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L Olson

Publications and source records attributed to L Olson.

At least 127 records · Page 7Linked to original sources
PubMed1997

Lingual deficits in BDNF and NT3 mutant mice leading to gustatory and somatosensory disturbances, respectively.

A combination of anatomical, histological and physiological data from wild-type and null-mutated mice have established crucial roles for BDNF and NT3 in gustatory and somatosensory innervation of the tongue, and indeed for proper development of the papillary surface of the tongue. BDNF is expressed in taste buds, NT3 in many surrounding epithelial structures. Absence of BDNF in mice leads to severely malformed taste bud-bearing papillae and severe reduction of taste buds, a loss of proper innervation of remaining taste buds and a loss of taste discrimination although not of the suckling reflex per se. In contrast, absence of NT3 leads to a massive loss of somatosensory innervation of lingual structures. These findings demonstrate distinct roles for BDNF and NT3 in the establishment of the complex innervation apparatus of the tongue with non-overlapping roles for the lingual gustatory and somatosensory systems. The distinction between different sensory modalities, being dependent on either BDNF or NT3 may also have clinical implications.

Animals↗
PubMed1997

Immunological aspects of kaolin-induced hydrocephalus.

Adult female Sprague Dawley rats were administrated 0.1 ml Kaolin (250 mg/ml) into cisterna magna. One, 4 and 8 weeks later, brains were analyzed using antibodies against MHC class I (OX18), MHC class II (OX6), CD4 (OX38), CD8 (OX8), OX42, ED1, NF, GFAP, AChE and TH. Remarkably high numbers of T lymphocytes, and OX42- and ED1-positive macrophages were found aggregated in subarachnoid spaces, and in the third and fourth ventricles. Marked aggregations of ED1-positive reactive microglial cells were also found in paraventricular structures, medial septum, retrosplenic cortex and commissural structures. However, no such cells were found in hippocampus. ED1-positive areas were also positive for round cells with a rim of MHC I fluorescent cytoplasm as well as for OX42-positive cells and MHC II positive microglial cells. At week 1, in ventro-frontal areas of cortex, CD8-positive cells and MHC I positive astroglial fibers were detected. At week 1, MHC I positive ramified microglial cells were also recognized in almost the entire brain. These positive cells gradually decreased with time and finally remained rounded with a rim of fluorescent cytoplasm. In addition, ED1 positive partly ramified microglial cells could be recognized in corpus callosum, probably representing cells in transition between ramified and reactive microglia. CD8+ cells entered ventral brain structures, and were found in the horizontal diagonal band at week 4, and had disappeared at week 8. Finally in cortex, ED1 positive microglial cells could be identified only in the retrosplenic cortex, and there were also "dark shrunken neurons" in light microscopic stainings. However, there was only a moderate GFAP positive gliosis. In conclusion, kaolin-induced hydrocephalus leads to immune reactions in several defined areas such as cholinergic systems, corpus callosum, circumventricular organs, pontine cerebellar peduncles and the vestibular nucleus.

Animals↗
PubMed1997

Trimethyltin exposure in the rat induces delayed changes in brain-derived neurotrophic factor, fos and heat shock protein 70.

Trimethyltin chloride (TMT) treatment in adult rats leads to limbic brain lesions that are detectable with classical neuropathological techniques 3 days after exposure. In particular, the hippocampal cells of the CA3c region are affected. The temporal and regional characteristics of TMT toxicity as reflected in changes of activity-dependent factors were studied in adult male Sprague-Dawley rats using quantitative in situ hybridization and immunohistochemistry. No significant alterations in the BDNF mRNA were detected in hippocampus and cerebral cortex 1 and 4 h after 8 mg TMT/kg. Three days after TMT, a significant increase in BDNF mRNA was detected in CA1, and increases in BDNF mRNA were also seen in cortical layers. An increase in BDNF hybridization signal was seen over scattered neurons within and outside CA3c at 3 days. Four h after 8 mg TMT/kg, BDNF immunoreactivity was reduced in the pyramidal cells of the CA3c and CA1 regions as well as in the dentate gyrus. No significant change in BDNF immunoreactivity was seen in hippocampus or cerebral cortex 3 days after TMT. BDNF interacts with the high-affinity receptor tyrosine kinase B (trkB). No immediate alteration in trkB mRNA was seen in hippocampus or cerebral cortex after 8 mg TMT/kg, while at 3 days trkB mRNA was significantly reduced in the CA3c pyramidal cell layer. No changes could be detected in neurotrophin-3 mRNA at either 1, 4 h or 3 days after TMT. Three days after 8 mg TMT/kg, a major induction of hsp70 mRNA occurred in a subset of neurons in the CA3c region, concomitant with an increased expression of c-fos mRNA as well as Fos protein in the hilar region of hippocampus. Hence, an early and transient decrease in BDNF appears to occur after TMT exposure, which is succeeded at 3 days by increases in BDNF, c-fos and hsp 70 mRNAs, concomitant with a decrease in trkB mRNA in regions known to be vulnerable to TMT. These results demonstrate that TMT causes a delayed, spatially restricted increase in activity-dependent gene expression, making TMT-induced disturbances an interesting model of neurodegenerative events.

Animals↗
PubMed1996

Differential expression of brain-derived neurotrophic factor and neurotrophin 3 mRNA in lingual papillae and taste buds indicates roles in gustatory and somatosensory innervation.

Although many studies have demonstrated the dependency of taste bud function and/or survival on intact innervation, relatively few have dealt with the development of taste bud innervation. Using in situ hybridization histochemistry, we show that brain-derived neurotrophic factor (BDNF) and neurotrophin 3 (NT3) mRNA are expressed in a specific pattern in the taste buds, tongue papillae, and lingual epithelium during development and that expression persists into adulthood. BDNF mRNA is expressed in a fraction of the taste cells of the developing and adult taste buds in rats, showing different labeling intensities among the labeled cells. NT3 and mRNA seems to be located in areas other than those where BDNF mRNA is expressed, mainly in the superior epithelial surfaces of circumvallate papillae, the outer surface epithelium of foliate papilae, the superior surface and the lateral epithelium of the fungiform papillae, and the epithelium of the filiform papillae. NT3 mRNA labeling is also observed among muscle and connective tissue of the tongue. The morphological appearance, expression of NT3 mRNA, and ramification of nerve fibers in defined epithelial structures in the posterior wall of the anterior filiform papillae suggest the existence of a mechanosensory apparatus in these papillae. Nerve growth factor and neurotrophin 4 probes did not give rise to selective labeling in tongue, although their presence cannot be totally excluded. Based on present and prior studies, we suggest that BDNF is needed during initiation and for maintenance of gustatory innervation of taste buds and gustatory papillae and that NT3 is mainly needed for somatosensory innervation of the tongue.

Animals↗
PubMed1996

Cellular expression of the immediate early transcription factors Nurr1 and NGFI-B suggests a gene regulatory role in several brain regions including the nigrostriatal dopamine system.

Nurr1 and NGFI-B are closely related orphan members of the steroid-thyroid hormone receptor family involved in immediate early responses to stimuli such as growth factors. In-situ hybridization in the developing and adult mouse and rat demonstrated Nurr1 mRNA in several regions during early central nervous system (CNS) development. Expression persisted through the pre- and postnatal periods and was also found in several areas in the adult CNS. Positive areas include the olfactory bulb, parts of the cortex, the hippocampal formation and substantia nigra where Nurr1 and tyrosine hydroxylase mRNAs were co-expressed. 6-Hydroxydopamine-induced degeneration of mesencephalic dopamine neurons led to a corresponding loss of Nurr1 mRNA, demonstrating a link between Nurr1 and dopaminergic neurons. NGFI-B mRNA was not found in the prenatal CNS but was highly expressed in the adult brain in many areas including the olfactory bulb, cortex, basal ganglia and hippocampus. The spatiotemporal distribution of Nurr1 and NGFI-B mRNAs suggests that these transcription factors are involved in the development and maturation of specific sets of CNS neurons. The experimental data imply that one of these functions may be to control gene regulatory events important for development and function of those neurons that degenerate in patients with Parkinson's disease.

Animals↗
PubMed1996

Spinal cord repair in adult paraplegic rats: partial restoration of hind limb function.

Complete spinal cord gaps in adult rats were bridged with multiple intercostal nerve grafts that redirected specific pathways from white to gray matter. The grafted area was stabilized with fibrin glue containing acidic fibroblast growth factor and by compressive wiring of posterior spinal processes. Hind limb function improved progressively during the first 6 months, as assessed by two scoring systems. The corticospinal tract regenerated through the grafted area to the lumbar enlargement, as did several bulbospinal pathways. These data suggest a possible repair strategy for spinal cord injury.

Animals↗
PubMed1996

Interactions of neurotrophic factors GDNF and NT-3, but not BDNF, with the immune system following fetal spinal cord transplantation.

Glial cell line-derived neurotrophic factor (GDNF) is known to stimulate survival of dopaminergic and spinal cord motor neurons. However, little is known of the possible immune sequelae of GDNF exposure, or that of other putative trophic factors. To address these questions we utilized in oculo grafts of spinal cord, wherein we could induce different levels of immune responses via allogeneic vs. syngeneic combinations. Adult female Sprague-Dawley and Fisher rats were used as hosts for allogeneic and syngeneic grafts, respectively. Embryonic age 14-15-day-old fetuses were taken from pregnant dams of each strain, and cervical spinal cords were removed and dissected. Pieces of the spinal cord were transplanted into the anterior chamber of the eye within each strain. At 5-day intervals, 0.5 microgram of GDNF, brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3) or cytochrome c (CC) was injected into the anterior chamber of the eye and the sizes of the transplants were measured for the Sprague-Dawley rats. The same injections and measurements, but only for GDNF and CC, were carried out using Fisher rats. As expected, GDNF increased transplant survival and growth in both the Sprague-Dawley and Fisher animals. At day 41-42, all rats were sacrificed. Cameral graft appearance was evaluated by cresyl violet and immunohistochemically using antibodies against neurofilament (NF), calcitonin gene-related peptide (CGRP) and glial fibrillary acidic protein (GFAP). To monitor immune responses, the following monoclonal antibodies were used: OX38 against CD4, OX18 against MHC class I (MHCI), OX8 against CD8, OX6 against MHC class II (MHCII), OX42 against CD11b, R73 against alpha and beta T cell receptor (TcR), and ED1. In the Sprague-Dawley grafts, significantly higher amounts of CD8+, T lymphocyte+, MHCI+ and MHCII+ antigen-presenting cells (APC) were observed in GDNF-treated transplants. These markers were also increased in NT-3-treated groups. There were two types of OX-42+ cells, one was the ordinary ramified microglial cell, the other appeared to be a phagocytic cell, looking like the interstitial proliferating variety. Interestingly, the phagocytic OX-42+ cells had the same distribution as ED1+ and MHCII+ cells. In contrast, there were few immunoreactive cells after GDNF treatment in the inbred Fisher animals, similar to the CC control group. These results suggest that GDNF and to some extent NT-3, can activate the immune system in allogeneic graft combinations, but that these trophic factors do not produce overt rejection, and do not per se induce immune responses.

Animals↗
PubMed1996

Microglial cell responses to fetal ventral mesencephalic tissue grafting and to active and adoptive immunizations.

Microglia express cytokines, major histocompatibility (MHC) loci, and several other immunologically important constituents. The aim of this study was to detect immunological responses of microglial cells following allogeneic dopaminergic transplantation using active and adoptive immunizations. Adult inbred Fisher 344 (F344 RT1) rats were unilaterally dopamine (DA) depleted in striatum by injection of 6-hydroxydopamine. The degree of degeneration was assessed by recording the rotational response to apomorphine. Fetal ventral mesencephalic tissue containing DA neuroblasts from Wistar-Furth (WF, RT1u) rat donors (9-12 mm CRL) were later implanted in striatum on the lesioned side. Lymph nodes and spleen cells were collected aseptically, resuspended, and diluted for isovolumetric injections. Animals selected for active immunization were injected intraperitoneally with varying amounts of WF lymphocytes. Animals selected for adoptive immunization (transferred immunity) were intraperitoneally injected with 10(8) F344 lymphocytes prepared from animals actively immunized 3 weeks previously. Monoclonal antibodies against CD4 (OX38), CD8 (OX8), CD11b (OX42), MHC class I (OX18), monomorphic MHC class II (OX-6), and ED1 and polyclonal antibodies against tyrosine hydroxylase (TH) were used for immunohistochemistry. We found that the degree of ED1-positive cell proliferation was well correlated to the immunization patterns. Groups that were actively immunized with or without prior adoptive immunization had a larger amount of reactive microglial proliferation. ED1 immunohistochemistry revealed patterns of immunolabeling of engrafted areas: 8-12 weeks after grafting in nonimmunized and adoptively immunized groups reactive microglial proliferation occurred only at the graft periphery. Active and adoptive + active immunization led to ED1-IR within the grafts themselves. At early stages nonimmunized groups had an ED1 pattern which was partially inside the grafts. At early time points nonimmunized groups contained ameboid microglial cells within the grafts which disappeared at later stages and were absent in the immunized groups. ED1-positive ameboid microglial cells within the grafts may be of graft origin and constitute a part of a continued normal development of the fetal tissue.

Animals↗
PubMed1996

Habrec1, a novel serine/threonine kinase TGF-beta type I-like receptor, has a specific cellular expression suggesting function in the developing organism and adult brain.

Members of the TGF-beta superfamily signal through a dual receptor system consisting of a type II receptor protein kinase that binds the ligand, after which this complex associates with a type I receptor to mediate intracellular signaling. In mammals, six type I and five type II receptors mediating responses to different TGF-beta family members have been identified to date. Using primers from conserved regions of the protein kinase domain of the serine/threonine kinase receptors in a low-stringency polymerase chain reaction-based screening procedure, and deselecting known receptors with colony hybridization, we now report cloning a novel receptor member. The novel receptor was found in a cDNA library prepared from the habenular nucleus area and was designated Habrec1. Although only a partial sequence is available, it fits the criteria for a TGF-beta type I serine/threonine kinase receptor. In situ hybridization of Habrec1 reveals mRNA expression in several distinct areas of the developing central nervous system, including cortex cerebri, cerebellum, hippocampus, striatum, and thalamic nuclei. Expression is also seen in the anterior pituitary. In the periphery, strong expression prenatally includes brown fat, the gastrointestinal tract, liver, pancreas, thymus, and nasal cavity epithelium. In the adult brain Habrec1 mRNA is prominently found in cerebellum, cortex cerebri, and striatum, but at lower levels in several additional areas. We conclude that Habrec1 is a member of the TGF-beta type I receptor family with expression patterns in the developing animal, suggesting specific functions in and outside the nervous system, and in the adult CNS, suggesting roles in both cortical and subcortical brain circuitry.

Adipose Tissue, Brown↗
PubMed1996

Microdialysis: a way to study in vivo release of neurotrophic bioactivity: a critical summary.

Microdialysis has been proven to be a valuable tool to study in vivo release of various neurotransmitters in the rat brain. Recently we demonstrated for the first time the release of neurotrophic bioactivity in the brains of awake rats. Neurotrophic factors, however, exist in extremely low concentrations in the brain compared to neurotransmitters, rendering their detection particularly difficult. This review summarizes knowledge about the use of microdialysis for the detection of neurotrophic bioactivity, its limits, and its problems.

Animals↗
PubMed1996

Differential immune responses to fetal intracameral spinal cord and cortex cerebri grafts.

While the central nervous system (CNS) has been characterized as an immunologically privileged site, there are also several reports describing immunological reactions within the CNS. A certain degree of immunological privilege has also been ascribed to the anterior chamber of the eye. We have used the intraocular transplantation model to study immunological reactions in transplants of embryonic neural tissue. Outbred Sprague-Dawley rats and inbred Fisher rats were used. Pieces of rat parietal cortex or the cervical spinal cord were prepared from embryonic day 14 and implanted into the eye chambers of adult rats of the same strain. Following intraocular maturation, grafts were analysed using antibodies against: major histocompatibility complex (MHC) class I, MHC class II; rat antigens CD4, CD8, CD11b; T-cell receptor; rat antigen ED1; and glial fibrillary acidic protein. Using this set of markers for immunological reactions, transplants were scored on a blind basis. We found no significant differences in immunological scores between transplants obtained from different litters of fetuses of the outbred animals. Grafting in the outbred strain led to increased numbers of immunologically reactive cells in the grafts. This was not seen in grafts in the inbred strain. Spinal cord transplants led to a significantly higher degree of cytotoxic immunity-related cells expressing MHC class II as well as CD4-positive cells. There was a positive correlation between ED1 negativity and well-developed ramified microglia. From these results we conclude also that well-developed intraocular CNS tissue grafts do contain cellular evidence of immunological events and that different areas of the CNS may provoke different degrees of response. Reactive microglial proliferation appears to be one of the most sensitive ways to monitor the immunological condition of grafted CNS tissue.

Animals↗
PubMed1996

Cellular hybridization for BDNF, trkB, and NGF mRNAs and BDNF-immunoreactivity in rat forebrain after pilocarpine-induced status epilepticus.

The messenger RNAs (mRNAs) for the neurotrophins, brain-derived neurotrophic factor (BDNF), and nerve growth factor (NGF), are upregulated during epileptic seizure activity, as visualized by in situ hybridization techniques. Neurotrophins might be protective against excitotoxic cell stress, and the upregulation during seizures might provide such cell protection. In this study, a high dose of pilocarpine (300 mg/kg) was used to induce long-lasting, limbic motor status epilepticus and a selective pattern of brain damage. The regulation of BDNF, trkB, and NGF mRNA was studied by in situ hybridization at 1, 3, 6, and 24 h after induction of limbic motor status epilepticus. BDNF immunoreactivity was examined with an anti-peptide antibody and the neuropathological process studied in parallel. BDNF mRNA increased in hippocampus, neocortex, piriform cortex, striatum, and thalamus with a maximum at 3-6 h. Hybridization levels increased earlier in the resistant granule and CA1 cells as compared to the vulnerable CA3 neurons. BDNF immunoreactivity was elevated in dentate gyrus at 3-6 h. trkB mRNA increased in the entire hippocampus. NGF mRNA in hippocampus appeared in dentate gyrus at 3-6 h and declined in hilar neurons at 6-24 h. Cell damage was found in the CA3 area, entire basal cortex, and layers II/III of neocortex. Endogenous neurotrophins are upregulated during status epilepticus caused by pilocarpine, which is related to the coupling between neuronal excitation and trophic factor expression. This upregulation of neurotrophic factors may serve endogenous protective effects; however, the excessive levels of neuronal hyperexcitation resulting from pilocarpine seizures lead to cell damage which cannot be prevented by endogenous neurotrophins.

Animals↗
PubMed1996

Cellular expression of GDNF mRNA suggests multiple functions inside and outside the nervous system.

Glial-cell-line-derived neurotrophic factor (GDNF) is a distant member of the transforming growth factor-beta family and has potent neurotrophic effects on several classes of neurons including dopamine neurons and motoneurons. Here, we have used in situ hybridization to describe the development of the cellular expression of GDNF mRNA pre- and postnatally. Consistent with dopaminotrophic activity, GDNF mRNA is expressed in the developing basal ganglia and the olfactory tubercle. It is also found in a thalamic nucleus, in neurons of the substantia innominata, in the developing Purkinje neurons and the developing locus coeruleus area, and in trigeminal brainstem nuclei. In the spinal cord, neuronal expression is found in Clarke's column. GDNF mRNA is also expressed in the dorsal horns during development. Additional GDNF mRNA expression in the head region includes the carotid body, the retina, the vibrissae, the inner ear, the ear canal, and epithelium in the nasal cavity. Prominent expression is also found in the developing teeth. The widespread expression of GDNF in developing skeletal muscle is consistent with trophic activity on alpha-motoneurons. The smooth muscle layers of the gastrointestinal tract are also strongly positive. A very strong signal is found in the outer mesenchyme of the developing metanephric kidney. We conclude that GDNF mRNA is expressed in many different cellular systems inside and outside the central nervous system during development, suggesting multiple functions of GDNF in the developing organism.

Animals↗
PubMed1996

Glial cell line-derived neurotrophic factor enhances survival and growth of prenatal and postnatal spinal cord transplants.

Glial cell line-derived neurotrophic factor was first described as a trophic factor for developing dopamine neurons. However, it has been shown that glial cell line-derived neurotrophic factor messenger RNA is also expressed in several areas of the developing brain and spinal cord, suggesting that it may have additional roles in the nervous system. Intraocular transplantation of neural tissue provides a unique method to examine in vivo effects of trophic factors. We have therefore studied the effects of glial cell line-derived neurotrophic factor on spinal cord survival and development following grafting to the anterior chamber of the eye of adult rats. We used spinal cord tissue from fetal stages (embryonic days 14 and 18) and postnatal days 1 and 14 as donors. The spinal cord tissue was allotransplanted to the anterior eye chamber of Sprague-Dawley host rats after incubation in buffered saline containing 100 micrograms glial cell line-derived neurotrophic factor/ml or 100 micrograms cytochrome C/ml. One group of postnatal day 1 spinal cord grafts was also treated with concentrations of 20 and 10 micrograms glial cell line-derived neurotrophic factor/ml. In all cases, 5 microliters of the same solution was injected into the anterior eye chamber on postgrafting days 5, 10, 15 and 20 (total amounts 0.5, 0.1 and 0.05 microgram/eye/injection, respectively). We found that all glial cell line-derived neurotrophic factor-treated spinal cord grafts grew more than controls. The effect of glial cell line-derived neurotrophic factor was most prominent in grafts from newborn rats. In these grafts we found a dose-dependent effect of glial cell line-derived neurotrophic factor on growth. Moreover, grafts treated with the highest dose (0.5 microgram) grew to sizes exceeding the initial size at transplantation. In these transplants we also found greater numbers of large neurons compared to controls. Glial fibrillary acidic protein immunoreactivity, in contrast, showed increased gliosis in controls. Similar results were found with syngeneic spinal cord postnatal day 1 grafts in Fisher hosts. Spinal cord tissue grafts from two-week-old rats treated with the highest glial cell line-derived neurotrophic factor dose every fifth day, through day 35 postgrafting, responded with increased growth and less necrotic tissue compared with controls; however, we could not detect neurofilament immunoreactivity in these transplants. Taken together, these results suggest that glial cell line-derived neurotrophic factor may be a potent trophic factor for neurons in the spinal cord and in spinal cord transplants. Of particular importance is that glial cell line-derived neurotrophic factor treatment can be used to obtain survival of postnatal spinal cord tissue, that would otherwise show minimal or no survival. Thus, glial cell line-derived neurotrophic factor allows successful transplantation of more mature spinal cord tissue, which may have important implications for both basic and clinical neuroscience.

Animals↗
PubMed1996

Comparative study of brain-derived neurotrophic factor messenger RNA and protein at the cellular level suggests multiple roles in hippocampus, striatum and cortex.

Brain-derived neurotrophic factor (BDNF) is important for the development and trophic support of several neuronal groups in the rat. In the present study, the distribution of BDNF messenger RNA was studied by in situ hybridization, and the cellular localization of BDNF protein was investigated with anti-peptide antibodies. Anatomical investigations were also made in animals with prolonged epileptic seizures which show an enhanced expression of BDNF messenger RNA. Major forebrain areas studied were the hippocampus, striatum and cortex. The messenger RNA coding for the putative high-affinity receptor, tyrosine kinase B, was also visualized using in situ hybridization with a probe specific for the full-length form. In the hippocampus, granule cells and pyramidal neurons expressed BDNF messenger RNA and BDNF-like immunoreactivity. Interneurons in dendritic layers did not show labelling with either method. Tyrosine kinase B messenger RNA was found within neurons in all these regions. In the medial septum-diagonal band, nucleus basalis and lateral hypothalamus, neurons with punctate cytoplasmic immunofluorescence were found, and neurons in the lateral septum were diffusely positive for BDNF. In striatum, positive labelling of medium-sized neurons was found with the antibody, whereas BDNF messenger RNA was only detectable during seizures. A laminar pattern of neuronal labelling for BDNF messenger RNA and protein was found in the neocortex. The analysis of the anatomical distribution of BDNF-producing cells suggests a number of possible cellular interactions. In the hippocampus, BDNF might act in an autocrine or paracrine manner for granule cells and pyramidal neurons, and, in addition, may serve as a signal from these principal cells to interneurons. BDNF could be a target-derived and a locally produced trophic factor for cholinergic neurons in the medial septum. The expression of BDNF in the striatum suggests that this factor could be a target-derived factor for dopaminergic neurons of substantia nigra and/or work as an autocrine/ paracrine factor within the striatum itself.

Animals↗
PubMed1996

Increasing emergency physician recognition of domestic violence.

STUDY OBJECTIVE: To determine whether recognition of domestic violence in the emergency department is affected by restructuring of the ED chart to include a specific question about domestic violence, to evaluate whether training concerning domestic violence further increases its recognition, and to develop a profile of women who present to the ED as a result of domestic violence. METHODS: We collected prospective data on all females aged 15 to 70 years who presented to an urban Level I trauma center during a 3-month period. Two keywords were used to define domestic violence: (1) mechanism (eg, kicked, hit, pushed) and (2) perpetrator (eg, current/former boyfriend, spouse). We used the first month to define the baseline number of domestic violence cases. We modified charts in the second and third months (intervention months) to include, "Is the patient a victim of domestic violence?" In addition, the third month included a 1-hour educational lecture on the identification of domestic violence in the ED. RESULTS: We identified 123 cases of domestic violence from a survey population of 4,073: 25 (2.0%) in the baseline month, 49 (3.4%) in the chart-modification month, and 49 (3.6%) in the education month. The proportion of cases identified during the intervention months was 1.8 times higher than during the control month (relative risk [RR], 1.78; 95% confidence interval [CI], 1.15 to 2.75), but did not differ between each other (RR, 1.06; 95% CI, .72 to 1.57). Women identified as domestic violence cases ranged in age from 15 to 61 years (median, 28.5 years). Most of the identified domestic violence patients presented with a triage classification of assault (54.5%), trauma (8.1%), or abdominal complaints (7.3%). Triage complaint differed for domestic violence and non-domestic violence cases (chi 2 = 830; P < .0001). Nearly one third of domestic violence patients (31.7%) presented between 11 PM and 6:59 AM, compared with 19.0% of non-domestic violence patients (chi 2 = 12.4; P = .005). CONCLUSION: Modification of the chart significantly increased the recognition rate of domestic violence. An education intervention did not significantly improve this rate. The profile of a woman presenting to the ED differs from those of other women with respect to chief complaint and time of presentation.

Adolescent↗
PubMed1996

Safe at home? Domestic violence and other homicides among women in New Mexico.

STUDY OBJECTIVE: To define the contribution of domestic violence (DV) to homicides in women in New Mexico and to examine differences in ethnicity, mechanism, previous documented injuries, incidence of sexual assault, and use of alcohol or illicit drugs between DV- and non-DV-related homicides. METHODS: We carried out a retrospective analysis of reports of the state office of the medical investigator (OMI) reports from all female homicides from 1990 to 1993 in New Mexico. A homicide was defined as being related to DV if the perpetrator was a current or former male intimate partner. The chi-squared and Mann-Whitney tests were used to analyze data. RESULTS: The OMI investigated 134 homicides in women for an overall fatality rate of 4.3 per 100,000. A male intimate partner was the perpetrator in 62 cases (46%). The rate of DV homicide among American Indians (4.9 per 100,000) was significantly higher than that among Hispanics (1.7) and non-Hispanic whites (1.8)(RR=2.8; 95% confidence interval (CI), 1.5 to 5.1). Firearms were almost two times as likely to be used in DV homicides as in non-DV homicides (RR=1.8; 95% CI, 1.2 to 2.6). Evidence of old injuries was found more often in DV homicide cases (35.5%) than in non-DV cases (83%) (RR=4.3; 95% CI, 1.8 to 9.8). The presence of alcohol or other drugs was higher among non-DV homicide victims (69%) than DV homicide victims (54.3%) (P=.03). CONCLUSION: American Indian women are at particularly high risk of homicide, including DV homicide. Firearms were overrepresented in DV homicides, suggesting that removing firearms from the homes of previous DV perpetrators would be a useful public health strategy. Alcohol or illicit drugs were found in approximately two thirds of New Mexico women who were victims of homicide. The high prevalence of history of previous injuries among DV homicide victims indicates that early identification of DV victims in the emergency department and other health care settings is an important point of intervention.

Domestic Violence↗