tbuckley/cabot-search huggingface dataset:
Peptic activity after the administration of Pentagastrin and in gastroduodenal disease.
Authors: M H Pritchard, A M Connell
Journal: Gut (1969)

The existence of more than one gastric pepsin has been reported by many authors. Herriott, Desreux, and Northrop (1940) separated two proteolytic fractions from human gastric juice by salt-fractionation methods, and similar results were described by Baker (1951) and Taylor (1959b). Using moving boundary electrophoresis, Kushner, Rapp, and Burtin (1964), Merten, Schramm, Grassmann, and Hannig (1952), and Taylor (1959a) have all identified two or more different proteolytic components in both swine and human gastric juice. Ryle and Porter (1959), Tang, Wolf, Caputto, and Trucco (1959) and Seijffers, Segal, and Miller (1963), using ion-exchange chromatography, have also isolated at least two different proteases in human gastric secretion. The two proteases most commonly isolated both digested proteins with two pH maxima, one near 2-0 the other around 3-5 (Taylor, 1959a). The third pepsin found by some authors was found by Tang and by Ryle to have a singlepH at 3.0. This, however, was only a minor component of gastric juice and was only occasionally found. There is good evidence therefore that two pepsins, and sometimes three, are present in human gastric juice. Furthermore, Taylor (1959b) has shown that these pepsins are obtainable from different parts of the stomach. Using material obtained at necropsy, he showed that one pepsin could be extracted from the fundic mucosa and the other from the pyloric mucosa. The fundic pepsin digested proteins with pH maxima at 2.2 and 3 5; the pyloric had more acidic peaks on thepH-activity curve at 1P7 and 3*1. Peptic activity/pH curves drawn in the present work have shown at some time or another five peaks of peptic activity below pH 4-5. However, three of these peaks occurred very rarely, and attention has been focused on the two peaks that were most frequently seen, namely, pH 1.8 and pH 2.2. This paper therefore first attempts to associate stimuli with the appearance of these peaks, and then to examine the occurrence of these pepsins in different conditions of the stomach in health and disease. METHOD
Hennekam syndrome: a rare and often ignored cause of intestinal lymphangiectasia
Authors: Shailendra Kapoor
Journal: Endoscopy (2014)

Hennekam syndrome is typically characterized by the presence of intestinal lymphangiectasia, mental retardation, and characteristic facial anomalies [2]. It is an autosomal recessive disorder, and consanguinity has been noted as a major contributing factor in transmission of the trait. In addition to the bowels, the lymphangiectasia may develop in renal tissue and endocrine glands such as the thyroid. A number of associated rare features may be seen in some patients. For example, Angle et al. have recently reported rectal prolapse as well as vesicoureteral reflux in a female patient with Hennekam syndrome [3].
Safety and Efficacy of First-Line Bevacizumab with Chemotherapy in Asian Patients with Advanced Nonsquamous NSCLC: Results from the Phase IV MO19390 (SAiL) Study
Authors: Chun-Ming Tsai, Joseph Siu-kie Au, Gee-Chen Chang, Ashley Chi-kin Cheng, Caicun Zhou, Yi-long Wu
Journal: Journal of Thoracic Oncology (2011)
Short-Term Psychotherapy for the Borderline Personality Disorder
Authors: Miguel A. Leibovich
Journal: Psychotherapy and Psychosomatics (1981)

This paper presents concepts of short-term therapy as utilized with borderline personality disorder. Criteria for patient selection as well as contraindications for its use are presented. Many clinical symptoms are rubricated under borderline disorders. One major consideration in diagnosis is based on the discernment of when developmental arrests have occurred. The author's opinion is that short-term integrative psychotherapeutic procedures can be beneficial for patients struggling with any of the developmental subphases. The concepts expressed in this paper are mostly applicable to more developed individuals, who have progressed in differentiating themselves from others, but who still present primitive characteristics and relationships.
Diagnosis of Obstructive Coronary Disease by Maximal Exercise and Atrial Pacing
Authors: MICHAEL H. KELEMEN, RONALD E. GILLILAN, RICHARD J. BOUCHARD, RICHARD L. HEPPNER, J. RICHARD WARBASSE
Journal: Circulation (1973)

The reliability of graded maximal exercise treadmill testing and right atrial pacing in diagnosing significant obstructive coronary artery disease was evaluated in 74 consecutive patients referred to a cardiac unit with chest pain consistent with angina pectoris. The results of maximal exercise testing and right atrial pacing, with regard to the presence or absence of the patient's characteristic chest pain or discomfort and ischemic ST segment depression, were compared with the findings determined by selective coronary arteriography. Ischemic ST segment depression was defined as a downward displacement of one full mm or more of a horizontal or downward sagging ST segment. Forty-nine of the 74 patients studied were found to have significant coronary arteriographic obstruction, i.e., greater than 75% obstruction of one major coronary artery. The occurrence of the patient's characteristic chest pain or discomfort during maximal exercise testing or right atrial pacing is an excellent indicator of the presence of obstructive coronary artery disease, since all of the 41 patients developing their characteristic pain on maximal exercise testing had coronary arteriograms positive for obstructive coronary disease (no false positives), and 46 of 47 patients with characteristic chest pain on right atrial pacing had selective coronary arteriograms positive for obstructive coronary disease. When present, one mm ST depression during maximal exercise treadmill testing also reliably indicates arteriographic obstructive coronary disease (26 of 27 patients). However, the presence or absence of ischemic ST depression during right atrial pacing is a particularly unreliable indication of the presence or absence of arteriographic obstructive coronary disease: 15 of 25 false positive tests, and 13 of 49 false negative tests.
Suppression of Histone Deacetylases Worsens Right Ventricular Dysfunction after Pulmonary Artery Banding in Rats
Authors: Harm J. Bogaard, Shiro Mizuno, Ayser A. Al Hussaini, Stefano Toldo, Antonio Abbate, Donatas Kraskauskas, Michael Kasper, Ramesh Natarajan, Norbert F. Voelkel
Journal: American Journal of Respiratory and Critical Care Medicine (2011)

Inhibitors of histone deacetylases (HDACs) reduce pressure-overload-induced left ventricular hypertrophy and dysfunction, but their effects on right ventricular (RV) adaptation to pressure overload are unknown.Determine the effect of the broad-spectrum HDAC inhibitors trichostatin A (TSA) and valproic acid (VPA) on RV function and remodeling after pulmonary artery banding (PAB) in rats.Chronic progressive RV pressure-overload was induced in rats by PAB. After establishment of adaptive RV hypertrophy 4 weeks after surgery, rats were treated for 2 weeks with vehicle, TSA, or VPA. RV function and remodeling were determined using echocardiography, invasive hemodynamic measurements, immunohistochemistry, and molecular analyses after 2 weeks of HDAC inhibition. The effects of TSA were determined on the expression of proangiogenic and prohypertrophic genes in human myocardial fibroblasts and microvascular endothelial cells.TSA treatment did not prevent the development of RV hypertrophy and was associated with RV dysfunction, capillary rarefaction, fibrosis, and increased rates of myocardial cell death. Similar results were obtained with the structurally unrelated HDAC inhibitor VPA. With TSA treatment, a reduction was found in expression of vascular endothelial growth factor and angiopoietin-1, which proteins are involved in vascular adaptation to pressure-overload. TSA dose-dependently suppressed vascular endothelial growth factor, endothelial nitric oxide synthase, and angiopoietin-1 expression in cultured myocardial endothelial cells, which effects were mimicked by selective gene silencing of several class I and II HDACs.HDAC inhibition is associated with dysfunction and worsened remodeling of the pressure-overloaded RV. The detrimental effects of HDAC inhibition on the pressure-overloaded RV may come about via antiangiogenic or proapoptotic effects.
Alteration of diastolic filling rate during exercise radionuclide angiography: a highly sensitive technique for detection of coronary artery disease.
Authors: L R Poliner, S H Farber, D H Glaeser, L Nylaan, M S Verani, R Roberts
Journal: Circulation (1984)

Diastolic and systolic parameters of left ventricular performance were characterized from high-frequency time-activity curves obtained in 10 normal volunteers (mean age 29 +/- 4 yr), in 25 patients with normal coronary arteries, and in 50 patients with coronary artery disease (CAD) at rest and during three stages of exercise radionuclide angiography. In the normal volunteers ejection fraction was 65 +/- 5% (SD) at rest and 78 +/- 5% with exercise (p less than .001). In patients with normal coronary arteries ejection fraction was 64 +/- 5% at rest and 72 +/- 8% with exercise (p less than .0001). In patients with CAD resting ejection fraction was 60 +/- 10% and that during exercise was 61 +/- 13% (p = NS). Peak diastolic filling rate in the first half of diastole, peak systolic ejection rate, and times to peak rates and to end-systole were measured. In the normal subjects resting peak diastolic filling rate was 3.1 +/- 0.6 end-diastolic counts/sec and it increased in all subjects with exercise to 3.6 +/- 0.7 (p less than .05). In patients with normal arteries and those with CAD peak diastolic filling rate was 2.3 +/- 0.8 at rest and with exercise this parameter increased to 3.2 +/- 1.1 (p less than .001) in patients with normal arteries and fell to 1.7 +/- 0.6 in those with CAD (p less than .001). Peak systolic ejection rate decreased from 2.5 +/- 0.8 to 1.9 +/- 0.8 with exercise in patients with CAD (p less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)
Is adrenaline safe and effective as a treatment for out of hospital cardiac arrest?
Authors: G. D. Perkins, P. Cottrell, S. Gates
Journal: BMJ (2014)

Adrenaline (epinephrine) has been an integral component of advanced resuscitation algorithms since the early 1960s. Initial guidelines for the treatment of cardiac arrest recommended the use of intracardiac adrenaline (0.5 mg) or high dose intravenous adrenaline (10 mg), repeating with larger doses if required.1 The mechanism of action for adrenaline in cardiac arrest is attributed to stimulation of α2 receptors in vascular smooth muscle, causing vasoconstriction. This increases aortic diastolic pressure, which in turn leads to increased coronary perfusion pressures, which improves short term survival. Experimental studies, however, suggest that adrenaline impairs cerebral macrovascular2 and microvascular blood flow,3 4 increases ventricular arrhythmias, and increases myocardial dysfunction after return of spontaneous circulation.5 This creates the paradox of better short term survival but at the potential cost of worse long term outcomes.

We searched Medline, Embase, the Cochrane Library, and trial registries for systematic reviews, randomised controlled trials, and observational studies relating to the use of adrenaline in the treatment of cardiac arrest.

A systematic review linked to the International Liaison Committee for Resuscitation 2010 evidence appraisal of vasoactive drugs in the treatment of cardiac arrest6 identified 53 articles, of which five compared adrenaline with placebo (three randomised trials6 7 8 and two observational studies9 10). The review concluded that adrenaline is associated with improved short term survival compared with placebo, but no long term survival benefit was seen. A more recent systematic review,11 which focused solely on adrenaline in cardiac arrest, identified 10 studies (two randomised trials6 8 and eight observational studies9 10 12 13 14 15 16 17). Meta-analysis found no significant effect on long term survival in randomised trials (odds …
The nuclear factor- B-interleukin-6 signalling pathway mediating vascular inflammation
Authors: A. R. Brasier
Journal: Cardiovascular Research (2010)

Vascular inflammation is a common pathophysiological response to diverse cardiovascular disease processes, including atherosclerosis, myocardial infarction, congestive heart failure, and aortic aneurysms/dissection. Inflammation is an ordered process initiated by vascular injury that produces enhanced leucocyte adherence, chemotaxis, and finally activation in situ. This process is coordinated by local secretion of adhesion molecules, chemotactic factors, and cytokines whose expression is the result of vascular injury-induced signal transduction networks. A wide variety of mediators of the vascular injury response have been identified; these factors include vasoactive peptides (angiotensin II, Ang II), CD40 ligands, oxidized cholesterol, and advanced glycation end-products. Downstream, the nuclear factor-κB (NF-κB) transcription factor performs an important signal integration step, responding to mediators of vascular injury in a stimulus-dependent and cell type-specific manner. The ultimate consequence of NF-κB signalling is the activation of inflammatory genes including adhesion molecules and chemotaxins. However, clinically, the hallmark of vascular NF-κB activation is the production of interleukin-6 (IL-6), whose local role in vascular inflammation is relatively unknown. The recent elucidation for the role of the IL-6 signalling pathway in Ang II-induced vascular inflammation as one that controls monocyte activation as well as its diverse signalling mechanism will be reviewed. These new discoveries further our understanding for the important role of the NF-κB–IL-6 signalling pathway in the process of vascular inflammation.
US women without health insurance are more likely to have late stage cervical cancer
Authors: M. Day
Journal: BMJ (2012)

Lack of health insurance has been strongly linked to the risk of late stage cervical cancer among US women in a new study in the American Journal of Public Health .1 The researchers say that the heightened risk is almost certainly due to uninsured women not being screened for the disease, which is associated with low mortality if detected early.

Their sample of 70 000 women from the US national cancer database who were given a diagnosis of cervical cancer between 2000 and 2007 found that lack of insurance was second only to age as a risk factor for a late stage (stages III and IV) cancer at diagnosis.

The American Cancer …
Changes in Antigenic Nature of Lymphocytes Caused by Common Viruses
Authors: E. Thompson, C. M. Lewis, G. D. Pegrum
Journal: BMJ (1973)

Healthy human lymphocytes were incubated in the presence of influenza A2/Singapore/57, herpes simplex type 1, or adenovirus type 2. After two days the cultures were inactivated by irradiation. Fresh lymphocytes taken from the same donor were then found to react to the virus-treated cells in short-term cultures. We suggest that this reactivity is due to a change in the surface characteristics of the lymphocytes brought about by the presence of the virus. This may account for anomalous reactions in mixed lymphocyte cultures, and a similar effect in vivo might cause accelerated graft rejection.
Diverse T-cell responses characterize the different manifestations of cutaneous graft-versus-host disease
Authors: Marie-Charlotte Brüggen, Irene Klein, Hildegard Greinix, Wolfgang Bauer, Zoya Kuzmina, Werner Rabitsch, Peter Kalhs, Peter Petzelbauer, Robert Knobler, Georg Stingl, Georg Stary
Journal: Blood (2013)
Mutations in<i>EDARADD</i>account for a small proportion of hypohidrotic ectodermal dysplasia cases
Authors: N. Chassaing, C. Cluzeau, E. Bal, P. Guigue, M-C. Vincent, G. Viot, D. Ginisty, A. Munnich, A. Smahi, P. Calvas
Journal: British Journal of Dermatology (2010)

Journal Article Mutations in EDARADD account for a small proportion of hypohidrotic ectodermal dysplasia cases Get access N. Chassaing, N. Chassaing INSERM, U563, Centre de Physiopathologie de Toulouse Purpan, Toulouse, F‐31300 FranceUniversité Toulouse III Paul‐Sabatier, Toulouse, F‐31400 FranceCHU Toulouse, Hôpital Purpan, Service de Génétique Médicale, Toulouse, F‐31300 France Search for other works by this author on: Oxford Academic Google Scholar C. Cluzeau, C. Cluzeau Université Paris Descartes and INSERM U781, Hôpital Necker‐Enfants Malades, Paris 75015, France Search for other works by this author on: Oxford Academic Google Scholar E. Bal, E. Bal Université Paris Descartes and INSERM U781, Hôpital Necker‐Enfants Malades, Paris 75015, France Search for other works by this author on: Oxford Academic Google Scholar P. Guigue, P. Guigue Université Paris Descartes and INSERM U781, Hôpital Necker‐Enfants Malades, Paris 75015, France Search for other works by this author on: Oxford Academic Google Scholar M‐C. Vincent, M‐C. Vincent CHU Toulouse, Hôpital Purpan, Service de Génétique Médicale, Toulouse, F‐31300 France Search for other works by this author on: Oxford Academic Google Scholar G. Viot, G. Viot Service Gynécologie Obstétrique, Maternité Port‐Royal, Hôpital Cochin AP‐HP, Paris, France Search for other works by this author on: Oxford Academic Google Scholar D. Ginisty, D. Ginisty Université Paris Descartes and Service de Chirurgie Maxillo‐faciale et Stomatologie Pédiatriques, Hôpital Saint‐Vincent‐de‐Paul, 75014 Paris, France Search for other works by this author on: Oxford Academic Google Scholar A. Munnich, A. Munnich Université Paris Descartes and INSERM U781, Hôpital Necker‐Enfants Malades, Paris 75015, France Search for other works by this author on: Oxford Academic Google Scholar A. Smahi, A. Smahi Université Paris Descartes and INSERM U781, Hôpital Necker‐Enfants Malades, Paris 75015, France Search for other works by this author on: Oxford Academic Google Scholar P. Calvas P. Calvas INSERM, U563, Centre de Physiopathologie de Toulouse Purpan, Toulouse, F‐31300 FranceUniversité Toulouse III Paul‐Sabatier, Toulouse, F‐31400 FranceCHU Toulouse, Hôpital Purpan, Service de Génétique Médicale, Toulouse, F‐31300 France Patrick Calvas. E‐mail: calvas.p@chu‐toulouse.fr Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 162, Issue 5, 1 May 2010, Pages 1044–1048, https://doi.org/10.1111/j.1365-2133.2010.09670.x Published: 01 May 2010
Abstract 637: Filling the gap between preclinical and clinical oncology drug evaluation- Molecular profiling and PD biomarkers on HuPrimeTM tumors models
Authors: Taiping Chen, Xiaoming Song, Dawei Chen, Shijun Yu, Jean-Pierre Wery, Yiyou Chen
Journal: Cancer Research (2010)

Abstract Most anticancer drug candidates, currently in clinical trials, have clear targets in molecular and cellular systems. However, such molecular targets are not always affected (or not correlated with efficacious endpoints) when the candidate is evaluated in a clinical setting. The gap between preclinical and clinical drug evaluation remains the bottle neck for anticancer drug development. There is an urgent need to develop better biological tools and models to ease the transition between in vitro and in vivo, and between preclinical and clinical settings. In our translational platforms, 170 human primary tumor models (HuPrimeTM) have been established directly from tumor fragments of the patients with many cancer types. In order to pick the best models for evaluation of targeted therapeutics, we have conducted a comprehensive molecular profiling of our models. This profiling includes Affymetrix whole genome expression, Illumina 1400 SNP of cancer related cancer genes for amplification, deletion, and allelic imbalance. Methylation statuses for selected gene sets were also analyzed by SuperArray platform. Genomic amplifications were further confirmed with protein analysis by western blot or immunohistochemistry. The models selected in this way have facilitated pharmacodynamic (PD) biomarker strategies. We have developed a unique platform combining our novel HuPrimeTM xenograft models with molecular profiling and PD biomarker exploration. We have now validated immunohistochemistry (IHC) assays on many molecules covering most signaling pathways that are involved in proliferation, apoptotic, necrotic, and cell cycle regulation, G2M phase arrest, DNA damage response, etc. Additional markers including angiogenesis have also been validated for certain therapeutic compounds. To illustrate the usefulness of our platform, we have applied it to understand the pharmacodynamic changes (at the molecular level) which are associated with the activity of Sunitinib, Sorafenib and Tarceva in several HuPrimeTM models. The PD biomarkers validated in this approach have potential for clinical application and patient stratification. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 637.
Resting heart rate as a predictive risk factor for sudden death in middle-aged men
Authors: X Jouven
Journal: Cardiovascular Research (2001)

A relative hyperadrenergic tone related to abnormalities of the autonomic nervous system is suspected in the mechanisms of sudden death. Therefore, we assessed the role of an elevated basal heart rate in the occurrence of sudden death in a long-term cohort study.7746 subjects aged 42--53 years, underwent ECG and physical examination conducted by a physician under standardized conditions, provided blood samples for laboratory tests, and answered questionnaires administered by trained interviewers. The vital status was obtained from specific inquiries up to the time of retirement and then by death certificates. Men with known ischemic heart disease were further excluded from analysis which was conducted on the 7079 remaining subjects.After an average follow-up period of 23 years, there were 2083 deaths, among which were 603 cardiovascular deaths including 118 sudden deaths and 192 following myocardial infarction. The crude risk of sudden death increased linearly with the level of resting heart rate and the risk in men in the highest quintile of heart rate was 3.8 fold than in those in the lowest quintile, whereas rates were approximatively twice higher for fatal myocardial infarction, cardiovascular and total mortality (all P<0.01). When age, body mass index, systolic blood pressure, tobacco consumption, parental history of myocardial infarction and parental history of sudden death, cholesterol level, diabetic status, and sport activity were simultaneously entered into the survival model, resting heart rate remained an independent risk factor for sudden death (P=0.03) but not for fatal myocardial infarction.An elevated heart rate at rest was confirmed as an independent risk factor for sudden death in middle-aged men.
Parasite uses host NFAT to co-opt immune response
Authors: Christopher Hunter, David Christian
Journal: The Journal of Experimental Medicine (2014)

![Figure][1] 

Insight from Christopher Hunter (left) and David Christian



Intracellular pathogens promote their survival by targeting host signaling pathways that either turn off antimicrobial activities or activate events that support their replication and/or survival of the host cell. The
William Rowland Murray Alexander B.Sc., M.B., Ch.B., F.R.C.P. (Edin.)
Authors: A. G. S. Hill
Journal: Annals of the Rheumatic Diseases (1970)

In September he was to have given the Heberden Round in Edinburgh and had deeply appreciated the invitation to perform this task.The Heberden Society owed a great deal to Rowland Alexander; his original papers, meticu- lously prepared, set a high standard and his dis- cussions revealed the clarity of his thinking and the depth of his knowledge.In 1969 he was senior Honorary Secretary to the Society, bringing to this office the same quiet efficiency which distinguished all his work.Many friends who were saddened by the news of his death will surely be glad that the Heberden Society, by inviting him to give the Round,