tbuckley/cabot-search huggingface dataset:
Is there agreement for optimal transbronchial sampling positions in lymph nodes
Authors: Kjetil Roth, Tomas Eagan, Jon Hardie
Journal: European Respiratory Journal (2014)

Background: Endobronchial ultrasound can visualize the position of the different lymph nodes and guide transbronchial needle aspiration (EBUS-TBNA). Knowledge of the lymph node positions is important for conventional TBNA and for teaching EBUS-TBNA.  Objective: To assess agreement for assumed optimal TBNA positions among physicians with EBUS-TBNA experience.  Methods: 46 experienced physicians who had performed more than 30 EBUS-TBNA were included in the study. 50% of these physicians had performed more than 500 EBUS-TBNA. The physicians marked the assumed optimal TBNA positions on standardized endobronchial pictures. The marked positions were digitalized and analyzed in Adobe Illustrator as pixels (px). The area of each marked position and the distance from an average x,y coordinate were calculated. Areas of agreement was drawn based on the visual impression of all drawings.  Results: There was good agreement of the optimal TBNA positions in stations 7 and 11R. The median distance from an average x,y position was 16.6px (0-52.0) for 7 from the right side and 15.9px (0-35.5) for 11R. It was possible to give a good description of station by the visual impression of the drawings in 7, 11R and 4R. Average 91% of each drawing in 4R was included in the area of agreement. The agreement was intermediate for 10L (27.1px (0-78.5), and 11L (23.5px (0-85.3)). There were low agreement for 4L (31.4px (0-55.3)), 10R (33,6px (0-85.1), 10L (0-78.5) and 12R.  Conclusion: There was good agreement for the optimal TBNA position in station 4R, 7, and 11R. The agreement for position 10, and 12 was low. Position 4R, 7, and 11R are optimal for conventional TBNA based on the agreement for these positions in this study.
Effect of oral terfenadine on the bronchoconstrictor response to inhaled histamine and adenosine 5'-monophosphate in non-atopic asthma.
Authors: G D Phillips, P Rafferty, R Beasley, S T Holgate
Journal: Thorax (1987)

Inhaled adenosine 5'-monophosphate (AMP) causes bronchoconstriction in atopic asthma, probably after in vivo conversion to adenosine. It has been suggested that adenosine potentiates preformed mediator release from mast cells on the mucosal surface of the airways by interacting with specific purinoceptors, without affecting the release of newly generated mediators. The airway response of nine non-atopic subjects with "intrinsic" asthma to inhaled AMP and the influence of the oral, selective H1 histamine receptor antagonist terfenadine on this response was investigated. The geometric mean provocation concentrations of histamine and AMP required to produce a 20% fall in FEV1 (PC20) were 1.82 and 13 mmol/l. In subsequent placebo controlled time course studies the FEV1 response to a single inhalation of the PC20 histamine was ablated after pretreatment with oral terfenadine 180 mg. This dose of terfenadine caused an 80% inhibition of the bronchoconstrictor response to the PC20 AMP when measured as the area under the time course-response curve and compared with the response to PC20 AMP preceded by placebo. Terfenadine 600 mg failed to increase protection against AMP further, but both doses of terfenadine delayed the time at which the mean maximum fall in FEV1 after AMP was achieved. Terfenadine 180 mg had no effect on methacholine induced bronchoconstriction in the same subjects. These data suggest that inhaled AMP may potentiate the release of preformed mediators from preactivated mast cells in the bronchial mucosa of patients with intrinsic asthma.
A mouse model for the delta F508 allele of cystic fibrosis.
Authors: B G Zeiher, E Eichwald, J Zabner, J J Smith, A P Puga, P B McCray, M R Capecchi, M J Welsh, K R Thomas
Journal: Journal of Clinical Investigation (1995)

The most common cause of cystic fibrosis is a mutation that deletes phenylalanine 508 in cystic fibrosis transmembrane conductance regulator (CFTR). The delta F508 protein is misprocessed and degraded rather than traveling to the apical membrane. We used a novel strategy to introduce the delta F508 mutation into the mouse CFTR gene. Affected epithelia from homozygous delta F508 mice lacked CFTR in the apical membrane and were Cl-impermeable. These abnormalities are the same as those observed in patients with delta F508 and suggest that these mice have the same cellular defect. 40% of homozygous delta F508 animals survived into adulthood and displayed several abnormalities found in human disease and in CFTR null mice. These animals should provide an excellent model to investigate pathogenesis and to examine therapies directed at correcting the delta F508 defect.
Targeted lung denervation for moderate to severe COPD: a pilot study
Authors: Dirk-Jan Slebos, Karin Klooster, Coenraad F N Koegelenberg, Johan Theron, Dorothy Styen, Arschang Valipour, Martin Mayse, Chris T Bolliger
Journal: Thorax (2015)

<h3>Background</h3> Parasympathetic pulmonary nerves release acetylcholine that induces smooth muscle constriction. Disruption of parasympathetic pulmonary nerves improves lung function and COPD symptoms. <h3>Aims</h3> To evaluate 'targeted lung denervation' (TLD), a novel bronchoscopic therapy based on ablation of parasympathetic pulmonary nerves surrounding the main bronchi, as a potential therapy for COPD. <h3>Methods</h3> This 1-year, prospective, multicentre study evaluated TLD in patients with COPD forced expiratory volume in 1 s (FEV<sub>1</sub>)/forced vital capacity (FVC) (FEV<sub>1</sub>/FVC &lt;0.70; FEV<sub>1</sub> 30%–60% predicted). Patients underwent staged TLD at 20 watts (W) or 15 W following baseline assessment off bronchodilators. Assessments were repeated on tiotropium before treatment and off bronchodilators at 30, 90, 180, 270 and 365 days after TLD. The primary endpoint was freedom from documented and sustained worsening of COPD directly attributable to TLD to 1 year. Secondary endpoints included technical feasibility, change in pulmonary function, exercise capacity, and quality of life. <h3>Results</h3> Twenty-two patients were included (n=12 at 20 W, n=10 at 15 W). The procedures were technically feasible 93% of the time. Primary safety endpoint was achieved in 95%. Asymptomatic bronchial wall effects were observed in 3 patients at 20 W. The clinical safety profiles were similar between the two energy doses. At 1 year, changes from baseline in the 20 W dose compared to the 15 W dose were: FEV<sub>1</sub> (+11.6%±32.3 vs +0.02%±15.1, p=0.324), submaximal cycle endurance (+6.8 min±12.8 vs 2.6 min±8.7, p=0.277), and St George9s Respiratory Questionnaire (−11.1 points ±9.1 vs −0.9 points ±8.6, p=0.044). <h3>Conclusions</h3> Bronchoscopic TLD, based on the concept of ablating parasympathetic pulmonary nerves, was feasible, safe, and well tolerated. Further investigation of this novel therapy is warranted. <h3>Trial registration number</h3> NCT01483534.
Parents for children.
Authors: A M Jepson
Journal: BMJ (1981)

Parents for Children is a specialist adoption agency set up to find homes for children with special needs--that is, those with physical, mental, and emotional handicaps; older children; and sibling groups. Of the first 38 children placed, one child died and six placements broke down, although four children were later re-placed. Almost all the children referred to the agency had been in care for most of their lives. A full assessment of each child is necessary before placement, but in several cases the medical assessment in care had been inadequate. Many of the prospective parents themselves had serious medical conditions. The agency has proved that homes can be found for children in need, but there have been problems and parents require advice and support in the management of the children after placement.
Studies on the anti‐allergic action of N‐(3′,4′dimethoxycinnamoyl) anthranilic acid (N‐5′)
Authors: R. Hamel, A. W. Ford‐Hutchinson, H. Piechuta
Journal: Allergy (1987)

The effects of the anti‐allergic compound N‐(3′,4′‐dimethoxycinnamoyl) anthranilic acid (N‐5′ or Tranilast) have been investigated upon antigen‐induced contractions of respiratory smooth muscle in vitro and bronchoconstriction in vivo. N‐5′ (3.1 × 10 −5 M) in vitro had no significant effect upon antigen‐induced contractions of the guinea pig trachea. However, when tested at concentrations of 9.2 and 3.1 × 10 −5 M, but not 0.9 × 10 −5 , N‐5′ significantly inhibited antigen‐induced contractions of the human parenchyma. In vivo N‐5′ (5 and 10 mg/kg p.o.) failed to inhibit antigen‐induced dyspnea in hyperreactive rats, N‐5′ (20 mg/kg p.o.) also failed to inhibit the immediate bronchoconstriction following ascaris challenge of conscious squirrel monkeys but significantly attenuated the reduction in dynamic compliance during the pulmonary late phase response observed between 4 and 10 h after antigen challenge. It is suggested that N‐5′ does not act as a “cromoglycate‐like” compound but may have novel mechanisms of action in human bronchial asthma.
The History of Witchcraft: A Review with Some Psychiatric Comments
Authors: ROBERT D. ANDERSON
Journal: American Journal of Psychiatry (1970)

Witchcraft, held to be an anti-Christian heresy with evil supernatural powers, is distinguished from common superstition and reviewed. The author suggests individual and group psychodynamics to explain the delusion, its inclusion of perverse sexuality, and its treatment by sadistic aggression. Opponents of the delusion are mentioned, and the role of mental illness among both the persecutors and the persecuted is defined.
INSIGHTS FROM IN VIVO MODIFICATION OF ADRENERGIC RECEPTOR GENE EXPRESSION
Authors: Daniel K. Rohrer, Brian K. Kobilka
Journal: The Annual Review of Pharmacology and Toxicology (1998)

▪ Abstract Adrenergic receptors are key targets within the autonomic nervous system, regulating a wide variety of physiological processes. The ability to modify adrenergic receptor expression patterns in vivo has added a powerful new tool to the functional analysis of these receptors. Modification of adrenergic receptor gene expression by overexpression, genetic ablation, or site-specific mutation has added new insight to models of receptor coupling behavior, pharmacology, and subtype-specific physiological function. This review highlights some of the recent advances resulting from such genetic approaches to the study of adrenergic receptors.
An epidemic of furniture-related dermatitis: searching for a cause
Authors: K. Lammintausta, E. Zimerson, T. Hasan, P. Susitaival, S. Winhoven, B. Gruvberger, M. Beck, J.D. Williams, M. Bruze
Journal: British Journal of Dermatology (2009)

Background Sitting in new chairs or sofas has elicited dermatitis in numerous patients in Finland and in the U.K. since autumn 2006. The cause of the dermatitis seemed to be an allergen in the furniture materials. Objectives To determine the cause of the dermatitis in patients with furniture-related dermatitis. Methods Altogether 42 patients with furniture-related dermatitis were studied. First, 14 Finnish patients were patch tested with the standardized series and with the chair textile material. A thin-layer chromatogram (TLC) strip and an extract made from the same textile material were tested in seven Finnish patients. The test positive spot of the TLC and the content of a sachet found inside a sofa in the U.K. were analysed by using gas chromatography-mass spectrometry. All chemicals analysed were patch tested in 37 patients. Results A positive patch test reaction to the chair textile and to its extract was seen in all patients tested, one-third of whom had concurrent reactions to acrylates. Positive reactions to the same spot of the TLC strip were seen in five of seven patients and dimethyl fumarate was analysed from the spot as well as from the sachet contents. Dimethyl fumarate (0.01%) elicited positive reactions in all the patients. The other chemicals analysed did not elicit positive reactions, but one patient in the U.K. had a positive reaction to tributyl phosphate. Conclusions Sensitization to dimethyl fumarate was seen in all the patients with furniture-related dermatitis. Concurrent sensitization or cross-reactions were common among the sensitized patients.
IgG, IgA and IgE autoantibodies against the ectodomain of desmoglein 3 in active pemphigus vulgaris
Authors: S. Spaeth, R. Riechers, L. Borradori, D. Zillikens, L. Budinger, M. Hertl
Journal: British Journal of Dermatology (2001)

Background IgG autoantibodies against desmoglein (Dsg) 3 play a key part in the pathogenesis of pemphigus vulgaris (PV), the most severe autoimmune bullous disorder. Objectives To determine whether immunoglobulin isotypes other than IgG are detectable in the sera of patients with PV and whether a particular immunoglobulin subtype is associated with a distinct clinical phenotype of PV. Methods Sera from 41 patients with acute-onset, chronic active, and remittent PV disease with mucosal and cutaneous lesions were assayed against a baculovirus-expressed Dsg3 protein by immunoblot analysis. Results In acute-onset PV, Dsg3-reactive IgG1 was detected in nine of 15 (60%), IgG4 in 14 of 15 (93%), IgA in nine of 15 (60%) and IgE in two of 15 (13%) sera. In chronic active PV, Dsg3-reactive IgG1 was detected in 11 of 18 (61%), IgG4 in 16 of 18 (89%), IgA in 13 of 18 (72%) and IgE in two of 18 (11%) sera. In contrast, sera from patients with remittent PV disease contained only Dsg3-reactive IgG1 in six of eight (75%) and IgG4 in four of eight (50%) cases, but not Dsg3-reactive IgA or IgE. Conclusions In extension of previous findings, our study demonstrates that, in addition to IgG autoantibodies, IgA and occasionally IgE autoantibodies reactive with Dsg3 are present in acute and chronic active PV. The detection of Dsg3-reactive autoantibodies of the IgG4, IgA and IgE subclasses in active PV provides additional evidence that PV is a T-helper 2-regulated autoimmune disorder.
Quantitation and characterization of plasma DNA in normals and patients with systemic lupus erythematosus.
Authors: L Raptis, H A Menard
Journal: Journal of Clinical Investigation (1980)

Using the in vitro DNA labeling technique of nick translation on purified plasma DNA, we have estimated the plasma DNA concentration in three normal individuals to be 266 +/- 57 ng/ml (mean +/- SD). This was not significantly different in three patients with a chronic inflammatory disease (209 +/- 14 ng/ml) or in five patients with steroid-inactivated systemic lupus erythematosus (SLE) (293 +/- 57 ng/ml). In two untreated, newly diagnosed, active SLE patients, however, the plasma DNA concentration was considerably higher (4,024 and 2,437 ng/ml, respectively). Characterization of these in vitro labeled DNA preparations by neutral sucrose-gradient sedimentation analysis showed a sedimentation coefficient of 6-8S, corresponding to a molecular weight of similar to or approximately 0.2-0.45 x 10(6). No difference was observed between normal subjects or patients. In addition, the relative size uniformity of these DNA molecules might suggest some form of specific protection of the DNA from blood DNAases. Further characterization in terms of buoyant density in cesium chloride did not reveal a difference between normal or SLE plasma and the human (HEp-2 cell) DNA used as marker. Taking into account the limitations of the method, no indication of a possible exogenous origin of the DNA circulating in SLE patients could be found. The physiological or pathophysiological role of this plasma DNA remains to be determined.
rNAPc2 Inhibits Colorectal Cancer in Mice through Tissue Factor
Authors: Jingsong Zhao, Gerard Aguilar, Servando Palencia, Elizabeth Newton, Arie Abo
Journal: Clinical Cancer Research (2008)

Recombinant nematode anticoagulant protein c2 (rNAPc2) is a specific inhibitor of tissue factor (TF)/factor VIIa complex with novel antithrombotic activity. TF is highly expressed in human colorectal tumors, and levels are positively correlated with disease progression.To explore the therapeutic potential and mechanism of action of rNAPc2 during tumor growth and metastasis, we tested rNAPc2 in several experimental colorectal cancer models in mice.Administration of rNAPc2 inhibited pulmonary metastasis in mice systemically disseminated with CT26 murine colon carcinoma cells in a dose-dependent fashion. Combining rNAPc2 with the cytotoxic agent 5-fluorouracil or bevacizumab (humanized anti-vascular endothelial growth factor monoclonal antibody) resulted in additive growth inhibition and simultaneous reduction of microvessel density in HCT116 human colorectal tumor xenografts in nude mice. Furthermore, rNAPc2 potentiated CPT-11 in inhibiting hepatic metastasis in nude mice with portal vein injection of HCT116 tumor cells. Long-term administration of rNAPc2 significantly suppressed spontaneous formation of intestinal tumors in Apc(Min/+) mice. Using a RNA interference approach, we showed that TF expression is necessary for rNAPc2-mediated inhibition of HCT116 human colorectal tumor xenograft growth in nude mice, indicating that the antitumor effect of rNAPc2 may be transduced through TF that is expressed on tumor cells.rNAPc2 is a potent anticancer agent when used in combination with chemotherapy or antiangiogenic therapy in mouse models of colorectal cancer, and TF positivity appears to be required for its activity.
Recombinant Annexin II Modulates Impaired Fibrinolytic Activity In Vitro and in Rat Carotid Artery
Authors: Hideto Ishii, Masayuki Yoshida, Megumi Hiraoka, Katherine A. Hajjar, Akira Tanaka, Yukio Yasukochi, Fujio Numano
Journal: Circulation Research (2001)

Fibrinolytic activity has been reported to be decreased in atherosclerosis. Recently, annexin II was identified as a coreceptor on endothelial cells for plasminogen and tissue plasminogen activator. In this study, we examined whether recombinant annexin II (rAN II) protein can modulate fibrinolytic activity on vascular endothelium in vitro and in vivo. The effect of rAN II on human umbilical vein endothelial cells (HUVECs) was measured. Addition of a fluorescent plasmin substrate revealed that HUVECs treated with rAN II exhibited significantly more plasmin generation than those treated with BSA. Moreover, rAN II treatment of HUVECs restored plasmin generation impaired by plasminogen activator inhibitor-1 or homocysteine pretreatment. In a rat carotid artery thrombus model, the patency of thrombosed carotid arteries was significantly enhanced by rAN II injection, in contrast to BSA injection, without systemic blood coagulation dysregulation. We found that rAN II enhanced plasmin generation on vascular endothelium in vitro and reduced thrombus formation in vivo, and concluded that enhancement of endothelial fibrinolytic activity by annexin II could modulate the hypercoagulable state of atherosclerosis. Further study of rAN II in vitro and in vivo may lead to the establishment of novel therapeutic approaches to thrombogenic vascular disease.
Screening for coronary artery disease after mediastinal irradiation in Hodgkin lymphoma survivors: phase II study of indication and acceptance
Authors: L.A. Daniëls, A.D.G. Krol, M.A. de Graaf, A.J.H.A. Scholte, M.B. van't Veer, H. Putter, A. de Roos, M.J. Schalij, C.L. Creutzberg
Journal: Annals of Oncology (2014)
Slaying the CVD dragon with steroids
Authors: D.D. Sin, S.F. Van Eeden, S.F.P. Man
Journal: European Respiratory Journal (2010)

<h3>Background</h3> The Pharmacy and Therapeutics Committee approved in May 2017 a protocol for the prescription of intravenous iron in order to achieve the correct use of it in the hospital, and the establishment of an iron sucrose complex as first choice in admitted patients. <h3>Purpose</h3> The objective of this study was to assess the degree of adaptation of the prescriptions to the protocol. <h3>Material and methods</h3> We conducted a retrospective observational study from May 2017 to July 2018. In order to assess the degree of adaptation of the prescriptions it was checked if the requests were received correctly completed for type of patient (inpatient or outpatient), medical service, diagnosis and cause and patient’s bodyweight, and if there were iron metabolism data (transferrin saturation, serum ferritin and iron) previous to the request.We also recorded the pharmaceutical product prescribed (ferric carboxymaltose or sucrose). Likewise, we reviewed if administered doses were correct, taking into account the theoretical deficiency calculated according to the Ganzoni formula. Dosage was considered correct if the difference between the administered dose and the theoretical deficiency did not exceed ±500 mg in ferric carboxymaltose and ±200 mg in sucrose. <h3>Results</h3> A total of 271 prescriptions were analysed (outpatients 51.3%). The internal medicine department was the main service prescriber (47.2%), followed by the gastroenterology department (21.8%). The principal medical diagnosis was anaemia. The cause was unknown in 35.5% of patients. Concerning the three main reasons for prescription, in descending order they were: need for fast iron replenishment (56.5%), inefficiency or intestinal malabsorption syndromes (14.7%) and intolerance to oral iron or impossibility to an oral regimen (11.4%) The reasons were unknown in 4.1%. Data of iron metabolism was not available in 34.7% of requests. Ferric carboxymaltose was the pharmaceutical product chosen in most of the patients (54.6%), of which 62% were outpatients. The total dose administered did not match the theoretical deficiency calculated in 41.3% of cases. <h3>Conclusion</h3> The lack of data in many orders received in the pharmacy department makes it difficult to verify the appropriateness of the prescription to the protocol in many cases. This highlights that protocolisation is a dynamic process which requires a continuous assessment to ensure its utility. Ferric carboxymaltose was used more frequently in iron replenishment in outpatients and iron sucrose in hospitalised patients. <h3>References and/or acknowledgements</h3> No conflict of interest.
Increased Activity of Activator Protein-1 Transcription Factor Components ATF2, c-Jun, and c-Fos in Human and Mouse Autosomal Dominant Polycystic Kidney Disease
Authors: Ngoc Hang Le, Annemieke van der Wal, Paola van der Bent, Irma S. Lantinga-van Leeuwen, Martijn H. Breuning, Hans van Dam, Emile de Heer, Dorien J.M. Peters
Journal: Journal of the American Society of Nephrology (2005)

Autosomal dominant polycystic kidney disease is a common inherited disorder that predominantly manifests with the formation of fluid-filled cysts in both kidneys. The disease can be accounted for by a mutation in either the PKD1 or the PKD2 gene. It was demonstrated previously that aberrant expression of the PKD1 gene product, polycystin-1, results in modification of activator protein-1 (AP-1) transcription factor activity in cultured renal epithelial cells. Here, it is reported that activity of the AP-1 components c-Jun, ATF2, and c-Fos is altered in renal cystic tissue of patients with autosomal dominant polycystic kidney disease and of hypomorphic Pkd1 mice with polycystic kidney disease. Data were obtained using immunohistochemical and Western blot analysis. Significant upregulation of Thr71- and Thr69/71-phosphorylated ATF2 and Ser73-phosphorylated c-Jun and increased c-Fos were detected in small cysts and (dilated) ducts and tubules surrounded by fibrotic interstitium. The data indicate that various AP-1 components are constitutively activated in polycystic kidney disease and suggest that aberrant AP-1 activity is relevant for cyst formation.