tbuckley/cabot-search huggingface dataset:
Telehealthcare for long term conditions
Authors: S. McLean, D. Protti, A. Sheikh
Journal: BMJ (2011)

#### Summary points

Telehealthcare is the provision of personalised healthcare over a distance.1 It has the three following essential components2w1:

Telehealthcare can be delivered by both synchronous and asynchronous (such as store and forward) technologies (fig 1⇓). For example, telephone and video conferencing enable consultations in real time. An example of asynchronous communication would be storing two weeks’ of spirometry results in a batch and forwarding these on to a healthcare provider, who responds by email or telephone. 

Telehealthcare is related to, but distinct from telemedicine, where technology is used to share information over a distance between healthcare providers.2



Fig 1 Key elements of telehealthcare



#### Sources and selection criteria

We identified systematic reviews and original research studies on telehealthcare and long term conditions. We used searches from our ongoing Cochrane systematic reviews to find randomised controlled trials for telehealthcare interventions for asthma and chronic obstructive pulmonary disease. Search terms were telehealth, tele-health, telemedicine, tele-medicine, internet, computer, web, interactive, telecommunication, telephone, …
House dust mite avoidance measures improve peak flow and symptoms in patients with allergy but without asthma: A possible delay in the manifestation of clinical asthma?
Authors: S.M. Cloosterman, I.D. Hofland, H.M. Lukassen, M.H. Wieringa, H.M. Folgering, S. van der Heide, B. Brunekreef, C.P. van Schayck
Journal: Journal of Allergy and Clinical Immunology (1997)
Effects of formoterol on histamine induced plasma exudation in induced sputum from normal subjects
Authors: L. Greiff, P. Wollmer, M. Andersson, C. Svensson, C. G A Persson
Journal: Thorax (1998)

BACKGROUND A number of studies have shown that β2 agonists, including formoterol, inhibit plasma exudation induced by the inflammatory stimulus in animal airways. Whether clinical doses of β2 agonists inhibit plasma exudation in human bronchial airways is unknown. METHODS In order to explore the microvascular permeability and its potential inhibition by β2 agonists in human bronchial airways a dual induction method was developed: plasma exudation induced by histamine inhalation followed by sputum induction by hypertonic saline (4.5%) inhalation. Sixteen healthy subjects received formoterol (18 μg) in a placebo controlled, double blind, crossover study. Sputum was induced on five occasions: once at baseline and four times after histamine challenge (30 minutes and eight hours after both formoterol and placebo treatments). Sputum levels of α2-macroglobulin were determined to indicate microvascular-epithelial exudation of bulk plasma. RESULTS Histamine induced plasma exudation 30 minutes after placebo was considerably greater than at baseline (median difference 11.3 μg/ml (95% confidence interval 0.9 to 90.0)). At 30 minutes after formoterol the effect of histamine was reduced by 5.1 (0.9 to 61.9) μg/ml compared with placebo. At eight hours histamine produced less exudation and inhibition by formoterol was not demonstrated. CONCLUSION This study shows for the first time an anti-exudative effect of a β2 agonist in healthy human bronchial airways. Through its physical and biological effects, plasma exudation is of multipotential pathogenic importance in asthma. If the present findings translate to disease conditions, it suggests that an anti-exudative effect may contribute to the anti-asthmatic activity of formoterol.
New insights into atopic dermatitis
Authors: Donald Y.M. Leung, Mark Boguniewicz, Michael D. Howell, Ichiro Nomura, Qutayba A. Hamid
Journal: Journal of Clinical Investigation (2004)

Atopic dermatitis is a chronic inflammatory skin disease associated with cutaneous hyperreactivity to environmental triggers and is often the first step in the atopic march that results in asthma and allergic rhinitis. The clinical phenotype that characterizes atopic dermatitis is the product of interactions between susceptibility genes, the environment, defective skin barrier function, and immunologic responses. This review summarizes recent progress in our understanding of the pathophysiology of atopic dermatitis and the implications for new management strategies.
Left Ventricular Lead Position and Clinical Outcome in the Multicenter Automatic Defibrillator Implantation Trial–Cardiac Resynchronization Therapy (MADIT-CRT) Trial
Authors: Jagmeet P. Singh, Helmut U. Klein, David T. Huang, Sven Reek, Malte Kuniss, Aurelio Quesada, Alon Barsheshet, David Cannom, Ilan Goldenberg, Scott McNitt, James P. Daubert, Wojciech Zareba, Arthur J. Moss
Journal: Circulation (2011)

Background— An important determinant of successful cardiac resynchronization therapy for heart failure is the position of the left ventricular (LV) pacing lead. The aim of this study was to analyze the impact of the LV lead position on outcome in patients randomized to cardiac resynchronization-defibrillation in the Multicenter Automatic Defibrillator Implantation Trial–Cardiac Resynchronization Therapy (MADIT-CRT) study. Methods and Results— The location of the LV lead was assessed by means of coronary venograms and chest x-rays recorded at the time of device implantation. The LV lead location was classified along the short axis into an anterior, lateral, or posterior position and along the long axis into a basal, midventricular, or apical region. The primary end point of MADIT-CRT was heart failure (HF) hospitalization or death, whichever came first. The LV lead position was assessed in 799 patients, (55% patients ≥65 years of age, 26% female, 10% LV ejection fraction ≤25%, 55% ischemic cardiomyopathy, and 71% left bundle-branch block) with a follow-up of 29±11 months. The extent of cardiac resynchronization therapy benefit was similar for leads in the anterior, lateral, or posterior position ( P =0.652). The apical lead location compared with leads located in the nonapical position (basal or midventricular region) was associated with a significantly increased risk for heart failure/death (hazard ratio=1.72; 95% confidence interval, 1.09 to 2.71; P =0.019) after adjustment for the clinical covariates. The apical lead position was also associated with an increased risk for death (hazard ratio=2.91; 95% confidence interval, 1.42 to 5.97; P =0.004). Conclusion— LV leads positioned in the apical region were associated with an unfavorable outcome, suggesting that this lead location should be avoided in cardiac resynchronization therapy. Clinical Trial Registration— URL: http://clinicaltrials.gov . Unique identifier: NCT00180271.
Performance of new alternative providers of primary care services in England: an observational study
Authors: Felix Greaves, Anthony A Laverty, Utz Pape, Anenta Ratneswaren, Azeem Majeed, Christopher Millett
Journal: Journal of the Royal Society of Medicine (2015)

Summary Objectives Health system reforms in England are opening broad areas of clinical practice to new providers of care. As part of these reforms, new entrants – including private companies – have been allowed into the primary care market under ‘alternative provider of medical services’ contracting mechanisms since 2004. The characteristics and performance of general practices working under new alternative provider contracts are not well described. We sought to compare the quality of care provided by new entrant providers to that provided by the traditional model of general practice. Design Open cohort study of English general practices. We used linear regression in cross-sectional and time series analyses, adjusting for practice and population characteristics, to compare quality in practices using alternative provider contracts to traditional practices. We created regression models using practice fixed effects to estimate the impact of practices changing to the new contract type. Setting The English National Health Service. Participants All general practices open from 2008/2009 to 2012/2013. Main outcome measures Seventeen established quality indicators – covering clinical effectiveness, efficiency, access and patient experience. Results In total, 4.1% (347 of 8300) of general practices in England were run by alternative contract providers. These practices tended to be smaller, and serve younger, more diverse and more deprived populations than traditional providers. Practices run by alternative providers performed worse than traditional providers on 15 of 17 indicators after adjusting for practice and population characteristics ( p &lt; 0.01 for all). Switching to a new alternative provider contract did not result in improved performance. Conclusions The introduction of new alternative providers to deliver primary care services in England has not led to improvements in quality and may have resulted in worse care. Regulators should ensure that new entrants to clinical provider markets are performing to adequate standards and at least as well as traditional providers.
A phase II trial of pemetrexed plus gemcitabine in locally advanced and/or metastatic transitional cell carcinoma of the urothelium
Authors: H. von der Maase, J. Lehmann, G. Gravis, H. Joensuu, P.F. Geertsen, J. Gough, G. Chen, M. Kania
Journal: Annals of Oncology (2006)
Alveolar proteinosis: diagnosis and treatment over a 10-year period.
Authors: R M Du Bois, W A McAllister, M A Branthwaite
Journal: Thorax (1983)

Ten years9 experience of using bronchoalveolar lavage in the treatment of 10 patients with alveolar proteinosis is reported. The diagnosis was often missed. The interval between onset of symptoms and diagnosis varied from six weeks to six years (median 2 years), so that the start of treatment was often delayed. Some patients experienced severe progressive disability before they had treatment. Whole-lung lavage proved to be a safe, repeatable procedure which provided symptomatic, physiological, and radiological improvement and allowed all 10 patients treated to return to full-time employment.
Suppression of Epidermal Growth Factor Receptor Signaling by Protein Kinase C-α Activation Requires CD82, Caveolin-1, and Ganglioside
Authors: Xiao-qi Wang, Qiu Yan, Ping Sun, Ji-Wei Liu, Linda Go, Shauntae M. McDaniel, Amy S. Paller
Journal: Cancer Research (2007)

Abstract Activation of protein kinase C (PKC)-α decreases normal and neoplastic cell proliferation by inhibiting epidermal growth factor receptor (EGFR)-related signaling. The molecular interactions upstream to PKC-α that influence its suppression of EGFR, however, are poorly understood. We have found that caveolin-1, tetraspanin CD82, and ganglioside GM3 enable the association of EGFR with PKC-α, ultimately leading to inhibition of EGFR signaling. GM3- and CD82-induced inhibition of EGFR signaling requires PKC-α translocation and serine/threonine phosphorylation, which eventually triggers EGFR Thr654 phosphorylation and receptor internalization. Within this ordered complex of signaling molecules, the ability of CD82 to associate with PKC-α requires the presence of caveolin-1, whereas the interaction of caveolin-1 or PKC-α with EGFR requires the presence of CD82 and ganglioside GM3. Disruption of the membrane with methyl-β-cyclodextrin dissociates the EGFR/GM3/caveolin-1/CD82/PKC-α complex and prevents the inhibitory effect of PKC-α on EGFR phosphorylation, suggesting that caveolin-1, CD82, and ganglioside interact with EGFR and PKC-α within intact cholesterol-enriched membrane microdomains. Given the role of these membrane molecules in suppressing EGFR signaling, up-regulation of GM3, caveolin-1, and CD82 function may be an effective adjunctive therapy for treating epithelial cell malignancies. [Cancer Res 2007;67(20):9986–95]
Effective Suicide Gene Therapy for Leukemia in a Model of Insertional Oncogenesis in Mice
Authors: Martina Blumenthal, Dianne Skelton, Karen A Pepper, Thomas Jahn, Emily Methangkool, Donald B Kohn
Journal: Molecular Therapy (2006)

The safety of gene therapy using hematopoietic stem cells may be increased by including a suicide gene in the therapeutic vector to eliminate adverse events like insertional oncogenesis while retaining the clinical benefits. We have developed a model of experimental insertional oncogenesis by transducing the murine factor-dependent leukemia cell line Ba/F3 with a bicistronic Moloney murine leukemia virus retroviral vector encoding a murine oncogene (cKit(D814V)) in addition to one of three suicide genes: Herpes simplex virus thymidine kinase (HSV-TK); SR39, an HSV-TK mutant with an increased affinity for the drug substrate Ganciclovir (GCV); or sc39, a splice-corrected version of SR39. Following intravenous challenge with transduced Ba/F3 clones and treatment with GCV, leukemia developed in mice given cells expressing HSV-TK, but not SR39 or sc39. In vitro GCV resistance was observed in heterogeneously transduced Ba/F3 pools at 2.5-14%, and single-nucleotide changes or partial loss of the suicide gene were identified as mechanisms of drug escape. However, GCV treatment resulted in 80-100% survival of mice challenged even with pools of partially resistant Ba/F3 cells expressing SR39 or sc39. Thus, in this model of vector-driven insertional oncogenesis, a suicide gene approach was effective for eliminating leukemia using modified HSV-TK variants with improved biological activity.
Antiviral CD8+ T cell effector activities in situ are regulated by target cell type
Authors: Matthew M. Hufford, Taeg S. Kim, Jie Sun, Thomas J. Braciale
Journal: The Journal of Experimental Medicine (2010)

Cytotoxic T lymphocytes (CTLs) play a prominent role in the resolution of viral infections through their capacity both to mediate contact-dependent lysis of infected cells and to release soluble proinflammatory cytokines and chemokines. The factors controlling these antiviral effector activities in vivo at infection sites are ill defined. Using a mouse model of influenza infection, we observed that the expression of CTL effector activity in the infected lungs is dictated by the target cell type encountered. CD45+ lung infiltrating inflammatory mononuclear cells, particularly CD11chi dendritic cells, trigger both CTL cytotoxicity and release of inflammatory mediators, whereas CD45− influenza-infected respiratory epithelial cells stimulate only CTL cytotoxicity. CTL proinflammatory mediator release is modulated by co-stimulatory ligands (CD80 and CD86) expressed by the CD45+ inflammatory cells. These findings suggest novel mechanisms of control of CTL effector activity and have potentially important implications for the control of excess pulmonary inflammation and immunopathology while preserving optimal viral clearance during respiratory virus infections.
Anti-EGFR monoclonal antibodies in the treatment of non-small cell lung cancer
Authors: A. Sartore-Bianchi, G. Cerea, I. Schiavetto, L. Giannetta, R. Ricotta, M.R. Maugeri, M. Moroni, G. Marrapese, S. Siena
Journal: Annals of Oncology (2006)
Acute perforated duodenal ulcer is not associated with Helicobacter pylori infection.
Authors: D H Reinbach, G Cruickshank, K E McColl
Journal: Gut (1993)

Most patients with chronic duodenal ulcer disease have Helicobacter pylori infection and eradicating it considerably reduces the relapse rate. The prevalence of H pylori in 80 patients (mean age = 52 years, range 17-85) presenting with acute perforated duodenal ulcer was examined and compared with age and sex matched hospital control patients. H pylori state was assessed by serum anti-H pylori IgG (Helico-G kit, Porton) using a titre of 18 or less as negative with a specificity of 89% and sensitivity of 88%. Only 47% of the perforated duodenal ulcer patients were positive for H pylori and this was similar to the value of 50% in the controls. In 51 of the perforated duodenal ulcer patients 14C-urea breath tests were also performed 4-10 weeks after surgery and this confirmed that only 49% were positive for H pylori. None of these patients had received perioperative drugs that might have eradicated the infection. The H pylori positive and H pylori negative perforated duodenal ulcer patients were similar with respect to age (53, 51), smoking (84%, 83%), and consumption of more than 15 units of alcohol per week (42%, 38%). Duodenal ulcer disease had been diagnosed before acute perforation in only 24% of those with H pylori and also 24% of those without the infection. Regular non-steroidal anti-inflammatory drug (NSAID) use was common in both those with (44%) and without (45%) H pylori. In conclusion, the lack of association of acute perforated duodenal ulcer and H pylori infection suggests that perforated duodenal ulcer has a different pathogenesis from chronic duodenal ulcer disease, and that the first should not be regarded simply as a complication of the second.
Relevance of the tubuloglomerular feedback mechanism in pathophysiology.
Authors: B Braam, K D Mitchell, H A Koomans, L G Navar
Journal: Journal of the American Society of Nephrology (1993)

The balance between a high filtration rate and high reabsorption rate in the kidney is critical in the maintenance of extracellular fluid volume. One of the mechanisms that maintain this balance is the tubuloglomerular feedback (TGF) mechanism, which operates at the level of the macula densa assessing the load and/or solute concentration coming out of the loop of Henle and controlling this load by adjusting the GFR. This review discusses the potential role of the TGF system with respect to volume homeostasis in various conditions where GFR is maintained, decreased, or increased. In most of the states discussed, the TGF system seems to act appropriately regarding volume control; however, trade-off effects occasionally occur. After acetazolamide administration, during extracellular fluid volume contraction or expansion or acute hyperkalemia, the TGF mechanism responds appropriately with regard to volume balance. After a large reduction of renal mass, the system adjusts to function at a higher level of GFR and distal delivery. In chloride-depletion metabolic alkalosis, glomerulonephritis, diabetes mellitus, and acute renal failure, the adaptation of the TGF system appears to be appropriate with regard to volume control; however, it may lead to trade-off effects, such as maintenance of metabolic alkalosis, glomerular hypertension and sclerosis, or depression of GFR, respectively. Because the TGF mechanism often contributes to compensatory adjustments to or development of disease, it can be appreciated that any in-depth evaluation of the mechanisms responsible for various pathophysiologic conditions should include an assessment of the potential role of the TGF mechanism.
DNA Polymerase η Is Involved in Hypermutation Occurring during Immunoglobulin Class Switch Recombination
Authors: Ahmad Faili, Said Aoufouchi, Sandra Weller, Françoise Vuillier, Anne Stary, Alain Sarasin, Claude-Agnès Reynaud, Jean-Claude Weill
Journal: The Journal of Experimental Medicine (2004)

Base substitutions, deletions, and duplications are observed at the immunoglobulin locus in DNA sequences involved in class switch recombination (CSR). These mutations are dependent upon activation-induced cytidine deaminase (AID) and present all the characteristics of the ones observed during V gene somatic hypermutation, implying that they could be generated by the same mutational complex. It has been proposed, based on the V gene mutation pattern of patients with the cancer-prone xeroderma pigmentosum variant (XP-V) syndrome who are deficient in DNA polymerase η (pol η), that this enzyme could be responsible for a large part of the mutations occurring on A/T bases. Here we show, by analyzing switched memory B cells from two XP-V patients, that pol η is also an A/T mutator during CSR, in both the switch region of tandem repeats as well as upstream of it, thus suggesting that the same error-prone translesional polymerases are involved, together with AID, in both processes.
Evaluating the Role of Computed Tomography
Authors: Martin A. Schreiber
Journal: JAMA Surgery (2013)

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Mycobacterium avium-intracellulare: A Cause of Disseminated Life-Threatening Infection in Homosexuals and Drug Abusers
Authors: JEFFREY B. GREENE
Journal: Annals of Internal Medicine (1982)

Five men developed disseminated infection with Mycobacterium avium-intracellulare. These patients all lived in the New York City area and presented with their illnesses between January 1981 and September 1981; four were homosexual and one was an intravenous drug abuser. Four patients died. All five patients had defects in the cell-mediated immune response. The infections were characterized histopathologically by poor or absent granulomatous tissue reaction. Clinical isolates of M. avium-intracellulare from all five patients agglutinated with type 8 antisera. The organisms were resistant to most commonly used antimycobacterial drugs. The spectrum of opportunistic infections among populations of homosexuals and drug abusers should be expanded to include disseminated disease due to M. avium-intracellulare.