tbuckley/cabot-search huggingface dataset:
The Early Repolarization Pattern
Authors: Peter W. Macfarlane, Charles Antzelevitch, Michel Haissaguerre, Heikki V. Huikuri, Mark Potse, Raphael Rosso, Frederic Sacher, Jani T. Tikkanen, Hein Wellens, Gan-Xin Yan
Journal: Journal of the American College of Cardiology (2015)
Clinical Evidence
Authors: F. Godlee, R. Smith, D. Goldmann
Journal: BMJ (1999)

Clinical review p 1600 See advertisement opposite p 1598 (CR edition), p 1621 (GP), p 1567 (Compact and International)

This week's BMJ carries a sample of information from a new resource for clinicians, Clinical Evidence , which will be launched later this month (p 1600). The inspiration for Clinical Evidence came in a phone call in 1995. Tom Mann and his colleagues at the NHS Executive asked the BMJ to explore the possibility of developing an evidence “formulary” along the lines of the British National Formulary . They recognised that clinicians were under increasing pressure to keep up to date and to base their practice more firmly on evidence but that few had the necessary time or skills to do this. Their idea was to provide a pocket-size book containing concise and regularly updated summaries of the best available evidence on clinical interventions.

A small team at the BMJ set …
Sustained Erythroid Response Associated With Red Cell Transfusion and Progressive Growth Factor Independence Is Feasible With Adjuvant Sertraline In Low-Risk Myelodysplastic Syndrome (LR-MDS)
Authors: Rui Li, Matthew Zheng, Sarvari Venkata Yellapragada, Ruben Hernandez Perez, Martha Mims, Gustavo A. Rivero
Journal: Blood (2013)
Abstract 21075: Percutaneous Closure of Patent Foramen Ovale for Systemic Hypoxemia: Patient Characteristics and Results in 104 Patients
Authors: Bryant H Nguyen, Leighton Satterfield, Michael S Kim, Brett Fenster, Howard Weinberger, Kern Buckner, Andrew Freeman, John D Carroll
Journal: Circulation (2010)

Right to left shunting (RTLS) across a PFO is a known but uncommon cause of hypoxemia. The role of closure is not well studied. We present the largest, single-center retrospective study of patients...
腹胀-纳差-巩膜黄疸
Authors: 甄真, 刁青, 米立军
Journal: BMJ (2011)

患者男,57岁,机关干部.主因间断腹胀、纳差伴巩膜黄疸、尿黄3个月入院.无发热、恶心、呕吐、腹痛、腹泻,肝区不适等,外院查甲、乙、丙、戊型肝炎痛毒标志物均阴性,肝功能:ALT 772 U/L,AST 467 U/L,血清总胆红素(TBIL)84.8μmol/L,直接胆红素(DBIL)60.2 μmol/L,白蛋白36 g/L,球蛋白53.8 g/L;γ-谷氨酰转肽酶(γ-GT)183 U/L;血常规正常.予保肝、降酶及退黄等综合治疗,病情无明显好转。
Prioritisation of infectious diseases in public health: feedback on the prioritisation methodology, 15 July 2008 to 15 January 2009
Authors: A Gilsdorf, G Krause
Journal: Eurosurveillance (2011)

In 2004, the German public health institute, the Robert Koch Institute (RKI), prioritised pathogens by public health criteria and presented the methodology and findings. In order to further improve the methodology, the RKI invited experts to give feedback on this via a structured web-based questionnaire. The survey was completed by 72 participants during 15 July 2008 to 15 January 2009. Prioritisation of pathogens was considered as useful for public health purposes by 68 participants and for both surveillance and epidemiological research by 64 participants. Additional pathogens were suggested, including some that are resistant to antimicrobials. The criteria incidence, severity, outbreak potential, emerging potential and preventability were each considered as useful or very useful for the prioritisation (by more than 65 participants for each criterion). Weighting of the criteria was judged as relevant or very relevant by 67 of participants, but needs more explanation. It was also suggested that the group carrying out the prioritisation be composed of a median of 15 experts (range: 5–1,000). The feedback obtained in the survey has been taken into account in the modification of the methodology for the next round of prioritisation, which started in December 2010.
Abstract 5: Indirect Brain Injury Resulting from Severe Burns Results in Estrogen-Reversible Elevations of Markers of Alzheimer's Disease
Authors: Jane G Wigginton, Paul E Pepe, Kareem R AbdelFattah, David L Maass, Ahamed H Idris, Joseph P Minei, Joshua W Gatson, James W Simpkins
Journal: Circulation (2011)

Background: Prior studies have found that patients with severe burns may suffer neurocognitive changes. While frequently attributed to psycho-social issues, recent data from our lab revealed a substantial, rapid and sustained (30 min - 7 day) increase in rat brain inflammation following burns that is blunted by a single post-burn dose of estrogen. Other brain injury processes, such as TBI and stroke have shown an accelerated accumulation of Aβ40, Aβ42, and pTau, leading to a clinical picture of early Alzheimer's disease (AD). We hypothesized that similar AD processes may be triggered in severe burn injury, and altered by post-burn estrogen. Methods: 149 male rats were given a 3° 40% TBSA scald burn. Rats were randomized into 3 groups: Group 1 (0.5mg/kg of 17β estradiol (E2) 15 min after injury); Group 2 (placebo); and Group 3 (sham-burn control). These rats were sequentially sacrificed at 0.5, 1, 2, 4, 6, 8, 12, 18, 24 hours post-burn. An additional 24 rats were sacrificed 7 days post-burn. Brain tissue IL-6, Aβ40, Aβ42, and pTau were measured using ELISA. Results: Compared to placebo, early estrogen treatment significantly decreases (~90%) brain levels of IL-6 at all measured time points. At 7 days post-burn, rats receiving E2 exhibited similar Aβ40, Aβ42, and pTau to the unburned group, while those receiving placebo were significantly elevated. Conclusions: 17β estradiol not only mitigates the early-onset, sustained brain inflammation following burn injury in a rat model, but also significantly decreases brain levels of Aβ40, Aβ42, and pTau. We hypothesize that other injuries causing acute, remote brain inflammation (such as cardiac arrest) may trigger similar AD-like brain changes.
Abstract 17842: Relationship Between Novel Angiographic Endpoint of Endovascular Therapy and Clinical Result of Patients with Critical Limb Ischemia
Authors: Makoto Utsunomiya, Masato Nakamura, Kaoru Sugi
Journal: Circulation (2011)

Objectives Several reports have been published of the acceptable patency and limb salvage rates following infra-popliteal interventions for the treatment of critical limb ischemia (CLI). However, the optimal angiographic endpoint of endovascular therapy (EVT) remains unclear. The aim of this study was to assess the relationship between the appearance of wound blush as an angiographic endpoint and the limb salvage rate in patients with CLI. Methods “Wound blush” was defined as contrast opacification of the vessels around the wound in digital subtraction angiograms obtained immediately after the EVT through the catheter introduced into the popliteal artery. We analyzed the data of 77 consecutive patients (93 limbs) with ischemic ulcerations classified as Rutherford category 5 or 6, who underwent EVT alone, without bypass surgery. Patients were divided into two groups depending on whether or not wound blush was obtained in the angiogram obtained immediately after the procedure, and the ‘freedom from amputation’ rate was compared between the two groups. Results The overall limb salvage rate was 81.7%. The limb salvage rate was significantly higher in the wound blush-positive group than in the wound blush-negative group, and remained so for at least 3 years after the EVT (96.4% vs. 56.8%, P&lt;0.001). Conclusion Presence of wound blush after EVT is associated with higher SPP, both of which are associated with higher rates of limb salvage. Wound blush as an angiographic endpoint in EVT may be a novel predictor of limb salvage in patients with CLI.
Urinary Concentrating Defect of Adrenal Insufficiency
Authors: Michael J. Schwartz, Juha P. Kokko
Journal: Journal of Clinical Investigation (1980)

Mineralo- and glucocorticoid-deficient states, such as Addison's disease, are partly characterized by an inability to generate a maximally concentrated urine. The purpose of the present study was to develop a model of adrenal insufficiency and to determine whether changes in the intrinsic function of the collecting duct could partly account for this concentrating defect. Two kinds of experiments were performed: an assessment of the in vivo ability of adrenal-ectomized rabbits to concentrate their urine, and an examination of the intrinsic hydroosmotic responsiveness of in vitro perfused collecting ducts isolated from normal and adrenalectomized rabbits. The present study demonstrates that adrenalectomized rabbits are unable to concentrate their urine maximally, and that the in vivo administration of either deoxycorticosterone, 250 μg/kg, or dexamethasone, 50 μg/kg, restored to or toward normal their concentrating ability. When cortical collecting tubules from adrenalectomized rabbits were perfused in vitro, they demonstrated a markedly blunted hydroosmotic response to antidiuretic hormone (ADH), which was corrected by the in vitro addition of either aldosterone (50 pM) or dexamethasone (50 pM), but not progesterone (50 pM). The steroids by themselves, in the absence of ADH, had no intrinsic effect on the water permeability of the collecting duct. The blunted hydroosmotic response across cortical collecting tubules from adrenal-ectomized rabbits was corrected by the addition of either 8-bromo cyclic AMP or a potent phosphodiesterase inhibitor, 1-methyl-3-isobutylxanthine. The present studies show that the cortical collecting tubules obtained from adrenalectomized rabbits do not respond normally to ADH. The poor hydroosmotic response to ADH was corrected by exogenous aldosterone, dexamethasone, an analog of cyclic AMP, or a phosphodiesterase inhibitor. In conclusion, the present studies are consistent with the view that the concentrating defect seen in adrenal insufficiency is at least partly the result of the absence of the permissive effect that adrenal steroids exert on the ADH-induced reabsorption of water across the collecting duct. The absence of adrenal steroids results in a diminished rate of cyclic AMP accumulation in the cells of the collecting duct, either as a result of an augmented activity of cyclic AMP phosphodiesterase or a diminished rate of cyclic AMP generation.
A Novel Mechanism of Megakaryopoiesis from Pre-Adipocytes: Involvement of Transferrin/ CD71/ TPO Pathways
Authors: Yukako Ono-Uruga, Keiichi Tozawa, Sahoko Matsuoka, Tadashi Horiuchi, Shinichiro Okamoto, Mitsuru Murata, Yasuo Ikeda, Toshio Suda, Yumiko Matsubara
Journal: Blood (2014)
Abstract 13739: Increased Psychological Demands of Work are Associated with Poor Adherence and Poor Health-Related Quality of Life Among Workers with Cardiovascular Disease
Authors: Victoria V Dickson, Alexandra Howe, Joshua Deal, Margaret M McCarthy
Journal: Circulation (2010)

Over 3.5 million workers have cardiovascular disease (CVD) with significant work limitations and increased disability. Workers must meet the challenges of today's work processes including increased...
ACCF/ASNC Appropriateness Criteria for Single-Photon Emission Computed Tomography Myocardial Perfusion Imaging (SPECT MPI)
Authors: Ralph G. Brindis, Pamela S. Douglas, Robert C. Hendel, Eric D. Peterson, Michael J. Wolk, Joseph M. Allen, Manesh R. Patel, Ira E. Raskin, Robert C. Hendel, Timothy M. Bateman, Manuel D. Cerqueira, Raymond J. Gibbons, Linda D. Gillam, John A. Gillespie, Robert C. Hendel, Ami E. Iskandrian, Scott D. Jerome, Harlan M. Krumholz, Joseph V. Messer, John A. Spertus, Stephen A. Stowers
Journal: Journal of the American College of Cardiology (2005)
Abstract 4351: Albuminuria is a Risk Factor for Adverse Events in Heart Failure Independent of the Presence of Chronic Kidney Disease
Authors: Adheesh Agnihotri, Kalkidan Bishu, James Arnold, Gary Gustafson, Inder S Anand
Journal: Circulation (2008)

Background : Chronic kidney disease (CKD) is a known risk factor for adverse events in patients with heart failure (HF). Whether albuminuria defined as urine albumin creatinine ratio ≥30 mg/g with or without CKD is also a risk factor for adverse events, is unclear. Methods : Data was abstracted from the electronic medical records of 442 patients admitted to the Minneapolis VA Medical Center with a primary diagnosis of HF, and an outpatient measurement of albumin creatinine ratio between September 2002 and March 2006. Multivariable Cox regression analysis was used to determine the impact of albuminuria on mortality and hospitalizations for HF at 1-year. Results : Albuminuria was seen in 54% (238/442) patients at baseline. Patients with albuminuria were more likely to have edema, higher systolic blood pressure, left ventricular hypertrophy, lower eGFR and use of beta-blockers (all p&lt;0.05). Albuminuria correlated (p&lt;0.05) with serum creatinine (rho=0.23), systolic blood pressure (0.37), and LVEF (0.13). The presence of albuminuria did not increase the risk of death (HR 0.65, 95% CI 0.38 –1.11), but was strongly associated with the risk of hospitalization for HF at 1-year (HR 1.77, 95% CI 1.11–2.82, p=0.017) independent of age, gender, h/o HTN, DM, CAD, PVD, COPD, CKD, atrial fibrillation, EF, use of ACE-I, spironolactone and beta-blocker. Conclusion : The presence of albuminuria is an independent prognostic marker for hospitalizations for heart failure.
Abstract 5572: Endothelial-Selective Deletion of Neuregulin-1 Leads to Impaired Tolerance of Ischemic Injury
Authors: Qunhua Huang, April Kalinowski, Kashif Jafri, Monica Palmeri, Raymond R Russell, Kerry S Russell
Journal: Circulation (2008)

The neuregulin-1 (NRG)/erbB signaling axis is emerging as an important mediator of endothelial/myocyte crosstalk. We have previously shown that NRG can protect cardiac myocytes from apoptosis induced by hypoxic injury and that endothelial cells can provide this NRG in an ex vivo co-culture model. To extend this observation to an intact animal system, we have generated mice with inducible and endothelial-selective deletion of NRG. We hypothesized that animals with decreased endothelial NRG expression would be more susceptible to ischemic injury. Mice carrying a transgene for tamoxifen-inducible expression of cre recombinase under control of the Tie2 promoter were crossed with those carrying homozygously floxed NRG-1 genes. Serial echocardiographic measurements of cardiac function were performed before, during and after tamoxifen induction. There was no significant decrease in cardiac function following the completion of the induction (NRG knockout) protocol. Hearts from these mice underwent a global ischemia/reperfusion protocol in the Langendorff mode. Both resting and post-ischemic +/−dP/dT and left ventricular developed pressure were impaired in the animals with endothelial selective NRG deletion compared to non-induced transgenics or tamoxifen-induced controls. Hearts from the NRG deleted animals released more CPK and contained significantly more apoptotic nuclei compared to controls after ischemia/reperfusion, supporting the idea that endothelial-derived NRG can protect myocytes against apoptosis in vivo. Another mechanism by which loss of NRG may contribute to cardiac dysfunction in the setting of ischemia is by altering cardiac myocyte glucose uptake. We have shown that adult rat cardiomyocyte glucose uptake is significantly increased in response to NRG and that this response is abrogated partially by wortmannin, but completely by wortmannin plus compound C (an inhibitor of AMP-activated protein kinase), suggesting that both AKT and AMPK dependent pathways of glucose uptake may be activated by NRG in adult myocytes. Thus, we conclude that NRG plays an important role in preservation of cardiac myocyte function in vivo and that this may occur as a result of both protection against apoptosis and enhanced glucose metabolism.
Abstract 12223: Regulation of Acat2 Expression by Hnf4 and its Cofactors Pgc1{alpha} and Shp
Authors: Zhu-Qin Zhang, Yang Xi, Rui-Feng Yang, Hou-Zao Chen, Zhen-Ya Li, Ran Zhang, Yu-Yan Jia, De-Long Hao, Zhi-Chen Guo, Depei Liu, Chih-Chuan Liang
Journal: Circulation (2011)

ACAT2, one member of ACAT family catalyzing formation of cholesterol esters, is important for cholesterol ester synthesis and VLDL/ApoB secretion. To explore how ACAT2 quantity is regulated, we studied the mechanism for controlling ACAT2 expression at transcriptional level. We found that HNF4, one liver enriched transcription factor, positively regulated ACAT2 expression. In luciferase reporter assay, HNF4 overexpression stimulated ACAT2 promoter activity. However, mutation of two response elements of HNF4 profoundly antagonized HNF4 effect. Moreover, HNF4 binds to these two elements in the promoter of ACAT2 as evidenced by EMSA and ChIP assays, In HuH7 cells, overexpression of HNF4 increased ACAT2 mRNA levels, whereas knockdown of HNF4 inhibited ACAT2 mRNA expression. ACAT2 expression was also upregulated by PGC1α, coactivator of HNF4, but decreased by SHP, corepsressor of HNF4. SHP competed with PGC1α to regulate ACAT2 promoter activity in luciferase reporter assay. Moreover, ACAT2 expression was regula...
Abstract 3377: Modulation of Vessel Stability by the ELR-negative Chemokine IP-10
Authors: Richard J Bodnar, Cecelia C Yates, Xiaoping Du, Alan Wells
Journal: Circulation (2008)

Angiogenesis plays a critical role in tissue development and wound repair. Regulation of the vascular tree is critical to organogenesis and neo-organogenesis. The initial vigorous vessel proliferation and arborization that occurs during tissue development and wound repair must be pruned to form mature tissue. The signals that trigger this vascular regression are still ill-defined. Mitotic endothelial cells express the CXC receptor 3 (CXCR3), which binds the ELR-negative chemokines IP-10 (CXCL10), platelet factor 4 (PF4, CXCL4), IP-9/I-TAC (CXCL11), and MIG (CXCL9), with IP-9 and IP-10 being expressed during the later remodeling phases of wound repair when vascular involution occurs. We hypothesized that not only does this signaling system limit angiogenesis, but that CXCR3 signaling also compromises endothelial cell tube integrity contributing to regression. Treatment of newly formed tubes/cords on Matrigel (in vitro) or vessels in a subcutaneous Matrigel plug (in vivo) with IP-10 in either presence or absence of VEGF caused a dissociation of the tubes and subsequent vascular involution. This followed CXCR3 induced cleavage of β3 integrin in endothelial cells. CXCR3 triggering of mu-calpain activity caused cleavage of the cytoplasmic tail of human β3 integrins at the calpain cleavage sites NPLY747 and TSTF754. IP-10 stimulation was also found to activate caspase 3, blockage of which prevented cell death but not tube dissociation. Thus, CXCR3 activation in newly formed vessels results in endothelial dissociation from matrix, followed by anoikis. This is the first direct evidence for an extracellular signaling mechanism through CXCR3 causing the dissociation of newly formed blood vessels. This study was supported by funds from VA Medical Research Program and National Institute of General Medical Sciences (NIH, USA).
Hypomethylation Status of CpG Sites at the Promoter Region and Overexpression of the Human MDR1 Gene in Acute Myeloid Leukemias
Authors: Masaharu Nakayama, Morimasa Wada, Taishi Harada, Jun Nagayama, Hitoshi Kusaba, Koichi Ohshima, Mitsuo Kozuru, Hirokazu Komatsu, Ryuzo Ueda, Michihiko Kuwano
Journal: Blood (1998)
Abstract 2758: Image Quality of Coronary CT Angiography in 256-slice CT
Authors: Sadako Motoyama, Masayoshi Sarai, Hirofumi Anno, Takahisa Sato, Kaori Inoue, Hiroto Harigaya, Yoshihiro Sanda, Hitoshi Hishida, Yukio Ozaki, Kazuhiro Katada
Journal: Circulation (2007)
Abstract 1459: Safety and Efficacy of Ezetimibe/Simvastatin Combination versus Atorvastatin in Older Patients
Authors: JoAnne M Foody, W. V Brown, Franklin Zieve, Adeniyi J Adewale, Doreen Flaim, Robert S Lowe, Charlotte Jones-Burton, Andrew M Tershakovec
Journal: Circulation (2009)

While over 80% of CHD related mortality occurs in patients ≥65 years of age, use of statins to mitigate CHD risk has been suboptimal, due in part to concerns for increased side effects in older pat...
Dasatinib Plus Smoothened (SMO) Inhibitor BMS-833923 in Chronic Myeloid Leukemia (CML) with Resistance or Suboptimal Response to a Prior Tyrosine Kinase Inhibitor (TKI): Phase I Study CA180323
Authors: Neil P. Shah, Jorge E. Cortes, Giovanni Martinelli, B. Douglas Smith, Emer Clarke, Mhairi Copland, Lewis Strauss, Moshe Talpaz
Journal: Blood (2014)
The results of the immunomorphological study of the placenta in women with asthma
Authors: Yulia R. Dymarskaya, Olga V. Lavrova, Ludmila B. Zubzhitskaya, Elena A. Shapovalova
Journal: European Respiratory Journal (2014)

Placenta is known to be a natural protective barrier for the unborn child and studying its status in patients with allergic diseases is particularly interesting.

The purpose of the study was to assess immunomorphological status of placenta in women with asthma.

Materials and methods . We conducted an immunomorphological analysis of 90 samples of placenta of women with asthma with varying severity. We used specific serum cytokines against IL-4, IL-6, IL-10, fibrinogen, C3 fraction of complement, and monoclonal antibodies against IgA, IgM, IgG.

Results .Our study showed that in cases of moderate to severe asthma fixation of pathogenic immune complex (C3 fraction of complement), IL-4, IL-6 in placenta were significantly higher, than in cases of mild intermittent and mild persistent asthma (p<0.05)

Conclusion . The severity of asthma is directly correlated with the presence of immune deposits in the placenta. These findings can be considered as the result of immune inflammation in placenta and may be the reason of complications of the course of pregnancy, labor. All these factors may play role in the prenatal development of allergic phenotype of newborns.
Clofarabine Plus Low-Dose Cytarabine For The Treatment Of Patients Withhigher-Risk Myelodysplastic Syndrome (MDS) Who Have Been Relapsing After, Or Are Refractory To, Hypomethylator Agent Therapy
Authors: Aziz Nazha, Guillermo Garcia-Manero, Hagop M. Kantarjian, Farhad Ravandi, Gautam Borthakur, Tapan M. Kadia, Elias Jabbour, Naveen Pemmaraju, Naval G. Daver, Courtney D. DiNardo, Darla Miller, Stefan H. Faderl
Journal: Blood (2013)
Vorinostat, Bortezomib, Cyclophosphomide, Thalidomide, and Dexamethasone in Relapsed/Refractory Multiple Myeloma Patients
Authors: Charise Gleason, Jonathan L. Kaufman, Ajay K. Nooka, Kelly Valla, Leonard T Heffner, Aditya Singh Bisht, Sanjay Manubolu, Melanie Watson, Lawrence H. Boise, Sagar Lonial
Journal: Blood (2014)