[Clinical analysis of 18 children with aggressive mature B-cell lymphoma after liver transplantation].

Objective: To summarize the clinical characteristics, prognostic factors and treatment outcomes of childhood aggressive mature B-cell lymphoma after liver transplantation. Methods: This retrospective study included 18 children with newly diagnosed aggressive mature B-cell lymphoma after liver transplantation and treated from June 2018 to June 2022 in the Department of Hematology and Oncology of Shanghai Children's Medical Center, Shanghai Jiao Tong University School of Medicine. Clinical characteristics, treatment and outcomes of patients at last evaluation were analyzed. Overall survival (OS) and event free survival (EFS) rates were calculated by Kaplan-Meier method and Log-Rank analysis was performed to find factors of poor prognosis. Results: Among all 18 patients, there were 6 males and 12 females, and the age of onset was 40 (35, 54) months. The interval from transplant to tumor diagnosis was 21 (17, 35) months and 5 patients had early onset disease (<1 year since transplant). Seventeen patients had abdominal lesions. Diarrhea, vomiting and abdominal masses were the main clinical manifestations. All patients were Epstein-Barr virus (EBV) related posttransplant lymphoproliferative disorders (PTLD). One patient received individualized therapy due to critical sick at diagnosis, and the remaining 17 patients received CP (cyclophosphamide, methylprednisolone plus rituximab) and (or) modified EPOCH (prednisone, etoposide, doxorubicin, vincristine, cyclophosphamide plus rituximab) regimens. Of all 18 patients, 15 cases got complete response, 2 cases got partial response, 1 patient died of severe infection. The 2-year OS and EFS rates of 18 patients were (94±5)% and (83±8)%, respectively. None of age, gender or early onset disease had effect on OS and EFS rates in univariate analysis (all P>0.05). Conclusions: The symptoms of PTLD were atypical. Close surveillance of EBV-DNA for patients after liver transplantation was crucial to early stage PTLD diagnosis. CP or modified EPOCH regimen was efficient for pediatric patients with aggressive mature B cell lymphoma after liver transplantation.

[Emphasis on multidisciplinary collaboration in clinical diagnosis and treatment of autoimmune disease-related ulcers].

The global prevalence and incidence of autoimmune diseases are increasing year by year, and the autoimmune diseases have become a major threat to public health. In the progression of the diseases, persistent and complex abnormal immune responses often lead to long-term unhealed skin ulcers, which not only affect the life quality of patients, but also lead to the aggravation of primary diseases. Therefore, doctors in burn surgery and other wound repair surgeries should pay attention to the understanding of autoimmune diseases. In the treatment of autoimmune disease-related ulcers, it is recommended to formulate a unified treatment plan according to the law of occurrence and development of the diseases, and multidisciplinary cooperation is needed to accelerate wound healing and improve the quality of wound healing.

Histone methyltransferase DOT1L coordinates AR and MYC stability in prostate cancer.

The histone methyltransferase DOT1L methylates lysine 79 (K79) on histone H3 and is involved in Mixed Lineage Leukemia (MLL) fusion leukemogenesis; however, its role in prostate cancer (PCa) is undefined. Here we show that DOT1L is overexpressed in PCa and is associated with poor outcome. Genetic and chemical inhibition of DOT1L selectively impaired the viability of androgen receptor (AR)-positive PCa cells and organoids, including castration-resistant and enzalutamide-resistant cells. The sensitivity of AR-positive cells is due to a distal K79 methylation-marked enhancer in the MYC gene bound by AR and DOT1L not present in AR-negative cells. DOT1L inhibition leads to reduced MYC expression and upregulation of MYC-regulated E3 ubiquitin ligases HECTD4 and MYCBP2, which promote AR and MYC degradation. This leads to further repression of MYC in a negative feed forward manner. Thus DOT1L selectively regulates the tumorigenicity of AR-positive prostate cancer cells and is a promising therapeutic target for PCa.

Data on the comprehensive first-principles diffusion study of the aluminum-magnesium system.

First-principles calculation of diffusion coefficients between Mg and Al is investigated comprehensively using density functional theory (DFT). The effect of different uncertainty sources arising from first principles calculations has been investigated systematically. These sources include the diffusion model, energetic, entropic and attempt frequency calculations. Variation in self and impurity diffusion coefficients of Mg and Al in stable phases are quantified using different DFT settings and compared with the experiments. Using the optimal DFT settings, diffusion coefficients in metastable phases of Al and Mg are predicted. The dataset refers to "An integrated experimental and computational study of diffusion and atomic mobility of the aluminum-magnesium system" [1].

[Female reproductive system dysplasia: a clinical study of 924 cases].

Objective: To explore the relationship between different types of female reproductive system dysplasia and age of visit, clinical manifestations, common types of combined malformations and endometriosis. Methods: The patient's medical records in the Second Hospital of Hebei Medical University from December 2002 to June 2016 were collected and retrospectively analyzed. Results: Among 924 cases of genital tract dysplasia, uterine dysplasia (65.3%, 824/1 261) was the most common, followed by vaginal dysplasia (28.3%, 357/1 261), hymen atresia and urogenital fistula (3.7%, 47/1 261), and cervical dysplasia (2.6%, 33/1 261). (1) The youngest age was in patients with hymen atresia and urogenital fistula, with a median of 14.5 years old, while the older age were in patients with uterine, vaginal and cervical dysplasia, with median age of 25.0, 24.0 and 23.0 years old, respectively. (2) The clinical manifestations were lack of specificity, mainly abnormal findings of physical examination or accessory examination, primary amenorrhea, lower abdominal pain, infertility, adverse pregnancy history. (3) About other systemic malformations, urological malformations were the most common (4.8%, 44/924), followed by spinal malformations (0.5%, 5/924), inguinal hernia (0.4%, 4/924), heart malformations (0.2%, 2/924), cleft lip and palate (0.2%, 2/924). Oblique vaginal septal syndrome and MRKH syndrome were the most likely to be associated with other system malformations. (4) About combination with endometriosis, there was no significant difference between obstructive genital tract malformations (2.3%, 9/385) and non obstructive genital tract malformations (1.7%, 9/539; P=0.469). Conclusions: Female reproductive system dysplasia is the most common in uterine dysplasia, followed by vaginal dysplasia, hymen atresia and urogenital fistula, and cervical dysplasia. The age of visit is generally older, often found by abnormal findings of physical examination or accessory examination, primary amenorrhea, lower abdominal pain, infertility, adverse pregnancy history;and could be combined with a variety of other system malformations, most seen by urinary system malformations,there is also the risk of endometriosis.

PKK deficiency in B cells prevents lupus development in Sle lupus mice.

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by the production of autoantibodies that can result in damage to multiple organs. It is well documented that B cells play a critical role in the development of the disease. We previously showed that protein kinase C associated kinase (PKK) is required for B1 cell development as well as for the survival of recirculating mature B cells and B-lymphoma cells. Here, we investigated the role of PKK in lupus development in a lupus mouse model. We demonstrate that the conditional deletion of PKK in B cells prevents lupus development in Sle1Sle3 mice. The loss of PKK in Sle mice resulted in the amelioration of multiple classical lupus-associated phenotypes and histologic features of lupus nephritis, including marked reduction in the levels of serum autoantibodies, proteinuria, spleen size, peritoneal B-1 cell population and the number of activated CD4 T cells. In addition, the abundance of autoreactive plasma cells normally seen in Sle lupus mice was also significantly decreased in the PKK-deficient Sle mice. Sle B cells deficient in PKK display defective proliferation responses to BCR and LPS stimulation. Consistently, B cell receptor-mediated NF-κB activation, which is required for the survival of activated B cells, was impaired in the PKK-deficient B cells. Taken together, our work uncovers a critical role of PKK in lupus development and suggests that targeting the PKK-mediated pathway may represent a promising therapeutic strategy for lupus treatment.

FOXA1 inhibits prostate cancer neuroendocrine differentiation.

Neuroendocrine prostate cancer (NEPC) has increasingly become a clinical challenge. The mechanisms by which neuroendocrine (NE) cells arises from prostate adenocarcinoma cells are poorly understood. FOXA1 is a transcription factor of the forkhead family that is required for prostate epithelial differentiation. In this study, we demonstrated that FOXA1 loss drives NE differentiation, demarcated by phenotypical changes and NEPC marker expressions. Mechanistically, this is mediated by FOXA1 binding to the promoter of interleukin 8 (IL-8), a chemokine previously shown elevated in NEPC, to directly inhibit its expression. Further, IL-8 upregulation activates the MAPK/ERK pathway, leading to ERK phosphorylation and enolase 2 (ENO2) expression. IL-8 knockdown or ERK inhibition, on the other hand, abolished FOXA1 loss-induced NE differentiation. Analysis of xenograft mouse models confirmed FOXA1 loss in NEPC tumors relative to its adenocarcinoma counterparts. Importantly, FOXA1 is downregulated in human NEPC tumors compared to primary and castration-resistant prostate cancers, and its expression is negatively correlated with that of ENO2. These findings indicate that FOXA1 transcriptionally suppresses IL-8, the expression of which would otherwise stimulate the MAPK/ERK pathway to promote NE differentiation of prostate cancer cells. Our data strongly suggest that FOXA1 loss may play a significant role in enabling prostate cancer progression to NEPC, whereas IL-8 and MAPK/ERK pathways may be promising targets for therapeutic intervention.

FOXA1 acts upstream of GATA2 and AR in hormonal regulation of gene expression.

Hormonal regulation of gene expression by androgen receptor (AR) is tightly controlled by many transcriptional cofactors, including pioneer factors FOXA1 and GATA2, which, however, exhibit distinct expression patterns and functional roles in prostate cancer. Here, we examined how FOXA1, GATA2 and AR crosstalk and regulate hormone-dependent gene expression in prostate cancer cells. Chromatin immunoprecipitation sequencing analysis revealed that FOXA1 reprograms both AR and GATA2 cistrome by preferably recruiting them to FKHD-containing genomic sites. By contrast, GATA2 is unable to shift AR or FOXA1 to GATA motifs. Rather, GATA2 co-occupancy enhances AR and FOXA1 binding to nearby ARE and FKHD sites, respectively. Similarly, AR increases, but not reprograms, GATA2 and FOXA1 cistromes. Concordantly, GATA2 and AR strongly enhance the transcriptional program of each other, whereas FOXA1 regulates GATA2- and AR-mediated gene expression in a context-dependent manner due to its reprogramming effects. Taken together, our data delineated for the first time the distinct mechanisms by which GATA2 and FOXA1 regulate AR cistrome and suggest that FOXA1 acts upstream of GATA2 and AR in determining hormone-dependent gene expression in prostate cancer.

LncRNA HOTAIR enhances ER signaling and confers tamoxifen resistance in breast cancer.

Tamoxifen, an estrogen receptor (ER) antagonist, is the mainstay treatment of breast cancer and the development of resistance represents a major obstacle for a cure. Although long non-coding RNAs such as HOTAIR have been implicated in breast tumorigenesis, their roles in chemotherapy resistance remain largely unknown. In this study, we report that HOTAIR (HOX antisense intergenic RNA) is upregulated in tamoxifen-resistant breast cancer tissues compared to their primary counterparts. Mechanistically, HOTAIR is a direct target of ER-mediated transcriptional repression and is thus restored upon the blockade of ER signaling, either by hormone deprivation or by tamoxifen treatment. Interestingly, this elevated HOTAIR increases ER protein level and thus enhances ER occupancy on the chromatin and potentiates its downstream gene regulation. HOTAIR overexpression is sufficient to activate the ER transcriptional program even under hormone-deprived conditions. Functionally, we found that HOTAIR overexpression increases breast cancer cell proliferation, whereas its depletion significantly impairs cell survival and abolishes tamoxifen-resistant cell growth. In conclusion, the long non-coding RNA HOTAIR is directly repressed by ER and its upregulation promotes ligand-independent ER activities and contributes to tamoxifen resistance.

[The expression of MiR-148a in nasopharyngeal carcinoma and its effect on tumor cell biology functions in nasopharyngeal carcinoma].

Objective:Nasopharyngeal carcinoma(NPC) is a common malignant tumor, in recent years,most of studies have found that micro RNA played an important role in the development of NPC.This study was to explore the expression level of MiR-148a and its effect on the biological functions of NPC cells.Method:The expression of MiR-148a in NPC cell line CNE2 was detected by Real-time PCR method.MTT,clone formation assay and flow cytometry were applied to detect cell proliferation and apoptosis. We predicted that EGFR was the downstream target genes of MiR-148a through the analysis of bioinformatics software. Then the expression change of EGFR was measured by Real-time PCR and Western blot.Result:Comparing with normal nasopharyngeal epithelial tissue cells,MiR-148a expression level was significantly reduced in NPC cell line CNE2.MTT,clone formation assay and flow cytometry test show that overexpression of MiR-148a can inhibit cell proliferation and promote cell apoptosis.Real-time PCR and Western blot test show that MiR 148a can reduce the expression of EGFR.Conclusion:MiR-148a can affect the proliferation and apoptosis of NPC cell,and it is likely to be involved in the development and progression of NPC.

[The clinical application of balloon dilation Eustachian tuboplasty in patients with Eustachian tube dysfunction].

Objective:To evaluate the clinical application of balloon dilation Eustachian tuboplasty (BET) in patients with Eustachian tube dysfunction (ETD). Method:Twenty-five patients who were diagnosed as ETD and reserved BET surgery were retrospectively analyzed in this study. Result:After 1-year's follow-up, among 25 ETD patients, the total cure rate was 55.9% and the effective rate was 85.3%. The cure rate and effective rate was 52.9% and 76.5% in the delayed opening of the ET group; 58.8% and 94.1% in the unopened group, which was higher than the other one. Conclusion:BET surgery is safe and effective in the treatment of BET patients.

TMPRSS2-ERG gene fusions induce prostate tumorigenesis by modulating microRNA miR-200c.

Chromosomal translocations that juxtapose the androgen-sensitive transmembrane protease, serine 2 (TMPRSS2) gene promoter to the oncogenic ETS-family transcription factor ERG result in excessive ERG overexpression in approximately 50% of prostate cancer (PCa) patients. Although numerous studies have investigated ERG-downstream genes, such studies have not attempted to examine miRNAs, which however are emerging to be important regulators of cancer. Through bioinformatics analysis of ChIP-Seq ERG data and miRNA expression profiling data we nominated miR-200c as a direct target of ERG. Experimentation of PCa cells with ERG overexpression or knockdown demonstrated that ERG directly repressed miR-200c expression by physically binding to the erythroblast transformation-specific (ETS) motif within its promoter. Consequently, miR-200c was downregulated in ERG-positive PCa, and miR-200c target gene expression was restored. In addition, the expression pattern of miR-200c target genes predicted ERG status in clinical PCa specimens. Furthermore, miR-200c was found to be important in modulating ZEB1 upregulation by ERG. Most importantly, miR-200c reconstitution fully reversed ERG-induced epithelial-to-mesenchymal transition (EMT), cell migration and invasion. Therefore, our study report miR-200c as the first miRNA target of ERG and a critical inhibitor of PCa cell motility. Therapeutic delivery of miR-200c may provide personalized treatment for patients with the molecular subtype of PCa that harbors TMPRSS2-ERG gene fusions.

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.

Body mass index evaluating donor hepatic steatosis in living donor liver transplantation.

INTRODUCTION: Evaluation of graft hepatic steatosis is important for the safety of the donor and the recipient in living donor liver transplantation. It is necessary to establish a noninvasive evaluation method to avoid performing a liver biopsy for donor safety. The aim of this study was to identify independent factors that correlated with hepatic steatosis to create a noninvasive method to evaluate hepatic steatosis. METHODS: We retrospectively collected data from 105 living donors. No prisoners were used to obtain the grafts, all of which underwent postoperative histological evaluation for hepatic steatosis. Preoperative clinical and biochemical variables were examined with univariate analyses, and filtered variables further examined with ordinal regression analysis. RESULTS: Eighty (76.2%) donors showed no hepatic steatosis, 15 (14.3%), mild steatosis, and 10 (9.5%), moderate steatosis. In ordinal stepwise regression analysis, body mass index (BMI; P = .000) was the only independent factor that correlated with the grade of hepatic steatosis. Preoperative biochemical parameters were not significantly correlated with hepatic steatosis. A regression model based on BMI was created to evaluate hepatic steatosis grade. Furthermore, individuals with a BMI > 27.5 were most likely to show moderate steatosis, and those with BMI < 23 likely to display no or mild steatosis. CONCLUSION: BMI can help to identify the grade of hepatic steatosis among living donors. BMI is also useful to select living donors for a preoperative liver biopsy before liver transplantation.

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.

Preliminary experience with indications for liver transplantation for hepatolithiasis.

OBJECTIVE: The aim of this study was to explore the indications for liver transplantation among patients with hepatolithiasis. PATIENTS AND METHODS: Data from 1,431 consecutive patients who underwent surgical treatment from January 2000 to December 2006 were retrospectively collected for analysis. Surgical procedures included T-tube insertion combined with intraoperative cholangioscopic removal of intrahepatic stones, hepatectomy, cholangiojejunostomy, and liver transplantation. RESULTS: Nine hundred sixty-one patients who had a stone located in the left or right intrahepatic duct underwent hepatectomy or T-tube insertion combined with intraoperative cholangioscopic removal of intrahepatic stones. The rate of residual stones was 7.5%. Four hundred seventy patients who had a stone located in the bilateral intrahepatic ducts underwent surgical procedures other than liver transplantation; the rate of residual stones was 21.7%. Only 15 patients with hepatolithiasis underwent liver transplantation; they all survived. According to the degree of biliary cirrhosis, recipients were divided into 2 groups: a group with biliary decompensated cirrhosis (n = 7), or group with compensated cirrhosis or no cirrhosis (n = 8). There were significant differences in operative times, transfusion volumes, and blood losses between the 2 groups (P < .05). In the first group, 6 of 7 patients experienced surgical complications, and in the second, 8 recipients recovered smoothly with no complications. Health status, disability, and psychological wellness of all recipients (n = 15) were significantly improved at 1 year after transplantation compared with pretransplantation (P < .05). CONCLUSIONS: Liver transplantation is a possible method to address hepatolithiasis and secondary decompensated biliary cirrhosis or difficult to remove, diffusely distributed intrahepatic duct stones unavailable by hepatectomy, cholangiojejunostomy, and choledochoscopy.

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.