tbuckley/cabot-search huggingface dataset:
Characterization of Endocardial Electrophysiological Substrate in Patients With Nonischemic Cardiomyopathy and Monomorphic Ventricular Tachycardia
Authors: Henry H. Hsia, David J. Callans, Francis E. Marchlinski
Journal: Circulation (2003)

Although catheter mapping has been used to define the endocardial electrogram characteristics in patients with ventricular tachycardia (VT) and coronary disease, characterization of the electrophysiological substrate in patients with VT and nonischemic cardiomyopathy is limited.Left ventricular endocardial electroanatomical mapping was performed in 19 patients with nonischemic cardiomyopathy and monomorphic VT with an average of 178+/-83 sites per chamber mapped. Abnormal bipolar electrogram was defined as endocardial voltage signal amplitude of <1.8 mV. The extent and location of abnormal endocardium was estimated by measuring areas of abnormal electrogram recordings from 3D voltage maps. The origin of VT was approximated by identifying sites of entrainment with concealed fusion or early presystolic activity and/or by pace mapping. Abnormal electrograms were recorded over a 41+/-28 cm2 area that represented 20+/-12% of total endocardial surface. The majority of patients (14/19 patients) had only a modest area (<25%) of endocardial abnormality. All patients had abnormal low-voltage endocardial areas located near the ventricular base in the perivalvular region. There were 3+/-1 VT morphologies per patient. The majority (88%) of the 57 mapped VTs originated from the ventricular base, corresponding to regions with abnormal endocardial electrograms.Electroanatomical mapping in patients with monomorphic VT and nonischemic cardiomyopathy typically demonstrates a modest-sized basal area of endocardial electrogram abnormalities. The VT site of origin corresponds to these basal electrogram abnormalities. These findings have important implications regarding strategies for VT ablation in this setting.
University-Based Science and Biotechnology Products
Authors: Aaron S Kesselheim, Jerry Avorn
Journal: JAMA (2005)

The pharmaceutical and biotechnology industries have long relied on patenting as the primary means of allocating ownership and control over new discoveries. Yet, patent protection is a double-edged sword that has major implications for the future of innovation in biomedical science in the United States. Excessive "upstream" patenting of genes and molecular targets could hinder further research by creating a need for expensive and inefficient cross-licensing. However, limiting such basic science patenting could allow private entities to use the results of years of costly publicly funded research to produce and market lucrative products without compensating university- or public sector-based innovators. Academic and other nonprofit research centers would, therefore, be deprived of revenue for pursuing novel therapeutics or other seminal research work that may not be patentable. Recent court cases illustrate the inherent conflicts in allocating ownership and control of basic biomedical discoveries. Several options exist to avoid the complex problems of overlapping basic science patents while still rewarding pivotal discoveries and encouraging further innovation. These include establishing basic science patent pools and mandating arbitration arrangements that would assign credit and royalties for biotechnology innovations that depend on prior research that was performed, financed, or both in the public sector.
Vaccination Effort Targets Middle East After Polio Outbreak in Syria
Authors: M. J. Friedrich
Journal: JAMA (2013)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Effect of methylprednisolone sodium succinate on hypoxic heart muscle
Authors: W. G. NAYLER, R. SEABRA-GOMES
Journal: Cardiovascular Research (1976)

The ability of 30 mg/litre methylprednisolone sodium succinate (MPSS) to modify the effects of hypoxia on isolated Langendorff-perfused rat hearts was investigated. When perfused under hypoxic conditions (pO2 less than 0.8 kPa[6 mmHg]) these hearts lose intracellular enzymes, including creatine phosphokinase (CPK) and succinic dehydrogenase (SDH). The size of the extracellular space is enhanced, the cells gain Na+ and Ca2+ and lose K+, and the endogenous stores of ATP and CP are depleted. Initially the resistance to flow in the coronary circulation falls but after 75 min of hypoxic perfusion it increases so that coronary flow is reduced. MPSS failed to prevent hypoxic muscle from either gaining Na+ and Ca2+ or losing K+. It did, however, delay the release of CPK and SDH from the hypoxic muscle, prolong the phase of increased coronary flow, and decrease the rate of depletion of the energy-rich phosphate stores. MPSS potentiated the hypoxic-induced gain in Ca2+. Whilst the effects of MPSS on coronary flow and tissue Ca2+ were probably due to the steroid part of the complex, the other changes, including the protection of the ATP and CP stores and the delayed enzyme release, were probably due to the presence of the sodium succinate.
Joint mobility changes due to low frequency vibration and stretching exercise
Authors: J. Atha, D. W. Wheatley
Journal: British Journal of Sports Medicine (1976)

It has been shown that fifteen minutes of locally applied cycloid vibration of low amplitude and frequency is equally as effective as a fifteen minute programme of flexibility exercises in increasing short term mobility of the hip flexors. It is suggested that this mobility change may occur as a result of improved muscle relaxation.
Violent Deaths of Iraqi Civilians, 2003–2008: Analysis by Perpetrator, Weapon, Time, and Location
Authors: Madelyn Hsiao-Rei Hicks, Hamit Dardagan, Gabriela Guerrero Serdán, Peter M. Bagnall, John A. Sloboda, Michael Spagat
Journal: PLoS Medicine (2011)

Armed violence is a major public health and humanitarian problem in Iraq. In this descriptive statistical analysis we aimed to describe for the first time Iraqi civilian deaths caused by perpetrators of armed violence during the first 5 years of the Iraq war: over time; by weapon used; by region (governorate); and by victim demographics.We analyzed the Iraq Body Count database of 92,614 Iraqi civilian direct deaths from armed violence occurring from March 20, 2003 through March 19, 2008, of which Unknown perpetrators caused 74% of deaths (n = 68,396), Coalition forces 12% (n = 11,516), and Anti-Coalition forces 11% (n = 9,954). We analyzed the subset of 60,481 civilian deaths from 14,196 short-duration events of lethal violence to link individual civilian deaths to events involving perpetrators and their methods. One-third of civilian violent death was from extrajudicial executions by Unknown perpetrators; quadratic regression shows these deaths progressively and disproportionately increased as deaths from other forms of violence increased across Iraq's governorates. The highest average number of civilians killed per event in which a civilian died were in Unknown perpetrator suicide bombings targeting civilians (19 per lethal event) and Coalition aerial bombings (17 per lethal event). In temporal analysis, numbers of civilian deaths from Coalition air attacks, and woman and child deaths from Coalition forces, peaked during the invasion. We applied a Woman and Child "Dirty War Index" (DWI), measuring the proportion of women and children among civilian deaths of known demographic status, to the 22,066 civilian victims identified as men, women, or children to indicate relatively indiscriminate perpetrator effects. DWI findings suggest the most indiscriminate effects on women and children were from Unknown perpetrators using mortar fire (DWI = 79) and nonsuicide vehicle bombs (DWI = 54) and from Coalition air attacks (DWI = 69). Coalition forces had higher Woman and Child DWIs than Anti-Coalition forces, with no evidence of decrease over 2003-2008, for all weapons combined and for small arms gunfire, specifically.Most Iraqi civilian violent deaths during 2003-2008 of the Iraq war were inflicted by Unknown perpetrators, primarily through extrajudicial executions that disproportionately increased in regions with greater numbers of violent deaths. Unknown perpetrators using suicide bombs, vehicle bombs, and mortars had highly lethal and indiscriminate effects on the Iraqi civilians they targeted. Deaths caused by Coalition forces of Iraqi civilians, women, and children peaked during the invasion period, with relatively indiscriminate effects from aerial weapons. Please see later in the article for the Editors' Summary.
Naevogenesis: new thoughts based on dermoscopy
Authors: I. Zalaudek, R. Hofmann-Wellenhof, H.P. Soyer, G. Ferrara, G. Argenziano
Journal: British Journal of Dermatology (2006)

Journal Article Naevogenesis: new thoughts based on dermoscopy Get access I. Zalaudek, I. Zalaudek Department of Dermatology, Medical University of Graz, Graz, AustriaDepartment of Dermatology, Second University of Naples, Nuovo Policlinico, Edificio 13, Via S. Pansini 5, I‐80131 Naples, Italy Search for other works by this author on: Oxford Academic Google Scholar R. Hofmann‐Wellenhof, R. Hofmann‐Wellenhof Department of Dermatology, Medical University of Graz, Graz, Austria Search for other works by this author on: Oxford Academic Google Scholar H.P. Soyer, H.P. Soyer Department of Dermatology, Medical University of Graz, Graz, Austria Search for other works by this author on: Oxford Academic Google Scholar G. Ferrara, G. Ferrara Pathologic Anatomy Service, Gaetano Rummo General Hospital, Benevento, Italy E‐mail: iris.zalaudek@meduni‐graz.at Search for other works by this author on: Oxford Academic Google Scholar G. Argenziano G. Argenziano Department of Dermatology, Second University of Naples, Nuovo Policlinico, Edificio 13, Via S. Pansini 5, I‐80131 Naples, Italy Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 154, Issue 4, 1 April 2006, Pages 793–794, https://doi.org/10.1111/j.1365-2133.2006.07152.x Published: 01 April 2006
S74 Is bronchoscopy needed in children with persistent bacterial bronchitis?
Authors: RK Narang, K Bakewell, J Peach, S Clayton, M Samuels, J Alexander, W Lenney, FJ Gilchrist
Journal: Thorax (2013)

<h3>Introduction and Objectives</h3> Persistent bacterial bronchitis (PBB) is increasingly recognised as a cause of chronic cough in young children but there is lack of consensus about investigation and treatment. At UHNS, children with a wet cough for &gt;6 weeks unresponsive to oral antibiotics prescribed by the GP are investigated with CXR, baseline immune function and flexible bronchoscopy with bronchoalveolar lavage (FB-BAL). Patients with confirmed PBB are then treated with a prolonged course of an appropriate antibiotic. Some centres reserve FB-BAL for those who do not respond to blind treatment with co-amoxiclav or clinically relapse. The objective was to review bronchoscopic findings and immune function in children with chronic cough to determine which investigations are necessary. <h3>Methods</h3> A retrospective case note review of all children investigated for chronic cough between May 2011 and June 2013. <h3>Results</h3> The notes of 44 children with chronic cough were reviewed. BAL samples were taken from 6 lobes in every patient. Median (IQR) age at bronchoscopy was 3.3 (1.8–4.4) years. Positive BAL cultures were obtained from 35 patients (80%). Ten patients (23%) isolated ≥2 organisms. <i>Haemophilus influenza</i> was identified in 20 (46%), <i>Moraxella catarrhalis</i> in 11 (25%), <i>Staphylococcusl aureus</i> in 10 (23%) and <i>Streptococcus pneumoniae</i> in 6 (14%). <i>Candida albicans, Group A Streptococcus, Haemophilus parainfluenzae</i> and a <i>gram negative bacillus</i> were each identified in 1 patient (2%). In 13 (30%) at least 1 organism was isolated that was unlikely to respond to co-amoxiclav. If the right middle lobe (RML) had been the only lobe sampled (as per ERS guidance) organisms would have been missed in 14 patients (32%). Suboptimal functional antibodies to <i>Haemophilus influenza </i>or <i>Pneumococcus</i> were identified in 7 patients (16%). Appropriate antibiotics were prescribed for all patients with a positive culture. Co-amoxiclav was the most commonly prescribed antibiotic and was used in 20 patients (57%). Treatment duration varied between 4 and 8 weeks. <h3>Conclusions</h3> FB-BAL is a useful investigation to aid the diagnosis and guide treatment in PBB. The best time to perform FB-BAL is not known. In PBB a number of organisms will be missed if BAL is only taken from the RML.
Filaggrin expression in epidermolytic ichthyosis (epidermolytic hyperkeratosis)
Authors: A. ISHIDA-YAMAMOTO, R.A.J. EADY, R.A. UNDERWOOD, B.A. DALE, K.A. HOLBROOK
Journal: British Journal of Dermatology (1994)

To evaluate the role of filaggrin in keratin filament aggregation in epidermolytic ichthyosis (epidermolytic hyperkeratosis, EH), we studied EH skin by light and electron microscopic immunohistochemistry, and biochemical analysis using sodium dodecylsulphate-polyacrylamide gel electrophoresis and immunoblotting. Immunohistochemical staining showed an increased number of filaggrin-immunoreactive cell layers, but the reaction was still confined to the mid- and upper epidermal layers, whereas an abnormal granular pattern of staining for K10 began in the lower suprabasal cell layers. This suggests that the aggregation of keratin filaments precedes, and occurs independently of, profilaggrin synthesis during epidermal differentiation. Although keratohyalin granules were frequently associated with clumped filaments, immunoelectron microscopy showed that K10 labelling was confined to keratin filaments (including clumped filaments), and that antifilaggrin antibodies stained only keratohyalin granules, at least in the living cells. Certain keratin aggregates in the cornified cells were still devoid of filaggrin staining. However, in some cells which appeared partially cornified, filaggrin immunoreactivity occurred over the aggregated keratin filaments. Immunoblotting showed a clear increase of filaggrin/profilaggrin expression, without evidence for a qualitative abnormality. It seems unlikely, therefore, that filaggrin is primarily involved in the keratin filament clumping in EH, but that in some EH cases it interacts with keratins in a defective manner, possibly due to premature cell death and profilaggrin processing and/or altered keratin filament structure involving the interaction points of keratin with filaggrin.
Mutant p53 Protects Cells from 12-<i>O</i>-Tetradecanoylphorbol-13-Acetate–Induced Death by Attenuating Activating Transcription Factor 3 Induction
Authors: Yosef Buganim, Eyal Kalo, Ran Brosh, Hila Besserglick, Ido Nachmany, Yoach Rais, Perry Stambolsky, Xiaohu Tang, Michael Milyavsky, Igor Shats, Marina Kalis, Naomi Goldfinger, Varda Rotter
Journal: Cancer Research (2006)

Abstract Mutations in p53 are ubiquitous in human tumors. Some p53 mutations not only result in loss of wild-type (WT) activity but also grant additional functions, termed “gain of function.” In this study, we explore how the status of p53 affects the immediate response gene activating transcription factor 3 (ATF3) in the 12-O-tetradecanoylphorbol-13-acetate (TPA)-protein kinase C (PKC) pathway. We show that high doses of TPA induce ATF3 in a WT p53-independent manner correlating with PKCs depletion and cell death. We show that cells harboring mutant p53 have attenuated ATF3 induction and are less sensitive to TPA-induced death compared with their p53-null counterparts. Mutagenesis analysis of the ATF3 promoter identified the regulatory motifs cyclic AMP-responsive element binding protein/ATF and MEF2 as being responsible for the TPA-induced activation of ATF3. Moreover, we show that mutant p53 attenuates ATF3 expression by two complementary mechanisms. It interacts with the ATF3 promoter and influences its activity via the MEF2 site, and additionally, it attenuates transcriptional expression of the ATF3 activator MEF2D. These data provide important insights into the molecular mechanisms that underlie mutant p53 gain of function. (Cancer Res 2006; 66(22): 1750-9)
SUDDEN DEATH FROM PNEUMONIA WITHOUT APPARENT SYMPTOMS
Authors: J. A. Stephen, E. R. C. Walker
Journal: BMJ (1929)

Tnz BmTrL of, lassitude, headaches, and constipation for about two montlhs.Thero was no family history of tuberculosis, and no signs or symptoms of this disease could be discovered in the child.A radiograph of the lungs showed nothing abnormal.He had never suffered from " bilious attacks," and was an only child.As will be seen from the accompanying chart, the temperature becamiie .FAH, t |IFEH I M 1EPIEI!g!1JIK E !EMIEI!f | fl | N!ILi af4 I _ .__ e ._ I 104.~~~~~~~~~~~~~~~~~~~~1 03 t ,_o ._998 ;,I I 'A iZf V q7 , ..I0 1 Chart showing subsidence of prolonged uinexplained pyrexia on administration of sugar.normal almost immediately after giving extra sugar (3 drachms of glucose powder in lemonade three times a day).It will be seen also that he at once began to gain in weight.Since then he has attended as an out-patient at intervals, and now (October, 1928) he is apparently in normal health, having had no further symptorms.During the whole of this period he has continued to take glucose.The following conclusions would appear to be justified.
CONGENITAL CIRSOID ANEURYSM OF THE LEG
Authors: Mont R. Reid
Journal: JAMA (1933)

Among the conditions that can have the effect of causing an overgrowth of an extremity during the growing period of life may be mentioned chronic osteomyelitis and abnormal arteriovenous communications. This effect is apparently due to an abnormal increase of the arterial blood supply.  An increased length of the limb resulting from abnormal arteriovenous communications has been reported by Giraldes,1Cordonnier,2Davis,3Hewett,4Franz5and Reid.6In four of the cases reported by these authors the etiology of the condition was trauma, while in two cases it was congenital. In a congenital case,6in a woman, aged 36, the affected leg was 6 cm. longer than the normal leg.  These cases have been reported under the various titles of abnormal arteriovenous communications, arteriovenous aneurysm, cirsoid aneurysm, racemose aneurysm and pulsating angioma. In all instances the cause has been abnormal communications between the arteries
Abstract 844: Peroxisome proliferator-activated receptor γ agonists abrogate tumor invasion and promote TRAIL-induced apoptosis in malignant glioma.
Authors: Kyungsun Choi, Kyuha Chong, Jungwhoi Lee, Hojun Choi, Chulhee Choi
Journal: Cancer Research (2013)

Abstract Glioblastoma multiforme is the most common brain tumors and have a worse prognosis, so it is needed to develop effective treatments. Peroxisome proliferator-activated receptor gamma (PPAR-γ) agonists, including 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2) and synthetic ligands, troglitazone and rosiglitazone, are known to sensitize tumor cells to apoptosis via various molecular mechanisms. In this study, we investigated the therapeutic potentials of combined treatment with PPAR-γ agonists and TRAIL in TRAIL-resistant astrocytoma cells. TRAIL alone and each PPAR-γ agonist exhibited no cytotoxic effects; while the pre-incubation with PPAR-γ agonists enhanced dramatically TRAIL-induced cell death, which was abrogated by a broad spectrum caspase inhibitor, z-VAD-fmk. And also, the combined treatment with PPAR-γ agonists and TRAIL increased the enzymatic activity of caspase-3. These results indicate that PPAR-γ agonists might promote TRAIL-mediated apoptosis by modulating the caspase activity. In addition, the expression of anti-apoptotic proteins including FLIP, Bcl-2, Bcl-xL and XIAP was suppressed by the combined treatment. Besides the cytotoxic effect, treatment with PPAR-γ agonists significantly inhibited glioma invasion in vitro and in vivo. These results collectively suggest that PPAR-γ agonists may provide a promising strategy to treat malignant glioma. Citation Format: Kyungsun Choi, Kyuha Chong, Jungwhoi Lee, Hojun Choi, Chulhee Choi. Peroxisome proliferator-activated receptor γ agonists abrogate tumor invasion and promote TRAIL-induced apoptosis in malignant glioma. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 844. doi:10.1158/1538-7445.AM2013-844
Glibenclamide, a Selective Inhibitor of ATP-Sensitive K <sup>+</sup> Channels, Attenuates Metabolic Coronary Vasodilatation Induced by Pacing Tachycardia in Dogs
Authors: Yousuke Katsuda, Kensuke Egashira, Hideki Ueno, Yutaka Akatsuka, Takahiro Narishige, Yukinori Arai, Tsuneo Takayanagi, Hiroaki Shimokawa, Akira Takeshita
Journal: Circulation (1995)

We previously reported that glibenclamide (a selective inhibitor of ATP-sensitive K+ channels [K+ATP channels]) inhibited metabolic coronary vasodilatation induced by beta 1-adrenoceptor stimulation. However, the role of K+ATP channels in metabolic coronary vasodilatation induced by tachycardia is still unknown. This study aimed to determine whether glibenclamide attenuates metabolic coronary vasodilatation induced by pacing-induced tachycardia.In anesthetized dogs, increasing heart rate from 103 +/- 1 to 160 beats per minute with atrial pacing increased coronary blood flow without altering arterial pressure and left ventricular pressure. Intracoronary infusion of glibenclamide at 1.5 and 5.0 micrograms.kg-1.min-1 did not alter basal coronary blood flow but significantly attenuated (P < .01) the tachycardia-induced coronary vasodilatation without altering the tachycardia-induced increase in myocardial oxygen consumption (MVO2). In conscious dogs, intracoronary glibenclamide at 5.0 micrograms.kg-1.min-1 attenuated (P < .05) coronary vasodilatation induced by ventricular pacing from 85 +/- 6 to 150 beats per minute. Glibenclamide markedly attenuated coronary vasodilation evoked with the K+ATP channel opener pinacidil.These data indicate that blockade of coronary vascular K+ATP channels with glibenclamide inhibited metabolic coronary vasodilatation induced by pacing tachycardia in dogs, suggesting that K+ATP channels are involved in the mechanism mediating metabolic coronary vasodilatation associated with pacing tachycardia.