Biomedical subjects

L J Martin

Publications and source records attributed to L J Martin.

At least 163 records · Page 9Linked to original sources

PubMed1990

Effect of a program to facilitate parent-child communication about sex.

U.S. teens have high rates of premarital sexual activity resulting in alarming rates of teenage pregnancy and sexually transmitted disease. One possible way to combat the problem of teenage sexual activity is to promote sexuality education within the family. The purpose of this study was to increase parent-child communication about sex through an educational program for parents. The effect of the educational program was evaluated by a nonrandomized, controlled trial. Volunteer parents were recruited from three middle schools (grade six through eight) located in middle to upper-middle socioeconomic class neighborhoods. The parents participated in four 2-hour sessions which included factual information about sexuality and exercises to improve communication skills. The experimental group (N = 47) were requested to fill out questionnaires immediately before and one month after the program. The control group (N = 17) were requested to fill out questionnaires one month before and again immediately before the program. Parents were asked to report the number of times they talked with their adolescents about 11 sex-related topics. The difference in reported frequency of communication before and after the program was compared using a two-tailed, matched pairs t-test. Twenty-four (51%) experimental group parents and eight (47%) control group parents completed both questionnaires. There was a significant increase in communication reported by the experimental group. The mean difference of the number of topics discussed was 10.9 (SD 7.3) for participants versus -2.5 (SD 5.9) for controls (p = .00053). This study shows that parent-child communication about sex can be facilitated by an educational program for parents.

Adolescent↗

PubMed1990

Neuronal disorders: studies of animal models and human diseases.

The peripheral nervous system and the central nervous system (CNS) are comprised of assemblies of neurons that communicate via electrical and chemical signals. Different disease processes selectively affect specific populations of neurons and/or specific cell functions (i.e., "selective vulnerability" of neurons is a principal determinant of phenotypes of disease). New cellular and molecular biological approaches have begun to clarify some of the mechanisms of selective cell injury in human diseases and their animal models. Following a brief review of the normal biology of nerve cells, we use illustrations drawn from studies of experimental and human diseases to discuss the mechanisms of structural/chemical abnormalities that occur in a variety of neuronal disorders.

Animals↗

PubMed1990

The count rate performance of a multiwire gamma camera measured by a decaying source method with 9.3-minute tantalum-178.

The multiwire gamma camera (MWGC) operates at high count rates with radionuclides of low energy and short half-life. We evaluate the count rate performance of the MWGC with tantalum-178 (178Ta) by a decaying source method. Data acquired dynamically by the camera from a 178Ta source in the NEMA Standards scatter phantom were corrected for deadtime loss by a trial paralyzing deadtime and converted to their natural logarithms. The trial deadtime, tau, was adjusted iteratively after curve fittings until a straight line was achieved. The paralyzing deadtime determined by this method was 0.41 microsecond. Therefore, the camera can be operated up to 850,000 cps with 178Ta without exceeding 50% data loss. This rate is 10 times greater than the performance of the typical scintillation camera. Moreover, high count rates are achieved without significant loss of spatial resolution.

Evaluation Studies as Topic↗

PubMed1988

Topographic, non-collateralized basal forebrain projections to amygdala, hippocampus, and anterior cingulate cortex in the rhesus monkey.

Projections of the basal forebrain magnocellular complex to the limbic telencephalon of the primate were studied by combining double-retrograde tracing with immunocytochemistry. Tracers were injected into anterior cingulate cortex and hippocampus or into hippocampus and amygdala. Retrogradely labeled populations of neurons were topographically arranged but intermingled peripherally. Double-labeled neurons, found only after amygdala-hippocampus injections, were very rare. Approximately 30% of hippocampopetal, 50-70% of amygdalopetal, and 50-90% of cingulopetal neurons were cholinergic; percentages varied among different regions of basal forebrain. These findings further support the concept of a system with a highly organized efferent circuitry.

Amidines↗

PubMed1988

Effects of oxotremorine on neuronal RNA and chromatin in thalamic cholinoceptive sites.

Neuronal nucleic acid responses were examined within the rat thalamic ventrobasal nuclear complex (VBC) and nucleus reticularis (NR) following single intraperitoneal injections of the central muscarinic-cholinergic (M2) receptor agonist oxotremorine (0.1, 0.7, or 1.0 mg/kg). After stoichiometric azure B and Feulgen staining of brain sections, scanning-integrating cytophotometry was used to quantify azure B-ribonucleic acid (RNA) content, Feulgen-DNA levels, and changes in the susceptibility of chromatin to Feulgen acid hydrolysis (F-DNA yield) of neurons on an individual basis. Changes in neuronal nucleolar volume were also determined histometrically. Within the VBC, oxotremorine produced marked dose-dependent elevations in neuronal RNA content and nucleolar volume with increased F-DNA yield (chromatin activation) in a proportion of VBC neurons. In contrast, within the NR, oxotremorine elicited reductions in RNA levels, F-DNA yield and nucleolar volume. The data demonstrate that oxotremorine-induced central muscarinic receptor stimulation is associated with metabolic correlates of thalamic VBC neuroexcitation and NR neuron depression. The overall study lends further credence to the hypothesis that muscarinic-cholinergic mechanisms are operative within the mammalian thalamus.

Animals↗

PubMed1988

Middle latency response to a 500-Hz tone pip in normal-hearing and in hearing-impaired subjects.

Measurement of middle latency responses (MLR) appears to be one of the most useful ways of determining low-frequency auditory threshold. It is known that analog filtering can drastically affect MLR and since most laboratories use different recording characteristics, we carried out these measurements with a number of filter configurations. Ten subjects with normal hearing sensitivity were tested. The stimuli were 500-Hz tone pips (alternating in polarity) with a 4-ms rise-fall time and a plateau of 2 ms, presented at the rate of 9.3/s. The MLR were recorded with filter settings of 10-100, 10-250, 10-1,500, 10-3,000, 30-100 and 30-250 Hz at 12 dB per octave roll-off with a time base of 100 ms. MLR threshold was found between 8.0 and 11.5 dB nHL. The Wilcoxon statistical test showed that mean MLR thresholds did not differ significantly at the various bandpass configurations. An additional objective of this study was to compare hearing sensitivity based on MLR threshold to tone pips at 500 Hz and behavioural results obtained by conventional pure-tone audiometry. Although the correlation coefficient between the behavioural and electrophysiological measurements was statistically significant (r = 0.85), further studies are required in order to determine the real magnitude of the predicted errors obtained, before this electrophysiological measure can be applied clinically.

Adolescent↗

PubMed1987

Effects of sodium fluoride on uptake of T-2 mycotoxin in cultured cells.

We examined the effect of sodium fluoride on uptake of tritium-labeled T-2 toxin (molecules of toxin/cell) in Chinese hamster ovary (CHO) and African green monkey kidney (VERO) cells. Correlations were made to temperature (22 and 37 degrees C) and toxin concentration (0.001 and 0.01 microgram/ml) over time (0-180 min). As expected, toxin uptake increased in both cell types with increasing time and temperature. VERO cells exhibited significant (P less than 0.05) increases in the rate (i.e. slope) of toxin uptake under all parameters, while the rate of toxin uptake in both cell types was generally greater at 37 degrees C compared to 22 degrees C. The rate of equilibrium was affected by both temperature and sodium fluoride. At 37 degrees C toxin uptake plateaued by 30 min in the presence of sodium fluoride. At 22 degrees C the rate of toxin uptake was slower, with or without sodium fluoride present. Statistical analysis of individual time points along the curve demonstrated that sodium fluoride significantly increased cell-associated toxin at most time points. Analysis of the slopes of uptake curves from 0 to 20 min indicated significant (P less than 0.05) differences in the rates of T-2 uptake in both cell types and toxin doses in the presence of sodium fluoride. The increase in toxin uptake in the presence of sodium fluoride was not due to altered cell membrane permeability caused by sodium fluoride. This study demonstrates that sodium fluoride significantly increases cell-associated T-2 toxin and the rate of toxin uptake in two cultured cell lines.

Animals↗

PubMed1986

Scanning cytophotometric analysis of brain neuronal nuclear chromatin changes in acute T-2 toxin-treated rats.

Male Sprague-Dawley rats (200 g) were injected intraperitoneally with T-2 toxin, a trichothecene mycotoxin protein synthesis inhibitor, at dosages of 0.75, 1.0, 1.5, and 6.0 mg/kg (1 LD50 = 0.9 mg/kg) before decapitation at 8-hr postexposure. Correlative data were obtained on changes in physicochemical properties of nuclear chromatin, chromatin dispersion, and nuclear volume of cerebrocortical (layer III) and striatal neurons using Feulgen-DNA (F-DNA) cytophotometry and ocular filar micrometry. Decreased lability of neurons to F-DNA acid hydrolysis (reduced F-DNA yield), nuclear shrinkage, and chromatin aggregation (decreased chromophore area) were used as indices of suppression of genomic template activity, i.e., neuronal nuclear functioning. Conversely, increased F-DNA yield, chromophore area, and nuclear volume signify enhanced neuronal activation. At 8 hr following T-2 toxin exposure, cerebrocortical and striatal neurons exhibited a dose-dependent decrease in F-DNA hydrolyzability, i.e., impaired chromatin activity, and increases in both chromatin dispersion and nuclear volume. Microscopic observation revealed no gross evidence of T-2 induced neurotoxicity. These data indicate that T-2 toxin elicits both neurochemical injury and adaptive or compensatory processes simultaneously. The toxicological importance of observed nuclear alterations and the role of impairments in central nervous system metabolism in acute T-2 toxicity remain to be ascertained.

Animals↗

PubMed1986

Brain neuronal chromatin responses in acute soman intoxicated rats.

Male Sprague-Dawley rats (200 g) were injected subcutaneously with soman, a potent neuronal acetylcholinesterase (AChE) inhibitor, at doses of 0.5, 0.8 and 1.0 LD50 (1 LD50 = 135 micrograms/kg) before decapitation at 1 and 24 h post-exposure. Correlative data were obtained on the severity of brain AChE inactivation and physicochemical changes in nuclear chromatin of cerebrocortical (layer V) and striatal neurons using Feulgen-DNA (F-DNA) cytophotometry and ocular filar micrometry. Decreased lability of neurons to F-DNA acid hydrolysis (reduced F-DNA yield), nuclear shrinkage and chromatin aggregation (decreased chromophore area) were used as indices of suppression of genomic template activity; conversely, increases in F-DNA yield and chromophore area signify enhanced neuroexcitation. At 1 hr post-soman there was a dose-dependent inactivation of AChE with a moderate increase in chromatin activation, i.e., nuclear hypertrophy and chromatin dispersion. At 24 hr post-soman there was a partial restoration of AChE activity, notably in striatal neurons, with a suppression in chromatin template activity. These data indicate that actions of soman on neuronal functioning are time-dependent. The absence of any dose-related neuronal chromatin changes may signify existence of non-cholinergic mediated events.

Acetylcholinesterase↗

PubMed1986

Quantitative cytophotometric analysis of brain neuronal RNA and protein changes in acute T-2 mycotoxin poisoned rats.

Male Sprague-Dawley rats (200 g) injected intraperitoneally with T-2 toxin, a trichothecene mycotoxin protein synthesis inhibitor, at dosages of 0.75, 1.0, 1.5 and 6.0 mg/kg (1 LD50 = 0.9 mg/kg) were decapitated at 8 hr post-exposure. Data were obtained on changes in neuronal (perikaryal) RNA levels, protein contents and nucleolar volumes in cerebrocortical (layer III) and striatal (caudate-putamen) brain regions using quantitative azure B-RNA and Coomassie-protein cytophotometry and ocular filar micrometry. Correlative observations were made on changes in brain cytomorphology. Reductions in neuronal RNA/protein contents and nucleolar volume were used as indices of impaired perikaryal functioning. At 8 hr after T-2 toxin poisoning the following results were obtained in cerebrocortical and striatal brain compartments: neuronal RNA contents were generally maintained at control values in both brain regions, however, moderate RNA depletion was evidenced in the cerebral cortex with 1.5 mg/kg T-2 and in the striatum with a 6.0 mg/kg dose; neuronal protein levels were suppressed in a dose-dependent fashion within the cerebrocortex, while in the striatum there was no direct correspondence between protein loss and T-2 dosage; neuronal nucleolar volumes were typically maintained at control levels in both neuronal compartments. Microscopic observations revealed no gross evidence of T-2-induced brain cytopathology. These data indicate that T-2 toxin does not elicit direct cytopathic actions in these two brain regions, thus indicating that cerebrocortical and striatal compartments do not represent primary target sites of T-2 toxicant action.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1986

Cytophotometric analysis of neuronal chromatin and RNA changes in oxotremorine-treated rats.

Neuronal nucleic acid responses were examined within the rat striatum and sensorimotor cortex (layer V) following single intraperitoneal injections of the central cholinergic-muscarinic agonist oxotremorine (0.1, 0.7, or 1.0 mg/kg). After stoichiometric Feulgen and azure B staining of brain sections, scanning-integrating microdensitometry was used to quantify Feulgen-deoxyribonucleic acid levels, changes in the susceptibility of chromatin to Feulgen acid hydrolysis (F-DNA yield) and azure B-ribonucleic acid (RNA) content of neurons on an individual basis. Changes in neuronal nuclear and nucleolar volumes were also determined histometrically. Within the striatum and sensorimotor cortex, oxotremorine produced marked dose-dependent elevations in both F-DNA yield and RNA content. These metabolic increases were typically paralleled by elevations in nuclear and nucleolar volumes. The data demonstrate that the oxotremorine-induced central muscarinic activation is associated with dose-related enhancements in neuronal chromatin template activity, RNA content, and protein synthetic capacity.

Animals↗

PubMed1985

Effects of diazepam on soman-induced brain neuronal RNA depletion and lethality in rats.

Studies were conducted to determine effects of the benzodiazepine anticonvulsant diazepam on soman induced brain neuronal RNA depletion and lethality in rats. Quantitative azure B-RNA cytophotometry was used to monitor RNA responses of cerebrocortical (layer V) and striatal neurons following dosages of 0.5, 0.9 and 1.5 LD50 soman (LD50 = 135 micrograms/kg, sc), whereas mean time of death and 24-h survival following 0.8, 1.2 and 1.5 LD50 were used to assess the antidotal efficacy of diazepam (2.2 mg/kg, im) pretreatment. Soman produced dose-dependent RNA depletion in both brain regions. This RNA impairment was almost completely prevented by diazepam, although neuronal RNA contents were generally slightly lower than corresponding control values. However, diazepam pretreatment was not associated with any change in mean time of death or in 24-h survival. The overall data suggest that excessive neural activity per se may underlie the genesis of soman-induced central metabolic impairments, but also appear to effectively dissociate epileptiform activity from lethal actions of soman.

Acetylcholinesterase↗

PubMed1985

Protective effect of diazepam pretreatment on soman-induced brain lesion formation.

Histopathological analyses of brains of rats receiving a single 0.9 LD50 injection of soman, a potent anticholinesterase neurotoxin, revealed massive widespread lesions in the cerebral cortex and thalamus 4 weeks post-injection. Such lesions were not evidenced in rats receiving diazepam (2.2 mg/kg, i.m.) 10 min prior to soman treatment. Thus, anticonvulsant antidotes may aid in preventing extensive or permanent brain damage in rats surviving near-lethal soman dosages.

Animals↗

PubMed1985

Effects of HI-6 and pralidoxime on neuronal RNA in thalamic cholinergic sites.

Quantitative azure B-RNA cytophotometry was employed to compare effects of the oximes HI-6 and pralidoxime (2-PAM) to those of atropine sulfate (AS) on neuronal RNA metabolism in the thalamic ventrobasal nuclear complex (VBC) and nucleus reticularis (NR). The ability of these compounds to mitigate soman (pinacolyl methylphosphonofluoridate)-induced neuronal RNA alterations (i.e., VBC-RNA depletion/NR-RNA elevation) in these muscarinic cholinergic sites was also determined. Generally, HI-6 (125 mg/kg, i.p.) and 2-PAM (43.2 mg/kg, i.m.) elicited similar patterns of neuronal RNA changes, i.e., diminution of VBC-RNA and NR-RNA with oximes alone; partial amelioration of soman (1.5 LD50, s.c.)-induced VBC-RNA loss; and slight or no effect on soman induced NR-RNA accumulation. HI-6 produced more severe RNA reduction than 2-PAM in both brain regions of non-poisoned rats, whereas 2-PAM was more effective in reversing the effects of soman in these two regions. The muscarinic antagonist, AS, also produced VBC-RNA depletion and partially counteracted the VBC-RNA loss in soman intoxicated rats. Unlike the oximes, however, AS resulted in NR-RNA accumulation and it also antagonized soman induced NR-RNA elevation. Neither oxime reactivated soman inhibited brain acetylcholinesterase but HI-6 did reactivate appreciable plasma cholinesterase. The overall data suggest that HI-6 and 2-PAM do exert pharmacologic actions on cholinergic neurons in the rat CNS. However, the greater effectiveness of HI-6 over 2-PAM in countering lethal actions of soman does not appear to be correlated with oxime mediated restoration of neuronal RNA levels in these two cholinergic regions.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1984

Cytophotometric analyses of thalamic neuronal RNA in soman intoxicated rats.

Quantitative azure B-RNA cytophotometry was used to monitor metabolic responses of individual neurons within the ventrobasal nuclear complex (VBC) and nucleus reticularis (NR) of the rat thalamus following administration of soman (0.5, 0.9 or 1.5 LD50, sc). A dose-dependent depression in brain acetylcholinesterase (AChE) was evidenced. With respect to thalamic RNA responses, a complex pattern of RNA alterations was evidenced, with these two regions generally exhibiting opposite patterns of dose-related RNA changes. With sub-lethal dosages of soman, RNA accumulation was evidenced in the acetylcholine (ACh) mediated excitatory VBC region and RNA depletion in the ACh mediated inhibitory NR neurons. With a lethal dose, an opposite RNA response pattern was observed in both thalamic regions. It is postulated that the observed RNA response pattern with sub-lethal dosages of soman is what one would anticipate with cholinergic brainstem reticular formation activation. The absence of such a response with lethal doses strongly suggests some disruption of functional excitatory cholinergic activity and perhaps also an impairment of inhibitory cholinergic synaptic activity.

Acetylcholinesterase↗

PubMed1984

Scanning cytophotometric analysis of myocardial nucleic acid and chromatin changes in soman toxicated rabbits.

Myocardial nucleic acid responses were analysed in New Zealand White rabbits 20 min-1 h and 6-8 h following single subcutaneous injections of soman (20, 30, or 40 micrograms kg-1). Scanning-integrating microdensitometry was used to quantify Azure B-RNA and Feulgen-DNA (F-DNA) levels, and changes in the susceptibility of chromatin to Feulgen acid hydrolysis (F-DNA reactivity) of individual ventricular myocardial cells. With a dosage of 20 micrograms kg-1 soman, no RNA alterations were evidenced at 1 h whereas at 6-8 h myocardial cells exhibited higher RNA levels and an increase in F-DNA reactivity of chromatin. With dosages of 30 and 40 micrograms kg-1 soman there was an augmentation in RNA levels and in the acid hydrolysability of nuclear chromatin at both 20 min-1 h and 6-8 h. It is postulated that the observed cellular transformations represent a compensatory augmentation in myocardial metabolic functioning presumably in response to an increased functional demand on the ventricular myocardium. The absence of cytopathic or cytochemical evidence of impairment in nucleic acid metabolism is inconsistent with the premise that soman exerts direct cytotoxic effects on rabbit myocardium.

Animals↗

PubMed1984

Soman toxication in hypoxia acclimated rats: alterations in brain neuronal RNA and survival.

Effects of prior hypoxia acclimation (14-day at 380 mm Hg) on soman (pinacolyl methylphosphonofluoridate) induced brain neuronal RNA and acetylcholinesterase (AChE) depletion and lethality were monitored in rats following their return to ambient oxygenation. Quantitative cytochemical techniques were used to measure RNA and AChE changes in individual cerebrocortical (Layer III) and striatal (caudate plus putamen) neurons. In ambient Po2 controls, soman eventuated in a moderate diminution of neuronal RNA in both brain regions and severe, dose-dependent suppression of AChE activity. Hypoxia acclimation per se induced RNA alterations as manifested in cortical RNA depletion and increased variability of striatal neuron RNA contents. In hypoxia acclimated rats, the extent of neuronal RNA depletion following soman injection was attenuated in both brain regions, yet there were no discernible differences in saline control AChE levels or in the extent of soman-induced AChE inhibition in ambient control versus hypoxia acclimated treatment groups. Hypoxia acclimated rats, however, were found to be even more susceptible to lethal actions of soman as assessed using 24- and 48-hour survival following a three-point treatment regimen. These data indicate that while compensatory systemic and central metabolic adjustments associated with 14d acclimation to reduced oxygen availability may retard soman-induced neuronal RNA depletion, resistance to lethal or near-lethal soman exposure is not enhanced. It is postulated that hypoxia acclimation is associated with complex adaptive and maladaptive neurophysiological alterations influencing CNS responsiveness to soman toxication, and that detrimental consequences exceed protection afforded by metabolic adaptation.

Acclimatization↗

PubMed1984

Effects of HI-6 on brain neuronal RNA and acetylcholinesterase: metabolic responses during acute soman intoxication.

Quantitative cytochemical techniques were used to monitor effects of the bis-pyridinium oxime HI-6 with and without atropine sulfate (AS) on soman-induced cerebrocortical (layer V) and striatal neuron RNA and acetyl-cholinesterase (AChE) impairments. In addition, plasma cholinesterase (ChE) activity was measured to determine the extent of peripheral enzyme reactivation. Antidotal pretreatment effected complete (HI-6) or partial (AS) amelioration of neuronal RNA depletion evidenced following 1.5 LD50 (195 micrograms/kg) soman, whereas combined HI-6 + AS treatment only partially restored (cortical) or did not change (striatal) neuron RNA contents. HI-6 produced appreciable plasma ChE reactivation but brain AChE activity was not significantly altered. In rats treated only with antidotes, HI-6 or AS alone significantly reduced neuronal RNA in both brain regions. These data indicate that HI-6 influences the metabolic status of central cholinergic compartments and can completely protect against soman-induced neuronal RNA depletion. However, there are no precise relationships among RNA restitution, AChE reactivation or the protective potency of antidotal treatments. Effects of HI-6 on neuronal RNA may signify central cholinolytic activity in vivo, but indirect effects mediated by peripheral mechanisms can not be excluded at present.

Acetylcholinesterase↗