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Biomedical subjects

L Borda

Publications and source records attributed to L Borda.

12 recordsLinked to original sources
PubMed2003

Kondo effect in the presence of itinerant-electron ferromagnetism studied with the numerical renormalization group method.

The Kondo effect in quantum dots (QDs)-artificial magnetic impurities-attached to ferromagnetic leads is studied with the numerical renormalization group method. It is shown that the QD level is spin split due to the presence of ferromagnetic electrodes, leading to a suppression of the Kondo effect. We find that the Kondo effect can be restored by compensating this splitting with a magnetic field. Although the resulting Kondo resonance then has an unusual spin asymmetry with a reduced Kondo temperature, the ground state is still a locally screened state, describable by Fermi liquid theory and a generalized Friedel sum rule, and transport at zero temperature is spin independent.

Journal Article↗
PubMed2003

Quantum magnetic impurities in magnetically ordered systems.

We discuss the problem of a spin 1/2 impurity immersed in a spin S magnetically ordered background. We show that the problem maps onto a generalization of the dissipative two level system with two independent heat baths, associated with the Goldstone modes of the magnet, that couple to different components of the impurity spin operator. Using analytical perturbative renormalization group methods and accurate numerical renormalization group we show that contrary to other dissipative models there is quantum frustration of decoherence and quasiscaling even in the strong coupling regime. We make predictions for the behavior of the impurity magnetic susceptibility. Our results may also have relevance to quantum computation.

Journal Article↗
PubMed2002

Dynamics of a tunneling magnetic impurity: Kondo effect induced incoherence.

We study how the formation of the Kondo compensation cloud influences the dynamical properties of a magnetic impurity that tunnels between two positions in a metal. The Kondo effect dynamically generates a strong tunneling impurity-conduction electron coupling, changes the temperature dependence of the tunneling rate, and may ultimately result in the destruction of the coherent motion of the particle at zero temperature. We find an interesting two-channel Kondo fixed point as well for a vanishing overlap between the electronic states that screen the magnetic impurity. We propose experiments where the predicted features could be observed.

Journal Article↗
PubMed1994

[Treatment of trigeminal neuralgia with glycerin injected into Meckel's cavity].

The authors of the present study report on their results with glycerol gained over the past 9 years in 142 cases of trigeminal neuralgia. Initial pain relief was achieved in 64.5% of the cases. The average pain-free interval was 18.6 +/- 5.4 months, in other terms, 50% of the patients remained pain-free at 15 months after the procedure. However, a half-life of 23 months could be observed in a subgroup of patients with typical neuralgia if glycerol injection was the only way of operation during the course of the disease. Facial sensory loss which persisted for more than one year was found in 9.6% of the patients, corneal hypaesthesia occurred in 5.7%. Despite the relatively frequent recurrences, the technical simplicity and the low rate of complications may render this method to be useful in the treatment of trigeminal neuralgia.

Administration, Topical↗
PubMed1994

Evaluation of cerebral vasoreactivity by SPECT and transcranial Doppler sonography using the acetazolamide test.

rCBF SPECT with 99mTc-HMPAO was performed prospectively in 29 patients (3 controls and 26 stroke patients) as well as TCD studies in 20 patients (3 controls and 17 stroke patients) before and after 1 g i.v. acetazolamide. The sensitivity of rCBF SPECT increased from 62% to 77% after acetazolamide provocation in stroke patients. In patients with a reversible neurological deficit, the sensitivity under resting conditions was 50% which increased to 71%, while in cases with a permanent deficit it increased from 75% to 83%. In the evaluation of the cerebrovascular reserve capacity the results of rCBF SPECT and TCD coincided in 91% of the hemispheres. The correlation was statistically significant.

Acetazolamide↗
PubMed1993

[The effect of carotid endarterectomy on the reserve capacity of cerebral blood flow velocity].

Cerebral blood flow velocity was measured by transcranial Doppler sonography at rest and during cerebral vasodilatation evoked with acetazolamide in 14 patients before and after carotid endarterectomy. Before surgery the vasoreactivity in the affected middle cerebral artery territories was reduced and abnormal (asymptomatic side: 35.9 +/- 25.6% [mean +/- SD; n = 14]; symptomatic side: 25.6 +/- 10.7%), but the difference between the two hemispheres was not significant however, vasoreactivity was normalized 5 days after surgery (asymptomatic side: 46.9 +/- 22.3% symptomatic side: 58.9 +/- 23%) (p < 0.001). The increase in cerebral reserve capacity and changes in Gosling's index of pulsatility correlated significantly in both hemispheres (p < 0.02). This findings indicate an improved perfusion reserve on the fifth day following carotid endarterectomy in patients with an internal carotid artery diameter reduction of at least 70%.

Blood Flow Velocity↗
PubMed1992

[Determination of the cerebrovascular reserve capacity by using acetazolamide as well as transcranial Doppler and SPECT tests].

The aim of this study was the development of a simple bedside test to assess cerebrovascular reserve capacity using transcranial Doppler sonography. We tried to validate the increase in blood flow velocity as cerebrovascular reserve capacity in 20 (3 normal, 7 TIA, 10 completed stroke) patients. They were studied using transcranial Doppler sonography and rCBF SPECT before and after injection of 1 g acetazolamide. Their increases in blood flow velocity and changes in cerebral blood flow correlated significantly in the symptomatic hemispheres (p less than 0.001). Blood flow velocity between the two hemispheres (symptomatic and asymptomatic) was not significantly different at rest. We offer these simple and reliable methods in clinical studies to clarify the frequency of ischemic stroke of hemodynamic origin.

Acetazolamide↗
PubMed1987

Inhibition of electroshock-induced seizures by cholecystokinin-related peptides in mice.

The effects of several doses of cholecystokinin octapeptide sulphate ester (CCK-8-SE) and nonsulphated cholecystokinin octapeptide (CCK-8-NS), and two CCK-related peptide analogues Ac-Thr5-caerulein, and nonsulphated Ac-Thr5-caerulein were investigated on electroshock-(ES)-induced seizures after intraperitoneal administration in mice. As parameters, the duration of the tonic and clonic phase of the fit, and those of postictal coma and behavioural depression were measured. CCK-8-SE decreased the duration of the clonic phase; its highest dose, 3.2 mumol/kg, shortened the coma. CCK-8-NS antagonized only slightly the clonic phase of seizure. Ac-Thr5-caerulein did not influence ES-induced seizures in any dose, only increased the duration of behavioural depression. Similarly to CCK-8-NS, the nonsulphated form of Ac-Thr5-caerulein inhibited selectively the clonic phase of seizures. The reference drugs, diazepam and phenobarbital, antagonized dose-dependently and most effectively the tonic phase of ES-induced seizures, but in much higher doses than did the CCK-related peptides. Besides, diazepam increased and phenobarbital decreased the duration of postictal coma. The results showed that the tested CCK-related peptides inhibit prevalently the clonic phase of ES-induced seizures after peripheral administration.

Animals↗
PubMed1985

Cataleptogenic and anticataleptic activity produced by cholecystokinin octapeptides in mice.

The catalepsy induced by subcutaneously (sc.) and intracerebroventricularly (icv.) administered cholecystokinin octapeptide sulfate ester (CCK-8-SE) and desulfated cholecystokinin octapeptide (CCK-8-NS), and the effects of CCK-8-SE and CCK-8-NS on haloperidol-induced catalepsy, were investigated in mice. The results demonstrate the bimodal effect of CCK octapeptides in a catalepsy test. With sc. administration CCK-8-SE in the doses of 0.4 or 0.8 mumole/kg, but not CCK-8-NS at any dose, induced catalepsy. Furthermore, the catalepsy induced by CCK-8-SE was of short duration. With icv. administration only 40 pmole CCK-8-NS induced significant catalepsy. When 0.2, 0.4 and 0.8 mumole/kg sc. doses of CCK-8-NS or 0.4 pmole icv. dose of CCK-8-SE or CCK-8-NS was given in combination with intraperitoneal (ip.) administration of 1.0 mg/kg haloperidol, the total duration of catalepsy was suppressed. Finally, CCK-8-SE sc. when given in combination with haloperidol ip., exerted a biphasic, synergistic-antagonistic effect on the haloperidol-induced catalepsy.

Animals↗
PubMed1982

Inotropic and chronotropic effects of vasodilators.

Although vasodilators are used with increasing frequency for the treatment of heart failure and myocardial ischemia, their direct effects on cardiac muscle have not been completely characterized. To delineate the action of vasodilators on mammalian myocardium, the chronotropic and inotropic effects of vasodilators on isolated guinea-pig atria (n = 163) have been determined. The spontaneous frequency and the peak rate of isometric force development at a fixed frequency of 200/min were used as indexes of chronotropy and inotropy. The potency series for negative chronotropy was diltiazem greater than D600 greater than verapamil greater than lidoflazine greater than bepridil greater than prenylamine greater than perhexiline greater than nifedipine. The potency series for negative inotropy differed substantially, exhibiting the sequence nifedipine greater than D600 greater than verapamil greater than bepridil greater than lidoflazine greater than prenylamine greater than perhexiline greater than diltiazem. Therefore, nifedipine acted as an "inoselective" and diltiazem as a "chrono-selective" depressant. Other vasodilators, including papaverine, nitroglycerin, nitroprusside, adenosine, dipyridamole, diazoxide and hydralazine exerted no or negligible negative chronotropic or inotropic effects even at high concentration (10(-5) M). Therefore, only vasodilators classified among the calcium antagonists proved to have appreciable direct myocardial effects. This supports the view that these drugs constitute a category of agents distinct from classical vasodilators.

Animals↗