7 Here we used homozygosity mapping with SNP microarray genotyping as an initial genetic test to pinpoint the causative mutation in this family. With the increasing use of SNP microarrays for whole genome scanning, homozygosity

mapping has become easy and rapid. This approach is particularly powerful in situations where there is an increased likelihood of inheriting two alleles identical-by-descent, such as consanguinity or inbreeding. Although the likelihood of homozygosity is smaller in outbred populations, homozygosity mapping has become easy and rapid and widely available through the use of SNP microarrays for routine cytogenetic analysis. The extent of homozygosity found in this family confirmed a high degree of consanguinity. Offspring of first cousins are expected to be homozygous for ≈6% (or 1/16th) of their genome. However, in populations with a history of DZNeP consanguineous matings the proportion of the genome Ku 0059436 that is homozygous can reach 11% when considering only homozygous regions that are greater than 3 cM.27 In this family, individuals III.5, III.6, and III.14, whose DNA was used for homozygosity mapping, were offspring of first cousins. Their genome homozygosity associated with recessive disease was estimated to be 21%, 9.5%, and

10%, respectively, indicating that consanguinity was practiced for generations in this family. An alternative genetic approach that could have been used to identify the causative gene in this family is whole exome (or whole genome) sequencing.28 This approach has the potential added advantage of revealing modifier genes that contribute to the phenotypic variability of this disorder. Unfortunately, it is unlikely that

exome sequencing would have been helpful in identifying modifier genes contributing to the phenotypic variability in this family, given the small number of affected individuals (n = 2) available for study and the large number of sequence variations found in genomes. A large-scale sequencing Sitaxentan study that includes large numbers of carefully phenotyped patients with 3β-HSD deficiency may provide the opportunity to identify modifier genes for this disorder. In conclusion, we present here a highly consanguineous Arab-Iranian pedigree with four individuals suffering from 3β-HSD deficiency, caused by a recurrent mutation. The clinical presentation was extremely variable, with both prolonged asymptomatic and fatal course occurring in the different affected family members. Increased awareness of possible 3β-HSD deficiency in clinical evaluation of cirrhosis in young adults, as well as in children, is essential, because this condition has an excellent prognosis with primary bile acid treatment. We thank Dr. Jennifer Cuthbert for the referral of this patient. We thank David Russell for helpful discussions and Barbara Gilbert for assistance collecting blood samples from the family.

Methods: ① The luciferease gene coding sequence was amplified from PMIR-luciferase using polymerase chain

reaction (PCR). The amplified product was digested with BamH1 and Kpn1 and cloned into the Bam H1 and Kpn1 sites in Psmp8 plasmid under an αSMA promoter component. INK 128 chemical structure The recombinant was sequenced to assess the orientation of the insert and the correctness of the sequence. We named this recombinant Psmp8+Luciferase. ② Mouse hepatic stellate cells (HSCs) were isolated from kunming mice’s livers using the way of density gradient centrifugation. Isolated HSCs were activated after being cultured and passaged numbers of days. Expression of αSMA was determined by western blot and immunofluorescence. ③ Psmp8+Luciferase and Renilla luciferase vector were co-transfected HSCs, hepatic cells and kuffer cells. PeGFP plasmid and Renilla luciferase vector were co-transfected the above cells as the negative control. Using Dual-Luciferase Reporter Assay System detected the expression of the two plasmids in HSCs, hepatic cells, kuffer cells. Results: ① The Psmp8+Luciferase sequence and the orientation of the insert were sequenced correct. ② The cells isolated from mice livers could

express αSMA determined by western blot and immunofluorescence. So the isolated cells were HSCs and had been activated. LDK378 order ③ The Psmp8+Luciferase could express luciferase in HSCs, but not in kuffer cells and hepatic cells detected by Dual-Luciferase Reporter

Assay System. Conclusion: The Psmp8+Luciferase containing the αSMA promoter could express specifically in activated HSCs. This suggested that Psmp8+Luciferase containing Ribose-5-phosphate isomerase αSMA promoter could be used as an specific vector targeted activation HSCs, further more it may be recombined and used in the fibrosis gene therapy. Key Word(s): 1. targeted therapy; 2. HSCs; 3. αSMA promoter; 4. liver fibrosis; Presenting Author: WUPENG BO Additional Authors: TANSHI YUN, ZHANG BO Corresponding Author: WUPENG BO Affiliations: wuhan university; guangxi renmin hospital Objective: Objective To explore the effects of ursodeoxycholic acid in rats’ chronic hepatic injury and it’s mechanism. Methods: Methods Rat s’ chronic hepatic injury model was induced by subcutaneous inject ion of CCl4 for 6 weeks. Suspension of ursodeoxycholic acid preprared with normal saline was given orally to the rats, 20 mg●kg-1●d-1 for 4 weeks. HE staining was done to characterize the change of hepatic pathology. Masson staining was used to qualitatively analyse the accumulation of extracellular matrix. The levels o f serum ALT, AST, TBIL and MAO were detected. And western blotting was also performed to detect the expression level of autophagic molecular signals including ATG-5, beclin-1 and LC3 II.

The liver inflammation check details and injury in 3xTg-iHAP mice were spontaneously resolved through liver regeneration and restitution within 5 days after low-dose Dox challenging. Taken together, we have developed and validated a new murine model of hepatocyte apoptosis-induced sterile liver inflammation and wound healing response. In a pilot study, we further revealed that 3xTg-iHAP mice chronically fed with alcohol-containing Lieber-DeCarli liquid diet developed profound steatohepatitis after treatment with a single low-dose of Dox. This finding suggests that our novel mouse model for sterile liver inflammation

can be combined with other liver disease models for studying the exact role of multi-hits in the pathogenesis of numerous inflammatory liver diseases such as alcoholic hepatitis and nonalcoholic steatohepatitis. Thus, 3xTg-iHAP mice is a novel in vivo research tool and may have a broad range of applications from exploring insights into the pathogenesis of sterile liver inflammation to testing new therapies for various liver diseases and complications (Supported in part by grants from the NIH). The following people have nothing to disclose: Heng-Fu Bu, Fangyi Liu, Xiao Wang, Pauline M. Chou, Catherine Marek, Ke Tian, Peng

Wang, Hua Geng, M. S. Rao, Suhail Akhtar, Monique E. De Paepe, Xiao-Di Tan Background/Aims: Nerve growth factor (NGF) has pro-inflammatory effects in lung and skin inflammatory diseases. During liver regeneration, NGF secreted learn more by hepatocytes

induces hepatic stellate cell apoptosis. However, NGF involvement in models of liver damage and inflammation has not yet been assessed. We investigated the possible inflammatory effects of NGF on isolated hepatic stellate cells (HSC), as well as the in vivo effect of silencing NGF on acute liver damage and inflammation. Methods: Primary HSC from rats and mice were isolated and cultured for 7d and 14d to CYTH4 obtain activated and fully activated HSC, respectively. HSC were treated with 100ng/ ml NGF and proNGF and inflammatory cytokine expression was assessed by qRT-PCR and ELISA. Acute liver damage was induced by two i.p. injections of CCl4 (1 μl/g body weight) or by bile duct ligation (BDL) and mice received daily treatment with antisense oligodeoxynucleotide to NGF (ODN)(25mg/kg body weight). Results: Both NGF and proNGF induced expression of pro-inflammatory cytokines TNFα and IL-6 in activated and fully activated primary rat and murine HSC. Administration of antisense ODN to NGF in the acute CCl4 and BDL models reduced liver damage, as demonstrated by significantly reduced serum liver enzymes. In addition, antisense ODN to NGF resulted in dramatically reduced (6- fold) hepatic mRNA expression of pro-inflammatory cytokines IL-6, TNFα and MCP1 in the acute CCl4 model.

We acknowledge the utility of responsiveness to steroids in aiding the diagnosis of AIH; however, these criteria were formulated to allow “bedside” diagnosis in routine clinical practice and to guide management. Application of the criteria after steroid therapy has been instituted would only be useful in retrospect. In addition, including response to steroid therapy would render the two criteria near identical in their applicability and ease of use. Finally, the authors emphasize the lower sensitivity of the simplified criteria for ‘definite’ diagnosis of AIH (70%) compared to “overall” diagnosis of AIH (90%) and suggest this as the major limitation. However, since majority of the patients

diagnosed as “probable” AIH using the simplified criteria would be treated in a fashion similar to those diagnosed as “definite” AIH, we would argue that the sensitivity for “overall” diagnosis of AIH is more relevant. In summary, the results of this study are difficult Selleck Talazoparib to interpret because

the accuracy of AIH diagnosis in study patients is unknown. Until a reliable gold standard test for AIH is devised to accurately assess the sensitivity and specificity of these criteria, it would be prudent to limit their use as an adjunct to clinical judgement in guiding diagnosis and management of patients with AIH. MK1775 Rajan Kochar*, Michael Fallon*, * Division of Gastroenterology & Nutrition Hepatology, The University of Texas Health Science Center at Houston, Houston, TX. “
“A 32-year-old Histidine ammonia-lyase woman presented in week 31 of her pregnancy with a 7-day history of nausea, intermittent vomiting, and fever. Investigations revealed significantly abnormal liver function (bilirubin: 45 μmol/L [normal: <18 μmol/L]; alkaline phosphatase: 211 U/L; alanine aminotransferase (ALT) = 2360 U/L; gamma-glutamyl transferase: 74 U/L; international normalized ratio: 1.6). The provisional diagnosis was fatty liver of pregnancy. ALT, alanine aminotransferase; AST, aspartate aminotransferase; HSV, herpes simplex virus.

Despite emergency caesarian section, the patient’s condition deteriorated and intubation was required on day 2 for hepatic encephalopathy. Computed tomography scan of the abdomen demonstrated patent hepatic vessels and an enlarged liver with parenchymal changes suggestive of fatty infiltration. Hepatitis A/B/C serology returned negative, and because of the diagnostic uncertainty at that point, both intravenous acyclovir and N-acetyl-cysteine were commenced. On postpartum day 3, the patient underwent urgent transplantation for acute liver failure. A diagnosis of fulminant liver failure from herpes simplex virus (HSV) was confirmed following pathological examination of the explanted liver. Figure 1 is a section of explanted liver. The liver is enlarged and congested. The yellow mottled areas correspond to the only residual viable parenchyma. In Figure 2, extensive geographic pauci-inflammatory, hemorrhagic necrosis is demonstrated.

Non-adherence to IS therapy leading to graft rejection is well-recognized. We aim to study adherence to IS treatments and patient preferences in adolescent and adult liver recipients in a multi-ethnic Asian centre. Methods Liver recipients (age >18) on IS therapy on active follow up at our institution

were identified. An anonymous questionnaire form (available in English, Mandarin, selleck chemicals llc Malay, Arabic) was given to each patient during a clinic visit (survey period Oct 2013 – Apr 2014). Completed forms were returned in unmarked sealed envelope. Results One hundred questionnaires were distributed; sixty-eight were returned fully completed and included in the present analysis. Based on the validated Morisky Adherence Score, only 5% of our cohort were considered to have “high adherence”; while 31% had “low adherence”. Liver recipients aged 20-39 were more likely to have low adherence compared to those between 40-69 years. Respondents were predominantly male (84%), with high school education (44%). Time from LT ranged

from <1 year to >10 years. 30% did not know the names of their current IS. 37% check details admitted to missing IS doses; selleck kinase inhibitor 7% missed doses once in 2 weeks; 12% missed doses once in 3 months. Evening doses were most commonly missed (18%). 57% felt once daily morning dosing regimen would improve IS adherence. Common reasons

for missed doses include “forgot” (19%), “too busy” (13%). 68% prefer to have their number of doses reduced and 28% found it difficult to take their evening dose on time. Patient’s ethnicity and primary language used, education level, occupation status, number of IS agents and amount spent on IS were not associated with adherence. Conclusion Adherence to immunosuppression is often under-reported by liver recipients. Extra vigilance and patient education by the transplant team is needed to improve adherence among younger liver recipients (20-39 years). Simplified immunosuppression dosing regimens with once daily regimens and a reduced pill burden may improve adherence to immunosuppressive therapy. Disclosures: Kieron B.

[27, 29] From a multicenter study of ALD in China, the incidence of ALD among hospitalized patients with liver diseases each year from 2000 to 2004 were 2.7%, 2.9%, 3.0%, 3.6%, and 4.4%, respectively. Among 902 patients with ALD, 11.2% exhibited mild ALD, 22.6% exhibited a fatty liver, 28.8% suffered from hepatitis, and 37.4% were classified as

having cirrhosis. The severity of liver Alectinib damage correlates with the amount and duration of alcohol use.[31] There has been a gradual increase in the number of patients with end-stage ALD undergoing liver transplantation in mainland China in the past 10 years.[32] Therefore, alcohol-induced liver injury has become an important issue in China, which cannot be neglected. The prevalence of NAFLD among adults in the general population in China is approximately 15% (6.3–27.0%), depending on the population studied, and has paralleled the increase in both obesity and T2D observed in these regions (Table 2).[20-24] selleck NAFLD is found in over a quarter of the general adult Chinese population in Hong Kong, but the proportion of patients with advanced fibrosis in NAFLD patients is low (3.7%).[24] Based on liver ultrasound, the prevalence of NAFLD is 2.1% among the 1180 surveyed schoolchildren age 6–14 years. The prevalence of NAFLD was higher in overweight and obese students

than in students with a normal body mass index (BMI). Male students were more likely to have NAFLD than female students.[33] In addition, compared with the nonobese controls, mixed obesity had the strongest association with NAFLD and dyslipidemia, followed by abdominal obesity and peripheral obesity in Chinese school-aged children.[34]

Coproporphyrinogen III oxidase The prevalence of NAFLD among 861 obese children (6–16 years old) was 68.2%, and the prevalence increased to 84.6% (187/222) in obese patients with MetS.[35] In contrast with the vast epidemiological data on the prevalence of NAFLD, there is minimal data available on the incidence of this disease in China. Fan et al. studied the incidence of ultrasound-defined NAFLD in 5402 nonalcoholic healthy subjects (4633 men, mean age 37 years) after a 2-year follow-up and observed 327 subjects (6.1%) with new cases of NAFLD.[36] The incidence of NAFLD increased significantly with the changes in BMI at baseline: 1.4% in subjects with normal weight, 6.4% in overweight patients, 16.8% in obese patients, and 24.5% in patients with severe obesity. Logistic regression analysis revealed a significant interaction between the incidence of NAFLD and age, BMI and serum triglycerides at baseline, and the subtle gain in BMI and triglycerides during follow-up. The other study by Zhou et al. revealed that the annual incidence of NAFLD is 9.1%, and the MetS components represent risk factors for the development and progression of NAFLD.

Fluorescent microscope was employed

to observe the transfection results. At 48 hours after transfection, RNAs and proteins R428 cost were extracted; Then the expressions of XPD, DNp73 and GADD45β were detected by RT-PCR and Western blotting, respectively. The cell proliferation was assessed by MTT assay. The changes in cell apoptosis were evaluated by flow cytometry. Results:  Green Fluorescent Protein (GFP) was expressed in SMMC-7721-pEGFP-N2-XPD group cells and SMMC-7721-pEGFP-N2 group cells. In contrast, GFP was undetectable in Lip group and Blank group cells by fluorescent microscope. Compared with Blank group, Lip group and N2 group, the expression of DNp73 mRNA decreased significantly in XPD group (P < 0.01), but the expressions of XPD and GADD45β mRNAs were enhanced obviously in XPD group (P < 0.01). There was no statistical diffirences of XPD, DNp73 and GADD45βmRNAs expressions among Blank group, Lip group and N2 group (P > 0.05). The trend of XPD, DNp73 and GADD45β proteins detected by Western blotting were consistent with the trend of their mRNAs. The proliferation of SMMC-7721 cells

was markedly inhibited (P < 0.01) and the apoptosis of SMMC-7721 cells was increased after transfected by XPD (P < 0.01). Conclusion:  The wild-type XPD as an tumor suppressor gene plays an inhibitory role in the carcinogenesis of HCC. The expression Vincristine of DNp73 decreased and the expression of GADD45βincreased with the overexpression of XPD, suggests that both of them may play a key role in the mechanism of XPD inhibiting the carcinogenesis of HCC. Key Word(s): 1. Hepatoma; 2. XPD gene; 3. DNp73 gene; 4. GADD45b gene;

Presenting Author: ANILK JOHN Additional Authors: MADIHAEMRAN SOOFI, SAADAL KAABI, ESRAMOHD AL ADHAL, SALWA KANDATH, MOUTAZ DERBALA, MT BUTT, RAFIE YAKOOB, Flavopiridol (Alvocidib) MUNEERA MOHANNADI, HAMID WANI Corresponding Author: ANILK JOHN Affiliations: Hamad Medical Corporation; Hamad Medical Corporation; Hamad Medical Corporation; Hamad Medical Corporation; Hamad Medical Corporation; Hamad Medical Corporation; Hamad Medical Corporation; Hamad Medical Corporation; Hamad Medical Corporation; Hamad Medical Corporation Objective: Percutaneous liver biopsy is the standard of care for obtaining hepatic tissue for histopathological assessment of parenchymal liver disease. Today percutaneous liver biopsies are mostly performed under real time ultra sound guidance by radiologists. We prospectively audited our practice of blind outpatient liver biopsies, performed without image guidance by gastroenterologists for its safety and adequacy, in this era of high tech imaging. Methods: All patients who underwent blind percutaneous liver biopsies without image guidance by gastroenterologists for grading and staging of chronic hepatitis B/C were audited prospectively for the safety of the procedure and the adequacy of tissue samples for proper grading and staging.

022, respectively, Fisher’s exact test) (Fig. 7). There was, however, no association between SP1 and MMP2 expression using immunohistochemistry (P = 0.740). No association between the clinicopathologic features and SP1 and

MMP2 overexpression was found. Despite the fact that PTEN has been extensively studied and is implicated in cell migration,15-19 its underlying molecular mechanisms in HCC progression and metastasis have not been clearly TSA HDAC order elucidated. Therefore, it is of strategic importance to characterize the functional consequence of PTEN underexpression and the deregulated downstream signaling. In line with our clinical findings, the metastatic cell line H2M had a lower PTEN protein expression compared with its primary HCC counterpart cell line H2P.10 To study the functional consequences of PTEN loss in HCC, two HCC cell lines, SMMC-7721 and BEL-7402, with relatively higher endogenous PTEN levels were used to establish the stable PTEN-knockdown clones. ACP-196 concentration Because more than one stable knockdown clone was used, this likely eliminated clonal effect in the assays. We documented that knockdown of PTEN significantly promoted cell migration and invasion

in vitro, suggesting its possible role in HCC metastasis. Similar results were obtained with both cell lines, which suggests that the enhanced cell migration and invasion associated with loss of PTEN expression was not cell line–specific. In addition, our PTEN-deficient MEFs also exhibited increased cell migration and invasion compared with wild-type

MEFs. This indicates that the association of PTEN loss with metastasis is not cell type–specific. Overall, our in vitro results were consistent with our clinical observation that PTEN underexpression was significantly associated with more frequent tumor microsatellite formation in human HCCs. Tumor microsatellite formation in human HCCs is one of the histologic features of tumor metastasis. Furthermore, we observed that the PTEN−/− MEFs also possessed enhanced PIK3C2G proliferation rate (Supporting Fig. 2), and this was consistent with our finding of p-AKT activation, thereby triggering the prosurvival pathways. The enhanced cell proliferation is in agreement with our finding of an association of PTEN underexpression with increased tumor size in human HCCs. To eliminate the additive effect or cell proliferation in contribution to the enhanced cell migration and invasion observed, mitomycin C, a drug that blocks cell proliferation, was added in these assays. To move across the Matrigel layer in the cell invasion assay, cells need to secrete certain enzymes to degrade the extracellular matrix. Indeed, the Matrigel coated onto the invasion chamber in the cell invasion assay comprise three main substances: 56% laminin, 31% collagen IV, and 8% entactin, all by weight. MMP2 and MMP9 gelatinases primarily act to destroy the major constituent collagen IV.

8, 9, 26 When Lombardi et al. combined CD with azaserine27 (not known to be a hepatocarcinogen) or with either of the liver carcinogens ethionine10 and acetylaminofluorene28 and fed to Sprague-Dawley rats at approximately 8 weeks of age, they reported rapid development of HCC, with an incidence of up to 80% after 6 months, and only selleck screening library a 38% incidence of CCAs.28 When initiation by diethylnitrosamine was followed by CDE, Takahashi et al. obtained similar results.29 Mikol et al.30 found a 90%-100% incidence of HCC in Fischer 344 rats initiated with diethylnitrosamine and fed a diet devoid of methionine and choline. We have no clear explanation

for why our present finding of a high incidence of CCA in rats fed cyclic CDE beginning at 3 weeks of age but no HCC in either the rats started on CDE at 3 weeks or 8 weeks, is different from other results previously reported. Clearly, most investigators have reported HCC in the various hepatocarcinogenic regimens that induce oval cell proliferation. However, AG-014699 order to the best of our knowledge,

no other study used cyclic CDE exposure. Perhaps the week off during each cycle allows putative liver stem cells to evade death or differentiation and thus be able to give rise to CCAs; in contrast, with continuous CDE exposure, the stem cells would be forced to differentiate, such that they give rise to relatively few CCAs and more HCCs. An alternative explanation is that the default differentiation pathway of oval cells is to form ducts. If this Niclosamide is true, then when hepatocarcinogenic regimens induce large numbers of oval cells, CCAs would be expected rather than HCCs. We chose a cyclic CDE dietary schedule for two principal reasons. The main reason was to reduce morbidity and mortality during a chronic feeding schedule, based on previous studies using a cyclic feeding of acetylaminofluorene.31, 32 Rats continuously fed CDE for more than 2 weeks in our previous studies died with massive oval cell proliferation.33 A secondary reason was as an attempt to augment oval cell proliferation and tumor development, by repetitive exposure to a CD diet.10, 28 Choline deficiency induces a state of fat deposition, apoptosis, and compensatory regeneration; in this

abnormal situation, hepatocytes are forced to divide repeatedly, such that the deficiency has been termed a nutritional partial hepatectomy.34 The aberrant hepatocyte proliferation within the liver is believed to be the fundamental alteration that is ultimately responsible for the development of HCC from a methyl-deficient diet.35 As discussed above, our results are in contrast to those found previously. In a study entailing a CD diet, only 51% of male F344 rats fed that CD diet for 13-24 months had developed HCC by the end of the 24-month period.36 Three months duration on a continuous CD diet has been considered to be the minimum period required to induce HCC.34 It is thus possible that we did not expose the rats to total CDE for a sufficiently long enough period.

[29, 30] High genomic similarity between genotype 4 HEV strains isolated from our patient and those previously reported from Aichi may support the zoonotic food-borne transmission of HEV from wild boar infected with genotype 4 HEV to our patient. INCB024360 in vivo In the present study, raw pig liver as food sold in grocery stores in Mie was found to be contaminated with HEV at the frequency of 4.9% of the total examined packages (12/243). The detection of HEV RNA in raw pig liver intended for human consumption in Mie is not surprising, because

contamination of commercially sold pig livers with HEV has been reported not only in Japan,[11] but also in the USA,[15] the Netherlands,[31] India,[32] France[33] and Germany.[34] However, this finding was contrary to our assumptions, because HEV RNA was detected significantly more frequently in commercially sold pig livers in Mie than in Hokkaido (4.9% vs 1.9% [7/363], P = 0.0372), where hepatitis E is endemic and approximately one-third of hepatitis E patients in Japan have been reported annually.[14] Some Japanese people Romidepsin have a habit of eating raw pig liver, and it is served

at some restaurants in Japan. Based on the evidence that HEV infection is distributed widely in domestic pigs in Japan,[8, 35] it is very likely that the raw pig livers as food sold in grocery stores or supermarkets throughout Japan are contaminated with HEV, although the rate of virus contamination may differ by region, and should be examined

in various areas in Japan, including both endemic and non-endemic regions (northern and southern parts, respectively, of Japan),[36] to assess the actual Thiamet G risk of HEV transmission from pig livers to humans. Importantly, the contaminating virus in commercial pig livers sold in local grocery stores remains infectious when inoculated into pigs[15] and cultured cells.[37] Of note, the virus sequences recovered from pig livers (nos. 152 and 193) were 99.5–100% identical to the viruses recovered from hepatitis E patients (nos. 13 and 17). However, these two patients did not remember consuming pig liver before the onset of hepatitis E (Table 2). The route of HEV transmission was unknown for patient nos. 13 and 17, although patient no. 17 reported frequent ingestion of raw horse meat and sushi. The HEV sequences recovered from the two patients and two pig liver specimens differed by 7.8% or more from the deposited HEV sequences as of June 2013, thus suggesting the uniqueness of these human and swine HEV sequences, and that the source of the HEV in the patients was likely pigs. It is now evident that pigs constitute a major reservoir, and are able to shed the virus into the environment.[12, 38] Contrary to our expectation, the distribution of HEV genotype/subgenotype was different between hepatitis E patients and purchased pig liver packages (Table 4). The reason for this discrepancy remains unknown.