Biomedical subjects

C A Castro

Publications and source records attributed to C A Castro.

At least 19 recordsLinked to original sources

PubMed2001

Enteral feeding in stable chronic obstructive pulmonary disease patients.

OBJECTIVE: The study aimed to compare the effectiveness of a defined formula diet with a blenderized diet on nutritional and respiratory function parameters and to determine the bacteriological load of the two formulations. METHODOLOGY: Seventeen patients, aged 50-75 years, admitted to the University of the Philippines-Philippine General Hospital for chronic bronchitis and/or emphysema, were studied. They were divided into two groups according to dietary regimens. Each group of patients received either the standardized commercial formula or the blenderized formula for 2 weeks. Evaluation of dietary intake, anthropometric measurements, laboratory examinations and lung function were assessed. Subjective evaluation (patient's and physician's assessment) was also sought. Microbiological examinations were performed on the prepared enteral formulas. RESULTS: There was a slight increase in weight and in pulmonary function in both groups but these results did not differ significantly. Possible formula contamination was confirmed. Furthermore, in the overall assessment, the physician and patients rated both formulas as comparable.

Aged↗

PubMed1999

The Oklahoma Postmenopausal Women's Health Study: recruitment and characteristics of American Indian, Asian, Black, Hispanic, and Caucasian women.

Since 1994, the National Institutes of Health has required the inclusion of women and minorities in all of its sponsored clinical research. This study describes a workable recruitment strategy that embraces the National Institutes of Health requirement. We describe the recruitment pattern of the Oklahoma Postmenopausal Women's Study conducted in the general community of Oklahoma City and in surrounding areas that are both urban and rural. For the period 1994 through 1997, 491 postmenopausal women from all racial/ethnic groups in the community have participated in this study. Over 4 years of recruitment, the percentage of minority women in the study population has risen annually from 31% in 1994 to 81% in 1997. The overall percentage of minority women in the study population is currently 63.3%: American Indian, 21.8%; Asian, 3.7%; Black, 14.9%; Hispanic, 9.4%; White/American Indian Blend, 13.6%; and White, 36.7%. The recruitment approach described may be implemented in a variety of research settings. Specific recruitment approaches are described, as well as the distribution of sociodemographic and health behaviors across and within ethnic/racial groups.

Black or African American↗

PubMed1998

Primacy and recency effects in rhesus monkeys (Macaca mulatta) using a serial probe recognition task. III. A developmental analysis.

In children, the recency effect emerges prior to the primacy effect. To determine whether this dissociation is also seen in nonhuman primates, we evaluated the development of the primacy and recency effect in 3 young adult (35 months) and 4 adolescent (21 months) male rhesus monkeys (Macaca mulatta) using a six-item serial probe recognition (SPR) task. As predicted, the young adult monkeys displayed both effects, while the adolescent monkeys only displayed the recency effect. Not until after 26 months of training on the SPR task did the adolescent monkeys exhibit both the primacy and recency effect. Interference and strategy differences are discussed in terms of the results along with an interpretation of Rudy's (1992) configural association theory of cognitive development. Additional possible explanations for this developmental dissociation include the delayed maturation of the neocortical, hippocampal, and/or cholinergic systems, the latter two having been shown to be important in the expression of the primacy but not the recency effect.

Age Factors↗

PubMed1997

Primacy and recency effects in rhesus monkeys (Macaca mulatta) using a serial probe recognition task: II. Effects of atropine sulfate.

Nonhuman primates display both a primacy and a recency effect when trained on a 6-item serial probe recognition task. The author has previously shown that in the rhesus monkey, diazepam (3.2 mg/kg im) interferes with the memory processes that mediate the recency effect without affecting those memory processes involved in the primacy effect (C. A. Castro, 1995). This study assessed the effects of atropine sulfate (0.2, 0.3, and 0.4 mg/kg im) on the primacy and recency effects in these same monkeys. Opposite the effects of diazepam, atropine disrupted the primacy component of the serial position curve and had no measurable effect on the recency component. In addition, the 2 highest doses of atropine disrupted accuracy on the nonmatching probe trials, whereas all 3 doses of atropine resulted in increased response latencies. These reports indicate that the primacy and recency effects in the nonhuman primate can be pharmacologically dissociated.

Animals↗

PubMed1995

Primacy and recency effects in rhesus monkeys (Macaca mulatta) using a serial probe recognition task. I. Effects of diazepam.

In this study, we evaluated the effects of diazepam (0.2, 0.8, 1.6 and 3.2 mg/kg; IM) on the primacy and recency memory effects in four rhesus monkeys trained on a six-item serial probe recognition (SPR) task. Only the highest dose of diazepam (3.2 mg/kg) consistently affected the shape of the monkeys' serial position curves. Accuracy on the probe trials was disrupted for list items which occurred in the middle portion and recency memory component of the serial position curve, without affecting the primacy component. Diazepam, however, also produced several nonspecific effects on SPR performance. Both the 1.6 and 3.2 mg/kg diazepam doses disrupted accuracy on the non-matching probe trials, and the 3.2 mg/kg dose caused an increase in response latencies which were unrelated to any one component of the serial position curve. This is the first demonstration in nonhuman primates showing that the primacy and recency memory effects can be differentiated on the basis of diazepam dose.

Animals↗

PubMed1995

Behavioral effects of vehicles: DMSO, ethanol, Tween-20, Tween-80, and emulphor-620.

Experimental drugs and compounds that do not easily dissolve in water or saline are frequently combined with vehicles like solvents, detergents, or vegetable oils. Yet very little has been reported on the behavioral effects of vehicles. In this study, we assessed the effects of a vegetable oil (emulphor-620), two detergents (Tween-20 and Tween-80), and two solvents [dimethyl sulphoxide (DMSO) and ethanol] on the locomotor activity in CD2F1 male mice. Locomotor activity was monitored for 12 h after vehicle administration (IP). The concentrations for each vehicle were expressed as percent of vehicle in saline (v/v). Emulphor-620 did not affect locomotor activity at any concentration tested (2%, 4%, 8%, 16%, and 32%). Tween-20 significantly decreased locomotor activity at a concentration of 16% and Tween-80 at 32%. DMSO significantly decreased locomotor activity at concentrations of 32% and 64%. In contrast, ethanol produced a biphasic behavioral response: increased activity at a concentration of 16% and decreased activity at a concentration of 32%. These results will facilitate the selection and concentration of vehicles to be used in combination with experimental drugs or test agents.

Animals↗

PubMed1993

Cholinesterases as scavengers for organophosphorus compounds: protection of primate performance against soman toxicity.

The present treatment for poisoning by organophosphates consists of multiple drugs such as carbamates, antimuscarinics, and reactivators in pre- and post-exposure modalities. Recently an anticonvulsant, diazapam, has been included as a post-exposure drug to reduce convulsions and increase survival. Most regimens are effective in preventing lethality from organophosphate exposure but do not prevent toxic effects and incapacitation observed in animals and likely to occur in humans. Use of enzymes such as cholinesterases as pretreatment drugs for sequestration of highly toxic organophosphate anticholinesterases and alleviation of side effects and performance decrements was successful in animals, including non-human primates. Pretreatment of rhesus monkeys with fetal bovine serum acetylcholinesterase protected them against lethal effects of soman (up to 5 LD50) and prevented signs of OP toxicity. Monkeys pretreated with fetal bovine serum acetylcholinesterase were devoid of behavioral incapacitation after soman exposure, as measured by serial probe recognition or primate equilibrium platform performance tasks. Use of acetylcholinesterase as a single pretreatment drug provided greater protection against both lethal and behavioral effects of potent organophosphates than current multicomponent drug treatments that prevent neither signs of toxicity nor behavioral deficits. Although use of cholinesterases as single pretreatment drugs provided complete protection, its use for humans may be limited, since large quantities will be required, due to the approximately 1:1 stoichiometry between organophosphate and enzyme. Bisquaternary oximes, particularly HI-6, have been shown to reactivate organophosphate-inhibited acetylcholinesterase at a rapid rate. We explored the possibility that enzyme could be continually reactivated in animals pretreated with fetal bovine serum acetylcholinesterase, followed by an appropriate dose of reactivator, and challenged with repeated doses of sarin. In in vitro experiments, stoichiometry greater than 1:400 for enzyme:sarin was achieved; in vivo stoichiometry in mice was 1:65. Pretreatment of mice with fetal bovine serum acetylcholinesterase and HI-6 amplified the effectiveness of exogenous enzyme as a scavenger for organophosphate.

Acetylcholinesterase↗

PubMed1993

Impaired short-term memory resulting from postnatal undernutrition is attenuated by physostigmine.

Early-life undernutrition impairs the short-term memory capacity of adult rats (90 days of age) trained on a conditional-spatial discrimination task (Castro, Tracy, & Rudy, Behavioral Brain Research, 32, 255-264, 1989). While well-nourished control animals perform above 90% correct when the interval separating the forced run and choice run is 180 s, the performance of the undernourished animals falls to chance (50%) when the delay interval is increased to 90 s. We now report that this performance decrement can be attenuated by the administration of the anticholinesterase, physostigmine. However, the effects of physostigmine were dose dependent. While 0.02 mg/kg of physostigmine improved the performance of the undernourished animals so that they performed significantly above chance at the 180-s delay interval, neither 0.2 nor 0.002 mg/kg of physostigmine improved performance. We concluded that this effect was centrally mediated since scopolamine hydrobromide (1.0 mg/kg) which blocks both central and peripheral cholinergic receptors blocked physostigmine's performance-improving effect, while methyl-scopolamine (1.0 mg/kg) which blocks only peripheral receptors did not. These are the first results which suggest that the short-term memory impairments produced by early-life undernutrition can be attenuated by enhancing central cholinergic functioning.

Animals↗

PubMed1992

Protection of rhesus monkeys against soman and prevention of performance decrement by pretreatment with acetylcholinesterase.

The ability of acetylcholinesterase from fetal bovine serum (FBS AChE) to protect against soman, a highly toxic organophosphorus (OP) compound, was tested in rhesus monkeys. Intravenous administration of FBS AChE produced a minimal behavioral effect on the serial probe recognition task, a sensitive test of cognitive function and short-term memory. Pharmacokinetic studies of injected FBS AChE indicated a plasma half-life of 40 hr for FBS AChE in monkeys. Both in vitro and in vivo titration of FBS AChE with soman produced a 1:1 stoichiometry between organophosphate-inhibited FBS AChE and the cumulative dose of the toxic stereoisomers of soman. Administration of FBS AChE protected monkeys against the lethal effects of up to 2.7 LD50 of soman and prevented any signs of organophosphate intoxication, e.g., excessive secretions, respiratory depression, muscle fasciculations, or convulsions. In addition, monkeys pretreated with FBS AChE were devoid of any behavioral incapacitation after soman challenge, as measured by the serial probe recognition task. Compared to the current multicomponent drug treatment against soman, which does not prevent the signs or the behavioral deficits resulting from OP intoxication, use of FBS AChE as a single pretreatment drug provides significantly effective protection against both the lethal and the behavioral effects of soman.

Acetylcholinesterase↗

PubMed1992

Behavioral efficacy of diazepam against nerve agent exposure in rhesus monkeys.

The possibility that nerve agents will be used on the battlefield is real. The traditional therapy against nerve agent exposure consists of pyridostigmine pretreatment and atropine-pralidoxime chloride therapy administered after nerve agent exposure. This therapy regimen is extremely effective in preventing mortality in laboratory animals exposed to multilethal concentrations of nerve agent, yet these animals often display convulsions, brain damage, and behavioral incapacitation. We report here that the addition of diazepam to the traditional therapy for nerve agent (soman) exposure not only decreases the incidence of convulsions, but also attenuates the cognitive impairments of rhesus monkeys trained on a Serial Probe Recognition (SPR) task. Monkeys which received diazepam treatment required only 6 days before their performance on the SPR task returned to presoman exposure levels, compared to nondiazepam-treated monkeys which required 15 days. Moreover, only 1 out of the 5 monkeys which received diazepam treatment suffered tonic-clonic convulsions; in contrast all 5 monkeys which did not receive diazepam treatment experienced severe convulsive episodes. These results suggest that diazepam would be an excellent adjunct to traditional nerve agent therapy to facilitate behavioral recovery from nerve agent intoxication that might be encountered by US military personnel on the battlefield or accidental organophosphate poisoning encountered in industrial or agricultural accidents.

Acetylcholinesterase↗

PubMed1992

Primacy and recency effects in nonhuman primates.

The reports of primacy and recency memory effects in nonhuman primates have been criticized because they have all used an initiating response. That is, the presentation of the to-be-remembered list of items was always contingent on a response being initiated by the nonhuman primate. It has been argued that this initiating response improves performance for early items in the list, resulting in the occurrence of the primacy effect, independent of any memory processing mechanism. This criticism was addressed in the present study by not using an initiating response prior to the presentation of the list. Nevertheless, both a primacy and a recency effect were observed in all 6 rhesus monkeys evaluated using a serial probe recognition task. Thus, the results are similar to those for humans, in that both primacy and recency effects can be obtained in nonhuman primates. A brief literature review is included, and it is proposed that the primacy and recency effects observed in humans, nonhuman primates, and infraprimates can be explained within the context of the configural-association theory.

Animals↗

PubMed1991

Competition between Li+ and Mg2+ for ATP and ADP in aqueous solution: a multinuclear NMR study.

We used 7Li NMR spin-lattice relaxation times and 31P NMR chemical shifts to study the binding of Li+ and Mg2+ to the phosphate moieties of ATP and ADP. To examine the binding of Li+ and Mg2+ to the base and ribose moieties, we used 1H and 13C NMR chemical shifts. The 7Li NMR relaxation times of Li+/Mg2+ mixtures of ATP or ADP increased with increasing concentrations of Mg2+, suggesting competition between the two ions for adenine nucleotides. No significant binding of Li+ and Mg2+ to the base and ribose moieties occurred. At the pH and ionic strength used, 2:1 and 1:1 species of the Li(+)-ATP and Li+-ADP complexes were present, with the 2:1 species predominating. In contrast, 1:1 species predominated for the Mg(2+)-ADP and Mg(2+)-ATP complexes. We calculated the Li(+)-nucleotide binding constants in the presence and absence of Mg2+ and found them to be somewhat greater in the presence of Mg2+. Although competition between Li+ and Mg2+ for ATP and ADP phosphate binding sites in solution is consistent with the 31P chemical shift data, the possibility that the Li+ and Mg2+ form mixed complexes with the phosphate groups of ATP or ADP cannot be ruled out.

Adenosine Diphosphate↗

PubMed1991

Protection by butyrylcholinesterase against organophosphorus poisoning in nonhuman primates.

Butyrylcholinesterase (BuChE) was examined as an in vivo exogenous scavenger for highly toxic organophosphorus (OP) poisons. Protection studies with equine BuChE were carried out in rhesus monkeys trained to perform a Serial Probe Recognition task. The pharmacokinetics of equine BuChE administered i.v. in rhesus monkeys revealed an elimination T1/2 of approximately 620 hr. Animals given 503 nmol of BuChE i.v. and then challenged with 220 to 260 nmol of soman (two LD50; a lethal dose in untreated animals) all survived with no clinical signs of OP poisoning. Serial Probe Recognition performance was depressed after enzyme administration and at 1 hr postsoman. However, all monkeys performed the task at base-line levels at 8 hr after soman and throughout the remainder of the experimental period. Two different monkeys each were given two doses of sarin, 183 nmol/dose (one LD50) after 460 nmol of BuChE. No signs were observed. A third group of monkeys given 253 or 340 nmol (three and four LD50, respectively) of soman after 460 nmol of BuChE required 1 mg/kg of atropine i.v. 10 min postsoman, but recovered completely within 24 hr. Our results indicate that BuChE has the required properties to function as a biological scavenger to protect against the pharmacological and behavioral toxicity of OP poisons.

Animals↗

PubMed1990

Undernutrition during the brain growth period of the rat significantly delays the development of processes mediating Pavlovian trace conditioning.

Pavlovian trace conditioning procedures allow one to assess the ability of animals to associate events that are temporally separated because the conditioned stimulus terminates prior to the occurrence of the unconditioned stimulus. We report that undernutrition during Postnatal Days 2-18 significantly delays the development of trace conditioning to a visual stimulus. Previously undernourished 20-day-old rats conditioned when no temporal interval separated the termination of the CS and US onset (0-s trace interval). However, it was not until the undernourished pups were 30 days old that they conditioned when the trace interval was 10 or 30 s. In contrast, control pups only 20 days old were able to condition when a 10-s trace interval separated the CS and US events, and 25-day-old control pups conditioned when the interval was either 10 or 30 s. These results suggest that undernutrition delays the development of processes that enable the rat to sustain a representation of a visual CS during the trace interval.

Animals↗

PubMed1990

The cholinergic agent physostigmine enhances short-term-memory-based performance in the developing rat.

There are age-related differences in the rat's short-term memory processes. Rats 24-25 days old are 90% correct when the delay interval separating the forced run and choice run of a trial is either 10 or 30 s, but they perform at chance when the delay interval is 60 s. In contrast, the choice performance of 30-day-old rats remains constant across all delay intervals. It is reported that the cholinergic agent physostigmine dramatically improved the short-term-memory-based performance of rats 24-25 days old such that they displayed no loss in choice accuracy even when the delay interval was 60 s. No such enhanced performance was seen in rats treated with neostigmine, a peripherally acting anticholinesterase. The results support the hypothesis that postnatal maturational differences in central cholinergic systems may contribute to age-related differences in short-term memory.

Age Factors↗

PubMed1989

Recovery of spatial learning deficits after decay of electrically induced synaptic enhancement in the hippocampus.

A widespread interest in a long-lasting form of synaptic enhancement in hippocampal circuits has arisen largely because it might reflect the activation of physiological mechanisms that underlie rapid associative learning. As its induction normally requires the 'Hebbian' association of activity on a number of input fibres, we refer to the process as long-term enhancement (LTE) rather than long-term potentiation (LTP), to emphasize its distinction from the ubiquitous, non-associative 'potentiation' phenomena that occur at most synapses, including those exhibiting LTE. Among other evidence that LTE might actually have a role in associative memory is the demonstration that repeated high-frequency stimulation, which saturated the inducible LTE, caused a severe deficit in spatial learning, although it had no effect on well established spatial memory. These results were consistent with a widespread view that information need only temporarily be stored in the hippocampal formation in order for long-term memories to be established in neocortical circuits. In this context, it is important to understand whether the possible underlying synaptic changes are of a permanent character, or are relatively transient. A second question is whether the actual cause of the observed learning deficit is the distruption of the synaptic weight distribution, and/or the limitation of further synaptic change, which presumably results from experimental saturation of the LTE mechanism. Alternatively, the deficit could be a consequence of some unobserved secondary effect of the high-frequency electrical stimulation. Here we demonstrate that learning capacity recovers in about the same time that it takes LTE to decay, which strongly favours the first possibility and supports the idea that LTE-like processes actually underlie associative memory.

Animals↗

PubMed1989

Spatial selectivity of rat hippocampal neurons: dependence on preparedness for movement.

The mammalian hippocampal formation appears to play a major role in the generation of internal representations of spatial relationships. In rats, this role is reflected in the spatially selective discharge of hippocampal pyramidal cells. The principal metric for coding spatial relationships might be the organism's own movements in space, that is, the spatial relationship between two locations is coded in terms of the movements executed in getting from one to the other. Thus, information from the motor programming systems (or "motor set") may contribute to coding of spatial location by hippocampal neurons. Spatially selective discharge of hippocampal neurons was abolished under conditions of restraint in which the animal had learned that locomotion was impossible. Therefore, hippocampal neuronal activity may reflect the association of movements with their spatial consequences.

Animals↗

PubMed1989

Early-life undernutrition impairs the development of the learning and short-term memory processes mediating performance in a conditional-spatial discrimination task.

Previously undernourished and well-nourished control rats 23, 30, 40, and 90 days old were compared in a win-shift version of a conditional-spatial discrimination task. Control animals at each age were able to reach criterion on this problem. In contrast, the underfed rats were unable to solve this problem until they were at least 40 days old. The short-term memory of the 40- and 90-day-olds was further evaluated by increasing the interval between the forced run and choice run to 30, 60, and 180 s. Control animals could bridge all intervals; however, the undernourished animals' performance fell to chance when the interval was only 60 s. Thus, early-life undernutrition severely impaired the development of the ability of animals to solve spatial-conditional discrimination tasks and permanently impaired their short-term memory capacity. A simple threshold model relating undernutrition, brain development, and behavior is proposed to account for these data.

Animals↗