tbuckley/cabot-search huggingface dataset:
Abstract 20212: MicroRNA-34a Impairs Endothelial Progenitor Cell-Mediated Angiogenesis through Silent Information Regulator 1 Inhibition during Aging
Authors: Ting Zhao, Jian Li, Alex F Chen
Journal: Circulation (2010)

Background: Aging impairs angiogenesis and accelerates vascular disease with reduced eNOS function. EPCs are critically regulated by eNOS for angiogenesis, but have reduced proliferation and survival in aging. MiR-34a, a tumor suppressor, has been found to target silent information regulator 1 (Sirt1), leading to cell cycle arrest and apoptosis. However, whether miR-34a regulates EPC angiogenesis related to eNOS essential cofactor BH4 in aging is unknown. We tested the hypothesis that miR-34a impairs EPC angiogenesis through Sirt1 inhibition in aging. Methods and Results: Bone marrow-derived EPCs from young (8 weeks), aged C57BL/6 and eNOS/GTP cyclohydrolase I (endothelial-specific GTPCH, the rate-limiting enzyme for BH4) double-transgenic mice (18 months, all males) were used. In vitro EPC angiogenesis was impaired by 56% in aged vs. young mice (Matrigel tube formation, n=4, p<0.01). MiR-34a level in EPCs was increased by ∼1 fold in aged vs. young mice (real time PCR, n=4, p<0.01), paralleled with 46% re...
Prognostic Value of C-Reactive Protein in Unstable Angina
Authors: Pierfrancesco Agostoni, Giuseppe G.L Biondi-Zoccai
Journal: Circulation (2000)

the Editor:We appreciate the work by Ferreirós et al 1 in confirming the strong prognostic value of C-reactive protein (CRP) in unstable angina.However, we believe that some issues should be raised.First, the authors did not exclude patients with Braunwald type C unstable angina and they did not provide an explanation of this choice.Class C unstable angina has a strong prognostic role in prospective studies. 2,3Confirming this fact, in their Table 1, the time between prior acute myocardial infarction (AMI) and the occurrence of unstable angina was not specified, and the group of patients with raised CRP (Ͼ1.5 mg/dL) had a higher, yet not statistically significant, prevalence of prior AMI.In fact, the pathophysiological meaning of a raised CRP titer is quite different in a patient recovering from a recent AMI than in a patient with unstable angina without previous myocardial necrosis.Moreover, in the Results and Discussion sections, the authors did not emphasize the prognostic value of CRP in refractory angina alone.Instead, several prospective studies considered, in the outcome analysis, either major cardiac events (AMI/death) alone 4 or minor (recurrence of angina) and major cardiac events evaluated as different end points. 5
A novel antibody–drug conjugate targeting SAIL for the treatment of hematologic malignancies
Authors: S Y Kim, J-W Theunissen, J Balibalos, S Liao-Chan, M C Babcock, T Wong, B Cairns, D Gonzalez, E H van der Horst, M Perez, Z Levashova, L Chinn, J A D'Alessio, M Flory, A Bermudez, D Y Jackson, E Ha, J Monteon, M F Bruhns, G Chen, T-S Migone
Journal: Blood Cancer Journal (2015)

Abstract Although several new therapeutic approaches have improved outcomes in the treatment of hematologic malignancies, unmet need persists in acute myeloid leukemia (AML), multiple myeloma (MM) and non-Hodgkin’s lymphoma. Here we describe the proteomic identification of a novel cancer target, SAIL (Surface Antigen In Leukemia), whose expression is observed in AML, MM, chronic lymphocytic leukemia (CLL), diffuse large B-cell lymphoma (DLBCL) and follicular lymphoma (FL). While SAIL is widely expressed in CLL, AML, MM, DLBCL and FL patient samples, expression in cancer cell lines is mostly limited to cells of AML origin. We evaluated the antitumor activity of anti-SAIL monoclonal antibodies, 7-1C and 67-7A, conjugated to monomethyl auristatin F. Following internalization, anti-SAIL antibody–drug conjugates (ADCs) exhibited subnanomolar IC 50 values against AML cell lines in vitro . In pharmacology studies employing AML cell line xenografts, anti-SAIL ADCs resulted in significant tumor growth inhibition. The restricted expression profile of this target in normal tissues, the high prevalence in different types of hematologic cancers and the observed preclinical activity support the clinical development of SAIL-targeted ADCs.
Abstract 1535: Immunohistochemistry predicts presence and type of TP53 mutation in high-grade serous carcinoma
Authors: Martin Köbel, Anna Piskorz, Shuhong Liu, James D. Brenton
Journal: Cancer Research (2014)

Abstract TP53 mutations are ubiquitous to ovarian high-grade serous carcinomas (HGSC) but uncommon in other types such as endometrioid carcinomas. Despite the advances in direct sequencing, this technology is not widely available for routine diagnostics. Significant improvements in standardization of immunohistochemistry (IHC) have dramatically improved sensitivity. We hypothesized that the pattern of p53 expression by IHC can predict the presence and group of TP53 mutations: complete absence indicating null mutations versus overexpression indicating missense mutation. DNA extracted from 91 fresh frozen HGSC samples obtained from the Canadian Ovarian Experimental Unified Resource (COEUR) and from 66 formalin fixed paraffin embedded HGSC samples obtained from Calgary Laboratory Services were sequenced using TAmSeq methods for NGS. Additional Sanger sequencing was performed for confirmation or for identification of indel mutations. Accompanying tissue microarrays with 0.6 mm cores were constructed and immunohistochemistry for p53 was performed on a Leica Bond MAX platform using the DO-7 monoclonal antibody. The expression of p53 was scored in a 3-tier system: complete absence, wild type (any staining from 1-70%), overexpression (&amp;gt;70% strong nuclear staining). Cytoplasmic localization was noted separately. TP53 mutations were detected in 147/157 HGSC (94%). The type of mutation in descending order were missense 104/147 (71%), frameshift 17/147 (12%), stopgain 13/147 (9%), and splice site 13/147 (13%). 101/104 cases with TP53 missense mutations showed p53 overexpression (98% concordance) while 12/17 cases with frameshift, 11/13 cases with stopgain, and 7/13 with splicing (combined 70% concordance) showed the expected complete absence of p53 expression. The overall sensitivity of p53 IHC to predict the group of mutation was 89% (131/147). Only 6/147 (4%) cases with TP53 mutations showed a p53 wild type pattern, four those were splice site mutations, hence the sensitivity of p53 IHC to predict the presence of mutation is 94%. Interestingly, 7/10 cases with TP53 wild type or synonymous silent mutations showed aberrant p53 expression as either complete absence or overexpression, suggesting alternative abnormalities in the p53 pathway. The three cases with TP53 wild type and p53 wild type expression may not be HGSC. We conclude that contemporary p53 immunohistochemistry is a useful, widely accessible, inexpensive complimentary test for direct TP53 sequencing. Citation Format: Martin Köbel, Anna Piskorz, Shuhong Liu, James D. Brenton. Immunohistochemistry predicts presence and type of TP53 mutation in high-grade serous carcinoma. [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 1535. doi:10.1158/1538-7445.AM2014-1535
Housing for Homeless Adults With Mental Illness—Reply
Authors: Vicky Stergiopoulos, Stephen W. Hwang, Agnes Gozdzik
Journal: JAMA (2015)

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
Screening for Psychological Illness in the Military—Reply
Authors: Simon Wessely, Kenneth C. Hyams, Roberto J. Rona
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
CYCLIC 3',5' ADENOSINE MONOPHOSPHATE-DEPENDENT PROTEIN KINASE OF SKIN.
Authors: P. D. MIER, J. HURK
Journal: British Journal of Dermatology (1972)

Journal Article CYCLIC 3′,5′ ADENOSINE MONOPHOSPHATE‐DEPENDENT PROTEIN KINASE OF SKIN: I. MEASUREMENT AND PROPERTIES Get access P. D. MIER, P. D. MIER Department of Dermatology (Professor Dr J. W. H. Mali), Nijmegen University, Netherlands Search for other works by this author on: Oxford Academic Google Scholar J. van den HURK J. van den HURK Department of Dermatology (Professor Dr J. W. H. Mali), Nijmegen University, Netherlands Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 87, Issue 6, 1 December 1972, Pages 571–576, https://doi.org/10.1111/j.1365-2133.1972.tb07447.x Published: 01 December 1972 Article history Accepted: 20 June 1972 Published: 01 December 1972
Audit of antibiotic prescribing in two governmental teaching hospitals in Indonesia
Authors: U. Hadi, D.O. Duerink, E.S. Lestari, N.J. Nagelkerke, M. Keuter, D. Huis in't Veld, E. Suwandojo, E. Rahardjo, P. van den Broek, I.C. Gyssens
Journal: Clinical Microbiology and Infection (2008)
647. AP20817-Inducible Activation of a Chimeric Insulin Receptor Mimics Insulin Action in Hepatocytes Transduced with AAV
Authors: Iñigo Narvaiza, María Vera, Nerea Razquin, Mikel Zaratiegui, Jesús Prieto, Puri Fortes
Journal: Molecular Therapy (2004)

RNA interference (RNAi) is a natural process, originally described in Caenorhabditis elegans and plants, initiated by the cleavage of long double stranded RNA (dsRNAs) by the ribonuclease III Dicer generating short interfering RNAs (siRNAs). siRNAs induce selective degradation of mRNAs that are homologous to their sequence. In mammalian cells, RNAi interference can be achieved by transfection of chemically synthesized siRNAs or short-hairpin RNA (shRNAs) precursor expressing plasmids. In-vivo gene silencing of endogenous and exogenous genes has been proven by hydrodynamics injection of both shRNAs and synthetic siRNAs, or by using shRNA expressing viral vectors such as lentivirus or adenoviruses.
Abstract 16460: Enhanced Trpc Channel-Mediated Ca2+ Influx in the Cells With Phospholipase C-δ1 Overexpression
Authors: Kazuo Murakami, Tomohiro Osanai, Makoto Tanaka, Kimitaka Nishizaki, Ikuyo Narita, Takahiko Kinjo, Tomohiro Tanno, Hirofumi Tomita, Ken Okumura
Journal: Circulation (2014)

Background: We recently showed that ergometrine induces coronary spasm in the mice with enhanced phospholipase C (PLC)-δ1 activity, which was detected in patients with coronary spasm (Circulation 2012), and PLC-mediated Ca2+ entry is involved in the genesis of coronary spams. We examined the role of enhanced PLC-δ1 in extracellular Ca2+ entry and its underlying mechanisms in human embryonic kidney (HEK)-293 cells and human coronary arteries smooth muscle cells (CASMC). Methods and Results: The cells were stimulated with acetylcholine (ACh) in a extracellular Ca2+-free condition, and the increase in intracellular free Ca2+ concentration ([Ca2+]i) after addition of extracellular Ca2+ was defined as Ca2+ influx. [Ca2+]i was measured by fura-2. In HEK-293 cells, ACh-induced Ca2+ influx (nM ) was 21±2 in the control and 52±6 in the cells with PLC-δ1 overexpression (p&lt;0.05). ACh-induced Ca2+ influx in the cells with PLC-δ1 overexpression was suppressed by nifedipine in a dose-dependent manner but was partially by 36±13% at 10-5M (p&lt;0.05), thereby even after treatment with nifedipine at 10-5M, ACh-induced Ca2+ influx was increased by 2.9±0.1 times by enhanced PLC-δ1 compared with the control (p&lt;0.05). To clarify the role of diacylglycerol (DAG) in Ca2+ influx, the effect of blockers for DAG-activated transient receptor potential (TRPC) channel was examined. ACh-induced Ca2+ influx in the cells with PLC-δ1 overexpression was suppressed by 2-APB, an inhibitor of non-selective cation channel TRPC, in a dose-dependent manner, and was almost completely blocked by 89±12% at 10-4M (p&lt;0.05). While TRPC3 siRNA did not affect ACh-induced Ca2+ influx (59±27 vs 75±23 nM, p=ns), TRPC6 siRNA suppressed Ca2+ influx to 37±28 nM (p&lt;0.05). In human CASMC, ACh-induced Ca2+ influx was 41±11 in the control and 64±15 in the cells with PLC-δ1 overexpression (p&lt;0.05). Like HEK-293 cells, pretreatment with nifedipine partially suppressed Ca2+ influx, whereas either 2-APB or TRPC6 siRNA almost completely blocked it. Conclusion: ACh-induced Ca2+ influx, mediated by both voltage-gated Ca2+ channels and non-selective cation channels TRPC6, is enhanced by PLC-δ1 overexpression. Inhibition of TRPC may be effective in enhanced PLC-δ1-mediated coronary spasm.
Does litigation make you ill
Authors: Kevin Barraclough
Journal: BMJ (2001)

It's often well into the consultation when their lower lip begins to quiver. This is the physical sign that alerts us astute physicians that something is up, and that it might be a long morning. However, when they start to speak of “my case,” you know that they are suffering from WLD and you reach for the Prozac pad. There are in fact two variations of the condition: WLD—whiplash, litigation, depression—or its variant, WLBBD—whiplash, litigation, breakup with …
Peripheral Calcitonin Gene‐Related Peptide Receptor Activation and Mechanical Sensitization of the Joint in Rat Models of Osteoarthritis Pain
Authors: Craig M. Bullock, Peter Wookey, Andrew Bennett, Ali Mobasheri, Ian Dickerson, Sara Kelly
Journal: Arthritis & Rheumatology (2014)

To investigate the role of the sensory neuropeptide calcitonin gene-related peptide (CGRP) in peripheral sensitization in experimental models of osteoarthritis (OA) pain.Experimental knee OA was induced in rats by intraarticular injection of monosodium iodoacetate (MIA) or by transection of the medial meniscus (MMT). Single-unit recordings of joint-innervating nociceptors were obtained in MIA- and saline-treated rats following administration of CGRP or the CGRP receptor antagonist CGRP 8-37. Effects of CGRP 8-37 were also examined in rats that underwent MMT and sham operations. Protein and messenger RNA (mRNA) levels of CGRP receptor components in the L3-L4 dorsal root ganglion (DRG) were investigated following MIA treatment.In both the MIA and MMT groups, the mechanical sensitivity of joint nociceptors was enhanced compared to that in the control groups. Exogenous CGRP increased mechanical sensitivity in a greater proportion of joint nociceptors in the MIA-treated rats than in the saline-treated rats. Local blockade of endogenous CGRP by CGRP 8-37 reversed both the MIA- and MMT-induced enhancement of joint nociceptor responses. Joint afferent cell bodies coexpressed the receptor for CGRP, called the calcitonin-like receptor (CLR), and the intracellular accessory CGRP receptor component protein. MIA treatment increased the levels of mRNA for CLR in the L3-L4 DRG and the levels of CLR protein in medium and large joint afferent neurons.Our findings provide new and compelling evidence implicating a role of CGRP in peripheral sensitization in experimental OA. Our novel finding of CGRP-mediated control of joint nociceptor mechanosensitivity suggests that the CGRP receptor system may be an important target for the modulation of pain during OA. CGRP receptor antagonists recently developed for migraine pain should be investigated for their efficacy against pain in OA.
Enoxaparin vs Unfractionated Heparin in Acute Coronary Syndrome
Authors: Balavenkatesh Kanna, Puneeta Sharma
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
Intensive management of high-utilizing adults with sickle cell disease lowers admissions
Authors: Kathryn L. Koch, Matthew S. Karafin, Pippa Simpson, Joshua J. Field
Journal: American Journal of Hematology (2014)

A minority of super-utilizing adults with sickle cell disease (SCD) account for a disproportionate number of emergency department (ED) and hospital admissions. We performed a retrospective cohort study comparing the rate of admission before and after the opening of a clinic for adults with SCD. Unique to this clinic was an intensive management strategy, focusing on super-utilizing adults with 12 or more admissions per year. ED/hospital and 30 days re-admission rates were compared, 1 year pre- and post-intervention, for those adults who established in the clinic. Prior to the intervention, 17 super-utilizers, comprising 15% of the pre-intervention cohort (n = 115), accounted for 58% of the total admissions and had an admission rate of 28 per patient-year. When pre- and post-intervention years were compared, rate of ED/hospital admission per patient-year for super-utilizers decreased from 27.9 to 13.5 (P < 0.001), while there was not a significant reduction for the entire cohort (7.1 vs. 6.1, P = 0.84). Similarly, the decrease in rate of 30 day re-admission was larger for the super-utilizers (13.5 per patient-year to 1.8, P < 0.001), than the whole cohort (2.6 per patient-year to 0.7, P = 0.006). Among the super-utilizers, the reduced rate of admission from the pre- to post-clinic intervention year equated to 252 fewer ED/hospital admissions and 227 fewer 30 day re-admissions. This management strategy focusing on super-utilizing adults with SCD lowered admission and 30 day re-admission rate.
Abstract 18425: Preventing Allogeneic Immune Rejection by Transplanting MHC-homo Induced Pluripotent Stem Cell-derived Cardiomyocytes to an MHC-matched non-Human Primate
Authors: Takuji Kawamura, Shigeru Miyagawa, Satsuki Fukushima, Shigeo Masuda, Noriyuki Kashiyama, Ai Kawamura, Emiko Ito, Atsuhiro Saito, Akira Maeda, Koichi Toda, Shuji Miyagawa, Yoshiki Sawa
Journal: Circulation (2014)

Introduction: Allogeneic, “ready-made” induced pluripotent stem cells (iPSCs) can be efficiently used for treating cardiac disease, although the immune response produced against the allogenicity is still a concern. Major histocompatibility complex (MHC)-matched allogeneic implantation (MMAI) performed with “ready-made” iPSCs that have homozygous MHC haplotypes can be theoretically used for diminishing the immune rejection. We thus explored the efficacy of this MMAI therapy using a non-human primate, Macaca fascicularis model. Methods: IPSCs constitutively expressing GFP were derived from Macaca fascicularis with homozygous MHC haplotypes (HT1). All alleles constituting MHC genes were homozygous. Cardiomyogenic differentiation was induced in the iPSCs in vitro. More than 80% of iPSCs were positive for troponin T. The derivatives were then subcutaneously transplanted to the Macaca fascicularis with heterozygous HT1, who served as MMAI models. The immunosuppressants included tacrolimus (TAC), mycophenolate m...
Alcoholism. A Practical Treatment Guide.
Authors: Stanley E. Gitlow, Herbert S. Peyser
Journal: Annals of Internal Medicine (1980)

This second edition of a 1980 textbook comes very close to being what it claims to be: a practical treatment guide to alcoholism. The editors, a wellknown internist and a psychiatrist, respectively, both of whom have extensive experience in the treatment of alcoholism, enlisted the help of physicians and other professionals to compile this volume. The chapter titles accurately reflect the broad content of the text, which ranges from diagnosis and motivation of the alcoholic patient to the physician's role in rehabilitation, medical complications, and long-term management. Spe­ cial chapters are devoted to the woman with alcoholism and the family in crisis. The disease model is also given provocative attention by psychiatrist Peyser, who discusses its implica­ tions for psychotherapy and counseling. The book contains an appendix that includes a repro­ duction in entirety of the 1972 landmark article by the National Council on Alcoholism entitled Criteria for Diagnosis of Alcoholism. The one new chapter in this edition is Peyser's review of alcoholism and clinical psychiatry.