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Inclusion of entire pancreas in the composite liver and intestinal graft in pediatric intestinal transplantation.

An entire pancreatico-duodenal complex was included in the liver and intestinal graft in eight children who received small-size grafts. This method showed several advantages compared to the traditional approach. They included reducing time for graft preparation by eliminating donor pancreas resection, no necessity of biliary reconstruction and leaving natural tissue support for blood vessels. The method was not associated with an increased risk of complications such as pancreatitis or rejection. It should be considered in pediatric liver and intestinal transplant recipients who require small-size grafts.

Age Factors↗

Inhibition of leucocyte migration in patients with large intestinal cancer by extracts prepared from large intestinal tumours and from normal colonic mucosa.

The degree of migration inhibition in response to tissue extracts has been examined in leucocyte preparations obtained from patients with large intestinal cancer and from age and sex matched control individuals. A greater degree of migration inhibition was observed in response to a colorectal tumour extract in cells obtained from the cancer patients. Inhibition also tended to be more marked in response to the tumour extract than in response to a normal colonic mucosal extract in these patients. These results suggest that altered cellular immune reactivity is demonstrable by this simple in vitro technique in patients with large intestinal cancer.

Aged↗

Localization of intestinal trefoil-factor mRNA in rat stomach and intestine by hybridization in situ.

A cDNA encoding rat intestinal trefoil factor (rITF) was prepared by reverse transcription and PCR amplification. The sequence obtained was well conserved with that of other trefoil peptides. An antisense riboprobe produced from the clone was used to localize the sites of ITF expression in the rat gastrointestinal tract using hybridization in situ. We found rITF mRNA in goblet cells in the small intestine and colon; a gradient of signal strength greatest near the crypt base was sometimes present. We found no evidence for rITF expression in Brunner's glands, the pancreas, or most regions of the gastric mucosa. Surprisingly, strong signals for rITF mRNA were detected in a region of stomach at the junction of the squamous fore-stomach with the glandular gastric mucosa. This region, which may correspond to the cardiac region, formed part of a larger area of cells staining positive for acid mucins. We hypothesize that concerted expression occurs of particular trefoil peptides with specific mucins, and that this organization reflects a functional relationship between mucins and trefoil peptides.

Amino Acid Sequence↗

[Sonographic structure of the intestinal wall--significance for the diagnosis of inflammatory intestinal diseases].

Sonography can depict the transformation of the intestinal wall in Crohn's disease, esp. its layers. Besides demonstrating the transmural aspect of inflammation it also shows typical mesenteritis and complications such as fistula, abscess, inflammatory tumour, stenosis and ileus. Sonography proves invaluable in following up Crohn's disease. Differential diagnosis against other diseases of the bowel wall (ulcerous colitis, radiogenic, ischaemic, infectious and pseudomembranous colitis, as well as some types of lymphoma and carcinoma of the intestine) on a purely morphological basis is difficult, but nevertheless possible.

Colitis, Ulcerative↗

[Function tests of the lower small intestine with 75selenium-labeled homotaurocholic acid in Crohn disease and resections of the small intestine].

UNLABELLED: Faecal excretion of bile acids was investigated using 75Se-homotaurocholic acid (75SeHCAT) in a total of 75 patients: 9 with irritable colon, 58 with Crohn's disease and 8 with small-bowel resection due to various indications but without Crohn's disease. Bile acid malabsorption, taken as a pathological bile acid retention of less than 19%, was found present in 43 patients with diseased terminal ileum or with more than 20 cm resection of this organ, except in one case (12 cm). On the other hand a normal bile acid retention (21 to 27%) was found in 29 of 72 patients (including 9 patients with irritable colon) who showed either no radiologically detectable lesion of the ileum (n = 21) or changes involving an extension of up to 30 cm (inflammation or resection) in the terminal ileum (n = 8), with the exception of one case (50 cm). Three patients had a raised bile acid excretion contrary to clinical expectation: they had colitis Crohn without radiologically detectable involvement of the small intestine. Thus using the 75SeHCAT-retention test it seems possible to recognize functional disorders in diseased segments of the bowel before the appearance of radiologically detectable changes. CONCLUSION: 75SeHCAT is a suitable substance for investigations on the function of the lower small intestine.

Adolescent↗

Intestinal epithelial lesions associated with signet ring cell carcinoma of the colon and small intestine.

AIMS: The purpose of this study was to investigate the epithelial lesions associated with signet ring cell carcinoma (SRCC) of the colon and small intestine and the possible mechanism of tumour development. METHODS: Twenty-seven cases of adenocarcinoma with a signet ring cell (SRC) component of the colon and small intestine were divided into three groups depending on the association of the SRCC with: (1) epithelium without definite epithelial dysplasia, (2) adenoma, and (3) common type of adenocarcinoma (CTCA) with SRCC component occupying more than 50%, 30%, or less than 30% of the tumour. RESULTS: Most carcinomas were of T3 or T4 type, using the TNM standard staging system. The SRCC component was histopathologically similar in all groups. In group 1 (four cases, linitis plastica type), the overlying epithelium was normal or showed indefinite epithelial dysplasia and occasionally contained intra-epithelial SRCs. In groups 2 and 3 (two and 21 cases, respectively), seven cases contained multiple foci of intra-epithelial SRCs in areas separated from the invasive carcinoma. Transitional areas between SRCC and adenoma or CTCA were also identified. Immunostaining for p53 showed a varied extent of positive reactivity in 23 SRCC. The degree and the extent of reactivity appeared to increase with the stage of the carcinoma. Most intra-epithelial SRCs were immunoreactive for p53. Linitis plastica SRCC was associated with extensive p53 reactivity of the 'atypical' and the adjacent 'normal' epithelium. CONCLUSIONS: SRCC may arise from either CTCA, adenoma, 'atypical' epithelium or a combination of these epithelia. SRCC accounts for the bulk of carcinoma in each of these categories. In linitis plastica SRCC, positive reactivity for p53 is extensive in the adjacent 'normal' colonic epithelium and extends as far as 3cm from the microscopically identified SRCC margin.

Adenoma↗

Protective effects of ischemic preconditioning on the intestinal mucosal microcirculation following ischemia-reperfusion of the intestine.

OBJECTIVE: The small bowel villi are extremely sensitive to ischemia-reperfusion (IR) injury and a range of microcirculatory disturbances contribute to structural and functional changes. The aim of this study was to determine the protective effects of ischemic preconditioning (IPC) of the intestine on the mucosal villous microcirculation during IR injury of the intestine and whether heme oxygenase (HO) is involved in the protection. METHODS: Rats were allocated into 4 groups: (1) sham, (2) IR consisting of 30 min of ischemia followed by 2 h of reperfusion, (3) IPC, as in IR group, but preceded by 10 min of ischemia and 10 min of reperfusion, and (4) with administration of zinc protoporphyrin, an HO inhibitor before IPC and IR. The mucosa of an exteriorized segment of ileum was visualized. Mucosal perfusion index (MPI), red blood cell (RBC) velocity and leukocyte-endothelial interactions during reperfusion were assessed continuously using in vivo fluorescence microscopy. HO activity in the ileum was assessed at the end of the reperfusion period. RESULTS: IPC improved the MPI by 26% and the RBC velocity by 29% on comparison to IR. IR led to a 52% increase in leukocyte-endothelial interactions on comparison to IPC. The administration of zinc protoporphyrin reversed the beneficial effects of IPC. There was a two fold increase of HO activity in IPC compared to IR, whereas zinc protoporphyrin significantly reduced the HO activity. CONCLUSIONS: IPC conferred a protective effect on the villous microcirculation possibly via HO and might prove to be an effective strategy for the amelioration of IR injury.

Animals↗

[Nitrogen metabolism in the large intestine of ruminants. 2. Metabolism of i.v. infused 15N-urea by additional supply of fermentable material to the large intestine of bulls].

The experiment was carried out on 3 bulls with body weights of 201, 168 and 190 kg, respectively. The animals were equipped with a ileo caecal re-entrant cannula and with catheters in the jugular veins on both sides. The pelleted ration was composed of straw 70-72%, cereals 10%, molasses 12-41%, ammoniumhydrogencarbonate 3%, urea 2% and mineral mixture 1%. During a preliminary period ileal digesta were collected, deep-freezed and stored. During the main experiment 15N-urea was infused intravenously for 24 hours. In this period and during the following 6 hours outflowing ideal digesta were collected quantitatively. At the same time precollected, unlabelled digesta together with a supplement of partly hydrolysed straw meal were reintroduced into the caecal part of the cannula. Plasma urea-N, urinary-N as well as several N-fractions of faeces and digesta were analysed for 15N abundance. A urea flux rate of 27.9 +/- 3.4 mumol per minute per kg 0.75 was estimated. It was calculated that 52% of this amount of urea was transferred into the digestive tract. In both, digesta and faeces NH3-N was highest 15N-labelled indicating a direct urea entry and degradation in both segments of the digestive tract. The amounts of 15N-excess found during the period of digesta replacement were in faeces 0.25 and in ileal digesta 4.02% of the infused amount of 15N. Although the microbial utilization of endogenous urea-N was generally low in the large intestine there was a clear stimulation of this process due to the additional supply of the large intestine with a fermentable source.

Animals↗

Liver-intestine cadherin: molecular cloning and characterization of a novel Ca(2+)-dependent cell adhesion molecule expressed in liver and intestine.

A novel member of the cadherin family of cell adhesion molecules has been characterized by cloning from rat liver, sequencing of the corresponding cDNA, and functional analysis after heterologous expression in nonadhesive S2 cells. cDNA clones were isolated using a polyclonal antibody inhibiting Ca(2+)-dependent intercellular adhesion of hepatoma cells. As inferred from the deduced amino acid sequence, the novel molecule has homologies with E-, P-, and N-cadherins, but differs from these classical cadherins in four characteristics. Its extracellular domain is composed of five homologous repeated domains instead of four characteristic for the classical cadherins. Four of the five domains are characterized by the sequence motifs DXNDN and DXD or modifications thereof representing putative Ca(2+)-binding sites of classical cadherins. In its NH2-terminal region, this cadherin lacks both the precursor segment and the endogenous protease cleavage site RXKR found in classical cadherins. In the extracellular EC1 domain, the novel cadherin contains an AAL sequence in place of the HAV sequence motif representing the common cell adhesion recognition sequence of E-, P-, and N-cadherin. In contrast to the conserved cytoplasmic domain of classical cadherins with a length of 150-160 amino acid residues, that of the novel cadherin has only 18 amino acids. Examination of transfected S2 cells showed that despite these structural differences, this cadherin mediates intercellular adhesion in a Ca(2+)-dependent manner. The novel cadherin is solely expressed in liver and intestine and was, hence, assigned the name LI-cadherin. In these tissues, LI-cadherin is localized to the basolateral domain of hepatocytes and enterocytes. These results suggest that LI-cadherin represents a new cadherin subtype and may have a role in the morphological organization of liver and intestine.

Amino Acid Sequence↗

Ontogeny of the Thy-1-, Lyt-2+ murine intestinal intraepithelial lymphocyte. Characterization of a unique population of thymus-independent cytotoxic effector cells in the intestinal mucosa.

Murine intestinal intraepithelial lymphocytes (IEL) from unprimed thymus-bearing and athymic nude mice were characterized according to the expression of murine lymphocyte antigenic markers and cytotoxic activity. The majority of IEL from thymus-bearing mice were Lyt-2+, L3T4- lymphocytes, over half of which did not express Thy-1 surface antigens. Nude IEL and spleen cells were void of Thy-1+ cells; however, Lyt-2 antigens were expressed on a significant proportion of IEL, but not splenic lymphocytes. Overall, 40-70% of IEL from either thymus-bearing or athymic mice expressed the cytotoxic activation antigen, CT-1, and the J11d lymphocyte marker, both of which were associated with a population of Thy-1-, Lyt-2+ cytotoxic IEL. These data are taken to mean that the intestinal epithelium is a site uniquely enriched for activated cytotoxic cells, a significant proportion of which originate as non-thymus-derived lymphocytes with acquired lytic activity.

Animals↗

Dietary retinoic acid supplementation stimulates intestinal tumour formation and growth in multiple intestinal neoplasia (Min)/+ mice.

Chemopreventive activity by retinoic acid (RA) has been demonstrated previously in rat colon. The spontaneous tumourigenesis in the Min/+ mouse, which harbours a germline mutation in the tumour suppressor gene adenomatous polyposis coli (Apc), is characterized by inactivation of Apc, nuclear accumulation of beta-catenin and the enhanced expression of specific genes activated by T cell factor (TCF)/beta-catenin signalling. Recently it was reported that beta-catenin interacts with retinoic acid receptor in a retinoid-dependent manner, reducing beta-catenin/TCF regulated transcription. Our hypothesis was therefore that dietary supplementation with all-trans RA may inhibit the Apc-driven tumourigenesis in Min/+ mice. Surprisingly, in two different experiments the results showed that dietary RA significantly stimulated both the formation and growth of small intestinal tumours. In the first experiment Min/+ mice were exposed to 50 mg 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine/kg bodyweight at day 3-6 after birth and then treated with 50 mg/kg dietary RA in 1-3 weeks from the age of 2 weeks. In the second experiment the mice were not treated with carcinogen, and the diet was supplemented with 5 or 10 mg/kg RA from the age of 4 weeks until termination of the experiment at 11 weeks. Immunohistochemical studies revealed no differences in beta-catenin, cyclin D1 or proliferating cell nuclear antigen staining following RA treatment. There was no intestinal toxicity in mice fed 10 mg/kg RA, indicating that the increased tumourigenesis in Min/+ mice is a specific effect of all-trans RA.

Animals↗

Purification and cDNA cloning of UDP-GlcNAc:GlcNAcbeta1-3Galbeta1-4Glc(NAc)-R [GlcNAc to Gal]beta1,6N-acetylglucosaminyltransferase from rat small intestine: a major carrier of dIGnT activity in rat small intestine.

A rat intestinal beta1,6N-acetylglucosaminyltransferase (beta1-6GnT) responsible for the formation of the beta1,6-branched poly-N-acetyllactosamine structure has been purified to apparent homogeneity by successive column chromatographic procedures using an assay wherein pyridylaminated lacto- N-triose II (GlcNAcbeta1-3Galbeta1-4Glc-PA) was used as an acceptor substrate and the reaction product was GlcNAcbeta1-3(GlcNAcbeta1-6)Galbeta1-4Glc-PA. The purified enzyme catalyzed the conversion of the polylactosamine acceptor GlcNAcbeta1-3'LacNAc into GlcNAcbeta1-3'(GlcNAcbeta1-6') LacNAc (dIGnT activity), but it could not transfer GlcNAc to LacNAcbeta1-3'LacNAc (cIGnT activity). This enzyme could also convert mucin core 1 and core 3 analogs, Galbeta1-3GalNAcalpha1-O-paranitrophenyl (pNP) and GlcNAcbeta1-3GalNAcalpha1-O-pNP, into Galbeta1-3(GlcNAcbeta1-6) GalNAcalpha1-O-pNP (C2GnT activity) and GlcNAcbeta1-3(GlcNAcbeta1-6)GalNAcalpha1-O-pNP (C4GnT activity), respectively. Based on the partial amino acid sequences of the purified protein, the cDNA encoding this enzyme was cloned. The COS-1 cells transiently transfected with this cDNA had high dI/C2/C4GnT activities in a ratio of 0.34:1.00:0.90, compared with non- or mock-transfected cells. The primary structure shows a significant homology with human and viral mucin-type core 2 beta1-6GnTs (C2GnT-Ms), indicating that this enzyme is the rat ortholog of human and viral C2GnT-Ms. This is the first identification and purification of this enzyme as a major carrier of dIGnT activity in the small intestine. This rat ortholog should mostly be responsible for making distal I-branch structures on poly-N-acetyllactosamine sequences in this tissue, as well as making mucin core 2 and core 4 structures, given that it also has high C2/C4GnT activities.

Amino Acid Sequence↗

Jejunal dilatation in Crohn's disease. Intestinal obstruction or intestinal edema?

Although dilatation of the jejunum is a well-recognized feature of Crohn's disease there has been no systematic inquiry as to whether this is related simply to distal intestinal obstruction or to other factors such as hypoalbuminemia and mucosal disease. Barium follow-up examinations of 21 patients with Crohn's disease who had serum albumin concentrations of 2.1-4.4 g/dl were reviewed. Fourteen of these patients (67%) had increased mean jejunal width. All patients with direct radiologic evidence of a stricture (six patients) had increased jejunal caliber, but this only accounted for 43% of patients with this abnormality. Of the remaining eight patients, six had hypoalbuminemia, three of whom had serum albumin concentrations less than or around 2.7 g/dl, the previously determined "albumin threshold" for jejunal dilatation. We conclude that increased jejunal caliber in Crohn's disease not only occurs in association with distal intestinal stenosis but also with severe hypoalbuminemia in the absence of obstruction. We were unable to define a cause of jejunal dilatation in 36% of these patients, but propose that functional obstruction due to distal nonstenosing inflammatory disease may be a factor.

Adult↗

Anatomic variability of rejection in intestinal allografts after pediatric intestinal transplantation.

BACKGROUND: Rejection of the allograft is a major contributor to morbidity and mortality in children who undergo a small intestinal transplant. Operational definitions for histologic rejection have been established, but little is known about the anatomic variability of the histologic abnormalities. STUDY DESIGN: Biopsy reports were reviewed retrospectively from more than 1200 endoscopies performed on the 41 children who received intestinal transplantation between 1990 and 1995. RESULTS: Biopsies were performed in the proximal jejunum and distal ileum allograft simultaneously on 248 occasions. In 168 biopsies, neither site was histologically abnormal; in 80, rejection was found. In 42, both regions were abnormal; however, in 17 only the jejunum was involved and in 21 the rejection exclusively involved the ileum. Among children whose allograft included colon, rejection was absent in colon and ileum in 34 biopsies, involved both in 6, involved ileum but not colon in another 6 and involved colon but not ileum in only one. When the allograft included stomach, rejection was absent in the stomach and jejunum 39 times, involved both sites 8 times, involved jejunum and not the stomach 10 times, but involved the stomach and not jejunum only once. Endoscopic appearance correctly predicted histologic rejection 63% of the time. CONCLUSION: Anatomic variability may exist in the rejection process. Sampling the jejunum and ileum seems to have similar sensitivity in detecting rejection, whereas sampling stomach and the colon is less sensitive. When allograft rejection is suspected on clinical grounds, sampling more than one area of the graft may be necessary for histologic confirmation.

Adolescent↗

Hypertonic/hyperoncotic resuscitation after intestinal superior mesenteric artery occlusion: early effects on circulation and intestinal reperfusion.

The objective of the study was to determine the early effects of hypertonic/hyperoncotic starch resuscitation after 2 h occlusion of the superior mesenteric artery (SMA) in comparison to animals reperfused without treatment and isotonic resuscitation. SMA was clamped (18 pigs, 19-23 kg) for 2 h followed by a 2-h reperfusion period, which was initiated with isotonic (ISO) (35 mL/kg 0.9% NaCl and 5 mL/kg 10% hydroxyethyl starch within 30 min) or hypertonic/hyperoncotic resuscitation (HHES) (7.5% NaCl/10% hydroxyethyl starch within 5 min). Cardiac output (CO), mean arterial blood pressure (MAP), serum lactate, antimesenteric serosal Laser-Doppler values (LD), and intramural pHi (tonometry) were measured. Without resuscitation at the onset of reperfusion MAP (70 +/- 3 mmHg) decreased to 40 +/- 3 mmHg and CO to 31% of baseline values after 30 min. Serum lactate increased to 5.1 +/- 1.6 mmol/L without improvement. The decrease of CO was attenuated only during the initial 30 min of reperfusion in the ISO group, but significantly better counteracted by hypertonic/hyperoncotic resuscitation. Without treatment, LD flow of the ileum (baseline 23-27 LD units) recovered but intramural pH (pHi) remained significantly decreased (7.26 +/- 0.05). With isotonic resuscitation LD values (21.8 +/- 2.1 LD units) and intramural pHi (7.09 +/- 0.14) decreased even more (P < 0.05) whereas the HHES group showed a significant hyperemic reaction and a normalization of the intramural pHi and serum lactate within 30 min. Hypertonic/hyperoncotic resuscitation significantly improves MAP and CO during reperfusion shock and induces an immediate hyperemic reperfusion reaction of the intestinal microcirculation. Adequate isotonic fluid replacement in order to restore the postischemic plasma volume loss may cause a pronounced deterioration of intestinal perfusion.

Animals↗

Immune responses that adapt the intestinal mucosa to commensal intestinal bacteria.

Animals contain an enormous load of non-pathogenic bacteria in the lower intestine, which exploit an environment with a stable temperature and abundant carbon sources. Our load of bacteria outnumbers our own cells. In order to survive with such a high number of organisms in very close proximity to host tissues the intestinal mucosa and its immune system is highly adapted. Mucosal immune responses are induced by small numbers of live commensal organisms penetrating the Peyer's patches and persisting in dendritic cells (DC). These DC can induce immunoglobulin A+ (IgA+) B cells, which recirculate through the lymph and bloodstream to populate the lamina propria and secrete protective IgA. Because DC loaded with commensal bacteria do not penetrate further than the mesenteric lymph nodes, immune induction to commensals is confined to the mucosa, allowing strong mucosal immune responses to be induced whilst the systemic immune system remains relatively ignorant of these organisms.

Adaptation, Physiological↗

Effects of the peripherally acting NK receptor antagonist, SB-235375, on intestinal and somatic nociceptive responses and on intestinal motility in anaesthetized rats.

We investigated the effects of the selective NK(3) tachykinin receptor antagonist, SB-235375, on noxious signalling from gut and skin and on intestinal motility in anaesthetized rats. We also measured penetrance into brain and spinal cord. Nociceptive responses in reaction to colorectal distension and skin pinch were assessed by recording the electromyogram (EMG) from the external oblique muscle (a visceromotor response). Motility was measured by recording intraluminal pressure waves during changes in baseline pressure in the jejunum. Colorectal compliance was assessed by measuring luminal pressure change during isovolumic distension. SB-235375 (20 mg kg(-1), by i.v. bolus) reduced the EMG response to colorectal distension by over 90%. The reduction was slow at onset, peaked at about 60 min, and lasted for over 2 h. Responses to noxious skin pinch were unchanged. Amplitudes of propulsive waves in the jejunum were slightly reduced, but their frequency of occurrence was unchanged. SB-235375 decreased colorectal compliance by 5-10%. There was undetectable penetration of i.v. SB-235375 into brain or spinal cord. We conclude that SB-235375 acts peripherally to substantially reduce nociceptive signalling from colorectum without affecting noxious signalling from skin and with little effect on intestinal motility.

Acetates↗

Intestinal cell adhesion molecules. Liver-intestine cadherin.

The cadherin superfamily comprises a large number of cell adhesion molecules, several of which are expressed in the gastrointestinal tract. LI-cadherin represents a novel type of cadherin within the cadherin superfamily distinguished from other cadherins by structural and functional features described in this review. In the mouse and human, LI-cadherin is selectively expressed on the basolateral surface of enterocytes and goblet cells in the small and large intestine, whereas in the rat this cadherin is additionally detectable in hepatocytes. LI-cadherin is capable of mediating Ca(2+)-dependent homophilic cell-cell adhesion independent of interactions with the cytoskeleton, indicating that the adhesive function of this novel cadherin is complementary to that of E-cadherin and desmosomal cadherins co expressed in the intestinal mucosa.

Cadherins↗