tbuckley/cabot-search huggingface dataset:
Multidisciplinary approach to management of postintubation tracheal stenoses
Authors: A. Brichet, C. Verkindre, J Dupont, M.l Carlier, J Darras, A Wurtz, P Ramon, C.h Marquette
Journal: European Respiratory Journal (1999)

The optimal management of postintubation tracheal stenosis is not well defined. A therapeutic algorithm was designed by thoracic surgeons, ear, nose and throat (ENT) surgeons, anaesthetists and pulmonologists. Rigid bronchoscopy with neodymium-yttrium aluminium garnet (Nd-YAG) laser resection or stent implantation (removable stent) was proposed as first-line treatment, depending on the type of stenosis (web-like versus complex stenosis). In patients with web-like stenoses, sleeve resection was proposed when laser treatment (up to three sessions) failed. In patients with complex stenoses, operability was assessed 6 months after stent implantation. If the patient was judged operable, the stent was removed and the patient underwent surgery if the stenosis recurred. This algorithm was validated prospectively in a series of 32 consecutive patients. Three patients died from severe coexistent illness shortly after the first bronchoscopy. Of the 15 patients with web-like stenosis, laser resection was curative in 10 (66%). Among the 17 patients with complex stenoses, three remained symptom-free after stent removal. Bronchoscopy alone was thus curative in more than one-third of the patients. Six patients underwent surgery, two after failure of laser resection and four after failure of temporary stenting. Surgery was always performed with the patient in good operative condition. Palliative stenting was the definitive treatment in nine cases. Tracheostomy was the definitive solution in two cases. This approach, including an initial conservative treatment, depending on the type of the stenosis, appears to be applicable to almost all patients and allows secondary surgery to be performed with the patient in good condition.
Aspirin and the Stomach
Authors: DAVID Y. GRAHAM
Journal: Annals of Internal Medicine (1986)

Aspirin often causes acute gastric mucosal damage that can be seen endoscopically or assessed indirectly (for example, by measuring increased gastrointestinal blood loss). The occurrence of most adverse effects is apparently related to the dose administered. This dose-response effect, evident in both endoscopic and microbleeding studies done after acute or short-term aspirin administration, is also associated with the risk of developing chronic gastric ulcer. The occurrence of gastric adaptation, or lessening injury with continued treatment, obscures the interpretation of results from studies of acute administration. Moreover, evidence of dose-response effects has frequently been ignored when lists of complications and side effects are compiled. The absence of symptoms does not correlate with acute or chronic mucosal damage and appears to have no predictive value. Endoscopic studies linking the extent and degree of acute mucosal injury to various nonsteroidal anti-inflammatory drugs have little or no value in predicting the frequency or severity of chronic gastric ulcer or gastrointestinal bleeding.
Immunohistochemical profiling of caspase signaling pathways predicts clinical response to chemotherapy in primary nodal diffuse large B-cell lymphomas
Authors: Jettie J. F. Muris, Saskia A. G. M. Cillessen, Wim Vos, Inge S. van Houdt, J. Alain Kummer, Johan H. J. M. van Krieken, N. Mehdi Jiwa, Patty M. Jansen, Hanneke C. Kluin-Nelemans, Gert J. Ossenkoppele, Chad Gundy, Chris J. L. M. Meijer, Joost J. Oudejans
Journal: Blood (2004)
A phase II trial of thymidine and carboplatin for recurrent malignant glioma: A North American Brain Tumor Consortium Study
Authors: H. Ian Robins, Susan M. Chang, Michael D. Prados, W.K. Alfred Yung, Kenneth Hess, David Schiff, Harry Greenberg, Karen Fink, Kelly Nicolas, John G. Kuhn, Timothy Cloughesy, Larry Junck, Minesh Mehta
Journal: Neuro-Oncology (2002)

This phase II study in recurrent high-grade glioma evaluated the response rate, toxicities, and time to treatment failure of high-dose carboplatin modulated by a 24-h infusion of thymidine (75 g/m(2)). The trial was based on preclinical data and a prior phase I study ( J. Clin. Oncol. 17, 2922-2931, 1999); a phase II recurrent high-grade glioma study was initiated in July of 1998. Thymidine was given over 24 h; carboplatin was given over 20 min at hour 20 of the thymidine infusion. The starting dose of carboplatin had a value of 7 for the area under the curve (AUC), with allowance for dose escalation of 1 AUC unit per cycle if grade 2 toxicity was observed. Treatment cycles were repeated every 4 weeks. Accrual as of September 1999 was 45 patients [4 were unevaluable]: 76% with glioblastoma multiforme (GBM), 20% with anaplastic oligodendroglioma, 2% with mixed type, and 2% with anaplastic astrocytoma. Most patients had prior chemotherapy (78%). As observed in the earlier phase I study (in which carboplatin pharmacokinetics were unaltered by thymidine or antiseizure medications), thymidine was myeloprotective, resulting in a minimal need for dose reduction for patients having a >2 grade toxicity (in only 4% of the courses of treatment). Of 101 total courses, the number of courses (at the AUCs) was 3 (5), 4 (6), 58 (7), 20 (8), 11 (9), and 5 (10). Grade 3 nonhematologic toxicities included headache (4%), altered consciousness (3%), fatigue (1%), and nausea (3%). Responses included 2 partial (1 oligodendroglioma, 1 GBM; 5%); 3 minor (1 anaplastic astrocytoma, 2 GBM; 7.3%); 6 stable disease (14.6%); and 30 progressive disease (73.2%). For GBM patients, median survival was 23 weeks (with a 95% confidence interval of 20 to 50 weeks), and progression-free survival was 8 weeks (with a 95% confidence interval of 7-16 weeks). These results in GBM were comparable to other phase II GBM trials and thus do not represent a therapeutic advance in the treatment of GBM. Taken collectively, however, results are consistent with continued investigation of thymidine in combination with chemotherapeutic agents for high-grade glioma and other malignant diseases. The significant myeloprotection afforded by thymidine may have particular relevance to polychemotherapeutic regimens.
The increasing incidence of basal cell carcinoma
Authors: P. Wallberg, E. Skog
Journal: British Journal of Dermatology (1994)

Journal Article The increasing incidence of basal cell carcinoma Get access P. Wallberg, P. Wallberg Department of Dermatology and Venereology, Södersjukhuset, 118 83 Stockholm, Sweden Search for other works by this author on: Oxford Academic Google Scholar E. Skog E. Skog Department of Dermatology and Venereology, Södersjukhuset, 118 83 Stockholm, Sweden Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 131, Issue 6, 1 December 1994, Pages 914–915, https://doi.org/10.1111/j.1365-2133.1994.tb08607.x Published: 01 December 1994
The Metabolic Syndrome and 11-Year Risk of Incident Cardiovascular Disease in the Atherosclerosis Risk in Communities Study
Authors: Ann Marie McNeill, Wayne D. Rosamond, Cynthia J. Girman, Sherita Hill Golden, Maria I. Schmidt, Honey E. East, Christie M. Ballantyne, Gerardo Heiss
Journal: Diabetes Care (2005)

OBJECTIVE— To assess the magnitude of the association between the National Cholesterol Education Program’s Third Adult Treatment Panel Report (ATP III) definition of the metabolic syndrome and cardiovascular disease (CVD). RESEARCH DESIGN AND METHODS— Cox regression was used to estimate the relative risk of incident coronary heart disease (CHD) and stroke among 12,089 black and white middle-aged individuals in the Atherosclerosis Risk in Communities (ARIC) study. RESULTS— The metabolic syndrome was present in ∼23% of individuals without diabetes or prevalent CVD at baseline. Over an average of 11 years of follow-up, 879 incident CHD and 216 ischemic stroke events occurred. Among the components of the metabolic syndrome, elevated blood pressure and low levels of HDL cholesterol exhibited the strongest associations with CHD. Men and women with the metabolic syndrome were ∼1.5 and 2 times more likely to develop CHD than control subjects after adjustment for age, smoking, LDL cholesterol, and race/ARIC center (sex interaction P &amp;lt; 0.03). Similar associations were found between the metabolic syndrome and incident ischemic stroke. Comparison of receiver operating characteristic curves indicated that the metabolic syndrome did not materially improve CHD risk prediction beyond the level achieved by the Framingham Risk Score (FRS). CONCLUSIONS— Individuals without diabetes or CVD, but with the metabolic syndrome, were at increased risk for long-term cardiovascular outcomes, although statistical models suggested that most of that risk was accounted for by the FRS. Nevertheless, identification of individuals with the metabolic syndrome may provide opportunities to intervene earlier in the development of shared disease pathways that predispose individuals to both CVD and diabetes.
Labour's “Black report” moment?
Authors: Mary Shaw, Danny Dorling, Richard Mitchell, George Davey Smith
Journal: BMJ (2005)

EDITOR—The release of the government's latest report on health inequalities on 11 August was curious.1 2 Reminiscent of the covert release of the Black report on August bank holiday in 1980, the report appeared when the minister for public health was on holiday and her deputy unavailable.

In July 2003 the government stated that there would be an annual report from the Department of Health on health inequality indicators related to the health inequality targets. Nothing appeared for more than two years, although the data that were eventually released had been available for some time,3 and when they did appear it was, conveniently, after the election. Even stranger, the press release for the latest report deflected attention from the key finding of widening inequalities in life expectancy and infant mortality by headlining the 12 “early adopter sites” with their “health trainers.”4 The minister said, “Many people have difficulty in changing to …
Cognition does not affect perception: Evaluating the evidence for “top-down” effects
Authors: Chaz Firestone, Brian J. Scholl
Journal: Behavioral and Brain Sciences (2015)

What determines what we see? In contrast to the traditional "modular" understanding of perception, according to which visual processing is encapsulated from higher-level cognition, a tidal wave of recent research alleges that states such as beliefs, desires, emotions, motivations, intentions, and linguistic representations exert direct, top-down influences on what we see. There is a growing consensus that such effects are ubiquitous, and that the distinction between perception and cognition may itself be unsustainable. We argue otherwise: None of these hundreds of studies - either individually or collectively - provides compelling evidence for true top-down effects on perception, or "cognitive penetrability." In particular, and despite their variety, we suggest that these studies all fall prey to only a handful of pitfalls. And whereas abstract theoretical challenges have failed to resolve this debate in the past, our presentation of these pitfalls is empirically anchored: In each case, we show not only how certain studies could be susceptible to the pitfall (in principle), but also how several alleged top-down effects actually are explained by the pitfall (in practice). Moreover, these pitfalls are perfectly general, with each applying to dozens of other top-down effects. We conclude by extracting the lessons provided by these pitfalls into a checklist that future work could use to convincingly demonstrate top-down effects on visual perception. The discovery of substantive top-down effects of cognition on perception would revolutionize our understanding of how the mind is organized; but without addressing these pitfalls, no such empirical report will license such exciting conclusions.
Decline of Childhood Haemophilus influenzae Type b (Hib) Disease in the Hib Vaccine Era
Authors: William G. Adams
Journal: JAMA (1993)

<h3>Objective.</h3> —Effective<i>Haemophilus influenzae</i>type b (Hib) conjugate vaccines were first licensed for use in US children at least 18 months old in December 1987 and for infants at least 2 months old in October 1990. We evaluated trends in Hib disease associated with licensure of Hib conjugate vaccines. <h3>Design.</h3> —Data from two sources, an intensive laboratory-based active surveillance system and the National Bacterial Meningitis Reporting System (NBMRS), were used separately to evaluate disease incidence. Data from vaccine manufacturers on Hib vaccine doses distributed in the United States were compared with trends in Hib disease incidence. <h3>Results.</h3> —The age-specific incidence of Hib disease among children less than 5 years old decreased by 71% from 37 per 100 000 persons in 1989 to 11 per 100 000 persons in 1991 (active surveillance data).<i>Haemophilus influenzae</i>meningitis incidence decreased by 82% between 1985 and 1991 (NBMRS data). Increases in doses of Hib vaccine distributed in the United States coincided with steep declines in Hib disease. Both surveillance systems showed decreased rates of Hib disease in infants less than 1 year old before vaccine was licensed for use in this age group.<i>Haemophilus influenzae</i>type b disease incidence in persons at least 12 years old and pneumococcal meningitis incidence in children less than 5 years old did not change substantially during the same period; therefore, decreased Hib disease in children less than 5 years old is not likely to be explained solely by changes in surveillance sensitivity or decreases in bacterial disease due to changes in medical practice. <h3>Conclusion.</h3> —Our data suggest that conjugate vaccines have already had a marked impact on the incidence of Hib disease in the United States, preventing an estimated 10 000 to 16 000 cases of Hib disease in 1991. The decline of disease in infants less than 1 year old before licensure for this age group warrants further investigation. (<i>JAMA</i>. 1993;269:221-226)
Bronchoalveolar lavage pepsin in acute exacerbation of idiopathic pulmonary fibrosis
Authors: J.S. Lee, J.W. Song, P.J. Wolters, B.M. Elicker, T.E. King, D.S. Kim, H.R. Collard
Journal: European Respiratory Journal (2011)

Some patients with idiopathic pulmonary fibrosis experience acute exacerbations in their respiratory status leading to substantial morbidity and mortality. Occult aspiration of gastric contents has been proposed as one possible mechanism leading to these acute exacerbations. We sought to determine whether pepsin, a marker of gastric aspiration, is elevated in bronchoalveolar lavage fluid obtained from patients during acute exacerbation of idiopathic pulmonary fibrosis, compared with that obtained in stable disease. Lavage samples were obtained in a case-control study of well-characterised patients. Acute exacerbation was defined using standard criteria. Levels of lavage pepsin were compared in cases and controls, and were correlated with clinical features and disease course. 24 cases with acute exacerbations and 30 stable controls were identified. There were no significant differences in baseline demographics between the two groups. Pepsin level was an indicator of acute exacerbation status (p=0.04). On average, pepsin appeared higher in patients with acute exacerbations compared with stable controls. This difference was driven by a subgroup of eight patients (33%) with pepsin levels ≥70 ng·mL(-1). Pepsin level was not an independent predictor of survival time. These results suggest occult aspiration may play a role in some cases of acute exacerbation of idiopathic pulmonary fibrosis.
Simvastatin reduces human atrial myofibroblast proliferation independently of cholesterol lowering via inhibition of RhoA
Authors: K Porter
Journal: Cardiovascular Research (2004)

Objective: Adverse atrial and ventricular myocardial remodeling is characterized by fibrosis, myocyte death or hypertrophy and fibroblast proliferation. HMG-CoA reductase inhibitors (statins) are widely prescribed cholesterol-lowering drugs that also appear to have beneficial effects on myocardial remodeling. Although statins are known to reduce myocyte hypertrophy, their effect on cardiac fibroblast proliferation is unknown. The purpose of this study was to investigate the effects of simvastatin on human atrial myofibroblast proliferation. Methods: Cardiac myofibroblasts were cultured from biopsies of human right atrial appendage. Proliferation was quantified by cell counting and cell cycle progression determined by immunoblotting for Cyclin A. The expression, activation and intracellular localization of RhoA were investigated using immunoblotting and immunocytochemistry. Results: Simvastatin (0.1–1.0 μmol/l) inhibited serum-induced myofibroblast proliferation in a concentration-dependent manner at a point upstream of Cyclin A expression. These effects were reversed by mevalonate or geranylgeranyl pyrophosphate (GGPP), but not squalene or farnesyl pyrophosphate (FPP), indicating a mechanism involving inhibition of Rho-family GTPases and independent of cholesterol synthesis. The effects of simvastatin were mimicked by inhibiting Rho geranylgeranylation or Rho-kinase activation. Furthermore, we demonstrated that simvastatin inhibited RhoA function by preventing its association with the plasma membrane and hence, its interaction with downstream effectors required for cell proliferation. Conclusions: Simvastatin reduced proliferation of cultured human atrial myofibroblasts independently of cholesterol synthesis via a mechanism involving inhibition of RhoA geranylgeranylation. Statins may therefore have an important role in preventing adverse myocardial remodeling associated with cardiac myofibroblast proliferation.
Survivorship and Quality of Life in Head and Neck Cancer
Authors: Jolie Ringash
Journal: Journal of Clinical Oncology (2015)

Head and neck cancer is becoming more common, and survival rates are improving. Human papillomavirus–associated oropharyngeal cancer, in particular, is increasing in incidence and is associated with an excellent prognosis. However, toxicity from disease and treatment leads to long-term impairment, disability, and handicap. Currently, more than 60% of survivors have unmet needs. As the numbers of survivors increase, current models of care will be increasingly inadequate to meet their needs. Exploration of new strategies and models of care to better address quality-of-life issues and meet the needs of survivors of head and neck cancer is urgently required.
Who is your general practitioner?
Authors: J Shaw, J Holloway
Journal: BMJ (1991)

pain in the chest or tip of the shoulder should be examined and have chest radiography performed.If pneumothorax is confirmed the patient should be referred to a respiratory physician.Such patients tend not to have primary lung disease and so their case will be amenable to observation or simple aspiration of the pneumothorax, which can often be performed as an outpatient procedure, avoiding the trauma of chest drainage.When the pneumothoraces in our series were managed by general physicians chest drainage was used, which generally amounts to overtreatment in such cases.Clinicians should be aware that pneumothorax is an accepted but rare complication of fine needle aspiration of lumps in the breast.We thank the surgeons concerned for allowing us to report these cases.
Inhibition of nitric oxide synthase by nasal decongestants
Authors: G.J. Westerveld, H-P. Voss, R.M. van der Hee, G.J.N. de Haan-Koelewijn, G.J.M. den Hartog, R.a Scheeren, A Bast
Journal: European Respiratory Journal (2000)

The nasal decongestants oxymetazoline and xylometazoline are frequently used in the topical treatment of rhinitis and sinusitis. As nitric oxide (NO) is thought to play a role in inflammation of the upper respiratory tract, the aim of this study was to examine the in vitro effects of these compounds on the activity and the expression of NO producing enzymes, including the inducible form of NO synthase (iNOS) and the constitutive isoform of NO synthase (cNOS). Experiments concerning the effects of both compounds on enzymatic activity and enzyme induction of iNOS were performed in a lipopolysaccharide (LPS) induced rat alveolar macrophage cell line (NR8383) using the Griess assay and the 3H-citrulline assay respectively. The effects on cNOS were examined in fresh rat synaptosomes using the 3H-citrulline assay. The direct scavenging properties of both compounds were investigated using a amperometric NO sensor. Oxymetazoline and xylometazoline were shown to have a dose dependent inhibitory effect on total iNOS activity indicated by nitrite/nitrate formation in the Griess assay. This effect was found to be due to an inhibition of induction of the enzyme rather than inhibition of the enzyme activity, as was investigated in two separate experiments using the 3H-citrulline assay. Inhibition of cNOS was moderate and in the same order of magnitude as the inhibition of enzymatic iNOS activity. Direct scavenging of NO could not be detected. As constitutive nitric oxide synthase activity is thought to serve beneficial physiological functions, and exaggerated inducible nitric oxide synthase activity may cause exacerbation of the inflammatory process, pharmacological treatment influencing the nitric oxide generating system should focus on inhibition of inducible nitric oxide synthase alone. The specific characteristics of these decongestants in vitro suggests suitability for this application and may indicate an additional beneficial effect in the treatment of upper respiratory tract inflammation.
Biological and clinical changes in premanifest and early stage Huntington's disease in the TRACK-HD study: the 12-month longitudinal analysis
Authors: Sarah J Tabrizi, Rachael I Scahill, Alexandra Durr, Raymund AC Roos, Blair R Leavitt, Rebecca Jones, G Bernhard Landwehrmeyer, Nick C Fox, Hans Johnson, Stephen L Hicks, Christopher Kennard, David Craufurd, Chris Frost, Douglas R Langbehn, Ralf Reilmann, Julie C Stout
Journal: The Lancet Neurology (2010)
Metabolic similarities between fertilization and phagocytosis. Conservation of a peroxidatic mechanism.
Authors: S J Klebanoff, C A Foerder, E M Eddy, B M Shapiro
Journal: The Journal of Experimental Medicine (1979)

At the time of fertilization, sea urchin eggs release a peroxidase which, together with H2O2 generated by a respiratory burst, is responsible for hardening of the fertilization membrane. We demonstrate here that the ovoperoxidase of unfertilized eggs is located in cortical granules and, after fertilization, is concentrated in the fertilization membrane. Fertilization of sea urchin eggs or their parthenogenetic activation with the ionophor A23187 also results in (a) the conversion of iodide to a trichloroacetic acid-precipitable form (iodination), (b) the deiodination of eggs exogenously labeled with myeloperoxidase and H2O2, (c) the degradation of thyroxine as measured by the recovery of the released radioiodine at the origin and in the inorganic iodide spot on paper chromatography, and (d) the conversion of estradiol to an alcohol-precipitable form (estrogen binding). The iodination reaction and the binding of estradio occurs predominantly in the fertilization membrane where the ovoperoxidase is concentrated. From the estimation of the kinetics of incorporation of iodine, we determine that the peroxidative system is active for 30 min after fertilization, long after hardening of the fertilization membrane is complete. Most of the bound iodine is lost during the hatching process. Iodination of albumin is catalyzed by the material released from the egg during fertilization, when combined with H2O2 and iodide. Iodination, thyroxine degradation, and estradiol binding are inhibited by azide, cyanide, aminotriazole, methimazole, ascorbic acid and ergothioneine, all of which can inhibit peroxidase-catalyzed reactions. These responses of the sea urchin egg to fertilization are strikingly similar to the changes induced in polymorphonuclear leukocytes by phagocytosis and, in both instances, a peroxidative mechanism may be involved.