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Biomedical subjects

Carol Anderson

Publications and source records attributed to Carol Anderson.

10 recordsLinked to original sources
PubMed2006

Impact of maternal mental health status on child mental health treatment outcome.

This study examined the effect of maternal depression and anxiety on child treatment outcome. Psychiatric assessments were conducted on 180 mother-child pairs when the child entered treatment in a community mental health center and six months later. Children whose mothers were depressed or anxious were significantly more impaired than children of mentally healthy mothers at both time points. Both groups of children improved at approximately the same rate. The findings suggest that early mental health screening of children and their mothers may be important preventive practices. Addressing the mental health needs of mothers and children simultaneously may be an effective method of reducing their mental health problems.

Adolescent↗
PubMed2006

Effect of maternal mental health problems on child treatment response in community-based services.

OBJECTIVE: Many mothers bringing children for community mental health treatment need mental health services themselves. Moreover, children of mothers with mental health problems enter treatment with more severe symptomatology than do other children. However, little is known about how maternal mental health problems affect children's response to treatment. This study examined the impact of maternal mental health status on the child's treatment response. METHODS: The mental health of 272 mother-child pairs was assessed twice, when children entered treatment at three community mental health clinics and again three months later. Analysis of variance was used to examine the impact of maternal mental health status on children's rate of improvement. RESULTS: Children of mothers with mental health problems had significantly greater behavior problems (F=34.54, p<.001) and demonstrated less improvement over time (F=4.44, p=.04) than children of mentally healthy mothers. CONCLUSION: These findings suggest that treatment for mothers as well as children could be beneficial for this population.

Adolescent↗
PubMed2005

Computer-based testing of the Braden Scale for Predicting Pressure Sore Risk.

The Detroit Medical Center nursing documentation system requires all staff nurses to complete the Braden Scale for Predicting Pressure Sore Risk on an Acute Care Flow Record or Critical Care Flow Sheet on every patient, every day. An audit of these records raised concern as to whether staff nurses accurately used the Braden Scale to calculate pressure sore risk. Advanced Practice and ET Nurses noted that staff nurses were rating patients at lower levels of pressure sore risk than was warranted by the patient condition. In response, a computer-based learning module with case study examples was developed and tested to teach nursing staff to accurately evaluate pressure ulcer risk by using the Braden Scale and its subscales and to identify preventive interventions based on the patient's Braden subscale scores. Following revisions of those case study example narratives that were found to be problematic, the learning/assessment module was instituted in 2002. More than 2,500 nurses at the facility were tested regarding their knowledge of pressure ulcer risk assessment and prevention using this program. On average, nurses correctly rated the Braden Scale level of risk 75.6% of the time. The percentage of correct responses was highest for very high (92%) and very low (78%) levels of risk. This finding is consistent with the observation that most nosocomial pressure ulcers in this facility occur in patients who are rated in the "mild risk" level on the Braden scale. Subscales with the lowest percentage of correct answers were moisture and sensory perception. Correct clinical identification of a Stage I pressure ulcer as it was described in writing occurred only 53% of the time. These results indicate that training and practice are needed to use an assessment scale accurately. The Detroit Medical Center plans to include the Braden Scale in annual nursing education and competency testing.

Clinical Competence↗
PubMed2004

Neuronal apoptosis is mediated by CXCL10 overexpression in simian human immunodeficiency virus encephalitis.

Inflammatory mediators play a crucial role in the pathophysiology of several neurodegenerative diseases including acquired immune deficiency syndrome dementia complex. In the present study we identified a link between CXCL10 overexpression in the brain and human immunodeficiency virus dementia and demonstrated the presence of the chemokine CXCL10 and its receptor, CXCR3, in the neurons in the brains of macaques with simian human immunodeficiency virus encephalitis. Using human fetal brain cultures, we showed that treatment of these cells with either SHIV89.6P or viral gp120 resulted in induction of CXCL10 in neurons. Cultured neurons treated with the chemokine developed increased membrane permeability followed by apoptosis via activation of caspase-3. We confirmed the relevance of these findings in sections of human and macaque brains with encephalopathy demonstrating that neurons expressing CXCL10 also expressed caspase-3.

Animals↗
PubMed2004

Cyclooxygenase-mediated generation of free radicals during hypoxia in the cerebral cortex of newborn piglets.

Previous studies have demonstrated that free radicals are formed under hypoxic conditions in newborn piglet brain. To test the hypothesis that the cyclooxygenase pathway serves as a source of free radical generation during hypoxia studies were performed on 24 piglets divided into four groups. Six saline (group 3) and six indomethacin treated (group 4) were exposed to hypoxia (FiO2 0.05-0.07) for 60 min. Cerebral hypoxia was documented biochemically by determination of ATP and phosphocreatine. Fluorescent compounds and conjugated dienes were determined as indices of lipid peroxidation. Free radical formation was determined by using n-tert butyl phenyl nitrone (PBN) as a spin trap agent and measuring spin adduct formation in duplicate using a Varian E-109 spectrometer. Groups 1 and 2 (normoxic) showed no spin adduct formation. Group 3 showed a significant increase in spin adduct formation compared to normoxia (372+/-125 vs. 63+/-15, P<0.001). Hypoxic animals pretreated with indomethacin had a spin adduct level of 197+/-132 and were similar to normoxic animals. ATP/PCr levels were the same in groups 3 and 4 denoting the same degree of cerebral hypoxia in all hypoxic animals. Conjugated dienes increased significantly during hypoxia as compared to normoxia (0.142+/-0.017 vs. 0.0+/-0.0) and were decreased insignificantly with indomethacin treatment. Fluorescent compounds were not significantly different among the four groups. Na+,K+-ATPase activity decreased during hypoxia but was not preserved in hypoxic animals pretreated with indomethacin. These data provide direct evidence of the presence of free radicals during hypoxia and the contribution of cyclooxygenase metabolism to their formation.

Animals↗
PubMed2004

Lateral rotation mattresses for wound healing.

Continuous lateral rotation therapy utilizes mattresses and beds that move the patient in a regular pattern around a longitudinal axis. Although these devices have been used for several decades for other medical purposes, literature is scant regarding their role in the treatment of skin breakdown in the bedridden, difficult-to-reposition patient. A descriptive study was undertaken to ascertain the rate of wound healing and number of weeks to achieve wound closure when continuous lateral rotation therapy was employed in patients with partial-thickness (n=10) and full-thickness (n=20) ulcers on the trunk or pelvis. Patients receiving the services of Advanced Therapy Surfaces in home or long-term care between March 15, 2002 and April 1, 2003 were enrolled. Partial-thickness wounds healed at an average rate of 16.68% per week, with an average time for continuous lateral rotation therapy of 9.25 weeks. Full-thickness wounds healed at an average rate of 14.38% per week (time to healing 11.25 weeks). No additional areas of skin breakdown were observed. These encouraging results suggest that additional research is warranted.

Beds↗
PubMed2003

Matrix metalloproteinase 1 interacts with neuronal integrins and stimulates dephosphorylation of Akt.

Several studies have demonstrated that matrix metalloproteinases (MMPs) are cytotoxic. The responsible mechanisms, however, are not well understood. MMPs may promote cytotoxicity through their ability to disrupt or degrade matrix proteins that support cell survival, and MMPs may also cleave substrates to generate molecules that stimulate cell death. In addition, MMPs may themselves act on cell surface receptors that affect cell survival. Among such receptors is the alpha(2)beta(1) integrin, a complex that has previously been linked to leukocyte death. In the present study we show that human neurons express alpha(2)beta(1) and that pro-MMP-1 interacts with this integrin complex. We also show that stimulation of neuronal cultures with MMP-1 is associated with a rapid reduction in the phosphorylation of Akt, a kinase that can influence caspase activity and cell survival. Moreover, MMP-1-associated dephosphorylation of Akt is inhibited by a blocking antibody to the alpha(2) integrin, but not by batimastat, an inhibitor of MMP-1 enzymatic activity. Such dephosphorylation is also stimulated by a catalytic mutant of pro-MMP-1. Additional studies show that MMP-1 causes neuronal death, which is significantly diminished by both a general caspase inhibitor and anti-alpha(2) but not by batimastat. Together, these results suggest that MMP-1 can stimulate dephosphorylation of Akt and neuronal death through a non-proteolytic mechanism that involves changes in integrin signaling.

Antibodies↗
PubMed2003

Temporal relationships between HIV-1 Tat-induced neuronal degeneration, OX-42 immunoreactivity, reactive astrocytosis, and protein oxidation in the rat striatum.

HIV-1 transactivating protein Tat is neurotoxic and is believed to play a role in the development of AIDS-associated dementia complex. Neurotoxicity of Tat may be associated with oxidative stress. In this study we examined temporal progression of histopathological changes induced by a single microinjection of Tat 1-72 into the rat striatum. Degenerating neural cells, detected by Fluoro-Jade B staining and increased protein oxidation, determined by protein carbonyl immunostaining, were observed in the striatum as soon as 2 h following the microinjection. Further progression of neuronal degeneration was associated with pronounced infiltration of the area surrounding Tat 1-72 injection site by OX-42 positive macrophages/microglia, which was evident at the 24 h time point. Signs of reactive astrocytosis were found in the striatum of Tat 1-72 injected animals as late as 7 days following the single microinjection. Increased GFAP immunoreactivity and changes in the morphology of astrocytes coincided with a second phase of increased protein carbonyl formation, but not with neuronal degeneration. Control polypeptide, nontoxic Tat delta 31-61, did not cause any cell death, inflammatory reaction or oxidative damage. Results of our study support the hypothesis that oxidative stress may be an early step in the mechanism of Tat neurotoxicity.

Acetyltransferases↗
PubMedDate not supplied

Temporal lobe, autism, and macrocephaly.

BACKGROUND AND PURPOSE: Because of increased prevalence of macrocephaly in autism, head size must be controlled for in studies that examine volumetric findings of the temporal lobe in autistic subjects. We prospectively examined temporal lobe structures in individuals with autism who were normocephalic or macrocephalic (head circumference > 97th percentile) and in control subjects who were normocephalic or macrocephalic or who had a reading disorder (unselected for head size). The rationale for the reading disorder group was to have control subjects with potential temporal lobe anomalies, but who were not autistic. METHODS: In individuals aged 7-31 years, autism was diagnosed on the basis of standardized interview and diagnostic criteria. Control subjects ranged in age from 7 to 22 years. All subjects were male. MR morphometrics of the major temporal lobe structures were based on ANALYZE segmentation routines, in which total brain volume and total intracranial volume (TICV) were calculated. Both group comparisons and developmental analyses were performed. RESULTS: No distinct temporal lobe abnormalities of volume were observed once head size (TICV) was controlled for. In autistic and control subjects, robust growth patterns were observed in white and gray matter that differed little between the groups. Although subtle differences were observed in some structures (ie, less white matter volume in the region of the temporal stem and overall temporal lobe), none was statistically significant. CONCLUSION: No major volumetric anomalies of the temporal lobe were found in cases of autism when IQ, TICV, and age were controlled. Temporal lobe abnormalities that may be associated with autism are likely to be more related to functional organization within the temporal lobe than to any gross volumetric difference.

Adolescent↗