[When conventional medicine is not sufficient. Even physicians are interested in alternative treatment methods].
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Biomedical subjects
Publications and source records attributed to T Svensson.
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Today different issues of medical ethics are in focus of the debate. A theoretical sequence starting at a "prepathogenic" level, ending in terminal care, is delineated to clarify the different characteristics of medical interventions. In this article we will discuss some ethical problems concerning interventions in the first parts of this sequence. Preventive measures at the population level are contrasted to the situation when the patient feels ill and calls for an intervention. Certain elements of paternalism are often interwoven in preventive medicine and health promotion.-The field of preventive medicine calls for a vivid theoretical and ethical discussion, which can mean better opportunities for effective prevention.
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At routine post mortem examinations performed at the National Veterinary Institute (NVI), Uppsala, Sweden, during November 1983-May 1984, a syndrome principally characterized by an acute hepatosis was found in 85 out of 177 brown hares (Lepus europaeus P.). The hepatic lesions consisted of periportal or extensive necrosis and haemorrhages. Concomitant changes in other organs were tubular necrosis in the kidneys, acute catarrhal enteritis, severe congestion, oedema and haemorrhages of the lungs, hyperemia of the spleen, and in some cases jaundice. A supplementary retrospective study of liver sections from another 388 brown hares and 202 mountain hares (Lepus timidus L.), autopsied at NVI during 1980-1985, revealed 35 additional cases of the acute hepatosis, 32 being in brown hares and 3 in mountain hares. The histopathology of the liver lesions may suggest a toxic etiology.
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Previous studies have indicated that brain noradrenaline (NA) neurons in spontaneously (genetically) hypertensive rats (SHR) are implicated in the development of hypertension. Thus, a number of biochemical aberrations in the metabolism of NA in the SHR brain have been detected although the data are not in total agreement. We report here experiments utilizing single cell recording techniques which show directly a reduction in neuronal activity of brain NA neurons in the locus coeruleus (LC) of SHR. This reduction develops gradually with age and in parellel with the increased blood pressure (BP), but is not altered by acute alterations in BP. The SHR were found to display an increased intraneuronal monoamine oxidase (MAO) activity as well as a specifically reduced sensitivity of inhibitory alpha 2-receptors within the LC. It is suggested that in SHR the LC system, in spite of a reduced basal activity displays increased responsiveness to sensory stimuli, a phenomenon that may contribute to the development of hypertension.
Central catecholamine (CA)-neuropeptide Y (NPY) interactions and their regulation by glucocorticoids have been analyzed in vivo and in vitro, especially in the dorsal cardiovascular center of the medulla oblongata, including the nucleus tractus solitarius (nTS), using immunocytochemical, receptor autoradiographical, biochemical, and physiological techniques. Intraventricular (i.v.t.) injections of NPY in a low (7.5 pmol) or a high (1.25 nmol) dose increased adrenaline levels 4 h later in the caudal part of the dorsomedial medulla. Furthermore, NPY immunoreactivity (IR) tended to decrease in the rostral part of the dorsomedial medulla 5 min after injection of clonidine (1 microgram) in the alpha-chloralose anaesthetized rat. Thus, presynaptic interaction between NPY and adrenaline (A) mechanisms may exist in the dorsal cardiovascular center taking place at the network local circuit level or the membrane level of the NPY/A costoring synapses of the dorsomedial medulla. In vitro NPY (10 nM) reduced the affinity of the alpha 2-adrenergic agonist binding sites in the nTS, and clonidine (10 nM) reduced the 125I-NPY binding in the dorsomedial medulla. These results indicate the existence of postsynaptic receptor-receptor interactions between alpha 2-adrenergic and NPY receptors in the dorsal cardiovascular center. This interaction may in part take place at the level of the Ni protein, since NPY (300 nM) inhibited cyclic AMP (cAMP) accumulation in slices of the dorsomedial medulla. However, the interactions also probably take place at the proteins carrying the recognition sites, since NPY and adrenaline together given i.v.t. significantly antagonized the hypotensive effects of one another. Thus, the reduced affinity of the alpha 2-adrenergic receptor induced by NPY may reflect a reduced efficiency of this receptor and not an increased coupling of Ni protein to the adenylate cyclase. Thus, the postsynaptic interaction between the two receptors represents inter alia a sensitivity regulation of the two receptors. Evidence is also presented for the existence of a glucocorticoid regulation of NPY IR neurons, especially of those innervating the locus coeruleus, since after 2 weeks adrenalectomy reduced NPY IR in this area. Furthermore, glucocorticoid receptor IR was demonstrated in the nuclei of NPY nerve cell bodies of the nTS. Thus, glucocorticoids exert direct actions on cardiovascular NPY/CA costoring neurons, actions that may contribute to their hypertensive effects in humans.(ABSTRACT TRUNCATED AT 400 WORDS)
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Previous work has shown that clonidine effectively suppresses many of the signs of opiate withdrawal. The present study was designed to test the hypothesis that the suppression of opiate withdrawal by clonidine is mediated by forebrain noradrenergic projections of the locus coeruleus. Two groups of 24 rats each were subjected to either a 6-hydroxydopamine lesion of the dorsal noradrenergic bundle (Lesion group) or a sham, vehicle injection (Sham group). All rats were made dependent on morphine by subcutaneous implantation of one 75 mg silastic morphine pellet for three days followed by 3 more days with two additional 75 mg pellets. Following removal of the morphine pellet, withdrawal was precipitated in all rats by subcutaneous injection of 4 mg/kg of naloxone. Pretreatment 10 min. before withdrawal with clonidine (0.1 or 0.2 mg/kg) produced a significant attenuation of withdrawal signs as compared to saline injected rats; this effect was equally significant in both sham and lesion groups. Lesions of the locus coeruleus had no effect on withdrawal, nor did they affect the ameliorating action of clonidine. These results substantiate the observation that clonidine can effectively attenuate signs of opiate withdrawal in the rat, but fail to support the hypothesis that these effects are mediated by the forebrain projections of the locus coeruleus.
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The present paper reviews some recent experiments with relevance to the functional significance of brain noradrenergic systems with bearing on three clinically relevant topics: 1. The withdrawal and abstinence reactions after the antihypertensive agent clonidine as well as after opiates. 2. The mental reactions associated with alterations in blood volume and acid-base balance. 3. The central actions and side-effects of beta-adrenoceptor blocking agents. The available evidence indicates that central NA neurons may serve a function within the CNS analogous to that of the peripheral sympathetic nerves, i.e. to alert and alarm the individual to significant events in the external and internal environment. Thus, the largest brain NA system, which emanates from locus coeruleus and innervates vast regions of the neuroaxis, is largely activated in the same situations and by the same mechanisms (e.g. blood-volume and chemoreceptors) as the sympathetic system, and may provide part of the central machinery for the anxiety reaction associated with hypercapnia as well as the withdrawal reactions after clonidine or morphine. Some, but not all centrally active beta-adrenoreceptor blocking agents were found to affect the activity of brain NA systems. This result suggests that there may be significant differences with respect to the clinical, central side effects of these drugs.
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An assessment scale consisting of 10 questions was constructed from an initial 20 questions. The scale encompassed orientation to time, place and person and was intended for geriatric patients and patients suffering from psychogeriatric disorders who had been institutionalized for at least 14 days. The reliability according to the Kuder-Richardson formula number KR20 was 0.83 and the test-retest reliability was 0.84. The scale differentiated between patients with senile dementia and/or cerebral arteriosclerosis and patients without such disorders.
The purpose of this study was to gather knowledge in order to provide a basis for the future planning of local nursing homes in Sweden. A total of 306 patients, residents and staff of six nursing homes and four old age homes were interviewed. The interview was combined with questions regarding a model for the design of a nursing home. The subjects were found to have opinions on the designs on the design which, in some cases, differed significantly from what is generally assumed to be true today in Sweden.
Inhibition of cell proliferation by leucocyte extracts containing the granulocytic chalone has been monitored in various ways. Target cells were rat bone marrow cells and chloroleukaemia cells cultured on cover glasses, as well as mouse marrow cells cultured in vivo and in vitro in diffusion chambers. Provided that the technique is optimized, the in vitro rat cell assays yielded reliable results with different types of radioactive DNA precursors. With the diffusion chamber techniques cells synthesizing DNA were killed specifically by hydroxyurea, rather than labelling them with e.g. 3H-thymidine. Inhibition of proliferation then showed up as a decreased cell killing, as compared with the controls. Inhibition of proliferation of both progenitor and transit cells could be demonstrated in this way, without interference by added thymidine.
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