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Biomedical subjects

G Hauser

Publications and source records attributed to G Hauser.

At least 73 records · Page 4Linked to original sources
PubMed1983

Somatovariants of females from Northern India.

On the basis of the somatometric data of a series of healthy females (126 individuals 20-30 years old; 219 individuals 31-49 years old) from Northern India (Punjab) a new method is demonstrated for the indication of habitus variants. This method is based on only three measurements. In this study stature, weight and biepicondylar breadth of the humerus were used. This simple method permits instant visualization of the actual class-memberships of each individual (somatovariants). The applicability of the method is shown for intragroup and intergroup comparison. The results are discussed with respect to possible indications of pathologic cases, undernourishment, population specific criteria and age-depending effects. The authors emphasize, however, that this method still needs further elaboration.

Adult↗
PubMed1982

[Methodological contributions to craniometric studies of some early medieval populations of the upper Donau region. II. Comparison of early medieval populations on absolute skull measurements].

On the basis of the means of 10 cranial measurements of 7 medieval populations different methodical approaches of the two commonly used distance estimation methods are compared with respect to their relevance. In addition also the results obtained by the same methods but based on different data (5 indices or 10 measurements, respectively) were compared. In spite of the fact that (DD)2 distances and the dendrograms (after Creel) give better results than the other methodical and graphic variants, the choice of qualified characters is more important than a certain distance method according to the authors' opinion. Thus the groupings and the clustering on the basis of the means of only 5 cranial indices show the best accordance with the ethnogenetic and historical conditions. An additional examination of the segregative values of cranial measurements revealed that the omission of the smallest frontal breadth and probably also the nasal height and breadth does not result in a reduction of the segregative accuracy.

Cephalometry↗
PubMed1982

Phospholipid metabolism changes in rat tissues in vitro after injections of propranolol.

When added to incubations in vitro. (+/-)-propranolol, a cationic amphiphilic drug, causes profound alterations in incorporation of [32P] orthosphosphate into rat cerebral cortex phospholipids. These include increases in the labeling of phosphatidic acid and polyphosphoinositides abd a decrease in the labeling of phosphatidylcholine. Similar changes occurred in a dose-dependent manner in incubations of cerebral cortex mince, prepared from animals injected i.p. 30 min before death with doses of propranolol ranging from 7.5 to 45 mg/kg. All changes in total incorporation and in labeling pattern had disappeared 3 hr after injection, indicating the reversibility of the effect. Repeated injections of low doses of propranolol (7.5 mg/kg) brought about significant changes in the labeling of brain cortex mince phospholipids, and especially a reduction in total incorporation. Addition of propranolol to kidney and liver minces caused reductions in the labeling of phosphatidylcholine and phosphatidylethanolamine and selective increases in the labeling of acidic lipids, restricted to phosphatidic acid in liver and phosphatidylinositol in kidney. After injection of 45 mg of propranolol per kg, but not at 15 mg/kg, some alterations in the labeling pattern were observed in liver and kidney minces. The differential response of tissues to propranolol injections can be explained on the basis of the pharmacokinetics of drug distribution and clearance and metabolic capacities of the tissues. Changes in phospholipid metabolism may be in part responsible for deleterious side effects that can occur during therapy with high doses of propranolol.

Animals↗
PubMed1981

[Plantar creasing and assessment of gestational age of the newborn (author's transl)].

Plantar creasing was graded (degrees I to IV) in 178 healthy newborn infants (males and females) and compared with gestational age and age of the mother. No significant correlation was found between these parameters. Thus, the importance attributed to plantar creasing as a parameter for the gestational age in paediatric scoring systems is doubtful. The misinterpretation of the appearance of "laundress hands" as increased plantar creasing is pointed out.

Dermatoglyphics↗
PubMed1981

Characteristics of the norepinephrine-stimulated phosphatidylinositol turnover in rat pineal cell dispersions.

Dispersed rat pineal cells can be used for the study of the phosphatidylinositol effect. The response to ( - )-norepinephrine of the incorporation of 32Pi into phospholipids is linear with time and cell concentration, stereospecific, and mediated through alpha-1-adrenergic receptors. Na+ in the incubation medium is obligatory for labeling of phosphatidylinositol and phosphatidylcholine by 32P. In the absence of K+, incorporation of 32P is drastically lowered and no stimulation by norepinephrine occurs. Rb+ can replace K+. Omission of Ca2+ or substitution with Sr2+ preferentially lowers incorporation of radioactivity into phosphatidylcholine. Mg2+ is not required for basal or stimulated labeling.

Animals↗
PubMed1981

Effects of changes in calcium concentration on basal and stimulated 32P incorporation into phospholipids in rat pineal cells.

The Ca2+ requirement for alpha-agonist stimulation of 32P incorporation into acidic phospholipids (the phosphatidylinositol effect) of dispersed pineal cells was evaluated by means of several different compounds that interfere with Ca2+ disposition. Simple omission of Ca2+ led to slight increases in basal and norepinephrine-stimulated phosphatidyl-CMP (CDP-diacylglycerol) and phosphatidylglycerol labeling without affecting phosphatidylinositol labeling. In the absence of Ca2+, EGTA (200 microM) or the ionophore for divalent cations A23187 (10 microM) elicited large increases in phosphatidic acid, phosphatidyl-CMP, and phosphatidylglycerol labeling while strongly inhibiting the phosphatidylinositol effect. The Ca2+ translocation inhibitor LaCl3 also reduced the magnitude of this effect. The phosphatidylinositol effect is, however, not induced by increased Ca2+ entry into the cytosol, since A23187 did not mimic the effect of norepinephrine. Under conditions where membrane Ca2+ was lowered, the addition of 1 mM-inositol greatly reduced phosphatidic acid, phosphatidylglycerol, and phosphatidyl-CMP labeling with concomitant increases in basal and norepinephrine-stimulated phosphatidylinositol labeling approaching that observed in the presence of norepinephrine and 2.5 mM-Ca2+. In the presence of 2.5 mM-Ca2+, inositol had negligible effects on phosphatidylinositol labeling. It was concluded that changes in membrane Ca2+ availability and/or disposition alter phospholipid metabolism and concurrently reduce the magnitude of the phosphatidylinositol effect, perhaps by making the pool of readily available inositol in pinealocytes rate-limiting.

Animals↗
PubMed1981

Alterations of phospholipid metabolism in rat cerebral cortex mince induced by cationic amphiphilic drugs.

Cationic amphiphilic drugs (CADs) of varied clinical use were screened to determine their capacity to alter the pattern of labeling with 32Pi of cerebral cortex mince phospholipids. The altered phospholipid labeling patterns were qualitatively similar, the prominent features being reduced incorporation into phosphatidylcholine and increased incorporation into phosphatidic acid. Relative potencies were: (/-+)-propranolol greater than chlorpromazine = 4,4'-bis(diethylaminoethoxy) alpha,beta-diethyldiphenylethane greater than desipramine greater than dibucaine greater than pimozide greater than oxymetazoline = fenfluramine = haloperidol = chloroquine greater than amphetamine = no drug added. Propranolol was used to study the action of CADs further. Its effect was time- and dose-dependent but in contrast with pineal gland, no label appeared in phosphatidyl-CMP (CDP-diacylglycerol), nor did dialysis of the mince to reduce diffusible substrates or exogenous addition of substrates cause appearance of liponucleotide. Thus lack of diffusible precursors is not responsible for CAD effects in vitro. Pulse-chase experiments with 32Pi and [2-3H]glycol suggested that inhibition of phosphatidate phosphohydrolase may be partly responsible for the observed alterations in phospholipid labeling in the presence of CADs.

Animals↗
PubMed1981

Jordi Folch-Pi.

Explore the source record for details and available documents.

History, 20th Century↗
PubMed1981

Cyclopia with trisomy 13 under special consideration of dermatoglyphics and flexion creases.

Report on a case of cyclopia with trisomy 13 (Patau-syndrome with cyclopia completa microphthalmica) and survey of relevant cases published in literature are presented. In addition to a combination of dermatoglyphic patterns and flexion creases typical for trisomy 13, some--so far not described--varieties are shown, above all a missing triradius d on the left and additional digital flexion creases on three phalanges. The possibility that the last mentioned observation might rather be due to population differences is discussed.

Abnormalities, Severe Teratoid↗
PubMed1981

[Methodologic problems in the measurement of somatometric characteristics].

With respect to difficult research conditions the problems of taking biologically relevant somatometric measurements for the determination of habitus variants are discussed. Under consideration of these difficulties several somatometric characters are selected by comparing the correlations based on the data of two series measured by the authors and three series taken from literature. However, attention is drawn to the fact that no complete characterization of habitus variants will result by means of these few measurements but yet some important relevant criteria.

Anthropometry↗
PubMed1979

The mechanism of modification by propranolol of the metabolism of phosphatidyl-CMP (CDP-diacylglycerol) and other lipids in the rat pineal gland.

The mechanism underlying the alteration of phospholipid metabolism in rat pineal gland in vitro produced by propranolol and tertiary amine local anesthetics was investigated. 0.1 mM propranolol did not affect either the levels or specific activity of [32P]ATP in glands. In the presence of the drug, the incorporation of cytidine, but not of inorganic phosphate, into phosphatidyl-CMP (CDP-diacylglycerol) was dependent on the cytidine concentration. The incorporation of glycerol into phosphatidyl-CMP, phosphatidylinositol and phosphatidylglycerol was enhanced by propranolol, whereas labeling of phosphatidylcholine was decreased. When both 1 mM propranolol and 1 mM inositol were present, labeling of phosphatidylinositol was further increased, stimulation of phosphatidyl-CMP and phosphatidylglycerol labeling was reduced and incorporation into phosphatidylcholine and triacylglycerol was depressed. The incorporation of [3H]inositol into pineal lipids was also enhanced by propranolol. 10 microM propranolol inhibited rat liver phosphatidic acid phosphohydrolase by 50%, while local anesthetics were less potent in the decreasing order: dibucaine greater than tetracaine greater than lidocaine greater than procaine. The propranolol-induced accumulation of phosphatidyl-CMP was prevented by supplying adequate freely diffusible inositol in the medium. The phosphatidyl-CMP which accumulated was not utilized for the enhanced formation of phosphatidylinositol brought about by norepinephrine. The results indicate that propranolol and local anesthetics redirect pineal phospholipid metabolism in part by inhibition of phosphatidic acid phosphohydrolase.

Adenosine Triphosphate↗
PubMed1979

[Mechanisms common to the development of malformation in congenital and sporadic forms of atrial septal defect (type II) (author's transl)].

Familial prevalence of some congenital cardiopathies leads to the conclusion that genetic factors might be involved. The case histories are presented of three families with atrial septal defect, Type II (ASD II) in which autosomal dominant inheritance was assumed on account of the pedigree analysis. Each family member was examined serologically, morphologically and morphometrically. One family was also tested for cytogenetic abnormalities. It is highly probable that the gene responsible for the defect is linked to the HLA system (Lod score = + 3.612) and is, therefore, located on the short arm of chromosome 6. The morphological examinations demonstrated uniformity of individual ear traits in related patients; moreover, the palmar dermatoglyphics showed a tendency to shortening of main line C, to ulnar and distal shifting of the carpal triradius and to an increase in hypothenar patterns. In addition a study was carried out of patients with apparently sporadic cardiopathy. A similar trend as to palmar configuration was observed. An attempt was made to connect known factors causing malformations with the results of this investigations.

Adolescent↗