Biomedical subjects

J E Thornton

Publications and source records attributed to J E Thornton.

At least 19 recordsLinked to original sources

PubMed2001

A continuous improvement process for health providers of victims of domestic violence.

BACKGROUND: Health care providers can play an important role in the prevention of domestic violence through established processes of identification, safety assessment, validation, documentation, and referral. In 1998 the Safe Family Project, funded by University Health System (UHS), affiliated with University of Texas Health Science Center at San Antonio, provided for a clinical review of existing services for victims of domestic violence. A subsequent review of the health system's policy and clinical practice supported the need for resources and training and for an improved care process for victims of domestic violence. THE CONTINUOUS IMPROVEMENT PROCESS (CIP) MODEL: UHS adapted the Shewhart cycle of activities popularly referred to as PDSA (plan change, do change, study results, act on results), a systematic, process-focused approach to achieving continuous and measurable improvement, as its CIP model, and it formed a process improvement team. This process led to translation of research findings into best practice guidelines for treatment of domestic violence and staff education. RESULTS: Significant improvements were made in the overall qualitative chart reviews, although the diagnostic coding (using ICD-9 codes and e-codes) did improve. The CIP can be replicated in other settings to improve the care of victims of domestic violence. DISCUSSION: The CIP effort is being extended to outpatient facilities, and managers have requested that the training manual be replicated and placed throughout UHS as a resource manual. Other activities are intended to improve prevention of domestic violence and intervention when it occurs.

Community Networks↗

PubMed2001

A reassessment of leptin's role in triggering the onset of puberty in the rat and mouse.

Leptin is an adipocyte-derived hormone that has been implicated to serve as a metabolic signal to the reproductive axis. The role of leptin in pubertal maturation, however, has been a much-debated topic. We have previously reported that leptin serves as a permissive signal to the onset of puberty in the female rat. In an attempt to further understand the mechanics of leptin during pubertal maturation in rodent species, we had three experimental objectives: first, to describe the temporal relationship of leptin with development in the male and female rat; second, to seek evidence for an increase in responsiveness of the neuroendocrine axis to leptin by assessing for possible changes in leptin receptor expression during pubertal developmental in the female rat; and, third, to reevaluate the possible role of leptin as a permissive signal to the onset of puberty in the mouse. We found that serum leptin levels remain relatively constant during the prepubertal and postpubertal stages of both sexes. In addition, we could not detect any significant developmental changes in leptin receptor gene expression in the hypothalamus of the female rat. Lastly, we corroborated our findings in the female rat that leptin reversed the delay in pubertal maturation secondary to food restriction but did not advance the onset of puberty in female mice. Together, these results suggest that leptin is not a metabolic trigger for the onset of puberty in the rodent; instead, leptin is one of several permissive factors, whose presence may be necessary but alone is not sufficient to initiate sexual maturation in these species.

Animals↗

PubMed2000

Domestic violence.

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Confidentiality↗

PubMed1999

Evaluation of the effect of peptidyl membrane-interactive molecules on avian coccidia.

This study examined the lytic effect of seven different synthetic peptidyl membrane-interactive molecules (Peptidyl-MIMs) on sporozoites of five different species of Eimeria infecting chickens and merozoites of two different species that infect chickens. All Peptidyl-MIMs (pMIMs) demonstrated antiparasitic effects at concentrations of 1-50 microM during incubation periods varying from 1 to 20 min. In addition, electron microscopy showed that ultrastructural degeneration of the pellicle of sporozoite stages of the parasites occurred within 5-10 min of exposure to 5-microM concentrations of three different pMIMs. Pore-like openings were seen in the pellicle of the sporozoites at the ultrastructural level, which indicated that the pMIMs had the same mechanism of action on the parasites as that reported from studies done on bacteria. A reduction in lesion scores was seen in chickens treated orally with 10-, 50-, or 75-microM concentrations of two different proteolytic stabilized (methylated) pMIMs after challenge with three different species of avian coccidia in battery-cage trials. Collectively these data indicate that pMIMs may be useful in the control of coccidiosis in poultry.

Animals↗

PubMed1997

Regulation of hypothalamic proopiomelanocortin mRNA by leptin in ob/ob mice.

The hormone leptin acts on the brain to regulate feeding, metabolism, and reproduction; however, its cellular targets and molecular mechanisms of action remain to be fully elucidated. The melanocortins, which are derived from the precursor proopiomelanocortin (POMC), are also implicated in the physiological regulation of body weight. POMC-containing neurons express the leptin receptor, and thus it is conceivable that the POMC gene itself may be part of the signaling pathway involved in leptin's action on the brain. Using in situ hybridization and computerized image analysis, we tested the hypothesis that the POMC gene is a target for regulation by leptin by comparing cellular levels of POMC mRNA in the hypothalamus among groups of leptin-deficient (ob/ob) mice, leptin-treated ob/ob mice, and wild-type controls. POMC mRNA levels were significantly reduced throughout the arcuate nucleus in vehicle-treated ob/ob mice relative to wild-type controls, whereas POMC mRNA levels in leptin-treated ob/ob mice were indistinguishable from wild-type controls. These observations suggest that one or more products of POMC serve as an integrative link between leptin and the central mechanisms governing body weight regulation and reproduction.

Animals↗

PubMed1997

Leptin is a metabolic gate for the onset of puberty in the female rat.

The timing of puberty onset in mammals is tightly coupled to the animal's nutritional and metabolic state. We conducted two experiments to test the hypothesis that leptin acts as a metabolic signal for the onset of puberty. In the first experiment, we administered leptin (6.3 micrograms/g twice daily) to a group of normal prepubertal female rats and compared their rate of sexual maturation to that of two control groups. The group of leptin-treated animals and one group of control animals were allowed to eat ad lib, while the other group of control animals was pair-fed to the leptin-treated group. Food intake in the leptin-treated group was reduced to approximately 80% of the ad lib-fed control group, resulting in retarded growth in both leptin-treated and pair-fed animals. All measured indices of pubertal maturation-age at vaginal opening, age at first estrus, ovarian weight, ovulatory index (corpora lutea/ovarian section), uterine weight, and uterine cross-sectional area-were significantly delayed in the pair-fed group but not different between the leptin-treated group and ad lib-fed controls. The second experiment was similar to the first, except that both the leptin-treated group and the pair-fed group were fed at 70% of the ad lib-fed controls. Under these conditions, leptin only partially reversed the delay in sexual maturation, as reflected by the age at vaginal opening and first estrus. These results suggest that leptin is not the primary signal that initiates the onset of puberty but that instead, it acts in a permissive fashion, as a metabolic gate, to allow pubertal maturation to proceed-if and when metabolic resources are deemed adequate; moreover, these observations suggest that other metabolic factors, besides leptin, influence the timing of puberty onset under conditions of more severe dietary stress.

Animals↗

PubMed1994

Effects of estrogen on the number of neurons expressing beta-endorphin in the medial basal hypothalamus of the female guinea pig.

The distribution pattern of immunoreactive beta-endorphin neurons was studied in female guinea pigs that were ovariectomized, and one week later were injected with 25 micrograms estradiol benzoate or oil. The animals (5 from each group) were perfused after 24 hours with 4% paraformaldehyde. The locations of beta-endorphin cells and fibers were determined using avidin-biotin immunohistochemistry on free-floating vibratome sections. beta-endorphin-immunoreactive fibers were distributed widely throughout specific regions of the rostral forebrain, similar to what has been described in other species. beta-endorphin cell bodies were found in the arcuate nucleus and in adjacent ventrolateral areas throughout the rostrocaudal extent of the basal hypothalamus. Cells immunoreactive to beta-endorphin were also present in the caudal part of the ventromedial nucleus of the hypothalamus. The number of beta-endorphin neurons was quantified in anatomically matched sections through the rostral, medial and caudal basal hypothalamus of estradiol benzoate- and oil-treated guinea pigs. Analysis of variance revealed that the number of immunoreactive beta-endorphin cells was significantly increased in all regions of the basal hypothalamus of estrogen-treated guinea pigs as compared to vehicle-treated animals (P < 0.01). These data indicate that in the guinea pig, the number of neurons expressing beta-endorphin is increased in the arcuate nucleus 24 hours after estrogen treatment.

Animals↗

PubMed1993

Idazoxan decreases estrogen-induced lordosis in female but not "hormone-independent" lordosis in male guinea pigs of an inbred strain.

This experiment examined whether the imidazoline idazoxan (which binds to alpha-noradrenergic receptors and to imidazoline-preferring sites) interferes with hormone-dependent or hormone-independent lordosis responses. Ovariectomized (ovx) Strain 2 female guinea pigs which were sexually receptive after receiving estradiol benzoate (EB; 3 micrograms/d for 3 days) were injected with either idazoxan (10 mg/kg) or with vehicle at 24 hr after the last EB injection. Idazoxan significantly decreased EB-facilitated lordosis responses in these females. Castrated Strain 2 males, which show lordosis behavior without gonadal hormone administration, were injected with the same dosage of idazoxan (10 mg/kg) or with vehicle. Idazoxan did not inhibit lordosis behavior in these males.

Adrenergic alpha-Antagonists↗

PubMed1993

Age-related deficits in brain estrogen receptors and sexual behavior of male rats.

Neural estrogen receptors (ER), serum testosterone (T), estradiol (E2) and luteinizing hormone (LH), and masculine sexual behavior were measured in young (5 months) and old (24 1/2 months) Fischer 344 male rats. We found that old intact males, which displayed significantly lower levels of sexual behavior, T, and LH than young intact males, also had lower levels of nuclear ER (ERn) in the amygdala (AMG). The age difference in ER binding did not appear to be a consequence of altered blood E2 levels because circulating E2 did not differ between the two age groups. Gonadectomy eliminated ejaculatory behavior and significantly reduced ERn in young males. When we administered exogenous T to gonadectomized males in doses that approximated levels found in young intact males, we found that sexual performance of old males was stimulated to precastration levels but not to levels found in young males. Moreover, such treatment failed to increase ERn in the AMG of old males to the levels measured in the AMG of young males. These results suggest that there is an association between the inability of T to increase ERn concentration in the AMG and the deficits in sexual performance that are characteristic of old males. Thus, the capacity of neural tissue to bind estrogen, presumably derived from circulating T, may be a limiting factor in the determination of androgen responsiveness in aging males.

Aging↗

PubMed1992

Monochromatism determined at a long-wavelength/middle-wavelength cone-antagonistic locus.

The foveal increment threshold spectral sensitivity function for a 500 msec raised cosine stimulus without spatial edges exhibits a sharp drop or "notch" in sensitivity that coincides with the wavelength of a long-wavelength adapting field. An appropriate name for this phenomenon is the "Sloan notch", after Louise Sloan, who first observed a notch in a foveal threshold spectrum. We have examined suprathreshold discriminability on both sides of the Sloan notch produced by a 6700 td, 578 nm adapting field. In a temporal two-alternative forced-choice paradigm, a suprathreshold 650 nm low-frequency "standard" stimulus was paired with low-frequency "test" stimuli, of wavelength between 600 and 670 nm and varied intensity; the observer's task was to identify the interval containing the standard. Discriminability of the test and standard typically dropped to chance for some particular test intensity, producing "indiscriminability action spectra", up to 0.7 log units above threshold. Truncated spectra (between about 530 and 560 nm) were also obtained from observers on the middle wavelength side of the Sloan notch, for a 550 nm standard. The indiscriminability action spectra of each observer were identical, up to scaling, with the observer's threshold action spectrum. Analysis of the action spectra shows that the indiscriminable stimuli are rendered equivalent at the input to a neural pathway where L- and M-cone signals converge with opposite sign. We also investigated discriminability in the spectral region containing and immediately surrounding the Sloan notch. Suprathreshold stimuli in the spectral region near the notch produce percepts that are always discriminable from 650 and 550 nm standards (and from one another), and thus we conclude that in this spectral region, perception is mediated in part by a pathway distinct from that which signals the standards. The action spectrum of this latter pathway was estimated with a variant of the discrimination procedure, and found similar to V lambda over the spectral region 575-610 nm.

Adaptation, Ocular↗

PubMed1991

Effects of prenatal antiandrogen treatment on masculinization and defeminization of guinea pigs.

Gonadectomized (gdx) guinea pigs which had received the antiandrogen flutamide prenatally were tested for female-typical and male-typical sexual behavior in adulthood. In tests for lordosis behavior, gdx males and females were injected with estradiol benzoate and progesterone. Prenatally flutamide-treated females showed a longer mean lordosis response than control females. This was true whether they were given either a high or a low dose of EB. No male ever showed a lordosis response. In tests for male-typical sexual behavior, gdx adult males were treated with testosterone propionate and tested with stimulus females. The prenatally flutamide-treated males showed significantly decreased levels of ejaculation, a lower intromission rate and a decreased percentage of mounts which included pelvic thrusts, when compared to control males. Mount rate and rate of pericopulatory behavior did not differ between the flutamide and control males. The fact that prenatal administration of flutamide increased female-typical behavior in adult females suggests that the female guinea pig is normally partially defeminized by androgens in utero. The male guinea pig appears to be resilient to attempts to block defeminization with prenatal antiandrogens. However, some aspects of masculinization can be blocked.

Androgen Antagonists↗

PubMed1991

Adjunctive lithium carbonate in nortriptyline-resistant elderly depressed patients.

Recent reports supporting the use of lithium carbonate as an adjunct to tricyclic antidepressants for the treatment of refractory depression have not utilized standardized tricyclic antidepressant therapy, nor have they addressed the efficacy of lithium augmentation in a geriatric population. A 3-week open trial was added to the medication regimen of 15 elderly depressed inpatients who had already failed 4 weeks of therapeutic levels of nortriptyline. Treatment response was determined by the 17-item Hamilton Rating Scale for Depression (HAM-D). Two of 15 partial responders before lithium augmentation became complete responders. Of the remaining 13 "nonresponders" before lithium augmentation, one had a complete response, 7 had a partial response and 5 remained nonresponders. Although there was a mean HAM-D change of 8.3 points after lithium augmentation (24.7 +/- 5.9 to 16.4 +/- 6.8, p less than .001), when considering the previously reported similar efficiency of extended nonaugmented nortriptyline, these data do not strongly support lithium augmentation in elderly subjects who fail to respond after 4 weeks of nortriptyline. Further study is needed to determine what role, if any, lithium augmentation should play in the treatment of geriatric depression.

Aged↗

PubMed1990

Factor analysis and preliminary validation of the mini-mental state examination from a longitudinal perspective.

The Mini-Mental State Examination (MMSE) is a commonly used instrument for assessing mental impairment. Previous proposals for its underlying structure have focused on scores obtained from a single administration of the test. Because the MMSE is widely used in longitudinal studies, we examined the pattern of relations among the rates of chance of the items. Data were obtained from 63 subjects for 1.5 years or more. The relations among the rates of change of the MMSE items were described by a five-factor solution that accounted for 75% of the variance and comprised factors pertaining to orientation and concentration, obeying commands, learning and repetition, language, and recall. This was in contrast to the structure of the scores obtained from a single administration of the MMSE, which was best described by a two-factor solution. In order to provide a clinical validation, factor scores derived from the MMSE factors were used to predict scores on the Memory and Behavior Problems Checklist and the Brief Cognitive Rating Scale.

Aged↗

PubMed1989

Sex differences in cytosolic progestin receptors in microdissected regions of the hypothalamus/preoptic area of guinea pigs.

Cytosolic progestin receptors (CPRs) were measured in microdissected nuclei of the hypothalamus and preoptic area of male and female guinea pigs. Adult gonadectomized animals were given 3 daily injections of 20 micrograms/day estradiol benzoate (EB) or oil vehicle. 24 h later, animals were sacrificed and cytosolic progestin receptors were measured using the synthetic progestin 3H-R5020. CPR levels did not differ significantly between oil treated males and oil treated females in any brain areas examined. With EB treatment, males showed significant increases in CPRs in most of the brain areas in which females showed increases, i.e. in the medial preoptic area, the periventricular part of the preoptic area, the periventricular part of the anterior hypothalamus, the ventromedial nucleus of the hypothalamus, the periventricular part of the medial hypothalamus and the arcuate-median eminence. However, EB treated males showed significantly lower CPR levels than EB treated females in both the periventricular part of the preoptic area and the periventricular part of the medial hypothalamus.

Animals↗

PubMed1989

Alpha 1 noradrenergic antagonism decreases hormonally-induced and hormonally-independent lordosis.

Manipulations of the alpha noradrenergic (NE) system affect both lordosis and the concentration of hypothalamic steroid receptors. The present studies explored whether NE affects lordosis in guinea pigs via changes in hypothalamic estrogen or progestin receptors or through some other mechanism. The alpha 1 NE antagonist prazosin blocked lordosis which was induced with estradiol benzoate (EB) followed by progesterone (P), lordosis which was induced by EB alone and lordosis which is not dependent upon gonadal hormones for its display. These results suggest that NE modulation of lordosis in the guinea pig is not exerted solely through progestin receptors or estrogen receptors. Because prazosin blocked hormonally-independent lordosis, it is apparent that the NE system modulates some nonhormonal component of lordosis in guinea pigs.

Animals↗

PubMed1989

Different roles of alpha-noradrenergic receptor subtypes in regulating lordosis.

Ovariectomized guinea pigs were given free estradiol (E) at hr 0 and 28, and progesterone (P) at hr 39. Experiment 1: The alpha-1 noradrenergic antagonist prazosin, but not the alpha-2 noradrenergic antagonist idazoxan, prevented display of lordosis behavior when administered systemically 30 min prior to E injections at either hr 0 or 28, or 30 min prior to both injections. Experiment 2: Multiple injections of idazoxan (i.e., 30 min prior to and 60 and 120 min after each E injection) failed to prevent display of lordosis. Experiment 3: E-primed animals were given a single injection of idazoxan 1 hr before P, or 5 hr after P. In those animals given idazoxan 1 hr before P, display of lordosis was not prevented. However, in animals given idazoxan once lordosis display had begun (i.e., 5 hr after P) ongoing lordosis behavior was blocked. These data suggest differential roles of alpha-noradrenergic receptor subtypes in regulation of lordosis: noradrenergic transmission through the alpha-1 subtype may mediate hormone-priming processes leading to lordosis, whereas transmission through the alpha-2 subtype may modulate ongoing lordosis responses.

Adrenergic alpha-Antagonists↗

PubMed1988

Facilitation of lordosis in guinea pigs by an alpha-noradrenergic agonist is independent of progestin receptor stimulation.

Because manipulations of the noradrenergic system affect both lordosis behavior and progestin receptor levels in female guinea pigs, the present study attempted to determine if the noradrenergic (NE) system affects lordosis solely because of its impact on progestin receptors. Although the progestin receptor antagonist RU486 significantly reduced progesterone-facilitated lordosis, it had no effect on lordosis induced by the alpha-NE agonist clonidine in estrogen-primed female guinea pigs. This indicates that although progesterone may facilitate lordosis in female guinea pigs via activation of progestin receptors, the alpha-noradrenergic agonist clonidine does not mediate lordosis through the same mechanism.

Animals↗

PubMed1988

Subjective health in relation to aging and disease in a representative sample at ages 70, 75 and 79.

This study explores the relationship between perception of health in 70-79-year-olds and documented functional ability/disability as well as prevalence of definable disorders. Two thirds of both men and women declared themselves healthy at age 70, 2/3-3/4 at age 75 and 3/4 at age 79. Subjective health correlated significantly with the results of an extensive clinical examination for men at age 75 and for women at ages 75 and 79. In both sexes the correlation coefficients between the number of definable diseases and subjective health scoring was statistically significant as well as between mortality and subjective health. Some correlations were also found between subjective health and certain parameters of organ system functions. Contrary to objective findings, the proportion of those who declared themselves healthy was not decreasing by increasing age, and sex difference in consumption of care was not reflected in any sex difference in subjective health. The correlation between subjective health and number of disorders illustrates that the subjective health answers were influenced by knowledge obtained at previous clinical examinations and from drug prescriptions. Many elderly with functional disorders and drug treatment reported, however, that they were well. Subjective evaluation of health seemed to be markedly influenced by their willingness to accept impairment, disability and handicaps as being normal for their age.

Aged↗