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Biomedical subjects

R Herold

Publications and source records attributed to R Herold.

At least 19 recordsLinked to original sources
PubMed2004

A meta-model of chemotherapy planning in the multi-hospital/multi-trial-center-environment of pediatric oncology.

OBJECTIVE: Chemotherapy planning in pediatric oncology is complex and time-consuming. The correctness of the calculation according to state-of-the-art research is crucial for curing the child. Computer-assistance can be of great value. The objective of our research was to work out a meta-model of chemotherapy planning based on the Unified Modeling Language (UML). The meta-model is used for the development of an application system which serves as a knowledge-acquisition tool for chemotherapy protocols in pediatric oncology as well as for providing protocol-based care. METHODS: We applied evolutionary prototyping, software reengineering techniques and grounded theory, a qualitative method in social research. We repeated the following steps several times over the years: Based on a requirements analysis (i) a meta-model was developed or adapted, respectively (ii). The meta-model served as a basis for implementing evolutionary prototypes (iii). Further requirements were identified (i) from clinical use of the systems. RESULTS: We developed a comprehensive UML-based meta-model for chemotherapy planning in pediatric oncology (chemoMM). We implemented it and introduced evolutionary prototypes (CATIPO and DOSPO) in several medical centers. Systematic validation of the prototypes enabled us to derive a final meta-model which covers the requirements that have turned out to be necessary in clinical routine. CONCLUSIONS: We have developed an application system that fits well into clinical routine of pediatric oncology in Germany. Validation results have shown that the implementation of the meta-model chemoMM can adequately support the knowledge acquisition process for protocol-based care.

Antineoplastic Agents↗
PubMed2002

Theory of mind deficit in people with schizophrenia during remission.

BACKGROUND: The authors' goal was to investigate the presence or absence of theory of mind impairments among people with schizophrenia during remission. Recent research results interpret theory of mind deficits as state rather than trait characteristics, connecting these impairments mainly to the acute episode of psychosis. METHODS: Twenty patients with schizophrenia in remission and 20 matched control subjects were evaluated. Participants were presented with one first-order theory of mind task, one second-order theory of mind task, two metaphor and two irony tasks adapted from previous studies. RESULTS: The schizophrenic patients performed a statistically significant impairment in the irony task, as there were no significant differences in the cases of the other evaluated tasks. CONCLUSIONS: These preliminary results suggest that theory of mind impairments can be detected not only in the acute phase as found in previous research studies, but also in remission.

Case-Control Studies↗
PubMed2001

[Olanzapine and pregnancy].

The appearance of psychosis during pregnancy means a challenge for clinicians, either untreated psychiatric disorders or pharmacological treatment of pregnant psychotic females increase risk of complications. Controlled clinical trials can't be evaluated because of ethical considerations, so case reports have higher scientific values than in other clinical issues. The authors inform about a delivery of a young psychotic female, who was treated with olanzapine (atypical antipsychotic) after the 25th weeks of her pregnancy. A healthy newborn was born in the observed case, the Apgar score was 7 at the first minute and 9 at fifth minute.

Adult↗
PubMed2001

Increased cerebrospinal fluid concentrations of soluble Fas (CD95/Apo-1) in hydrocephalus.

BACKGROUND AND AIMS: The ventricular enlargement observed in children with chronically raised intracranial pressure (ICP) causes a secondary loss of brain tissue. In animal studies of hydrocephalus, programmed cell death (apoptosis) has been found as a major mechanism of neuronal injury. One of the regulators of the apoptotic cell death programme is the receptor mediated Fas/Fas ligand interaction. METHODS: The apoptosis regulating cytokines soluble Fas (sFas) and soluble Fas ligand (sFasL) were studied in the cerebrospinal fluid (CSF) of 31 hydrocephalic children undergoing shunt surgery for symptomatic hydrocephalus and 18 controls. RESULTS: High concentrations of sFas were observed in children with hydrocephalus (median 252 ng/ml); in controls sFas was below the detection limit (0.5 ng/ml). sFasL was undetectable in all but one sample. CONCLUSION: High concentrations of sFas in the CSF of children with hydrocephalus suggest intrinsic sFas production, potentially antagonising pressure mediated Fas activation.

Adolescent↗
PubMed1998

Quantification of cerebrospinal fluid proteins in children by high-resolution agarose gel electrophoresis.

Physiologic alterations in cerebrospinal fluid proteins occur inter alia with aging. Agarose gel electrophoresis discriminates many cerebrospinal fluid proteins and in addition quantifies concentration alterations. This study aimed to investigate the time course of these alterations in children and to establish normative values for cerebrospinal fluid protein properties. In 202 children without diseases known to alter cerebrospinal fluid, normative protein properties were quantified using nephelometry, ultrafiltration, high-resolution electrophoresis, and Gaussian curve fit densitometry. Total protein and protein concentrations (albumin and gamma-globulins) decreased from birth until 7 months age, and, from then on, increased slightly (transthyretin, albumin, and alpha2-proteins) or strongly (gamma-globulins). Protein proportions (transthyretin and transferrin) increased until about 3 years of age and decreased from then on. These normative values for children as quantified by high-resolution agarose gel electrophoresis are presented in a significance-structured percentile table. The time courses of these cerebrospinal fluid properties reflect physiologic alterations of the blood-brain barrier function during childhood.

Adolescent↗
PubMed1998

[A score in transference. BIP--experiencing the relationship in psychoanalysis].

The (emotional) experience of reference in psychoanalyses, presented here, has been developed by the author in continuation of a method evolved by Gill and Hoffman 1982 in Chicago, which they termed "The Patient's Experience of the Relationship with the Therapist", to describe the course of analytical work on patient resistance against transference. The "Experience of reference in psychoanalyses" is a rating method that links by means of its two manuals quantitative methods (which are empirical in the conventional sense) with qualitative, clinical-hermeneutical research approaches. After reliable coding of categorial data of a tape recorder transcription, a condensed description of the course and a clinical comment are obtained, the graphic representation of which reads like a score transference.

Defense Mechanisms↗
PubMed1996

Cerebrospinal fluid soluble L-selectin (sCD62L) in meningoencephalitis.

The leucocyte adhesion molecule L-selectin (CD62L) is rapidly cleaved off proteolytically after cell activation, generating soluble L-selectin (sCD62L) molecules. sCD62L concentrations were determined in 185 cerebrospinal fluid (CSF) samples obtained from children aged 1 month to 17 years. In 36 CSF samples of children with meningoencephalitis, sCD62L was significantly higher (median 209 fmol/ml) than in samples of children with other febrile diseases (n = 67, median 50 fmol/ml) or non-febrile disorders (n = 82, median 44 fmol/ml). There was a positive correlation between CSF protein and CSF sCD62L (rS = 0.68), suggesting that a disturbed blood-brain barrier contributes to raised sCD62L concentrations in the CSF. However, the CSF sCD62L/protein ratio of children with meningoencephalitis was significantly higher than in children with other febrile diseases or non-febrile disorders, indicating that sCD62L concentrations in children with meningoencephalitis were higher than expected from plasma leakage alone. It is concluded that both an impaired blood-brain barrier and the generation of sCD62L by infiltrating leucocytes contribute to raised CSF sCD62L concentrations in children with meningoencephalitis.

Acute Disease↗
PubMed1991

Structure and expression of the bovine amelogenin gene.

In order to define further the mechanisms responsible for tooth amelogenin heterogeneity, seven bovine amelogenin cDNAs were sequenced. On the basis of these sequences, five of the cDNAs could be grouped into one class which differed appreciably in sequence from the second group of two cDNAs. Two overlapping bovine genomic clones were then isolated and shown by sequencing to contain six exons encoding the entire consensus sequence of the class I cDNA. Southern blot analysis of DNA from male and female animals using class I or class II specific oligonucleotide probes suggested that the class I gene sequence was located on the X chromosome while the class II sequence was located on the Y chromosome. Therefore, these results also suggest that the genes on the X and Y chromosomes are both transcribed. Furthermore, the results are consistent with alternative splicing of the class I primary transcript as a potential mechanism for generating amelogenin heterogeneity.

Amelogenin↗
PubMed1989

Phylogenetic distribution of enamel proteins: immunohistochemical localization with monoclonal antibodies indicates the evolutionary appearance of enamelins prior to amelogenins.

The hard covering tissues, enamel or enameloid, of representative vertebrate teeth were immunohistochemically stained using specific monoclonal antibodies against bovine amelogenins and bovine enamelins in order to determine the phylogenetic distribution of enamelin and amelogenin proteins. Immunohistochemically, only enamelin proteins were present in lower vertebrate (shark, bony fish, and larval amphibian) teeth and dermal denticles. Both enamelin and amelogenin proteins were present in higher vertebrate (mammal, reptile, and adult amphibian) teeth. Large hydroxyapatite crystal size and high levels of mineralization, characteristics common to both enamel and enameloid, are probably due to the presence of the common protein enamelin. The evolution of enamel from enameloid in the tetrapods seems to have involved the development of the gene for amelogenin.

Amelogenin↗
PubMed1988

Inhibition of embryonic palatal shelf horizontalization and medial edge epithelial breakdown by cortisol: role of H-2 in the mouse.

We have investigated the effect of glucocorticoids on the development of the embryonic palate in vivo and of glucocorticoids and diphenylhydantoin (DPH) in culture in the cleft palate-sensitive B10.A strain and its resistant congenic partner strain, B10, as well as the effect of glucocorticoids in vivo in the sensitive A/J strain. The B10.A (H-2a) strain differs from its congenic partner strain, B10 (H-2b), only in the H-2 region of chromosome 17, and thus, differences between the two strains in the responses to the drugs can be ascribed to H-2-linked genes. The degree of corticoid-induced inhibition of shelf horizontalization in vivo is only slightly (if at all) greater in B10.A than in B10, but the degree of corticoid-induced inhibition of fusion following contact in vivo and the inhibition by cortisol and DPH of programmed cell death and breakdown of the medial edge epithelium (MEE) in vitro are much greater in B10.A than in B10. The corticoid-induced delay of shelf horizontalization produced in vivo in the A/J (H-2a) strain is considerably greater than that produced in either B10.A or B10. Thus, H-2-linked genes appear to influence slightly, if at all, the degree of corticoid-induced delay of shelf elevation, but they have a major effect on the corticoid-induced inhibition of fusion via the inhibition of breakdown of the medial edge epithelia. The delay of corticoid-induced shelf horizontalization appears to be a trait influenced primarily by non H-2-linked genes.

Animals↗
PubMed1986

Production of a monoclonal antibody to enamelins which does not cross-react with amelogenins.

Developing enamel matrix contains a complex mixture of proteins whose characterization is essential to an understanding of amelogenesis. It is not known whether each component is the product of an individual gene, or whether they are interrelated by physiologic or artifactual breakdown. To define these relationships, monoclonal antibodies were prepared to enamel proteins and we have previously reported the characterization of six antibodies to amelogenins which did not react with enamelins (Christner et al. (1985) Arch. Oral Biol. 30:849-854). We now report the isolation of antibody to enamelins which stains the enamel matrix but does not cross-react with amelogenins. These results suggest that amelogenins and enamelins are distinct classes of proteins.

Amelogenin↗
PubMed1985

Hyperglycemia-induced teratogenesis is mediated by a functional deficiency of arachidonic acid.

Congenital malformations now represent the largest single cause of mortality in the infant of the diabetic mother. The mechanism by which diabetes exerts its teratogenic effects is not known. This study evaluated whether arachidonic acid might be involved, a possibility raised by the role of arachidonic acid in palatal elevation and fusion, processes analogous to neural tube folding and fusion. This hypothesis was tested in two animal models of diabetic embryopathy, the in vivo pregnant diabetic rat and the in vitro hyperglycemic mouse embryo culture. The subcutaneous injection of arachidonic acid (200-400 mg/kg per day) into pregnant diabetic rats during the period of organ differentiation (days 6-12) did not alter the maternal glucose concentration, the maternal weight gain, or the weight of the embryos. However, the incidence of neural tube fusion defects was reduced from 11% to 3.8% (P less than 0.005), the frequency of cleft palate was reduced from 11% to 4% (P less than 0.005), and the incidence of micrognathia was reduced from 7% to 0.8% (P less than 0.001). The addition of arachidonic acid to B10.A mouse embryos in culture also resulted in a reversal of hyperglycemia-induced teratogenesis. The teratogenic effect of D-glucose (8 mg/ml) in the medium resulted in normal neural tube fusion in only 32% of the embryos (P less than 0.006 when compared to controls). Arachidonic acid supplementation (1 or 10 micrograms/ml) produced a rate of neural tube fusion (67%) that was not significantly different from that observed in controls. The evidence presented indicates that arachidonic acid supplementation exerts a significant protective effect against the teratogenic action of hyperglycemia in both in vivo (rat) and in vitro (mouse) animal models. These data therefore suggest that the mechanism mediating the teratogenic effect of an increased glucose concentration involves a functional deficiency of arachidonic acid at a critical stage of organogenesis.

Animals↗
PubMed1984

Glucocorticoid-induced phospholipase A2-inhibitory proteins mediate glucocorticoid teratogenicity in vitro.

Dexamethasone induces the synthesis of a phospholipase A2-inhibitory protein (PLIP) of molecular weight approximately equal to 55,000 from calf thymus and PLIPs of molecular weights 55,000, 40,000, 28,000, and 15,000 from A/J mouse thymus and from 12-day embryonic B10. A mouse palates. Sufficient quantities of calf thymus PLIP and of the 15,000 molecular weight mouse thymus and palate PLIPs were prepared and tested as inhibitors of programmed cell death in the medial-edge epithelium of single mouse embryonic palatal shelves in culture. All of the proteins tested prevent the loss of the medial-edge epithelium and, thus, produce the teratogenic effects of glucocorticoids in the palatal culture model. This teratogenic action of both PLIP and glucocorticoids is reversed by arachidonic acid, the precursor of prostaglandins and thromboxanes, suggesting that PLIP mediates the effects of glucocorticoids by inhibiting phospholipase A2.

Animals↗
PubMed1984

[Enteral protein loss in regional enteritis of the terminal ileum: treatment by segmental resection of the small intestine].

A case report is given of a 37 year old patient who suffered from excessive intestinal protein losses caused by inflammatory changes of the terminal ileum. Conservative treatment improved neither hypoproteinemia nor weight loss. Finally surgical removal of the afflicted intestinal segment did lead to healing. This rare indication for surgical removal of an intestinal segment is discussed on the basis of literature reviewed.

Adult↗
PubMed1983

Cortisol inhibition of development of various lysosomal enzymes in cultured palatal shelves from mouse embryos.

The lysosomal enzymes, non-specific esterases, beta-glucuronidase, N-acetyl-beta-glucosaminidase and aryl sulphatases A and B, were examined histochemically in medial-edge epithelia (MEE) of single palatal shelves in vitro. Activities of most enzymes increased gradually in MEE with a peak at 24-26 h of culture. Aryl sulphatase B activities were lower than the others and aryl sulphatase A activities could not be detected in the palatal cells during the entire culture period. By 48 h, MEE cells degenerated and were lost. Cortisol suppressed increased activities of these hydrolytic enzymes and prevented programmed breakdown of the palatal epithelium.

Acetylglucosaminidase↗
PubMed1983

Inhibition of programmed cell death in mouse embryonic palate in vitro by cortisol and phenytoin: receptor involvement and requirement of protein synthesis.

In an in vitro model cortisol and phenytoin inhibit the precisely timed process of palatal development, the lysosomally mediated cell death of the medial edge palatal epithelium. This inhibition of programmed cell death of the palatal midline epithelium by each drug is virtually completely blocked by the antiglucocorticoid, cortexolone, whose blocking action results from competitive binding of the glucocorticoid receptor site. The inhibition produced by each of these drugs is prevented by the protein synthesis blocker, cycloheximide. Thus, blockade of programmed cell death by each of these drugs involves the glucocorticoid receptor site and requires protein synthesis.

Animals↗