Biomedical subjects

Jie Zhou

Publications and source records attributed to Jie Zhou.

At least 37 records · Page 2Linked to original sources

PubMed2006

Solution structure of Urm1 and its implications for the origin of protein modifiers.

Protein modifiers are involved in diverse biological processes and regulate the activity or function of target proteins by covalently conjugating to them. Although ubiquitin and a number of ubiquitin-like protein modifiers (Ubls) in eukaryotes have been identified, no protein modifier has been found in prokaryotes; thus, their evolutionary origin remains a puzzle. To infer the evolutionary relationships between the protein modifiers and sulfur carrier proteins, we solved the solution NMR structure of the Urm1 (ubiquitin-related modifier-1) protein from Saccharomyces cerevisiae. Both structural comparison and phylogenetic analysis of the ubiquitin superfamily, with emphasis on the Urm1 family, indicate that Urm1 is the unique "molecular fossil" that has the most conserved structural and sequence features of the common ancestor of the entire superfamily. The similarities of 3D structure and hydrophobic and electrostatic surface features between Urm1 and MoaD (molybdopterin synthase small subunit) suggest that they may interact with partners in a similar manner, and similarities between Urm1-Uba4 and MoaD-MoeB establish an evolutionary link between ATP-dependent protein conjugation in eukaryotes and ATP-dependent cofactor sulfuration.

Models, Molecular↗

PubMed2006

Identification of nuclear localization signal that governs nuclear import of BRD7 and its essential roles in inhibiting cell cycle progression.

BRD7, a novel bromodomain gene, is identified to be associated with nasopharyngeal carcinoma (NPC). Decreased or loss of expression of BRD7 was detected in NPC biopsies and cell lines. Overexpression of BRD7 could inhibit NPC cell growth and arrest cells in cell cycle by transcriptionally regulating some important molecules involved in ras/MEK/ERK and Rb/E2F pathway, and downregulate the promoter activity of E2F3. In the present study, the subcellular localization of BRD7 was investigated. It was found that BRD7 was mainly localized in nucleus without distinct cell-specific difference between COS7 and HNE1. Furthermore, a functional nuclear localization signal (NLS) sequence ranging from amino acid 65 to 96 was identified and characterized. The NLS is composed of a cluster of four bipartite nuclear targeting sequences, which are tightly linked and extremely overlapped. We found that whether the entire NLS or the four bipartite nuclear targeting sequences could respectively determine the nuclear import of green fluorescent protein (GFP). The most important is that NLS-deleted BRD7 shifted the nuclear localization to be mostly in cytoplasm, and failed or reduced to negatively regulate the expression of cell cycle related molecules, cyclin D1 and E2F3, and cell cycle progression from G1 to S phase. In conclusion, NLS is an essential motif affecting BRD7 nuclear distribution, and the nuclear localization of BRD7 is critical for the expression of cell cycle related molecules and cell biological function.

Active Transport, Cell Nucleus↗

PubMed2006

A novel pregnane X receptor-mediated and sterol regulatory element-binding protein-independent lipogenic pathway.

The pregnane X receptor (PXR) was isolated as a xenosensor regulating xenobiotic responses. In this study, we show that PXR plays an endobiotic role by impacting lipid homeostasis. Expression of an activated PXR in the livers of transgenic mice resulted in an increased hepatic deposit of triglycerides. This PXR-mediated lipid accumulation was independent of the activation of the lipogenic transcriptional factor SREBP-1c (sterol regulatory element-binding protein 1c) and its primary lipogenic target enzymes, including fatty-acid synthase (FAS) and acetyl-CoA carboxylase 1 (ACC-1). Instead, the lipid accumulation in transgenic mice was associated with an increased expression of the free fatty acid transporter CD36 and several accessory lipogenic enzymes, such as stearoyl-CoA desaturase-1 (SCD-1) and long chain free fatty acid elongase. Studies using transgenic and knock-out mice showed that PXR is both necessary and sufficient for Cd36 activation. Promoter analyses revealed a DR-3-type of PXR-response element in the mouse Cd36 promoter, establishing Cd36 as a direct transcriptional target of PXR. The hepatic lipid accumulation and Cd36 induction were also seen in the hPXR "humanized" mice treated with the hPXR agonist rifampicin. The activation of PXR was also associated with an inhibition of pro-beta-oxidative genes, such as peroxisome proliferator-activated receptor alpha (PPARalpha) and thiolase, and an up-regulation of PPARgamma, a positive regulator of CD36. The cross-regulation of CD36 by PXR and PPARgamma suggests that this fatty acid transporter may function as a common target of orphan nuclear receptors in their regulation of lipid homeostasis.

Animals↗

PubMed2006

The transcriptional regulation role of BRD7 by binding to acetylated histone through bromodomain.

Studies showed that the bromodomain binds to acetyl-lysines on histone tails, which is involved in deciphering the histone codes. BRD7, a novel bromodomain gene, is the first described bromodomain gene involved in nasopharyngeal carcinoma (NPC). Previous studies showed that ectopic expression of BRD7 inhibited cell growth and cell cycle progression from G1 to S phase in HNE1 cells (a NPC cell line) by transcriptionally regulating some cell cycle related genes including E2F3 gene. In the present study, we revealed the co-localization between acetylated H3 and BRD7 and found that the bromodomain of BRD7 is required for this co-localization. More importantly, wild-type BRD7 interacted with H3 peptide acetylated at Lys14, while the bromodomain deleted mutant lost this ability. We also found that the mutant BRD7 failed to regulate E2F3 promoter activity and inhibit cell cycle progression. These results indicated that the transcriptional regulation role of BRD7 was achieved by binding to acetylated histone H3 and that the bromodomain was essential for this role. In addition, no obvious changes were observed in the acetylated level of histone H3 after transfection with BRD7, indicating that chromatin remodeling, not chromatin modification, is the major mechanism of BRD7 mediated gene transcription. Taken together, the present work shed light on the fact that a novel bromodomain gene, BRD7, is of importance in transcriptional regulation and cellular events including cell cycle.

Acetylation↗

PubMed2006

Calpain mediates a von Hippel-Lindau protein-independent destruction of hypoxia-inducible factor-1alpha.

Hypoxia-inducible factor 1 (HIF-1) is controlled through stability regulation of its alpha subunit, which is expressed under hypoxia but degraded under normoxia. Degradation of HIF-1alpha requires association of the von Hippel Lindau protein (pVHL) to provoke ubiquitination followed by proteasomal digestion. Besides hypoxia, nitric oxide (NO) stabilizes HIF-1alpha under normoxia but destabilizes the protein under hypoxia. To understand the role of NO under hypoxia we made use of pVHL-deficient renal carcinoma cells (RCC4) that show a high steady state HIF-1alpha expression under normoxia. Exposing RCC4 cells to hypoxia in combination with the NO donor DETA-NO (2,2'-(hydroxynitrosohydrazono) bis-ethanimine), but not hypoxia or DETA-NO alone, decreased HIF-1alpha protein and attenuated HIF-1 transactivation. Mechanistically, we noticed a role of calpain because calpain inhibitors reversed HIF-1alpha degradation. Furthermore, chelating intracellular calcium attenuated HIF-1alpha destruction by hypoxia/DETA-NO, whereas a calcium increase was sufficient to lower the amount of HIF-1alpha even under normoxia. An active role of calpain in lowering HIF-1alpha amount was also evident in pVHL-containing human embryonic kidney cells when the calcium pump inhibitor thapsigargin reduced HIF-1alpha that was stabilized by the prolyl hydroxylase inhibitor dimethyloxalylglycine (DMOG). We conclude that calcium contributes to HIF-1alpha destruction involving the calpain system.

Amino Acid Sequence↗

PubMed2006

Reactive oxygen species attenuate nitric-oxide-mediated hypoxia-inducible factor-1alpha stabilization.

Tissue hypoxia/ischemia are major pathophysiological determinants. Conditions of decreased oxygen availability provoke accumulation and activation of hypoxia-inducible factor-1 (HIF-1). Recent reports demonstrate a crucial role of HIF-1 for inflammatory events. Regulation of hypoxic responses by the inflammatory mediators nitric oxide (NO) and reactive oxygen species (ROS) is believed to be of pathophysiolgical relevance. It is reported that hypoxic stabilization of HIF-1alpha can be antagonized by NO due to its ability to attenuate mitochondrial electron transport. Likely, the formation of ROS could contribute to this effect. As conflicting results emerged from several studies showing either decreased or increased ROS production during hypoxia, we used experiments mimicking hypoxic intracellular ROS changes by using the redox cycling agent 2,3-dimethoxy-1,4-naphthoquinone (DMNQ), which generates superoxide inside cells. Treatment of A549, HEK293, HepG2, and COS cells with DMNQ resulted in a concentration-dependent raise in ROS which correlated with HIF-1alpha accumulation. By using a HIF-1alpha-von Hippel-Lindau tumor suppressor protein binding assay, we show that ROS produced by DMNQ impaired prolyl hydroxylase activity. When HIF-1alpha is stabilized by NO, low concentrations of DMNQ (<1 microM) revealed no effect, intermediate concentrations of 1 to 40 microM DMNQ attenuated HIF-1alpha accumulation and higher concentrations of DMNQ promoted HIF-1alpha stability. Attenuation of NO-induced HIF-1alpha stability regulation by ROS was mediated by an active proteasomal degradation pathway. In conclusion, we propose that scavenging of NO by ROS and vice versa attenuate HIF-1alpha accumulation in a concentration-dependent manner. This is important to fully elucidate HIF-1alpha regulation under inflammatory conditions.

Acetylcysteine↗

PubMed2006

Effect of truncated-ApoE4 overexpression on tau phosphorylation in cultured N2a cells.

The carboxyl-terminal amino acids 272-299-truncated apoE4 (delta272-299) is the main fragments of apoE4 hydrolysate in neurons. The effects of truncated-ApoE4 (delta272-299) overexpression on tau phosphorylation in cultured N2a cells were investigated. The truncated-apoE4 (delta272-299) cDNA was subcloned into pEGFP-c3 to form recombinant pEGFP-T-apoE4. pEGFP-c3, pEGFP-T-apoE4 and pEGFP-apoE4 were transfected into N2a cells respectively by lipofectamine 2000 method. After 24--48 h, tau phosphorylation was detected by Western blot assay and glycogen synthase kinase-3 (GSK-3) activity by using GSK-3 activity assay. The results showed that the overexpression of both full length-apoE4 and truncated apoE4 fragments in N2a cells induced a dramatic increase in phosphorylation of tau at Ser202 sites and the activation of GSK-3 as compared with untransfected cells, most significantly in the cells transfected with pEGFP-T-apoE4 (P < 0.05). It was concluded that in vitro overexpression of truncated-ApoE4 (delta272-299) can result in tau hyperphosphorylation in N2a cells by activating GSK-3, suggesting truncated-ApoE4 (delta272-299) might contribute the pathogenesis of Alzheimer disease.

Animals↗

PubMed2006

Adsorption of microcystins by carbon nanotubes.

The production of cyanobacterial toxins microcystins (MCs) by cyanobacterial bloom which may promote the growth of tumor in human liver is a growing environmental problem worldwide. In this paper, the adsorption of MC-RR and LR, which were extracted from cyanobacterial cells in Dianchi Lake in China, by carbon nanotubes (CNTs), wood-based activated carbon (ACs) and clays were investigated. Compared with ACs and clay materials of sepiolite, kaolinite and talc tested, CNTs were found to have a strong ability in the adsorption of MCs. At the concentrations of 21.5 mg l(-1) MC-RR and 9.6 mg l(-1) MC-LR in 50 mmol phosphate buffer solution (pH 7.0), the adsorption amounts of MCs by CNTs with the range of outside diameter from 2 to 10nm were 14.8 and 5.9 mg g(-1), which were about four times higher than those by other adsorbents tested. It was shown that with the decrease of CNTs outside diameters from 60 to 2 nm, the adsorption amount of MCs was apparently increased, however the size of CNTs particles formed in solution declined. This result implies that the size of CNTs tube pore that is fit for the molecular dimension of MCs plays a dominant role. Furthermore the specific surface area of CNTs was also found to be a factor in the adsorption of MCs. The results suggested that the selection of suitable size of CNTs as a kind of adsorbent is very important in the efficient eliminating MCs from drinking water in future.

Adsorption↗

PubMed2006

Differential expression of Epstein-Barr virus-encoded RNA and several tumor-related genes in various types of nasopharyngeal epithelial lesions and nasopharyngeal carcinoma using tissue microarray analysis.

Studies have revealed that Epstein-Barr virus (EBV) infection, genetic aberration, and environmental factors are of importance in the development of nasopharyngeal carcinoma (NPC), although the definite mechanism remains to be fully elucidated. The aim of our study is to investigate using tissue microarray analysis whether differential expression of EBV-encoded small RNA-1 (EBER-1) and several tumor-related genes were associated with NPC carcinogenesis. Immunohistochemistry and in situ hybridization were performed on tissue microarrays containing 148 NPCs and 164 noncancerous nasopharyngeal epithelia (NPE) with different morphologic features. We found that overexpressions of EBER-1 hybridization signals, p53, p21ras, and bcl-2 proteins and loss expressions of p16 and p27 proteins were significantly increased in NPC tissues compared with normal NPE and hyperplastic NPE (P </= .001). The overexpressions of EBER-1 and p53 (P < .001) and the loss expressions of P16 (P < .001) and P27 (P = .005) were also significantly higher and more frequently observed in NPC than in dysplastic NPE. The positive expression of EBER-1 hybridization signals in NPC had significant associations with overexpressions of p53 (P < .001), p21ras (P = .041), and bcl-2 proteins (P < .001) and loss expression of p16 protein (P = .001). Further analysis confirmed that the abnormal expression of p53, p16, and p27 proteins occurred in the earliest stage of nasopharyngeal epithelial carcinogenesis. In the final logistic regression analysis model, the positive hybridization signals of EBER-1 and the abnormal expression of p53, p16, and p27 proteins were independent contributions for nasopharyngeal carcinogenesis, and EBER-1 was the most significant, independent predictor of nasopharyngeal carcinogenesis (hazard ratio = 13.412, 95% confidence interval 6.179-29.111, P < .001). In conclusion, EBV infection, together with overexpressions of p53, and loss expressions of p16 and p27 proteins are involved in the multistep process of human nasopharyngeal epithelial carcinogenesis.

Adenocarcinoma↗

PubMed2006

Cloning and characterization of the BRD7 gene promoter.

BRD7, a novel bromodomain gene, encodes a protein that inhibits cell growth and cell cycle progression by transcriptional regulation of some cell cycle-related genes. Its transcriptional down-expression has been shown to be critical to the pathogenesis of Nasopharyngeal carcinoma (NPC). Little is known about the transcriptional mechanisms controlling BRD7 gene expression. In this paper, we have characterized the 5' regulatory region of the BRD7 gene in order to understand the molecular mechanisms regulating its expression. Transient transfection results suggested that the analyzed upstream sequences of the BRD7 gene might contain some important but not sufficient sequence information to confer the cell-type specificity of BRD7 gene expression. Further analysis with a series of deletions demonstrated that a 125-bp region was required for the basal promoter activity of the BRD7 gene. Results from ChIP and EMSA indicated that the promoter was responsive to Sp1, E2F, and E2F6. All of these suggest a possible mechanism that transcriptional factor Sp1, E2F, and E2F-6 are associated in the BRD7 promoter region and regulate BRD7 promoter activity. Taken together, these results will help to better understand the role of the BRD7 gene in signal-dependent transcriptional regulation, and to develop new reagents for therapeutic upregulation of the BRD7 gene in NPC.

Base Sequence↗

PubMed2006

Fingerprint recognition using model-based density map.

Utilizing more information other than minutiae is much helpful for large-scale fingerprint recognition applications. In this paper, we proposed a polynomial model to approximate the density map of fingerprints and used the model's parameters as a novel kind of feature for fingerprint representation. Thus, the density information can be utilized into the matching stage with a low additional storage cost. A decision-level fusion scheme is further used to combine the density map matching with conventional minutiae-based matching and experimental results showed a much better performance than using single minutiae-based matching.

Algorithms↗

PubMed2006

Fingerprint recognition by combining global structure and local cues.

As an important feature, orientation field describes the global structure of fingerprints. It provides robust discriminatory information other than traditional widely-used minutiae points. However, there are few works explicitly incorporating this information into fingerprint matching stage, partly due to the difficulty of saving the orientation field in the feature template. In this paper, we propose a novel representation for fingerprints which includes both minutiae and model-based orientation field. Then, fingerprint matching can be done by combining the decisions of the matchers based on the global structure (orientation field) and the local cue (minutiae). We have conducted a set of experiments on large-scale databases and made thorough comparisons with the state-of-the-arts. Extensive experimental results show that combining these local and global discriminative information can largely improve the performance. The proposed system is more robust and accurate than conventional minutiae-based methods, and also better than the previous works which implicitly incorporate the orientation information. In this system, the feature template takes less than 420 bytes, and the feature extraction and matching procedures can be done in about 0.30 s. We also show that the global orientation field is beneficial to the alignment of the fingerprints which are either incomplete or poor-qualitied.

Algorithms↗

PubMed2006

Multibody grouping by inference of multiple subspaces from high-dimensional data using oriented-frames.

Recently, subspace constraints have been widely exploited in many computer vision problems such as multibody grouping. Under linear projection models, feature points associated with multiple bodies reside in multiple subspaces. Most existing factorization-based algorithms can segment objects undergoing independent motions. However, intersections among the correlated motion subspaces will lead most previous factorization-based algorithms to erroneous segmentation. To overcome this limitation, in this paper, we formulate the problem of multibody grouping as inference of multiple subspaces from a high-dimensional data space. A novel and robust algorithm is proposed to capture the configuration of the multiple subspace structure and to find the segmentation of objects by clustering the feature points into these inferred subspaces, no matter whether they are independent or correlated. In the proposed method, an Oriented-Frame (OF), which is a multidimensional coordinate frame, is associated with each data point indicating the point's preferred subspace configuration. Based on the similarity between the subspaces, novel mechanisms of subspace evolution and voting are developed. By filtering the outliers due to their structural incompatibility, the subspace configurations will emerge. Compared with most existing factorization-based algorithms that cannot correctly segment correlated motions, such as motions of articulated objects, the proposed method has a robust performance in both independent and correlated motion segmentation. A number of controlled and real experiments show the effectiveness of the proposed method. However, the current approach does not deal with transparent motions and motion subspaces of different dimensions.

Algorithms↗

PubMed2006

Differential gene expression in mouse sclera during ocular development.

PURPOSE: Ocular development involves changes in extracellular matrix components of the scleral wall as it expands. This study was conducted to determine scleral gene expression profiles during mouse ocular development to identify genes involved in normal scleral growth. METHODS: Sample sets of pooled sclerae of 3- and 8-week-old mice were microdissected, and total RNA was isolated. After reverse transcription, the cDNA was in vitro transcribed to produce biotin-labeled cRNA. The purified biotin-labeled cRNA samples were hybridized to microarray chips (GeneChip Mouse Genome 430 2.0; Affymetrix, Santa Clara, CA). Gene transcript expression profiles were determined, and eight differentially expressed genes between the two age groups underwent further confirmation by real-time PCR analysis. RESULTS: Differential regulation of 4884 gene transcripts in mouse sclera with less than 5% false-discovery rate (FDR) was identified. The top 1000 with the lowest FDR among the 4884 probe sets were filtered for threefold changes between the two age groups, and 718 gene transcripts were identified. Among these 718 gene transcripts, 210 were upregulated and 508 downregulated in adult relative to juvenile mouse sclera. TGF-beta1 and several collagen genes were significantly downregulated. Microarray differential expression by real-time PCR validation of eight extracellular matrix-associated gene transcripts was confirmed. CONCLUSIONS: This is the first study to demonstrate gene expression profiles in mouse sclera during ocular growth. These findings support the role of TGFbeta1 as a signaling molecule in modulating extracellular matrix during ocular development. This endeavor may be helpful in furthering understanding of how scleral remodeling is regulated during eye growth.

Animals↗

PubMed2006

Genomewide scan and fine mapping of quantitative trait loci for intraocular pressure on 5q and 14q in West Africans.

PURPOSE: High intraocular pressure (IOP) is a major risk factor for glaucoma, one of the leading causes of blindness worldwide. Because it has been demonstrated that African populations are at increased risk for glaucoma, the authors investigated the genetic basis of IOP in a sample of West Africans with type 2 diabetes (T2D) from Ghana and Nigeria. METHODS: Genomewide linkage analysis was conducted for loci linked to IOP (measured by applanation tonometry) in 244 affected sibling pairs with T2D using 372 autosomal short-tandem repeat markers at an average spacing of 9 cM. RESULTS: Multipoint variance components linkage analyses revealed suggestive linkage on chromosome 5 (5q22) with a logarithm of odds (LOD) score of 2.50 (nominal P = 0.0003; empiric P = 0.0004) and on chromosome 14 (14q22) with an LOD score of 2.95 (nominal P = 0.0001; empiric P = 0.0003). Fine mapping at a marker density of 2 cM in the 5q region confirmed the linkage signal, with an increase in peak LOD score to 4.91. CONCLUSIONS: The strong signal on chromosome 5 lies in the region in which a novel gene, WDR36, in the GLC1G locus was recently identified as causative for adult-onset primary open-angle glaucoma and provides additional evidence that chromosome 5 contains susceptibility loci for glaucoma in multiple human populations. The evidence provided in this study is particularly important given the evolutionary history of these West African populations and the recent ancestral relationship to African Americans-a population with one of the highest rates of diabetes and associated complications (including glaucoma) in the world.

Chromosome Mapping↗

PubMed2006

Cytokines and hormones in the regulation of hypoxia inducible factor-1alpha (HIF-1alpha).

Hypoxia inducible factor-1 (HIF-1) is a central component of the oxygen sensing system that coordinates cellular responses to conditions of decreased oxygen availability. The hypoxia inducible transcription factor HIF-1 is a heterodimer composed of the helix-loop-helix-Per-Arnt-Sim (bHLH-PAS) proteins HIF-1alpha and the aryl hydrocarbon nuclear translocator (ARNT) also known as HIF-1beta. Transactivation of HIF-1 transmits a hypoxic signal into patho-physiological responses such as angiogenesis, erythropoiesis, vasomotor control, an altered energy metabolism, as well as cell survival decisions by regulating a staidly growing number of target genes. Among recent advances are the discoveries that cytokines and growth factors make use of the 'hypoxic signaling system' under normoxia. Here we summarize current knowledge and existing concepts that help to understand how cytokines and hormones affect protein accumulation of HIF-1alpha and discuss potential implications of activating HIF-1 under normoxia. Considering the fundamental role of cytokines during inflammation may predict a role of HIF-1alpha in coordinating cellular responses to pathogens and point to the connection of cancer and inflammation. Moreover, we will address potential feed-back mechanisms showing an impact of HIF-1 on cytokine production. These considerations suggest an intimate signaling cross-talk between cytokines and the HIF-1 system.

Cytokines↗

PubMed2006

[Inhibition of nuclear translocation and binding activity of nuclear factor-kappaB by oligodeoxynucleotides in THP-1 cells].

OBJECTIVE: To observe the inhibitory effect of oligodeoxynucleotides (ODN) on nuclear translocation and nuclear binding activity of nuclear factor (NF)-kappaB in THP-1 cells. METHODS: Oligodeoxynucleotides were transfected via liposome into THP-1 cells followed by stimulation of the cells with lipopolysaccharide (LPS). Immunocytochemistry, electrophoretic mobility shift assay (EMSA) and reverse transcription (RT)-PCR were performed to detect the nuclear translocation and nuclear binding activity of NF-kappaB. RESULTS: Immunocytochemical results showed that after LPS stimulation of the ODN-transfected cells, NF-kappaB expression was still localized in cytoplasma. EMSA demonstrated inhibited nuclear binding activity of NF-kappaB in the ODN-transfected cells, and ODN inhibited the mRNA expression of tumor necrosis factor (TNF)-alpha, a NF-kappaB-associated inflammatory factor, as shown by RT-PCR. CONCLUSION: ODN can inhibit the nuclear translocation and binding activity of NF-kappaB in THP-1 cells, whereby the transcription and expression of the related inflammation factor genes is suppressed, which shed light on a new solution for clinical treatment of acute pancreatitis.

Cell Line↗

PubMed2006

[Analysis of factors for bacterial infection following liver transplantation].

OBJECTIVE: To investigate the association of surgical skills, anhepatic time and preoperative hepatic function grading with bacteria infection after the liver transplantation and identify the common bacterial flora involved for effective prevention and treatment of the posttransplant bacterial infection. METHODS;The clinical records of 31 cases of liver transplantation from August 2004 to August 2005 were reviewed and the collected data were analyzed statistically. RESULTS; Among the 31 cases, posttransplant bacterial infection occurred in 16 cases accounting for a total incidence of 51.61%, with the incidence of multi-system (or multi-organ) infection of 22.58%. The earlier cases had longer average surgery time and anhepatic period than the later cases, with also higher incidence of infection. Among the 19 patients with hepatic function class A before surgery, 7 acquired bacterial infection involving one system or organ, 2 had infections compromising multiple system or organ. In the 8 patients of hepatic function class B before surgery, 2 had single-system or -organ infection and 1 multi-system or -organ infection. Four out of the 5 patients with hepatic function class C before surgery acquired posttransplant bacterial infections, all involving multiple systems or organs. Pseudomonas aeruginosa was the most common bacteria responsible for the infections in these cases. CONCLUSION: Improvement of surgical skills can obviously reduce the incidence of bacterial infection after liver transplantation. No evidences suggest the correlation between the incidence of infections (including severe ones) and hepatic function class A or B before the operation, whereas patients with preoperative hepatic function class C seems to be at higher risk for infection involving multiple systems or organs. The anhepatic time does not significantly impact on the incidence or severity of the posttransplant infections, and Pseudomonas aeruginosa is the most common bacteria causing the infections.

Adult↗