tbuckley/cabot-search huggingface dataset:
925-40 Increased Plasma Brain Natriurtic Peptide Predicts Vascular Response in Patients with Hypertophic Cardiomyopathy
Authors: Krishna Prasad, Andrew Grace, Alistair K.B. Slade, David Gordon, Carol A. Page, A. John Camm, David W. Holt, William J. McKenna
Journal: Journal of the American College of Cardiology (1995)
1,25-dihydroxyvitamin D3 potentiates the decreased response of lymphocytes from atopic subjects to agents that increase intracellular cyclic adenosine monophosphate
Authors: Amiram Ravid, Rami Tamir, Uri A. Liberman, Carmela Rotem, Albert I. Pick, Abraham Novogrodsky, Ruth Koren
Journal: Journal of Allergy and Clinical Immunology (1990)
A novel 120-kD surface antigen expressed by a subset of human lymphocytes. Evidence that lymphokine-activated killer cells express this molecule and use it in their effector function.
Authors: M R Zocchi, C Bottino, S Ferrini, L Moretta, A Moretta
Journal: The Journal of Experimental Medicine (1987)

A human cell clone (SF-16) displaying strong cytolytic activity against fresh tumor target cells was used for production of murine mAbs against surface antigens expressed by lymphokine-activated killer (LAK) cells and their peripheral blood precursors. The preliminary screening of hybridoma supernatants was performed according to the ability to bind SF-16 cells. Selected mAbs were further analyzed for their reactivity with several T and B cell lines and with peripheral blood T and non-T cell populations. A selected mAb, termed anti-LAK-1, only reacted with some T cell lines and with 15-30% of PBMC. Approximately 10-15% E-rosetting (T) cells and 40-50% E-rosette-negative cells were LAK-1+, as determined by cytofluorometric analysis. As the fluorescence distribution of LAK-1 antigen was clearly bimodal, LAK-1+ and LAK-1- cells could be separated by FACS. Positive cells were composed of large granular lymphocytes (LGL), whereas negative cells were mostly small lymphocytes and monocytes without LGL. After culture in rIL-2, purified LAK-1+ (but not LAK-1-) cells acquired the ability to lyse NK-resistant fresh melanoma target cells. In addition, only the LAK-1+ fraction of PBMC cultured for 5 d in rIL-2 lysed fresh tumor targets, thus indicating that the LAK-1 antigen is expressed also on LAK effector cells. Unlike some other LGL/NK cell markers, LAK-1 antigen is characterized by a stable expression: thus, LAK-1+ cell populations cultured for up to 20 d in rIL-2 maintained the LAK-1 antigen expression, whereas HNK-1 and, partially, CD16 were lost. Finally the cytolytic activity of LAK effector cells generated from PBMC cultured for 3 d in rIL-2 was susceptible to inhibition by the anti-LAK-1 mAb.
EVEN AFTER PERCUTANEOUS CORONARY INTERVENTION OF ANGIOGRAPHICALLY SIGNIFICANT LESIONS, IVUS-DEFINED HIGH-GRADE STENOSES ARE COMMON. A BASELINE IVUS ANALYSIS FROM THE PROSPECT TRIAL
Authors: Akiko Maehara, Gary S. Mintz, Ecaterina Cristea, Alexandra J. Lansky, Roxana Mehran, George Dangas, Barry Templin, Wai-Fung Cheong, John McPherson, Bernard de Bruyne, Naim Farhat, Steven Marso, Jean Fajadet, Michael Foster, Patrick W. Serruys, Gregg W. Stone
Journal: Journal of the American College of Cardiology (2010)
TCT-585 Circulating CD31+CD45- endothelial but not endothelial progenitor cells relate to re-endothelialization of drug-eluting stents: results from 40 patients undergoing optical coherence tomography
Authors: Thomas G. Nuehrenberg, Michael Amann, Harald Binder, Michael Gick, Franz-Josef Neumann, Christian Stratz, Dietmar Trenk, Christian M. Valina, Min Zhao
Journal: Journal of the American College of Cardiology (2013)
Points: Anticholinergic intoxication syndrome: potentiation by ethanol
Authors: G P Pullen
Journal: BMJ (1984)

but no obstructing lesion or other abnormality were found.He had an uneventful recovery.Acute pseudo-obstruction of the large bowel is a recognised, potentially fatal, clinical syndrome.'The mechanism is unknown, but the condition may be associated with serious pathology inside or outside the abdomen.'-3Our experience suggests that pulmonary thromboembolism may lead to this condition.1 Addison NV.Pseudo-obstruction of the large bowel.
Immunosuppression Enhances Oncolytic Adenovirus Replication and Antitumor Efficacy in the Syrian Hamster Model
Authors: Maria A Thomas, Jacqueline F Spencer, Karoly Toth, John E Sagartz, Nancy J Phillips, William SM Wold
Journal: Molecular Therapy (2008)

We recently described an immunocompetent Syrian hamster model for oncolytic adenoviruses (Ads) that permits virus replication in tumor cells as well as some normal tissues. This model allows exploration of interactions between the virus, tumor, normal organs, and host immune system that could not be examined in the immunodeficient or nonpermissive animal models previously used in the oncolytic Ad field. Here we asked whether the immune response to oncolytic Ad enhances or limits antitumor efficacy. We first determined that cyclophosphamide (CP) is a potent immunosuppressive agent in the Syrian hamster and that CP alone had no effect on tumor growth. Importantly, we found that the antitumor efficacy of oncolytic Ads was significantly enhanced in immunosuppressed animals. In animals that received virus therapy plus immunosuppression, significant differences were observed in tumor histology, and in many cases little viable tumor remained. Notably, we also determined that immunosuppression allowed intratumoral virus levels to remain elevated for prolonged periods. Although favorable tumor responses can be achieved in immunocompetent animals, the rate of virus clearance from the tumor may lead to varied antitumor efficacy. Immunosuppression, therefore, allows sustained Ad replication and oncolysis, which leads to substantially improved suppression of tumor growth. We recently described an immunocompetent Syrian hamster model for oncolytic adenoviruses (Ads) that permits virus replication in tumor cells as well as some normal tissues. This model allows exploration of interactions between the virus, tumor, normal organs, and host immune system that could not be examined in the immunodeficient or nonpermissive animal models previously used in the oncolytic Ad field. Here we asked whether the immune response to oncolytic Ad enhances or limits antitumor efficacy. We first determined that cyclophosphamide (CP) is a potent immunosuppressive agent in the Syrian hamster and that CP alone had no effect on tumor growth. Importantly, we found that the antitumor efficacy of oncolytic Ads was significantly enhanced in immunosuppressed animals. In animals that received virus therapy plus immunosuppression, significant differences were observed in tumor histology, and in many cases little viable tumor remained. Notably, we also determined that immunosuppression allowed intratumoral virus levels to remain elevated for prolonged periods. Although favorable tumor responses can be achieved in immunocompetent animals, the rate of virus clearance from the tumor may lead to varied antitumor efficacy. Immunosuppression, therefore, allows sustained Ad replication and oncolysis, which leads to substantially improved suppression of tumor growth.
Abstract 3699: Multi-walled carbon nanotubes induce apoptosis in normal human small airway epithelial cells through proteasome-mediated Mcl-1 protein degradation
Authors: Bao-Zhu Yuan, Joshua Chapman, Yon Rojanasakul, Vincent Castranova, Steven H. Reynolds
Journal: Cancer Research (2010)

Abstract Engineered carbon nanotubes (CNTs) are emerging as the major building blocks in nanotechnology thanks to their unique physical and chemical properties. However, widespread application of CNTs, including single- and multi-walled (SWCNTs and MWCNT), has resulted in increased public concern regarding potential toxicities from occupational or environmental exposures to CNTs. Recently, both SWCNTs and MWCNTs have been observed to exhibit pulmonary toxicities. To better understand CNT-related pulmonary toxicities, the present in vitro study used normal human small airway epithelial cells (SAEC), which constitute a primary target of respiratory exposure to CNTs, as a model to investigate cell death effects of either SWCNTs or MWCNTs. We observed that, at 24 h after exposure, greater than 5 μg/cm2 MWCNT, but not SWCNT, induced a significant dose-dependent cell death in primary cultured SAEC cells as assayed by WST-1. The cell death was accompanied by DNA damage, as indicated by the appearance of sub G0/G1 cells in a flow cytometry assay, and protein cleavages for PARP, caspases 3, 7 and 9, as revealed by Western blotting. It was further observed that the pro-apotpotic activities of MWCNT were reduced by caspase specific inhibitors, demonstrating that MWCNT, but not SWCNT, can induce a caspase-dependent apoptosis in SAEC cells. To understand regulation of the MWCNT-induced apoptosis, we then examined expression of the anti-apoptotic Bcl-2 family proteins and found that only Mcl-1 was significantly reduced in protein level by MWCNT, but not SWCNT, and such reduction was blocked by proteasome inhibitor MG132. Furthermore, it was found that reduction of Mcl-1 protein expression through Mcl-1 siRNA enhanced sensitivity of SAEC cells to MWCNT-induced apoptosis, suggesting that proteasome-mediated Mcl-1 protein degradation contributes to MWCNT-induced apoptosis. This study reveals a difference in cell death effects on normal human SAEC cells between SWCNT and MWCNT. It also provides new insights into understanding of the MWCNT-induced pulmonary toxicity. Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3699.
Feature article contains many inaccuracies
Authors: M. N. Sawka
Journal: BMJ (2012)

Cohen’s feature article contains many inaccuracies.1 I am repeatedly named for my supposed role in a poorly disguised conspiracy to dupe the public for personal gain. I will comment only on matters that I have personal experience of.

The feature implies that I have inappropriate “links” (conflicts of interest) with the sports drink industry because I work for the US military (referred to as “the biggest customer of Gatorade”), I receive monetary benefits (“not clear he receives funding directly”), and I attended exclusive Quaker Oats meetings in the 1990s. 

In answer, I do work for the US army but am not aware of (or would have any role in) any contract or arrangement that the US army might have with the makers of Gatorade …
Chemical modification of DNA with muta-carcinogens. I. 3-Amino-1-methyl-5H-pyrido[4,3-b]indole and 2-amino-6-methyldipyrido[1,2-a:3',2'-d]imidazole: metabolic activation and structure of the DNA adducts.
Authors: Y Hashimoto, K Shudo
Journal: Environmental Health Perspectives (1985)

3-Amino-1-methyl-5H-pyrido[4,3-b]indole (Trp-P-2) and 2-amino-6-methyldipyrido[1,2-a:3',2'-d]imidazole (Glu-P-1) are potent mutagen/carcinogens isolated from pyrolyzates of tryptophan and glutamic acid, respectively, and they have been found to exist in many cooked foods. Trp-P-2 and Glu-P-1 bind to DNA covalently after metabolic activations. The compounds are oxidized to the corresponding hydroxylamines (N-OH-Trp-P-2 and N-OH-Glu-P-1) by microsomes. N-OH-Trp-P-2 and N-OH-Glu-P-1 are the proximate forms of Trp-P-2 and Glu-P-1, respectively. They are further activated by cytosol to the O-acyl derivatives, which bind covalently with DNA. The structures of the modified nucleic acid bases were identified as 3-(C8-guanyl)amino-1-methyl-5H-pyrido[4,3-b]indole (Gua-Trp-P-2) and 2-(C8-guanyl)amino-6-methyldipyrido[1,2-a:3',2'-d]imidazole (Gua-Glu-P-1). These initial events caused by Trp-P-2 and Glu-P-1 were established chemically, both in vitro and in vivo.
TCT-656 Beneficial Effects Of Manual- Versus Pump Contrast Injection On Image Quality And ContRast Demand During Optical Coherence Tomography: The BIRD Study
Authors: Bert Lenaerts, Gabor Toth, Els Van Laer, Stylianos Pyxaras, De Vroey Frederic, William C. Wijns, Emanuele Barbato, Bernard De Bruyne
Journal: Journal of the American College of Cardiology (2013)
311. Target-Specific Knockdown and Enhanced Anti-Tumor Outcome by an Oncolytic Virus- Delivered Small Interfering RNA (siRNA)
Authors: Alex W. Tong, Yu-An Zhang, Shirley Samuel, Patrick Chen, Yuqiao Shen, John Nemunaitis
Journal: Molecular Therapy (2006)

Small interfering RNAs (siRNA) are small double stranded RNA molecules that mediate specific and highly potent post- transcriptional gene knockdown. siRNA-mediated knockdown of relevant genes resulted in tumor growth inhibition in a variety of human cancer cell types. However, clinical applicability of this technology has been hindered by the lack of an optimal delivery platform. We examined the use of the conditional replicative, oncolytic virus ONYX-411 to deliver an siRNA that knocks down the K-rasv-12 mutant oncogene overexpressed in many cancer cells. ONYX-411 carries an E1A deletion and E2F-1 conditional promoters in the E1 and E4 regions, hence limiting replication to cancer cells with a defective retinoblastoma tumor suppressor protein (pRB) pathway and E2F-1 overexpression. Viral oncolysis and replication lead to tumor cell reinfection, which is expected to amplify siRNA-knockdown effects. In proof-of-principle studies, we observed additive tumor growth inhibitory responses through siRNA-mediated K-ras knockdown and ONYX-411 infection. siRNA expression at the late infectious phase did not negatively impact viral replicative activity. A novel construct (Internavec) was generated by placing the K-rasv-12-specific siRNAras-4 hairpin construct under the control of endogenous, viral E3B late gene regulatory elements of ONYX-411. When tested against a panel of viral permissive human cancer lines (H79, H441, SW480, H522, H596), Internavec displayed a significantly elevated anti-tumor response (as compared with parental ONYX-411) only in host cells expressing the relevant K- rasv-12 mutation. The required Internavec dose (MOI of 1.03) for attaining 50% tumor cell growth inhibition (ED50) was 11-fold- lower than parental ONYX-411 (MOI of 11.6) and 14x lower than the control construct containing an siRNA against the green fluorescence protein (ONYX-411-siRNAGFP, MOI of 14.7). By comparison, Internavec remains attenuated in non-malignant HMEC cells. Hence the restricted viral activity within the tumor microenvironment can potentially serve to safeguard against previously reported "off target" siRNA effects. Daily intratumoral injections with Internavec (5 @ 1×108 pfu) significantly reduced H79 pancreatic cancer xenograft growth by 85.5 %, including complete growth suppression in 3 of 5 mice. Parental ONYX-411 or ONYX-411-siRNAGFP was markedly less effective (47.8% growth reduction, p=0.03; and 44.1% growth reduction, p=0.03, respectively). These findings indicate that Internavec can generate a two-pronged attack on tumor cells through oncogene knockdown and viral oncolysis, leading to significantly enhanced antitumor outcomes.
Abstract C55: Investigating mechanisms of gastrointestinal polyposis and osteoblastic tumor formation induced by mesenchymal Lkb1 deficiency
Authors: Kaisa Laajanen, Saara Ollila, Iris PL Wong, Kari Vaahtomeri, Gustavo Leone, Benoit Viollet, Makela P. Tomi
Journal: Cancer Research (2013)

Abstract Lkb1 has emerged as an important tumor suppressor gene in both sporadic and hereditary cancer. Inactivating germline mutations in the LKB1 gene underlie familial Peutz-Jeghers Syndrome (PJS), a cancer-prone disorder characterized by predisposition to gastrointestinal polyposis. Targeted disruption of Lkb1 in mesenchymal smooth muscle cells was sufficient to recapitulate PJS-type polyposis in mice (Katajisto et al, 2008) and Lkb1 heterozygous mice develop osteoblastic tumors (Robinson et al, 2008). To investigate the mechanism(s) by which Lkb1 loss in mesenchymal tissues drives tumorigenesis, we deleted Lkb1 using two mesenchymal deletors (Fsp1-Cre and Twist2-Cre) expressed in mesenchymal progenitors. Heterozygous deletion of Lkb1 with either Fsp1-Cre (Lkb1flox/+;Fsp1-Cre) or Twist2-Cre (Lkb1flox/+;Twist2-Cre) results in both polyposis and osteoblastic tumor. Homozygous Lkb1 deletion using Fsp1-Cre (Lkb1flox/flox;Fsp1-Cre) leads to rapid polyposis and osteoblastic tumors with complete penetrance, indicating that complete loss of Lkb1 is advantageous for tumorigenesis. AMPK, a key substrate of Lkb1 connected to several other tumor suppressors, has been proposed to mediate Lkb1 tumor suppressive function. However, homozygous deletion of both AMPKα1 and AMPKα2 using Fsp1-Cre does not lead to tumorigenesis. These results implicate other Lkb1 substrate kinases in tumor suppression and suggest Lkb1 loss in a common progenitor underlies mesenchymal tumorigenesis. Katajisto P, et al., (2008) LKB1 signaling in mesenchymal cells required for suppression of gastrointestinal polyposis. Nat Genet, 40(4): p. 455-9 Robinson J, et al., (2008) Osteogenic tumours in Lkb1-deficient mice. Exp Mol Pathol, 85(3): p. 223-6 Citation Format: Kaisa Laajanen, Saara Ollila, Iris PL Wong, Kari Vaahtomeri, Gustavo Leone, Benoit Viollet, Makela P. Tomi. Investigating mechanisms of gastrointestinal polyposis and osteoblastic tumor formation induced by mesenchymal Lkb1 deficiency. [abstract]. In: Proceedings of the Third AACR International Conference on Frontiers in Basic Cancer Research; Sep 18-22, 2013; National Harbor, MD. Philadelphia (PA): AACR; Cancer Res 2013;73(19 Suppl):Abstract nr C55.
Prevalence of Major Vascular Complications at the Initial Visit Among Japanese Diabetic Patients
Authors: Eishi Miki, Yasuo Akanuma, Yasunori Kanazawa, Hiroyuki Sando, Masatoshi Kikuchi, Shoji Kawazu, Kinori Kosaka
Journal: Diabetes Care (1979)

The frequencies of retinopathy, proteinuria, hypertension, and electrocardiographic (ECG) abnormalities in 2025 diabetic subjects new to our clinic in Tokyo were analyzed in relation to status at initial visit with respect to age, estimated duration of diabetes, and fasting blood glucose. Frequency and severity of retinopathy increased markedly with duration of diabetes. A relationship was found between retinopathy at first visit and level of blood glucose at that time. Proteinuria also clearly increased with duration; its frequency was generally higher in older age groups. Frequency of hypertension increased with age up to 60 yr, but there was no association between prevalence of hypertension and duration of diabetes. ECG abnormalities also increased with age, although serious abnormalities were rare even in older subjects. Hypertension and ECG abnormalities were not more common in those with higher initial blood glucose values, and the frequencies of these aberrations did not increase with the duration of diabetes. ECG abnormalities were more common among hypertensives, especially in younger age groups. Despite the clear effect of degree and duration of hyperglycemia on microvascular complications, there was no evidence of a direct effect of hyperglycemia on macrovascular abnormalities in this study.
Radiation-associated impotence. A clinical study of its mechanism
Authors: I. Goldstein
Journal: JAMA (1984)

External beam pelvic irradiation in men is frequently complicated by erectile dysfunction. We tested the erectile function in 23 patients (mean age, 65 years) who received radiation therapy for prostate cancer. Fifteen patients experienced changes in erectile potency following radiotherapy. Neurological, endocrine, and vascular testing revealed abnormalities in 0, 5, and 15 of these patients, respectively. In two, arteriography revealed bilateral occlusive disease in the distal internal pudendal and penile arteries overlying the pelvic radiation field. A significant difference with cigarette smoking was found among the 15 patients whose erectile capacity decreased and the four patients whose capacity remained unchanged. Vasculogenic impotence is the most consistent organic erectile abnormality in RAI. (<i>JAMA</i>1984;251:903-910)
DARK FIELD EXAMINATION OF TUBERCLE BACILLI
Authors: Edward W. Schoenheit
Journal: JAMA (1923)

This method of microscopic examination is chiefly used for demonstrating<i>Spirochaeta pallida</i>in the unstained specimen, but certain investigators have found it valuable in the study of stained specimens. Hoffmann<sup>1</sup>found the dark field useful in demonstrating the spirochetes of yellow fever and jaundice in stained specimens, and likewise believes that it is valuable for studying tissue sections. Ficker<sup>2</sup>used Hoffmann's method for examining flagellates. Silberstein<sup>3</sup>and Zorn<sup>4</sup>applied the method in examining other forms of bacteria, among them the tubercle bacillus, and state that they could find them much more easily and in greater numbers than in the luminous field. We have tried this method for examining specimens of sputum and urine sediment for tubercle bacilli, and found that we could see them more quickly, in greater numbers and with greater facility than with the light field, and bacilli in thick specimens could be more
1122-165 Dimerization of mitrogen-activated protein kinase and auto-phosphorylation of akt occur in the newly differentiated endothelial-like cells from adult bone marrow stem cells in vitro
Authors: Zhenguo Liu, Rong Lou, Yuehua Jing, Kapla Gupta, Catherine Verfaillie, Robert J Bache
Journal: Journal of the American College of Cardiology (2004)
Cardiorenal and neurohumoral function in a canine model of early left ventricular dysfunction.
Authors: M M Redfield, L L Aarhus, R S Wright, J C Burnett
Journal: Circulation (1993)

BACKGROUND Recent studies have reported that asymptomatic left ventricular dysfunction (ALVD) in humans is characterized by early neurohumoral activation. Specifically, atrial natriuretic factor (ANF) and norepinephrine are activated without activation of the renin-angiotensin-aldosterone system (RAAS). The current study describes hemodynamic and renal function associated with this neurohumoral profile in a canine model of early and presumably "asymptomatic" ventricular dysfunction. We hypothesized that the neurohumoral profile observed in ALVD is associated with preservation of renal function despite significant hemodynamic compromise. METHODS AND RESULTS ALVD was produced by ventricular pacing at 180 beats per minute for 10 days. Intravascular volume expansion was performed before and after producing ALVD in eight conscious dogs. The model of ALVD was characterized by decreases in ejection fraction (48 +/- 2 to 29 +/- 4%), cardiac output (4.64 +/- 0.29 to 2.89 +/- 0.17 L/min), and mean arterial pressure (119 +/- 4 to 108 +/- 4 mm Hg). Atrial pressures and systemic vascular resistance were increased. ANF (60 +/- 19 to 165 +/- 27 pg/mL) and norepinephrine (382 +/- 127 to 690 +/- 211 pg/mL) were activated, whereas the RAAS was not. Creatinine clearance and sodium excretion (UNa V) were unchanged after producing ALVD. The natriuretic response to volume expansion in ALVD was completely intact, with increases in UNa V similar to that observed with volume expansion in ALVD was completely intact, with increases in UNa V similar to that observed with volume expansion before producing ALVD. CONCLUSIONS The current study demonstrates that significant ventricular dysfunction with peripheral vasoconstriction can be associated with normal renal function and thus suggests an important functional role for the neurohumoral profile of ALVD in preserving sodium balance.
The Dynamics of Eisenmenger's Complex
Authors: H. GOLDBERG, E. N. SILBER, A. GORDON, L. N. KATZ
Journal: Circulation (1951)

Pulmonary venous blood and pulmonary venous pressure were obtained by catheterization technic in a case of Eisenmenger's complex with anomalous pulmonary venous drainage into the right auricle. This made possible measurement of the true total pulmonary vascular resistance and evaluation of a pulmonary factor in the cyanosis accompanying this anomaly. No evidence for inadequate oxygenation in the lungs was apparent, and it is concluded that the cyanosis in Eisenmenger's complex is due solely to venoarterial shunting.