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Biomedical subjects

A Rosenkranz

Publications and source records attributed to A Rosenkranz.

At least 19 recordsLinked to original sources
PubMed2005

Impact of steroid withdrawal on metabolic parameters in a series of 112 enteric/systemic-drained pancreatic transplants.

BACKGROUND: New immunosuppressive protocols and advanced surgical techniques have brought major improvements in pancreas transplantation outcomes. Steroid withdrawal might have a beneficial long-term effect on metabolic parameters. METHODS: We retrospectively analyzed 112 enteric-drained pancreas transplants (PTx) performed between March 1997 and October 2001. Prophylactic imunosuppression consisted of ATG induction, tacrolimus, MMF, and steroids. RESULTS: Actuarial patient, pancreas, and kidney graft survivals at 1 year were 96.4%, 86.7%, and 95.3%, respectively. The 5-year pancreatic graft survival was 77%. In addition to four patients who died with functioning grafts, eight grafts were lost due to intraabdominal infection; ten due to rejection; and the remaining three, due to other complications. One-year follow-up was available for 89 patients, Including 22 (25%) withdrawn from steroids. Significantly lower median serum cholesterol values were measured among patients off steroids (158 mg/dL [range 135 to 231 mg/dL] versus 188 mg/dL [range 91 to 278 mg/dl]; P = .005). In contrast, the difference in triglycerides did not reach statistical significance; that is, at last follow-up, at a median of 41.3 months posttransplant, 64 patients (70% of the available study population) were off steroids. Cessation of steroids resulted in significantly lower cholesterol (median 176 mg/dL [range 101 to 229 mg/dL] versus 196 mg/dL [range 107 to 339 mg/dL]; P = .047) and triglyceride values (median 74 mg/dL [range 34 to 299 mg/dL] versus 98 mg/dL [range 47 to 565 mg/dL]; P = .008), but had no impact on rejection rate, serum creatinine and urea, HbA(1c), or fasting blood glucose levels. CONCLUSIONS: Steroid withdrawal after pancreatic transplantation can be performed in the majority of cases without risking an immunologic complication, but it seems to be associated also with the benefit of improved lipid metabolism.

Adult↗
PubMed2004

Acute effects of glucose and insulin on vascular endothelium.

AIMS/HYPOTHESIS: Chronic exposure to high concentrations of glucose has consistently been demonstrated to impair endothelium-dependent, nitric oxide (NO)-mediated vasodilation. In contrast, several clinical investigations have reported that acute exposure to high glucose, alone or in combination with insulin, triggers vasodilation. The aim of this study was to examine whether elevated glucose itself stimulates endothelial NO formation or enhances insulin-mediated endothelial NO release. METHODS: We measured NO release and vessel tone ex vivo in porcine coronary conduit arteries (PCAs). Intracellular Ca(2+) was monitored in porcine aortic endothelial cells (PAECs) by fura-2 fluorescence. Expression of the Na(+)/glucose cotransporter-1 (SGLT-1) was assayed in PAECs and PCA endothelium by RT-PCR. RESULTS: Stimulation of PCAs with D: -glucose, but not the osmotic control L: -glucose, induced a transient increase in NO release (EC(50) approximately 10 mmol/l), mediated by a rise in intracellular Ca(2+) levels due to an influx from the extracellular space. This effect was abolished by inhibitors of the plasmalemmal Na(+)/Ca(2+) exchanger (dichlorobenzamil) and the SGLT-1 (phlorizin), which was found to be expressed in aortic and coronary endothelium. Alone, D: -glucose did not relax PCA, but did augment the effect of insulin on NO release and vasodilation. CONCLUSIONS/INTERPRETATION: An increased supply of extracellular D: -glucose appears to enhance the activity of the endothelial isoform of nitric oxide synthase by increasing intracellular Na(+) concentrations via SGLT-1, which in turn stimulates an extracellular Ca(2+) influx through the Na(+)/Ca(2+) exchanger. This mechanism may be responsible for glucose-enhanced, insulin-dependent increases in tissue perfusion (including coronary blood-flow), thus accelerating glucose extraction from the blood circulation to limit the adverse vascular effects of prolonged hyperglycaemia.

Amiloride↗
PubMed1999

Glomerular inflammation: use of genetically deficient mice to elucidate the roles of leukocyte adhesion molecules and Fc-gamma receptors in vivo.

Single gene knock-outs in mice have been used to define the biological role of leukocyte adhesion receptors, Fc-gamma receptors and complement in animal models of immune complex glomerulonephritis. These studies have shown important differences in the role of P-selectin in glomerular inflammation and inflammation at other sites, and have given a new appreciation of the dominant role played by Fc-gamma receptors in immune complex-induced glomerular injury.

Animals↗
PubMed1997

A role for Mac-1 (CDIIb/CD18) in immune complex-stimulated neutrophil function in vivo: Mac-1 deficiency abrogates sustained Fcgamma receptor-dependent neutrophil adhesion and complement-dependent proteinuria in acute glomerulonephritis.

Mac-1 (alphambeta2), a leukocyte adhesion receptor, has been shown in vitro to functionally interact with Fcgamma receptors to facilitate immune complex (IC)-stimulated polymorphonuclear neutrophil (PMN) functions. To investigate the relevance of Mac-1-FcgammaR interactions in IC-mediated injury in vivo, we induced a model of Fc-dependent anti-glomerular basement membrane (GBM) nephritis in wild-type and Mac-1-deficient mice by the intravenous injection of anti-GBM antibody. The initial glomerular PMN accumulation was equivalent in Mac-1 null and wild-type mice, but thereafter increased in wild-type and decreased in mutant mice. The absence of Mac-1 interactions with obvious ligands, intercellular adhesion molecule 1 (ICAM-1), and C3 complement, is not responsible for the decrease in neutrophil accumulation in Mac-1- deficient mice since glomerular PMN accumulation in mice deficient in these ligands was comparable to those in wild-type mice. In vitro studies showed that spreading of Mac-1-null PMNs to IC-coated dishes was equivalent to that of wild-type PMNs at 5-12 min but was markedly reduced thereafter, and was associated with an inability of mutant neutrophils to redistribute filamentous actin. This suggests that in vivo, Mac-1 is not required for the initiation of Fc-mediated PMN recruitment but that Mac-1-FcgammaR interactions are required for filamentous actin reorganization leading to sustained PMN adhesion, and this represents the first demonstration of the relevance of Mac-1-FcgammaR interactions in vivo. PMN-dependent proteinuria, maximal in wild-type mice at 8 h, was absent in Mac-1 mutant mice at all time points. Complement C3-deficient mice also had significantly decreased proteinuria compared to wild-type mice. Since Mac-1 on PMNs is the principal ligand for ic3b, an absence of Mac-1 interaction with C3 probably contributed to the abrogation of proteinuria in Mac-1-null mice.

Actins↗
PubMed1997

Orellanine poisoning: rapid detection of the fungal toxin in renal biopsy material.

BACKGROUND: Mushroom poisoning by some species of the Cortinarius (Agaricales) often lead to irreversible renal failure caused by the nephrotoxin orellanine. In 1994 and 1995, six poisoning outbreaks involving ten individuals in Northern Italy and in Austria were investigated. METHODS: A total of 87 clinical samples (urine and blood samples including renal biopsy material of three patients) were examined for the presence of orellanine by thin layer chromatography. RESULTS: Orellanine can be detected after a relatively long period following poisoning by performing a simple thin layer chromatography technique using small quantities of renal biopsy material. No toxin was found in urine or blood samples. CONCLUSIONS: Orellanine is rapidly concentrated in the kidneys in a relatively soluble form and cannot be detected in urine, blood and dialysis fluids at the time when first symptoms appear.

2,2'-Dipyridyl↗
PubMed1995

Granulocyte activation via a binding site near the C-terminal region of complement receptor type 3 alpha-chain (CD11b) potentially involved in intramembrane complex formation with glycosylphosphatidylinositol-anchored Fc gamma RIIIB (CD16) molecules.

We report that engagement of a particular epitope near the C-terminal region of complement receptor type 3 (CR3, CD11b/CD18) alpha-chain with CD11b mAb VIM12 induces granulocyte activation with a rise in cytosolic-free Ca2+, actin polymerization, an up-regulation of CR3 cell surface expression and enhanced adhesiveness. Induction of enhanced adhesiveness and homotypic aggregation of human granulocytes represents an active process. It is temperature and energy dependent, requires divalent cations, and an intact cytoskeleton. The mAb VIM12-induced enhanced adhesiveness seems to be mediated, at least in part, by activated CR3 molecules. It can be significantly inhibited, although not completely abolished, with blocking mAbs against adhesiotopes of CR3. VIM12-induced adhesion could be blocked with the serine/threonine inhibitors okadaic acid and calyculin A and with dibuturyl-cAMP but not with the protein kinase inhibitors herbimycin A and staurosporine. We further present evidence that the particular molecular region of CR3 recognized by mAb VIM12 might be involved in the reported intramembrane sugar-lectin type interaction and complex formation between transmembrane CR3 and glycosylphosphatidylinositol (GPI)-anchored Fc gamma RIIIB (CD16) molecules on human granulocytes. Binding of mAb VIM12 to CR3 on granulocytes enhances the release of GPI-anchored Fc gamma RIIIB molecules from granulocytes upon phosphoinositol-phospholipase C treatment. The sugar preparation N-acetyl-D-glucosamine, previously shown to dissociate CR3-Fc gamma RIIIB complex formation, inhibits mAb VIM12 binding. Engagement of CR3 with mAb VIM12 may thus mimic a biologically relevant intramembrane cooperation between two distinct receptor molecules on human granulocytes.

Actins↗
PubMed1994

Effective stimulation of neutropoiesis with rh G-CSF in dyskeratosis congenita: a case report.

Dyskeratosis congenita (DC) is a rare congenital X-linked disorder. The major clinical manifestations are abnormal skin pigmentation, nail dystrophy, and leukoplakia of mucosal membranes. About 50% of the patients develop bone marrow failure, which is partly responsible for the poor prognosis. Recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF) has been administered to some neutropenic patients with DC, but only a moderate stimulation of neutropoiesis has been observed. We report on a patient with DC treated with recombinant human granulocyte-colony-stimulating factor (rhG-CSF). This treatment resulted in a substantial dose-dependent increase in the neutrophil count.

Adult↗
PubMed1993

Monoclonal antibodies to the carbohydrate structure Lewis(x) stimulate the adhesive activity of leukocyte integrin CD11b/CD18 (CR3, Mac-1, alpha m beta 2) on human granulocytes.

Several carbohydrate structures on human granulocytes have been discussed as potential ligands for C-type lectins (selectins) on endothelial cells. Among them are the lacto-series type II chain antigens sialyl-Lewis(x) (SLe(x), Lewis(x) (Le(x)), and VIM2. We demonstrated in this study that monoclonal antibodies (mAbs) to Le(x) and to SLe(x), but not other anticarbohydrate mAbs (VIM2, CDw17, CD24), can stimulate granulocytes to form homotypic aggregates. This effect was particularly noticeable with three distinct anti-Le(x) mAbs (3C6, 4D1, 6C7). Much less impressive effects were also seen with nine other anti-Le(x) mAbs and with the anti-SLe(x) mAb CSLEX1. Aggregation was shown to be an active process. It is temperature and energy dependent, requires divalent cations, and is selective in terms of mAb specificity. Anti-Le(x)-induced homoaggregate formation could be inhibited with CD11b mAb JML-H11 and CD54 (ICAM1) mAb LB-2 and thus seems to be associated with activation of the beta 2-integrin cytoadhesion pathway.

Antibodies, Monoclonal↗
PubMed1990

Prophylaxis of necrotizing enterocolitis by oral IgA-IgG: review of a clinical study in low birth weight infants and discussion of the pathogenic role of infection.

Necrotizing enterocolitis, a severe gastrointestinal disease in the neonatal period, affects primarily premature infants. Perinatal complications that predispose the neonate to systemic hypoxia are frequent in infants with necrotizing enterocolitis. Ischemia of the intestinal mucosa may facilitate the invasion of enteric microorganisms in stressed low birth weight infants. Geographical and temporal clustering of outbreaks of the disease and the termination of epidemics by standard infection control underline the importance of infectious agents in the development of this disease. Several studies have established the immunoprotective effect of orally administered antibodies against infection of the gastrointestinal mucosa in children and adults. Anecdotal evidence suggested that feeding of human immune globulin might have a positive effect on the incidence of necrotizing enterocolitis in premature infants. This paper reviews a prospective, randomized, controlled trial of the efficacy of an oral immune globulin preparation (published in detail in the New England Journal of Medicine, Vol. 319, pp 1-7, 1988) and discusses the pathogenic role of infection in necrotizing enterocolitis.

Administration, Oral↗
PubMed1989

[Systemic side effects in immunotherapy of allergic diseases--a comparative study].

Data on systemic side effects (SSE) of specific immunotherapy of allergic diseases recorded in 99 publications over the past 10 years were evaluated and compared with the figure of 0.4% SSE, according to number of injections, published in 1987 by the authors of the present study. The latter figure ranks among the lowest of comparable publications and under present conditions represents the standard. Reasons for the small number of side effects may be found in persistent use of antihistamine premedication before each injection and reduction of vaccination dosage to 50,000 SQ units maximally. Chemically modified allergens are by no means less liable to produce side effects than other allergens. The comparison was undertaken with respect to the following preparations: Alavac P, Allergovit, Allpyral, Alutard, Aquagen (ALK aqueous), Conjuvac, Diephuis, Migen, Novo Helisen, Pangramin Depot, Pharmalgen, Pollinex, Reless, Spectralgen, Stallergenes Depot, and some vaccines, prepared by the authors themselves.

Desensitization, Immunologic↗
PubMed1988

Prevention of necrotizing enterocolitis in low-birth-weight infants by IgA-IgG feeding.

In a randomized clinical trial, we evaluated the efficacy of an oral immunoglobulin preparation (73 percent IgA and 26 percent IgG) in reducing the incidence of necrotizing enterocolitis in infants of low birth weight for whom breast milk from their mothers was not available. A total of 434 infants weighing between 800 and 2000 g were eligible for entry in the study. Of these, 255 were withdrawn - 234 during the first week of the study because breast milk from their mothers became available (123 in the treatment group and 111 in the control group), and 21 because of violations of protocol or because breast milk became available after the first week. The duration of follow-up was 28 days. Among the infants for whom breast milk did not become available during the study, there were no cases of necrotizing enterocolitis among the 88 receiving oral IgA-IgG, as compared with six cases among the 91 control infants (P = 0.0143). Of the infants withdrawn from the study, two assigned to the control group had necrotizing enterocolitis. We conclude that the oral administration of IgA-IgG may prevent the development of necrotizing enterocolitis in low-birth-weight infants.

Administration, Oral↗
PubMed1988

Hemorrhagic and hypoxic-ischemic intracranial lesions in neonates diagnosed by realtime sonography: incidence and short-term outcome.

887 neonates at risk, referred to our neonatal unit underwent serial cranial ultrasound examinations and neurological follow-up over a period of 2 years. Our study focused on the prognosis of hemorrhagic and hypoxic-ischemic intracranial lesions. 194 patients with hemorrhages (subependymal hemorrhages [SEH] I degree-IV degrees according to Papile, hemorrhages of the choroid plexus [CPH], primarily intraparenchymal hemorrhages [PIH]) and/or hypoxic-ischemic lesions (infarcts of the major intracranial arteries and lesions of the periventricular white matter) were neurologically followed-up 12 to 24 months postnatally. A group of 266 patients with normal ultrasound scans out of the same population was equally followed-up and served as a control group. At the age of 12 months a preliminary neurodevelopmental diagnosis was made and the patients were divided into 3 groups. Group N (normal) had a normal neuromotor outcome, group S (suspect) showed minor neurological abnormalities without evidence of cerebral palsy and/or a developmental quotient between 80 and 90. Group A (abnormal) included patients with any degree of cerebral palsy (CP) and/or a development quotient below 80. A normal neurological outcome was seen in 88.3% of patients without intracranial lesion and in a comparable proportion of patients with SEH I degree (88.9%), SEH II degrees (84.8%) and CPH (81.3%). Patients with SEH III degrees developed normally in 72.7%, whereas only 25% of patients with SEH IV degrees and PIH were neurological normal at 12 months of age. For detailed statistical evaluation only preterm neonates (birthweight below 2500 grms) with and without hemorrhagic lesions were compared. Concerning the neurological short-term outcome our analysis revealed no statistically significant difference between patients with SEH I degrees, II degrees, III degrees, CPH and the control group. SEH IV degrees and PIH showed a unfavourable outcome. Only 2/8 surviving patients had a normal development, but small numbers of patients made a statistical analysis impossible. Two children with infarcts of the middle cerebral artery developed spastic hemiplegia of the contralateral body side. One child with an infarct of the posterior cerebral artery developed normally until the age of 1 year, but could not be followed-up further. Patients with periventricular lesions showed a normal neuromotor development in 88.9% and 75% when they had solitary periventricular cysts or wedge-shaped periventricular lesions, whereas none of 9 children who suffered from extensive cystic periventricular leucomalacia was neurologically normal at the age of 1 year.(ABSTRACT TRUNCATED AT 400 WORDS)

Brain↗
PubMed1987

[Comparison of continuously monitored labor to unmonitored labor with reference to mortality and morbidity of the infant].

The aim of this retrospective study was to investigate differences with respect to infant morbidity and mortality following cardiotocographically monitored versus non-monitored deliveries. The observation period was 2 years. In particular, mortality was significantly higher in the non-monitored group of neonates weighing over 2500 g than in the monitored group of the same birth weight. The incidence of brain oedema in the group of infants where no cardiotocography had been employed during delivery was also higher. The results of this study are discussed.

Birth Weight↗
PubMed1986

Renal haemodynamics in spontaneously hypertensive rats with superficial glomeruli.

Spontaneously hypertensive rats (SHR) were mated with Munich-Wistar rats (MW), and the F1 hybrids were called Escola Paulista de Medicina (EPM) rats. The EPM rats present spontaneous hypertension and superficial glomeruli, allowing a study of glomerular haemodynamics. Mean whole kidney (GFR) and single nephron glomerular filtration rate (SNGFR), and mean total and glomerular plasma flow, were similar in EPM and MW rats. However, a higher glomerular capillary hydraulic pressure and a reduced ultrafiltration coefficient (Kf) of EPM rats were observed. The glomerular hypertension may be the cause of low Kf, a possible initial lesion of glomerular sclerosis. When mean arterial pressure levels were reduced to about 90 mmHg, a maintenance of SNGFR, with a 40% reduction in GFR, in EPM rats were achieved, suggesting an autoregulatory mechanism in the superficial but not in the juxtamedullary nephrons. The decrease on urinary sodium excretion (UNaV) in this condition, which was also lower than in MW rats, showed an impaired sodium handling by EPM kidneys, a possible role in the hypertension genesis. Thus, the data suggest that EPM rats can be a useful model for glomerular haemodynamics and microcirculatory studies in the spontaneously hypertensive state.

Animals↗
PubMed1985

Characteristics of spontaneously hypertensive, Wistar Kyoto and Munich Wistar rats bred in Brazil.

The breeding of imported strains of isogenic rats was started in 1981 because of the lack of experimental rat models in Brazil. The imported strains were: Spontaneously Hypertensive Rats (SHR) and their normotensive controls Wistar Kyoto Rats (WKY) from the National Institutes of Health, Bethesda, MD, and Munich Wistar (MW) rats which present superficial renal glomeruli, from Simonsen Laboratories, Gilroy, CA. Breeding of these strains was carried out without strict barriers (conventional breeding), under Standard Operating Procedures and strict inbreeding. Environmental factors such as ration, light, temperature, type of shavings and bedding, size of cages and their population were constant. Body weight growth curves were constructed for the three strains. The productivity of imported rats and local breeding colonies in 1981, 1982 and 1983 was compared on the basis of the following parameters: mean litter size, productivity of the females, pre- and post-weaning mortality, and effective yield. Systolic blood pressure was also measured for SHR and WKY rats. MW rats showed a high and relatively stable reproduction performance. The productivity of SHR and especially WKY animals declined progressively during the first three years, making the breeding of these strains of isogenic rats very difficult.

Animals↗
PubMed1983

[Pediatric aspects of success and failure of anti-D-prophylaxis].

During the last 10 years 485 exchange transfusions have been performed in the Children's Hospital of the City of Vienna--Glanzing, about 25% for rhesus immunization. While the frequency of exchange transfusions due to hyperbilirubinaemia and ABO incompatibility could be reduced by 90% by phototherapy and phenobarbital prophylaxis, only 55% reduction was observed in connection with rhesus immunization. Anti-D prophylaxis after the 1. pregnancy had only been carried out in 5 mothers (seen as secunda or multi para). In the 221 cases where exchange transfusion became necessary, 196 mothers of these children never had anti-D prophylaxis. This corresponds to 98%. There were 126 women with multiple pregnancies without abortion and 70 mothers, where anti-D prophylaxis had not been carried out after abortion. Consequently anti-D prophylaxis, especially including abortions both natural and induced, could substantially reduce the number of rhesus-sensitized newborns, requiring exchange transfusion.

Abortion, Spontaneous↗