“
“Melanistic leopards Panthera pardus are common in south-east Asian forests but the exact frequency of this variant phenotype is difficult to assess. Records from camera-trapping studies conducted at 22 locations in Peninsular Malaysia and southern Thailand between 1996 and 2009 show that only melanistic leopards were present in samples south of the Isthmus of Kra. During 42 565 trap-nights, we collected 445 Selleckchem Bafilomycin A1 photos of melanistic leopards and 29 photos of the spotted or non-melanistic morph. All 29 photos of spotted leopards came from study sites north of the Isthmus. These results indicate that this recessive trait may be nearly fixed in P. pardus populations

of the Malay Peninsula, suggesting a unique evolutionary history of leopards in the region. Assuming a very small effective population size (Ne=100) and a high initial allelic frequency, at least 1000 years would be expected to elapse until a neutral allele became fixed. The severe bottleneck implied by this scenario provides a testable hypothesis that can be addressed using molecular markers and evidence of past glacioeustatic changes across the region. Although natural selection might lead to rapid

fixation of melanism within Malayan leopards, had their effective population Napabucasin size been much larger (e.g. Ne=5000) and stable, with a lower allelic frequency, the fixation would require a longer time span (e.g. 20 000 years) if induced by genetic drift alone. “
“Human habitation in deserts can create rich novel resources that may be used by native desert species. However, at night such resources may lose attractiveness when they are in artificially lit areas. For bats, attraction to such manmade habitats might be species specific.

In an isolated village in the Negev desert that is known for its high bat activity we investigated the effects of artificial lighting on flight behaviour of two aerial insectivorous bat species: Pipistrellus kuhlii, a non-desert synanthropic bat, common in urban environments and Eptesicus bottae, a desert-dwelling species. Using an acoustic tracking system we reconstructed flight trajectories for bats that flew under artificial lights [Light treatment (L)] versus in natural darkness [Dark treatment (D)]. Under L both P. kuhlii and E. bottae flew significantly faster than under D. Under L, P. kuhlii also flew at significantly lower altitude (i.e. 上海皓元医药股份有限公司 away from a floodlight) than under D. Whereas P. kuhlii foraged both in L and D, E. bottae only foraged in D. In L, activity of E. bottae decreased and it merely transited the illuminated area at commuting rather than foraging speed. Thus, under artificially lighted conditions the non-desert synanthropic species may have a competitive advantage over the native desert species and may outcompete it for aerial insect prey. Controlling light pollution in deserts and keeping important foraging sites unlit may reduce the synanthropic species’ competitive advantage over native desert bats.

[68, 69] Risk factors that require careful assessment include patient age and weight, nutritional status, hypoalbuminemia, hepatopulmonary syndrome, and cardiomyopathy associated with cirrhosis.[69,

70] Pediatric conditions and their associated comorbidities that may heighten anesthetic risk include Alagille syndrome (cardiac disease, vascular and renal abnormalities, and moyamoya), biliary atresia with splenic malformation (complex heart disease, interrupted inferior vena cava), and primary hyperoxaluria (renal and cardiac dysfunction).[69] A specialized LT anesthesia team has been associated with more favorable patient outcomes in adults, although pediatric centers were excluded from this study.[71] The United Network for Organ Sharing (UNOS) has recently modified policy to require liver transplant programs to designate a Director of Liver Transplant Anesthesia who has expertise in the area of perioperative care Epigenetics Compound Library datasheet of liver transplant patients and can serve as an advisor to other members of the team. 20. An anesthesiologist familiar with pediatric indications for LT and associated comorbidities should ensure the LT evaluation includes appropriate disease-specific assessments to minimize intraoperative and postoperative anesthetic risk. (2-B) Children with chronic liver disease are often not fully immunized prior to LT.[72, 73] Development of a vaccine

Alectinib preventable disease (VPD) either before or after LT will increase morbidity and mortality and heightened the risk of graft injury or loss.[74, 75] Timing of immunization administration in the LT candidate is important, as vaccines are more immunogenic before the development of endstage liver disease and more immunogenic before than after LT. Humoral immunity to rubella, measles, and varicella vaccines is significantly decreased in children with biliary atresia compared to healthy controls.[76] VPD can develop in immunized children with chronic liver disease

when antibody titers are low.[77] There is a paucity of data related to influenza vaccine in patients with MCE chronic liver disease.[78] Hepatic decompensation has been reported with influenza,[79] and influenza vaccination in adults with cirrhosis significantly reduced the frequency of hepatic decompensation compared to those who did not receive the vaccine.[80] Guidelines for vaccination of liver transplant candidates and recipients are published periodically by the American Society of Transplantation.[81] Clinical practice guidelines for vaccination of the immunocompromised host were recently published by the Infectious Diseases Society of America.[82] Vaccination of household contacts provides additional protection to the child.[83] Paralytic polio has been described in household contacts of oral polio vaccine recipients.[84] Data suggest that administration of live virus vaccines to household contacts, other than oral polio, poses minimal risk to the child.

These cells undergo cell replication at a significantly faster rate than other hepatocytes. Importantly, these cells are present peri-centrally

in the normal liver lobule, are not dependent on injury and thereby distinct from injury-induced oval cells and Lgr5+ cells. In addition, we have identified the Wnt ligands that act on these progenitor hepatocytes and show that endothelial cells at the central vein of the liver are the Wnt producing niche cells. We hypothesize that this specialized population of peri-central hepatocyte stem cells is responsible for homeostatic renewal in the liver. Disclosures: The following people have nothing to disclose: Bruce M. Wang, Roel Nusse Induced pluripotent stem cell-derived BMN 673 cell line human hepatocyte-like cells (iHLCs) have learn more great potential for applications such as studying the mechanisms underlying human liver development and disease, testing the efficacy and safety of pharmaceuticals across different patients (i.e. personalized medicine), and enabling cell-based therapies such as bioartificial liver devices and implantable cell-laden constructs. However, current in vitro protocols

that utilize growth factors and extracellular matrices (ECM) alone yield iHLCs with fetal levels of liver functions relative to adult primary human hepatocytes (PHHs). Furthermore, these low hepatic functions in iHLCs are difficult to maintain for prolonged times in culture. Here, we have engineered a micropatterned co-culture (iMPCC) platform in a multi-well format (24- and 96-well plates) that significantly enhanced the functional maturation and longevity of fresh and cryopreserved iHLCs in culture for at least 4 weeks in

vitro when compared to standard confluent cultures. In particular, iHLCs were micro-patterned onto ECM-coated domains of empirically optimized dimensions using soft lithographic techniques and subsequently surrounded by supportive 3T3-J2 murine embryonic fibroblasts. Overlaying the iMPCCs with an ECM gel further improved iHLC functions. 上海皓元医药股份有限公司 We assessed iHLC maturity via liver gene expression (i.e. HNF4a), secretion of albumin and urea (5-6 ug/hr/million iHLCs in iMPCCs), basal CYP450 activities (i.e. up to 73% CYP3A4 activity in iMPCCs as compared to stable PHH cultures), phase II conjugation, drug-mediated CYP450 induction, and hepatocyte polarity (LDL uptake, canalicular transport). Moreover, we showed for the first time that the predictive power for classifying drugs as liver-toxic or non-toxic in iMPCCs was remarkably similar to stable cultures of PHHs (∼65-70% sensitivity, 100% specificity), thereby demonstrating iHLC utility in early stages of drug development where a paucity of healthy human liver tissues limits PHH use.

1%∼6.5%). Some of our microbiome samples were enriched in both Bacteroides and Prevotella and did not fit into the enterotypes described above. Therefore, we designated these samples as enterotype H, a hybrid between enterotypes 1 and 2. From the QIIME-generated

OTU table, all OTUs assigned to Escherichia were examined. The most abundant Escherichia OTU was identified to be OTU#20341. The DNA sequence of OTU#20341 was retrieved from a QIIME-generated FASTA file containing a representative sequence for each OTU. This sequence was used as the input for Blast search (available at: http://blast.ncbi.nlm.nih.gov), against the current 16S rRNA database (search performed on April 9, 2012). A single blood sample was collected from each patient at the time of liver biopsy (from July 26, 2010 through RG7204 ic50 June 1, 2011). A single blood sample from

each healthy and non-NASH obese subject was collected at the same period. Serum alcohol concentration was determined in subsets of obese and Selleckchem Abiraterone NASH patients in the microbiome study and a new cohort of healthy subjects. Serum samples were stored at −80 °C before ethanol concentrations were measured with an ethanol assay kit from BioVision (Milpitas, CA), following the manufacturer’s instructions. Briefly, alcohol was oxidized by alcohol oxidase, and the product was subsequently measured by a colorimetric probe (at 570 nm). A linear standard curve between alcohol concentrations and OD570 was generated and used to calculate alcohol concentrations in serum samples. One-way analysis of variance (ANOVA) and post-hoc Tukey’s honest significant difference tests for multiple comparisons were performed to evaluate differences in taxonomic abundance, alpha diversities, and serum ethanol concentrations among three groups. Fisher’s exact test was performed to examine a possible association between enterotypes and health status. ANOVA, Tukey’s, and Fisher’s tests were performed with R version 上海皓元 2.14.0. A P value less than 0.05 was considered statistically significant. Gut microbiomes of healthy, obese, and NASH children and adolescents (Table

1) were analyzed by 16S rRNA pyrosequencing. A total of 835,591 sequencing reads were obtained from a total of 63 samples. Ecological diversity within each sample was evaluated by a phylogenetic distance metric (Supporting Fig. 1A). No significant difference was observed among three groups. However, as a measurement of species richness, Chao1 metric revealed significant differences among three groups (Supporting Fig. 1B). P(ANOVA) values were <0.05 at sampling sizes 1,268, 2,526, 3,784, and 5,042 OTUs. Post-hoc Tukey’s tests indicated that differences were significant between obese and healthy controls (Tukey’s P < 0.05 at sampling sizes 1,268, 2,526, 3,784, and 5,042 OTUs). Species abundance in the NASH group was marginally lower than that of the healthy group, with Tukey’s P values of approximately 0.1. Ecological diversities within each group were accessed by UniFrac analysis.

1%∼6.5%). Some of our microbiome samples were enriched in both Bacteroides and Prevotella and did not fit into the enterotypes described above. Therefore, we designated these samples as enterotype H, a hybrid between enterotypes 1 and 2. From the QIIME-generated

OTU table, all OTUs assigned to Escherichia were examined. The most abundant Escherichia OTU was identified to be OTU#20341. The DNA sequence of OTU#20341 was retrieved from a QIIME-generated FASTA file containing a representative sequence for each OTU. This sequence was used as the input for Blast search (available at: http://blast.ncbi.nlm.nih.gov), against the current 16S rRNA database (search performed on April 9, 2012). A single blood sample was collected from each patient at the time of liver biopsy (from July 26, 2010 through ABT737 June 1, 2011). A single blood sample from

each healthy and non-NASH obese subject was collected at the same period. Serum alcohol concentration was determined in subsets of obese and check details NASH patients in the microbiome study and a new cohort of healthy subjects. Serum samples were stored at −80 °C before ethanol concentrations were measured with an ethanol assay kit from BioVision (Milpitas, CA), following the manufacturer’s instructions. Briefly, alcohol was oxidized by alcohol oxidase, and the product was subsequently measured by a colorimetric probe (at 570 nm). A linear standard curve between alcohol concentrations and OD570 was generated and used to calculate alcohol concentrations in serum samples. One-way analysis of variance (ANOVA) and post-hoc Tukey’s honest significant difference tests for multiple comparisons were performed to evaluate differences in taxonomic abundance, alpha diversities, and serum ethanol concentrations among three groups. Fisher’s exact test was performed to examine a possible association between enterotypes and health status. ANOVA, Tukey’s, and Fisher’s tests were performed with R version 上海皓元 2.14.0. A P value less than 0.05 was considered statistically significant. Gut microbiomes of healthy, obese, and NASH children and adolescents (Table

1) were analyzed by 16S rRNA pyrosequencing. A total of 835,591 sequencing reads were obtained from a total of 63 samples. Ecological diversity within each sample was evaluated by a phylogenetic distance metric (Supporting Fig. 1A). No significant difference was observed among three groups. However, as a measurement of species richness, Chao1 metric revealed significant differences among three groups (Supporting Fig. 1B). P(ANOVA) values were <0.05 at sampling sizes 1,268, 2,526, 3,784, and 5,042 OTUs. Post-hoc Tukey’s tests indicated that differences were significant between obese and healthy controls (Tukey’s P < 0.05 at sampling sizes 1,268, 2,526, 3,784, and 5,042 OTUs). Species abundance in the NASH group was marginally lower than that of the healthy group, with Tukey’s P values of approximately 0.1. Ecological diversities within each group were accessed by UniFrac analysis.

While conventional magnetic resonance imaging did not show any sign of involvement in the other components of GMT, DTI demonstrated signal changes in all anatomical components of the GMT. Main DTI findings in GMT of patients with HOD were an increase in radial diffusivity representing demyelination and an increase in axial diffusivity that is reflective of neuronal hypertrophy. DTI parameters can reflect the spatiotemporal evolution of transneuronal degeneration associated with HOD in a manner consistent with the

known pathologic stages of HOD. Hypertrophic selleck olivary degeneration (HOD), usually characterized by symptomatic palatal tremor, is a rare and unique type of transneuronal degeneration involving the inferior olivary (IO) nucleus, which occurs secondary to lesions in the components of the Guillain-Mollaret triangle (GMT).1 GMT is composed of the contralateral dentate nucleus, the ipsilateral red nucleus, and the inferior olivary nucleus.1 The ipsilateral central tegmental tract, the contralateral superior cerebellar peduncle, and the inferior cerebellar peduncle form the connecting pathways of these three structures.1 Lesions anywhere on this network may result in HOD. On conventional magnetic resonance imaging (MRI), signal intensity changes in the IO are typically observed about 1 month after lesion SP600125 mouse onset in the GMT.2–5 IO gradually increases in size, reaching a peak at

about 8.5 months.2 From this stage on, the size remains stable until the 24th month. Thereafter, IO gradually starts to decrease in size. Olivary hyperintensity on T2 weighted images usually persists for years.2 But even at a very late stage conventional MRI rarely demonstrates changes in the central tegmental tract, the superior cerebellar peduncle, the dentate, and red nucleuses, if they are not host of the inciting MCE lesion.6 In contrast, post-mortem studies of HOD reveal that there is

an ongoing dynamic process, starting just after the occurrence of the inciting lesion and extending several years thereafter.4,5 Although conventional MRI is a valuable tool in the diagnosis of HOD, it is not sensitive to dynamic histopathological changes known to occur in these patients. Therefore, we have hypothesized that these complex changes in patients with HOD, including hypertrophic changes in neurons, axonal degeneration, demyelination, and astrocytic hypertrophy, could be investigated by DTI.7 The aim of the study is to assess the pattern of DTI parameters in GMT of patients with HOD, and to relate the directional diffusivities with the known underlying pathologic stages of HOD. Ten patients (3 female and 7 male) who were diagnosed as HOD according to clinical symptoms and MRI findings at our hospital between January 2005 and June 2009 were selected for the study. Mean patient age was 49 (range 16–77). Internal review board of our hospital approved the study, and written informed consent was obtained from all subjects.

HFE gene mutations were linked to Hereditary Hemochromatosis. They were associated with hepatic iron overload, liver fibrosis, and response to interferon in chronic HCV patients. The aim of this study is to evaluate the effect of HFE mutation on response to standard of care (SOC) treatment of Egyptian patients. Patients and Methods the study comprised 657 patients with HCV who took SOC treatment and were accordingly divided into responders(301) and non-responders(356), as well as 160 age and sex

matched healthy controls. The following parameters were measured: complete iron profile, hepatic iron content, as well as frequency of HFE 187C>G and HFE193A>T genotypes. Results There was a statistically significant difference

in the Everolimus clinical trial frequency of HFE187C>G and HFE193A>T genotypes between responders, nonresponders and controls. There was a statistically significant association between the C allele of HFE187C>G and Selleckchem AZD6244 response to interferon. Carriers of G allele had a 9.3 odds ratio for non-response to SOC treatment than C allele. Carriers of T allele of HFE193A>T gene mutation had a 9.2 time risk for nonre-sponse to treatment. Conclusion Determination HFE gene polymorphism in chronic HCV patients may become an important tool in patient selection for theapy as it appears to play a role in the response to treatment. Frequency of the genotypes of HFE gene polymorphisms in the studied groups: Disclosures: The following people have nothing to disclose: Mazen I. Naga, Mona A. Amin, Dina A. Algendy, Ahmed I. El Badry, Mai M. Fawzi, Ayman R. Foda, Serag M. Esmat, Dina Sabry, Laila A. Rashed, Samia M. Gabal, Manal Kamal Background: Although many studies have tried to clarify the association between hepatitis C virus (HCV) infection and metabolic syndrome, few studies have comprehensively assessed their relationship stratified by different demographic characteristics.

Aims: To investigate the correlation between metabolic syndrome and HCV infection in Taiwan. Methods: We enrolled consecutive subjects who had received health check-up services at Taipei Veterans General Hospital from 2002 to 2009. Metabolic syndrome was diagnosed according to the criteria defined by the International Diabetes Federation Task Force on Epidemiology and Prevention. Results: 上海皓元医药股份有限公司 Among the 30616 subjects enrolled in this study, the prevalence of positive anti-HCV serology was 2.7%, and 28.8% were diagnosed with metabolic syndrome. In compared to those without HCV infections, patients with HCV infection were older in age and more females, with higher serum alanine aminotransferase (ALT), aspartate aminotransferase, gamma-glutamyltransferase, and fasting glucose levels, higher systolic and diastolic blood pressure, and lower cholesterol, high-density lipoprotein-cholesterol (HDL), low-density lipoprotein, and triglycerides levels, and lower platelet counts.

dubliniensis and S. mutans only (p= 0.046 and 0.043, respectively). MFC/MBC values were similar for all species except C. albicans; in that case, MUPB presented significantly higher values (p= 0.046). MUPB presented higher cytotoxicity than MMA for all tested concentrations (p < 0.001) except at 0.01 g/L. Irrespective of the concentration incorporated and species, there was no inhibition halo around the specimens. The incorporation of MUPB influenced the adhesion of C. albicans only (p= 0.003), with lower

CFU counts for the click here 0.6% group. Conclusions: It was concluded that non-polymerized MUPB has an antimicrobial capacity close to that of CPC and high cytotoxicity when compared with MMA. The antimicrobial activity of MUPB after incorporation within a denture base acrylic resin did not depend on its elution, but was shown to be restricted

to C. albicans. “
“Purpose: This study evaluated the effect of the incorporation of the antimicrobial monomer methacryloyloxyundecylpyridinium bromide (MUPB) on the hardness, roughness, flexural strength, and color stability of a denture base material. Materials and Methods: Ninety-six disk-shaped (14-mm diameter × 4-mm thick) and 30 rectangular (65 × 10 × 3.3 mm3) heat-polymerized acrylic resin specimens were divided into three groups according to the concentration of MUPB (w/w): (A) 0%, (B) 0.3%, (C) 0.6%. Hardness was assessed by a hardness tester equipped with a Vickers diamond ICG-001 solubility dmso penetrator. Flexural strength and surface roughness were tested on a universal testing machine and a surface roughness tester, respectively. Color alterations (ΔE) were measured by a portable spectrophotometer after 12 and 36 days of immersion in water, coffee, or wine. Variables were analyzed by ANOVA/Tukey HSD test (α= 0.05). Results: MCE公司 The following mean results (±SD) were obtained for hardness (A: 15.6 ± 0.6, B: 14.6 ±

1.7, C: 14.8 ± 0.8 VHN; ANOVA: p= 0.061), flexural strength (A: 111 ± 17, B: 105 ± 12, C: 88 ± 12 MPa; ANOVA: p= 0.008), and roughness (A: 0.20 ± 0.11, B: 0.20 ± 0.11, C: 0.24 ± 0.08 μm; ANOVA: p= 0.829). Color changes of immersed specimens were significantly influenced by solutions and time (A: 9.1 ± 3.1, B: 14.8 ± 7.5, C: 13.3 ± 6.1 ΔE; ANOVA: p < 0.05). Conclusions: The incorporation of MUPB affects the mechanical properties of a denture base acrylic resin; however, the only significant change was observed for flexural strength and may not be critical. Color changes were slightly higher when resin containing MUPB was immersed in wine for a prolonged time; however, the difference has debatable clinical relevance. "
“Purpose: In the tooth- and implant-supported fixed dental prosthesis (FDP), rigid and nonrigid connector (NRC) designs have been preferred by clinicians for many years.

5 Under all conditions and with all the types of stem/progenitors identified, the edges of the colonies contained cells that were larger and more differentiated than those in the colony interiors mimicking the formation of liver tissue from ductal plates4 and that of islets from

the edges of pancreatic ducts during organogenesis.11 Biliary tree stem/progenitors are logical precursors for mature cells of liver, bile duct, and pancreas given known events in organogenesis and in studies on pathologies of these tissues.6 They overcome many, if not all, of the ongoing controversies selleck products about whether or not there are stem cells in adult tissues for pancreas.11 The inability to identify true stem cells in adult pancreas10, 11, 23, 24 has fueled attempts to lineage restrict ES cells, induced pluripotent stem (iPS) cells, amniotic fluid-derived stem cells (AFSCs), or mesenchymal stem cells (MSCs), often with genetic manipulation to direct these cells to an endodermal fate; to find ways to reprogram adult pancreatic acinar cells; or to elicit proliferation of existing pancreatic islet beta cells.11, 25, 26 The process of driving www.selleckchem.com/products/pexidartinib-plx3397.html these various stem cell populations to a

mature endodermal tissue fate is inefficient, requiring up to 4-6 weeks in culture, and yielding adult cells with muted functions or with overexpression of or absence of expression of some genes. In the cases of the MSCs, the resulting adult cells are phenotypic hybrids of mesenchymal cells and the desired adult cell type.27 Moreover, for reasons unknown, the phenotype of the adult cells generated is distinct with every preparation and source. Fully mature hepatocytes or glucose-regulated MCE公司 β-cells from these precursors occur only with in vivo maturation of transplanted cells after several months. Moreover, any therapy based on ES or iPS cells may be limited by the potential of teratoma formation, usually ascribed to residual

undifferentiated stem cells.28, 29 Our findings that there are endodermal stem/progenitors in the biliary trees of all donor ages; that they clonogenically expand in vitro under wholly defined conditions; and that they readily and efficiently lineage restrict to liver, biliary tree, or pancreatic adult fates in culture with sets of wholly definable microenvironmental cues or in vivo suggest that they will become preferred choices for clinical programs and most experimental studies. The speed at which the differentiation occurs, even in culture, is an indication that these biliary tree stem/progenitors have progressed through most of the developmental stages for a liver or pancreatic fate. Indeed, their phenotypic characteristics in situ and in vitro indicate that they are mostly at stage 4 of the 5 stages during the progress of human ES cell stepwise-differentiation toward an islet fate.

We evaluated 61 patients (25 NASH and 36 CHC) who had undergone

liver biopsy for clinical purposes and 20 subjects without liver disease. Serum 25(OH)D3 was measured via colorimetric assay. Expression of VDR, CYP2R1, and CYP27A1 was evaluated via immunohistochemistry in hepatocytes, cholangiocytes, and liver inflammatory cells. Parenchymal and inflammatory cells from liver biopsies of patients with NASH and CHC expressed VDR, CYP2R1, and CYP27A1. In NASH patients, VDR expression on cholangiocytes was inversely correlated with steatosis severity Acalabrutinib supplier (P < 0.02), lobular inflammation (P < 0.01), and nonalcoholic fatty liver disease score (P < 0.03). Moreover, expression of CYP2R1 in hepatocytes correlated strongly with VDR positivity on liver inflammatory cells. In CHC subjects, fibrosis stage was associated with low hepatic CYP27A1 expression, whereas portal inflammation was significantly higher in patients with VDR-negative inflammatory cells (P < 0.009) and low VDR expression in hepatocytes (P < 0.03). Conclusion: VDR is widely expressed in the liver and inflammatory cells of chronic liver disease patients and its expression is negatively associated with the severity of liver histology in both NASH and CHC

patients. These data suggest that vitamin D/VDR system may play a role in the progression of metabolic and viral chronic liver damage. (HEPATOLOGY 2012;56:2180–2187) Recent studies have suggested a direct association between low serum 25-hydroxy-vitamin D3 [25(OH)D3] levels and the presence, severity, and prognosis of several liver diseases.1-7 Targher et al.1 and Manco et al.2 reported MCE公司 low serum 25(OH)D3 Apoptosis inhibitor concentrations among adults and children affected by

nonalcoholic steatohepatitis (NASH). Furthermore, we demonstrated the existence of a strong association between nonalcoholic fatty liver disease (NAFLD) and low 25(OH)D3 levels in a large adult population with normal serum liver enzymes.3 Recently, other studies have shown the presence of low serum 25(OH)D3 levels in patients affected by chronic hepatitis C (CHC) along with a failure to achieve sustained antiviral responses after standard therapy in CHC subjects with hypovitaminosis D.4-6 Vitamin D is present in the diet and dietary supplements, but its primary source is the photo-mediated conversion of 7-dehydrocholesterol in the skin.8 To become biologically active, vitamin D requires 25-hydroxylation in the liver and subsequent 1-hydroxylation in the kidney.9, 10 The 25-hydroxylation occurs exclusively in hepatocytes and is mediated by CYP27A1 and CYP2R1, two liver-expressed cytochromes characterized by different intracellular location, specificity, and affinity for vitamin D3.11, 12 Low serum 25(OH)D3 levels and hypovitaminosis D–related diseases have been shown to be associated with CYP2R1 polymorphisms by some authors,13, 14 but only one study to date has investigated liver 25-hydroxylase expression.