Pop-Up Safety Town: Leveling the Playing Field for Children in Underserved Communities Through Injury Prevention Education.

BACKGROUND: Unintentional injuries are the leading cause of morbidity and mortality among children and adolescents in the United States. Traditional injury education interventions for children often are inaccessible due to cost and logistics in underserved communities, exacerbating injury disparities. A new approach is needed to close this gap for families with preschool children. CONTRIBUTIONS TO THEORY: Collaborating with Head Start preschools optimizes engagement and accessibility to families in underserved communities. Involving caregivers and community organizations addresses the limitations of conventional interventions and community-specific injury prevention concerns. IMPLICATIONS FOR SCHOOL HEALTH POLICY, PRACTICE, AND EQUITY: Pop-up Safety Town offers a more affordable model for injury prevention education, particularly in underserved regions. The model's approach, using adaptable education, mobile and reusable materials, and volunteer staffing, offers greater potential for achieving sustainable impact in these underserved communities. CONCLUSIONS: Pop-up Safety Town presents a novel upstream solution to address disparities in injury prevention education in underserved communities.

Research Collaboration in a Communication Rights Campaign: Lessons Learned.

In building public support for social change, activists in communities of color routinely approach broader audiences via news media. Communities of color, however, routinely face disparities that limit their access to media including local news media outlets. This lack of access mirrors inequalities in political, social, and economic arenas and can slow public awareness campaigns to address disparities in health, environmental, and other quality-of-life issues. I describe two community-based collaborative action research studies that documented and challenged how local television newscasts underrepresented and misrepresented three communities of color in Boston. The linkage between communication rights and campaigns to address quality-of-life issues is presented, as well as unresolved challenges in the collaborative research process. The study has implications for environmental health campaigns.

A critical role for the protein kinase PKK in the maintenance of recirculating mature B cells and the development of B1 cells.

Protein kinase C associated kinase (PKK) regulates NF-κB activation and is required for the survival of certain lymphoma cells. Mice lacking PKK die soon after birth, and previous studies suggest that the role of PKK in B cell development might be context dependent. We have generated a mouse strain harboring conditional null alleles for PKK and a Cre-recombinase transgene under the control of the endogenous CD19 promoter. In the present study, we show that knockout of PKK in B cells results in the reduction of long-lived recirculating mature B cell population in lymph nodes and bone marrow as well as a decrease in peritoneal B1 cells, while PKK deficiency has no apparent effect on early B cell development in bone marrow or the development of follicular and marginal zone B cells in the spleen. In addition, we demonstrate that PKK-deficient B cells display defective proliferation and survival responses to stimulation of B cell receptor (BCR), which may underlie the reduction of recirculating mature B cells in PKK mutant mice. Consistently, BCR-mediated NF-κB activation, known to be required for the survival of activated but not resting B cells, is attenuated in PKK-deficient B cells. Thus, our results reveal a critical role of PKK in the maintenance of recirculating mature B cells as well as the development of B1 cells in mice.

Diagnostic value of HMGAs, p53 and ß-catenin in discriminating adenocarcinoma from adenoma or reactive atypia in ampulla and common bile duct biopsies.

AIMS: Biopsies from the ampulla of Vater and the common bile duct often pose diagnostic challenges. The aim of this study was to investigate the expression patterns of HMGA1, HMGA2, ß-catenin and p53 in biopsy specimens, in order to evaluate the potential diagnostic value of these proteins in differentiating adenocarcinoma from reactive atypia or adenoma. METHODS AND RESULTS: Forty-eight biopsies (10 from the common bile duct and 38 from the ampulla) were selected for immunohistochemical studies; they included 14 cases of reactive atypia, 12 adenomas, and 22 adenocarcinomas. Expression of HMGA1 was seen in 21% of the reactive atypia cases, 42% of adenomas, and 91% of adenocarcinomas. HMGA2 was positive in 14% of reactive atypias, 42% of adenomas, and 86% of adenocarcinomas. The staining intensity of HMGA1 and HMGA2 was also significantly higher in adenocarcinomas than in adenomas or reactive atypias. Interestingly, coexpression of HMGA1 and HMGA2 was found in 86% of adenocarcinomas, 0% of reactive atypias, and 8% of adenomas. p53 and ß-catenin expression seemed not to provide additional value for discriminating adenocarcinoma from reactive atypia or adenoma. CONCLUSIONS: HMGA1 and HMGA2 might serve to discriminate between reactive atypia, adenoma and adenocarcinoma in ampulla and common bile duct biopsies.

Shear wave dispersion measures liver steatosis.

Crawling waves, which are interfering shear wave patterns, can be generated in liver tissue over a range of frequencies. Some important biomechanical properties of the liver can be determined by imaging the crawling waves using Doppler techniques and analyzing the patterns. We report that the dispersion of shear wave velocity and attenuation, that is, the frequency dependence of these parameters, are strongly correlated with the degree of steatosis in a mouse liver model, ex vivo. The results demonstrate the possibility of assessing liver steatosis using noninvasive imaging methods that are compatible with color Doppler scanners and, furthermore, suggest that liver steatosis can be separated from fibrosis by assessing the dispersion or frequency dependence of shear wave propagations.

Comparative analysis of hepatitis C recurrence and fibrosis progression between deceased-donor and living-donor liver transplantation: 8-year longitudinal follow-up.

BACKGROUND: Hepatitis C virus (HCV) recurrence is universal after liver transplantation (LT). Whether the progression of recurrent HCV is faster after live-donor LT (LDLT) compared with deceased-donor LT (DDLT) is debatable. METHODS AND RESULTS: We retrospectively examined 100 consecutive LTs (65 DDLTs and 35 LDLTs) performed between July 2000 and July 2003. A total of 147 liver biopsies were performed between 6 months post-LT and last follow-up. Mean donor age and model for end-stage liver disease (MELD) score were significantly lower in LDLT (P<0.01). On a mean follow-up of 86.6±6.8 months, overall patient and graft survivals were 61% (51% DDLT vs. 77.1% LDLT; P=0.026) and 56% (46.2% DDLT vs. 71.4% LDLT; P=0.042), respectively. Eight of 39 (20.5%) deaths (7 DDLT and 1 LDLT) and two of nine (22.2%) retransplants (one in each group) were related to recurrent HCV. Mean fibrosis scores for DDLT and LDLT were 1.9±1.7 and 1.6±1.4, respectively (P=0.01). When donor age less than 50 years and MELD score less than 25 were matched among 64 patients (32 DDLT and 32 LDLT), the overall patient and graft survivals were 73.4% (68.8% DDLT vs. 78.1% LDLT; P=0.439) and 71.9% (71.9% DDLT vs. 71.9% LDLT; P=0.978), respectively. CONCLUSIONS: Long-term survival rates were better, and fibrosis scores were lower for LDLT. The survivals between LDLT and DDLT were comparable for patients with MELD score less than 25 and donor age less than 50 years.

Living donor and deceased donor liver transplantation for autoimmune and cholestatic liver diseases--an analysis of the UNOS database.

INTRODUCTION: Autoimmune hepatitis and cholestatic liver diseases have more favorable outcomes after liver transplantation as compared to viral hepatitis and alcoholic liver diseases. However, there are only few reports comparing outcomes of both living donor liver transplants (LDLT) and deceased donor liver transplants (DDLT) for these conditions. AIM: We aim to study the survival outcomes of patients undergoing LT for autoimmune and cholestatic diseases and to identify possible risk factors influencing survival. Survival outcomes for LDLT vs. DDLT are also to be compared for these diseases. PATIENTS AND METHODS: A retrospective analysis of the UNOS database for patients transplanted between February 2002 until October 2006 for AIH, PSC, and PBC was performed. Survival outcomes for LDLT and DDLT patients were analyzed and factors influencing survival were identified. RESULTS: Among all recipients the estimated patient survival at 1, 3, and 5 years for LDLT was 95.5%, 93.6%,and 92.5% and for DDLT was 90.9%, 86.5%, and 84.9%, respectively (p = 0.002). The estimated graft survival at 1, 3, and 5 years for LDLT was 87.9%, 85.4%, and 84.3% and for DDLT 85.9%, 80.3%, and 78.6%, respectively (p = 0.123). On multivariate proportional hazard regression analysis after adjusting for age and MELD score, the effect of donor type was not found to be significant. CONCLUSION: The overall survival outcomes of LDLT were similar to DDLT in our patients with autoimmune and cholestatic liver diseases. It appears from our study that after adjusting for age and MELD score donor type does not significantly affect the outcome.

Androgen receptor promotes hepatitis B virus-induced hepatocarcinogenesis through modulation of hepatitis B virus RNA transcription.

Hepatitis B virus (HBV)-induced hepatitis and carcinogen-induced hepatocellular carcinoma (HCC) are associated with serum androgen concentration. However, how androgen or the androgen receptor (AR) contributes to HBV-induced hepatocarcinogenesis remains unclear. We found that hepatic AR promotes HBV-induced hepatocarcinogenesis in HBV transgenic mice that lack AR only in the liver hepatocytes (HBV-L-AR(-/y)). HBV-L-AR(-/y) mice that received a low dose of the carcinogen N'-N'-diethylnitrosamine (DEN) have a lower incidence of HCC and present with smaller tumor sizes, fewer foci formations, and less alpha-fetoprotein HCC marker than do their wild-type HBV-AR(+/y) littermates. We found that hepatic AR increases the HBV viral titer by enhancing HBV RNA transcription through direct binding to the androgen response element near the viral core promoter. This activity forms a positive feedback mechanism with cooperation with its downstream target gene HBx protein to promote hepatocarcinogenesis. Administration of a chemical compound that selectively degrades AR, ASC-J9, was able to suppress HCC tumor size in DEN-HBV-AR(+/y) mice. These results demonstrate that targeting the AR, rather than the androgen, could be developed as a new therapy to battle HBV-induced HCC.

Effect of liver transplant on pulmonary functions in adult patients with alpha 1 antitrypsin deficiency: 7 cases.

OBJECTIVES: Alpha 1 antitrypsin (A1A) is a 52 kD glycoprotein that is mainly synthesized in the liver. As a major protease inhibitor, it binds to and neutralizes neutrophil elastase, thereby limiting the damage to the normal tissues after an inflammatory response. A deficiency in A1A leads to end-stage liver disease, both in children and in adults. In addition, the deficiency also has a detrimental effect in the lungs of the adult population. Alpha 1 antitrypsin deficiency is corrected with hepatic replacement; however, the changes in pulmonary functions have not been studied before and after liver transplant. The purpose of this study was to observe the changes in the pulmonary functions of patients who underwent liver transplant for the treatment of A1A deficiency. MATERIALS AND METHODS: Nine patients underwent liver transplant for A1A deficiency. Seven patients (5 men, 2 women; mean age, 49.95 -/+ 7.09 years) had their pulmonary function tests available before the liver transplant (mean, 5.6 -/+ 3.4; range, 0.9-10.1 months) and after the liver transplant (mean, 30.3 -/+ 18.4, range 7.8-48.1 months) for analysis. RESULTS: The mean, preliver, transplant, FEV1 was 2.69 -/+ 0.9 L, which was nearly unchanged after the liver transplant to a mean of 2.7 -/+ 1.2 L. During the mean total interval of nearly 3 years, an estimated decline of 250 mL in FEV1 was expected. CONCLUSIONS: It appears from the results of our study that liver transplant probably prevented the progression of pulmonary disease in A1A-deficient patients. Further study and close, postliver, transplant follow-up is warranted to support our initial findings.

Response to antiviral therapy in liver transplant recipients with recurrent hepatitis C viral infection: a single center experience.

INTRODUCTION: Recurrence of hepatitis C virus (HCV) in hepatic allograft is a major concern after successful liver transplant (LTx). AIM: To examine the response rate to pegylated interferon (PEG-IFN) and ribavirin in post-LTx patients with HCV recurrence. PATIENTS AND METHODS: Between January 2003 and September 2006, 60 patients with biopsy proven HCV recurrence (46 males and 14 females) received PEG-IFN 2a (n = 40) or IFN 2b (n = 20) with ribavirin. All patients were followed until July 2007. RESULTS: Fourteen patients (23.3%) tolerated antiviral therapy for less than six months and 10 (16.7%) discontinued therapy between six and 11 months. PEG-IFN dose was reduced in 21 (35%) patients and ribavirin dose was reduced in 16 (26.7%) patients. Overall, 55% patients achieved end of treatment response (EOT) and 35% sustained virological response (SVR). Mean Hepatitis Activity Index and Fibrosis Score pre-therapy was 5.8 +/- 1.9 and 1.7 +/- 1.3 and post-therapy, it was 4.4 +/- 2.1 and 2.4 +/- 1.6, respectively. Overall, three yr patient and graft survival was 73.9% and 69.2%, respectively. The patients with SVR had significantly lower viral load compared with other groups (p = 0.028). CONCLUSION: PEG-IFN and ribavirin therapy achieved 55% EOT and 35% SVR; 60% patients tolerated therapy. Biochemical response was observed in all groups of patients irrespective of virological response.

Liver grafts from donors with central nervous system tumors: a single-center perspective.

Traditionally, patients who die with a malignancy have been excluded from donation. However, it has become a common practice to accept organs from donors that have low-grade tumors or tumors with low metastatic potential. The aim of this study was to analyze our experience with the use of liver grafts from donors with central nervous system (CNS) tumors. A retrospective review of 1173 liver transplants performed between 1992 and 2006 identified 42 donors diagnosed with a CNS tumor. Thirty-two tumors were malignant, and 10 tumors were benign. Forty-two liver transplant recipients received livers from these donors. All patients were followed until May 2007 with a mean follow-up of 29 +/- 17 months. Among 42 donors, there were 28 males and 14 females. The mean donor risk index was 1.78 +/- 0.39. Twenty (47.6%) of the CNS tumors were glioblastoma multiforme (astrocytoma grade IV), 11 (26.2%) were other astrocytomas, and 1 (2.4%) was an anaplastic ependymoma. Twenty (62.5%) neoplasms were grade IV tumors, 8 (25%) were grade II tumors, and 4 (12.5%) were grade III tumors. Over 80% of the patients had at least 1 kind of invasive procedure violating the blood-brain barrier. The rate of recurrence for the entire group was 2.4% (all CNS tumors). There were 7 (7.2%) deaths in all. The most common cause of death was sepsis (n = 3, 7.2%). There was no difference in survival between recipients of grafts from donors with CNS tumors and recipients of grafts from donors without CNS tumors (1 year: 82% versus 83.3%, P = not significant; 3 years: 77.4% versus 72%, P = not significant). In conclusion, in our experience, despite violation of the blood-brain barrier and high-grade CNS tumors, recurrence was uncommon. Grafts from these donors are often an overlooked source of high-quality organs from younger donors and can be appropriately used, particularly in patients who, despite low Model for End-Stage Liver Disease scores, carry a high risk of mortality.

Comparative analysis of outcomes in living and deceased donor liver transplants for primary sclerosing cholangitis.

INTRODUCTION: Primary sclerosing cholangitits (PSC) is a progressive fibrosing cholangiopathy eventually leading to end-stage liver disease (ESLD). While literature for deceased donor liver transplantation (DDLT) for PSC abounds, only a few reports describe live donor liver transplant (LDLT) in the setting of PSC. We present a single-center experience on survival outcomes and disease recurrence for LDLT and DDLT for ESLD secondary to PSC. AIM: The aim of this study was to analyze survival outcomes and disease recurrence for LDLT and DDLT for ESLD secondary to PSC. PATIENTS AND METHODS: A retrospective review of 58 primary liver transplants for PSC-associated ESLD, performed between May 1995 and January 2007, was done. Patients were divided into two groups based on donor status. Group 1 (n = 14) patients received grafts from living donors, while group 2 (n = 44) patients received grafts from deceased donors. An analysis of survival outcomes and disease recurrence was performed. Recurrence was confirmed based on radiological and histological criteria. RESULTS: Recurrence of PSC was observed in four patients in LDLT group and seven in DDLT group. Retransplantation was required in one patient in LDLT group and nine patients in DDLT group. One patient (7%) among LDLT and six patients (14%) among DDLT died. The difference in patient and graft survival was not statistically significant between the two groups (patient survival, p = 0.60; graft survival, p = 0.24). CONCLUSION: This study demonstrates equivalent survival outcomes between LDLT and DDLT for PSC; however, the rate of recurrence may be higher in patients undergoing LDLT.

Tissue factor and VEGF expression in prostate carcinoma: a tissue microarray study.

Tissue factor (TF) is the principal physiologic initiator of coagulation. It also plays an important role in tumor growth and metastasis possibly by contributing to angiogenesis. We evaluated the expression of TF in benign and malignant prostate tissue and correlated it with the expression of the pro-angiogenic protein, vascular endothelial growth factor (VEGF). We used a tissue microarray (TMA) constructed from 80 archival prostatectomy specimens. Core samples were collected from benign prostate tissue (BP) (n= 77), high-grade prostatic intraepithelial neoplasia (PIN) (n= 26), and carcinoma (PCa) (n= 93). TMA sections were stained with an immunopurified polyclonal TF antibody and a rabbit polyclonal VEGF. Two pathologists manually scored staining in epithelial cells using the German Immunoreactive Score. Positive staining for TF was seen predominantly in PCa with rare positive glands in BP and PIN. TF expression was significantly lower in BP versus PCa specimens (p< .001) and in PIN versus PCa specimens (p< .001). Positive staining for VEGF was seen in PCa, BP, and PIN. Rates of VEGF expression were also significantly lower in BP versus PCa specimens (p= .003) but not in PCa versus PIN (p= .430). The majority of PCa samples positive for TF were also positive for VEGF (p< .001). Our findings reinforce the link between angiogenesis and TF expression in PCa. We suggest further exploration of TF-mediated pathways leading to increased tumor aggressiveness in PCa, and the possible use of anti-TF agents in PCa.

Structural studies on the Pseudomonas aeruginosa sialidase-like enzyme PA2794 suggest substrate and mechanistic variations.

Pseudomonas aeruginosa encodes an enzyme (PA2794) that is annotated as a sialidase (or neuraminidase), as it possesses three bacterial neuraminidase repeats that are a signature of nonviral sialidases. A recent report showed that when the gene encoding this sialidase is knocked out, this led to a reduction in biofilm production in the lungs of mice, and it was suggested that the enzyme recognizes pseudaminic acid, a sialic acid analogue that decorates the flagella of Pseudomonas, Helicobacter, and Campylobacter species. Here, we present the crystal structure of the P. aeruginosa enzyme and show that it adopts a trimeric structure, partly held together by an immunoglobulin-like trimerization domain that is C-terminal to a classical beta-propeller sialidase domain. The recombinant enzyme does not show any sialidase activity with the standard fluorogenic sialic-acid-based substrate. The proposed active site contains certain conserved features of a sialidase: a nucleophilic tyrosine with its associated glutamic acid, and two of the usual three arginines that interact with the carboxylic acid group of the substrate, but is missing the first arginine and the aspartic acid that acts as an acid/base in all sialidases studied to date. We show, by in silico docking, that the active site may accommodate pseudaminic acid but not sialic acid and that this is due, in part, to a phenylalanine in the hydrophobic pocket that selects for the alternative stereochemistry of pseudaminic acid at C5 compared to sialic acid. Mutation of this phenylalanine to an alanine converts the enzyme into a sialidase, albeit a poor one, which we confirm by kinetics and NMR, and this allowed us to probe the function of other amino acids. We propose that a histidine plays the role of the acid/base, whose state is altered through a charge-relay system involving a novel His-Tyr-Glu triad. The location of this relay system precludes the presence of one of the three arginines usually found in a sialidase active site.

Should trichrome stain be used on all post-liver transplant biopsies with hepatitis C virus infection to estimate the fibrosis score?

Recurrent hepatitis C is virtually universal after liver transplantation; however, an individual patient's clinical course and disease burden are highly variable and difficult to predict. The fibrosis score determined on posttransplant biopsies appears to be a sensitive and specific marker of disease progression and severity. Currently, the fibrosis score is determined from hematoxylin and eosin (H&E)-stained tissue sections supplemented by variable use of trichrome stain or other connective tissue-specific stains. In this study, we compare the fibrosis score on H&E stain with that obtained with trichrome stain in posttransplant liver biopsies of patients with hepatitis C. A total of 197 liver biopsies from 105 allograft patients with hepatitis C were reviewed. The mean fibrosis stage was 1.0 +/- 1.25 with H&E stain versus 1.69 +/- 1.42 with trichrome stain (P < 0.00001). The trichrome staging score was higher in 53.3%, lower in 3%, and the same in 43.7%. The fibrosis stage was raised by 2 or more points in 17.8% and elevated into a bridging category in 14.7%. No significant differences in clinical and laboratory levels were measured in patients with higher fibrosis scores. In conclusion, the hepatic fibrosis score is significantly underestimated by H&E stain in the posttransplant setting in patients with hepatitis C. The fibrosis stage may be an indicator of significant liver damage in these patients. Accuracy of its determination may be most easily facilitated by employment of a connective tissue stain.

Potential immunological advantage of intravenous mycophenolate mofetil with tacrolimus and steroids in primary deceased donor liver transplantation and live donor liver transplantation without antibody induction.

With the current immunosuppressive regimens, graft loss secondary to immunological reasons after successful liver transplantation is a rarity; acute rejections, however, do occur, with the majority of them being steroid-responsive. The aim of the present study is to examine the rate of acute rejection with tacrolimus, intravenous (IV) mycophenolate mofetil (MMF), and steroids in primary deceased donor liver transplant (DDLT) and live donor liver transplant (LDLT) recipients. During the year 2005, 130 patients (mean age: 54.9 +/- 10.8, males: 84, females: 46, 112 DDLT and 18 LDLT) received primary liver transplantation. They were followed up for the incidence of acute rejection in the first 12 months. Liver biopsies were performed as clinically indicated; protocol liver biopsies were never performed. A total of 127 liver biopsies were performed. Thirty-two had a rejection activity index (RAI) score of > or =3, of which 24 biopsies in 20 patients were not treated with a steroid bolus. Eight (6.1%) patients (mean RAI score: 5.1 +/- 1.4) received 750 to 1500 mg of methylprednisolone over 3 days. Out of these, 2 were noncompliant, 4 were off MMF, and 1 was on cyclosporine. All patients responded to steroid therapy. None of the patients required any antibody preparation. In conclusion, IV MMF with tacrolimus and steroids is useful and required antirejection therapy in 6.1% of liver transplant recipients.

Tissue factor expression, angiogenesis, and thrombosis in pancreatic cancer.

PURPOSE: Hemostatic activation is common in pancreatic cancer and may be linked to angiogenesis and venous thromboembolism. We investigated expression of tissue factor (TF), the prime initiator of coagulation, in noninvasive and invasive pancreatic neoplasia. We correlated TF expression with vascular endothelial growth factor (VEGF) expression, microvessel density, and venous thromboembolism in resected pancreatic cancer. EXPERIMENTAL DESIGN: Tissue cores from a tri-institutional retrospective series of patients were used to build tissue microarrays. TF expression was graded semiquantitatively using immunohistochemistry in normal pancreas (n=10), intraductal papillary mucinous neoplasms (n=70), pancreatic intraepithelial neoplasia (n=40), and resected or metastatic pancreatic adenocarcinomas (n=130). RESULTS: TF expression was observed in a majority of noninvasive and invasive pancreatic neoplasia, including 77% of pancreatic intraepithelial neoplasias, 91% of intraductal papillary mucinous neoplasms, and 89% of pancreatic cancers, but not in normal pancreas. Sixty-six of 122 resected pancreatic cancers (54%) were found to have high TF expression (defined as grade >or=2, the median score). Carcinomas with high TF expression were more likely to also express VEGF (80% versus 27% with low TF expression, P<0.0001) and had a higher median MVD (8 versus 5 per tissue core with low TF expression, P=0.01). Pancreatic cancer patients with high TF expression had a venous thromboembolism rate of 26.3% compared with 4.5% in patients with low TF expression (P=0.04). CONCLUSIONS: TF expression occurs early in pancreatic neoplastic transformation and is associated with VEGF expression, increased microvessel density, and possibly clinical venous thromboembolism in pancreatic cancer. Prospective studies evaluating the role of TF in pancreatic cancer outcomes are warranted.

Incidence of arterial injuries detected by arteriography following percutaneous right-lobe ultrasound-guided core liver biopsies in human subjects.

PURPOSE: To determine the incidence and significance of arterial injuries detected by angiography subsequent to ultrasound-guided random core liver biopsies in normal healthy adults. MATERIALS AND METHODS: Retrospective analysis of 55 potential living related liver donors who underwent an ultrasound-guided random liver biopsy and a visceral angiogram was performed (January, 1999 to May, 2002). All liver biopsy samples (obtained by 2-3 18-gauge needle passes) were re-evaluated prospectively by a transplant pathologist for adequacy (defined: >or=5 complete portal triads). Subjects who underwent angiograms before the biopsy or >7 days after the biopsy were excluded from the arterial injury evaluation. Angiograms were reviewed by two angiographers. Arterial injuries were identified and classified by consensus into contusions, active bleeding, arterial-venous fistulae, and pseudoaneurysms. RESULTS: Mean needle pass was 2.1. No major complications were encountered. All samples were deemed pathologically adequate. Forty-eight potential donors were included for the arterial injury evaluation. Three arterial injuries (two arterioportal fistulae, 4.2%) were found in 48 angiograms (6.3%). None of the three injuries required intervention. CONCLUSION: The incidence of arterioportal fistulae following core liver biopsies has not changed over the past three decades despite improvement in biopsy needle technology, reduction of needle caliber, and the use of image guidance.

Characterization of CD4, CD8, CD56 positive lymphocytes and C4d deposits to distinguish acute cellular rejection from recurrent hepatitis C in post-liver transplant biopsies.

INTRODUCTION: Hepatitis C viral (HCV) infection is the most common cause for liver transplantation (LTx) in USA. Hepatitis C viral recurrence in liver allograft is almost universal, which is often difficult to distinguish from acute cellular rejection (ACR). AIM: Aim of the present study is to examine the differences between distribution of CD4, CD8, CD56 positive lymphocytes, and C4d deposits in patients with ACR and recurrent HCV. PATIENTS AND METHODS: As a pilot project, a group of five post-LTx HCV RNA negative patients, strongly suspicious for ACR based on clinical findings and history of medication non-compliance and another group of five post-LTx HCV positive, medication compliant patients with abnormal liver function were retrospectively selected. Liver biopsies of these patients were stained with monoclonal CD4, CD8, CD56, and polyclonal C4d antibodies and compared. RESULTS: Mean CD4, CD8, and CD56 counts in ACR group were 156.7 +/- 17.6, 35.4 +/- 8.8, and 1.0 +/- 1.8/HPF, respectively and were 89.7 +/- 41.3, 20.3 +/- 23.2, and 0.6 +/- 0.9/HPF, respectively in HCV recurrence group. Biopsies of four of five patients with ACR demonstrated moderate to strong C4d staining, whereas all patients with recurrent HCV had none to mild C4d staining. CONCLUSION: Mean CD4, CD8, and CD56 were similar for acute rejection and recurrent HCV infection. However, 80% of patients with ACR showed moderate to strong staining for C4d and all recurrent HCV patients showed none to mild C4d staining.