tbuckley/cabot-search huggingface dataset:
p53 Acts as a Safeguard of Translational Control by Regulating Fibrillarin and rRNA Methylation in Cancer
Authors: Virginie Marcel, Sandra E. Ghayad, Stéphane Belin, Gabriel Therizols, Anne-Pierre Morel, Eduardo Solano-Gonzàlez, Julie A. Vendrell, Sabine Hacot, Hichem C. Mertani, Marie Alexandra Albaret, Jean-Christophe Bourdon, Lee Jordan, Alastair Thompson, Yasmine Tafer, Rong Cong, Philippe Bouvet, Jean-Christophe Saurin, Frédéric Catez, Anne-Catherine Prats, Alain Puisieux, Jean-Jacques Diaz
Journal: Cancer Cell (2013)
Beale Street Blues
Authors: Colleen M. Hubona
Journal: JAMA (1976)

<h3>To the Editor.—</h3> If Beale Street had talked, or yelled, or even whispered, I would have listened and would not have committed such a ghastly geographic faux pas as to locate it in New Orleans instead of Memphis (235:888, 1976). I have not gone unpunished, however. Numerous alert readers have pointed out the mistake, and, as a result, I have changed my name and moved to another city. I have tried to buy a hair shirt, but they only come in "large." My apologies to Memphis and New Orleans.
Surgery for Renovascular Hypertension
Authors: Joseph J. Kaufman, Morton H. Maxwell
Journal: JAMA (1964)

In this study, 67 cases of renovascular hypertension were followed from one to six years after vascular repair or nephrectomy. Twenty-five patients became normotensive and another 30 patients showed significant improvement. There were 18 failures and three deaths in this series. The results obtained in this series were compared with those obtained from other centers and have been analyzed in regard to the percentage of cases treated by nephrectomy versus those treated by arterial reconstruction procedures. The data indicate certain pitfalls in the preoperative diagnosis of renovascular hypertension, employing the currently available tests of radiorenography, intravenous urography, and divided kidney studies.
Atorvastatin attenuates hepatic fibrosis in rats after bile duct ligation via decreased turnover of hepatic stellate cells
Authors: Jonel Trebicka, Martin Hennenberg, Margarete Odenthal, Khanwali Shir, Sabine Klein, Michaela Granzow, Annabelle Vogt, Hans-Peter Dienes, Frank Lammert, Jürg Reichen, Jörg Heller, Tilman Sauerbruch
Journal: Journal of Hepatology (2010)
Injury prevention in people with disabilities
Authors: S. N Forjuoh
Journal: BMJ (2001)

Clinical review p 975 

Some risk of injury exists for almost every human activity, and this risk may be increased for people with impairments, disabilities, or other special healthcare needs. The mechanism of injury is insensitive to the presence or type of disability, whether the injury involves transfer of excessive kinetic energy to the body, as in physical trauma, or deprivation of an essential element such as oxygen, as in submersion. However, the additional risk associated with the underlying condition changes the dynamics of the injury process. Epidemiological studies have, for example, found that people with epilepsy have a greater risk of drowning and burns than those without the disease1–3 and that individuals with a sensory deficit are at greater risk of pedestrian injury.4 Besag's description in this week's BMJ of the death by drowning of a 14 year old boy who suffered from tonic seizures (p 975)5 raises questions about injury prevention strategies in an area where there is not much evidence. …
Abstract 1012: Osteopontin mediates loss of tumor suppressive activity of Merlin in breast cancer
Authors: K. Adam Morrow, Brandon J. Metge, Shamik Das, Keqiang Ye, Madhuri S. Mulekar, J. Allan Tucker, Rajeev S. Samant, Lalita A. Shevde
Journal: Cancer Research (2011)

Abstract The neurofibromatosis type 2 (NF2) tumor suppressor gene encodes a cytoskeletal/membranous protein, Merlin. Inactivation of the NF2 gene is known to cause tumors of the nervous system in humans and multiple cancers in mice. Although Merlin's role as a tumor suppressor has been well studied in other systems, its function in breast cancer is unknown. In this study, we have determined that the expression of Merlin protein is decreased in breast cancer tissues. Concomitantly, we observed increased expression of osteopontin (OPN), a malignancy-promoting protein that induces activation of Akt phosphorylation. Thus, there is an inverse correlation between the expression of Merlin and OPN in breast cancer. Ectopic restoration of Merlin in breast cancer cells significantly reduced attributes of malignant behavior as assessed in vitro by foci formation, soft agar colony formation, and invasion. In vivo, breast cancer cells stably expressing Merlin displayed reduced tumor growth and progression in athymic mice. Further, our investigations reveal that OPN-initiated activation of Akt signaling results in phosphorylation of Merlin at Serine 315 that targets it for proteasome-mediated degradation. Thus, our studies elucidate the utility of Merlin as an important biomarker in breast cancer and also identify a novel mechanism for the loss of Merlin expression in breast cancer. Moreover, our studies demonstrate the ability of Merlin to act as a tumor suppressor in breast cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1012. doi:10.1158/1538-7445.AM2011-1012
Coronary Angiography and Angioplasty after Acute Myocardial Infarction
Authors: David W. Bates, Elizabeth Miller, Steven J. Bernstein, Paul J. Hauptman, Lucian L. Leape
Journal: Annals of Internal Medicine (1997)

Purpose: To assess the data that support the use of coronary angiography and angioplasty after acute myocardial infarction, that identify the risks of these procedures, and that analyze their use and costs. Data Sources: English-language articles published between 1970 and June 1995 identified through a search of the MEDLINE database. Study Selection: Studies that contained information about benefits, risks, use, and costs of coronary angiography and angioplasty after acute myocardial infarction. Data Extraction: Descriptive and analytic data from each study were collected. Data Synthesis: The outcome for patients who have complications of myocardial infarction (such as shock) is poor. Such patients usually undergo angiography, although the evidence that supports this practice is weak. Preliminary data suggest that patients who immediately have angiography and angioplasty after acute myocardial infarction have better outcomes than do patients who receive thrombolytic therapy with angioplasty only for specific indications in experienced centers. After the acute phase of myocardial infarction, patients who have noninvasive evidence of persistent or recurrent ischemia are believed to benefit from angiography. In the remaining patients, however, angiography after myocardial infarction has not been shown to be beneficial. Coronary angiography is done in 30% to 81% of patients after acute myocardial infarction in different settings and regions; for many of these patients, the benefit is questionable. Better outcomes are not always associated with more frequent use of the procedure. In the United States, catheterizations after myocardial infarction cost approximately $1 billion per year. Conclusions: Although many patients benefit from angiography and angioplasty after myocardial infarction, others probably do not. Substantial resources are at stake.
Functional characteristics of intramyocardial capacitance vessels during diastole in the dog.
Authors: F Kajiya, K Tsujioka, M Goto, Y Wada, X L Chen, M Nakai, S Tadaoka, O Hiramatsu, Y Ogasawara, K Mito
Journal: Circulation Research (1986)

In order to evaluate the functional characteristics of the intramyocardial capacitance vessels during prolonged diastole, we analyzed the response of coronary vein flow after stepwise changes of coronary artery pressure in anesthetized open-chest dogs by using our newly developed laser Doppler velocimeter with an optical fiber. The peripheral portion of the great cardiac vein was isolated and the optical fiber tip was inserted into the vessel. The left anterior descending coronary artery was cannulated and connected to a reservoir to regulate coronary perfusion pressure. Intracoronary adenosine administration was carried out to avoid any change in coronary vasomotor tone. After 15 seconds of occlusion of the perfusion route, the heart was arrested by pacing-off. Two seconds later, coronary perfusion pressure was increased stepwise to a preset target pressure. This procedure was repeated by changing target pressure at 4 (or 5) different pressure levels (31-105 mm Hg). The great cardiac vein flow became zero due to the cardiac arrest and remained at zero for a moment (dead time) after the initiation of reperfusion. Then the flow reappeared and increased with first order time delay. The presence of dead time indicates the existence of unstressed volume, and the first order time delay represents the product of resistance and capacitance. The unstressed volume with a minimal vasomotor tone for perfusion pressure of 60-90 mm Hg was 5.2 +/- 2.2 ml per 100 g left ventricle, which is comparable to coronary blood flow for several beats. The capacitance at perfusion pressure of 60-90 mm Hg was 0.08 +/- 0.04 ml/mm Hg per 100 g left ventricle, while that at low perfusion pressure (30-50 mm Hg) was 0.14 +/- 0.09 ml/mm Hg per 100 g left ventricle. These results indicate that the intramyocardial capacitance vessels have two functional components, and that the phasic nature of coronary vein flow is solely the result of the myocardial squeezing of the blood in the capacitance vessels.
The Major Receptor for C-Reactive Protein on Leukocytes Is Fcγ Receptor II
Authors: Dwaipayan Bharadwaj, Mary-Pat Stein, Michael Volzer, Carolyn Mold, Terry W. Du Clos
Journal: The Journal of Experimental Medicine (1999)

C-reactive protein (CRP) is an acute phase serum protein that shares several functions with immunoglobulin (Ig)G including complement activation and binding to receptors on monocytes and neutrophils. The identity of the receptor for CRP has been the target of extensive research. We previously determined that CRP binds to the high affinity receptor for IgG, FcγRI (CD64). However, this interaction could not account for the majority of binding of CRP to neutrophils or monocytic cells. We now determine that CRP also interacts with FcγRIIa (CD32), the low affinity receptor for IgG on monocytes and neutrophils. COS-7 cells were transfected with a construct containing the human FcγRIIA cDNA. CRP binding and the presence of CD32 were detected by mAb and analyzed by two-color flow cytometry. Cells expressing CD32 bound CRP in a dose-dependent and saturable manner consistent with receptor binding. CRP bound to transfectants and K-562 cells with similar kinetics, and in both cases binding was completely inhibited by aggregated IgG. On monocytic cell lines, treatment with Bt2cAMP increased FcγRII expression and enhanced CRP binding. CRP also specifically precipitated FcγRI and FcγRII from the monocytic cell line, THP-1. It is suggested that the major receptor for CRP on phagocytic cells is FcγRII.
Telangiectasia and von Willebrand's Disease in Two Families
Authors: Charles L. Conlon, Ronald S. Weinger, Philip L. Cimo, Joel L. Moake, John D. Olson
Journal: Annals of Internal Medicine (1978)

Two families are described with members who have both von Willebrand's disease and telangiectasias. Family A has four members in three consecutive generations that have both von Willebrand's disease and telangiectasias. von Willebrand's disease in this family is characterized by decreased ristocetin cofactor (FVIII-vWF), variably depressed factor VIII coagulant (FVIII-AHG), and factor Vlll-related antigen (FVIII-AGN) levels. FVIII-AGN mobility on two-dimensional crossed immunoelectrophoresis was found to be normal. Four generations in Family B have von Willebrand's disease characterized by decreased FVIII-AHG, FVIII-vWF, FVIII-AGN, and prolonged template bleeding times. Two members of this family also have telangiectasias and recurrent gastrointestinal bleeding. Results in these two families suggest an association between von Willebrand's disease and telangiectasia—perhaps a defect in vascular endothelial cell function.
Pericardioscopy in the Etiologic Diagnosis of Pericardial Effusion in 141 Consecutive Patients
Authors: Olivier Nugue, Alain Millaire, Henri Porte, Pascal de Groote, Philippe Guimier, Alain Wurtz, Ge´rard Ducloux
Journal: Circulation (1996)

Although previous small series have documented the utility of pericardioscopy for accurate etiologic diagnosis of pericardial effusion, this technique remains underused. The aim of our study was to assess the benefits and risks of surgical pericardioscopy in a large prospective series.One hundred forty-one consecutive patients with unexplained pericardial effusion underwent 142 pericardioscopies with a rigid mediastinoscope. For each patient, the etiologic data obtained by pericardioscopy (visualization of pericardium, guided biopsies, subxiphoid window biopsy, and fluid analysis) were compared with the results that would have been obtained with only conventional surgical drainage and biopsy (subxiphoid window biopsy and fluid analysis). After complete workup, a specific cause was found in 69 cases (48.6%); the other 73 cases were considered idiopathic effusions (51.4%). Procedural and in-hospital mortality was 8 of 141 patients (5.6%). No death was directly attributable to pericardioscopy. During long-term follow-up (median duration, 24 months; range, 6 to 96), a previously unrecognized cause was discovered in 6 patients (4%). By comparing the areas under the receiver-operating characteristic curves, the diagnostic advantage of pericardioscopy was significant for the whole series (pericardioscopy, 0.98 +/- 0.011; conventional surgical drainage, 0.89 +/- 0.029; P < .001). The increase in sensitivity was more marked for some types such as neoplastic (21%), radiation-induced (100%), or purulent (83%) effusions.Our data demonstrate that pericardioscopy increases the diagnostic sensitivity of surgical pericardial drainage and biopsy without specific risk.
Extracorporeal albumin dialysis with the molecular adsorbent recirculating system in acute-on-chronic liver failure: The RELIEF trial
Authors: Rafael Bañares, Frederik Nevens, Fin Stolze Larsen, Rajiv Jalan, Agustín Albillos, Matthias Dollinger, Faouzi Saliba, Tilman Sauerbruch, Sebastian Klammt, Johann Ockenga, Albert Pares, Julia Wendon, Tanja Brünnler, Ludwig Kramer, Philippe Mathurin, Manuel de la Mata, Antonio Gasbarrini, Beat Müllhaupt, Alexander Wilmer, Wim Laleman, Martin Eefsen, Sambit Sen, Alexander Zipprich, Teresa Tenorio, Marco Pavesi, Hartmut H.-J. Schmidt, Steffen Mitzner, Roger Williams, Vicente Arroyo
Journal: Hepatology (2012)

Acute-on-chronic liver failure (ACLF) is a frequent cause of death in cirrhosis. Albumin dialysis with the molecular adsorbent recirculating system (MARS) decreases retained substances and improves hemodynamics and hepatic encephalopathy (HE). However, its survival impact is unknown. In all, 189 patients with ACLF were randomized either to MARS (n=95) or to standard therapy (SMT) (n=94). Ten patients (five per group) were excluded due to protocol violations. In addition, 23 patients (MARS: 19; SMT: 4) were excluded from per-protocol (PP) analysis (PP population n=156). Up to 10 6-8-hour MARS sessions were scheduled. The main endpoint was 28-day ITT and PP survival. There were no significant differences at inclusion, although the proportion of patients with Model for Endstage Liver Disease (MELD) score over 20 points and with spontaneous bacterial peritonitis (SBP) as a precipitating event was almost significantly greater in the MARS group. The 28-day survival was similar in the two groups in the ITT and PP populations (60.7% versus 58.9%; 60% versus 59.2% respectively). After adjusting for confounders, a significant beneficial effect of MARS on survival was not observed (odds ratio [OR]: 0.87, 95% confidence interval [CI] 0.44-1.72). MELD score and HE at admission and the increase in serum bilirubin at day 4 were independent predictors of death. At day 4, a greater decrease in serum creatinine (P=0.02) and bilirubin (P=0.001) and a more frequent improvement in HE (from grade II-IV to grade 0-I; 62.5% versus 38.2%; P=0.07) was observed in the MARS group. Severe adverse events were similar.At scheduled doses, a beneficial effect on survival of MARS therapy in patients with ACLF could not be demonstrated. However, MARS has an acceptable safety profile, has significant dialysis effect, and nonsignificantly improves severe HE.
Repeated “non-invasive” cardiac output measurements using an implanted right ventricular oxygen sensor and a hemodynamic monitor in heart failure patients
Authors: Åke Ohlsson, Rolf Nordlander, Hans Åström, Barbro Kjellström, Brian Lee, Mark Claxton, Bob Beck, Frans Ottenhoff, Tom Bennett, Lars Rydén
Journal: Journal of the American College of Cardiology (1996)
Genomic landscape of copy number aberrations enables the identification of oncogenic drivers in hepatocellular carcinoma
Authors: Kai Wang, Ho Yeong Lim, Stephanie Shi, Jeeyun Lee, Shibing Deng, Tao Xie, Zhou Zhu, Yuli Wang, David Pocalyko, Wei Jennifer Yang, Paul A. Rejto, Mao Mao, Cheol-Keun Park, Jiangchun Xu
Journal: Hepatology (2013)

Cancer is a genetic disease with frequent somatic DNA alterations. Studying recurrent copy number aberrations (CNAs) in human cancers would enable the elucidation of disease mechanisms and the prioritization of candidate oncogenic drivers with causal roles in oncogenesis. We have comprehensively and systematically characterized CNAs and the accompanying gene expression changes in tumors and matched nontumor liver tissues from 286 hepatocellular carcinoma (HCC) patients. Our analysis identified 29 recurrently amplified and 22 recurrently deleted regions with a high level of copy number changes. These regions harbor established oncogenes and tumor suppressors, including CCND1 (cyclin D1), MET (hepatocyte growth factor receptor), CDKN2A (cyclin-dependent kinase inhibitor 2A) and CDKN2B (cyclin-dependent kinase inhibitor 2B), as well as many other genes not previously reported to be involved in liver carcinogenesis. Pathway analysis of cis-acting genes in the amplification and deletion peaks implicates alterations of core cancer pathways, including cell-cycle, p53 signaling, phosphoinositide 3-kinase signaling, mitogen-activated protein kinase signaling, Wnt signaling, and transforming growth factor beta signaling, in a large proportion of HCC patients. We further credentialed two candidate driver genes (BCL9 and MTDH) from the recurrent focal amplification peaks and showed that they play a significant role in HCC growth and survival.We have demonstrated that characterizing the CNA landscape in HCC will facilitate the understanding of disease mechanisms and the identification of oncogenic drivers that may serve as potential therapeutic targets for the treatment of this devastating disease.
Transmission of occult hepatitis B virus by transfusion to adult and pediatric recipients in Taiwan
Authors: Chun-Jen Liu, Shyh-Chyi Lo, Jia-Horng Kao, Ping-Tsung Tseng, Ming-Yang Lai, Yen-Hsuan Ni, Shiou-Hwei Yeh, Pei-Jer Chen, Ding-Shinn Chen
Journal: Journal of Hepatology (2005)
Epigenetic regulation of 11β-hydroxysteroid dehydrogenase type 2 expression
Authors: Rasoul Alikhani-Koopaei, Fatemeh Fouladkou, Felix J. Frey, Brigitte M. Frey
Journal: Journal of Clinical Investigation (2004)

The enzyme 11β-hydroxysteroid dehydrogenase type 2 (11βHSD2) is selectively expressed in aldosterone target tissues, where it confers aldosterone selectivity for the mineralocorticoid receptor by inactivating 11β-hydroxyglucocorticoids. Variable activity of 11βHSD2 is relevant for blood pressure control and hypertension. The present investigation aimed to elucidate whether an epigenetic mechanism, DNA methylation, accounts for the rigorous control of expression of the gene encoding 11βHSD2, HSD11B2. CpG islands covering the promoter and exon 1 of HSD11B2 were found to be densely methylated in tissues and cell lines with low expression but not those with high expression of HSD11B2. Demethylation induced by 5-aza-2′-deoxycytidine and procainamide enhanced the transcription and activity of the 11βHSD2 enzyme in human cells in vitro and in rats in vivo. Methylation of HSD11B2 promoter–luciferase constructs decreased transcriptional activity. Methylation of recognition sequences of transcription factors, including those for Sp1/Sp3, Arnt, and nuclear factor 1 (NF1) diminished their DNA-binding activity. Herein NF1 was identified as a strong HSD11B2 stimulatory factor. The effect of NF1 was dependent on the position of CpGs and the combination of CpGs methylated. A methylated-CpG–binding protein complex 1 transcriptional repression interacted directly with the methylated HSD11B2 promoter. These results indicate a role for DNA methylation in HSD11B2 gene repression and suggest an epigenetic mechanism affecting this gene causally linked with hypertension.
Brachial plexus neuropathy after radiotherapy for breast cancer
Authors: M. F Spittle
Journal: BMJ (1995)

Lower doses and surgical management of the axilla may be the answer

It is tragic when patients are permanently harmed by a complication of treatment. One such complication, which has recently received publicity, is brachial plexus neuropathy after radiotherapy for early breast cancer.1 A group of women who perceived themselves damaged in this way formed a pressure group called RAGE (Radiotherapy Action Group Exposure). In response the Royal College of Radiologists commissioned an independent survey by two senior oncologists funded by the NHS Executive.2

The committee of RAGE received more than 1000 letters after publicity surrounding litigation and formed an action group with 800 members. Of 556 women who thought they had sustained nerve damage the college contacted those who had been treated at 15 representative centres. These women were asked if they would agree to have their medical records reviewed in order to establish whether they were suffering from a condition related to the disease process …
Failure of Transfer-Factor Therapy in Chronic Active Type B Hepatitis
Authors: Myron J. Tong, J. Scott Nystrom, Allan G. Redeker, G June Marshall
Journal: New England Journal of Medicine (1976)

Chronic active type B hepatitis, a disorder caused by the hepatitis B virus, is characterized by progressive hepatocellular damage leading to cirrhosis, portal hypertension and, in some cases, to hepatocellular carcinoma.1 Factors that allow persistent viral replication and continuous liver-cell necrosis in these patients are poorly understood, although it has been postulated that a deranged cellular immune response to invasion by the hepatitis B virus2 or decreased interferon production3 in the host may be involved. Abnormal lymphocyte-mediated responses to HBs Ag have recently been demonstrated in patients with chronic active Type B hepatitis.4 5 6 7 8 We attempted to correct the immune . . .
DIFFERENTIAL IMPACT OF FEMALE GENDER ON MORTALITY BY PRESENCE OR ABSENCE OF CHRONIC KIDNEY DISEASE FOLLOWING PCI: RESULTS FROM A SINGLE–CENTER REGISTRY WITH 15,990 PATIENTS
Authors: Usman Baber, Jason Kovacic, Pedro Moreno, Swathi Roy, Swapna Sayeneni, George Dangas, Roxana Mehran, Samin Sharma, Annapoorna Kini
Journal: Journal of the American College of Cardiology (2013)
Cardioprotective Effects of Granulocyte Colony-Stimulating Factor in Swine With Chronic Myocardial Ischemia
Authors: Hiroshi Hasegawa, Hiroyuki Takano, Koji Iwanaga, Masashi Ohtsuka, Yingjie Qin, Yuriko Niitsuma, Kazutaka Ueda, Tomohiko Toyoda, Hiroyuki Tadokoro, Issei Komuro
Journal: Journal of the American College of Cardiology (2006)