tbuckley/cabot-search huggingface dataset:
Hydroxyurea Can Be Used to Increase Mouse c-kit+Thy-1.1loLin−/loSca-1+ Hematopoietic Cell Number and Frequency in Cell Cycle In Vivo
Authors: Nobuko Uchida, Annabelle M. Friera, Dongping He, Michael J. Reitsma, Ann S. Tsukamoto, Irving L. Weissman
Journal: Blood (1997)

Abstract The DNA synthesis inhibitor hydroxyurea (HU) was administered to determine whether it induces changes in the cell-cycle status of primitive hematopoietic stem cells (HSCs)/progenitors. Administration of HU to mice leads to bone marrow accumulation of c-kit+Thy-1.1loLin−/loSca-1+ (KTLS) cells in S/G2/M phases of the cell cycle. HU is a relatively nontoxic, reversible cell-cycle agent that can lead to approximately a threefold expansion of KTLS cells in vivo and approximately an eightfold increase in the number of KTLS cells in S/G2/M. HSCs in HU-treated mice have undiminished multilineage long-term and short-term clonal reconstitution activity.
Sustaining the graft-versus-tumor effect through posttransplant immunization with granulocyte-macrophage colony-stimulating factor (GM-CSF)–producing tumor vaccines
Authors: Ivan Borrello, Eduardo M. Sotomayor, Frédérique-Marie Rattis, Sara K. Cooke, Lingping Gu, Hyam I. Levitsky
Journal: Blood (2000)
Abstract 4338: SYNTAX Score Predicts Major Adverse Cardiovascular and Cerebrovascular Event (MACCE)-free Survival, but Not Overall Survival, in Unprotected Left Main Coronary Artery (ULMCA) Patients Undergoing Percutaneous Coronary Revascularization (PCI): 3-Year Follow-up Analysis
Authors: Tarun Chakravarty, Mamta H Buch, Hursh Naik, James S Forrester, Niraj Doctor, James M Mirocha, Raj Makkar
Journal: Circulation (2009)
Suicide, stressors, and the life cycle [published erratum appears in Am J Psychiatry 1991 Jul;148(7):960]
Authors: C L Rich, G M Warstadt, R A Nemiroff, R C Fowler, D Young, G M Warsradt
Journal: American Journal of Psychiatry (1991)

Relationships between stressors and suicide might be expected to vary with stages of the life cycle. The purpose of this study was to examine this possibility.The authors examined the first 204 consecutive cases from the San Diego Suicide Study, a federally funded investigation of 283 suicides, for possible relationships between suicide and age and the frequency of specific stressors. Information was gathered from family members, spouses, acquaintances, employers, other witnesses, physicians, and other professionals by trained interviewers using a structured format. Hospital, physician, therapist, school, and police records were also included when available. DSM-III diagnoses were made by consensus of two investigators. Life events information was also reviewed independently by the investigators to determine stressors (if any) for each case.Of the 202 subjects for whom data were available, 195 (97%) had one or more stressors; 137 male subjects had a total of 272 stressors, and 58 female subjects had a total of 115 stressors. The authors found predictable patterns of the three most common stressor groups--conflict-separation-rejection, economic problems, and medical illness. The majority of the stressors among subjects 80 years old or older were illnesses. The only significant difference between the sexes was that more men than women had economic problems as a stressor.The variations in the patterns of stressors found in this study of suicides coincide with adult development theory. The lack of population comparison subjects and stressor scoring validation, however, limits the predictive value of these data in assessing suicidal persons.
Hemoglobin level is an independent predictor for adverse cardiovascular outcomes in women undergoing evaluation for chest pain
Authors: Christopher B Arant, Timothy R Wessel, Marian B Olson, C.Noel Bairey Merz, George Sopko, William J Rogers, Barry L Sharaf, Steven E Reis, Karen M Smith, B.Delia Johnson, Eileen Handberg, Sunil Mankad, Carl J Pepine
Journal: Journal of the American College of Cardiology (2004)
Inhibition of Caspase Cascade by HTLV-I Tax Through Induction of NF-κB Nuclear Translocation
Authors: Atsushi Kawakami, Tomoki Nakashima, Hideaki Sakai, Satoshi Urayama, Satoshi Yamasaki, Ayumi Hida, Masahiko Tsuboi, Hideki Nakamura, Hiroaki Ida, Kiyoshi Migita, Yojiro Kawabe, Katsumi Eguchi
Journal: Blood (1999)
Abstract 1472: Genetic Deficiency in Caveolin-3 Alters Stress Hormone-activated Membrane Signaling in Mouse Hearts
Authors: Masahiro Doi, Youyang Zhao, Takeharu Hayashi, Nancy Dalton, Yusu Gu, Kirk L Peterson, Masahiko Hoshijima
Journal: Circulation (2007)

Caveolin-3 is a primary molecular component that forms caveolae, flask-shaped plasma membrane domains in cardiac and skeletal myocytes. Caveolae provide a critical micro-environment to receptors, ion channels and other membrane-bound molecules. In this study, we established a new caveolin-3 knockout (cav3−/−) mouse line and tested whether disruption of caveolin-3 alters the regulation of cardiac excitation-contraction coupling (ECC) by G-protein coupled receptor (GPCR) agonists, including beta-adrenergic agonists and urocortin 2 (Ucn2), a member of the corticotropin-releasing factor, which we have shown to have strong inotropic and lusitropic actions in normal and failing hearts (Bale TL. PNAS. 2004, 101: 3697–3702). We tested baseline phenotypes of our cav3−/− mice by echocardiography at 8, 20, 35 weeks old, as well as challenged with trans-aortic banding for 1 week and confirmed there is no overt cardiac dysfunction developed in these mice, in which missing of caveolae in cardiomyocytes was confirmed by electron microscopy. Cav3−/− mice (10–16 weeks old) and age-matched control C57BL/6 mice (wild type; WT) were first tested in in vivo hemodynamic studies. No obvious difference was observed at baseline between 2 groups. Ucn2 strongly enhanced cardiac contractility in WT. However, the response to Ucn2 was attenuated in cav3−/− (max dP/dt: 18869+−851 mmHg/sec in WT vs. 16797+−1891 in cav3−/−, p=0.01, min dP/dt: −10023+−1023 in WT vs. −8376+−716 in cav3−/−, p&lt;0.01 (ANOVA), n=3). We also tested single adult cardiomyocytes isolated from both animal groups. Consistently with hemodynamic results, Ucn2-dependent enhancement of cell shortening was significantly suppressed in cav3−/− (% sarcomere length shortening, %SLS: 15.17+−3.35% in WT vs. 9.78+−3.41% in cav3−/−, p&lt;0.01, n=26). In contrast, beta2 stimulant (combination of isoproterenol and CGP20712A) response was augmented in cav3−/− (%SLS: 7.44+−2.66% in WT vs. 9.65+−2.92% in cav3−/−, p=0.011, n=21). Calcium transient analyses with Fura2 supported these data. We conclude that caveolin-3 associated membrane micro-environment is critical for normal GPCR signaling and speculate their disease-related alterations affect ECC regulation by various stress-hormones.
Sarcoidosis presenting with pyoderma gangrenosum
Authors: P. Banerjee, C.A. Holden
Journal: British Journal of Dermatology (2002)

Journal Article Sarcoidosis presenting with pyoderma gangrenosum Get access P. Banerjee, P. Banerjee Department of Dermatology, Epsom and St Helier NHS Trust, Carshalton, Surrey, SM5, U.K. E‐mail: piu_b@hotmail.com Correspondence: Dr Piu Banerjee, Department of Dermatology, Queen Elizabeth Hospital Trust, Stadium Road, London SE18 4QH, U.K Search for other works by this author on: Oxford Academic Google Scholar C.A. Holden C.A. Holden Department of Dermatology, Epsom and St Helier NHS Trust, Carshalton, Surrey, SM5, U.K. E‐mail: piu_b@hotmail.com Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 146, Issue 1, 1 January 2002, Pages 169–171, https://doi.org/10.1046/j.1365-2133.2002.4513_6.x Published: 01 January 2002
Abstract 20407: Restoration of p21-Activated Kinase (Pak1) Activity Attenuates Arrhythmic Activity in a Dog Model of Atrial Fibrillation
Authors: Jaime DeSantiago, Dan J Bare, Yunbo Ke, R. J Solaro, Boaz Avitall, Rishi Arora, Kathrin Banach
Journal: Circulation (2014)

Introduction:  The mechanisms underlying the genesis of atrial fibrillation (AF) are not fully understood. Activation of the small GTPase Rac1 through production of reactive oxygen species (ROS) is believed to contribute to the development of an AF substrate. We identified Pak1 as an endogenous negative regulator of Rac1 and hypothesized that stimulation of Pak1 activity attenuates atrial arrhythmia by antagonizing ROS induced changes in Ca handling.   Method:  Tissue and isolated myocytes (left superior pulmonary vein, LSPV) were obtained from dogs with persistent AF (atrial tachypacing, 600bpm, 3 weeks) or sinus rhythm (SR) and changes in Pak1 expression were quantified by western blotting. Changes in [Ca] i  (fluo-4/AM) or ROS (fluorescent29,79-dichlorofluorescein, DCF) were monitored by confocal microscopy in isolated atrial myocytes (AMs). AMs from WT and Pak1 -/-  mice were used to determine the mechanism by which a decrease in Pak1 enhances arrhythmic activity.   Results:  For the first time we demonstrate that Pak1 is down regulated in the atria of the canine AF model (adjusted density: SR: 85.6±7.2 % vs. AF 50±8.1%, n=3; p -/-  mice and an increased number of delayed after depolarizations during Ctrl and AngII stimulation in isolated Pak1 -/-  AMs. On a cellular level Rac1 stimulation by AngII (1microM) induced exaggerated ROS production in Pak1 -/-  AMs (DCF(au): WT AngII : 4572±487, n=20 vs. Pak1 -/-  AngII : 11231±838, n=16, p i  (F/F 0 : WT AngII : 3.4±0.4 n=6 vs. Pak1 -/-  AngII : 4.1±0.4 n=9, p AF s prevented the AngII induced increase in DADs that was based on spontaneous Ca release.   Conclusion:  In AF ROS production is enhanced by down-regulation of Pak1, an endogenous negative regulator of Rac1. Restoring Pak1 activity could be a therapeutic strategy to attenuate ROS induced arrhythmia and remodeling.
Abstract 1356: Is Human Ventricular Fibrillation Different From Experimental Models?
Authors: Martyn P Nash, Ayman Mourad, Chris P Bradley, David J Paterson, Richard H Clayton, Peter M Sutton, Martin Hayward, Peter Taggart
Journal: Circulation (2007)

Introduction: There is a paucity of data on wavefront dynamics during human VF. Some experimental models show multiple small wavelets, whilst others implicate a single stationary rotor. We have studied human VF using phase and wavefront analysis based on global epicardial mapping. Methods: VF was induced by burst pacing in 10 patients undergoing routine cardiac surgery. For each subject, a 20 – 40 s episode of VF activity was sampled at 1 kHz using an epicardial sock containing 256 unipolar contact electrodes connected to a UnEmap system. Wavefronts were determined from the phase plane (based on de-trended voltage versus its Hilbert transform) using an active-edge algorithm to track the isolines of zero phase. Wavefront sizes and rotor statistics were tallied across all patients. Results: As illustrated, one or more wavefronts of at least 10 cm in size were present for 90% of the VF duration. Insert shows a polar projection of wavefronts between pairs of phase singularities. Large convoluted wavefronts were predominant with at least one wavefront of size &gt; 20 cm present for over half of the VF duration. Persistent epicardial rotors (defined as those with lifetimes greater than 1000 ms, or approximately 5 rotations) were present for more than 78% of the total VF duration, whilst two or more persistent rotors were present more than half of the time. Conclusion: Epicardial mapping in humans suggests that neither multiple wavelets nor a single persistent stationary rotor, as seen in experimental models, drive VF. Instead, in all subjects the predominant characteristic was multiple mobile rotors of moderate duration (1000 –7000 ms), which generated large make and break wavefronts.
Atopy and current intestinal parasite infection: a systematic review and meta‐analysis
Authors: J. Feary, J. Britton, J. Leonardi‐Bee
Journal: Allergy (2010)

To cite this article: Feary J, Britton J, Leonardi‐Bee J. Atopy and current intestinal parasite infection: a systematic review and meta‐analysis. Allergy 2011; 66 : 569–578. Abstract Background: The rate of increase in prevalence of allergic disease in some countries implies environmental exposures may be important etiological factors. Our aim was to undertake a systematic review and meta‐analysis of epidemiological studies to quantify the association between current intestinal parasite infection and the presence of atopy and to determine whether this relation is species specific. Methods: We searched MEDLINE, EMBASE, LILIACS and CAB Abstracts (to March 2009); reviews; and reference lists from publications. No language restrictions were applied. We included studies that measured current parasite infection using direct fecal microscopy and defined atopy as allergen skin sensitization or presence of specific IgE. We estimated pooled odds ratios (OR) and 95% confidence intervals (95% CI) using data extracted from published papers using random‐effects model. Results: Twenty‐one studies met our inclusion criteria. Current parasite infection was associated with a reduced risk of allergen skin sensitization OR 0.69 (95% CI 0.60–0.79; P &lt; 0.01). When we restricted our analyses to current geohelminth infection, the size of effect remained similar OR 0.68 (95% CI 0.60–0.76; P &lt; 0.01). In species‐specific analysis, a consistent protective effect was found for infection with Ascaris lumbricoides , Tricuris trichuria , hookworm and Schistosomiasis . There were insufficient data to pool results for atopy defined by the presence of specific IgE. Conclusion: Intestinal parasite infection appears to protect against allergic sensitization. Work should continue to identify the mechanisms of this effect and means of harnessing these to reduce the global burden of allergic disease.
Biosensors: Simple and Sensitive Point‐of‐Care Bioassay System Based on Hierarchically Structured Enzyme‐Mimetic Nanoparticles (Adv. Healthcare Mater. 9/2015)
Authors: Miju Kim, Min Su Kim, Soon Ho Kweon, Sanha Jeong, Mi Hyun Kang, Moon Il Kim, Jinwoo Lee, Junsang Doh
Journal: Advanced Healthcare Materials (2015)

An enzyme-mimetic nanoparticle-based point of care bioassay device is developed by J. Lee, J. Doh, and colleagues on page 1311 for rapid and sensitive detection of analytes. Digital images acquired by smart cellular phones allow quantifying the amounts of analytes. Using this new device, quantitative analysis of liquid sample is performed within 15 min with an order of magnitude enhancement of sensitivity compared with conventional Au nanoparticle-based devices.
Novel sequences and epitopes of diagnostic value derived from the <i>Anisakis simplex</i> Ani s 7 major allergen*
Authors: E. Rodríguez, A. M. Anadón, E. García‐Bodas, F. Romarís, R. Iglesias, T. Gárate, F. M. Ubeira
Journal: Allergy (2008)

Background: Anisakis simplex allergens may cause severe allergic reactions in infected patients. Human anisakiasis can be specifically diagnosed by detection of immunoglobulin E (IgE) antibodies against O ‐deglycosylated nAni s 7 allergen captured by monoclonal antibody (mAb) UA3 (UA3‐ELISA), although the nature of this important allergen is unknown. The aim of this study was to clone and characterize the Ani s 7 major allergen, and to obtain a recombinant fragment suitable for serodiagnosis. Methods: An Anisakis cDNA library was screened with mAb UA3 and a cDNA clone (rAni s 7) encoding a 1096‐amino acid fragment of Ani s 7 (GenBank: EF158010 ) was identified. Bioinformatic tools and immunological and biochemical techniques were used to characterize the allergen obtained. Results: The rAni s 7 fragment comprised 19 repeats of a novel C X 17−25 C X 9−22 C X 8 C X 6 tandem repeat motif not seen in any previously reported protein sequence. An internal 435 Met– 713 Arg fragment of the rAni s 7 (t‐Ani s 7) was expressed in Escherichia coli and evaluated for serodiagnostic utility. Indirect enzyme‐linked immunosorbent assay (ELISA) with t‐Ani s 7 identified as positive the same 60 sera as UA3‐ELISA. The sequence MCQCVQKYGTEFCKKRLA from rAni s 7 was identified as the epitope recognized by mAb UA3, and is the target for over 60% of human IgE antibodies that react with O ‐deglycosylated nAni s 7. Conclusions: In addition to their clear value for serodiagnosis of human anisakiasis, the nature of the novel sequences and epitopes identified in the Ani s 7 allergen are of interest for a better understanding of the mechanisms operating in Anisakis ‐induced allergy.
Mast cells are critically involved in serum-mediated vascular leakage in chronic urticaria beyond high-affinity IgE receptor stimulation
Authors: F. Bossi, B. Frossi, O. Radillo, M. Cugno, A. Tedeschi, P. Riboldi, R. Asero, F. Tedesco, C. Pucillo
Journal: Allergy (2011)

To cite this article: Bossi F, Frossi B, Radillo O, Cugno M, Tedeschi A, Riboldi P, Asero R, Tedesco F, Pucillo C. Mast cells are critically involved in serum-mediated vascular leakage in chronic urticaria beyond high-affinity IgE receptor stimulation. Allergy 2011; 66: 1538–1545. Background: Chronic urticaria (CU) is one of the most common skin disorders whose pathogenic mechanisms are not fully clarified. Autoimmune aetiology can be ascribed to 45% of patients with CU, and basophil histamine release is positive in 40% of cases. Our aim was to use a novel approach to evaluate the serum permeabilizing effect to identify the mediators of endothelial cell (EC) leakage and to define the role of mast cells (MCs) in the process. Methods: Permeabilizing activity of sera from 19 patients with CU and 11 healthy blood donors was evaluated by measuring serum-induced degranulation of two MC lines, expressing (LAD2) or lacking (HMC-1) the IgE receptor. Mast cell supernatant (SN) was then incubated with an EC monolayer, and endothelial permeability was evaluated by Fluorescein isothiocyanate–bovine serum albumin leakage in a transwell system. Results: All 19 patient sera failed to induce direct EC leakage, but 15/19 and 17/19 promoted degranulation of HMC-1 and LAD2, respectively. Interestingly, 85% of autologous serum skin test-negative sera were able to cause MC degranulation. Also, 17/19 SNs from HMC-1 and all SNs from LAD2 incubated with CU sera increased endothelial permeability. Endothelial cell leakage remained unchanged after Ig depletion and was prevented by antihistamine, platelet-activating factor or leukotriene antagonist. Conclusions: Our study shows that CU sera are able to degranulate MCs through an IgE- and IgG-independent mechanism. The nature of histamine-releasing factors involved is still unclear, but our finding opens new ways to the understanding of the pathogenesis of CU, particularly in patients not showing circulating autoantibodies to FcεRI or IgE.
Modern Aspects of the Diagnosis, Classification and Treatment of Tuberculosis.
Authors: J. H. Elliott
Journal: JAMA (1928)

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
MRI Reveals Gene Activity In Vivo
Authors: Bridget M Kuehn
Journal: JAMA (2005)

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
High-concentration all-trans retinoic acid induces dermal inflammation and reduces the accumulation of type I procollagen in human skin in vivo
Authors: H.S. Yoon, Y.K. Kim, J.H. Chung
Journal: British Journal of Dermatology (2011)

Background Because inflammation is a factor promoting ageing, all‐trans retinoic acid (RA)‐induced irritation may have a negative influence on collagen accumulation in human skin despite its stimulation of collagen production. Objectives To determine whether RA‐induced irritation detrimentally affects RA efficacy as represented by new collagen synthesis. Methods Retinoic acid (0·01%, 0·025% or 0·05%) or vehicle was applied to the buttock skin of elderly male volunteers three times a week for 8 weeks under continuous occlusion. Every 2 weeks, biopsy specimens were obtained and immunohistochemical analysis was performed to determine levels of type I procollagen expression and inflammatory cell infiltration. Results Topical RA regardless of concentration increased type I procollagen expression in human skin in vivo after 2 weeks. However, only 0·01% RA continuously increased type I procollagen expression up to 8 weeks. After 4 weeks, significant infiltrations of macrophages and neutrophils were observed in 0·025% and 0·05% RA‐treated skin, and procollagen expression had returned to baseline. Conclusions Excessive RA‐induced inflammation might prevent collagen accumulation in aged skin despite the positive effect of RA on collagen production.