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ABSTRACT: The animal model of the whole-size and reduced-size liver transplantation in both rat and mouse has been successfully established. Because of the difficulties and complexities in microsurgical technology, the animal model of dual liver transplantation was still not established for twelve years since the first human dual liver transplantation has been made a success. There is an essential need to establish this animal model to lay a basic foundation for clinical practice. To study the physiological and histopathological changes of dual liver transplantation, "Y" type vein from the cross part between vena cava and two iliac of donor and "Y' type prosthesis were employed to recanalize portal vein and the bile duct between dual liver grafts and recipient. The dual right upper lobes about 45-50% of the recipient liver volume were taken as donor, one was orthotopically implanted at its original position, the other was rotated 180° sagitally and heterotopically positioned in the left upper quadrant. Microcirculation parameters, liver function, immunohistochemistry and survival were analyzed to evaluate the function of dual liver grafts. No significant difference in the hepatic microcirculatory flow was found between two grafts in the first 90 minutes after reperfusion. Light and electronic microscope showed the liver architecture was maintained without obvious features of cellular destruction and the continuity of the endothelium was preserved. Only 3 heterotopically positioned graft appeared patchy desquamation of endothelial cell, mitochondrial swelling and hepatocytes cytoplasmic vacuolization. Immunohistochemistry revealed there is no difference in hepatocyte activity and the ability of endothelia to contract and relax after reperfusion between dual grafts. Dual grafts made a rapid amelioration of liver function after reperfusion. 7 rats survived more than 7 days with survival rate of 58.3.%. Using "Y" type vein and bile duct prosthesis, we successfully established a novel rat model of dual right upper liver lobe transplantation.
PLoS ONE 01/2012; 7(7):e40818. · 4.09 Impact Factor
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ABSTRACT: Sepsis due to Enterobacter aerogenes (E. aerogenes) is rare after liver transplantation but is also a serious infection that may cause liver abscess. The purpose of this case report is to relate an unusual presentation of liver transplantation to show how successive treatment can be an appropriate option in septic patients after liver transplantation.
We report on a patient with liver transplantation who developed sepsis due to extended spectrum beta-lactamases and AmpC-producing E. aerogenes.
A 39-year-old man had a biliary fistula and then was found to have multiple liver abscesses through abdominal ultrasound and an abdominal computed tomography scan, and carbapenem-sensitive E. aerogenes infection was confirmed. The patient was not successfully treated with conservative treatment consisting of intravenous carbapenems, percutaneous transhepatic cholangial drainage, and biliary stent placement by endoscopic retrograde cholangiopancreatography, so a second liver transplantation followed. Carbapenem-resistant E. aerogenes was detected in bile and blood after a five-week course of carbapenem therapy. The patient developed septic shock and multiple organ dysfunction syndrome.
We first report an unusual case of sepsis caused by E. aerogenes after liver transplantation in China. Carbapenem-resistant E. aerogenes finally leads to uncontrolled sepsis with current antibiotics. We hypothesize that the infection developed as a result of biliary fistula and predisposing immunosuppressive agent therapy. Further research is progressing on the aspect of immunomodulation therapy.
Hepatobiliary & pancreatic diseases international: HBPD INT 07/2009; 8(3):320-2. · 1.08 Impact Factor
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The Journal of Infectious Diseases 02/2009; 199(2):289. · 6.41 Impact Factor
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ABSTRACT: Liver transplantation is an effective treatment for end-stage liver disease, but a huge gap remains between the number of people who need a liver transplant and the number of organs available. In order to maximize donor organ access for adult and pediatric recipients, novel surgical and liver replacement procedures have evolved. Newer surgical techniques include split cadaveric liver transplantation and living donor liver transplantation (LDLT). With marginal and abnormal donor livers, despite tremendous advances in surgical technology, individual surgical procedure can not be completely brought into play unless effective measurements and basal studies are undertaken.
A literature search of MEDLINE and the Web of Science database using "liver transplantation" and "expanding donor pool" was conducted and research articles were reviewed.
Therapies directed toward scavenging O2-, inhibiting nicotinamide adenine dinucleotide phosphate oxidase, and/or immuno-neutralizing tumor necrosis factor-alpha may prove useful in limiting the liver injury induced by surgical procedures such as split liver transplantation or LDLT. Improved donor organ perfusion and preservation methods, modulation of inflammatory cytokines, energy status enhancement, microcirculation amelioration, and antioxidant usage can improve non-heart beating donor liver transplantation. Effective measures have been taken to improve the local conditions of donor cells with steatosis, including usage of fat-derived hormone and inflammatory mediators, ischemic preconditioning, depletion of Kupffer cells, and cytokine antibody and gene therapy. Double-filtration plasmapheresis can effectively reduce HCV viremia and prevent HCV recurrence in patient with high HCV RNA levels after LDLT.
Shortage of grafts and poor function of marginal and abnormal donor grafts put many patients at risk of death in waiting for liver transplantation. Advances in surgical technology, combined with improvement and breakthroughs in basic studies hold a promise in expanding the liver donor pool.
Hepatobiliary & pancreatic diseases international: HBPD INT 01/2009; 7(6):571-80. · 1.08 Impact Factor
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ABSTRACT: An armA-producing Klebsiella oxytoca isolate, strain 157, was detected after screening of 447 extended-spectrum beta-lactamase-producing Enterobacteriaceae isolates in China. K. oxytoca 157 was resistant to aminoglycosides, ciprofloxacin and most beta-lactams. Resistance to aminoglycosides and beta-lactams could be transferred to recipient Escherichia coli by conjugation. armA, blaCTX-M-15 and blaTEM-1 genes were detected in K. oxytoca 157 and transconjugant E. coli strain 600(pEC157). Mutation of aa 87 in GyrA was found in K. oxytoca 157. A plasmid of approximately 55 kb was extracted from K. oxytoca 157(pKO157) and E. coli 600(pEC157). Southern blot hybridization confirmed that the armA, blaCTX-M-15 and blaTEM-1 genes were all located on this conjugative plasmid (pEC157). PCR mapping was also performed to investigate the genetic environment of armA. The armA gene was found to be flanked by the same putative transposable elements as reported previously in E. coli, Klebsiella pneumoniae and Citrobacter freundii isolates from different countries.
Journal of Medical Microbiology 11/2008; 57(Pt 10):1273-6. · 2.50 Impact Factor
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ABSTRACT: The aim of this study was to evaluate the potential efficacy of therapy with thymosin alpha(1) and ulinastatin for patients with sepsis due to carbapenem-resistant bacteria.
Prospective, randomized, parallel controlled clinical study.
A total of 120 patients received a diagnosis of sepsis caused by infection with carbapenem-resistant bacteria and satisfied the study enrollment criteria. Sixty patients received carbapenems combined with thymosin alpha(1) and ulinastatin (the CTU group), and the other 60 patients were treated with carbapenems and placebo (the CP group). For both groups, flow cytometry was used to enumerate lymphocyte subsets, and ELISA was used to determine cytokine concentrations.
When the 2 groups were compared, the CTU group exhibited a better performance with respect to organ failure scores such as the Acute Physiology and Chronic Health Evaluation II score, the Multiple Organ Failure Score, and the Glasgow Coma Scale. The CTU group also showed significant improvements in CD4(+)CD8(+) count after initiation of treatment. In addition, compared with the CP group, in the CTU group the balance between proinflammatory mediators (such as tumor necrosis factor-alpha, interleukin [IL]-1beta, IL-6, and IL-8) and anti-inflammatory cytokines (including IL-4 and IL-10) was better modulated, and the cumulative survival rate of the CTU group exceeded that of the CP group by 17.8% at day 28, 25.9% at day 60, and 27.4% at day 90.
Immunomodulatory therapy that combines thymosin alpha(1) and ulinastatin appears to improve the survival rate for patients infected with carbapenem-resistant bacteria. The number of patients in this study was relatively small, and although the same number of patients was initially enrolled in each study group, the groups were not the same size at the end of the study. Therefore, a larger clinical trial should be conducted to validate this conclusion.
The trial was registered with the Chinese State Food and Drug Administration (Peking Science and Technology Development Plan, 2002[641]), (registration number 2007Y0211).
The Journal of Infectious Diseases 08/2008; 198(5):723-30. · 6.41 Impact Factor
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ABSTRACT: Four clinical strains of extended-spectrum beta-lactamase- and AmpC-producing Enterobacter aerogenes were isolated successively from a liver transplantation patient. Isolates C(1) and C(2) were isolated prior to carbapenem therapy, whilst isolates C(3) and C(4) were recovered after 40 days of carbapenem therapy. The homology of these strains was analysed by pulsed-field gel electrophoresis (PFGE). beta-Lactamases were analysed by isoelectric focusing, polymerase chain reaction (PCR) and sequencing. Outer membrane proteins were analysed by PCR, sequencing, sodium dodecyl sulphate-polyacrylamide gel electrophoresis and Western blot. Disruption of OmpE36 in C(1) in vitro was also performed by homologous gene recombination. The isolates demonstrated an indistinguishable PFGE pattern. Molecular characterisation revealed that, in addition to the pre-existing multiple beta-lactamases (DHA-1, TEM-1, SHV-5, CTX-M-3 and CTX-M-14) found in C(1) and C(2), isolates C(3) and C(4) failed to express OmpE36 owing to insertional inactivation by an IS903-like insertion sequence. Other resistance mechanisms, such as production of carbapenem-hydrolysing enzymes or expression of chromosomal efflux, were apparently not involved. Completely replacing OmpE36 by the kanamycin resistance gene (kan) resulted in a significant increase in carbapenem minimum inhibitory concentrations of an ompE36 mutant. Thus, C(3) and C(4) were apparently derived from the previously imipenem-susceptible isolates C(1) and C(2). Following carbapenem exposure, depletion of OmpE36 expression resulted in the collateral effect of carbapenem resistance.
International Journal of Antimicrobial Agents 07/2008; 32(4):302-7. · 4.13 Impact Factor
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ABSTRACT: To identify the aminoglycoside resistance gene in the high-level gentamicin resistant (HLGR) enterococcus and its transmission mechanism.
A HLGR strain, HZ95, of Enterococcus casseliflavus was screened by agar dilution method. The aminoglycoside activation enzyme genes were screened by PCR. The PCR products underwent purification, cloned, and sequenced. Plasmids were extracted and underwent Southern hybridization. Plasmid-mediated aminoglycoside modifying enzymes were cloned. The resistance of the HZ05 strain to different antimicrobial agents was determined by K-B method or agar dilution method.
A new aminoglycosides-modifying enzyme, APH (2'')-Ie, leading to HLGR, was found in the plasmid of the HZ95 bacteria. The aph (2'')-Ie gene and partial sequence of a streptomycin adenylyltransferase gene (str) were contained in the 8.7-kb cloned fragment, and the transposase gene (tnpA) was on the upper stream. The aph (2'')-Ie gene was located on the 16-kb plasmid with the amino acid sequence 96.1% homologous with chromosome-mediated APH (2'')-Id aminoglycoside-modifying enzyme.
HLGR can be caused by a new plasmid-mediated aminoglycosides-modifying enzyme, APH (2'')-Ie, which can be transmitted among plasmids or chromosome with other resistant genes through transposase.
Zhonghua yi xue za zhi 04/2006; 86(9):596-9.
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ABSTRACT: To determine the antibiotics resistance, aminoglycoside-modifying enzymes and homology of high-level gentamycin resistant enterococcus in clinical specimens.
The high-level gentamicin resistant (HLGR) isolates were screened by the agar method and the resistance of 14 antimicrobial agents was determined by K-B method. The aminoglycoside-modifying enzyme genes were detected by polymerase chain reaction (PCR). Pulsed-field gel electrophoresis (PFGE) was used to analyze the homology of HLGR isolates.
The ratio of HLGR was 64.2% (68/106). Among the HLGR,there were no isolates resistant to linezolid, vancomycin and tecoplanin, and Enterococcus faecium was more resistant to beta-lactam antibiotics and quinolone than Enterococcus faecalis. The positive rate of aac(6')-Ie-aph(2')-Ia was 92.6% and 3 isolates had the resistance gene mostly similar to aph(2')-Id. And among 51 HLGR isolates from the hospitalized patients, PFGE grouped 17 E. faecalis isolates into 4 clusters (A-D), and 33 E. faecium isolates into 8 clusters (A-H) with A cluster as predominant.
HLGR has become the important antibiotic resistance bacteria which results in nosocomial infection; and aac(6')-Ie-aph(2')-Ia is the main aminoglycoside-modifying enzyme gene which causes HLGR.
Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences 01/2006; 35(1):76-82.
