共查询到20条相似文献,搜索用时 203 毫秒
1.
Background and objectives
The pathophysiological mechanism of sarcopenia in the elderly has not yet been fully understood. Here, we aim to explore the relationship between sarcopenia and the inflammatory cytokine interleukin-6 (IL-6), and the anti-inflammatory cytokine interleukin-10 (IL-10) in an elderly population.Methods
Our study comprised 118 males and 46 females aged between 61 and 90 who had received a general medical examination in Tianjin First Central Hospital. Subjects were divided into a sarcopenia group and a non-sarcopenia group, defined according to the criteria of the Asian Working Group for Sarcopenia (AWGS). We compared body composition, handgrip strength (HS), gait speed (GS), biochemical indexes, levels of IL-6 and IL-10, living habits, and disease status between these groups.Results
Non-sarcopenia subjects undertook more regular physical exercise than sarcopenia patients. Sarcopenia subjects had higher nutrition risk but lower body mass index (BMI), serum albumin (ALB), triglyceride (TG), and creatinine (Cr) levels compared to non-sarcopenia subjects. Sarcopenia subjects were older and had higher visceral fat tissue (VFA) than non-sarcopenia subjects (P?<?0.05), along with higher IL-6 and IL-10 levels. Furthermore, IL-6/IL-10 ratios were higher in subjects with sarcopenia (P?<?0.05). Age, BMI, levels of physical activity, nutritional risk, VFA, IL-6, IL-10, IL-6/IL-10 ratio were independently associated with the presence of sarcopenia in univariate regression analyses. Following adjustment for confounding factors, the presence of sarcopenia was positively correlated with IL-6, IL-10, IL-6/IL-10 ratio and inversely correlated with BMI. Age is associated with increased presence of sarcopenia.Conclusions
The levels of inflammation cytokine IL-6, anti-inflammatory IL-10 and IL-6/IL-10 ratio were increased in elderly sarcopenia subjects. Sarcopenia was associated with increased levels of inflammatory cytokine IL-6, anti-inflammatory cytokine IL-10, and IL-6/IL-10 ratios.2.
Purpose of the Review
Proinflammatory cytokines are consistently elevated in congestive heart failure. In the current review, we provide an overview on the current understanding of how tumor necrosis factor-α (TNFα), a key proinflammatory cytokine, potentiates heart failure by overwhelming the anti-inflammatory responses disrupting the homeostasis.Recent Findings
Studies have shown co-relationship between severity of heart failure and levels of the proinflammatory cytokine TNFα and one of its secondary mediators interleukin-6 (IL-6), suggesting their potential as biomarkers. Recent efforts have focused on understanding the mechanisms of how proinflammatory cytokines contribute towards cardiac dysfunction and failure. In addition, how unchecked proinflammatory cytokines and their cross-talk with sympathetic system overrides the anti-inflammatory response underlying failure.Summary
The review offers insights on how TNFα and IL-6 contribute to cardiac dysfunction and failure. Furthermore, this provides a forum to begin the discussion on the cross-talk between sympathetic drive and proinflammatory cytokines and its determinant role in deleterious outcomes.3.
Susanna?Nikolaus Georg?H.?Waetzig Sven?Butzin Monika?Ziolkiewicz Natalie?Al-Massad Florian?Thieme Ulf?L?vgren Birgitte?B.?Rasmussen Torsten?M.?Reinheimer Dirk?Seegert Philip?Rosenstiel Silke?Szymczak Stefan?Schreiber
Purpose
Interleukin-6 (IL-6) production and signalling are increased in the inflamed mucosa in inflammatory bowel diseases (IBD). As published serum levels of IL-6 and its soluble receptors sIL-6R and sgp130 in IBD are from small cohorts and partly contradictory, we systematically evaluated IL-6, sIL-6R and sgp130 levels as markers of disease activity in Crohn’s disease (CD) and ulcerative colitis (UC).Methods
Consecutive adult outpatients with confirmed CD or UC were included, and their disease activity and medication were monitored. Serum from 212 CD patients (815 measurements) and 166 UC patients (514 measurements) was analysed, and 100 age-matched healthy blood donors were used as controls.Results
IL-6 serum levels were significantly elevated in active versus inactive CD and UC, also compared with healthy controls. However, only a fraction of IBD patients showed increased serum IL-6. IL-6 levels ranged up to 32.7 ng/mL in active CD (>?5000-fold higher than in controls), but also up to 6.9 ng/mL in inactive CD. Increases in active UC (up to 195 pg/mL) and inactive UC (up to 27 pg/mL) were less pronounced. Associations between IL-6 serum levels and C-reactive protein concentrations as well as leukocyte and thrombocyte counts were observed. Median sIL-6R and sgp130 levels were only increased by up to 15%, which was considered of no diagnostic significance.Conclusions
Only a minority of IBD patients shows elevated IL-6 serum levels. However, in these patients, IL-6 is strongly associated with disease activity. Its soluble receptors sIL-6R and sgp130 do not appear useful as biomarkers in IBD.4.
Giacomo Emmi Maria Letizia Urban Massimo Imazio Marco Gattorno Silvia Maestroni Giuseppe Lopalco Luca Cantarini Domenico Prisco Antonio Brucato 《Current cardiology reports》2018,20(8):61
Purpose of Review
This review aims to summarize the role of the interleukin-1 (IL-1) blocking agents in cardiovascular diseases, briefly describing the pathogenetic rationale and the most relevant clinical studies.Recent Findings
IL-1 is a pivotal cytokine of the innate immune system. Anti-IL-1 agents are currently used for the treatment of several autoimmune and autoinflammatory conditions. Recently, the role of IL-1 has also emerged in cardiovascular diseases. Indeed, two recent randomized controlled trials have shown that the IL-1 receptor antagonist anakinra is effective for the treatment of idiopathic recurrent pericarditis and the IL-1β blocking agent canakinumab is effective in reducing myocardial infarction in people at risk. Interestingly, interfering with IL-1 has proved to be also effective in other cardiovascular manifestations, such as myocarditis, arrhythmias, and heart failure.Summary
Blocking the IL-1 pathway is a possible new therapeutic strategy, potentially leading to innovative therapies in many acute and chronic cardiovascular diseases.5.
Minghao Xie Huabo Qin Qianxin Luo Xiaosheng He Xiaowen He Ping Lan Lei Lian 《Digestive diseases and sciences》2017,62(1):115-123
Background
Mesenchymal stromal cells (MSCs) have been used in the treatment of Crohn’s disease (CD) because of the immunomodulatory ability.Aim
The aim of this study was to investigate the therapeutic effect of adipose-derived MSCs (AD-MSCs) and to compare the therapeutic effect of AD-MSCs with that of bone marrow MSCs (BM-MSCs) in a murine model of CD.Methods
Murine colitis model of CD was created by trinitrobenzene sulfonic acid (TNBS). Twelve hours after treatment with TNBS, the mouse model was injected with MSCs intraperitoneally. Real-time polymerase chain reaction and immunohistochemistry staining were used to measure the expression levels of inflammatory cytokines in colonic tissues to investigate the therapeutic effect of AD-MSCs. The ten-day survival was recorded after infusion of MSCs.Results
Intraperitoneal injection of MSCs alleviated the clinical and histopathologic severity of intestinal inflammation, and improved the survival of the TNBS-induced mouse model of CD. AD-MSCs could effectively increase the expression of interleukin-10 and reduce the secretion of pro-inflammatory cytokines including tumor necrosis factor-α, interleukin-12, and vascular endothelial growth factor. The mucosal injury was repaired by AD-MSCs. These effects were comparable between AD-MSCs and BM-MSCs.Conclusions
The therapeutic effect appears similar between AD-MSCs and BM-MSCs in treating CD. AD-MSCs may be a potential alternative of cell-based therapy for CD.6.
Sezin Günaltay Mohammed Ghiboub Olof Hultgren Elisabeth Hultgren Hörnquist 《Digestive diseases and sciences》2017,62(5):1204-1215
Background and Aim
Microscopic colitis, comprising collagenous colitis and lymphocytic colitis, is a common cause of chronic diarrhea. Previously, we showed enhanced chemokine productions in microscopic colitis patients, indicating dysregulated immune cell chemotaxis in the immunopathogenesis. We also showed decreased mRNA of IL-37, mainly regarded as an anti-inflammatory cytokine, in the colonic mucosa of these patients, potentially an important factor for the chronicity of the colitis. Our aim in this study was to understand the possible role of IL-37 in chemokine production using a cell line model.Methods
A colon epithelial cell line, T84, was stimulated with the TLR5 ligand flagellin. IL-37 protein production was reduced 20% using the CRISPR/Cas9 system, and the changes in chemokine mRNA and protein expressions were compared to cells transfected with empty plasmid.Results
The 20% reduction in IL-37 protein levels spontaneously increased CCL5, CXCL8, CXCL10, and CXCL11 mRNA and protein expressions. CCL2 mRNA and protein levels were enhanced upon TLR5 stimulation. CCL3, CCL20, and CX3CL1 mRNA expressions were increased either spontaneously or following TLR5 stimulation, whereas CCL4 and CCL22 mRNA expressions were significantly decreased.Conclusions
Even a minor decrease in the ability of colon epithelial cells to produce IL-37 results in altered chemokine expression, mainly an increase in the production of several chemokines. Our results indicate that a decreased IL-37 expression by colon epithelial cells may be an important factor for increasing the recruitment of immune cells and subsequently developing microscopic colitis.7.
Purpose
Interleukin (IL)-25 and IL-33 induce IL-5 production by various types of cells, such as type 2 helper T (Th2) cells and type 2 innate lymphoid cells. The number of Th2 cells and concentration of IL-5 in the bronchoalveolar lavage fluid (BALF) are increased in patients with eosinophilic pneumonia (EP). To examine the contribution of IL-25 and IL-33 to eosinophilic inflammation of the lung in humans, we evaluated IL-5, IL-25 and IL-33 levels in the BALF of patients with EP.Methods
IL-5, IL-25, and IL-33 concentrations in the BALF were measured by enzyme-linked immunosorbent assay in patients with acute eosinophilic pneumonia (AEP), chronic eosinophilic pneumonia (CEP), idiopathic pulmonary fibrosis (IPF), and sarcoidosis.Results
The absolute number of eosinophils, and IL-5 levels, but not IL-33 levels, in the BALF were significantly higher in patients with EP than in patients with IPF and sarcoidosis. IL-25 levels in the BALF were significantly higher in patients with CEP, but not in patients with AEP, than in patients with IPF and sarcoidosis. The absolute number of eosinophils was significantly correlated with the IL-5 concentration in the BALF of patients with EP. IL-5 concentrations were significantly correlated with IL-25 concentrations in the BALF of patients with CEP, but not in patients with AEP. IL-5 levels were not correlated with IL-33 levels in the BALF of patients with EP.Conclusions
Our findings suggest that IL-25 plays an important role via IL-5 in eosinophilic lung inflammation in patients with CEP.8.
Yoon Seok Roh Surim Park Chae Woong Lim Bumseok Kim 《Digestive diseases and sciences》2015,60(7):2009-2018
Background
Accumulating evidence suggests that Foxp3+ regulatory T (Treg) cells act as inhibitory mediators of inflammation; however, the in vivo mechanism underlying this protection remains elusive in liver diseases.Aims
To clarify the in vivo role of Foxp3+ Treg cells in liver fibrosis, we used the DEREG mouse, which expresses the diphtheria toxin receptor under control of the Foxp3 promoter, allowing for specific deletion of Foxp3+ Treg cells.Methods
Bile duct ligation-induced liver injury and fibrosis were assessed by histopathology, fibrogenic gene expression, and measurement of cytokine and chemokine levels.Results
Depletion of Foxp3+ Treg cells enhanced Th17 cell response as demonstrated by the increase of IL-17+ cells and related gene expressions including Il17f, Il17ra, and Rorgt in the fibrotic livers of DEREG mice. Of note, infiltration of CD8+ T cells and Cd8 gene expression was significantly increased in the livers of DEREG mice. Consistent with increased IL-17+ and CD8+ T cell responses, DEREG mice generated higher levels of inflammatory cytokines (TNF-α, IL-6, and IL-12p70) and chemokines (MCP-1, MIP-1α, and RANTES). These results were concordant with severity of liver fibrosis and hepatic enzyme levels (ALT and ALP).Conclusions
The present findings demonstrate that Foxp3+ Treg cells inhibit the profibrogenic inflammatory milieu through suppression of pro-fibrogenic CD8+ and IL-17+ T cells.9.
Background
Inflammatory bowel disease (IBD) is an intestinal disorder, involving chronic and relapsing inflammation of the digestive tract. Dysregulation of the immune system based on genetic, environmental, and other factors seems to be involved in the onset of IBD, but its exact pathogenesis remains unclear. Therefore, radical treatments for ulcerative colitis and Crohn’s disease remain to be found, and IBD is considered to be a refractory disease.Aims
The aim of this study is to obtain novel insights into IBD via metabolite profiling of interleukin (IL)-10 knockout mice (an IBD animal model that exhibits a dysregulated immune system).Methods
In this study, the metabolites in the large intestine and plasma of IL-10 knockout mice were analyzed. In our analytical system, two kinds of analysis (gas chromatography/mass spectrometry and liquid chromatography/mass spectrometry) were used to detect a broader range of metabolites, including both hydrophilic and hydrophobic metabolites. In addition, an analysis of lipid mediators in the large intestine and ascites of IL-10 knockout mice was carried out.Results
The levels of a variety of metabolites, including lipid mediators, were altered in IL-10 knockout mice. For example, high large intestinal and plasma levels of docosahexaenoic acid (DHA) were observed. In addition, arachidonic acid- and DHA-related lipid cascades were upregulated in the ascites of the IL-10 knockout mice.Conclusions
Our findings based on metabolite profiles including lipid mediators must contribute to development of researches about IBD.10.
Giovanni B. Gaeta Massimo Puoti Nicola Coppola Teresa Santantonio Raffaele Bruno Antonio Chirianni Massimo Galli 《Infection》2018,46(2):183-188
Aim
This paper is aimed at providing practical recommendations for the management of acute hepatitis C (AHC).Methods
This is an expert position paper based on the literature revision. Final recommendations were graded by level of evidence and strength of the recommendations.Results
Treatment of AHC with direct-acting antivirals (DAA) is safe and effective; it overcomes the limitations of INF-based treatments.Conclusions
Early treatment with DAA should be offered when available.11.
Renata Kopach-Konrad Mark Lawley Mike Criswell Imran Hasan Santanu Chakraborty Joseph Pekny Bradley N. Doebbeling 《Journal of general internal medicine》2007,22(3):431-437
Background
In a highly publicized joint report, the National Academy of Engineering and the Institute of Medicine recently recommended the systematic application of systems engineering approaches for reforming our health care delivery system. For this to happen, medical professionals and managers need to understand and appreciate the power that systems engineering concepts and tools can bring to redesigning and improving health care environments and practices.Objective
To present and discuss fundamental concepts and tools of systems engineering and important parallels between systems engineering, health services, and implementation research as it pertains to the care of complex patients.Design
An exploratory, qualitative review of systems engineering concepts and overview of ongoing applications of these concepts in the areas of hemodialysis, radiation therapy, and patient flow modeling.Results
In this paper, we describe systems engineering as the process of identifying the system of interest, choosing appropriate performance measures, selecting the best modeling tool, studying model properties and behavior under a variety of scenarios, and making design and operational decisions for implementation.Conclusions
We discuss challenges and opportunities for bringing people with systems engineering skills into health care.12.
Background
Patients with cancer and recommendations for aftercare are increasing worldwide.Objectives
Presentation of the current follow-up guidelines of selected gastrointestinal tumors.Materials and methods
The current German S3 guidelines for colorectal cancer, pancreatic cancer, hepatocellular carcinoma, and gastric cancer are analyzed.Results
The S3 guidelines for colorectal cancer and hepatocellular carcinoma favor structured aftercare. For a period of 2–5 years, a combination of case history, physical examination, imaging, endoscopy, and determination of tumor markers is recommended. Advocacy for structured aftercare for pancreatic or gastric cancer must be decided individually. In general, the follow-up time and interval should be adjusted to the complaints of the patient, regardless of the tumor type.Conclusions
Structured aftercare makes sense and is already part in the monitoring of selected gastrointestinal tumors.13.
Franklin Correa Barcellos Bruno Pereira Nunes Luciana Jorge Valle Thiago Lopes Bianca Orlando Cintia Scherer Marcia Nunes Gabriela Araújo Duarte Maristela Böhlke 《Infection》2017,45(2):139-145
Background
Central venous catheters (CVC) are the only option when hemodialysis is needed for patients without definitive vascular access. However, CVC is associated with complications, such as infection, thrombosis, and dysfunction, leading to higher mortality and expenditures. The aim of this study was to compare the effectiveness of 30 % trisodium citrate (TSC30 %) with heparin as CVC lock solutions in preventing catheter-related bloodstream infections (CRBSI) and dysfunction in hemodialysis patients.Methods
Randomized, double-blind controlled trial comparing the event-free survival of non-tunneled CVC locked with heparin or TSC30 % in adult hemodialysis patients.Results
The study included 464 catheters, 233 in heparin group, and 231 in TSC30 % group. The CRBSI-free survival of TSC30 % group was significantly shorter than that of heparin group. When stratified by insertion site, heparin was better than TSC30 % only in subclavian CVC. The dysfunction-free survival was not different between groups in the main analysis, but there is also a shorter survival among subclavian CVC locked with TSC30 % in stratified analysis.Conclusion
There was no difference on CRBSI-free or dysfunction-free survival between jugular vein CVC locked with heparin or 30 % citrate. However, subclavian CVC locked with 30 % citrate presented shorter event-free survival. This difference may be related to anatomical and positional effects, CVC design, and hydraulic aspects of the lock solution.ClinicalTrials.gov identifier
NCT02563041.14.
Background
Little is known about self-help associations and their possibilities. Obstacles often prevent early contacts between affected people.Objectives
The psychosocial support given by self-help associations in different phases is evaluated.Materials and methods
Based on the experience of the Deutsche ILCO and from cooperation with other organizations and institutions, various dimensions of self-help groups are investigated.Results
On the professional side, there is a lack of knowledge and of attitude. Suitable structures are rare.Conclusions
The removal of barriers and development of effective structures are overdue.15.
Ting Zhang Min Xia Qiang Zhan Qunyan Zhou Guomin Lu Fangmei An 《Digestive diseases and sciences》2015,60(7):1991-1999
Objective
The present study was designed to evaluate the effect of sodium butyrate on pancreas damage and to investigate the role of high-mobility group box-1 (HMGB1) and nuclear factor-κB (NF-κB) in the development of severe acute pancreatitis (SAP) in a mouse model.Methods
The SAP model was established by intraperitoneal injection of two doses of 20 % L-2 arginine (200 mg/g). Female Sprague–Dawley mice were randomly allocated into three groups (n = 48/group): the control, untreated SAP, and sodium butyrate-treated SAP groups. The animals were euthanized at 0, 12, 24, and 48 h after the establishment of the SAP. Histopathology of the pancreas was performed, and the NF-κB levels were determined by immunohistochemistry. The serum levels of tumor necrosis factor (TNFα), interleukin-6 (IL-6), and HMGB1 were measured by ELISA. The HMGB1 mRNA levels were determined by qRT-PCR.Results
The sodium butyrate-treated SAP animals showed significantly improved pancreas histopathology and lower serum amylase levels than the untreated SAP animals. In the SAP group, the mRNA levels of HMGB1 were remarkably increased at the 12 h, peaked at 24 h, and remained at a high level up to 48 h after L-2 arginine injection. The levels of TNFα and IL-6 were decreased at 48 h. Treatment with sodium butyrate reduced the pathological lesions, the serum levels of HMGB1, TNFα, and IL-6, the HMGB1 mRNA levels, and NF-κB activity.Conclusion
Sodium butyrate inhibits the NF-κB activation and reduces pancreas injury in SAP through the modulation of HMGB1 and other inflammatory cytokine responses.16.
J. Daryl Thornton Catherine Sullivan Jeffrey M. Albert Maria Cedeño Bridget Patrick Julie Pencak Kristine A. Wong Margaret D. Allen Linda Kimble Heather Mekesa Gordon Bowen Ashwini R. Sehgal 《Journal of general internal medicine》2016,31(8):832-839
BACKGROUND
Low organ donation rates remain a major barrier to organ transplantation.OBJECTIVE
We aimed to determine the effect of a video and patient cueing on organ donation consent among patients meeting with their primary care provider.DESIGN
This was a randomized controlled trial between February 2013 and May 2014.SETTING
The waiting rooms of 18 primary care clinics of a medical system in Cuyahoga County, Ohio.PATIENTS
The study included 915 patients over 15.5 years of age who had not previously consented to organ donation.INTERVENTIONS
Just prior to their clinical encounter, intervention patients (n?=?456) watched a 5-minute organ donation video on iPads and then choose a question regarding organ donation to ask their provider. Control patients (n?=?459) visited their provider per usual routine.MAIN MEASURES
The primary outcome was the proportion of patients who consented for organ donation. Secondary outcomes included the proportion of patients who discussed organ donation with their provider and the proportion who were satisfied with the time spent with their provider during the clinical encounter.KEY RESULTS
Intervention patients were more likely than control patients to consent to donate organs (22 % vs. 15 %, OR 1.50, 95%CI 1.10–2.13). Intervention patients were also more likely to have donation discussions with their provider (77 % vs. 18 %, OR 15.1, 95%CI 11.1–20.6). Intervention and control patients were similarly satisfied with the time they spent with their provider (83 % vs. 86 %, OR 0.87, 95%CI 0.61–1.25).LIMITATION
How the observed increases in organ donation consent might translate into a greater organ supply is unclear.CONCLUSION
Watching a brief video regarding organ donation and being cued to ask a primary care provider a question about donation resulted in more organ donation discussions and an increase in organ donation consent. Satisfaction with the time spent during the clinical encounter was not affected.TRIAL REGISTRATION
clinicaltrials.gov Identifier: NCT0169713717.
Mitsuaki Ishioka Kouichi Miura Shinichiro Minami Yoichiro Shimura Hirohide Ohnishi 《Digestive diseases and sciences》2017,62(2):396-406
Background
Although several types of diet have been used in experimental steatohepatitis models, comparison of gut microbiota and immunological alterations in the gut among diets has not yet been performed.Aim
We attempted to clarify the difference in the gut environment between mice administrated several experimental diets.Methods
Male wild-type mice were fed a high-fat (HF) diet, a choline-deficient amino acid-defined (CDAA) diet, and a methionine-choline-deficient (MCD) diet for 8 weeks. We compared the severity of steatohepatitis, the composition of gut microbiota, and the intestinal expression of interleukin (IL)-17, an immune modulator.Results
Steatohepatitis was most severe in the mice fed the CDAA diet, followed by the MCD diet, and the HF diet. Analysis of gut microbiota showed that the composition of the Firmicutes phylum differed markedly at order level between the mice fed the CDAA and HF diet. The CDAA diet increased the abundance of Clostridiales, while the HF diet increased that of lactate-producing bacteria. In addition, the CDAA diet decreased the abundance of lactate-producing bacteria and antiinflammatory bacterium Parabacteroides goldsteinii in the phylum Bacteroidetes. In CDAA-fed mice, IL-17 levels were increased in ileum as well as portal vein. In addition, the CDAA diet also elevated hepatic expression of chemokines, downstream targets of IL-17.Conclusions
The composition of gut microbiota and IL-17 expression varied considerably between mice administrated different experimental diets to induce steatohepatitis.18.
Joseph J. Gallo Seungyoung Hwang Jin Hui Joo Hillary R. Bogner Knashawn H. Morales Martha L. Bruce Charles F. ReynoldsIII 《Journal of general internal medicine》2016,31(4):380-386
Background
Two-thirds of older adults have two or more medical conditions that often take precedence over depression in primary care.Objective
We evaluated whether evidence-based depression care management would improve the long-term mortality risk among older adults with increasing levels of medical comorbidity.Design
Longitudinal analyses of the practice-randomized Prevention of Suicide in Primary Care Elderly: Collaborative Trial (PROSPECT). Twenty primary care practices randomized to intervention or usual care.Patients
The sample included 1204 older primary care patients completing the Charlson Comorbidity Index (CCI) and other interview questions at baseline.Intervention
For 2 years, a depression care manager worked with primary care physicians to provide algorithm-based care for depression, offering psychotherapy, increasing the antidepressant dose if indicated, and monitoring symptoms, medication adverse effects, and treatment adherence.Main Measures
Depression status based on clinical interview, CCI to evaluate medical comorbidity, and vital status at 8 years (National Death Index).Key Results
In the usual care condition, patients with the highest levels of medical comorbidity and depression were at increased risk of mortality over the course of the follow-up compared to depressed patients with minimal medical comorbidity [hazard ratio 3.02 (95 % CI, 1.32 to 8.72)]. In contrast, in intervention practices, patients with the highest level of medical comorbidity and depression compared to depressed patients with minimal medical comorbidity were not at significantly increased risk [hazard ratio 1.73 (95 % CI, 0.86 to 3.96)]. Nondepressed patients in intervention and usual care practices had similar mortality risk.Conclusions
Depression management mitigated the combined effect of multimorbidity and depression on mortality. Depression management should be integral to optimal patient care, not a secondary focus.19.
Hui-Jing Zhang Yi-Ning Zhang Huan Zhou Lin Guan Yue Li Ming-Jun Sun 《Digestive diseases and sciences》2018,63(11):2898-2909
Background
Intestinal fibrosis is a common complication of Crohn’s disease (CD). Its exact mechanism is still unclear, and effective treatments to control or reverse the fibrosis process are unavailable. Epithelial–mesenchymal transition (EMT) may promote intestinal fibrosis by increasing deposition of extracellular matrix protein. IL-17A is a pro-inflammatory cytokine, and it has been shown as a profibrotic factor as its association with fibrosis of multiple organs was reported.Aims
To assess the roles of IL-17A and EMT in the initiation and development of intestinal fibrosis and to verify the potential inductive effect of IL-17A on EMT.Methods
In this study, we evaluated the expression of IL-17A and EMT-related genes in colonic mucosal biopsy tissues of CD patients and control individuals. Then, we examined the changes of EMT-related genes and fibrosis-related genes of IEC-6 cells which cultured for 72 h under increasing concentrations of IL-17A or with TGF-β1, to verify the potential inductive effect of IL-17A on EMT in vitro. We blocked the IL-17A of the mouse model of TNBS-induced experimental intestinal colitis and fibrosis to further verify the potential inductive effect of IL-17A on EMT in vivo.Results
We found the occurrence of EMT and high-level expression of IL-17A in intestinal mucosa of CD patients. Using IEC-6 cells, we showed that IL-17A may induce EMT in intestinal epithelial cells that come with reduced E-cadherin expression and increased expression of vimentin, snail, and α-SMA. We further found that anti-IL-17A treatment alleviated intestinal fibrosis through reducing EMT in mouse intestine.Conclusions
Our study confirmed the involvement of IL-17A in the development of intestinal fibrosis through inducing EMT.20.
Denny Miley Cárdenas Angie Carolina Sánchez Daris Angélica Rosas Esmeralda Rivero Massiel Dayana Paparoni Mildred Andreína Cruz Yeicy Paola Suárez Nestor Fabián Galvis 《BMC gastroenterology》2018,18(1):184