Additionally, RNA from these cells was harvested and qPCR was performed as previously Proteasome inhibitors in cancer therapy described. Paired Student’s t tests were used to determine the statistical significance of the data in all figures except Fig. 6, where an unpaired Student’s t test used.

Statistical analysis was performed using Prism 4 v. 4.0c. P < 0.05 was considered significant. HCV clone, JFH-1, can infect Huh-derived hepatoma cells in cell culture and produce infectious virus.21-23 By using this system, we determined the effect of HCV-infected hepatocytes on the generation of suppressive CD33+ monocytes/macrophages. We first infected Huh7.5.1 cells with HCV (JFH-1) virus; infection was then confirmed by immunofluorescence

(IF) for the expression of HCV core protein (Fig. 1A). HCV-infected cells (HCV+ hepatocytes) were reseeded and cultured for 24 hours. After the coculture of HCV+ or HCV− hepatocytes with PBMCs for 7 days, CD33+ cells were subsequently selected and then cocultured with autologous PD0325901 mouse CD4+ and CD8+ T cells. Interestingly, CD33+ cells cocultured with HCV+ hepatocytes significantly inhibited the production of IFN-γ by both CD4+ and CD8+ T cells using ELISA (Fig. 1B). In contrast, there was no significant difference in T-cell proliferation when T cells were cocultured with HCV+ hepatocytes as compared with those with HCV− hepaotcytes (data not shown). These results suggest that HCV impairs antiviral T-cell responses through the generation of suppressive CD33+ M/Mφ. To examine the effect of infectious virus on the generation of suppressive CD33+ cells, we treated PBMCs with varying doses of JFH-1 virus isolated using an Amicon filter system and CD33+ cells were then selected and cocultured with autologous CD4+ T cells. These results indicate that CD33+ cells are Urocanase not altered by

treatment with isolated virus (Supporting Fig. 1). Furthermore, CD33+ cells cocultured with HCV+ hepatocytes in the presence of a transwell modestly, but not significantly, suppress CD4+ T-cell activation as compared with control (Supporting Fig. 2), suggesting that close contact of CD33+ cells with HCV+ hepatocytes is required for optimal MDSC induction. Based on a report that CD33+ MDSCs, generated from human PBMCs following exposure to immunosuppressive factors for 7 days, suppress T-cell responsiveness, we assessed whether the immunomodulatory protein, extracellular HCV core, could induce MDSCs to impair T-cell responses.13 To this end, we treated human PBMCs with recombinant extracellular HCV core or control β-galactosidase (β-gal) for 7 days and then selected CD33+ cells using magnetic beads. The cells were then cocultured with CD4+ or CD8+ T cells for 3 days. HCV core-treated CD33+ cells inhibited the proliferation of both CD4 and CD8 T cells (Fig. 2A,B).

Additionally, RNA from these cells was harvested and qPCR was performed as previously CFTR activator described. Paired Student’s t tests were used to determine the statistical significance of the data in all figures except Fig. 6, where an unpaired Student’s t test used.

Statistical analysis was performed using Prism 4 v. 4.0c. P < 0.05 was considered significant. HCV clone, JFH-1, can infect Huh-derived hepatoma cells in cell culture and produce infectious virus.21-23 By using this system, we determined the effect of HCV-infected hepatocytes on the generation of suppressive CD33+ monocytes/macrophages. We first infected Huh7.5.1 cells with HCV (JFH-1) virus; infection was then confirmed by immunofluorescence

(IF) for the expression of HCV core protein (Fig. 1A). HCV-infected cells (HCV+ hepatocytes) were reseeded and cultured for 24 hours. After the coculture of HCV+ or HCV− hepatocytes with PBMCs for 7 days, CD33+ cells were subsequently selected and then cocultured with autologous see more CD4+ and CD8+ T cells. Interestingly, CD33+ cells cocultured with HCV+ hepatocytes significantly inhibited the production of IFN-γ by both CD4+ and CD8+ T cells using ELISA (Fig. 1B). In contrast, there was no significant difference in T-cell proliferation when T cells were cocultured with HCV+ hepatocytes as compared with those with HCV− hepaotcytes (data not shown). These results suggest that HCV impairs antiviral T-cell responses through the generation of suppressive CD33+ M/Mφ. To examine the effect of infectious virus on the generation of suppressive CD33+ cells, we treated PBMCs with varying doses of JFH-1 virus isolated using an Amicon filter system and CD33+ cells were then selected and cocultured with autologous CD4+ T cells. These results indicate that CD33+ cells are Docetaxel concentration not altered by

treatment with isolated virus (Supporting Fig. 1). Furthermore, CD33+ cells cocultured with HCV+ hepatocytes in the presence of a transwell modestly, but not significantly, suppress CD4+ T-cell activation as compared with control (Supporting Fig. 2), suggesting that close contact of CD33+ cells with HCV+ hepatocytes is required for optimal MDSC induction. Based on a report that CD33+ MDSCs, generated from human PBMCs following exposure to immunosuppressive factors for 7 days, suppress T-cell responsiveness, we assessed whether the immunomodulatory protein, extracellular HCV core, could induce MDSCs to impair T-cell responses.13 To this end, we treated human PBMCs with recombinant extracellular HCV core or control β-galactosidase (β-gal) for 7 days and then selected CD33+ cells using magnetic beads. The cells were then cocultured with CD4+ or CD8+ T cells for 3 days. HCV core-treated CD33+ cells inhibited the proliferation of both CD4 and CD8 T cells (Fig. 2A,B).

There were 117 patients with chronic hepatitis and 13 patients with compensated liver cirrhosis (Child–Pugh score < 6). Patients were treated with lamivudine (GlaxoSmithKline, Brentford, UK) 100 mg daily. Lamivudine treatment was started on day 1 to day 5 on admission (median day 3). One hundred and thirty patients did not receive lamivudine in the historical control cohort selected from our database. With SAS ver. 8.2 software (SAS Institute, Cary, NC, USA), patients in the control group were matched for sex, age and

imaging finding (cirrhosis or not) with the lamivudine treatment group. The match ratio was 1:1. There were 117 patients with chronic hepatitis and 13 patients with compensated liver cirrhosis. All patients of the historical control group met the aforementioned NVP-LDE225 chemical structure inclusion and exclusion criteria. The

protocol of our study conformed to the ethical guidelines of the 1975 Declaration of Helsinki and was approved by the Clinical Research Ethics Committee of the Harbin Medical University. All the patients or their relatives in the lamivudine treatment group gave written informed consent before enrolment. The level of serum creatinine, INR for prothrombin time and the level of serum total bilirubin of each ACLF patient on admission were recorded. The MELD score was calculated according to the original formula proposed by the Mayo Clinic group: 3.8 × loge (bilirubin [mg/dL]) + 11.2 × loge (INR) + 9.6 × loge (creatinine [mg/dL]) + 6.4 × (etiology:

AZD3965 0 if cholestatic or alcoholic, 1 otherwise). Hepatitis B e-antigen and antibody to HBeAg were detected by a qualitative oxyclozanide HBeAg enzyme immunoassay (Abbott Laboratories, Chicago, IL, USA). Serum HBV DNA was measured by polymerase chain reaction (PCR) assay (Amplicor HBV Monitor Test; Roche Diagnostics, Mannheim, Germany). The detection limit was 1 × 103 copies/mL. HBV DNA levels of the patients were evaluated before and after the 4-week treatment. HBV genotyping was determined by PCR using type-specific primers. The tyrosine, methionine, aspartate, aspartate (YMDD) motif mutant was detected by PCR assay and restriction fragment length polymorphism (RFLP) assay at baseline and 3-month follow up. With the use of PCR and RFLP assay for mixed viral-genotype populations (wild-type and mutant virus), the lower limit of detection for differentiating between the two viral genotypes has been determined to be 5% of the viral population. The assay has a lower limit of detection of approximately 1 × 104 copies of viral DNA per mL of serum. The patients were questioned about adverse events. All the adverse events, regardless of their possible association with lamivudine, were recorded. The 260 patients with ACLF were followed up for at least 3 months. The outcome (recovery, bridging to liver transplantation, or death) of each patient was recorded.

Recent advances provide additional support for the liver TISC concept and, importantly, may aid therapeutic decision making by allowing risk assessment. Targeted anti-TISC therapies hold significant promise, but a better understanding of the origin and phenotype of www.selleckchem.com/products/MG132.html these cells appears necessary. Significant progress has been made in liver stem cell and liver cancer

stem cell research in the last 2 years. Although normal and cancerous liver stem cells or LPCs naturally share many characteristics and markers, on most accounts, the two fields have been moving forward independently. The dual focus of the conference provided an opportunity to gather insight or update one’s knowledge of the other field. In addition, the conference

identified commonalities that may serve as a basis for future advances. For Lumacaftor example, new markers of normal LPCs may be useful for further fractionation of heterogeneous TISC populations. Conversely, signaling pathways and transcription factors regulating TISC characteristics may also play a role in noncancerous liver regeneration. In addition, new cell-culture or in vivo cell-delivery systems will likely benefit research on both normal and cancerous liver stem cells or LPCs. The hope is that increased exchange and collaboration between the two fields will accelerate the development of therapies for patients with liver disease and liver cancer. The American Association for the Study of Liver Disease Henry M. and Lillian Stratton Basic Research Single Topic Conference “Stem Cells in Liver Diseases and Cancer: Discovery and Promise” was held in Atlanta, GA, March 19-20, 2011. The meeting provided an overview and update on ongoing research efforts seeking to obtain a detailed

understanding of stem cell biology in liver disease and cancer for the development of new therapies. This review is dedicated to Nelson Fausto, a leader in the field. “
“Ischemia-reperfusion injury (IRI) is a major limiting event for successful Cyclooxygenase (COX) liver transplantation, and CD4+ T cells and invariant natural killer T (iNKT) cells have been implicated in promoting IRI. We hypothesized that hepatic overexpression of CD39, an ectonucleotidase with antiinflammatory functions, will protect liver grafts after prolonged cold ischemia. CD39-transgenic (CD39tg) and wildtype (WT) mouse livers were transplanted into WT recipients after 18 hours cold storage and pathological analysis was performed 6 hours after transplantation. Serum levels of alanine aminotransferase and interleukin (IL)-6 were significantly reduced in recipients of CD39tg livers compared to recipients of WT livers. Furthermore, less severe histopathological injury was demonstrated in the CD39tg grafts. Immune analysis revealed that CD4+ T cells and iNKT cells were significantly decreased in number in the livers of untreated CD39tg mice.

35, 36 To

confirm viperin’s anti-HCV activity, we knocked down viperin expression, using an RNA interference (RNAi) approach, and were able to demonstrate, for the first time, Depsipeptide that viperin plays an important, but not exclusive, role in the anti-HCV activity of IFN-α. Considering that many genes are differentially regulated in Huh-7 cells after IFN-α stimulation, it is highly likely that a coordinated ISG response is responsible for the control of HCV replication. A number of studies have suggested that viperin has an ER distribution18, 23; however, we and others have observed that viperin localizes to both LDs and, in our studies, the HCV NS5A-positive RCs.24 LDs have recently been shown to be an essential component of the HCV life cycle,25 and it is thought that the

close association of the LD and ER membranes provides a microenvironment essential for HCV RNA replication and virion production. It has been hypothesized that the interaction of viperin with NS5A at the LD surface is the possible mechanism whereby viperin exerts its antiviral effect through the disruption of virion assembly.12, 13 However, a number of lines of evidence suggest that this is unlikely. First, viperin exerts its anti-HCV effect against the HCV subgenomic replicon, which lacks the HCV structural proteins and is defective in virion assembly. This would also suggest click here that the viperin-core acetylcholine interaction we observed is not fundamental to viperin antiviral activity, and that the interaction with NS5A is critical. It is plausible that the observed interaction between viperin and core at the surface of the LD is mediated by the ability of core to recruit and interact with NS5A at the LD surface to initiate virion assembly. Second,

viperin is antiviral against a genotype 2a HCV subgenomic replicon (SGRm-JFH1BlaRL), in which the HCV IRES drives the expression of the luciferase reporter gene to allow for the quantitative measurement of HCV RNA replication kinetics uncoupled from virion assembly after transfection of in vitro transcribed HCV RNA.10 Expression of viperin significantly suppressed luciferase output from this HCV subgenomic replicon, suggesting that the anti-HCV effect of viperin was at the level of HCV replication and not virion assembly. Finally, through confocal miscroscopy and FRET analysis, we have conclusively shown that viperin interacts with both NS5A and the proviral host factor, VAP-A, within the HCV RC. VAP-A (also known as hVAP-33) is a known interacting partner with NS5A (and NS5B) and is required for the efficient replication of HCV genomic RNA.

The fact that almost a third of the patients in either group received further TACE sessions after they went off protocol further outlines the danger of inadequate retreatment criteria for protocol compliance and consequently the success of multicenter

TACE studies. The ART score developed here is able to identify patients with good prognosis despite the presence of Child-Pugh stage B 7-9 points (Fig. 4B,C) or ascites (Fig. 4D) and would therefore provide a robust and objective evidence based tool to guide retreatment with TACE in future clinical trials. Finally, regarding the association of higher ART score values with SAEs and unplanned admissions (Table 4) and poorer OS (Figs. 3, 4), the application of this score may spare patient suffering see more and consequential costs by avoiding treatment-related side effects. The retrospective nature and the heterogeneous TACE types (TAE, cTACE, DEB-TACE) in the training cohort may be potential limitations of this study. However, we confirmed the results in all three TACE types in the training cohort (Fig. 3C-E) and in a completely independent external (Table 1, Figs. 3F, 4) patient GSI-IX cohort in

which most patients received conventional TACE. Additionally, the outcome of our patient population within the different Child-Pugh stages (Table 2) matches the published survival data reported in prospective clinical trials tuclazepam and meta-analysis3 and, thus,

further confirms the validity of our data. Another limitation may be the ART score assessment at heterogeneous timepoints between the first and second TACE (13-90 days), since the ART score is composed of laboratory changes that may be potentially reversible over time. However, time-related sensitivity analysis (Supporting Table 1-2) revealed no significant hint that the time of the ART score assessment influenced the results of this study. Finally, the ART score was developed by using the radiologic EASL-response criteria. Although the prognostic performance of EASL criteria in the setting of TACE seems to be equal to the performance of mRECIST criteria,25 the latter may be more adequate to dissect the prognosis of patients with partial response from that of subjects with stable disease.26 This could rely on a different definition of partial response in the two models: greater than 50% tumor reduction for EASL and greater than 30% for mRECIST criteria. Given that radiologic response is a parameter of the ART score, there is a need for prospective studies validating the ART score which include mRECIST criteria to the study design. In summary, we developed a novel and externally validated, noninvasive, objective, widely applicable prognostic (ART) score for patients with HCC allocated to retreatment with TACE. Patients with 2.

Methods: 10 Bama minipigs were divided into control group and stent group, one pig of each group died in the procedure. Every pig Dabrafenib order underwent endoscope, then laryngopharyngeal and distal esophageal pH monitoring for 4 hours, and at last been taken specimens from laryngopharyngeal mucosa. We repeat this procedure after 14 days. For stent group, between the procedures, we implant stents into their esophaguses, then laryngopharyngeal and distal esophageal pH monitoring for 2 hours, at last took away stents 3 days later. Cell interspaces were analyzed by transmission electron

microscope. Results: 1) There are no LPR in control group, at begin or last; but in stent group, LPR happened when stent implanted and can be detected after taking stent at the fourteenth day. (p < 0.05). 2) There are only some GER in control group, at begin or last; but in stent group, More GER happened when stent implanted and can be detected after

taking stent away at the fourteenth day. (p < 0.05). 3) There are no difference in intercellular space and desmosomes in the control group between begin and last. But in the stent group, the intercellular space increased, and the desmosomes counts decreased. Conclusion: According to these Vadimezan mw result, an animal model of LPR was established by implanting stent, at the same time, we established an animal model of GERD. Of course, LPR destroy the Laryngopharyngeal mucosal barrier. Key Word(s): 1. Laryngopharyngeal; 2. Reflux; 3. animal model; 4. intercellular space; Presenting Author: NING ZHONG Additional Molecular motor Authors: XUETING ZHENG, FENGYAN LIU, XUEFENG LU, YANQING LI Corresponding Author: NING ZHONG Affiliations: Qilu Hospital; Qiluhospital; Qilu hospital Objective: The management of lesions adjacent to the upper gastrointestinal tract with unknown origin is challengeable. Endoscopic ultrasound guided fine needle aspiration (EUS-FNA)

is one of the emerging methods to acquire histological diagnosis. The aim of this study was to evaluate accuracy and safety of EUS-FNA for those lesions. Methods: Thirty-seven patients with lesions adjacent to the upper gastrointestinal tract with unknown origin were identified retrospectively. All underwent EUS-FNA using a 19 or 22 gauge needle, with 2–3 needle passes. Ultrasonic characteristics were assessed. EUS-FNA diagnoses were made on the basis of cytologic-histologic analysis.(Picture) The results were compared with the final surgical pathology or follow-up. Results: Most EUS-FNA (35/37, 95%) acquired adequate samples for diagnosis. In compared with the final diagnosis, the sensitivity, specificity, positive predictive value, negative predictive value of EUS-FNA in differentiating benign and malignant were 92%, 100%, 100%, and 85%, respectively. Final diagnosis confirmed the diagnoses of malignancy in 25.

Methods: 10 Bama minipigs were divided into control group and stent group, one pig of each group died in the procedure. Every pig SCH772984 manufacturer underwent endoscope, then laryngopharyngeal and distal esophageal pH monitoring for 4 hours, and at last been taken specimens from laryngopharyngeal mucosa. We repeat this procedure after 14 days. For stent group, between the procedures, we implant stents into their esophaguses, then laryngopharyngeal and distal esophageal pH monitoring for 2 hours, at last took away stents 3 days later. Cell interspaces were analyzed by transmission electron

microscope. Results: 1) There are no LPR in control group, at begin or last; but in stent group, LPR happened when stent implanted and can be detected after taking stent at the fourteenth day. (p < 0.05). 2) There are only some GER in control group, at begin or last; but in stent group, More GER happened when stent implanted and can be detected after

taking stent away at the fourteenth day. (p < 0.05). 3) There are no difference in intercellular space and desmosomes in the control group between begin and last. But in the stent group, the intercellular space increased, and the desmosomes counts decreased. Conclusion: According to these Alvelestat mw result, an animal model of LPR was established by implanting stent, at the same time, we established an animal model of GERD. Of course, LPR destroy the Laryngopharyngeal mucosal barrier. Key Word(s): 1. Laryngopharyngeal; 2. Reflux; 3. animal model; 4. intercellular space; Presenting Author: NING ZHONG Additional Bcl-w Authors: XUETING ZHENG, FENGYAN LIU, XUEFENG LU, YANQING LI Corresponding Author: NING ZHONG Affiliations: Qilu Hospital; Qiluhospital; Qilu hospital Objective: The management of lesions adjacent to the upper gastrointestinal tract with unknown origin is challengeable. Endoscopic ultrasound guided fine needle aspiration (EUS-FNA)

is one of the emerging methods to acquire histological diagnosis. The aim of this study was to evaluate accuracy and safety of EUS-FNA for those lesions. Methods: Thirty-seven patients with lesions adjacent to the upper gastrointestinal tract with unknown origin were identified retrospectively. All underwent EUS-FNA using a 19 or 22 gauge needle, with 2–3 needle passes. Ultrasonic characteristics were assessed. EUS-FNA diagnoses were made on the basis of cytologic-histologic analysis.(Picture) The results were compared with the final surgical pathology or follow-up. Results: Most EUS-FNA (35/37, 95%) acquired adequate samples for diagnosis. In compared with the final diagnosis, the sensitivity, specificity, positive predictive value, negative predictive value of EUS-FNA in differentiating benign and malignant were 92%, 100%, 100%, and 85%, respectively. Final diagnosis confirmed the diagnoses of malignancy in 25.

RIPC was able to mitigate pancreatitis, indicating that it can protect beyond ischemic insults.

Conclusions: We have identified a platelet-serotonin-Vegf-Il10/Mmp8 axis that mediates the protective effects of RIPC. The systemic action, the conservation of RIPC effects among mice and humans, and the protection beyond ischemic insults suggest that the platelet-dependent axis has evolved as a preemptive response to local stress, priming the body against impending harm. (Hepatology 2014;60:1409–1417) “
“A Venetoclax systematic review and meta-analysis were conducted to explore the role of the methylenetetrahydrofolate reductase (MTHFR) C677T gene mutation and hyperhomocysteinemia in patients with Budd–Chiari syndrome (BCS) and portal vein thrombosis (PVT). PubMed, EMBASE, Cochrane Library and ScienceDirect databases were searched. Eligible studies should compare the prevalence of the MTHFR C677T mutation or hyperhomocysteinemia GSI-IX chemical structure or the homocysteine levels between BCS or non-cirrhotic PVT patients and healthy controls or between cirrhotic patients with and without PVT. A pooled odds ratio or weighted mean difference with 95% confidence interval was calculated. Of the 484 articles retrieved, 20 were included.

BCS and non-cirrhotic PVT patients had a higher prevalence of homozygous MTHFR mutation than healthy controls. The difference was statistically significant in BCS patients, but not in non-cirrhotic PVT

patients. BCS and non-cirrhotic PVT patients had a significantly higher prevalence of hyperhomocysteinemia and homocysteine level than healthy controls. Cirrhotic patients with PVT had a significantly higher prevalence of homozygous MTHFR mutation than those without PVT. However, the association between homocysteine level and PVT in cirrhotic patients was inconsistent among three studies. Homozygous MTHFR mutation and hyperhomocysteinemia may be associated with the occurrence of BCS and non-cirrhotic ADP ribosylation factor PVT. In addition, homozygous MTHFR mutation may increase the risk of PVT in cirrhotic patients. However, the current evidence failed to support the association of hyperhomocysteinemia with PVT in cirrhotic patients. The methylenetetrahydrofolate reductase (MTHFR) plays an important role in the remethylation pathway of the homocysteine metabolism.[1, 2] MTHFR is responsible for catalyzing the reduction of 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate in the folate cycle, which further produces the active form of folate for the remethylation of homocysteine to methionine.[1] MTHFR gene mutation is associated with the defective function of the MTHFR enzyme.[3] The most common MTHFR mutation is a C to T substitution at the nucleotide position 677 (C677T) of the MTHFR gene, converting from an alanine to valine in this enzyme.

Outcomes included discharge disposition and number and timing of readmissions. Covari-ates included demographics, donor age, graft type, MELD, etiology of liver disease, Charlson Comorbidity Index (CCI), pre-transplant depression, pretransplant pain and opioid use, ischemia time, and self-reported pre-transplant disability. Covariates were evaluated using the following multivariable models:

logistic regression for discharge disposition after transplant, competing risk Cox proportional-hazards regression for time to rehospitalization, IWR-1 and negative binomial regression for number of rehospitalizations (using followup time as an offset). Results: Of 1085 transplant recipients, 679 (63%) were discharged home, 233 (21%) required long-term acute care, and 61 (5%) required nursing home care. The statistically significant predictors of long-term care requirements included age at transplant (OR=1.04 per year, 95%CI=1.02,1.06),

female gender (OR=1.79, 95%CI=1.23,2.63), depression pre-transplant (OR=1.71, 95%CI=1.07,2.60), and MELD at transplant (OR=1.08,95%,CI=1.05,1.10). Discharge to a location other than home was associated with significantly decreased time to rehospitalization (median time 17 vs. 71 days p<0.01). Over the period of followup, 74% of patients were rehospitalized. The median number of rehospitalization was 2 (IQR=0,4), with a median of 4.6 years of follow-up (IQR=1.8,7.6). Excluding disposition after transplant, the only significant predictor Selleck Dabrafenib of time from discharge to rehospitalization was the CCI (HR=1.07 per point, p<0.01). There was a non-significant trend towards pretransplant depression predicting shorter time to readmis-sion (HR=1.18, p=0.07). The number of rehospitalizations were associated with pre-transplant depression (IRR=1.18, CI=1.17,1.18), pre-transplant opioid use (IRR=1.30, CI=1.29,1.31), warm ischemia time (IRR per minute=1.003, 1.00,1.00), CCI (IRR=1.16, CI=1.15,1.16),

and etiology of liver disease. Conclusions: Pre-transplant depression and pre-transplant opioid use are potentially modifiable risk factors for increased healthcare utilization after liver transplantation. Disclosures: The following people have nothing to disclose: Shari S. Rogal, Gautam Mank-aney, Viyan Udawatta, Christopher B. Hughes, Amit D. Tevar, Mark Sturdevant, Abhinav Humar, Andrea DiMartini Background Pneumococcal disease Tryptophan synthase is a leading cause of vaccine- preventable illness and death in the United States. The Centers for Disease Control and Prevention (CDC) recommends vaccination of any patient with cirrhosis between age 2 and 64 and any adult older than 65. Our objective is to determine pneumococcal vaccination (Pneumovax) prevalence in patients with liver cirrhosis. Methods This was a retrospective study utilizing the “Explorys” database, an open private cloud based platform that electronically integrates non-identified patient data used by 14 major healthcare systems.