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OBJECTIVES: To examine colorectal cancer (CRC) survivors' symptom characteristics (occurrence, frequency, and severity) during acute cancer survivorship. PARTICIPANTS & SETTING: A cross-sectional study of 117 CRC survivors was conducted at a National Cancer Institute-designated cancer center in South Florida. METHODS & VARIABLES: Symptom characteristics were assessed by the Therapy-Related Symptom Checklist. Participants completed a 25-item demographic questionnaire. Mann-Whitney U and Kruskal-Wallis H tests assessed between-group differences based on sex, age, education, and months since diagnosis. Exploratory factor analysis was performed to identify preliminary symptom clusters. RESULTS: 117 CRC survivors completed the study (age range = 21-88 years, 56% male, and 79% stage IV). Common symptoms included peripheral neuropathy, fatigue/feeling sluggish, and skin changes. Significance was found between months since diagnosis and number of symptoms (p = 0.03), suggesting that symptoms accumulate with time. Chemotherapy (85%) was the most common treatment type, and exploratory factor analysis identified two chemotherapy-related symptom clusters. IMPLICATIONS FOR NURSING: Nurses are poised to identify, prevent, and promote self-management skills to reduce symptoms. [ABSTRACT FROM AUTHOR]

Background: Neuroinflammation is an important feature of traumatic brain injury (TBI) that remains poorly understood in the 3- to 12-month period post-TBI., Objective: The purpose of our pilot study was to examine the relationships between biomarkers of neuroinflammation and functional outcomes in TBI patients 3 to 12 months postinjury., Methods: TBI patients (n = 36) 3 to 12 months post-TBI were recruited from a South Florida TBI clinic from May 2022 to June 2023. The Disability Rating Scale, Satisfaction with Life Scale, NIH Toolbox Sorting Working Memory, Neuro-Quality of Life Cognitive Function, Anxiety, Depression, and Sleep assessments were performed. Multiple plasma biomarkers were assayed. Analysis of variance was used to compare between-group results. Linear regression was performed to analyze relationships between biomarkers and outcomes., Results: Brain-derived neurotrophic factor concentrations were higher as postinjury time interval increased and were associated with cognitive battery outcomes. S-100β and glial fibrillary acidic protein were associated with anxiety score and hospital length of stay; S-100β was also associated with depression. Interleukin 6 was associated with cognitive function score and time since injury., Conclusions: We found S-100β, glial fibrillary acidic protein, Interleukin 6, and brain-derived neurotrophic factor to play a larger role in the TBI recovery period than other biomarkers examined. Clinicians should continue to monitor for symptoms post-TBI, as the neuroinflammatory process continues to persist even into the later rehabilitation stage., Competing Interests: The authors declare no conflicts of interest related to this manuscript., (Copyright © 2024 Wolters Kluwer Health, Inc. All rights reserved.)

Traditional machine learning (ML) approaches learn to recognize patterns in the data but fail to go beyond observing associations. Such data-driven methods can lack generalizability when the data is outside the independent and identically distributed (i.i.d) setting. Using causal inference can aid data-driven techniques to go beyond learning spurious associations and frame the data-generating process in a causal lens. We can combine domain expertise and traditional ML techniques to answer causal questions on the data. In this paper, we estimate the causal effect of Pre-Exposure Prophylaxis (PrEP) on mortality in COVID-19 patients from an observational dataset of over 120,000 patients. With the help of medical experts, we hypothesize a causal graph that identifies the causal and non-causal associations, including the list of potential confounding variables. We use estimation techniques such as linear regression, matching, and machine learning (meta-learners) to estimate the causal effect. On average, our estimates show that taking PrEP can result in a 2.1% decrease in the death rate or a total of around 2,540 patients' lives saved in the studied population.

Background: Telomeres are structures at the end of chromosomes that shorten with each cell division. The purpose of this pilot project is to report changes in telomere length (T/S ratio), indicators of oxidative stress (serum protein carbonyl, vitamin C, GSH:GSSG, and total antioxidant capacity) from Intensive Care Unit (ICU) admission to ICU discharge, and to explore their association with ICU-related morbidities among critically ill mechanically ventilated adults., Methods: Blood was collected from mechanically ventilated patients ( n = 25) at enrollment and within 48 hours of ICU discharge. Telomere length from peripheral blood mononuclear cells (PBMCs) was determined using RTqPCR. ELISAs were used to measure indicators of oxidative stress. Descriptive analysis, paired t-tests, and Pearson's correlations were performed., Results: Mean age was 62.0 ± 12.3 years, 28.6% were male, and 76.2% were White with disease severity using APACHE III (74.6 ± 24.6) and SOFA (7.6 ± 3.2). Mean T/S ratios shortened (ICU: 0.712, post-ICU: 0.683, p < 0.001, n = 19) and serum protein carbonyl increased (ICU: 7437 nmol/mg ± 3328, post-ICU: 10,254 nmol/mg ± 3962, p < 0.005) as did the oxidative stress index (protein carbonyl/GSH:GSSG, ICU: 1049.972 ± 420.923, post-ICU: 1348.971 ± 417.175, p = 0.0104). T/S ratio was positively associated with APACHE III scores (ICU: r = 0.474, post-ICU: r = 0.628, p < 0.05)., Conclusions: Pilot findings suggest that critical illness significantly correlates with telomere attrition, perhaps due to increased oxidative stress. Future larger and longitudinal studies investigating mechanisms of telomere attrition and associations with clinical outcomes are needed to identify potential modifiable factors for subsequent intervention to improve outcomes for critically ill patients.

Objectives: To examine colorectal cancer survivors' positive psychology and symptom characteristics, and to assess for potential impact of prior trauma on these relationships during acute cancer survivorship., Sample & Setting: A cross-sectional study of 117 colorectal cancer survivors was conducted at a National Cancer Institute-designated cancer center., Methods & Variables: Participants completed a demographic questionnaire, and the Carver Benefit Finding Scale and Posttraumatic Growth Inventory assessed positive psychology. Descriptive statistics and multiple linear regression analyses were performed., Results: 49 symptoms were reported and varied based on prior trauma. Significance was found between positive psychology and symptom frequency (p < 0.001); symptoms reported almost daily and daily were inversely related to positive psychology., Implications for Nursing: Nurses should prioritize symptoms; less frequent symptoms improve positive psychology. Early identification of positive changes may promote survivors' self-awareness and management skills to mitigate adverse symptoms.

The world has been affected by COVID-19 coronavirus. At the time of this study, the number of infected people in the United States is the highest globally (31.2 million infections). Within the infected population, patients diagnosed with acute respiratory distress syndrome (ARDS) are in more life-threatening circumstances, resulting in severe respiratory system failure. Various studies have investigated the infections to COVID-19 and ARDS by monitoring laboratory metrics and symptoms. Unfortunately, these methods are merely limited to clinical settings, and symptom-based methods are shown to be ineffective. In contrast, vital signs (e.g., heart rate) have been utilized to early-detect different respiratory diseases in ubiquitous health monitoring. We posit that such biomarkers are informative in identifying ARDS patients infected with COVID-19. In this study, we investigate the behavior of COVID-19 on ARDS patients by utilizing simple vital signs. We analyze the long-term daily logs of blood pressure (BP) and heart rate (HR) associated with 150 ARDS patients admitted to five University of California academic health centers (containing 77,972 samples for each vital sign) to distinguish subjects with COVID-19 positive and negative test results. In addition to the statistical analysis, we develop a deep neural network model to extract features from the longitudinal data. Our deep learning model is able to achieve 0.81 area under the curve (AUC) to classify the vital signs of ARDS patients infected with COVID-19 versus other ARDS diagnosed patients. Since our proposed model uses only the BP and HR, it would be possible to review data prior to the first reported cases in the U.S. to validate the presence or absence of COVID-19 in our communities prior to January 2020. In addition, by utilizing wearable devices, and monitoring vital signs of subjects in everyday settings it is possible to early-detect COVID-19 without visiting a hospital or a care site.

Background: Preterm birth is a risk factor for elevated blood pressure in childhood and the development of hypertension and cardiometabolic disease in adulthood; however, mechanisms for the development of both are poorly understood. Rapid weight gain early in childhood may serve as a driver directly and indirectly through cortisol levels found to be elevated in early childhood in individuals born preterm., Objectives: The objective of this pilot study was to examine the effect sizes of the relationships between weight gain and blood pressure in toddlers born very preterm. A secondary aim was to note any mediating effect of cortisol on the relationships between weight gain and blood pressure., Methods: A cross-sectional design with a convenience sample of 36 toddlers who were born very preterm was used to examine the relationships between postnatal weight gain, cortisol, and blood pressure at follow-up., Results: Many of the participants experienced rapid weight gain in the first 12 months of life. Mean systolic and diastolic readings were 94 and 56.6, respectively. Diastolic blood pressure readings were obtained from 23 participants, and the majority were elevated. Weight gain was associated with diastolic blood pressure with a medium effect size. A mediating role with cortisol was not supported., Discussion: Although findings need to be validated in a larger sample, the blood pressure elevations in this sample were alarming. If readings continue to amplify as these children age, the fact that elevations are already present during the toddler period could indicate more significant cardiovascular disease in adulthood for this population. Rapid weight gain in early life may be a driver for elevated blood pressure even during early childhood in individuals born preterm.

Background: There is a compelling unmet medical need for biomarker-based models to risk-stratify patients with acute respiratory distress syndrome. Effective stratification would optimize participant selection for clinical trial enrollment by focusing on those most likely to benefit from new interventions. Our objective was to develop a prognostic, biomarker-based model for predicting mortality in adult patients with acute respiratory distress syndrome., Methods: This is a secondary analysis using a cohort of 252 mechanically ventilated subjects with the diagnosis of acute respiratory distress syndrome. Survival to day 7 with both day 0 (first day of presentation) and day 7 sample availability was required. Blood was collected for biomarker measurements at first presentation to the intensive care unit and on the seventh day. Biomarkers included cytokine-chemokines, dual-functioning cytozymes, and vascular injury markers. Logistic regression, latent class analysis, and classification and regression tree analysis were used to identify the plasma biomarkers most predictive of 28-day ARDS mortality., Results: From eight biologically relevant biomarker candidates, six demonstrated an enhanced capacity to predict mortality at day 0. Latent-class analysis identified two biomarker-based phenotypes. Phenotype A exhibited significantly higher plasma levels of angiopoietin-2, macrophage migration inhibitory factor, interleukin-8, interleukin-1 receptor antagonist, interleukin-6, and extracellular nicotinamide phosphoribosyltransferase (eNAMPT) compared to phenotype B. Mortality at 28 days was significantly higher for phenotype A compared to phenotype B (32% vs 19%, p = 0.04)., Conclusions: An adult biomarker-based risk model reliably identifies ARDS subjects at risk of death within 28 days of hospitalization.

Background: Precision health is a population-based approach that incorporates big-data strategies to understand the complex interactions between biological, environmental, lifestyle, and psychosocial factors that influence health., Purpose: A promising tool to facilitate precision health research and its dissemination is the ConNECT Framework., Methods: Here, we discuss the relationship of the five broad and synergistic principles within the ConNECT Framework as they may apply to nursing science research: (1) Integrating Context, (2) Fostering a Norm of Inclusion, (3) Ensuring Equitable Diffusion of Innovations, (4) Harnessing Communication Technology, and (5) Prioritizing Specialized Training., Discussion/conclusion: The principles within this framework can be used by nurse scientists and educators to guide and disseminate precision health research., (Copyright © 2019. Published by Elsevier Inc.)

Purpose: Long-term consequences of prematurity are a public health concern. A pattern of slow initial weight gain followed by a period of rapid weight gain has been associated with poor cardiometabolic health outcomes. The purpose of this study was to examine the relationships between infant feeding practices and weight gain in a sample of 18-to-24-month olds corrected age born very preterm., Design and Methods: A cross-sectional design was used to examine the relationships between infant feeding practices and weight gain. Estimates of effect sizes and model fit estimates were the primary parameters of interest., Results: Most of the participants received human milk after birth, but most had transitioned to formula before three months. Slightly less than half received complementary foods prior to four months corrected age. Gains in weight and head circumference were rapid after discharge from the neonatal intensive care unit, while gains in length lagged behind. Infant feeding practices did not have a clinically meaningful effect on weight gain., Conclusions: While the initiation of human milk feedings was encouraging, the duration fell short of recommendations. Practices such as the early introduction of complementary feedings and the addition of rice cereal to the bottle are troubling. Additionally, the rapid increase in weight gain may have a negative impact on future cardiometabolic health., Practice Implications: Clinical recommendations include ensuring support for the use of human milk before and after hospital discharge, close monitoring of physical growth, and ensuring adherence to the guidelines for the introduction of complementary foods., (Copyright © 2018 Elsevier Inc. All rights reserved.)

The receptor for advanced glycation end-products (RAGE) is a pattern recognition receptor and member of the immunoglobulin superfamily. RAGE is constitutively expressed in the distal lung where it co-localizes with the alveolar epithelium; RAGE expression is otherwise minimal or absent, except with disease. This suggests RAGE plays a role in lung physiology and pathology. We used proteomics to identify and characterize the effects of RAGE on rat alveolar epithelial (R3/1) cells. LC-MS/MS identified 177 differentially expressed proteins and the PANTHER Classification System further segregated proteins. Proteins involved in gene transcription (RNA and mRNA splicing, mRNA processing) and transport (protein, intracellular protein) were overrepresented; genes involved in a response to stimulus were underrepresented. Immune system processes and response to stimuli were downregulated with RAGE knockdown. Western blot confirmed RAGE-dependent changes in protein expression for NFκB and NLRP3 that was functionally supported by a reduction in IL-1β and phosphorylated p65. We also assessed RAGE's effect on redox regulation and report that RAGE knockdown attenuated oxidant production, decreased protein oxidation, and increased reduced thiol pools. Collectively the data suggest that RAGE is a critical regulator of epithelial cell response and has implications for our understanding of lung disease, specifically acute lung injury., Significance Statement: In the present study, we undertook the first proteomic evaluation of RAGE-dependent processes in alveolar epithelial cells. The alveolar epithelium is a primary target during acute lung injury, and our data support a role for RAGE in gene transcription, protein transport, and response to stimuli. More over our data suggest that RAGE is a critical driver of redox regulation in the alveolar epithelium. The conclusions of the present work assist to unravel the molecular events that underlie the function of RAGE in alveolar epithelial cells and have implications for our understanding of RAGE signaling during lung injury. Our study was the first proteomic comparison showing the effects of RAGE activation from alveolar epithelial cells that constitutively express RAGE and these results can affect a wide field of lung biology, pulmonary therapeutics, and proteomics., (Copyright © 2018 Elsevier B.V. All rights reserved.)

The amiloride-sensitive epithelial sodium channel (ENaC) has been characterized in a variety of non-epithelial tissues. In the current study we sought to understand the effect of angiotensin II on δ ENaC function using human umbilical vein endothelial cells (HUVECs). The δ ENaC subunit is found in humans, but notably absent in rat and most mouse epithelial tissues. In this study we report the presence of δ ENaC in HUVECS with a half-life of ~80min and a change in δ ENaC abundance when HUVECs were treated with angiotensin II. We also observed that angiotensin II increased apical membrane expression of δ ENaC and decreased protein ubiquitination. Equivalent short circuit current measurements showed angiotensin II increased δ ENaC ion transport in HUVEC cells. Treatment with the antioxidant apocynin attenuated angiotensin II mediated effects indicating an important role for angiotensin-derived H 2 O 2 in δ ENaC subunit regulation. Whole cell recordings from oocytes injected with δβγ ENaC shows H 2 O 2 -sensitive current. These results suggest that δ ENaC subunits can make up functional channel in HUVEC cells that are regulated by angiotensin II in a redox-sensitive manner. The novel findings have significant implications for our understanding of the role of ENaC in vascular conditions in which oxidative stress occurs., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Amiloride-sensitive epithelial Na(+) channels (ENaC) regulate fluid balance in the alveoli and are regulated by oxidative stress. Since glutathione (GSH) is the predominant antioxidant in the lungs, we proposed that changes in glutathione redox potential (Eh) would alter cell signaling and have an effect on ENaC open probability (Po). In the present study, we used single channel patch-clamp recordings to examine the effect of oxidative stress, via direct application of glutathione disulfide (GSSG), on ENaC activity. We found a linear decrease in ENaC activity as the GSH/GSSG Eh became less negative (n = 21; P < 0.05). Treatment of 400 μM GSSG to the cell bath significantly decreased ENaC Po from 0.39 ± 0.06 to 0.13 ± 0.05 (n = 8; P < 0.05). Likewise, back-filling recording electrodes with 400 μM GSSG reduced ENaC Po from 0.32 ± 0.08 to 0.17 ± 0.05 (n = 10; P < 0.05), thus implicating GSSG as an important regulatory factor. Biochemical assays indicated that oxidizing potentials promote S-glutathionylation of ENaC and irreversible oxidation of cysteine residues with N-ethylmaleimide blocked the effects of GSSG on ENaC Po. Additionally, real-time imaging studies showed that GSSG impairs alveolar fluid clearance in vivo as opposed to GSH, which did not impair clearance. Taken together, these data show that glutathione Eh is an important determinant of alveolar fluid clearance in vivo., (Copyright © 2015 the American Physiological Society.)

The receptor for advanced glycation end-products (RAGE), a multiligand member of the Ig family, may play a crucial role in the regulation of lung fluid balance. We quantified soluble RAGE (sRAGE), a decoy isoform, and advanced glycation end-products (AGEs) from the bronchoalveolar lavage fluid of smokers and nonsmokers, and tested the hypothesis that AGEs regulate lung fluid balance through protein kinase C (PKC)-gp91(phox) signaling to the epithelial sodium channel (ENaC). Human bronchoalveolar lavage samples from smokers showed increased AGEs (9.02 ± 3.03 μg versus 2.48 ± 0.53 μg), lower sRAGE (1,205 ± 292 pg/ml versus 1,910 ± 263 pg/ml), and lower volume(s) of epithelial lining fluid (97 ± 14 ml versus 133 ± 17 ml). sRAGE levels did not predict ELF volumes in nonsmokers; however, in smokers, higher volumes of ELF were predicted with higher levels of sRAGE. Single-channel patch clamp analysis of rat alveolar epithelial type 1 cells showed that AGEs increased ENaC activity measured as the product of the number of channels (N) and the open probability (Po) (NPo) from 0.19 ± 0.08 to 0.83 ± 0.22 (P = 0.017) and the subsequent addition of 4-hydroxy-2, 2, 6, 6-tetramethylpiperidine-N-oxyl decreased ENaC NPo to 0.15 ± 0.07 (P = 0.01). In type 2 cells, human AGEs increased ENaC NPo from 0.12 ± 0.05 to 0.53 ± 0.16 (P = 0.025) and the addition of 4-hydroxy-2, 2, 6, 6-tetramethylpiperidine-N-oxyl decreased ENaC NPo to 0.10 ± 0.03 (P = 0.013). Using molecular and biochemical techniques, we observed that inhibition of RAGE and PKC activity attenuated AGE-induced activation of ENaC. AGEs induced phosphorylation of p47(phox) and increased gp91(phox)-dependent reactive oxygen species production, a response that was abrogated with RAGE or PKC inhibition. Finally, tracheal instillation of AGEs promoted clearance of lung fluid, whereas concomitant inhibition of RAGE, PKC, and gp91(phox) abrogated the response.

In vivo imaging is an important tool for preclinical studies of lung function and disease. The widespread availability of multimodal animal imaging systems and the rapid rate of diagnostic contrast agent development have empowered researchers to noninvasively study lung function and pulmonary disorders. Investigators can identify, track, and quantify biological processes over time. In this review, we highlight the fundamental principles of bioluminescence, fluorescence, planar X-ray, X-ray computed tomography, magnetic resonance imaging, and nuclear imaging modalities (such as positron emission tomography and single photon emission computed tomography) that have been successfully employed for the study of lung function and pulmonary disorders in a preclinical setting. The major principles, benefits, and applications of each imaging modality and technology are reviewed. Limitations and the future prospective of multimodal imaging in pulmonary physiology are also discussed. In vivo imaging bridges molecular biological studies, drug design and discovery, and the imaging field with modern medical practice, and, as such, will continue to be a mainstay in biomedical research., (Copyright © 2014 the American Physiological Society.)

Ion channels perform a variety of cellular functions in lung epithelia. Oxidant- and antioxidant-mediated mechanisms (that is, redox regulation) of ion channels are areas of intense research. Significant progress has been made in our understanding of redox regulation of ion channels since the last Experimental Biology report in 2003. Advancements include: 1) identification of nonphagocytic NADPH oxidases as sources of regulated reactive species (RS) production in epithelia, 2) an understanding that excessive treatment with antioxidants can result in greater oxidative stress, and 3) characterization of novel RS signaling pathways that converge upon ion channel regulation. These advancements, as discussed at the 2013 Experimental Biology Meeting in Boston, MA, impact our understanding of oxidative stress in the lung, and, in particular, illustrate that the redox state has profound effects on ion channel and cellular function.

Cigarette smoke contains high levels of reactive species. Moreover, cigarette smoke can induce cellular production of oxidants. The purpose of this study was to determine the effect of cigarette smoke extract (CSE)-derived oxidants on epithelial sodium channel (ENaC) activity in alveolar type 1 (T1) and type 2 (T2) cells and to measure corresponding rates of fluid clearance in mice receiving a tracheal instillation of CSE. Single-channel patch clamp analysis of T1 and T2 cells demonstrate that CSE exposure increases ENaC activity (NPo), measured as the product of the number of channels (N) and a channels open probability (Po), from 0.17 ± 0.07 to 0.34 ± 0.10 (n = 9; P = 0.04) in T1 cells. In T2 cells, CSE increased NPo from 0.08 ± 0.03 to 0.35 ± 0.10 (n = 9; P = 0.02). In both cell types, addition of tetramethylpiperidine and glutathione attenuated CSE-induced increases in ENaC NPo. Biotinylation and cycloheximide chase assays indicate that CSE-derived ROS increases channel activity, in part, by maintaining cell surface expression of the α-ENaC subunit. In vivo studies show that tracheal instillation of CSE promoted alveolar fluid clearance after 105 minutes compared with vehicle control (n = 10/group; P < 0.05).

β-Adrenergic receptors (β-AR) increase epithelial sodium channel (ENaC) activity to promote lung fluid clearance. However, the effect of selective β-AR agonist on highly selective cation (HSC) channels or nonselective cation (NSC) channels in alveolar type 1 (T1) and type 2 (T2) cells is unknown. We hypothesized that stimulation with β(1)-AR agonist (denopamine) or β(2)-AR agonist (terbutaline) would increase HSC and/or NSC channel activity in alveolar epithelial cells. We performed single-channel measurements from T1 and T2 cells accessed from rat lung slices. Terbutaline (20 μM) increased HSC ENaC activity (open probability, NP(o)) in T1 (from 0.96 ± 0.61 to 1.25 ± 0.71, n = 5, P <0.05) and T2 cells (from 0.28 ± 0.14 to 1.0 ± 0.30, n = 8, P = 0.02). Denopamine (20 μM) increased NSC NP(o) in T1 cells (from 0.34 ± 0.09 to 0.63 ± 0.14, n = 7, P = 0.02) and in T2 cells (from 0.47 ± 0.09 to 0.68 ± 0.10, P = 0.004). In vivo X-ray imaging of lung fluid clearance and ICI 118,551 selective inhibition of β(2)-ARs confirmed patch-clamp findings. cAMP concentrations increased following treatment with denopamine or terbutaline (n = 3, P < 0.002). The effects of systemic (intraperitoneal, IP) and local (intratracheal, IT) modes of delivery on lung fluid clearance were assessed. IT delivery of denopamine promoted alveolar flooding, whereas IP delivery promoted delayed fluid clearance. In summary, β-AR agonists differentially regulate HSC and NSC in T1 and T2 cells to promote lung fluid clearance in vivo, and the mode of drug delivery is critical for maximizing β-AR agonist efficacy.

There is a lack of cell culture models using primary alveolar type I (AT I) cells. The purpose of this study was to develop cell culture models using rat AT I cells and microvascular endothelial cells from the lung (MVECL). Two types of model systems were developed: single and co-culture systems; additionally a 3-dimensional model system was developed. Pure AT I cell (96.3 ± 2.7%) and MVECL (97.9 ± 1.1%) preparations were used. AT I cell morphology, mitochondrial number and distribution, actin filament arrangement and number of apoptotic cells at confluence, and telomere attrition were characterized. AT I cells maintained their morphometric characteristics through at least population doubling (PD) 35, while demonstrating telomere attrition through at least PD 100. Furthermore, AT I cells maintained the expression of their specific markers, T1α and AQ-5, through PD 42. For the co-cultures, AT I cells were grown on the top and MVECL were grown on the bottom of fibronectin-coated 24-well Transwell Fluroblok™ filter inserts. Neither cell type transmigrated the 1 μm pores. Additionally, AT I cells were grown in a thick layer of Matrigel(®) to create a 3-dimensional model in which primary AT I cells form ring-like structures that resemble an alveolus. The development of these model systems offers the opportunities to investigate AT I cells and their interactions with MVECL in response to pharmacological interventions and in the processes of disease, repair and regeneration., (Copyright © 2011 Elsevier Ltd. All rights reserved.)

Scientists and clinicians frequently use immunological methods (IMs) to investigate complex biological phenomena. Commonly used IMs include immunocytochemistry (IC), enzyme-linked immunosorbent assays (ELISA) and flow cytometry. Each of these methodologies exploits a common principle in IMs -the binding of an antibody to its antigen. Scientists continue to develop new methodologies, such as high-throughput immunohistochemistry (IHC) and in vivo imaging techniques, which exploit antibody-antigen binding, to more accurately answer complex research questions involving single cells up to whole organ systems. The purpose of this paper is to discuss established and evolving IMs and to illustrate the application of these methods to nursing research.

Purpose: To describe available methods for assessing functional capacity in persons with chronic obstructive pulmonary disease (COPD)., Data Sources: An extensive literature review is used to provide pertinent information., Conclusions: COPD disease affects millions of Americans and is physically and psychologically distressing. The hallmark of chronic obstructive pulmonary disease is irreversible airflow limitation and dyspnea. Dyspnea is a major contributor to decreased exercise capacity and functional status in this population. Understanding the methods to complete a functional assessment is important for all practitioners caring for this population., Implications for Practice: This paper provides an overview of current methods used to assess functional status, including pulmonary function testing, exercise testing, and anthropomorphic and self-report measurements. In addition, there is discussion of the indications and contraindications for exercise testing in chronic obstructive pulmonary disease and the clinical significance of performing a global composite of functional ability., (©2011 The Author(s) Journal compilation ©2011 American Academy of Nurse Practitioners.)

Postdoctoral training is vital to a successful career for nurse researchers with a biological or biobehavioral focus. Such training provides structured time to devote to gaining substantive knowledge, expanding one's biological-methods repertoire, and writing grants. However, for unknown reasons, relatively few nurses pursue postdoctoral training. A few plausible explanations include a near critical shortage of nursing faculty coupled with an aging population in need of health care, a lack of available mentoring for predoctoral students to pursue postdoctoral training, and the difficulty of navigating the process of finding and choosing the right match for a postdoctoral experience. The purposes of this article are to provide a rationale for choosing postdoctoral training, review common fellowship opportunities, and discuss the process of finding and choosing the right match for postdoctoral training. The authors provide two prospective plans for postdoctoral training and include a plan for staying on track during the postdoctoral experience.

Although adults with HIV are at risk of developing cognitive impairments, the literature suggests that nurses and clinicians should be cautious about relying on patients' perceptions of their mental abilities. However, these findings are based on a questionnaire of cognitive complaints that may not lend itself easily to a clinical setting. In this pilot study, the relationship between a single item of self-reported cognitive ability and a global cognitive performance composite based on 7 neuropsychological tests was examined in 50 adults with HIV. Depressive symptomatology predicted lower self-reported cognitive ability; however, lower self-reported cognitive ability was also related to poorer cognitive performance but to a lesser extent. These results suggest that adults with HIV who report their cognitive ability as being poor may be experiencing depression, but they may also be experiencing declines in cognitive performance. These findings also suggest that a single item of self-reported cognitive ability may have some clinical value in detecting problems with global cognitive performance, as well as depression. Interventions for assessing patients and improving mood or cognition can be considered by nursing professionals treating individuals with HIV who report their cognitive ability as poor.

Purpose: The purpose of this article is to provide a comprehensive review of the current modalities employed in diagnosing and treating chronic obstructive pulmonary disease (COPD). Special emphasis is placed on current guidelines, as defined by the Global Initiative for Chronic Obstructive Lung Disease., Data Source: A comprehensive literature review for COPD serves as the basis for this article., Conclusions: According to the National COPD Coalition (2004), there are nearly 24 million Americans who suffer from COPD. The incidence of COPD is rising globally and is associated with increased morbidity and mortality. COPD is characterized by progressive decline in function, resulting in concomitant diseases, which increase healthcare dollar expenditures, thus making COPD a concern for healthcare providers in the United States and abroad., Implications for Practice: Once a diagnosis of COPD is made, healthcare providers should explore multiple treatment options in an effort to find the most beneficial regimen. It is only when the treatments are individualized, including physiological therapies and cognitive approaches to lessen risks as well as to reduce exacerbations, that the patient with COPD is able to potentially experience a reasonable quality of life.