tbuckley/cabot-search huggingface dataset:
Effectiveness of acute geriatric units on functional decline, living at home, and case fatality among older patients admitted to hospital for acute medical disorders: meta-analysis
Authors: J. J Baztan, F. M Suarez-Garcia, J. Lopez-Arrieta, L. Rodriguez-Manas, F. Rodriguez-Artalejo
Journal: BMJ (2009)

<b>Objective</b> To assess the effectiveness of acute geriatric units compared with conventional care units in adults aged 65 or more admitted to hospital for acute medical disorders. <b>Design</b> Systematic review and meta-analysis. <b>Data sources</b> Medline, Embase, and the Cochrane Library up to 31 August 2008, and references from published literature. <b>Review methods</b> Randomised trials, non-randomised trials, and case-control studies were included. Exclusions were studies based on administrative databases, those that assessed care for a single disorder, those that evaluated acute and subacute care units, and those in which patients were admitted to the acute geriatric unit after three or more days of being admitted to hospital. Two investigators independently selected the studies and extracted the data. <b>Results</b> 11 studies were included of which five were randomised trials, four non-randomised trials, and two case-control studies. The randomised trials showed that compared with older people admitted to conventional care units those admitted to acute geriatric units had a lower risk of functional decline at discharge (combined odds ratio 0.82, 95% confidence interval 0.68 to 0.99) and were more likely to live at home after discharge (1.30, 1.11 to 1.52), with no differences in case fatality (0.83, 0.60 to 1.14). The global analysis of all studies, including non-randomised trials, showed similar results. <b>Conclusions</b> Care of people aged 65 or more with acute medical disorders in acute geriatric units produces a functional benefit compared with conventional hospital care, and increases the likelihood of living at home after discharge.
Supplemental oxygen in COPD
Authors: T RINGBAEK
Journal: Thorax (2001)

Myositis associated with graft-versus-hostdisease (GVHD) typically presents with proximal muscle weakness, myalgias, and a raised creatinine phosphokinase (CPK) level.We report a case of a 51 year old man who developed respiratory muscle weakness five years after an allogeneic bone marrow transplant for multiple myeloma.His symptoms included tachypnoea, abdominal paradox, and orthopnoea.Pulmonary function tests revealed diminished vital capacity and maximal inspiratory and expiratory pressures.Serum CPK levels were raised and a peripheral muscle biopsy specimen was consistent with GVHD.He improved with immunosuppressive therapy.
Central nervous system site of action for the respiratory depressant effect of diacetylmorphine (heroin) in the cat.
Authors: A M Taveira da Silva, J D Souza, J A Quest, F D Pagani, J M Moerschbaecher, A Buller, P Hamosh, R A Gillis
Journal: Journal of Clinical Investigation (1983)

The purpose of our study was to identify central nervous system sites involved in the respiratory depressant effect of drugs that stimulate opioid receptors. Diacetylmorphine (heroin) was administered into several cerebroventricular regions of chloralose-anesthetized cats, while monitoring pulmonary ventilation with a Fleisch pneumotachograph. Administration of heroin (17, 50, 150, and 450 micrograms) into the forebrain ventricles, which was restricted to these ventricles, resulted in no significant respiratory effects. In contrast, administration of heroin into either the fourth ventricle or the cisterna magna resulted in a significant (P less than 0.05) decrease in respiratory minute volume (VE). In the fourth ventricle this was because of a decrease in frequency (f) and in the cisterna magna, to a decrease in tidal volume (VT). Intravenous administration of heroin in the same dose-range produced a decrease in VE, which was primarily due to a decrease in f. Bilateral application of heroin (70 micrograms/side) to each of three ventral medullary surface sites (Mitchell's, Schlaefke's, and Loeschcke's areas) known to influence respiration elicited a decrease in VE only at Mitchell's area. This decrease was due to decreases in f and VT. The role of this site in the action of intravenously administered heroin was tested by topical application of naloxone to this area in animals with respiratory depression evoked by intravenous heroin. Bilateral application of naloxone (15 micrograms/side) to Mitchell's area restored breathing to normal. These results lead us to suggest that the site of heroin-induced respiratory depression is a specific area (Mitchell's area) on the ventral surface of the medulla.
Sustained delivery of a HIF-1 antagonist for ocular neovascularization
Authors: Takeshi Iwase, Jie Fu, Tsunehiko Yoshida, Daisuke Muramatsu, Akiko Miki, Noriyasu Hashida, Lili Lu, Brian Oveson, Raquel Lima e Silva, Christopher Seidel, Ming Yang, Sheila Connelly, Jikui Shen, Bing Han, Mingsheng Wu, Gregg L. Semenza, Justin Hanes, Peter A. Campochiaro
Journal: Journal of Controlled Release (2013)
Limitations of calculating "true" regression slope: impact on estimates of minimal important difference
Authors: J.W. Dodd, P. Jones
Journal: European Respiratory Journal (2011)

Limitations of calculating ''true'' regression slope: impact on estimates of minimal important differenceTo the Editors:We read with interest the recent article [1] that addresses the important question of minimal important difference (MID) for exercise tests in chronic obstructive pulmonary disease.PUHAN et al.[1] use both distribution-and anchor-based methods, and it is the anchor-based methodology that we would like to consider here.Those authors use linear regression analysis between change in the dependent variable, in this case 6-min walk distance, and change in an anchor variable (St George's Respiratory Questionnaire and University of California San Diego Shortness of Breath Questionnaire) as the independent variable.We would like to highlight limitations of this approach and demonstrate, with example data, the potential impact on estimates of MID.The problem is based on the assumption that the independent variable (X) is measured without error, but the slope of linear regression will be a measure of the ''true'' relationship only if all variance of X is due to the regression and not due to measurement error.Although no measurement is free from error, some signals are rather more ''noisy'' than others.The presence of high correlation between the variables will indicate the reduction in such a potential error.This point is made by the authors, who suggest an r-value of 0.5 as a cut-off and a linear relationship between the two variables.
Socio-demographic inequalities in stage of cancer diagnosis: evidence from patients with female breast, lung, colon, rectal, prostate, renal, bladder, melanoma, ovarian and endometrial cancer
Authors: G. Lyratzopoulos, G.A. Abel, C.H. Brown, B.A. Rous, S.A. Vernon, M. Roland, D.C. Greenberg
Journal: Annals of Oncology (2012)

BackgroundUnderstanding socio-demographic inequalities in stage at diagnosis can inform priorities for cancer control.Patients and methodsWe analysed data on the stage at diagnosis of East of England patients diagnosed with any of 10 common cancers, 2006–2010. Stage information was available on 88 657 of 98 942 tumours (89.6%).ResultsSubstantial socio-demographic inequalities in advanced stage at diagnosis (i.e. stage III/IV) existed for seven cancers, but their magnitude and direction varied greatly by cancer: advanced stage at diagnosis was more likely for older patients with melanoma but less likely for older patients with lung cancer [odds ratios for 75–79 versus 65–69 1.60 (1.38–1.86) and 0.83 (0.77–0.89), respectively]. Deprived patients were more likely to be diagnosed in advanced stage for melanoma, prostate, endometrial and (female) breast cancer: odds ratios (most versus least deprived quintile) from 2.24 (1.66–3.03) for melanoma to 1.31 (1.15–1.49) for breast cancer. In England, elimination of socio-demographic inequalities in stage at diagnosis could decrease the number of patients with cancer diagnosed in advanced stage by ∼5600 annually.ConclusionsThere are substantial socio-demographic inequalities in stage at diagnosis for most cancers. Earlier detection interventions and policies can be targeted on patients at higher risk of advanced stage diagnosis.
Inflammation in the Genesis and Perpetuation of Cancer: Summary and Recommendations from a National Cancer Institute–Sponsored Meeting
Authors: Richard M. Peek, Suresh Mohla, Raymond N. DuBois
Journal: Cancer Research (2005)

The Inflammation and Cancer Think Tank Meeting was organized by the National Cancer Institute with the purpose of identifying research advances, gaps, and opportunities for the study and clinical application of the role of inflammation on tumorigenesis. The format of this meeting consisted of brief presentations that focused on concepts, with extensive discussion periods to allow participants to identify issues and barriers limiting progress in this area. The strong relationship between inflammation and cancer in the gastrointestinal tract prompted several presentations that were focused on carcinogenesis within this organ system; however, many of the same immune mediators that influence esophageal, gastric, and colorectal carcinoma were also shown to influence inflammation-related malignancies at other anatomic sites. This article summarizes the findings of this Think Tank Meeting, which highlight the intimate relationship between malignant cells and their inflammatory microenvironment and specifically address opportunities to manipulate the host immune response and therefore intervene at different points along the tumorigenic cascade.
985 COMBINATION OF SERUM BIOCHEMICAL MARKERS FOR EARLY DIAGNOSIS OF HEPATITIS B VIRUS-ASSOCIATED HEPATOCELLULAR CARCINOMA: ONE STEP BEYOND ALPHA-FETOPROTEIN
Authors: Y.-J. Lin, M.-H. Lee, H.-I. Yang, C.-L. Jen, S.-L. You, L.-Y. Wang, S.-N. Lu, C.-J. Chen
Journal: Journal of Hepatology (2011)
Decreased expression of keratinocyte beta1 integrins in chronically sun-exposed skin in vivo
Authors: S. Bosset, M. Bonnet-Duquennoy, P. Barre, A. Chalon, K. Lazou, R. Kurfurst, F. Bonte, S. Schnebert, F. Disant, B. Le Varlet, J.F. Nicolas
Journal: British Journal of Dermatology (2003)

Chronic exposure to ultraviolet (UV) radiation induces changes in the skin structure which are mostly found in the superficial dermis and at the dermal-epidermal junction. Keratinocytes and fibroblasts contribute both to the synthesis and to the degradation of the molecules important for the integrity of this skin site. While several studies have reported on alterations of dermal components and of the functions of fibroblasts in vivo and in vitro after UV exposure, recent data suggested that keratinocytes could be the main skin cell type involved in the photoageing process.In this study, we analysed the expression of two keratinocyte molecules namely, beta1 integrin (a proliferation marker) and involucrin (a differentiation marker) in sun-exposed and sun-protected facial skin of 16 healthy patients undergoing facial lifting.Methods included histology, immunohistochemistry and quantitative reverse transcriptase-polymerase chain reaction analysis.Sun-exposed skin displayed the characteristic morphological and molecular features of dermal photoageing, compared with sun-protected skin, including dermal elastosis, diminished fibrillin and type VII collagen expression. Analysis of the epidermis in sun-exposed vs. sun-protected skin showed no histological differences, but dramatic changes in the expression of beta1 integrin and involucrin. In sun-exposed skin, expression of beta1 integrin protein by epidermal basal cells was reduced, paralleling a downregulation of beta1 integrin mRNA, whereas involucrin protein expression was greatly enhanced in the superficial epidermal cell layers. Interestingly, the ratio between involucrin and beta1 integrin protein expression was consistently increased in sun-exposed skin sites.Collectively these results demonstrate that epidermal homeostasis is impaired by chronic UV exposure, and define beta1 integrin expression as a molecular marker of the epidermal photoageing process.
Fracture of the Bronchus
Authors: J. L. Griffith
Journal: Thorax (1949)

Traumatic rupture of the bronchus is an unusual condition, and is sufficiently rare to justify the reporting of one further case.The case presented shows many unusual features.The injury sustained may be termed simple frac- ture rather than rupture, or laceration of the bronchus.The common complications of this type of injury did not arise.Pneumothorax, bleeding into the pleural cavity, surgical emphysema, and collapse of the lung did not occur, presumably because the mucosa and membranous wall of the bronchus remained intact.
Comparative study of the intestinal mucus barrier in normal and inflamed colon
Authors: A. Swidsinski, V. Loening-Baucke, F. Theissig, H. Engelhardt, S. Bengmark, S. Koch, H. Lochs, Y. Dorffel
Journal: Gut (2006)

<b>Aim:</b> To study the role of mucus in the spatial separation of intestinal bacteria from mucosa. <b>Patients and methods:</b> Mucus barrier characteristics were evaluated using histological material obtained by biopsy from purged colon, colon prepared with enema and material from untreated appendices fixed with non-aqueous Carnoy solution. Bacteria were evaluated using fluorescence in situ hybridization, with bacterial 16S RNA probes and related to the periodic acid Schiff alcian blue stain. Biopsies from controls (n = 20), patients with self-limiting colitis (SLC; n = 20), ulcerative colitis (n = 20) and 60 randomly selected appendices were investigated. <b>Results:</b> The mucosal surface beneath the mucus layer was free of bacteria in ⩾80% of the normal appendices and biopsies from controls. The thickness of the mucus layer and its spread decreased with increasing severity of the inflammation; the epithelial surface showed bacterial adherence, epithelial tissue defects and deep mucosal infiltration with bacteria and leucocytes. Bacteria and leucocytes were found within mucus in all biopsy specimens from patients with ulcerative colitis, SLC, and acute appendicitis. The concentration of bacteria within mucus was inversely correlated to the numbers of leucocytes. <b>Conclusions:</b> The large bowel mucus layer effectively prevents contact between the highly concentrated luminal bacteria and the epithelial cells in all parts of the normal colon. Colonic inflammation is always accompanied by breaks in the mucus barrier. Although the inflammatory response gradually reduces the number of bacteria in mucus and faeces, the inflammation itself is not capable of preventing bacterial migration, adherence to and invasion of the mucosa.
Tolerization of Anti–Galα1-3Gal Natural Antibody–forming B Cells by Induction of Mixed Chimerism
Authors: Yong-Guang Yang, Emil deGoma, Hideki Ohdan, Jennifer L. Bracy, Yuanxin Xu, John Iacomini, Aron D. Thall, Megan Sykes
Journal: The Journal of Experimental Medicine (1998)

Xenotransplantation could overcome the severe shortage of allogeneic organs, a major factor limiting organ transplantation. Unfortunately, transplantation of organs from pigs, the most suitable potential donor species, results in hyperacute rejection in primate recipients, due to the presence of anti–Galα1-3Gal (Gal) natural antibodies (NAbs) in their sera. We evaluated the ability to tolerize anti-Gal NAb–producing B cells in α1,3-galactosyltransferase knockout (GalT KO) mice using bone marrow transplantation (BMT) from GalT+/+ wild-type (WT) mice. Lasting mixed chimerism was achieved in KO mice by cotransplantation of GalT KO and WT marrow after lethal irradiation. The levels of anti-Gal NAb in sera of mixed chimeras were reduced markedly 2 wk after BMT, and became undetectable at later time points. Immunization with Gal+/+ xenogeneic cells failed to stimulate anti-Gal antibody production in mixed chimeras, whereas the production of non–Gal-specific antixenoantigen antibodies was stimulated. An absence of anti-Gal–producing B cells was demonstrated by enzyme-linked immunospot assays in mixed KO+WT→ KO chimeras. Thus, mixed chimerism efficiently induces anti-Gal–specific B cell tolerance in addition to T cell tolerance, providing a single approach to overcoming both the humoral and the cellular immune barriers to discordant xenotransplantation.
Income Inequality and Health: What Does the Literature Tell Us?
Authors: Adam Wagstaff, Eddy van Doorslaer
Journal: Annual Review of Public Health (2000)

▪ Abstract This paper reviews the large and growing body of literature on the apparently negative effects of income inequality on population health. Various hypotheses are identified and described that explain the empirically observed association between measures of income inequality and population health. We have concluded that data from aggregate-level studies of the effect of income inequality on health, i.e. studies at the population and community (e.g. state) levels, are largely insufficient to discriminate between competing hypotheses. Only individual-level studies have the potential to discriminate between most of the advanced hypotheses. The relevant individual-level studies to date, all on U.S. population data, provide strong support for the “absolute-income hypothesis,” no support for the “relative-income hypothesis,” and little or no support for the “income-inequality hypothesis.” Results that provide some support for the income-inequality hypothesis suggest that income inequality at the state level affects mainly the health of the poor. There is only indirect evidence for the “deprivation hypothesis,” and no evidence supports the “relative-position hypothesis.” Overall, the absolute-income hypothesis, although &gt;20 years old, is still the most likely to explain the frequently observed strong association between population health and income inequality levels.
Toward a general psychobiological theory of emotions
Authors: Jaak Panksepp
Journal: Behavioral and Brain Sciences (1982)

Abstract Emotions seem to arise ultimately from hard-wired neural circuits in the visceral-limbic brain that facilitate diverse and adaptive behavioral and physiological responses to major classes of environmental challenges. Presumably these circuits developed early in mammalian brain evolution, and the underlying control mechanisms remain similar in humans and “lower” mammals. This would suggest that theoretically guided studies of the animal brain can reveal how primitive emotions are organized in the human brain. Conversely, granted this cross-species heritage, it is arguable that human introspective access to emotional states may provide direct information concerning operations of emotive circuits and thus be a primary source of hypotheses for animal brain research. In this article the possibility that emotions are elaborated by transhypothalamic executive (command) circuits that concurrently activate related behavior patterns is assessed. Current neurobehavioral evidence indicates that there are at least four executive circuits of this type – those which elaborate central states of expectancy, rage, fear, and panic. The manner in which learning and psychiatric disorders may arise from activities of such circuits is also discussed.
The histone deacetylase inhibitor suberoylanilide hydroxamic acid reduces cardiac arrhythmias in dystrophic mice
Authors: Claudia Colussi, Roberta Berni, Jessica Rosati, Stefania Straino, Serena Vitale, Francesco Spallotta, Silvana Baruffi, Leonardo Bocchi, Francesca Delucchi, Stefano Rossi, Monia Savi, Dante Rotili, Federico Quaini, Emilio Macchi, Donatella Stilli, Ezio Musso, Antonello Mai, Carlo Gaetano, Maurizio C. Capogrossi
Journal: Cardiovascular Research (2010)

The effect of histone deacetylase inhibitors on dystrophic heart function is not established. To investigate this aspect, dystrophic mdx mice and wild-type (WT) animals were treated 90 days either with suberoylanilide hydroxamic acid (SAHA, 5 mg/kg/day) or with an equivalent amount of vehicle. The following parameters were evaluated: (i) number of ventricular arrhythmias in resting and stress conditions (restraint test) or after aconitine administration; (ii) cardiac excitability, conduction velocity, and refractoriness; (iii) expression and distribution of connexins (Cxs) and Nav1.5 sodium channel. Ventricular arrhythmias were negligible in all resting animals. During restraint, however, an increase in the number of arrhythmias was detected in vehicle-treated mdx mice (mdx-V) when compared with SAHA-treated mdx (mdx-SAHA) mice or normal control (WT-V). Interestingly, aconitine, a sodium channel pharmacologic opener, induced ventricular arrhythmias in 83% of WT-V mice, 11% of mdx-V, and in 57% of mdx-SAHA. Epicardial multiple lead recording revealed a prolongation of the QRS complex in mdx-V mice in comparison to WT-V and WT-SAHA mice, paralleled by a significant reduction in impulse propagation velocity. These alterations were efficiently counteracted by SAHA. Molecular analyses revealed that in mdx mice, SAHA determined Cx remodelling of Cx40, Cx37 and Cx32, whereas expression levels of Cx43 and Cx45 were unaltered. Remarkably, Cx43 lateralization observed in mdx control animals was reversed by SAHA treatment which also re-induced Nav1.5 expression. SAHA attenuates arrhythmias in mdx mice by a mechanism in which Cx remodelling and sodium channel re-expression could play an important role.
Identification of Hypertension-Related Genes Through an Integrated Genomic-Transcriptomic Approach
Authors: Chana Yagil, Norbert Hubner, Jan Monti, Herbert Schulz, Marina Sapojnikov, Friedrich C. Luft, Detlev Ganten, Yoram Yagil
Journal: Circulation Research (2005)

In search for the genetic basis of hypertension, we applied an integrated genomic-transcriptomic approach to identify genes involved in the pathogenesis of hypertension in the Sabra rat model of salt-susceptibility. In the genomic arm of the project, we previously detected in male rats two salt-susceptibility QTLs on chromosome 1, SS1a ( D1Mgh2-D1Mit11 ; span 43.1 cM) and SS1b ( D1Mit11-D1Mit4 ; span 18 cM). In the transcriptomic arm, we studied differential gene expression in kidneys of SBH/y and SBN/y rats that had been fed regular diet or salt-loaded. We used the Affymetrix Rat Genome RAE230 GeneChip and probed &gt;30 000 transcripts. The research algorithm called for an initial genome-wide screen for differentially expressed transcripts between the study groups. This step was followed by cluster analysis based on 2×2 ANOVA to identify transcripts that were of relevance specifically to salt-sensitivity and hypertension and to salt-resistance. The two arms of the project were integrated by identifying those differentially expressed transcripts that showed an allele-specific hypertensive effect on salt-loading and that mapped within the defined boundaries of the salt-susceptibility QTLs on chromosome 1. The differentially expressed transcripts were confirmed by RT-PCR. Of the 2933 genes annotated to rat chromosome 1, 1102 genes were identified within the boundaries of the two blood pressure QTLs. The microarray identified 2470 transcripts that were differentially expressed between the study groups. Cluster analysis identified genome-wide 192 genes that were relevant to salt-susceptibility and/or hypertension, 19 of which mapped to chromosome 1. Eight of these genes mapped within the boundaries of QTLs SS1a and SS1b . RT-PCR confirmed 7 genes, leaving TcTex1, Myadm, Lisch7, Axl-like, Fah, PRC1-like, and Serpinh1 . None of these genes has been implicated in hypertension before. These genes become henceforth targets for our continuing search for the genetic basis of hypertension.