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PubMedDate not supplied

Peptidergic nerves in the colon of patients with ulcerative colitis.

BACKGROUND/AIMS: The cause of impaired motility, such as diarrhea and toxic megacolon, in patients with ulcerative colitis is unknown. Neuropeptides have recently been shown to be a neurotransmitter in the non-adrenergic non-cholinergic inhibitory and excitatory nerves in the human gut. To clarify the physiological significance of vasoactive intestinal polypeptide, substance P and neurotensin in the colon of patients with ulcerative colitis, we investigated the enteric nerve responses on lesional and normal bowel segments derived from patients with ulcerative colitis and patients who underwent colon resection for colonic cancers. METHODOLOGY: Twenty-four specimens were obtained from the lesional colon of 6 patients with ulcerative colitis (4 male, 2 female; ages 14-51 years, mean: 40.3 years). The patients with ulcerative colitis had chronic disease (4 with moderate disease, 2 with severe disease). Seventy-two specimens were obtained from the normal colon of 10 patients with colonic cancer (8 men and 2 women; ages 40-56 years, mean: 51.2 years). A mechanographic technique was used to evaluate in vitro muscle responses to these peptides of adrenergic and cholinergic nerves before and after treatment with various autonomic nerve blockers. RESULTS: (1) Peptidergic nerves such as vasoactive intestinal polypeptide, substance P, and neurotensin nerves were found to act on both normal colon and ulcerative colitis colon; (2) the colon with ulcerative colitis was more strongly innervated by vasoactive intestinal polypeptide nerves than the normal colon; (3) Substance P and neurotensin nerves act more weakly in the UC colon that the normal colon. CONCLUSIONS: These findings suggest that peptidergic nerves play an important role in the impaired motility observed in patients with UC.

Adolescent↗
PubMed2001

Nizatidine enhances the gastrocolonic response and the colonic peristaltic reflex in humans.

Animal studies demonstrate that nizatidine, an H2-receptor inhibitor, may enhance colonic activity independent of its effect on acid secretion. The effect of nizatidine on human colonic motility is unknown. We evaluated the potential prokinetic property of nizatidine in 12 healthy subjects (10 men and 2 women, age 21-46 years). Each subject received either nizatidine (600 mg), famotidine (80 mg, a H2-receptor inhibitor used as a control), or a placebo, on separate days in randomized order at least 3 days apart. Following an overnight fast, a three-lumen catheter fitted with a stimulus balloon and two barostat bags was placed in the descending colon. The gastrocolonic response was tested by antral balloon inflation and the colonic peristaltic reflex was evaluated by colonic distension. Changes in colonic motility were assessed by volume changes in the barostat bags. Antral distension evoked volume-dependent increases in colonic motility, maximal at a 300-ml inflation, as demonstrated by a reduced bag volume. Nizatidine enhanced colonic motility in response to antral distension at 200 and 300 ml, compared with famotidine and placebo. Colonic distension evoked volume-dependent increases in colonic motility proximal to the stimulus balloon. Compared with famotidine and placebo, nizatidine enhanced the ascending and descending contractile limbs of the peristaltic reflex but did not affect relaxation distal to the balloon. In conclusion, nizatidine enhanced the gastrocolonic response and the colonic peristaltic reflex in healthy subjects. Further research on the prokinetic action of nizatidine in the colon may lead to novel treatments for idiopathic constipation.

Adult↗
PubMed2002

Down-regulation of PLK3 gene expression by types and amount of dietary fat in rat colon tumors.

Epidemiological studies suggest that high intake of dietary fat rich in saturated fatty acids increases the colon cancer risk whereas dietary fish oil high in omega-3 fatty acids reduces the colon cancer risk. Previously, we reported that consumption of omega-6 fatty acid rich diets such as corn oil strongly promotes azoxymethane (AOM)-induced colon carcinogenesis in rats as compared to ingestion of a diet with equivalent amount of fat containing fish oil (HFFO) or low-fat diet (LFCO). Expression of PLK3 (Polo-like kinase-3, previously named Prk) is negatively correlated with the development of certain cancers. Ectopic expression of human PLK3 results in cell cycle arrest or induces apoptosis. To understand the role of PLK3 in colon carcinogenesis and to study the effect of types and amount of dietary fat on the expression levels of PLK3 in colon tumors, we analyzed the colon tumors and mucosa of rats administered the diets containing fish oil and corn oil for PLK mRNA expression. Here we report that expression of PLK3 was down-regulated in rat colon tumors. Quantitative polymerase chain reaction demonstrated that PLK3 mRNA levels were significantly lower in carcinogen (azoxymethane)-induced rat colon tumors than their uninvolved normal colonic mucosa. Among the normal mucosa isolated from rats fed on diets with various levels of fat (LFCO, or high fat diet with corn oil, HFCO, or supplemented with fish oil, HFFO), no significant changes in PLK3 mRNA expression was detected. Tumors isolated from rats fed with HFCO diet contained a very low level of PLK3 mRNA expression. Interestingly, tumors from rats fed the HFFO diet did not exhibit as dramatic down-regulation of PLK3 as the tumors of animals fed the HFCO diet. Furthermore, our results also indicate that the ectopic expression of a kinase active PLK3 construct induced apoptosis in HT-29 colon carcinoma cells. These observations suggest for the first time that a decreased activity of PLK3 may play a key role in colon tumor development as well as in HFCO-induced colon tumorigenesis.

Animals↗
PubMed1991

[A case of a right-sided sigmoid colon].

During dissecting practice by students at Chiba University in 1991, a rare anomaly was found in a cadaver of a 50-year-old Japanese male. The distal part of the colon, including the sigmoid colon, was excessively long and formed a loop behind the ascending colon. This anomalous colon consisted of four parts. The first part began in the left iliac fossa and passed across the lower posterior abdominal wall into the right iliac fossa; the second turned upward and ascended along the posterior surface of the ascending colon to the inferior surface of the right lobe of the liver; the third turned backward and descended to the right iliac fossa and was in contact with the posterior abdominal wall; the fourth curved medially and downward and ended in the rectum at the median line. Only the anterior surface of the anomalous colon was covered with the peritoneum, and its mesocolon was not found. The inferior mesenteric artery gave off four branches toward the distal three-fourths of the excessively long colon and the superior rectal artery to the upper part of the rectum. Since it did not directly give off any branches toward the descending colon and the first part of the anomalous colon (these portions were supplied by a marginal artery), the branch supplying the second part was considered to be equivalent to the left colic artery. Thus, the proximal half of the long colon (parts 1 and 2) can be regarded as a part of the descending colon, and the distal half as the sigmoid colon.(ABSTRACT TRUNCATED AT 250 WORDS)

Colon, Sigmoid↗
PubMed1981

Effect of volatile fatty acids on blood flow and oxygen uptake by the dog colon.

The effects of volatile fatty acids on colonic hemodynamics and oxygen uptake were examined in a denervated autoperfused dog colon preparation. While measuring arterial pressure, colonic blood flow, venous pressure, and arteriovenous O2 difference, a Tyrode's solution containing acetic (75 mM), propionic (30 mM), and butyric acids (30 mM) was placed into the colon lumen. The volatile fatty acid mixture increased colonic blood flow (23.5%) and oxygen uptake (18.4%), yet did not affect oxygen extraction. Of the three fatty acids, only acetic acid (75 mM) could mimic the effects of the entire mixture on colonic hemodynamics and oxygen uptake. Butyric (30 mM) and propionic (30 mM) acids were without appreciable effects on colonic blood flow and oxygen uptake. The vehicle for the volatile fatty acids, Tyrode's did not alter blood flow, yet increased colonic oxygen uptake (18.7%) through an increase in oxygen extraction (18.3%). When compared with Tyrode's, acetic acid increased blood flow, yet did not alter oxygen uptake, while butyric and propionic acids did not alter colonic blood flow, yet inhibited colonic oxygen uptake. Close intraarterial infusion of acetic acid increased colonic blood flow and oxygen uptake. These data suggest that physiologic concentrations of volatile fatty acids (particularly acetic acid) significantly alter colonic flow.

Acetates↗
PubMed1981

Electromyogram of rabbit colon and cecum in vitro.

The rabbit colon is unique in that the proximal colon has taenia coli, but the distal colon has none. Electromyograms were studied from the mucosal and serosal sides of the proximal (taenial) and distal (nontaenial) rabbit colon and cecum. In the proximal colon, similar electromyograms could be obtained from either the mucosal (circular muscle) or serosal (taenia coli) side. Spike bursts occurred in 18.6% of slow waves from the serosal side; however, there were none from the mucosal side. Unlike the proximal colon, the serosal side of the distal colon gave a better electromyographic recording which showed electrical silent periods and variable amplitudes of slow waves. Recordings could also be obtained equally well from both the mucosal and serosal sides of the rabbit cecum. Acetylcholine significantly increased (p less than 0.05) the percentage of slow waves with spikes in taenial colon and the electrical active period in nontaenial colon, whereas atropine, phenylephrine, isoproterenol, and tetrodotoxin produced a significant decrease (p less than 0.05). This study showed that the electromyograms of the rabbit colon and cecum were complex. Although differences existed between the taenial and nontaenial colon, they exhibited similar responses to some autonomic drugs. Furthermore, recordings could be obtained from both sides of the proximal colon and cecum.

Acetylcholine↗
PubMed1995

A study of the safety and clinical efficacy of flexible sigmoidoscopy and colonoscopy after recent colonic surgery in 52 patients.

OBJECTIVE: Our objective was to evaluate the safety of lower endoscopy after colonic surgery, which has been unstudied and unknown. Endoscopy could promote suture breakdown at sites of colonic anastomoses, ostia, or repair by colonic abrasion or stretch from endoscopic intubation, torque, and insufflation. METHODS: Risks versus benefits of lower endoscopy performed within 3 wk of colonic surgery were retrospectively analyzed at five medical centers in 36 patients undergoing sigmoidoscopy and 72 age-and-sex-matched controls, and in 16 patients undergoing colonoscopy and 32 age-and-sex-matched controls. RESULTS: Sigmoidoscopy indications included rectal bleeding in 14, distal colonic obstruction in 12, and other in 10. Sigmoidoscopy provided the diagnosis in 18 (54%) of 33 cases (excluding three therapeutic sigmoidoscopies, control rate = 30%, p < 0.01, X2, including colon cancer in six and benign stricture in five. Sigmoidoscopy led to colonic surgery in nine and medical therapy changes in four. Colonoscopy indications included colonic bleeding in seven, colonic obstruction in five, and other in four. Colonoscopy provided the diagnosis in nine (56%, control rate = 56%, NS, X2). Colonoscopy led to colonic surgery in three and chemotherapy in one. Two endoscopic complications, unrelated to suture breakdown, occurred: An acutely ill patient developed hypotension during sigmoidoscopy which resolved with intravenous fluid resuscitation. A contained sigmoid diverticular perforation became a free perforation (requiring laparotomy) after colonoscopy. Both control groups had no endoscopic complications (NS, Fisher's exact test). CONCLUSION: In this study, the benefits outweighed the risks of postoperative sigmoidoscopy and colonoscopy. Clinicians should use discretion and perform colonoscopy or sigmoidoscopy after colonic surgery, particularly bowel anastomosis, only for clinically important indications. Endoscopy is contraindicated when colonic wound dehiscence or bowel perforation is suspected.

Colon↗
PubMedDate not supplied

Reduced nonspecific steroidal esterase activity in human malignant tumor tissue from liver, colon and breast when compared to peritumoral and normal tissue levels.

The levels of a nonspecific steroidal esterase estimated as alpha naphthyl acetate esterase (ANAE) activity were measured in apparently normal (peritumoral) tissue of liver, colon and breast cancer patients, in malignant tumor tissue from the same patients and in normal colon tissue from healthy individuals who never had colon cancer. Cancer tissue from all three organs showed 35-79% reduced levels of ANAE activity when compared to peritumoral tissue of the same organ (p < 0.03). When ANAE activity of normal colon tissue from healthy individuals who never had colon cancer was compared with peritumoral colon tissue from colon cancer patients, which were combined with colonic biopsies from cancer-free patients previously operated on for colon cancer, a 50% reduced ANAE activity was observed in these tissues compared to the normal (p < 0.005). A highly significant reduction of enzyme activity was also found when malignant colon tissue from the cancer patients was compared to normal colon tissue from healthy individuals who never had colon cancer.

Adenocarcinoma↗
PubMed1996

The capability of rat colon tissue slices to metabolize the cooked-food carcinogen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine.

A major target tissue for carcinogenesis from the cooked-food carcinogen 2-amino-l-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) in rodents is the colon, yet the role of colon metabolism on the carcinogenicity of PhIP is not clearly understood. The mutagenic potency of PhIP is highly dependent upon cytochrome P450 N-hydroxylation. In the present study, the ability of rat colon tissue to activate PhIP to a mutagen was investigated in Salmonella typhimurium (strains TA98 and YGI024) and rat colon tissue slices. In the Ames/Salmonella assay, using rat colon S9 as the activating system, no mutations were evident from bacteria exposed to PhIP at any concentration tested. However, mutations were observed when bacteria were exposed to 2-aminoanthracene (2AA) and colon S9, indicating sufficient P450 activity in the S9 to activate 2AA but not PhIP. In rat colon slice preparations, the sulfotransferase and acetyltransferase inhibitors pentachlorophenol (PCP) and 2,6-dichloro-4-nitrophenol (DCNP) were used to modulate DNA adduct and metabolite formation. Incubations of 3-methylcholanthrene-induced colon slices dosed with 50 microMolar [(3)H]PhIP produced no detectable metabolites. However, incubations of uninduced slices exposed to 10 microMolar of the reactive intermediate, [(3)H]2-(hydroxyamino)-l-methyl-6-phenylimidazo[4,5-b]pyridine (N-hydroxy-PhIP), produced a single detectable metabolite, a glucuronide conjugate of N-hydroxy-PhIP. This metabolite decreased when PCP or DCNP was added to the incubation medium. DNA adducts were detected in colon slices exposed to N-hydroxy-PhIP at approximately 33 adducts/10(7) nucleotides. Interestingly, when PCP was added to the incubation mixture, an increase in DNA adduct levels was detected, whereas DCNP produced a decrease in adducts. Because these inhibitors are thought to have similar mechanisms with regard to sulfotransferase inhibition, the inverse relationship in DNA adduct levels due to PCP or DCNP treatment is at present unexplainable. The formation of DNA adducts and metabolites from colon slices exposed to N-hydroxy-PhIP but not PhIP implies that there is insufficient P450 activity in the rat colon to activate PhIP to hydroxylated metabolites, suggesting that the rat colon is a site of Phase II metabolism for PhIP and that the liver is the primary source for hydroxylation.

Animals↗
PubMed1996

The deleted in colon cancer (DCC) gene is consistently expressed in colorectal cancers and metastases.

The DCC (deleted in colorectal cancer) gene was originally identified as a candidate tumour suppressor gene in colon carcinogenesis on the basis of allelic losses in chromosome 18q.21 in 70% of colon cancers. Reverse transcriptase polymerase chain reaction (RT-PCR) of DCC mRNA suggests that DCC expression may also be reduced in colon cancers. We have used monoclonal antibodies generated against the DCC immunoglobulin-like domain to investigate DCC isoforms and DCC protein expression during colon cancer progression. Normal mucosa and colonic tumour specimens representative of the range of colonic tumour progression from benign adenomatous polyps to metastases were compared by Western blot analyses. We show that while M(r) 194 000 DCC is present in normal colonic mucosa and adenomatous polyps, it is also similarly expressed in colorectal carcinomas and colonic metastases in the liver. The presence of DCC protein is consistent with the presence of DCC mRNA transcripts in the same tissue specimens. Notably DCC was not completely lost in any colonic tumour specimens examined, even those that had progressed to metastatic cancers. Quantitation of DCC protein expression in tissue specimens by densitometry demonstrated that both normal and malignant specimens exhibit a wide range of DCC protein levels and there was no significant correlation between diminished DCC protein expression and colon cancer progression. These results demonstrate the pattern of expression of the DCC gene product in colonic tumour progression and show that absence of DCC expression is not associated with colonic tumour progression.

Base Sequence↗
PubMed1998

The role of "colonization pressure" in the spread of vancomycin-resistant enterococci: an important infection control variable.

OBJECTIVE: The spread of nosocomial multiresistant microorganisms is affected by compliance with infection control measures and antibiotic use. We hypothesized that "colonization pressure" (ie, the proportion of other patients colonized) also is an important variable. We studied the effect of colonization pressure, compliance with infection control measures, antibiotic use, and other previously identified risk factors on acquisition of colonization with vancomycin-resistant enterococci (VRE). METHODS: Rectal colonization was studied daily for 19 weeks in 181 consecutive patients who were admitted to a single medical intensive care unit. A statistical model was created using a Cox proportional hazards regression model including length of stay in the medical intensive care unit until acquisition of VRE, colonization pressure, personnel compliance with infection control measures (hand washing and glove use), APACHE (Acute Physiology and Chronic Health Evaluation) 11 scores, and the proportion of days that a patient received vancomycin or third-generation cephalosporins, sucralfate, and enteral feeding. RESULTS: With survival until colonization with VRE as the end point, colonization pressure was the most important variable affecting acquisition of VRE (hazard ratio [HR], 1.032; 95% confidence interval [C1], 1.012-1.052; P=.002). In addition, enteral feeding was associated with acquisition of VRE (HR, 1.009; 95% CI, 1.000-1.017; P=.05), and there was a trend toward association of third-generation cephalosporin use with acquisition (HR, 1.007; 95% CI, 0.999-1.015; P=.11). The effects of enteral feeding and third-generation cephalosporin use were more important when colonization pressure was less than 50%. Once colonization pressure was 50% or higher, these other variables hardly affected acquisition of VRE. CONCLUSIONS: Acquisition of VRE was affected by colonization pressure, the use of antibiotics, and the use of enteral feeding. However, once colonization pressure was high, it became the major variable affecting acquisition of VRE.

APACHE↗
PubMed2000

Postoperative colonic motility and tone in patients after colorectal surgery.

PURPOSE: Colonic motility is crucial for the resolution of postoperative ileus. However, few data are available on postoperative colonic motility and no data on postoperative colonic tone. We aimed to characterize postoperative colonic tone and motility in patients. METHODS: Nineteen patients were investigated with combined barostat and manometry recordings after left colonic surgery. During surgery a combined recording catheter was placed in the colon with two barostat bags and four manometry channels cephalad to the anastomosis. Recordings were performed twice daily from Day 1 to Day 3 after surgery. RESULTS: Manometry showed an increasing colonic motility index, which was a mean (+/- standard error of the mean) of 37 +/- 5 mmHg/minute on Day 1, 87 +/- 19 mmHg/minute on Day 2, and 102 +/- 13 mmHg/minute on Day 3 (P < 0.05 for Day 1 vs. Day 2 and Day 2 vs. Day 3). Low barostat bag volumes indicating a high colonic tone were observed on Day 1 after surgery and increased subsequently (barostat bag I was 19 +/- 4, 32 +/- 6, and 32 +/- 6 ml; barostat bag II was 13 +/- 1, 19 +/- 3, and 22 +/- 5 ml on Days 1, 2, and 3, respectively; for both barostat bags P < 0.05 for Day 1 vs. Day 2 but not Day 2 vs. Day 3). CONCLUSIONS: Colonic motility increased during the postoperative course. The low barostat bag volumes indicated a high colonic tone postoperatively which would correspond to a contracted rather than to a distended colon. High colonic tone postoperatively may be relevant for pharmacologic treatment of postoperative ileus.

Adult↗
PubMed2002

Acetic acid-derived prostaglandin-dependent colonic adaptive cytoprotection is preserved in chronic colitis: role of cyclo-oxygenase.

BACKGROUND AND AIMS: We recently reported the phenomenon of prostaglandin-dependent colonic adaptive cytoprotection (CAP) against acute colonic injury induced by acetic acid (AA) in the normal colon. This study investigated whether the CAP is preserved in the chronic inflamed colon. MATERIALS AND METHODS: Normal rats and a chronic colitis model, induced by trinitrobenzene sulfonic acid, received an intracolonal administration (0.5 ml) of saline or AA at low concentration (1%) followed by high concentration (8%) 30 min later. The distal colon was removed 48 h after 8% AA administration, and colitis was assessed by macroscopic scoring and measurement of the myeloperoxidase (MPO) activity. Indomethacin (5 mg/kg), a nonselective cyclo-oxygenase (COX) inhibitor, or N-[2-cyclohexyloxy-4-nitrophenyl] methane-sulfonamide (NS398, 1 mg/kg), a COX type 2 selective inhibitor, was injected intraperitoneally 1 h before pretreatment with 1% AA. RESULTS: Intracolonal administration of 8% AA induced colonic mucosal damage (macroscopic score 10.0+/-0.9) and elevated MPO activity (2.8+/-0.2 U/g), which were significantly reduced to 3.3+/-0.8 and 1.8+/-0.2 U/g by 1% AA pretreatment, respectively. Indomethacin abolished the gross mucosal protective effect by 1% AA pretreatment in 8% AA-derived colitis in normal rats while the NS398 had no effect. Both indomethacin and NS398 reversed the MPO activity reduction induced by 1% AA pretreatment. In chronic inflamed colon 8% AA treatment resulted in an increase in the macroscopic score to 11.5+/-0.4 from 4.7+/-0.4, but not the MPO activity, which was significantly reduced to 5.7+/-0.9 by 1% AA pretreatment. This gross mucosal protective effect by 1% AA pretreatment in chronic inflamed colon was reversed by indomethacin while the NS398 had no effect. CONCLUSION: These data show that COX-1 and COX-2 derived prostaglandins induced by low concentration AA pretreatment reduce the colonic mucosal injury and the increase in the MPO activity in colitis, respectively. The protective effect of COX-1 is preserved in chronic inflamed colon. These findings support the existence of a low concentration of AA-derived prostaglandin-dependent CAP and suggest that colonic AA, which is derived from bacterial breakdown of carbohydrate and protein in the colon, plays a crucial role in the endogenous defense mechanisms.

Acetic Acid↗
PubMed1998

Pulmonary evolution of cystic fibrosis patients colonized by Pseudomonas aeruginosa and/or Burkholderia cepacia.

UNLABELLED: We analysed the pulmonary evolution (radiological scores and pulmonary function) of 81 cystic fibrosis (CF) patients colonized by Pseudomonas aeruginosa (PA), by Burkholderia cepacia (BC) or by both these bacteria, compared to a control group. Pulmonary function was compared in the age bracket 6-13 years. Functional vital capacity (FVC) and forced expiratory volume (FEV1) values for PA colonized patients were significantly worse than for the control group but better than for children colonized by both organisms. In this last group, the evolution of radiological scores and pulmonary function showed a greater decline 2 years after the first colonization compared to the other groups. FVC and FEV1 values in patients colonized by BC were not worse than these of patients colonized by PA. Moreover, BC affected older patients with advanced lung disease and often previously colonized with PA. These results suggested that co-colonization by PA and BC could be a more deleterious factor on the pulmonary evolution than the isolated colonization by PA or BC, and that BC could be a severity marker rather than a cause. In addition, after starting the utilization of mouthpieces with filter at single use for spirometry in 1993 (without any other change in preventive measures already taken during hospitalization), incidence of BC decreased from 8.2% to zero, and no new case of BC colonization has been observed over the last 4 years. CONCLUSION: Co-colonization of CF patients by PA and BC is more deleterious for pulmonary evolution than colonization by one of these bacteria alone. Re-inforcement of environmental measures during hospitalization (e.g. use of disposable mouthpieces for spirometry) was sufficient to reduce the transmission of BC.

Adolescent↗
PubMed2006

Congenital pouch colon: follow-up and functional results after definitive surgery.

PURPOSE: In this study, functional results with regard to fecal continence levels and other parameters were studied in 22 patients with congenital pouch colon associated with anorectal agenesis (CPC) more than 3 years old who had undergone definitive pull-through surgery 1 to 13 years earlier. An attempt was made to formulate treatment protocols for management of fecal incontinence and other problems associated with CPC. METHODS: The study sample consisted of 14 males and 8 females. Three of the 8 female patients had had a cloacal malformation. The medical records of the patients were scrutinized and they were classified into 4 subtypes based on the length of normal colon proximal to the colonic pouch. The patients were further categorized into 3 groups based on the terminal bowel that had been pulled-through, namely, the ileum or colon proximal to the colonic pouch or a tubularized segment of the colonic pouch. The somatic growth of the patients was studied. Clinical assessment of fecal continence was performed by the Kelly and the Kiesewetter and Chang scoring systems. A computed tomographic scan of the pelvis with a barium enema was performed to assess the terminal bowel and its placement as well as the bony and muscular anatomy of the pelvis. The urinary system was assessed by a clinical history as well as by abdominal ultrasound and a micturating cystourethrogram. Various treatment modalities including dietary modifications, drugs, and enemas were instituted in patients with poor continence levels, and the response to treatment studied. RESULTS: Thirteen patients (59.2%), all with an ileal pull-through, had height and weight less than 50% of that expected for their ages. Overall fecal continence was "poor" in 17 patients and "fair" in only 5 patients. Patients with pull-through of either ileum or normal colon often had very frequent passage of liquid or semisolid stools, whereas the 4 patients with pull-through of tubularized colon had infrequent passage of semisolid stools with abdominal distension and bloating. One of these 4 patients had massive colonic redilatation necessitating surgical correction. Mucosal prolapse and perineal excoriations were frequent findings. Ultrasonography and micturating cystourethrogram showed hydroureteronephrosis and vesicoureteric reflux in 5 patients. Radiologic assessment revealed that there were no significant sacral abnormalities and the striated sphincteric musculature was well developed, although the levator ani was thinner than normal in 15 patients (68%). The bowel was very well placed in the sphincteric complex in 19 patients (86%). In 7 of the 13 patients who had pull-through of normal ileum or colon, some improvement in continence levels was seen 3 to 6 months after institution of dietary measures, loperamide, and saline-water enemas. Two of 3 patients with pull-through of tubularized colon improved to some extent with colonic washouts alone. Overall, quality of life was poor in the 22 patients. CONCLUSIONS: Despite the fact that the sacrum is usually normal, the sphincteric musculature well developed, and the terminal bowel well placed without any anal strictures, long-term prognosis with regard to fecal continence, growth and development, and quality of life appears to be dismal for all subtypes of CPC, irrespective of the type of definitive surgery performed. Corrective measures also appear to be of limited value. Various newer management modalities for management of fecal incontinence may be considered, but in several patients a permanent abdominal stoma may be a more practical solution.

Adolescent↗
PubMed2001

Microbiology and risk factors for catheter exit-site and -hub colonization in neonatal intensive care unit patients.

OBJECTIVE: To identify risk factors and describe the microbiology of catheter exit-site and hub colonization in neonates. DESIGN: During a period of 2 years, we prospectively investigated 14 risk factors for catheter exit-site and hub colonization in 862 central venous catheters in a cohort of 441 neonates. Cultures of the catheter exit-site and hub were obtained using semiquantitative techniques at time of catheter removal. SETTING: A neonatal intensive care unit at a university hospital. RESULTS: Catheter exit-site colonization was found in 7.2% and hub colonization in 5.3%. Coagulase-negative staphylococci were predominant at both sites. Pathogenic flora were found more frequently at the catheter hub (36% vs 14%; P<.05). Through logistic regression, factors associated with exit-site colonization were identified as umbilical insertion (odds ratio [OR], 8.1; 95% confidence interval [CI95], 2.35-27.6; P<.001), subclavian insertion (OR, 54.6; CI95, 12.2-244, P<.001), and colonization of the catheter hub (OR, 8.9; CI, 3.5-22.8; P<.001). Catheter-hub colonization was associated with total parenteral nutrition ([TPN] OR for each day of TPN, 1.056; CI95, 1.029-1.083; P<.001) and catheter exit-site colonization (OR, 6.11; CI95, 2.603-14.34; P<.001). No association was found between colonization at these sites and duration of catheterization and venue of insertion, physician's experience, postnatal age and patient's weight, ventilation, steroids or antibiotics, and catheter repositioning. CONCLUSION: These data support that colonization of the catheter exit-site is associated with the site of insertion and colonization of the catheter hub with the use of TPN. There is a very strong association between colonization at both catheter sites.

Analysis of Variance↗
PubMed1997

Specific flavonoids promote intercellular root colonization of Arabidopsis thaliana by Azorhizobium caulinodans ORS571.

The ability of Azorhizobium caulinodans ORS571 and other diazotrophic bacteria to internally colonize roots of Arabidopsis thaliana has been studied. Strains tagged with lacZ or gusA reporter genes were used, and the principal colonization sites were found to be the points of emergence of lateral roots, lateral root cracks (LRCs). High frequencies of colonization were found; 63 to 100% of plants were colonized by ORS571, and 100% of plants were colonized by Herbaspirillum seropedicae. After LRCs were colonized, bacteria moved into intercellular spaces between the cortical and endodermal cell layers. Specific flavonoids, naringenin and daidzein, at 5 x 10(-5) M, significantly promoted colonization by ORS571. By using a nodC and a nodD mutant of ORS571, it was shown that neither Nod factors nor NodD are involved in colonization or flavonoid stimulation of colonization. Flavonoids did not appear to be stimulating LRC colonization by their activity as nutritional factors. LRC and intercellular colonization by H. seropedicae was stimulated by naringenin and daidzein at the same concentration that stimulated colonization by ORS571.

Arabidopsis↗
PubMed1992

Bacterial and fungal colonization of endotracheal tubes in children: a prospective study.

OBJECTIVES: To evaluate both the frequency and route of endotracheal colonization of intubated children by pathogens and to assess the usefulness of Pediatric Risk of Mortality scoring and measurement of gastric pH in predicting this colonization. DESIGN: Prospective data collection. SETTING: A multidisciplinary pediatric ICU. PATIENTS: Nineteen children with medical/surgical problems who were intubated for at least 4 days. INTERVENTIONS: Buccal mucosa, and endotracheal and gastric aspirates were cultured for pathogens immediately after endotracheal intubation and daily for 4 to 5 days. Pediatric Risk of Mortality scores were calculated at the time of endotracheal intubation; gastric pH was measured each time that the cultures were obtained. MEASUREMENTS AND MAIN RESULTS: The buccal mucosae of ten (53%) of 19 children were colonized with Candida species at the time of endotracheal intubation. This colonization correlated with the degree of physiologic instability as measured by Pediatric Risk of Mortality scores (12.9 +/- 2.8 SEM for those patients colonized vs. 4.9 +/- 1.0 for those patients not colonized; p = .01), but not with preintubation antibiotic therapy. Eleven (58%) children acquired 27 endotracheal pathogens after the day of intubation. The buccal mucosa was the initial site of colonization of 19 (70%) of 27 of the acquired pathogens. A gastric pH of > 3.0 at the time of intubation correctly predicted colonization in nine of 11 children (p < .025, Fisher's exact test); a Pediatric Risk of Mortality score of > 8 at the time of endotracheal intubation correctly predicted colonization in eight of 11 patients (p < .05, Fisher's exact test). CONCLUSIONS: Colonization of the buccal mucosa appears to be the crucial antecedent to endotracheal colonization in children. In children, gastric pH and Pediatric Risk of Mortality scores at the time of endotracheal intubation can predict pathogenic endotracheal colonization within 4 days of intubation. Selective decontamination regimes may be appropriate for these patients, especially those regimes that are directed to the buccal mucosa.

Adolescent↗