia of the right hindlimb followed by 5-min reperfusion,and then the model of ALI was established.In group α-BGT,α-BGT 1 μg/kg was injected intraperitoneally before establishment of the model.In group P+α-BGT,limb ischemic preconditioning was performed,α-BGT 1 μg/kg was then injected intraperitoneally,and the model of ALI was established.At 24 h after LPS instillation,6 mice were selected from each group and sacrificed,and lungs were removed for microscopic examination and for determination of wet and dry lung weight,myeloperoxidase (MPO) activities,contents of interleukin-lbeta (IL-1β),tumor necrosis factoralpha (TNF-α) and IL-6,and expression of α7nAChR and high mobility group box-1 (HMGB1) in lung tissues.The lung water content was calculated.The survival of the left 10 mice in each group was observed at 7 days after establishment of the model,and the survival rate was calculated.Results Compared with group C,the lung water content,MPO activities,contents of IL-1β,TNF-α and IL-6,and HMGB1 expression were significantly increased,α7nAChR expression was significantly down-regulated,and the 7-day survival rate was significantly decreased in group ALI(P＜0.05).Compared with group ALI,the lung water content,MPO activities,contents of IL-1β,TNF-α and IL-6,and HMGB1 expression were significantly decreased,α7nAChR expression was significantly up-regulated,and the 7-day survival rate was significantly increased in group P (P＜0.05).Compared with group P,the lung water content,MPO activities,contents of IL-1β,TNF-α and IL-6,and HMGB1 expression were significantly increased,α7nAChR expression was significantly down-regulated,and the 7-day survival rate was significantly decreased in group P+α-BGT (P＜0.05).Conclusion The mechanism by which limb ischemic preconditioning inhibits inflammatory responses and reduces endotoxin-induced ALI is related to activation of α7nAChR in mice.

Objective:To evaluate the cytotoxicity of different dental bonding agents to human dental pulp cells. Methods:Four dental bonding agents(Prime & Bond NT,Single Bond,Xeno Ⅲ and iBond) were diluted with the culture medium by a ratio of 1∶1 000,1∶2 000 and 1∶4 000(v/v), and the fourth passage of dental pulp cells were then exposed to agent dilutions for 12, 24 and 48 h respectively, then the morphological changes of pulp cells were observed with microscopy and cytotoxicity was analyzed with modified 3-(4,5-dimethyl-thiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) assay.Results:There was significant influence of the type of dental bonding agents,exposure time and concentration on the cell morphology. Total-etch system was more toxic than self-etch system.Conclusion:Dental bonding agents are toxic to pulp cells,Single Bond is the strongest cytotoxic agent among the 4 adhesive agents.

Objective To evaluate the role of nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway in remote ischemic preconditioning-induced reduction of lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice.Methods Sixty-eight healthy male C57BL/6 mice,aged 6-8 weeks,weighing 22-26 g,were divided into 4 groups (n =17 each) using a random number table:control group (group C),ALI group,remote ischemic preconditioning group (group RIPC) and brusatol plus remote ischemic preconditioning group (group B+RIPC).Normal saline 100 μl was intratracheally instilled in group C.ALI was induced by intratracheal instillation of LPS 5 mg/kg in group ALI.Mice in group RIPC were subjected to 6 cycles of 5-min ischemia followed by 5-min reperfusion in the right hindlimbs using a tourniquet,and 1 h later the model of ALI was established.Nrf2 inhibitor brusatol 2 mg/kg (in 100 μl of 1％ dimethyl sulfoxide) was intraperitoneally injected every other day for 10 days prior to establishment of the ALI model in group B.Brusatol 2 mg/kg was intraperitoneally injected every other day for 10 days prior to establishment of the ALI model,and remote ischemic preconditioning was performed at 1 h before establishment of the ALI model in group B+RIPC.Seven mice in each group were selected at 24 h after establishment of the ALI model,and bronchoalveolar lavage fluid (BALF) was collected for determination of protein concentrations and neutrophil count.Mice were then sacrificed and lungs were removed for determination of lung water content,myeloperoxidase (MPO) activity,contents of interleukin-1beta (IL-1β) and tumor necrosis factor-alpha (TNF-α),and expression of Nrf2,HO-1 and high-mobility group box 1 protein (HMGB1) in lung tissues (by Western blot) and for examination of pathological changes (with a light microscope).Results Compared with group C,the lung water content,MPO activity,contents of IL-1β and TNF-α,and neutrophil count and protein concentrations in BALF were significantly increased,and the expression of Nrf2,HO-1 and HMGB1 was up-regulated in group ALI (P＜ 0.05).Compared with group ALI,the lung water content,MPO activity,contents of IL-1β and TNF-α,and neutrophil count and protein concentrations in BALF were significantly decreased,the expression of Nrf2 and HO-1 was up-regulated,and the expression of HMGB1 was down-regulated (P＜0.05),and the pathological changes were significantly attenuated in group RIPC.Compared with group RIPC,the lung water content,MPO activity,contents of IL-1β and TNF-α,and neutrophil count and protein concentrations in BALF were significantly increased,the expression of Nrf2 and HO-1 was down-regulated,and the expression of HMGB1 was up-regulated (P＜0.05),and the pathological changes were aggravated in group B+RIPC.Conclusion The activation of Nrf2/HO-1 signaling pathway is involved in remote ischemic preconditioning-induced reduction of LPS-induced ALI in mice.

Objective:To explore the resistance of common clinical isolates to chlorhexidine gluconate (CHG) and the clinical characteristics of patients with the infections.Methods:A total of 1 000 isolates from the First Affiliated Hospital of Wenzhou Medical University in 2018 (from January to May) were collected, which included 200 strains each of Escherichia coli ( E. coli), Acinetobacter baumanii ( A. baumanii), Pseudomonas aeruginosa ( P. aeruginosa), Staphylococcus aureus ( S. aureus), and Enterococcus spp.. Minimum inhibitory concentration (MIC) of CHG against 1 000 isolates were determined by the agar dilution method. The correlation between the resistance of isolates and clinical characteristics of infected patients was analyzed. Chi-square test or Fisher exact probability test were used for statistical analysis. Results:A total of 57 CHG resistant strains were detected in 1 000 clinical isolates. These CHG-resistant strains were mainly isolated from sputum and intensive care unit ward, accounting for 49.1%(28/57)and 38.6%(22/57), respectively. The resistance rates of P. aeruginosa, A. baumanii, Enterococcus spp., S. aureus, and E. coli to CHG were 16.0%(32/200), 7.0%(14/200), 3.0%(6/200), 1.5%(3/200) and 1.0%(2/200), respectively. The CHG-resistant rates of P. aeruginosa to ceftazidime, ciprofloxacin, levofloxacin and gentamicin were 53.1%(17/32), 78.1%(25/32), 65.6%(21/32) and 50.0%(16/32), respectively, which were all higher than those of CHG-sensitive P. aeruginosa (25.0%(8/32), 25.0%(8/32), 21.9%(7/32) and 15.6%(5/32), respectively), with statistical significance ( χ2=5.317, 18.080, 12.444 and 8.576, respectively, all P<0.05). The hospital mortality was 22.8%(13/57) in patients infected with CHG-resistant bacteria, which was higher than that in patients infected with CHG-sensitive bacteria ((7.0%(4/57); Fisher exact probability test, P=0.018)). CHG-resistant group had a higher history of CHG exposure and antimicrobial treatment (61.4%(35/57) and 70.2%(40/57), respectively), which were both higher than those with CHG-susceptible isolates (17.5%(10/57) and 47.4%(27/57), respectively), the differences were both statistically significant ( χ2=22.947 and 6.118, respectively, both P<0.05). In addition, the multi-drug resistance rate of CHG-resistant strains was 54.4%(31/57), which was higher than that of CHG-susceptible strains (35.1%(20/57)), the difference was statistically significant ( χ2=4.293, P=0.039). Conclusions:CHG resistant strains have higher antimicrobial resistance. Hospital mortality in patients infected with CHG-resistant bacteria is higher than patients infected with CHG-sensitive bacteria. The important risk factors are CHG exposure and antimicrobial therapy.