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Value of Butyrylcholinesterase as a Marker of Surgical Site Infection Following Surgery for Colorectal Diseases

ABSTRACT: Butyrylcholinesterase (BChE) is an α-glycoprotein synthesized in the liver. BchE’s serum level decreases in many clinical conditions such as acute and chronic liver damage, inflammation, injury and infections, and malnutrition. The Investigators prospectively evaluate patients undergoing elective procedures for colorectal diseases. Blood samples are collected preoperatively (at day 0), post-operatively in the recovery room (day 1), and on the subsequent four days (days 2, 3, 4, and 5) for assessment of BChE, C-reactive protein, and white blood cell concentrations. The same surgical team operates all patients and is blinded to the study. Patients are monitored for post-operative infection by using standard laboratory and clinical methods. If surgical site infection (SSI) is suspected the wound is swabbed and empirical antibiotics are started. The aim of the current trial is to study whether BChE is a reliable marker for the presence of SSI in patients undergoing colorectal surgery.

DISEASE(S): Colorectal Disorders,Colorectal Neoplasms,Surgical Wound Infection

PROVIDER: 2366924 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

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2019-12-02 | PXD011122 | Pride

Effect of Vitamin E Ointment on Incisional SSI in Colorectal Surgery

Project description:A prospective, randomized study was performed. The patients were randomized into 2 groups: those patients undergoing subcutaneous vitamin E ointment application (Group 1) and those patients who not (Group 2). Incisional surgical site infection (SSI), microbiological cultures from the infected surgical wounds, postoperative pain and acute phase reactants were investigated.

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Single-cell RNA-sequencing of CD4+ T cells from lung and draining lymph node of flu-infected mice

Project description:We performed a single-cell transcriptome analysis of pooled samples from lung and lymph node of 4-12 mice per time point in days post infection (d9, d14, d30) sorted for I-Ab NP311-325 specific CD4 T cells. Additionally we include mRNA counts from liver cells from LCMV infected mice day 37 post-infection, which were sequenced simultaneously with spleen cells from GSE134157.

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Transcriptomics coupled proteomics reveals the critical signaling pathways regulating OVA antigen-specific CD8+ T cells in mouse spleen and liver

Project description:Background: Antigen-specific T cells are particularly important for eliminating bacterial infection, and the dynamics in this process help uncover the mechanisms by which bacteria are eliminated.Results: In this study, we sorted the antigen-specific CD8+ T cell in the mouse liver and spleen at 5, 7, and 14 days after infection of Listeria monocytogenes expressing the OVA protein, finding that antigen-specific CD8+ T cell expansion after infection peaked on Day 7. Through the RNAseq analysis, we identified 355 genes whose expression peaked on 7 days post-infection shared in both of spleen and liver. For these shared genes, the KEGG pathway analysis showed a notable enrichment in the metabolic pathway. We also discovered 1621 proteins shared in the mouse liver and spleen that peaked seven days after infection by the LC-MS/MS analysis. The KEGG pathway analysis for these proteins revealed a significant enrichment in Splicesome, RNA transport, Ubiquitin mediated proteolysis, and Huntington disease. Transcriptomics coupled proteomics reveals 45 genes/proteins that were elevated on day 7 post listeria infection both in the spleen and liver. These 45 molecules were enriched in Human T-cell leukemia virus 1 infection and T cell activation, which played an important role in the activation of T cells and the anti-infection process.Conclusion: Transcriptomics coupled proteomics reveals the key signaling pathways to regulate antigen-specific CD8+ T cells by infection of Listeria monocytogenes expressing the OVA protein in mouse spleen and liver.

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Renal transcriptome profiles from mice infected with Leptospira spp.

Project description:Leptospirosis caused by pathogenic Leptospira spp. leads to kidney damage that may progress to chronic kidney disease. However, how leptospiral infections lead to renal damage is unclear. Here, we apply microarray platforms to determine the murine renal transcriptome-wide investigation of gene expression changes and biological pathways associated with leptospiral infection-related kidney damage. The aims of this study are to investigate a global analysis of renal gene expression associated with renal damage that was induced by leptospiral infection using experimental murine models. The result of microarray analysis showed that 467 and 927 genes to be differentially expressed in mice kidney with pathogenic leptospiral infection after day 7 and 28, respectively. Moreover, the result also showed that the 508 significantly differentially expressed genes in the kidneys of mice after infection with non-pathogenic leptospires at 7 days post-infection, and the 1,067 transcripts significantly differentially expressed in these kidneys at 28 days post-infection. Biological pathways performed using KEGG pathway enrichment analysis (P-value < 1E-5) showed that a total of 6 and 7 pathways were significantly enriched at 7 and 28 days post-infection with pathogenic leptospires, respectively. A total of 25 pathways were significantly enriched at day 28 following the non-pathogenic leptospiral infection. However, none of pathways were found in microarray data at day 7 post-infection with non-pathogenic leptospires. In addition, the antigen processing and presentation pathways was significantly enriched at 7 and 28 days post-infection with pathogenic leptospires, and at day 28 following the non-pathogenic leptospiral infection.

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