Biomedical subjects

H van Goor

Publications and source records attributed to H van Goor.

At least 91 records · Page 5Linked to original sources

PubMed1996

SIRS, MODS and tertiary peritonitis.

Some patients with peritonitis develop a septic response without a detectable infective focus. It is suggested that an immunological dysfunction is responsible for this so called tertiary peritonitis. The role of the gastrointestinal tract in the development of multiple organ dysfunction syndrome (MODS) is discussed. In patients with tertiary peritonitis treatment should be directed towards restoration of the immunological balance, which is probably more important than the elimination of microorganisms with antibiotics.

Anti-Bacterial Agents↗

PubMed1995

Results of vascular reconstructions for atherosclerotic arterial occlusive disease of the lower limbs in young adults.

OBJECTIVE: To evaluate early and long-term results of vascular reconstructions for arterial atherosclerotic occlusive disease (AOD) of the lower limb in young patients under the age of 40 years. DESIGN: Retrospective study. SETTING: University hospital. MATERIALS: Twenty-nine young adults, who underwent vascular reconstruction for histologically proven AOD of the aortoiliac and/or femoropopliteal segments in a 15-year period. CHIEF OUTCOME MEASURES: Early and late mortality, failure of vascular reconstructions, additional procedures, other manifestations of atherosclerosis, recurrence of symptoms. MAIN RESULTS: Nine patients (31%) died, seven related to atherosclerotic disease. In 21 patients (72%) initial vascular reconstruction(s) failed. Twenty-two patients (76%) underwent surgery for failures and/or progression of AOD in other segments of the lower limb. Amputation was performed in five patients (17%). At the end of the follow-up period only 25% of surviving patients were asymptomatic. CONCLUSION: Young patients undergoing vascular reconstructions for AOD of the lower limbs, in particular those who initially have extensive and progressive atherosclerosis, have a poor outcome in terms of a high mortality and a high operative failure rate. A liberal attitude towards reconstructive surgery, particularly in claudication, is not warranted.

Adult↗

PubMed1995

Proteinuria, lipoproteins and renal apolipoprotein deposits in uninephrectomized female analbuminemic rats.

To elucidate the pathogenetic role of hyperlipidemia per se in the development of glomerulosclerosis, severely hyperlipidemic female analbuminemic rats (NAR) and mildly hyperlipidemic male NAR were studied for a period of 37 weeks after uninephrectomy (UNX). Plasma cholesterol increased from 6.3 +/- 0.4 (week 4) to 11.9 +/- 0.6 mmol/liter (week 37) in the female NAR, and from 4.3 +/- 0.1 to 6.4 +/- 0.5 mmol/liter in the male NAR in the same period. Plasma protein concentration was also consistently higher in female NAR (60 +/- 1 g/liter) as compared to male NAR (52 +/- 1 g/liter). Plasma viscosity was higher in female NAR than in male NAR, but there were no differences in blood viscosity. Proteinuria increased progressively in the UNX female NAR from 25 weeks after surgery, reaching a final value of 141 +/- 37 mg/day. No proteinuria occurred in the UNX male NAR (final value 15 +/- 2 mg/day). Glomerular capillary pressure, measured prior to the onset of proteinuria, was not significantly different in UNX female NAR and UNX male NAR. At the end of the study glomerulosclerosis and lipid deposition was only found in the UNX female NAR. Throughout the study hyperfiltration and hyperperfusion, relative to the one-kidney clearances of the sham-operated (2K) animals, were not different in UNX male and female NAR. No differences were observed in blood pressure. Hypertrophy, evaluated by glomerular diameters, was less pronounced in UNX female NAR (174 +/- 3 microns) than in UNX male NAR (190 +/- 7 microns). Glomerular diameters in 2K female and male NAR were similar (respectively 158 +/- 2 and 157 +/- 4 microns). Plasma apo B levels were similar (2K female NAR: 204 +/- 8 U; 2K male NAR 204 +/- 13 U), but cholesterol and triglyceride content of apo B-containing lipoproteins, namely VLDL, IDL and LDL, was increased twofold in the female NAR as compared to the male NAR, implying a larger particle size in the female NAR. Deposition of apo B and apo E was observed in the glomerular mesangium of UNX female NAR, particularly in sclerotic lesions. Glomerular apo A-I deposits were localized primarily in visceral epithelial cells and were not associated with sclerotic lesions. The development of proteinuria and glomerulosclerosis after UNX in female NAR but not in male NAR may depend upon differences in plasma lipoprotein composition, but is apparently not related to differences in whole kidney hyperfiltration and hyperperfusion, glomerular capillary pressure, or blood viscosity.

Animals↗

PubMed1995

Differential mRNA expression of renal cortical tissue inhibitor of metalloproteinase-1, -2, and -3 in experimental hydronephrosis.

The pathophysiologic sequelae of both acute and chronic experimental unilateral ureteral obstruction (UUO) in the rat are the result of a variety of complex humoral and cellular interactions. The development of interstitial fibrosis is dependent on the tightly coupled regulation of synthesis and degradation of extracellular matrix proteins. This laboratory, among others, has shown an up-regulated expression of renal cortical transforming growth factor (TGF)-beta 1 within hours of the onset of UUO. Because a potential contribution of TGF-beta to fibrosis may be its ability to increase the expression of proteinase inhibitors such as members of the tissue inhibitor of metalloproteinase (TIMP) family, this laboratory now sought to delineate the kinetics of TIMP-1, TIMP-2, and TIMP-3 mRNA expression in the renal cortex after UUO. There was a marked elevation of TIMP-1 mRNA expression after UUO, which was first noted at 12 h after ureteral ligation. By 96 h after UUO; there was a 30-fold increment in TIMP-1 mRNA in the obstructed kidneys compared with the contralateral unobstructed kidney or sham-operated rat specimens. In contradistinction to TIMP-1, a decrease in TIMP-3 mRNA levels was noted at 12 h after ureteral obstruction and persisted at the 24-, 48-, and 96-h time intervals. TIMP-2 gene expression remained at a relatively constant level during the entire study. It is proposed that the increased expression of TGF-beta 1 post-UUO induces a profibrogenic state and initiates a cascade of dysregulatory events including the up-regulation of TIMP-1.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1995

Gentamycin reduces bacteremia and mortality rates associated with the treatment of experimental peritonitis with recombinant tissue plasminogen activator.

BACKGROUND: Recombinant tissue plasminogen activator (rtPA), administered intraperitoneally, reduces intra-abdominal abscess formation in rats with fecal peritonitis at the costs of increased mortality and early Escherichia coli bacteremia. It was determined whether or not mortality and bacteremia could be prevented by gentamycin in these rats. STUDY DESIGN: Fecal peritonitis was induced by intraperitoneal injection of sterile feces contaminated with 10(8) (experiment 1) or 10(4) (experiment 2) colony forming units (cfu) E. coli and 10(4) cfu Bacteroides fragilis. Male Wistar rats were randomly assigned to receive either methyl hydroxy propyl cellulose (MHPC) gel alone (M) or 0.5 mg/mL rtPA dissolved in MHPC gel (M-tPA). Three hours after inoculation, one-half of the rats in each of these groups received 6 mg/kg gentamycin sulfate (G) intramuscularly (group M-G and M-tPA-G). At one, three, six, 12, and 24 hours after inoculation, blood cultures were taken. At five days after inoculation, intra-abdominal abscess formation was assessed and abscesses were cultured (experiment 2). RESULTS: All rats in groups M and M-tPA in experiment 1 developed bacteremia and died within 24 hours. Bacteremia occurred significantly earlier in group M-tPA compared with group M (p < 0.05). Gentamycin significantly reduced the number of rats with bacteremia, the bacteria concentration in the blood, and mortality rates. Although in experiment 2 none of the rats developed bacteremia, gentamycin prevented mortality associated with the use of rtPA. The number of abscesses in groups M-tPA and M-tPA-G was significantly lower than in those in groups M and M-G (p < 0.01). Gentamycin did not influence the number of abscesses. CONCLUSIONS: Gentamycin reduces bacteremia and mortality rates in rats with fecal peritonitis treated with rtPA intraperitoneally to prevent intra-abdominal abscess formation.

Abdominal Abscess↗

PubMed1995

Myofibroblasts in experimental hydronephrosis.

Interstitial fibrosis is a common outcome of longterm ureteral obstruction. One pathological arm of the fibrotic reaction in diverse tissue loci and experimental models is the retraction of granulation tissue. The role of the myofibroblast in granulation tissue contraction and fibrocontractive diseases has been well established, but the mechanisms leading to differentiation of fibroblastic cells into myofibroblasts during the evolution of inflammation are not yet fully clarified. Investigators using other model systems have shown that macrophage-derived transforming growth factor-beta 1 (TGF-beta 1) may be pivotal in the process of myofibroblast modulation. Our laboratory has shown that the unilateral ureteral obstruction in the rat is characterized by a 20-fold increment in infiltrating renal cortical interstitial macrophages, an increase in cortical TGF-beta 1 gene expression, which parallels the infiltrating macrophage burden, and immunolocalization of this peptide growth factor in close proximity to resident interstitial fibroblasts. Because of this model's features, it was our aim to assess whether a myofibroblastic modulation was operant in the renal cortex of obstructed rat kidneys versus the control contralateral unobstructed kidney specimens. Immunolabeling for alpha-smooth muscle actin and the intermediate filament protein, desmin, was detected and steadily intensified from 24 to 96 hours after unilateral ureteral obstruction in obstructed kidneys only. In temporal concert with the detection of alpha-smooth muscle actin protein, the mRNA expression for this cytoskeletal component exhibited 3.7-, 15.7-, and 4.1-fold increments in the renal cortex of obstructed kidneys versus the contralateral unobstructed kidney specimens at 24, 48, and 96 hours after unilateral ureteral obstruction, respectively. Whole body X-irradiation, administered to rats 11 days before proximal left ureteral ligation, significantly lowered cortical interstitial macrophage number, cortical TGF-beta and alpha-smooth muscle actin mRNA levels as well as the intensity of immunolabeling for alpha-smooth muscle actin from 12 to 96 hours after unilateral ureteral obstruction. These data support a postulate that renal cortical TGF-beta 1, derived from the infiltrating macrophage, in part, contributes to the subsequent interstitial fibrosis response to renal injury by fostering the modulation of fibroblasts to myofibroblasts within the renal cortex after ureteral obstruction.

Actins↗

PubMed1995

High lipid levels in very low density lipoprotein and intermediate density lipoprotein may cause proteinuria and glomerulosclerosis in aging female analbuminemic rats.

BACKGROUND: Male rats are generally more prone to developing renal disease than female rats. However, female Nagase analbuminemic rats (NAR) are profoundly hyperlipidemic and develop proteinuria and glomerulosclerosis after uninephrectomy. Male NAR are less hyperlipidemic and are resistant to developing renal damage after uninephrectomy. Ovariectomy markedly decreases hepatic triglyceride secretion and plasma triglyceride levels in the female NAR. EXPERIMENTAL DESIGN: In this study, we investigated the relationship between plasma lipids and lipoprotein composition as well as the development of proteinuria, glomerular apolipoprotein and lipid deposition, and glomerulosclerosis in aging female and male analbuminemic rats. We also studied whether ovariectomy in female NAR at an early age would protect their renal function in old age. RESULTS: Aging hyperlipidemic female NAR with high triglyceride and cholesterol levels in very low density lipoprotein (VLDL) and intermediate density lipoprotein (IDL) were found to develop spontaneous proteinuria at 9 months of age. Glomerular lipid deposition and glomerulosclerosis were observed at 18 months of age. In male NAR that had lower lipid levels in VLDL and IDL, only mild proteinuria and no glomerular lipid deposition or glomerulosclerosis were observed up to the age of 22 months. Concurrently ovariectomized NAR demonstrated profound and persistent decreases in triglyceride and cholesterol content of VLDL and IDL as well as total plasma triglycerides, without much change in LDL, high density lipoprotein, total plasma cholesterol, or apolipoprotein B, and they remained completely free of proteinuria and glomerulosclerosis. Apolipoprotein B deposition in glomeruli was not different in the oldest female, male, or ovariectomized NAR. No important differences were observed in glomerular diameter between the three different groups up to the age of 1 year. CONCLUSIONS: These findings point to an important role of elevated lipid content of the triglyceride-rich lipoproteins VLDL and IDL in the pathogenesis of proteinuria and glomerulosclerosis in the female NAR.

Aging↗

PubMed1994

Translocation of bacteria and endotoxin in organ donors.

OBJECTIVE: To determine if bacterial translocation and endotoxin absorption occur in organ donors with an anatomically intact gastrointestinal tract. DESIGN: Case series. SETTING: Intensive care units in general and university hospitals. PATIENTS: Twenty-one (multiple) organ donors. INTERVENTION: None. MAIN OUTCOME MEASURES: Occurrence of factors that may promote bacterial translocation and/or endotoxin absorption. Bacterial concentration in mesenteric lymph nodes, abdominal fluid, blood, liver, lung, and spleen. Endotoxin level in abdominal fluid, peripheral blood, and portal blood. Anatomical integrity of the bowel wall. RESULTS: Factors that may promote bacterial translocation and/or endotoxin absorption were present in all organ donors. Culture specimens revealed bacteria in 14 organ donors (67%). In 210 (81%) of 260 culture specimens, the bacteria isolated were identical to those isolated from the bowel content, demonstrating bacterial translocation. Endotoxin was found in nine (53%) of 17 abdominal fluid samples, in four (19%) of 21 peripheral blood samples, and in two (10%) of 21 portal blood samples. Light- and electron-microscopic examination of the bowel wall showed no anatomical abnormalities. CONCLUSION: Bacterial translocation and endotoxin absorption are frequent among organ donors and may adversely influence organ function in transplant recipients and other critically ill patients.

Ascitic Fluid↗

PubMed1994

Fibrinolytic activity in the abdominal cavity of rats with faecal peritonitis.

Generalized peritonitis causes a reduction in abdominal fibrinolytic activity, resulting in persistence of intraabdominal fibrin with subsequent adhesion and abscess formation. The activities of tissue plasminogen activator (tPA) and plasminogen activator inhibitor (PAI) were measured in the peritoneal fluid of rats with faecal peritonitis and correlated with the extent of peritoneal damage to determine the cause of decreased fibrinolysis. Activity of tPA was low during the study period of 8 days, but higher in rats with peritonitis than in controls. The activity of PAI in rats with peritonitis was significantly increased compared with that of controls during the whole study period (P < 0.001). Histological signs of damage to the peritoneum were similar in rats with peritonitis and controls. There was no correlation between the extent of peritoneal damage and tPA or PAI activity. The increased activity of PAI in the peritoneal fluid of rats with faecal peritonitis may be the main cause of reduced fibrinolysis in the abdominal cavity. Activities of tPA and PAI may originate not only from the mesothelium but from other sources.

Animals↗

PubMed1994

Neutrophil activation in vitro and in vivo in Wegener's granulomatosis.

The mechanisms underlying glomerular capillary wall injury in Wegener's granulomatosis (WG) are not well understood. Anti-neutrophil cytoplasmic antibodies (ANCA), present in sera from patients with WG, are known to stimulate respiratory burst and degranulation of primed polymorphonuclear neutrophils (PMN) in vitro. Experimental studies have shown that oxygen radical production and lysosomal enzymes are important mediators of glomerular capillary wall injury. In the present study we investigated the presence of activated PMN and the extracellular localization of lysosomal enzymes in 28 consecutive renal biopsies from patients with WG. The presence of activated PMN within the renal biopsies was compared with the capacity of ANCA, isolated from simultaneously drawn serum samples, to activate primed PMN obtained from a normal donor. Both parameters were also related to renal function. Renal biopsies were obtained from newly diagnosed WG patients before therapy had started. Activation of PMN in the biopsies was assessed by measuring hydrogen peroxide production in situ. The number of activated PMN in the biopsy correlated with the extent of impairment of renal function. Proteinase 3, myeloperoxidase, and elastase, all targets of ANCA, were localized extracellularly in renal tissue and were also found within tubular epithelial cells. All ANCA positive samples were capable of activating primed PMN. The amount of activation correlated with the ANCA titer in those samples. No correlation, however, was found between the in vitro capacity of ANCA-positive IgG fractions to activate primed PMN and the number of activated PMN present in the renal biopsy. We conclude that activated PMN producing toxic oxygen metabolites and releasing lysosomal enzymes, are present in renal biopsies from patients with WG. The amount of activated PMN present within the kidney, and not the capacity of the corresponding ANCA to activate PMN, correlates with renal tissue damage as assessed by serum creatinine levels.

Antibodies, Antineutrophil Cytoplasmic↗

PubMed1994

Transforming growth factor-beta expression in macrophages during hypercholesterolemic states.

Macrophage infiltration into the glomerular mesangium is a prominent feature of various glomerulopathies. Recent evidence suggests that infiltrating macrophages may play a role in propagating initial glomerular injury to the development of glomerulosclerosis via transforming growth factor-beta (TGF-beta)-stimulating matrix accumulation. Rats with the acute puromycin aminonucleoside (PA) nephrosis exhibit an elevated gene expression of glomerular TGF-beta 1; however, the cellular origin of this upregulation is unknown. Using polymerase chain reaction (PCR), we detected that the TGF-beta 1 isoform is expressed in glomerular macrophages isolated from experimental rats made hypercholesterolemic by either diet or by induction of PA nephrosis. Peritoneal macrophages from nephrotic or dietary-hypercholesterolemic animals also exhibited a significant increment in the expression of TGF-beta 1 mRNA on Northern analysis, in contrast to similar cells obtained from normal control rats. PCR analysis of glomerular RNA also detected the expression of the TGF-beta 2 mRNA isoform. TGF-beta 2 mRNA expression was not observed in isolated glomerular macrophages from either glomeruli of PA-nephrotic rats or from glomeruli of animals with dietary hypercholesterolemia. Expression of the TGF-beta 3 mRNA isoform was only observed by PCR in J774 A.1 cells. Thus the as a cellular source for the enhanced expression of TGF-beta 1 during the acute nephrotic phase of our toxic, progressive glomerulopathy model and within several days of inducing only hypercholesterolemia by dietary means.

Albuminuria↗

PubMed1994

Effect of recombinant tissue plasminogen activator on intra-abdominal abscess formation in rats with generalized peritonitis.

BACKGROUND: During generalized peritonitis, intraabdominal fibrin deposition is stimulated whereas fibrinolytic activity is reduced, which predisposes intra-abdominal abscess formation. We investigated the effects of increasing the intra-abdominal fibrinolytic activity on abscess formation by intra-abdominal administration of recombinant tissue plasminogen activator (rt-PA). Potential side effects, such as bacteremia and bleeding, were also assessed. STUDY DESIGN: A rat model of generalized peritonitis, induced by intraperitoneal injection of sterile feces contaminated with 10(4) cfu per mL Escherichia coli (E. coli) and 10(4) cfu per mL Bacteroides fragilis, was used. RESULTS: Rats treated with rt-PA dissolved in methyl hydroxy propyl cellulose (MHPC) gel (0.5 mg per mL), had significantly less intra-abdominal abscesses than rats in the control group, treated with either Ringer's lactate solution or MHPC gel alone (p < 0.01). Other than E. coli, cultures of abscesses revealed species originating from the intestine, demonstrating bacterial translocation. The mortality rate was significantly higher in the rats treated with rt-PA as compared with rats in the control group (p < 0.01), which was surprising considering the absence of bacteremia. By challenging the rats with a higher dose of E. coli, early bacteremia was observed in the rats treated with rt-PA, not related to increased mortality rates. Intraabdominal use of rt-PA was not associated with an increased incidence of bleeding events. CONCLUSIONS: Recombinant tissue plasminogen activator prevents abscess formation in rats with generalized peritonitis. However, early bacteremia and increased mortality rates are serious drawbacks of the intra-abdominal use of rt-PA in this rat model.

Abdominal Abscess↗

PubMed1993

Pathobiology of focal sclerosis.

This paper briefly reviews recent experimental data derived from work in animals and cell cultures that have increased our understanding of the pathobiologic pathways leading to focal sclerosis. These pathways include glomerular visceral epithelial cell damage, leukocyte infiltration, hyperplasia and matrix accumulation in the mesangium, and endothelial injury.

Animals↗

PubMed1993

Plasma lipoproteins and renal apolipoproteins in rats with chronic adriamycin nephrosis.

The relation between plasma lipoprotein composition and renal apolipoprotein deposition was studied in nephrotic rats in which stable renal function had been monitored for 7 months after a single low dose of adriamycin (ADR, 3 mg/kg). Proteinuria was observed 3 weeks after ADR and increased progressively up to about 0.5 g/day (versus 0.07 g/day in controls; P < 0.001), while the creatinine clearance remained stable at about 80% of control values. Hypercholesterolaemia was observed 6 weeks after ADR, and increased progressively up to 7.0 +/- 1.0 mmol/l (versus 2.3 +/- 0.1 mmol/l in controls; P < 0.001). Cholesterol was primarily located in LDL2 and HDL2 lipoproteins. Plasma apolipoprotein (apo) A-I increased by more than 400% in the nephrotic rats (P < 0.001). Apo B and apo E increased by about 60% (P < 0.01), whereas apo A-IV remained unchanged. Focal sclerotic lesions in glomeruli had an incidence of 50 +/- 10% in ADR rats versus 2 +/- 1% in controls (P < 0.001). Immunohistochemistry revealed apo A-I and apo A-IV in the visceral epithelium. Apo E immunoreactivity and lipid deposits were observed in focal glomerular sclerotic lesions of ADR rats. Neither apolipoproteins nor lipids were detected in glomeruli of controls. Proximal tubular localization of apolipoproteins was extensive for apo A-I, apo A-IV and apo E, but no differences were observed in tubular deposition of apolipoproteins between ADR and control rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Renal apolipoproteins in nephrotic rats.

Recent experimental data suggest a role for lipids in the pathogenesis of glomerulosclerosis. In this study, we examined the main apolipoproteins (apo) of high density lipoproteins (A-I, A-IV, E), low density lipoproteins (B), and very low density lipoproteins (B,E) in plasma and kidney tissue of rats with puromycin aminonucleoside or adriamycin nephrosis. In full-blown nephrosis, plasma concentrations of apo A-I and apo B were significantly elevated, apo A-IV and apo E levels did not change. Immunohistological studies in plastic sections revealed increased apo A-I, apo A-IV, and apo E immunoreactivity in glomerular visceral epithelial cells both in puromycin aminonucleoside and adriamycin nephrosis. This was confirmed by immunoelectronmicroscopy. In addition, apo B and apo E were encountered in increased amounts in the mesangium and colocalized with Oil Red O-positive lipid deposits, particularly in puromycin aminonucleoside nephrosis rats. Double-staining showed a preferential localization of apo B and apo E at sites of increased mesangial matrix in close proximity to ED1-positive foam cells, i.e., the mesangial macrophages. The close topographic association between apo B and apo E, lipid deposits, and macrophages in the mesangium lend further support to the concept of lipid-mediated glomerular injury in nephrosis.

Animals↗

PubMed1992

Glomerular macrophage modulation affects mesangial expansion in the rat after renal ablation.

Recent studies have provided evidence for the involvement of macrophages (m phi) in various types of human and experimental glomerular disease. The aim of the present study was to examine the effect of m phi depletion on glomerular injury after 3/4 renal ablation in the rat. This "remnant kidney" model is a widely used experimental model of focal and segmental glomerulosclerosis. Sustained glomerular m phi depletion was induced in remnant kidney rats by a regimen of sublethal triple systemic X-irradiation with shielding of the kidney remnants. Groups of 8 X-irradiated and 8 non-irradiated rats were studied at 5, 9, and 13 weeks after renal ablation. X-irradiated rats showed severe peripheral blood leukopenia at 5 and 9 weeks which had normalized at 13 weeks. The number of remnant glomerular m phi (immunohistochemistry with the monoclonal antibody ED1) in X-irradiated rats at 5 weeks was significantly lower when compared to non-irradiated remnant kidney rats. A rebound effect occurred at 9 and 13 weeks with increased m phi in remnant glomeruli of X-irradiated rats. Light microscopic examination disclosed significantly lower semiquantitative scores for mesangial cellularity and mesangial matrix expansion in remnant glomeruli of X-irradiated rats at 5 weeks when compared to non-irradiated remnant kidney rats. Mesangial matrix expansion had increased in X-irradiated rats at 9 and 13 weeks after ablation coincident with elevated glomerular m phi at these intervals. Multiple linear regression analysis indicated a highly significant contribution of m phi to the best fitting regression model predicting mesangial matrix expansion (multiple r2 = 0.81). In conclusion, these data provide evidence for a contributory role of m phi in the evolution of glomerular injury in the rat after renal ablation.

Animals↗

PubMed1992

Antibodies defining rat endothelial cells: RECA-1, a pan-endothelial cell-specific monoclonal antibody.

We have been searching for antibodies reactive with rat endothelial cells. Two monoclonal antibodies (mAb), named RECA-1 and RECA-2 were produced and tested in immunoperoxidase staining on frozen sections of various rat tissues. Staining patterns were compared to those obtained with the mAbs OX-2, OX-26, OX-43, and the polyclonal antibody to von Willebrand Factor (vWF), which all have been described to react with rat endothelial cells. The RECA-2 mAb showed staining patterns similar to those obtained with OX-2. RECA-1 showed to be the only antibody reactive with all vascular endothelium in the tested tissues. In addition, RECA-1 was endothelial cell-specific whereas all other antibodies crossreacted with one or more other cell types. No reactivity of RECA-1 was found in various tested species other than rat. The RECA-1 antibody was successfully applied in staining of paraformaldehyde fixed, plastic embedded tissue material. Immunofluorescence staining of viable endothelial cells demonstrated that RECA-1 recognizes a cell surface antigen. This was supported by intravenous injection of RECA-1, which showed the antibody to localize along the endothelium lining the vasculature in various organs tested. No reactivity of the antibody was seen when applied in immunoblotting of PAGE-run lysates from endothelial cell cultures and stromal cell preparations. We believe RECA-1 to be a promising antibody for rat endothelial cell studies, and in particular for further defining nature and function of endothelial cell-specific antigens.

Animals↗

PubMed1991

Bezoars: a special cause of ileal obstruction in mentally retarded patients.

Abdominal symptoms in mentally retarded patients may pose difficult diagnostic problems due to an unreliable history of disease and incooperation of the patients. The case histories are presented of three patients with bezoars in the ileum. Delayed diagnosis and signs of peritonitis necessitated emergency surgery. All patients could successfully be treated by small bowel resection and primary anastomosis. In mentally retarded patients with abdominal pain a bezoar must be considered.

Adolescent↗