Therefore, MMN is a good procedure, using routine assessment in neurophysiological settings, to diagnose attention deficits and MHE and follow their course in patients with liver cirrhosis. Patients with MHE show a wide array of neurologic-neuropsychiatric alterations, PD0325901 molecular weight including reduced attention,

psychomotor slowing, reduced motor coordination, and so on. Each alteration is the result of impairment of different neuronal circuits and processes, of which modulation involves different brain areas, neurotransmitter systems, and mechanisms. Also, different pathogenic mechanisms could be involved in the different neurological alterations in the same patient. This is nicely illustrated by a recent report39 showing that in patients with MHE, alterations in the PHES performance strongly correlated with Epigenetics Compound Library elevated inflammatory markers, but not with increased ammonia. However, EEG abnormalities correlated with high ammonia levels, but not with inflammation. This shows that different cerebral and neurological alterations

are the result of different mechanisms. This has been demonstrated in more detail in animal models of MHE. Hypokinesia is caused by increased extracellular glutamate in substantia nigra,40 whereas impairment of learning a Y maze task is the result of reduced function of the glutamate/nitric oxide/cGMP pathway in the cerebellum.41 The MMN wave is generated by multiple neuronal elements. Latency depends on the neurons with faster response. Amplitude represents the maximum response of the sum of all neurons responding at the same time point. The area represents the accumulated response of all neurons from the beginning of the wave until its return to basal levels. In patients with MHE, latency and amplitude are not altered, but the area is reduced, indicating that the neurons

respond in a similar way to control subjects, but a lower number of neurons are activated and during shorter periods. Impairment of MMN in patients with MHE could be caused by similar mechanisms as in patients with schizophrenia. Understanding the mechanisms leading to attention deficits in MHE may help to design treatments to eliminate these deficits. In summary, the data reported show that MMN is a good procedure, MCE using routine neurophysiological techniques, to diagnose attention deficits and MHE with good sensitivity and specificity and follow their course in patients with liver cirrhosis. “
“Gallstone prevalence ranges from 10% to 15% in the Western world, with a great variety of genetic and environmental risk factors. Gallbladder or common bile-duct stones can result in biliary pain, which may be accompanied by systemic infection and jaundice in the case of cholecystitis and/or cholangitis. The primary work-up includes investigation of clinical signs (e.g.

Results.— Headache of non-migraine type was associated with low levels of serum 25(OH)D with an odds ratio (OR) of 1.20 (1.04-1.39) in the lowest quartile as compared to the highest serum 25(OH)D quartile. No significant association was found between migraine and serum 25(OH)D. Conclusion.— Non-migraine

headache was associated with low levels of serum Daporinad cost 25(OH)D. Although adjustment were done for possible confounders, this finding may still reflect lifestyle rather than causality, and further studies are needed to investigate this. No association was found between serum 25(OH)D and migraine. “
“A broadening of the clinical and imaging features of the spontaneous cerebrospinal fluid (CSF) leaks is now well recognized, far beyond what was thought only two decades ago. This has resulted in increasing number of patients with atypical and unusual features who, not unexpectedly, are directed to headache specialists and tertiary referral centers. In many cases, obviously the fundamental question of presence or absence of CSF leak will need to be addressed prior to proceeding with further and often more involved, more invasive, and more costly diagnostic and therapeutic considerations. Radioisotope cisternography often proves to be very helpful in these situations by demonstrating reliable, although indirect, evidences of CSF leak while it is less helpful in directly identifying the exact site of the CSF leakage. In this overview

article, the expectations from and the limitations of this diagnostic method are described along PKC inhibitor with some personal observations in the past 25 years. “
“This study aims to determine why patients with migraine present to an emergency department (ED). While migraine accounts for 上海皓元医药股份有限公司 over 800,000 ED visits annually, no prospectively gathered data characterize patients’ reasons for presenting to an ED. We prospectively interviewed 309 consecutive

patients presenting to an urban ED for headache. Patients were asked 100 closed-ended questions regarding sociodemographics, headache history, and current headache attack. We performed descriptive analyses on patients fulfilling International Classification of Headache Disorders 2 migraine criteria. Of 186 patients who met migraine criteria, 77% (95% confidence interval [CI]: 71, 83%) had a primary care provider (PCP), 87% (95% CI: 82, 92%) had medical insurance, and 83% (95% CI: 77, 88%) had drug coverage. Fifty-three percent (95% CI: 46, 60%) reported that they previously visited a doctor for headache. Fifty-five percent (95% CI: 48, 62%) previously received a migraine diagnosis. Twenty-two percent (95% CI: 16, 28%) sought medical care for the current headache prior to ED presentation. Fifty-five percent (95% CI: 48, 63%) took abortive medication for migraine on the day of the ED visit. Median headache duration was 24 hours (IQR: 12-72). Forty-nine percent (95% CI: 42, 57%) screened positive for depression.

2802, P = 0.0213) and 7.9 (95%CI: 1.0225–62.2802, P = 0.0213) were estimated in AH for the DRB1*16 and DQB1*0502 alleles, respectively (Fig. 1). For the other two alleles, DRB1*15 and DQB1*0602, the OR in relation to AH was calculated as 0.2 (95%CI: 0.0731–0.3929, P = 0.0001). Thus, these comparative results revealed that the high risk alleles in patients with AH, DRB1*16 and DQB1*0502, represent low risk alleles in patients

with congenital haemophilia A and inhibitors and conversely, the low risk alleles in AH, DRB1*15 and DQB1*0602, are associated with high risk for inhibitor patients with congenital haemophilia A. The DRB1*15 allele is known to present efficiently a specific selleck surface loop peptide comprising amino acids 1706 through 1721 of the FVIII light chain. This is currently considered to be an established mechanism for inhibitor formation in patients with congenital HA and lack of endogenous FVIII protein synthesis [17,24]. It might be speculated that this allele is protective in patients with endogenous FVIII as is the case with AH. The DQB1*0602 allele was found to be in strong linkage disequilibrium with DR1*15. In conclusion, AH is a multifactorial disease resulting from the combined influence of multiple Pim inhibitor susceptibility genes and additionally, not very clearly understood environmental factors. The association

of HLA class II-DR1*16 and DQB1*0502 alleles with AH in our cohort of patients is in contradiction to associative allele profiles for inhibitor patients with congenital haemophilia A and might be related to the synthesis of normal amounts of endogenous FVIII protein in AH opposed to the

absence of FVIII in congenital haemophilia A. The authors stated that they had no interests which might be perceived as posing a conflict or bias. “
“About 10% of mutations in haemophilia A cases generate a premature termination codon in the factor VIII gene (F8). Upon therapeutic FVIII substitution, it was noted that the risk of 上海皓元医药股份有限公司 developing inhibitors is higher when the nonsense mutation is located in the light chain (LC) of the factor VIII (FVIII) protein than in the heavy chain (HC). We analysed the impact of six different nonsense mutations distributed over the six FVIII domains on recombinant FVIII expression to elucidate the process of inhibitor formation in haemophilic patients. Full-length F8 mRNA was transcribed from all constructs despite the presence of nonsense mutations. Polyclonal antigen assays revealed high antigen levels in transfection experiments with constructs truncated in LC whereas low antigen was detected from constructs truncated in HC. Those results were supported by FVIII localization experiments. These findings suggest that F8 transcription occurs in a usual way despite nonsense mutations, whereas translation appears to be interrupted by the premature stop codon. We hypothesize that the inclusion of the B domain enables proteins truncated in LC to accumulate in the ER.

Approximately half of the patients with positive polysomy develop CCA, but not all do. Follow-up testing with ERCP should depend on occurrence of mass on MRI, stricture development on MRC, presence of prominent CA 19-9 elevation, and whether other clinical symptoms that might be associated with CCA are present. In conclusion, the results of FISH tests need to be interpreted with caution in PSC patients. FISH trisomy/tetrasomy-positive results have very limited implications in PSC patients. A positive FISH polysomy test result does enhance the sensitivity of cytology testing for CCA, especially

if a dominant stricture is present. Results of FISH should be interpreted in association BIBW2992 purchase with patient’s clinical, laboratory, and cholangiographic Galunisertib features. “
“NorUDCA (24-norursodeoxycholic acid), the C23-homolog of ursodeoxycholic acid (UDCA), showed remarkable therapeutic effects

in cholestatic Mdr2 (Abcb4) (multidrug resistance protein 2/ATP-binding cassette b4) knockout mice with sclerosing/fibrosing cholangitis. In contrast to UDCA, norUDCA is inefficiently conjugated in human and rodent liver, and conjugation has been discussed as a key step for the anticholestatic action of UDCA in cholestasis. We compared the choleretic, anticholestatic, and antiapoptotic properties of unconjugated and taurine-conjugated UDCA (C24) and norUDCA (C23) in isolated perfused rat liver (IPRL) and in natrium/taurocholate cotransporting polypeptide (Ntcp)-transfected human hepatoma (HepG2) cells. Taurolithocholic acid (TLCA) was used to induce a predominantly hepatocellular cholestasis in IPRL. Bile flow was determined gravimetrically; bile acids determined by gas chromatography and liquid chromatography/tandem mass spectrometry; the Mrp2 model substrate, 2,4-dinitrophenyl-S-glutathione

(GS-DNP) was determined spectrophotometrically; and apoptosis was determined immunocytochemically. The choleretic effect of C23-bile acids was comparable to their C24-homologs in IPRL. In contrast, TnorUDCA, but not norUDCA antagonized the cholestatic effect of TLCA. Bile flow (percent of controls) was 8% with TLCA-induced cholestasis, and unchanged by coinfusion 上海皓元医药股份有限公司 of norUDCA (14%). However, it was increased by TnorUDCA (83%), UDCA (73%) and TUDCA (136%). Secretion of GS-DNP was markedly reduced by TLCA (5%), unimproved by norUDCA (4%) or UDCA (17%), but was improved modestly by TnorUDCA (26%) or TUDCA (58%). No apoptosis was observed in IPRL exposed to low micromolar TLCA, but equivalent antiapoptotic effects of TUDCA and TnorUDCA were observed in Ntcp-HepG2 cells exposed to TLCA. Conclusion: Conjugation is essential for the anticholestatic effect of norUDCA in a model of hepatocellular cholestasis.

Using a gene silencing approach, the authors

convincingly show that cellular DGAT1 depletion results in a marked decrease of infection and viral spread in the HCV cell culture (HCVcc) model system. Interestingly, this effect was not observed when viral spreading was analyzed following DGAT2 depletion in the same conditions. Similarly, the treatment of HCV-producing cells with a well characterized DGAT1 inhibitor,11 conferred a marked decrease in viral spread in HCV permissive cells. Because the DGAT1 inhibitor had no effect on HCV protein expression and RNA synthesis, the authors conclude that this molecule affects a life cycle step following viral replication. Additional functional studies uncovered that DGAT1 is this website involved in the very early steps of viral assembly. To further elucidate the molecular mechanism of DGAT1-mediated HCV production, Herker et al. performed coimmunoprecipitation and colocalization assays. In their mechanistic studies, the authors observed that DGAT1 interacts with HCV core protein at the ER and that

DGAT1 is required for the trafficking of core to LD surface, allowing early steps of viral assembly to occur. These observations support a model where packaging of viral genomes into progeny virions requires DGAT1 (Fig. 1). What are the clinical implications of this important study? First, the results of Herker et al.9 identify DGAT1 as an important host factor for HCV infection. This discovery does not only advance our understanding of the viral life cycle but may selleckchem also have implications for the understanding of pathogenesis of HCV-induced liver disease. Further studies are needed to investigate the relevance of the uncovered virus-host MCE公司 interactions for HCV-associated steatosis and modulation of treatment response. In this regard it is of interest to note that DGAT1 has been previously identified as a specific

factor for hepatic steatosis12 and the HCV core protein has been suggested to modulate triglyceride accumulation in hepatocytes (for review, see Negro1). Second, by demonstrating that a DGAT1 inhibitor decreases HCV particle assembly and production, the results of Herker et al. have uncovered a promising novel target for antiviral therapy. Because specific DGAT1-inhibitors do not affect LD composition, their further development might not be limited by potential off-target effects. As shown previously for micro-RNA122, cyclophilin A, and claudin-1, targeting host factors is an attractive antiviral strategy which may increase the genetic barrier for viral resistance (for review see Georgel et al.2). Proof-of-concept studies in HCV animal models are clearly the next step to demonstrate the efficacy and the antiviral resistance profile for the DGAT1-inhibitor in vivo. Clinical trials in HCV-infected patients may ultimately address its clinical relevance within the widening arsenal of antiviral strategies for HCV infection.

The letter also provided information about HCV transmission, effect on the liver, and effect on general health. In addition, beginning in 2005-2006, serum samples from participants with a positive or indeterminate result for anti-HCV were tested for hepatitis C RNA (HCV-RNA);

starting in 2007, participants with an indeterminate test result for anti-HCV and a positive HCV-RNA also were sent an ROF letter. Because a primary aim of the follow-up survey was to assess what actions participants this website took after becoming aware of their first positive test result, attempts to administer a follow-up telephone questionnaire to all those who were sent an ROF letter began 6 months after examination (approximately 4-5 months after the ROF letter was mailed) to allow participants time to have initiated or implemented actions after notification. Persons ≥18 years of age were interviewed directly; an adult proxy provided information

for participants who were <18 years of age and for individuals unable to answer the questions themselves. The HCV Follow-up Questionnaire (available at: www.cdc.gov/nchs/nhanes/nhanes2003-2004/questexam03_04.htm) was mentioned in the informed consent and also in the ROF letter. Bilingual AP24534 mouse (i.e., English and Spanish) trained interviewers contacted eligible participants by telephone for the interview. Participants who lived in households with no telephones were sent a letter asking them to call a toll-free number to answer a few questions about their hepatitis C results. Participants with communication

or cognitive difficulties that made it impossible to respond to the questionnaire, and for whom a parent or guardian was not available to complete the interview, were excluded. For the main NHANES survey, participants were interviewed in their homes to ascertain demographic characteristics, access to care, and health insurance coverage, using the Computer-Assisted Personal Interviewing (i.e., interviewer-administered) system. Having a usual source of medical care was determined by responses to the question: “Is there a place that medchemexpress you/sampled person usually go/goes when you are/he/she is sick or you/s/he needs advice about your/his/her health? Qualitative determination of anti-HCV in blood serum or plasma was measured using direct solid-phase enzyme immunoassay with an anti-HCV screening enzyme-linked immunosorbent assay (ELISA) (Ortho CD VITROS Anti-HCV Immunodiagnostic System; Ortho Clinical Diagnostics, Raritan, NJ). Positive specimens were repeated in duplicate according to the same procedure. Repeatedly positive specimens were then tested using a confirmatory recombinant immunoblotting assay (RIBA) (Chiron RIBA Processor System, Chiron RIBA HCV 3.0 Strip SIA; Chiron Corporation, Inc., Emeryville, CA), an in vitro qualitative enzyme immunoassay for the detection of anti-HCV in human serum or plasma.

Also, it shows that early education of oral and dental health in comprehensive care services for CBD and their regular supervision lead to even better results for these children compared with normal population. One limitation Vismodegib cell line of this study is whether it was appropriate

to use general questionnaires for the CBD population. As far as we are aware, a disease-specific questionnaire is not available to assess OHR-QoL in CBD patients. Validated questionnaires are necessary for adequate assessment of quality of life, as, due to limited population of CBD patients, we applied the above-mentioned validated Iranian version of age-specific questionnaires, and this study can be assumed as a pilot for further investigations. However, further studies with larger group of subjects and new approaches to assess the children with bleeding disorders compared with healthy controls are needed. The authors acknowledge Mrs. Fatemeh Gorgi and Mrs. Zahra Poorhabibi for statistical analyses,

and Mrs. Behnaz Habibpanah, head nurse of Mofeed Comprehensive Care center for Children with CBD, for her contribution to the study. This study was designed by Katayoun check details Salem and Peyman Eshghi; the manuscript was written by Katayoun Salem and revised by Peyman Eshghi. The authors also appreciate the collaboration of Professor Ghasem Ansari, head of Hospital Dentistry Department, in the management of multidisciplinary approach. The authors stated that they had no interests which might be perceived as posing a conflict or bias. “
“Summary.  Dogs with haemophilia A or haemophilia B exhibit spontaneous bleeding comparable with the spontaneous bleeding phenotype

that occurs in humans with severe haemophilia. The phenotypic and genotypic characteristics of haemophilic dogs have been well-described, and such dogs are suitable for testing prophylactic 上海皓元 protein replacement therapy and gene transfer strategies. In dogs with haemophilia, long-term effects on spontaneous bleeding frequency (measured over years) can be used as an efficacy endpoint in such studies. Although complete correction of coagulopathy has not been achieved, published data show that prophylactic factor replacement therapy and gene transfer can markedly reduce the frequency of spontaneous bleeding in haemophilic dogs. Further studies are currently ongoing. “
“PEGylation of B-domain deleted factor VIII (PEG-FVIII-BDD) prolongs the half-life of the molecule by approximately twofold in animals (Mei et al., Blood 2010; 116: 270). To investigate the role of von Willebrand factor (vWF) in the catabolism of PEG-FVIII-BDD in vivo, a FVIII-BDD mutant (F8V), which is incapable of binding vWF, was generated by deleting the vWF-binding region in the a3 domain of FVIIII-BDD. F8V was expressed, purified and PEGylated by site-specific conjugation.

Conclusion:  Endoplasmic reticulum stress might be involved in lipogenesis in

fatty acids-induced hepatic steatosis. Talazoparib mouse Therefore, endoplasmic reticulum stress might serve as a novel target in the pathogenesis and therapy of non- alcoholic fatty liver disease. “
“Heo J, Reid T, Ruo L, Breitbach CJ, Rose S, Bloomston M, et al. Randomized dose-finding clinical trial of oncolytic immunotherapeutic vaccinia JX-594 in liver cancer. Nat Med 2013;19:329-336. (Reprinted with permission.) Oncolytic viruses and active immunotherapeutics have complementary mechanisms of action (MOA) that are both self amplifying in tumors, yet the impact of dose on subject outcome is unclear. JX-594 (Pexa-Vec) is an oncolytic and immunotherapeutic vaccinia virus. To determine the optimal JX-594 dose in subjects with advanced hepatocellular carcinoma (HCC), we conducted a randomized phase 2 dose-finding trial (n = 30). Radiologists infused low- or high-dose JX-594 into liver tumors (days 1, 15 and 29); infusions resulted in acute detectable intravascular JX-594 genomes. Objective intrahepatic Modified Response Evaluation Criteria in Solid Tumors (mRECIST) (15%) and Choi (62%) response rates and intrahepatic disease control (50%) were Selleck Epigenetics Compound Library equivalent

in injected and distant noninjected tumors at both doses. JX-594 replication and granulocyte-macrophage colony-stimulating factor (GM-CSF) expression preceded the induction of anticancer immunity. In contrast to tumor response rate and immune endpoints, subject survival duration was significantly related to dose (median survival of 14.1 months compared to 6.7 months on the high and low dose, respectively;

hazard ratio 0.39; P = 0.020). JX-594 demonstrated oncolytic and immunotherapy MOA, tumor responses and dose-related survival in individuals with HCC. Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related death in men and claims more than 700,000 lives per year worldwide.[1, 2] The age-adjusted incidence of HCC in the U.S. more than doubled within the past 35 years, and it is medchemexpress projected to continue to be the fastest-growing cancer in the U.S. for at least another 15 years. However, the prognosis remains dismal, with a 5-year survival rate slightly above 10%.[2] The risk factors for HCC can be divided into two major groups: (1) viral hepatitis, including chronic hepatitis B and chronic hepatitis C infection; and (2) chronic nonviral hepatic inflammation, such as alcoholic and nonalcoholic fatty liver disease, autoimmune hepatitis, and primary biliary cirrhosis. Approximately 85% of HCCs arise in livers with chronic hepatitis or cirrhosis. In clinical practice, cirrhosis is recognized as a high-risk preneoplastic condition and HCC surveillance with abdominal ultrasound every 6 months is recommended for all individuals with cirrhosis by both the American Association for the Study of Liver Diseases (AASLD) and the European Association for the Study of the Liver (EASL).

Early hepatocellular carcinomas with a high incidence of iso-density or low density (signal) areas throughout the arterial, portal and equilibrium phases (LF1213816

level 1), hepatocellular carcinoma with a nodule-in-nodule finding (LF1214517 level 1), and dysplastic nodules (LF1214018) were not included in the studies. Of the articles adopted this time, the histological diagnostic criteria for hepatocellular carcinoma were mentioned in five articles. Three articles (LF121031 level 1, LF105467 level 1, LF0620011 level 1) cited the International Working Party (LF1214018), and two articles (LF058794 level 1, LF020016 level 1) made a reference to the diagnostic criteria established by Ferrell et al. (LF1213919

level 1). Of the three articles on lipiodol CT, only lipiodol was used in two studies (LF058794 level 1, LF103715 level 1), Cilomilast ic50 and lipiodol plus anticancer drug plus/minus gelatin sponge were used in the third study (LF004742 level 1). With regard to the diagnostic performance of each diagnostic imaging technique, the merits and demerits of studies using isolated or resected livers as the gold standards may be as follows: (1) Usually, the sensitivity is higher for resected livers than for BMS-907351 price isolated livers. This is probably attributable to small cancer nests not being identifiable at the time of surgery but being found in the explanted livers. More sensitive diagnosis is considered to be possible in isolated livers. However, (2) the time 上海皓元医药股份有限公司 from the final imaging test to liver transplantation (range : 32 days to 6 months, Table 1) is generally longer than that from the final imaging to resection. If a new focus develops during the waiting period for transplantation, the preoperative diagnostic imaging examination may have yielded a false-negative

result, reducing the sensitivity of diagnosis. (3) The main candidates for liver transplantation in Western countries are patients with advanced cirrhosis (Child–Pugh class C), and hepatocellular carcinoma is only a secondary indication. The diagnostic performance of imaging decreases as the severity of cirrhosis increases. Whereas, hepatectomy is often performed in patients with good liver function (Child–Pugh class A). (4) A section of resected liver and a CT/MRI image plane can be compared relatively easily, whereas it is difficult to maintain an isolated liver in a 3-D anatomical form as it is in the body after explantation. Therefore, comparison with CT/MRI is not always easy. (5) The slice thickness of an isolated liver tends to be generally thicker than that of a resected liver, and small lesions may be missed in thicker slices.

All immigrants from the former USSR had one or more Jewish ancestors in various generations (or were Jews themselves). However, individuals from these separate geographical regions had very distinct cultural and socioeconomic characteristics, resembling their former non-Jewish neighbours (and are assimilated to various extents with these non-Jewish neighbours). Four HCV-infected haemophiliac siblings (Ashkenazi-1; Sephardi-3) had identical haplotype at rs12979860 – and therefore excluded. Inclusion of relatives would introduce bias and for a cohort of patients with a genetic disease this becomes a major issue. Genotypic frequencies were obtained

using AZD0530 research buy direct counting, and statistical analysis was performed using the chi-squared test with Fisher’s exact. C-allele frequencies were calculated using the Hardy–Weinberg Equilibrium equation. The duration of HCV infection in each haemophiliac patient was estimated using a method described elsewhere [23]. P-values less than 0.05 were considered statistically significant. Calculations

were performed using sas software (SAS 9.1.3; SAS buy AP24534 Institute Inc., Cary, NC, USA). The demographic and clinical characteristics of a cohort of 130 patients with haemophilia and other coagulation disorders testing positive for hepatitis C serology are presented in Table 1. Their mean age was 41 years, with an estimated duration of HCV infection of 27.1 years. There were 84 (80.8%) patients infected with HCV genotype 1:26 (20%) of the entire group were co-infected with HIV (61.5% with HCV genotype 1). A high viral load was found in 59 (56.7%), whereas 38 (29.2%) patients had advanced fibrosis (F3–F4).

Twenty-six (20%) patients tested persistently HCV RNA-negative, and were considered to have cleared HCV infection spontaneously. Fifty-one (39.2%) patients completed at least 80% of the recommended PEG–IFN/RBV dose, and 19 (37.3%) of the treated medchemexpress patients achieved SVR. The distribution of the various polymorphisms at SNPs rs12979860 and rs8099917 is shown in Table 2. The minor haplotype CC at SNP rs12979860 was found in 40 (30.8%) patients, whereas the major rs8099917 TT genotype was detected in 74 (56.9%) patients. Of note, genotyping was not feasible for laboratory technical issues at SNP rs12979860 in one patient, or at rs8099917 in 12 (9.2%) patients. The GG genotype at rs8099917 was only found in one patient, and therefore, for further analysis, we considered this patient together with the TG genotype, which was found in 43 (33.1%) HCV-infected haemophiliacs. SVR was achieved in 7 (70%) treated haemophilia patients who were CC homozygotes at SNP rs12979860 vs. 12 (38.7%) of the TC heterozygotes. No patient with the TT haplotype achieved an SVR (CC vs. CT or TT; P = 0.0196). Likewise, the CC haplotype was detected in seven (36.8%) of those patients achieving SVR and in only three (9.4%) non-responders.