tbuckley/cabot-search huggingface dataset:
The Neurologic Assessment in Neuro-Oncology (NANO) scale: a tool to assess neurologic function for integration into the Response Assessment in Neuro-Oncology (RANO) criteria
Authors: Lakshmi Nayak, Lisa M. DeAngelis, Alba A. Brandes, David M. Peereboom, Evanthia Galanis, Nancy U. Lin, Riccardo Soffietti, David R. Macdonald, Marc Chamberlain, James Perry, Kurt Jaeckle, Minesh Mehta, Roger Stupp, Alona Muzikansky, Elena Pentsova, Timothy Cloughesy, Fabio M. Iwamoto, Joerg-Christian Tonn, Michael A. Vogelbaum, Patrick Y. Wen, Martin J. van den Bent, David A. Reardon
Journal: Neuro-Oncology (2017)

The Macdonald criteria and the Response Assessment in Neuro-Oncology (RANO) criteria define radiologic parameters to classify therapeutic outcome among patients with malignant glioma and specify that clinical status must be incorporated and prioritized for overall assessment. But neither provides specific parameters to do so. We hypothesized that a standardized metric to measure neurologic function will permit more effective overall response assessment in neuro-oncology. An international group of physicians including neurologists, medical oncologists, radiation oncologists, and neurosurgeons with expertise in neuro-oncology drafted the Neurologic Assessment in Neuro-Oncology (NANO) scale as an objective and quantifiable metric of neurologic function evaluable during a routine office examination. The scale was subsequently tested in a multicenter study to determine its overall reliability, inter-observer variability, and feasibility. The NANO scale is a quantifiable evaluation of 9 relevant neurologic domains based on direct observation and testing conducted during routine office visits. The score defines overall response criteria. A prospective, multinational study noted a >90% inter-observer agreement rate with kappa statistic ranging from 0.35 to 0.83 (fair to almost perfect agreement), and a median assessment time of 4 minutes (interquartile range, 3-5). The NANO scale provides an objective clinician-reported outcome of neurologic function with high inter-observer agreement. It is designed to combine with radiographic assessment to provide an overall assessment of outcome for neuro-oncology patients in clinical trials and in daily practice. Furthermore, it complements existing patient-reported outcomes and cognition testing to combine for a global clinical outcome assessment of well-being among brain tumor patients.
Comparison of the Phadebas RAST with the Pharmacia CAP system for insect venom
Authors: S. Jeep, E. Kirchhof, A. O'Connor, G. Kunkel
Journal: Allergy (1992)

Determination of specific IgE by RAST is a well‐established method in the diagnosis of immediate allergic reactions. In this study, we have compared the RAST with the ImmunoCAP, a novel test system which is based on a new type of solid phase. A total of 123 sera from 111 insect venom‐allergic patients (74% female) were investigated. All patients had their diagnosis confirmed on the basis of their history and skin tests with insect venom. The patients’ age showed a mean ± S of 44.2 ± 14.6 years. The total serum IgE levels ranged from 4‐1712 kU/1, with a median of 108 kU/1. The results of specific IgE, as determined by RAST and CAP, showed a significantly higher sensitivity, by almost one class, with the CAP compared with the RAST system. The quotient of specific IgE to total IgE, determined with the CAP system, could not be shown to be an expression of sensitization, compared with the severity of sting reactions (Müller classification (16)). A conversion factor for vespid venom RAST to CAP was calculated from the present data by subtracting the RAST from the CAP values. The mean delta value ± SD was found to be 0.9 ± 0.65, with a range from −0.8 to 2.7 and a median of 0.9. The data clearly show the differences between RAST and CAP‐RAST classes, indicating that the CAP‐system has a higher sensitivity and that patients with a low level sensitization are missed by the RAST method.
The absence of effect of chemical sympathectomy on ventricular hypertrophy induced by hypoxia in young rabbits
Authors: E M V. WILLIAMS, I D DUKES
Journal: Cardiovascular Research (1983)

Young rabbits, eight at a time, were exposed to 203 and 208 h (groups I and II) and 283 and 298 h (groups III and IV) of hypoxia (O2 at 70 to 80 mmHg), at atmospheric pressure. The animals were injected ip with 25 mg·kg−1 on the first day, and with 50 mg·kg−1 on the second day and every 48 h thereafter of guanethidine (G) or 6-hydroxy dopamine (6-OHDA) (O), or an equivalent volume of saline (H=hypoxic controls, or N=normoxic controls). This regime of treatment abolished, in normoxic and hypoxic animals alike, the effect of sympathetic nerve stimulation on the pupil at voltages which produced maximum dilatation in control animals. Injection of atenolol reduced heart rate by 32% in control animals, but had no effect in the guanethidine treated animals, and a very small effect in the 6-OHDA treated group. The animals in each group were litter mates of those in the other groups. In the first series the dry weight of the hypoxic right ventricles increased, relative to the normoxic controls, by 38.8% (H), 40.5% (G) and 40.9% (O). There was no left ventricular hypertrophy in the hypoxic animals, but there was a small, but not statistically significant, rise in the haematocrit (Hct). In the second series the right ventricular hypertrophy was greater (+98% (H), +89% (G) and +102% (O)). There was also a significant left ventricular hypertrophy (+38% (H), +40.3% (G) and +41% (O)) and a highly significant increase in haematocrit in all the hypoxic groups. The right atria were only slightly hypertrophied in the first series, but greatly hypertrophied in the second series (+103%, H), an effect attenuated by the treatment (+34%, G, and +39%, O). When each treated hypoxic animal was compared with its untreated hypoxic littermate (n=12), the mean treated/untreated ratio for the right ventricular dry weight was 0.991 ±0.022 for the guanethidine group (n=11) and 1.023 ± 0.043 for the 6-hydroxy dopamine (n=11). Such identity of the extent of the hypertrophy in all the hypoxic groups, irrespective of the duration of hypoxia, implies that the hypertrophy was not conditional upon sympathetic activity.
Synthesis of Tunable Theranostic Fe<sub>3</sub>O<sub>4</sub>@Mesoporous Silica Nanospheres for Biomedical Applications
Authors: Yang Zhao, Li‐Ning Lin, Yang Lu, Huai‐Ling Gao, Shao‐Feng Chen, Ping Yang, Shu‐Hong Yu
Journal: Advanced Healthcare Materials (2012)

Tunable theranostic Fe3O4@mesoporous silica nanospheres: Tunable theranostic Fe3O4@mesoporous silica nanospheres for diagnosis and gene therapy have been designed. The tunable delivery doses of imaging probe and gene by Fe3O4@mesoporous silica nanospheres can be realized by the tunable magnetic cores and modification of surface charges. These Fe3O4@mesoporous silica nanospheres may act as a theranostic nanosystem due to good biocompatibility, effective MRI diagnosis and gene delivery capabilities.
The Combined Hyperlipidemia Caused by Impaired Wnt-LRP6 Signaling Is Reversed by Wnt3a Rescue
Authors: Gwang-woong Go, Roshni Srivastava, Antonio Hernandez-Ono, Gyoungok Gang, Stephen B. Smith, Carmen J. Booth, Henry N. Ginsberg, Arya Mani
Journal: Cell Metabolism (2014)
Cryosurgical treatment of atrioventricular node reentrant tachycardia.
Authors: J L Cox, W L Holman, M E Cain
Journal: Circulation (1987)

Paroxysmal supraventricular tachycardia most commonly arises from reentry within the atrioventricular (AV) node. Although ablation of the His bundle has gained popularity for treating patients with AV node reentrant tachycardia refractory to medical therapy, undesirable sequelae include complete heart block and the necessity for a permanent pacemaker. To obviate this limitation, we have developed a discrete cryosurgical procedure that interrupts the reentrant circuit responsible for AV node reentrant tachycardia without blocking AV conduction. After first characterizing the salutary effects of this approach in experimental animals, we performed this procedure in eight patients with AV node reentrant tachycardia. Preoperative, intraoperative, and postoperative electrophysiologic studies were performed in each patient. Under conditions of normothermic cardiopulmonary bypass and during atrial pacing at a constant rate with continuous monitoring of AV conduction, nine separate 3 mm cryolesions (-60 degrees C for 2 min) were placed at predetermined sites around the triangle of Koch in the lower right atrial septum. Postoperatively, each patient had a single AV node conduction curve. No patient had AV node reentrant tachycardia induced or has experienced AV node reentrant tachycardia clinically during a follow-up of up to 5 years. The cryosurgical procedure had no detrimental effects on the AH or HV interval or on the paced cycle length at which AV node Wenckebach occurred. Based on these results, this curative operation offers promise for patients with AV node reentrant tachycardia that is refractory to medical treatment.
Ronald Victor Walley
Authors: C. Mackenzie
Journal: BMJ (2002)

Former consultant in infectious diseases and respiratory intensive care Ham Green Hospital, Bristol (b Sussex 1921; q Cambridge/University College Hospital 1945; MD), d 26 September 2001. 

Ronnie was a pioneer in the measurement of pulmonary function and in positive pressure respiration. An accomplished inventor and engineer, he designed and built most of his own equipment, including an early kidney machine. As well as a wooden disposable smallpox unit, he installed a high risk infectious disease unit at Ham Green. He was well ahead of his time, living in a Corbusier style house, which he helped to design and build. His true passion was motor cycles, of which he owned many exotic types. Predeceased by a son, he leaves a wife, Betty; and two children.
Heterogeneity of the Ro/SSA antigen. Different molecular forms in lymphocytes and red blood cells.
Authors: M D Rader, C O'Brien, Y S Liu, J B Harley, M Reichlin
Journal: Journal of Clinical Investigation (1989)

Ro(SSA) is an intracellular ribonucleoprotein against which autoantibodies are found in a portion of patients with Sjögren's syndrome and systemic lupus erythematosus. A form of Ro(SSA) is described in red blood cells that shares a line of identity with purified Ro(SSA) from bovine spleen and human lymphocytes in counterimmunoelectrophoresis, but has different molecular properties. Ro(SSA) from red blood cells exists in association with only two small RNAs as opposed to four in other cell types, as determined by RNA extraction of protein A-assisted immunoprecipitates. In addition to the common 60-kD Ro(SSA) protein, Western blot analysis revealed an additional 52-kD protein in lymphocytes and a 54-kD protein in red blood cells. The 60-kD form of Ro(SSA) in red cells was found to be antigenically distinct from that in the lymphocyte, because sera were identified that bound each exclusively. Finally, a rabbit antibovine Ro(SSA) serum distinguished red cell from lymphocyte Ro(SSA). These results suggest two distinctive populations of Ro(SSA) proteins and distributions of Ro(SSA) RNAs in the lymphocyte and red blood cell.
THE ACTION OF THE HUNTINGDON COUNTY, PA., MEDICAL SOCIETY.
Authors: Geo. C. Borst
Journal: JAMA (1891)

At the annual meeting of the Huntingdon County Medical Society, held at Huntingdon, Pa., on April 14, 1891, the following resolution was unanimously adopted: <i>Resolved</i>, That it is the opinion of the Huntingdon County Medical Society that the office of publication ofThe Journal of the American Medical Associationshould not be removed from Chicago. Illinois, and that the delegates to the American Medical Association from the Huntingdon County Medical Society, of the State of Pennsylvania, are hereby instructed to vote against the removal of the office of publication. Attest,
Phase II Study of Imatinib in Advanced Chordoma
Authors: Silvia Stacchiotti, Alessandra Longhi, Virginia Ferraresi, Giovanni Grignani, Alessandro Comandone, Roger Stupp, Alexia Bertuzzi, Elena Tamborini, Silvana Pilotti, Antonella Messina, Carlo Spreafico, Alessandro Gronchi, Paola Amore, Vincenza Vinaccia, Paolo Giovanni Casali
Journal: Journal of Clinical Oncology (2012)

Purpose To explore the antitumor activity of imatinib in patients with advanced platelet-derived growth factor β (PDGFB)/PDGF receptor β (PDGFRB)–positive chordomas. Patients and Methods In a collaborative Italian-Swiss, prospective, phase II clinical study conducted from November 2004 through April 2006, 56 patients with advanced PDGFB and/or PDGFRB chordoma received 800 mg/d of imatinib until progression. The primary end point was the overall tumor response rate (ORR), defined by RECIST. Secondary, exploratory end points included tissue response (ie, changes in tumor density or signal intensity/contrast enhancement, and/or [18F]-fluorodeoxyglucose positron emission tomography [PET] uptake), overall survival, progression-free survival (PFS), and pain score. Results Among 50 patients evaluable by RECIST, the best response was one partial response (PR) obtained at 6 months (ORR, 2%). There were 35 patients with stable disease (SD, 70%) and a 64% clinical benefit rate (ie, RECIST complete response + PR + SD ≥ 6 months). A minor dimensional response (&lt; 20%) was detected in nine patients. A maximum standard uptake value decrease ≥ 25% was observed in 10 (39%) of 26 patients evaluable for PET response at 3 months. Changes in the Brief Pain Inventory score were consistent with the response assessment. Median PFS (intention-to-treat population, 56 patients) was 9 months. No unexpected toxicities were observed. Conclusion This is the largest phase II study in chordoma to date. It confirms anecdotal evidence that imatinib has antitumor activity in this orphan disease, and therefore, it is worth further investigation.
Problems of Hyperuricemia
Authors: Solomon Fisch
Journal: JAMA (1966)

<h3>To the Editor:—</h3> We would like to comment on the interesting article by Brest et al (<b>195</b>:42, 1966). We are reluctant to endorse blanket prophylactic administration of uricosuric agents to patients with diuretic-induced hyperuricemia for the following reasons: Except for gout and uric acid stone formation, there is no evidence that hyperuricemia is causally related to the other listed diseases. In the latter conditions hyperuricemia could be a coincidental chemical finding. In our Diuretic Clinic where we have studied hundreds of patients, receiving a variety of diuretics, for very long periods of time, the incidence of hyperuricemia is about 50%, yet the overwhelming majority of these patients showing persistent hyperuricemia have not shown any ill effects from this deviation, including gout. Indeed, considering the vast clinical use of these drugs over the last several years, one should have begun to see by now a heightened incidence of
Adenovirus-mediated expression of p35 prevents hypoxia/reoxygenation injury by reducing reactive oxygen species and caspase activity
Authors: T Date
Journal: Cardiovascular Research (2002)

This study aimed to examine the effects of adenovirus-mediated expression of p35, a baculovirus gene, on apoptosis induced by hypoxia/reoxygenation (H/R) in cardiomyocytes.Neonatal rat cardiomyocytes were infected with recombinant adenoviral vectors expressing p35 (Ad2/CMVp35) or no transgene (Ad2/CMVEV) and were then subjected to H/R. Separate groups of non-infected cardiomyocytes were treated with pharmacological caspase inhibitors or antioxidants. Cell viability, apoptosis, caspase activity, and cellular reactive oxygen species (ROS) were measured using various assays.H/R decreased cell viability and increased cellular ROS levels, caspase activity, and cell apoptosis. Infection with Ad2/CMVp35 effectively inhibited the increase in cellular ROS levels, the activities of caspases 3 and 8, apoptosis, and cell death following H/R, whereas Ad2/CMVEV had no effect. Despite its ability to abolish the increase in caspase activity and partially inhibit apoptosis, the pan-caspase inhibitor ZVAD-fmk (100 microM) failed to significantly reduce cell death induced by H/R. N-acetyl-L-cysteine, an antioxidant, completely inhibited H/R-induced increase in cellular ROS levels, but reduced apoptosis and cell death by 30% only.Adenovirus-mediated expression of p35 effectively inhibits H/R-induced cardiomyocyte apoptosis by reducing cellular ROS levels and inhibiting caspase activity.
Immunosuppression — The Promise of Specificity
Authors: Julie R. Ingelfinger, Robert S. Schwartz
Journal: New England Journal of Medicine (2005)

The success of organ transplantation owes much to improvements in the immunosuppressive regimens that prevent or suppress allograft rejection. Nevertheless, the potent immunosuppressive drugs that are now in general use increase susceptibility to infection and cancer and can also have adverse effects not directly related to immunosuppression.Conventional immunosuppressive agents affect not only immune cells but also other cells. Glucocorticoids, for example, can cause a myriad of side effects,1 but these harmful actions are often minimized by combining glucocorticoids with other immunosuppressive medications. In use since the early days of transplantation, small-molecule immunosuppressive drugs act by targeting DNA or proteins . . .
Acute Cardiovascular Management: Anesthesia and Intensive Care
Authors: Ronald M. Meyer
Journal: JAMA (1983)

This is a large book whose authors come from all parts of the country, though most are from Stanford's anesthesia department. It covers much of what is currently accepted about the perioperative management of the patient having cardiac surgery. I think this book achieves the goal of elucidating the contemporary theory and practice of acute cardiovascular therapeutics. The opus presents a mass of observations, concepts, and knowledge, which has accumulated so rapidly and in so many places that it has been hard for the trainee or practitioner to master. In fact, organized access to thousands of recent and relevant references may be the greatest strength of this volume. The topics of the 28 chapters range from myocardial energetics and cellular physiology to pacing and cardiac catheterization, management of heart transplants and ventricular mapping, and even the education of the cardiac anesthesiologist. In my view, opinion is not always adequately separated
The effect of mannitol following permanent coronary occlusion.
Authors: H O Hirzel, E S Kirk
Journal: Circulation (1977)

Quantitative comparisons of infarcts 24 hours after ligation of the left anterior descending coronary artery (LAD) via thoracotomy were made in 13 control and 13 dogs treated with i.v. 25% mannitol, 2 ml/min for 4 hours following occlusion. Mannitol increased serum osmolarity by 44+/-4 mOsm/L (mean +/- 1 SE) with hemodynamic effects limited to a small increase in left ventricular dP/dt. Nonperfusible tissue measured by planimetry at 24 hours was similar in both groups (46+/-4% of area defined with dye injected into the distal LAD for control versus 48+/-5% for mannitol treated dogs, P = NS). Creatine phosphokinase activity in infarcted tissues was also similar in both groups. Myocardial blood flows measured with radioactive microspheres were also similar in both groups. Collateral conductance calcultaed from retrograde flow and aortic pressure increased with the 24 hour period by 146+/-23% in the control dogs; in the mannitol treated dogs, collateral increased only 38+/-14% (P less than 0.001). Thus mannitol had no effect on ultimate infarct size. Moreover, mannitol appeared to hinder the development of collateral vessels.
Depressed Bronchoalveolar Urokinase Activity in Patients with Adult Respiratory Distress Syndrome
Authors: Paul Bertozzi, Birgir Astedt, Laura Zenzius, Karen Lynch, Françoise LeMaire, Warren Zapol, Harold A. Chapman
Journal: New England Journal of Medicine (1990)

Abundant deposition of bronchoalveolar fibrin and fibronectin occurs during the exudative phase of the adult respiratory distress syndrome (ARDS), promoting hyaline-membrane formation and subsequent alveolar fibrosis. To explore the mechanisms that account for the persistence of bronchoalveolar fibrin and fibronectin, we compared the activity of urokinase, which is necessary for plasminogen activation and fibrin degradation, in cell-free bronchoalveolar-lavage fluid from 8 patients with ARDS, 9 patients with acute pulmonary diseases other than ARDS, and 10 normal subjects.
Chronic Ischemic Gastritis: Case Report of a Difficult Diagnosis and Review of the Literature
Authors: V. Quentin, N. Dib, F. Thouveny, P. L’Hoste, A. Croue, J. Boyer
Journal: Endoscopy (2006)

Chronic ischemic gastritis is an unusual entity that is rarely distinguished from other forms of intestinal ischemia. On the basis of a case encountered and a subsequent review of the literature, the main features of this rare condition are described here. A better understanding and awareness of the disease should improve the diagnosis and ultimately also the prognosis.
US hospital mergers threaten reproductive services
Authors: J. H. Tanne
Journal: BMJ (1997)

Mergers and affiliations between Catholic and non-sectarian hospitals are threatening reproductive health care in the United States. Driven by managed care, hospitals are merging to reduce costs, increase efficiency, obtain a larger share of the market, and improve their negotiating strength.

“Chief operating officers are confronted by demands to follow religious rules to achieve business success,” said Lois Uttley, director of Family Planning Advocates of New York state.

Catholic institutions do not provide abortions, tubal ligations, vasectomies, contraceptive counselling, in vitro fertilisation, condoms …
RM-04 * RETINOBLASTOMA BINDING PROTEIN 4 (RBBP4) MODULATES TEMOZOLOMIDE RESPONSE THROUGH REGULATION OF MGMT EXPRESSION IN GLIOBLASTOMA
Authors: G. Kitange, M. Schroeder, J. Sarkaria
Journal: Neuro-Oncology (2014)

Through shRNA library screen we identified RBBP4 as a modulator of TMZ response in glioblastoma (GBM). Consequently, we investigated the mechanisms whereby RBBP4 modulates TMZ response using shRNA to silence this gene in MGMT-expressing T98G and U138 GBM cells. The cytotoxicity was evaluated using fluorescence-based CYQUANT proliferation assay. A total of 4 shRNA constructs significantly suppressed RBBP4 in both T98G and U138. Cells expressing non-specific targeting shRNA (NT-shRNA) were used as control. RBBP4 knockdown significantly sensitized TMZ both in T98G and U138 cells; the relative fluorescence for the TMZ-treated (100 µM) control T98NT-shRNA cells was 1.17 ± 0.15, whereas for T98RBBP4-shRNA clones were 0.54 ± 0.02, 0.29 ± 0.03, 0.36 ± 0.05, and 0.34 ± 0.03, respectively (p < 0.001). Similar sensitization was observed in U138 cells; relative fluorescence for the TMZ-treated (300 µM) control U138NT-shRNA cells was 0.70 ± 0.05 and for U138RBBP4-shRNA clones were 0.42 ± 0.06, 0.27 ± 0.01, 0.28 ± 0.02, and 0.30 ± 0.01, respectively (p < 0.001). Interestingly, knockdown of RBBP4 in T98G was accompanied with a synthetic lethality to PARP inhibition and increased response to TMZ-induced DNA damage, as evidenced by increased phosphorylation of KAP1, CHK1 and CHK2. Moreover, phosphorylation of H2AX in response to TMZ treatment was significantly higher in T98RBBP4-shRNA clones. Consistent with deficient homologous recombination (HR), T98RBBP4-shRNA clones significantly expressed less RAD51 compared with the control T98NT-shRNA cells. Even more interesting, RBBP4 knockdown silenced MGMT expression in both T98G and U138, which was accompanied by decreased recruitment of acetylated H3K9 coupled with increased recruitment of tri-methylated H3K9. Moreover, RBBP4 knockdown was coupled with loss of p300 recruitment to bind MGMT promoter region. Collectively, these findings suggest that RBBP4 modulates TMZ response in GBM cells through epigenetic regulation of MGMT, and perhaps through RAD51-mediated HR repair of DNA damage in selected GBM cells.