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ABSTRACT: Recent studies have highlighted a significant association between the severity of atherosclerosis and bone mineral density (BMD) among healthy subjects, although its connection to angiographically determined peripheral artery disease (PAD) has never been investigated. We evaluated the connection between the angiographic severity and site specificity of peripheral atherosclerosis and osteoporosis among patients with chronic lower limb ischemia. In our cross-sectional study we investigated 172 patients with PAD. The anatomic sites of the lesions were analyzed. The severity of atherosclerosis was diagnosed using the Bollinger angiographic score (BS). BMD was measured at the lumbar spine (l-BMD) and at femoral (f-BMD) and radial (r-BMD) sites by dual-energy X-ray absorptiometry. Dyslipidemia, the level of vitamin D3, and different bone turnover markers were also noted. Among PAD patients, regardless of the lesion site, we did not find any association between BMD and BS. Among patients with iliac disease, BS was associated with l-BMD (p = 0.038, r = -0.467) and with f-BMD (p = 0.002, r = -0.642). The level of r-BMD among patients with iliac disease was not associated with BS (p = 0.233, r = -0.306). We did not find any difference between the group of patients with and that without dyslipidemia and low or normal levels of vitamin D3. Our results show a connection between the severity of atherosclerosis and osteoporosis among patients with PAD, specific to the site of the lesion. The findings regarding dyslipidemia, bone markers, and site specificity support the hypothesis that reduced blood flow is the key factor responsible for the inverse association of BMD with atherosclerosis.
Calcified Tissue International 04/2013; · 2.38 Impact Factor
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Loránd Eross,
Gábor Fekete, László Entz,
Dániel Fabó,
Csaba Borbély,
Lajos Rudolf Kozák,
Mónika Andrejkovics,
Sándor Czirják,
Imre Fedorcsák,
László Novák,
László Bognár
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ABSTRACT: To summarize the results gained with awake craniotomies, which were performed in either low grade glioma patients or epilepsy surgical patients whose tumor or epileptogenic zone, was in the vicinity of eloquent, mostly language, cortices. PATIENT SELECTION AND METHODS: In our retrospective study we selected 16 patients who were operated awake between 1999-2011 at the Neurosurgical Department of MAV Kórház Budapest, or at the National Institute of Neurosciences in Budapest, or at the Neurosurgical Department of the University of Debrecen in Debrecen. In the presurgical evaluation if it was possible we performed functional magnetic resonance imaging, tractography and detailed neuropsychological testing. At the National Institute of Neurosciences all patients were operated with the aid of MR guided neuronavigation.
Anesthesia was carried out without complications in all of the 16 cases. Monitoring of sleep deepness has significantly contributed to the safety of anesthesia during the superficial anesthezied states of the operation. The intraoperative neuropsychological tasks used for testing language were sensitive enough to judge the little disturbances in speech during stimulation. Stimulation evoked seizures could be adequately managed during surgery and did not influence the outcome of the procedures. The use of neuronavigation helped significantly by planning the optimal place for the craniotomy and by intraoperative orientation.
Awake craniotomies require well practiced surgical teams, which requires the cooperation of neuro-anesthesiologits, neurosurgeons, neuropsychologist and electrophysiologists. It has two goals, first to reduce the time of surgery to minimize surgical complications, secondly the detailed intraoperative mapping of cognitive and motor functions to avoid any neurological deficit. The intraoperative anatomical data provided by the neuronavigation and the functional data provided by awake intraoperative stimulation of the patient together serve the safety of the patient which is essential in the neurologically minimal invasive neurosurgical approach of the 21st century.
Ideggyógyászati szemle 09/2012; 65(9-10):333-41. · 0.49 Impact Factor
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ABSTRACT: Cortical electrical activity during nonrapid eye movement (non-REM) sleep is dominated by slow-wave activity (SWA). At larger spatial scales (∼2-30 cm), investigated by scalp EEG recordings, SWA has been shown to propagate globally over wide cortical regions as traveling waves, which has been proposed to serve as a temporal framework for neural plasticity. However, whether SWA dynamics at finer spatial scales also reflects the orderly propagation has not previously been investigated in humans. To reveal the local, finer spatial scale (∼1-6 cm) patterns of SWA propagation during non-REM sleep, electrocorticographic (ECoG) recordings were conducted from subdurally implanted electrode grids and a nonlinear correlation technique [mutual information (MI)] was implemented. MI analysis revealed spatial maps of correlations between cortical areas demonstrating SWA propagation directions, speed, and association strength. Highest correlations, indicating significant coupling, were detected during the initial positive-going deflection of slow waves. SWA propagated predominantly between adjacent cortical areas, albeit spatial noncontinuities were also frequently observed. MI analysis further uncovered significant convergence and divergence patterns. Areas receiving the most convergent activity were similar to those with high divergence rate, while reciprocal and circular propagation of SWA was also frequent. We hypothesize that SWA is characterized by distinct attributes depending on the spatial scale observed. At larger spatial scales, the orderly SWA propagation dominates; at the finer scale of the ECoG recordings, non-REM sleep is characterized by complex SWA propagation patterns.
Journal of Neuroscience 06/2011; 31(24):8770-9. · 7.11 Impact Factor
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ABSTRACT: Prosthetic graft infection or the need for reconstructive arterial surgery in septic condition is a challenging situation in vascular surgery. Recent introduction of silver coated polyester graft has meant a new therapeutic option in selecting the type of graft for revascularization. In this study we analyzed the short and midterm outcome of using silver coated grafts in aortic and lower extremity arterial reconstructions (mortality, graft occlusion, graft infection, amputation).
In a single center retrospective study we implanted 42 silver coated Dacron grafts (InterGard Silver Dacron prosthesis). The indication of silver graft implantation was graft infection in 17, aorto-duodenal fistula in 7, septic condition caused by gangrene in 16 cases and in 2 cases infection was not established.
Forty silver grafts were implanted in 40 patients with diagnosed infection. The mean age was 62 years (35-81 years), 70% were men. Long term follow-up data were available in 29 patients; the mean follow-up time was 36.76 months. Early (within 30 days of surgery) death occurred in 3 and late death in 11 cases (8 and 38%). Early graft occlusion was noticed in 8 and late occlusion in 2 cases (20 and 7%). Reinfection was diagnosed in 7% of the cases in the early and the midterm period as well. Eight amputations were indicated in the early postoperative period (5 major and 3 minor) and 28% of the patients required major amputation during the follow-up.
Silver coated Dacron graft means a valuable therapeutic option with good rate of infection control in the treatment of graft infection and septic condition in the lack of autologous graft material in this high risk population.
Magyar Sebészet (Hungarian Journal of Surgery) 12/2010; 63(6):369-73.
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Richárd Csercsa,
Balázs Dombovári,
Dániel Fabó,
Lucia Wittner,
Loránd Eross, László Entz,
András Sólyom,
György Rásonyi,
Anna Szucs,
Anna Kelemen, [......],
László Grand,
Andor Magony,
Péter Halász,
Tamás F Freund,
Zsófia Maglóczky,
Sydney S Cash,
László Papp,
György Karmos,
Eric Halgren,
István Ulbert
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ABSTRACT: Brain electrical activity is largely composed of oscillations at characteristic frequencies. These rhythms are hierarchically organized and are thought to perform important pathological and physiological functions. The slow wave is a fundamental cortical rhythm that emerges in deep non-rapid eye movement sleep. In animals, the slow wave modulates delta, theta, spindle, alpha, beta, gamma and ripple oscillations, thus orchestrating brain electrical rhythms in sleep. While slow wave activity can enhance epileptic manifestations, it is also thought to underlie essential restorative processes and facilitate the consolidation of declarative memories. Animal studies show that slow wave activity is composed of rhythmically recurring phases of widespread, increased cortical cellular and synaptic activity, referred to as active- or up-state, followed by cellular and synaptic inactivation, referred to as silent- or down-state. However, its neural mechanisms in humans are poorly understood, since the traditional intracellular techniques used in animals are inappropriate for investigating the cellular and synaptic/transmembrane events in humans. To elucidate the intracortical neuronal mechanisms of slow wave activity in humans, novel, laminar multichannel microelectrodes were chronically implanted into the cortex of patients with drug-resistant focal epilepsy undergoing cortical mapping for seizure focus localization. Intracortical laminar local field potential gradient, multiple-unit and single-unit activities were recorded during slow wave sleep, related to simultaneous electrocorticography, and analysed with current source density and spectral methods. We found that slow wave activity in humans reflects a rhythmic oscillation between widespread cortical activation and silence. Cortical activation was demonstrated as increased wideband (0.3-200 Hz) spectral power including virtually all bands of cortical oscillations, increased multiple- and single-unit activity and powerful inward transmembrane currents, mainly localized to the supragranular layers. Neuronal firing in the up-state was sparse and the average discharge rate of single cells was less than expected from animal studies. Action potentials at up-state onset were synchronized within +/-10 ms across all cortical layers, suggesting that any layer could initiate firing at up-state onset. These findings provide strong direct experimental evidence that slow wave activity in humans is characterized by hyperpolarizing currents associated with suppressed cell firing, alternating with high levels of oscillatory synaptic/transmembrane activity associated with increased cell firing. Our results emphasize the major involvement of supragranular layers in the genesis of slow wave activity.
Brain 09/2010; 133(9):2814-29. · 9.46 Impact Factor
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ABSTRACT: Vagus nerve stimulation (VNS) is a nonpharmacologic therapeutic option for patients with intractable epilepsy. Better clinical outcomes were recorded in nonfocal and Lennox-Gastaut syndrome (LGS). We conducted a 2-year, open label, prospective study to measure the seizure outcome of 26 VNS patients. The seizure numbers were assessed using clinician's global impression scale (CGI) and patient diaries. The average seizure reduction was 23% at the first year and 22% at the second year. Seizure reduction was more pronounced among patients with nonfocal than with focal epilepsy. The response rate was 50% at first year and 30% at the second year. The best CGI record for clinically significant improvement was 15% in the LGS group. The only statistically significant result was the reduction of the generalized tonic-clonic seizures (GTCS). The side-effect profile was good; however, the large number of mild and reversible effects influenced the stimulation parameters and thus probably the effectiveness of the therapy. We suggest that VNS is an optional treatment mostly in cases of therapy-resistant Lennox-Gastaut syndrome. Patients with GTCS may experience improvement such as reduction of seizure severity. We conclude that VNS is a safe neuromodulatory treatment, but future developments of neuromodulatory approaches are needed.
Epilepsia 07/2010; 51 Suppl 3:98-101. · 3.96 Impact Factor
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ABSTRACT: Although the association between vulnerable lesions and cardiovascular events is well established, little is known about their relationship to postsurgery restenosis. To address this issue, we initiated a prospective, nonrandomized study to examine the femoral plaques on both sides in patients who were undergoing eversion carotid endarterectomy (CEA) and were longitudinally followed-up for early restenosis development.
The final analysis enrolled 321 patients (189 women) with a median age of 67.0 years (interquartile range, 59.0-73.0 years), who underwent eversion CEA (2005 to 2007). Using duplex ultrasound scanning, we evaluated 321 common femoral atherosclerotic lesions on the day before CEA. A quantitative scale was used to grade the size of plaques as grade 1, one or more small plaques (<20 mm2); grade 2, moderate to large plaques; and grade 3, plaques giving flow disturbances. The plaque morphology in terms of echogenicity was graded as echolucent, 1; predominantly echolucent, 2; predominantly echogenic, 3; echogenic 4; or calcified, 5. The plaque surface was categorized as smooth, irregular, or ulcerated. The patients underwent carotid duplex ultrasound imaging at 6 weeks and at 6, 12, and 24 months after CEA. Mann-Whitney U test, chi2 test, and multivariate logistic regression were used for statistical evaluation.
Internal carotid artery restenosis of > or = 50% was detected in 33 patients (10.28%) in the operated region. Neither the size (grade 1, P = .793; grade 2, P = .540; grade 3, P = .395) nor the surface characteristics of the femoral plaques (smooth, P = .278; irregular, P = .281; ulcerated, P = .934) were significantly different between the patients with and without carotid restenosis. Echolucent-predominantly echolucent femoral lesions were an independent predictor of recurrent carotid stenosis (adjusted odds ratio, 5.63; 95% confidence interval, 2.14-10.89; P < .001).
Ultrasound evaluation of femoral plaque morphology before CEA can be useful for identifying patients at higher risk for carotid restenosis.
Journal of vascular surgery: official publication, the Society for Vascular Surgery [and] International Society for Cardiovascular Surgery, North American Chapter 02/2010; 51(2):345-50. · 3.52 Impact Factor
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Lucia Wittner,
Gilles Huberfeld,
Stéphane Clémenceau,
Loránd Eross,
Edouard Dezamis, László Entz,
István Ulbert,
Michel Baulac,
Tamás F Freund,
Zsófia Maglóczky,
Richard Miles
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ABSTRACT: The dentate gyrus, the cornu ammonis 2 region and the subiculum of the human hippocampal formation are resistant to the cell loss associated with temporal lobe epilepsy. The subiculum, but not the dentate gyrus, generates interictal-like activity in tissue slices from epileptic patients. In this study, we asked whether a similar population activity is generated in the cornu ammonis 2 region and examined the electrophysiological and neuroanatomical characteristics of human epileptic cornu ammonis 2 neurons that may be involved. Hippocampal slices were prepared from postoperative temporal lobe tissue derived from epileptic patients. Field potentials and multi-unit activity were recorded in vitro using multiple extracellular microelectrodes. Pyramidal cells were characterized in intra-cellular records and were filled with biocytin for subsequent anatomy. Fluorescent immunostaining was made on fixed tissue against the chloride-cation cotransporters sodium-potassium-chloride cotransporter-1 and potassium-chloride cotransporter-2. Light and electron microscopy were used to examine the parvalbumin-positive perisomatic inhibitory network. In 15 of 20 slices, the hippocampal cornu ammonis 2 region generated a spontaneous interictal-like activity, independently of population events in the subiculum. Most cornu ammonis 2 pyramidal cells fired spontaneously. All cells fired single action potentials and burst firing was evoked in three cells. Spontaneous excitatory postsynaptic potentials were recorded in all cells, but hyperpolarizing inhibitory postsynaptic potentials were detected in only 27% of the cells. Two-thirds of cornu ammonis 2 neurons showed depolarizing responses during interictal-like events, while the others were inhibited, according to the current sink in the cell body layer. Two biocytin-filled cells both showed a pyramidal-like morphology with axons projecting to the cornu ammonis 2 and cornu ammonis 3 regions. Expression of sodium-potassium-chloride cotransporter-1 and potassium-chloride cotransporter-2 was reduced in some cells of the epileptic cornu ammonis 2 region, but not to an extent corresponding to the proportion of cells in which hyperpolarizing postsynaptic potentials were absent. Numbers of parvalbumin-positive inhibitory cells and axons were shown to be decreased in the epileptic tissue. Electron microscopy showed the preservation of somatic inhibitory input of cornu ammonis 2 cells, and confirmed the loss of parvalbumin from the interneurons rather than their death. An extra excitatory input (partly coming from sprouted mossy fibres) was demonstrated to innervate cornu ammonis 2 cell bodies. Our results show that the cornu ammonis 2 region of the sclerotic human hippocampus can generate an independent epileptiform activity. Inhibitory and excitatory signalling were functional but modified in epileptic cornu ammonis 2 pyramidal cells. Overexcitation and the altered functional properties of perisomatic inhibitory network, rather than a modified chloride homeostasis, may account for the perturbed gamma-aminobutyric acid-ergic signalling and the generation of interictal-like activity in the human epileptic cornu ammonis 2 region.
Brain 09/2009; 132(Pt 11):3032-46. · 9.46 Impact Factor
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Loránd Eross, László Entz,
Dániel Fabó,
Rita Jakus,
Anna Szucs,
György Rásonyi,
Anna Kelemen,
Gábor Barcs,
Vera Juhos,
Attila Balogh,
Péter Barsi,
Zsófia Clemens,
Péter Halász
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ABSTRACT: To investigate interhemispheric propagation of mesial temporal lobe epilepsy seizures in patients undergoing long-term video-EEG monitoring with combined scalp and foramen ovale electrodes.
To reveal possible interhemispheric propagation patterns in mesial temporal lobe epilepsy, to improve presurgical evaluation of temporal epileptic patients.
Sixty-five seizures from 20 patients were analyzed. We defined two contralateral seizure propagation patterns: Type I for those seizures that spread to the contralateral foramen ovale electrodes earlier than to the contralateral scalp electrodes, and type II for the opposite.
Twenty drug resistant epileptic patients were investigated in frame of their presurgical evaluation.
The majority of seizures (80%) were classified as type I. Inter-foramen ovale electrode propagation time was significantly shorter for type I compared to type II seizures. Ninety percent of patients had either type I or type II seizures only. Patients with type I seizures significantly more often had mesiotemporal structural alterations evident on magnetic resonance imaging scans, and became more often seizure-free after surgery compared to patients with type II seizures whose surgical outcome was less favorable or surgery could not be indicated because of independent bilateral ictal seizure-onset.
The two types of contralateral propagation patterns we are describing seem to represent two subtypes of mesial temporal lobe epilepsy with different morphological and prognostic features. The predominance of type I over type II seizures together with shorter propagation times for type I seizures indicate a role of a more direct and dominant interhemispheric pathway in mesial temporal lobe epilepsy.
Ideggyógyászati szemle 09/2009; 62(9-10):319-25. · 0.49 Impact Factor
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ABSTRACT: Intrapericardial (IP) administration of certain cardioactive agents allows investigation of local pharmacological actions on the heart and may carry potential benefit to influence myocardial function. The cardioprotective adenosine (ADO) and inosine (INO) may be the most representative candidates. Elimination and cardiovascular effects of IP and intravenously (IV) applied ADO and INO were compared on anesthetized dogs. Their pericardial and systemic concentrations were measured after consecutive administration of increasing ADO and INO doses. In the case of IP administration at the end of the incubation period, pericardial concentrations of adenine nucleosides significantly exceeded the control values. However, the IV applied ADO and INO were rapidly metabolized in the systemic plasma. As characteristic hemodynamic effects, small but sustained decrease in heart rate (IP ADO) and increase in myocardial contractility (IP INO) were observed. During IV administration, ADO and INO exerted remarkable effects on all hemodynamic variables, which then gradually disappeared in 15 minutes. In summary, the elimination of ADO and INO was significantly slower in the pericardial fluid than in the plasma. Considering the balanced cardiac actions and lack of strong systemic hemodynamic effects, IP administration of adenine nucleosides may suggest a promising approach in the local treatment of the diseased heart.
Journal of cardiovascular pharmacology 09/2009; 54(4):341-7. · 2.83 Impact Factor
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ABSTRACT: Restenosis following endovascular interventions is the main limitation of their long-term success. The incidence of restenosis varies according to the method (stenting, endarterectomy) and the treated vascular region, but the pathomechanism and risk factors are similar. The current article reviews of the author's previous studies in this field. In clinical studies, we compared the restenosis rate after carotid artery stenting and carotid endarterectomy. We also analyzed the complement activation profile after these interventions. In another study, we investigated the role of two polymorphisms of the estrogen receptor alpha in the occurrence of carotid restenosis after either carotid artery stenting or carotid endarterectomy. In an animal model of carotid endarterectomy, we studied the role of the nitrite-oxide-cyclic guanosine monophosphate signaling and the effect of the phosphodiesterase-5 inhibitor therapy in neointimal hyperplasia. Our results suggest that higher incidence of restenosis following carotid endarterectomy can be correlated with the more highly expressed complement activation after this type of carotid intervention. Polymorphisms in the estrogen receptor alpha gene could contribute to the restenosis formation, especially in women. Neointimal hyperplasia can be attenuated by increased cyclic guanosine monophosphate signaling.
Orvosi Hetilap 08/2009; 150(28):1307-12.
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ABSTRACT: Long-term results of surgical vessel reconstruction are compromised by restenosis caused by neointimal hyperplasia. Recent studies suggest that reduced cyclic guanosine monophosphate signaling is associated with neointima formation. In a rat model of endarterectomy, we investigated the effect of pharmacologic inhibition of cyclic guanosine monophosphate degradation on neointima formation by using the selective phosphodiesterase-5 inhibitor vardenafil.
Carotid endarterectomy was performed in male Sprague-Dawley rats by means of incision of the right common carotid artery with removal of intima. Four groups were studied: unoperated control rats (n = 4), sham-operated rats (n = 9), control rats with endarterectomy (n = 9), or endarterectomized rats treated with vardenafil (10 mg/kg/day) postoperatively (n = 9). After 3 weeks, vessel compartment areas were measured by means of conventional microscopy with hematoxylin and eosin staining. Immunohistochemical analysis was performed to confirm neointima formation and the local cyclic guanosine monophosphate content. Plasma levels of cyclic guanosine monophosphate were determined by means of enzyme immunoassay. Student's t test was used for statistical evaluation.
Immunohistochemical analysis demonstrated intensive staining for transforming growth factor beta1 and alpha-smooth muscle actin in the control neointima. Vardenafil significantly reduced the stenosis grade (24.64% +/- 7.46% vs 54.12% +/- 10.30% in the control group, P < .05) and expression of transforming growth factor beta1, as well as alpha-smooth muscle actin, in the neointima. The immunohistochemical score for cyclic guanosine monophosphate was higher in the treated neointima (4.80 +/- 0.76 vs 2.84 +/- 0.40 in the control group, P < .05), and increased plasma cyclic guanosine monophosphate levels were found by means of enzyme immunoassay as well (84.65 +/- 12.77 pmol/mL vs 43.50 +/- 3.30 pmol/mL in the control group, P < .05).
Treatment with vardenafil can be considered a new possibility to prevent neointimal hyperplasia after endarterectomy.
The Journal of thoracic and cardiovascular surgery 06/2009; 137(6):1508-14. · 3.41 Impact Factor
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ABSTRACT: Our aim was to identify the role of PvuII and XbaI polymorphisms of the ESR1 (estrogen receptor alpha) gene in the occurrence of early restenosis after carotid endarterectomy and carotid artery stenting.
In a non-randomized prospective study we analysed blood samples from 172 patients (105 men) with severe stenosis of the internal carotid artery, using the PCR-RFLP method. Patients were treated either by carotid endarterectomy (n=82) or carotid artery stenting (n=90), and were followed-up by ultrasonography with a median follow-up time of 12 months (7.32-14.65 months). Conventional laboratory parameters were also recorded. Restenosis (>50%) rates were compared between patients carrying different genotypes and risk factors were calculated by using multivariate logistic regression.
Allelic frequencies were similar between sexes (C/T allele, 0.40/0.60 and 0.43/0.57; p=0.67; G/A allele, 0.35/0.65 and 0.32/0.68; p=0.65; in men and women, respectively). Significantly higher restenosis rate was observed in patients homozygous for the A-allele of the XbaI polymorphism as compared to carriers of AG and GG genotypes (23.4% vs. 10.5%, p=0.02). TT and TC genotypes of the PvuII polymorphism were also associated with greater restenosis rate, as compared with genotype CC (19.3% vs. 3.1%, p=0.02). Associations for both polymorphisms were more expressed in women and in CEA patients. At multivariate analysis, T-A haplotype was a predictor of restenosis in the whole patient cohort (adjusted odds ratio, 7.85; 95% CI, 1.01-60.98).
Presence of A and T alleles (of the XbaI and PvuII polymorphisms, respectively) were associated with higher incidence of carotid restenosis, while the presence of G and C alleles (of the XbaI and PvuII polymorphisms, respectively) were associated with lower incidence of carotid restenosis.
Atherosclerosis 02/2009; 206(1):186-92. · 3.79 Impact Factor
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ABSTRACT: For localization of the epileptogenic zone in cases of focal epilepsy, detailed clinical investigations, imaging studies, and electrophysiological methods are used. If the noninvasive presurgical evaluation provides insufficient data, intracranial electrodes are necessary. Computed tomography and MR imaging techniques are the gold standard for localization of the postoperative position of the implanted intracranial electrode contacts. If the electrode strips are inserted through a bur hole, however, the exact localization of the electrode contacts on the patient's brain remains uncertain for the surgeon during insertion. Therefore, the authors developed a simple method to visualize the electrodes during the procedure. In this method they combine neuronavigation and intraoperative fluoroscopy for parallel visualization of the cortex, electrodes, and the navigation probe. The target region is searched with neuronavigation, a bur hole is made over the optimal entry point, and using real-time fluoroscopy the strip electrode is slid to the tip of the navigation probe, which was kept over the area of interest. At the authors' institution 26 strips in 8 patients have been inserted with this technique, and none of the strips had to be repositioned. There were no complications with this procedure and the prolongation of surgery time is acceptable. Compared to previously published electrode placement methods, this one enhances the accuracy of electrode placement at occipital, parietal, frontal, or interhemispheric regions as well. Intraoperative visualization of the electrodes with fluoroscopy combined with neuronavigation during positioning through a bur hole gives the neurosurgeon the ability to control the real position of the electrode over the gyri during the procedure.
Journal of Neurosurgery 12/2008; 110(2):327-31. · 2.96 Impact Factor
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Gábor Széplaki,
Róbert Szegedi,
Kristóf Hirschberg,
Tímea Gombos,
Lilian Varga,
István Karádi, László Entz,
Zoltán Széplaki,
Peter Garred,
Zoltán Prohászka,
George Füst
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ABSTRACT: According to data from animal models, complement activation plays a major role in the brain injury after acute ischemic stroke. Scarce findings are, however, available on the detection of complement activation products in stroke patients.
We have measured plasma levels of the five complement activation products (C1rC1sC1inh, C4d, C3a, C5a and SC5b-9) in samples of 26 patients with ischemic stroke upon admission. Twenty-six patients with severe carotid atherosclerosis served as patient controls.
Levels of two activation products (SC5b-9 and C4d)) were significantly elevated in the plasma of stroke patients, SC5b-9 levels, exhibited significant positive correlation with the clinical severity of stroke, the severity of neurological deficit, as well as with the level of functional disability.
These findings suggest that complement activation plays an active role in the development of brain infarct. The measurement of complement activation products might help to determine the clinical prognosis after acute ischemic stroke. Furthermore, there is potential usefulness of complement modulating therapy in ischemic stroke.
Atherosclerosis 09/2008; 204(1):315-20. · 3.79 Impact Factor
