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IntroductionProactive outreach offering tobacco treatment is a promising strategy outside of clinical settings, but little is known about factors for engagement. The study objective is to examine the impact of caller area code in a proactive, phone-based outreach strategy on consenting low-income smokers to a quitline e-referral.Aims and methodsThis pragmatic randomized trial included unassisted adult smokers (n = 685), whose preferred language was English or Spanish, in a Los Angeles safety-net health system. Patients were randomized to receive a call from a local or generic toll-free area code. Log-binomial regression was used to examine the association between area code and consent to a quitline e-referral, adjusted for age, gender, language, and year.ResultsOverall, 52.1% of the patients were contacted and, among those contacted, 30% consented to a referral. The contact rate was higher for the local versus generic area code, although not statistically significant (55.6% vs. 48.7%, p = .07). The consent rate was higher in the local versus generic area code group (adjusted prevalence ratio 1.29, 95% CI 1.01-1.65) and also higher for patients under 61 years old than over (adjusted prevalence ratio 1.47, 95% CI 1.07-2.01), and Spanish-speaking than English-speaking patients (adjusted prevalence ratio 1.40, 95% CI 1.05-1.86).ConclusionsProactive phone-based outreach to unassisted smokers in a safety net health system increased consent to a quitline referral when local (vs. generic) area codes were used to contact patients. While contact rate did not differ by area code, proactive phone-based outreach was effective for engaging younger and Spanish-speaking smokers.ImplicationsPopulation-based proactive phone-based outreach from a caller with a local area code to unassisted smokers in a safety net health system increases consent to an e-referral for quitline services. Findings suggest that a proactive phone-based outreach, a population-based strategy, is an effective strategy to build on the visit-based model and offer services to tobacco users, regardless of the motivational levels to quit.

BackgroundSince the advent of COVID-19, accelerated adoption of systems that reduce face-to-face encounters has outpaced training and best practices. Electronic consultations (eConsults), structured communications between PCPs and specialists regarding a case, have been effective in reducing face-to-face specialist encounters. As the health system rapidly adapts to multiple new practices and communication tools, new mechanisms to measure and improve performance in this context are needed.ObjectiveTo test whether feedback comparing physicians to top performing peers using co-specialists' ratings improves performance.DesignCluster-randomized controlled trial PARTICIPANTS: Eighty facility-specialty clusters and 214 clinicians INTERVENTION: Providers in the feedback arms were sent messages that announced their membership in an elite group of "Top Performers" or provided actionable recommendations with feedback for providers that were "Not Top Performers."Main measuresThe primary outcomes were changes in peer ratings in the following performance dimensions after feedback was received: (1) elicitation of information from primary care practitioners; (2) adherence to institutional clinical guidelines; (3) agreement with peer's medical decision-making; (4) educational value; (5) relationship building.Key resultsSpecialists showed significant improvements on 3 of the 5 consultation performance dimensions: medical decision-making (odds ratio 1.52, 95% confidence interval 1.08-2.14, p

While much is known about governance models for research informatics programs in academic medical centers and similarly situated cancer centers, community and public health systems have been less well-characterized. As part of implementing an enterprise research governance framework, leaders in the Los Angeles County Department of Health Services established a research informatics program, including research data warehousing. The strategy is focused on high-priority, patient-centered research that leverages the investment in health IT and an efficient, sustained contribution from 2 affiliated Clinical Translational Sciences Institutes. This case study describes the foundational governance framework and policies that were developed. We share the results of several years of planning, implementation, and operations of an academically funded research informatics service core embedded in a large, multicenter county health system. We include herein a Supplementary Appendix of governance documents that may serve as pragmatic models for similar initiatives.

ImportanceFor critically ill patients with advanced medical illnesses and poor prognoses, overuse of invasive intensive care unit (ICU) treatments may prolong suffering without benefit.ObjectiveTo examine whether use of time-limited trials (TLTs) as the default care-planning approach for critically ill patients with advanced medical illnesses was associated with decreased duration and intensity of nonbeneficial ICU care.Design, setting, and participantsThis prospective quality improvement study was conducted from June 1, 2017, to December 31, 2019, at the medical ICUs of 3 academic public hospitals in California. Patients at risk for nonbeneficial ICU treatments due to advanced medical illnesses were identified using categories from the Society of Critical Care Medicine guidelines for admission and triage.InterventionsClinicians were trained to use TLTs as the default communication and care-planning approach in meetings with family and surrogate decision makers.Main outcomes and measuresQuality of family meetings (process measure) and ICU length of stay (clinical outcome measure).ResultsA total of 209 patients were included (mean [SD] age, 63.6 [16.3] years; 127 men [60.8%]; 101 Hispanic patients [48.3%]), with 113 patients (54.1%) in the preintervention period and 96 patients (45.9%) in the postintervention period. Formal family meetings increased from 68 of 113 (60.2%) to 92 of 96 (95.8%) patients between the preintervention and postintervention periods (P

[This corrects the article DOI: 10.1017/cts.2020.23.].

A primary barrier to translation of clinical research discoveries into care delivery and population health is the lack of sustainable infrastructure bringing researchers, policymakers, practitioners, and communities together to reduce silos in knowledge and action. As National Institutes of Health's (NIH) mechanism to advance translational research, Clinical and Translational Science Award (CTSA) awardees are uniquely positioned to bridge this gap. Delivering on this promise requires sustained collaboration and alignment between research institutions and public health and healthcare programs and services. We describe the collaboration of seven CTSA hubs with city, county, and state healthcare and public health organizations striving to realize this vision together. Partnership representatives convened monthly to identify key components, common and unique themes, and barriers in academic-public collaborations. All partnerships aligned the activities of the CTSA programs with the needs of the city/county/state partners, by sharing resources, responding to real-time policy questions and training needs, promoting best practices, and advancing community-engaged research, and dissemination and implementation science to narrow the knowledge-to-practice gap. Barriers included competing priorities, differing timelines, bureaucratic hurdles, and unstable funding. Academic-public health/health system partnerships represent a unique and underutilized model with potential to enhance community and population health.

There is scarce information about the link between specific single-nucleotide polymorphisms (SNPs) and risk of liver disease among Latinos, despite the disproportionate burden of disease among this population. Our aim was to investigate nine SNPs in or near the following genes: PNPLA3, LYPLAL1, PPP1R3B, GCKR, NCAN, IRS1, PPARG, and ADIPOR2 and examine their association with persistently elevated alanine aminotransferase (ALT) or aspartate aminotransferase (AST) levels in Mexican adults. Data and samples were collected from 741 participants in the Mexican Health Worker Cohort Study, in Cuernavaca, Mexico. We identified 207 cases who had persistently elevated levels of ALT or AST (≥40 U/L) and 534 controls with at least two consecutive normal ALT or AST results in a 6 month period, during 2004-2006 and 2011-2013. TaqMan assays were used to genotype the SNPs. The risk allele of PNPLA3 rs738409 was found to be associated with persistently elevated levels of ALT or AST, adjusting for age, sex, BMI, type 2 diabetes, and ancestry: (OR 2.28, 95 % CI 1.13, 4.58). A significant association was found between the LYPLAL1, PPP1R3B, and GCKR risk alleles and elevated ALT or AST levels among overweight/obese adults. These results suggest that among Mexicans, the PNPLA3 (rs738409), LYPLAL1 (rs12137855), PPP1R3B (rs4240624), and GCKR (rs780094) polymorphisms may be associated with a greater risk of chronic liver disease among overweight adults. This study is the first to examine these nine SNPs in a sample of adults in Mexico.

Abstract Background Little is known about endoscopic services provided or operational practice variation within California public hospital endoscopy centers. Methods A survey was distributed to all 18 California public hospitals with endoscopy centers to assess operational practices. Results Eight of 18 hospitals responded to the survey. Six of the eight responding hospitals used a closed access system for patient referrals. Mean wait time for an endoscopic procedure was 42.4 ± 37.7 days (N = 8) with a mean procedure no-show/cancellation rate of 14.5 ± 8.0% (N = 7). All responding public hospitals performed colonoscopy, esophagogastroduodenoscopy, PEG tube placement, and endoscopic retrograde cholangiopancreatography (ERCP) with two hospitals performing endoscopic ultrasound. There was significant practice variation in the documentation of endoscopic quality and performance measurements among the responding hospitals. Multiple methods were used to communicate pathology results to patients: GI clinic visit (6/8), primary physician (4/8), telephone (2/8) or letter (1/8). Conclusion Our study highlights the diversity and practice variations of endoscopy center operations at California public hospitals and serves as a catalyst for future collaborations among safety-net hospitals.

BackgroundPreconsultation exchange is an emerging model of specialty care proposed by the American College of Physicians that seeks to answer a clinical question without a formal patient visit to the specialty clinic. This form of specialty care has been little studied. We sought to determine the appropriateness of preconsultation exchange for ambulatory hepatology consultations within our urban health care system.MethodsRetrospective study of referrals for ambulatory hepatology consultation in the safety net health care system of San Francisco, Calif from January 2007 through April 2010.ResultsOf the 500 referrals reviewed, 87 were excluded as repeat requests. The most common reasons for referral were hepatitis B (34.9%) and hepatitis C (32.0%). Fifty-six referrals (13.6%) were appropriate for preconsultation exchange, and 190 (46.0%) were inappropriate for preconsultation exchange. One hundred sixty-seven (40.4%) referrals did not include enough information to determine appropriateness for preconsultation exchange. Most of these (83.8%) were made for hepatitis B or hepatitis C, despite the presence of explicit referral guidelines. Midlevel providers were more likely than physicians to provide enough information to determine appropriateness for preconsultation exchange.ConclusionIn our urban health care system, preconsultation exchange appears to be an appropriate form of specialty care for some ambulatory hepatology consultations. Communication between primary care provider and specialist appears to be an important barrier to broader implementation of preconsultation exchange. Optimizing the preconsultation exchange is critical to improve the primary-specialty care interface, and to build a true Patient-Centered Medical Home Neighborhood.

Inflammatory bowel disease (IBD) patients display elevated levels of intraluminal nitric oxide (NO). NO can react with other molecules to form toxic compounds, which has led to the idea that NO may be an important mediator of IBD. However, the cellular source of NO and how its production is regulated in the intestine are unclear. In this study we aimed to determine if intestinal myofibroblasts produce NO in response to the IBD-associated cytokines IL-1β, TNFα, and IFNγ. Intestinal myofibroblasts were isolated from mice and found to express inducible nitric oxide synthase (iNOS) mRNA, but not endothelial NOS or neuronal NOS. Individual treatment of myofibroblasts with IL-1β, TNFα, or IFNγ had no effect on NO production, but stimulation with combinations of these cytokines synergistically increased iNOS mRNA and protein expression. Treatment with TNFα or IFNγ increased cell surface expression of IFNγRI or TNFRII, respectively, suggesting that these cytokines act in concert to prime NO production by myofibroblasts. Impairment of NF-κB activity with a small molecule inhibitor was sufficient to prevent increased expression of IFNγRI or TNFRII, and inhibition of Akt, JAK/STAT, or NF-κB blocked nearly all NO production induced by combinatorial cytokine treatment. These data indicate that intestinal myofibroblasts require stimulation by multiple cytokines to produce NO and that these cytokines act through a novel pathway involving reciprocal cytokine receptor regulation and signaling by Akt, JAK/STAT, and NF-κB.

UnlabelledWe have developed a novel model for depleting mouse hepatic stellate cells (HSCs) that has allowed us to clarify their contributions to hepatic injury and fibrosis. Transgenic (Tg) mice expressing the herpes simplex virus thymidine kinase gene (HSV-Tk) driven by the mouse GFAP promoter were used to render proliferating HSCs susceptible to killing in response to ganciclovir (GCV). Effects of GCV were explored in primary HSCs and in vivo. Panlobular damage was provoked to maximize HSC depletion by combining CCl(4) (centrilobular injury) with allyl alcohol (AA) (periportal injury), as well as in a bile duct ligation (BDL) model. Cell depletion in situ was quantified using dual immunofluorescence (IF) for desmin and GFAP. In primary HSCs isolated from both untreated wild-type (WT) and Tg mice, GCV induced cell death in ≈ 50% of HSCs from Tg, but not WT, mice. In TG mice treated with CCl(4) +AA+GCV, there was a significant decrease in GFAP and desmin-positive cells, compared to WT mice (≈ 65% reduction; P < 0.01), which was accompanied by a decrease in the expression of HSC-activation markers (alpha smooth muscle actin, beta platelet-derived growth factor receptor, and collagen I). Similar results were observed after BDL. Associated with HSC depletion in both fibrosis models, there was marked attenuation of fibrosis and liver injury, as indicated by Sirius Red/Fast Green, hematoxylin and eosin quantification, and serum alanine/aspartate aminotransferase. Hepatic expression of interleukin-10 and interferon-gamma was increased after HSC depletion. No toxicity of GCV in either WT or Tg mice accounted for the differences in injury.ConclusionActivated HSCs significantly amplify the response to liver injury, further expanding this cell type's repertoire in orchestrating hepatic injury and repair.

AbstractBackgroundStudies document increasing rates of hospitalization among patients with inflammatory bowel disease, but temporal trends for in-hospital mortality among patients with inflammatory bowel disease are not characterized. We sought to determine whether in-hospital mortality changed over a 13-year period among nationwide hospitalizations associated with inflammatory bowel disease. We additionally sought to identify factors correlated with mortality.MethodsWe used the National Hospital Discharge Survey, a large nationally representative database, for the years 1994 through 2006. Age- and mortality-adjusted rates of in-hospital mortality and standardized mortality ratios were calculated for four time periods. Logistic regression analysis was used to assess associations between advancing time and mortality in adjusted analyses.Results150 (0.9%) of 17,393 hospitalizations for patients with inflammatory bowel disease ended in death. Age-adjusted in-hospital mortality decreased from 3.6 deaths per 1,000 hospital days in 1994–96 to 2.4 per 1,000 in 2003–06; standardized mortality ratio decreased from 0.33 to 0.27. Similar trends were seen for patients with ulcerative colitis, but mortality did not change over time among patients with Crohn’s disease. Multivariable logistic regression analysis confirmed the significance of these changes in mortality, with 17% decreased odds of in-hospital death per three-year period (P = 0.012). Subject age (OR 1.06 per year, P

Inflammatory bowel disease (IBD) is increasingly common among non-Caucasian populations, but interracial differences in disease characteristics and management are not well-characterized.We tested the hypothesis that disease characteristics and management vary by race among IBD patients in an ethnically diverse healthcare system.A retrospective study of the safety net healthcare system of San Francisco, CA, from 1996 to 2009 was undertaken. Patient records with International Classification of Diseases, 9th Revision (ICD9) codes 555.xx, 556.xx, and 558.xx were reviewed. Adult patients with confirmed IBD diagnoses were included. Interracial variations in disease characteristics and management were assessed broadly; focused between-race comparisons identified specific differences.The 228 subjects included 77 (33.4%) with Crohn’s disease (CD), 150 (65.8%) with ulcerative colitis, and 1 (0.4%) with IBD, type unclassified. The race distribution included 105 (46.1%) white, 34 (14.9%) black, 35 (15.4%) Hispanic, and 51 (22.4%) Asian subjects. Asians and Hispanics were diagnosed at older ages (41.0 and 37.1 years, respectively) and had shorter disease durations (5.4 and 5.2 years, respectively) than whites (30.5 years at diagnosis and 8.6 years duration, P

Poor communication between referring clinicians and specialists may lead to inefficient use of specialist services. San Francisco General Hospital implemented an electronic referral system (eReferral) that facilitates iterative pre-visit communication between referring and specialty clinicians to improve the referral process.The purpose of the study was to determine the impact of eReferral (compared with paper-based referrals) on specialty referrals.The study was based on a visit-based questionnaire appended to new patient charts at randomly selected specialist clinic sessions before and after the implementation of eReferral.Specialty clinicians.The questionnaire focused on the self-reported difficulty in identifying referral question, referral appropriateness, need for and avoidability of follow-up visits.We collected 505 questionnaires from speciality clinicians. It was difficult to identify the reason for referral in 19.8% of medical and 38.0% of surgical visits using paper-based methods vs. 11.0% and 9.5% of those using eReferral (p-value 0.03 and

The National Center for Health Statistics (NCHS) is the principal health statistics agency for the United States. It seeks to provide accurate, relevant, and timely data on health status and utilization of health care. As such, the NCHS represents a tremendous repository of behavioral, biological, and clinical data that can be employed to identify issues and effect change in public policy related to liver health and disease. By providing an understanding of the rich, publicly available data systems within the NCHS, investigators may capitalize on an efficient means to shape current knowledge of liver disease.

Electronic referrals can improve access to subspecialty care in safety net settings. In January 2007, San Francisco General Hospital (SFGH) launched an electronic referral portal that incorporated subspecialist triage, iterative communication with referring providers, and existing electronic health record data to improve access to subspecialty care.We surveyed primary care providers (PCPs) to assess the impact of electronic referrals on workflow and clinical care.We administered an 18-item, web-based questionnaire to all 368 PCPs who had the option of referring to SFGH.We asked participants to rate time spent submitting a referral, guidance of workup, wait times, and change in overall clinical care compared to prior referral methods using 5-point Likert scales. We used multivariate logistic regression to identify variables associated with perceived improvement in overall clinical care.Two hundred ninety-eight PCPs (81.0%) from 24 clinics participated. Over half (55.4%) worked at hospital-based clinics, 27.9% at county-funded community clinics, and 17.1% at non-county-funded community clinics. Most (71.9%) reported that electronic referrals had improved overall clinical care. Providers from non-county-funded clinics (AOR 0.40, 95% CI 0.14-0.79) and those who spent ≥6 min submitting an electronic referral (AOR 0.33, 95%CI 0.18-0.61) were significantly less likely than other participants to report that electronic referrals had improved clinical care.PCPs felt electronic referrals improved health-care access and quality; those who reported a negative impact on workflow were less likely to agree. While electronic referrals hold promise as a tool to improve clinical care, their impact on workflow should be considered.

Chemotaxis (i.e., directed migration) of hepatic stellate cells to areas of inflammation is a requisite event in the liver's response to injury. Previous studies of signaling pathways that regulate stellate cell migration suggest a key role for focal adhesions, but the exact function of these protein complexes in motility remains unclear. Focal adhesions attach a cell to its substrate and therefore must be regulated in a highly coordinated manner during migration. To test the hypothesis that focal adhesion turnover is an essential early event for chemotaxis in stellate cells, we employed a live-cell imaging technique in which chemotaxis was induced by locally stimulating the tips of rat stellate cell protrusions with platelet-derived growth factor-BB (PDGF). Focal adhesions were visualized with an antibody directed against vinculin, a structural component of the focal adhesion complex. PDGF triggered rapid disassembly of adhesions within 6.25 min, subsequent reassembly by 12.5 min, and continued adhesion assembly in concert with the spreading protrusion until the completion of chemotaxis. Blockade of adhesion disassembly by growing cells on fibronectin or treatment with nocodazole prevented a chemotactic response to PDGF. Augmentation of adhesion disassembly with ML-7 enhanced the chemotactic response to PDGF. These data suggest that focal adhesion disassembly is an essential early event in stellate cell chemotaxis in response to PDGF. platelet-derived growth factor; migration; microtubules; myosin light chain kinase; fibronectin

The contractile force generated by hepatic stellate cells in response to endothelin-1 contributes to sinusoidal blood flow regulation and hepatic fibrosis. This study's aim was to directly test the widely held view that changes in cytosolic [Ca.sup.2+] concentration ([[[Ca.sup.2+]].sub.i] mediate stellate cell force generation. Contractile force generation by primary cultures of rat hepatic stellate cells grown in three-dimensional collagen gels was directly and quantitatively measured using a force transducer. Stellate cell [[[Ca.sup.2+]].sub.i], myosin activation, and migration were quantified using standard techniques. [[[Ca.sup.2+]].sub.i] was modulated using ionomycin, BAPTA, KC1, and removal of extracellular [Ca.sup.2+]. Removal of extracellular [Ca.sup.2+] did not alter endothelin-1-stimulated force development or [[[Ca.sup.2+]].sub.i]. Ionomycin, a [Ca.sup.2+] ionophore, triggered an increase in [[[Ca.sup.2+]].sub.i] that was three times greater than that stimulated by endothelin-1, but only induced 16% of the force and 38% of the myosin regulatory light chain (MLC) phosphorylation induced by endothelin-1. Physiological increases in [[[Ca.sup.2+]].sub.i] induced by hyperkalemia had no effect on contractile force. Loading BAPTA, a [Ca.sup.2+] chelator, in stellate cells completely blocked endothelin-l-induced increases in [[[Ca.sup.2+]].sub.i] but had no effect on endothelin-1-stimulated force generation or MLC phosphorylation. In contrast, Y-27632, a selective rho-associated kinase inhibitor, inhibited endothelin-1-stimulated force generation by at least 70% and MLC phosphorylation by at least 80%. Taken together, these observations indicate that changes in [[[Ca.sup.2+]].sub.i] are neither necessary nor sufficient for contractile force generation by rat stellate cells. Our results challenge the current model of contractile regulation in hepatic stellate cells and have important implications for our understanding of hepatic pathophysiology. myosin light chain phosphorylation; myosin light chain kinase; rho-associated kinase; cytosolic calcium concentration

Intestinal response to injury requires coordinated regulation of the tension exerted by subepithelial myofibroblasts (SEM). However, the signals governing relaxation of intestinal SEM have not been investigated. Our aim was to test the hypothesis that signal transduction pathways initiated by C-type natriuretic peptide (CNP) induce intestinal SEM relaxation. We directly quantified the effects of CNP on isometric tension exerted by cultured human colonic SEM. We also measured the effects of CNP on cGMP content, myosin regulatory light chain (MLC) phosphorylation, and cytosolic [Ca.sup.2+] concentration. CNP induced relaxation of SEM within 10 s. By 10 min, relaxation reached a plateau that was sustained for 2 h. CNP-induced relaxation was saturable, with a maximal decrease in tension (51.7 [+ or -] 3.8 dyn) observed at 250 nM. SEM relaxation in response to CNP constituted ~23% of total basal tension. CNP increased intracellular cGMP content and reduced MLC phosphorylation. Effects of CNP on cGMP and MLC exhibited the same dose dependence as CNP-induced relaxation. MLC phosphorylation decreased within 2 min of CNP exposure and was sustained for at least 45 min. CNP also stimulated a large transient increase in cytosolic [Ca.sup.2+] concentration that occurred within 30 s and was nearly complete by 1 min. We also observed that calyculin-A, a potent inhibitor of MLC phosphatase, completely abolished the reduction in MLC phosphorylation induced by CNP. These results suggest that CNP induces intestinal SEM relaxation through cGMP-associated reductions in MLC phosphorylation. Moreover, these findings raise the possibility that CNP plays a role in intestinal wound healing. guanosine 3',5'-cyclic monophosphate; contraction; myosin; subepithelial myofibroblast; intestine

The role of G protein-coupled receptors and their ligands in intestinal epithelial cell signaling and proliferation is poorly understood. Here, we demonstrate that arginine vasopressin (AVP) induces multiple intracellular signal transduction pathways in rat intestinal epithelial IEC-18 cells via a [V.sub.1A] receptor. Addition of AVP to these cells induces a rapid and transient increase in cytosolic [Ca.sup.2+] concentration and promotes protein kinase D (PKD) activation through a protein kinase C (PKC)-dependent pathway, as revealed by in vitro kinase assays and immunoblotting with an antibody that recognizes autophosphorylated PKD at [Ser.sup.916]. AVP also stimulates the tyrosine phosphorylation of the nonreceptor tyrosine kinase proline-rich tyrosine kinase 2 (Pyk2) and promotes Src family kinase phosphorylation at [Tyr.sup.418], indicative of Src activation. AVP induces extracellular signal-related kinase (ERK)-1 ([p44.sup.mapk]) and ERK-2 ([p42.sup.mapk]) activation, a response prevented by treatment with mitogen-activated protein kinase kinase (MEK) inhibitors (PD-98059 and U-0126), specific PKC inhibitors (GF-I and Ro-31-8220), depletion of [Ca.sup.2+] (EGTA and thapsigargin), selective epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (tyrphostin AG-1478, compound 56), or the selective Src family kinase inhibitor PP-2. Furthermore, AVP acts as a potent growth factor for IEC-18 cells, inducing DNA synthesis and cell proliferation through ERK-, [Ca.sup.2+]-, PKC-, EGFR tyrosine kinase-, and Src-dependent pathways. arginine vasopressin; protein kinase D; protein kinase C; Src; proline-rich tyrosine kinase 2; intestinal epithelial proliferation

Research was conducted to examine the hypothesis that hepatic stellate cell (HSC) contraction and relaxation around the sinusoid control hepatic blood flow by regulating sinusoidal resistance. The objective was to directly quantitate contractile force development by HSC. Results provide evidence that the magnitude and rate of HSC contraction and relaxation are enough to modulate sinusoidal blood flow.

Abstract Background Studies document increasing rates of hospitalization among patients with inflammatory bowel disease, but temporal trends for in-hospital mortality among patients with inflammatory bowel disease are not characterized. We sought to determine whether in-hospital mortality changed over a 13-year period among nationwide hospitalizations associated with inflammatory bowel disease. We additionally sought to identify factors correlated with mortality. Methods We used the National Hospital Discharge Survey, a large nationally representative database, for the years 1994 through 2006. Age- and mortality-adjusted rates of in-hospital mortality and standardized mortality ratios were calculated for four time periods. Logistic regression analysis was used to assess associations between advancing time and mortality in adjusted analyses. Results 150 (0.9%) of 17,393 hospitalizations for patients with inflammatory bowel disease ended in death. Age-adjusted in-hospital mortality decreased from 3.6 deaths per 1,000 hospital days in 1994–96 to 2.4 per 1,000 in 2003–06; standardized mortality ratio decreased from 0.33 to 0.27. Similar trends were seen for patients with ulcerative colitis, but mortality did not change over time among patients with Crohn’s disease. Multivariable logistic regression analysis confirmed the significance of these changes in mortality, with 17% decreased odds of in-hospital death per three-year period (P = 0.012). Subject age (OR 1.06 per year, P P P = .042) were also associated with in-hospital mortality. Conclusions The odds of in-hospital mortality among hospitalized patients with inflammatory bowel disease decreased by 17% per 3-year period from 1994 to 2006 in analysis adjusted for age and comorbidity status, in this large, nationally representative database. Multiple factors likely contribute to these trends.