tbuckley/cabot-search huggingface dataset:
Abstract 16190: National Trends in RSV Hospitalizations in Children With Hemodynamically Significant Heart Disease, 1997-2009
Authors: Patricia Y Chu, Christoph P Hornik, Jennifer S Li, Michael J Campbell, Kevin D Hill
Journal: Circulation (2014)

Background: Children with hemodynamically significant heart disease (HS-HD) are at risk for morbidities and mortality due to respiratory syncytial virus (RSV). Palivizumab was approved for RSV prophylaxis in 1998. Guidelines released in December 2003 recommend palivizumab for all children &lt; 2 yrs with HS-HD. We sought to define the impact of RSV prophylaxis in children with HS-HD by evaluating trends in U.S. RSV hospitalizations. Methods: The 1997, ’00, ’03, ’06 and ’09 Healthcare Cost and Utilization Project (HCUP) Kids’ Inpatient Databases (KID) were used to estimate U.S. RSV hospitalizations in children &lt; 2 yrs, overall and in those with HS-HD, using standard HCUP weighting methods. RSV was defined by ICD-9-CM codes for RSV infection. HS-HD was defined using ICD-9-CM codes from the Clinical Classifications Software for congestive heart failure, or an ICD-9-CM code for pulmonary hypertension, common truncus, common ventricle, or hypoplastic left heart syndrome. Results: Our cohort included an estimated 461,491 RSV hospitalizations; 2,132 in children with HS-HD. Figure 1 depicts hospitalizations over time. There was no evident trend in number of overall RSV hospitalizations, however RSV hospitalizations in children with HS-HD declined by 39% from ’97 to ‘09. The largest decline was from ’97-’03. RSV hospitalizations in children with HS-HD relative to overall hospitalizations in children with HS-HD declined annually from ’97-’06 with a small increase in ‘09 (3.8%, 3.5%, 3.0%, 2.3% and 2.6% for successive analytic years). In 2009 mean hospital length of stay for children with HS-HD and RSV was 22.5 ± 2.1 days. Conclusions: RSV disease burden in children with HS-HD has declined since palivizumab approval. Much of this decline occurred before palivizumab was recommended for use in HS-HD, perhaps reflecting early adoption of prophylaxis, or greater awareness of alternative preventative strategies. RSV remains a significant cause of morbidity in children with HS-HD.
God Save the Child
Authors: C Atkins
Journal: JAMA (1998)

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 4273: An enhanced microRNA backbone for potent single-copy RNAi
Authors: Christof Fellmann, Thomas Hoffmann, Vaishali Sridhar, Barbara Hopfgartner, Dan Y. Lai, Johannes Zuber
Journal: Cancer Research (2014)

Abstract Short-hairpin RNA (shRNA) technology enables stable and regulated gene repression through RNA interference (RNAi). Synthetic shRNAs can be embedded into the context of an endogenous microRNA (miRNA) to create natural substrates of RNAi pathways and minimize cellular toxicities. While such “shRNAmir” reagents provide an experimentally versatile RNAi system, their design remains challenging due to our limited understanding of miRNA processing factors. Consequently, shRNAmir reagents often fail to trigger potent target knockdown, especially when expressed from a single genomic integration (“single-copy”), a common scenario in pool-based screens and other key applications. To tackle this issue, we recently developed a high-throughput Sensor assay that enables functional identification of effective shRNAs and has been used to establish shRNA-specific prediction rules. Following these advances in design of the synthetic shRNA stem, here we take a systematic approach to improve the experimental miR-30 backbone. Among several sequence features enhancing knockdown efficiency, we identify a conserved element 3′ of the basal stem that is critically required for optimal shRNAmir processing. Implementation of this feature in an optimized backbone termed “miR-E” results in a 10-30 fold increase in mature shRNA levels, and generally boosts knockdown efficacy. Importantly, combination of the enhanced miR-E backbone with Sensor-based design rules establishes a validated and easily accessible platform for generating single-copy effective shRNAs for pool-based RNAi screening and transgenic animals, and will facilitate the functional annotation of the genome. Citation Format: Christof Fellmann, Thomas Hoffmann, Vaishali Sridhar, Barbara Hopfgartner, Dan Yu Lai, Johannes Zuber. An enhanced microRNA backbone for potent single-copy RNAi. [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 4273. doi:10.1158/1538-7445.AM2014-4273
Clinical Strategies in Adult Asthma.
Authors: Charles H. Scoggin, Thomas L. Petty
Journal: Annals of Internal Medicine (1982)

second edition of "Ultrastructural Pathology" is somewhat restricted to transmission electron microscopy, with little reference to scanning or to other modes of electron microscopy, such as high-voltage.As a result, the chapters on cytoskeleton contain no mention of microtrabeculae (a much debated topic in recent years).I also wish that a special section had covered the subject of virus-like particles, an area of interpretation of electron micrographs that has been puzzling ultrastructural pathologists for quite some time.These are minor remarks that should in no way minimize the general impression one gets from reading Ghadially's new book -that it is a mine of ultrastructural information, critically presented and most efficiently illustrated.I expect that this book will help many electron microscopists in their continual effort to refine the critical and precise interpretation of their micrographs.It will without any doubt substantiate a statement made by Ghadially in his introduction -"Electron microscopy is a science in its own right.
Abstract 4349: Regulation of proliferation and platelet-derived growth factor expression in desmoid tumors by microRNA-29
Authors: Mushriq Al-Jazrawe, Raymond Poon, Jessica Liu, Benjamin Alman
Journal: Cancer Research (2014)

Abstract Desmoid tumors (DT), also called aggressive fibromatosis, are a rare, locally invasive soft tissue tumors. While DTs harbor mutations that activate β-catenin, a major effector molecule of canonical Wnt signaling, they also display elevated levels of both Platelet-Derived Growth Factor Receptor Beta (PDGFRβ) and its PDGF-B ligand. We hypothesize that active PDGFRβ signaling maintains DT progression. We studied the effect of PDGFRβ inhibition on DT growth. Primary cultures of DTs treated with the PDGFRβ inhibitor Sunitinib show a decrease in proliferation rate as measured by bromodeoxyuridine (BrdU) incorporation assay. In vivo, Sunitinib treatment of Apc1638N/+ mice, a mouse model of DT, also decreased the number and size of tumors. To investigate the relationship of β-catenin activation and PDGFRβ activation, we treated human skin fibroblasts with Wnt3a to activate canonical Wnt signaling, and utilized transgenic murine skin fibroblasts harboring an activated form of β-catenin. In both systems, PDGF-B ligand expression increased both at the mRNA and protein level. However, this increase was not observed immediately, suggesting an indirect mode of regulation. The PDGF-B gene contains a conserved microRNA-29 (miR29) binding site in its 3′ untranslated region. In silico miRacts analysis of five independent DT microarray studies predicted miR29 family deregulation. As such, we studied whether miR29 deregulation in DT leads to PDGF-B overexpression and tumor proliferation. By performing quantitative PCR on human DT samples, we observed that the levels of mature forms of all miR29 family members (MIR29A, B, and C) are significantly down-regulated. Overexpressing miR29 in DT cells decreases PDGF-B ligand levels as well as BrdU incorporation rate. Finally, β-catenin-induced modulation of the PDGF-B ligand is abrogated upon inhibiting miR29. Taken together, these data suggest that PDGFRβ signaling is a potentially important pathway in DT progression. PDGFRβ may be linked to β-catenin by the novel discovery of microRNA-29 down-regulation in DT tumors. This work will offer new perspectives on the molecular biology underlying DT development and help identify novel targets for therapy. Citation Format: Mushriq Al-Jazrawe, Raymond Poon, Jessica Liu, Benjamin Alman. Regulation of proliferation and platelet-derived growth factor expression in desmoid tumors by microRNA-29. [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 4349. doi:10.1158/1538-7445.AM2014-4349
FDA Warns Antipsychotic Drugs May Be Risky for Elderly
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
Abstract 4274: High fidelity copy number analysis of formalin-fixed and paraffin-embedded tissues using Affymetrix CytoScan HD chip
Authors: Jian-Hua Luo, Amantha Michalopoulos, Ying Ding, Yan P. Yu
Journal: Cancer Research (2014)

Abstract Detection of human genome copy number variation (CNV) is one of the most important analyses in diagnosing human malignancies. Genome CNV detection in formalin-fixed and paraffin-embedded (FFPE) tissues remains challenging task. Here, we report that a modified method to analyze CNV in FFPE tissues using Affymetrix Cytoscan HD chips. Our analysis showed a 91% overlap in CNV detection between FFPE and the karyotype analysis on 8 cases of lymphoma samples. The CNV overlap between frozen and the matched FFPE tissues reached 93.8%. When the analyses were restricted to regions containing genes, 87.1% concordance between FFPE and fresh frozen tissues was found. The results suggest that the modified method using Affymetrix Cytoscan HD chip represents a significant improvement over most of the previous methods in terms of accuracy in detecting CNV in FFPE tissues. This FFPE methodology may hold promise for wide application of CNV analysis on clinical samples. Citation Format: Jian-Hua Luo, Amantha Michalopoulos, Ying Ding, Yan P. Yu. High fidelity copy number analysis of formalin-fixed and paraffin-embedded tissues using Affymetrix CytoScan HD chip. [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 4274. doi:10.1158/1538-7445.AM2014-4274
Self-complementary Adeno-associated Virus 2 (AAV)–T Cell Protein Tyrosine Phosphatase Vectors as Helper Viruses to Improve Transduction Efficiency of Conventional Single-Stranded AAV Vectors in Vitro and in Vivo
Authors: Li Zhong, Linyuan Chen, Yanjun Li, Keyun Qing, Kirsten A. Weigel-Kelley, Rebecca J. Chan, Mervin C. Yoder, Arun Srivastava
Journal: Molecular Therapy (2004)

Recombinant vectors based on adeno-associated virus type 2 (AAV) target the liver efficiently, but the transgene expression is limited to ∼5% of hepatocytes. The lack of efficient transduction is due, in part, to the presence of a cellular protein, FKBP52, phosphorylated forms of which inhibit the viral second-strand DNA synthesis. We have documented that dephosphorylation of FKBP52 at tyrosine residues by the cellular T cell protein tyrosine phosphatase (TC-PTP) enhances AAV-mediated transduction in primary murine hematopoietic cells from TC-PTP-transgenic mice. We have also documented that AAV-mediated transduction is significantly enhanced in hepatocytes in TC-PTP-transgenic as well as in FKBP52-deficient mice because of efficient viral second-strand DNA synthesis. In this study, we evaluated whether co-infection of conventional single-stranded AAV vectors with self-complementary AAV-TC-PTP vectors leads to increased transduction efficiency of conventional AAV vectors in established human cell lines in vitro and in primary murine hepatocytes in vivo. We demonstrate here that scAAV-TC-PTP vectors serve as a helper virus in augmenting the transduction efficiency of conventional AAV vectors in vitro as well as in vivo which correlates directly with the extent of second-strand DNA synthesis of conventional single-stranded AAV vectors. Toxicological studies following tail-vein injections of scAAV-TC-PTP vectors in experimental mice show no evidence of any adverse effect in any of the organs in any of the mice for up to 13 weeks. Thus, this novel co-infection strategy should be useful in circumventing one of the major obstacles in the optimal use of recombinant AAV vectors in human gene therapy.
Abstract 4256: Characterization of the cellular inhibitor of apoptosis 1 (cIAP1) IRES trans-acting factors and their contribution to apoptotic resistance in rhabdomyosarcomas
Authors: Mame Daro Faye, Tyson E. Graber, Shawn Beug, Xiao Xiang, Benjamin Wild, Stephanie Langlois, Kyle N. Cowan, Robert G. Korneluk, Martin Holcik
Journal: Cancer Research (2014)

Abstract The cellular inhibitor of apoptosis protein 1 (cIAP1) is a key regulator of the NFκB signaling pathway and of caspase-8 mediated cell death in mammalian cells. cIAP1 expression is regulated at the translation level via an internal ribosome entry site (IRES). We have previously identified and characterized two IRES trans-acting factors - NF45 and IGF2BP1 - that bind specifically to the cIAP1 IRES and regulates its activity in the context of cell division and apoptosis. In this study, we characterized the minimal requirement of the cIAP1 IRES for these IRES trans-acting factors as well as other canonical translation factors. We also studied the contribution of cIAP1 expression regulation by these IRES trans-acting factors on the apoptotic resistance of rhabdomyosarcoma cancer cells. In particular, we show that the IRES trans-acting factor IGF2BP1 is overexpressed in a panel of rhabdomyosarcoma primary tumors and cell lines where it drives cIAP1 IRES-mediated translation, contributing to increased resistance to cell death. We also show that targeting cIAP1 by either IGF2BP1 knock-down or IAP antagonists delay RMS tumour growth in the presence of TNFα and improve survival in mice. Citation Format: Mame Daro Faye, Tyson E. Graber, Shawn Beug, Xiao Xiang, Benjamin Wild, Stephanie Langlois, Kyle N. Cowan, Robert G. Korneluk, Martin Holcik. Characterization of the cellular inhibitor of apoptosis 1 (cIAP1) IRES trans-acting factors and their contribution to apoptotic resistance in rhabdomyosarcomas. [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 4256. doi:10.1158/1538-7445.AM2014-4256
Abstract 3701: High All-Cause Mortality in Patients with Peripheral Arterial Disease in Primary Care: Five-Year Results of the getabi Study
Authors: Curt Diehm, Jens-Rainer Allenberg, Roman Haberl, Harald Darius, Matthias Mahn, Gerhart Tepohl, Tim Holland-Letz, David Pittrow, Hans-Joachim Trampisch
Journal: Circulation (2007)

Peripheral arterial disease (PAD) is widely accepted as an indicator for generalized atherosclerosis. We aimed to quantify the excess mortality risk borne by symptomatic and asymptomatic PAD patien...
Emerging Agents for the Treatment of Advanced, Imatinib-Resistant Gastrointestinal Stromal Tumors: Current Status and Future Directions
Authors: Sebastian Bauer, Heikki Joensuu
Journal: Drugs (2015)

Imatinib is strongly positioned as the recommended first-line agent for most patients with advanced gastrointestinal stromal tumor (GIST) due to its good efficacy and tolerability. Imatinib-resistant advanced GIST continues to pose a therapeutic challenge, likely due to the frequent presence of multiple mutations that confer drug resistance. Sunitinib and regorafenib are approved as second- and third-line agents, respectively, for patients whose GIST does not respond to imatinib or who do not tolerate imatinib, and their use is supported by large randomized trials. ATP-mimetic tyrosine kinase inhibitors provide clinical benefit even in heavily pretreated GIST suggesting that oncogenic dependency on KIT frequently persists. Several potentially useful tyrosine kinase inhibitors with distinct inhibitory profiles against both KIT ATP-binding domain and activation loop mutations have not yet been fully evaluated. Agents that have been found promising in preclinical models and early clinical trials include small molecule KIT and PDGFRA mutation-specific inhibitors, heat shock protein inhibitors, histone deacetylase inhibitors, allosteric KIT inhibitors, KIT and PDGFRA signaling pathway inhibitors, and immunological approaches including antibody-drug conjugates. Concomitant or sequential administration of tyrosine kinase inhibitors with KIT signaling pathway inhibitors require further evaluation, as well as rotation of tyrosine kinase inhibitors as a means to suppress drug-resistant cell clones.
PEP Talk: Treating Nonoccupational HIV Exposure
Authors: Joan Stephenson
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 Journals 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
Decade of Work Shows Depression Is Physical
Authors: Brian Vastag
Journal: JAMA (2002)

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
Ventilatory exercise response at low altitude
Authors: Jerica Sinkeldam, Gwenda Commandeur, Herman Groepenhoff
Journal: European Respiratory Journal (2011)

Introduction: At medium and high altitude there is an increased ventilatory response at sub maximal exercise tolerance due to a decreased aerobic capacity. However little is known about the ventilatory exercise response to sub maximal exercise at low altitude compared to sealevel. Therefore we conducted this study to test if the ventilatory response at sub maximal exercise differs at low altitude compared to sea level.

Methods: Nine healthy women were included to perform a submaximal cardio pulmonary exercise test (3 min, 50 and 100 watt), with gas exchange, heart rate and oxygen saturation measurements on a cycle ergometer at sea level and identical measurements at 1560 meters above sea level (Davos, Switzerland).

Results: See Table 1.

View this table:

Table 1





Conclusion: For an equal sub maximal oxygen uptake at low altitude there is already an increased ventilation compared to sea level. This is likely explained by impaired gas exchange.