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Biomedical subjects

B Bucher

Publications and source records attributed to B Bucher.

At least 19 recordsLinked to original sources
PubMed2002

Radiation doses of Swiss population from external sources.

The outdoor radiation exposure of the population in Switzerland from external sources results from cosmic background as well as from natural and artificial ground radiation. The geographical distribution of these components and of the total dose rate are represented on maps consisting of 2 kmx2 km grid cells. The average dose rate on Swiss territory outdoors is 147 nSv/h (1.29 mSv/a). The distributions are then related to the population density distribution by GIS application. The population is exposed to an average dose rate of 108 nSv/h (0.95 mSv/a) per capita which is just below the threshold for man-made dose rate given by national regulation. The lower value (relative to the country average 147 nSv/h) arises from the fact that most of the population lives north of the Alps where the lithology is dominated by rocks of relatively low radioactivity and where the cosmic radiation is low relative to the Alps.

Environmental Exposure↗
PubMed2001

The neurokinin A receptor activates calcium and cAMP responses through distinct conformational states.

G protein-coupled receptors are thought to mediate agonist-evoked signal transduction by interconverting between discrete conformational states endowed with different pharmacological and functional properties. In order to address the question of multiple receptor states, we monitored rapid kinetics of fluorescent neurokinin A (NKA) binding to tachykinin NK2 receptors, in parallel with intracellular calcium, using rapid mixing equipment connected to real time fluorescence detection. Cyclic AMP accumulation responses were also monitored. The naturally truncated version of neurokinin A (NKA-(4-10)) binds to the receptor with a single rapid phase and evokes only calcium responses. In contrast, full-length NKA binding exhibits both a rapid phase that correlates with calcium responses and a slow phase that correlates with cAMP accumulation. Furthermore, activators (phorbol esters and forskolin) and inhibitors (Ro 31-8220 and H89) of protein kinase C or A, respectively, exhibit differential effects on NKA binding and associated responses; activated protein kinase C facilitates a switch between calcium and cAMP responses, whereas activation of protein kinase A diminishes cAMP responses. NK2 receptors thus adopt multiple activatable, active, and desensitized conformations with low, intermediate, or high affinities and with distinct signaling specificities.

Calcium↗
PubMed2001

Airborne surveys of Swiss nuclear facility sites.

Annually since 1989, biannually since 1994, the environs (approximately 50 km2) of the Swiss nuclear facilities are surveyed (by helicopters) flying the same survey lines. The equipment and the data processing software used for these surveys were built and developed at the Institute of Geophysics, ETH Zurich. For mapping of man-made radiation at or around nuclear facility sites a pixel representation and the MMGC (man-made gross count) ratio is used. So far no artificial radioactivity that could not be explained by the Chernobyl event (1986) or by earlier nuclear weapon tests was detected outside the fenced sites of the nuclear facilities.

Air Pollution, Radioactive↗
PubMed2001

Role of pre-operative assessment in the surgical management of leiomyoma extended to the right heart chambers: a compendium of information from isolated reports.

Recurrent intravenous leiomyoma extending to the right heart chambers is extremely rare. A large range of surgical techniques and approaches (i.e. two-step procedure, hypothermia and circulatory arrest) have been previously described. We report a recent case where the tumour was excised in a one-step procedure under normothermic cardiopulmonary bypass. This report associated to a comprehensive literature review allows us to discuss the role of pre-operative assessment and to propose refinement of surgical techniques according to the anatomy of the tumour.

Female↗
PubMed2001

Wine polyphenols decrease blood pressure, improve NO vasodilatation, and induce gene expression.

The effects of short-term oral administration of red wine polyphenolic compounds on hemodynamic parameters and on vascular reactivity were investigated in rats. Endothelial function and vascular smooth muscle contractility were studied in association with the induction of gene expression in the vascular wall. Rats were treated daily for 7 days by intragastric administration of either 5% glucose or red wine polyphenolic compounds (20 mg/kg). Administration of these compounds produced a progressive decrease in systolic blood pressure, which became significantly different on day 4. Aortas from rats treated with red wine polyphenolic compounds displayed increased endothelium-dependent relaxation to acetylcholine that was related to increased endothelial NO activity and involved a mechanism sensitive to superoxide anion scavengers. However, no increase in whole-body oxidative stress has been observed in rats treated with red wine polyphenolic compounds, as shown by plasma glutathione assay. Also, in the aorta, red wine polyphenolic compounds increased the expression of cyclooxygenase-2 and increased the release of endothelial thromboxane A(2), which compensated for the extraendothelial NO-induced hyporeactivity in response to norepinephrine, resulting from enhanced inducible NO synthase expression. The present study provides evidence that short-term oral administration of red wine polyphenolic compounds produces a decrease in blood pressure in normotensive rats. This hemodynamic effect was associated with an enhanced endothelium-dependent relaxation and an induction of gene expression (of inducible NO synthase and cyclooxygenase-2) within the arterial wall, which together maintain unchanged agonist-induced contractility. These effects of red wine polyphenolic compounds may be a potential mechanism for preventing cardiovascular diseases.

Animals↗
PubMed1999

Vasoconstrictor effects of various melatonin analogs on the rat tail artery in the presence of phenylephrine.

We performed a pharmacologic analysis of the increase in perfusion pressure induced by melatonin and related analogues in the perfused rat tail artery precontracted by 1 microM phenylephrine. Melatonin, 2-iodomelatonin, 6-chloromelatonin, and S20098 (N-[2-(7-methoxy-1-naphthyl)ethyl]acetamide) produced a concentration-dependent enhancement of the vasoconstrictor response evoked by 1 microM phenylephrine with a rank order of potency compatible with the pharmacologic profile defined for high-affinity melatonin receptors. Melatonin had no effect on electrically induced [3H]noradrenaline release, but the neurogenic vasoconstriction was increased at melatonin concentrations of 100 and 300 nM. Increasing concentrations of the naphthalenic-based antagonist S20928 (N-[2-(1-naphthyl)ethyl]cyclobutanecarboxamide) caused a parallel rightward shift in the melatonin concentration-response curve without depressing the maximal response. The pA2 value of S20928 was 7.01 +/- 0.08. Luzindole, 1 microM, an antagonist of Mel1b melatonin receptors, was without effect on melatonin-induced responses. By using reverse transcription-polymerase chain reaction (RT-PCR), we found that messenger RNA (mRNA) encoding for Mel1a is transcribed in the rat tail artery. In conclusion, the results show that melatonin produced an enhancement of the contractile response elicited by phenylephrine in the perfused rat tail artery. This vasoconstrictor response appears to be mediated through activation of Mel1a receptors located on smooth-muscle cells. No evidence for an action of melatonin on either the endothelium or sympathetic nerve endings was found.

Acetamides↗
PubMed1999

Conservative surgery for atrioventricular valve myxoma.

Patients with valvular myxoma are usually candidates for surgery because of the high incidence of life-threatening embolism. In some cases, the tumor is sessile or presents with a large peduncle: complete excision may then lead to valve replacement. We report two cases of atrioventricular valve myxoma where replacement was avoided. In one patient, a mitral myxoma appended from the edge of the anterior leaflet close to the chordae insertion; safe excision implied destruction of the two chordae and a peritumoral section of the anterior leaflet. A chordal transposition technique was used to preserve valve competence. In a second patient, a tricuspid myxoma causing syncopal episodes was resected; this was characterized by a large stalk, located on the anterior tricuspid leaflet away from chordal attachment and the valvular annulus. Treatment was by resection and the leaflet reconstructed with a pericardial patch. Techniques for conservative treatment of degenerative valvular disease or endocarditis, when monitored peroperatively by transesophageal echocardiography, may be successful in the surgical resection of atrioventricular myxoma.

Adult↗
PubMed1998

Quality of life and psychosocial adjustment of young patients after treatment of bone cancer.

BACKGROUND: The aim of this study was to collect information about the psychosocial situation of young patients after multimodality therapy for bone cancer. METHODS: Selection criteria for patients were ages 15-30 years, tumor localization at the extremities, and an interval of at least 1 year since the end of treatment. Of 110 patients, 60 were willing to participate. Evaluation of psychosocial quality of life included assessment of psychosocial adjustment and age-appropriate achievements as well as identification of problems typical for this patient group. RESULTS: Approximately 80% of patients revealed, at the very most, only minor psychosocial problems. They were able to adapt well to their new living conditions, although strong efforts were necessary for them to deal with problems such as restricted mobility, catching up with school, or changing jobs or job orientation. Differences between patients and control subjects emerged in the areas of marital status, independent living, and parenthood. The most recently determined levels of education and income were similar. Neither clinical data nor physical or functional sequelae affected psychosocial adjustment, with one exception: patients diagnosed in adolescence had significantly more problems, especially in the area of social well-being, than patients diagnosed in childhood or early adulthood. CONCLUSIONS: Given the limitations of this study, the findings suggest that survivors of bone cancer are not necessarily at risk of developing long term emotional or social problems and are not precluded from leading active and independent lives.

Adaptation, Psychological↗
PubMed1998

ORL1 receptor-mediated inhibition by nociceptin of noradrenaline release from perivascular sympathetic nerve endings of the rat tail artery.

In the present study the effect of the opioid heptadecapeptide nociceptin, also termed orphanin FQ, an endogenous ligand for the orphan receptor named ORL1 (opioid receptor-like 1) receptor, was investigated on [3H]noradrenaline release induced by electrical field stimulation (24 pulses at 0.4 Hz, 200 mA, 0.3 ms duration) in the rat tail artery in the absence and presence of an alpha2-adrenoceptor antagonist, rauwolscine 3 microM. Nociceptin inhibited the electrically-evoked tritiated noradrenaline release in a concentration-dependent manner from rat tail arteries. This inhibitory effect of nociceptin was enhanced in the presence of the alpha2-adrenoceptor antagonist rauwolscine (maximum inhibition by 25% and 50% in the absence and presence of rauwolscine, respectively). At a supramaximal concentration (10 microM), the inhibitory action of DAGO, a selective micro-opioid receptor agonist, was less pronounced than that of nociceptin. The inhibitory effect of nociceptin was counteracted by naloxone benzoylhydrazone (3 microM) which by itself did not change the stimulation-evoked noradrenaline overflow. Naloxone (10 microM), a non-selective opioid receptor antagonist, did not affect the inhibitory effect of nociceptin whereas it abolished that of DAGO. In conclusion, these results suggest that nociceptin modulates noradrenergic neurotransmission by acting on prejunctional ORL1 receptors located on nerve terminals innervating the rat tail artery. They also demonstrate that prejunctional ORL1 receptors interact with prejunctional alpha2-adrenoceptors. The physiological significance of this phenomenon remains to be determined.

Animals↗
PubMed1997

Neuropeptide Y modulates ATP-induced increases in internal calcium via the adenylate cyclase/protein kinase A system in a human neuroblastoma cell line.

The modulatory effects of neuropeptide Y (NPY) on ATP-induced increases in cytosolic free-calcium concentration ([Ca2+]i) were investigated in the CHP-234 human neuroblastoma cell line. Pretreatment of cells with 100 nM NPY potentiated the increase in [Ca2+]i evoked subsequently by 20 microM ATP, compared with initial application of ATP in a control experiment, whereas a similar pretreatment with 1 microM NPY attenuated the subsequent response to ATP. Both actions of NPY were completely blocked by H-89 [N-[2-((3-(4-bromo-phenyl)-2-propenyl)-amino)-ethyl]-5 isoquinoline sulphonamide dihydrochloride], a selective antagonist of protein kinase A. The effects of 100 nM NPY were mimicked by H-89, while forskolin and 8-Br-cAMP mimicked the effects of 1 microM NPY. Both basal and forskolin-stimulated cAMP levels were inhibited by 100 nM NPY and by 100 nM NPY(13-36), a selective agonist of the NPY Y2-receptor subtype. In contrast, at 1 microM such inhibition was not observed for either NPY or NPY(13-36). It is concluded that NPY has a biphasic modulatory effect on increases in [Ca2+]i produced by ATP, which probably involves the cAMP/protein kinase A cascade.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1997

Cannabinoid CB1 receptor-mediated inhibition of the neurogenic vasopressor response in the pithed rat.

The effects of two cannabinoid receptor agonists, R(+)-[2,3-dihydro-5-methyl-3-[(morpholinyl)methyl]pyrrolo[1,2,3-de]-1,4- benzoxazin-yl]-(1-naphthalenyl)-methanone (WIN 55,212-2) and (-)-cis-3-[2-hydroxy-4-(1,1-dimethylheptyl)phenyl]-trans-4-(3-hydr oxypropyl)-cyclohexanol (CP-55,940), were studied on (i) the vasopressor response elicited in pithed rats by electrical stimulation of the sympathetic outflow and (ii) the release of 3H-noradrenaline and the vasoconstriction elicited in isolated rat tail arteries by transmural electrical stimulation. In pithed rats, the electrical (1 Hz for 10 s) stimulation of the preganglionic sympathetic nerve fibres increased diastolic blood pressure by about 30 mmHg. This neurogenic vasopressor response (which under the conditions of our study was almost exclusively due to the release of catecholamines) was decreased by WIN 55-212,2 and CP-55,940 in a dose-dependent manner (inhibition by WIN 55,212-2 and CP-55,940, 0.1 micromol/kg each, about 25-30%). The inhibition was identical in adrenalectomized rats and in animals with intact adrenals. The inhibitory action of WIN 55,212-2 and CP-55,940 was abolished by a dose of 0.03 micromol/kg of the CB1 receptor antagonist N-piperidino-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-3-pyrazo le-carboxamide (SR 141716), which, by itself, had no effect. WIN 55,212-2, CP-55,940 and SR 141716 failed to affect the vasopressor response to exogenous noradrenaline (1 nmol/kg), which also increased diastolic blood pressure by about 30 mmHg. In isolated rat tail arteries, the electrically (0.4 Hz) evoked tritium overflow and vasoconstriction were not modified by WIN 55,212-2 and CP-55,940 (1 micromol/l each). In conclusion, the neurogenic vasopressor response in the pithed rat can be modulated via cannabinoid CB1 receptors probably located presynaptically on the postganglionic sympathetic nerve fibres innervating resistance vessels.

Action Potentials↗
PubMed1997

Identification of histamine H3 receptors in the tail artery from normotensive and spontaneously hypertensive rats.

We examined the possible existence of prejunctional histamine H3 receptors on sympathetic nerve fibers innervating rat tail artery. The stimulation-evoked tritium outflow from isolated vessels preincubated with [3H]-noradrenaline and perfused/superfused in the presence of the alpha2-adrenoceptor antagonist rauwolscine, 3 microM, was inhibited by histamine 10 microM (by 8%) and the H3 agonists R-(-)-alpha-methylhistamine, 10 microM (by 18%), and imetit, 0.1-10 microM (by < or =20%). The inhibitory effect of imetit, which did not occur in the absence of rauwolscine, was counteracted by thioperamide, 1 microM. In the presence of rauwolscine, 3 microM, the inhibitory effect of imetit also occurred when the current strength or the Ca2+ concentration in the medium was reduced to compensate for the increase in tritium overflow elicited by rauwolscine, indicating that the inhibitory action of imetit is not associated with the increase in noradrenaline release produced by rauwolscine. In spontaneously hypertensive rats (SHRs), imetit also inhibited the overflow of tritium. This inhibitory effect was comparable to that observed in Wistar-Kyoto (WKY) rats and indicates that the sympathetic nerves of the rat tail artery in SHRs, like those in normotensive rats, are endowed with prejunctional histamine H3 receptors.

Adrenergic alpha-2 Receptor Antagonists↗
PubMed1997

Inhibition of [Ca2+]i transients in rat adrenal chromaffin cells by neuropeptide Y: role for a cGMP-dependent protein kinase-activated K+ conductance.

The effects of neuropeptide Y on the intracellular level of Ca2+ ([Ca2+]i) were studied in cultured rat adrenal chromaffin cells loaded with fura-2. A proportion (16%) of cells exhibited spontaneous rhythmic [Ca2+]i oscillations. In silent cells, oscillations could be induced by forskolin and 1,9-dideoxyforskolin. This action of forskolin was not modified by H-89, an inhibitor of protein kinase A. Spontaneous [Ca2+]i fluctuations and [Ca2+]i fluctuations induced by forskolin- and 1,9-dideoxyforskolin were inhibited by neuropeptide Y. Increases in [Ca2+]i induced by 10 and 20 mM KCI but not by 50 mM KCI were diminished by neuropeptide Y. However, neuropeptide Y had no effect on [Ca2+]i increases evoked by (-)BAY K8644 and the inhibitory effect of neuropeptide Y on responses induced by 20 mM KCI was not modified by omega-conotoxin GVIA, consistent with neither L- nor N-type voltage-sensitive Ca2+ channels being affected by neuropeptide Y. Rises in [Ca2+]i provoked by 10 mM tetraethylammonium were not decreased by neuropeptide Y, suggesting that K+ channel blockade reduces the effect of neuropeptide Y. However, [Ca2+]i transients induced by 1 mM tetraethylammonium and charybdotoxin were still inhibited by neuropeptide Y, as were those to 20 mM KCI in the presence of apamin. The actions of neuropeptide Y on [Ca2+]i transients provoked by 20 and 50 mM KCI, 1 mM tetraethylammonium, (-)BAY K8644 and charybdotoxin were mimicked by 8-bromo-cGMP. In contrast, 8-bromo-cAMP did not modify responses to 20 mM KCI or 1 mM tetraethylammonium. The inhibitory effects of neuropeptide Y and 8-bromo-cGMP on increases in [Ca2+]i induced by 1 mM tetraethylammonium were abolished by the Rp-8-pCPT-cGMPS, an inhibitor of protein kinase G, but not by H-89. A rapid, transient increase in cGMP level was found in rat adrenal medullary tissues stimulated with 1 microM neuropeptide Y. Rises in [Ca2+]i produced by DMPP, a nicotinic agonist, but not by muscarine, were decreased by neuropeptide Y. Our data suggest that neuropeptide Y activates a K+ conductance via a protein kinase G-dependent pathway, thereby opposing the depolarizing action of K+ channel blocking agents and the associated rise in [Ca2+]i.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1996

The role of chronic alcohol abuse in the development of acute respiratory distress syndrome in adults.

OBJECTIVE: To determine the effect of a history of chronic alcohol abuse on the incidence of acute respiratory distress syndrome (ARDS) and in-hospital mortality. DESIGN: Prospective cohort study. PATIENTS: A total of 351 medical and surgical intensive care unit patients with one of seven at-risk diagnoses for the development of ARDS. MAIN OUTCOME MEASURES: The development of ARDS and in-hospital mortality. RESULTS: Of the 351 patients enrolled in the study, the incidence of ARDS in patients with a history of alcohol abuse was significantly higher than in patients without a history of alcohol abuse (43% vs 22%) (P < .001; relative risk [RR], 1.98; 95% confidence interval [Cl], 1.32 to 2.85). In patients with sepsis, ARDS developed in 52% of the patients with a prior history of alcohol abuse compared with only 20% in patients without a history of alcohol abuse (P < .001; RR, 2.59; 95% Cl, 1.29 to 5.12). Fifty-one percent (52/102) of the patients who developed ARDS died compared with only 14% (36/249) of patients who did not develop ARDS (P < .001). In the subset of patients who developed ARDS, the in-hospital mortality rate was 65% in patients with a prior history of alcohol abuse. This mortality rate was significantly higher (P = .003) than the mortality rate in patients without a history of alcohol abuse (36%). CONCLUSIONS: A prior history of chronic alcohol abuse significantly increases the risk of developing ARDS in critically ill patients with an identified at-risk diagnosis. Our results may be useful in the earlier and more accurate identification of patients at high risk for developing ARDS.

APACHE↗