tbuckley/cabot-search huggingface dataset:
Abstract 16518: Inhibition of Inositol (1,4,5)-Trisphosphate Signaling in the Mouse Heart Attenuates Cardiac Hypertrophy after GPCR Stimulation.
Authors: Hiroyuki Nakayama, Ilona Bodi, Jeffery D Molkentin
Journal: Circulation (2010)

Introduction: Alterations in intracellular calcium (Ca2+) handling is hypothesized to underlie cardiac disease through activating calcium-dependent signaling pathways such as calcineurin. However the true nature of the Ca2+ alteration that induces reactive signaling remains unknown, especially given the backdrop of cyclical release of Ca2+ in the heart. Ca2+ release from cardiac inositol (1,4,5)-trisphosphate (IP3) receptors may produce a specialized microdomain for activating calcium-sensitive signaling pathways. IP3-sponge (IP3SP) is a recombinant protein generated from IP3 binding core in IP3 receptor (IP3R) which displays 500-fold higher affinity to IP3 compared with IP3Rs and inhibits IP3 signaling by chelating IP3 in vitro. Hypothesis and Methods: To determine if inhibition of Ca2+ release from IP3R attenuates cardiac growth and deleterious signaling, we generated transgenic (TG) mice with cardiac-specific expression of the IP3SP protein. [Results] Two TG lines were obtained and the higher expressin...
Grand Rounds: Outbreak of Hematologic Abnormalities in a Community of People Exposed to Leakage of Fire Extinguisher Gas
Authors: Shih-Hsiang Lo, Chang-Chuan Chan, Wei-Chin Chen, Jung-Der Wang
Journal: Environmental Health Perspectives (2006)

Although there are ample data on the respiratory effects of exposure to fire extinguisher gas, the potential hematologic effects have not been fully documented. We conducted this study to determine the possible etiologic agent(s) for a decrease in red blood cells among community residents in Taipei, Taiwan, after they were exposed to leakage of mixed fire extinguishants containing bromotrifluoromethane (CF3Br, Halon 1301), bromochlorodifluoromethane (CF2BrCl, Halon 1211), and dichlorodifluoromethane (CCl2F2, CFC-12).We studied 117 exposed residents who came into one hospital for physical examinations. We also selected age- and sex-matched referents for comparison from residents who came to the same hospital for health examinations. Nine months after the exposure to mixed fire extinguishants, 91 of the exposed residents came back for a second physical examination. In the first examination of the exposed residents, we found a significant reduction in red blood cell count and hemoglobin and a relationship between dose and response.After excluding iron-deficiency anemia, thalassemia, and other possible agents, we suspected that the hematologic effects might have resulted from pyrolytic products of CFC-12 and Halon 1211, which may contain phosgene, among other products.The acute transient hematologic effects observed in the exposed residents were associated with the incident of leakage of mixed fire-extinguisher gases and were most likely caused by a small amount of pyrolytic products, probably phosgene. Nine months after the exposure, we found a significant improvement in the abnormalities without any specific treatment.
Prednisolone Resistance in Childhood Acute Lymphoblastic Leukemia: Vitro-Vivo Correlations and Cross-Resistance to Other Drugs
Authors: G.J.L. Kaspers, R. Pieters, C.H. Van Zantwijk, E.R. VanWering, A. Van Der Does-Van Den Berg, A.J.P. Veerman
Journal: Blood (1998)
Child and Adolescent Obesity: Causes and Consequences, Prevention and Management
Authors: Youfa Wang
Journal: JAMA (2003)

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
Measuring symptoms of grief and bereavement
Authors: Sidney Zisook, Richard A. Devaul, Maurice A. Click
Journal: American Journal of Psychiatry (1982)

As part of an effort to develop an instrument to measure grief, a 58-item questionnaire was completed by 211 subjects who had lost a loved one because of death. The results demonstrated wide individual variations in specific symptoms and in their intensity and duration. Long after the immediate grief period, most bereaved individuals continued to feel upset, empty, or tearful; many experienced anniversary reactions and/or physical symptoms; and some had persistent identification phenomena. Although the acute dysphoria peaked between 1 and 2 years, several grief-related feelings, symptoms, and behaviors continued indefinitely. The relevance of present work and directions for future studies are discussed.
LAHB obscuring RBBB.
Authors: A Mayorga-Cortes, A Castellanos, R J Myerburg
Journal: Circulation (1980)

procainamide.We clearly showed in dogs1 and have recently confirmed in man2 that the two drugs have different electrophysiologic effects.Woosley et al.3 have recently reported that antiarrhythmic response to one drug does not necessarily mean response to the other.Thus, just because a patient responds to procainamide there is absolutely no guarantee that that patient will respond to NAPA, because the drugs probably have different mechanisms of action.To date there are only a small number of publications in relatively small numbers of patients indicating that NAPA is an efficacious antiarrhythmic agent.We would prefer to await the results of further clinical trials which might help to establish its appropriate role as an antiarrhythmic agent before recommending its widespread use.
IgG-induced clustering of desmogleins 1 and 3 in skin of patients with pemphigus fits with the desmoglein nonassembly depletion hypothesis
Authors: D.A.M. Oktarina, G. van der Wier, G.F.H. Diercks, M.F. Jonkman, H.H. Pas
Journal: British Journal of Dermatology (2011)

Background In pemphigus circulating IgG is present with the desmosomal cadherins desmoglein (Dsg) 1 and 3. In the epidermis of patients, this IgG deposits in a pattern that is often partly granular and does not reflect the normal Dsg distribution. Objective To understand why the IgG deposits in a granular pattern in the skin of patients with pemphigus. Patients/Methods We analysed the distribution of IgG and desmosomal adhesion molecules in skin biopsies of 18 patients with pemphigus vulgaris (PV) and 10 with pemphigus foliaceus (PF) by double staining immunofluorescence. The effect of IgG on desmosomal proteins was studied in an in vitro skin model. Results In PF skin Dsg1, but not Dsg3, was aberrantly distributed in the same partly granular pattern as the IgG. Vice versa, in skin of PV patients with anti‐Dsg3 antibodies, Dsg3, but not Dsg1, colocalized with the granular IgG. Plakoglobin also coclustered with IgG and Dsg, but this was far more prominent with Dsg1 than with Dsg3. In areas of heavy Dsg1 clustering, but not in areas of heavy Dsg3 clustering, intercellular widening between keratinocytes was present. Patient IgG, but not Fab fragments, induced the same Dsg clustering in vitro. Conclusions The IgG‐induced clustering of the Dsg autoantigens underlies the granular IgG deposition in patient skin. In PF and in mucocutaneous PV, Dsg1 clustering, but not Dsg3 clustering, correlates with nonacantholytic intercellular widening between desmosomes. In the patient the Dsg becomes sequestered from desmosomal components which fits in with the desmoglein nonassembly depletion hypothesis, indicating that targeted nonjunctional Dsg is no longer available to be incorporated into desmosomes and this leads to disturbed assembly, and Dsg‐depleted desmosomes.
Abstract 838: Establishment, identification and treatment data of TCGA glioblatoma xenograft subtypes
Authors: Stephen T. Keir, B Ahmed Rasheed, Katherine A. Hoadley, Martin A. Roskoski, Danuta Gasinski, Patrick J. Killela, Hai Yan, Madan M. Kwatra, Henry S. Friedman, Darell D. Bigner
Journal: Cancer Research (2014)

Abstract The Cancer Genome Atlas (TCGA) Network recently catalogued recurrent genomic abnormalities in glioblastoma (GBM). This genomic profiling lead to the molecular classification of GBMs into four subtypes: Proneural, Neural, Classical and Mesenchymal. The importance of identifying these subtypes helps researchers and clinicians to better understand GBMs with the potential to personalize treatment options and explore different therapeutic approaches that each subtype may require. In addition, the TCGA identified possible mechanisms that can cause some GBM tumors to become resistant to therapy, including the standard of care alkylating agent temozolomide (TMZ). For this project, we established xenografts using patient derived tissue and passaged these xenografts until reliable growth characteristics were obtained. Established GBM xenografts were classified into TCGA-defined subtypes first by obtaining global gene expression data using the GeneChip Human Genome U133A 2.0 array from Affymetrix. Microarray data was then quantile normalized and probes were summarized as gene expression levels using RMA. Then data was log2 transformed and genes median centered. Xenografts were subsequently classified into one of four previously defined subtypes as described using Classification to the Nearest Centroid (ClaNC) with the TCGA GBM data as the training dataset. Using established xenografts from each subtype, a panel of standard of care treatment agents (including TMZ) was assessed by delay in tumor growth and by tumor regression. Statistical analysis was performed using a SAS statistical analysis program, the Wilcoxon rank order test for growth delay, and Fisher's exact test for tumor regression. Data regarding each xenografts BRAF, EGFR, EGFRvIII, IDH1, PIK3CA, PIK3R1, PTEN, RB1, TERT and TP53 status is reported within. The identification of these valid xenograft models represents an important contribution toward the ability of studying GBM subtypes, in particular for modeling and predicting therapeutic response. Citation Format: Stephen T. Keir, B Ahmed Rasheed, Katherine A. Hoadley, Martin A. Roskoski, Danuta Gasinski, Patrick J. Killela, Hai Yan, Madan M. Kwatra, Henry S. Friedman, Darell D. Bigner. Establishment, identification and treatment data of TCGA glioblatoma xenograft subtypes. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 838. doi:10.1158/1538-7445.AM2014-838
Abstract P5-20-04: Autophagy promotes escape from PI3K inhibition in ER+ breast cancer
Authors: Wei Yang, Todd W Miller
Journal: Cancer Research (2015)

Abstract PI3K inhibitors have shown promise for the treatment of ER+ breast cancers. Autophagy has been suggested to promote resistance to PI3K inhibitors. Interestingly, cancer cells often exhibit basal levels of autophagy, which is thought to serve as a mechanism to manage oxidative stress and remove damaged organelles (e.g., mitochondria). Pharmacodynamic analysis of the orally available pan-PI3K inhibitor GDC-0941 at low (100 mg/kg) and high (800 mg/kg) doses, and 2 low doses administered 12 hours apart (BID), in combination with fulvestrant in mice bearing MCF-7 xenografts revealed that treatment induced accumulation of LC-3 II (marker of autophagy) after 24-48 h. In ER+ breast cancer cells cultured in hormone-depleted medium, PI3K inhibition gradually induced apoptosis while increasing LC-3 II. Autophagy promotes glucose metabolism, and PI3K activation is a major driver of glucose uptake. We thus hypothesized that inhibition of autophagy will potentiate the anti-tumor effects of PI3K inhibition by suppressing glucose metabolism. Chloroquine (CQ) is an anti-malarial drug that inhibits autophagy in mammalian cells by an unknown mechanism. CQ inhibited proliferation and autophagy in ER+ breast cancer cells in vitro. CQ treatment potentiated GDC-0941-induced inhibition of cell proliferation and promotion of apoptosis in growth conditions (10% FBS) with or without fulvestrant, and in hormone-depleted conditions (10% DCC-FBS). CQ treatment increased PI3K inhibitor-induced mitochondrial membrane depolarization, suggesting that this drug combination engages an intrinsic apoptotic pathway. PI3K inhibition also induced autophagy in fulvestrant-resistant MCF-7/FR and CAMA-1/FR cells. CQ increased GDC-0941-induced apoptosis in MCF7/FR and CAMA-1/FR cells, offering combined targeting of PI3K and autophagy as a promising therapeutic strategy for the treatment of anti-estrogen resistant breast cancer. Mice bearing ZR75-1 xenografts are currently being treated with vehicle, CQ (2 mg/day via drinking water), 800 mg/kg GDC-0941 QW, or the combination. Thus far, single-agents treatments significantly inhibit tumor growth. However, the drug combination has not shown synergistic effects in vivo. Analysis of different doses and schedules of GDC-0941 plus CQ, with or without anti-estrogen treatment, is ongoing. Citation Format: Wei Yang, Todd W Miller. Autophagy promotes escape from PI3K inhibition in ER+ breast cancer [abstract]. In: Proceedings of the Thirty-Seventh Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2014 Dec 9-13; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2015;75(9 Suppl):Abstract nr P5-20-04.
Abstract 12602: Silent Ischemic Brain Lesions Related to the Presence of Atrial High Rate Episodes in Patients With Cardiac Implantable Electronic Devices
Authors: Juan Benezet-Mazuecos, Jose Manuel Rubio, Jose Antonio Iglesias, Juan Jose de la Vieja, Soraya Calle, Marcelino Cortes, Miguel Angel Quiñones, Pepa Sanchez-Borque, Jeronimo Farre
Journal: Circulation (2014)

Introduction:  The enhanced monitoring capabilities of cardiac implantable electronic devices (CIED) have revealed that a large proportion of patients present silent atrial fibrillation (AF) detected as atrial high rate episodes (AHRE).   Hypothesis:  AHRE >5min have been linked to increased risk of clinical stroke, but a high proportion of ischemic brain lesions could be subclinical and thromboembolic risk underestimated. Cranial CT-scan can detect silent lesions to determine the real risk these patients are exposed to.   Methods:  We analyzed prospectively the incidence of AHRE > 5 min compatible AF in patients in sinus rhythm with dual chamber cardiac devices and the presence of ischemic brain lesions on CT-scan.   Results:  125 patients (54% men, aged 75 ± 10 years) were evaluated. Mean CHADS2 and CHA2DS2VASc scores were 2,3 ± 1,4 and 4,0 ± 1,7 respectively. History of AF was present in 27 patients (21%). After 12 months, 40 patients (32%) showed at least one AHRE >5min. Patients with AHREs were more likely to have history of AF (40% vs 13%). CT-scan showed silent ischemic brain lesions in 32 (25%). The presence of silent infarcts was significantly related to older patients, prior history of AF or stroke/TIA, higher CHADS2 or CHA2DS2VASc scores, small vessel disease and the presence of AHRE >5min. Table. Multivariable analyses demonstrated that the presence of AHRE >5min was an independent predictors for silent ischemic lesions in overall population (OR 3.39 [1.12 - 10.25; p    Conclusions:  CIED can accurately detect AF as AHRE. AHRE were independently associated to a higher incidence of silent ischemic brain lesions on CT-scan. Moreover, patients without history of AF or stroke/TIA presenting AHRE showed a higher risk for silent ischemic brain lesions. AHRE represent a kind of silent AF where management recommendations are lacking despite the fact that a higher embolic risk is present.
Bronchial stump insufficiency after pneumonectomy in purulent-destructive diseases of lungs
Authors: Shuhrat Hudaybergenov, Georgy Pahomov, Rustem Hayaliev, Ortikali Irisov, Otabek Eshonhodjaev, Sharif Rahimiy
Journal: European Respiratory Journal (2011)

As is well known, bronchial stump insufficiancy (BSI), bronchopleural fistulas (BPF) and connected with them empyema pleura are the main reasons of the reduction to efficiency of the surgical treatment of lung cancer, purulent-destructive diseases of lungs (PDDL) and other surgical pathology of thorax.

Material and methods: Results of complex examination and treatment of 684 patients had comparative analysed, from which 575 (84,1%) patients underwent pneumonectomy (PE) on cause oncological pathology or PDDL, but 109 (15,9%) patients were treated on cause BPF after PE. The average age 56,4±4,1 years. The main group has formed 98 patients, admitted for 2006-2008 and undertaken designed tactics of the surgical treatment, founded on determination of the groups of the risk of the development BSI after PE.

Results: The frequency BSI after PE depending on presence different factor among 87 patients with PDDL was apart considered. PE is on the right made in 25 (28,7%) patients, on the left in 62 (71,3%) patients. BSI after PE is revealled in 4 (16,0%) and 7 (11,3%) accordingly. PE on cause PDDL noted increasing of the frequency BSI from 10,5% to 12,6% (11 from 87 patients), and risk of the development of this complication, depending on side of the operations forms - 16,0% after right-side and 11,3% after leftside PE.

Conclusions: In patients of oncological profile, which is planned PE, frequency of accompanying COPD forms 53,8% patient then in patients with PDDL this factor reaches 75,2%, in turn exacerbation COPD after performing PE noted in 48,8% and 63,6% patients accordingly, but risk of the development BSI on this background reaches 16,5% that requires including in the treatment nebulised therapy.
Abstract 16279: Traumatic Brain Injury-Induced Increased Pial Venular Permeability is Ameliorated With Endothelial Progenitor Cells and the Stromal Vascular Fraction Cells in Mice
Authors: Nino Muradashvili, Reeta Tyagi, Jacob Dale, Richard L Benton, Suresh C Tyagi, Timothy E O’Toole, James B Hoying, David Lominadze
Journal: Circulation (2014)

Traumatic brain injury (TBI) is a devastating public health problem worldwide. It is accompanied with an increased cerebrovascular permeability to blood proteins. It is suggested that impairment in endothelial cell properties can be a main cause of enhanced vascular permeability, and thus vasculo-neuronal degeneration. We tested the hypothesis that TBI-induced an increase in cerebrovascular permeability can be ameliorated by repairing vascular endothelium via increasing number of endothelial progenitor cells (EPCs) or injecting the stromal vascular fraction cells (SVFCs) based on their capacity of self-regeneration. Permeability of pial venules in pericontusional area was studied in C57BL/6J mice brain after mild TBI. Mouse bone marrow-derived cells were grown on tissue culture plates to confluence and Flk-1+/Sca-1+ (markers of endothelial and stem cell phenotype, respectively) EPCs were isolated by flow cytometry sorting. SVFCs from mouse adipose tissue were collected via enzymatic tissue dissociation. After induction of mild TBI, mice were infused with EPCs or with SVFCs (~106 cells) suspended in 100 μl of phosphate buffered saline (PBS) or with PBS alone (control group) through the tail vein. After 10-14 days, pial venular permeability in these mice was assessed by measuring the extravascular accumulation of fluorescently-labeled bovine serum albumin (BSA) using an intravital fluorescence microscope. The protein leakage to interstitium was analyzed by changes in the ratio of fluorescence intensity in the interstitium to that inside the respective vascular segment. The measurements were done 1 hour after injection of BSA and were expressed as a percent of baseline (10 minutes after BSA injection). Cerebrovascular leakage was lesser in mice infused with EPCs (136 ± 4 % of baseline) and with SVFCs (131 ± 3 %) compared to that in mice infused with PBS alone (186 ± 6 %). These results suggest that TBI-induced increased cerebrovascular permeability can be reversed by enhancing the number of EPCs and with SVFCs, which can restore impaired property of vascular endothelium or cerebral microvascular network in pericontusional area. Our data indicate a novel functional role of EPCs and SVFCs in post-TBI treatment of cerebrovascular pathology.
Hypnotism. Its History, Practice and Theory.
Authors: Bramwell, J. Milne , b.
Journal: JAMA (1904)

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