Biomedical subjects

V Palma

Publications and source records attributed to V Palma.

At least 19 recordsLinked to original sources

PubMed2001

Calcium mediates dorsoventral patterning of mesoderm in Xenopus.

Calcium signals participate in the differentiation of electrically excitable and nonexcitable cells; one example of this differentiation is the acquisition of mature neuronal phenotypes. For example, transient elevations of the intracellular calcium concentration have been recorded in the ectoderm of early embryos, and this elevation has been proposed to participate in neural induction. Here, we present molecular evidence indicating that voltage-sensitive calcium channels (VSCC) are involved in early developmental processes leading to the establishment of the dorsoventral (D-V) patterning of a vertebrate embryo. We report that alpha1S VSCC are expressed selectively in the dorsal marginal zone at the early gastrula stage. The expression of the VSCC correlates with elevated intracellular calcium levels, as evaluated by the fluorescence of the intracellular calcium indicator Fluo-3. Misexpression of VSCC leads to a strong dorsalization of the ventral marginal zone and induction of the secondary axis but no direct neuralization of the ectoderm. Moreover, specific inhibition of VSCC by the use of calcicludine results in ventralization of the dorsal mesoderm. Together, these results indicate that calcium channels regulate mesodermal patterning by specificating the D-V identity of the mesodermal cells. The D-V patterning of the mesoderm has been shown to depend on a gradient of BMPs activity. We discuss the possibility that VSCC affect or act downstream of BMPs activity.

Animals↗

PubMed2001

Fluoro derivatives of bis(salicylideneaminato-N,O)copper(II) and -oxovanadium(IV).

The structures of five complexes of fluorine-containing bidentate salicylideneamine Schiff base ligands are reported. These are the bis-ligand copper(II) complexes of the Schiff bases derived from salicylaldehyde and 4-fluoro-, [Cu(C(13)H(9)FNO)(2)], 3-fluoro-4-methyl-, [Cu(C(14)H(11)FNO)(2)], 3,5-bis(trifluoromethyl)-, [Cu(C(15)H(8)F(6)NO)(2)], and 4-trifluoromethoxyanilines, [Cu(C(14)H(9)F(3)NO(2))(2)], and the bis-ligand oxovanadium(IV) complex of the Schiff base derived from salicylaldehyde and 4-trifluoromethoxyaniline, [VO(C(14)H(9)F(3)NO(2))(2)]. Three of the copper complexes have square-planar coordination at the metal, imposed by the virtue of symmetry, but the immediate coordination environment of the copper in the 3,5-bis(trifluoromethyl) complex is intermediate between square planar and tetrahedral. The coordination environment at the metal of the vanadium complex can be described as distorted square pyramidal.

Journal Article↗

PubMed2001

The Sonic Hedgehog-Gli pathway regulates dorsal brain growth and tumorigenesis.

The mechanisms that regulate the growth of the brain remain unclear. We show that Sonic hedgehog (Shh) is expressed in a layer-specific manner in the perinatal mouse neocortex and tectum, whereas the Gli genes, which are targets and mediators of SHH signaling, are expressed in proliferative zones. In vitro and in vivo assays show that SHH is a mitogen for neocortical and tectal precursors and that it modulates cell proliferation in the dorsal brain. Together with its role in the cerebellum, our findings indicate that SHH signaling unexpectedly controls the development of the three major dorsal brain structures. We also show that a variety of primary human brain tumors and tumor lines consistently express the GLI genes and that cyclopamine, a SHH signaling inhibitor, inhibits the proliferation of tumor cells. Using the in vivo tadpole assay system, we further show that misexpression of GLI1 induces CNS hyperproliferation that depends on the activation of endogenous Gli1 function. SHH-GLI signaling thus modulates normal dorsal brain growth by controlling precursor proliferation, an evolutionarily important and plastic process that is deregulated in brain tumors.

Animals↗

PubMed1999

Hyperkalemic periodic paralysis M1592V mutation modifies activation in human skeletal muscle Na+ channel.

Mutations in the human skeletal muscle Na+ channel underlie the autosomal dominant disease hyperkalemic periodic paralysis (HPP). Muscle fibers from affected individuals exhibit sustained Na+ currents thought to depolarize the sarcolemma and thus inactivate normal Na+ channels. We expressed human wild-type or M1592V mutant alpha-subunits with the beta1-subunit in Xenopus laevis oocytes and recorded Na+ currents using two-electrode and cut-open oocyte voltage-clamp techniques. The most prominent functional difference between M1592V mutant and wild-type channels is a 5- to 10-mV shift in the hyperpolarized direction of the steady-state activation curve. The shift in the activation curve for the mutant results in a larger overlap with the inactivation curve than that observed for wild-type channels. Accordingly, the current through M1592V channels displays a larger noninactivating component than does that through wild-type channels at membrane potentials near -40 mV. The functional properties of the M1592V mutant resemble those of the previously characterized HPP T704M mutant. Both clinically similar phenotypes arise from mutations located at a distance from the putative voltage sensor of the channel.

Animals↗

PubMed1998

Brainstem involvement in obsessive-compulsive disorder.

We investigated the possible involvement of the brainstem in the pathology of obsessive-compulsive disorder. Brainstem auditory evoked potentials (BAEPs) were collected from a population of neurotics (100 patients), including a group of 50 subjects suffering from obsessive-compulsive disorder (OCD) and the rest having generalized anxiety disorder. Twenty-five, age- and sex-matched, healthy volunteers served as controls. BAEPs were recorded by standard techniques as recommended by the AEEGS Clinical Evoked Potentials Guidelines. A one-way analysis of variance and the Fisher least-significant difference test were used for statistical analysis of the data. After stimulation of the right ear, a significant increase of wave I-V interpeak latency was found in the two groups of patients as compared with that of controls. Moreover OCD patients had a significantly reduced amplitude of wave III when compared to that of the control group. Our electrophysiological data suggest a possible involvement of brainstem in OCD pathogenesis. We discuss our findings in relation to biochemical, anatomical and physiological alterations described in the literature for serotonin-dependent systems.

Adult↗

PubMed1996

Sperm interaction with human oviductal cells in vitro.

In this article we describe the in-vitro interaction between human spermatozoa and oviductal epithelial cell monolayers. Freshly obtained spermatozoa were added to culture dishes containing human oviductal cells (co-culture), culture medium (control) or culture medium which had previously been used for culture of oviductal cells (conditioned medium). At 0, 5, 24, and 48 h of incubation the percentage of motile spermatozoa was determined and their motion characteristics analysed. Aliquots were taken to determine the percentage of acrosome-reacted spermatozoa. The spermatozoa were motile for a longer period in the presence of oviductal cells (54 +/- 9% co-culture versus 18 +/- 3% control, at 48 h) and the kinetics of the acrosome reaction exhibited a different pattern. In the control the percentage of reacted spermatozoa increased progressively throughout incubation. In co-culture, there was an increase only at 5 h; thereafter, the percentage of acrosome reactions did not change. Spermatozoa incubated in conditioned medium exhibited a behaviour halfway between the control and the co-culture. The pattern of sperm movement was not different in any of the experimental conditions. Although there was no binding between spermatozoa and oviductal epithelial cells, the frequency of the ciliary beat increased after spermatozoa were added to the oviductal cell monolayers. These results suggest that incubation with oviductal cells increases sperm survival, stabilizes the acrosome, and modifies the frequency of ciliary beat.

Acrosome↗

PubMed1994

Somatosensory evoked potentials in non-insulin-dependent diabetics with different degrees of neuropathy.

Changes in median nerve somatosensory evoked potential (SEP) in diabetic patients have amply been reported. However the relationships between the diabetic polyneuropathy and the abnormalities of SEPs are still a matter of discussion. To elucidate these relationships, we have studied SEPs in 38 non-insulin-dependent diabetics with mild or severe degree of peripheral neuropathy. Our principal findings are as follows. (i) The wrist-Erb point (EP) conduction velocity (WECV) and the EP-N13 interpeak latency are significantly altered in diabetics. The N11-N13, N13-N20 and N13-P22, interpeak latencies are within the normal range. (ii) The WECV is more reduced in patients with severe neuropathy than in those with mild neuropathy, whereas the degrees of neuropathy have no influence on the alterations of EP-N13 interpeak latency. (iii) No significant correlation is found between the WECV and the EP-N13 interpeak latency. (iv) The WE conduction velocity was significantly correlated with both motor and sensory peripheral nerve conduction velocities. On the contrary, no correlation is found between these latter peripheral parameters and the EP-N13 interpeak latency. These findings indicate that the alteration in the tract from brachial plexus to the posterior column could not be a parallel process of distal neuropathy of non-insulin-dependent diabetic patients.

Adult↗

PubMed1994

An electrophysiological study in obsessional compulsive disorders.

Recent anatomoclinical and neuroimaging studies have suggested a possible relation between obsessional compulsive disorders (OCD) and some brain damage, such as frontolenticular lesions, basal ganglia cavitations and local glucose metabolism impairment. A poor frontocaudal regulation of the left hemisphere and an autonomic nervous system dysfunction in OCD patients have been supposed. To absess these morphofunctional abnormalities, an electrophysiological approach has been performed in 100 consecutive neurotic patients, screened with various neuropsychological tests and divided in two groups, 50 with OCD and 50 with anxious neurosis (ANX). Patients were submitted to EEG spectral analysis and BAEP studies and comparated with 25 age-matched normal controls. The mean alpha power in occipital regions was significantly higher in OCD patients and reduced in ANX patients. A significant reduction of the beta activity was recorded in frontal regions in both patient groups as compared to controls. A slight (p < 0.11) increase in I-V interpeak latency (IPL) vs. control group was observed in BAEP from left ear. A significant increase of the same IPL in OCD vs. controls (p < 0.025) was observed in BAEP from right ear. A slight n.s. reduction in III wave amplitude in OCD patients was observed in BAEP from left ear, whereas a highly significant reduction in the same wave amplitude from BAEP from right ear was observed in OCD patients. The above findings cold be account for both a frontotemporal and brainstem dysfunction with a probable involvement of serotoninergic central pathways, with a significant impairment of pontine segment in ANX patients and of mesencephalic region in OCD patients.

Basal Ganglia↗

PubMed1994

S.P.E.C.T., E.E.G. and M.R.I. investigations in complex partial epilepsy.

We present SPECT, electroencephalography (EEG) and magnetic resonance imaging (MRI) data of a homogeneous group of 12 young adults with rare focal seizures and a good response to carbamazepine. Our data suggest that the alterations of the rCBF are independent of severity and duration of the epilepsy and of the frequency of seizures. Based on our experimental data, it may be suggested that complex partial epilepsy is a good biological model to investigate the neurogenic control of cerebral flow and metabolism.

Adolescent↗

PubMed1993

Methods for the analysis of cellular kinetics in PHA-stimulated blood lymphocytes using BrdU incorporation. A comparative study.

The cellular cycle (cc) span was measured by using differential sister-chromatid staining (DSCS) and applying the following methods: cellular cycle time (cct) according to the graphic method of Dutrillaux and Fosse (G-cct); the analytical equation (A-cct) proposed in the present paper, and the average generation time (AGT) suggested by Ivett and Tice. The mean values obtained by the three methods were 12.5, 12.7, and 19.5 h, respectively. A-cct is the more precise method, since the equation of the analytical procedure allows the utilization of numerical data, and when the graphical method is used, the values plotted in a graph may vary according to the employed scale. Cct is the choice over AGT because the first evaluates actively dividing cells and only considers those at M2 or M3. It will be useful to study cell proliferation kinetics in genetic pathological conditions and to investigate with accuracy the effect of cytostatic and cytotoxic drugs.

Adolescent↗

PubMed1993

Hindbrain hernia headache and syncope in type I Arnold-Chiari malformation.

We describe two young women affected with syncopal episodes and occipital headache exacerbated by cough, sneezing, rising, or effort. MRI revealed in both patients type I Arnold-Chiari malformation. A craniospinal pressure dissociation with brainstem compression may be involved in the pathogenesis of headache and syncope.

Adult↗

PubMed1992

Dopaminergic regulation of epileptic activity.

We evaluated the role of dopamine systems in the propagation of epileptic Focal, limbic seizures were produced by systemically administered pilocarpine (200 mg/kg, i.p.); as previously described this dose produces limbic stereotypes but neither convulsions nor seizure-related brain damage. The systemic pretreatment with D-1, but not D-2, agonists induced convulsions identical to those produced by a higher, convulsant dose of pilocarpine (400 mg/kg). Conversely, the pretreatment with D-1 receptor antagonists prevented the convulsions whereas the D-2 antagonists facilitated the pilocarpine-induced seizures. Furthermore, we studied the effects of intracerebral injections of dopamine agents on seizures induced by pilocarpine. Nigral microinjection of D-1 agonists strongly induced motor seizures in rats treated with the low dose of pilocarpine. On the other hand, microinjection of D-1 antagonists prevented the motor seizures induced by the high dose of pilocarpine. This study indicates that the two dopamine receptor subtypes, D-1 and D-2, exert opposing roles in the control of epilepsy propagation. Substantia nigra pars reticulata appears to be primarily involved in the dopamine-mediated modulation of seizures.

Animals↗

PubMed1992

Sneddon's syndrome, anticardiolipin antibodies and anticardiolipin cofactor. A case report.

Sneddon's syndrome is a rare entity characterized by idiopathic livedo reticularis and cerebrovascular lesions. A case of a young woman with livedo reticularis and progressive cerebral arteriopathy is described. Abnormalities of sexual and gonadotropic hormones were present. Anticardiolipin and anticardiolipin-cofactor complex antibodies were not found.

Abortion, Spontaneous↗

PubMed1992

Spinal cord injury: some epidemiological data. A review of 233 cases.

Two hundred thirty-three consecutive cases of traumatic para- and tetraplegia admitted to a department of Neurosurgery in Naples within ten years were reviewed and categorized according to etiology, level of lesion and clinical features. The age of the patients at the time of injury varied from 7 to 74 years with a mean age of 37.1 +/- 17.1 (male mean age = 35.8 +/- 16.7; female mean age = 41.5 +/- 18.2). The male/female sex ratio was 4.8. Of these patients 66 were paraplegic and 167 were tetraplegic. The analysis of the various causes of the spinal cord injury showed that the occupational activities take the first place (32.2%); injuries in recreational activities and road accidents accounted for the majority of the remaining cases.

Adolescent↗

PubMed1991

Dopamine D1 and D2 receptors mediate opposite functions in seizures induced by lithium-pilocarpine.

The effect of selective dopamine receptor blockade on epileptic activity was tested in rats, using the lithium-pilocarpine seizure model. One day after lithium pretreatment, systemic administration of the dopamine D1 antagonist, SCH 23390, prevented the convulsive activity induced by either 10 or 15 mg/kg of pilocarpine in a dose-dependent manner as revealed by behavioral and electroencephalographic alterations. No anticonvulsant effect was observed when SCH 23390 was injected at the same time as lithium and 24 h prior to pilocarpine. Furthermore, the D2 antagonists, raclopride and haloperidol, potently reduced the threshold for convulsions induced by 10 mg/kg of pilocarpine, following lithium pretreatment. Neither dopamine D1 nor D2 antagonists altered the limbic stereotypies induced by pilocarpine, supporting the view that the dopamine system is primarily involved in the mechanisms of convulsion generation and seizure spreading. These results indicate that dopamine receptor subtypes exert opposite functions on the regulation of convulsive activity.

Animals↗

PubMed1991

Evoked potentials in shoe-workers with minimal polyneuropathy.

The aim of the present research was to investigate early impairments of central nervous system in subjects exposed to a low toxic level of industrial solvents for several years. Therefore a group of fifteen shoe-workers, with symptoms of minimal polyneuropathy, and a group of twenty, sex and age matched, healthy volunteers were selected for multimodal evoked potentials studies. The statistical analysis revealed a decrease of VEP and SEP amplitudes as well as a significant higher percentage of cases with BAEP V/I ratio between 0.5 and 1 among patients. The wrist-Erb's point conduction velocity was, also, found lowered in them. In accordance with the experimental results, the systematic employment of multimodal evoked potentials is proposed for screening the subjects exposed to neurotoxic influence of industrial solvents.

Adolescent↗

PubMed1991

Steroid myopathy: clinical and immunohistochemical study of a case.

A 42 year old woman with foot process disease, was treated with corticosteroids for 6 years. She had been suffering, for about 3 years from progressive muscle weakness of the limbs, accompanied by general paresthesia, cramps of the calves and burning muscle pain both at rest and an effort. The clinical, neurophysiological and histochemical examination indicated noninflammatory myopathic damage. The progressive reduction of corticosteroid dosage led rapidly to a distinct improvement, but not to a remission, of symptoms. Clinical and laboratory findings were consistent with those observed in most cases of steroid myopathy described in literature. We discuss the possible pathogenetic role of corticosteroids in this affection.

Adult↗

PubMed1990

Dopamine D1 receptor modulation of pilocarpine-induced convulsions.

The contribution of dopaminergic mechanisms to the generalization of epileptic activity was studied in rats given pilocarpine after pretreatment with selective dopamine agonists. At the dose of 200 mg/kg, pilocarpine produced limbic stereotypes but not convulsions or seizure-related brain damage. Pilocarpine, 200 mg/kg, following pretreatment with the D1 agonist (RS)-2,3,4,5-tetrahydro-7,8-dihydroxy-1-phenyl-1H-3 benzazepine, but not its (S)-enantiomer, induced convulsive activity as revealed by behavioral, electroencephalographic alterations and widespread brain damage. These features were identical to those produced by a higher, convulsant dose of pilocarpine (400 mg/kg). On the other hand, pretreatment with the D2 agonist 4,4a,5,6,7,8,8a,9-octahydro-5-n-propyl-2H-pyrazolo-3,4-g-quinoline failed to induce convulsions. Furthermore, the D1 receptor antagonist (R)-(+)-8-chloro-2,3,4,5-n-tetrahydro-3-methyl-5-phenyl-1H-3-benzazepine -7-ol prevented the convulsive activity induced by both 2,3,4,5-tetrahydro-7,8-dihydroxy-1-phenyl-1H-3 benzazepine plus pilocarpine (200 mg/kg) and pilocarpine (400 mg/kg), given alone. However, neither dopamine agonists nor antagonists altered the limbic stereotypes induced by pilocarpine, suggesting a dopamine system involvement primarily in the mechanisms of epilepsy generalization. The results suggest that pharmacological manipulation of dopaminergic transmission may provide an alternative approach to therapy of secondarily generalized epilepsy.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗