tbuckley/cabot-search huggingface dataset:
Lung function in bronchiectasis: the influence of Pseudomonas aeruginosa
Authors: SA Evans, SM Turner, BJ Bosch, CC Hardy, MA Woodhead
Journal: European Respiratory Journal (1996)

Sputum isolation of Pseudomonas aeruginosa (PA) is associated with extensive disease in bronchiectasis. It is not known, however, whether infection with P. aeruginosa is the result or the cause of severe disease. We compared spirometry in patients with bronchiectasis before and after infection with P. aeruginosa, with that of patients infected by other organisms. All patients (n=12) with chronic colonization by P. aeruginosa (PA group) were studied. These were compared with other patients with bronchiectasis with no isolations of P. aeruginosa (n=37, non-PA group). In the PA group, forced expiratory volume in one second (FEV1) and forced vital capacity (FVC) were lower than in the non-PA group. The PA group, however, also had lower values at the time of initial colonization with P. aeruginosa than the current values for the non-PA group. Change in FEV1 and FVC over time was faster in the PA group than in the non-PA group. Reduction of FEV1 and FVC over time in the PA group prior to P. aeruginosa colonization was intermediate, not being statistically different from either value above. Our results confirm the association of chronic P. aeruginosa colonization with poor lung function, but conclude that patients with bronchiectasis who become colonized by P. aeruginosa have poorer lung function when first colonized than those colonized by other organisms. Decline in lung function is faster in those chronically colonized by P. aeruginosa than in those colonized by other organisms. It is not clear whether chronic P. aeruginosa colonization causes an accelerated decline in lung function or whether it is simply a marker of those whose lung function is already declining rapidly.
Neurogenic sympathetic vasoconstriction of the rabbit basilar artery.
Authors: T J Lee, C Su, J A Bevan
Journal: Circulation Research (1976)

When examined by fluorescence microscopy the rabbit basilar artery contains a rich adrenergic-like plexus at the adventitiomedial junction. The fluorescence disappears upon chronic reserpinization and bilateral superior cervical ganglionectomy. Transmural stimulation of intramural nerves a results in a response which is predominantly constrictor but also contains a small, inconstant dilator component. The constrictor response is abolished by chronic reserpinization, bilateral superior cervical ganglionectomy, and cold storage of the preparation. The constriction is prevented by the adrenergic neuron blocking agents guanethidine and bretylium but not by such alpha-adrenergic receptor blocking agents as phenoxybenzamine (PBZ), phentolamine, and tolazoline. Our results show that doses of the three latter agents sufficient to abolish contractions to norepinephrine (NE) in concentrations of up to 10(-2) M only potentiate and prolong the contractile response to nerve stimulation. The beta-adrenergic receptor blocking agent, propranolol, and inhibitors of NE neuronal uptake, such as desipramine (desmethylimipramine, DMI) and cocaine, do not influence the size of the neurogenic response. These results suggest that the vasoconstrictor component of the rabbit basilar artery response to transmural nerve stimulation (TNS) is mediated via sympathetic adrenergic-like neurons, but at the same time also raise the question whether the transmission process is typical of classic adrenergic neuroeffector mechanisms.
Agitation Associated with Acute Bladder Obstruction
Authors: Gabriele Carmine De Luca, Eelco F M Wijdicks
Journal: New England Journal of Medicine (2010)

A 61-year-old man with mild cognitive impairment and a seizure disorder from traumatic brain injury sustained 3 years earlier presented to the emergency department while having a cluster of complex partial seizures. He had been receiving levetiracetam monotherapy as an outpatient. In the emergency department, he was treated with intravenous fosphenytoin and transferred to our institution. He subsequently became agitated and combative, requiring mechanical restraints. Physical examination revealed abdominal distention. Serum levels of amylase and creatinine were elevated. A computed tomographic scan of his abdomen and pelvis revealed marked bladder enlargement (Panel A) and entrapment of a Foley catheter that . . .
The development of a preference-based measure of health in children with atopic dermatitis
Authors: K.J. Stevens, J.E. Brazier, S.P. McKenna, L.C. Doward, M.J. Cork
Journal: British Journal of Dermatology (2005)

Outcomes of health care interventions can be measured in many different ways, but there has been growing interest in the role that quality-adjusted life-years (QALYs) can play in informing priorities in health care. While existing generic preference-based measures can be used to obtain QALYs, these measures may often be inappropriate for some conditions such as atopic dermatitis (AD). These measures are also usually developed for adults and may not capture the domains pertinent to children.To develop a preference-based quality-of-life measure for use in children with AD.Items generated from interviews conducted with parents of children with AD were used to form a health state classification system that gives 16 unique health states. One hundred and fifty members of the general population were interviewed to derive preference weights for these states, following the methods used in the valuation of the Health Utilities Index 2 (HUI 2). Each person valued 10 health states using the standard gamble technique. The primary analysis was the estimation of mean health state values for each of the 16 states.Mean values across the 16 health states range from 0.36 (SD = 0.36) for the worst state to 0.84 (SD = 0.19) on a scale from zero to one, where zero is for health states thought to be as bad as being dead and one is for perfect health. There was some support for the validity of the values from the fact that the values were logically consistent with the ordering of the health state classification system.These results show the perceived importance of the defined health states of childhood AD to the general population. The resultant health state classification and values can be used to calculate QALYs for use in assessing the cost-effectiveness of interventions for children with AD.
Investigation of rheumatoid arthritis susceptibility loci in juvenile idiopathic arthritis confirms high degree of overlap
Authors: Anne Hinks, Joanna Cobb, Marc Sudman, Stephen Eyre, Paul Martin, Edward Flynn, Jonathon Packham, Anne Barton, Jane Worthington, Carl D Langefeld, David N Glass, Susan D Thompson, Wendy Thomson
Journal: Annals of the Rheumatic Diseases (2012)

Rheumatoid arthritis (RA) shares some similar clinical and pathological features with juvenile idiopathic arthritis (JIA); indeed, the strategy of investigating whether RA susceptibility loci also confer susceptibility to JIA has already proved highly successful in identifying novel JIA loci. A plethora of newly validated RA loci has been reported in the past year. Therefore, the aim of this study was to investigate these single nucleotide polymorphisms (SNP) to determine if they were also associated with JIA.Thirty-four SNP that showed validated association with RA and had not been investigated previously in the UK JIA cohort were genotyped in JIA cases (n=1242), healthy controls (n=4281), and data were extracted for approximately 5380 UK Caucasian controls from the Wellcome Trust Case-Control Consortium 2. Genotype and allele frequencies were compared between cases with JIA and controls using PLINK. A replication cohort of 813 JIA cases and 3058 controls from the USA was available for validation of any significant findings.Thirteen SNP showed significant association (p<0.05) with JIA and for all but one the direction of association was the same as in RA. Of the eight loci that were tested, three showed significant association in the US cohort.A novel JIA susceptibility locus was identified, CD247, which represents another JIA susceptibility gene whose protein product is important in T-cell activation and signalling. The authors have also confirmed association of the PTPN2 and IL2RA genes with JIA, both reaching genome-wide significance in the combined analysis.
Autoimmunity and pulmonary hypertension: a perspective
Authors: M. R. Nicolls, L. Taraseviciene-Stewart, P. R. Rai, D. B. Badesch, N. F. Voelkel
Journal: European Respiratory Journal (2005)

The association between autoimmunity and pulmonary arterial hypertension (PAH) has been appreciated for &gt;40 yrs, but how autoimmune injury might contribute to the pathogenesis of this disease has only been examined in a case-specific manner. It is becoming increasingly clear that a variety of diverse clinical diseases, ranging from viral infections to connective tissue disorders, can culminate in pulmonary vascular pathology that is indistinguishable. Is there a hitherto unappreciated biology that unites these seemingly unrelated conditions? The answer to this question may come from the increasing body of evidence concerned with the central importance of regulatory T-cells in preventing inappropriate B-cell activity. Two striking similarities between conditions associated with severe angioproliferative pulmonary hypertension are a defect in the CD4 T-cell compartment and auto-antibody production. Pathogenic auto-antibodies targeting endothelial cells are capable of inducing vascular endothelial apoptosis and may initiate the development of PAH. The present review will focus on what is known about autoimmune phenomena in pulmonary arterial hypertension patients, in order to better consider whether an early loss of self-tolerance followed by autoimmune injury could influence the early development of severe angioproliferative pulmonary hypertension.
Should Selection of Adjuvant Chemotherapy for Patients With Breast Cancer Be Based on erbB-2 Status?
Authors: Gary M. Clark
Journal: JNCI Journal of the National Cancer Institute (1998)

It has been more than 10 years since the initial report of an association between amplification of erbB-2 (also known as HER-2/neu and ERBB2) and poor clinical outcome of patients with primary breast cancer (1). Dozens of papers involving thousands of patients have now been published on this topic, and the general conclusion is that erbB-2 abnormalities, either gene amplification or protein overexpression, are associated with worse prognosis of patients with lymph node-positive breast cancer, but the relationship for patients with lymph node-negative disease is weak, at best. Since most of these correlative studies were retrospective and many of the patients were treated before adjuvant therapy was widely administered to patients with lymph node-negative disease, several clinical researchers speculated that these associations were due, in part, to specific adjuvant therapies received by lymph node-positive patients. The first studies that examined the potential role of erbB-2 status for predicting response to adjuvant chemotherapy concentrated on regimens that contained CMF (cyclophosphamide, methotrexate, and 5-fluorouracil) (2,3). The general trend reported in these and subsequent studies is that patients whose tumors have little or no detectable levels of erbB-2 derive considerable benefit from CMF regimens, but patients whose tumors have amplified erbB-2 genes or overexpress erbB-2 protein do not benefit from these therapies. However, it must be stressed that these conclusions are based on retrospective analyses, and they have not been validated in prospective studies with sufficient statistical power to detect interactions between treatment and erbB-2 status. In 1994, Muss et al. (4) published, to our knowledge, the first analysis of an interaction between expression of erbB-2 and adjuvant therapy with doxorubicin-containing regimens. The finding that tumors with high expression of erbB-2 responded better to dose-intensive treatment with CAF (cyclophosphamide, doxorubicin [Adriamycin], and 5-fluorouracil) was contrary to the previous results with the CMF regimens and spurred international efforts to validate or refute the published data and to understand the biologic mechanisms that might explain such results. But such validation studies are difficult to perform, and analyses of interactions between treatments and potential predictive factors can be accomplished only within a randomized clinical trial. Without the protection of randomization, selection biases will result in confounding effects between treatments administered and potential predictive factors that cannot be overcome with the most sophisticated multivariate statistical analyses.
Inhibition of coronary artery superoxide dismutase attenuates endothelium-dependent and -independent nitrovasodilator relaxation.
Authors: H A Omar, P D Cherry, M P Mortelliti, T Burke-Wolin, M S Wolin
Journal: Circulation Research (1991)

Isolated bovine coronary arteries were treated with 10 mM diethyldithiocarbamate (DETCA) for 30 minutes to deplete the cytosolic ZnCu form of superoxide dismutase (SOD). This treatment completely inhibited the endothelium- and cGMP-dependent relaxation to acetylcholine (mediated via the endothelium-derived relaxing factor, which is thought to be nitric oxide) without significantly inhibiting endothelium-dependent relaxation to arachidonic acid (mediated by prostaglandins). DETCA treatment of endothelial cells cultured from the coronary arteries inhibited bradykinin-elicited release of endothelium-derived relaxing factor, which was detected by bioassay on an isolated rabbit aorta in the presence of extracellular SOD. DETCA also inhibited cGMP-associated relaxations to nitric oxide and to vasodilators thought to function via the generation of this mediator (nitroglycerin and nitroprusside), but cAMP-associated relaxations to isoproterenol and papaverine were not altered. The inhibitory effects of DETCA against the relaxation to nitroprusside and nitroglycerin were attenuated by severe hypoxia. DETCA treatment of isolated coronary arterial smooth muscle or cultured endothelial cells produced an increase of chemiluminescence elicited in the presence of lucigenin, a detector of superoxide anion generation. The addition of SOD markedly attenuated the effects of DETCA treatment on arterial relaxation and chemiluminescence. Therefore, control of cellular superoxide anion levels by endogenous SOD appears needed for the release of endothelium-derived relaxing factor and relaxation of vascular smooth muscle to nitrovasodilators mediated via cGMP in the bovine coronary artery, but SOD is not critical for other endothelium-dependent or cAMP-associated relaxant mechanisms.
Pleural procedures and patient safety: a national BTS audit of practice: Table 1
Authors: Clare E Hooper, Sally A Welham, Nick A Maskell
Journal: Thorax (2014)

The BTS pleural procedures audit collected data over a 2-month period in June and July 2011. In contrast with the 2010 audit, which focussed simply on chest drain insertions, data on all pleural aspirations and local anaesthetic thoracoscopy (LAT) was also collected. Ninety hospitals submitted data, covering a patient population of 33 million. Twenty-one per cent of centres ran a specialist pleural disease clinic, 71% had a nominated chest drain safety lead, and 20% had thoracic surgery on site. Additionally, one-third of centres had a physician-led LAT service.
Cancer Patients Seeking a Second Surgical Opinion: Results of a Study on Motives, Needs, and Expectations
Authors: W.A.M. Mellink, A.M.V. Dulmen, Th. Wiggers, P.M.M. Spreeuwenberg, A.M.M. Eggermont, J.M. Bensing
Journal: Journal of Clinical Oncology (2003)

To explore the sociodemographic and clinical characteristics of cancer patients seeking a second-opinion consultation and to analyze their second opinion-related motives, needs, and expectations.In 212 consecutive patients seeking a second opinion at the Surgical Oncology Outpatient Clinic, satisfaction with the first specialist, motivation for the second opinion, need for information, preference for decision participation, and hope for and expectation of a different second opinion were assessed with a questionnaire.The mean age was 53 years. Most patients were women (82%), of whom 76% were diagnosed with breast cancer. Half of the patients (51%) had a low educational level. The majority of patients (62%) only had internal motives for second-opinion seeking associated with the need for reassurance and more certainty, whereas a substantial minority of patients (38%) also had external motives related to negative experiences or unfulfilled needs. The externally motivated patients had a higher anxiety disposition, were less satisfied with their first specialist, preferred a more active role in medical decision making, and more often hoped for and expected a different second opinion.Motives for second-opinion consultations differ greatly. Understanding the difference between internal and external motivation is necessary to develop strategies to prevent unnecessary second-opinion seeking. Additional studies are warranted to evaluate the objective and subjective outcomes of second-opinion consultations.
Serotonin and embolization by small blood clots in dogs.
Authors: R Marshall
Journal: Thorax (1966)

Serotonin is one of the few substances which has a strong vasoconstrictor action on the pulmonary circulation ; it can also cause bronchoconstriction.Serotonin in the blood is contained almost en- tirely in the platelets, but this is released during the process of clot formation.Several investigators (Comroe, van Lingen, Stroud, and Roncoroni, 1953; Smith and Smith, 1955; Cobb and Nanson, 1960) have suggested that serotonin may be re- sponsible for many of the effects of embolization of the lungs by blood clot or thrombus.The present experiments were carried out to investigate further the role of serotonin in the effect of small blood clot emboli on anaesthetized dogs.Normal blood clots and serotonin-depleted clots have been injected into normal dogs, and autogenous blood clots have been injected into serotonin-depleted dogs. METHODSMongrel dogs of 10-8 to 15 0 kg.were used in the experiments.Morphine, 1 mg./kg., was used as a premedication before anaesthesia in dogs I and 2. but this was omitted from later experiments since morphine may liberate histamine from the tissues (Nasmyth and Stewart, 1950). SEROTONIN-DEPLETION OF INJECTED BLOOD CLOTSThe serotonin stores of the body can be depleted by treat- ment of the animal with reserpine (Haverback, Dutcher, Shore, Tomich, Terry, and Brodie, 1957: Shore, Pletscher, Tomich, Carlsson Kuntzman, and Brodie, 1957).Blood with a low serotonin content was obtained by giving a dog a single dose of 20 mg.reserpine approximately 16 hours before the start of the main experiment.Before giving the reserpine blood samples were taken for estimation of initial serotonin levels.SEROTONIN DEPLETION OF RECIPIENT DOGS To three INJECTION OF BLOOD CLOT INTO NORMAL DOGS Bloodwas taken from the femoral vein of the normal (recipient) dog and the reserpine-treated dog.From each dog 20 ml. of blood was put into each of three tubes and allowed to clot.Blood samples were also taken for serotonin assay.The normal dog was connected to a closed-circuit spirometer system, using a cuffed endotracheal tube.An oesophageal balloon was used to record intra- thoracic pressure changes.The intra-oesophageal pressure and the tidal volume trace from the spiro- meter were recorded from a double-beam oscillo-266 on August 18, 2023 by guest.
Tennis ranking related to exercise capacity: Figure 1
Authors: W Banzer, C Thiel, A Rosenhagen, L Vogt
Journal: British Journal of Sports Medicine (2008)

The physical demands upon players in professional tennis have been increasing over the past few years. Currently, average intensities range between 60% and 70% of maximum oxygen uptake.1 Tennis can be classified as a mainly anaerobic activity with emphasis on glycolysis and glycogenolysis.2 However, taking into consideration incomplete physiological regeneration between points, as well as between matches and tournaments, a high cardiorespiratory capacity may help to avoid fatigue3 and aid in recovery, thus promoting continuous success in professional tennis.1 4 The relative importance of aerobic capacity may depend on an individual athlete’s preferred strategy, as the proportion of playing time versus total match time varies with playing style.5 Average point duration may reach more than 15 seconds when baseline players are in control of a rally, as opposed to <5 seconds when attacking players are in control.6

Professional players have a cardiorespiratory capacity of 55–65 mL/min/kg.5–7 Players attend up to 40 tournaments/year, during which athletic training sessions are necessarily reduced in volume and intensity. Thus, the preparation period at the end of the year offers the best, if not the only chance to systematically develop athletic capabilities.8 Improving the aerobic capacity in this period may have a strong bearing on tennis performance. This study aimed to examine the relationship between VO2max during preparation and the following year’s entry ranking, focusing on a single top athlete, to explore the research potential for future systematic evaluation.

The athlete (180 cm, 74 kg) has competed at Association of Tennis Professionals (ATP) tour level since 1994. He prefers to play most points from …
Modulation of Elastase Binding to Elastin by Human Alveolar Macrophage–derived Lipids
Authors: JIRO FUJITA, C. MAGNUS SKÖLD, DAVID M. DAUGHTON, RONALD F. ERTL, JIRO TAKAHARA, STEPHEN I. RENNARD
Journal: American Journal of Respiratory and Critical Care Medicine (1999)

Human neutrophil elastase (HNE), an enzyme secreted by activated neutrophils, can bind to and degrade extracellular matrix including human lung elastin. This protease is believed to play an important role in several destructive processes including pulmonary emphysema. In this study, we hypothesized that an alveolar macrophage (AM) product or products may interact with neutrophil elastase (NE) and modulate its binding to elastin. Elastase binding to elastase was evaluated by a modified elastase functional assay using a synthetic substrate. Supernatants from cultured AM inhibited elastase binding to elastin at a dose-dependent manner without inhibiting functional elastase activity. The AM products had a heterogeneous molecular weight ranging from 440,000 to 54,000. The activity was heat-stable, but was lost after ultracentrifugation. After lipid fractionation, neither the aqueous nor the lipid fractions contained activity, suggesting that the factor may be a lipid complex. Culture supernatants from smokers' AM released significantly higher amounts of the factor than nonsmokers. In addition, high-molecular-weight elastase was present in bronchoalveolar lavage fluid (BALF) obtained from patients with pneumonia. Most of the in vivo high-molecular-weight elastase was lost after lipid extraction. In conclusion, macrophages release a factor or factors, probably lipid, which can interact with NE and inhibit its binding to human lung elastin without inhibiting elastase activity. This macrophage-derived factor may play a role in protecting the lung from NE by partitioning elastase into the airspace and thus protecting the interstitial connective tissue matrix from elastase degradation.