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N Reuter

Publications and source records attributed to N Reuter.

16 recordsLinked to original sources
PubMed2003

Orexins and their receptors: structural aspects and role in peripheral tissues.

Orexins, also named hypocretins, were discovered in 1998 by subtractive cDNA cloning or orphan receptor technologies. Prepro-orexin is enzymatically matured into two peptides, orexin-A and orexin-B which are 33- and 28-amino-acid peptides, respectively. Two cloned orexin receptors OX1R and OX2R are serpentine G-protein-coupled receptors, both of which bind orexins and are coupled to Ca2+ mobilization. Orexins are neuropeptides present in hypothalamic neurons that project throughout the central nervous system to nuclei involved in the control of feeding, sleep-wakefulness, neuroendocrine homeostasis and autonomic regulation. The interest of investigators in orexins has focused on narcolepsy, since genetic or experimental alterations of the orexin system are associated with this sleep disorder. However, orexins are not restricted to the hypothalamus and together with their receptors they are expressed in peripheral tissues. This new multifaceted aspect of orexin biology is reviewed here in descriptions of (i) the proform, maturation and structure of orexins, (ii) the structure, signal transduction and pharmacology of orexin receptors and (iii) the expression of orexins and orexin receptors as well as their biological role in the hypothalamus-pituitary-adrenal axis, gastrointestinal tract, endocrine pancreas and other peripheral tissues.

Amino Acid Sequence↗
PubMed2001

The search for a new model structure of beta-factor XIIa.

We present the search for a new model of beta-factor XIIa, a blood coagulation enzyme, with an unknown experimental 3D-structure. We decided to build not one but three different models using different homologous proteins as well as different techniques and different modelers. Additional studies, including extensive molecular dynamics simulations on the solvated state, allowed us to draw several conclusions concerning homology modelling, in general, and beta-factor XIIa, in particular.

Amino Acid Sequence↗
PubMed1998

Protein kinase C regulates nutrient uptake and growth in hepatoma cells.

BACKGROUND: Human hepatoma cells extract glutamine at rates severalfold greater than normal hepatocytes through a high-affinity transporter encoded by the ATB0 gene, which contains two putative phosphorylation sites for protein kinase C (PKC). The studies presented here were undertaken to determine whether System B0-mediated glutamine uptake regulates hepatoma growth and whether PKC regulates the activity of this transporter. METHODS: SK-Hep cells were treated with the PKC activator phorbol 12-myristate 13-acetate (PMA) and the initial-rate transport of glutamine and other nutrients measured at specific times thereafter. Growth rates were monitored during culture +/- PMA or an excess of system B0 substrates relative to glutamine. RESULTS: PMA treatment exerted a rapid (half-life approximately 15 minutes) concentration-dependent inhibition of glutamine uptake rates to 50% of control values via a posttranslational mechanism that decreased transporter maximum velocity. This effect persisted after 24 hours and was abrogated by the PKC inhibitor staurosporine. PMA also significantly decreased amino acid transport System y+ and System L activities but no System A. Chronic treatment with PMA (PKC depletion) inhibited SK-Hep growth, as did attenuation of System B0-mediated glutamine uptake with other B0 substrates. CONCLUSIONS: System B0-mediated glutamine uptake regulates hepatoma cell growth, whereas PKC influences both processes.

Amino Acid Transport Systems↗
PubMed1996

[Splenic infarction caused by paradoxical emboli in severe pulmonary hypertension].

HISTORY AND CLINICAL FINDINGS: A 55-year-old woman developed increasing shortness of breath and breath-independent pain in the left lower chest. 20 years previously she had had an episode of pulmonary embolism and 10 years previously a central venous thrombosis in the left eye. No cause of the increased thrombogenesis had been found. On admission she had resting dyspnoea but a stable circulation. On auscultation the breath sounds were diminished over the left base and there was a diastolic murmur over the pulmonary area with an accentuated second sound. There was also marked tenderness below the left costal margin. Recurrent pulmonary embolism or left-sided pleuropneumonia was suspected. INVESTIGATION: Arterial blood gases (without additional oxygen) showed severe hypoxaemia (pO2 42.3 mm Hg, pCO2 27.8 mm Hg, pH 7.455, oxygen saturation 80.5%). Transthoracic and transoesophageal echocardiography showed normal left ventricular dimensions, right atrial and ventricular dilatation, and an atrial septal aneurysm with a right to left interatrial shunt. Right heart catheterisation demonstrated severe pulmonary hypertension. Sonography, computed tomography and scintigraphy revealed multiple splenic infarcts. TREATMENT AND COURSE: Heparinisation was instituted (partial thromboplastin time 70-90 s) and overlapping oral anticoagulation to a Quick value of 20%. Subsequently the calcium antagonist felodipine (15 mg daily) was given. The mean pulmonary artery pressure was 61 mm Hg before and 57 mm Hg after treatment. CONCLUSION: Splenic infarction resulting from paradoxical embolisation is rare, but should be routinely considered in the presence of thromboembolic phenomena.

Angiography↗
PubMed1976

[Heart and circulatory effects of quinidine stereoisomers].

Quinidine sulfate shows dose-related activity. On the cardio-vascular system of anaesthetized cats. It reduces heart rate, prolongs QRS and QT of the ECG, lowers peripheral blood pressure and depresses slightly myocardial contractility. Quinidine hydrochloride lowers blood pressure but alters the ECG only in very high doses. Epiquinidine has no blood pressure lowering activity. According to the Easson and Stedman hypothesis this may be the result of stereoselectivity of alpha-adrenergic receptors. Only very high doses of the epimer produce a transient decrease of blood pressure. The ECG-waves are, however, markedly altered. QT is prolonged only with epiquinine-epiquinidine-sulfate. The salts of epiquinidine tested are much better water-soluble than those of quinidine.

Animals↗
PubMed1976

[Local anesthesia after percutaneous application. II].

Cyclohexane and hexadecane have been found to accelerate the penetration of local anesthetics (lidocaine, fomocaine, procaine) through the intact skin of guinea-pigs. Dissolved in cyclohexane, the potency of lidocaine is twice that of fomocaine, the latter being more active than procaine. When dissolved in hexadecane, the activity of the local anesthetics in markedly reduced. In combination with 2-butanone, (30% w/w), a solvent without any apparent effect on the permeability of skin, enhanced anesthetic effects are noted. The anesthetic bases, dissolved in dimethyl sulfoxide, produce a much deeper and longer local anesthetic effect than the solutions of their salts.

Administration, Topical↗
PubMed1976

[Effects of pentaformylgitoxin (gitoformate) on the cardiovascular system of anesthetized cats].

In small and medium doses 3 beta, 14 beta-dihydroxy-16 beta-formyloxy-5 beta-card-20-[22]-enolide-3-tetraformyltridigitoxoside (pentaformylgitoxin; gitoformate) shows a greater positive inotropic and blood pressure increasing potency than do digitoxin and beta-acetyldigoxin. In high doses this influence on contractility is exceeded by digitoxin, that on blood pressure is equalled. None of the substances tested changes heart rate. Arrhythmias with gitoformate are only seen in lethal doses, with digitoxin and beta-acetyldigoxin two dose levels earlier.

Animals↗
PubMed1975

[Action of fomocaine on heart and circulation (author's transl)].

Fomocaine shows antiarrhythmic properties. It prolongs the periods of the ECG (anaesthetized cats) and the functional refractory period (left atria of guinea-pigs, electrically driven). Effects on these parameters are qualitatively the same as with quinidine. Quantitatively fomocaine prolongs the functional refractory period in the same, the PQ-interval to a greater extent than does quinidine. In contrast quinidine has a greater effect on QRS- and QT-interval. Up to higher doses fomocaine's efficacy on contractility (dp/dtmax) and blood pressure is opposite to quinidine because they are increased by fomocaine and decreased by quinidine. The lack of toxic ECG-signs prior to lethal dosis makes fomocaine dangerous in overdosage.

Animals↗
PubMedDate not supplied

[Early detection of hepatobiliary involvement in children with mucoviscidosis using duplex sonography of the portal system].

To investigate early signs of hepatobiliary disease in CF, we measured portal, splenic, superior mesenteric vein and hepatic artery diameters, maximal flow velocity (Vmax) and time average velocity (TAV) in 25 males and 17 females with CF. Hepatic artery resistance, regional blood flow and liver perfusion were calculated. According to liver enzyme data (aminotransferases raised greater than 30 U/l) and sonographic findings (nodular changes), there were 17 CF-patients (mean age 11.4 yrs; range 0.75-31) with and 25 CF-patients (mean age 7.8 yrs; range 0.25-32) without liver involvement (L+/L-). No patient had clinical signs of portal hypertension. 61 healthy children were studied for control. Diameter of portal vein (PVD) and flow data for portal vein showed consistent abnormalities (mean +/- SD): CF-L+ CF-L- Control PVC (mm/m2) 10.7 +/- 3.9*** 10.5 +/- 3.4*** 7.2 +/- 1.3 Vmax (m/sec) 0.23 +/- 0.06*** 0.30 +/- 0.06*** 0.40 +/- 0.14 TAV (m/sec) 0.12 +/- 0.04*** 0.16 +/- 0.04* 0.18 +/- 0.05 Differences were statistically significant (* p less than 0.05, *** p less than 0.001) for CF-patients versus controls. Data for splenic and mesenteric veins and for hepatic artery were moderately alterated, with a significant reduction in TAV and Vmax of splenic vein for CF-L+ versus controls. Liver perfusion and portal vein flow showed no relevant differences in CF-patients versus controls. It is concluded that portal system abnormalities, especially a decrease in Vmax and TAV of portal vein shown by duplex sonography, may be earlier indicators of CF liver disease than biochemical and clinical signs.

Adolescent↗