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At least 19 recordsLinked to original sources
PubMed1976

The effects of mechanical preparation and acidification of the colon on the healing of colonic anastomoses.

The results of clinical studies have suggested that inadequate preoperative mechanical preparation of the colon is a significant factor in the pathogenesis of disruption of colonic and colorectal anastomoses. A possible explanation for the adverse effect of poor mechanical preparation is that ammonia released from feces has a cytotoxic effect on the healing anastomosis. It has been suggested that acidification of the colonic lumen prevents the release of fecal ammonia and protects the anastomoses. The effects of mechanical preparation of the colon and colonic acidification were studied in anastomoses in the left colon of rats. Colonic acidification was produced by the oral administration of a synthetic disaccharide lactulose solution. Mechanical preparation resulted in a significant increase in the bursting wall tension in anastomoses on the seventh postoperative day. The oral administration of lactulose resulted in a reduction in the colonic mucosal pH, but this was not accompanied by improved healing of anastomoses, as judged by measurements of colonic bursting pressure, bursting wall tension and total challagen content. Mechanical preparation of the colon is an important factor in the safety of colonic anastomosis. However, the results do not suggest that acidification of the colonic lumen significantly improves the quality of colonic healing.

Administration, Oral↗
PubMed1979

Cell population kinetics of 1,2-dimethylhydrazine-induced colonic neoplasms and their adjacent colonic mucosa in the mouse.

The parameters of cell population kinetics of symmetrical 1,2-dimethylhydrazine-induced colonic neoplasms and their adjacent colonic mucosa in the mouse were analyzed using the fraction labeled-mitoses curve method and compared with those of three groups of epithelial cells in the crypt of the descending colon of normal mouse. The analysis of three groups of epithelial cells in the crypt of normal mouse indicates that differentiation of epithelial cells was associated not only with a smaller proliferative pool of cells but also with a shortening of the duration of G2 phase and a prolongation of mitotic time. Other parameters of cell cycle did not change significantly. The mean cell cycle time of neoplastic cells in chemically induced colonic neoplasms was similar to that of epithelial cells in normal colon, but the variance was much greater in neoplastic cells. In neoplastic cells, the proliferative pool was greater, the G1 phase prlonged, and the S phase and the mitotic time became shorter as compared to epithelial cells in normal colon. The duration of G2 phase of neoplastic cells fell between the values of presumptive stem cells and differentiating cells in normal colon, compatible with the hypothesis that neoplastic cells are transformed stem cells defective in cellular differentiation. In the colonic mucosa immediately adjacent to neoplasms, the fraction-labeled-mitoses curve showed a flat second wave, indicating that the group of cells initially labeled by the pulse became a mixture of cells, some continuing the proliferative cycle normally, some going out of cycle, some slowing down in their passage from S through G2 to M, and some being arrested in mitotic phase. Such heterogeneous behavior of cells may be closely related to expansion of neoplasms. With some assumptions, however, cell cycle parameters of those normally cycling cells were estimated: the cell cycle time and the duration of G1 phase and mitotic phase were prolonged as compared to neoplastic cells and epithelial cells of normal colon.

Adenocarcinoma↗
PubMed1978

Management of colon ischemia following colon interposition for esophageal substitution.

During the past four years three patients have been seen with ischemia of the colon segment following colon interposition. Colon interposition was done for esophageal cancer in two patients and for esophageal stricture following ingestion of lye. Colon ischemia was manifested as early as two weeks in one patient and as late as eight weeks in the others. Colon ischemia presented a frank gangrene with cervical fistula or as dysphagia due to stricture formation. Dysphagia in two patients prompted mechanical dilatation of the colon segment which led to perforation in both cases. All three patients had empyemas. The management of these patients includes proper diagnosis, drainage of abscesses and antibiotic treatment, hyperalimentation and visceral arteriography to delineate the residual colon for reinterposition. Two of the three patients in the series are long-term survivors and are well.

Abscess↗
PubMed1975

Studies on the kinetics of glycosidases from chemically-induced rat colonic tumours and normal rat colon.

K-m values of beta-N-acetylglucosaminidase (2-acetamido-2-deoxy-beta-D-glucoside acetamidodeoxyglucohydrolase EC 3.2.1.30), beta-N-acetylgalactosaminidase (EC 3.2.1.53), beta-galactosidase (beta-D-galactoside galactohydrolase EC 3.2.1.23) and alpha-L-fucosidase (alpha-L-fucoside fucohydrolase EC 3.2.1.51) of distal colonic tumours, induced in rats by 1,2-dimethylhydrazine, were found to be significantly different compared with the values for the enzymes of the colonic mucosa of the control and tumour-bearing animals and of the proximal colonic tumours. The inhibition kinetics data also showed a significant difference between the enzymes of the distal colon tumours and of other experimental tissues. The data on the effect of pH on enzyme kinetics (pK values) showed no significant difference in the catalytic groups of the active centres of enzymes from tumours and from the control colonic mucosa. Tumour beta-N-acetylglucosaminidase and beta-N-acetylgalactosaminidase compared with the enzymes from other experimental tissues were found to be different in their thermal inactivation kinetics. K-m values of 14 days old foetal intestinal beta-N-acetylglucosaminidase and beta-N-acetylgalactosaminidase were significantly different from the values obtained for the adult mucosal enzymes but were similar to those of the distal colonic tumour enzymes.

Acetylgalactosamine↗
PubMed1977

Evidence for common and distinct determinants of colon carcinoembryonic antigen, colon carcinoma antigen-III, and molecules with carcinoembryonic antigen activity isolated from breast and ovarian cancer.

This study was designed to answer the question, do molecules with carcinoembryonic antigen (CEA) activity from colon, breast, and ovarian cancer differ? Extracts of two breast and three ovarian cancers with CEA activity were compared to three colon cancer CEA preparations and to the related antigen, colon carcinoma antigen-III, in terms of lectin- and antiserum-binding properties. With the use of Farr-type radioimmunoassays with the lectins, concanavalin A and wheat germ agglutinin, the iodinated colon CEA and CEA-like preparations from breast and ovarian cancer all showed distinctly different patterns of binding. Specificity of binding was confirmed by inhibition studies with the relevant monosaccharides. Similarly, with antisera prepared against colon CEA, colon carcinoma antigen-III, or breast CEA, it was shown that, although all preparations shared some antigens, unique antigenic determinants were also present on all preparations. These data are consistent with the concept of a series of closely related CEA and CEA-like molecules with distinct characteristics for each tissue source of CEA.

Antibodies, Neoplasm↗
PubMed1978

[Phenotypic expression of colon polymorphic antigens (WZ) in human colon adenocarcinomas].

Human colon adenocarcinomas from 52 patients were investigated for the presence of the colon polymorphic antigens WZ. The patients were typed for their WZ phenotype, using the immunofluorescence method on non tumoral colon mucosa sections: 27 patients were found W+ Z+, 18 W- Z+, and 7 W- Z-. The tumors were tested for the presence of the WZ phenotypes, using the immunofluorescence method and a radio-immunoassay. The WZ phenotypes were not expressed in the non secreting tumors, whatever the patient's phenotype. They were expressed in the secreting tumors and had the same phenotype as found in the corresponding normal mucosa. The WZ phenotypes were present in human developed into "nude" Mice inoculated either with differentiated colon carcinomas, or with a human colon carcinoma cell line (HT-29).

Adenocarcinoma↗
PubMedDate not supplied

The influence of serotonin on the mitotic rate in the colonic crypt epithelium and in colonic adenocarcinoma in rats.

1. The mitotic rate in the crypts of Lieberkühn of the descending colon and in dimethylhydrazine-induced adenocarcinomata of the descending colon of rat was measured using a stathmokinetic technique. 2. Intraperitoneal injection of a small dose (10 microgram/kg) of serotonin resulted in an increase in the tumour cell mitotic rate. 3. Blockade of serotonin receptors by 2-bromolysergic acid diethylamide and depletion of tissue serotonin levels following injection of DL-6-fluorotryptophan both result in a decrease in the tumour cell mitotic rate. 4. Treatment with serotonin, 2-bromolysergic acid diethylamide and DL-6-fluorotryptophan were all without effect on the colonic crypt cell mitotic rate.

Adenocarcinoma↗
PubMed1979

Scanning electron microscopy of interaction of peripheral blood lymphocytes from colonic cancer patients with human colonic cancer-derived cells; P-4788.

Peripheral blood lymphocytes and the various lymphocyte fractions from patients with cancer of the colon were cultivated with target cells (P-4788) derived from the colon cancer. Changes in the surface ultrastructure during tumor cell destruction were studied by scanning electron microscopy (SEM). P-4788 cells adhering to the coverslip showed various surface activity. The surfaces of some cells were relatively flat; others were smooth or had fine granules. Still other cells were villous, round or had marked blebs. When host lymphocytes were added to the target cells, adhesion of the two cell groups began by many fine projections. After incubation for 6 h, some lymphocytes had adhered to the target cells. Many lymphocytes had adhered to the target tumor cells by 24--48 h incubation. Ultimately the tumor cells became swollen and disrupted. Most lymphocytes adherent to the target cells had few microvilli. Lymphocytes after elimination of phagocytes by carbonyl iron treatment also adhered readily. Some target cells showed adhesion with lymphocytes passed through nylon-wool columns, although the number of lymphocytes adhering was fewer than in the case of lymphocytes not passed through nylon-wool columns. T cells were collected from lymphocytes that form rosettes with SRBC by isolation with NH4Cl. They had markedly elongated microvilli which in places were sparsely scattered and tended to be localized on the side, a finding which suggests loss of cell activity by the time of SEM. Only a few T cells adhered to target cells and they seemed to be T cells without activity. It was thought that there are cytotoxic cells among T cells and that the co-existence of T cells, non-T cells and monocytes caused target cell destruction.

Adenocarcinoma↗
PubMed1978

Acidification of rat colon with lactulose. Its effects on the healing of colonic anastomoses.

Preoperative preparation of rats with lactulose, 2.5 ml/kg of a 52.5% w/w solution, for two days resulted in increased bursting pressure and bursting wall tension of low colonic anastomoses three days postoperatively when compared with unprepared controls (85.8, viz, 36.1 mm Hg and 0.55, viz, 0.19 dynes/cm X 10(-5). After seven days, there was no appreciable difference in the rats with colonic acidification and in the controls.

Animals↗
PubMed1975

Crohn's disease of the colon. III. Toxic dilatation of the colon in Crohn's colitis.

In a group of 160 patients with Crohn's disease involving the colon, there were seven patients with toxic dilatation, four with granulomatous colitis and three with ileocolitis, all successfully treated without mortality. This complications is more common than previously recognized in Crohn's colitis. In Crohn's disease, toxic dilatation is less likely to proceed to perforation of the bowel, because of the nature of the pathology and is more likely to respond to conservative measures: intubation, with decompression, corticotropin, steroids and high-dose antibiotic administration. Although patients do recover from this life-threatening complication with conservative management, the majority of patients, if not all, will ultimately come to surgical excision of the colon. If surgery is mandatory, it should be carried out early, rather than late, in the patient who is failing to respond to medical therapy, certainly before the development of perforation, massive hemorrhage, or gram negative sepsis with shock. The surgical therapy will depend upon the state of the bowel at laparotomy. Thus, an intact bowel in a young patient, would favor subtotal colectomy or proctocolectomy; a sealed perforation, a diverting ileostomy with skin level colostomy decompression as suggested by Turnbull and a free perforation, the minimum adequate procedure which will tide the patient over the early postoperative period. Diverting ileostomy alone has been effective in two of our patients but should be avoided in ulcerative colitis. The critically ill patient with the ominous finding of "disintegrating colitis" and multiple leaks, will require nothing less than total radical excision of the diseased bowel in the hope of immediate salvage.

Adrenocorticotropic Hormone↗
PubMed2026

Difficult-to-treat resistant Gram-negative bacteria and genomic resemblances between colonization and infection among patients in an intensive care unit of a tertiary care hospital in Bangladesh.

Colonization with difficult-to-treat-resistant Gram-negative bacteria (DTR-GNB) increases the risk of subsequent infections with limited treatment options. This study aimed to assess the burden of DTR-GNB colonization in ICU patients, explore its association with clinical outcomes, and examine genomic similarities. This secondary analysis included patients enrolled within 24 h of ICU admission between July 2023 and January 2024. Rectal swabs were collected at enrollment, on days 3, 7, and weekly during ICU stay to detect colonization. Bacterial isolates grown on selective chromogenic agar media were identified and tested for antimicrobial susceptibility using matrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF MS) and automated broth microdilution, respectively. Blood, urine, and/or tracheal aspirate cultures were performed if clinically suspected sepsis. Whole-genome sequencing (WGS) was performed on paired colonization and infection isolates, and genomic relatedness was assessed using FastANI, core-genome single-nucleotide polymorphism (SNP) analysis, and phylogenetic reconstruction. Among 373 patients, 181 (48.5%) were colonized with DTR-GNB; 76 (20.4%) at enrollment, and 105 (53.0%) acquired during hospital stay. Among 52 (13.9%) patients evaluated for suspected infection, 30 (57.7%) had positive cultures, predominantly Acinetobacter baumannii (n = 15) and Klebsiella pneumoniae (n = 11) of DTR-phenotypes. Compared to non-colonized patients, patients colonized with DTR-GNB had higher risks of infections (risk ratio [RR]: 2.18, 95% CI: 1.27-3.76) and longer ICU stays (median 7 vs 2 days, P < 0.001). DTR-GNB-infected patients had a higher risk of death (RR: 1.57, 95% CI: 1.34-1.84) compared to patients without DTR-GNB infection. WGS revealed that 13 of 14 paired colonization-infection isolates were conspecific, with three pairs being highly clonal; whereas the remaining pairs showed greater genomic divergence, consistent with the SNP and phylogenetic analyses. While common, more than half acquired DTR-GNB colonization from the ICU. Its association with subsequent infection and prolonged ICU stays underscores the need for enhanced infection prevention and control measures to mitigate nosocomial transmission and improve patient outcomes.IMPORTANCEThis study underscores the growing threat posed by difficult-to-treat resistant Gram-negative bacteria (DTR-GNB) in intensive care units. Nearly half of critically ill patients were colonized, with a considerable proportion acquiring these multidrug-resistant organisms during their ICU stay. Colonization with these pathogens substantially increased the risk of subsequent infections, even by the same colonizing strain, prolonged ICU stays, and likely worsened clinical outcomes due to the unavailability of susceptible antibiotics. Alarmingly, more than 90% of patients infected with DTR-GNB expired in the hospital. These findings highlight the urgent need for robust infection prevention and control strategies to curb nosocomial transmission and mitigate the impact of DTR-GNB on vulnerable patient populations. Addressing this emerging resistance phenotype is critical to improving patient safety and reducing the burden on healthcare systems.

Humans↗
PubMed2026

Tumor Suppressive Role of Hsa-miR-328-3p in Colon Cancer by Regulating EN2.

BACKGROUND/AIM: Colon cancer is a prevalent and life-threatening malignancy worldwide. Recent studies have focused on how microRNAs (miRNAs) act as post-transcriptional modulators in colon cancer progression. Herein, this study aimed to identify the impact of miRNAs that are decreased in colon cancer and to investigate their regulatory mechanisms. MATERIALS AND METHODS: Differentially expressed miRNAs (DEmiRNAs) and genes (DEGs) were identified through analysis of miRNA sequencing and RNA sequencing data from normal and tumor tissues in The Cancer Genome Atlas (TCGA). Expression levels were validated by quantitative polymerase chain reaction (qPCR) in both tissues and cell lines. Functional effects of miRNAs were evaluated by assessing cell viability, proliferation, migration, and invasion following transfection with miRNA mimics. RESULTS: Analysis of miRNA-seq data from the TCGA database identified hsa-miR-328-3p as a miRNA consistently downregulated across all stages of colon cancer. This downregulation was independently validated in colon cancer patient tissues by qPCR. Functional assays demonstrated that enforced expression of hsa-miR-328-3p significantly reduced cell viability, proliferation, migration, and invasion in colon cancer cell lines, supporting its tumor-suppressive role. To elucidate the molecular mechanism underlying these inhibitory effects, target gene analysis was performed. Engrailed homeobox 2 (EN2) was identified as a potential target of hsa-miR-328-3p, and a dual-luciferase assay confirmed that EN2 is directly regulated by hsa-miR-328-3p. CONCLUSION: Collectively, these findings indicate that hsa-miR-328-3p is frequently downregulated in colon cancer and functions as a tumor suppressor by negatively regulating its target gene, EN2, thereby contributing to colon cancer malignancy. EN2 may serve as a potential diagnostic biomarker for colon cancer, while restoration of hsa-miR-328-3p expression represents a promising therapeutic strategy. Further studies are needed to clarify the precise molecular mechanisms linking the hsa-miR-328-3p/EN2 axis to colon cancer progression.

Humans↗
PubMed1976

An electrophysiological study of the sacral parasympathetic pathway to the colon of the cat.

1. Electrophysiological techniques were used to study the sacral parasympathetic pathway to the colon of the cat. 2. Electrical stimulation of the sacral ventral roots or the pelvic nerve elicited contractions of the colon and firing in nerve filaments on the serosal surface of the colon. Both responses were markedly reduced by the administration of ganglionic blocking agents. It is concluded that sacral preganglionic fibres to the colon make synaptic contacts with extramural ganglion cells. These cells were identified histologically in small ganglia on the serosal surface of the distal colon and rectum. 3. Transmission in extramural colonic ganglia was cholinergic and mediated by nicotinic receptors. Colonic ganglia did not exhibit large recruiting responses during repetitive (1-4 c/s) preganglionic nerve stimulation or an adrenergic inhibitory mechanism, both of which have been identified in bladder parasympathetic ganglia. It is concluded that colonic ganglia unlike bladder function primarily as simple relay stations and have little potential for modulating the neral activity arising in the central nervus system. 4. The preganglionic input to colonic ganglia was mediated by C fibres with maximal conduction velocities ranging from 0-5 to 1-4 m/sec. Bladder ganglia, on the other hand, received a preganglionic input composed of B fibres with maximal conduction velocities ranging from 8 to 10 m/sec. The possible physiological significance of different types of preganglionic fibres in the sacral outflow is discussed.

Action Potentials↗
PubMed2025

MicroRNA-122 overexpression suppresses the colon cancer cell proliferation by downregulating the astrocyte elevated gene-1/metadherin oncoprotein.

BACKGROUND: MicroRNAs (miRNAs) are small non-coding RNAs that regulate essential cellular functions, such as cell adhesion, proliferation, migration, invasion, and programmed cell death, and therefore, alterations in miRNAs can contribute to carcinogenesis. Previous studies have shown that miRNA-122 is abundant in the liver and regulates cell proliferation, migration, and apoptosis. However, the expression pattern and mechanism of actions of miR-122 remain primarily unknown in colon cancer. METHODS: In this study, we analyzed The Cancer Genome Atlas Colon Adenocarcinoma (TCGA-COAD) database to assess the clinical significance of astrocyte elevated gene-1 (AEG-1)/metadherin (MTDH) and miR-122 in colon cancer. MiR-122 overexpression studies were performed in HCT116, SW480, and SW620 cell lines. Dual-luciferase assay was carried out to confirm the interaction between AEG-1 and miR-122. In vivo-JetPEI-transfection reagent was used for in-vivo transient transfection of miR-122 in the AOM/DSS-induced colon tumor mouse model. RESULTS: Our results demonstrate that miR-122 was downregulated in colon cancer cells, and it influences the expressions of apoptotic factors and inflammatory cytokines. MiR-122 overexpression in HCT116, SW480, and SW620 cells showed upregulation of Caspase 3, Caspase 9, and BAX and decreased expression of BCL2, which are pro-apoptotic and anti-apoptotic members that maintain a ratio between cellular survival and cell death. In vivo transient transfection of miR-122 mimic in AOM/DSS induced colon tumor mouse model showed less inflammation and disease activity. The TCGA-COAD data indicated that AEG-1 expression was higher in patients with low expression of miR-122 and lower AEG-1 expression in patients with higher expression miR-122. CONCLUSION: Our findings highlight the key role of miR-122 in the high grade of colonic inflammation, and possibly in colon cancer, and the use of miR-122 mimic might be a therapeutic option.

MicroRNAs↗