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PubMed1998

In birds, NHE2 is major brush-border Na+/H+ exchanger in colon and is increased by a low-NaCl diet.

We previously reported that mammalian small intestinal and colonic brush borders (BBs) contained both epithelial Na+/H+ exchangers NHE2 and NHE3. We now show that, in the avian (chicken) colon, NHE2 is the major functional isoform under basal conditions and when stimulated by a low-NaCl diet. Hubbard chickens were maintained for 2 wk on a high- or low-NaCl diet. After the chickens were killed, the ileum and colon were removed, and BBs were prepared by Mg2+ precipitation and 22Na and D-[14C]glucose uptake determined in the BB vesicles. NHE2 and NHE3 were separated by differential sensitivity to HOE-694 (NHE2 defined as Na+/H+ exchange inhibited by 50 microM HOE-694). Chickens on a low-Na+ diet have increased plasma aldosterone (10 vs. 207 pg/ml). On the high-NaCl diet, both NHE2 and NHE3 contributed to ileal and colonic apical Na+/H+ exchange, contributing equally in ileum, but NHE2 being the major component in colon (86%). Low-NaCl diet significantly increased ileal and colonic BB Na+/H+ exchange; the increase in BB Na+/H+ exchange in both ileum and colon was entirely due to an increase in NHE2 with no change in NHE3 activity. In contrast, low-NaCl diet decreased ileal and colonic Na+-dependent D-glucose uptake. Western analysis showed that low-Na+ diet increased the amount of NHE2 in the ileal and colonic BB and decreased the amount of ileal Na+-dependent glucose transporter SGLT1. Both NHE2 and NHE3 were present in the apical but not basolateral membranes (BLM) of ileal and colonic epithelial cells. In summary, 1) NHE2 and NHE3 are both present in the BB and not BLM of chicken ileum and colon; 2) NHE2 is the major physiological colonic BB Na+/H+ exchanger under basal conditions; 3) low-NaCl diet, which increases plasma aldosterone, increases ileal and colonic BB Na+/H+ exchange and decreases Na+-dependent D-glucose uptake; 4) the stimulation of colonic BB Na+/H+ exchange is due to increased activity and amount of NHE2; and 5) the inhibition of ileal D-glucose uptake is associated with a decrease in SGLT1 amount. NHE2 is the major chicken colonic BB Na+/H+ exchanger.

Animals↗
PubMed1993

Identifying the low-risk patient with penetrating colonic injury for selective use of primary repair.

As the mortality rate for penetrating colonic injuries approaches zero, emphasis has shifted toward reducing associated morbidity. This study was done to identify patients at low risk for colon-related extensive morbidity after primary repair of a penetrating colonic injury. The records of 100 consecutive patients admitted to the District of Columbia General Hospital (DCGH) between 1984 to 1990, surviving more than 24 hours after full-thickness penetrating colonic injuries, were retrospectively reviewed. Data collection included mechanism, management and anatomic location of the colonic injury. Severity of injury was evaluated by the Trauma Score (TS), Penetrating Abdominal Trauma Index (PATI), Flint Colon Injury Score (FCIS), time in the operating room, blood transfused during the first 24 hours and presence of preoperative shock (systolic blood pressure less than 90 millimeters of mercury). Mechanism of injury included 97 gunshot wounds and three stab wounds. Fifty-seven patients had primary repair (17 having resection and anastomosis) and 43 had colostomy. The anatomic location of injury was right colon in 37, transverse colon in 27, left colon in 35 and multiple sites (two) in one patient. In this series, only two patients had colon-related extensive morbidity--a parastomal hernia and wound dehiscence, both requiring operative intervention. There were no instances of intraperitoneal abscess formation. One patient died from overwhelming pneumonia after segmental resection of the colon with primary anastomosis. The literature reports a 12 to 42 percent colon-related morbidity rate in patients sustaining penetrating colonic injuries. This series from DCGH represents the lowest colon-related extensive morbidity and mortality rates reported to date in any substantial series of penetrating abdominal trauma. We attribute the 2 percent extensive morbidity rate to high TS (mean of 15.7), low PATI (mean of 24.2), low FCIS (mean of 1.9) and few associated intra-abdominal injuries (59 percent of patients with less than two). We have identified a group of patients with full-thickness penetrating injuries to the colon, few associated intra-abdominal injuries, high TS, low PATI and low FCIS who can be managed safely and judiciously by primary repair without undue morbidity and mortality.

Colon↗
PubMed2004

Methicillin-resistant Staphylococcus aureus (MRSA) nares colonization at hospital admission and its effect on subsequent MRSA infection.

BACKGROUND: Asymptomatic colonization with methicillin-resistant Staphylococcus aureus (MRSA) has been described as a risk factor for subsequent MRSA infection. MRSA is an important nosocomial pathogen but has currently been reported in patients without typical risk factors for nosocomial acquisition. This study was designed to evaluate the impact of asymptomatic nares MRSA colonization on the development of subsequent MRSA infection. The incidence of MRSA infection was examined in patients with and patients without MRSA or methicillin-susceptible S. aureus (MSSA) colonization at admission to the hospital and in those who developed colonization during hospitalization. METHODS: Patients admitted to 5 representative hospital units were prospectively evaluated. Nares samples were obtained for culture at admission and during hospitalization. Laboratory culture results were monitored to identify all MRSA infections that occurred during the study period and 1 year thereafter. RESULTS: Of the 758 patients who had cultures of nares samples performed at admission, 3.4% were colonized with MRSA, and 21% were colonized with MSSA. A total of 19% of patients with MRSA colonization at admission and 25% who acquired MRSA colonization during hospitalization developed infection with MRSA, compared with 1.5% and 2.0% of patients colonized with MSSA (P<.01) and uncolonized (P<.01), respectively, at admission. MRSA colonization at admission increased the risk of subsequent MRSA infection, compared with MSSA colonization (relative risk [RR], 13; 95% confidence interval [CI], 2.7-64) or no staphylococcal colonization (RR, 9.5; 95% CI, 3.6-25) at admission. Acquisition of MRSA colonization also increased the risk for subsequent MRSA infection, compared with no acquisition (RR, 12; 95% CI, 4.0-38). CONCLUSION: MRSA colonization of nares, either present at admission to the hospital or acquired during hospitalization, increases the risk for MRSA infection. Identifying MRSA colonization at admission could target a high-risk population that may benefit from interventions to decrease the risk for subsequent MRSA infection.

Adolescent↗
PubMed2005

Colonic response to food in constipation.

OBJECTIVES: Colonic response to food is possibly abnormal in constipation. METHODS: The colonic response to food was evaluated in 323 patients and 60 healthy subjects by following the movements of radiopaque markers after ingestion of a standard 1,000-cal test meal. Constipated patients were divided into four groups: one with a normal, and three with a delayed colorectal transit time. When the delay was found mainly in the ascending colon, the group was labeled as suffering from "colonic inertia". In "hindgut dysfunction", the delay was predominantly found in the descending colon, whereas the term "outlet obstruction" was reserved for constipated patients whose major site of delay was the rectosigmoid area. Colonic response to food was quantified by evaluating the variation of markers in a given abdominal region and the evolution of the geometric center on the entire plain film of the abdomen. RESULTS: Emptying of the caecum-ascending colon and filling of the rectosigmoid area characterize the colonic response to food in healthy subjects. Constipated patients also filled the rectosigmoid, but different patterns were found in the colon. In constipated patients with transit in the normal range, there was a frequent (41%) absence of colonic response to food as compared to controls (13%) and constipated patients with delayed transit (p<0.0001). The response to food of patients with colonic inertia was similar to that of healthy subjects in terms of distal progression, but less marked. The hindgut dysfunction group emptied the entire left colon but failed to empty the caecum and ascending colon. In the outlet obstruction group, there was no distal progress of the geometric center after meal. CONCLUSIONS: Abnormal colonic response to food is frequently found in constipated patients, with different patterns according to the type of constipation.

Adolescent↗
PubMed2001

Estrogen metabolism and malignancy: analysis of the expression and function of 17beta-hydroxysteroid dehydrogenases in colonic cancer.

Age and sex differences in the incidence of gastrointestinal cancers suggest the involvement of sex steroids. Post-menopausal loss of estrogen in women appears to be associated with a lower risk of colonic cancer, and studies in vitro have shown that estradiol (E2) stimulates the growth of colonic cancer cell lines. Paradoxically more recent epidemiological data have shown that hormone replacement therapy (HRT) is associated with a lower risk of colonic cancer, although this may reflect differences in the composition and route of administration of HRT regimes. The precise mechanism by which estrogens influence colonic cancer in vivo remains unclear, although E2-induced growth of colonic cancer cells in vitro appears to be dependent on estrogen receptor (ER) expression. We have previously demonstrated differential responses to E2 in pre-malignant and malignant colonic cancer cell lines, without any apparent difference in ER expression. Analogous to well documented studies in breast cancer, we have postulated that local steroid metabolism in the colon may play a key role in modulating the effects of oestrogens by determining the tissue availability of active E2. Using biopsy material we have shown that the normal colonic mucosa has a high level of 17beta-hydroxysteroid dehydrogenase (17beta-HSD)-mediated E2 metabolism. Furthermore, the predominant enzyme activity, inactivation of E2 to estrone (E1), was significantly decreased in paired tumor biopsies. The presence of 17beta-HSD activity in the colon appears to be due to expression of the type 2 and 4 isozymes of 17beta-HSD (17beta-HSD2 and 4), and expression of mRNA for the latter was shown to be significantly decreased in tumours compared to normal mucosa. Further studies have characterised the expression of 17beta-HSD2 and 4 in colonic epithelial cells and in colonic cancer cell lines, and have suggested a link between estrogen metabolism and colonic cell proliferation. Data reviewed here provide evidence for the importance of 17beta-HSD isozymes as attenuators of E2 bioavailability in the colon, and emphasise a possible role for 17beta-HSD2 and 4 in the pathogenesis of colon cancer.

17-Hydroxysteroid Dehydrogenases↗
PubMed1991

A fish oil diet inhibits colon cancer in mice.

High-fat, high-cholesterol diets have been linked to colon cancer in both epidemiological and animal studies. Saturated and N-6 polyunsaturated fats have both been implicated as playing causative roles. Epidemiological studies have shown a reduced colon cancer incidence in populations consuming a large quantity of N-3 polyunsaturated fat. This study asked whether N-3 polyunsaturated fat found in fish oil would also be associated with reduced colon cancer in animal studies. 1,2-Dimethylhydrazine was used to induce colon cancer in mice fed three high-fat, high-cholesterol diets (beef tallow, safflower oil, and fish oil) and one low-fat, cholesterol-free diet (soybean oil). Colon adenocarcinomas developed in 55% of mice fed tallow, 48% of those fed low-fat diets, 33% of those fed safflower oil, and 18% of those fed fish oil (p less than 0.05). Tumors per animal were also greatest in mice fed tallow and fewest in those fed fish oil (p less than 0.05). Plasma cholesterol levels were significantly higher in mice fed tallow than in mice fed fish oil, but this did not show any association with tumors. Plasma triglyceride levels were not significantly different among groups but were strongly correlated with colon cancers (r = 0.90, p less than 0.025). In both plasma and colon mucosa cells, saturated fat levels were similar. Monounsaturated fat was highest in plasma of mice fed tallow and correlated strongly with colon cancers (r = 0.84, p less than 0.005). N-6 polyunsaturated fat was highest in plasma and colon mucosa cells of both mice fed safflower oil and those fed low-fat (soybean oil) diet, but there was no association with tumors. N-3 polyunsaturated fat was highest in plasma and colon mucosa cells of mice fed fish oil and showed a negative association with tumors (r = -0.57, p less than 0.05). Thus, in this model of colon cancer, a diet high in fish oil was associated with less colon cancer. Monounsaturated fat was most strongly correlated with tumors. This study suggests monounsaturated fat promotes colon tumors and N-3 polyunsaturated fat inhibits colon tumors.

Analysis of Variance↗
PubMed2000

Application of confocal laser scanning microscopy to detect oxidative stress in human colon cells.

INTRODUCTION: Excess of intracellular reactive oxygen species in relation to antioxidative systems results in an oxidative environment which may modulate gene expression or damage cellular molecules. These events are expected to greatly contribute to processes of carcinogenesis. Only few studies are available on the oxidative/reductive conditions in the colon, an important tumour target tissue. It was the objective of this work to further develop methods to assess intracellular oxidative stress within human colon cells as a tool to study such associations in nutritional toxicology. METHODS: We have measured H2O2-induced oxidative stress in different colon cell lines, in freshly isolated human colon crypts, and, for comparative purposes, in NIH3T3 mouse embryo fibroblasts. Detection was performed by loading the cells with the fluorigenic peroxide-sensitive dye 6-carboxy-2',7'-dichlorodihydrofluorescein diacetate (diacetoxymethyl ester), followed by in vitro treatment with H2O2 and fluorescence detection with confocal laser scanning microscopy (CLSM). Using the microgel electrophoresis ("Comet") Assay, we also examined HT29 stem and clone 19A cells and freshly isolated primary colon cells for their relative sensitivity toward H2O2-induced DNA damage and for steady-state levels of endogenous oxidative DNA damage. RESULTS: A dose-response relationship was found for the H2O2-induced dye decomposition in NIH3T3 cells (7.8-125 microM H2O2) whereas no effect occurred in the human colon tumour cell lines HT29 stem and HT29 clone 19A (62-1000 M H2O2). Fluorescence was significantly increased at 62microM H2O2 in the human colon adenocarcinoma cell line Caco-2. In isolated human colon crypts, the lower crypt cells (targets of colon cancer) were more sensitive towards H2O2 than the more differentiated upper crypt cells. In contrast to the CLSM results, oxidative DNA damage was detected in both cell lines using the Comet Assay. Endogenous oxidative DNA damage was highest in HT29 clone 19A, followed by the primary colon cells and HT29 stem cells. CONCLUSIONS: Oxidative stress in colon cells leads to damage of macromolecules which is sensitively detected in the Comet Assay. The lacking response of the CLSM-approach in colon tumour cells is probably due to intrinsic modes of protective activities of these cells. In general, however, the CLSM method is a sensitive technique to detect very low concentrations of H2O2-induced oxidative stress in NIH3T3 cells. Moreover, by using colon crypts it provides the unique possibility of assessing cell specific levels of oxidative stress in explanted human tissues. Our results demonstrate that the actual target cells of colon cancer induction are indeed susceptible to the oxidative activity of H2O2.

3T3 Cells↗
PubMed1997

Chemoprevention of azoxymethane-induced rat colon carcinogenesis by a xanthine oxidase inhibitor, 1'-acetoxychavicol acetate.

In our studies to find natural compounds with chemopreventive efficacy in foods, using azoxymethane (AOM)-induced colonic aberrant crypt foci and colonic mucosal cell proliferation as biomarkers, a xanthine oxidase inhibitor, 1'-acetoxychavicol acetate (ACA), present in the edible plant Languas galanga from Thailand was found to be effective. This study was conducted to test the ability of ACA to inhibit AOM-induced colon tumorigenesis when it was fed to rats during the initiation or post-initiation phase. Male F344 rats were given three weekly s.c. injections of AOM (15 mg/kg body weight) to induce colonic neoplasms. They were fed diet containing 100 or 500 ppm ACA for 4 weeks, starting one week before the first dosing of AOM (the initiation feeding). The other groups were fed the ACA diet for 34 weeks, starting one week after the last AOM injection (the post-initiation feeding). At the termination of the study (week 38), AOM had induced 71% incidence of colonic adenocarcinoma (12/17 rats). The initiation feeding with ACA caused significant reduction in the incidence of colon carcinoma (54% inhibition by 100 ppm ACA feeding and 77% inhibition by 500 ppm ACA feeding, P = 0.03 and P = 0.001, respectively). The post-initiation feeding with ACA also suppressed the incidence of colonic carcinoma (45% inhibition by 100 ppm ACA feeding and 93% inhibition by 500 ppm ACA feeding, P = 0.06 and P = 0.00003, respectively). Such inhibition was dose-dependent and was associated with suppression of proliferation biomarkers, such as ornithine decarboxylase activity in the colonic mucosa, and blood and colonic mucosal polyamine contents. ACA also elevated the activities of phase II enzymes, glutathione S-transferase (GST) and quinone reductase (QR), in the liver and colon. These results indicate that ACA could inhibit the development of AOM-induced colon tumorigenesis through its suppression of cell proliferation in the colonic mucosa and its induction of GST and QR. The results confirm our previous finding that ACA feeding effectively suppressed the development of colonic aberrant crypt foci. These findings suggest possible chemopreventive ability of ACA against colon tumorigenesis.

Animal Feed↗
PubMed2000

Impact of KRAS and TP53 mutations on survival in patients with left- and right-sided Dukes' C colon cancer.

OBJECTIVE: It has been suggested that KRAS and TP53 mutated tumors might influence the phenotypic behavior of left- and right-sided colon tumors. We investigated the incidence of these mutations in left- and right-sided colon tumors and their possible influence on survival in a homogeneous group of patients with Dukes' C colon cancers. METHODS: The primary tumors of 55 patients with a sporadic Dukes' C colon cancer, all treated with adjuvant chemotherapy were analyzed for the presence of KRAS and TP53 mutations. Mutation detection of the KRAS and TP53 genes was performed on paraffin-embedded tumor material, using denaturating gradient gel electrophoresis. The 5-yr survival rates of KRAS and TP53 mutated tumors were analyzed regarding right-sided tumors (defined as tumors up to the splenic flexure) and left-sided tumors (defined as tumors from the splenic flexure to the rectosigmoid peritoneal reflection). RESULTS: KRAS mutations occurred more frequently in the right colon compared to the left colon (R = 38% (10/26); L = 10% (3/29); chi2 test: p = 0.014). KRAS mutations did not influence survival in patients with right-sided colon tumors. Patients with KRAS mutation-negative tumors in the right colon, however, had a significantly worse survival than patients with left-sided KRAS mutation-negative tumors (5-yr survival; R: 34% vs L: 65%, log-rank test: p = 0.007). TP53 mutations of a possible causative nature were found in 24 tumors (44%). Neither the incidence (R = 42% (11/26); L = 45% (13/29)) nor the survival of TP53 mutated tumors differed significantly between left- and right-sided tumors. Furthermore, survival of patients with TP53 mutation-negative tumors did not differ significantly between left- and right-sided tumors. CONCLUSIONS: There seems to be no difference in survival rate between patients with KRAS mutated and KRAS negative Dukes' C colon tumors; however, KRAS mutations are more frequently found in the right colon compared to the left colon. TP53 mutations do not have predominance for either side of the colon, and there are no differences in survival in patients with left-sided versus right-sided tumors. Patients with KRAS-nonmutated tumors in the right colon did have a worse survival compared to those with such tumors in the left colon. This suggests that other genetic factors may play a role in tumor genesis in this subgroup of patients.

Adenocarcinoma↗
PubMed2002

Molecular changes in the early stage of colon carcinogenesis in rats treated with azoxymethane.

To elucidate early molecular events related to colon carcinogenesis, we examined alterations in the expression of colon cancer-related genes such as cyclooxygenase (COX)-2, APC and c-Myc, cell proliferation and apoptosis in the background colon mucosa, and K-ras mutation at aberrant crypt foci (ACF) in the colons of azoxymethane (AOM)-treated rats 4 weeks after the first exposure to AOM. About 40 ACF/colon were induced in the colons of rats treated with AOM (Group 1); however, rats not treated with AOM (Group 2) showed no ACF formation in the colon. The level of AgNORs in the colonic mucosa was significantly higher in Group 1 than in Group 2 (P<0.01). The colonic mucosa in Group 1 looked macroscopically and histologically normal, but the proliferative activity of the mucosa of rats treated with AOM was clearly elevated. COX-2 mRNA expression was not detected in normal colonic mucosa in Group 2, but 3 out of 10 rats in Group 1 showed COX-2 mRNA expression in their colons by reverse transcription (RT)-polymerase chain reaction (PCR). There was a tendency toward an increased expression level of COX-2 in the AOM-treated group. The level of APC mRNA expression in Group 1 was significantly lower than that in Group 2 (P<0.01). Moreover, the level of c-Myc mRNA expression in Group 1 was significantly higher than that in Group 2 (P<0.01). An average of 0.034+/-0.006% apoptosis in colonic mucosa was detected in Group 1; the incidence of apoptosis in Group 2 was 0.021+/-0.005%. The difference between Groups 1 and 2 was significant (P<0.01). These results indicate that apoptosis was possibly induced to eliminate cells damaged by AOM administration. Six out of 22 (27%) ACF with 4 or more crypts showed K-ras mutations at codon 12; all mutations were G to A transitions (GGT to GAT). ACF with 1-3 crypts showed no mutations in the K-ras gene. In conclusion, AOM caused an increase in COX-2 and c-Myc mRNA expression, a decrease in APC mRNA expression, induction of apoptosis in normal-appearing colonic mucosa, and a K-ras mutation in ACF with 4 or more crypts. These findings may help to identify key targets in the early steps of colon carcinogenesis, against which drugs that would be broadly effective for chemoprevention of colon cancer could be developed.

Adenomatous Polyposis Coli Protein↗
PubMedDate not supplied

Electrophysiologic identification of the location of the colonic pacemakers in humans: further study.

We recently defined the sites of four colonic pacemakers that appear to generate the electric waves assumed to be responsible for the colonic motility. We hypothesized that a dysfunction of one or more of these pacemakers might interfere with the generation of electric waves and the colonic motility. This hypothesis was investigated in the current communication. The tests were performed during the repair of huge incisional hernia of 8 subjects (5 F, 3 M; mean age 42.8 +/- 3.3 SD years). Two electrodes were applied to each of the terminal ileum (TI), cecum (C), and ascending (AC), transverse (TC), descending (DC), and sigmoid (SC) colon. The electric activity of the TI and the various colonic segments was recorded using surface silver-silver chloride electrodes applied to the colon. The site of change of the wave variables between the TI and the C and between the different other colonic segments was determined by changing the position of the electrodes placed over the segments to be examined. Presumably, the sites where the wave variables changed represent the potential location of the pacemakers. We anesthetized these sites individually by injection of 2% Xylocaine, and then recorded the electric activity after 20 min in all the subjects and after 2 h in only 5 subjects. Electric waves in the form of pacesetter and action potentials were recorded from the TI and the colon. The sites of potential pacemakers could be defined at the ileocecal and cecocolonic junctions, at the mid third of the TC, and at the colosigmoid junction. Anesthetization of the cecal pole resulted in disappearance of the cecal electric waves, with persistence of the waves from the other colon segments. Anesthetization of the cecocolonic junction eliminated the electric waves of the AC and the right half of the TC, while the waves in the rest of the colon persisted. The remaining two pacemaker sites produced similar results when anesthetized. The electric waves reappeared after the anesthetic effect had waned. Thus, the colon possesses at least four pacemakers that appear to mediate the colonic motor activity. Individual pacemaker block by anesthetization effected disappearance of electric waves in the relative colonic segment, which reappeared after waning of the anesthetic effect. The disappearance of these waves upon pacemaker anesthetization supports a relationship between the pacemakers at the anesthetized site and the electric waves. The electric waves seem to be generated by these pacemakers. We suggest that colonic inertia, segmental or total, results from the dysfunction of one or more pacemakers, and that an artificial pacemaker could be applied for the treatment of such conditions. These suggestions need to be further studied.

Action Potentials↗
PubMedDate not supplied

Comparison of the classical autoradiographic and the immunohistochemical methods with BrdU for measuring proliferation parameters in colon cancer.

In vivo labelling with bromodeoxyuridine (BrdU) was compared with 3H-thymidine (3HTdR) labelling for the study of cell proliferation in normal colon epithelium and in colon cancer tissue. Twenty-four BDIX rats with implanted subcutaneous tumors of DHD/K12 colon cancer cells were subdivided into 3 groups. Each rat received an intraperitoneal injection of either 5-bromo-2'deoxyuridine (50 mg/kg), or 3H-thymidine (1mCi/kg) or both precursors (double labelling). Immunoperoxidase staining with a monoclonal antibody to BrdU, or autoradiography were used. In the colonic crypts, similar patterns of spatial distributions of the labelled colonic epithelial cells were observed after each kind of labelling. The mean labelling indices (LI) by BrdU and by 3HTdR were similar in the normal colon as well as in the implanted tumors. The validity of BrdU labelling in vivo was further investigated by using BrdU+3HTdR double labelling technique. In the colonic crypts, the total BrdU labelled colonic epithelial cells were 11.85%, whereas the total 3HTdR labelled cells were 11.99% (p > 0.05). In the implanted tumors of colon cancer, the total BrdU and 3HTdR labelled cells accounted for 19.40% and 20.10% respectively of the colon cancer cells (p > 0.05). There was a close correlation between BrdU LI and 3HTdR LI in colonic epithelial cells (r = 0.99, p < 0.0001) as well as in colon cancer cells (r = 0.97, p < 0.001). There data indicate that the labelling index of BrdU is equivalent to that of 3HTdR not only in normal colonic epithelium but also in colon cancer. BrdU may thus be used for measuring proliferation parameters in cancer tissues.

Adenocarcinoma↗
PubMed2001

[Hydrocolonic sonography--potentials and limitations of ultrasonographic diagnosis of colon diseases].

Hydrocolonic sonography - potentials and limitations of ultrasonographic diagnosis of colon diseases. Ultrasonic examination has become increasingly important in the diagnosis of diseases of the gastrointestinal tract. In neoplastic diseases of the large intestine, however, the diagnostic value of conventional transabdominal sonography is limited. The sonographic evaluation of the colon could be improved by the retrograde instillation of water into the colon in a procedure called hydrocolonic sonography. This technique allows the visualization of the colon sonographically from the rectosigmoid transition to the cecum. Hydrocolonic sonography enables a detailed sonographic examination of the hypoechoic colonic lumen, the five individual layers of the colon wall and the surrounding connective tissue, thus providing additional information and allowing a more precise diagnosis of many diseases of the colon. Colonic polyps and carcinomas appear sonographically as echogenic structures projecting from the intestinal wall into the lumen. Colonic polyps larger than 7 mm in diameter and carcinomas of the colon can be detected with great sensitivity. In addition, detailed evaluation of the structure of the bowel wall permits more precise staging of tumors of the colon. Aside from such localized changes, hydrocolonic sonography can also demonstrate changes in the wall structure in chronic inflammatory large bowel diseases such as Crohn's disease and ulcerative colitis. In addition hydrocolonic sonography has been proven to be of great value for the ultrasonographically-guided hydrostatic reduction of intussusception in children. On the other hand virtual colonoscopy is another promising new imaging method for the diagnosis of colon diseases. The differences between hydrcolonic sonography and virtual colonoscopy and their potential for screening purposes of colon cancer will be discussed.

Colon↗
PubMed2005

Distribution of cytochrome P450 2C, 2E1, 3A4, and 3A5 in human colon mucosa.

BACKGROUND: Despite the fact that the alimentary tract is part of the body's first line of defense against orally ingested xenobiotica, little is known about the distribution and expression of cytochrome P450 (CYP) enzymes in human colon. Therefore, expression and protein levels of four representative CYPs (CYP2C(8), CYP2E1, CYP3A4, and CYP3A5) were determined in human colon mucosa biopsies obtained from ascending, descending and sigmoid colon. METHODS: Expression of CYP2C, CYP2E1, CYP3A4, and CYP3A5 mRNA in colon mucosa was determined by RT-PCR. Protein concentration of CYPs was determined using Western blot methods. RESULTS: Extensive interindividual variability was found for the expression of most of the genes. However, expression of CYP2C mRNA levels were significantly higher in the ascending colon than in the sigmoid colon. In contrast, mRNA levels of CYP2E1 and CYP3A5 were significantly lower in the ascending colon in comparison to the descending and sigmoid colon. In sigmoid colon protein levels of CYP2C8 were significantly higher by ~73% than in the descending colon. In contrast, protein concentration of CYP2E1 was significantly lower by ~81% in the sigmoid colon in comparison to the descending colon. CONCLUSION: The current data suggest that the expression of CYP2C, CYP2E1, and CYP3A5 varies in different parts of the colon.

Adult↗
PubMed2002

Role of nitric oxide in the colon of patients with slow-transit constipation.

PURPOSE: The cause of dysmotility in patients with slow-transit constipation is unknown. Nitric oxide has recently been shown to be a neurotransmitter in the nonadrenergic, noncholinergic inhibitory nerves of the human gut. To clarify the physiologic significance of nitric oxide in the colon of patients with slow-transit constipation, we investigated the enteric nerve responses in lesional and normal bowel segments derived from patients with slow-transit constipation and patients who underwent colon resection for colonic cancers. METHODS: Twenty-six preparations were taken from colonic lesions in eight patients with slow-transit constipation (2 men; age, 23 to 69 (mean, 44.8) years). Forty-two preparations were taken from the normal colons of 14 patients with colonic cancer (8 men; age, 40 to 66 (mean, 52.4) years). A mechanographic technique was used to evaluate in vitro muscle responses to electric field stimulation before and after treatment with various autonomic nerve blockers, NG-nitro-L-arginine, and L-arginine. RESULTS: The colons of patients with slow-transit constipation were more strongly innervated by nonadrenergic, noncholinergic inhibitory nerves than were normal colons (P <0.05). Nitric oxide was found to act on both normal and slow-transit constipation colons. The colons of patients with slow-transit constipation were more strongly innervated by nitric oxide nerves than were normal colons (P < 0.01). Responses to electric field stimulation were the same in each case among the normal colons and were also the same in each case among the slow-transit constipation colons. CONCLUSION: These findings suggest that an increase of nitric oxide mediates nonadrenergic, noncholinergic inhibitory nerves and plays an important role in the dysmotility observed in the colons of patients with slow-transit constipation.

Adult↗
PubMed2003

Experimental colonic obstruction increases collagen degradation by matrix metalloproteinases in the bowel wall.

PURPOSE: Emergency resections for colonic obstruction are accompanied with increased risk of anastomotic dehiscence. Elevated local degradation of submucosal collagens by matrix metalloproteinases may predispose to anastomotic leakage. This study was designed to study the effect of colon obstruction and surgical trauma on matrix metalloproteinase activities and correlate these results to collagen concentration in the colon wall. METHODS: Colonic obstruction was induced in male, Sprague-Dawley rats (n = 58) by applying a constricting silicone ring around the left colon 3 cm above the peritoneal reflection. After four days of obstruction, 2-mm wide colonic segments were resected approximately 3 mm proximal and 3 mm distal to the stenosis for biochemical analyses. Colonic segments at corresponding locations were obtained from sham-operated rats (n = 5) without obstruction but with silicone ring placed adjacent to colon and from normal, nontraumatized rats (n = 10). Matrix metalloproteinase activity was determined by liberation of fragmented collagens from homogenized colonic tissue incubated ex vivo. Matrix metalloproteinase-2 specifically was analyzed by gelatin zymography. RESULTS: Endogenous collagenolysis by matrix metalloproteinases increased (P < 0.001) in colon as a consequence of obstruction (4.1-fold) and trauma (1.7-fold) compared with normal colon. In the proximity of the colon stenosis, total matrix metalloproteinase activity and matrix metalloproteinase-2 were significantly (P < 0.05) higher above than below the obstruction. Total activity was 22.9 (13.1-32.9) units/mg collagen proximal and 16.6 (12.7-18.4) units/mg collagen distal to the stenosis. Collagen concentration correlated inversely (r = -0.76; P < 0.001) with total matrix metalloproteinase activity. CONCLUSION: Colonic obstruction and trauma up-regulated matrix metalloproteinases and decreased collagen concentration in colonic wall.

Animals↗
PubMed1992

Muscarinic receptor subtypes in human and rat colon smooth muscle.

Muscarinic receptor subtypes in human and rat colon smooth muscle homogenates were characterized with [3H]N-methylscopolamine ([3H]NMS) by ligand binding studies. [3H]NMS saturation experiments show the existence of a homogeneous population of non-interacting binding sites with similar affinity (KD values of 1.38 +/- 0.20 nM in human colon smooth muscle and 1.48 +/- 0.47 nM in rat colon smooth muscle) and with Hill slopes close to unity in both samples of tissue. However, a significant (P less than 0.01) increase in muscarinic receptor density (Bmax) is found in human colon (29.9 +/- 2.9 fmol/mg protein) compared with rat colon (17.2 +/- 1.5 fmol/mg protein). Inhibition of [3H]NMS binding by non-labelled compounds shows the following order in human colon: atropine greater than AF-DX 116 greater than pirenzepine. Whereas in rat colon the rank order obtained is atropine greater than pirenzepine greater than AF-DX 116. Atropine and pirenzepine bind to a homogeneous population of binding sites, although pirenzepine shows higher affinity to bind to the sites present in rat colon (Ki = 1.08 +/- 0.08 microM) than those in human colon (Ki = 1.74 +/- 0.02 microM) (P less than 0.05). Similarly, IC50 values obtained in AF-DX 116 competition experiments were significantly different (P less than 0.01) in human colon (IC50 = 1.69 +/- 0.37 microM) than in rat colon (IC50 = 3.78 +/- 0.75 microM). Unlike atropine and pirenzepine, the inhibition of [3H]NMS binding by AF-DX 116 did not yield a simple mass-action binding curve (nH less than 1, P less than 0.01) suggesting the presence of more than one subtype of muscarinic receptor in both species. Computer analysis of these curves with a two binding site model suggests the presence of two populations of receptor. The apparent Ki1 value for the high affinity binding site is 0.49 +/- 0.07 microM for human colon smooth muscle and 0.33 +/- 0.05 microM for rat colon smooth muscle. The apparent Ki2 for the low affinity binding site is 8.01 +/- 1.0 microM for human samples and 6.07 +/- 1.1 microM for rat samples. These values are close enough to suggest that the first subtype of muscarinic receptor may be considered cardiac (M2) and the second subtype glandular (M3). The relative densities of the receptor subtypes are significantly different for both species. Human colon samples show the major densities of subtype M2, 22.62 +/- 1.11 fmol/mg protein, this represents 75.66 +/- 3.73% of the total receptors.(ABSTRACT TRUNCATED AT 400 WORDS)

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PubMed1985

Localization of carbonic anhydrase activity in the developing rat colon.

Carbonic anhydrase activity was localized histochemically by light and electron microscopy in the proximal and distal colon of developing rats. Fixed tissue was taken for normal morphology and carbonic anhydrase localization from fetal (20-22 days gestation), suckling (1-19 days postnatal), weanling (20-25 days postnatal), and adult rats. The proximal colon had distinct villi at birth which were diminished between days 5 and 11 postnatally. The distal colon lacked villi at birth but had rudimentary crypts (ridges and furrows) which were replaced during the suckling period by a flat mucosa interspersed with true crypts. Carbonic anhydrase first appeared in both proximal and distal colonic epithelial cells on the day of birth (22 days gestation). Goblet cells were nonreactive at each developmental period. In neonatal rats, epithelial cells in the upper half of the villi of the proximal colon and on the surface and upper crypts of the distal colon were positive for carbonic anhydrase throughout the cytoplasm. Cells at the villar base (proximal colon) or in the deep crypt (distal colon) had reaction product in the intercellular spaces but not the cytoplasm. By 11 days postnatal, cytoplasmic reaction product was present in proximal colonic cells in the upper three-fourths of the crypt and was concentrated in a heavy band in the apical cytoplasm. In the distal colon, cytoplasmic positive cells did not extend as deeply into the crypts and the apical banding pattern was weak. Intercellular spaces in the deeper crypt epithelium were positive in both proximal colon and distal colon, suggesting a membrane-bound carbonic anhydrase. It was concluded that carbonic anhydrase appeared suddenly at birth and was continuously present in mid- to upper-crypt (or upper villus in early neonatal proximal colon) non-goblet cells into adulthood. This suggests a functional role for carbonic anhydrase in chloride-bicarbonate exchange across the neonatal and adult colonic mucosa.

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