tbuckley/cabot-search huggingface dataset:
Logistic Time Constant of Isovolumic Relaxation Pressure–Time Curve in the Canine Left Ventricle
Authors: Hiromi Matsubara, Miyako Takaki, Shingo Yasuhara, Junichi Araki, Hiroyuki Suga
Journal: Circulation (1995)

Background The time constant of left ventricular (LV) relaxation derived from a monoexponential model has been widely used as an index of LV relaxation rate or lusitropism, although this model has several well-recognized problems. In the present study, we proposed a logistic model and derived a “logistic” time constant ( T L ) as a better alternative to the conventional “exponential” time constant ( T E ). Methods and Results A total of 189 beats (147 isovolumic and 42 ejecting beats) were investigated in seven canine excised cross–circulated heart preparations. We found that the logistic model fitted much more precisely all the observed LV isovolumic relaxation pressure–time [P(t)] curves than the monoexponential model ( P &lt;.05). The logistic model also fitted well both the time curve of the first derivative of the observed P(t) (dP/dt) and the dP/dt–P(t) phase–plane curve. Like T E , T L indicated that volume loading depressed LV lusitropism and that increasing heart rate and ejection fraction augmented it. T L was independent of the choice of cutoff point defining the end of isovolumic relaxation; T E was dependent on that choice. Conclusions We conclude that the logistic model better fits LV isovolumic relaxation P(t) than the monoexponential model in the present heart preparation. We therefore propose T L as a better alternative to T E for evaluating LV lusitropism.
NOTE ON A MOLD, COCCIDIOIDES IMMITIS, FOUND IN A CASE OF GENERALIZED INFECTION IN MAN
Authors: WARD J. MacNEAL
Journal: JAMA (1913)

A sample of pus, obtained by incision of a subcutaneous abscess in the case reported by Dr. Morris in this issue of The Journal, was sent to the laboratory for examination on April 23, 1913, Laboratory No. 8511. Microscopic examination of stained preparations of the pus was negative. Plate cultures on ascitic-fluid agar brought to development, after incubation for forty-eight hours, numerous colonies of radiating mycelial threads and a very few bacterial colonies. The appearance of the colonies suggested the possibility of oidiomycosis. The patient was seen by us on April 25 at the invitation of, and in consultation with, Dr. B. Lattin. The clinical condition of the patient, as well as the history of the illness, was found to be quite in accord with the indication of the laboratory examination. At this time a second specimen of pus was obtained from a closed subcutaneous abscess by aspiration into a
Prolongation of a Preterm Pregnancy Complicated by Death of a Single Twin in Utero and Disseminated Intravascular Coagulation
Authors: Roberto Romero, Thomas P. Duffy, Richard L. Berkowitz, Effie Chang, John C. Hobbins
Journal: New England Journal of Medicine (1984)

Medical Intelligence from The New England Journal of Medicine — Prolongation of a Preterm Pregnancy Complicated by Death of a Single Twin in Utero and Disseminated Intravascular Coagulation — Effects of Treatment with Heparin
A germline variant in the TP53 polyadenylation signal confers cancer susceptibility
Authors: Simon N Stacey, Patrick Sulem, Aslaug Jonasdottir, Gisli Masson, Julius Gudmundsson, Daniel F Gudbjartsson, Olafur T Magnusson, Sigurjon A Gudjonsson, Bardur Sigurgeirsson, Kristin Thorisdottir, Rafn Ragnarsson, Kristrun R Benediktsdottir, Bjørn A Nexø, Anne Tjønneland, Kim Overvad, Peter Rudnai, Eugene Gurzau, Kvetoslava Koppova, Kari Hemminki, Cristina Corredera, Victoria Fuentelsaz, Pilar Grasa, Sebastian Navarrete, Fernando Fuertes, Maria D García-Prats, Enrique Sanambrosio, Angeles Panadero, Ana De Juan, Almudena Garcia, Fernando Rivera, Dolores Planelles, Virtudes Soriano, Celia Requena, Katja K Aben, Michelle M van Rossum, Ruben G H M Cremers, Inge M van Oort, Dick-Johan van Spronsen, Jack A Schalken, Wilbert H M Peters, Brian T Helfand, Jenny L Donovan, Freddie C Hamdy, Daniel Badescu, Ovidiu Codreanu, Mariana Jinga, Irma E Csiki, Vali Constantinescu, Paula Badea, Ioan N Mates, Daniela E Dinu, Adrian Constantin, Dana Mates, Sjofn Kristjansdottir, Bjarni A Agnarsson, Eirikur Jonsson, Rosa B Barkardottir, Gudmundur V Einarsson, Fridbjorn Sigurdsson, Pall H Moller, Tryggvi Stefansson, Trausti Valdimarsson, Oskar T Johannsson, Helgi Sigurdsson, Thorvaldur Jonsson, Jon G Jonasson, Laufey Tryggvadottir, Terri Rice, Helen M Hansen, Yuanyuan Xiao, Daniel H Lachance, Brian Patrick O′Neill, Matthew L Kosel, Paul A Decker, Gudmar Thorleifsson, Hrefna Johannsdottir, Hafdis T Helgadottir, Asgeir Sigurdsson, Valgerdur Steinthorsdottir, Annika Lindblom, Robert S Sandler, Temitope O Keku, Karina Banasik, Torben Jørgensen, Daniel R Witte, Torben Hansen, Oluf Pedersen, Viorel Jinga, David E Neal, William J Catalona, Margaret Wrensch, John Wiencke, Robert B Jenkins, Eduardo Nagore, Ulla Vogel, Lambertus A Kiemeney, Rajiv Kumar, José I Mayordomo, Jon H Olafsson, Augustine Kong, Unnur Thorsteinsdottir, Thorunn Rafnar, Kari Stefansson
Journal: Nature Genetics (2011)
Cardiac Transplantation in an 8-Month-Old Female Infant With Subendocardial Fibroelastosis
Authors: Denton A. Cooley
Journal: JAMA (1986)

On Nov 1, 1984, an orthotopic cardiac transplantation was performed in an 8-month-old female infant with subendocardial fibroelastosis. Because of the advanced state of cardiac failure, the operation was done despite a positive tissue crossmatch for antitoxic donor-specific antibodies. Immunosuppression consisted of high doses of cyclosporine (up to 550 mg/m2 or 30 mg/kg) and steroids. Hypertension and tremor of the extremities, which were attributed to cyclosporine, occurred during the first week but resolved after seven days. No signs of nephrotoxic effects have been noted; however, a severe episode of allograft rejection was detected by endomyocardial biopsy on the seventh postoperative day, and a moderate rejection episode was noted on the 22nd postoperative day. Histologic improvement was seen after treatment with conventional steroid pulses. The patient was discharged on Nov 29, 1984. Complications consisted of four episodes of otitis media caused by Staphylococcus aureus and one rejection episode that was treated on an outpatient basis with an intravenous methylprednisolone sodium succinate pulse. Our experience emphasizes both the feasibility and importance of performing endomyocardial biopsies in infant recipients. Through biopsy, episodes of rejection can be discovered when clinical signs are not yet apparent. Eighteen months after transplantation, the child was developing and growing normally.
Outcomes of Acute Retrograde Type A Aortic Dissection With an Entry Tear in Descending Aorta
Authors: Joon Bum Kim, Suk Jung Choo, Wan Kee Kim, Ho Jin Kim, Sung-Ho Jung, Cheol Hyun Chung, Jae Won Lee, Jae-Kwan Song
Journal: Circulation (2014)

Optimal management strategy of acute aortic dissection (AD) with retrograde extension from entry tear in the descending aorta into the ascending aorta remains undetermined.Of the 538 patients who were diagnosed as having acute AD from 1999 through 2011, 49 patients (37 men; 52.5±13.1 years) were identified as having entry tear in the descending aorta with retrograde extension of AD into the ascending aorta. Sixteen patients who were clinically stable with thrombosed false lumen in the ascending aorta were treated medically (MED group), whereas 33 patients underwent aortic replacement (SURG group) on an intention-to-treat basis. In the MED group, 1 patient was converted to urgent aortic surgery and 2 patients underwent endovascular stent grafting in the descending aorta during the initial hospitalization. The early (30-day or in-hospital) mortality rates were 0% and 9.1% in the MED and SURG group, respectively (P=0.54). Follow-up was complete in all patients (median, 61.4 months; Q1-Q3, 28.2-99.1 months). The 5-year 100% survival rate in the MED group was higher than that in the SURG group (81.2±7.0%; P=0.080), in the surgically treated patients with antegrade type A AD (74.5±2.8%; P=0.038), and in the patients with type B AD (75.3±3.3%; P=0.045). Aortic event-free survival at 5 years was 52.7±14.8% and 69.6±8.0% in the MED and SURG groups, respectively (P=0.98).Patients with acute retrograde type A AD showed a more favorable prognosis than patients with antegrade AD. In selected patients with retrograde type A AD, excellent outcomes could be achieved with initial medical management combined with timely interventions.
Quantification of Coronary Artery Lumen Volume by Digital Angiography
Authors: Sabee Molloi, Ghassan S. Kassab, Yifang Zhou
Journal: Circulation (2001)

Background Coronary artery lumen volume may potentially have several advantages over the commonly used variables, such as percent stenosis or minimal lumen diameter, in the assessment of coronary artery disease. The goal of this study is to validate a quantitative assessment of lumen volume using a video densitometry technique. Methods and Results Coronary arteriography was performed in 9 swine (body weight 20 to 55 kg) after power injection of contrast material (2 mL/s for 3 seconds) into the left main coronary artery. Phase-matched subtracted images were used to quantify regional lumen volume by a video densitometry technique. The in vivo volume measurements were validated by a polymer cast of the coronary arterial tree made at physiological pressure. The measured cast volume (V C ) and video densitometric regional lumen volume (V VD ) were related by V VD =1.06 V C −0.01 mL ( r =0.99). The root mean square and systematic errors for these measurements were 17% and −3%, respectively. Conclusions A video densitometry technique for quantification of coronary lumen volume was validated both in vitro and in vivo in a swine animal model. The present results demonstrated the feasibility and potential utility of the video densitometry technique for accurate measurement of regional lumen volume in vivo. This study contributes to the understanding of the angiographic methods used for the assessment of coronary artery disease and indicates that this technique can potentially be used for quantification of diffuse coronary artery disease during routine coronary arteriography.
17β-Estradiol Mobilizes Bone Marrow–Derived Endothelial Progenitor Cells to Tumors
Authors: Robert Suriano, Devyani Chaudhuri, Raja Singh Johnson, Erin Lambers, Badithe T. Ashok, Raj Kishore, Raj K. Tiwari
Journal: Cancer Research (2008)

Abstract Neovascularization is critical for tumor growth and development. The cellular mediators for this process are yet to be defined. We discovered that bone marrow–derived endothelial progenitor cells (BM-EPC), having the phenotype (CD133+, CD34+, VEGFR-2+), initiate neovascularization in response to TG1-1 mammary cells implanted in the inguinal mammary gland of Tie-2 GFP transgenic mice. The fluorescence tag allowed for tracing the migration of green fluorescent protein–tagged endothelial progenitor cells to tumor tissues. We discovered that 17-β estradiol supplementation of ovariectomized mice significantly enhanced BM-EPC–induced neovascularization and secretion of angiogenic factors within the tumor microenvironment. Cell-based system analyses showed that estrogen-stimulated BM-EPCs secreted paracrine factors which enhanced TG1-1 cell proliferation and migration. Furthermore, TG1-1 cell medium supplemented with estrogen-induced BM-EPC mediated tubulogenesis, which was an experimental in vivo representation of the neovasculature. Our data provide evidence of BM-EPC mammary tumor cell interactions and identify a novel cellular mediator of tumor progression that can be exploited clinically. [Cancer Res 2008;68(15):6038–42]
If preventable why not prevented?
Authors: J Primrose
Journal: BMJ (1979)

surgeons), who would no doubt be happy to co-operate.In one town the surgeon in charge of the accident unit gave police officers tuition in airway control at the hospital, and this was greatly appreciated.Equipment of most police cars was inadequate and often consisted only of first- aid boxes containing bandages and dressings.Patrol cars attending road accidents should have modern respiratory resuscitation equip- ment, spinal boards, cervical collars, inflatable splints, and waterproof sheets.They should also carry light rescue and cutting equipment for the release of trapped casualties, particu- larly in rural districts.
Income inequality and mortality: why are they related?
Authors: G. D. Smith
Journal: BMJ (1996)

The long held belief that household income is an important indicator of risk of death has recently received strong support from a series of large prospective studies.1 2 Income inequality within a population has also been suggested to be an important determinant of population mortality. In a cross national comparison, Rodgers found associations between income inequality and three mortality indicators—infant mortality, life expectancy at birth, and life expectancy at age 5—after taking overall gross national product into account.3 Several replications of this, across both a wide range of countries and within industrialised nations alone, using a variety of health indicators, have appeared.4 5 6 7 These studies have related income inequality to infant mortality,4 life expectancy,5 height,6 and morbidity,7 with a consistent finding that the less equitable the income distribution in a country, the less favourable the health outcome.

In this week's issue of the BMJ, two studies relate income inequality between states in the United States to mortality rates within these states. Kennedy and colleagues (p 1004) show that greater income inequality is associated with higher mortality from several broad causes of death, although taking levels of poverty and smoking prevalence into account attenuates these associations.8 Kaplan et al find associations between level of inequality and mortality in both 1980 and 1990 (p 999), with trends in mortality differences between states over this decade being inconsistently related to changes in income inequality.9

In Britain, reliable data on income inequality by area are not readily available. Also in this issue, Ben-Shlomo et al (p 1013) have used the variation in small area deprivation scores within local authority areas in Britain as their …
SURGICAL VS. MEDICAL TREATMENT OF HYPERTENSION-Reply
Authors: Max M. Peet
Journal: JAMA (1941)

To  Editor:—  May we first express our appreciation to Dr. Weiss for  keen interest he has shown in our paper and for his penetrating criticisms, indicating a thorough knowledge of  therapeutics of hypertension.  The question is not at all a matter of   medical treatment of hypertension but rather of determining  point in  progress of  disease when surgical treatment should be called on to replace accepted medical treatment which has failed. In confirmation of this point of view may we agree with  author that we do not see the kinds of patients who comprise most of  cases seen in private practice but instead are asked to treat those patients who have not gained relief after a thorough trial of medical treatment. The term versus arises only when persistent medical therapy has proved inadequate for too long and has allowed irreversible damage
Potential Role of FDG PET/CT in Evaluating Patients With Hepatic Incidentalomas
Authors: Gaia Grassetto, Maria Cristina Marzola, Sotirios Chondrogiannis, Anna Margherita Maffione, Lucia Rampin, Fabrizio Galeotti, Patrick M. Colletti, Domenico Rubello
Journal: Clinical Nuclear Medicine (2013)

This review article is focused on the role of FDG PET/CT in diagnosing and characterizing hepatic incidentalomas. A large variety of unsuspected lesions can be detected in the liver both with ultrasound and CT performed for other reasons; the prevalence of liver incidentalomas increases in patients with chronic liver disease or preexisting oncologic history. The major challenge is to discriminate benign from malignant lesions. There is a large body of literature indicating that FDG PET/CT is a useful tool to this purpose even if it is unspecific (ie, it cannot differentiate a primary tumor from a secondary lesion). Occasionally, FDG PET/CT can be useful for biopsy guidance.
The Influence of Sociopathology in Childhood Asthma
Authors: Ph. Pinkerton
Journal: Psychotherapy and Psychosomatics (1970)

Asthmatic children do not constitute a homogeneous group. They show wide variations in severity of physiological involvement, in parental attitudes to the disorder and in the attitude of the child himself to his disability. Each of these factors has been shown to affect the therapeutic outcome. This paper seeks to demonstrate that in addition, adversity of life circumstances may equally influence the pattern of clinical response. Two groups of juvenile asthmatics were studied; 161 referred to a children's hospital, and 55 accomodated within a residental open-air school. Both groups showed the characteristic alternation between relative improvement under hospital supervision or in boarding school and the tendency to relapse if discharged prematurely. Both groups were similarly comparable in their constituent physiological grades. By contrast, a much higher incidence of sociopathic stress was found to operate within the residential open-air school group than within the hospital based group, this difference being highly significant statistically. Among a number of general implications, which emerge from this study, the conclusion of most immediate import is that sociopathology, where it exists, should never be dismissed as trivial or irrelevant to the clinical course of the individual asthmatic case. On the contrary, adverse life circumstances can be shown on occasion to be as important in the genesis of clinical intractability as the more familiar variants of psychopathology based upon interpersonal or intrapsychic considerations. In effect, we have to consider the whole patient within his family and social environment rather than just his efficiency in ventilatory function if we are to achieve the optimum therapeutic response in childhood asthma.
A key role for autoreactive B cells in the breakdown of T-cell tolerance to pyruvate dehydrogenase complex in the mouse
Authors: Amanda J. Robe, John A. Kirby, David E. J. Jones, Jeremy M. Palmer
Journal: Hepatology (2005)

The key immunological event in the pathogenesis of the autoimmune liver disease primary biliary cirrhosis is breakdown of T-cell self-tolerance to pyruvate dehydrogenase complex (PDC). The mechanism resulting in this breakdown of tolerance remains unclear. Mice exposed to self-PDC mount no immune response; however, animals coexposed to self-PDC and PDC of foreign origin (which in isolation induces a cross-reactive antibody but not an autoreactive T-cell response) show breakdown of T-cell as well as B-cell tolerance. This observation raises the possibility that a cross-reactive antibody response to self-PDC can promote breakdown of T-cell tolerance. The aim of this study was to address the hypothesis that breakdown of T-cell tolerance to PDC can be driven by the presence of B cells and/or antibodies cross-reactive with this self-antigen. Naive female SJL/J mice were exposed to self-PDC alone and in the presence of purified splenic B cells from animals primed with foreign PDC (or controls) or purified immunoglobulin (Ig) G from the same animals. Breakdown of T-cell tolerance was assessed by splenic T-cell proliferative response to antigen at 5 weeks. CD4(+) T-cell proliferative responses indicative of breakdown of T-cell tolerance to self-PDC were seen in the majority (7 of 9, 78%) of animals receiving self-PDC together with purified PDC-reactive B cells. Tolerance breakdown was not seen in animals receiving self-PDC with purified anti-PDC IgG or with B cells from animals sensitized with an irrelevant antigen. In conclusion, breakdown of T-cell tolerance to the highly conserved self-antigen PDC may be mediated by high-level presentation of self-derived epitopes by activated cross-reactive B cells.
Failure to control venereal disease.
Authors: A King
Journal: BMJ (1970)

<h3>Objective</h3> To evaluate if defective activation of renal functional reserve (RFR) in systemic sclerosis (SSc) without clinical signs of renal involvement predicts the risk of developing clinically relevant renal damage. <h3>Methods</h3> Twenty-eight normotensive SSc patients with normal renal function and no urinary abnormalities were submitted to an intravenous amino acid load to activate RFR. Nineteen patients (six with diffuse cutaneous SSc (dcSSc)) had an RFR activation defect, while nine (two with dcSSc) showed normal RFR. All patients were followed up for 5 years, with periodic evaluation of renal function, urinary protein excretion and systemic blood pressure (BP). <h3>Results</h3> At admission, patients with normal RFR had lower BP than those with abnormal RFR; no age, disease duration or creatinine clearance (CCr) differences were found. Five years later, patients with abnormal RFR showed, with respect to basal values, a significantly higher CCr reduction than patients with normal RFR (mean percent decrease 15.4±9.5 vs 2.6±3.8, p&lt;0.001). Among patients with abnormal RFR, 13 (68.4%) showed a CCr reduction of ≥2 ml/min/year, with a final CCr of ≤70 ml/min in eight cases; two patients developed microalbuminuria and 10 grade 1 or 2 systemic hypertension. Significant CCr reduction rates were found in eight patients with high BP and in five patients who remained normotensive. No patient with normal RFR had proteinuria or high BP during follow-up. <h3>Conclusions</h3> Lack of RFR activation is an early sign of renal involvement in SSc, and is a harbinger of an increased risk of developing renal insufficiency and systemic hypertension.
Abstract 3559: A new selective ALK inhibitor CH5424802 shows potent efficacy against ALK-positive cancers including the gatekeeper mutant-driven tumors
Authors: Hiroshi Sakamoto, Toshiyuki Tsukaguchi, Sayuri Hiroshima, Tatsushi Kodama, Takamitsu Kobayashi, Takaaki A. Fukami, Nobuhiro Oikawa, Takuo Tsukuda, Nobuya Ishii, Yuko Aoki
Journal: Cancer Research (2011)

Abstract The recent development of targeted protein kinase inhibitors has provided new opportunity in cancer treatment. However, certain factors limit the efficacy of cancer therapies, such as a narrow therapeutic index caused by inhibition of multiple kinases, and the emergence of resistant mutants. Thus, kinase inhibitors with more potent and selective properties and effectiveness against resistant mutants need to be developed. Anaplastic lymphoma kinase (ALK) is a tyrosine kinase that is constitutively activated in certain cancers following gene alterations such as chromosomal translocation, amplification, or point mutation. Here, we identified CH5424802, a potent, selective, and orally available ALK inhibitor with a new chemical scaffold, showing preferential antitumor activity against cancers with gene alterations of ALK, such as non-small cell lung cancer (NSCLC) cells expressing EML4-ALK fusion and anaplastic large-cell lymphoma (ALCL) cells expressing NPM-ALK fusion in vitro and in vivo. CH5424802 inhibited ALK L1196M, which corresponds to the gatekeeper mutation conferring common resistance to kinase inhibitors, and blocked EML4-ALK L1196M-driven tumors. Our results support the potential for the clinical evaluation of CH54242802 for long-term treatment of patients with ALK-driven tumors. CH5424802 is currently being investigated in Phase I/II clinical trials for patients with ALK-positive NSCLC. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 3559. doi:10.1158/1538-7445.AM2011-3559