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<title>Biological Research For Nursing</title>
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<item rdf:about="http://brn.sagepub.com/cgi/reprint/11/2/117?rss=1">
<title><![CDATA[The Value of Research Group Meetings]]></title>
<link>http://brn.sagepub.com/cgi/reprint/11/2/117?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Vincent, M. A.]]></dc:creator>
<dc:date>Mon, 21 Sep 2009 23:17:34 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1099800409337525</dc:identifier>
<dc:title><![CDATA[The Value of Research Group Meetings]]></dc:title>
<prism:number>2</prism:number>
<prism:volume>11</prism:volume>
<prism:endingPage>118</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>117</prism:startingPage>
<prism:section>Articles</prism:section>
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<item rdf:about="http://brn.sagepub.com/cgi/content/abstract/11/2/119?rss=1">
<title><![CDATA[Clinical Signs of Infection in Diabetic Foot Ulcers With High Microbial Load]]></title>
<link>http://brn.sagepub.com/cgi/content/abstract/11/2/119?rss=1</link>
<description><![CDATA[<p>Aims. One proposed method to diagnose diabetic foot ulcers (DFUs) for infection is clinical examination. Twelve different signs of infection have been reported. The purpose of this study was to examine diagnostic validity of each individual clinical sign, a combination of signs recommended by the Infectious Disease Society of America (IDSA), and a composite predictor based on all signs of localized wound infection in identifying DFU infection, among a sample of DFUs. Methods. A cross-sectional research design was used. Sixty-four individuals with DFUs were recruited from a Department of Veterans Affairs Medical Center and an academic-affiliated hospital. Each DFU was independently assessed by 2 research team members using the clinical signs and symptoms checklist. Tissue specimens were then obtained via wound biopsy and quantitatively processed. Ulcers with more than 10<sup>6</sup> organisms per gram of tissue were defined as having high microbial load. Individual signs and the IDSA combination were assessed for validity by calculating sensitivity, specificity, and concordance probability. The composite predictor was analyzed using c-index and receiver operating curves. Results. Twenty-five (39%) of the DFUs had high microbial loads. No individual sign was a significant predictor of high microbial load. The IDSA combination was not a significant predictor either. The c-index of the composite predictor was .645 with a 95% confidence interval of .559-.732. Conclusions. Individual signs of infection do not perform well nor does the IDSA combination of signs. However, a composite predictor based on all signs provides a moderate level of discrimination, suggesting clinical use. Larger sample sizes and alternate reference standards are recommended.</p>]]></description>
<dc:creator><![CDATA[Gardner, S. E., Hillis, S. L., Frantz, R. A.]]></dc:creator>
<dc:date>Mon, 21 Sep 2009 23:17:34 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1099800408326169</dc:identifier>
<dc:title><![CDATA[Clinical Signs of Infection in Diabetic Foot Ulcers With High Microbial Load]]></dc:title>
<prism:number>2</prism:number>
<prism:volume>11</prism:volume>
<prism:endingPage>128</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>119</prism:startingPage>
<prism:section>Articles</prism:section>
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<item rdf:about="http://brn.sagepub.com/cgi/content/abstract/11/2/129?rss=1">
<title><![CDATA[Effects of Low-Intensity Exercise Conditioning on Blood Pressure, Heart Rate, and Autonomic Modulation of Heart Rate in Men and Women with Hypertension]]></title>
<link>http://brn.sagepub.com/cgi/content/abstract/11/2/129?rss=1</link>
<description><![CDATA[<p>Untreated hypertension increases cardiovascular risk 2-fold to 3-fold, leading to serious cardiovascular problems that include left ventricular hypertrophy, stroke, ischemic heart disease, myocardial infarction, vascular disease, renal disease, and death. Exercise conditioning is recommended as one of the initial treatments for hypertension. The purpose of this pretest&mdash;posttest study was to quantify the effects of a 12-week home-based low-intensity exercise conditioning (walking) program in hypertensive men and women on systolic and diastolic blood pressure, heart rate, and autonomic modulation of heart rate. A total of 20 mildly hypertensive men and women who were assigned to a structured exercise (walking) program were compared with a control group of 20 nonexercising mildly hypertensive participants. Electrocardiographic heart rate and R-R interval data and beat-by-beat arterial blood pressure data were collected continuously for 10 min with participants in the supine and standing postures and during low-intensity steady-state exercise. The results show that systolic and diastolic blood pressure and R-R interval decreased and spontaneous baroreflex sensitivity increased in the exercise group. The decline in blood pressure was significant statistically and clinically. The increase in spontaneous baroreflex sensitivity indicates that the ability of the cardiovascular system to respond rapidly to changing stimuli improved after the 12-week walking protocol. The low-intensity exercise conditioning program achieved a training effect in this population.</p>]]></description>
<dc:creator><![CDATA[Hua, L. P.T., Brown, C. A., Hains, S. J.M., Godwin, M., Parlow, J. L.]]></dc:creator>
<dc:date>Mon, 21 Sep 2009 23:17:34 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1099800408324853</dc:identifier>
<dc:title><![CDATA[Effects of Low-Intensity Exercise Conditioning on Blood Pressure, Heart Rate, and Autonomic Modulation of Heart Rate in Men and Women with Hypertension]]></dc:title>
<prism:number>2</prism:number>
<prism:volume>11</prism:volume>
<prism:endingPage>143</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>129</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://brn.sagepub.com/cgi/content/abstract/11/2/144?rss=1">
<title><![CDATA[Influence of Seated Rocking on Blood Pressure in the Elderly: A Pilot Clinical Study]]></title>
<link>http://brn.sagepub.com/cgi/content/abstract/11/2/144?rss=1</link>
<description><![CDATA[<p>Patients with Alzheimer&rsquo;s disease (AD) who rock for 1&mdash;2 hr per day in a rocking chair demonstrate significant improvements in depression, anxiety, and balance and a decrease in pain medication usage; however, the underlying basis for their responses remains unclear. Rocking with plantar flexion uses the calf muscles, enhancing lower limb fluid return to the heart, which should increase blood pressure (BP) and may, then, also increase cerebral perfusion. Accordingly, we tested the efficacy of rocking activity for increasing BP in healthy, older persons. In a pilot laboratory study of 24 healthy, White men and women aged 55&mdash;87 years, we observed that 30 min of steady rocking led to an average 12 mmHg increase in systolic blood pressure (SBP, p &lt; .001) and a 3.6 mmHg average increase in diastolic blood pressure (DBP, p &lt; .001). To determine the effect of using this intervention in a nonclinical setting, we tested a similar group of 7 participants at a senior center. In this setting, we observed an average increase in SBP of 27 mmHg (p &lt; .001) and in DBP of 2.5 mmHg (p &lt; .001) after 30 min of rocking. In a subgroup (n = 8) of hypotensive individuals (SBP &lt; 110 mmHg after sitting quietly for 30 min) extracted from both settings, rocking raised the average SBP from &lt;100 mmHg to approximately 120 mmHg. These results are consistent with the hypothesis that rocking can increase BP and, therefore, may enhance cerebral perfusion. This observation may play a fundamental role in designing nursing interventions focused on improvement of symptoms associated with AD.</p>]]></description>
<dc:creator><![CDATA[Pierce, C., Pecen, J., McLeod, K. J.]]></dc:creator>
<dc:date>Mon, 21 Sep 2009 23:17:34 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1099800409334264</dc:identifier>
<dc:title><![CDATA[Influence of Seated Rocking on Blood Pressure in the Elderly: A Pilot Clinical Study]]></dc:title>
<prism:number>2</prism:number>
<prism:volume>11</prism:volume>
<prism:endingPage>151</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>144</prism:startingPage>
<prism:section>Articles</prism:section>
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<item rdf:about="http://brn.sagepub.com/cgi/content/abstract/11/2/152?rss=1">
<title><![CDATA[Propofol Protects Against Hemorrhagic Shock-Induced Organ Damage in Conscious Spontaneously Hypertensive Rats]]></title>
<link>http://brn.sagepub.com/cgi/content/abstract/11/2/152?rss=1</link>
<description><![CDATA[<p>Patients with hypertension have higher mortality rates from hemorrhagic shock (HS) than normotensive patients. Several inflammatory mediators such as tumor necrosis factor a (TNF-a) and interleukin 10 (IL-10) can be produced by HS and lead to multiple organ dysfunction and death. We investigated the effects of high dose (10 mg/kg/hr) and low dose (1 mg/kg/hr) propofol treatment after HS in conscious spontaneously hypertensive rats (SHRs). By withdrawing 40% of total blood volume from a femoral arterial catheter (6 ml/100 g body weight [BW]) for more than 30 min, HS was induced. The mean arterial pressure (MAP) and heart rate (HR) were monitored continuously for 24 hr after the start of blood withdrawal. Levels of biochemical parameters, including glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), blood urea nitrogen (BUN), creatinine (Cre), creatine phosphokinase (CPK), and lactic dehydrogenase (LDH) were measured 30 min before and 0, 1, 3, 6, 9, 12, 18, and 24 hr after the 30-min blood withdrawal period. Cytokine levels, including TNF-a and IL-10 in the serum, were measured 1 hr after HS. The kidney, liver, and lung were removed for pathology assessment at 48 hr after HS. HS significantly increased blood GOT, GPT, BUN, LDH, CPK, TNF-a, and IL-10 levels in conscious SHRs. Posttreatment propofol decreased serum TNF-a level, increased serum IL-10 level, attenuated the severity of organ damage, and improved survival rate after HS. This treatment protected SHRs against HS-induced organ damage. Moreover, high-dose propofol had a more protective effect than low-dose propofol against HS in conscious SHRs.</p>]]></description>
<dc:creator><![CDATA[Lee, C.-J., Lee, R.-P., Subeq, Y.-M., Lee, C.-C., Peng, T.-C., Hsu, B.-G.]]></dc:creator>
<dc:date>Mon, 21 Sep 2009 23:17:34 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1099800409334750</dc:identifier>
<dc:title><![CDATA[Propofol Protects Against Hemorrhagic Shock-Induced Organ Damage in Conscious Spontaneously Hypertensive Rats]]></dc:title>
<prism:number>2</prism:number>
<prism:volume>11</prism:volume>
<prism:endingPage>162</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>152</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://brn.sagepub.com/cgi/content/abstract/11/2/163?rss=1">
<title><![CDATA[Inflammatory Protein Levels and Depression Screening After Coronary Stenting Predict Major Adverse Coronary Events]]></title>
<link>http://brn.sagepub.com/cgi/content/abstract/11/2/163?rss=1</link>
<description><![CDATA[<p>Background: Traditional risk factors cannot account for the majority of future major adverse coronary events (MACE) in patients diagnosed with heart disease. We examined levels of inflammatory proteins to be possible predictors of future MACE and physiological and psychological factors that initiate temporal increases in inflammatory protein levels. Methods: Peripheral blood samples and depression data were collected 4 to 12 hr after elective coronary stent insertion in 490 patients. Depression screening was assessed by a single-question screening tool. Predictive modeling for future MACE was performed by using survival analysis, with time from the index event (placement of the stent) to future MACE as the dependent variable. Results: Patients with high-sensitivity c-reactive protein (hsCRP) in the second and third quartiles were 3 and 2.5 times more likely to have a MACE than patients with hsCRP in the first quartile, respectively. As levels of vascular cell adhesion molecule and monocyte chemoattractant protein-1 increased, so did the risk of future MACE. Patients who screened positive for depression were approximately 2 times more likely to have a MACE within 24 months after stent placement than were patients who did not screen positive. Conclusions: Our results suggest that hsCRP, vascular cell adhesion molecule, and monocyte chemoattractant protein-1 levels, measured after coronary stent insertion in patients with coronary heart disease, are prognostic of future MACE. Furthermore, positive depression screening is an independent predictor of future MACE.</p>]]></description>
<dc:creator><![CDATA[Frazier, L., Vaughn, W. K., Willerson, J. T., Ballantyne, C. M., Boerwinkle, E.]]></dc:creator>
<dc:date>Mon, 21 Sep 2009 23:17:34 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1099800409332801</dc:identifier>
<dc:title><![CDATA[Inflammatory Protein Levels and Depression Screening After Coronary Stenting Predict Major Adverse Coronary Events]]></dc:title>
<prism:number>2</prism:number>
<prism:volume>11</prism:volume>
<prism:endingPage>173</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>163</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://brn.sagepub.com/cgi/content/abstract/11/2/174?rss=1">
<title><![CDATA[Intracranial Pressure Waveform Analysis During Rest and Suctioning]]></title>
<link>http://brn.sagepub.com/cgi/content/abstract/11/2/174?rss=1</link>
<description><![CDATA[<p>Cerebral compliance is a measure of cerebral adaptability to increases in volume within the intracranial space and an indicator of risk for neurological deterioration. However, no direct measurement of compliance exists in clinical practice to guide nursing care or treatment decisions. Current use of mean intracranial pressure (MICP) and gross morphological intracranial pressure waveform (ICPW) analysis have great variability in predicting outcomes. The purpose of this review and pilot study was to evaluate the effects of suctioning on MICP and other measures estimating cerebral compliance derived from analysis of ICPW on patient outcome. We analyzed arterial blood pressure waveforms (ABPWs), ICPWs, and respiratory cycle variations using Fourier Transform analysis, to explore the potential benefits of studying ICPWs across single cardiac and respiratory cycles using linear modeling and calculation of correlation coefficients. ABPWs, ICPWs, and MICP were measured over individual cardiac cycles across multiple respiratory phases in five critically ill neurological patients. Both direct and derived ICP measures, including Fourier analysis of ABP and ICP and the cross-transform between ABP and ICP, were correlated with patient outcome. This more complex waveform analysis of individual ABPW and ICPW together, and derived measures during both single cardiac and respiratory cycles, may provide information relevant to cerebral compliance and patient outcomes. Pending confirmation with additional data sets, this technique may be a useful real-time clinical tool to provide a measure of compliance and risk of neurological deterioration for clinicians.</p>]]></description>
<dc:creator><![CDATA[Hickey, J. V., Olson, D. M., Turner, D. A.]]></dc:creator>
<dc:date>Mon, 21 Sep 2009 23:17:34 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1099800409332902</dc:identifier>
<dc:title><![CDATA[Intracranial Pressure Waveform Analysis During Rest and Suctioning]]></dc:title>
<prism:number>2</prism:number>
<prism:volume>11</prism:volume>
<prism:endingPage>186</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>174</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://brn.sagepub.com/cgi/content/abstract/11/2/187?rss=1">
<title><![CDATA[Is Shock a Key Element in the Pathology of Sudden Infant Death Syndrome (SIDS)?]]></title>
<link>http://brn.sagepub.com/cgi/content/abstract/11/2/187?rss=1</link>
<description><![CDATA[<p>In developed countries, sudden infant death syndrome (SIDS) is the most common cause of death for infants between 1 month and 1 year of age. The etiology of SIDS is likely to be multifactorial, and current paradigms often describe three overlapping elements of risk. Those elements are a critical developmental period, a vulnerable infant, and one or more exogenous stressors. In the triple-risk model, SIDS infants are described as having an underlying vulnerability in cardiorespiratory control in the central nervous system during a critical period when autonomic control is developing. This vulnerability might affect the response to exogenous stressors, including prone sleeping position, hypoxia, and increased carbon dioxide. In the common bacterial hypothesis and fatal triangle, the focus is on the stressors. In the first, a combination of common respiratory infections can cause SIDS in an infant during a developmentally vulnerable period. This theory also includes 3 factors of vulnerability: a genetic predisposition, a vulnerable developmental age, and infectious stressors. In the fatal triangle theory, infection, inflammation, and genetics each play a role in triggering a SIDS fatality. From our work in an animal model, we have found that rat pups die from a combination of infectious insults during a critical time of development. This is exacerbated by perinatal nicotine exposure, a condition shown to alter the autonomic response in exposed offspring. We are proposing that shock and cardiovascular collapse is a key element that links these theories.</p>]]></description>
<dc:creator><![CDATA[Blood-Siegfried, J., Bowers, M. T., Lorimer, M.]]></dc:creator>
<dc:date>Mon, 21 Sep 2009 23:17:34 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1099800408324854</dc:identifier>
<dc:title><![CDATA[Is Shock a Key Element in the Pathology of Sudden Infant Death Syndrome (SIDS)?]]></dc:title>
<prism:number>2</prism:number>
<prism:volume>11</prism:volume>
<prism:endingPage>194</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>187</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://brn.sagepub.com/cgi/content/abstract/11/2/195?rss=1">
<title><![CDATA[Basic Concepts of Optical Mapping Techniques in Cardiac Electrophysiology]]></title>
<link>http://brn.sagepub.com/cgi/content/abstract/11/2/195?rss=1</link>
<description><![CDATA[<p>Optical mapping is a tool used in cardiac electrophysiology to study the heart&rsquo;s normal rhythm and arrhythmias. The optical mapping technique provides a unique opportunity to obtain membrane potential recordings with a higher temporal and spatial resolution than electrical mapping. Additionally, it allows simultaneous recording of membrane potential and calcium transients in the whole heart. This article presents the basic concepts of optical mapping techniques as an introduction for students and investigators in experimental laboratories unfamiliar with it.</p>]]></description>
<dc:creator><![CDATA[Attin, M., Clusin, W. T.]]></dc:creator>
<dc:date>Mon, 21 Sep 2009 23:17:34 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1099800409338516</dc:identifier>
<dc:title><![CDATA[Basic Concepts of Optical Mapping Techniques in Cardiac Electrophysiology]]></dc:title>
<prism:number>2</prism:number>
<prism:volume>11</prism:volume>
<prism:endingPage>207</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>195</prism:startingPage>
<prism:section>Articles</prism:section>
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<item rdf:about="http://brn.sagepub.com/cgi/content/abstract/11/2/208?rss=1">
<title><![CDATA[Biosignatures of Health]]></title>
<link>http://brn.sagepub.com/cgi/content/abstract/11/2/208?rss=1</link>
<description><![CDATA[<p>The term health is commonplace in both everyday parlance and professional discourse. Unfortunately, the term has little objective specification, especially in physiologic terms. When critically examined, even time-honored terms such as homeostasis lack specific measurable referents. The last three decades, however, have witnessed an explosion of information from diverse fields regarding the dynamical basis of biology. This brief review explores a few main ideas, which appear to be coming together to provide biosignatures of health.</p>]]></description>
<dc:creator><![CDATA[Zbilut, J. P.]]></dc:creator>
<dc:date>Mon, 21 Sep 2009 23:17:34 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1099800409341176</dc:identifier>
<dc:title><![CDATA[Biosignatures of Health]]></dc:title>
<prism:number>2</prism:number>
<prism:volume>11</prism:volume>
<prism:endingPage>220</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>208</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://brn.sagepub.com/cgi/reprint/11/1/5?rss=1">
<title><![CDATA[Genetics and Genomics in Nursing Research]]></title>
<link>http://brn.sagepub.com/cgi/reprint/11/1/5?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Conley, Y. P.]]></dc:creator>
<dc:date>Mon, 22 Jun 2009 02:33:55 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1099800409336293</dc:identifier>
<dc:title><![CDATA[Genetics and Genomics in Nursing Research]]></dc:title>
<prism:number>1</prism:number>
<prism:volume>11</prism:volume>
<prism:endingPage>6</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>5</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://brn.sagepub.com/cgi/content/abstract/11/1/7?rss=1">
<title><![CDATA[Genome-Wide Screen Identifies Drug-Induced Regulation of the Gene Giant Axonal Neuropathy (Gan) in a Mouse Model of Antiretroviral-Induced Painful Peripheral Neuropathy]]></title>
<link>http://brn.sagepub.com/cgi/content/abstract/11/1/7?rss=1</link>
<description><![CDATA[<p>Painful peripheral neuropathy is a debilitating complication of the treatment of HIV with nucleoside reverse transcriptase inhibitors (NRTIs). Patients are living longer with these drugs; however many develop excruciating, unremitting, and often treatment-limiting neuropathy that is resistant to conventional pain management therapies. Improving patient comfort and quality of life is paramount and depends on a clearer understanding of this devastating side effect. The mechanisms underlying the development of NRTI-induced neuropathy, however, remain unclear. Using a mouse model of NRTI-induced neuropathy, the authors conducted an unbiased whole-genome microarray screen to identify molecular targets in the spinal dorsal horn, which is the location where integration of ascending sensory transmission and descending modulatory effects occur. Analysis of the microarray data identified a change in the gene giant axonal neuropathy 1 (Gan1). Mutation of this gene has been linked to the development of giant axonal neuropathy (GAN), a rare autosomal recessive condition characterized by a progressive sensorimotor neuropathy. Gan1 has not been previously linked to nerve pathologies in other populations. In this study, downregulation of the Gan1 gene and the gene protein product, gigaxonin, was validated via quantitative polymerase chain reaction ([qPCR] gene expression) and Western blot analyses (protein level). Our report is the first to suggest that Gan1 might be a novel molecular target in the development of NRTI-induced peripheral neuropathy with implications for new therapeutic approaches to preventing or reducing a significant side effect of HIV treatment.</p>]]></description>
<dc:creator><![CDATA[Dorsey, S. G., Leitch, C. C., Renn, C. L., Lessans, S., Smith, B. A., Wang, X. M., Dionne, R. A.]]></dc:creator>
<dc:date>Mon, 22 Jun 2009 02:33:55 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1099800409332726</dc:identifier>
<dc:title><![CDATA[Genome-Wide Screen Identifies Drug-Induced Regulation of the Gene Giant Axonal Neuropathy (Gan) in a Mouse Model of Antiretroviral-Induced Painful Peripheral Neuropathy]]></dc:title>
<prism:number>1</prism:number>
<prism:volume>11</prism:volume>
<prism:endingPage>16</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>7</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://brn.sagepub.com/cgi/content/abstract/11/1/17?rss=1">
<title><![CDATA[Altered Beta-2 Adrenergic Receptor Gene Expression in Human Clinical Hypertension]]></title>
<link>http://brn.sagepub.com/cgi/content/abstract/11/1/17?rss=1</link>
<description><![CDATA[<p>Objectives: The beta-2 adrenergic receptor is involved in mediating vasodilatation via neurohumoral and sympathetic nervous system pathways. Alterations in beta-2 adrenergic receptor gene expression (mRNA transcription) may contribute to the hypertensive phenotype. Human gene expression in clinical phenotypes remains largely unexplored due to ethical constraints involved in obtaining human tissue. We devised a method to obtain normally discarded internal mammary artery tissue from coronary artery bypass graft patients. We then investigated differences in hypertensive and normotensive participants' beta-2 adrenergic receptor gene expression in this tissue. Methods: We collected arterial tissue samples from 46 coronary artery bypass patients in a surgical setting. Using 41 of the samples, we performed TaqMan real-time polymerase chain reaction (RT-PCR) and used the delta delta cycle threshold (Ct) relative quantitation method for determination of fold-differences in gene expression between normotensive and hypertensive participants. The beta-2 adrenergic receptor target was normalized to glyceraldehyde-phosphate dehydrogenase. Results: Participants with hypertension had significantly less-expressed beta-2 adrenoceptor gene (2.76-fold, p &lt; .05) compared to normotensive participants. After Bonferroni correction, gene expression did not differ by race, gender, type/dose of &beta;-blocker prescribed, positive family history of hypertension, or diagnosis of diabetes mellitus type 2. Conclusions: These data support the possibility of a molecular basis for impaired adrenoceptor-mediated vascular tone in hypertension. Modification and extension of this research is required.</p>]]></description>
<dc:creator><![CDATA[Dungan, J. R., Conley, Y. P., Langaee, T. Y., Johnson, J. A., Kneipp, S. M., Hess, P. J., Yucha, C. B.]]></dc:creator>
<dc:date>Mon, 22 Jun 2009 02:33:55 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1099800409332538</dc:identifier>
<dc:title><![CDATA[Altered Beta-2 Adrenergic Receptor Gene Expression in Human Clinical Hypertension]]></dc:title>
<prism:number>1</prism:number>
<prism:volume>11</prism:volume>
<prism:endingPage>26</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>17</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://brn.sagepub.com/cgi/content/abstract/11/1/27?rss=1">
<title><![CDATA[Preliminary Evidence of a Genetic Association Between Tumor Necrosis Factor Alpha and the Severity of Sleep Disturbance and Morning Fatigue]]></title>
<link>http://brn.sagepub.com/cgi/content/abstract/11/1/27?rss=1</link>
<description><![CDATA[<p>Although fatigue and sleep disturbance are prevalent symptoms in oncology patients and their family caregivers, little is known about the factors that contribute to interindividual variability in symptom severity ratings as well as in their underlying biological mechanisms. In this study, we sought to determine whether a functional genetic variation in a prominent proinflammatory cytokine, tumor necrosis factor-alpha (TNFA-308G&gt;A [rs1800629] promoter polymorphism) was associated with overall ratings of sleep disturbance and fatigue as well as with the trajectories of these symptoms. Over 6 months, participants completed standardized measures of sleep disturbance and fatigue. Multiple linear regression was used to assess the effect of the TNFA genotype and other covariates on mean sleep disturbance and fatigue scores. Hierarchical linear modeling was used to determine the effect of TNFA genotype on the trajectories of these symptoms. Common allele homozygotes reported higher levels of sleep disturbance (p = .09) and morning fatigue (p = .02) than minor allele carriers. Multivariate analyses demonstrated that age and genotype were predictors of both mean symptom scores and the trajectories of these symptoms. Findings provide preliminary evidence of an association between a functional promoter polymorphism in the TNFA gene and the severity of sleep disturbance and morning fatigue in oncology patients and their family caregivers.</p>]]></description>
<dc:creator><![CDATA[Aouizerat, B. E., Dodd, M., Lee, K., West, C., Paul, S. M., Cooper, B. A., Wara, W., Swift, P., Dunn, L. B., Miaskowski, C.]]></dc:creator>
<dc:date>Mon, 22 Jun 2009 02:33:55 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1099800409333871</dc:identifier>
<dc:title><![CDATA[Preliminary Evidence of a Genetic Association Between Tumor Necrosis Factor Alpha and the Severity of Sleep Disturbance and Morning Fatigue]]></dc:title>
<prism:number>1</prism:number>
<prism:volume>11</prism:volume>
<prism:endingPage>41</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>27</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://brn.sagepub.com/cgi/content/abstract/11/1/42?rss=1">
<title><![CDATA[Endothelial Nitric Oxide Synthase Tagging Single Nucleotide Polymorphisms and Recovery From Aneurysmal Subarachnoid Hemorrhage]]></title>
<link>http://brn.sagepub.com/cgi/content/abstract/11/1/42?rss=1</link>
<description><![CDATA[<p>Aneurysmal subarachnoid hemorrhage (SAH) is a hemorrhagic stroke subtype with a poor recovery profile. Cerebral vasospasm (CV), a narrowing of the cerebral vasculature, significantly contributes to the poor recovery profile. Variation in the endothelial nitric oxide (NO) synthase (eNOS) gene has been implicated in CV and outcome after SAH. The purpose of this project was to explore the potential association between three eNOS tagging single nucleotide polymorphisms (SNPs) and recovery from SAH. We included 195 participants with a diagnosis of SAH and DNA and 6-month outcome data available but without preexisting neurologic disease/deficit. Genotyping was performed using an ABI Prism 7000 Sequence Detection System and TaqMan assays. CV was verified by cerebral angiogram independently read by a neurosurgeon on 118 participants. Modified Rankin Scores (MRS) and Glasgow Outcome Scale (GOS) scores were collected 6 months posthemorrhage. Data were analyzed using descriptive statistics, analysis of variance (ANOVA) and chi-square analysis as appropriate. The sample was primarily female (n = 147; 75.4%) and White (n = 178; 91.3%) with a mean age of 54.6 years. Of the participants with CV data, 56 (47.5%) developed CV within 14 days of SAH. None of the SNPs individually were associated with CV presence; however, a combination of the three variant SNPs was significantly associated with CV (p = .017). Only one SNP (rs1799983, variant allele) was associated with worse 6-month GOS scores (p &lt; .001) and MRS (p &lt; .001). These data indicate that the eNOS gene plays a role in the response to SAH, which may be explained by an influence on CV.</p>]]></description>
<dc:creator><![CDATA[Alexander, S., Poloyac, S., Hoffman, L., Gallek, M., Dianxu Ren,  , Balzer, J., Kassam, A., Conley, Y.]]></dc:creator>
<dc:date>Mon, 22 Jun 2009 02:33:55 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1099800409334751</dc:identifier>
<dc:title><![CDATA[Endothelial Nitric Oxide Synthase Tagging Single Nucleotide Polymorphisms and Recovery From Aneurysmal Subarachnoid Hemorrhage]]></dc:title>
<prism:number>1</prism:number>
<prism:volume>11</prism:volume>
<prism:endingPage>52</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>42</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://brn.sagepub.com/cgi/content/abstract/11/1/53?rss=1">
<title><![CDATA[Genetic and Environmental Risks for High Blood Pressure Among African American Mothers and Daughters]]></title>
<link>http://brn.sagepub.com/cgi/content/abstract/11/1/53?rss=1</link>
<description><![CDATA[<p>Objective: To determine the relationship between genetic and environmental lifestyle factors (physical activity and sodium) on blood pressure (BP) among African-American women. Method: In this cross-sectional study involving 108 African-American mothers and daughters from a Midwestern area, investigators obtained BP measurements, information on minutes of physical activity, amount of sodium intake, and buccal swab saliva samples. Results: Of the 4 single nucleotide polymorphisms (SNPs) on the sodium bicarbonate cotransporter gene (SLC4A5), rs8179526 had a statistically significant interaction with cytosine/thymine (C/T) genotype by sodium status on systolic BP (SBP; p = .0077). For gene <FONT FACE="arial,helvetica">x</FONT> physical activity interaction, 2 significant interactions (cytosine/adenine [C/A] genotype by physical activity and adenine/adenine [A/A] genotype by physical activity, p = .0107 and p = .0171, respectively) on SBP and 1 on diastolic BP (DBP; A/A genotype by physical activity, p = .0233) were found on rs1017783. Two significant guanine/adenine [G/A] genotype by physical activity interactions were found on rs6731545 for SBP and DBP (p = .0160 and p = .0492, respectively). Discussion: A gene <FONT FACE="arial,helvetica">x</FONT> environmental interaction with rs8179526 has a protective effect on SBP in African-American women with high sodium intake. Participants with C/T genotype of rs8179526 who consumed greater than 2,300 mg of sodium had lower SBP than those who consumed less than recommended. Women with thymine/thymine (T/T) genotype of rs8179526 who consumed greater than 2,300 mg had lower SBP than those who consumed less. Awareness of both the protective and deleterious properties of rs8179526 in African-American women may one day assist in determining appropriate treatment plans.</p>]]></description>
<dc:creator><![CDATA[Taylor, J. Y., Maddox, R., Chun Yi Wu,  ]]></dc:creator>
<dc:date>Mon, 22 Jun 2009 02:33:55 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1099800409334817</dc:identifier>
<dc:title><![CDATA[Genetic and Environmental Risks for High Blood Pressure Among African American Mothers and Daughters]]></dc:title>
<prism:number>1</prism:number>
<prism:volume>11</prism:volume>
<prism:endingPage>65</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>53</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://brn.sagepub.com/cgi/content/abstract/11/1/66?rss=1">
<title><![CDATA[Genetic Characterization of Familial CPVT After 30 Years]]></title>
<link>http://brn.sagepub.com/cgi/content/abstract/11/1/66?rss=1</link>
<description><![CDATA[<p>Introduction: Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a stress-related, bidirectional ventricular tachycardia and atrial tachyarrhythmia in the absence of either structural heart disease or prolonged QT interval. Autosomal dominant and recessive forms of CPVT because of mutations in the cardiac ryanodine receptor (RyR2) or calsequestrin 2 (CASQ2) have been reported. The objective of this study was the clinical and genetic characterization of the family of an individual initially diagnosed as a child in 1978. Method: We collected family medical history and recorded a four-generation pedigree. We performed mutation analysis of RyR2 ``critical regions'' in the N-terminus, FKBP12.6 binding domain, Ca<sup>2+</sup> binding domain, and transmembrane domains of the C-terminus by direct sequencing. Results: CPVT was diagnosed in two of the nine family members evaluated. Pedigree analysis suggested autosomal dominant disease transmission. There were no additional reports of seizures, pregnancy loss, neonatal death, or sudden cardiac death in family members. A novel RyR2 gene variant (W4645R) was found in four family members including two without symptoms. RyR2-W4645R segregates with disease in this family with incomplete penetrance. The W4645 residue is evolutionarily conserved in the transmembrane region adjacent to previously reported disease-causing mutations. Based on sorting intolerant from tolerant analysis of protein structure, RyR2-W4645R is predicted to be deleterious. Conclusions: All current evidence supports RyR2-W4645R as a disease-causing variant, which was silent in persons for two generations before causing symptoms in persons for the next two generations, beginning in 1978.</p>]]></description>
<dc:creator><![CDATA[Beery, T. A., Shah, M. J., Benson, D. W.]]></dc:creator>
<dc:date>Mon, 22 Jun 2009 02:33:55 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1099800409333369</dc:identifier>
<dc:title><![CDATA[Genetic Characterization of Familial CPVT After 30 Years]]></dc:title>
<prism:number>1</prism:number>
<prism:volume>11</prism:volume>
<prism:endingPage>72</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>66</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://brn.sagepub.com/cgi/content/abstract/11/1/73?rss=1">
<title><![CDATA[Introducing Systems Biology for Nursing Science]]></title>
<link>http://brn.sagepub.com/cgi/content/abstract/11/1/73?rss=1</link>
<description><![CDATA[<p>Systems biology expands on general systems theory as the ``omics'' era rapidly progresses. Although systems biology has been institutionalized as an interdisciplinary framework in the biosciences, it is not yet apparent in nursing. This article introduces systems biology for nursing science by presenting an overview of the theory. This framework for the study of organisms from molecular to environmental levels includes iterations of computational modeling, experimentation, and theory building. Synthesis of complex biological processes as whole systems rather than isolated parts is emphasized. Pros and cons of systems biology are discussed, and relevance of systems biology to nursing is described. Nursing research involving molecular, physiological, or biobehavioral questions may be guided by and contribute to the developing science of systems biology. Nurse scientists can proactively incorporate systems biology into their investigations as a framework for advancing the interdisciplinary science of human health care. Systems biology has the potential to advance the research and practice goals of the National Institute for Nursing Research in the National Institutes of Health Roadmap initiative.</p>]]></description>
<dc:creator><![CDATA[Founds, S. A.]]></dc:creator>
<dc:date>Mon, 22 Jun 2009 02:33:55 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1099800409331893</dc:identifier>
<dc:title><![CDATA[Introducing Systems Biology for Nursing Science]]></dc:title>
<prism:number>1</prism:number>
<prism:volume>11</prism:volume>
<prism:endingPage>80</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>73</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://brn.sagepub.com/cgi/content/abstract/11/1/81?rss=1">
<title><![CDATA[Can Heterogeneity of Chronic Sickle-Cell Disease Pain Be Explained by Genomics? A Literature Review]]></title>
<link>http://brn.sagepub.com/cgi/content/abstract/11/1/81?rss=1</link>
<description><![CDATA[<p>This literature review explores the potential of genomics to explain, or at least contribute to the discussion about, heterogeneity in chronic pain in sickle-cell disease (SCD). Background: Adults with SCD, a single-gene disorder, are living longer than in years past, yet report being burdened by chronic pain. With only a few studies on chronic pain in this population, the epidemiology is unclear. However, research in the area of pain genetics continues to advance since the conclusion of the Human Genome Project. Two pain susceptibility genes, catechol-O-methyltransferase (COMT) and cytochrome P450, have, to date, been discovered that can increase individual susceptibility to the development of chronic pain. Method: A search was conducted in PubMed, CINAHL, and EBSCO using the terms ``sickle cell,'' ``chronic pain,'' ``polymorphism,'' ``genetics,'' ``pain genetics,'' ``human,'' ``adult,'' ``association studies,'' and ``pain susceptibility genes'' to search for articles published between 1970 and 2008. Findings: Chronic pain generally is more prevalent and severe than previously reported, and individuals with SCD report daily pain. The genomic era has made it possible for scientists to identify pain susceptibility genes that contribute to variability in the interindividual experience of chronic pain. Conclusion: Nurses are well positioned to generate and translate genomic research, thus improving care delivery. Such research may lead to the identification of polymorphisms associated with pain sensitivity in individuals with SCD.</p>]]></description>
<dc:creator><![CDATA[Adegbola, M. A.]]></dc:creator>
<dc:date>Mon, 22 Jun 2009 02:33:55 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1099800409337154</dc:identifier>
<dc:title><![CDATA[Can Heterogeneity of Chronic Sickle-Cell Disease Pain Be Explained by Genomics? A Literature Review]]></dc:title>
<prism:number>1</prism:number>
<prism:volume>11</prism:volume>
<prism:endingPage>97</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>81</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://brn.sagepub.com/cgi/content/abstract/11/1/98?rss=1">
<title><![CDATA[Gene Therapy and Informed Consent Decision Making: Nursing Research Directions]]></title>
<link>http://brn.sagepub.com/cgi/content/abstract/11/1/98?rss=1</link>
<description><![CDATA[<p>Recent gene therapy clinical trials have demonstrated significant promise for treating a number of genetic neuromuscular disorders. Although nurses are experienced in educating patients and families about the benefits and risks of conventional therapeutics, there are significant challenges for guiding patients through the decision-making phase of gene therapy clinical trial participation. The first part of this review provides an overview and update on neuromuscular gene therapy, including viral delivery principles and historical progress. The second part discusses risk/benefit perception of gene therapy and factors affecting the decision making for patients interested in participating in a trial. Future challenges for gene therapy are targeted high-efficiency delivery, and additional research on developing patient-centered decision support interventions.</p>]]></description>
<dc:creator><![CDATA[Kaspar, R. W., Wills, C. E., Kaspar, B. K.]]></dc:creator>
<dc:date>Mon, 22 Jun 2009 02:33:55 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1099800409333169</dc:identifier>
<dc:title><![CDATA[Gene Therapy and Informed Consent Decision Making: Nursing Research Directions]]></dc:title>
<prism:number>1</prism:number>
<prism:volume>11</prism:volume>
<prism:endingPage>107</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>98</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://brn.sagepub.com/cgi/reprint/10/4/305?rss=1">
<title><![CDATA[In Support of the Overuse of Sustainability]]></title>
<link>http://brn.sagepub.com/cgi/reprint/10/4/305?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[St. Pierre Schneider, B.]]></dc:creator>
<dc:date>Tue, 24 Mar 2009 06:01:15 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1099800409333368</dc:identifier>
<dc:title><![CDATA[In Support of the Overuse of Sustainability]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>10</prism:volume>
<prism:endingPage>306</prism:endingPage>
<prism:publicationDate>2009-04-01</prism:publicationDate>
<prism:startingPage>305</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://brn.sagepub.com/cgi/content/abstract/10/4/307?rss=1">
<title><![CDATA[Cerebrovascular Disease and Patterns of Cerebral Oxygenation During Sleep in Elders]]></title>
<link>http://brn.sagepub.com/cgi/content/abstract/10/4/307?rss=1</link>
<description><![CDATA[<p><I>Purpose</I>: The aim of this descriptive exploratory study was to describe patterns of cerebral oxygen reserves during sleep and their association with cerebrovascular risk factors in elders. <I>Method</I>: Participants&mdash;115 elders, age 70<sup> +</sup> years&mdash;were monitored overnight using standard polysomnography. Measures included arterial oxyhemoglobin (SaO<SUB>2</SUB>) and regional measures of percentage of cerebral oxyhemoglobin saturation (rcSO<SUB>2</SUB>) via cerebral oximetry. Participants were classified based on the magnitude of change in rcSO<SUB>2</SUB> from resting baseline to the end of the first nonrapideye-movement (NREM) period. One-way ANOVA and Chi-square were used to test group differences in SaO<SUB>2</SUB> and the prevalence of cerebrovascular risk factors. <I>Findings</I>: 20 participants (Group 1) experienced an increase in rcSO<SUB>2</SUB> during sleep along with sleeping rcSO<SUB>2</SUB> levels !55%; 95 participants experienced a decline in rcSO<SUB>2</SUB>; 72 participants (Group 2) had sleeping rcSO<SUB>2</SUB> levels !55%; and 23 participants had sleeping rcSO<SUB>2</SUB> levels &lt;55% (Group 3). Although all three groups had equivalent declines in SaO<SUB>2</SUB> levels during sleep, Group 3 had more cardiovascular comorbidity than Groups 1 and 2. <I>Conclusions</I>: Although SaO<SUB>2</SUB> levels decline in most people during sleep, compensatory vascular responses to these drops in SaO<SUB>2</SUB> are important for preventing rcSO<SUB>2</SUB> from falling during sleep. Those entering sleep with lower baseline rcSO<SUB>2</SUB> levels and those with greater declines in cerebral oxygenation during sleep may have greater cardiovascular burden and be at greater risk for stroke and other forms of disabling cerebrovascular disease.</p>]]></description>
<dc:creator><![CDATA[Carlson, B. W., Neelon, V. J., Carlson, J. R., Hartman, M., Dogra, S.]]></dc:creator>
<dc:date>Tue, 24 Mar 2009 06:01:15 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1099800408330396</dc:identifier>
<dc:title><![CDATA[Cerebrovascular Disease and Patterns of Cerebral Oxygenation During Sleep in Elders]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>10</prism:volume>
<prism:endingPage>317</prism:endingPage>
<prism:publicationDate>2009-04-01</prism:publicationDate>
<prism:startingPage>307</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://brn.sagepub.com/cgi/content/abstract/10/4/318?rss=1">
<title><![CDATA[Biobehavioral Outcomes in Adolescents and Young Adults Prenatally Exposed to Cocaine: Evidence From Animal Models]]></title>
<link>http://brn.sagepub.com/cgi/content/abstract/10/4/318?rss=1</link>
<description><![CDATA[<p>Cocaine has been a popular illicit drug among drug-using pregnant women over the last three decades. Prenatal cocaine exposure (PCE) has significant effects on children's development throughout early childhood. Very few human studies, however, report the effects of PCE on adolescent or early-adult development. As knowledge about early childhood effects in human children was informed by animal studies, this review considers the effects of PCE on behavioral outcomes in adolescent and young adult animals and provides potential guidance for research in human children. Animal models prenatally exposed to cocaine manifest play deficits, decreased social interaction, and increased aggression during competition in adolescence and young adulthood. Altered behavioral adaptation after stress exposure, including hormonal response change, is also evident. Attention deficits are reported in adult offspring with PCE, not only in a novel environment, but also in a final task session, indicating effects of PCE on transition and maintenance of attention. Animal studies support that PCE effects may extend beyond early childhood and continue to adolescence and adulthood. Additionally, some studies highlight that behavioral changes in offspring with PCE born without teratogenesis remain latent and reveal themselves during adulthood when animals are under stress conditions. Based on the evidence from animal models, well-designed human studies are needed to elucidate the effects of PCE on older human children. Research models that combine behavioral measures with stressful challenges may hold potential in discerning a longer term influence of PCE.</p>]]></description>
<dc:creator><![CDATA[Chae, S.-M., Covington, C. Y.]]></dc:creator>
<dc:date>Tue, 24 Mar 2009 06:01:15 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1099800408330395</dc:identifier>
<dc:title><![CDATA[Biobehavioral Outcomes in Adolescents and Young Adults Prenatally Exposed to Cocaine: Evidence From Animal Models]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>10</prism:volume>
<prism:endingPage>330</prism:endingPage>
<prism:publicationDate>2009-04-01</prism:publicationDate>
<prism:startingPage>318</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://brn.sagepub.com/cgi/content/abstract/10/4/331?rss=1">
<title><![CDATA[Lateral Hypothalamic-Induced Alpha-Adrenoceptor Modulation Occurs in a Model of Inflammatory Pain in Rats]]></title>
<link>http://brn.sagepub.com/cgi/content/abstract/10/4/331?rss=1</link>
<description><![CDATA[<p>Previous work from our lab showed that stimulation of the lateral hypothalamus (LH) produces analgesia (antinociception) in a model of thermal nociceptive pain. This antinociceptive effect is mediated by 2-adrenoceptors in the spinal cord dorsal horn. However, a concomitant, opposing hyperalgesic (pro-nociceptive) response also occurs, which is mediated by 1-adrenoceptors in the dorsal horn. Antinociception predominates but is attenuated by the pronociceptive response. To determine whether such an effect occurs in a model of inflammatory pain, we applied mustard oil (allyl isothiocyanate; 20 &micro;l) to the left ankle of female Sprague-Dawley rats. We then stimulated the LH using carbamylcholine chloride (carbachol; 125 nmol). The foot withdrawal latencies were measured. Some rats received intrathecal -adrenoceptor antagonists to determine whether the opposing -adrenoceptor response was present. Mustard oil application produced hyperalgesia in the affected paw, while the LH stimulation increased the foot withdrawal latencies for the mustard oil paw as compared to the control group. Following carbachol microinjection in the LH, WB4101, an 1-adrenoceptor antagonist, produced significantly longer foot withdrawal latencies compared to saline controls, while yohimbine, an 2-antagonist, decreased the foot withdrawal latencies from 10 min postinjection (<I>p</I> &lt; .05). These findings support the hypothesis that the LH-induced nociceptive modulation is mediated through an -adrenoceptor opposing response in a model of inflammatory pain.</p>]]></description>
<dc:creator><![CDATA[Jeong, Y., Holden, J. E.]]></dc:creator>
<dc:date>Tue, 24 Mar 2009 06:01:15 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1099800408325053</dc:identifier>
<dc:title><![CDATA[Lateral Hypothalamic-Induced Alpha-Adrenoceptor Modulation Occurs in a Model of Inflammatory Pain in Rats]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>10</prism:volume>
<prism:endingPage>339</prism:endingPage>
<prism:publicationDate>2009-04-01</prism:publicationDate>
<prism:startingPage>331</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://brn.sagepub.com/cgi/content/abstract/10/4/340?rss=1">
<title><![CDATA[Association of Serum Prolactin and Oxytocin With Milk Production in Mothers of Preterm and Term Infants]]></title>
<link>http://brn.sagepub.com/cgi/content/abstract/10/4/340?rss=1</link>
<description><![CDATA[<p>The present study was designed to compare milk production and hormone responses (prolactin [PRL], oxytocin [OT]) and to determine associations of hormone levels with milk production in mothers of preterm (PT) and term (TM) infants during the first 6 weeks postpartum. Mothers of PT infants (<I>n</I> = 95) were all pump dependent; mothers of TM infants (<I>n</I> = 98) were all feeding their infant at breast. Mothers of nonnursing PT infants produced less milk over time compared to mothers of TM infants. A higher proportion of PT mothers had lower basal PRL levels compared with TM mothers. PRL and frequency of breast stimulation combined positively influenced milk production in PT mothers. OT levels were higher in PT versus TM mothers, but OT was not related to milk production. Further study is warranted regarding interventions to enhance milk production, particularly in pump-dependent mothers of PT infants.</p>]]></description>
<dc:creator><![CDATA[Hill, P. D., Aldag, J. C., Demirtas, H., Naeem, V., Parker, N. P., Zinaman, M. J., Chatterton, R. T.]]></dc:creator>
<dc:date>Tue, 24 Mar 2009 06:01:15 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1099800409331394</dc:identifier>
<dc:title><![CDATA[Association of Serum Prolactin and Oxytocin With Milk Production in Mothers of Preterm and Term Infants]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>10</prism:volume>
<prism:endingPage>349</prism:endingPage>
<prism:publicationDate>2009-04-01</prism:publicationDate>
<prism:startingPage>340</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://brn.sagepub.com/cgi/content/abstract/10/4/350?rss=1">
<title><![CDATA[Association Between Stress-Related Substances in Saliva and Immune Substances in Breast Milk in Puerperae]]></title>
<link>http://brn.sagepub.com/cgi/content/abstract/10/4/350?rss=1</link>
<description><![CDATA[<p><I>Objective</I>: We examined the association between biochemical parameters of stress in puerperae and immune substances in breast milk. <I>Methods</I>: The participants were 22 mothers 2 weeks after delivery, with normal pregnancy/delivery and a normal puerperal course. We measured the levels of secretory immunoglobulin A (SIgA) and cortisol in saliva and the level of SIgA and the leukocyte count in breast milk and investigated their association. <I>Results</I>: There was a positive correlation between the salivary and breast milk levels of SIgA (<I>r</I> = .536, <I>p</I> &lt; .05). However, there were no correlations among the salivary level of cortisol and the level of SIgA and leukocyte count in breast milk. <I>Conclusions</I>: The only association found in our study was between the salivary and breast milk SIgA. The lack of association among SIgA and cortisol may be related to a variety of factors such as production site, diurnal rhythms, and the interval between stress stimulation in mothers and the response of the biomarker.</p>]]></description>
<dc:creator><![CDATA[Kawano, A., Emori, Y., Miyagawa, S.]]></dc:creator>
<dc:date>Tue, 24 Mar 2009 06:01:15 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1099800409331892</dc:identifier>
<dc:title><![CDATA[Association Between Stress-Related Substances in Saliva and Immune Substances in Breast Milk in Puerperae]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>10</prism:volume>
<prism:endingPage>355</prism:endingPage>
<prism:publicationDate>2009-04-01</prism:publicationDate>
<prism:startingPage>350</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://brn.sagepub.com/cgi/content/abstract/10/4/356?rss=1">
<title><![CDATA[The Role of Impaired Mitochondrial Lipid Oxidation in Obesity]]></title>
<link>http://brn.sagepub.com/cgi/content/abstract/10/4/356?rss=1</link>
<description><![CDATA[<p>Obesity represents a disruption in balancing fuel intake with energy expenditure in favor of energy conservation. Adiposity is known to be carefully regulated and, over time, highly resistant to major changes, raising questions about how energy homeostasis can become dysregulated in favor of fat accumulation. In obesity, the excess lipid accumulation represents a surfeit of energy, but those who are obese often experience rapid fatigue and decreased physical endurance, reflecting an energy deficiency. To develop an explanation for this apparent contradiction in energy homeostasis and the chronic overeating relative to energy used in obesity, a review of the literature was conducted. The resulting model of obesity is based on a growing body of research demonstrating that altered mitochondrial energy production, particularly in skeletal muscles, is a major anomaly capable of setting off a chain of metabolic events leading to obesity. Alterations in skeletal muscle mitochondria distribution and their oxidative and glycolytic energy capacities in obesity are described. The metabolic responses of obese and normal individuals to exercise are contrasted, and the effects of weight loss on energy production are presented. The effect of altered fat oxidation is considered in relation to energy regulation by the central nervous system and the development of major obesity comorbidities, including systemic inflammation, insulin resistance and diabetes, and cardiovascular disease. Recommendations for clinical intervention and additional research are proposed based on the model presented of impaired mitochondrial function in obesity.</p>]]></description>
<dc:creator><![CDATA[Rogge, M. M.]]></dc:creator>
<dc:date>Tue, 24 Mar 2009 06:01:16 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1099800408329408</dc:identifier>
<dc:title><![CDATA[The Role of Impaired Mitochondrial Lipid Oxidation in Obesity]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>10</prism:volume>
<prism:endingPage>373</prism:endingPage>
<prism:publicationDate>2009-04-01</prism:publicationDate>
<prism:startingPage>356</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://brn.sagepub.com/cgi/content/abstract/10/4/374?rss=1">
<title><![CDATA[Long-Term Exercise Training Selectively Alters Serum Cytokines Involved in Fever]]></title>
<link>http://brn.sagepub.com/cgi/content/abstract/10/4/374?rss=1</link>
<description><![CDATA[<p>Long-term exercise training selectively alters serum cytokines involved in fever. Chronic exercise training has a number of effects on the immune system that may mimic the physiological response to fever. Female rats that voluntarily exercise on running wheels develop an elevated daytime core temperature after several weeks of training. It remains to be seen whether the elevation in daytime temperature involves inflammatory patterns characteristic of an infectious fever. We assessed whether chronic exercise training in the rat would alter levels of cytokines involved in fever. Female Sprague Dawley rats at 45 days of age weighing 90&mdash;110 g were divided into two groups (exercise and sedentary) and housed at an ambient temperature of 22<sup>&deg;</sup>C. Interleukin-1 beta (IL-1&beta;), interleukin-6 (IL-6), interleukin-10 (IL-10), tumor necrosis factor alpha (TNF-), iron, and zinc levels were analyzed. Rats underwent 8 weeks of exercise on running wheels. Exercise led to altered levels of some key cytokines that are involved in fever. Exercise animals had significantly higher IL-1&beta; levels and lower IL-10 levels compared to sedentary animals. Although IL-6 levels were slightly lower in the exercise animals, these levels were not significantly affected by training. TNF- activity was similar in the two groups. Training also led to a slight increase in serum zinc and decrease in serum unsaturated iron binding capacity (UIBC). The data suggest that chronic exercise training evokes immune responses that mimic some, but not all, aspects of fever. This may explain why exercise leads to elevated daytime core temperature.</p>]]></description>
<dc:creator><![CDATA[Rowsey, P. J., Metzger, B. L., Carlson, J., Gordon, C. J.]]></dc:creator>
<dc:date>Tue, 24 Mar 2009 06:01:16 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1099800408329409</dc:identifier>
<dc:title><![CDATA[Long-Term Exercise Training Selectively Alters Serum Cytokines Involved in Fever]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>10</prism:volume>
<prism:endingPage>380</prism:endingPage>
<prism:publicationDate>2009-04-01</prism:publicationDate>
<prism:startingPage>374</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://brn.sagepub.com/cgi/content/abstract/10/4/381?rss=1">
<title><![CDATA[A Biobehavioral Model for the Study of Exercise Interventions in Cancer-related Fatigue]]></title>
<link>http://brn.sagepub.com/cgi/content/abstract/10/4/381?rss=1</link>
<description><![CDATA[<p>Cancer-related fatigue (CRF) is a multifactorial, biobehavioral phenomenon experienced by the majority of persons with cancer. It has negative consequences on the individual's physical functioning and quality of life. An array of biological, psychobehavioral, and functional mechanisms contributes to its occurrence. A relatively large number of studies have examined the effect of physical exercise on CRF over the past few decades. Most of these studies did not specifically examine the effect of physical exercise on the biobehavioral mechanisms underlying CRF. For the most part, these studies have not been guided by a consistent theoretical model. Consequently, the mechanisms by which exercise may ameliorate CRF are not fully elucidated. A theoretical model incorporating fatigue-related biobehavioral variables that could be affected by physical exercise will allow for effective knowledge development in this area and could lead to the development and refinement of exercise protocols that specifically target these mechanisms. Thus, the purpose of this paper is to present a comprehensive theoretical model to guide future research on the effectiveness of exercise interventions in CRF. The proposed model incorporates the biological, psychobehavioral, and functional variables implicated in the induction of CRF.</p>]]></description>
<dc:creator><![CDATA[Al-Majid, S., Gray, D. P.]]></dc:creator>
<dc:date>Tue, 24 Mar 2009 06:01:16 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1099800408324431</dc:identifier>
<dc:title><![CDATA[A Biobehavioral Model for the Study of Exercise Interventions in Cancer-related Fatigue]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>10</prism:volume>
<prism:endingPage>391</prism:endingPage>
<prism:publicationDate>2009-04-01</prism:publicationDate>
<prism:startingPage>381</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://brn.sagepub.com/cgi/content/abstract/10/4/392?rss=1">
<title><![CDATA[The Interplay Between Secondhand Cigarette Smoke, Genetics, and Cervical Cancer: A Review of the Literature]]></title>
<link>http://brn.sagepub.com/cgi/content/abstract/10/4/392?rss=1</link>
<description><![CDATA[<p>Research has suggested a link between smoking and cervical cancer; however, little data are available on secondhand smoke (SHS) exposure and cervical cancer risk. This article reviews the literature on the links among smoking, SHS exposure and cervical cancer. The review was based on a search of electronic databases. The research reviewed clearly showed that smoking increases cervical cancer risk through myriad mechanisms that interact with genetics and the pathologic processes leading to cervical cancer. However, less is understood about the role of SHS in cervical cancer. With new technology enabling scientists to examine how genomic structure responds to environmental stimuli, more information should be forthcoming on links between SHS exposure, biomarkers, and genetic changes involved in the development of cervical cancer.</p>]]></description>
<dc:creator><![CDATA[Pate Capps, N., Stewart, A., Burns, C.]]></dc:creator>
<dc:date>Tue, 24 Mar 2009 06:01:16 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1099800408330849</dc:identifier>
<dc:title><![CDATA[The Interplay Between Secondhand Cigarette Smoke, Genetics, and Cervical Cancer: A Review of the Literature]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>10</prism:volume>
<prism:endingPage>399</prism:endingPage>
<prism:publicationDate>2009-04-01</prism:publicationDate>
<prism:startingPage>392</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://brn.sagepub.com/cgi/content/abstract/10/4/400?rss=1">
<title><![CDATA[Conceptualizing Compensatory Responses: Implications for Treatment and Research]]></title>
<link>http://brn.sagepub.com/cgi/content/abstract/10/4/400?rss=1</link>
<description><![CDATA[<p>Many scientists approach the discovery and application of knowledge of physiological processes from a reductionistic paradigm. A reductionistic approach focuses on treating one or a few key disease-related variables but overlooks the interaction of systems and their dependency on one another to produce homeostasis. The purposes of this article are to examine the current paradigm underlying treatment and its effect on patient outcome and to present an alternative perspective for understanding the body's compensatory responses and their implications for treatment and research. Chaos theory and nonlinear methods are presented as possible ways to conceptualize and explore the complex integration of physiological patterns in response to disease, aging, and treatment.</p>]]></description>
<dc:creator><![CDATA[Fisher, E. M., Wineman, N. M.]]></dc:creator>
<dc:date>Tue, 24 Mar 2009 06:01:16 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1099800408324612</dc:identifier>
<dc:title><![CDATA[Conceptualizing Compensatory Responses: Implications for Treatment and Research]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>10</prism:volume>
<prism:endingPage>408</prism:endingPage>
<prism:publicationDate>2009-04-01</prism:publicationDate>
<prism:startingPage>400</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://brn.sagepub.com/cgi/content/abstract/10/4/409?rss=1">
<title><![CDATA[A Feasibility Study of Valerian Extract for Sleep Disturbance in Person With Arthritis]]></title>
<link>http://brn.sagepub.com/cgi/content/abstract/10/4/409?rss=1</link>
<description><![CDATA[<p><I>Objectives</I>: To present a pilot study of valerian to explore issues of feasibility and efficacy in studies of sedative herbs for arthritis-related sleep disturbance. Methods: Fifteen persons with arthritis and mild sleep disturbance were randomized to receive 600 mg valerian (<I>Valeriana officinalis, n</I> = 7) or placebo (<I>n</I> = 8) for five nights.</p><p><I>Results</I>: Protocol adherence (dosing and data collection) was high. Allocation concealment was successful using a novel approach for matching the placebo on the distinctive odor of valerian. Nonsignificant differences between the groups were found on all sleep outcomes, measured by daily diaries and wrist actigraphy.</p><p><I>Conclusion</I>: The study methods were feasible, except for recruitment issues (addressed in the discussion), and may guide the testing of other sedative herbs for persons with arthritis. Although efficacy outcomes were inconclusive due to the small sample size of this study, recent evidence from larger trials of valerian also does not support its efficacy.</p>]]></description>
<dc:creator><![CDATA[Taibi, D. M., Bourguignon, C., Gill Taylor, A.]]></dc:creator>
<dc:date>Tue, 24 Mar 2009 06:01:16 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1099800408324252</dc:identifier>
<dc:title><![CDATA[A Feasibility Study of Valerian Extract for Sleep Disturbance in Person With Arthritis]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>10</prism:volume>
<prism:endingPage>417</prism:endingPage>
<prism:publicationDate>2009-04-01</prism:publicationDate>
<prism:startingPage>409</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://brn.sagepub.com/cgi/reprint/10/4/420?rss=1">
<title><![CDATA[Reviewer Acknowledgment]]></title>
<link>http://brn.sagepub.com/cgi/reprint/10/4/420?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>Tue, 24 Mar 2009 06:01:16 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1099800409331999</dc:identifier>
<dc:title><![CDATA[Reviewer Acknowledgment]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>10</prism:volume>
<prism:endingPage>421</prism:endingPage>
<prism:publicationDate>2009-04-01</prism:publicationDate>
<prism:startingPage>420</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://brn.sagepub.com/cgi/reprint/10/3/201?rss=1">
<title><![CDATA[The Evolving Contribution of Nurse Researchers to Genetics, as Seen Through the Prism of Biological Research for Nursing]]></title>
<link>http://brn.sagepub.com/cgi/reprint/10/3/201?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Yucha, C. B., Wiss, M.]]></dc:creator>
<dc:date>Mon, 15 Dec 2008 23:55:31 PST</dc:date>
<dc:identifier>info:doi/10.1177/1099800408327994</dc:identifier>
<dc:title><![CDATA[The Evolving Contribution of Nurse Researchers to Genetics, as Seen Through the Prism of Biological Research for Nursing]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>10</prism:volume>
<prism:endingPage>204</prism:endingPage>
<prism:publicationDate>2009-01-01</prism:publicationDate>
<prism:startingPage>201</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://brn.sagepub.com/cgi/content/abstract/10/3/205?rss=1">
<title><![CDATA[APOE Genotype and Functional Outcome Following Aneurysmal Subarachnoid Hemorrhage]]></title>
<link>http://brn.sagepub.com/cgi/content/abstract/10/3/205?rss=1</link>
<description><![CDATA[<p>Apolipoprotein E (apoE), the major apolipoprotein in the central nervous system, has been shown to influence neurologic disease progression and response to neurologic injury in a gene-specific manner. Presence of the APOE4 allele is associated with poorer response to traumatic brain injury and ischemic stroke, but the association between APOE genotype and outcome following aneurysmal subarachnoid hemorrhage (SAH) remains unclear. The purpose of this project was to investigate the association between APOE genotype and outcome after SAH. We also explored the association of APOE4 genotype and cerebral vasospasm (CV) presence in a subsample of our population with available angiographic data. A sample of 206 aneurysmal SAH participants had APOE genotyping performed, Glasgow outcome scores (GOS) and modified Rankin scores (MRS) collected at 3 and 6 months after aneurysm rupture. No significant association was found between the presence of the APOE4 genotype and functional outcomes controlling for age, race, size of hemorrhage (Fisher grade), and severity of injury (Hunt &amp; Hess grade). However when controlling for CV and the covariates listed above, individuals with the APOE4 allele had worse functional outcomes at both time points. The presence of the APOE2 allele was not associated with functional outcomes even when considering presence of CV. There was no difference in mortality associated with APOE4 presence, APOE2 presence, or presence of CV. These findings suggest APOE4 allele is associated with poor outcome after aneurysmal SAH.</p>]]></description>
<dc:creator><![CDATA[Gallek, M. J., Conley, Y. P., Sherwood, P. R., Horowitz, M. B., Kassam, A., Alexander, S. A.]]></dc:creator>
<dc:date>Mon, 15 Dec 2008 23:55:31 PST</dc:date>
<dc:identifier>info:doi/10.1177/1099800408323221</dc:identifier>
<dc:title><![CDATA[APOE Genotype and Functional Outcome Following Aneurysmal Subarachnoid Hemorrhage]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>10</prism:volume>
<prism:endingPage>212</prism:endingPage>
<prism:publicationDate>2009-01-01</prism:publicationDate>
<prism:startingPage>205</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://brn.sagepub.com/cgi/content/abstract/10/3/213?rss=1">
<title><![CDATA[Functional Status, Chronic Stress, and Cortisol Response After Mild-to-Moderate Traumatic Brain Injury]]></title>
<link>http://brn.sagepub.com/cgi/content/abstract/10/3/213?rss=1</link>
<description><![CDATA[<p>It is well known that individuals experience difficulties with depressive symptoms and functional status after traumatic brain injury. However, it is unclear what the relationship is between these 2 phenomena and whether there is a biological explanation for. In this secondary analysis, we examined whether depressive symptoms explained postinjury functional status and whether chronic stress and salivary cortisol influenced this relationship. Participants included 75 persons within 24 months of their injury dates who were evaluated or treated in specialty clinics. All participants and a family member or significant other completed survey data, and 50 of the participants provided cortisol data. Results indicated that chronic stress, measured using Cohen's Perceived Stress Scale, completely mediated the relationship between depressive symptoms, measured using the Center for Epidemiological Studies Depression Scale, and psychological functioning, measured using the Patient Competency Rating Scale. Furthermore, those who provided cortisol data displayed hypocortisolemia in their 12-hr profile. Results from this analysis suggest that interventions focused on addressing the chronic stress experience may be important in limiting depressive symptoms and improving psychological functioning. Longitudinal study of this phenomenon is required to understand the progression of chronic stress after traumatic brain injury.</p>]]></description>
<dc:creator><![CDATA[Bay, E., Sikorskii, A., Fuli Gao,  ]]></dc:creator>
<dc:date>Mon, 15 Dec 2008 23:55:31 PST</dc:date>
<dc:identifier>info:doi/10.1177/1099800408326453</dc:identifier>
<dc:title><![CDATA[Functional Status, Chronic Stress, and Cortisol Response After Mild-to-Moderate Traumatic Brain Injury]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>10</prism:volume>
<prism:endingPage>225</prism:endingPage>
<prism:publicationDate>2009-01-01</prism:publicationDate>
<prism:startingPage>213</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://brn.sagepub.com/cgi/content/abstract/10/3/226?rss=1">
<title><![CDATA[Coregulation in Salivary Cortisol During Maternal Holding of Premature Infants]]></title>
<link>http://brn.sagepub.com/cgi/content/abstract/10/3/226?rss=1</link>
<description><![CDATA[<p>Purpose: The purpose of this study was to examine coregulation between mothers and preterm infants in hypothalamic-pituitary-adrenocortical (HPA) system activity, as indicated by salivary cortisol levels, while mothers held their infants. The research questions were (a) does mother&mdash;infant coregulation in HPA activity occur during holding? and (b) if mother&mdash; infant coregulation in HPA activity exists during holding, do type of holding, antenatal steroids, sound level, and maternal touch influence this coregulation? Sample: The sample consisted of 20 mother&mdash; infant dyads with infants at a mean postconceptional age of 34.7 weeks (+0.7) and average postnatal age of 15 days (+9) at the time of cortisol sampling. Design: The design was exploratory using convenience sampling. Maternal and infant cortisol levels were obtained at Time 1 (baseline) and Time 2 (end of holding); at each time, the absolute differences in levels between mother and infant were determined. Coregulation was operationalized as less difference between maternal-infant cortisol levels immediately after holding (Time 2) as compared to before holding (Time 1). Results: The two variables with the highest correlation with the Time 1/Time 2 difference score included antenatal steroids and ambient sound level, which were entered into a linear regression equation as predictor variables. A coregulatory relationship in cortisol levels existed between mothers and infants during holding, which was moderated by sound levels. Nurses in the neonatal intensive care unit (NICU) can facilitate the mother&mdash;infant relationship, as reflected in coregulatory measures, by promoting a quiet environment, particularly around mothers who are holding their infants.</p>]]></description>
<dc:creator><![CDATA[Neu, M., Laudenslager, M. L., Robinson, J.]]></dc:creator>
<dc:date>Mon, 15 Dec 2008 23:55:31 PST</dc:date>
<dc:identifier>info:doi/10.1177/1099800408327789</dc:identifier>
<dc:title><![CDATA[Coregulation in Salivary Cortisol During Maternal Holding of Premature Infants]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>10</prism:volume>
<prism:endingPage>240</prism:endingPage>
<prism:publicationDate>2009-01-01</prism:publicationDate>
<prism:startingPage>226</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://brn.sagepub.com/cgi/content/abstract/10/3/241?rss=1">
<title><![CDATA[The Potential Role of Glucose Transport Changes in Hot Flash Physiology: A Hypothesis]]></title>
<link>http://brn.sagepub.com/cgi/content/abstract/10/3/241?rss=1</link>
<description><![CDATA[<p>Purpose: The purpose of this article is to detail a novel hypothesis regarding the role of changes in brain glucose delivery in menopausal hot flashes. Organizing Framework: The impaired glucose delivery hypothesis of menopausal hot flashes is presented as a potential model of hot flash physiology. As foundational to the hypothesis, brain glucose physiology, specifically neurobarrier coupling, is presented in detail. With brain activation, glucose needs immediate increase; additional glucose is supplied through increased production of glucose transporter 1 (GLUT1) at the blood&mdash;brain barrier (BBB) and through vasodilation. Estrogen is important to this system in stimulating production of GLUT1. As estrogen declines at menopause, upregulation of GLUT1 is less efficient. As a consequence, neurobarrier coupling overcompensates with an excess neurovascular response, or a hot flash. Research supporting this hypothesis is briefly reviewed and new questions raised are reviewed. Conclusions: The impaired glucose hypothesis of menopausal hot flashes proposes an inadequate neurobarrier response to neurometabolic stimulation as estrogen declines, resulting in additional neurometabolic stimulation with consequent neurovascular stimulation. In this model, the menopausal woman has diminished ability to respond to fluctuations in blood glucose over the course of the day, which results in hot flashes as a counter-regulatory response. This perspective accounts for observed physiological changes that have not been previously detailed. New research directions are identified.</p>]]></description>
<dc:creator><![CDATA[Dormire, S. L.]]></dc:creator>
<dc:date>Mon, 15 Dec 2008 23:55:31 PST</dc:date>
<dc:identifier>info:doi/10.1177/1099800408324558</dc:identifier>
<dc:title><![CDATA[The Potential Role of Glucose Transport Changes in Hot Flash Physiology: A Hypothesis]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>10</prism:volume>
<prism:endingPage>247</prism:endingPage>
<prism:publicationDate>2009-01-01</prism:publicationDate>
<prism:startingPage>241</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://brn.sagepub.com/cgi/content/abstract/10/3/248?rss=1">
<title><![CDATA[Allostatic Load and Frailty in the Women's Health and Aging Studies]]></title>
<link>http://brn.sagepub.com/cgi/content/abstract/10/3/248?rss=1</link>
<description><![CDATA[<p>Background: Frailty involves decrements in many physiologic systems, is prevalent in older ages, and is characterized by increased vulnerability to disability and mortality. It is yet unclear how this geriatric syndrome relates to a preclinical cumulative marker of multisystem dysregulation. The purpose of this study was to evaluate whether allostatic load (AL) was associated with the geriatric syndrome of frailty in older community-dwelling women. Methods: We examined the cross-sectional relationship between AL and a validated measure of frailty in the baseline examination of two complementary population-based cohort studies, the Women's Health and Aging studies (WHAS) I and II. This sample of 728 women had an age range of 70&mdash;79. We used ordinal logistic regression to estimate the relationship between AL and frailty controlling for covariates. Results: About 10% of women were frail and 46% were prefrail. AL ranged from 0 to 8 with 91% of participants scoring between 0 and 4. Regression models showed that a unit increase in the AL score was associated with increasing levels of frailty (OR = 1.16, 95% CI = 1.04&mdash;1.28) controlling for race, age, education, smoking status, and comorbidities. Conclusion: This study suggests that frailty is associated with AL. The observed relationship provides some support for the hypothesis that accumulation of physiological dysregulation may be related to the loss of reserve characterized by frailty.</p>]]></description>
<dc:creator><![CDATA[Szanton, S.L., Allen, J.K., Seplaki, C.L., Bandeen-Roche, K., Fried, L.P.]]></dc:creator>
<dc:date>Mon, 15 Dec 2008 23:55:31 PST</dc:date>
<dc:identifier>info:doi/10.1177/1099800408323452</dc:identifier>
<dc:title><![CDATA[Allostatic Load and Frailty in the Women's Health and Aging Studies]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>10</prism:volume>
<prism:endingPage>256</prism:endingPage>
<prism:publicationDate>2009-01-01</prism:publicationDate>
<prism:startingPage>248</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://brn.sagepub.com/cgi/content/abstract/10/3/257?rss=1">
<title><![CDATA[The Effect of a Senior Jazz Dance Class on Static Balance in Healthy Women Over 50 Years of Age: A Pilot Study]]></title>
<link>http://brn.sagepub.com/cgi/content/abstract/10/3/257?rss=1</link>
<description><![CDATA[<p>The purpose of this pilot study is to assess the impact of a senior jazz dance class on static balance for healthy women over 50 years of age using the NeuroCom Smart Balance Master System (Balance Master). A total of 12 healthy women aged 54&mdash;88 years completed a 15-week jazz dance class which they attended 1 time per week for 90 min per class. Balance data were collected using the Sensory Organization Test (SOT) at baseline (pre), at 7 weeks (mid), and after 15 weeks (post). An equilibrium score measuring postural sway was calculated for each of six different conditions. The composite equilibrium score (all six conditions integrated to 1 score) was used as an overall measure of balance. Repeated measures analyses of variance (ANOVAs) were used to compare the means of each participant's SOT composite equilibrium score in addition to the equilibrium score for each individual condition (1&mdash;6) across the 3 time points (pre, mid, post). There was a statistically significant difference among the means, p &lt; .0005. Pairwise (Bonferroni) post hoc analyses revealed the following statistically significant findings for SOT composite equilibrium scores for the pre (67.33 + 10.43), mid (75.25 + 6.97), and post (79.00 + 4.97) measurements: premid (p = .008); prepost (p &lt; .0005); midpost (p = .033). In addition, correlational statistics were used to determine any relationship between SOT scores and age. Results indicated that administration of a 15-week jazz dance class 1 time per week was beneficial in improving static balance as measured by the Balance Master SOT.</p>]]></description>
<dc:creator><![CDATA[Wallmann, H. W., Gillis, C. B., Alpert, P. T., Miller, S. K.]]></dc:creator>
<dc:date>Mon, 15 Dec 2008 23:55:31 PST</dc:date>
<dc:identifier>info:doi/10.1177/1099800408322600</dc:identifier>
<dc:title><![CDATA[The Effect of a Senior Jazz Dance Class on Static Balance in Healthy Women Over 50 Years of Age: A Pilot Study]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>10</prism:volume>
<prism:endingPage>266</prism:endingPage>
<prism:publicationDate>2009-01-01</prism:publicationDate>
<prism:startingPage>257</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://brn.sagepub.com/cgi/content/abstract/10/3/267?rss=1">
<title><![CDATA[Hemodynamic Response to Postural Shift in Women with Multiple Chemical Sensitivities]]></title>
<link>http://brn.sagepub.com/cgi/content/abstract/10/3/267?rss=1</link>
<description><![CDATA[<p>Multiple chemical sensitivity (MCS) is a chronic condition prevalent in women; the symptoms are reproducible with repeated low-level chemical exposure. Evidence gathered through clinical observations suggests that women with MCS may be at risk for autonomic nervous system dysfunction as evidenced by abnormal heart rate and pulse pressure responses to exercise. The primary objective of this study was to describe the hemodynamic response to postural shift in 17 women with MCS. Using impedance cardiography, hemodynamic measures were taken while sitting and immediately upon standing. The hemodynamic response to standing was increased heart rate (p &lt; .0001), decreased stroke volume (p = .002), decreased left ventricular ejection time (p &lt; .0001), increased diastolic blood pressure (p = .01), and increased systemic vascular resistance (p =.002). Although this pattern of hemodynamic response was normal, the magnitude of the changes was considerably less than those observed previously in healthy participants. These findings warrant further investigation.</p>]]></description>
<dc:creator><![CDATA[McFetridge-Durdle, J. A., Routledge, F. S., Sampalli, T., Fox, R., Livingston, H., Adams, B.]]></dc:creator>
<dc:date>Mon, 15 Dec 2008 23:55:31 PST</dc:date>
<dc:identifier>info:doi/10.1177/1099800408324251</dc:identifier>
<dc:title><![CDATA[Hemodynamic Response to Postural Shift in Women with Multiple Chemical Sensitivities]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>10</prism:volume>
<prism:endingPage>273</prism:endingPage>
<prism:publicationDate>2009-01-01</prism:publicationDate>
<prism:startingPage>267</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://brn.sagepub.com/cgi/content/abstract/10/3/274?rss=1">
<title><![CDATA[A Comparison of Field Methods to Assess Body Composition in a Diverse Group of Sedentary Women]]></title>
<link>http://brn.sagepub.com/cgi/content/abstract/10/3/274?rss=1</link>
<description><![CDATA[<p>Accurate assessment of body composition is essential in the evaluation of obesity. While laboratory methods are commonly used to assess fat mass, field measures (e.g., skinfold thickness [SKF] and bioelectrical impedance [BIA]) may be more practical for screening large numbers of individuals in intervention studies. In this study, a correlational design was used among 46 racially and ethnically diverse, sedentary women (mean age = 25.73 years) to (a) compare the percentage of body fat as determined by SKF and the upper body BIA and (b) examine the effects of body mass index (BMI), racial/ethnic background, age, and stage of the menstrual cycle on differences in the estimated percentage of body fat obtained using the SKF and BIA. Overall, a significant correlation between SKF and BIA (r = .98, p &lt; .001) was found, with similar findings among Black, Hispanic and White non-Hispanic women. The mean differences between BIA and SKF were not significantly correlated with BMI, age, race/ethnicity or stage of the menstrual cycle. Data from this study suggest that BIA showed similar body fat prediction values compared with SKF and may be a viable alternative to SKF among diverse groups of healthy women. Additional testing and comparison of these field methods with the laboratory methods of hydrodensitometry or dual energy X-ray absorptiometry is recommended to further determine whether BIA devices can be routinely recommended as an alternative to the SKF.</p>]]></description>
<dc:creator><![CDATA[D'Alonzo, K. T., Aluf, A., Vincent, L., Cooper, K.]]></dc:creator>
<dc:date>Mon, 15 Dec 2008 23:55:31 PST</dc:date>
<dc:identifier>info:doi/10.1177/1099800408326583</dc:identifier>
<dc:title><![CDATA[A Comparison of Field Methods to Assess Body Composition in a Diverse Group of Sedentary Women]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>10</prism:volume>
<prism:endingPage>283</prism:endingPage>
<prism:publicationDate>2009-01-01</prism:publicationDate>
<prism:startingPage>274</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://brn.sagepub.com/cgi/content/abstract/10/3/284?rss=1">
<title><![CDATA[Placental Insufficiency: Programming of Leptin Secretion, Blood Pressure, and Postnatal Growth in Two Generations of Sprague-Dawley Rats]]></title>
<link>http://brn.sagepub.com/cgi/content/abstract/10/3/284?rss=1</link>
<description><![CDATA[<p>Regulatory process may be altered in response to the intrauterine environment, leading to the development of altered growth trajectory and disease later in life. Previously, our lab reported reduced leptin levels in pregnant hypertensive Sprague-Dawley rat dams with placental insufficiency. The purposes of this study were to investigate the relationship between leptin levels, growth and hypertension in two generations of offspring exposed to placental insufficiency. Leptin levels were significantly different only at 12 weeks in female first generation offspring (p &lt; 0.05). Variations in postnatal body and organ weights were evident in first generation females at 3 and 12 weeks of age. There were no significant correlations with plasma leptin levels and systolic blood pressure in offspring groups at any age point. Our findings indicate that fetal exposure to maternal hypertension and hypoleptinemia is associated with altered leptin and growth patterns in mature female offspring and not perpetuated to a second generation.</p>]]></description>
<dc:creator><![CDATA[Anderson, C. M., Lopez, F., Sandeen, A., Johnson, L.]]></dc:creator>
<dc:date>Mon, 15 Dec 2008 23:55:31 PST</dc:date>
<dc:identifier>info:doi/10.1177/1099800408324127</dc:identifier>
<dc:title><![CDATA[Placental Insufficiency: Programming of Leptin Secretion, Blood Pressure, and Postnatal Growth in Two Generations of Sprague-Dawley Rats]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>10</prism:volume>
<prism:endingPage>291</prism:endingPage>
<prism:publicationDate>2009-01-01</prism:publicationDate>
<prism:startingPage>284</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://brn.sagepub.com/cgi/content/abstract/10/3/292?rss=1">
<title><![CDATA[Ascorbic Acid Does Not Influence Consciousness Recovery After Anesthesia]]></title>
<link>http://brn.sagepub.com/cgi/content/abstract/10/3/292?rss=1</link>
<description><![CDATA[<p>Several studies have examined the influence of general anesthesia on changes in consciousness and unconscious cognitive processes. However, much remains to be learned about potential moderators of general anesthetic agents, such as antioxidants including ascorbic acid, and their influence on the recovery of consciousness following general anesthesia. General anesthesia potentially affects plasma ascorbic acid levels and may impair consciousness during the postoperative period; however, published literature regarding these relationships is equivocal. Ascorbic acid is important for brain function and may be related to the return of postoperative consciousness through action on the synaptic receptors in the brain. This study was designed as a pretest&mdash;posttest repeated measures investigation. Ascorbic acid levels were measured at four time periods in patients (N = 50) undergoing surgery and general anesthesia. Following surgery, patients were administered a paper-and-pencil measure of concentration that served as an index of post-anesthesia consciousness. The results suggest that changes occur in plasma ascorbic acid levels at different time points during the anesthesia regimen in nonemergent surgical patients. No statistically significant relationships were found between plasma ascorbic acid levels and improved post-anesthesia consciousness, suggesting that ascorbic acid does not influence recovery of consciousness following general anesthesia.</p>]]></description>
<dc:creator><![CDATA[Talley V, H. C., Wicks, M. N., Carter, M., Roper, B.]]></dc:creator>
<dc:date>Mon, 15 Dec 2008 23:55:31 PST</dc:date>
<dc:identifier>info:doi/10.1177/1099800408323222</dc:identifier>
<dc:title><![CDATA[Ascorbic Acid Does Not Influence Consciousness Recovery After Anesthesia]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>10</prism:volume>
<prism:endingPage>298</prism:endingPage>
<prism:publicationDate>2009-01-01</prism:publicationDate>
<prism:startingPage>292</prism:startingPage>
<prism:section>Article</prism:section>
</item>

</rdf:RDF>