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PubMed1998

Enhanced levels of oleate-dependent and Arf-dependent phospholipase D isoforms in experimental colon cancer.

Phospholipase D (PLD) (EC 3.1.4.4) is one of the intracellar signal transduction enzymes and plays an important role in a variety of cellular functions. In order to clarify the role of PLD in proliferation and tumorigenesis of colon cancer, we investigated the activities of oleate-dependent and ADP-ribosylation factor (Arf)-dependent types of PLD in experimental colon cancer of the rat. We produced colon cancer in Wistar rats by injecting the carcinogen, dimethylhydrazine dihydrochloride (DMH). The control rats were injected with physiological saline. Mucosal scrapings from the colon were homogenized and centrifuged to obtain the microsomal or membrane fraction. We measured the two types of PLD activities in these fractions using the transphosphatidylation reaction. Both oleate-dependent and Arf-dependent PLD activities were significantly higher in the colon cancer tissue than normal colonic mucosa. The mean specific activity of oleate-dependent PLD) in colon cancers was 1.66 +/- 0.75 (SD) nmol/min/mg whereas the value for normal colonic mucosa was 0.18 +/- 0.09 nmol/min/mg (P < 0.01; Mann-Whitney U-test). On the other hand, the mean specific activity of Arf-dependent PLD in colon cancers was 76.36 +/- 29.37 pmol/min/mg whereas the value for normal colonic mucosa was 19.90 +/- 11.97 pmol/min/mg (P < 0.01; Mann-Whitney U-test). These results suggest that PLD is implicated in the proliferation and tumorigenesis of colon cancer. The present study provides the first evidence for the enhanced levels of two types of PLD in colon cancer and raises the possibility that these PLDs can be used as the potential target for the treatment of colon cancer.

1,2-Dimethylhydrazine↗
PubMed2001

Modulation of experimental colon tumorigenesis by types and amounts of dietary fatty acids.

Epidemiological studies and laboratory animal model assays suggest that a high intake of dietary fat promotes colorectal cancer. Several in vivo and in vitro studies support the hypothesis that omega-6 fatty acids promote colon tumorigenesis, whereas omega-3 fatty acids lack promoting activity. Fat intake in the United States traditionally includes high amounts (30% of total caloric intake) of saturated fat rather than omega-6 fatty acids. Therefore, the present study was designed to compare the modulatory effects of a high-fat diet containing mixed lipids (HFML), a diet rich in saturated fatty acids (the average American diet), a diet with fish oil (HFFO) that is rich in omega-3 fatty acids, and a low-fat corn oil diet (LFCO) on the formation of chemically induced colonic aberrant crypt foci (ACF) and tumors, cyclooxygenase (COX)-2 activity, and apoptosis during experimental colon carcinogenesis. At 5 weeks of age, groups of male F344 rats were fed a 5% corn oil diet (LFCO). At 7 weeks of age, rats intended for carcinogen treatment received s.c. injections of azoxymethane at a dose level of 15 mg/kg of body weight once weekly for 2 weeks. Beginning 1 day after the carcinogen treatment, groups of rats were then maintained on experimental diets containing 20% HFML or 20% HFFO. Rats were killed at 8, 23, or 38 weeks after azoxymethane treatment. Colonic ACF and tumors were evaluated histopathologically, and apoptosis was evaluated by the terminal deoxynucleotidyl transferase-mediated nick end labeling method. Colonic mucosae and tumor samples harvested at week 38 were analyzed for COX-2 synthetic activity and expression. The rats fed the HFML diet showed significantly increased total colonic ACF (P < 0.001-0.0001) with a multiplicity of > or = 4 aberrant crypts/focus (P < 0.0001) compared with the effects of the HFFO or LFCO diets at week 8, 23, and 38. Interestingly, there was a 2- to 3-fold increase (> or = 4) in multicrypt foci in rats given the HFML diet as compared with such foci in rats fed the HFFO or LFCO diets. By week 23, the HFML diet had significantly increased the incidence of colonic tumors (30-60%) and their multiplicity (100-141%) when compared with the effects of the LFCO or HFFO diets. At week 38, the HFML diet had induced 100% colon tumor incidence and a 4-fold multiplicity of adenocarcinomas compared with the LFCO and HFFO diets. At weeks 23 and 38, a significantly lower percentage of apoptotic colonic epithelial cells were observed in the tumors of animals fed the HFML diet as compared with those fed the HFFO diet. The HFML diet caused significantly increased levels of COX-2 activity in colon tumors (P < 0.05-0.01), and these tumors had enhanced levels of COX-2 expression as compared with those in assays with LFCO or HFFO diets. These observations demonstrate for the first time that HFML diets containing high levels of saturated fatty acids (such as those in Western diets) promote colon carcinogenesis. Although the mechanisms involved in colon tumor promotion by a HFML diet are not fully known, our results indicate that the modulation of eicosanoid production via the influence on COX activity and the suppression of apoptosis may play a key role in HFML diet-induced colon tumorigenesis.

Animals↗
PubMedDate not supplied

Regulation of the enteric nervous system in the colon of patients with slow transit constipation.

BACKGROUND/AIMS: The cause of impaired motility in patients with slow transit constipation is unknown. To clarify the physiological significance of cholinergic, adrenergic, non-adrenergic non-cholinergic inhibitory nerves in the colon of patients with slow transit constipation, we investigated the enteric nerve responses on lesional and normal bowel segments derived from patients with slow transit constipation and patients who underwent colon resection for colonic cancers. METHODOLOGY: Twenty preparations were taken from the lesional colon of 6 patients with slow transit constipation (2 men and 4 women, aged 23 to 68 years, with a mean age of 44.0 years). Thirty-six preparations were taken from the normal colon of 12 patients with colonic cancer (6 men and 6 women, aged 40 to 60 years, with a mean age of 52.2 years). A mechanographic technique was used to evaluate in vitro muscle responses to acetylcholine, adrenalin, electrical field stimulation of adrenergic and cholinergic nerves before and after treatment with various autonomic nerve blockers. RESULTS: The contraction reaction to acetylcholine in the colon with slow transit constipation was significantly weaker than in the normal colon (P < 0.01). The relaxation reaction to adrenalin in the colon with slow transit constipation was stronger than in the normal colon. The colon with slow transit constipation was more strongly innervated by non-adrenergic non-cholinergic inhibitory nerves than the normal colon, significantly (P < 0.05). CONCLUSIONS: These findings suggest that a decrease of cholinergic nerve and an increase of non-adrenergic non-cholinergic inhibitory nerve play an important role in the impaired motility observed in the colon of patients with slow transit constipation.

Acetylcholine↗
PubMed1992

Characterization of insulinlike growth factor I receptors in human colon cancer.

A possible role of insulinlike growth factor I (IGF-I) and IGF-I receptors in the proliferation of human colon cancer has, to the best of the authors' knowledge, not been examined as yet. To determine a role of IGF-I in colon cancer, several human colon cancer cell lines and colon cancers were screened for specific binding to 125I-IGF-I. Almost all the human colon cancer cells examined were variably positive for specifically binding 125I-IGF-I. Almost half the colon cancer cell lines examined showed significant growth response to 6.6 nmol/L IGF-I. Dose-dependent growth effects of exogenously added IGF-I (0.05-3.3 nmol/L) were shown in a representative human colon cancer cell line (Colo-205). To determine if IGF-I binding sites on colon cancer cells were similar or different from that described on other cells, the binding affinity, binding specificity, and molecular size of the IGF-I binding sites were characterized in representative human colon cancer cell lines (HCT-116 and Colo-205). The optimal binding assay conditions for measuring maximum number of 125I-IGF-I binding sites on the cells, in vitro, were determined and found to be similar to that described on other cells. Scatchard analysis of the specific binding data showed the presence of a single class of high-affinity binding sites [disassociation constant (Kd) = approximately 1.0-2.0 nmol/L], with a binding capacity of 1.0-2.0 x 10(5) sites per cell. The molecular weight of IGF-I receptors on cell membranes was determined by gel electrophoresis of the affinity cross-linked proteins, followed by autoradiography. A single band of binding proteins with a molecular mass of approximately 300 kilodaltons was evident under nonreducing conditions and separated out into two bands of approximately 240 and approximately 130 kilodaltons under reducing conditions. The 130-kilodalton band represents the alpha subunit of IGF-I receptors, and the 240-kilodalton band may represent aggregates of the receptor subunits that were not reduced completely. The widespread existence of high-affinity binding sites for IGF-I in established human colon cancer cell lines and freshly resected human colon cancers and the proliferative effect of IGF-I in several colon cancer cell lines, in vitro, reflect that IGF-I may be an important endocrine/paracrine/autocrine factor in the growth regulation of colon cancers in situ.

Cell Division↗
PubMed1991

Adenocarcinoma in the ascending colon of ACI strain rat foster bred by WF-Osaka female rat.

We now keep HFRSV free WF-Osaka rats and ACI rats together in the separate three animal rooms (animal room 1, 2 and 3) and the incidence of colon carcinoma is still high on the WF-Osaka rats in animal room 1 with the high humidity. Two female ACI rats developed colon carcinomas in the ascending colon. The gross and the histological appearance of the colon carcinoma were completely the same as those of WF-Osaka rats. ACI and WF-Osaka rat strain together have been kept bred in neighborhood of each other in different racks in the identical animal room 1. To obtain HFRSV free ACI rat strain, Antecedents born by cesarean section of ACI female pregnant rat were foster-bred by WF-Osaka female nursing rat incidentally, and at the fourth mating generation after the start of foster-breeding, they developed colon carcinomas at the age of four months. Before five out of eight F1 hybrids by WF-Osaka cancer carrying female rat x male ACI rat had developed the same colon carcinoma, but none of F1 hybrids by the contrary mating had developed colon carcinomas in this same animal room 1. Animal room 1 and 2 where there was a high incidence of colon carcinomas, had happened to be kept moistened. However, after disinfection of these animal rooms, the animal room 2 and 3 occurred to be kept dried, and rats of WF-Osaka strain ceased to develop colon carcinomas in the animal room 2. Thereafter, animal room 2 and 3 were adjusted to be kept moistened again. Subsequently WF-Osaka rats in the animal room 2 began to have colon carcinomas in the ascending colon as before, but none of rats developed colon carcinomas in the animal room 3. Based on these findings, we consider that milk factor at the time of foster-breeding played an important role first and high moistened condition of the animal room resulted in promoting effect on colon carcinogenesis on ACI rats and WF-Osaka rats as well.

Adenocarcinoma↗
PubMed2005

[Cell balance between apoptosis and proliferation in colon cancer and its correlation with prognosis].

BACKGROUND & OBJECTIVE: In normal tissues and organs, cell apoptosis and proliferation maintain a homeostasis. Alterations of this physiologic balance may lead to malignant transformation of cells and tumorigenesis. This study was to investigate cell balance (ratio of apoptosis index to proliferation index, AI/PI) in colon cancer and its correlation with prognosis. METHODS: The apoptotic population and the proliferating population of colon cancer cells were quantitatively analyzed by Sub-G1 method and Ki-67/DNA bivariate analysis of flow cytometry. Cell proliferation was observed under confocal microscope. Kaplan-Meier method and log-rank test were used to analyze patients' survival. RESULTS: AI/PI ratio of cells was significantly higher in normal colon tissue than in colon adenoma tissue, Dukes' A colon cancer, Dukes' B colon cancer, and Dukes' C and D colon cancer (0.45+/-0.19 vs. 0.30+/-0.07, 0.29+/-0.11, 0.28+/-0.10, and 0.26+/-0.07, respectively, P < 0.01). AI/PI ratio showed a down-regulating trend in variables tested including tumor size, pathologic type, differentiation grade, Dukes' stage, and nodal involvement. AI/PI ratio of peripheral lymphocytes was significantly higher in colon cancer patients than in healthy people (0.64+/-0.11 vs. 0.49+/-0.12, P < 0.01). The expression of Ki-67 was observed in normal colon tissue, colon adenoma, and colon cancer under confocal microscope. Survival rate of patients with AI/PI ratio of < 0.285 (using the median value as the cutoff) and >/= 0.285 was not significantly different (P> 0.05). CONCLUSIONS: Dysregulation (down-regulation or up-regulation) of cell balance between apoptosis and proliferation in colon cancer cells and lymphocytes might play an important role in tumorigenesis and tumor progression. AI/PI ratio can' t be used as a prognostic factor of colon cancer.

Adenocarcinoma↗
PubMed1991

Use of the lectin from Amaranthus caudatus as a histochemical probe of proliferating colonic epithelial cells.

A newly isolated lectin, Amaranthus caudatus agglutinin (also called amaranthin or ACA), which binds to the Thomsen-Friedenreich antigen (T-antigen) and its sialylated variants, was used as a histochemical probe for proliferating cells in sections of human colonic tissues. Binding inhibition studies revealed that ACA binds to different sites on histological sections when compared to peanut agglutinin, which also recognizes the T-antigen. ACA bound selectively to the cells at the base of the colonic crypt [46 +/- 4% (SEM) of glands] which is the zone of proliferation in this tissue and preferentially labeled cytoplasmic and apical membrane glycoconjugates. Only 7 +/- 2% of the upper portions of the colonic crypts were labeled (P less than 0.001 compared to the base), and this was largely a result of extensive labeling in 2 of 23 samples studies. A marked increase in histochemical labeling by ACA was seen in adenomatous polyps and adenocarcinomas of the colon, in which 82 +/- 7 and 97 +/- 2% of the glandular units were labeled, respectively. Transitional mucosa and connective tissue adjacent to cancers were also labeled by ACA. Neuraminidase studies indicated that removal of sialic acid residues enhanced binding by peanut agglutinin, but not ACA, to glycoconjugates in cancer specimens. Specimens of colonic tissue from patients with familial adenomatous polyposis (FAP) were examined with ACA; 83 +/- 7% of adenomatous glands and 60 +/- 7% of glands in flat, normal-appearing tissue were labeled. Colonic tissues from persons at 50% risk for hereditary nonpolyposis colorectal cancer (HNPCC), FAP, and normal colons were studied and given "weighted average" labelling scores that ranged from 0-400 to accommodate variable intensity and distribution of labeling. Normal colons had a weighted average score of 65 +/- 33; FAP tissues had a score of 224 +/- 76 (P less than 0.001 compared to normal colon) and HNPCC tissues had a score of 74 +/- 70 (P less than 0.05 compared to normal colon). A group of five HNPCC cases had scores of 203 +/- 43 (P less than 0.001 compared to normal colon). ACA labels glycoconjugates in the proliferative region of normal human colonic epithelium and neoplastic lesions of the colon. The results of FAP and HNPCC tissues suggest that it may be useful for identifying foci of abnormal proliferation in familial colorectal cancer syndromes.

Adenocarcinoma↗
PubMed1981

Campylobacter fetus ss. Jejuni, a newly recognized enteric pathogen: morphology and intestinal colonization.

Campylobacter fetus ss. jejuni has recently been recognized as a frequent enteric pathogen of man. Although long known as a significant pathogen of domestic animals, little is known regarding mechanisms of colonization and pathogenesis. In an effort to study the colonization and morphology of this organism, we used scanning electron microscopy to examine ilea and colons from mice in which a human isolate of C. fetus ss. jejuni had been inoculated. When inoculated into the ileum of the mice, a transient colonization was observed by 24 hours and had disappeared by 48 hours. Colonization of the colon first appeared at 48 hours and persisted at least three weeks. When inoculated directly into the colon, colonization appeared within 24 hours in the colon and persisted at least 16 days. Severe colonic necrosis and mucosal degeneration were observed in colons only in those mice which were inoculated via the colon. In the infected colons, the C. fetus ss. jejuni organisms were enmeshed in a fibrous network which may play a role in the attachment of bacteria to the mucosal surface. Differences between the morphology of C. fetus ss. jejuni in the mouse model and that found in pure culture were observed and may represent distinct tissue and culture phases of growth.

Animals↗
PubMed1993

[Screening of principal enzymes involved in the metabolism of anticancer drugs in human and murine colonic tumors].

Since drug-metabolizing enzymes may influence the toxic response of tissues or organs to drugs, we studied their expression in human and colon tumor tissues, in an attempt to find new targets for chemotherapy and also to explain the intrinsic drug-insensitivity of most colon tumors to anticancer drugs. In the present work, we compared human colorectal tumors and peritumoral tissues to a mouse colorectal tumor (Co38) and normal murine colon with regard to their main drug-metabolizing enzyme systems. We investigated cytochromes P-450 (1A1/1A2, 2B1/B2, 2C, 2E1, 3A) and epoxide hydrolase (EH) by immunoblotting. Total glutathione (GSH) and the activities of the following enzymes: total GST, selenium-independent glutathione peroxidase (GPX), 1,2-dichloro-4-nitrobenzene-GST (DCNB-GST), ethacrynic acid-GST (EA-GST), UDP-glucuronosyltransferase 1 (UDPGT), beta-glucuronidase (beta G), sulfotransferase (ST) and sulfatase (S) were investigated by fluorometric and spectrophotometric assays. Results obtained by immunoblotting showed that mouse colon tumor Co38 did not express any of the probed cytochromes P-450, whereas human tumors showed the presence of cytochrome P-450 3A. EH was not expressed in either mouse colon tumor Co38 or normal mouse colon, whereas it was expressed in human peritumoral and tumoral colon tissues at similar levels. GPX and EA-GST were detected in all tumoral and non tumoral tissues of both species. DCNB-GST was expressed in all murine tissues investigated, but was not found in human tissues. For human peritumoral and tumoral colorectal tissues there was no significant difference between GST isoenzymes levels, whereas mouse colon tumor Co38 had a lower expression of DCNB-GST and EA-GST compared to normal mouse colon. No significant difference was observed between human tumors and peritumoral tissues for total GST, UDPGT1, beta G, ST and S activities. For murine colon tissues, the conjugation pathways (total GST, UDPGT1 and ST) were lower in Co38, whereas the opposite was observed for the hydrolytic enzymes (beta G and S). In conclusion, despite similarities between human and murine colon tumors, mouse colon tumor Co38 appears different from human colon tumors for many drug-metabolizing enzyme systems. These interspecies differences may have implications with regard to drug screening methodologies and preclinical evaluation of candidate anticancer drugs useful in the chemotherapy of human colorectal tumors.

Aged↗
PubMedDate not supplied

Differential activation of total and EGF receptor (EGF-R) tyrosine kinase (tyr-k) in the rectal mucosa in patients with adenomatous polyps, ulcerative colitis and colon cancer.

BACKGROUND/AIMS: Tyrosine kinase and a number of growth factors, especially EGF and TGF-alpha are known to stimulate proliferation in much of the gastrointestinal tract, including colon. In humans increased colonic mucosal proliferative activity has been observed in numerous premalignant lesions including adenomatous polyps and ulcerative colitis. The aim of the present study was to determine the differences of proliferative patterns in patients with adenomatous polyps, ulcerative colitis and colonic adenocarcinoma as reflected by rectal mucosa tyrosine kinase, EGF receptor tyrosine kinase and PCNA and to evaluate the role of tyr-k in colonic mucosal cell proliferation during carcinogenic process. MATERIALS AND METHODS: The study population comprised 40 patients, aged 17-74 years (mean 57), in which 10 patients had adenomatous polyps, 10-ulcerative colitis in remission phase, 10- colon adenocarcinoma and 10 healthy controls. After informed consent 6-8 rectal mucosal biopsy specimen were obtained at 10 cm from the anal verge at the beginning of the colonoscopy examination and at least 10 cm away from any macroscopic mucosal changes. RESULTS: Mean PCNA labeling indices in patients with colon adenocarcinoma, adenomatous polyps, ulcerative colitis ulcerosa and healthy controls were respectively: 27.6% +/- 5.75; 12.18% +/- 6.76; 10.9% +/- 5.34 and 1.5% +/- 0.97. PCNA labeling index in rectal mucosa of patients with adenomatous polyps, ulcerative colitis and colon cancer was significantly higher (p < 0.01) than in the control group. An upward expansion of the proliferative compartment was also observed in patients with premalignant and malignant colon conditions as regards to the control group. Total tyrosine kinase activity in the rectal mucosa of patients with polyps was elevated by 219%, with ulcerative colitis by 224% and with colorectal carcinoma by 600% as regards to the control group. EGF receptor tyrosine kinase was increased in colonic mucosa by 35.2% in patients with adenomatous polyps, by 40.6% in patients with ulcerative colitis and by 123% in patients with colon cancer. CONCLUSIONS: Increased values of this enzyme in the above mentioned group of patients may suggest that tyrosine phosphorylation represents an early sign of colonic mucosa susceptibility for cancer development. We conclude, that overall an EGF receptor-associated tyrosine kinase plays an important role in the development of hyperproliferative state of the colonic mucosa and colon carcinogenesis.

Adenocarcinoma↗
PubMed1990

Low diacylglycerol values in colonic adenomas and colorectal cancer.

The biochemical events that make colonic epithelial cells proceed along the adenoma-carcinoma sequence are not well understood. The phosphoinositol signal transduction pathway is involved in the regulation of cell growth and differentiation. To determine its role in colonic neoplasias we performed mass measurements of its second messenger sn-1,2-diacylglycerol in biopsy specimens from normal mucosa and neoplasias of the colon. Normal colonic mucosa was also investigated in patients without colonic abnormalities (n = 10). Compared with pooled diacylglycerol values from five colonic sites (100%), values in patients with a normal colon were highest in the ascending colon (120 (5)%, p less than 0.05) and lowest in the rectum (81 (5)%, p less than 0.01). Absolute diacylglycerol values in patients with normal colons (2.62 (0.16) nmol/mg protein) were not significantly different from those found in the normal mucosa of patients with colorectal neoplasias (2.45 (0.17) nmol/mg protein). Both colonic adenomas (n = 15) and colorectal carcinomas (n = 14) showed significantly decreased diacylglycerol values compared with the adjacent normal mucosa of each patient (72 (4)%, p less than 0.001, and 71 (4)%, p less than 0.001 respectively). The appreciable decrease in mass diacylglycerol values clearly distinguishes adenomas and carcinomas of the colon from the surrounding normal mucosa. This finding suggests that profound metabolic changes of the phosphoinositol signal transduction pathway occur early in the adenoma-carcinoma sequence and may be important in colonic carcinogenesis.

Adenocarcinoma↗
PubMed2003

Colonization of lower respiratory tract with anaerobic bacteria in mechanically ventilated patients.

OBJECTIVE: To study lower respiratory tract colonization by anaerobic bacteria in ICU patients on prolonged mechanical ventilation using two types of protected tracheal sampling methods. DESIGN AND SETTING: Prospective clinical investigation in the intensive care unit of a university hospital. PATIENTS: Twenty-six consecutive patients mechanically ventilated within 24 h after their admission in ICU and with expected duration of mechanical ventilation longer than 7 days. MEASUREMENTS AND RESULTS: Two types of protected tracheal sampling methods were obtained without the use of bronchoscopic guidance on the day following intubation and twice a week until extubation: protected tracheal aspiration and protected tracheal specimen brush. Specific methods for anaerobic isolation were used. Early colonization was defined if colonization occurred within the first 5 days after intubation. Of the 26 patients studied 22 were colonized by at least one bacterial strain. Twenty-one patients were colonized by aerobic and 15 by anaerobic bacteria. Twenty-eight anaerobic strains were identified, with bacterial counts higher than 10(3) cfu/ml in 11 cases. Of the 15 patients colonized by anaerobes 14 were also colonized by aerobic bacteria. The use of protected specimens ruled out oropharyngeal contamination. Early onset colonization occurred in 16 of 22 patients colonized by aerobes and in 8 of 15 patients colonized by anaerobes. Five patients developed ventilatory-acquired pneumonia following colonization (by anaerobic bacteria in two cases). In eight patients colonization by anaerobic bacteria occurred despite antimicrobial therapy. CONCLUSIONS: These results show that anaerobic bacteria frequently colonize the lower respiratory tract of mechanically ventilated patients and underline the potential importance of the anaerobic bacteria in ventilatory acquired pneumonia.

Anti-Bacterial Agents↗
PubMed1990

Pulmonary function and clinical course in patients with cystic fibrosis after pulmonary colonization with Pseudomonas aeruginosa.

To evaluate the relationship between Pseudomonas aeruginosa colonization and the development of lung disease, we studied 895 patients who attended our cystic fibrosis clinic between 1975 and 1988. The prevalence of P. aeruginosa colonization was 82%. Patients who acquired P. aeruginosa in the first year of life had a similar 10-year survival rate (85%) to that in patients who were colonized between the ages of 1 and 7 years (87%), and to that in patients colonized after the age of 7 years (78%). One year before colonization, mean age, forced expiratory volume in 1 second (FEV1), forced vital capacity, and forced expiratory flow in the mid-expiratory phase were similar to those in a group of patients who remained free of P. aeruginosa. No significant change in pulmonary function variables could be demonstrated 1 year and 2 years after the colonization. The rate and duration of hospitalization did not increase in the years after P. aeruginosa colonization compared with the years before colonization. By the age of 7 years, the mean percentage of predicted FEV1 was lower by 10% in patients who were already colonized by P. aeruginosa compared with those who were not colonized (p less than 0.01). A similar reduction in FEV1 was observed at all ages from 7 to 35 years, but no precipitate rate of decline in FEV1 could be associated with P. aeruginosa colonization. We conclude that although P. aeruginosa colonization is associated with 10% lower lung function, it does not cause an immediate and rapid reduction, as has been previously reported. The clinical course and the pulmonary deterioration in cystic fibrosis after P. aeruginosa colonization is a gradual and variable process.

Adolescent↗
PubMed1987

Recognition and treatment of patients with hereditary nonpolyposis colon cancer (Lynch syndromes I and II).

Primary genetic factors are etiologic in at least 5-10% of patients with colon cancer. The polyposis syndromes (FPC) are easily identified examples because of the spectacular number of polyps. The hereditary nonpolyposis syndromes (HNPCC), although five times more common than FPC, are usually not recognized because they do not have such a distinctive clinical, premonitory genetic marker. Colorectal cancer expression was surveyed in 10 extended, thoroughly documented HNPCC kindreds. One hundred sixteen patients were found to have 183 colorectal cancers. Despite the striking family history, less than 5% were correctly treated by subtotal colectomy. This provided a unique opportunity to study the natural history. Five findings differed significantly (p less than 0.05) from patients with sporadic colon cancer: (1) mean age of initial colon cancer diagnosed was 45.6 years; (2) 69.1% of first colon cancers were located proximal to the splenic flexure of the colon; (3) 18.1% had synchronous colon cancer; (4) 24.2% had metachronous colon cancer develop with life table analysis showing the risk for a metachronous lesion at 10 years to be 40%; and (5) only 23.3% of cancers were located in the sigmoid colon or rectum. Based on this data, it is recommended that the family history of all patients with a newly diagnosed colon cancer be evaluated for evidence of this syndrome. If an autosomal dominant inheritance pattern emerges, an in-depth genetic investigation is indicated. When HNPCC is confirmed, the following recommendations apply: a subtotal abdominal colectomy is indicated at the time of the initial colon cancer because of the risk of synchronous and metachronous lesions. The rectum should be spared in favor of careful lifetime surveillance because of the proclivity for proximal colon cancer involvement. As yet unaffected members of a newly diagnosed HNPCC kindred who are in the "direct genetic line" should be cautioned that they are at 50% risk and must begin an intensive surveillance program beginning in the third decade with careful attention to the right colon. Patients from newly diagnosed HNPCC families who have had a previous conventional colectomy for colon cancer should, at the very least, enter an intensive surveillance program; a prophylactic completion subtotal colectomy should be considered for patients who are less than totally compliant.

Adolescent↗
PubMed1990

Risk factors for Pseudomonas aeruginosa colonization in cystic fibrosis patients.

In an attempt to study the association between Pseudomonas aeruginosa colonization and clinical factors present before colonization, we studied 502 patients who attended our cystic fibrosis (CF) clinic between 1975 and 1988 and who were not colonized with P. aeruginosa before the study period. Twelve percent of the patients became colonized with P. aeruginosa before the age of 1 year and 44% by the age of 7 years. In a birth cohort followed from diagnosis during the study period, 23% were colonized with P. aeruginosa before age 1 year and 67% before age 7 years. Early P. aeruginosa colonization was associated with early diagnosis of CF. Presence of meconium ileus, gastrointestinal symptoms and pancreatic insufficiency at the time of diagnosis was also associated with early colonization. There was no association between the presence of respiratory symptoms at the time of diagnosis and age at first P. aeruginosa colonization. In families in which more than one sibling had CF, the age of P. aeruginosa acquisition was similar in the first colonized and the subsequently colonized siblings. In the year before the colonization patients with P. aeruginosa who were older than 1 year had higher rates of hospitalization and spent more days in hospital compared with patients without P. aeruginosa. In conclusion most P. aeruginosa colonization occurs at a younger age than previously reported. Early age at diagnosis and presence of CF-associated gastrointestinal abnormalities increase the likelihood of earlier colonization of P. aeruginosa.

Age Factors↗
PubMed2006

Patterns of fungal colonization in preterm infants weighing less than 1000 grams at birth.

BACKGROUND: Colonization with Candida spp. is an important risk factor for systemic infection in very low birth weight (VLBW; <1500 g) and extremely low birth weight (ELBW, <1000 g) infants. ELBW infants are at a higher risk than VLBW infants for fungal sepsis and its associated mortality, but few studies have examined fungal colonization exclusively in ELBW infants. METHODS: Fungal colonization data were analyzed retrospectively in 50 high risk ELBW infants. Weekly surveillance fungal cultures of the skin, gastrointestinal tract, respiratory tract and umbilicus had been performed from birth through the first 6 weeks of life. Colonization was analyzed for time of initial colonization, site, species and spread of Candida from one site to another. RESULTS: Candida was isolated from surveillance cultures in 31 of 50 (62%) infants. Colonization was inversely proportional to gestational age. Initial week of both the fungal colonization of the skin [1 (0-6) week, median (range)] and gastrointestinal tract [2 (0-6)] preceded colonization of the respiratory tract [3 (1-6)] (P = 0.0001). Among infants colonized by only 1 of the species, colonization at 2 or more sites occurred similarly with Candida albicans (77%) and Candida parapsilosis (85%), whereas colonization at 3 or more sites occurred more frequently with C. albicans (69%) compared with C. parapsilosis (23%) (P = 0.047). CONCLUSIONS: Fungal colonization occurs on the skin and gastrointestinal tract before the respiratory tract. In addition, C. albicans is more likely than C. parapsilosis to colonize multiple sites.

Antifungal Agents↗
PubMed2003

Amylase-binding proteins A (AbpA) and B (AbpB) differentially affect colonization of rats' teeth by Streptococcus gordonii.

Streptococcus gordonii produces two alpha-amylase-binding proteins, AbpA and AbpB, that have been extensively studied in vitro. Little is known, however, about their significance in oral colonization and cariogenicity (virulence). To clarify these issues, weanling specific pathogen-free Osborne-Mendel rats, TAN : SPFOM(OM)BR, were inoculated either with wild-type strains FAS4-S or Challis-S or with strains having isogenic mutations of abpA, abpB, or both, to compare their colonization abilities and persistence on the teeth. Experiments were done with rats fed a sucrose-rich diet containing low amounts of starch or containing only starch. The mutants and wild-types were quantified in vivo and carious lesions were scored. In 11 experiments, S. gordonii was a prolific colonizer of the teeth when rats were fed the sucrose (with low starch)-supplemented diet, often dominating the flora. Sucrose-fed rats had several-fold higher recoveries of inoculants than those eating the sucrose-free, starch-supplemented diet, regardless of inoculant type. The strain defective in AbpB could not colonize teeth of starch-only-eating rats, but could colonize rats if sucrose was added to the diet. Strains defective in AbpA surprisingly colonized better than their wild-types. A double mutant deficient in both AbpA and AbpB (abpA/abpB) colonized like its wild-type. Wild-types FAS4-S and Challis-S had no more than marginal cariogenicity. Notably, in the absence of AbpA, cariogenicity was slightly augmented. Both the rescue of colonization by the AbpB- mutant and the augmentation of colonization by AbpA- mutant in the presence of dietary sucrose suggested additional amylase-binding protein interactions relevant to colonization. Glucosyltransferase activity was greater in mutants defective in abpA and modestly increased in the abpB mutant. It was concluded that AbpB is required for colonization of teeth of starch-eating rats and its deletion is partially masked if rats eat a sucrose-starch diet. AbpA appears to inhibit colonization of the plaque biofilm in vivo. This unexpected effect in vivo may be associated with interaction of AbpA with glucosyltransferase or with other colonization factors of these cells. These data illustrate that the complex nature of the oral environment may not be adequately modelled by in vitro systems.

Animals↗
PubMed1994

Colonization and infection with antibiotic-resistant bacteria in a long-term care facility.

OBJECTIVE: To assess colonization and infection with methicillin-resistant Staphylococcus aureus (MRSA), high-level gentamicin-resistant enterococci (R-ENT) and gentamicin and/or ceftriaxone-resistant Gram-negative bacilli (R-GNB) and the factors that are associated with colonization and infection with these organisms. DESIGN: Monthly surveillance for colonization and infection over a period of 2 years. In the second year, an intervention to decrease MRSA colonization by the use of mupirocin ointment was carried out. SETTING: Long-term care facility attached to an acute care Veterans Affairs Medical Center. PATIENTS: A total of 551 patients in the facility were followed for a period of 2 years. MEASUREMENTS: Colonization and infection rates with MRSA, R-ENT, and R-GNB. Analysis of risk factors associated with colonization and infection with these three groups of organisms. MAIN RESULTS: In the first year, colonization rates were highest for MRSA (22.7 +/- 1% patients colonized each month) and R-ENT (20.2 +/- 1%) and lower for R-GNB (12.6 +/- 1%). After introduction of decolonization of nares and wounds with mupirocin, the rate of MRSA colonization fell significantly to 11.5 +/- 1.8%, but rates remained unchanged for R-ENT and R-GNB. Risk factors for MRSA colonization included the presence of wounds and decubitus ulcers. For R-ENT, the presence of wounds, renal failure, intermittent urethral catheterization, low serum albumin, and poor functional level were significant. For R-GNB, intermittent urethral catheterization, chronic renal disease, inflammatory bowel disease, presence of wounds, and prior pneumonia were significantly associated with colonization. Overall, of infections caused by known organisms, 49.6% were due to MRSA, R-ENT, or R-GNB, and 50.4% were due to susceptible organisms. Infections were more commonly due to R-GNB (21.1% of all infections) than to R-ENT (8.3%) or MRSA (4.6%). The most common infections were urinary tract infections (42.9% of all infections) and skin and soft tissue infections (31.9% of all infections). Risk factors for MRSA infections were diabetes mellitus and peripheral vascular disease, for R-GNB infections were intermittent urethral catheterization and indwelling urethral catheters, and no one factor was associated with R-ENT infection. CONCLUSIONS: In our long-term care facility, colonization with resistant MRSA and R-ENT was more common than R-GNB, but infections were more often due to R-GNB than R-ENT and MRSA. Several host factors, which potentially could be modified in order to prevent infections, emerged as important in colonization and infection with these antibiotic-resistant organisms.

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