tbuckley/cabot-search huggingface dataset:
Abstract 17840: Progression of Cardiovascular Risk Factors Across the Menopausal Transition - Results from Study of Women’s Health Across the Nation
Authors: Zubair A Khan, Imke Janssen, Lynda H Powell, Andrius Dumasius, Susan A Everson-Rose, Emma J Barinas-Mitchell, Perry J Weinstock, Steven M Hollenberg
Journal: Circulation (2014)

Objectives: To correlate arterial compliance and measures of subclinical atherosclerosis with menopausal status during menopausal transition. Background: Cardiovascular risk increases in women after the menopausal transition. To assess factors that might explain this increased risk, we used radial tonometry to measure arterial compliance in SWAN (Study of Women’s Health Across the Nation), a longitudinal study of women in the menopausal transition. Methods: Raw waveforms were digitized and a generalized transfer function was utilized to calculate central Augmentation Pressure (cAP) &amp; aortic Augmentation index (AIx) adjusted for heart rate of 75bpm. Carotid intima-media thickness (cIMT) was calculated using B-mode ultrasound. Coronary artery calcium (CAC) and thoracic aortic calcium (TAC) scores were obtained by computed tomography. Pulse wave velocity (PWV) was recorded as time taken for the arterial pulse to propagate from the carotid to the femoral artery. Results: Mean age was 52±9, BMI 28±6; 7% of women were premenopausal, 48% perimenopausal, and 45% were postmenopausal. PWV, cAP, cIMT, CAC and TAC were higher in post-menopause than peri-menopause and lowest in the premenopausal group with a similar trend for AIx (see Table). Higher PWV correlated significantly with higher cIMT (r=0.32), cAP (r=0.34), AIx (0.17), CAC (r=0.13) &amp; TAC (r=0.19). Conclusion: Physiologic measures of arterial stiffness were higher through the menopausal transition along with morphologic measures of subclinical atherosclerosis, with a correlation between the two. Such changes may help to explain the increased risk of cardiovascular disease in women after menopause and may be assessed using a combination of physiologic and morphologic parameters. Supported by NIH/DHHS (grants U01AG012505, U01AG012546, R01HL065581, R01HL065591, R01HL089862).
The effects of weapons and the Solferino cycle
Authors: R. M Coupland
Journal: BMJ (1999)

When designers of weapons want to know if their creations are effective they observe the simulated effects of those weapons so they can modify and develop them and, in a cycle of activities, test them again. They then want to observe the real effects after the weapons have been produced, transferred into the hands of users, and used against their intended human target. Observing and documenting the real effects of weapons in the field, however, falls to health professionals rather than to weapons designers. The observation and documentation of the effects of weapons then forms an essential part of another cycle of activities. Instead of providing feedback about weapon design, this second cycle works in the interests of the victims of weapons by generating policies and laws that impose limits on the design, production, transfer, or use of weapons.

The original turn of this second cycle was initiated by Henry Dunant, who observed the effects of munitions on soldiers at the Battle of Solferino in 1859. Until then Europe's aristocracy had seen war as glorious. Dunant's documentation of the reality in A Memory of Solferino changed this perception.1 In 1863 he and four other Genevan dignitaries created the International Committee of the Red …
Abstract 13350: Cardiac-specific Deletion of GSK-3α and GSK-3β Leads to Fatal Dilated Cardiomyopathy With Mitotic Catastrophe
Authors: Jibin Zhou, Firdos Ahmad, Hind Lal, Shan Parikh, Nichole E Hoffman, Sudarsan Rajan, Santhanam Shanmughapriya, Xiaoxiao Zhang, Yuanjun Guo, Ancai Yuan, Jianliang Song, Xiongwen Chen, Muniswamy Madesh, James R Woodgett, Raj Kishore, Thomas L Force
Journal: Circulation (2014)

In mammals, glycogen synthase kinase-3 (GSK-3) exists as two homologs, GSK-3α and GSK-3β, encoded by independent genes which share similar kinase domains but differ substantially in their N and C termini. Previously we have shown that cardiomyocyte specific deletion of 2 functional GSK-3α or 2 functional GSK-3β alleles has a negligible role in normal homeostasis of myocardial biology. In contrast, herein we describe the creation of mice that are specifically targeted to lack 3 or 4 GSK-3 alleles. Mice lacking any 3 of the alleles live longer than 120 days but develop cardiac hypertrophy and display impaired cardiac function assessed by hemodynamics. Mice lacking all four alleles (double knockout, DKO) develop profound dilated cardiomyopathy and heart failure, leading to death. Pathologically, the hearts of DKOs show giant myocardial nuclei, multi-nucleation, metabolic abnormalities including excess glycogen deposition, degeneration and cell death; and fibrotic remodeling. Microarray and functional pathway analysis demonstrate that these disturbances arise from marked disorders of the cell cycle. Western blot and immunofluorescence confocal microscopy show dysregulated expression of major cell cycle/checkpoint markers, apoptotic proteins and DNA damage markers. These findings indicate that the cardiomyocyte undergoes cell cycle initiation, but this is followed by mitotic catastrophy, DNA damage and apoptosis. This study confirms that GSK-3 is a central regulator of the cell cycle in the heart.
Polio Eradication Goal Still Elusive
Authors: Mike Mitka
Journal: JAMA (2004)

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
Evidence for bone marrow-derived endothelial cells incorporation into perfused blood vessels in tumors
Authors: Dan G. Duda, Kenneth S. Cohen, Sergey V. Kozin, Jean Y. Perentes, Dai Fukumura, David T. Scadden, Rakesh K. Jain
Journal: Cancer Research (2006)

3991   The contribution of bone marrow-derived endothelial cells (BMD-ECs) to blood vessels in postnatal life (adult vasculogenesis) remains controversial. BMD-EC involvement in tumor neovascularization has been reported to be significant to undetectable in some of the same tumor models. Other studies have identified hematopoietic cells incorporated into the endothelial lining of tumor vessels. In this context, the extent to which bone marrow-derived cells incorporate as bona fide endothelial (non-hematopoietic) cells into perfused tumor vessels, or any new vessels formed postnatally (vasculogenesis), is unclear. To this end, we developed models to characterize local vessel-derived and bone marrow-derived endothelial cells (BMD-ECs) using detection of a fluorescence reporter gene by in vivo multiphoton and ex vivo confocal microscopy techniques, as well as flow cytometry of enzymatically-digested tissues. Then, we quantified their contribution to perfused blood vessels in tumors using three transplanted tumor models, as well as in four spontaneous primary tumors and two metastatic models. By defining the endothelial cells based on their morphology, phenotype (i.e., endothelial markers such as Tie2, CD31, lack of CD45 expression), and function (i.e., blood perfusion), we demostrate that the process of neovascularization directly involves BMD-ECs. We demonstrate that BMD-ECs incorporate in perfused tumor vessels to a highly variable degree (from less than 1% to 58%). BMD-EC contribution to functional vessels was different for the same tumor type in different organ site, and varied with mouse strain. Furthermore, we observed that adipose tissue vasculature in aging obese mice||but not in young obese mice||contains BMD-ECs. This suggests a long-term re-population in certain tissues by bone marrow-derived cells. Collectively, these findings offer direct evidence for vasculogenesis during isografted tumor growth and metastasis in genetically unaltered mice. Many tumors are associated with extensive bone marrow-derived cell infiltration and thus, characterization of the roles of different subsets of bone marrow-derived cells in tumor growth, progression, metastasis and response to treatment may identify new therapeutic targets.
Abstract 3620: Neuropeptide signaling activates Type-1 immunity through the NK1 and NK2 receptors on human dendritic cells
Authors: Hidemitsu Kitamura, Junya Ohtake, Shun Kaneumi, Kazutaka Masuko, Kentaro Sumida, Satoshi Terada, Takuto Kishikawa, Yosuke Ono, Toshiyuki Kita, Hiroya Kobayashi
Journal: Cancer Research (2014)

Abstract Dendritic cells (DCs), representative antigen-presenting cells, effectively induce antigen-specific immune responses through activation of CD4+T and CD8+T cells. In tumor microenvironments, DCs uptake tumor-derived antigens, and generate helper T cells and cytotoxic T lymphocytes (CTLs), which recognize and kill the target tumor cells in response to the antigens. Thus, proper regulation of DC function is important for tumor immunology. Substance P (SP) and Neurokinin A (NKA), neurotransmitters, are widely distributed in both central and peripheral nervous system. Recently, we demonstrated that IFN-γ remarkably induced neurokinin-2 receptor (NK2R) expression human monocyte-derived dendritic cells. These findings strongly suggested that neuropeptide-signaling cascade might be closely related with regulation of DC-mediated immune responses. To elucidate the precise role of such neuro-immune crosstalk, we further investigated the effect of neuropeptide signaling on function of human DCs. At first, we found that both neurokinin-1 receptor (NK2R) and NK2R mRNA expressions were significantly enhanced by IFN-β, IFN-γ, LPS, or poly I:C stimulation with human DCs generated from peripheral blood mononuclear cells (PBMCs). In addition, we confirmed that the upregulation of NK1R and NK2R mRNA expressions was induced in a STAT-1-dependent manner. Surface expression levels of HLA-DR and costimulatory molecules on DCs, augmented by poly I:C, were modulated in the presence of specific inhibitors against NK1R or NK2R. On the other hand, we confirmed that blockade of NK1R- and NK2R-mediated signaling cascade significantly suppressed cytokine productions by antigen-specific CD4+ T cells after the antigen stimulation with DCs. Finally, we found that human DCs also enhanced expression level of TAC-1 gene, which encodes SP and NKA, after the IFN-γ stimulation. Thus, these findings indicate that NK1R- and NK2R-dependent neuropeptide signaling regulate Type-1 immunity through the activation of DC function, suggesting that such neuro-immune cross-talk through SP-NK1R and NKA-NK2R cascade might be involved in various diseases caused by excessive Type-1-dominant immunity including cancer and infection with chronic inflammation. Citation Format: Hidemitsu Kitamura, Junya Ohtake, Shun Kaneumi, Kazutaka Masuko, Kentaro Sumida, Satoshi Terada, Takuto Kishikawa, Yosuke Ono, Toshiyuki Kita, Hiroya Kobayashi. Neuropeptide signaling activates Type-1 immunity through the NK1 and NK2 receptors on human dendritic cells. [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 3620. doi:10.1158/1538-7445.AM2014-3620
Abstract 2841: Characterization of ALK fusions in circulating tumor cells (CTCs) of NSCLC
Authors: David Lu, Rachel Krupa, Natalee Bales, Jessica Louw, Dena Marrinucci, Ryan Dittamore
Journal: Cancer Research (2014)

Abstract Background: Many NSCLC patients have insufficient tumor sample or have high co-morbidities preventing access to tissue biopsies for FISH or IHC to determine ALK fusion and subsequent eligibility to Crizotinib therapy. We developed a gene/protein assay for the ALK fusion and examined CTCs and CTC subpopulation incidence and molecular characterization in newly diagnosed NSCLC patients. Methods: 10 samples from newly diagnosed NSCLC patients prior to therapy were recruited and blood specimens were collected and shipped to Epic Sciences. 2/10 had known ALK rearrangement through tissue analysis. All nucleated cells were plated onto glass slides and subjected to IF staining and CTC identification by fluorescent scanners and algorithmic analysis. CTCs, defined as classic (CK+ CD45- w/intact DAPI nuclei and morphologically distinct), apoptotic (CK+, CD45-, non-intact nuclei) and CK- (CK-, CD45-, intact and distinct) were identified. Samples were characterized with ALK IF to assess expression. Patients with known ALK rearrangements in tissue also had their CTCs assessed with ALK FISH. Results: Assays for the ALK protein and ALK gene rearrangement were developed and specificity confirmed utilizing H2228 (ALK positive) &amp; A549 (ALK negative) cells spiked into donor blood and run through the Epic Assay. Expression of ALK fusions was visualized in CTCs of 1/2 patients with known ALK rearrangements and 0/8 patients with no ALK rearrangements. ALK fusion protein expression was seen in classic, apoptotic, small and CK- CTCs. Conclusion: ALK fusion protein and ALK rearrangement assessment with FISH utilizing the Epic CTC platform demonstrates sensitivity and specificity to identification of patients eligible to Crizotinib. The identification of ALK in CTC subpopulations identifies unique tumor cell morphology and suggests evidence of epithelial plasticity. Further clinical studies are ensuing to determine the sensitivity and specificity of ALK in CTCs and the relevance of CTC subpopulations related to Crizotinib therapy and NSCLC progression. Citation Format: David Lu, Rachel Krupa, Natalee Bales, Jessica Louw, Dena Marrinucci, Ryan Dittamore. Characterization of ALK fusions in circulating tumor cells (CTCs) of NSCLC. [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 2841. doi:10.1158/1538-7445.AM2014-2841
A pilot study of high-dose interleukin-3 treatment of relapsed follicular small cleaved-cell lymphoma: hematologic, immunologic, and clinical results [published erratum appears in Blood 1996 Jun 1;87(11):4922]
Authors: A Younes, A Sarris, U Consoli, A Rodriguez, P McLaughlin, Y Huh, S Starry, F Cabanillas, M Andreeff
Journal: Blood (1996)
Abstract 18520: Can Left Atrial Wall Area Strain Obtained by Three-dimensional Speckle Tracking Imaging Assess Left Ventricular Filling Pressure in Patients with Normal Left Ventricular Ejection Fraction?
Authors: Noriyuki Ikehara, Kazuaki Wakami, Toshihiko Goto, Tomonori Sugiura, Hidekatsu Fukuta, Tomomitsu Tani, Nobuyuki Ohte
Journal: Circulation (2014)

Left atrial (LA) reservoir and booster pump function plays substantially important roles in optimizing left ventricular (LV) filling pressure. Our hypothesis was that elevated LV filling pressure deteriorates LA deformation in patients with impaired LV relaxation, even if the LV ejection fraction (EF) is preserved. We investigated this issue by assessing LA wall area strain (AS) using the 3-dimensional speckle tracking imaging (3D-STI).   Methods:  Study subjects were 82 patients with sinus rhythm who underwent diagnostic cardiac catheterization and 3D-STI (Artida TM , Toshiba) on the same day. Twenty-seven of them were prior myocardial infarction, 7 were dilated cardiomyopathy, while remaining 48 had no localized LV wall motion abnormality. The temporal changes of global LA-AS were drawn offline using an echo image analyzer (Ultra-Extend TM , Toshiba). Both the peak LA-AS value at LV end-systole (peak AS) and the LA-AS value just before LA contraction (AS-preA) were measured as the parameters of LA function. Early mitral annular velocities (e’) at the both septal and lateral corners of the mitral annulus were obtained using tissue Doppler imaging. The patients with lateral e’   Results:  In all patients, the peak AS and the AS-preA significantly correlated with the m-LVDP (r=-0.70, p 50%, n=53), the peak AS and the AS-preA also significantly correlated with the m-LVDP (r=-0.67, p   Conclusions:  This study indicates that an elevated LA pressure could deteriorate both LA reservoir and booster pump function. LA-AS obtained by 3D-STI is an emerging parameter for the noninvasive prediction of m-LVDP, even in patients with preserved LVEF.
Characterization of a murine monoclonal antibody that mimics heparin-induced thrombocytopenia antibodies
Authors: G. M. Arepally, S. Kamei, K. S. Park, K. Kamei, Z. Q. Li, W. Liu, D. L. Siegel, W. Kisiel, D. B. Cines, M. Poncz
Journal: Blood (2000)
1918 Killer Flu Virus Reconstructed, May Help Prevent Future Outbreaks
Authors: Mike Mitka
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
Abstract 13649: Protective Role of Stat3 in Vascular Smooth Muscle Cells During the Development of Acute Aortic Dissection
Authors: Saki Hirakata, Hiroki Aoki, Michihide Nishihara, Satoko Ohno, Aya Furusho, Norifumi Nishida, Sohei Ito, Yoshihiro Fukumoto
Journal: Circulation (2014)

Acute aortic dissection (AAD) is a common and fatal disease for which pathogenesis is largely unknown. Recently we and others reported that JAK/STAT-activating cytokines are highly expressed in human and mouse models of AAD. We also reported in this meeting last year that STAT3 is activated both in macrophages and in vascular smooth muscle cells (VSMCs) during AAD development, and STAT3 activation in macrophages promotes AAD progression. However, the role of STAT3 in VSMCs is unknown in the context of AAD. To address this question, we used a mouse model of AAD that was induced by continuous infusion of beta-aminopropionitrile, an inhibitor of lysyl oxidase that cross-links collagen and elastin, and angiotensin II (BAPN+AngII). BAPN+AngII caused thoracic and suprarenal AAD starting at 7 days of the administration, and most of the mice developed AAD within 14 days. We first performed the transcriptome analysis 3 days after the BAPN+AngII infusion, when aorta showed no obvious structural changes. The induced genes by BAPN+AngII were enriched for those encoding proinflammatory cytokines. The suppressed genes by BAPN+AngII were enriched for those encoding extracellular matrix proteins that are normally maintained by VSMCs and cytoskeletons of VSMCs, indicating that profound changes in VSMCs function precedes AAD development. To investigate into the function of STAT3 in VSMCs, we used the smooth muscle-specific knockout mice for STAT3 (smSTAT3-KO). We also used the smooth muscle-specific knockout mice for SOCS3, a negative feedback regulator of STAT3, to enhance the STAT3 signal specifically in smooth muscle cells (smSOCS3-KO). We determined the AAD severity by the length of the lesions with enlarged aortic diameter. BAPN+AngII caused more severe AAD in smSTAT3-KO mice compared with wild type mice in the descending aorta (WT; 0.069±0.024 vs. smSTAT3; 0.214±0.084 mm/g body weight, P=0.028). In contrast, smSOCS3-KO mice developed less severe AAD in the aortic arch (WT; 0.093±0.018 vs. smSOCS3-KO; 0.018±0.013 mm/g body weight, P=0.014). These results indicate that dysfunction of VSMCs with proinflammatory response precedes the AAD development, and STAT3 activation in VSMCs protects aorta from AAD, possibly by maintaining the VSMC function.
Die experimentelle Pharmakologie als Grundlage der Arzneibehandlung.
Authors: Hans H. Meyer, R. Gottlieb, Ernst Peter Pick
Journal: JAMA (1926)

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