ABSTRACT
In recent years, the use of fluorescent contrast agents staining to guide surgery has flourished in various fields of surgery under the concept of precision surgery, which is helpful to guide surgery and provide surgeons with actual visible fluorescence imaging.Clinically, fluorescent contrast agent can be used to display tumor’s outline with high recognition degree, guide operation in real time, locate lymph node metastasis, detect small metastases, and identify important anatomical structures during the operation to avoid possible side-injury. Great progress has been made in the study of fluorescent contrast agents that can mediate surgery, including the study and surgical application development of classical fluorescent contrast agents such as indocyanine green and methylene blue, etc, as well as the discovery and clinical application of new targeted fluorescent contrast agents such as folate receptor targeting contrast agents, monoclonal antibody based fluorescent targeting contrast agents and intelligent contrast agents, etc. This paper will review the research and surgical application of fluorescent contrast agents in two aspects: classical fluorescent contrast agents and new targeted fluorescent contrast agents.
ABSTRACT
In recent years,the use of fluorescent contrast agents staining to guide surgery has flourished in various fields of surgery under the concept of precision surgery,which is helpful to guide surgery and provide surgeons with actual visible fluorescence imaging.Clinically,fluorescent contrast agent can be used to display tumor's outline with high recognition degree,guide operation in real time,locate lymph node metastasis,detect small metastases,and identify important anatomical structures during the operation to avoid possible side-injury.Great progress has been made in the study of fluorescent contrast agents that can mediate surgery,including the study and surgical application development of classical fluorescent contrast agents such as indocyanine green and methylene blue,etc,as well as the discovery and clinical application of new targeted fluorescent contrast agents such as folate receptor targeting contrast agents,monoclonal antibody based fluorescent targeting contrast agents and intelligent contrast agents,etc.This paper will review the research and surgical application of fluorescent contrast agents in two aspects:classical fluorescent contrast agents and new targeted fluorescent contrast agents.
ABSTRACT
Objective@#To investigate the bacterial flora distribution and antimicrobial resistance of patients with pyogenic liver abscess (PLA) in multi-centers of China.@*Methods@#The retrospective and descriptive study was conducted. The clinical data of 897 patients with PLA at 3 medical centers in China from October 2007 to April 2018 were collected, including 656 cases in the First Hospital of Harbin Medical University, 109 cases in Tongji Hospital Affiliated to Tongji Medical College of Huazhong University of Science and Technology and 132 cases in the Eastern Hepatobiliary Surgery Hospital of Naval Military Medical University. There were 582 males and 315 females, aged (59±11)years, with a range of 6-86 years. Observation indicators: (1) bacterial flora distribution; (2) bacterial resistance. Measurement data with normal distribution were represented as Mean±SD and measurement data with skewed distribution were represented as M (range). Count data were described as absolute numbers or percentages.@*Results@#(1) Bacterial flora distribution: among 897 patients, 733 cases of Klebsiella pneumoniae, 75 cases of Escherichia coli, 11 cases of Staphylococcus aureus, 10 cases of Streptococcus viridians, 9 cases of Klebsiella pneumoniae subsp. pneumoniae, 7 cases of β-emolytic streptococcus, 6 cases of Acinetobacter baumannii, 5 cases of Streptococcus intermadius, 5 cases of Enterococcus faecium, 3 cases of Alcaligenes xylosoxidans subsp. xylosoxidans, 2 cases of Proteus mirabilis, 2 cases of Streptococcus isthmus, 2 cases of Enterobacter cloacae subsp. cloacae, 1 case of Citrobacter koseri, 1 case of Proteus vulgaris, 1 case of Pasteurella pneumotropica, 1 case of Curobacter freudii, 1 case of Enterobacter amnigenus, 1 case of Stenotrophomonas maltophilia, 1 case of Acinetobacter lwoffii, 1 case of Streptococcus salivarius, 1 case of Streptococcus bacterium, 1 case of Enterococcus avium, 1 case of Enterococcus faecalis, 1 case of Klebsiella oxytoca, and 1 case of Staphylococcus epidermidis were cultured in the pus respectively. There were 12 cases of double bacterial infection, and 2 cases of multiple bacterial infections. (2) Bacterial resistance. ① Resistance of Klebsiella pneumoniae and Escherichia coli: the drug resistance rates of Klebsiella pneumoniae to ampicillin, piperacillin, cefazolin, cefuroxime, cefotaxime, ceftriaxone, ceftazidime, cefotetan, cefepime, cefoxitin, amoxicillin/carat Retinoic acid, ampicillin/sulbactam, piperacillin/tazobactam, cefoperazone/sulbactam, aztreonam, imipenem, meropenem, ertapenem, gentamicin, tobramycin, amikacin, tigaricycline, ciprofloxacin, levofloxacin, and trimethoprim sulfamethoxazole were 99.79%(474/475), 4.09%(7/171), 12.18%(82/673), 7.34%(49/668), 2.34%(4/171), 1.96%(11/562), 5.85%%(10/171), 0(0/562), 0.55%(4/733), 1.42%(9/635), 0(0/733), 2.46%(18/733), 0.55%(4/733), 0.27%(2/733), 1.36%(10/733), 0.14%(1/733), 0(0/733), 0.36%(2/562), 0.95%(7/733), 0.41%(3/733), 0(0/733), 0(0/562), 1.64%(12/733), 0.95%(7/733), and 4.50%(33/733), respectively. The drug resistance rates of Escherichia coli to above antibiotics were 78.67%(59/75), 40.91%(18/44), 65.33%(49/75), 56.00%(42/75), 38.64%(17/44), 41.94%(13/31), 20.00%(15/75), 3.23%(1/31), 25.33%(19/75), 5.77%(3/52), 18.67%(14/75), 32.00%(24/75), 8.00%(6/75), 16.00%(12/75), 37.33%(28/75), 1.33%(1/75), 0(0/75), 0(0/31), 40.00%(30/75), 14.67%(11/75), 1.33%(1/75), 0(0/31), 54.67%(41/75), 37.33%(28/75), and 52.00%(39/75), respectively. ② Drug resistance of other Gram-negative bacteria: the drug resistance rates of Klebsiella pneumoniae subsp. pneumoniae to ampicillin, cefazolin, cefuroxime, ceftriaxone, ceftazidime, cefotetan, cefepime, amoxicillin/carat Retinoic acid, ampicillin/sulbactam, piperacillin/tazobactam, cefoperazone/sulbactam, aztreonam, imipenem, meropenem, ertapenem, gentamicin, tobramycin, amikacin, ciprofloxacin, levofloxacin, and trimethoprim sulfamethoxazole were 8/8, 0/5, 0/5, 0/1, 0/9, 0/2, 0/9, 0/8, 0/9, 0/9, 0/6, 0/9, 0/9, 0/7, 0/1, 0/9, 0/8, 0/9, 0/9, 0/9, and 0/9. The drug resistance rates of Acinetobacter baumannii to ceftriaxone, ceftazidime, cefepime, ampicillin/sulbactam, piperacillin/tazobactam, cefoperazone/sulbactam, aztreonam, imipenem, meropenem, gentamicin, tobramycin, amikacin, tigaricycline, ciprofloxacin, levofloxacin, and trimethoprim sulfamethoxazole were 2/6, 4/6, 3/6, 0/6, 4/6, 1/6, 2/6, 4/6, 2/6, 4/6, 4/6, 3/6, 0/6, 4/6, 2/6, and 3/6, respectively. The drug resistance rates of Alcaligenes xylosoxidans subsp. xylosoxidans to ampicillin, cefazolin, cefuroxime, ceftazidime, cefepime, amoxicillin/carat Retinoic acid, piperacillin/tazobactam, aztreonam, imipenem, gentamicin, tobramycin, amikacin, ciprofloxacin, and levofloxacin were 3/3, 3/3, 3/3, 1/3, 1/3, 1/3, 0/3, 3/3, 2/3, 3/3, 3/3, 3/3, 3/3, and 1/3. ③ Drug resistance of other Gram-positive bacteria: the drug resistance rates of Staphylococcus aureus to penicillin, ampicillin, piperacillin, cefazolin, cefuroxime, cefotaxime, ceftazidime, cefepime, cefoxitin, amoxicillin/carat Retinoic acid, ampicillin/sulbactam, piperacillin/tazobactam, cefoperazone/sulbactam, aztreonam, imipenem, meropenem, gentamicin, tobramycin, amikacin, tetracycline, tigaricycline, ciprofloxacin, levofloxacin, moxifloxacin, trimethoprim sulfamethoxazole, linezolid, erythromycin, clindamycin, vancomycin, teicoplanin, and rifampin were 2/6, 6/8, 4/5, 4/5, 4/5, 4/5, 4/5, 4/5, 4/5, 4/5, 4/5, 4/5, 4/5, 3/5, 2/5, 2/5, 3/8, 3/5, 3/5, 0/8, 0/8, 3/8, 3/11, 0/5, 1/8, 0/8, 0/8, 2/6, 3/3, 1/3, and 0/3. The drug resistance rates of Streptococcus viridians to penicillin, ampicillin, ceftriaxone, cefoperazone/sulbactam, gentamicin, tetracycline, ciprofloxacin, levofloxacin, moxifloxacin, linezolid, erythromycin, clindamycin, vancomycin, teicoplanin, and rifampin were 3/10, 0/8, 0/7, 0/7, 2/8, 6/10, 0/8, 0/8, 0/7, 0/5, 4/10, 6/10, 0/5, 0/5, and 0/3. The drug resistance rates of β-emolytic streptococcus to antibacterial agents were 0. ④ Drug resistance of complex bacteria. For the 12 patients with double bacterial infection, in the Klebsiella pneumoniae combined with Gram-negative bacteria, the drug resistance rates of Klebsiella pneumoniae to cefotetan, cefoxitin, ampicillin/sulbactam, meropenem, ertapenem, tobramycin, tigecycline, and trimethoprim sulfamethoxazole were 0. The drug resistance rates of Acinetobacter baumannii to ertapenem, levofloxacin, and trimethoprim sulfamethoxazole were 0. The drug resistance rates of Escherichia coli to ceftazidime, cefoxitin, amoxicillin/clavulanic acid, piperacillin/tazobactam, imipenem, meropenem, ertapenem, tobramycin, amikacin, and tigecycline were 0. Citrobacter florida was sensitive to other antibiotics than levofloxacin and trimethoprim cotrimoxazole. In the Escherichia coli combined with Gram-positive bacteria, the drug resistance rates of Escherichia coli to cefotetan, cefepime, cefoxitin, cefoperazone/sulbactam, meropenem, tobramycin, and amikacin were 0. The drug resistance rates of Enterococcus faecalis to penicillin, ampicillin, levofloxacin, moxifloxacin, linezolid, vancomycin, and teicoplanin were 0. The drug resistance rates of Enterococcus casselifavus to ampicillin, tetracycline, levofloxacin, moxifloxacin, linezolid, and erythromycin were 0. The drug resistance rates of Staphylococcus hominis subspecies to levofloxacin, moxifloxacin, linezolid, vancomycin, teicoplanin, and rifampicin were 0. The drug resistance rates of Enterococcus faecium to tetracycline, linezolid, vancomycin, and teicoplanin were 0. In the multiple bacterial infections of Klebsiella pneumoniae + Escherichia coli + Staphylococcus aureus subspecies + Pseudomonas aeruginosa + Torulopsis glabrata, the drug resistance rates of Klebsiella pneumoniae to ceftriaxone, ceftazidime, cefotetan, cefepime, cefoxitin, ampicillin/sulbactam, piperacillin/tazobactam, cefoperazone/sulbactam, aztreonam, imipenem, tobramycin, amikacin, and levofloxacin were 0. The drug resistance rates of Escherichia coli to ceftazidime, cefotetan, cefepime, ampicillin/sulbactam, piperacillin/tazobactam, cefoperazone/sulbactam, aztreonam, imipenem, and amikacin were 0. The drug resistance rates of Staphylococcus aureus subspecies to ceftriaxone, ceftazidime, cefotetan, cefepime, ampicillin/sulbactam, piperacillin/tazobactam, cefoperazone/sulbactam, aztreonam, imipenem, tobramycin, amikacin, tigecycline, moxifloxacin, cotrimoxazole, teicoplanin, vancomycin, linezolid, and clindamycin were 0. The drug resistance rates of Pseudomonas aeruginosa to ceftazidime, cefepime, piperacillin/tazobactam, imipenem, gentamicin, tobramycin, amikacin, ciprofloxacin, and levofloxacin were 0. The drug resistance rates of Torulopsis glabrata to 5-fluorocytosine, fluconazole, itraconazole, and voriconazole were 0. In the multiple bacterial infections of Klebsiella pneumoniae + Escherichia coli + Acinetobacter baumannii, the drug resistance rates of Klebsiella pneumoniae to cefotetan, cefepime, piperacillin/tazobactam, imipenem, ertapenem, tobramycin, ciprofloxacin, and levofloxacin were 0. The drug resistance rates of Escherichia coli to amoxicillin/clavulanic acid, piperacillin/tazobactam, imipenem, meropenem were 0. The drug resistance ratets of Acinetobacter baumannii to trimethoprim sulfamethoxazole was 0.@*Conclusions@#Klebsiella pneumoniae is the main pathogen of PLA, followed by Escherichia coli. Klebsiella pneumoniae and Escherichia coli are sensitive to meropenem and tigecycline. Klebsiella pneumoniae subsp. pneumoniae and other Gram-negative bacteria are sensitive to ertapenem. Staphylococcus aureus are sensitive to Linezolid. Antibiotics are selected after drug sensitivity test for patients.
ABSTRACT
Objective To investigate the bacterial flora distribution and antimicrobial resistance of patients with pyogenic liver abscess (PLA) in multi-centers of China.Methods The retrospective and descriptive study was conducted.The clinical data of 897 patients with PLA at 3 medical centers in China from October 2007 to April 2018 were collected,including 656 cases in the First Hospital of Harbin Medical University,109 cases in Tongji Hospital Affiliated to Tongji Medical College of Huazhong University of Science and Technology and 132 cases in the Eastern Hepatobiliary Surgery Hospital of Naval Military Medical University.There were 582 males and 315 females,aged (59± 11) years,with a range of 6-86 years.Observation indicators:(1) bacterial flora distribution;(2) bacterial resistance.Measurement data with normal distribution were represented as Mean±SD and measurement data with skewed distribution were represented as M (range).Count data were described as absolute numbers or percentages.Results (1) Bacterial flora distribution:among 897 patients,733 cases of Klebsiella pneumoniae,75 cases of Escherichia coli,11 cases of Staphylococcus aureus,10 cases of Streptococcus viridians,9 cases of Klebsiella pneumoniae subsp.pneumoniae,7 cases of β-emolytic streptococcus,6 cases of Acinetobacter baumannii,5 cases of Streptococcus intermadius,5 cases of Enterococcus faecium,3 cases of Alcaligenes xylosoxidans subsp.xylosoxidans,2 cases of Proteus mirabilis,2 cases of Streptococcus isthmus,2 cases of Enterobacter cloacae subsp.cloacae,1 case of Citrobacter koseri,1 case of Proteus vulgaris,1 case of Pasteurella pneumotropica,1 case of Curobacter freudii,1 case of Enterobacter amnigenus,1 case of Stenotrophomonas maltophilia,1 case of Acinetobacter lwoffii,1 case of Streptococcus salivarius,1 case of Streptococcus bacterium,1 case of Enterococcus avium,1 case of Enterococcus faecalis,1 case of Klebsiella oxytoca,and 1 case of Staphylococcus epidermidis were cultured in the pus respectively.There were 12 cases of double bacterial infection,and 2 cases of multiple bacterial infections.(2) Bacterial resistance.① Resistance of Klebsiella pneumoniae and Escherichia coli:the drug resistance rates of Klebsiella pneumoniae to ampicillin,piperacillin,cefazolin,cefuroxime,cefotaxime,ceftriaxone,ceftazidime,cefotetan,cefepime,cefoxitin,amoxicillin/carat Retinoic acid,ampicillin/sulbactam,piperacillin/tazobactam,cefoperazone/sulbactam,aztreonam,imipenem,meropenem,ertapenem,gentamicin,tobramycin,amikacin,tigaricycline,ciprofloxacin,levofloxacin,and trimethoprim sulfamethoxazole were 99.79％ (474/475),4.09％ (7/171),12.18％ (82/673),7.34％(49/668),2.34％(4/171),1.96％(11/562),5.85％％(10/171),0(0/562),0.55％(4/733),1.42％(9/635),0(0/733),2.46％(18/733),0.55％(4/733),0.27％(2/733),1.36％(10/733),0.14％ (1/733),0 (0/733),0.36％ (2/562),0.95％ (7/733),0.41％ (3/733),0 (0/733),0 (0/562),1.64％ (12/733),0.95％ (7/733),and 4.50％ (33/733),respectively.The drug resistance rates of Escherichia coli to above antibiotics were 78.67％ (59/75),40.91％ (18/44),65.33％ (49/75),56.00％ (42/75),38.64％ (17/44),41.94％ (13/31),20.00％ (15/75),3.23％ (1/31),25.33％ (19/75),5.77％ (3/52),18.67％ (14/75),32.00％(24/75),8.00％(6/75),16.00％(12/75),37.33％(28/75),1.33％(1/75),0(0/75),0(0/31),40.00％(30/75),14.67％(11/75),1.33％(1/75),0(0/31),54.67％(41/75),37.33％ (28/75),and 52.00％ (39/75),respectively.② Drug resistance of other Gram-negative bacteria:the drug resistance rates of Klebsiella pneumoniae subsp.pneumoniae to ampicillin,cefazolin,cefuroxime,ceftriaxone,ceftazidime,cefotetan,cefepime,amoxicillin/carat Retinoic acid,ampicillin/sulbactam,piperacillin/tazobactam,cefoperazone/sulbactam,aztreonam,imipenem,meropenem,ertapenem,gentamicin,tobramycin,amikacin,ciprofloxacin,levofloxacin,and trimethoprim sulfamethoxazole were 8/8,0/5,0/5,0/1,0/9,0/2,0/9,0/8,0/9,0/9,0/6,0/9,0/9,0/7,0/1,0/9,0/8,0/9,0/9,0/9,and 0/9.The drug resistance rates of Acinetobacter baumannii to ceftriaxone,ceftazidime,cefepime,ampicillin/sulbactam,piperacillin/tazobactam,cefoperazone/sulbactam,aztreonam,imipenem,meropenem,gentamicin,tobramycin,amikacin,tigaricycline,ciprofloxacin,levofloxacin,and trimethoprim sulfamethoxazole were 2/6,4/6,3/6,0/6,4/6,1/6,2/6,4/6,2/6,4/6,4/6,3/6,0/6,4/6,2/6,and 3/6,respectively.The drug resistance rates of Alcaligenes xylosoxidans subsp.xylosoxidans to ampicillin,cefazolin,cefuroxime,ceftazidime,cefepime,amoxicillin/carat Retinoic acid,piperacillin/tazobactam,aztreonam,imipenem,gentamicin,tobramycin,amikacin,ciprofloxacin,and levofloxacin were 3/3,3/3,3/3,1/3,1/3,1/3,0/3,3/3,2/3,3/3,3/3,3/3,3/3,and 1/3.③ Drug resistance of other Gram-positive bacteria:the drug resistance rates of Staphylococcus aureus to penicillin,ampicillin,piperacillin,cefazolin,cefuroxime,cefotaxime,ceftazidime,cefepime,cefoxitin,amoxicillin/carat Retinoic acid,ampicillin/sulbactam,piperacillin/tazobactam,cefoperazone/sulbactam,aztreonam,imipenem,meropenem,gentamicin,tobramycin,amikacin,tetracycline,tigaricycline,ciprofloxacin,levofloxacin,moxifloxacin,trimethoprim sulfamethoxazole,linezolid,erythromycin,clindamycin,vancomycin,teicoplanin,and rifampin were 2/6,6/8,4/5,4/5,4/5,4/5,4/5,4/5,4/5,4/5,4/5,4/5,4/5,3/5,2/5,2/5,3/8,3/5,3/5,0/8,0/8,3/8,3/11,0/5,1/8,0/8,0/8,2/6,3/3,1/3,and 0/3.The drug resistance rates of Streptococcus viridians to penicillin,ampicillin,ceftriaxone,cefoperazone/sulbactam,gentamicin,tetracycline,ciprofloxaein,levofloxaein,moxifloxacin,linezolid,erythromycin,clindamycin,vancomycin,teicoplanin,and rifampin were 3/10,0/8,0/7,0/7,2/8,6/10,0/8,0/8,0/7,0/5,4/10,6/10,0/5,0/5,and 0/3.The drug resistance rates of β-emolytic streptococcus to antibacterial agents were 0.④ Drug resistance of complex bacteria.For the 12 patients with double bacterial infection,in the Klebsiella pneumoniae combined with Gramnegative bacteria,the drug resistance rates of Klebsiella pneumoniae to cefotetan,cefoxitin,ampicillin/sulbactam,meropenem,ertapenem,tobramycin,tigecycline,and trimethoprim sulfamethoxazole were 0.The drug resistance rates of Acinetobacter baumannii to ertapenem,levofloxacin,and trimethoprim sulfamethoxazole were 0.The drug resistance rates of Escherichia coli to ceftazidime,cefoxitin,amoxicillin/clavulanic acid,piperacillin/tazobactam,imipenem,meropenem,ertapenem,tobramycin,amikacin,and tigecycline were 0.Citrobacter florida was sensitive to other antibiotics than levofloxacin and trimethoprim cotrimoxazole.In the Escherichia coli combined with Gram-positive bacteria,the drug resistance rates of Escherichia coli to cefotetan,cefepime,cefoxitin,cefoperazone/sulbactam,meropenem,tobramycin,and amikacin were 0.The drug resistance rates of Enterococcus faecalis to penicillin,ampicillin,levofloxacin,moxifloxacin,linezolid,vancomycin,and teicoplanin were 0.The drug resistance rates of Enterococcus casselifavus to ampicillin,tetracycline,levofloxacin,moxifloxacin,linezolid,and erythromycin were 0.The drug resistance rates of Staphylococcus hominis subspecies to levofloxacin,moxifloxacin,linezolid,vancomycin,teicoplanin,and rifampicin were 0.The drug resistance rates of Enterococcus faecium to tetracycline,linezolid,vancomycin,and teicoplanin were 0.In the multiple bacterial infections of Klebsiella pneumoniae + Escherichia coli + Staphylococcus aureus subspecies + Pseudomonas aeruginosa + Torulopsis glabrata,the drug resistance rates of Klebsiella pneumoniae to ceftriaxone,ceftazidime,cefotetan,cefepime,cefoxitin,ampicillin/sulbactam,piperacillin/tazobactam,cefoperazone/sulbactam,aztreonam,imipenem,tobramycin,amikacin,and levofloxacin were 0.The drug resistance rates of Escherichia coli to ceftazidime,cefotetan,cefepime,ampicillin/sulbactam,piperacillin/tazobactam,cefoperazone/sulbactam,aztreonam,imipenem,and amikacin were 0.The drug resistance rates of Staphylococcus aureus subspecies to ceftriaxone,ceftazidime,cefotetan,cefepime,ampicillin/sulbactam,piperacillin/tazobactam,cefoperazone/ sulbactam,aztreonam,imipenem,tobramycin,amikacin,tigecycline,moxifloxacin,cotrimoxazole,teicoplanin,vancomycin,linezolid,and clindamycin were 0.The drug resistance rates of Pseudomonas aeruginosa to ceftazidime,cefepime,piperacillin/tazobactam,imipenem,gentamicin,tobramycin,amikacin,ciprofloxacin,and levofloxacin were 0.The drug resistance rates of Torulopsis glabrata to 5-fluorocytosine,fluconazole,itraconazole,and voriconazole were 0.In the multiple bacterial infections of Klebsiella pneumoniae + Escherichia coli + Acinetobacter baumannii,the drug resistance rates of Klebsiella pneumoniae to cefotetan,cefepime,piperacillin/tazobactam,imipenem,ertapenem,tobramycin,ciprofloxacin,and levofloxacin were 0.The drug resistance rates of Escherichia coli to amoxicillin/clavulanic acid,piperacillin/tazobactam,imipenem,meropenem were 0.The drug resistance ratets of Acinetobacter baumannii to trimethoprim sulfamethoxazole was 0.Conclusions Klebsiella pneumoniae is the main pathogen of PLA,followed by Escherichia coli.Klebsiella pneumoniae and Escherichia coli are sensitive to meropenem and tigecycline.Klebsiella pneumoniae subsp.pneumoniae and other Gram-negative bacteria are sensitive to ertapenem.Staphylococcus aureus are sensitive to Linezolid.Antibiotics are selected after drug sensitivity test for patients.
ABSTRACT
Objective To observe the effect of heparin on the cellular morphology and the expressions of nitric oxide (NO) and reactive oxygen species (ROS) in renal microvascular endothelial cells (RMVECs) stimulated by lipopolysaccharide (LPS). Methods The three step gradient screen method was used to primarily culture rat RMVECs, and the 3rd and 4th generation cells with excellent growth were collected. The cells were divided into blank control group, 10 mg/L LPS treatment group and 2.5, 5, 10 kU/L heparin pretreatment groups (the corresponding dose of heparin was given 0.5 hour before LPS stimulation). The morphology of the cells at 24 hours after LPS stimulation was observed by transmission electron microscope, the expression of ROS in RMVECs was determined by immunofluorescence at 5, 15, 30, 45 minutes after LPS stimulation, and the expression of NO in RMVECs was determined by nitrate reductase method. Results ① In blank control group, the RMVECs membrane was intact, and the mitochondria and endoplasmic reticulum in cells were clearly visible. The nuclear membrane was complete, and nucleolus was obvious. Cell bubble deformation was obvious at 24 hours after LPS stimulation, especially in the mitochondria and cell membrane. After 10 kU/L heparin pretreatment, the vacuolar degeneration of organelles was significantly reduced, and the cell membrane morphology was stable. ② The increases in ROS and NO in RMVECs could be detected at 5 minutes after LPS stimulation, showed an increase tendency with time prolongation, ROS expression peaked at 30 minutes, NO expression peaked at 45 minutes, which showed significant differences as compared with those of blank control group [30-minute ROS (mean density): 76.2±5.8 vs. 1.5±0.1, 45-minute NO (μmol/L): 70.3±8.6 vs. 1.8±0.1, both P < 0.01]. The expression of ROS and NO production in RMVECs were significantly reduced by heparin, showed a decrease tendency with heparin dose elevation, and the most obvious effect was 10 kU/L of heparin, with significant difference as compared with those of LPS treatment group [30-minute ROS (mean density): 16.8±1.7 vs. 76.2±5.8, 45-minute NO (μmol/L): 11.8±8.6 vs. 70.3±8.6, both P < 0.01]. Conclusions Unfractionated heparin ameliorates LPS induced expressions of NO and ROS in RMVECs and protects the cell morphology. The effect of 10 kU/L heparin is most obvious.
ABSTRACT
Objective To study unfractionated heparin (UFH) effect on the expression of HOXA9 in activation of human umbilical vein endothelial cells (HUVECs) induced by lipopolysaccharide (LPS). Methods HUVECs were cultured and they were randomly divided into four groups (n = 5) for the challenge respectively: ① control group (with an equal volume of phosphate buffer saline); ② LPS group (LPS 10 mg/L); ③UFH group (UFH 10 kU/L);④ UFH+LPS group (10 kU/L UFH 30 minutes + LPS 10 mg/L). After treatment for 3 hours, the expressions of HOXA9, E-selectin and nuclear factor-κB (NK-κB) in endothelial cells were detected by Western Blot. Results Compared with the control group, the expression of HOXA9 in LPS group was significantly decreased, the expressions of E-selectin and NF-κB were significantly increased (HOXA9/β-actin: 0.082±0.009 vs. 0.199±0.067, E-selectin/β-actin:0.113±0.055 vs. 0.047±0.030, NF-κB/β-actin: 0.845±0.025 vs. 0.664±0.092, all P < 0.05). Compared with LPS group, the expression of HOXA9 in UFH+LPS group was significantly increased, the expressions of E-selectin and NF-κB were significantly decreased (HOXA9/β-actin: 0.190±0.096 vs. 0.082±0.009, E-selecin/β-actin: 0.057±0.017 vs. 0.113±0.055, NF-κB/β-actin: 0.544±0.060 vs. 0.845±0.025, all P < 0.05). Each protein expression of UFH group were in accordance with the control group. Conclusions In LPS stimulated endothelial cells, HOXA9 expression is down regulated, E-expression is reduced, and endothelial cell activation is inhibited. UFH can inhibit the activation of endothelial cells by decreasing the degree of HOXA9 reduced expression.
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Objective To compare risk factors and bacterial etiology in patients with early-onset versus late-onset ventilator-associated pneumonia (VAP) in intensive care unit (ICU).Methods This prospective cohort study enrolled mechanically ventilated patients hospitalized for more than 48 hours in the first affiliated hospital,China Medical University from Jan 2012 to Jun 2016.Subjects were classified by ventilator status:early-onset VAP (＜ 5 d ventilation,E-VAP) or late-onset VAP (≥ 5 d ventilation,L-VAP).Potential risk factors and pathogen were evaluated.Results A total of 4 179 patients in adult ICU were screened,3 989 (95.5％) of whom were mechanically ventilated,962 patients with mechanical ventilation time ≥ 48 h.VAP developed in 142 patients.E-VAP and L-VAP had different potential risk factors based on statistical analysis.Independent risk factors for E-VAP included male (OR =1.825,95％ CI 1.006-3.310),chronic obstructive pulmonary disease (COPD;OR =3.746,95％ CI 1.795-7.818),emergency intubation (OR =1.932,95％ CI 1.139-3.276),aspiration (OR =3.324,95％ CI 1.359-8.130).Whereas independent risk factors for L-VAP were coma (OR =2.335,95％ CI 1.300-4.194),renal dysfunction (OR =0.524,95％ CI O.290-O.947),emergency intubation (OR =2.184,95％ CI 1.334-3.574).Mortality in E-VAP and L-VAP group were both higher than the non-VAP group[30.2％(19/63)vs 19.8％ (162/820),P=0.044;29.1％ (23/79) vs 19.8％(162/820),P=0.046].The pathogens isolated from early-onset versus late-onset VAP were not significantly different between groups,which the most common ones were acinetobacter baumannii,pseudomonas aeruginosa and klebsiella pneumoniae.Conclusion E-VAP and L-VAP have different risk factors,however related pathogens are similar.Different specific preventive strategies are suggested based on different onset of VAP.
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Objective To compare risk factors and bacterial etiology in patients with early-onset versus late-onset ventilator-associated pneumonia (VAP) in intensive care unit (ICU).Methods This prospective cohort study enrolled mechanically ventilated patients hospitalized for more than 48 hours in the first affiliated hospital,China Medical University from Jan 2012 to Jun 2016.Subjects were classified by ventilator status:early-onset VAP (＜ 5 d ventilation,E-VAP) or late-onset VAP (≥ 5 d ventilation,L-VAP).Potential risk factors and pathogen were evaluated.Results A total of 4 179 patients in adult ICU were screened,3 989 (95.5％) of whom were mechanically ventilated,962 patients with mechanical ventilation time ≥ 48 h.VAP developed in 142 patients.E-VAP and L-VAP had different potential risk factors based on statistical analysis.Independent risk factors for E-VAP included male (OR =1.825,95％ CI 1.006-3.310),chronic obstructive pulmonary disease (COPD;OR =3.746,95％ CI 1.795-7.818),emergency intubation (OR =1.932,95％ CI 1.139-3.276),aspiration (OR =3.324,95％ CI 1.359-8.130).Whereas independent risk factors for L-VAP were coma (OR =2.335,95％ CI 1.300-4.194),renal dysfunction (OR =0.524,95％ CI O.290-O.947),emergency intubation (OR =2.184,95％ CI 1.334-3.574).Mortality in E-VAP and L-VAP group were both higher than the non-VAP group[30.2％(19/63)vs 19.8％ (162/820),P=0.044;29.1％ (23/79) vs 19.8％(162/820),P=0.046].The pathogens isolated from early-onset versus late-onset VAP were not significantly different between groups,which the most common ones were acinetobacter baumannii,pseudomonas aeruginosa and klebsiella pneumoniae.Conclusion E-VAP and L-VAP have different risk factors,however related pathogens are similar.Different specific preventive strategies are suggested based on different onset of VAP.
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The diagnosis of nonparasitic hepatic cysts has been significantly improved with the development of imaging techniques,however,the successful differential diagnosis depends on more careful consideration.The differential diagnosis of multiple hepatic cysts and polycystic liver disease depends on the family heredity,number of cysts,combination of polycystic kidney,division and the results of B ultrasound.The differential diagnosis of hepatic cyst and hepatic cystic adenocarcinoma depends on the imaging features and results of histopathological examination.Recently,laparoscopic surgery has been widespread-ly used in the management of hepatic cystic disease,while it still cannot replace open surgery.The individualized and various treatment should be selected according to the condition of the patients.
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Objective To investigate the pulmonary microvascular responsiveness of diabetic animals to sepsis and the potential mechanism of NO system.Methods Sixty-four Wistar rats of clean grade were randomly (random number) divided into 4 groups,namely normal control group (group A,n =16),diabetes group (group B,n =16),sepsis group (group C,n =16),diabetes and sepsis group (group D,n =16).Diabetic mellitus model was made in rats with injection of streptozotocin,STZ (65 mg/kg).Successful model was defined as the blood glucose value≥ 16.67 mmol/L 48 hours after injection of STZ.All animals were fed 4 weeks before initiation of next experiment.The sepsis model was established by intravenous injection of LPS (10 mg/kg) in rats.RT-PCR was used to determine the mRNA expression of Tie-2 in rats'blood.The ratio of dry/wet of lung tissue and the extravasation of Evans blue dye into the lung were detected.Quantitation of NO in lung tissue and serum was measured by using Griess method.RT-PCR was also used for determination of iNOS,eNOS,DDAH2 mRNA expressions in lung tissue.Data were analyzed with ANONA and LSD method for comparison between groups,and P ＜ 0.05 was considered statistically significant.Results Compared with septic group.,the diabetic rats with sepsis group demonstrated higher expression of Tie-2 mRNA in blood (19.72 ± 0.70) vs.(3.99 ± 0.92),P =0.00,lower ratio of dry/wet in lung tissue (0.19 ±0.01) vs.(0.22 ±0.01),P =0.000,higher permeability of Evans blue dye into lung tissue (3.76 ± 0.77) vs.(1.74 ± 0.24),P =0.000.Serum NO level was lower in group D than that in group C (123.13 ±4.24) vs.(188.30 ±5.18),P =0.000,however,NO levels in lung tissue of both group D and group C were higher than that in control group (53.62 ± 6.70),(23.63± 3.92) vs.(10.37 ± 1.29),P =0.00,and NO level in group D was higher in 2 times than that in group C (P =0.00).However,there were no differences in eNOS expression among groups A,B and C,but the difference in eNOS expression was present between group D with lower expression and group A,that lower in group D (0.07 ±0.02) vs.(0.38 ±0.05),P=0.017.Compared with group C,the expression of iNOS was higher in group D (80.23 ±2.49),(32.48±5.37) vs.(1.74±0.23),P=0.00),and the expression of DDAH2 was lower in group D (0.49 ±0.13),(7.26 ±0.50) vs.(11.96 ±0.55).Conclusions Diabetic rats with sepsis enhanced endothelial cell damages.Diabetes deteriorates the regulatory activity of NO system,suggesting the potential mechanism of the worsened damages of EC in diabetic sepsis host.
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Objective To evaluate the efficacy and safety of itraconazole injection in treatmeat of invasive fungal infections.Methods The clinical trial was conducted in 16 patients(17 times)with invasive fungal infection from August 2003 to August 2005,including 1 case confirmed,11 cases(12 times)suspected and 4 cases for empiric treatment.They were treated with iv itraconazole injection in a dose of 200 mg twice daily in the first and the second day,from the third day to 14th day they were given iv itraconazole injection in a dose of 200 mg once daily,and then treated with capsule in a dose of 200 mg twice daily for another 28 days.Two cases were treated with iv itraconazole injection in a dose of 200 mg twice daily for 9 days and 14 days;1 case in a dose of 200 mg once daily for 21 days.Results 62 strains were isolated from 16 patients with invasive fungal infection,including 40 strains in urine cultivate,and 21 strains of tropic candida were primacy.In confirmed and suspected patients,the cure rate was 6/13,the effective rate was 11/13 and the eradication rate was 6/13.The incidence of adverse reaction was 3/24.Conclusion Itraconazole injection is effective and safe in treatment of severe invasive fungal infections,especially in severe ill,old patients for long time use.