tbuckley/cabot-search huggingface dataset:
Abstract 2152: Close Bidirectional Relationship Between Chronic Kidney Disease and Atrial Fibrillation: The Niigata Preventive Medicine Study
Authors: Hiroshi Watanabe, Toru Watanabe, Shigeru Sasaki, Kojiro Nagai, Yoshifusa Aizawa
Journal: Circulation (2008)

Atrial fibrillation (AF) and chronic kidney disease share risk factors including obesity, hypertension, diabetes, and the metabolic syndrome as well as pathophysiologic mechanisms including persistent inflammation and oxidative stress. We tested the hypothesis here that two conditions are risk factors for each other. This is a prospective community-based observational cohort study based upon an annual health check-up in Niigata prefecture, Japan. We studied the association of kidney dysfunction with new-onset AF and the association of AF with development of kidney disease in 235,818 subjects (mean age, 60.9 ± 11.7 years). Development of kidney dysfunction was defined by an elevation of serum creatinine level (≥1.4 mg/dL for men, ≥1.2 mg/dL for women) or an GFR reduction (&lt;60 ml/min/1.73 m 2 ) in subjects without baseline kidney dysfunction. Kidney disease as risk of AF During a follow-up of 5.9 ± 2.4 years, AF developed in 2,947 subjects (1.3%). Baseline serum creatinine and GFR were associated with risk of subsequent AF (adjusted hazard ratios, HRs [95% confidence interval, CI], 1.09 [1.02–1.17] for serum creatinine [1 mg/dL increment] and 1.02 [1.00 –1.03] for GFR [10 ml/min/1.73 m 2 decline]). The HRs for AF increased inversely with GFR: 1.32 (95% CI, 1.08 –1.62) for GFR 30 –59 ml/min/1.73 m 2 and 1.57 (95% CI, 0.89 –2.77) for GFR &lt;30 ml/min/1.73 m 2 . The effect of chronic kidney disease on risk of new-onset AF was significant after eliminating subjects with treated hypertension or diabetes. AF as risk of kidney disease During a 5.9 year follow-up, 7,791 subjects (4.0%) developed kidney dysfunction and 11,307 subjects (5.8%) developed proteinuria. Baseline AF was associated with development of kidney dysfunction (HRs [95% CI], 1.84 [1.30 –2.61] for serum creatinine-based model and 1.77 [1.50 –2.10] for GFR-based model) and proteinuria (HR [95% CI], 2.20 [1.92–2.52]). The association remained significant in subjects without treated hypertension and diabetes. Kidney dysfunction increased the risk of new-onset of AF and AF increased risk of development of kidney disease. This finding supports the concept that the two conditions share common abnormal molecular signaling pathways contributing to their pathogenesis.
Inserting central venous catheters
Authors: D. Young, M. Kettlewell, H. Hamilton
Journal: BMJ (1995)

Case for angiographically guided placement is not proved

EDITOR,--Andy Adam's editorial suggesting that long term central venous catheters (Hickman lines) should be placed only by interventional radiologists contains many errors that seriously weaken his argument.1 His description of “traditional” surgical placement is incorrect: the lines are placed into the internal jugular vein or, less commonly, the cephalic vein and not, as he suggests, into the subclavian vein. The risks of arterial puncture in patients with coagulopathies is overstated, simply because coagulopathies should always be corrected before insertion of a central venous catheter, and the use of imaging …
Abstract P29: Impaired Systemic but Preserved Cerebral Microcirculation Following Hemorrhagic Shock and Fluid Resuscitation
Authors: Zhi Wan, Shijie Sun, Giuseppe Ristagno, Yongqin Li, Max H Weil, Wanchun Tang
Journal: Circulation (2008)

Background: Decreases in buccal microcirculation are associated with severity and outcomes of circulatory shock. However, there is evidence that cerebral function is unimpaired after even severe states of hemorrhagic shock. We therefore hypothesized that in severe states of hemorrhagic shock with profound decreases in buccal microcirculation, the cerebral microcirculation may be preserved. Method: Craniotomies were performed in 15 male Sprague-Dawley rats, weighing 450–550g, to expose the parietal cortex for visualization of microcirculation. Animals were then bled via a catheter advanced into the descending aorta. An estimated 35% or 25% of blood volume was bled over 60 minutes and measurements were compared with unbled control. Sixty minutes after onset of hypotension, bled animals received normal saline infused over 30 minutes in amounts equivalent to two times the volume of shed blood. Cerebral and buccal microcirculations were visualized with orthogonal polarization spectral imaging. Result: Reductions in mean arterial pressure (MAP) were partially reversed after fluid infusion (Figure 1 ). Buccal microcirculation was restored to baseline level after the 25% blood loss and partially restored after the 35% loss. The cerebral microcirculation, however, was unchanged during both hemorrhagic hypotension and following volume repletion. Conclusion: In contrast to the striking reduction in arterial pressure and systemic microcirculation, the cerebral microcirculatory blood flow was preserved during hemorrhagic shock of moderate and severe degrees. These findings confirm a dissociation between the macrocirculation and the cerebral microcirculation.
Immune response with sipuleucel-T in patients (pts) with metastatic castration-resistant prostate cancer (mCRPC): Phase II ProACT study.
Authors: Thomas A. Gardner, Daniel Peter Petrylak, John M. Corman, Simon Hall, Ralph Weinstein, Robert Keyser, Robert Brownell Sims, Amanda Sanders, Nadeem A. Sheikh, Celestia S. Higano
Journal: Journal of Clinical Oncology (2013)

148 Background: Sipuleucel-T is an autologous cellular immunotherapy for asymptomatic or minimally symptomatic mCRPC. Sipuleucel-T prepared using 10μg/mL PA2024 (PAP-GM-CSF antigen) stimulates immune responses and prolongs overall survival (OS). ProACT is an ongoing phase 2 study to evaluate immune responses and OS of sipuleucel-T when manufactured using 3 different concentrations of PA2024. Here we report data from the FDA-approved concentration, 10μg/mL PA2024 (n=40). Methods: Pts with asymptomatic or minimally symptomatic mCRPC (n=120) received sipuleucel-T manufactured using 2, 5 or 10μg/mL PA2024 for a total of 3 infusions with 2-wk intervals. Peripheral immune responses were evaluated 2, 4 and 6 mo after 1 st infusion by serum ELISA (n=40), and B cell activation phenotype was characterized during the manufacture of the product by flow cytometry (n=19). Results: During product manufacture both mature and memory B cells were activated; the percentage of B cells that had a mature phenotype (defined as CD20 + IgD + CD27 + CD86 + ) was increased only after culture of each successive treatment. Activated memory B cells (defined as CD20 + IgD - CD27 + CD86 + ) were also increased after culture of each successive treatment and in pre-culture cells at the 3 rd treatment. At mo 2, median serum anti-PA2024 and anti-PAP titers (IgG and IgM combined) were 128 and 32-fold higher vs baseline respectively, compared to median serum anti-GM-CSF titers, which were 16-fold higher vs baseline. Median serum anti-PA2024 titers (IgG and IgM combined) were significantly higher than those for anti-GM-CSF (p&lt;0.001) at all timepoints and correlated with anti-PAP titers (r=0.840). PA2024 and PAP responder frequencies (IgG and IgM titers combined &gt;12,800) were 79% and 47% of pts, respectively. Anti-tetanus titers were predominantly IgG and did not differ between timepoints. Conclusions: These data indicate that sipuleucel-T induces an activated memory phenotype, evident after each culture in vivo after the first two treatments. Sipuleucel-T also appears to generate robust, long lasting anti-PA2024 and anti-PAP responses. Analyses comparing the 3 dosing cohorts will be reported in future publications. Clinical trial information: NCT00715078.
Resveratrol in the diet regulates IGF-1 signaling proteins in the prostate of rats
Authors: Leah M. Cook, Curt Harper, Coral Lamartiniere
Journal: Cancer Research (2006)

2261  Prostate cancer is the second leading cause of cancer death among men, exceeded only by lung cancer. Resveratrol, a phytoalexin, is found in red grapes and red wine. In vitro studies have shown that resveratrol can inhibit the initiation, promotion, and progression stages of carcinogenesis. Recently, resveratrol has been used in cancer chemoprevention studies to target various mitogens such as the insulin-like growth factor 1(IGF-1) signaling pathway. IGF-1 has been reported to stimulate cell cycle progression and inhibit apoptosis, two factors that are believed to contribute to cancer. In our study, Sprague Dawley rats were treated with resveratrol to investigate its mechanism of action on the IGF-1 signaling proteins in the rat ventral prostate. We hypothesized that resveratrol would suppress IGF-1 signaling. Starting at birth, Sprague Dawley rats were fed 1000 mg resveratrol/kg AIN-76A diet, a dose demonstrated by our lab to suppress prostate cancer development in mice. Control animals received phytoestrogen-free AIN-76A diet. Ventral prostates were dissected from 70 day old rats and flash frozen via liquid nitrogen until further analysis. The samples were analyzed via immuno-blot analysis and Enzyme-Linked Immunoabsorbant Assay (ELISA). Resveratrol significantly down-regulated IGF-1 receptor expression, up-regulated IGF-1 binding protein 3, and down-regulated total extracellular signaling regulating kinase 2 (ERK-2) but not significantly. It had no significant change on IGF-1, phospho-ERKs 1 and 2, and total ERK-1. The ERKs are mitogenic proteins associated with cell proliferation and tumor growth. Our results show that resveratrol suppresses the IGF-1 signaling pathway, possibly contributing to its chemopreventive actions in the prostate. Supported by DOD DAMD17-0301-0153. PR2 Diet and Cancer
Long-Term Clinical Outcome Based on Aspirin and Clopidogrel Responsiveness Status After Elective Percutaneous Coronary Intervention
Authors: Gianluca Campo, Luca Fileti, Nicoletta de Cesare, Emanuele Meliga, Alessandro Furgieri, Filippo Russo, Salvatore Colangelo, Salvatore Brugaletta, Roberto Ferrari, Marco Valgimigli
Journal: Journal of the American College of Cardiology (2010)
切尔诺贝利事件25周年祭 教训还未被汲取，对整个公共卫生的影响仍未知
Authors: Keith, Baverstock, 王富华, 张拓红
Journal: BMJ (2011)

1986年4月26号，在前苏联的切尔诺贝利发生了一场核事故。1957年英国温斯克尔核事故中获得的放射线数据，十年以来一直被用于紧急情况下的参照水平，以求在类似事故后保护英国人民的健康。在事故发生后这些数据可用于决定是否疏散民众以及实行食品控制政策。
Abstract A24: CD133 initiates tumors, induces epithelial-mesenchymal transition, and increases metastasis in pancreatic cancer
Authors: Alice Nomura, Sulagna Banerjee, Veena Sangwan, Rohit Chugh, Vikas Dudeja, Selwyn M. Vickers, Ashok K. Saluja
Journal: Cancer Research (2015)

Abstract CD133 has been implicated as a cancer stem cell (CSC) surface marker in several malignancies including pancreatic cancer, however, the functional role in the cancer stem cell remains elusive. In this study, we overexpressed CD133 CSC marker in a cell line with minimal endogenous CD133 in order to determine its functional role within a cancer context. We determined that CD133 expression led to increased tumorigenicity down to 10 cells. Progression of tumors derived from cells overexpressing CD133 increased in volume quicker than controls. Additionally, the number of lesions and sites of metastasis were increased in the orthotopic tumors derived from CD133 overexpressing cells. In vitro, CD133 expression induced epithelial-mesenchymal transition (EMT). Mesenchymal marker genes such as SNAI1, ZEB1, CDH2, and VIM increased upon CD133 overexpression and led to increased in vitro invasion by Boyden chamber invasion assay. Furthermore, our results indicate EMT induction and increased invasiveness were mediated by increased NF-κB activation upon CD133 overexpression, as inhibition of NF-κB mitigated these effects. In conclusion, this study demonstrated a functional role of CD133 in pancreatic cancer: its expression increases tumorigenicity; induces EMT; and increases invasion and metastasis. Citation Format: Alice Nomura, Sulagna Banerjee, Veena Sangwan, Rohit Chugh, Vikas Dudeja, Selwyn M. Vickers, Ashok K. Saluja. CD133 initiates tumors, induces epithelial-mesenchymal transition, and increases metastasis in pancreatic cancer. [abstract]. In: Proceedings of the AACR Special Conference on Pancreatic Cancer: Innovations in Research and Treatment; May 18-21, 2014; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2015;75(13 Suppl):Abstract nr A24.
Diagnosis and management of migraine
Authors: A. D Brown, P. M Dodson, J. R Ainsworth
Journal: BMJ (1996)

develop the intermediate neurotoxic syndrome while other equally seriously intoxicated patients do not.Paraoxon polymorphism (the genetic capability of humans to detoxify organophos- phates), toxic liposolubility, and interaction with other toxins, among other possibilities, would contribute to the development of the intermediate neurotoxic syndrome in people with atypical butyrylcholinesterase.Therefore, pseudocholinesterase activity is worth studying in further epidemiological and toxicological follow up studies on pesticide intoxication, including those recommended by
Author’s reply to English and Potter
Authors: Lilana Keith
Journal: BMJ (2015)

I would like to add a few remarks to the discussion on the efficacy of provisions for testing for and treating particular infectious diseases, such as tuberculosis, for undocumented migrants.1 2 3 Such provisions exist in several European countries, although in a few countries only testing is available, and not treatment, which has obvious medical and ethical implications.

Although certain services …
Abstract 3217: Prasugrel 60/10 mg Compared with Clopidogrel 600/75 mg Results in Fewer Poor Responders Using Definitions of Platelet Reactivity Associated with Clinical Outcomes
Authors: David Erlinge, Christoph Varenhorst, Oscar O Braun, Stefan James, Kenneth J Winters, John T Brandt, Joseph A Jakubowski, Tim Costigan, Agneta Siegbahn, Wallentin Lars
Journal: Circulation (2007)
特発性左室心室頻拍(ILVT)の心筋焼灼術においてdiastolic potentialが有用であった1例
Authors: 小田望, 小田登, 中野由紀子, 梶原賢太, 末成和義, 日高貴之, 尾木浩, 平位有恒, 寺川宏樹
Journal: Circulation (2009)
Self-reported paresthesias, Raynaud’s phenomena, tinnitus, and hearing impairment in a large cohort of long-term testicular cancer (TC) survivors
Authors: M. Brydoy, J. Oldenburg, O. Klepp, R. M. Bremnes, E. Wist, O. Dahl, S. D. Fossa
Journal: Journal of Clinical Oncology (2006)

4547 Background: Persisting side-effects of treatment may impair the well-being of TC survivors. The aim of this study was to assess long-term Raynaud’s phenomena, oto-, and neurotoxicity related to prior therapy. Methods: A follow-up survey was conducted in men treated for TC 1980–1994 in Norway. The 1319 eligible responders had a median follow-up time of 11 years (range 4–21) and were allocated to four separate treatment groups: Surgery (Surg), Radiotherapy (Rt), and chemotherapy (Cisplatin [Cis] ≤ 850 mg and Cis &gt; 850 mg). The questionnaire included six items assessing the relevant toxicities. The responders’ scores were dichotomized [minor (“not at all” or “a little”) vs. major (“quite a bit” or “very much”)] and analyzed by logistic regression with Surg as reference. Results: The proportion of cases (%) reporting major symptoms and the corresponding Odds ratios (OR) varied significantly between treatment groups ( table ). Rt was not statistically significantly different from Surg for any symptom, but showed a trend for higher scores of paresthesias in the feet. Cis &gt; 850 mg differed significantly for all symptoms with major symptoms reported by 25–49% with the highest OR (8.1) for Raynaud’s phenomena in hands. Apart from Raynaud’s phenomena, paresthesias in feet were the only symptom significantly different in Cis &lt; 850 mg compared to Surg. Conclusions: Toxicities induced by cisplatin-based chemotherapy persist in many TC survivors. A cold climate may contribute to the high perception of Raynaud’s phenomena in Norwegian TC survivors. [Table: see text] No significant financial relationships to disclose.
Self defined ethnicity is unhelpful
Authors: J. McAuley, L. De Souza, V. Sharma, I. Robinson, C. J Main, A O Frank
Journal: BMJ (1996)

the Hungarian case-control surveillance of congenital abnormalities, however, was unable to confirm that griseofulvin used during pregnancy has a teratogenic effect.6In my opinion, the anxiety and fear created by the notion that nearly all drugs cause congenital abnormalities may be more harmful than the drugs themselves.
Abstract 1292: Osteopontin Mediates The Estradiol Effect On Endothelium Regrowth By Increasing The Capacity Of Bone Marrow-derived Cells To Adhere To Endothelial Cells
Authors: Laetitia Lam Shang Leen, Cedric Filipe, Audrey Billon, Sandra Jalvy, Daniele Daret, Cecile Allieres, Laurent Brouchet, Pascale Dufourcq, Susan R Rittling, Claude Desgranges, Pierre Gourdy, Jean Francois Arnal, Alain Pierre Gadeau
Journal: Circulation (2007)

The improvement of the reendothelialization process could prevent atherosclerosis initiationand stent-induced neointima formation. We and others have demonstrated that estrogens (E2)accelerate the reendothelialization process through estrogen receptor α. However, the mechanisms involved are still poorly understood. In this work, we asked whether the multipotent protein osteopontin (OPN), which induces endothelial cells (EC) adhesion, proliferation and survival, was involved in E2 effect on reendothelialization. For this purpose, we compared the effect of E2 in wild type (OPN+/+) and OPN deficient (OPN−/−) mice. We demonstrated that OPN was required for the accelerative effect of E2 on endothelium regrowth. Moreover, we showed that E2 induced a 30% increase in EC proliferation in OPN+/+ mice but in OPN−/− mice, confirming that OPN is required for E2-mediated endothelium healing. Since E2 has been shown to act on endothelium regrowth through bone marrow (BM)-derived cells, we used a graft strategy and showed that OPN presence in the BM cells was absolutely required for the accelerative effect of E2. Since OPN was involved in adhesion processes, we hypothesized that OPN contribution in reendothelialization could be mediated through its capacity to induce a better adhesion of BM cells to the injured carotid in presence of E2. Indeed, we showed that E2 increased the adhesion of OPN using OPN+/+ and OPN−/− BM cells, that OPN was required for adhesion of these cells to EC (adhered BM cells numbering after 24h: 67 ± 44 OPN+/+ cells, 38 ± 24 OPN−/− cells and 50 ± 22 OPN−/− cells when human recombinant OPN (rOPN) was added, p<0.01). Furthermore, we showed that E2 action depended on OPN to increase adhesion of BM-derived cells on collagen I, a low-adhesive matrix for these cells compared to fibronectin. Indeed, E2 increased OPN expression in BM cells and OPN−/− BM cells showed an impaired adhesion on collagen I, which was reversed by addition of rOPN. Moreover, blocking anti-OPN antibody inhibited this E2-mediated effect. Altogether, our results suggest that E2 accelerates reendothelialization through OPN production by BM-derived cells, allowing them to adhere on the EC of the regenerating endothelium.
Abstract 15263: Myocardial Perfusion Reserve is Impaired in Patients with Chronic Obstructive Pulmonary Disease: a Quantitative Myocardial Perfusion MRI Study
Authors: Shiro Nakamori, Katsuya Onishi, Hiroshi Nakajima, Motonori Nagata, Masaki Ishida, Kakuya Kitagawa, Kaoru Dohi, Mashio Nakamura, Hajime Sakuma, Masaaki Ito
Journal: Circulation (2011)

Background: Chronic obstructive pulmonary disease (COPD) is associated with atherosclerosis and cardiovascular disease. However, limited data is available regarding the association between COPD and...
Abstract 20886: Impact of Pre-Dialysis Chronic Kidney Disease on Response to Clopidogrel in Patients Undergoing Coronary Angiography
Authors: Usman Baber, Kapil Yadav, Jeffrey Bander, Annapoorna S Kini, Jaime Uribarri, Juan J Badimon, Paul Muntner, Rucha Karajgikar, Samin K Sharma
Journal: Circulation (2010)

Background: Response to clopidogrel is highly variable and patients with increased post-treatment residual platelet reactivity (RPR) are at increased risk for adverse events. Patients with chronic ...
Abstract 9303: Dodecafluoropentane Emulsion Decreases Cerebral Infarcts in a Rabbit Embolic Stroke Model
Authors: Sean D Woods, Robert D Skinner, Aliza T Brown, John D Lowery, Paula K Roberson, William C Culp
Journal: Circulation (2011)

Introduction Dodecafluoropentane emulsion (DDFPe) absorbs, transports, and delivers very high levels of oxygen in vitro and in vivo, with the potential to protect tissues during varied ischemic episodes including stroke. DDFPe may be beneficial by protecting cells during hypoxic perturbations such as myocardial infarction, cardiac surgery, carotid interventions, or stroke. For clinical success in current stroke therapy, tPA must be given within 4.5-hours of onset. Agents that can extend this time frame by delaying ischemic damage have the potential to increase access to thrombolysis treatment and improve outcomes. Using a rabbit model of acute insoluble embolic stroke, we describe the efficacy of DDFPe at decreasing infarct volumes. Hypothesis We assessed the hypothesis that treatment with DDFPe effectively decreases infarct volumes without lysis of the arterial occlusion. Methods New Zealand White rabbits (N=45, 5.1±0.50 kg) received angiography and three embolic spheres (700-900 µm diameter) were injected into the internal carotid artery, permanently occluding the middle cerebral artery. Rabbits were randomly assigned to control (N=7, embolized without treatment) or one of three DDFPe treatment start times: pre-treatment 30-min before stroke (N=7), hyperacute treatment 0-30 min after stroke (N=13) or acute treatment 1-3 hours after stroke (N=18). DDFPe dose was 2% w/v intravenous injection, 0.6 ml/kg, at the group start time and repeated every 90 minutes as time allowed. Following euthanasia at 4 hours infarct volume was measured using vital stains on brain sections. Results Percent infarct volumes were decreased (P=0.001) for all DDFPe treated rabbits (0.73±0.51%, N=38) compared with controls (3.57±0.67%). DDFPe pre-treatment (0.64±0.65%), hyperacute treatment (0.73±0.48%) and acute treatment (0.76±0.40%) all significantly decreased infarct volumes compared to controls (P=0.021, 0.021, and 0.005, respectively). Conclusions DDFPe protects ischemic brain from hypoxia and decreases infarct volumes. Further testing is warranted of DDFPe as a therapeutic agent where delivery of oxygen may be of great benefit. Potential clinical applications may be much broader and development is urgently needed.
Stereotypy After Acute Thalamic Infarct
Authors: Sanjay Pandey, Neelav Sarma
Journal: JAMA Neurology (2015)

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