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<title>Biological Research For Nursing current issue</title>
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<prism:coverDisplayDate>October 2009</prism:coverDisplayDate>
<prism:publicationName>Biological Research For Nursing</prism:publicationName>
<prism:issn>1099-8004</prism:issn>
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<title>Biological Research For Nursing</title>
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<link>http://brn.sagepub.com</link>
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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>
</item>

<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>
</item>

<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>
</item>

<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>
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