PubMed Health⌕ Search

Biomedical subjects

A M Martino

Publications and source records attributed to A M Martino.

At least 19 recordsLinked to original sources
PubMed2000

Allozyme variation and divergence in the phyllotine rodent Calomys hummelincki (Husson, 1960).

The aim of the present study was to assess the degree of genetic variation and divergence among six populations of Calomys hummelincki, a phyllotine rodent distributed in northern South America. With this information we will try to evaluate the two hypotheses of possible colonization and differentiation of this group of rodents postulated by Baskin and Reig. We studied 34 loci by electrophoretic analysis: 21 were monomorphic for all populations and 13 were polymorphic in at least one population, being P1% = 21.6% the mean value for all populations. The mean value of heterozygosity per locus was H = 0.075. Low values of genetic distance were observed among populations of the Llanos region (0.001 < D < 0.006). There was a larger genetic distance (D = 0.024) between the population from Isiro, in the northwestern semiarid region, and those from the Llanos region. The insular population of Aruba displayed the lowest value of genetic distance with the population from Isiro (D=0.014). The specimens from Sipao, on the right side of the Orinoco river, displayed the highest values of genetic distances in comparison with other populations of C. hummelincki (0.070 < D < 0.095). The relatively high differentiation was due to the fixation of new alleles, not found in other populations of C. hummelincki, at loci Idh-1 and Est-2. F-statistics and Nm values indicated reduced gene flow among the populations sampled. Despite the limited data, the results seem to support Reig's hypothesis about south to north colonization of genus Calomys in South America.

Alleles↗
PubMed1998

In search of a new ethic for treating patients with chronic pain: what can medical boards do?

Author argues that a complex "ethic of underprescribing" underlies the continued reluctance of physicians to use opioids to treat chronic pain. She contends that state medical boards are uniquely positioned to promote a new ethic for pain management, but stresses the difficulties for boards in attaining this goal. She thinks success may hinge on whether boards can change their approach to pain management and persuade a skeptical medical community that adopting a risk for underprescribing will serve the long-term interests of patients and the profession.

Analgesics, Opioid↗
PubMed1995

Characterization of superior sagittal sinus blood flow velocity using color flow Doppler in neonates and infants.

The objective of the investigation was to determine what effect intracranial pathology has on alterations of superior sagittal sinus blood flow, and to determine the role of color flow Doppler imaging of the superior sagittal sinus in the diagnosis of intracranial pathology in the neonate and infant. One hundred examinations were performed prospectively in 96 patients. The velocity was determined with an angle correction at 30-60 degrees and was obtained with and without gentle transducer compression. Superior sagittal sinus thrombosis was identified in two patients by the absence of flow. Multiple t-tests for independent measures showed no clinically significant differences between flow velocities with regard to intracranial hemorrhage, ventriculomegaly, extracorporeal membrane oxygenation therapy or prematurity. The authors conclude that color flow Doppler can accurately diagnose superior sagittal sinus thrombosis and may be used to screen high risk neonates such as those with thrombosis elsewhere or those treated with extracorporeal membrane oxygenation. No clinically significant associations were found between superior sagittal sinus flow velocity and any of the parameters evaluated in this study.

Blood Flow Velocity↗
PubMed1994

Intracerebral hemorrhage after evacuation of a subdural hematoma in an infant.

Intracerebral hematomas following evacuation of a subdural hematoma have been described in adults resulting from sudden decompression during the drainage of the hematoma. In infants an open fontanelle and patent sutures are expected to offer protection against sudden decompression. We report the occurrence of intracerebral hematoma in an infant following evacuation of a subdural hematoma. The multiplicity and centripetal spread of the postoperative hematomas suggested that they had resulted from sudden decompression.

Brain↗
PubMed1994

[Neonatal abstinence syndrome and maternal toxicological profile].

Neonatal abstinence syndrome (NAS) is one of the most frequent manifestations in the neonates of drug-addicted mothers. It is caused by the abrupt interruption of the transplacentar passage of drugs from the mother to the fetus. The aim of this study was to evaluate the correlation between drugs taken during pregnancy and NAS. Data were examined relating to 223 neonates born during 1975-1992 to drug-addict mothers. Neonates were subdivided into four groups according to the maternal toxicological profile. It was thus possible to observe that there is a greater prevalence of NAS in cases of polypharmacomania and that it gradually diminishes in the children of heroin addicts and those receiving methadone treatment. Moreover, the intensity of the syndrome is correlated to the high doses of methadone and/or heroin. In the group of neonates whose mothers had complied with the methadone treatment protocol, the severity of NAS was proportional to the dose taken by the mother. In conclusion, the management of pregnant drug addicts following a controlled methadone treatment programme is accompanied by improved obstetric help and is the most suitable way of reducing perinatal complications and the prevalence of NAS.

Dose-Response Relationship, Drug↗
PubMed1992

[The effects of lactitol in the treatment of intestinal stasis in childhood].

Thirty-nine children (18 males, 21 females) suffering from intestinal stasis were treated with lactitol or a reference drug (lactulose in crystalline form), according to a balanced randomization, for 15 days. The first group of children included 19 subjects treated with lactitol, the second group included 20 subjects treated with lactulose. The dosages of lactitol and lactulose were, respectively, of 150-350 mg/kg and of 150-300 mg/kg daily per os with a single administration in the morning. During the trial, the children did not take any concomitant drug. For each patient the tested parameters were: number of intestinal evacuations, consistency of stool and adverse reactions (abdominal swelling, abdominal pain, nausea, vomiting, meteorism) daily; routine laboratory tests at the beginning and at the end of the trials. The results showed that the subjects treated with lactitol have manifested, besides a proved therapeutic efficacy, a better tolerability and compliance than the subjects treated with lactulose.

Adolescent↗
PubMed1988

Reductions in acetylcholine and nicotine binding in several degenerative diseases.

Alzheimer's disease, Parkinson's disease, and progressive supranuclear palsy are all characterized by loss of neurons in the basal forebrain cholinergic system and by associated reductions in cortical presynaptic cholinergic markers, such as choline acetyltransferase. In this report, we identify that a major cortical receptor alteration in these disorders is a reduction in nicotinic receptors measured using both tritiated acetylcholine and levorotatory tritiated nicotine binding.

Acetylcholine↗
PubMed1988

Corticospinal projections from the medial wall of the hemisphere.

We injected wheat germ agglutinin conjugated to horseradish peroxidase into different segments of the spinal cord in order to examine the topographic organization of corticospinal projections from the medial wall of the hemisphere. We observed that substantial projections to the spinal cord originate not only from the supplementary motor area (SMA) in area 6, but also from 2 regions within the cingulate sulcus. The distribution of labeled neurons following tracer injections into different spinal cord segments indicates that corticospinal projections from the SMA and from the 2 cingulate regions are somatotopically organized. These findings together with other recent anatomical observations suggest that the corticospinal projections from the medial wall of the hemisphere provide the basal ganglia and limbic system with a somatotopically organized access to spinal cord mechanisms.

Animals↗
PubMed1988

Reductions in [3H]nicotinic acetylcholine binding in Alzheimer's disease and Parkinson's disease: an autoradiographic study.

In Alzheimer's disease (AD) and Parkinson's disease (PD), dysfunction in the basal forebrain cholinergic system is accompanied by a consistent loss of presynaptic cholinergic markers in cortex, but changes in cholinergic receptor binding sites are poorly understood. In the present study, we used receptor autoradiography to map the distribution of nicotinic [3H]acetylcholine binding sites in cortices of individuals with AD and PD and matched control subjects. In both diseases, a profound loss of nicotinic receptors occurs in all cortical layers, particularly the deepest layers.

Aged↗
PubMed1987

Corticospinal projections originate from the arcuate premotor area.

We investigated the patterns of corticospinal projection to different segments of the cervical spinal cord using retrograde transport of wheat germ agglutinin conjugated to horseradish peroxidase. We confirmed prior suggestions that the arcuate premotor area (APA) has a significant projection to the spinal cord. In addition, we observed that the corticospinal projection from the APA terminates in upper, but not lower segments of the cervical spinal cord. Furthermore, the region of the APA which projects to the cervical cord also projects to the arm area of the primary motor cortex on the crest of the precentral gyrus. Thus, we conclude that the APA projection to upper cervical segments is involved in the cortical control of arm movements.

Animals↗
PubMed1986

Nicotinic acetylcholine binding sites in Alzheimer's disease.

In Alzheimer's disease (AD), there is a loss of presynaptic cholinergic markers in the cerebral cortex, but the nature of cholinergic receptor changes is unclear. In this study, [3H]acetylcholine and [3H]nicotine were used to label nicotinic cholinergic binding sites in cerebral cortical tissues obtained at autopsy from patients with AD and from matched controls. A consistent and severe loss of nicotinic receptors was found in AD.

Acetylcholine↗
PubMed1985

A strong influence of serotonin axons on beta-adrenergic receptors in rat brain.

The role of serotonin axons in modulating the norepinephrine neurotransmission system in rat brain was investigated. Selective lesions of the forebrain serotonergic system were made by injecting 5,7-dihydroxytryptamine into the midbrain raphe nuclei. Four to six weeks after the lesion, the uptake of 3H-labeled serotonin in the frontal cortex and the hippocampus was reduced by more than 90 percent, while neither the uptake of 3H-labeled norepinephrine nor the content of norepinephrine was affected in either tissue. The number of beta-adrenergic receptors, as measured by radioligand binding with 3H-labeled dihydroalprenolol, was increased in the frontal cortex and hippocampus of rats with lesions. Similarly, specific lesions of central serotonin axons produced by systemically administered p-chloramphetamine resulted in an increase in the binding of 3H-labeled dihydroalprenolol to beta-adrenergic receptors and in the production of adenosine 3',5'-monophosphate in response to isoproterenol. These results indicate that serotonin axons may regulate beta-adrenergic receptor number and function in brain.

Animals↗
PubMed1985

High-affinity binding of [3H]acetylcholine to muscarinic cholinergic receptors.

High-affinity binding of [3H]acetylcholine to muscarinic cholinergic sites in rat CNS and peripheral tissues was measured in the presence of cytisin, which occupies nicotinic cholinergic receptors. The muscarinic sites were characterized with regard to binding kinetics, pharmacology, anatomical distribution, and regulation by guanyl nucleotides. These binding sites have characteristics of high-affinity muscarinic cholinergic receptors with a Kd of approximately 30 nM. Most of the muscarinic agonist and antagonist drugs tested have high affinity for the [3H]acetylcholine binding site, but pirenzepine, an antagonist which is selective for M-1 receptors, has relatively low affinity. The ratio of high-affinity [3H]acetylcholine binding sites to total muscarinic binding sites labeled by [3H]quinuclidinyl benzilate varies from 9 to 90% in different tissues, with the highest ratios in the pons, medulla, and heart atrium. In the presence of guanyl nucleotides, [3H] acetylcholine binding is decreased, but the extent of decrease varies from 40 to 90% in different tissues, with the largest decreases being found in the pons, medulla, cerebellum, and heart atrium. The results indicate that [3H]acetylcholine binds to high-affinity M-1 and M-2 muscarinic receptors, and they suggest that most M-2 sites have high affinity for acetylcholine but that only a small fraction of M-1 sites have such high affinity.

Acetylcholine↗
PubMed1983

Differential binding properties of adenosine receptor agonists and antagonists in brain.

The binding properties of N6-cyclohexyl [3H]adenosine ( [3H]CHA) and 1,3-diethyl-8-[3H]phenylxanthine ( [3H]DPX) in rat forebrain membrane are compared. The kinetic parameters of binding for each ligand are quite distinct, with [3H]CHA displaying two populations of binding sites (KD = 0.4 +/- 0.05 nM and 4.2 +/- 0.3 nM; Bmax = 159 +/- 17 and 326 +/- 21 fmol/mg protein), whereas [3H]DPX yielded monophasic Scatchard plots (KD = 13.9 +/- 1.1 nM; Bmax = 634 +/- 27 fmol/mg protein). The metals copper, zinc, and cadmium are potent inhibitors of [3H]CHA binding, with respective IC50 concentrations of 36 microM, 250 microM, and 70 microM. Copper is a much less potent inhibitor of [3H]DPX binding (IC50 = 350 microM). The inhibitory effect of copper on both [3H]CHA and [3H]DPX binding is apparently irreversible, as membranes pretreated with copper cannot be washed free of its inhibitory effect. The inhibitory effect of both copper and zinc on [3H]CHA binding was reversed by the guanine nucleotide Gpp(NH)p. [3H]DPX binding is only partially inhibited by zinc and cadmium (60% of specific binding remains unaffected), suggesting that this adenosine receptor ligand binds to two separate sites. Guanine nucleotides had no effect on the inhibition of [3H]DPX binding by either copper or zinc. Differential thermal and proteolytic denaturation profiles are also observed for [3H]CHA and [3H]DPX binding, with the former ligand binding site being more labile in both cases. Stereospecificity is observed in the inhibition of both [3H]CHA and [3H]DPX binding, with L-N-phenylisopropyladenosine (PIA) being 50-fold more potent than D-PIA in both cases. Evidence is therefore provided that adenosine receptor agonists and antagonists have markedly different binding properties to brain adenosine receptors.

Adenosine↗
PubMed1982

Specific calcium antagonist binding sites in brain.

The binding of the calcium antagonist [3H] nitrendipine ([3H] NDP) to brain and heart is described and the brain site is characterized. The binding is saturable, specific and of very high affinity with KD values of 0.16 nM in brain and 0.21 nM in heart. Our kinetic results are similar to those recently reported by two other groups (1, 2), indicating a saturable, high affinity binding site in brain. In brain the binding sites are enriched in crude nuclear and synaptosomal fractions. The highest levels of binding are seen in the hippocampus, caudate and cerebral cortex with much lower levels in the cerebellum and pons. Calcium has a marked stimulatory effect on [3H] NDP binding at 10(-4) M. Addition of 0.5 mM CaCl2 to EDTA treated membranes nearly doubles the number of binding sites. Of the many drugs and neurotransmitters tested only other calcium antagonists, i.e. verapamil, inhibit binding (IC50 = 250 nM). The inhibition of [3H] NDP binding by verapamil is apparently non-competitive and not complete, suggesting that [3H] NDP binds to several sites, only some of which are inhibited by verapamil. The [3H] NDP binding site is probably a protein since it is very sensitive to trypsin, heat and sulfhydryl reagents.

Animals↗
PubMed1982

Benzodiazepines are weak inhibitors of [3H]nitrobenzylthioinosine binding to adenosine uptake sites in brain.

Saturable, specific, high affinity binding of the potent adenosine uptake inhibitor [3H]nitrobenzylthioinosine ([3H]NBI) to brain membranes has been demonstrated. In an effort to test the hypothesis that benzodiazepine action may be due to the inhibition of adenosine uptake, the inhibition of [3H]NBI binding by diazepam, clonazepam and chlordiazepoxide was tested. The benzodiazepines are very weak inhibitors of [#H]NBI binding, having IC50 values several orders of magnitude above their therapeutic levels.

Adenosine↗