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Biomedical subjects

G Enders

Publications and source records attributed to G Enders.

At least 55 records · Page 3Linked to original sources
PubMed1999

Evaluation of two novel enzyme immunoassays using recombinant antigens to detect cytomegalovirus-specific immunoglobulin M in sera from pregnant women.

BACKGROUND: Two novel enzyme linked immunosorbent assays (ELISA) (Abbott IMx CMV IgM 2.0, and Cobas Core CMV IgM EIA recomb, research version) which use recombinant antigens to detect cytomegalovirus (CMV)-specific IgM antibodies were evaluated. OBJECTIVES: A new ELISA is normally evaluated against a gold standard commercial kit, which in this case does not exist. We therefore evaluated the two novel recombinant ELISA against four conventional ELISAs and a recently developed CMV IgM immunoblot containing four purified viral and four recombinant proteins. STUDY DESIGN: A total of 280 sera from pregnant women and 42 potentially cross-reactive sera were investigated using the six ELISAs, including 101 sera which were also tested using the new IgM immunoblot. RESULTS: Relative sensitivity, relative specificity and overall agreement differed according to the reference assay. The Cobas Core CMV EIA recomb showed much higher agreement with the ELISA consensus, and the IMx CMV IgM 2.0 with the immunoblot. CONCLUSION: The evaluation of these new IgM assays in terms of their agreement with either commercial ELISA kits or the IgM immunoblot demonstrates that the question 'which reference method?' is still open. However the recombinant IgM assays may improve the diagnosis of CMV infection in pregnancy since the recombinant technology offers helpful tools for identifying diagnostically relevant proteins and allows the use of standardized pure preparations of antigens. For serological diagnosis of CMV infection in pregnancy two IgM assays that can be relied upon should be performed. IgM positive sera should be tested with supplementary assays to differentiate primary from non-primary infection.

Antibodies, Viral↗
PubMed1999

Intrauterine management of fetal parvovirus B19 infection.

OBJECTIVES: The aim of our study was to determine the outcome of pregnancies after intrauterine management of fetal parvovirus B19 infection. DESIGN: Retrospective study. SUBJECTS: A total of 37 cases of maternofetal parvovirus B19 infection, 35 of which were associated with hydrops fetalis, were referred to our tertiary level center between 1989 and 1996. With regard to fetal hydrops, no apparent cause other than parvovirus B19 infection was found in any patient. METHODS: In all patients, cordocentesis was performed to assess the degree of fetal anemia. When anemia was present, cordocentesis was followed by intrauterine transfusion with packed red cells into the umbilical vein. Further management depended on the degree of fetal anemia and gestational age and included follow-up fetal blood sampling/transfusion as well as ultrasound examinations as deemed appropriate. RESULTS: Packed red cell transfusion was performed in 30 patients with significant fetal anemia (Z-score 1.6-7.8 below the mean for gestational age). The fetal hemoglobin values ranged from 2.1 to 9.6 g/dl. Serum levels of platelets in the transfusion group were 9-228 x 10(9)/l with Z-scores in the range of < 1 to 3.8 below the mean. During treatment and follow-up, there were five intrauterine deaths (13.5%), one neonatal death (2.7%) and 31 live births (83.8%). CONCLUSIONS: Fetal parvovirus infection can lead to marked anemia and hydrops formation. Cordocentesis allows precise assessment of fetal anemia which can then be corrected by intravenous transfusion. Under this regimen, the outcome proved favorable in the majority of fetuses, even those that were severely anemic.

Anemia↗
PubMed1999

Reduction of hepatic microcirculatory failure caused by normothermic ischemia/reperfusion-induced injury by means of heat shock preconditioning.

Transient sublethal hyperthermia and the recovery from this exposure to heat (heat shock preconditioning) provides a cytoprotective effect on oxidative insults through an intracellular protective response, heat shock response. The impact of heat shock preconditioning on hepatic microvascular failure, which is a causative determinant of ischemia/reperfusion-induced injury of the liver, was investigated by using intravital fluorescence microscopy. In Sprague-Dawley rats, normothermic ischemia was induced by totally clamping the hepatoduodenal ligament for 20 min, followed by 120 min of reperfusion. Heat shock preconditioning was performed by whole-body hyperthermia (42 degrees C for 15 min) and subsequent 48 h recovery. In accordance with the prominent induction of heat shock protein 70 in the liver tissue, the postischemic decrease in sinusoidal perfusion rate and sinusoidal diameter, and the postischemic increase in the number of stagnant leukocytes in sinusoids and adherent leukocytes in postsinusoidal venules were significantly attenuated in the heat shock-treated animals. Furthermore, liver enzyme release (glutamate pyruvate transaminase and alpha-glutathione S-transferase) was significantly reduced and postischemic deterioration of bile production was attenuated. The 7-day survival rate after 20-minute ischemia was significantly improved from 50% to 80% (heat shock-nontreated group vs. heat shock-treated group, P < 0.05). These results indicate that heat shock preconditioning attenuates ischemia/reperfusion-induced hepatic injury by preventing postischemic microvascular disturbances, and that its protective effect is circumstantially associated with the concomitant induction of heat shock protein 70.

Alanine Transaminase↗
PubMed1998

An enzyme linked immunoassay using recombinant antigens for differentiation of primary from secondary or past CMV infections in pregnancy.

BACKGROUND: As primary cytomegalovirus (CMV) infection in pregnancy may be associated with severe fetal outcome, the serological differentiation of primary infection from recurrent or previous infection is of major importance. OBJECTIVES: This differentiation was attempted with a CMV IgG enzyme immunoassay (EIA), which investigated the differential IgG immune response to recombinant proteins p52 and pp150. To express the IgG reactivity to either protein a ratio was calculated by OD p52/OD pp150. STUDY DESIGN: Serial samples from groups of pregnant women with primary infection (n = 18) were compared to those with recurrent (n = 7) or previous CMV infection (n = 189). RESULTS: In primary infected women a predominant IgG response to p52 (p52 alone or ratio > or = 1.5) was observed in early sera less than 4 weeks after seroconversion, whereas the IgG response to recombinant protein pp150 was delayed and appeared after 2-7 weeks. Women with secondary and those with past infection had either IgG antibodies to pp150 alone or a ratio of less than 1.5 in 85 and 89.1% respectively with no remarkable change of ratio over time. CONCLUSIONS: The IgG recombinant EIA was shown to be a useful supplementary assay for differentiation of primary up to 8 weeks after seroconversion from recurrent or past infections.

Antibodies, Viral↗
PubMed1998

Platelet-endothelial cell interactions during ischemia/reperfusion: the role of P-selectin.

Growing evidence supports a pathophysiological role for platelets during the manifestation of postischemic reperfusion injury; in the current study, we investigated the nature and the molecular determinants of platelet-endothelial cell interactions induced by ischemia/reperfusion (I/R). Platelet-endothelium and leukocyte-endothelium interactions after 1 hour of ischemia were monitored in vivo within mouse small intestine. By intravital fluorescence microscopy, we observed that platelets, like leukocytes, roll along or firmly adhere to postischemic microvascular endothelial cells. In contrast, few leukocyte-endothelial cell interactions were detected in sham-operated controls. Monoclonal antibodies against P-selectin significantly attenuated platelet rolling and adherence in response to I/R. To identify whether platelet or endothelial P-selectin plays the major role in mediating postischemic platelet-endothelial cell interactions, P-selectin-deficient or wild-type platelets were transfused into wild-type or P-selectin-deficient mice, respectively. Whereas platelets lacking P-selectin rolled along or adhered to postischemic wild-type endothelium, interactions between wild-type platelets with mutant endothelium were nearly absent, indicating that I/R-induced platelet-endothelium interactions are dependent on the expression of P-selectin by endothelial cells. Concomitantly, P-selectin expression in the intestinal microvasculature was enhanced in response to I/R, whereas no upregulation of P-selectin was observed on circulating platelets. In summary, we provide first in vivo evidence that platelets accumulate in the postischemic microvasculature early after reperfusion via P-selectin-ligand interactions. Platelet recruitment and subsequent activation might play an important role in the pathogenesis of I/R injury.

Animals↗
PubMed1998

Development of antibodies to the nonstructural protein NS1 of parvovirus B19 during acute symptomatic and subclinical infection in pregnancy: implications for pathogenesis doubtful.

At present little is known about the mechanisms influencing the course and severity of parvovirus B19 infection. Antibodies to the parvovirus nonstructural protein NS1 were reported in patients with parvovirus-associated arthritis and those with persisting infection but not in those without complications, suggesting a potential involvement of NS1 or anti-NS1 antibodies in pathogenesis. The immune response to NS1 was examined retrospectively in 33 pregnant women with acute parvovirus B19 infection, 14 of whom experienced symptomatic infection and 19 in whom the infection was subclinical. Antibodies to NS1 were found in 15 (45%) of the women, seven with symptomatic and eight with subclinical infection. No association was found between the development of anti-NS1 antibodies and the occurrence of fetal complications. Of the seven cases in which fetal complications were observed, anti-NS1 antibodies were detected in only three. The finding that an immune response to NS1 can also be demonstrated in patients with asymptomatic infection suggests that anti-NS1 antibodies do not appear to represent a marker for an altered or severe course of infection in pregnant women or to contribute significantly to pathogenesis. Since anti-NS1 antibodies first become detectable at least six weeks postinfection, their presence can be used to exclude acute infection in patients with unclear serology or be used to aid differential diagnosis of rashlike illnesses.

Acute Disease↗
PubMed1998

Endothelium-dependent microvascular vasomotion and its correlation with vasoactive mediators early after cardiac transplantation in humans.

Endothelial dysfunction precedes and predicts transplant vasculopathy. We investigated the relationship between endothelial dysfunction and the vasoactive mediators nitric oxide and endothelin, 33.7 +/- 2.0 days after heart transplantation. Coronary flow was measured in 18 patients to determine the endothelial microvascular vasomotor response to acetylcholine. Endomyocardial biopsies were taken to determine the levels of gene expression of isozymes of endothelin and nitric oxide synthases (NOS). Blood samples from the coronary sinus and aorta were withdrawn for measurement of endothelin, nitrite and cytokines. Five patients (30%) showed an impaired coronary flow reserve response to acetylcholine, significantly higher inducible NOS gene expression and significant transcardiac nitrite production. Plasma nitrite correlated with tumour necrosis factor-alpha levels in coronary sinus and a transcardiac net extraction of endothelin was noted in all patients. In conclusion, 30% of patients develop endothelial dysfunction early after heart transplantation; this correlates with the expression and activation of vasoactive and immunomodulatory mediators, which may predict the development of transplant vasculopathy.

Endothelin-1↗
PubMed1998

Quantitative analysis of small intestinal microcirculation in the mouse.

Impairment of intestinal nutritive perfusion and accumulation of inflammatory cells in the intestinal microvasculature are well-known sequelae of mesenteric ischemia/reperfusion, sepsis, and shock. However, the molecular mechanisms underlying these alterations are still not fully understood. The mouse is particularly suitable for the study of these mechanisms since in this species the involvement of, for example, adhesion receptors or pro-/anti-adhesive mediators can be selectively investigated by the use of monoclonal antibodies or gene-targeted strains. The aim of our present study was, therefore, to establish a model to investigate the microcirculation in the mouse small intestine. Under anesthesia by inhalation of isoflurane-N2O, Balb/c mice (n = 16) were laparotomized, and a segment of the jejunum was exteriorized for intrvital fluorescence microscopy. Using FITC-dextran (MW 150,000) as a plasma marker, functional capillary density (FCD) of both the intestinal mucosa and muscle layer was analyzed. Nutritive perfusion was homogeneous in both compartments with values for FCD of 512 +/- 15 cm-1 in mucosa and 226 +/- 21 cm-1 in the muscle layer. No significant changes were observed throughout the observation period of 2 h (FCD values at the end of the observation period: 524 +/- 31 cm-1 and 207 +/- 7 cm-1 in mucosa and muscle, respectively). Besides capillary perfusion, leukocyte-endothelial cell interaction was analyzed in postcapillary venules of the intestinal submucosa using rhodamine-6G as an in vivo leukocyte stain. Under physiological conditions only a few white blood cells were found rolling along or firmly adherent to the microvascular endothelium (number of rolling leukocytes 1 +/- 0.2 cells/mm per second; number of adherent leukocytes: 18 +/- 7 cells/mm2). In a separate group rhodamine-6G-labeled syngeneic platelets were infused to analyze platelet-endothelial cell interactions quantitatively in vivo. Platelets rolled along or attached to the endothelium in a manner similar to leukocytes. However, in contrast to leukocytes the interactions were not restricted to venules, but were also observed in small arterioles. The newly established model allows for the visualization and quantitative assessment of both nutritive perfusion and platelet/leukocytendothelial cell interactions within the distinct layers of the mouse small intestine. Using this model in combination with gene-targeted mice or monoclonal antibodies it is possible to investigate the molecular mechanisms of intestinal inflammation reactions.

Analysis of Variance↗
PubMed1998

Seroprevalence study of herpes simplex virus type 2 among pregnant women in Germany using a type-specific enzyme immunoassay.

In a German seroepidemiological study to determine the proportion of pregnant women infected with herpes simplex virus type 2 (HSV-2) and at risk of transmitting the infection to the newborn during delivery, IgG antibodies to HSV-2 in 1999 sera collected from pregnant women in 1996-1997 were measured using an automated type-specific enzyme immunoassay (Cobas Core HSV-2 IgG EIA; Roche Diagnostics, Switzerland). The seroprevalence of HSV-2 was 8.9%, and control studies with a type-common HSV assay measuring antibodies to HSV-1 and HSV-2 revealed that 20.7% of pregnant women were seronegative for HSV antibodies and are therefore at risk of acquiring primary genital HSV infection of either type.

Adolescent↗
PubMed1998

Life-threatening parvovirus B19-associated myocarditis and cardiac transplantation as possible therapy: two case reports.

Parvovirus B19 infection can cause a wide spectrum of disease syndromes. Two cases of parvovirus B19 infection were identified that resulted in life-threatening myocarditis shortly after acute infection in immunocompetent individuals. The diagnosis was made with serological and polymerase chain reaction techniques. One patient was successfully treated by heart transplantation. Sequence analysis showed that the parvovirus B19 cloned from the patients' sera had 99% homology with the prototype sequence. Clinicians should be alerted to the possible role of parvovirus B19 in myocarditis presenting in immunocompetent patients.

Adolescent↗
PubMed1998

[Effect of hypothermic preservation on ICAM-1 mRNA induction, leukocyte-endothelium interaction and microvascular perfusion after pancreas transplantation in the rat].

A prolonged period of 18 h hypothermic preservation in pancreas grafts led to a significant induction of ICAM-1 mRNA, enhanced leukocyte-adherence/-extravasation and compromised microvascular perfusion upon 2 h of reperfusion when compared to a 2 h preservation period. Therefore, during the period of prolonged cold ischemia changes within the graft must take place causing a reinforced ICAM-1 mRNA-induction already early after the onset of reperfusion. These results underline the relevance of the ischemia/reperfusion injury for the development of complications arising in the early course following pancreas transplantation.

Animals↗
PubMed1998

Differentiation between acute primary and recurrent human cytomegalovirus infection in pregnancy, using a microneutralization assay.

Acute primary human cytomegalovirus (HCMV) infection in pregnancy, the major cause of congenital symptomatic infection, is often difficult to differentiate from recurrent infection, which presents a considerably smaller risk to the fetus. Therefore, the diagnosis of primary infection in pregnancy is very important, especially if seroconversion is not documented and follow-up sera with declining IgM-titers are not available. To investigate the value of the neutralizing antibody response against HCMV in differentiating acute primary from recurrent and past infection, well-characterized sera from pregnant women were examined. Employing a microneutralization assay, it was found that neutralizing antibodies first appeared approximately 15 weeks after acute infection. However, serum samples of pregnant women with recurrent or past infection consistently displayed neutralizing activity. In conclusion, the neutralization assay can be used as a reliable method for discriminating acute primary from previous or recurrent infection in a single serum sample.

Antibodies, Viral↗
PubMed1997

The role of rubella-immunoblot and rubella-peptide-EIA for the diagnosis of the congenital rubella syndrome during the prenatal and newborn periods.

Rubella infection during the first trimester of pregnancy can cause the congenital rubella syndrome (CRS). Patients with CRS were shown to have a decreased humoral and cellular immunity. It is not known whether asymptomatic newborns who had experienced intrauterine infection with rubella virus (RV) differ in their antibody response from newborns with CRS. In this study we compared both groups for a difference which might be a useful diagnostic criterion for CRS during the prenatal and newborn periods. We used the nonreducing Rubella-Immunoblot and the Rubella-IgG-Peptide-Enzyme Immunoassay (EIA) to determine the antibodies directed to rubella proteins E1, E2 and C. The results showed that only newborns with CRS who had experienced RV infection during the first 12 weeks of gestation showed significantly reduced levels of antibodies directed to both the linear RV E1 epitope (SP 15) and the topographic RV E2 epitope. Asymptomatic newborns infected mostly later than week 10 of gestation showed normal levels of antibodies. These data suggest that the lack of antibody response in CRS is linked to the immaturity of the fetal immune system during the first trimester of gestation. Rubella-IgG-Peptide-EIA and Rubella-Immunoblot should be used additionally for CRS diagnosis in the prenatal/newborn periods. These results may have an impact on the early treatment of late-onset symptoms of CRS patients.

Antibodies, Viral↗
PubMed1997

Gastric antigen challenge releases gastrin and eicosanoids and protects against ethanol.

Various gastrointestinal functions such as mucosal blood flow and mucus secretion can be influenced immunologically. Rats were systemically sensitized with 4-hydroxy-3-iodo-5-nitro-phenylacetic acid (NIP), a synthetic antigen. Mucosal release of gastrin, prostaglandin F2 alpha, 6-keto-prostaglandin F1 alpha, and leukotriene C4 was measured after intragastric or in vitro antigen challenge. Gastric protection from ethanol was determined. In sensitized rats, intragastric antigen challenge increased release of gastrin from the antral mucosa ex vivo and tended to increase release of prostaglandin F2 alpha. Likewise, antral mucosa of sensitized rats released significantly more gastrin and prostaglandin F2 alpha during in vitro antigen challenge than during incubation in the absence of antigen. Release of 6-keto-prostaglandin F1 alpha and leukotriene C4 was not affected by the immunologic reaction. Topical antigen challenge in sensitized rats reduced gastric mucosal damage caused by ethanol by 50%. The immunologically induced gastroprotection was significantly attenuated by pretreatment with indomethacin. The findings show that specific antigen challenge renders the gastric mucosa more resistant against the injurious effect of ethanol indicating that the stomach is a target organ of immunological reactions. As gastrin and prostaglandins exert potent protective effects, release of these mediators may contribute to the protective response to gastric mucosal immune activation.

6-Ketoprostaglandin F1 alpha↗
PubMed1997

Mediators of antigen-induced gastrin release: role of antigen-antibody complexes and the complement system.

That orally administered antigen was shown to induce gastrin release in immunized animals was a new aspect of gastrointestinal physiology. The mediators responsible for this immunological effect are still unclear. In an attempt to discover more about the mechanisms regarding antigen-induced gastrin release, we developed an in vitro system where fragments of rat antral mucosa were challenged. This makes it possible to determine the role of antigen-antibody complexes and the complement system in the mechanism of antigen-induced gastrin release. Wistar rats were immunized in vivo with NIP-OVA and mucosal fragments were challenge, in vitro with NIP-HGG. Gastrin was determined after a preincubation and a challenged incubation period without supernatants. After antigenic challenge, supernatants were used for in vitro challenge in order to rule out the presence of a soluble mediator and activation of complement. In a second group of experiments Wistar rats were used to study in vitro the release of specific antibodies after antigenic challenge. With this experimental design we were able to show increased gastrin secretion after antigenic challenge in vitro in the presence of intact tissue. It is shown that the increased gastrin release is most probably mediated by activation of the complement system in the presence of antigen-antibody complexes. These are built up by specific anti-NIP antibodies and NIP-HGG used for the challenge. The complement system might be the final pathway of the observed increased gastrin release.

Animals↗
PubMed1997

Comparative investigation of the long non-coding M-F genome region of wild-type and vaccine measles viruses.

The sequence of the 300 nucleotides region of the measles virus genome was determined that includes a part of the 3'-untranslated region of the matrix (M) gene, the intergenic region and a part of the 5'-untranslated region of the fusion (F) gene [M-F region] for vaccine strain Leningrad-16 and 14 wild-type isolates. The data obtained demonstrate the variability of this long non-coding M-F region. No mutations in this region of the genome were found which seem to be specific for vaccine strains of measles virus (MV).

Animals↗