tbuckley/cabot-search huggingface dataset:
New providers in UK health care
Authors: Penelope Dash
Journal: BMJ (2004)

What effect will more competition have on the NHS? 

Over the past 5-10 years the European airline market has been completely transformed by the introduction of new players. Through a combination of adding capacity and radically changing traditional ways of working, Ryanair and Easyjet have effectively challenged the status quo among the traditional incumbents (British Airways, Alitalia, Air France, etc) and created a whole new approach to air travel across Europe. Can the same transformation happen in health care?

The current UK government hopes so. Since its election to office in 1997, the government has set itself an ambitious strategy to substantially improve health care. The strategy has three key planks—improvement of quality, expansion of capacity, and introduction of new incentives (in particular customer choice1) to drive through radical changes (box). This article explores how the expansion of capacity through opening up health care to new providers, combined with increasing consumer choice, will change the way in which health care is provided and used.

The NHS Plan focused on increasing capacity and put at its heart key targets for the reduction of waiting lists and waiting times for planned elective care.2 By 2005, no patient will have to wait more than six months for a routine operation, and by 2008, waiting times will be less than three months.



#### Mechanisms for implementing three key components of NHS strategy Improving quality

#### Increasing capacity

#### Creating incentives for change

Increased capacity will be achieved partly by expanding existing NHS services but also by purchasing services from non-NHS organisations—so called plurality of provision.3 The …
Inhibition of Tissue Angiotensin-Converting Enzyme With Quinapril Reduces Hypoxic Pulmonary Hypertension and Pulmonary Vascular Remodeling
Authors: Zengxuan Nong, Jean-Marie Stassen, Lieve Moons, De´sire´ Collen, Stefan Janssens
Journal: Circulation (1996)

Background Angiotensin II may contribute to hypoxic pulmonary hypertension via its vasoconstrictor and growth-stimulatory effects on vascular smooth muscle cells (VSMCs). Therefore, the use of ACE inhibitors might reduce hypoxic pulmonary hypertension by decreasing pulmonary vasomotor tone or vascular remodeling. Methods and Results Pulmonary hemodynamics and vascular remodeling were compared in chronically hypoxic (F io 2 =0.10) rats treated with 0, 1, and 10 mg·kg −1 ·d −1 quinapril, a potent tissue ACE inhibitor, both during and after the development of pulmonary hypertension. Quinapril reduced the development of pulmonary hypertension after 12 days of hypoxia from 26±1 to 19±1 mm Hg ( P &lt;.05). When started in established pulmonary hypertension, quinapril reduced pulmonary artery pressure and total pulmonary resistance index from 29±1 to 25±1 mm Hg and from 0.136±0.01 to 0.101±0.005 mm Hg·mL −1 ·min −1 per kg, respectively ( P &lt;.05). Chronically hypoxic rats showed a small pulmonary vasoconstrictor response that was not affected by quinapril. In contrast, percent medial thickness in alveolar duct blood vessels was reduced by quinapril treatment both in developing and in established pulmonary hypertension (10.0±0.2% versus 8.9±0.1% [ P &lt;.05] and 11.2±0.2% versus 9.1±0.2% [ P &lt;.05], respectively). 5′-Bromo-deoxyuridine–positive VSMCs were detected in 56±3% of hypoxic control pulmonary resistance vessels versus 41±3% of vessels after quinapril treatment ( P &lt;.05). Conclusions Pulmonary ACE and angiotensin II contribute to the development and maintenance of hypoxic pulmonary hypertension in rats. ACE inhibition with quinapril reduces the development of hypoxic pulmonary hypertension and in part reverses established pulmonary hypertension, most likely via inhibition of pulmonary VSMC proliferation and/or growth.
P54. Possible role of MDSC for the induction of tumour-specific T cells following LRAST
Authors: P Rose, JR Kovács, RA Hatz, H Winter, NK van den Engel
Journal: Journal for ImmunoTherapy of Cancer (2014)

Meeting abstracts L ymphodepletion with subsequent r econstitution and a ctive- s pecific t umour cell vaccination (LRAST) during the homeostatic proliferation is a promising approach in cancer immunotherapy. While tumour specific response is evident under LRAST regime, simultaneous induction of
Increase of laminin 5 synthesis in human keratinocytes by acute wound fluid, inflammatory cytokines and growth factors, and lysophospholipids
Authors: S. Amano, N. Akutsu, Y. Ogura, T. Nishiyama
Journal: British Journal of Dermatology (2004)

Journal Article Increase of laminin 5 synthesis in human keratinocytes by acute wound fluid, inflammatory cytokines and growth factors, and lysophospholipids Get access S. Amano, S. Amano Skin Biology Research Laboratories, Shiseido Life Science Research Center, 2‐12‐1 Fukuura, Kanazawa‐ku, Yokohama 236‐8643, Japan Satoshi Amano. E‐mail: satoshi.amano@to.shiseido.co.jp Search for other works by this author on: Oxford Academic Google Scholar N. Akutsu, N. Akutsu Skin Biology Research Laboratories, Shiseido Life Science Research Center, 2‐12‐1 Fukuura, Kanazawa‐ku, Yokohama 236‐8643, Japan Search for other works by this author on: Oxford Academic Google Scholar Y. Ogura, Y. Ogura Skin Biology Research Laboratories, Shiseido Life Science Research Center, 2‐12‐1 Fukuura, Kanazawa‐ku, Yokohama 236‐8643, Japan Search for other works by this author on: Oxford Academic Google Scholar T. Nishiyama T. Nishiyama Skin Biology Research Laboratories, Shiseido Life Science Research Center, 2‐12‐1 Fukuura, Kanazawa‐ku, Yokohama 236‐8643, Japan Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 151, Issue 5, 1 November 2004, Pages 961–970, https://doi.org/10.1111/j.1365-2133.2004.06175.x Published: 01 November 2004 Article history Accepted: 08 March 2004 Published: 01 November 2004
Erythropoietin Coming of Age
Authors: Allan Erslev
Journal: New England Journal of Medicine (1987)

Since 1957, when Jacobson and associates1 demonstrated the renal origin of erythropoietin, it has been assumed that the anemia of chronic renal disease is caused at least in part by a deficiency of this renal hormone and that it might be corrected if erythropoietin could be administered in large enough quantities. Molecular biology has now provided such quantities, and Eschbach and associates, in this issue of the Journal,2 and Winearls and associates, in a recent issue of The Lancet,3 have provided convincing evidence for the therapeutic effectiveness of recombinant erythropoietin in anemic patients on long-term hemodialysis. This is . . .
Cloning and characterization of a vertebrate cellular myosin regulatory light chain complementary DNA.
Authors: P J Zavodny, M E Petro, H K Lonial, S H Dailey, S K Narula, P J Leibowitz, C C Kumar
Journal: Circulation Research (1990)

We have isolated two series of complementary DNAs (cDNAs) from a chicken gizzard cDNA library encoding two isoforms of phosphorylatable myosin regulatory light chain (RLC). One of the cDNAs encodes a previously isolated smooth muscle myosin RLC (also referred to as LC20-A); the other encodes a protein that shares 92% homology with the LC20-A isoform. The phosphorylatable threonine and serine residues at positions 18 and 19 of the two myosin RLC sequences are conserved. The two cDNAs are 81% homologous at the nucleotide level over the coding region; the 5' and 3' untranslated regions are divergent. Most of the DNA nonhomology in the coding region does not affect the protein sequence, indicating strong evolutionary conservation pressure to maintain the myosin RLC structure. Northern blot analysis using 3' untranslated region probes reveals restrictive tissue specific expression of one myosin RLC isoform (LC20-A) in smooth muscle tissue and not in other tissues examined. In contrast, the novel myosin RLC isoform messenger RNA (mRNA) is uniformly expressed in all smooth and nonmuscle tissues examined and is designated as cellular myosin RLC for this reason. Our results indicate that cellular and smooth muscle myosin RLC isoforms are distinct and are encoded by separate genes. This report describes the cloning of a novel vertebrate cellular myosin RLC mRNA that differs from previously characterized smooth muscle RLC isoform mRNAs in both primary sequence and expression pattern.
South Africa to tighten control on drug trials after five deaths
Authors: P. Sidley
Journal: BMJ (2000)

South Africa's HIV/AIDS drug trials industry has been thrown into confusion after the government had to intervene and stop a trial in which five patients died. About 11% of patients in the trial showed signs of severe liver toxicity, and serious allegations were levelled against the trial organisers that women involved in one site of the trial had not given fully informed consent.

This problem has arisen amid serious soul searching among medicines'regulators, research ethics committees, drug companies, and doctors after research procedures had to be questioned when Werner Bezwoda falsified research results into …
Parental Stress as a Predictor of Wheezing in Infancy
Authors: ROSALIND J. WRIGHT, SHELDON COHEN, VINCENT CAREY, SCOTT T. WEISS, DIANE R. GOLD
Journal: American Journal of Respiratory and Critical Care Medicine (2002)

The role of stress in the pathogenesis of childhood wheeze remains controversial. Caretaker stress might influence wheeze through stress-induced behavioral changes in caregivers (e.g., smoking, breast-feeding) or biologic processes impacting infant development (e.g., immune response, susceptibility to lower respiratory infections). The influence of caregiver stress on wheeze in infancy was studied in a genetically predisposed prospective birth-cohort (n = 496). Caregiver-perceived stress and wheeze in the children were ascertained bimonthly from the first 2 to 3 mo of life. Greater levels of caregiver-perceived stress at 2 to 3 mo was associated with increased risk of subsequent repeated wheeze among the children during the first 14 mo of life (RR, 1.6; 95% CI, 1.3 to 1.9). Caregiver-perceived stress remained significant (RR, 1.4; 95% CI, 1.1 to 1.9) when controlling for factors potentially associated with both stress and wheeze (parental asthma, socioeconomic status, birth weight, and race/ethnicity) as well as mediators through which stress might influence wheeze (maternal smoking, breast-feeding, indoor allergen exposures, and lower respiratory infections). Furthermore, caregiver stress prospectively predicted wheeze in the infants, whereas wheeze in the children did not predict subsequent caregiver stress. The effect of caregiver stress on early childhood wheeze was independent of caregiver smoking and breast-feeding behaviors, as well as allergen exposure, birth weight, and lower respiratory infections. These findings suggest a more direct mechanism may be operating between stress and wheeze in early childhood. Stress may contribute significantly to the population burden of preventable childhood respiratory illness.
Reduction in Obesity and Related Comorbid Conditions after Diet-Induced Weight Loss or Exercise-Induced Weight Loss in Men
Authors: Robert Ross
Journal: Annals of Internal Medicine (2000)

Background: The independent effects of diet- or exercise-induced weight loss on the reduction of obesity and related comorbid conditions are not known. The effects of exercise without weight loss on fat distribution and other risk factors are also unclear. Objective: To determine the effects of equivalent diet- or exercise-induced weight loss and exercise without weight loss on subcutaneous fat, visceral fat, skeletal muscle mass, and insulin sensitivity in obese men. Design: Randomized, controlled trial. Setting: University research center. Participants: 52 obese men (mean body mass index [±SD], 31.3 ± 2.0 kg/m2) with a mean waist circumference of 110.1 ± 5.8 cm. Intervention: Participants were randomly assigned to one of four study groups (diet-induced weight loss, exercise-induced weight loss, exercise without weight loss, and control) and were observed for 3 months. Measurements: Change in total, subcutaneous, and visceral fat; skeletal muscle mass; cardiovascular fitness; glucose tolerance and insulin sensitivity. Results: Body weight decreased by 7.5 kg (8%) in both weight loss groups and did not change in the exercise without weight loss and control groups. Compared with controls, cardiovascular fitness (peak oxygen uptake) in the exercise groups improved by approximately 16% (P < 0.01). Although total fat decreased in both weight loss groups (P < 0.001), the average reduction was 1.3 kg (95% CI, 0.3 to 2.3 kg) greater in the exercise-induced weight loss group than in the diet-induced weight loss group (P = 0.03). Similar reductions in abdominal subcutaneous, visceral, and visceral fat–to–subcutaneous fat ratios were observed in the weight loss groups (P < 0.001). Abdominal and visceral fat also decreased in the exercise without weight loss group (P = 0.001). Plasma glucose and insulin values (fasting and oral glucose challenge) did not change in the treatment groups compared with controls (P = 0.10 for all comparisons). Average improvement in glucose disposal was similar in the diet-induced weight loss group (5.6 mg/kg skeletal muscle per minute) and in the exercise-induced weight loss group (7.2 mg/kg skeletal muscle per minute) (P > 0.2). However, these values were significantly greater than those in the control and exercise without weight loss groups (P < 0.001). Conclusions: Weight loss induced by increased daily physical activity without caloric restriction substantially reduces obesity (particularly abdominal obesity) and insulin resistance in men. Exercise without weight loss reduces abdominal fat and prevents further weight gain.
Prevention of Type 2 Diabetes
Authors: Thomas A. Buchanan
Journal: Diabetes Care (2003)

The current epidemic of type 2 diabetes in developed countries is occurring at three levels. First, more and more individuals are in positive calorie balance and accumulating fat in their bodies; they are becoming obese. Second, many of those obese individuals partition sufficient lipid in their livers and muscles and/or generate sufficient hormonal signals from fat cells to create insulin resistance. Third, pancreatic β-cells progressively fail in some individuals as they attempt to compensate for insulin resistance by increasing insulin output on a chronic basis. The β-cell failure tends to be slowly progressive over time and leads to progressively rising glucose levels that, when they become dangerous for eyes, kidneys, and nerves, define type 2 diabetes.

Prevention of type 2 diabetes requires arrest of the progressive β-cell dysfunction and stabilization of glucose concentrations at nondiabetic levels. Anything short of this arrest and stabilization will only delay the onset of type 2 diabetes. Theoretically, type 2 diabetes could be prevented or delayed by three types of interventions: 1 ) interventions that limit fat accumulation in the body (less obesity = less insulin resistance); 2 ) interventions that uncouple obesity from insulin resistance (less insulin resistance = less β-cell failure); and 3 ) interventions that directly preserve β-cell mass and/or function, despite the high secretory demands imposed by insulin resistance (better β-cell function = less diabetes).

Current efforts to prevent type 2 diabetes have used interventions that modify obesity and/or insulin resistance or that change glucose levels directly. The studies have generally not focused on the end points of stable glycemia and β-cell function. Rather, they have focused on reducing the fraction of patients with slightly elevated glucose levels (e.g., impaired glucose tolerance or “IGT”) who “cross the line” to diabetes, where the risk of microvascular complications begins. The studies have been conducted over periods …
On the Role of the cAMP Response Element Binding Protein in Long-Term Cardiac Memory
Authors: Kornelis W. Patberg, Michael R. Rosen
Journal: Circulation Research (2003)

To the Editor:Cardiac memory (CM) has been investigated extensively over the last decades. 1-3Whereas early studies focused on electrotonus as a central determinant of cardiac memory, 3 more recent work has considered changes in ion channels driven by to-be-determined transcriptional events. 4,5However, any transcriptional mechanisms involved remained largely unidentified.In the September 5 issue of the journal, we reported our first study investigating transcriptional mechanisms of CM. 6 Based on previously shown parallels between CM and memory in the CNS, 7 which incorporates the cAMP response element binding protein (CREB) as an important transcription factor, 8 we investigated the role of CREB in CM.Briefly, using 2 hours of ventricular pacing (VP) to induce short-term CM (STCM), we observed a decrease in nuclear CREB, with phosphorylated CREB levels remaining equal.This decrease was most marked close to the pacing electrode.We also showed reduced binding of nuclear proteins to CRE in dogs in which LTCM was induced by 3 weeks of VP and demonstrated binding of nuclear proteins to a CRE-like element in the Kv4.3 promoter.An erudite editorial by Folco et al 9 in the same issue of the journal notes that several members of the CREB family of transcription factors (including CREM and ATF-1) can compensate for a loss of CREB.They also state that a 50% reduction in CREB is not necessarily adequate to cause loss of function.We fully agree with both points, and accordingly never stated that the 50% CREB reduction observed during 2 hours of VP is responsible for STCM or uniquely responsible for LTCM.However, we do believe and did state (see page 477) that this reduction in CREB might initiate a cascade of events leading to LTCM.It remains to be elucidated whether LTCM would result from events downstream from CREB or from a direct influence of CREB on CM target genes (such as Kv4.3). 4 In support of the latter possibility was our observation of nuclear protein binding activity to a CRE-like element in the Kv4.3 promoter region.Folco and colleagues 9 state the Kv4.3 CRE (TGACGTCT) lacks the complete CRE core sequence (CGTCA), and on initial inspection this might seem the case.However, the complementary strand of the Kv4.3 sequence is 5Ј-AGACGTCA-3Ј, which does contain a CRE core sequence.Whether this element has comparable binding capacities as the consensus CRE is currently under investigation.Folco and colleagues were puzzled, as were we, that no increase in phosphorylated CREB occurred early in the 2 hours of VP.They offer the explanation that increased phosphorylation might be ob-
Europeans with poor "health literacy" are heavy users of health services
Authors: R. Watson
Journal: BMJ (2011)

Almost half of all Europeans have inadequate levels of “health literacy,” concludes a survey conducted by a consortium led by Maastricht University. 

The European health literacy survey measured people’s ability to access, understand, analyse, and apply health information to enable them to make informed decisions so as to maintain their health, prevent diseases, and seek treatment when ill.

The research, which was conducted in eight countries (Austria, Bulgaria, Germany, Greece, Ireland, Netherlands, Poland, and Spain) found that overall 47% of the 8000 people surveyed had limited health literacy. The results varied considerably between countries, …
The IPPB Trial
Authors: Bertrand J. Shapiro, Melvin A. Welch, Philip Mercurio
Journal: Annals of Internal Medicine (1984)

Letters and Corrections1 March 1984The IPPB TrialBERTRAND J. SHAPIRO, M.D., MELVIN A. WELCH JR, R.R.T., PHILIP MERCURIO, R.R.T.BERTRAND J. SHAPIRO, M.D.Search for more papers by this author, MELVIN A. WELCH JR, R.R.T.Search for more papers by this author, PHILIP MERCURIO, R.R.T.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-100-3-457_3 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: We are greatly disturbed by several points in the article (1) on the trial comparing intermittent positive pressure breathing (IPPB) and compressor nebulizer therapies. Seventy percent of screened candidates were not entered into the study, many because of refusal to participate or recent use of IPPB or compressor nebulizers. Our conjecture is that in these moderately to severely ill patients, most have used either IPPB or compressor nebulizers in the course of their illness. The candidates who were screened but not enrolled in the study may have included responders to the therapies. Responders, when faced with going...References1. . Intermittent positive pressure breathing therapy of chronic obstructive pulmonary disease: a clinical trial. Ann Intern Med. 1983;99:612-20. LinkGoogle Scholar2. BAKER J. Intermittent positive pressure breathing or compressor nebulizer therapy [Editorial]? Ann Intern Med. 1983;99:715-6. LinkGoogle Scholar3. WELCHSHAPIROMERCURIOWAGNERHIRAYAMA MBPWG. Methods of intermittent positive pressure breathing. Chest. 1980;78:463-87. CrossrefMedlineGoogle Scholar4. HODGKINZORNANTHONESENLEVINMURRAYSTEVENS JENDJP. The NIH Protocol—Is it vulnerable? Respir Care. 1982;27:995. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 March 1984Volume 100, Issue 3Page: 457-458KeywordsBreathing Issue Published: 1 March 1984 PDF DownloadLoading ...
Genome-wide scan for familial nasopharyngeal carcinoma reveals evidence of linkage to chromosome 4
Authors: Bing-Jian Feng, Wei Huang, Yin Yao Shugart, Ming K. Lee, Feng Zhang, Jian-Chuan Xia, Hui-Yun Wang, Teng-Bo Huang, Shao-Wen Jian, Ping Huang, Qi-Sheng Feng, Li-Xi Huang, Xing-Juan Yu, Duang Li, Li-Zheng Chen, Wei-Hua Jia, Yan Fang, Hui-Ming Huang, Jing-Liu Zhu, Xiao-Ming Liu, Yan Zhao, Wang-Qing Liu, Mang-Quan Deng, Wei-Han Hu, Shao-Xiong Wu, Hao-Yuan Mo, Ming-Fang Hong, Mary Claire King, Zhu Chen, Yi-Xin Zeng
Journal: Nature Genetics (2002)
Neuropeptide Y upregulates the adhesiveness of human endothelial cells for leukocytes.
Authors: C P Sung, A J Arleth, G Z Feuerstein
Journal: Circulation Research (1991)

The nervous system and the autonomic system in particular have been associated with stress-induced changes in host resistance to infections and inflammatory reactions. Since a key step in initiation of inflammation is adhesion of leukocytes to the endothelium, we hypothesized that neuron-derived factors might be involved in this process. Neuropeptide Y (NPY), a 36-amino acid neuropeptide that is colocalized and released with norepinephrine from sympathetic nerves, has already been implicated in inflammatory reactions via modulation of histamine release from mast cells. This study was undertaken to examine the potential role of NPY in proinflammatory processes via modulation of endothelium-leukocyte interaction. NPY (0.01-10 microM) increased the adhesion of 51Cr-labeled human neutrophils or the human monocytic U937 cell line to human umbilical vein endothelial cells in a dose- and time-dependent manner. The stimulation of human umbilical vein endothelial cell adhesiveness occurred as early as 30 minutes and lasted over 48 hours. The increase of leukocyte adhesion to human umbilical vein endothelial cells by NPY was not inhibited by protein synthesis inhibitor cycloheximide, nor was it associated with expression of intercellular adhesion molecule-1 on human umbilical vein endothelial cells; in contrast, strong expression of intercellular adhesion molecule-1 was induced by tumor necrosis factor alpha and lipopolysaccharide endotoxin. These data suggest that neuron-derived factors such as NPY may serve as modulators of not only the neuromuscular unit but also the interaction of endothelial cells with leukocytes. In this capacity, the sympathetic nervous system might play an important role in the regulation of proaggregatory and hemostatic activity of microvessels.