Quantitative image features of gadoxetic acid-enhanced MRI for predicting glypican-3 expression of small hepatocellular carcinoma ≤3 cm.

AIM: To explore the value of quantitative image features of gadoxetic acid-enhanced magnetic resonance imaging (MRI) for predicting Gglypican-3 (GPC3) expression of single hepatocellular carcinoma (HCC) ≤3 cm. MATERIALS AND METHODS: One hundred and forty-nine patients with histopathologically confirmed HCC were included retrospectively. Quantitative image features and clinicopathological parameters were analysed. The significant predictors for GPC3 expression were identified using multivariate logistic regression analyses. Nomograms were constructed from the prediction model and the progression-free survival (PFS) rate was evaluated by the Kaplan-Meier method. RESULTS: The tumour-to-liver signal intensity (SI) ratio on the hepatobiliary phase (HBP; odds ratio [OR] = 0.004; p=0.001), serum alpha-fetoprotein (AFP) > 20 ng/ml (OR=6.175; p<0.001), and non-smooth tumour margin (OR=4.866; p=0.002) were independent significant factors for GPC3 expression. When the three factors were combined, the diagnostic specificity was 97.7% (42/43). The nomogram based on the predictive model performed satisfactorily (C-index: 0.852). Kaplan-Meier curves showed that patients with GPC3-positive HCCs have lower PFS rates than patients with GPC3-negative HCCs (Log-rank test, p=0.006). CONCLUSION: The tumour-to-liver SI ratio on the HBP combined with serum AFP >20 ng/ml and non-smooth tumour margin are potential predictive factors for GPC3 expression of small HCC ≤3cm. GPC3 expression is correlated with a poor prognosis in HCC patients.

Expression of CALR mutants causes mpl-dependent thrombocytosis in zebrafish.

CALR mutations are identified in about 30% of JAK2/MPL-unmutated myeloproliferative neoplasms (MPNs) including essential thrombocythemia (ET) and primary myelofibrosis. Although the molecular pathogenesis of CALR mutations leading to MPNs has been studied using in vitro cell lines models, how mutant CALR may affect developmental hematopoiesis remains unknown. Here we took advantage of the zebrafish model to examine the effects of mutant CALR on early hematopoiesis and model human CALR-mutated MPNs. We identified three zebrafish genes orthologous to human CALR, referred to as calr, calr3a and calr3b. The expression of CALR-del52 and CALR-ins5 mutants caused an increase in the hematopoietic stem/progenitor cells followed by thrombocytosis without affecting normal angiogenesis. The expression of CALR mutants also perturbed early developmental hematopoiesis in zebrafish. Importantly, morpholino knockdown of mpl but not epor or csf3r could significantly attenuate the effects of mutant CALR. Furthermore, the expression of mutant CALR caused jak-stat signaling activation in zebrafish that could be blocked by JAK inhibitors (ruxolitinib and fedratinib). These findings showed that mutant CALR activates jak-stat signaling through an mpl-dependent mechanism to mediate pathogenic thrombopoiesis in zebrafish, and illustrated that the signaling machinery related to mutant CALR tumorigenesis are conserved between human and zebrafish.

Comprehensive analysis of RHD splicing transcripts reveals the molecular basis for the weak anti-D reactivity of Del -red blood cells.

BACKGROUND: Of the Rh blood type, Del is a rare variant that elicits the weakest anti-D reactivity. In this study, we revisit the genetic changes of Del allele and characterise the RHD splicing transcripts to realise the molecular basis of Del formation in the Taiwanese population. STUDY DESIGN AND METHODS: The RHD exons from Del and D-positive individuals were amplified by polymerase chain reaction (PCR) using different primer pairs followed by sequencing analyses. In addition, full-length RHD transcripts were reversed transcribed and amplified by nested-PCR. The type and frequency of the RHD splicing transcripts were analysed after sequencing the PCR products that were subcloned into a cloning vector. RESULTS: All Del individuals had a characteristic 1227G>A mutation. No deletion of the exon sequences was found. At least nine types of RHD splicing transcripts including exons 7/8/9 deletion, 7/9 deletion, 8/9 deletion, 9 deletion, 2/3/7/9 deletion, 2/3/7/8/9 deletion, exons 7/8/9 deletion with replacement of exon 3 with RHCE exon 3, exon 9 deletion with cryptic insertion of 170 bp of intron 7 and exons 7/8/9 deletion with cryptic insertion of 117 bp of intron 3 were identified in the Del -RBC. These aberrant splicing transcripts led to production of frame shift or truncated D antigen. Notably, no full-length RHD transcript was identified in the Del -RBC. CONCLUSION: The RHD 1227G>A mutation contributes to the molecular basis of Del phenotype in the Taiwanese population. The point mutation results in aberrant frame shift or exon deletion transcripts and generates D protein with weak antigen presenting function.

Genome-wide screen identified let-7c/miR-99a/miR-125b regulating tumor progression and stem-like properties in cholangiocarcinoma.

Cholangiocarcinoma (CCA), which is a poor prognosis malignancy that arises from the malignant transformation of cholangiocytes, is associated with chronic inflammation of the biliary epithelium. Thus far, the molecular mechanisms of the origin and neoplastic processes of CCA that are promoted by inflammation are still unclear and need to be fully elucidated. Here using small RNA sequencing to determine the microRNA (miRNA) expression profiles in CCA, we found that let-7c, miR-99a and miR-125b, which are three miRNAs of the same cluster, were downregulated in CCA and targeted interleukin 6 (IL-6), IL-6R and type 1 insulin-like growth factor, which are important cytokines and receptors of the IL-6/signal transducer and activator 3 (STAT3) pathway and have key roles in inflammation and CCA initiation. We also found that enforced expression of let-7c, miR-99a or miR-125b could reduce the activity of STAT3 and further suppress CCA tumorigenicity in vivo and inhibit the migration and invasion of CCA cells in vitro. Surprisingly, let-7c/miR-99a/miR-125b cluster also significantly decreased the ability of CCA cells for cancer stem cell-like mammosphere generation by downregulating CD133 and CD44, which suggests the pivotal roles of let-7c, miR-99a and miR-125b in CCA by regulating both inflammation and stem-like properties. Our findings showed potential links between miRNAs and inflammation, and provide a potential treatment strategy for developing an miRNA-based therapy via IL-6/STAT3 targeting for CCA.

De Novo Malignancies After Liver Transplantation With 14 Cases at a Single Center.

OBJECTIVE: To analyze the clinical characteristics, risk factors, and prevention of de novo malignant tumors after liver transplantation. METHODS: Fourteen patients who underwent liver transplantation were identified as having de novo malignancies. The clinical characteristics and survival of these patients were retrospectively reviewed. RESULTS: Fourteen cases of de novo malignancies after liver transplantation occurred for an incidence rate of 1.94% (14/722), including 11 men (78.6%, mean age, 48 y) and 3 women (21.4%, mean age, 50 y). The mean period from transplantation to cancer diagnosis was 55 ± 35 months. The distribution of tumor histologic types included colon cancer, lung cancer, esophageal cancer, nasopharyngeal cancer, liver cancer, parotid carcinoma, bone cancer, post-transplantation lymphoproliferative disorder, stomach cancer, bladder cancer, and laryngeal cancer. Twelve cases (85.7%) had hepatitis B. Five patients (35.7%) underwent operations, and the other 9 patients underwent chemotherapy or radiotherapy. During a mean follow-up period of 37 ± 26 months after the diagnosis of de novo malignancy, 8 patients (57.1%) died, with only 1 dying of causes not related to the de novo malignancy. The survival analysis showed 1-, 5-, and 7-year survival rates of 85.7%, 71.4%, and 42.9%, respectively. CONCLUSIONS: De novo malignancies after organ transplantation have been suggested to be a major cause of late mortality. De novo malignancy after orthotopic liver transplantation was found to be related to smoking, sex, and low immune function due to immunosuppressive agents. Solid tumors should be removed, and the patient should receive chemotherapy or radiotherapy as early as possible. Early diagnosis and treatment are very important for improving the prognosis.

Differential response of normal and malignant urothelial cells to CHK1 and ATM inhibitors.

While DNA damage response pathways are well characterized in cancer cells, much less is known about their status in normal cells. These pathways protect tumour cells from DNA damage and replication stress and consequently present potential therapeutic targets. Here we characterize the response of human telomerase reverse transcriptase (hTERT)-immortalized normal human urothelial (NHU) and bladder cancer cell lines to agents that disrupt the DNA damage response. Effects of replication and DNA damage response inhibitors on cell cycle progression, checkpoint induction and apoptosis were analysed in hTERT-NHU and bladder cancer cell lines. The primary signalling cascade responding to replication stress in malignant cells (ataxia telangiectasia-mutated (ATM) and Rad3-related-checkpoint kinase 1 (ATR-CHK1)) is not activated in hTERT-NHU cells after treatment with a replication inhibitor and these cells do not depend upon CHK1 for protection from apoptosis during replication stress. Instead, ATM signalling is rapidly activated under these conditions. Intriguingly, an ATM inhibitor suppressed S-phase checkpoint activation after exposure to replication inhibitors and stopped entry of cells into S-phase indicating G1 checkpoint activation. Consistent with this, hTERT-NHU cells treated with the ATM inhibitor showed increased levels of cyclin-dependent kinase inhibitor p19(INK4D), reduced levels of cyclin D1 and CDK4, and reduced phosphorylation of the retinoblastoma protein. In contrast, a bladder cancer cell line cotreated with ATM and replication inhibitors progressed more slowly through S phase and showed a marked increase in apoptosis. Taken together, our findings suggest that ATM and CHK1 signalling cascades have different roles in tumour and normal epithelial cells, confirming these as promising therapeutic targets.

Genetic and mechanistic evaluation for the weak A phenotype in Ael blood type with IVS6 + 5G>A ABO gene mutation.

BACKGROUND AND OBJECTIVES: Ael is a rare blood type that is characterized by weak agglutination of RBCs when reacts with anti-A antibody in adsorption-elution test. Although IVS6 + 5G→A mutation is known to associate with the Ael blood type, genetic and mechanistic evaluation for the weak agglutination of Ael with IVS6 + 5G→A mutation has not yet been completely addressed. MATERIALS AND METHODS: In this study, five cases of confirmed Ael individuals were analysed. The cDNAs for the A(el) alleles were obtained by cloning method for sequence analyses. The erythroleukemia K562 cells were used as the cell study model and were transfected with the A(el) expression construct. Flow cytometry analysis was then performed to determine the levels of surface antigen expression. RESULTS: The results indicated that IVS6 + 5G→A attributes to all cases of Ael . RT-PCR analyses revealed the presence of at least 10 types of aberrant A(el) splicing transcripts. Most of the transcripts caused early termination and produced non-functional protein during translation. Nevertheless, the transcript without exons 5-6 was predicted to generate functional Ael glycosyltransferase lacking 57 amino acids at the N-terminal segment. When the exons 5-6 deletion transcript was stably expressed in the K562 cells, weak agglutination of the cells can be induced by adding anti-A antibody followed by adsorption-elution test. CONCLUSION: This study demonstrates that aberrant splicing of A transcripts contributes to weak A expression and the weak agglutination of Ael -RBCs, adding to the complexity for the regulatory mechanisms of ABO gene expression.

The application of chromosome abnormality chip detection in male infertility / Aplicación de la detección de la anormalidad del cromosoma mediante biochips genéticos en la infertilidad masculina

OBJECTIVE: To discuss the application of microarray technology in the diagnosis of male infertility. METHODS: Sixteen loci, including a sex-determining region on the Y chromosome, were investigated by polymerase chain reaction (PCR) in infertile male patients. Chromosome abnormality chip with 180 000 probes was used to detect small deletion, small amplification and loss of heterozygosity. RESULTS: By PCR, nine of 103 infertile patients were found to have sequence-tagged site microdeletions. Microdeletions were not observed in control samples. The deletions detected by PCR were present in six azoospermic men (6/44, 13.6%) and in three oligoasthenoteratozoospermic (OATS) men (3/59, 5%). The overall frequency of microdeletions in infertile men was 8.7% (9/103). Chromosome abnormality chip detection 500+ detected more amplification or deletion in 51 infertile patients and the overall frequency of microdeletions in infertile men was 49.5% (51/103). CONCLUSION: Chromosome abnormality chip detection system provides a sensitive, economic and high-throughput method for detecting the deletion or amplification of genomic DNA sequences of infertile patients. Not only can it identify Yq deletions, but it can also find other chromosome abnormalities and facilitate the understanding of male infertility.

OBJETIVO: Analizar la aplicación de la tecnología de los microarreglos en el diagnóstico de la infertilidad masculina. MÉTODOS: Dieciséis loci, incluyendo una región determinante del sexo en el cromosoma Y, fueron investigados mediante reacción en cadena de la polimerasa (RCP) en pacientes hombres con problemas de infertilidad. Un biochip de la anormalidad cromosómica, con 180000 sondas, fue utilizado a fin de detectar pequeñas delecciones, pequeñas amplificaciones y pérdidas de heterocigosidad. RESULTADOS: Por medio de la RCP, se halló que nueve de 103 pacientes con infertilidad presentaban microdelecciones de sitios de secuencia marcada. Las microdelecciones no fueron observadas en las muestras de control. Las delecciones detectadas mediante RCP, estuvieron presentes en seis hombres azoospérmicos (6/44, 13.6%) y en tres hombres con oligoastenoteratozoospermia (OAT) (3/59, 5%). La frecuencia general de las microdelecciones en los hombres infértiles fue 8.7% (9/103). La detección con biochip de la anormalidad cromosómica de 500+ detectó más amplificación y delección en 51 pacientes, y la frecuencia general de microdelecciones en los hombres infértiles fue 49.5% (51/103). CONCLUSIÓN: El sistema de detección de la anormalidad del cromosoma mediante biochips genéticos representa un método sensible, económico, y de alto rendimiento, para detectar la delección o amplificación de las secuencias genómicas de ADN de pacientes infértiles. Este método puede no sólo identificar las delecciones Yq, sino también hallar otras anormalidades cromosómicas, facilitando así la comprensión de la infertilidad en los hombres.

The application of chromosome abnormality chip detection in male infertility.

OBJECTIVE: To discuss the application of microarray technology in the diagnosis of male infertility. METHODS: Sixteen loci, including a sex-determining region on the Y chromosome, were investigated by polymerase chain reaction (PCR) in infertile male patients. Chromosome abnormality chip with 180 000 probes was used to detect small deletion, small amplification and loss of heterozygosity. RESULTS: By PCR, nine of 103 infertile patients were found to have sequence-tagged site microdeletions. Microdeletions were not observed in control samples. The deletions detected by PCR were present in six azoospermic men (6/44, 13.6%) and in three oligoasthenoteratozoospermic (OATS) men (3/59, 5%).The overall frequency of microdeletions in infertile men was 8.7% (9/103). Chromosome abnormality chip detection 500+ detected more amplification or deletion in 51 infertile patients and the overall frequency of microdeletions in infertile men was 49.5% (51/103). CONCLUSION: Chromosome abnormality chip detection system provides a sensitive, economic and high-throughput method for detecting the deletion or amplification of genomic DNA sequences of infertile patients. Not only can it identify Yq deletions, but it can also find other chromosome abnormalities and facilitate the understanding of male infertility.

Neuronal Glud1 (glutamate dehydrogenase 1) over-expressing mice: increased glutamate formation and synaptic release, loss of synaptic activity, and adaptive changes in genomic expression.

Glutamate dehydrogenase 1 (GLUD1) is a mitochondrial enzyme expressed in all tissues, including brain. Although this enzyme is expressed in glutamatergic pathways, its function as a regulator of glutamate neurotransmitter levels is still not well defined. In order to gain an understanding of the role of GLUD1 in the control of glutamate levels and synaptic release in mammalian brain, we generated transgenic (Tg) mice that over-express this enzyme in neurons of the central nervous system. The Tg mice have increased activity of GLUD, as well as elevated levels and increased synaptic and depolarization-induced release of glutamate. These mice suffer age-associated losses of dendritic spines, nerve terminals, and neurons. The neuronal losses and dendrite structural changes occur in select regions of the brain. At the transcriptional level in the hippocampus, cells respond by increasing the expression of genes related to neurite growth and synapse formation, indications of adaptive or compensatory responses to the effects of increases in the release and action of glutamate at synapses. Because these Tg mice live to a relatively old age they are a good model of the effects of a "hyperglutamatergic" state on the aging process in the nervous system. The mice are also useful in defining the molecular pathways affected by the over-activation of GLUD in glutamatergic neurons of the brain and spinal cord.

A significant expansion of CD8+ CD28- T-suppressor cells in adult-to-adult living donor liver transplant recipients.

BACKGROUND: The appearance of human regulatory CD8(+) CD28(-) T-suppressor (Ts) cells has been associated with a reduced need for maintenance immunosuppression in cadaveric heart- kidney transplant recipients and pediatric liver-intestine transplant recipients. However, few data are available in adult-to-adult living donor liver transplantation (A-A LDLT). MATERIALS AND METHODS: To study the population of CD8(+) CD28(-) Ts cells in A-A LDLT, we performed flow cytometry on whole blood specimens obtained from 20 transplant recipients, 18 end-stage liver disease patients, and 20 normal controls. Meanwhile, we measured the trough levels of immunosuppressants and monitored graft function in transplant recipients. We retrospectively reviewed the clinical data of the 20 recipients. RESULTS: A significant expansion of CD8(+) CD28(-) Ts cells was observed among recipients of A-A LDLT as compared with a disease control group (P = .000) or healthy individuals (P = .000). All recipients were free of acute cellular rejection episodes. During the follow-up period, no grafts were lost due to acute or chronic rejection. CONCLUSION: Expansion of CD8(+) CD28(-) Ts cells in A-A LDLT seemed to be associated with a decreased occurrence of acute or chronic rejection and sustained good graft function. Based on our low dosages of immunosuppressants for recipients of A-A LDLT, we suggest that this strategy may promote expansion of CD8(+) CD28(-) Ts cells, which can conversely maintain the low immunosuppressant dosages.

Initial clinical effect of intraportal insulin administration on liver graft regeneration in adult patients underwent living donor right lobe liver transplantation.

OBJECTIVE: Insulin is one factor responsible for hepatotrophic regeneration in animal models. This study assessed the clinical effects of intraportal administration of insulin on liver graft regeneration in adult patients undergoing right lobe living donor liver transplantation (LDLT). METHODS: Between July 2005 and September 2007, 19 right lobe LDLT adult recipients voluntarily received posttransplant intraportal insulin administration. The present study describes 15 patients without postoperative vascular and bile duct complications, with more than 1 month survival and with complete clinical data who were enrolled to receive intraportal insulin therapy (group I; n = 15). Another consecutive 15 right lobe LDLT adult recipients without any stimulation regeneration who met the same criteria were enrolled in as noninsulin therapy control group (group NI; n = 15). Group I recipients were treated postoperatively with intraportal insulin infusion, as follows. An 18-gauge catheter was inserted into right gastro-omental vein during surgery, to administer regular insulin just after the operation at the rate of 2 U/h for 1 week. Graft volume (GV) was measured by computed tomography on postoperative days (POD) 7 and 30. Liver functions and serum insulin levels were also measured at POD 7 and POD 30. The liver graft regeneration rate was defined as ratio of posttransplant GV/harvested GV and posttransplant graft-to-recipient weight ratio (GRWR)/operative GRWR. RESULTS: The rate defined as ratio of POD 7 GV/harvested GV among group I was significantly greater than that of group NI (186.07 +/- 35.40% vs 160.61 +/- 22.11%; P < .05). The rate defined as ratio of POD 7 GRWR/operation GRWR was also significantly higher in group I than group NI (178.95 +/- 35.84% vs 156.56 +/- 18.53%; P < .05), whereas there was no significant difference in terms of regeneration rates at 1 month post-LDLT. Intraportal insulin administration may significantly downregulate POD 7 total bilirubin, aspartate aminotransferase, and alanine aminotransferase levels (P < .05). These results suggested that intraportal insulin administration augmented liver regeneration during the first postoperative week by improving hepatic function in LDLT recipients.

Using the Clavien grading system to classify the complications of right hepatectomy in living donors.

INTRODUCTION: The ratios of complications for living related liver donors after right hepatectomy differ widely among numerous single institutions. This study sought to use the Clavien classification system to define and graded the severity of these complications. MATERIALS AND METHODS: This study retrospectively analyzed the outcomes of 160 consecutive living donor right hepatectomies performed between July 2002 and February 2008. Complications among living donors for liver transplantation after right hepatectomy were stratified according to the Clavien classification of postoperative surgical complications. RESULTS: Fifty-two living donors displayed one or more perioperative complications Grade 1 complications were recorded in 18.1%; grade 2 in 6.3%; grade 3a in 5%; and grade 3b in 3.1%. Biliary complications were the most frequent. No donor mortality was present in this series. CONCLUSIONS: The Clavien grading system is useful to comparise surgical outcomes. This study demonstrated that donor right hepatectomy was a relatively safe procedure, but reducing donor complications after right hepatectomy has to be the first priority during the entire process of living related transplantation.

Asymmetric expression patterns of brain transthyretin in normal mice and a transgenic mouse model of Alzheimer's disease.

Brain asymmetry is linked with several neurological diseases, and transthyretin (TTR) is a protein sequestering beta-amyloid (Abeta) and helping to prevent the Alzheimer's disease (AD). We show, by real time reverse transcription-polymerase chain reaction (RT-PCR), in situ hybridization and Western blotting, that TTR exhibits a pattern of adult male-specific, leftward distribution in the mouse brain. This asymmetry appeared to be mainly due to the asymmetric distribution of the choroid plexus cells in the ventricles. Unlike the normal mice, however, the hemispheric levels of TTR transcripts of 2- and 6-month-old Tg2576 mice, a transgenic AD mouse model overexpressing Abeta, were symmetric in both sexes. Furthermore, at the age of 10 months when the pathological AD-like features had developed, the level of TTR transcripts in the left hemisphere of the male Tg2576 became significantly lower than the right one. This lowering of TTR transcript is accompanied with a higher Abeta level in the left hemisphere of the 10-month Tg2576 males. Finally, for both genders, the TTR transcript levels in the two hemispheres of aged Tg2576 mice were lower than either the adult Tg2576 or the aged nontransgenic controls. Based on the above, we suggest scenarios to correlate the changes in the levels and hemispheric patterns of TTR expression to the pathogenesis of AD.

Cloning, expression and location of RNase9 in human epididymis.

BACKGROUND: Mammalian spermatozoa become fully motile and fertile during transit through the luminal fluid of the epididymis. At least 200 proteins are present in the epididymal lumen, but the potential roles of these luminal proteins in male fertility are unknown. Investigation of the function of these proteins will elucidate the mechanism of sperm maturation, and also provide new drug targets for male contraception. We cloned RNase9 from a human epididymis cDNA library for characterization and analysis of its functions. FINDINGS: It was predicted that human RNase9 gene was located on chromosome 14q11.2 and encoded a 205 amino acids protein with a signal peptide of 26 amino acids at the N-terminus. The protein had eight conserved cysteine residues characteristic of the RNase A family members and several potential post-translational modification sites.At the transcriptional level, RNase9 was expressed in a wide variety of tissues, and the expression was higher in men than in boys. RNase9 was localized to the post-equatorial region of the sperms' head. Immunofluorescence staining showed that RNase9 protein was present mostly in the epithelium of the epididymal tubule. Recombinant RNase9 had no ribonuclease activity. In addition, RNase9 had no detectable effect on sperm motility and fertilization as demonstrated by blocking spermatozoa with anti-RNase9 polyclonal serum. CONCLUSION: RNase9 is expressed in a wide variety of tissues. It is located on the post-equatorial region of the sperm head and the epithelium of epididymal tubule. Although RNase9 belongs to the RNase A family, it has no ribonuclease activity.

University of California at San Francisco criteria can be applied to living donor liver transplantation for hepatocellular carcinoma: single-center preliminary results in 27 patients.

BACKGROUND: Living donor liver transplantation (LDLT) can provide life-saving therapy for many patients with hepatocellular carcinoma (HCC), who otherwise would succumb due to tumor progression. However, donor risk must be balanced against potential recipient benefit. METHODS: From January 2002 to December 2006, a total of 27 LDLT were performed for HCC patients in our center, including 25 right lobe grafts, and 2 dual grafts. Twenty-four (88.89%) met the University of California at San Francisco (UCSF) criteria, whereas 3 (11.11%) did not. RESULTS: Of our 29 donors, the overall complication rate was 17.24%. Two (6.90%) experienced major complications including intra-abdominal bleeding and portal vein thrombosis in 1, respectively; 3 (10.34%) experienced minor complications: wound steatosis, pleural effusion, and transient chyle leakage in 1, respectively. We did not observe any donor mortality; all donors fully recovered and returned to their previous occupations. No recipient developed small-for-size syndrome. The overall HCC patient survival rates at 1- and 3-years were 84.01% and 71.40%, respectively, similar to those of patients undergoing LDLT for various nonmalignant diseases during the same period (P > .05). CONCLUSIONS: Although further study is needed to fully assess the risks and benefits of LDLT for both HCC patients and donors, our preliminary results suggested that LDLT offered an acceptable chance and duration of survival for HCC patients. It was not only a relatively safe procedure provided that every effort was taken to minimize donor morbidities, but also beneficial for HCC recipients.

Arterial complications after living-related liver transplantation: single-center experience from West China.

Vascular complications after liver transplantation remain a major source of morbidity and mortality for recipients. In particular, patients receiving living-related liver transplantation (LRLT) experience a higher rate of vascular complications owing to the complex vascular reconstruction. Between July 2001 and December 2005, LRLTs were performed in our center on 33 patients with end-stage liver diseases. The 23 men and 10 women had a mean age of 32.6 +/- 11.3 years (range = 5 to 58 years). Of the 33 patients, the percentage of vascular complications was 9.09% (3 cases), including hepatic arterial thrombosis (HAT), hepatic arterial stenosis (HAS), or hepatic artery pseudoaneurysm (HAP) in one patient, respectively. No portal vein or hepatic vein complication occurred in our patients. Thrombectomy was performed in the patient with thrombosis. The patient with stenosis was treated with balloon angioplasty and endoluminal stent placement. The pseudoaneurysm was also successfully embolized to restore the blood flow toward the donor liver. Mean follow-up for all patients after LRLT was 18.0 +/- 5.4 months. The overall postoperative 30-day mortality rate was 6.06% (2/33). The 1-year survival rate was 86.36% in 22 patients with benign diseases and 72.73% in 11 patients with malignant diseases. However, no death was associated with vascular complications. Careful preoperative evaluation and intraoperative microsurgical technique for hepatic artery reconstructions are the keys to prevent vascular complications following LRLT. Immediate surgical intervention is required for acute vascular complications, whereas late complications may be treated by balloon angioplasty and endoluminal stent placement. Embolization may be a safe and effective approach in the treatment of a pseudoaneurysm of the hepatic artery.

Surgical procedures for management of right portal venous branching in right lobe living donor liver transplantation.

OBJECTIVE: This study sought to describe the surgical management of right portal venous (PV) branches encountered among 104 cases of right lobe living donor liver transplantation (LDLT). METHODS: From January 2002 to September 2007, we performed 104 cases of right-lobe LDLT including 11-donors who had anomalous right portal venous branches (APVB). One recipient had PV sponginess hemangioma. The donor right PV branches were type I in 93 cases, type II (trifurcation) in nine cases, and type III in two cases. Except one narrow bridge of tissue excision, the PV branches were transected on the principal of donor priority: PV branches were excised approximately 2 to 3 mm from the confluence while leaving the donor's main portal vein and confluence intact. In type II APVB, donor PV branches were obtained with two separate openings in six cases; with two separate openings joined as a common orifice at the back table in two cases, with one common opening with a narrow bridge of tissue in one case. In type III APVB, the donor right anterior and posterior PV branches were obtained with separate openings. The donor right PV branches with one common opening in 92 cases of type I PV branches and a joined common orifice in three cases of type II APVB were anastomosed to the recipient's main portal vein or to right branching. As the unavailable recipient PV for sponginess hemangioma, one case of type I right PV branches was end-to-end anastomosed to one of the variceal lateral veins of about 1 cm diameter in a pediatric patient. The PV were reconstructed as double anastomoses in six type II APVB and in one type III APVB obtained with two separate PV openings. In the another type III APVB reconstruction, we successfully utilized a novel U-shaped vein graft interposition. RESULTS: The type II APVB donor receiving a narrow bridge of portal vein tissue excision developed portal vein thrombosis on the third postoperative day and underwent reexploration for thrombectomy. There were no vascular complications, such as portal vein thrombosis or stricture among other donors or all recipients. The velocity of blood flow in the U-graft was normal. The anastomosis between the type I donor right portal vein and recipient variceal lateral vein was unobstructed. CONCLUSION: Right PV branches should be excised on the principal of donor priority while leaving the donor's main portal vein and confluence intact. Single anastomoses was the fundamental procedure of right branch reconstruction. Double anastomoses could be used as the main management for type II and type III APVB reconstruction. U-graft interposition may be a potential procedure for type III APVB reconstruction. Single anastomoses between the donor right portal vein and the recipient variceal lateral vein may be performed when recipient portal vein is unavailable. These innovations for excision and reconstruction of right PV branches were feasible, safe, and had good outcomes.