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F Velasco

Publications and source records attributed to F Velasco.

At least 19 recordsLinked to original sources
PubMed2007

Influence of motor symptoms upon the quality of life of patients with Parkinson's disease.

We studied the impact of various motor and nonmotor symptoms upon quality of life in patients with Parkinson's disease (PD). The study comprised 110 patients with PD (age: 68.6 years, course of the disease: 7.6 years). The Unified Parkinson Disease Rating Scale (UPDRS; I-IV) and Parkinson's Disease Questionnaire (PDQ-39) were recorded. We recorded the correlations between years of disease and UPDRS IV, as well as PDQ-39 and UPDRS I, II, III and IV. Introduction of all variables into a linear regression model showed that 3 variables accounted for 51% of the variance in PDQ-39. Mental condition, gait disorders and complications of dopaminergic drugs are the variables that most affect the quality of life of patients with PD.

Aged↗
PubMed2006

Monozygotic twins suffering from Huntington's disease show different cognitive and behavioural symptoms.

Monozygotic male twins, carrying the same number of trinucleotide repeats in the IT 15 Huntington disease (HD) gene, showed a different clinical course. Patient 1 presented with anxiety and chorea at the age of 40. Patient 2 showed persecution paranoia and motor impersistence at the age of 42. Both patients were monitored for 30 months using currently recommended motor and behaviour scales. No differences were observed in motor scoring besides small interevaluation fluctuations. However, on the cognitive and behaviour scales, patient 1 showed a significant worsening when compared with patient 2. Our cases support the belief that the motor symptoms and signs in HD are highly dependent on the trinucleotide expansion. However, the differences in the evolution of mental status in our patients suggest that other still unknown environmental factors are important in the phenotypic expression of Huntington's disease.

Adult↗
PubMed2006

Vascular endothelial growth factor expression in monocytes from patients with primary antiphospholipid syndrome.

BACKGROUND: One of the described mechanisms leading to thrombosis in antiphospholipid syndrome (APS) is overexpression of tissue factor (TF) in the monocytes and endothelial cells of patients with antiphospholipid antibodies (aPL). Vascular endothelial growth factor (VEGF) may stimulate monocyte TF expression through its receptor, the tyrosine kinase Flt-1. OBJECTIVES: This study aimed to analyze the following in monocytes of 55 primary APS patients: VEGF and Flt-1 expression levels, their potential regulation by aPL, and the association of VEGF and Flt-1 expression with the increased TF expression found in APS patients. RESULTS: Purified monocytes from APS patients showed higher levels of VEGF and Flt-1 than healthy donors, which further correlated with immunoglobulin G (IgG) anticardiolipin titers and TF expression rank. Moreover, monocyte VEGF and Flt-1 levels were significantly higher in patients with than in patients without previous thrombosis. In vitro, IgG from APS patients increased monocyte VEGF and Flt-1 expression in a dose-dependent manner. VEGF and Flt-1 expression was significantly inhibited by the p38 mitogen-activated protein kinase (MAPK) inhibitor SB203580; this suggests the involvement of this kinase in the aPL-induced VEGF and Flt-1 upregulation. CONCLUSIONS: Our data show, for the first time in vivo, that monocytes from primary APS patients have an increased expression of VEGF and Flt-1. Furthermore, in vitro results indicated that this cytokine is produced by monocytes when treated with aPL, and that the p38 MAPK signaling pathway plays an important role. Thus, VEGF might act as a regulatory factor in aPL-mediated monocyte activation and TF expression, thereby contributing to the proinflammatory-prothrombotic phenotype of APS patients.

Adolescent↗
PubMed2006

Tissue factor as an effector of angiogenesis and tumor progression in hematological malignancies.

In the last few years, it has become clear that the processes of tumor angiogenesis, metastasis and invasiveness are highly dependent on components of the blood coagulation cascade. One of the key proteins in coagulation is tissue factor (TF). In addition, TF is also known as a mediator of intracellular signaling events that can alter gene expression patterns and cell behavior. TF significantly participates in tumor-associated angiogenesis and its expression levels have been correlated with the metastatic potential of many types of hematological malignancies. Signaling pathways initiated by both, tissue factor-activated factor VII (TF-FVIIa) protease activation of protein-activated receptors (PARs), and phosphorylation of the TF-cytoplasmic domain, appear to regulate these tumoral functions. Advances in antiangiogenic therapies and preclinical studies with TF-targeted therapeutics are hopeful in the control of tumor growth and metastasis, but continued studies on the regulation of TF are still needed. In the last few years, the use of approaches of functional genomics and proteomics has allowed the discovery of new proteins involved in the origin of the neoplasia and their participation in the development of the disease. This review attempts to establish a cellular and molecular causal link between cancer coagulopathy, angiogenesis and tumor progression in hematological malignancies.

Animals↗
PubMed2006

Antiphospholipid syndrome and tissue factor: a thrombotic couple.

The antiphospholipid syndrome (APS) is characterized by thrombosis and/or pregnancy morbidity in the presence of antiphospholipid antibodies (aPL). Among the thrombogenic mechanisms proposed, it has been suggested that aPL can stimulate tissue factor (TF) expression by endothelial cells (ECs) and monocytes. Moreover, our in vivo studies have shown that APS patients (particularly those with thrombosis) have increased monocyte TF expression. Yet, the molecular mechanism(s) by which aPL induce TF expression has not been completely underscored. In a recent study, we have demonstrated that aPL induces TF expression in monocytes from APS patients by activating, simultaneously and independently, the phosphorylation of MEK-1/ERK proteins, and the p38 MAP kinase-depenent nuclear translocation and activation of NFkappaB/Rel proteins. Understanding the intracellular mechanism(s) of aPL-mediated monocyte activation may help to establish new therapeutic approaches, such as selective inhibition of MAP kinases, to reverse the prothrombotic state in APS. Furthermore, the contribution of TF to a protrombotic state in the APS provides a renewed focus on antithrombotic therapies in current use, including the oral anticoagulation and, more recently, the use of statins, which have been proven to be effective in the inhibition of EC and monocyte TF-expression.

Antibodies, Antiphospholipid↗
PubMed2006

[Utility of the study of the vegetative nervous system in the differential diagnosis between Parkinson's disease and multiple system atrophy].

INTRODUCTION: The aim of this study is to show if the exploration of the autonomic nervous system is useful to improve the specificity of clinical criteria of Parkinson's Disease (PD) and Multiple System Atrophy (MSA). PATIENTS AND METHODS: 20 patients with PD and 13 patients with MSA were studied. After 12 hours in off medication, NE and GH were measured in supine position and NE after 5 minutes standing. Later, GH levels were recorded at 15, 30, 45 and 60 minutes after a dose of 0.005 mg/kg of apomorphine. Finally, analysis of the symptoms of autonomic dysfunction and levodopa test were carried out. RESULTS: Sympathetic response to postural changes was significantly higher in patients with PD (NE increase in relation to basal: PD: 170.90 +/- 110.08 pg/ml; MSA: 91.33 +/- 73.79 pg/ml; p = 0.029). No differences were found in the response of GH to apomorphine (GH peak at 45 minutes: PD: 2.37 +/- 2.7 ng/ml; MSA: 1.69 +/- 1.90 ng/ml; ns). The symptoms of autonomic dysfunction were more frequently in patients with MSA. The stridor was specific to MSA. Improvement in motor scores in the levodopa test was higher in patients with PD (PD: 39.7 %; MSA: 17.89; p = 0.019). DISCUSSION: Sympathetic response to postural changes, description of symptoms of autonomic dysfunction, and motor response to levodopa test are useful tools in order to improve specificity of the diagnostic criteria of PD and MSA. The GH test with apomorphine was not useful for a differential diagnosis.

Aged↗
PubMed2005

Monitoring the Prestige oil spill impacts on some key species of the Northern Iberian shelf.

Selected key components of the continental shelf benthic and demersal communities were monitored for the two years following the Prestige oil spill (POS) in order to identify the possible ecological effects of the oil. This work includes the first results regarding changes in abundance, distribution and food habits of hake (Merluccius merluccius), four-spot megrim (Lepidorhombus boscii), Norway lobster (Nephrops norvegicus) and Pandalid shrimp (Plesionika heterocarpus) populations of Galician and Cantabrian Sea shelves following the POS. Significant reductions in the abundance of Norway lobster, Plesionika heterocarpus and four-spot megrim were detected in the POS maximum impact area, located over the Galician shelf. Noteworthy recoveries were observed in the 2004 abundance indices of four-spot megrim and Plesionika. On the other hand, no significant effects were detected in the abundance or distribution of hake juveniles even though the tar aggregates were bound by the same oceanographic drift events as the hake recruits were during the winter of 2003 (Navidad current) in different water column layers of the Cantabrian Sea. Feeding patterns of the four species analysed did not present apparent modifications that can be related to the POS.

Animals↗
PubMed2005

Phenotypic variability in familial prion diseases due to the D178N mutation.

BACKGROUND: Between January 1993 and December 2003, 19 patients with familial prion diseases due to the D178N mutation were referred to the regional epidemiological registry for spongiform encephalopathies in the Basque Country in Spain, a small community of some 2,100,000 inhabitants. METHODS: Ten further patients belonging to the same pedigrees were retrospectively ascertained through neurological or neuropathological records. In four of the patients, the diagnosis was confirmed by analysing DNA obtained from paraffin blocks. In this article, we report on the clinical, genetic, and pathological features of the 23 patients carrying the D178N mutation confirmed by genetic molecular analysis. Haplotyping studies suggest a founder effect among Basque born families, explaining in part this unusually high incidence of the D178N mutation in a small community. Only two patients (8%) lack familial antecedents. RESULTS: We have observed a phenotypic variability even among homozygous 129MM patients. Our findings challenge the currently accepted belief that MM homozygosity in codon 129 is always related to a fatal familial insomnia (FFI) phenotype. Indeed, seven out of 17 patients with a 129MM genotype in this series presented with a Creutzfeldt-Jakob disease (CJD) clinicopathological picture. CONCLUSIONS: The considerable clinical and pathological overlapping observed among homozygous 129MM patients favours the view that FFI and CJD178 are the extremes of a spectrum rather than two discrete and separate entities. Other genetic or environmental factors apart from the polymorphism in codon 129 may play a role in determining the phenotypic expression of the D178N mutation in the PRNP gene.

Adult↗
PubMed2004

[Asterixis in focal brain lesions].

Asterixis is a motor control disorder characterized by the presence of abnormal movements of the lower limbs in the vertical plane during posture maintenance. Asterixis is usually bilateral and associated with toxic-metabolic metabolic encephalopathies. Unilateral asterixis is less frequent and it normally indicates focal brain damage. We report the cases of four patients (two males/two females), aged 57 to 83 years, suffering from uni or bilateral asterixis associated with focal brain damage. All patients underwent CT brain scan and a neurophysiological study (parietal EMG and/or PES). In addition, any toxic-metabolic cause that could be produced by this clinical phenomenon was ruled out with the appropriate testing. Unilateral asterixis is a clinical symptom that may indicate the presence of focal brain damage. Often, it is ignored or overlooked during routine neurological examinations. On the other hand, the presence of a bilateral asterixis is not always indicative of a toxic-metabolic encephalopathy.Rarely, such as in one of the cases herein presented, bilateral asterixis can also appear associated with structural brain lesions. Although asterixis diagnosis is fundamentally clinical, the neurophysiological study contributes to verify the diagnosis.

Aged↗
PubMed2004

[Baroreflex failure after chemodectoma resection].

Baroreflex failure after chemodectoma resection We present a case of baroreflex failure secondary to a unilateral injury of the glossopharyngeal nerve. The patient was operated for a left-sided chemodectoma in the carotid body. Some months after surgery she started to report presyncopal episodes exacerbated by mental stress and when standing up. During these episodes, the patient presented hypertensive crises and tachycardia. However, blood pressure was below normal ranges at rest. The diagnosis was baroreflex failure secondary to unilateral injury of the glossopharyngeal nerve. The case reported herein illustrates the fact that the presence of a bilateral injury is not essential for the occurrence of this disorder.

Aged↗
PubMed2001

Antithrombin III prevents early pulmonary dysfunction after lung transplantation in the dog.

BACKGROUND: Ischemia-reperfusion injury with the resulting inflammatory response is a devastating complication of lung transplantation; much of the tissue damage could be diminished by control of the inflammatory response. Recent studies have show that antithrombin III (AT III) has an anti-inflammatory effect in addition to its established role in the regulation of blood coagulation. Thus, we hypothesized that the administration of AT III might help to prevent ischemia-reperfusion injury after lung transplantation. METHODS AND RESULTS: The study was performed in a dog model of orthotopic lung transplantation. Dogs were randomly assigned to receive either vehicle (controls) or AT III. We observed that in control dogs, during the 180-minute period after lung transplantation, the arterial O(2) partial pressure decreased and both the alveolar-arterial O(2) difference and the pulmonary vascular resistance increased. By contrast, these parameters remained unchanged in the group of dogs receiving AT III. Dogs with transplants receiving AT III did not show an increase in cell adhesion molecules, and histological examination revealed almost an absence of inflammatory response. The administration of AT III produced a marked increase in serum prostacyclin (PGI(2)) levels, whereas in control dogs, the PGI(2) levels did not change. The beneficial effect of AT III was not observed when dogs received indomethacin to prevent the stimulation of PGI(2) release by AT III. CONCLUSIONS: Our results demonstrate that AT III prevents ischemia-reperfusion injury in a dog model of lung transplantation and that this effect is conditioned by an increase in PGI(2) production.

6-Ketoprostaglandin F1 alpha↗
PubMed2001

Dementia, amyotrophy, and periodic complexes on the electroencephalogram: a diagnostic challenge.

BACKGROUND: The clinical diagnosis of neurodegenerative diseases is a challenge to the neurologist. In many cases the diagnosis becomes neuropathological only after the autopsy. Several consensus criteria have been defined for the clinical diagnosis of different neurodegenerative diseases, among them the various types of dementia as well as prion-induced diseases. When compared with neuropathological findings, these criteria have proved to be reasonably accurate for regular practice, research, and epidemiological studies. The problem arises when a combination of complementary and clinical data are obtained that do not easily match these diagnostic criteria. CASE DESCRIPTION: We describe a patient with dementia and periodic complexes on an electroencephalogram, suggesting a diagnosis of sporadic Creutzfeldt-Jakob disease. RESULTS: When the condition progressed, signs and symptoms of a motoneuron disease appeared. Thus, 2 different diagnoses were proposed: (1) an amyotrophic variant of a prion-induced disease; or (2) an ELA dementia syndrome with periodic complexes on the electroencephalogram, a finding that previously has not been described.

Autopsy↗
PubMed2001

Centromedian-thalamic and hippocampal electrical stimulation for the control of intractable epileptic seizures.

The following two different modulatory procedures to control intractable epileptic seizures are presented: (1) chronic electrical stimulation of the centromedian-thalamic nucleus (ESCM) for control of generalized tonic-clonic seizures and atypical absences, and (2) subacute hippocampal stimulation (SAHCS) and chronic hippocampal stimulation for control of nonlesional temporal lobe seizures. The ESCM antiepileptic effect seems to be the result of activation of a nonspecific reticulothalamocortical system responsible for generalized electrocortical responses (recruiting, desynchronization, negative direct current shifts, and three spike-wave complexes per second). The success of the ESCM procedure depends on the following predictor factors: case selection (primary and secondary tonic-clonic seizures and atypical absences of the Lennox Gastaut syndrome), ventriculographic and electrophysiologic definition of the optimal stereotactic targets (based on the anterior commissure, posterior commissure, and the vertical line perpendicular to the posterior commissure and electrocortical recruiting responses), periodic electrophysiologic monitoring of the reliability of ESCM in the absence of the patient's subjective sensations and with totally internalized subcutaneous stimulation systems (by recording scalp electrocortical recruiting, desynchronizing, and direct current responses), quantitative evaluation of clinical and EEG improvement, and analysis of the ON and OFF effects, taking into account a long-lasting (possibly plastic) effect of ESCM. SAHCS blocks clinical and EEG signs of temporal lobe epileptogenesis with no additional damage of the stimulated hippocampal tissue. Preliminary results suggest that this antiepileptic effect is, at least in part, the result of a physiologic inhibition of the stimulated hippocampal tissue, because after SAHCS the authors found the following: (1) increased threshold and decreased duration, propagation, and blockage of the clinical signs accompanied with the hippocampal afterdischarge; (2) flattening of the hippocampal-evoked response recovery cycles; (3) single photon emission computed tomographic hypoperfusion; and (4) increased concentration of benzodiazepine receptor binding at the stimulated hippocampal region. Chronic hippocampal stimulation persistently blocked temporal lobe epileptogenesis in one patient under open protocols during 24 months with no apparent additional alterations in recent memory.

Brain Mapping↗
PubMed2001

Electrical stimulation of the prelemniscal radiation in the treatment of Parkinson's disease: an old target revised with new techniques.

OBJECTIVE: In the treatment of tremor and rigidity in patients with Parkinson's disease (PD), the prelemniscal radiation (RAPRL), a subthalamic bundle of fibers, is an exquisite target that can be visualized easily on ventriculograms. We sought to evaluate the effect of electrical stimulation of the RAPRL on symptoms and signs of PD in a long-term trial and to determine the localization of the stimulated area by means of stereotactic magnetic resonance imaging studies. METHODS: Ten patients with PD predominantly on one side had tetrapolar electrodes stereotactically oriented through a frontal parasagittal approach to the RAPRL contralateral to the most prominent symptoms. Preoperative and postoperative evaluations at 3, 6, 9, and 12 months after surgery were performed using conventional PD scales and quantitative evaluations of tremor amplitude and reaction time. Stereotactic high-resolution magnetic resonance imaging studies with the electrodes in place were used for anatomic localization. RESULTS: In all patients, temporary suppression of tremor occurred when the electrodes reached the target. The most effective stimulation was obtained when the pair of contacts was placed in the RAPRL. Long-term stimulation at 130 Hz, 0.09 to 0.450 milliseconds, and 1.5 to 3.0 V produced significant improvement in tremor and rigidity and mild improvement in bradykinesia. CONCLUSION: The RAPRL is an effective target for the alleviation of tremor and rigidity in patients with PD by either lesioning or neuromodulation; however, neuromodulation has the advantage of not inducing an increase in bradykinesia. The stimulated area seems to be independent of the subthalamic nucleus.

Aged↗
PubMed2001

Electrical stimulation for epilepsy: stimulation of hippocampal foci.

Subacute and chronic continuous electrical stimulation at the epileptic focus in the hippocampus or parahippocampal cortex at 130 Hz, 0.21-1.0 ms, 2.5-3.5 V (about 200-300 microA) induces a decrease in focal EEG epileptic interictal activity and also in the occurrence of clinical seizures. This may represent an alternative for the treatment of temporal lobe seizures originated in bilateral independent temporal lobe foci or occurring in patients where one is uncertain whether memory deficit might result from ablative procedures.

Electric Stimulation Therapy↗
PubMed2001

Stimulation of the central median thalamic nucleus for epilepsy.

Electrical stimulation of the centromedian thalamic nucleus (ESCM) has been used in cases of difficult to control seizures with multifocal onset in frontal and temporal lobes, as well as in cases of seizures with no evidence of focal onset, such as Lennox-Gastaut syndrome. The stimulation program consists of 1 min stimulation on one side, 4 min interval OFF stimulation and 1 min stimulation on the other side, alternating from one side to the other for 24 h, at 60-130 Hz, 2.5-5.0 V, 0.21-0.45 ms. 49 cases have been treated and followed for periods of 6 months to 15 years. Results indicate that ESCM is highly efficient to control generalized tonic clonic seizures (GTC), atypical absences (AA) and tonic seizures (TS) and less efficient to control complex partial seizures (CxP).

Child↗