[Rectal palpation when justified--a final reply].
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Humans↗
Biomedical subjects
R Andersson
Publications and source records attributed to R Andersson.
The role of transient mucosal ischemia in acetic acid-induced colitis in the rat.
The importance of early microcirculatory changes in the rat colon after exposure to acetic acid was investigated. Administration of 4% acetic acid for 15 sec into an exteriorized colonic segment induced a marked, transient (starting 2 min after the challenge with acetic acid and persisting for 15 min) decrease in the colonic blood flow as estimated by a laser-Doppler flowmeter. Four days after acetic acid administration, a uniform colitis had developed in the exteriorized colonic segment with a total morphological score (TMS) of 15.1 +/- 0.8, myeloperoxidase activity (MPO) increased more than threefold, and plasma exudation into the colonic lumen increased sevenfold. Administration of hydrochloric acid (HCl) with the same pH as the acetic acid or sodium acetate (pH 7.0) did not affect colonic blood flow or produce colitis. Mechanical colonic ischemia, induced by a controlled increase in the intraluminal pressure, resulted in several pathological features of colitis with a TMS of 7.3 +/- 0.2, combined with a significant increase in MPO activity. The TMS and MPO were further increased when mechanical colonic ischemia was combined with HCl or sodium acetate. Pretreatment with SOD and catalase 5 or 15 min before acetic acid administration did not affect the transient ischemia immediately following acetic acid administration. However, it partially prevented the development of colitis. It is concluded that immediate transient ischemia accompanied by the generation of oxygen free radicals might be of importance in the pathogenesis of acetic acid-induced colitis in the rat.
Acetic Acid↗
[More penalties without reason by the disciplinary board. Criticism against the handling of appendicitis].
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Abdomen, Acute↗
Resection margins of 2 versus 5 cm for cutaneous malignant melanoma with a tumor thickness of 0.8 to 2.0 mm: randomized study by the Swedish Melanoma Study Group.
BACKGROUND: The traditional surgical treatment for primary malignant melanoma has often been a wide excision with a margin of about 5 cm. Since the risk of local recurrences is dependent on tumor thickness, thin tumors (<1 mm) have routinely been excised with a narrow margin. For thick tumors, the optimal resection margin is controversial, and can be determined only by prospective, randomized trials. METHODS: The Swedish Melanoma Study Group performed a prospective, randomized multicenter study to evaluate an excision margin of 2 versus 5 cm for patients with cutaneous malignant melanoma with tumor thickness > 0.8 and < or = 2.0 mm. The trial includes 769 patients. Patients with melanomas of the skin of the head, neck, hands, feet, or vulva were not included in the trial. In the event of an excision biopsy for diagnosis, radical surgery was completed within 6 weeks. The median follow-up time was 5.8 years for estimation of survival and 4.0 years for diagnosis of recurrent disease. RESULTS: No significant differences have been observed between the treatment groups regarding local or regional recurrences or survival. CONCLUSIONS: We recommend an excision with a margin of 2 cm for cutaneous malignant melanoma with a tumor thickness > 0.8 and < or = 2.0 mm.
Biopsy↗
Structural features of an arabinan fragment isolated from the water-soluble fraction of dehulled rapeseed.
A water-soluble polysaccharide fraction was prepared from dehulled rapeseed meal (winter rapeseed variety Casino). Further purification yielded two major fractions having a high content of arabinose and galactose residues, with Ara/Gal ratios of 5.4 (G1) and 1.8 (G2). The Ara/Gal ratio of the high molecular weight fraction G1 was stable over the whole gel filtration peak, indicating that the arabinose and galactose residues are part of the same polysaccharide. The high molecular weight fraction G1 was studied further by methylation analysis and several NMR techniques. Structural studies showed G1 to consist mainly of arabian fragments, which have terminal alpha-L-arabinofuranosyl groups with anomeric carbons bound (1-->5) (A) or (1-->2) (B), and 2,5-substituted arabinosyl residues with anomeric carbons bound (1-->5) (D) or (1-->2) (C) to adjacent arabinosyl residues. The A:B:C:D ratios were 2:1:1:1 according to results from NMR and methylation analysis.
Arabinose↗
Repeated liver resection for recurrent liver cancer.
Patients with cancer recurrence limited to the liver alone after a first liver resection may be candidates for a repeat resection. Some 191 second and ten third liver resections for recurrent colorectal metastases, and 128 second and ten third liver resections for recurrent hepatocellular carcinoma (HCC), were evaluated after reviewing the literature. The 5-year survival rate after second liver resection for colorectal metastases was 26 per cent with a median survival time of 30 months. Mortality and morbidity rates were 1.2 and 27.4 per cent respectively. The 5-year survival rate after second resection for HCC was 40 per cent with a median survival time of 40 months. The operative mortality rate was 2.3 per cent; morbidity occurred in 13 per cent of patients with HCC. Survival after primary colorectal resection was significantly better for patients with metachronous metastases than for those with synchronous disease; survival correlated with a long interval between the first and second liver resection (in both colorectal liver cancer and HCC). Repeated liver resection may be performed in selected patients and yield a similar survival to that obtained after first liver resection.
Adult↗
Alterations in intestinal function in acute pancreatitis in an experimental model.
Gastrointestinal tract failure may be involved in the development of systemic septic complications in acute pancreatitis. Systemic and intestinal circulation, intestinal permeability and absorptive function were evaluated in the early course of acute pancreatitis induced in rats by retrograde intraductal injection of 0.2 ml of 5 per cent sodium taurodeoxycholate and 0.4 nmol trypsin. A decrease in systemic arterial pressure and intestinal blood flow and an increase in intestinal permeability as measured by the leakage of 125I-labelled human serum albumin from blood to lumen were noted in the distal ileum and colon, reaching statistically significant differences 6 h after induction of pancreatitis. The transport of small molecular markers (sodium fluorescein and 51Cr-labelled ethylenediamine tetra-acetic acid) through the distal ileum and colon in vitro from the mucosal to the serosal site in Ussing chambers significantly increased in the early periodic (20-60 min) of incubation, while the passage of a macromolecular marker (ovalbumin) demonstrated a definite increase at 60-120 min of incubation. D-Xylose absorption from the gut lumen to the portal vein was significantly less in acute pancreatitis than after sham operation. Intravenous administration of the hydroxyl radical scavenger dimethylsulphoxide prevented the compromised intestinal permeability and gut absorptive capacity induced by acute pancreatitis, but did not affect the reduced arterial pressure and intestinal microcirculation. Cytotoxic oxygen-derived free radicals may contribute to the development of alterations in intestinal permeability and absorptive function found in the early stage of acute pancreatitis in the rat.
Acute Disease↗
Protein adsorption and bacterial adhesion to biliary stent materials.
Four biliary stents inserted for relief of jaundice in patients with biliary obstruction due to carcinoma of pancreatic head were examined for the adsorption of biliary proteins and bacterial colonization. Fibronectin and vitronectin (S-protein) were found to be the two main proteins adsorbed on the inner surface of the stents. Biliary isolates included Escherichia coli, Enterococcus faecalis, and Candida albicans. In vitro studies were performed to clarify the kinetics of biliary protein and bacterial adhesion. Biliary drains of polytetrafluorethylene, polyethylene, polyurethane, and rubber were placed in a flow cell and perfused with human bile at 37% C for 24 hr. The materials were subjected to either detection of adsorbed biliary proteins or perfusion with 3 H-labeled E. coli cells (1 X 10 6 cfu/ml). The results show that the adsorbed biliary proteins were detectable on the surface of biliary stents and able to enhance bacterial adhesion to the surface in the first 24 hrs after the exposure of stent materials to bile, and that both the adsorption of biliary proteins and the adhesion of bacterial cells were material- and strain-dependent. Furthermore, there was a clear correlation between the amount of adsorbed fibronectin and the number of adherent bacteria. The results indicate that, in the clinical situation, biliary proteins may be adsorbed on the surface of inserted stents within a short time after insertion, and some of them may be used by bacterial cells as receptors for adhesion to the surface, and thus involved in the process of bacterial adhesion.
Adsorption↗
Influence of colostomy on in vivo and in vitro permeability of the rat colon.
PURPOSE: Barrier properties of an isolated colon loop and the remnant colon in continuity with the gastrointestinal tract after colostomy were studied in the rat. METHODS: The in vivo absorption after colonic loop administration of the marker fluorescein sodium was measured as the urinary recovery. The in vitro permeability was measured in Ussing diffusion chambers as the transmucosal passage of [14C]mannitol and of human serum albumin in the isolated and the nonexcluded colonic segments and was compared with the corresponding colonic regions from sham-operated rats at 1 to 14 days after operation. RESULTS: Body weight gain of the rats decreased and diarrhea appeared from day 2 after colostomy. Histologic examination showed mucosal atrophy with decreased villus height in the isolated colonic loop and an increased villus height in the nonexcluded colon segment. Absorption of fluorescein sodium in the isolated loop was increased at 8 and 14 days. Moreover, permeability in the isolated loop was increased for both mannitol and human serum albumin from four days after colostomy compared with the corresponding colonic segments after the sham operation, whereas a decrease in the passage of mannitol was noted in the nonexcluded colon. CONCLUSIONS: Experimentally performed colostomy diversion in the rat induced alterations of the barrier function in both the isolated colonic loop and the nonexcluded colon in continuity with the fecal stream.
Animals↗
Carbon dioxide transport in rats with acute pancreatitis.
CONCLUSION: The production, release, and transport of carbon dioxide from tissues to blood are facilitated both systemically and in the gastrointestinal tract in acute pancreatitis. Red blood cells are responsible for the major exchange and transport of this increase in CO2. The existence of arteriovenous shunting within the intestine is associated with tissue ischemia, which may be involved in the etiology of gut barrier failure in acute pancreatitis. BACKGROUND: Hemodynamic alterations in acute pancreatitis have been described, while little is known about CO2 metabolism. METHODS: Carbon dioxide metabolism was evaluated by virtual values of venoarterial CO2 concentration differences in the early phase after sham operation or induction of acute pancreatitis by intraductal injection of 5% sodium taurocholate in rats. RESULTS: In acute pancreatitis, virtual values of the CO2 concentration increased in arterial RBC at 6 and 12 h as well as in caval and portal vein RBC and plasma. Virtual values of the dissolved CO2 concentration were reduced in arterial and portal vein blood. The increment in blood CO2 concentration related to the increase in CO2 tension from arterial to caval or portal vein valves at constant CO2 tension. The total increment in CO2 concentration from arterial to caval or portal vein blood increased. Whole body oxygen extraction increased, whereas gut oxygen extraction decreased in pancreatitis.
Acute Disease↗
Alterations in intestinal motility and microflora in experimental acute pancreatitis.
CONCLUSION: A delay in intestinal transit time appears as an early event in acute pancreatitis, preceding intestinal bacterial overgrowth and translocation. BACKGROUND: Septic complications, primarily caused by bacteria of enteric origin, are frequent in severe acute pancreatitis. Impairment in intestinal motility probably plays a pathophysiological role in the development of bacterial overgrowth and ensuing translocation. METHODS: In the present study, the influence of acute pancreatitis on intestinal motility was evaluated by measuring small intestinal transit time in the rat. Acute pancreatitis was induced by the retrograde intraductal infusion of 0.2 mL taurodeoxycholate. Intestinal transit time was studied by intraduodenal injection of Krebs' phosphate-buffered solution labeled with Na2(51)CrCO4, and 1 h small intestinal transit was measured at 1, 3, 12, and 24 h, after induction of pancreatitis. Bacterial overgrowth was evaluated by measuring Escherichia coli counts in the colon and distal small intestine, and bacterial translocation to mesenteric lymph nodes, the liver, spleen, and pancreas was determined. RESULTS: A delayed small intestinal transit time was noted from 3 h on after induction of acute pancreatitis, with most of the radioactivity retained in the first two intestinal segments. Overgrowth of E. coli was noted 12 h after induction of pancreatitis in both the colon and distal small intestine, and at the same time-point, a significant increase in the incidence of bacterial translocation to mesenteric lymph nodes was seen.
Acute Disease↗
Enhanced prevalence of T cell receptor V beta 7 gene family expression in human intestine-associated T lymphocytes.
Relative levels of expression of T cell receptor variable (V) beta and joining (J) beta gene segments were determined in T cells derived from intestinal biopsies of healthy mucosal areas, mesenteric lymph nodes and peripheral blood of the same individuals. Samples taken from patients suffering from inflammatory (n = 8) and non-inflammatory (n = 8) bowel diseases were analyzed by semi-quantitative polymerase chain reaction-based methods. In the intestine, fewer (median = 3.5) V beta gene segments constituted more than 50% of the T cell receptor V beta repertoire compared to that of peripheral blood T cells (median = 7, P < 0.001). Interestingly, in all sixteen individuals studied, intestinal T lymphocytes (IL-T) expressed the V beta 7 gene family to a higher degree than did T cells in the paired peripheral blood and mesenteric lymph nodes (P < 0.001). T cell receptor J beta gene segment analyses of V beta 7+ T cells revealed no significant difference in oligoclonality rates between peripheral blood (4/16) and intestine (7/16) (P = 0.46). Hence, overexpression of intestinal TCR V beta 7 message does not seem to be due to oligoclonal expansions in the majority of the samples.
Adolescent↗
Proliferation of distinct human T cell subsets in response to live, killed or soluble extracts of Mycobacterium tuberculosis and Myco. avium.
The proliferative responses of distinct cell subsets from healthy, bacille Calmette-Guérin (BCG)-vaccinated blood donors were assessed after in vitro stimulation with live or UV-killed Mycobacterium tuberculosis and Myco. avium or with soluble extracts obtained from either mycobacterial species. Proliferation of cell subsets was evaluated by flow cytometric determination of 5-bromo-2'-deoxy-uridine incorporation into DNA and simultaneous identification of surface phenotypic markers. In the presence of monocytes, the response to whole (live or killed) bacteria was characterized by a predominant proliferation of CD4+ alphabeta+ T cells and, to a lesser extent, of CD8+ alphabeta+ T cells. Proliferation of CD8+ alphabeta+ T cells was primarily elicited by live rather than killed bacilli (P < 0.05). Conversely, when soluble bacterial extracts were used as stimulators, a preferential proliferation of gammadelta+ T cells, expressing predominantly Vgamma9+ and Vdelta2+ T cell receptor chains, was recorded. Moreover, when monocyte-depleted cell populations were directly cultured with live bacteria, a marked proportion of CD3- CD16+ (natural killer (NK)) cells was detected among the responding cells. Although both alphabeta, gammadelta and NK cells have been previously shown to react with mycobacteria in vitro, their relative contributions to the response have been difficult to assess. Using a flow cytometric technique which allows direct identification of proliferating cells within complex cell populations, our study demonstrates significant differences in the ability of various mycobacterial antigen preparations to elicit proliferation of distinct cell subsets.
Antigens, Bacterial↗
Immune responses in congenic mice to multiple antigen peptides based on defined epitopes from the malaria antigen Pf332.
Repeat sequences from the Plasmodium falciparum blood stage antigen Pf332 frequently comprise the pentapeptide VTEEI, an epitope recognized by certain parasite neutralizing antibodies. This B-cell epitope was assembled in an octavalent multiple antigen peptide (MAP) system either as trimers (VTEEI)3 (MAP1) or as an integral part of a naturally occurring Pf332 undecamer repeat sequence SVTEEIAEEDK (MAP2). Characteristics of the immunogenicity of these subunit constructs were evaluated in H-2 congenic mice. MAP1 generated antibody responses in mice of the H-2d, H-2k and H-2q haplotypes, but not in H-2b or H-2s mice, whereas MAP2 only induced antibodies in mice of H-2k haplotype. When analysing T-cell responses induced by the MAP, lymph node cells from responder strains primed in vivo with MAP1 proliferated in response to restimulation with both MAP1 and the peptide (VTEEI)3. MAP2, however, did not induce a detectable T-cell proliferation. Additionally, the lack of antibody response to MAP1 in H-2b mice could be circumvented by combining the MAP1 peptide and a H-2b-restricted T-cell epitope in a diepitope MAP construct. Despite the fact that the motif VTEEI has not been identified in Pf332 sequences in the form of a trimer, MAP1 did induce Pf332 protein-reactive antibodies. Assembly of multimers of short defined epitopes in MAP constitutes an interesting approach for the design of polyvalent subunit immunogens.
Amino Acid Sequence↗
Biotransformation of the cyclopenta-fused polycyclic aromatic hydrocarbon benz[j]aceanthrylene in isolated rat liver cell: identification of nine new metabolites.
The biotransformation of benz[j]aceanthrylene (B[j]A) was studied in suspensions of hepatocytes isolated from Aroclor 1254-treated or untreated rats. Using radiolabeled cofactors and metabolic inhibitors combined with UV, mass and 1H-NMR spectroscopy, we have detected five known metabolites and characterized nine new metabolites: metabolite 1 was tentatively assigned as B[j]A-1,2-dihydrodiol-8-sulfate; metabolite 2, B[j]A-1,2,9,10-tetrahydrotetrol; metabolite 3, B[j]A-1,2-dihydrodiol-10-O-glucuronide; metabolite 4, B[j]A-1-one-8-sulfate; metabolite 5, B[j]A-1,2-dihydrodiol-10-sulfate; metabolite 6, the sulfate conjugate of B[j]A-dihydrodiol-phenol; peak 7 in the chromatogram is a mixture of one glutathione conjugate and two sulfate conjugates of a B[j]A-metabolite; metabolite 8, B[j]A-10-O-glucuronide; metabolite 8', B[j]A-1,2-dihydrodiol; metabolite 9, B[j]A-10-sulfate; metabolite 9', B[j]A-9,10-dihydrodiol and metabolite 10, B[j]A-9,10-dihydro-9-hydroxy-10-sulfate. The metabolites identified support the notion that epoxidation at the cyclopenta region is an important activation step of B[j]A. Furthermore, sulfation appears to play a very important role in the conversion of hydroxylated B[j]A metabolites into more polar excretable products.
Animals↗
Alterations in endothelial barrier permeability in multiple organs during overactivation of macrophages in rats.
Macrophage hyperactivity has been suggested to play an important role in septic complications and the development of multiple organ failure. Intraperitoneal administration of macrophage stimulants, e.g., zymosan, induce a systemic inflammatory response, with concomitant gut origin sepsis, and organ dysfunction. However, little is known about alterations in endothelial permeability during macrophage hyperactivation. In the present study, the effect of macrophage hyperactivation on endothelial permeability, assessed by 125I-labeled HSA and 51Cr-labeled EDTA, and the difference between cytolytic and noncytolytic inflammatory macrophages induced by i.p. injection of .25 or .50 mg/g of zymosan, concanavalin A (Con A) or thioglycollate medium (TM) diluted in 4 mL of paraffin, as well as the potential relationship with the doses used, were evaluated in the rat. Overactivation of cytolytic inflammatory macrophages induced a pronounced alteration in endothelial barrier permeability, characterized by a decrease in whole body plasma volume and an increase in whole body interstitial fluid volume, while overactivation of noncytolytic inflammatory macrophages only induced leakage of proteins and plasma to several of the organs studied. Macrophage activators, like zymosan, Con A and TM, exhibited varying effects on endothelial permeability related to the dose used. The results in the present study imply that overactivation of cytolytic inflammatory macrophages may play an important role in endothelial barrier injury and that zymosan possesses a more potent effect as compared to Con A when administered at the same dose.
Animals↗
Cisapride prevents enteric bacterial overgrowth and translocation by improvement of intestinal motility in rats with acute liver failure.
Enteric bacterial overgrowth resulting from compromised gastrointestinal motility has been suggested to be important for the development of enteric bacterial translocation. In the present study, the effect of cisapride, a 5-hydroxytryptamine-4-receptor agonist and stimulant of intestinal motility, was evaluated concerning intestinal motility, as measured by intestinal transit time, enteric bacterial overgrowth, and bacterial translocation from the gut in rats with acute liver failure induced by 90% hepatectomy. The results demonstrated that (1) the incidence of bacterial translocation to the systemic and portal circulation as well as to the liver, spleen, kidneys, and lungs was nil, and 17-33% to MLN in hepatectomized animals treated with cisapride, i.e. significantly lower than in hepatectomized rats administered saline; (2) overgrowth of E. coli in the intestine was noted in hepatectomized animals given saline, but not following cisapride treatment; (3) cisapride improved the otherwise delayed intestinal transit time following hepatectomy as shown by an increase in the leading edge of isotopic propulsion and the linear slope of the cumulative percent of radioactivity through each intestinal segment. Thus, we conclude that intravenous administration of cisapride prevents enteric bacterial overgrowth and bacterial translocation by improving intestinal motility in rats with acute liver failure induced by subtotal hepatectomy.
Animals↗
Cholecystokinin increases small intestinal motility and reduces enteric bacterial overgrowth and translocation in rats with surgically induced acute liver failure.
Enteric bacterial translocation into extraintestinal sites has been proposed as a potential route for bacterial infection in acute liver failure. Bacterial overgrowth in the intestine plays an important role in the etiology of bacterial translocation from the gut. The aim of the present study was to evaluate the influence of exogenous cholecystokinin (CCK) on intestinal transit time, enteric bacterial overgrowth and translocation in experimental acute liver failure induced by 90% hepatectomy. A delayed intestinal transit time was noted in animals subjected by subtotal hepatectomy after 1 h, followed by enteric bacterial overgrowth and translocation into the systemic circulation, mesenteric lymph nodes, and systemic organs at 2 and 4 h. Intravenous infusion of CCK stimulated intestinal transit time in animals with sham operation and subtotal hepatectomy, though a restoration to sham levels could not be obtained in the later. Moreover, enteric bacterial overgrowth and translocation were prevented in hepatectomized animals. The present data imply that impaired intestinal motility, followed by enteric bacterial overgrowth and translocation in experimental acute liver failure, could be prevented by CCK infusion.
Animals↗