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PloS One 2022It has been indicated that there is an association between inflammatory bowel disease (IBD) and hepatocellular carcinoma (HCC). However, the molecular mechanism...
It has been indicated that there is an association between inflammatory bowel disease (IBD) and hepatocellular carcinoma (HCC). However, the molecular mechanism underlying the risk of developing HCC among patients with IBD is not well understood. The current study aimed to identify shared genes and potential pathways and regulators between IBD and HCC using a system biology approach. By performing the different gene expression analyses, we identified 871 common differentially expressed genes (DEGs) between IBD and HCC. Of these, 112 genes overlapped with immune genes were subjected to subsequent bioinformatics analyses. The results revealed four hub genes (CXCL2, MMP9, SPP1 and SRC) and several other key regulators including six transcription factors (FOXC1, FOXL1, GATA2, YY1, ZNF354C and TP53) and five microRNAs (miR-124-3p, miR-34a-5p, miR-1-3p, miR-7-5p and miR-99b-5p) for these disease networks. Protein-drug interaction analysis discovered the interaction of the hub genes with 46 SRC-related and 11 MMP9- related drugs that may have a therapeutic effect on IBD and HCC. In conclusion, this study sheds light on the potential connecting mechanisms of HCC and IBD.
Topics: Biomarkers; Carcinoma, Hepatocellular; Gene Expression Regulation, Neoplastic; Humans; Inflammatory Bowel Diseases; Liver Neoplasms; MicroRNAs
PubMed: 35452485
DOI: 10.1371/journal.pone.0267358 -
Frontiers in Immunology 2019Gut-derived infection is among the most common complications in patients who underwent severe trauma, serious burn, major surgery, hemorrhagic shock or severe acute... (Review)
Review
Gut-derived infection is among the most common complications in patients who underwent severe trauma, serious burn, major surgery, hemorrhagic shock or severe acute pancreatitis (SAP). It could cause sepsis and multiple organ dysfunction syndrome (MODS), which are regarded as a leading cause of mortality in these cases. Gut-derived infection is commonly caused by pathological translocation of intestinal bacteria or endotoxins, resulting from the dysfunction of the gut barrier. In the last decades, the studies regarding to the pathogenesis of gut-derived infection mainly focused on the breakdown of intestinal epithelial tight junction and increased permeability. Limited information is available on the roles of intestinal microbial barrier in the development of gut-derived infection. Recently, advances of next-generation DNA sequencing techniques and its utilization has revolutionized the gut microecology, leading to novel views into the composition of the intestinal microbiota and its connections with multiple diseases. Here, we reviewed the recent progress in the research field of intestinal barrier disruption and gut-derived infection, mainly through the perspectives of the dysbiosis of intestinal microbiota and its interaction with intestinal mucosal immune cells. This review presents novel insights into how the gut microbiota collaborates with mucosal immune cells to involve the development of pathological bacterial translocation. The data might have important implication to better understand the mechanism underlying pathological bacterial translocation, contributing us to develop new strategies for prevention and treatment of gut-derived sepsis.
Topics: Animals; Bacterial Infections; Critical Illness; Dysbiosis; Gastrointestinal Microbiome; Humans; Immunity, Mucosal; Intestinal Mucosa; Permeability; Sepsis
PubMed: 31456801
DOI: 10.3389/fimmu.2019.01873 -
Annals of the Royal College of Surgeons... Feb 1968
Topics: Animals; Arm; Dogs; Humans; Ileum; Iodine Radioisotopes; Leg; Lymphatic Diseases; Lymphatic System; Lymphedema; Lymphography; Lymphoma; Radioisotope Dilution Technique; Rats; Sclerosis; Thyroid Function Tests
PubMed: 4170564
DOI: No ID Found -
Experimental Gerontology Feb 2022Advanced age is an independent risk factor for morbidity and mortality after burn injury. Following burn, the intestines can become permeable leading to the leakage of...
BACKGROUND
Advanced age is an independent risk factor for morbidity and mortality after burn injury. Following burn, the intestines can become permeable leading to the leakage of bacteria and their products from the lumen of the ileum to the portal and systemic circulation. Here, we sought to determine the effects of advanced age on intestinal permeability post burn injury and assess intestinal inflammatory biomarkers.
METHODS
Young (4-5 months) and aged (18-22 months) female BALB/cBy mice were subjected to a 12-15% total body surface area (TBSA) sham or burn injury. 24 h after injury, mice were euthanized, and organs collected. Colony-forming units (CFU) were counted from plated mesenteric lymph nodes (MLN). Gene expression of ileal tight junctional proteins, occludin and zonula occludens 1 (ZO-1), in addition to ileal damage associated molecular pattern (DAMP) proteins, S100A8 and S100A9, as well as ileal inflammatory markers IL-6 and TNF-α were measured by qPCR. Intestinal cell death was measured by ELISA. Intestinal permeability was determined by FITC fluorescence in serum; 4kD FITC-dextran was given by oral gavage 3 h before euthanasia.
RESULTS
Aged mice subjected to burn injury had increased intestinal permeability as evidenced by a 5.8-fold higher level of FITC-dextran in their serum when compared to all other groups (p < 0.05). In addition, aged burn-injured mice exhibited heightened bacterial accumulation in the MLN with a 15.5-fold increase over all other groups (p < 0.05). Histology of ileum failed to show differences in villus length among all groups. Analysis of ileal tight junctional proteins and inflammatory marker gene expression revealed no difference in Ocln, Tjp1, Il6, or Tnf expression among all groups, but 2.3 and 2.9-fold upregulation of S100a8 and S100a9, respectively, in aged burn-injured mice relative to both young groups and aged sham-injured mice (p < 0.05). Lastly, cell death in the ileum was elevated more than two-fold in aged burn-injured mice relative to young animals regardless of injury (p < 0.05).
CONCLUSIONS
These data demonstrate that advanced age exacerbates intestinal epithelial permeability after burn injury. Heightened apoptosis may be responsible for the elevated intestinal leakiness and accumulation of bacteria in mesenteric lymph nodes. In addition, S100a8/9 may serve as a biomarker of elevated inflammation within the intestine.
Topics: Animals; Female; Intestinal Mucosa; Intestines; Mice; Occludin; Permeability; Tight Junctions
PubMed: 34915110
DOI: 10.1016/j.exger.2021.111654 -
BMC Surgery Jul 2019The laparoscopic Roux-en-Y gastric bypass (LRYGBP) is the second most performed bariatric surgical procedure. With the increasing number of patients undergoing bariatric...
BACKGROUND
The laparoscopic Roux-en-Y gastric bypass (LRYGBP) is the second most performed bariatric surgical procedure. With the increasing number of patients undergoing bariatric surgery, the number of complications is also growing. Early diagnosis and treatment of the complications is crucial.
CASE PRESENTATION
A very unusual complication was met after an uneventful laparoscopic gastric bypass (LGBP) procedure due to an obstructing blood clot in the biliairy limb resulting in an acute pancreatitis and gastric distention, accompanied by an obstructing blood clot in the distal ileum causing small bowel obstruction. A review of the occurrence of these complications and the diagnosis and treatment is presented.
CONCLUSION
Post-bariatric acute pancreatitis is uncommon, but could be fatal. Blood clots should be considered as possible causes of small bowel obstruction, ileus or pancreatitis.
Topics: Adult; Female; Gastric Bypass; Humans; Ileal Diseases; Intestinal Obstruction; Laparoscopy; Obesity, Morbid; Pancreatitis; Postoperative Complications; Tomography, X-Ray Computed
PubMed: 31277624
DOI: 10.1186/s12893-019-0532-6 -
World Journal of Gastrointestinal... Sep 2015Various procedure-related adverse events related to colonoscopic treatment have been reported. Previous studies on the complications of colonoscopic treatment have... (Review)
Review
Various procedure-related adverse events related to colonoscopic treatment have been reported. Previous studies on the complications of colonoscopic treatment have focused primarily on perforation or bleeding. Coagulation syndrome (CS), which is synonymous with transmural burn syndrome following endoscopic treatment, is another typical adverse event. CS is the result of electrocoagulation injury to the bowel wall that induces a transmural burn and localized peritonitis resulting in serosal inflammation. CS occurs after polypectomy, endoscopic mucosal resection (EMR), and even endoscopic submucosal dissection (ESD). The occurrence of CS after polypectomy or EMR varies according previous reports; most report an occurrence rate around 1%. However, artificial ulcers after ESD are largely theoretical, and CS following ESD was reported in about 9% of cases, which is higher than that for CS after polypectomy or EMR. Most cases of post-polypectomy syndrome (PPS) have an excellent prognosis, and they are managed conservatively with medical therapy. PPS rarely develops into delayed perforation. Delayed perforation is a severe adverse event that often requires emergency surgery. Since few studies have reported on CS and delayed perforation associated with CS, we focused on CS after colonoscopic treatments in this review. Clinicians should consider delayed perforation in CS patients.
PubMed: 26380051
DOI: 10.4253/wjge.v7.i12.1055 -
Journal of Biomedical Optics Jun 2019Spatial frequency domain imaging (SFDI) has witnessed very rapid growth over the last decade, owing to its unique capabilities for imaging optical properties and... (Review)
Review
Spatial frequency domain imaging (SFDI) has witnessed very rapid growth over the last decade, owing to its unique capabilities for imaging optical properties and chromophores over a large field-of-view and in a rapid manner. We provide a comprehensive review of the principles of this imaging method as of 2019, review the modeling of light propagation in this domain, describe acquisition methods, provide an understanding of the various implementations and their practical limitations, and finally review applications that have been published in the literature. Importantly, we also introduce a group effort by several key actors in the field for the dissemination of SFDI, including publications, advice in hardware and implementations, and processing code, all freely available online.
Topics: Animals; Burns; Equipment Design; Hand; Humans; Image Processing, Computer-Assisted; Intestine, Large; Optical Imaging; Surgery, Computer-Assisted; Swine
PubMed: 31222987
DOI: 10.1117/1.JBO.24.7.071613 -
European Urology May 2019There are limited data examining the risk of prostate cancer (PCa) in patients with inflammatory bowel disease (IBD).
BACKGROUND
There are limited data examining the risk of prostate cancer (PCa) in patients with inflammatory bowel disease (IBD).
OBJECTIVE
To compare the incidence of PCa between men with and those without IBD.
DESIGN, SETTING, AND PARTICIPANTS
This was a retrospective, matched-cohort study involving a single academic medical center and conducted from 1996 to 2017. Male patients with IBD (cases=1033) were randomly matched 1:9 by age and race to men without IBD (controls=9306). All patients had undergone at least one prostate-specific antigen (PSA) screening test.
OUTCOME MEASUREMENTS AND STATISTICAL ANALYSIS
Kaplan-Meier and multivariable Cox proportional hazard models, stratified by age and race, evaluated the relationship between IBD and the incidence of any PCa and clinically significant PCa (Gleason grade group ≥2). A mixed-effect regression model assessed the association of IBD with PSA level.
RESULTS AND LIMITATIONS
PCa incidence at 10yr was 4.4% among men with IBD and 0.65% among controls (hazard ratio [HR] 4.84 [3.34-7.02] [3.19-6.69], p<0.001). Clinically significant PCa incidence at 10yr was 2.4% for men with IBD and 0.42% for controls (HR 4.04 [2.52-6.48], p<0.001). After approximately age 60, PSA values were higher among patients with IBD (fixed-effect interaction of age and patient group: p=0.004). Results are limited by the retrospective nature of the analysis and lack of external validity.
CONCLUSIONS
Men with IBD had higher rates of clinically significant PCa when compared with age- and race-matched controls.
PATIENT SUMMARY
This study of over 10000 men treated at a large medical center suggests that men with inflammatory bowel disease may be at a higher risk of prostate cancer than the general population.
Topics: Adult; Aged; Case-Control Studies; Humans; Incidence; Inflammatory Bowel Diseases; Male; Middle Aged; Neoplasm Grading; Prostate-Specific Antigen; Prostatic Neoplasms; Retrospective Studies; Risk Factors
PubMed: 30528221
DOI: 10.1016/j.eururo.2018.11.039 -
Pharmacology & Therapeutics Nov 2017The nervous system and immune system have broad and overlapping distributions in the body, and interactions of these ubiquitous systems are central to the field of... (Review)
Review
The nervous system and immune system have broad and overlapping distributions in the body, and interactions of these ubiquitous systems are central to the field of neuroimmunology. Over the past two decades, there has been explosive growth in our understanding of neuroanatomical, cellular, and molecular mechanisms that mediate central modulation of immune functions through the autonomic nervous system. A major catalyst for growth in this field was the discovery that vagal nerve stimulation (VNS) caused a prominent attenuation of the systemic inflammatory response evoked by endotoxin in experimental animals. This effect was mediated by acetylcholine (ACh) stimulation of nicotinic receptors on splenic macrophages. Hence, the circuit was dubbed the "cholinergic anti-inflammatory pathway". Subsequent work identified the α7 nicotinic ACh receptor (α7nAChR) as the crucial target for attenuation of pro-inflammatory cytokine release from macrophages and dendritic cells. Further investigation made the important discovery that cholinergic T cells within the spleen and not cholinergic nerve cells were the source of ACh that stimulated α7 receptors on splenic macrophages. Given the important role that inflammation plays in numerous disease processes, cholinergic anti-inflammatory mechanisms are under intensive investigation from a basic science perspective and in translational studies of animal models of diseases such as inflammatory bowel disease and rheumatoid arthritis. This basic work has already fostered several clinical trials examining the efficacy of VNS and cholinergic therapeutics in human inflammatory diseases. This review provides an overview of basic and translational aspects of the cholinergic anti-inflammatory response and relevant pharmacology of drugs acting at the α7nAChR.
Topics: Acetylcholine; Animals; Anti-Inflammatory Agents; Arthritis, Rheumatoid; Brain Injuries, Traumatic; Burns; Cholinergic Agents; Humans; Immunomodulation; Macrophages; Microglia; Sepsis; Stroke; Vagus Nerve Stimulation; alpha7 Nicotinic Acetylcholine Receptor
PubMed: 28529069
DOI: 10.1016/j.pharmthera.2017.05.002 -
Gastroenterology & Hepatology Oct 2019There is growing appreciation that functional gastrointestinal disorders (FGIDs) such as functional dyspepsia and irritable bowel syndrome are heterogeneous conditions...
There is growing appreciation that functional gastrointestinal disorders (FGIDs) such as functional dyspepsia and irritable bowel syndrome are heterogeneous conditions linked by subtle inflammation within the gastrointestinal (GI) tract. The literature suggests that while the symptoms of these diseases may manifest with similar clinical presentations, there are significant differences in triggers and disease severity among patients classified into the same subtype. It is hypothesized that the subtle inflammation observed in these patients is related to an imbalance in GI homeostasis. Disruption of the delicate homeostatic balance within the GI tract can result from any number or combination of factors, including dysbiosis, loss of barrier integrity, genetic predisposition, or immune responses to dietary or luminal antigens. This article discusses the interplay between the immune system, microbiota, and luminal environment in FGIDs. In addition, the article proposes emerging immune pathways, including those involving T-helper type 17 response and innate lymphoid cells, as potential regulators of the subtle inflammation characteristic of FGIDs that warrant investigation in future studies.
PubMed: 31802978
DOI: No ID Found