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Biomedical subjects

B Schmidt

Publications and source records attributed to B Schmidt.

At least 397 records · Page 22Linked to original sources
PubMed1990

[Long-term sequelae in the area of personality and achievement following bone marrow transplantations in children and adolescents--a pilot study].

Long-term sequeales after bone marrow transplantation of 13 children and adolescents are described from a psychological standpoint. The findings suggest that inspite of the aggressive treatment by the majority of the children fundamental changes in personality or mental ability are not to prove, with the exception of: 1. children, who receive poor psychosocial support by their parents, 2. children, who suffer from a graft-versus-host-reaction, 3. children, whose mental ability after transplantation is worse than before. These children need psychosocial management and appropriate intervention.

Achievement↗
PubMed1989

Alpha-2-macroglobulin is an important progressive inhibitor of thrombin in neonatal and infant plasma.

Antithrombin III (ATIII) is the main inhibitor of thrombin in adult plasma; alpha 2-macroglobulin (alpha 2M) and heparin cofactor II (HCII) are of lesser importance. The relative contributions of these inhibitors to the inactivation of thrombin may differ during the neonatal period and infancy, when plasma concentrations of alpha 2M are about twice as high as those of ATIII. We therefore compared the relative importance of these anti-proteases for the inhibition of 125I-thrombin in defibrinated pooled adult and neonatal plasma. Observations were also made in pooled plasma of 6 months old infants. 125I-thrombin-inhibitor complexes were quantitated after SDS-PAGE and autoradiography by scanning densitometry. Thrombin (2.5 NIH U/ml) was inhibited more slowly in neonatal than in adult plasma. However, both plasmas inhibited 88% of the added thrombin by 5 minutes. Alpha 2M inhibited consistently a larger fraction of thrombin in neonatal than in adult plasma. Consequently, the ratio of thrombin bound to ATIII over thrombin bound to alpha 2M was significantly lower in neonatal (less than 2.5) than in adult plasma (greater than 4.5; p less than 0.0001). In infant plasma, this ratio was less than 2.0. Upon addition of therapeutic amounts of heparin (0.4 U/ml), differences between the contributions of ATIII and alpha 2M to the inhibition of thrombin were no longer apparent, as over 90% of complexed thrombin was bound to ATIII in heparinized plasmas of all age groups. We conclude that alpha 2M is an important progressive inhibitor of thrombin in young infants. This finding may explain why healthy newborns rarely suffer from thrombosis, despite their low plasma ATIII levels.

Adult↗
PubMed1989

Cloning and expression of human steroid-sulfatase. Membrane topology, glycosylation, and subcellular distribution in BHK-21 cells.

A 2.4-kilobase cDNA clone for human steroid-sulfatase (STS) was isolated and sequenced, which encoded an enzymatically active protein. The deduced amino acid sequence comprises 583 amino acids with an N-terminal signal peptide of 21 or 23 residues and four potential N-glycosylation sites. Two of the N-glycosylation sites are utilized and were localized to the asparagine residues 47 and 259. STS has the solubility properties of an integral membrane protein. The resistance of STS toward proteinase K after translocation into microsomes suggests that most, if not all, sequences of STS are exposed at the luminal side of microsomes. The deduced amino acid sequence predicts two membrane-spanning domains (amino acids 185-211 and 213-237) separated by a helix-breaking proline residue. We propose for STS a three-domain model. Two glycosylated luminally oriented domains of 161 and 346 residues are separated by a hydrophobic domain spanning the membrane twice in opposite directions. STS expressed in BHK-21 cells is located predominantly in the endoplasmic reticulum; smaller fractions are found in the Golgi, at the cell surface, multivesicular endosomes, as well as in lysosomes. The stability of STS in lysosomes may be related to the high homology of the two luminal domains of STS with the lysosomal sulfatases, arylsulfatase A, and arylsulfatase B. In spite of its similarity with these two lysosomal sulfatases, STS does not contain mannose 6-phosphate residues and is transported to lysosomes by a mannose 6-phosphate receptor-independent mechanism.

Amino Acid Sequence↗
PubMed1989

Cloning and expression of human arylsulfatase A.

A full length cDNA for human arylsulfatase A was cloned and sequenced. The predicted amino acid sequence comprises 507 residues. A putative signal peptide of 18 residues is followed by the NH2-terminal sequence of placental arylsulfatase A. One of the arylsulfatase A peptides ends 3 residues ahead of the predicted COOH terminus. This indicates that proteolytic processing of arylsulfatase A is confined to the cleavage of the signal peptide. The predicted sequence contains three potential N-glycosylation sites, two of which are likely to be utilized. The sequence shows no homology to any of the known sequences of lysosomal enzymes but a 35% identity to human steroid sulfatase. Transfection of monkey and baby hamster kidney cells resulted in an up to 200-fold increase of the arylsulfatase A activity. The arylsulfatase A was located in lysosome-like structures and transported to dense lysosomes in a mannose 6-phosphate receptor-dependent manner. The arylsulfatase A cDNA hybridizes to 2.0- and 3.9-kilobase species in RNA from human fibroblasts and human liver. RNA species of similar size were detected in metachromatic leukodystrophy fibroblasts of two patients, in which synthesis of arylsulfatase A polypeptides was either detectable or absent.

Amino Acid Sequence↗
PubMed1989

Dystrophin immunocytochemistry in muscle culture: detection of a carrier of Duchenne muscular dystrophy.

Dystrophin is the gene product which is affected in Duchenne muscular dystrophy (DMD). We studied differentiating clonal muscle cultures derived from normal muscle and from the mother of a DMD patient by immunocytochemistry, using anti-dystrophin antibody. While clonal cultures derived from normal muscle expressed dystrophin in all myotubes, two populations of myogenic cells could be demonstrated in muscle from this possible DMD carrier; in 13 clones the myotubes expressed dystrophin and in 7 clones dystrophin was undetectable. No DNA deletion, duplication or rearrangement was detected by Southern blot analysis of DNA from this family using cDNA probes. Thus, immunocytochemical analysis of clonal muscle cultures may be a useful method to determine whether mothers of DMD patients are carriers of the DMD mutation, especially in the absence of demonstrable gene defects.

Adult↗
PubMed1989

Cough-cardiopulmonary resuscitation in the cardiac catheterization laboratory: hemodynamics during an episode of prolonged hypotensive ventricular tachycardia.

Cough-CPR, a deep rhythmic forceful cough repeated 30-60 times per minute, can be an effective resuscitative technique during emergencies occurring in the cardiac catheterization laboratory. We provide documented evidence on the potential of cough-CPR to maintain adequate systemic arterial blood pressure and consciousness during malignant ventricular arrhythmias, including the longest cough-CPR episode (75-90 sec), with continuous hemodynamics recorded. Results in three patients disclose that 1) mean arterial pressure during cough-CPR was 47-66% of nonarrhythmic baseline at a cough rate of 38-46% of normal sinus rhythm heart rate; 2) mean arterial pressure during hypotensive ventricular tachycardia was 17-60 mm Hg higher with than without cough-CPR; 3) at comparable diastolic pressures (33 vs. 31 mm Hg), systolic arterial pressure during cough-CPR was 40 mm Hg higher than basic CPR; and 4) consciousness can be maintained with cough-CPR during prolonged malignant ventricular arrhythmias. Thus cough-CPR can be a valuable adjunct in maintaining patient stability while definitive therapy for the malignant ventricular arrhythmia is administered.

Aged↗
PubMed1989

Sequential processing of lysosomal acid phosphatase by a cytoplasmic thiol proteinase and a lysosomal aspartyl proteinase.

BHK cells expressing human lysosomal acid phosphatase (LAP) transport LAP to lysosomes as an integral membrane protein. In lysosomes LAP is released from the membrane by proteolytic processing, which involves at least two cleavages at the C terminus of LAP. The first cleavage is catalysed by a thiol proteinase at the outside of the lysosomal membrane and removes the bulk of the cytoplasmic tail of LAP. The second cleavage is catalysed by an aspartyl proteinase inside the lysosomes and releases the luminal part of LAP from the membrane-spanning domain. The first cleavage at the cytoplasmic side of the lysosomal membrane depends on acidification of lysosomes and the second cleavage inside the lysosomes depends on prior processing of the cytoplasmic tail. These results suggest that the cytoplasmic tail controls the conformation of the luminal portion of LAP and vice versa.

Acid Phosphatase↗
PubMed1989

Serum-Zn-levels in prostatic cancer.

Zinc in serum of both patients with prostatic carcinoma and men without prostatic cancer was analyzed by flame atomic absorption spectrometry (FAAS). No significant differences were found between the group with prostatic carcinoma without metastasis and the group used for comparison. The Zn level in serum of patients with both prostatic carcinoma and metastases was decreased in comparison to the other groups. A decrease in the Zn concentration was also found for men without metastases after orchiectomy and hormone therapy.

Adenocarcinoma↗
PubMed1989

[Sports accidents in children and adolescents].

A total of 2617 sports injuries in children were analysed from a 2-year-period. The age-dependent rate of sports injuries in this material was 30% to 40% of all injuries in childhood. Although male children predominated over females with 2:1 depending from the type of sport, the sexual preponderance was very different. Horse riding injuries showed a female preponderance of 4:1. Most common occurrences were low-grade injuries such as contusions, distorsions or wounds. One-third of the injuries were fractures. 5% of the children had a brain injury such as commotio or contusio cerebri. Sequelae of accidents differed largely between different forms of sport. To quantify the extent of the injuries, a score was calculated from the rate of head injuries, times the rate of brain damage, times the rate of fractures of the long bones. By means of this score it can be shown that the most severe injuries occur during horse riding, skating, tobogganing and bicycle riding. A detailed analysis of different injury patterns allows recommendations for preventive measures.

Accidents↗
PubMed1989

[T2*-weighted MR images of gynecologic tumors with the FLASH sequence: the initial experiences at 1.5 T].

To speed up the time taken for MR examinations, 20 patients with malignant gynaecological lesions (carcinoma of the cervix, uterus or ovary) and two operative specimen (carcinoma of the cervix) were examined by T2*-weighted flash sequences; the results were compared with T2-weighted spin echo sequences. In ten out of 20 in vivo examinations, the flash method produced a similar contrast range between tumour and normal tissues, cystic lesions being particularly well seen in gradient echo sequences. In the remaining patients, and in the surgical specimen, demarcation of the tumour was significantly poorer on the flash sequences. There was also loss of anatomic detail and an increased susceptibility to artifacts. The flash sequence as used here can therefore not be regarded as of the same diagnostic value as T2-weighted spin echo sequences in the diagnosis of gynaecological malignancies.

Carcinoma↗
PubMed1989

Detection of "deleted" mitochondrial genomes in cytochrome-c oxidase-deficient muscle fibers of a patient with Kearns-Sayre syndrome.

Using in situ hybridization and immunocytochemistry, we studied a muscle biopsy sample from a patient with Kearns-Sayre syndrome (KSS) who had a deletion of mitochondrial DNA (mtDNA) and partial deficiency of cytochrome-c oxidase (COX; EC 1.9.3.1). We sought a relationship between COX deficiency and abnormalities of mtDNA at the single-fiber level. COX deficiency clearly correlated with a decrease of normal mtDNA and, conversely, deleted mtDNA was more abundant in COX-deficient fibers, especially ragged-red fibers. The distribution of mtRNA had a similar pattern, suggesting that deleted mtDNA is transcribed. Immunocytochemistry showed that the nuclear DNA-encoded subunit IV of COX was present but that the mtDNA-encoded subunit II was markedly diminished in COX-deficient ragged-red fibers. Because the mtDNA deletion in this patient did not comprise the gene encoding COX subunit II, COX deficiency may have resulted from lack of translation of mtRNA encoding all three mtDNA-encoded subunits of COX.

Base Sequence↗
PubMed1989

Transition metals, ferritin, glutathione, and ascorbic acid in parkinsonian brains.

The regional distributions of iron, copper, zinc, magnesium, and calcium in parkinsonian brains were compared with those of matched controls. In mild Parkinson's disease (PD), there were no significant differences in the content of total iron between the two groups, whereas there was a significant increase in total iron and iron (III) in substantia nigra of severely affected patients. Although marked regional distributions of iron, magnesium, and calcium were present, there were no changes in magnesium, calcium, and copper in various brain areas of PD. The most notable finding was a shift in the iron (II)/iron (III) ratio in favor of iron (III) in substantia nigra and a significant increase in the iron (III)-binding, protein, ferritin. A significantly lower glutathione content was present in pooled samples of putamen, globus pallidus, substantia nigra, nucleus basalis of Meynert, amygdaloid nucleus, and frontal cortex of PD brains with severe damage to substantia nigra, whereas no significant changes were observed in clinicopathologically mild forms of PD. In all these regions, except the amygdaloid nucleus, ascorbic acid was not decreased. Reduced glutathione and the shift of the iron (II)/iron (III) ratio in favor of iron (III) suggest that these changes might contribute to pathophysiological processes underlying PD.

Aged↗
PubMed1989

The impact of erythropoietin on hemodialyzer design and performance.

The present study investigated theoretically and experimentally the effects of increases in hematocrit on the clearance of urea by the Baxter ST15 hollow fiber dialyzer. In a theoretical model that incorporates the three component resistances for the overall mass transfer rate, namely, the resistance of the blood (Rb)-, membrane (Rm)-, and dialysate side (Rd), it was predicted that a change in hematocrit would alter only the blood side resistance. The overall impact of this alteration is expected to be determined by the relative contribution of Rb to the overall resistance (RO). The modest contribution of Rb to RO implies that a major change in Rb (50%) would have only a minor effect on RO (11%) and consequently on urea clearance (5%). These theoretical conclusions were tested experimentally and the results confirmed the theoretical predictions. Indeed, there was little change in urea clearance in the clinically relevant range of variations in hematocrit (19-39%). Possible ways of compensation by minor changes in the hollow fiber geometry are discussed as well as the more complex relationships with larger solutes (creatinine) or unequally distributed solutes (potassium, phosphate).

Equipment Design↗
PubMed1989

Anticoagulant effects of heparin in neonatal plasma.

Available data on the anticoagulant effects of heparin in neonatal plasma are scarce and conflicting: relative to adult plasma, neonatal plasma has been reported to show both resistance as well as sensitivity to heparin. We explored this apparent paradox by comparing how well heparin accelerated inhibition of exogenous thrombin and prevented thrombin generation in defibrinated neonatal and adult plasmas. Using amidolytic assays, we determined the effects of heparin on 1) the neutralization of exogenous human alpha-thrombin and on 2) the formation of endogenous thrombin activity after contact activation and recalcification. Neonatal plasma proved resistant to heparin (0.05 U/mL) during inhibition of added thrombin (15 NIH U/mL). Inhibition of thrombin in heparinized neonatal plasma became as efficient as in adult plasma only after raising the AT III activity to normal adult values. However, de novo generation of thrombin activity was very susceptible to inhibition by heparin, even in neonatal plasmas with physiologically low AT III levels. Peak thrombin activity generated in neonatal plasma in the absence of heparin was 50% or less of peak adult activity, and this already reduced ability of neonatal plasma to generate thrombin activity upon prothrombin activation was further decreased by heparin (0.05-0.2 U/mL). We conclude that due to the neonatal AT III deficiency, added thrombin is inactivated less effectively by heparin in neonatal than in normal adult plasma. Yet, the generation of thrombin activity is impaired in neonatal plasma and easily suppressed by heparin. We speculate that newborn infants may be resistant to heparin therapy during overt thrombotic disease, when neutralization of abnormal thrombin activity is the therapeutic goal.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

[Histochemical study of the skeletal muscle in chronic alcoholism].

Twenty-two chronic alcoholic patients were assessed by neurologic examination and muscle biopsy. The patients manifested proximal muscular weakness to a variable extent. One case presented as an acute bout of myopathy, according to the Manual Muscle Test, MMT. The most prominent histologic feature observed was muscle atrophy (95.3%) better evidenced through the ATPase stain with the predominance of type II A fibers (71.4%). Lack of the mosaic pattern (type grouping) seen in 76% of the cases and an important mitochondrial proliferation with intrasarcoplasmatic lipid accumulation in 63% of the patients. In case of acute presentation of muscle weakness the pathological substrate is quite different, i.e. presence of myositis mainly interstitial characterized by lymphoplasmocytic infiltrate and several spots of necrosis like Zencker degeneration. Based on histologic criteria, our data suggest that: the main determinant of muscle weakness seen in chronic alcoholic patients is neurogenic in origin (alcoholic polyneuropathy); the direct toxic action of ethanol under the skeletal muscle is closely related to the mitochondrial metabolism; the so-called acute alcoholic myopathy has probably viral etiology.

Adult↗
PubMed1989

[Histochemical study of the skeletal muscle in multiple sclerosis].

The authors present muscle histochemistry of ten patients of multiple sclerosis. The clinical diagnosis was based on criteria established by Poser et al. (1983). The main pathological findings observed were: lymphoplasmocitary vasculitis, increase in the number of 2B type fibers, inflammatory cells (macrophages) in the intramuscular ends of the motor nerves, amounts of lipids and 'moth-eaten' fibers. The presence of vasculitis observed in our cases contributes with the etiopathogenic hypothesis of an autoimmune lesion in multiple sclerosis. There is no correlation between the clinical and histological atrophy observed.

Adult↗
PubMed1989

Fluorescence polarization immunoassay of urinary 5-hydroxy-3-indoleacetic acid.

Fluorescence polarization immunoassay of 5-hydroxy-3-indoleacetic acid in urine is described and compared with liquid chromatography (electrochemical detection) and colorimetry. Reports of in-house performance data and results of clinical trials are included to emphasize the usefulness of the assay for routine work.

Chromatography, High Pressure Liquid↗