tbuckley/cabot-search huggingface dataset:
Competing Demands for Time and Self-Care Behaviors, Processes of Care, and Intermediate Outcomes Among People With Diabetes
Authors: Laura N. McEwen, Catherine Kim, Susan L. Ettner, William H. Herman, Andrew J. Karter, Gloria L. Beckles, Arleen F. Brown
Journal: Diabetes Care (2011)

To determine whether competing demands for time affect diabetes self-care behaviors, processes of care, and intermediate outcomes.We used survey and medical record data from 5,478 participants in Translating Research Into Action for Diabetes (TRIAD) and hierarchical regression models to examine the cross-sectional associations between competing demands for time and diabetes outcomes, including self-management, processes of care, and intermediate health outcomes.Fifty-two percent of participants reported no competing demands, 7% reported caregiving responsibilities only, 36% reported employment responsibilities only, and 6% reported both caregiving and employment responsibilities. For both women and men, employment responsibilities (with or without caregiving responsibilities) were associated with lower rates of diabetes self-care behaviors, worse processes of care, and, in men, worse HbA(1c).Accommodations for competing demands for time may promote self-management and improve the processes and outcomes of care for employed adults with diabetes.
Smear negative pulmonary tuberculosis in HIV: Over diagnosed or under investigated
Authors: Kavita Mody, Mandar Kubal, Ravindra Nath Sahay, Amita Athavale
Journal: European Respiratory Journal (2012)

Introduction: A significant proportion of HIV infected individuals with respiratory complaints and abnormal chest radiograph are labelled as tuberculosis and started empirical treatment without detailed investigations.  Aims: The aim of the study was to verify the empirical diagnosis of smear negative pulmonary tuberculosis in HIV infected individuals using diagnostic modalities available at a tertiary medical center in resource limited settings.  Methods: 50 HIV infected individuals with respiratory complaints, an abnormal chest radiograoh, and negative sputum for AFB and labelled smear negative pulmonary tuberculosis underwent detailed history, physical examination, and a series of microbiological investigations. HRCT scans of the chest were performed to verify the chest x-ray findings. In the absence of definitive diagnosis on the initial smears, the patients underwent bronchoscopy and sampling of respiratory secretions from the affected areas.  Results: Out of the fifty patients enrolled in the study, definitive diagnosis was reached in 47 patients of which 14 patients (28%) had bronchiectasis, 13 patients (26%) had Pneumocystis jiroveci pneumonia, 5 patients (10%) bacterial pneumonia, and 8 patients (16%) had fungal pneumonia. 6 patients (12%) had non infective conditions like cardiomyopathy (3 patients), bronchial asthma (1 patient), non small cell carcinoma (1 patient), and interstitial lund disease (1 patient). Only 1 patient was confirmed to have tuberculosis on sputum AFB culture and also on bronchial washings AFB smears.  Conclusion: A wide variety of respiratory conditions other then tuberculosis can be definitively diagnosed in HIV infected individuals if investigated in detail.
Antigenic specificity of the cytolytic T lymphocyte response to murine sarcoma virus-induced tumors. III. Characterization of cytolytic T lymphocyte clones specific for Moloney leukemia virus-associated cell surface antigens.
Authors: A Weiss, K T Brunner, H R MacDonald, J C Cerottini
Journal: The Journal of Experimental Medicine (1980)

Cytolytic T lymphocyte (CTL) clones specific for Moloney leukemia virus (MoLV)-derived tumor cells were generated by placing limiting numbers of C57BL/6 responder cells into mixed leukocyte-tumor cell microcultures. Under appropriate conditions (presence of stimulating tumor cells, accessory cells, and T cell growth factor), such cloned CTL could readily be expanded to provide large numbers of homogeneous, highly cytolytic CTL populations for further characterization. Using four target-cell types, three specificity patterns were observed: one reactive with the syngeneic MoLV-derived tumor only, one cross-reactive with an allogeneic MoLV-derived tumor, and one cross-reactive with normal allogeneic cells. Subclones derived from these three types of clones exhibited a high degree of stability in terms of lytic activity and specificity over a 4-mo period of observation. Three clones analyzed by flow cytofluorometry using monoclonal antibodies were all found to be of the Lyt-1+2+ phenotype. Furthermore, lysis of target cells by all of six clones tested was inhibited by anti-H-2Db (but not by anti-H-2Kb) monoclonal antibodies, demonstrating H-2Db-restriction at the clonal level.
Chlorine gas induced acute lung injury in isolated rabbit lung
Authors: A Menaouar, D Anglade, P Baussand, A Pelloux, M Corboz, S Lantuejoul, G Benchetrit, FA Grimbert
Journal: European Respiratory Journal (1997)

This study was designed to investigate the pathogenesis of chlorine gas (Cl2) induced acute lung injury and oedema. Isolated blood-perfused rabbit lungs were ventilated either with air (n=7) or air plus 500 parts per million (ppm) of Cl2 (n=7) for 10 min. Capillary pressure, measured by analysing the pressure/time transients of pulmonary arterial, venous and double (both arterial and venous) occlusions, was unchanged in both groups. In Cl2-exposed lungs, the fluid filtration rate increased from -0.228+/-0.25 to 1.823+/-1.23 mL min(-1) x 100 g(-1) (p&lt;0.001) and the filtration coefficient increased from 0.091+/-0.01 to 0.259+/-0.07 mL x min(-1) x cmH2O(-1) x 100 g(-1) (p&lt;0.001). No changes were observed in the control lungs. The extravascular lung water/blood-free dry weight ratio was 8.6+/-1.6 in the Cl2 group and 4.0+/-0.5 in the control group (p&lt;0.001), confirming that the increase in lung weight was related to accumulation of extravascular fluid. Although the alveolar flooding by oedema is explained, in part, by the Cl2-induced epithelial injury, our results suggest that Cl2 exposure induces acute lung injury and oedema due to an increased microvascular permeability.
Swine pericardium as dermal substrate for human keratinocyte culture
Authors: R. Oliveira-Prado, I.R. Caldas, G.M.V. Pereira, M.V. Andrade, J.R. Cunha-Melo
Journal: British Journal of Dermatology (2009)

Background Synthetic skin analogues or living allogeneic or autologous cells are used as dressings for the care of skin wounds, as well as temporary or permanent substitutes for damaged epithelia. Objectives To evaluate if keratinocyte growth on a swine pericardium substrate mimics the natural epithelial layers compared with cultures on allogeneic dermis, which is accepted as having appropriate physical and chemical properties for growth and differentiation. Methods Keratinocytes were cultured on a swine pericardium substrate and allogeneic dermis, either submerged or at the air–liquid interface. At 7, 14 and 21 days postseeding the cultures were evaluated by light microscopy after both haematoxylin and eosin staining and immunohistochemistry. Results Cell–substrate interactions led to growth, stratification and differentiation of cells, with the definition of epithelial layers. The submerged system showed a continuous growth rise on both composites, but this was more prominent with the swine pericardium substrate. An increase in the number of layers at the air–liquid interface with the dermis composites, in contrast to the submerged cultures, occurred only from days 7 to 14. The pattern of keratinocyte growth on swine pericardium substrate was much better in the submerged than in the air–liquid interface cultures. Conclusions The results indicate that swine pericardium is a better substrate than allogeneic dermis for keratinocyte cultures in submerged but not in air–liquid interface cultures. Swine pericardium as a substrate opens one more possibility for skin restoration after trauma or burns.
Early Reinfarction After Fibrinolysis
Authors: Michael P. Hudson, Christopher B. Granger, Eric J. Topol, Karen S. Pieper, Paul W. Armstrong, Gabriel I. Barbash, Alan D. Guerci, Alec Vahanian, Robert M. Califf, E. Magnus Ohman
Journal: Circulation (2001)

Background Trials report a 2% to 6% incidence of reinfarction after fibrinolysis for acute myocardial infarction (MI). We combined the Global Utilization of Streptokinase and Tissue plasminogen activator (alteplase) for Occluded coronary arteries (GUSTO I) and Global Use of Strategies To Open occluded coronary arteries (GUSTO III) populations to better define frequency, timing, and clinical predictors of in-hospital reinfarction. Methods and Results In 55 911 patients with ST-segment elevation myocardial infarction (MI) who were receiving fibrinolysis, we compared baseline characteristics and mortality rate by reinfarction incidence and developed multivariable logistic regression models to predict in-hospital reinfarction and composite of death or reinfarction. Reinfarction occurred in 2258 patients (4.3%) a median of 3.8 days after fibrinolysis; rates did not differ between GUSTO I (4.0%) and GUSTO III (4.2%) or by fibrinolytic assignment (streptokinase, 4.1%; alteplase, 4.3%; reteplase, 4.5%; combined streptokinase and alteplase, 4.4%; P =0.55). Advanced age, shorter time to fibrinolysis, non-US enrollment, nonsmoking status, prior MI or angina, female sex, anterior MI, and lower systolic blood pressure were associated significantly with reinfarction. Patients with reinfarction had higher mortality at 30 days (11.3% versus 3.5% without reinfarction; odds ratio, 3.5; P &lt;0.001) and from 30 days to 1 year (4.7% versus 3.2%; hazard ratio, 1.5; P &lt;0.001). Significant multivariate predictors of in-hospital death or reinfarction included age, Killip class, systolic and diastolic blood pressures, heart rate, anterior MI, smoking status, prior MI, sex, and country of enrollment (all P &lt;0.001). Conclusion Reinfarction occurs infrequently after fibrinolysis but confers increased risk of 30-day and 1-year mortality. Some predictors of reinfarction differ from known predictors of death after MI. Improved treatment and prevention strategies for reinfarction deserve study.
Protein Tyrosine Phosphatase 1B, a Major Regulator of Leptin-Mediated Control of Cardiovascular Function
Authors: Eric J. Belin de Chantemèle, Kenjiro Muta, James Mintz, Michel L. Tremblay, Mario B. Marrero, David J. Fulton, David W. Stepp
Journal: Circulation (2009)

Background— Obesity causes hypertension and sympathoactivation, a process proposed to be mediated by leptin. Protein tyrosine phosphatase 1B (PTP1B), a major new pharmaceutical target in the treatment of obesity and type II diabetes mellitus, constrains the metabolic actions of leptin, but the extent to which PTP1B regulates its cardiovascular effects is unclear. This study examined the hypothesis that PTP1B is a negative regulator of the cardiovascular effects of leptin. Methods and Results— PTP1B knockout mice had lower body fat but higher mean arterial pressure (116±5 versus 105±5 mm Hg, P &lt;0.05) than controls. Leptin infusion produced a greater anorexic effect in PTP1B knockout mice and a marked increase in mean arterial pressure (135±5 mm Hg) in PTP1B knockout mice only. The decrease in mean arterial pressure in response to ganglionic blockade was higher in PTP1B knockout mice (−38±3% versus −29±3%, P &lt;0.05), which suggests increased sympathetic tone. PTP1B deletion blunted mean arterial pressure responses to phenylephrine injection (55±10% versus 93±7%, P &lt;0.05). Phenylephrine-induced aortic contraction was reduced in PTP1B knockout mice (57.7±9% versus 96.3±12% of KCl, P &lt;0.05), consistent with desensitization to chronically elevated sympathetic tone. Furthermore, PTP1B deletion significantly reduced gene expression of 3 α 1 -adrenergic receptor subtypes, consistent with blunted constriction to phenylephrine. Conclusions— These data indicate that PTP1B is a key regulator of the cardiovascular effects of leptin and that reduced vascular adrenergic reactivity provides a compensatory limit to the effects of leptin on mean arterial pressure.
CHANGES IN CONNECTIVE TISSUE AND INTESTINE CAUSED BY VITAMIN A IN AMPHIBIA, AND THEIR ACCELERATION BY HYDROCORTISONE
Authors: Gerald Weissmann
Journal: The Journal of Experimental Medicine (1961)

In view of the theory that an excess of vitamin A causes release of cathepsins from intracellular lysosomes, hypervitaminosis A was induced orally in the larvae of Xenopus laevis. It was predicted that the tails of these amphibia would undergo resorption prior to metamorphosis, since the presence of abundant lysosomes, associated with measurable increases of catheptic activity, had previously been demonstrated in the resorbing tails of amphibia during metamorphosis. This prediction was confirmed; after 3 to 4 weeks of hypervitaminosis A, the tails of treated animals underwent partial resorption. Other transitory appendages, the rostral tentacles, collapsed after 2 weeks of treatment with an excess of vitamin A, an effect analogous to the collapse of rabbits' ears after intravenous papain. These effects were related to the loss of metachromatic extracellular material in these appendages. Excess of vitamin A caused kyphoscoliosis and prognathos in the larvae. The hypervitaminotic larvae always developed a mucinous diarrhea, which was associated with a remarkable overgrowth of metachromatic goblet cells of the intestine. The entire intestine of the treated animals was more advanced in development than that of control larvae at equivalent stages. All the effects of hypervitaminosis A were accelerated by the simultaneous administration of hydrocortisone. This was held to be due to liberation of vitamin A from hepatic stores by the steroid, and is in contrast to the retardation of hypervitaminosis A by hydrocortisone in vitro.
ATF4 is an oxidative stress–inducible, prodeath transcription factor in neurons in vitro and in vivo
Authors: Philipp S. Lange, Juan C. Chavez, John T. Pinto, Giovanni Coppola, Chiao-Wang Sun, Tim M. Townes, Daniel H. Geschwind, Rajiv R. Ratan
Journal: The Journal of Experimental Medicine (2008)

Oxidative stress is pathogenic in neurological diseases, including stroke. The identity of oxidative stress-inducible transcription factors and their role in propagating the death cascade are not well known. In an in vitro model of oxidative stress, the expression of the bZip transcription factor activating transcription factor 4 (ATF4) was induced by glutathione depletion and localized to the promoter of a putative death gene in neurons. Germline deletion of ATF4 resulted in a profound reduction in oxidative stress-induced gene expression and resistance to oxidative death. In neurons, ATF4 modulates an early, upstream event in the death pathway, as resistance to oxidative death by ATF4 deletion was associated with decreased consumption of the antioxidant glutathione. Forced expression of ATF4 was sufficient to promote cell death and loss of glutathione. In ATF4(-/-) neurons, restoration of ATF4 protein expression reinstated sensitivity to oxidative death. In addition, ATF4(-/-) mice experienced significantly smaller infarcts and improved behavioral recovery as compared with wild-type mice subjected to the same reductions in blood flow in a rodent model of ischemic stroke. Collectively, these findings establish ATF4 as a redox-regulated, prodeath transcriptional activator in the nervous system that propagates death responses to oxidative stress in vitro and to stroke in vivo.
Differences in antigen presentation to MHC class I-and class II-restricted influenza virus-specific cytolytic T lymphocyte clones.
Authors: L A Morrison, A E Lukacher, V L Braciale, D P Fan, T J Braciale
Journal: The Journal of Experimental Medicine (1986)

We have examined requirements for antigen presentation to a panel of MHC class I-and class II-restricted, influenza virus-specific CTL clones by controlling the form of virus presented on the target cell surface. Both H-2K/D- and I region-restricted CTL recognize target cells exposed to infectious virus, but only the I region-restricted clones efficiently lysed histocompatible target cells pulsed with inactivated virus preparations. The isolated influenza hemagglutinin (HA) polypeptide also could sensitize target cells for recognition by class II-restricted, HA-specific CTL, but not by class I-restricted, HA-specific CTL. Inhibition of nascent viral protein synthesis abrogated the ability of target cells to present viral antigen relevant for class I-restricted CTL recognition. Significantly, presentation for class II-restricted recognition was unaffected in target cells exposed to preparations of either inactivated or infectious virus. This differential sensitivity suggested that these H-2I region-restricted CTL recognized viral polypeptides derived from the exogenously introduced virions, rather than viral polypeptides newly synthesized in the infected cell. In support of this contention, treatment of the target cells with the lysosomotropic agent chloroquine abolished recognition of infected target cells by class II-restricted CTL without diminishing class I-restricted recognition of infected target cells. Furthermore, when the influenza HA gene was introduced into target cells without exogenous HA polypeptide, the target cells that expressed the newly synthesized protein product of the HA gene were recognized only by H-2K/D-restricted CTL. These observations suggest that important differences may exist in requirements for antigen presentation between H-2K/D and H-2I region-restricted CTL. These differences may reflect the nature of the antigenic epitopes recognized by these two CTL subsets.
A STUDY OF PNEUMONIA IN A RURAL AREA IN SOUTHERN ALABAMA
Authors: W. G. Smillie, E. L. Caldwell
Journal: The Journal of Experimental Medicine (1929)

1. Pneumococcus Type IV of low virulence was the prevailing organism in fifty-eight cases of pneumonia studied in southern Alabama. Fixed types of pneumococci were not common. 2. Pneumoma was more prevalent in children from 5 to 15 years of age than in adults. As a rule, the disease ran a mild course. 3. Most of the cases of pneumonia gave a definite history of an acute cold antedating the attack of pneumonia by a period of 5 to 8 days. Exposure alone did not seem to predispose to pneumonia, but those with an acute cold who were exposed to chilling of the body surface frequently developed pneumonia. 4. There were seven "family epidemics" of pneumonia. In each instance there was a family epidemic of colds antedating the pneumonia. The pneumococcus was found in large numbers in the nasopharynx of those suffering from colds as well as in the pneumonia patients. 5. The epidemiology of pneumonia in the pioneer days of American history has many points in common with the epidemiology of pneumonia in a rural isolated area in southern Alabama today. This suggests that the crowded conditions and frequent contacts of modern city life have built up a community resistance to avirulent strains of pneumococci.
Avoiding confusion in COPD: from risk factors to phenotypes to measures of disease characterisation
Authors: A. Agustí, B. Celli
Journal: European Respiratory Journal (2011)

Because chronic obstructive pulmonary disease (COPD) is a complex disorder with different pulmonary and extrapulmonary manifestations [1], there is great interest in better understanding the complexity of COPD in order to facilitate a more accurate risk stratification of patients and a better understanding of disease pathobiology, and eventually develop more targeted therapy and improved management of patients with the disease. One end-product of the great number of studies addressing the complexity of COPD has been the emergence of several concepts and terms that are often used (and misused) in scientific discussions and publications (table 1). The purpose of this article is to contribute to the clarification of these concepts by summarising the meaning of the terms, so the scientific community can communicate and discuss advances in the field of COPD, being confident that there is no uncertainty or misunderstanding in their use. We accept this to be only a first proposal and that some investigators may disagree with its content. We invite them to correspond with us in the European Respiratory Journal such that, eventually, a consensus may emerge.

View this table:

Table 1– Terms and definitions 

A risk factor is “an aspect of personal behaviour or lifestyle, environmental exposure, or inborn or inherited characteristic, which, on the basis of epidemiological evidence, is known to be associated with a health-related condition” [2]. Examples of well-established risk factors in COPD include age [9], smoking [10], …
Mitochondrial structure and function in CCl4-induced cirrhosis in the rat
Authors: Stephan Krählenbühl, Jürg Reichen, Arthur Zimmermann, Peter Gehr, Jörg Stucki
Journal: Hepatology (1990)

To investigate whether the impairment of mitochondrial function in cirrhosis is due to a reduction in liver cell mass or whether mitochondrial function is altered specifically, we analyzed mitochondrial volume and surface density of mitochondrial membranes in control and cirrhotic rats by stereological means. Cirrhosis was induced by long-term exposure to phenobarbital and CCl4. Hepatocellular and mitochondrial volumes were reduced to a similar extent, by 39% and 40%, respectively, in cirrhotic animals (p less than 0.01). Thus the fraction of hepatocytes occupied by mitochondria did not differ between the two groups. Both total outer (31 +/- 3 vs. 19 +/- 6 m2; p less than 0.01) and inner (87 +/- 24 vs. 45 +/- 12 m2; p less than 0.01) mitochondrial membranes were significantly reduced. Membrane surface was normal per unit of mitochondrial volume, however, suggesting intact mitochondrial structure. Matrix and outer membrane enzyme activities expressed per compartment did not differ between control and cirrhotic animals. Inner membrane, in contrast, had an increased enzyme content per unit area both for cytochrome oxidase (10.3 +/- 2.9 vs. 13.0 +/- 1.6; p less than 0.05) and ATPase (13.7 +/- 1.4 vs. 21.2 +/- 2.9; p less than 0.01). Basal oxygen consumption measured in the perfused liver in situ was significantly reduced in cirrhotic livers (1.6 +/- 0.1 vs. 1.1 +/- 0.4 mumol/min-1/gm-1) but was unchanged when expressed per square meter of inner membrane. Our results demonstrate that impaired mitochondrial function is mainly due to loss of hepatocellular mass. Increased enzyme activity per unit surface area of inner mitochondrial membrane may be important to maintain mitochondrial function of the cirrhotic liver.