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Biomedical subjects

J Peres

Publications and source records attributed to J Peres.

15 recordsLinked to original sources
PubMed1996

Niflumic acid-induced increase in potassium currents in frog motor nerve terminals: effects on transmitter release.

The actions of the nonsteroidal antiinflammatory drug niflumic acid were studied on frog neuromuscular preparations by conventional electrophysiological techniques. Niflumic acid reduced the amplitude and increased the latency of endplate potentials in a concentration-dependent manner. Neuromuscular junctions pretreated with niflumic acid (0.05-0.5 mM) showed much less depression than control when they were stimulated with trains of impulses. Inhibition of acetylcholine release was reverted by raising the extracellular Ca(2+) concentration but not by simply washing out the preparations with niflumic acid-free solutions. Pretreatment with indomethacin (0.1 mM), another nonsteroidal antiinflammatory drug, did not affect the niflumic acid-induced inhibition of evoked responses. Niflumic acid (0.1 mM) did not change the amplitude of miniature endplate potentials and had a dual action on the frequency of miniatures: it decreased their frequency at 0.1 mM whereas it produced an enormous increase in the rate of spontaneous discharge at 0.5 mM. Niflumic acid (0.1 - 1 mM) reversibly increased the amplitude and affected the kinetics of presynaptic voltage-activated K+ current and Ca(2+)-activated K(+) current in a concentration-dependent manner. Niflumic acid (0.1 - 1 mM) irreversibly decreased the amplitude and reversibly affected the kinetics of the nodal Na(+) current. Indomethacin (0.1 mM) had no effect on presynaptic currents. In conclusion, niflumic acid reduces acetylcholine release by increasing presynaptic K+ currents. This may shorten the depolarizing phase of the presynaptic action potential and may reduce the entry of Ca(2+) with each impulse.

Animals↗
PubMed1995

CSF somatostatin increase in patients with early parkinsonian syndrome.

Somatostatin-like immunoreactivity levels (SLI) in cerebrospinal fluid (CSF) were determined in twenty-three patients with untreated parkinsonian syndrome (15 with Idiopathic Parkinson's disease (IPD) and 8 with other forms of parkinsonism) at the moment of clinical diagnosis (mean duration of disease 1.1 +/- 0.2 years), and in 26 subjects without neurological symptoms. None of the IPD patients had a diagnosis of dementia at the moment of inclusion in the study. CSF-SLI content was found to be significantly higher in patients with parkinsonian syndrome (107.9 +/- 9.8 pg/ml) than in control subjects (73.5 +/- 8.4 pg/ml). The increase was also significant when controls were compared with IPD patients. In addition, a positive correlation between SLI and homovanillic acid was found in CSF of all patients. A test of learning memory was used to evaluate the mental state of patients and a significant increase in CSF-somatostatin levels was observed in patients with Idiopathic Parkinson's disease and severe affectation of memory. These results indicate that in the early steps of untreated parkinsonian syndrome, somatostatin concentration in cerebrospinal fluid may increase, probably due to the neurodegenerative depletion of somatostatin from striatal or cortical neurons.

Aged↗
PubMed1995

T cell subsets in multiple sclerosis: a serial study.

The relevance of abnormalities in the distribution of peripheral blood T lymphocyte subsets to the clinical manifestations of multiple sclerosis is not firmly established. A clinical and immunological follow-up of relapsing-remitting multiple sclerosis patients was performed in order to study the relationship of immune changes with the clinical course of the disease. Twenty patients were monitored monthly during a mean time of nine months for peripheral blood lymphocyte subsets (CD3, CD4, CD8, CD19), including the immunoregulatory subsets CD4CD29 (helper-inducer), and CD4CD25) by flow cytometry. A total of 14 untreated relapses was included. The most significant observations were a decrease in T suppressor-inducer CD4+ CD45RA+ subset during clinical relapses (P = 0.028) that was also detectable one month before (P = 0.020) and the lack of changes in CD4+ CD29+ and CD8+ T cells. In addition, variations in the percentage of CD4+ CD25+ activated T helper cells were not associated with clinical exacerbations. These results indicate the existence of a temporal association of immune changes in peripheral blood, but not activation, with the clinical manifestations of multiple sclerosis.

Adolescent↗
PubMed1994

Zinc ions block rectifier potassium channels and calcium activated potassium channels at the frog motor nerve endings.

The effect of Zn2+ on presynaptic currents was investigated on frog cutaneous pectoris nerve-muscle preparations. Nerve terminal spikes were recorded with extracellular electrodes placed in the perineurial sheaths of motor nerves. Zinc ions reversibly suppressed the component of the waveform associated with K+ currents--unmasking an inward current at the terminal--and induced repetitive firing when were applied to preparations perfused with calcium containing solutions. In experiments in which delayed rectifier channels were blocked by 3,4-diaminopyridine, Zn2+ caused a prolonged and reversible inward current associated with a slight decrease in the peak calcium current generated by 3,4-diaminopyridine. Zinc ions abolished the plateau calcium current produced by the simultaneous action of 3,4-diaminopyridine and tetraethylammonium. Finally, in all the preparations in which the exposure to Zn2+ was prolonged it was observed a dramatic and irreversible reduction of the presynaptic currents. These results suggest that Zn2+ has, at least, four different effects on presynaptic currents: (1) blockade of delayed rectifier potassium currents, (2) blockade of calcium-activated potassium currents, (3) blockade of calcium currents and (4) a delayed and irreversible disruption of all ionic conductances of the terminal.

4-Aminopyridine↗
PubMed1993

[Progressive infiltration of cranial nerves as first manifestation of primary meningeal lymphoma].

Primary meningeal lymphomas are an infrequent disease representing 1% of the primary cerebral lymphomas. Progressive paraparesia constitutes the most frequent presentation with progressive infiltration of the cranial nerves being an usual initial manifestation. The case of a primary meningeal lymphoma is presented in a 76 years old patient in whom the form of presentation involved progressive infiltration of cranial nerves. Repeated lumbar punctions demonstrated infiltration of cranial nerves. Repeated lumbar punctions demonstrated inflammatory changes with high protein levels and low sugar levels in cerebrospinal fluid and pleocytosis. No malignant cells were observed upon cytologic study of the LCR. The importance of the determination of tumor markers in LCR and the use of MR with gadolinium in the early diagnosis of this entity is commented upon.

Aged↗
PubMed1992

[Polymicrogyria and ulegyria. Diagnosis by magnetic resonance].

Three patients who had had epilepsy since the second decade of life were studied with cranial magnetic resonance (MR). Two patients had no antecedents of interest during pregnancy and the perinatal period and neurological examination was normal. The third patient had had dystocia and presented left hemiparesia since then, with normal intellectual development. None of the cases had any family history of neurological disease. Cranial magnetic resonance was performed in the three patients demonstrating polymicrogyria in two and ulegyria in the other, in addition to other lesions. The first patient presented an unilateral area of polymicrogyria related with a porencephalic cyst in the distal territory of the right sylvian artery and ipsilateral heterotopia of periventricular location. The second patient presented bilateral periventricular heterotopia, partial agenesis of the corpus callosum and an enlarged cisterna magna in addition to bilateral frontal-occipital polymicrogyria. Finally, ulegyria was observed in the third patient in the edges and neighboring regions of a right rolandic porencephalic cyst, as well as an enlarged cisterna magna.

Adult↗
PubMed1992

[Primary intraventricular hemorrhage in a patient with unilateral moyamoya disease].

According to the diagnostic criteria currently in use, the so-called "unilateral" forms of the moyamoya disease, or rather those in which the disorders of the disease itself--such as occlusion of the internal supraclinoid carotid artery or its terminal branches and development of abnormal collateral circulation in the region of the basal ganglia--are only found in one hemisphere and should be considered as "probable" forms of the disease with a much lower incidence than the bilateral or "defined" forms of the same. One patient with a primary intraventricular hemorrhage (PIVH) in whom an occlusion of the right internal carotid artery was angiographically demonstrated and in whom collateral type moyamoya circulation was found as was the presence of an aneurysm in the right coroid territory is presented. The association of PIVH, unilateral moyamoya disease and aneurysm is infrequent in the literature, with the origin of the bleeding, in some cases, having been attributed to rupture of the aneurysm. Since angiographic control was not available in the patient presented it cannot be excluded that the aneurysm was really a pseudoaneurysm therefore being a consequence, rather than a cause, of the arterial rupture. Thus one of the other mechanisms proposed must be invoked to explain the pathogenesis of the PIVH: rupture of a perforating artery or of a microaneurysm located in the subependimary periventricular region. The treatment recommended for these case of PIVH associated to aneurysm is chirurgical if persistence is demonstrated in successive arteriographies.

Adult↗
PubMed1991

[Magnetic resonance imaging and Cogan's syndrome].

We report the case of a 25-year old man with vestibulocochlear and ocular impairment compatible with Cogan's syndrome. Later on, severe headache developed. CT scan showed an ischaemic lesion in the right frontal lobe. Magnetic resonance imaging demonstrated multiple bilateral nodular lesions on T2-weighted sequences. These were unmodified at a second MRI examination performed six months later. Under corticosteroids, the neurological and ophthalmic symptoms disappeared, but the patient remained deaf. We believe that this patient had vasculitis involving the brain, with infarcts. To our knowledge, no case of Cogan's syndrome with cerebral magnetic resonance imaging has yet been reported.

Adult↗
PubMed1990

Giant basilar aneurysm in the course of subacute bacterial endocarditis.

We describe a man aged 42 years with mitral valve regurgitation who suffered from subacute bacterial endocarditis caused by Streptococcus morbillorum. The clinical picture began with a toxic syndrome. Five months later, the patient had an embolic episode and a right rostral pontine stroke, which was followed a few days later by an adversive focal seizure on the right. Despite antibiotic treatment, he suffered complete third nerve palsy. Arteriography, magnetic resonance imaging, and computed tomography of the brain showed a giant aneurysm in the rostral end of the basilar artery; the aneurysm was clipped. We discuss the clinical features, radiology, and characteristics of this aneurysm as a unique case of a giant bacterial aneurysm in the vertebrobasilar system.

Basilar Artery↗
PubMed1983

[Paroxysmal hemicrania. Post-stenotic dilatation of the subclavian artery].

A 50 year-old women presented with a history of increasingly frequent bouts of cervicofacial pain over the last 18 months, and a pulsatile tumor in the supraclavicular region. Angiography showed a stenosis of the left subclavian artery with post-stenotic dilatation related to a cervical rib. No further pain was experienced after removal of the rib. The probable rate of the autonomic nervous system in the physiopathology of this painful syndrome is discussed.

Angiography↗
PubMedDate not supplied

Cerebral infarction of the basal ganglia due to embolism from the heart.

We studied 8 patients with cerebral infarction in the deep territory of the middle cerebral artery (MCA). All patients had a definite cardiac source of emboli and no known factors for thrombosis. Mixed sensory and motor deficit was found in all but one patient and CT scan showed larger lesions than usually reported in lacunar infarcts. Contrast enhancement was seen in all cases in which CT scan was performed in the second or third week. It is concluded that embolic infarcts in deep cerebral territory of MCA from a cardiac source are more frequent than previously reported. This diagnosis has to be considered when CT scan demonstrates a deep cerebral infarct.

Adult↗