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This study explores the lived experiences of gays and lesbians at Central Mindanao University (CMU) through a narrative and descriptive research approach. It aims to document their challenges, coping mechanisms, and the extent of recognition they receive within the university community. By weaving together their personal stories, the research provides a critical understanding of the struggles and triumphs of the LGBTQIA+ community, contributing to a broader discourse on inclusion and diversity in higher education. Primary data were gathered through oral interviews with respondents and supplemented by written records from various colleges and the Office of Student Affairs (OSA). A thematic analysis revealed that discrimination, bullying, gossiping, and harassment remain persistent challenges faced by gays and lesbians. However, findings also highlight their remarkable resilience and adaptability, as they excel academically and actively participate in extracurricular activities despite these adversities. Significantly, the study notes a gradual yet meaningful shift in the university's acknowledgment of the achievements and contributions of gays and lesbians. This growing visibility within organizations and the broader CMU community is a testament to evolving attitudes toward inclusivity and respect. The findings underscore the need for enhanced institutional policies and advocacy efforts to promote equality and safeguard the rights of LGBTQIA+ individuals, providing a roadmap for fostering an inclusive and supportive academic environment. By documenting these experiences, the research sheds light on the intersection of identity, adversity, and success, offering valuable insights into queer history and institutional progress toward equality. [ABSTRACT FROM AUTHOR]

Discoidin domain receptor 1 (DDR1) is one of the receptors that belong to a family of non-integrin collagen receptors. In common, DDR1 is predominantly found in epithelial and smooth muscle cells and its mainly involved in organogenesis during embryonic development. However, it's also overexpressed in several pathological conditions, including cancer and inflammation. The DDR1 is reported in numerous cancers, including breast, prostate, pancreatic, bladder, lung, liver, pituitary, colorectal, skin, gastric, glioblastoma, and inflammation. DDR1 activates through the collagen I, IV, IGF-1/IGF1R, and IGF2/IR, regulating downstream signaling molecules such as MAPKs, PI3K/Akt, and NF-kB in diseases. Despite its biomedical importance, there is a lack of consolidated network map of the DDR1 signaling pathway, which prompted us for curation of literature data pertaining to the DDR1 system following the NetPath criteria. We present here the compiled pathway map comprises 39 activation/inhibition events, 17 catalysis events, 22 molecular associations, 65 gene regulation events, 35 types of protein expression, and two protein translocation events. The detailed DDR1 signaling pathway map is made freely accessible through the WikiPathways Database (https://www.wikipathways.org/index.php/ Pathway: https://www.wikipathways.org/index.php/Pathway:WP5288). [ABSTRACT FROM AUTHOR]

Interleukin-17A (IL-17A) is one of the member of IL-17 family consisting of other five members (IL-17B to IL-17F). The Gamma delta (γδ) T cells and T helper 17 (Th17) cells are the major producers of IL-17A. Aberrant signaling by IL-17A has been implicated in the pathogenesis of several autoimmune diseases including idiopathic pulmonary fibrosis, acute lung injury, chronic airway diseases, and cancer. Activation of the IL-17A/IL-17 receptor A (IL-17RA) system regulates phosphoinositide 3-kinase/AKT serine/threonine kinase/mammalian target of rapamycin (PI3K/AKT/mTOR), mitogen-activated protein kinases (MAPKs) and activation of nuclear factor-κB (NF-κB) mediated signaling pathways. The IL-17RA activation orchestrates multiple downstream signaling cascades resulting in the release of pro-inflammatory cytokines such as interleukins (IL)-1β, IL-6, and IL-8, chemokines (C-X-C motif) and promotes neutrophil-mediated immune response. Considering the biomedical importance of IL-17A, we developed a pathway resource of signaling events mediated by IL-17A/IL-17RA in this study. The curation of literature data pertaining to the IL-17A system was performed manually by the NetPath criteria. Using data mined from the published literature, we describe an integrated pathway reaction map of IL-17A/IL-17RA consisting of 114 proteins and 68 reactions. That includes detailed information on IL-17A/IL-17RA mediated signaling events of 9 activation/inhibition events, 17 catalysis events, 3 molecular association events, 68 gene regulation events, 109 protein expression events, and 6 protein translocation events. The IL-17A signaling pathway map data is made freely accessible through the WikiPathways Database (https://www.wikipathways.org/index.php/Pathway: WP5242). [ABSTRACT FROM AUTHOR]

Urotensin-II is a polypeptide ligand with neurohormone-like activity. It mediates downstream signaling pathways through G-protein-coupled receptor 14 (GPR14) also known as urotensin receptor (UTR). Urotensin-II is the most potent endogenous vasoconstrictor in mammals, promoting cardiovascular remodelling, cardiac fibrosis, and cardiomyocyte hypertrophy. It is also involved in other physiological and pathological activities, including neurosecretory effects, insulin resistance, atherosclerosis, kidney disease, and carcinogenic effects. Moreover, it is a notable player in the process of inflammatory injury, which leads to the development of inflammatory diseases. Urotensin-II/UTR expression stimulates the accumulation of monocytes and macrophages, which promote the adhesion molecules expression, chemokines activation and release of inflammatory cytokines at inflammatory injury sites. Therefore, urotensin-II turns out to be an important therapeutic target for the treatment options and management of associated diseases. The main downstream signaling pathways mediated through this urotensin-II /UTR system are RhoA/ROCK, MAPKs and PI3K/AKT. Due to the importance of urotensin-II systems in biomedicine, we consolidated a network map of urotensin-II /UTR signaling. The described signaling map comprises 33 activation/inhibition events, 31 catalysis events, 15 molecular associations, 40 gene regulation events, 60 types of protein expression, and 11 protein translocation events. The urotensin-II signaling pathway map is made freely accessible through the WikiPathways Database (https://www.wikipathways.org/index.php/Pathway:WP5158). The availability of comprehensive urotensin-II signaling in the public resource will help understand the regulation and function of this pathway in normal and pathological conditions. We believe this resource will provide a platform to the scientific community in facilitating the identification of novel therapeutic drug targets for diseases associated with urotensin-II signaling. [ABSTRACT FROM AUTHOR]

Bradykinin, a member of the kallikrein-kinin system (KKS), is associated with an inflammatory response pathway with diverse vascular permeability functions, including thrombosis and blood coagulation. In majority, bradykinin signals through Bradykinin Receptor B2 (B2R). B2R is a G protein-coupled receptor (GPCR) coupled to G protein family such as Gαqs, Gαq/Gα11, Gαi1, and Gβ1γ2. B2R stimulation leads to the activation of a signaling cascade of downstream molecules such as phospholipases, protein kinase C, Ras/Raf-1/MAPK, and PI3K/AKT and secondary messengers such as inositol-1,4,5-trisphosphate, diacylglycerol and Ca2+ ions. These secondary messengers modulate the production of nitric oxide or prostaglandins. Bradykinin-mediated signaling is implicated in inflammation, chronic pain, vasculopathy, neuropathy, obesity, diabetes, and cancer. Despite the biomedical importance of bradykinin, a resource of bradykinin-mediated signaling pathway is currently not available. Here, we developed a pathway resource of signaling events mediated by bradykinin. By employing data mining strategies in the published literature, we describe an integrated pathway reaction map of bradykinin consisting of 233 reactions. Bradykinin signaling pathway events included 25 enzyme catalysis reactions, 12 translocations, 83 activation/inhibition reactions, 11 molecular associations, 45 protein expression and 57 gene regulation events. The pathway map is made publicly available on the WikiPathways Database with the ID URL: https://www.wikipathways.org/index.php/Pathway:WP5132. The bradykinin-mediated signaling pathway map will facilitate the identification of novel candidates as therapeutic targets for diseases associated with dysregulated bradykinin signaling. [ABSTRACT FROM AUTHOR]

The C–C Motif Chemokine Ligand 18 (CCL18) is a beta-chemokine sub-family member with immunomodulatory functions in primates. CCL18-dependent migration and epithelial-to-mesenchymal transition of oral squamous cell carcinoma, squamous cell carcinoma of head and neck, breast cancer, hepatocellular carcinoma, non-small cell lung carcinoma, ovarian cancer, pancreatic ductal carcinoma and bladder cancer cells are well-established. In the tumor niche, tumor-associated macrophages produce CCL18 and its overexpression is correlated with reduced patient survival in multiple cancers. Although multiple receptors including C–C chemokine receptor type 3 (CCR3), type 6 (CCR6), type 8 (CCR8) and G-protein coupled estrogen receptor (GPER1) are reported for CCL18, the Phosphatidylinositol Transfer Protein, Membrane-Associated 3 (PITPNM3) receptor is currently considered as its predominant receptor. Characterization of the molecular events and check points associated with the immunosuppressive and cancer progression support functions induced by CCL18 for their potential towards therapeutic applications is an area of active research. Hence, in this study, we assembled 917 signaling events reported to be induced by CCL18 through their studied receptors in diverse cell types as an integrated knowledgebase for reference, data integration and gene-set enrichment analysis of global transcriptomic and/or proteomics datasets. [ABSTRACT FROM AUTHOR]

This article, published in the journal Endoscopy, presents the results of an international expert consensus on the referral of large non-pedunculated colorectal polyps for endoscopic resection. The study used a Delphi methodology to establish consensus among a panel of 24 experts from diverse continents. The experts agreed on 19 statements related to the referral process, including factors such as patient demographics, relevant medications, lesion characteristics, photodocumentation, and the presence of a tattoo. The consensus statements can help improve the triage and planning of resection techniques for large colorectal polyps, ultimately contributing to the reduction of colorectal cancer incidence and mortality. [Extracted from the article]

Elabela (ELA; also called Apela and Toddler) is one of the recently discovered ligand among the two endogenous peptide ligands (Apelin and Elabela) of the apelin receptor (APLNR, also known as APJ). Elabela-induced signaling plays a crucial role in diverse biological processes, including formation of the embryonic cardiovascular system and early placental development by reducing the chances of occurrence of preeclampsia during pregnancy. It also plays the major role in the renoprotection by reducing kidney injury and the inflammatory response and regulation of gene expression associated with heart failure and fibrosis. Elabela may be processed into different active peptides, each of which binds to APLNR and predominantly activates the signals through PI3K/AKT pathway. Owing to its biomedical importance, we developed a consolidated signaling map of Elabela, in accordance with the NetPath criteria. The presented Elabela signaling map comprises 12 activation/inhibition events, 15 catalysis events, 1 molecular association, 34 gene regulation events and 32 protein expression events. The Elabela signaling pathway map is freely made available through the WikiPathways Database (https://www.wikipathways.org/index.php/Pathway:WP5100). [ABSTRACT FROM AUTHOR]

The apelin receptor (APLNR) is a class A (rhodopsin-like) G-protein coupled receptor with a wide distribution throughout the human body. Activation of the apelin/APLNR system regulates AMPK/PI3K/AKT/mTOR and RAF/ERK1/2 mediated signaling pathways. APLNR activation orchestrates several downstream signaling cascades, which play diverse roles in physiological effects, including effects upon vasoconstriction, heart muscle contractility, energy metabolism regulation, and fluid homeostasis angiogenesis. We consolidated a network map of the APLNR signaling map owing to its biomedical importance. The curation of literature data pertaining to the APLNR system was performed manually by the NetPath criteria. The described apelin receptor signaling map comprises 35 activation/inhibition events, 38 catalysis events, 4 molecular associations, 62 gene regulation events, 113 protein expression types, and 4 protein translocation events. The APLNR signaling pathway map data is made freely accessible through the WikiPathways Database (https://www.wikipathways.org/index.php/Pathway:WP5067). [ABSTRACT FROM AUTHOR]

Coronavirus disease (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). COVID-19 has been declared a pandemic by WHO. The clinical manifestation and disease progression in COVID-19 patients varies from minimal symptoms to severe respiratory issues with multiple organ failure. Understanding the mechanism of SARS-CoV-2 interaction with host cells will provide key insights into the effective molecular targets for the development of novel therapeutics. Recent studies have identified virus-mediated phosphorylation or activation of some major signaling pathways, such as ERK1/2, JNK, p38, PI3K/AKT and NF-κB signaling, that potentially elicit the cytokine storm that serves as a major cause of tissue injuries. Several studies highlight the aggressive inflammatory response particularly 'cytokine storm' in SARS-CoV-2 patients. A depiction of host molecular dynamics triggered by SARS-CoV-2 in the form of a network of signaling molecules will be helpful for COVID-19 research. Therefore, we developed the signaling pathway map of SARS-CoV-2 infection using data mined from the recently published literature. This integrated signaling pathway map of SARS-CoV-2 consists of 326 proteins and 73 reactions. These include information pertaining to 1,629 molecular association events, 30 enzyme catalysis events, 43 activation/inhibition events, and 8,531 gene regulation events. The pathway map is publicly available through WikiPathways: https://www.wikipathways.org/index.php/Pathway:WP5115. [ABSTRACT FROM AUTHOR]

Kant suggested that Newton's Inverse Square Law (ISL) determines the dimensions of space to be three. Much has been written in the philosophical literature about Kant's suggestion, including specific arguments attempting to link the ISL to three-dimensionality. In this article, we explore one such argument and demonstrate that it fails to support the link Kant purports to make between the ISL and the three-dimensionality of space. At best, the link that can be made is between the ISL and symmetry. [ABSTRACT FROM AUTHOR]

Bleomycin (BLM) injury is associated with the severity of acute lung injury (ALI) leading to fibrosis, a high‐morbidity, and high‐mortality respiratory disease of unknown etiology. BLM‐induced ALI is marked by the activation of a potent fibrogenic cytokine transcription growth factor beta‐1 (TGFβ‐1), which is considered a critical cytokine in the progression of alveolar injury. Previously, our work demonstrated that a diet‐derived compound curcumin (diferuloylmethane), represents its antioxidative and antifibrotic application in TGF‐β1‐mediated BLM‐induced alveolar basal epithelial cells. However, curcumin‐specific protein targets, as well as its mechanism using mass spectrometry‐based proteomic approach, remain elusive. To elucidate the underlying mechanism, a quantitative proteomics approach and bioinformatics analysis were employed to identify the protein targets of curcumin in BLM or TGF‐β1‐treated cells. With subsequent in vitro experiments, curcumin‐related pathways and cellular processes were predicted and validated. The current study discusses two separate proteomics experiments using BLM and TGF‐β1‐treated cells with the proteomics approach, various unique target proteins were identified, and proteomic analysis revealed that curcumin reversed the expressions of unique proteins like DNA topoisomerase 2‐alpha (TOP2A), kinesin‐like protein (KIF11), centromere protein F (CENPF), and so on BLM or TGF‐β1 injury. For the first time, the current study reveals that curcumin restores TGF‐β1 induced peroxisomes like PEX‐13, PEX‐14, PEX‐19, and ACOX1. This was verified by subsequent in vitro assays. This study generated molecular evidence to deepen our understanding of the therapeutic role of curcumin at the proteomic level and may be useful to identify molecular targets for future drug discovery. [ABSTRACT FROM AUTHOR]

Calcium/calmodulin-dependent protein kinase kinase 2 (CAMKK2) is a serine/threonine-protein kinase belonging to the Ca2+/calmodulin-dependent protein kinase subfamily. CAMKK2 has an autocatalytic site, which gets exposed when Ca2+/calmodulin (CAM) binds to it. This results in autophosphorylation and complete activation of CAMKK2. The three major known downstream targets of CAMKK2 are 5′-adenosine monophosphate (AMP)-activated protein kinase (AMPKα), calcium/calmodulin-dependent protein kinase 1 (CAMK1) and calcium/calmodulin-dependent protein kinase 4 (CAMK4). Activation of these targets by CAMKK2 is important for the maintenance of different cellular and physiological processes within the cell. CAMKK2 is found to be important in neuronal development, bone remodeling, adipogenesis, and systemic glucose homeostasis, osteoclastgensis and postnatal myogensis. CAMKK2 is reported to be involved in pathologies like Duchenne muscular dystrophy, inflammation, osteoporosis and bone remodeling and is also reported to be overexpressed in prostate cancer, hepatic cancer, ovarian and gastric cancer. CAMKK2 is involved in increased cell proliferation and migration through CAMKK2/AMPK pathway in prostate cancer and activation of AKT in ovarian cancer. Although CAMKK2 is a molecule of great importance, a public resource of the CAMKK2 signaling pathway is currently lacking. Therefore, we carried out detailed data mining and documentation of the signaling events associated with CAMKK2 from published literature and developed an integrated reaction map of CAMKK2 signaling. This resulted in the cataloging of 285 reactions belonging to the CAMKK2 signaling pathway, which includes 33 protein–protein interactions, 74 post-translational modifications, 7 protein translocation events, and 22 activation/inhibition events. Besides, 124 gene regulation events and 25 activator/inhibitors involved in CAMKK2 activation were also cataloged. The CAMKK2 signaling pathway map data is made freely accessible through WikiPathway database (https://www.wikipathways.org/index.php/Pathway:WP4874). We expect that data on a signaling map of CAMKK2 will provide the scientific community with an improved platform to facilitate further molecular as well as biomedical investigations on CAMKK2 and its utility in the development of biomarkers and therapeutic targets. [ABSTRACT FROM AUTHOR]

This article is a compilation of all the books that have been listed in the "Recent Publications" section of The Methodist Review Newsletter since the first issue in January 2011. [ABSTRACT FROM AUTHOR]

Introduction: Esophageal squamous cell carcinoma (ESCC), a histopathologic subtype of esophageal cancer is a major cause of cancer-related morbidity and mortality worldwide. This is primarily because patients are diagnosed at an advanced stage by the time symptoms appear. The genomics and mass spectrometry-based proteomics continue to provide important leads toward biomarker discovery for ESCC. However, such leads are yet to be translated into clinical utilities. Areas covered: We gathered information pertaining to proteomics and proteogenomics efforts in ESCC from the literature search until 2020. An overview of omics approaches to discover the candidate biomarkers for ESCC were highlighted. We present a summary of recent investigations of alterations in the level of gene and protein expression observed in biological samples including body fluids, tissue/biopsy and in vitro-based models. Expert opinion: A large number of protein-based biomarkers and therapeutic targets are being used in cancer therapy. Several candidates are being developed as diagnostics and prognostics for the management of cancers. High-resolution proteomic and proteogenomic approaches offer an efficient way to identify additional candidate biomarkers for diagnosis, monitoring of disease progression, prediction of response to chemo and radiotherapy. Some of these biomarkers can also be developed as therapeutic targets. [ABSTRACT FROM AUTHOR]

Copyright of British Journal of Surgery is the property of Oxford University Press / USA and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

This article discusses the use of computer-aided detection (CADe) systems during colonoscopy to increase the adenoma detection rate (ADR) and potentially reduce the risk of post-colonoscopy colorectal cancer (PCCRC). The study analyzes the variability in the effectiveness of CADe systems across previous studies and the contradictory results in real-life experiences. The researchers conducted a meta-regression analysis of randomized controlled trials (RCTs) to investigate the factors that affect the impact of CADe-assisted colonoscopy on ADR. The analysis found that patient age, ADR in control arms, and withdrawal time were significant predictors of the CADe effect on ADR. The study concludes that the variability in colonoscopy quality performances contributes to the heterogeneity in CADe effectiveness, and the implementation of CADe-assisted colonoscopy can help reduce the gap in detection performances between high- and low-detectors. [Extracted from the article]

This article discusses a randomized trial that examined the use of cold snare endoscopic resection for large colon polyps. The study aimed to determine if cold resection without electrocautery reduces the risk of severe adverse events (SAEs) and provides complete resection. The trial involved 660 patients and found that while there was no significant safety benefit of universal cold resection, cold resection did have a lower SAE rate compared to hot resection when accounting for a high crossover rate. However, cold resection was associated with a higher rate of polyp recurrence, particularly for advanced pathology. The study concludes that the universal application of cold resection for large non-pedunculated colorectal polyps is not supported. [Extracted from the article]

Interleukin-33 (IL-33) is a member of the IL-1 family of cytokines that play a central role in the regulation of immune responses. Its release from epithelial and endothelial cells is mediated by pro-inflammatory cytokines, cell damage and by recognition of pathogen-associated molecular patterns (PAMPs). The activity of IL-33 is mediated by binding to the IL-33 receptor complex (IL-33R) and activation of NF-κB signaling via the classical MyD88/IRAK/TRAF6 module. IL-33 also induces the phosphorylation and activation of ERK1/2, JNK, p38 and PI3K/AKT signaling modules resulting in the production and release of pro-inflammatory cytokines. Aberrant signaling by IL-33 has been implicated in the pathogenesis of several acute and chronic inflammatory diseases, including asthma, atopic dermatitis, rheumatoid arthritis and ulcerative colitis among others. Considering the biomedical importance of IL-33, we developed a pathway resource of signaling events mediated by IL-33/IL-33R in this study. Using data mined from the published literature, we describe an integrated pathway reaction map of IL-33/IL-33R consisting of 681 proteins and 765 reactions. These include information pertaining to 19 physical interaction events, 740 enzyme catalysis events, 6 protein translocation events, 4 activation/inhibition events, 9 transcriptional regulators and 2492 gene regulation events. The pathway map is publicly available through NetPath (http://www.netpath.org/), a resource of human signaling pathways developed previously by our group. This resource will provide a platform to the scientific community in facilitating identification of novel therapeutic targets for diseases associated with dysregulated IL-33 signaling. Database URL: http://www.netpath.org/pathways?path_id=NetPath_120. [ABSTRACT FROM AUTHOR]

From the Fieldis a semi-regular column that explores what it means to be a local health professional on the front lines of an emergency. Typically, National Association of County and City Health Officials (NACCHO) members share their stories of preparing for and responding to disasters, epidemics, and other major health issues. Through exploring the analysis of the challenges faced and the solutions developed, readers can learn how these public health champions keep their communities safe even in extreme situations. Readers may submit topics of interest to the column's editor, Meghan McGinty, PhD, MPH, MBA, at mmcginty@naccho.org. [ABSTRACT FROM AUTHOR]

This article outlines an approach for teaching law students about advocacy beyond the judicial branch, with particular emphasis on legislative advocacy. Given the long and well-documented shift away from the judicial branch as the primary source of original public law, it is critical to teach law students that legislative advocacy is more than just an "alternative" or "non-traditional" legal career option and, instead, is one which regularly involves "real lawyering." Just as law students learn practical trial skills through moot court, shouldn't they learn practical legislative advocacy skills through simulated legislative hearings? Further, can law students move beyond traditional approaches for drafting legislative proposals in a classroom, setting to vetting and advancing student-developed legislative proposals in a legislative body ? This article outlines an effort to determine the limits of how far, and under what circumstances, law students can both develop original legislation and engage in actual legislative advocacy. [ABSTRACT FROM AUTHOR]

Objective To assess the efficacy and safety of endoscopic resection of large colorectal polyps. Design Relevant publications were identified in MEDLINE/EMBASE/Cochrane Central Register for the period 1966-2014. Studies in which ⩾20 mm colorectal neoplastic lesions were treated with endoscopic resection were included. Rates of postendoscopic resection surgery due to non-curative resection or adverse events, as well as the rates of complete endoscopic removal, invasive cancer, adverse events, recurrence and mortality, were extracted. Study quality was ascertained according to Newcastle-Ottawa Scale. Forest plot was produced based on random effect models. I2 statistic was used to describe the variation across studies due to heterogeneity. Meta-regression analysis was also performed. Results 50 studies including 6442 patients and 6779 large polyps were included in the analyses. Overall, 503 out of 6442 patients ( pooled rate: 8%, 95% CI 7% to 10%, I2=78.6%) underwent surgery due to non-curative endoscopic resection, and 31/6442 ( pooled rate: 1%, 95% CI 0.7% to 1.4%, I2=0%) to adverse events. Invasive cancer at histology, non-curative endoscopic resection, synchronous lesions and recurrence accounted for 58%, 28%, 2.2% and 5.9% of all the surgeries, respectively. Endoscopic perforation occurred in 96/6595 (1.5%, 95% CI 1.2% to 1.7%) polyps, while bleeding in 423/6474 (6.5%, 95% CI 5.9% to 7.1%). Overall, 5334 patients entered in surveillance, 502/5836 (8.6%, 95% CI 7.9% to 9.3%) being lost at follow-up. Endoscopic recurrence was detected in 735/5334 patients (13.8%, 95% CI 12.9% to 14.7%), being an invasive cancer in 14/5334 (0.3%, 95% CI 0.1% to 0.4%). Endoscopic treatment was successful in 664/735 cases (90.3%, 95% CI 88.2% to 92.5%). Mortality related with management of large polyps was reported in 5/6278 cases (0.08%, 95% CI 0.01% to 0.15%). Conclusions Endoscopic resection of large polyps appeared to be an extremely effective and safe intervention. However, an adequate endoscopic surveillance is necessary for its long-term efficacy. [ABSTRACT FROM AUTHOR]

Background Severe and severe/complicated Clostridium difficile infection ( CDI) can result in ICU admission, sepsis, toxic megacolon and death. In this setting, colectomy is the standard of care but it is associated with a 50% mortality. Aim To evaluate safety and efficacy of a sequential faecal microbiota transplantation ( FMT) and antibiotic protocol in severe and severe/complicated CDI patients who are at high risk for colectomy. Methods All patients with severe and severe/complicated CDI refractory to oral vancomycin ± rectal vancomycin and intravenous metronidazole therapy were offered FMT. Treatment consisted of sequential FMTs via colonoscopy with the need for repeat FMT and continued vancomycin guided by clinical response and pseudomembranes at colonoscopy. Results A total of 29 patients underwent FMT between July 2013 and August 2014. The overall treatment response of endoscopic sequential FMT was 93% (27/29), with 100% (10/10) for severe CDI and 89% (17/19) for severe/complicated CDI. A single FMT was performed in 62%, two FMTs were performed in 31% and three FMTs in 7% of patients. The use of non- CDI antibiotics predicted repeat FMT (odds ratio = 17.5). The 30-day all-cause mortality after FMT was 7%, and the cumulative 3-month survival was 76%. Of the two patients who died within 30 days, one underwent colectomy and succumbed to sepsis; the other died from septic shock related to CDI. Conclusion The success of a treatment protocol for severe and severe/complicated involving faecal microbiota transplantation and continued vancomycin in selected patients was high, and it warrants further evaluation. [ABSTRACT FROM AUTHOR]