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Biomedical subjects

G Schroeder

Publications and source records attributed to G Schroeder.

54 records · Page 3Linked to original sources
PubMed1991

[The "Alcomat" breath alcohol analyzer in a controlled drinking trial].

In controlled drinking tests according to a concrete forensic problem the residual-alcohol detector of the breath alcohol analyzer "ALCOMAT" was checked in relation to the actual blood alcohol concentration. The tests with non-alcoholic persons, rinsing the mouth with US-whiskey (40 ml, 30 seconds), showed first residual-alcohol indication and later blood alcohol levels up to 0.26%. The test groups with beforehand blood alcohol concentration showed either with mouth rinsing, or with real whiskey ingestion indicated devitations up to 2.07% according to 130% of the actual BAC. A correlation with the level of BAC was not found. The electronic precautionary fittings of the "ALCOMAT" are even under best possible controlled test conditions not sufficient reliable for forensic purpose.

Adult↗
PubMed1990

[The pedestrian-automobile accident at lower velocity. Experimental studies of biomechanical and clinico-prognostic topics].

The influence of bumper configuration on injury patterns resulting from car/pedestrian collisions were analyzed. 18 experimental settings were carried out on the deceleration device of the Institute of Forensic Medicine of the Medizinische Hochschule Hannover using a middle class passenger car at collision speed of 32 km/h. Three modifications of the standard bumper design did not reduce the severity of injuries induced by collision. Comparatively promising results were given by another bumper construction consisting of an additional bumper relatively easy to deform attached to the standard variant at a level of 12 cm below. Authors discuss findings regarding injury patterns, injury mechanisms and subsequent implications. Based on trauma surgeons' experience it is suggested not only to aim on reduction of bone injuries. Major attention has to be paid on improving rehabilitation prognosis and on reducing medical treatment expenses. According to data available soft tissue damage is of major importance and needs to be quantified before taking one particular bumper construction as pedestrian friendly design.

Accidents, Traffic↗
PubMed1989

Age-dependent changes of cerebral ventricular size. Part I: Review of intracranial fluid collections.

The age distributions of communicating hydrocephalus (CH), pseudotumour cerebri (PC) slit-ventricle syndrome (SVS), and chronic subdural haematomas (CSH) were reviewed in the medical literature. An age-related incidence was found: CH and CSH predominated in neonates less than 2 years and adults older than 55 years, while PC and SVS occurred mainly in older children and young adults. The latter two patient groups seem to show a greater resistance to ventricular dilatation in the presence of decreased CSF absorption. This may be related to larger volume and state of maturity of the cerebrum. On the other hand, neonates and the elderly more readily develop enlarged ventricles, in association with impairment of CSF absorption, or subdural fluid collections. Factors including status of cranial sutures, cerebral atrophy, cerebral water content, degree of cerebral myelination, and glial cell composition, may contribute to the age-related incidence of the four disorders investigated. Similarly, the development of ventriculomegaly may depend upon cerebral elastic properties besides the pri mary disturbance of CSF dynamics. The authors postulate that the size of cerebral ventricles in disorders of the cerebrospinal fluid (CSF) absorption is related to the elastic properties and volume of the brain. Furthermore, cerebral volume and elastic properties may also contribute to the age distribution of chronic subdural haematomas (CSH).

Adolescent↗
PubMed1988

Involvement of the conserved histidine-188 residue in the L-lactate dehydrogenase from Thermus caldophilus GK24 in allosteric regulation by fructose 1,6-bisphosphate.

The conserved histidine-188 residue of the L-lactate dehydrogenase of Thermus caldophilus GK 24, which is allosterically activated by fructose 1,6-bisphosphate, has been exchanged to phenylalanine by site-specific mutagenesis. In the mutant enzyme the strong stimulatory effect of fructose 1,6-bisphosphate is abolished. The analysis of the pH dependence of the activity indicates that the positive charge of the conserved His-188 residue is important for the interaction of the enzyme with the allosteric effector.

Binding Sites↗
PubMed1987

Atrial natriuretic factor inhibits central angiotensin II pressor responses.

Intracerebroventricular (i.c.v.) administration of human atrial natriuretic factor (ANF), fragment 1-25, in the dose range 3 to 20 micrograms/kg did not alter resting arterial pressure or heart rate in rats anesthetized with chloralose/urethan (60:600 mg/kg i.p.), while angiotensin II (ANG II), 1 microgram/kg, produced a significant increase in arterial pressure after i.c.v. application. This pressor effect induced by ANG II was abolished by simultaneous administration of ANF (3 micrograms/kg i.c.v.). In isolated strips of rabbit aorta preconstricted with ANG II (10 nM), ANF caused a dose-dependent relaxation. In intact rats, the increase in blood pressure following intravenously administered ANG II (0.1 and 1 microgram/kg) was not altered by the highest dose of ANF (20 micrograms/kg) given intracerebroventricularly. These results suggest that atrial peptides may play an important role in the regulation of blood pressure by interacting with both the central and peripheral actions of ANG II. Inhibition of the central pressor action of angiotensin by ANF appears to be independent of any direct peripheral effect of the atrial peptides.

Angiotensin II↗
PubMed1987

Angiotensin II-induced vasopressin release is attenuated by central atrial natriuretic factor.

Administration of angiotensin II (Ang II) into the cerebral ventricles (icv) of rats elicits vasopressin release and an increase in blood pressure. The effect of atrial natriuretic factor (ANF) on these actions of ANG II was studied in conscious spontaneously hypertensive rats. The magnitude and time course of the blood pressure increase following ANG II (50 and 100 ng) were not altered by ANF, icv. However, vasopressin levels which were stimulated from 10.8 +/- 1.5 to 62.1 +/- 6.4 pq/ml by ANG II (100 ng) were significantly suppressed by combined administration of ANG II (100 ng) and ANF (3 ug/kg) (33.0 +/- 4.3 pg/ml). The injection of ANF alone into the cerebral ventricles had no effect on resting blood pressure or vasopressin levels. Peripheral administration of ANF was unable to attenuate the ANG II-induced vasopressin release. These data suggest that there exists a central interaction of ANF and ANG II within the brain which cannot be mimicked by peripheral administration of ANF.

Angiotensin II↗
PubMed1977

[Isolation and structure determination of the metabolites of 2-(1,3-dimethyl-xanthinyl-(7)-methyl)-4-methyl-morpholine--a xantinol derivative--from rat urine (author's transl)].

In the urine of rats the following metabolites of the xantinol derivative 2-(1,3-dimethyl-xanthinyl-(7)-methyl)-4-methyl-morpholine were found: 2-[1,3-dimethyl-xanthinyl-(7)-methyl]-morpholine and 2-[1,3-dimethyl-xanthinyl-(7)-methyl]-4-methyl-morpholin-5-one. These compounds represent about 13.7% of the p.o. applied 2-[1,3-dimethyl-xanthinyl-(7)-methyl]-4-methyl-morpholine. Their structure has been elucidated by IR-, PMR- and mass spectrometry.

Animals↗
PubMedDate not supplied

Stopping when the experimental regimen does not appear to help.

We discuss a procedure that offers the possibility of reducing the number of patients assigned to experimental regimens which are no more effective than a standard regimen. The procedure is useful in advanced cancer trials in which the length of the accrual period might be more than twice the median survival time for the standard regimen. The procedure is intuitively appealing and offers a 50 per cent chance of stopping accrual to ineffective therapies, yet is associated with a loss of power of less than 0.02.

Antineoplastic Combined Chemotherapy Protocols↗
PubMedDate not supplied

[The role of tumor markers in prognosing transitional bladder cancer].

PURPOSE: Review the literature on tumor markers used for prognosis of transitional bladder cancer. The existing problems regarding grading and local staging of these tumors are also discussed. METHODS: The published literature on transitional bladder cancer markers was identified using a Medline search and critically analysed. RESULTS: There are significant interobserver differences in grading. There is a new grading system. There are also problems in local staging and low correlation between clinic stage and pathologic stage. Major tumor markers studied for prognosis of transitional bladder cancer are: flow cytometry, kariocytometric study, oncogenes (p53, bcl-2, Her2/Neu or c-erbB2), chromosomic alterations (chromosomes 9, 7 and 17), proliferation markers (Ki-67, MIB-1), cyclin-dependent kinases and its inhibitors (cyclin D1, cyclin E, p21Wafl, p27Kipl), vascular endothelial growth factor, other growth factors (fibroblastic, epidermal, hepatocyte, platelet-derived), metalloproteinases, cell adhesion molecules, and others. CONCLUSIONS: At present, there are no prognostic markers for bladder cancer that are superior to conventional grading and staging, despite its imperfections. Standarization of assay methods in bladder tumor markers is needed to permit more conclusive and reproducible results and become a clinic tool. Controversy resulting from several studies make the meaning of some putative prognostic markers in transitional bladder cancer questionable.

Biomarkers, Tumor↗
PubMedDate not supplied

[Experimental studies of the development of linear electric current marks].

UNLABELLED: By means of reconstructing electric current pathways electrophysical conditions were explored causing electrocution death in the bathtub, according to many authors quite often indicated by linear electric lesions. In our experimental settings we observed appearance of circumscribed linear marks of pallor similar to electric lesions in the region of postmortem lividity of corpses at the same level as bathtub water. None of typical histological indicators could be seen in skin samples. So no evidence was given for electric burns even under conditions of high density and extended duration of current. Similar linear marks and equivalent histological results were found when corpses were put into the bathtub filled with cold water without any experimental electric contact. CONCLUSIONS: Linear marks of pallor may occur at water level even without any electric contact to corpse or water neither bathtub. IMPLICATIONS: According to specific conditions mentioned above linear so called electric lesions at water level do not indicate electric current yet lethal electric damage.

Burns, Electric↗