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PubMed1978

[Intestinal amebiasis in children. I. Etiological study of colonic lesions of the rectosigmoid colon].

A total of 253 children from two months to 12 years old, who had diarrheic or dysenteric syndromes, were studied from the rectosigmoidoscopic and parasitologic points of view. In addition, 112 and 20 of these patients were also studied bacteriologically and virologically, respectively. Only in 28 patients torphozoites of Entamoeba histolytica were found by means of direct microscopic examination, staining techniques and amoebal cultures. Enteropathogenic bacteria were isolated in 41 of the 112 cases examined. No viral particles were detected in the 20 cases studied. From the discussion of these results, the conclusion is reached that the rectosigmoidal mucusal alterations which have been currently considered as suggesting amoebal lessions are not characteristic of invasive intestinal amebiasis in children.

Child↗
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↗
PubMed1979

Effects of age, antigen deprivation, and allograft rejection on epithelial cell kinetics in mouse colon.

A technique of microdissection of colonic mucosa has allowed the study of mitotic activity, measured by metaphase accumulation following colchicine blockade, in individual crypts of mouse colon. The changes occurring during growth and development of normal colon have been studied and compared with changes found in antigen free colon (colonic isografts) and in cell-mediated immune damage of the bowel (allograft rejection). Metaphase accumulation was steady at two metaphases per hour in baby mouse colon until 18 days after birth. Between 18 and 24 days a rapid, and significant increase in mitotic activity occurred (P less than 0.01), reached adult values, and changed no further. Metaphase accumulation in isografts was similar to normal colon for the first two weeks after transplantation but the rise in mitotic activity in the third week did not occur. Allografts of colon showed two- to three-fold increases in metaphase accumulation when compared with both normal colon and isografts (P less than 0.01). When crypt mitotic activity was compared with the length of crypts measured in histological sections of normal colon, isografts, and allografts, no clear relationship was observed. Both changes in the luminal environment of the gut at the time of weaning and cell-mediated immune reactions in the colonic wall appeared to be associated with increased mitotic activity in colonic crypts.

Age Factors↗
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↗
PubMed1979

Characterization of colonization of the rabbit gastrointestinal tract by Escherichia coli RDEC-1.

We have reported previously the isolation of an Escherichia coli strain (RDEC-1) that in rabbits is able to colonize the gut, adhere to mucosal epithelial cells of the ileum, cecum, and colon, and cause diarrhea by a novel mechanism. The purpose of the present study was to characterize more fully the colonization of the rabbit gut by strain RDEC-1. Colonization reached a maximum 3 to 4 days post-inoculation with strain RDEC-1 and did not decrease until 15 days post-inoculation. Diarrhea occurred 3 to 4 days after colonization reached its maximum intensity. Semiquantitative rectal swab cultures were found to be correlated with counts of colony-forming units of strain RDEC-1 per gram of ileum, cecum, and colon and their contents and were used to chart the course of colonization of the rabbit gut. The actual number of colony-forming units per gram was dependent on the stage of colonization and ranged from 4.0 X 10(3) to 2.4 X 20(6) in the ileum to 3.1 X 10(5) to 3.6 X 10(7) in the cecum. The number of colony-forming units per gram was not affected by the presence of diarrhea. E. coli RDEC-1 colonizes the ileum, cecum, and colon of rabbits heavily for a relatively long period of time.

Animals↗
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↗
PubMed1978

Colonic myoelectrical activity in irritable-bowel syndrome. Effect of eating and anticholinergics.

To determine the effect of a standard meal on colonic myoelectrical and motor activity in the irritable-bowel syndrome and to determine the effect of a single dose of an oral anticholinergic drug (clidinium bromide) on this response, we studied 10 patients. These patients showed a prolonged increase in both colonic spike (P less than 0.05) and motor activity (P less than 0.05) after eating as compared to normal subjects. Clidinium did not affect the frequency of colonic slow waves or the basal colonic spike and motor activity. However, the anticholinergic reduced the prolonged postprandial colonic spike and motor response in the patients and also reduced the postprandial increase in colonic contractions at 3 cycles per minute (P less than 0.05). These studies indicate that patients with the irritable-bowel syndrome show an abnormally prolonged post-prandial increase in colonic spike and motor activity. An anticholinergic drug reduces the duration and the magnitude of this abnormal colonic response.

Administration, Oral↗
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↗
PubMed1977

Gamma glutamyl transpeptidase in colon cancer induced by 1,2-dimethylhydrazine.

The study of the gamma-glutamyl transpeptidase (GTase) in colon of adult rats showed that in the sequence: duodenum, jejunum, ileum, cecum and colon, the colon has the lowest activity. There are, on the other hand, relatively small differences between GTase activities in the ascending, transverse and descending portions of the large intestine. GTase activity in the colon of neonatal rat is several times higher than in the colon of adult rats. Colon adenocarcinoma induced by 1,2-dimethylhydrazine were found to have a much higher GTase activity than the homologous normal tissue. Because these tumors resemble human colonic adenocarcinomas, it is suggested that the assay of GTase levels of human colon mucosa might be of potential value in the diagnosis of neoplastic changes.

Adenocarcinoma↗
PubMed1978

Cytomegalovirus D.N.A. and adenocarcinoma of the colon: Evidence for latent viral infection.

The cause of adenocarcinoma of the colon has not been proven and a viral association has not been reported with this disease. A sensitive biochemical technique for the detection of viral nucleic acid was used to determine whether one type of herpesvirus, namely a human strain of cytomegalovirus, was uniquely present in tumour tissue. 24 specimens of colon, obtained at surgery from 14 patients, were analysed by membrane CR.N.A.-D.N.A. hybridisation. 4 of 7 tumours of the colon were definitely positive for C.M.V. D.N.A. (2greater than or equal to 2 genome-equivalents/cell), or repeatedly showed more than 1 genome-equivalent/cell. Macroscopically normal colon 5 cm from the tumour, as well as histologically normal and abnormal colon from a control population with Crohn's disease were uniformly negative for C.M.V. D.N.A., except for 1 specimen which was macroscopically normal tissue from a patient with carcinoma of the colon. Among patients with conditions that predispose to adenocarcinoma of the colon, 1 of 2 patients with familial polyposis and 1 of 3 with ulcerative colitis harboured in their colon greater than or equal to 2 genome-equivalents of C.M.V. D.N.A. per cell, and another ulcerative colitis patient had 1-2 genome-equivalents/cell.

Adenocarcinoma↗
PubMed1977

Effects of saline infusion and acute metabolic acidosis and alkalosis on water and electrolyte transport in the human colon.

Both the kidney and colon secrete bicarbonate and transport water and electrolytes. The respective contributions of these two organs to acid-base and electrolyte balance in normal man has thus been studied in eight healthy male volunteers who underwent simultaneous renal clearance studies, and colonic perfusion with a 0.9% saline or 7.2% mannitol solution, during metabolic alkalosis and acidosis, extracellular volume expansion, and control conditions. There was no influence of these acid-base conditions on electrolyte transport in the colon. In the urine, preferential loss of chloride over sodium averaged 81, 143 (P less than 0.001), and 141 (P less than 0.05) muequiv./min, during control, metabolic acidosis, and extracellular volume expansion conditions, respectively. During alkalosis more sodium than chloride was lost (146 muequiv./min) (P less than 0.001). Colonic pH averaged 7.41 during saline and 6.75 (P less than 0.005) during mannitol perfusion. Titratable acid was not produced in the colon during saline perfusion, and averaged 18 muequiv./min during mannitol perfusion. Urinary titratable acid increased from 19 to 25 muequiv./min (P less than 0.01) during volume expansion. With saline perfusion, bicarbonate secretion rate in the colon rose from 249 muequiv./min during control conditions to 289 muequiv./min during metabolic alkalosis (P less than 0.05). More bicarbonate was excreted in the urine during alkalosis when mannitol was introduced in the colon (243 muequiv./min) than when saline was perfused (152 muequiv./min) (P less than 0.05). This study indicates that the response of the human colon is trivial compared with that of the kidney during acute changes in acid-base balance.

Acid-Base Equilibrium↗
PubMed1979

Comparison of proximal and distal colonic muscle of the rabbit.

Mechanical length-tension properties and response to neurohumoral agents were compared for proximal and distal colonic muscle. Resting tension during stretch, acetylcholine-stimulated tension, and the total tension were determined. Proximal circular muscle developed a maximum total tension of 0.96 +/- 0.18 kg/cm2 (mean +/- SE) compared to 0.86 +/- 0.06 kg/cm2 for the distal colon (P greater than 0.05). Resting tension was 0.33 +/- 0.03 kg/cm2 for the proximal colon and 0.05 +/- 0.01 kg/cm2 for the distal colon at the length of optimal acetylcholine-stimulated tension (Lo) (P less than 0.01). Longitudinal muscle showed a similar difference for the proximal and distal colon. The high resting tension in the proximal colonic muscle was reduced by nitroprusside or calcium-free Krebs with EGTA. Dose-response curves to acetylcholine, histamine, phenylephrine, and isoproterenol were similar for the muscle of either part of the colon. Gastrin or cholecystokinin had no effect on the muscle. In summary, the circular or longitudinal muscles of the proximal and distal colon have different length-tension properties but only minimal differences in response to neurohumoral agents.

Acetylcholine↗
PubMed1978

Inhibition of DNA synthesis by 1,2-dimethylhydrazine and methylazoxymethanol acetate in rabbit colon mucosa in organ culture.

When maintained in organ culture, colon mucosa from male New Zealand White rabbits showed a near-normal mucosal morphology and linear incorporation of [3H]thymidine into mucosal DNA up to 36 hours of incubation. Explants from the descending colon had a higher DNA synthetic activity than did other segments of the large bowel. Inhibition of DNA synthesis in colon explants by 1,2-dimethylhydrazine (DMH) and methylazoxymethanol (MAM) acetate was dose-dependent. When DNA synthesis was determined after an 18-hour incubation, MAM acetate inhibited DNA synthesis at concentrations of 50, 100, 150, and 200 microgram/ml. With the same concentration of DMH, little or no inhibition was observed. At the concentration of 200 microgram/ml, both carcinogens significantly inhibited DNA synthesis after 3 and 6 hours of incubation. With longer incubation, the inhibitory effect of DMH appeared to be reversible, whereas DNA synthesis was continuously inhibited by MAM acetate up to 18 hours of incubation. No altered uptake of [3H]thymidine by colon explants incubated in the presence of DMH or MAM acetate for 18 hours was observed. No morphologic changes were seen in colon explants treated with 200 microgram MAM acetate/ml for 18 hours. Physostigmine sulfate had no influence on MAM acetate-induced inhibition of DNA synthesis in colon explants. These in vitro observations reflected a direct action of DMH and MAM acetate on the colon mucosa and supported the possibilility that colon epithelial cells contain enzymes capable of activating DMH and MAM acetate to their alkylating carcinogens.

Animals↗