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Biomedical subjects

R Haller

Publications and source records attributed to R Haller.

17 recordsLinked to original sources
PubMed1989

[Synthesis, stereochemistry and analgesic action of 3,7-diazabicyclo[3.3.1] nonan-9-ones and 1,3-diazaadamantan-6-ones].

The 1,3-diazaadamantan-6-ones 13-18 are synthesized from the 4-piperidones 1-3. Different conditions lead to stereoisomeric structures. The 3,7-diazabicyclo[3.3.1]nonan-9-ones 8 and 9 show similar geometrical isomerisms. The configuration is determined by means of 1H-NMR and 13C-NMR spectroscopic data. Whereas the diazabicyclo[3.3.1]nonanones 7 and 12 show opioid-like effects, the diazaadamantanone 13 is a peripheral analgesic.

Adamantane↗
PubMed1988

[The action of aminobenzoic acid derivatives on the ion currents in myelinated nerves. 1. Dose-response relationship].

Effects of Aminobenzoic Acid Derivatives on the Ionic Currents in Myelinated Nerve/1st Communication: Dose-response curves Derivatives of aminobenzoic acid were modified and their blocking potencies on the ionic currents of single potential clamped myelinated nerve fibres were tested by means of dose-response curves. Starting from metacaine (ethyl m-aminobenzoate), derivatives of different basicity were produced by N-dimethylization, N-quarternization and by preparing a corresponding aliphatic amine. The corresponding free acids and the structural isomers of metacaine were tested as well. The physico-chemical properties of the derivatives were characterized by their pKa-values and their octanol/water partition coefficients. Our findings suggest that the site of action of the aminobenzoic acids tested is located at the inside of the nerve membrane. Moreover, no indications of binding to a receptor in a pharmacological sense were found.

Aminobenzoates↗
PubMed1978

Hypophosphatemia and rhabdomyolysis.

Clinical observations suggest that overt rhabdomyolysis may occur if severe hypophosphatemia is superimposed upon a pre-existing subclinical myopathy. To examine this possibility, a subclinical muscle cell injury was induced in 23 dogs by feeding them a phosphorus- and calorie-deficient diet until they lost 30% of their original weight. To induce acute, severe hypophosphatemia in the animals after partial starvation, 17 of the dogs were given large quantities of the same phosphorus-deficient diet in conjunction with an oral carbohydrate supplement, which together provided 140 kcal/kg per day. After phosphorus and caloric deprivation, serum phosphorus and creatine phosphokinase (CPK) activity were normal. Total muscle phosphorus content fell from 28.0+/-1.3 to 26.1+/-2.5 mmol/dg fat-free dry solids. Sodium, chloride, and water contents rose. These changes resembled those observed in patients with subclinical alcoholic myopathy. When studied after 3 days of hyperalimentation, the animals not receiving phosphorus showed weakness, tremulousness, and in some cases, seizures. Serum phosphorus fell, the average lowest value was 0.8 mg/dl (P <0.001). CPK activity rose from 66+/-357 to 695+/-1,288 IU/liter (P <0.001). Muscle phosphorus content fell further to 21.1+/-7.7 mmol/dg fat-free dry solids (P <0.001). Muscle Na and Cl contents became higher (P <0.01). Sections of gracilis muscle showed frank rhabdomyolysis.6 of the 23 phosphorus- and calorie-deprived dogs were also given 140 kal/kg per day but in addition, each received 147 mmol of elemental phosphorus. These dogs consumed their diet avidly and displayed no symptoms. They did not become hypophosphatemic, their CPK remained normal, and derangements of cellular Na, Cl, and H(2)O were rapidly corrected. The gracilis muscle appeared normal histologically in these animals. These data suggest that a subclinical myopathy may set the stage for rhabdomyolysis if acute, severe hypophosphatemia is superimposed. Neither acute hypophosphatemia nor rhabdomyolysis occur if abundant phosphorus is provided during hyperalimentation.

Animals↗
PubMed1977

Endogeneity and reactivity as orthogonal dimensions in depression.

Endogeneity and reactivity have long been considered polar opposites of a major dimension of depression. The present factor analytic study examines 35 distinct depressive symptoms in three depressed samples and supports the conceptualization of D. F. Klein (Endomorphic depression. Arch. Gen. Psychiatry, 31:447-454, 1974) that endogeneity and reactivity can be construed as orthogonal, independent dimensions. Symptoms consistently loading on an endogeneity factor are: 1) lacking in reactivity to environmental changes; 2)showing no interest in life; 3) retarded (slow, feeling tired, etc.); 4) feeling unable to act; 5) considering self lazy; 6) feeling helpless and powerless; and 7) perceiving depression as qualitatively different from ordinary sadness. Symptoms consistently loading on a reactivity factor are: 1) feeling that he or she is bearing troubles; 2) presence of precipitating stress; 3) crediting problems to excessive family and/or job responsiblitiies; 4) expressing concern for welfare of family and friends; 5) visceral symptoms; 6) feeling at "end of rope"; 7) having middle-of-the-night insomnia; and 8) showing self-pity. The results suggest a methodology for identifying depressives who are high-high, low-high, high-low, and low-low on the endogeneity and reactivity factors.

Adjustment Disorders↗
PubMed1975

Isolated glucocorticoid insufficiency.

Two cases of isolated glucocorticoid insufficiency or congenital adrenocortical unresponsiveness to ACTH-a variant of adrenocortical failure without mineralocorticoid insufficiency-are presented. Familial incidence was present only in case 1 since two of the siblings died after convulsions, possible related to hypoglycemia. The pathology specimens of one sibling were available for review showing complete lack of the fascicular zone and degenerative changes in the adrenals and evidence of increased ACTH secretion in the pituitary. In the patients who were given substitution therapy with hydrocortisone, studies of plasma renin and aldosterone revealed impairment of plasma aldosterone response to salt restriction, orthostatism and furosemide-induced diuresis combined with postural change. We conclude that in some cases of isolated glucocorticoid insufficiency, impairment of mineralocorticoid function may gradually develop, which is in contrast to the assumption of a congenital defect in the action of ACTH.

Adrenal Cortex Diseases↗
PubMed1975

[Interactions of some parasympatholytics and structurally similar drugs with bovine serum albumin].

The interactions of the parasympatholytic drugs adiphenin, adiphenin H and propanthelin and the structurally related compounds, diphenhydramine, D-propoxyphene and methadone with bovine serum albumin (BSA) are studied by equilibrium dialysis and ultracentrifugation. The results show that BSA has a few binding sites (n less than 10) for the mentioned drugs. The association between the compounds under study and BSA are relatively weak. The binding constants are in the range of 10(3) l/Mol.

Binding Sites↗
PubMed1975

[Studies on the binding of some parasympatholytics to bovine serum albumin/measurement of relaxation times (author's transl)].

The interactions of the parasympatholytic drugs adiphenin, adiphenin H and propantheline and the structurally related compounds diphenhydramine, D-propoxyphene and methadone with bovine serum albumin (BSA) are studied by means of 1H-NMR-spectroscopy. The relaxation rates of essential protons or proton groups of the bound ligands are obtained by a plot of the observed relaxation rates, which are determined from the alterations of the line widths in the presence of BSA, versus the biopolymer concentration. From the stabilization factors R thus obtained it can be concluded that there exist defined but relatively weak associations between these drugs and BSA; both the hydrophobic aryl moieties and the ionized amino groups are involved in these interactions.

Dextropropoxyphene↗