tbuckley/cabot-search huggingface dataset:
A STUDY OF CARDIOPULMONARY ALTERATIONS IN PATIENTS WITH SICKLE CELL DISEASE AND ITS VARIANTS1
Authors: Brian J. Sproule, E. Richard Halden, William F. Miller
Journal: Journal of Clinical Investigation (1958)

It has recently become apparent that a high proportion of individuals who possess S type he- moglobin exhibit significant desaturation of the arterial blood.In 1942 Klinefelter (1) found arterial oxygen saturations of 89 and 91 per cent in two patients, and in 1943 Reinhard, Moore, Dubach, and Wade (2) found values ranging from 74.2 to 90.8 per cent saturation in one pa- tient with sickle cell disease.Leight, Snider, Clifford, and Hellems (3) studied 13 patients with sickle cell disease in 1954, 10 of whom had arterial 02 desaturation.Within the past year reports from this laboratory (4, 5) and from Jen- sen, Rucknagel, and Taylor (6) indicate that de- saturation of arterial blood exists in most people who possess S type hemoglobin.The exact mech- anism responsible for this phenomenon has not been elucidated.The various possibilities may be distinguished with fair accuracy by determining alveolar and arterial oxygen tensions and calculating A-a oxy- gen tension gradients at three levels of oxygena- tion.If desaturation is due to hypoventilation, no appreciable gradient exists at any level of oxy- genation and CO2 retention is usually evident.Any increase in A-a gradient must, therefore, be due to some other mechanism.Lilienthal, Riley, Proemmel, and Franke (7) suggested that one might distinguish between a diffusion defect and veno-arterial admixture by measurement of the effective alveolar-arterial gradient at two levels of oxygenation, one of which produces significant desaturation of arterial blood.Low levels of in- spired 02 (12 to 14 per cent) exaggerate the ef- fects of impaired diffusion and minimize the ef- fects of veno-arterial admixture.Veno-arterial admixture, thus delineated, may be either through actual anatomical communications, or the result of reduction in the ventilation-perfusion ratios.
Correlation of Serum Creatinine Concentration and Kanamycin Half-Life
Authors: Ralph E. Cutler
Journal: JAMA (1969)

The serum half-life of kanamycin sulfate following an intramuscularly administered dose was compared to the serum creatinine concentration in ten adult patients with different degrees of renal failure. Because a linear correlation was found, the kanamycin half-life (in hours) could be estimated by multiplying the serum creatinine concentration (mg/100 ml) by three. As the apparent distribution volume for kanamycin is similar to the extracellular volume and averages 19% of body weight, an injection of 7 mg/kg of body weight will result in therapeutic drug levels. Kinetic analysis predicts that repetition of this loading dose every third half-life will result in therapeutic, nontoxic serum levels in patients with renal failure.
Chimeric NKG2D Receptor–Bearing T Cells as Immunotherapy for Ovarian Cancer
Authors: Amorette Barber, Tong Zhang, Leslie R. DeMars, Jose Conejo-Garcia, Katherine F. Roby, Charles L. Sentman
Journal: Cancer Research (2007)

Despite advancements in the treatment of ovarian cancer, this disease continues to be a leading cause of cancer death in women. Adoptive transfer of tumor-reactive T cells is a promising antitumor therapy for many cancers. We designed a chimeric receptor linking NKG2D, a natural killer (NK) cell-activating receptor, to the CD3zeta chain of the T-cell receptor to target ovarian tumor cells. Engagement of chimeric NKG2D receptors (chNKG2D) with ligands for NKG2D, which are commonly expressed on tumor cells, leads to T-cell secretion of proinflammatory cytokines and tumor cytotoxicity. In this study, we show that >80% of primary human ovarian cancer samples expressed ligands for NKG2D on the cell surface. The tumor samples expressed MHC class I-related protein A, MICB, and UL-16 binding proteins 1 and 3. ChNKG2D-expressing T cells lysed ovarian cancer cell lines. We show that T cells from ovarian cancer patients that express chNKG2D secreted proinflammatory cytokines when cultured with autologous tumor cells. In addition, we show that chNKG2D T cells can be used therapeutically in a murine model of ovarian cancer. These data indicate that treatment with chNKG2D-expressing T cells is a potential immunotherapy for ovarian cancer.
The Pyelogram-Urea Washout Test
Authors: Melvyn H. Schreiber, Harry E. Sarles, Maurice E. Herring, August R. Remmers
Journal: New England Journal of Medicine (1964)

RENAL-artery narrowing leading to decreased perfusion pressure may result in an exaggerated secretion of renin by the juxtaglomerular cells of the involved kidney,1 with subsequent production of angiotensin leading to systemic hypertension. Because the measurement of renin and angiotensin is extremely difficult several indirect tests have been employed to facilitate the diagnosis of insufficiency of the renal artery. acid concentrations are increased in the urine from the involved kidney. Modern urographic contrast mediums are filtered by the glomerulus but are not reabsorbed by the tubules.4 Therefore, in patients with unilateral renal-artery insufficiency, increased water reabsorption without reabsorption of contrast material . . .
Valvular Heart Disease and the Use of Dopamine Agonists for Parkinson's Disease
Authors: Renzo Zanettini, Angelo Antonini, Gemma Gatto, Rosa Gentile, Silvana Tesei, Gianni Pezzoli
Journal: New England Journal of Medicine (2007)

Ergot-derived dopamine receptor agonists, often used in the treatment of Parkinson's disease, have been associated with an increased risk of valvular heart disease.
ECHOCARDIOGRAPHIC ASSESSMENT OF LEFT VENTRICULAR ROTATION AS A PREDICTOR OF ADVERSE EVENTS IN HYPERTROPHIC CARDIOMYOPATHY
Authors: Jaroslaw D. Kasprzak, Adam Smialowski, Karina Wierzbowska, Paulina Wejner-Mik, Pawel Zycinski, Magorzata Kurpesa
Journal: Journal of the American College of Cardiology (2012)
Long-Term Results of Operative Treatment for Renal Hypertension.
Authors: Annette Fitz
Journal: Annals of Internal Medicine (1970)

Meeting Abstracts1 May 1970Long-Term Results of Operative Treatment for Renal Hypertension.Annette Fitz, M.D., Elizabeth Thompson, M.D., Walter Kirkendall, M.D., F.A.C.P.Annette Fitz, M.D.Search for more papers by this author, Elizabeth Thompson, M.D.Search for more papers by this author, Walter Kirkendall, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-72-5-803_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThree years ago we published a study of 50 patients operated on for renal hypertension. Postoperatively, nine were "cured" with a blood pressure of 140/90 mm Hg or below without therapy (average follow-up, 16.6 months), 16 were "improved" at 19.5 months average with a fall in mean blood pressure of at least 20 mm Hg without additional drug therapy. We have reevaluated these patients to better define the long-term benefits of operative treatment for renal hypertension. Of the cured patients, now followed an average of 43 months, five are still cured, and all had nonatherosclerotic renal artery stenosis. Two are... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Iowa City, Iowa PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 May 1970Volume 72, Issue 5Page: 803-803KeywordsBlood pressureDrug therapyFallsHypertensionRenal arteriesStenosis Issue Published: 1 May 1970 PDF DownloadLoading ...
Airway surface mycosis in chronic TH2-associated airway disease
Authors: Paul C. Porter, Dae Jun Lim, Zahida Khan Maskatia, Garbo Mak, Chu-Lin Tsai, Martin J. Citardi, Samer Fakhri, Joanne L. Shaw, Annette Fothergil, Farrah Kheradmand, David B. Corry, Amber Luong
Journal: Journal of Allergy and Clinical Immunology (2014)
Treatment without consent: emergency
Authors: C D Jolly
Journal: BMJ (1985)

naire), stress (mood adjective checklist), and depression (daily symptom record)).Thus, of the 28 variables reported on, only five (17 9%) were found to be significantly improved by progesterone during the first month of treatment (table II) and four (14 3%) overall during the four months of the study (table III).Secondly, and similarly, the apparently impres- sive graph of the total menstrual distress question- naire scores during the four months of treatment, by omitting any index of the range of the results, belies the fact that the difference between placebo and progesterone as judged by that particular value was actually statistically insignificant.This is clearly evident from the results quoted in tables II and III, which form the basis for the graph.Thirdly, for most symptoms of the premenstrual syndrome, including three of the four most commonly reported complaints quoted by the authors in table I, this controlled study has shown that progesterone is neither clinically nor statistic- ally superior to placebo.
Language and analogy in conceptual change
Authors: Dedre Gentner, Nina Simms
Journal: Behavioral and Brain Sciences (2011)

Abstract Carey proposes that the acquisition of the natural numbers relies on the interaction between language and analogical processes: specifically, on an analogical mapping from ordinal linguistic structure to ordinal conceptual structure. We suggest that this analogy in fact requires several steps. Further, we propose that additional analogical processes enter into the acquisition of number.
Abstract LB-220: The Integrinβ1/Src/Akt-driven bypass signaling pathway contributes to Erlotinib resistance in lung cancer.
Authors: Mayumi Ono, Rina Kanda, Kosuke Watari, Akihiko Kawahara, Masayoshi Kage, Hidetaka Uramoto, Michihiko Kuwano
Journal: Cancer Research (2013)

Abstract Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) such as gefitinib and erlotinib have improved therapeutic efficacies on non-small cell lung cancer (NSCLC) harboring activating EGFR mutations. However, appearance of drug resistant mutation limits patients' outcome. A secondary T790M mutation and MET amplification are two major mechanisms of acquired EGFR-TKI resistance. To develop novel therapeutics to overcome drug resistant tumors, we should further understand other mechanisms at molecular basis of intrinsic importance. We established erlotinib or gefitinib resistant cell lines from PC9 cells that harbor an activating EGFR deletion mutation by chronic exposure to these TKIs. We have previously identified that loss of PTEN or loss of activated EGFR gene allele is responsible for acquired resistance (Cancer Res., 2010; Nat Med., 2011; PLoS ONE, 2012; Cancer Sci., 2013). In our present study, one erlotinib-resistant subline from PC9 cells revealed following interesting characteristics; [1] The increased expression of integrins β1, α2, and α5 was observed, along with enhanced adhesion and migratory activity in the resistant sublines. [2] The increased expression and activation of Src was also observed. [3] Interestingly, integrinβ1 knockdown markedly restored sensitivity to erlotinib and reduced the activation of Src and Akt upon treatment with erlotinib. [4] Furthermore, Src knockdown suppressed Akt phosphorylation and cell growth, and this inhibitory effect was further augmented by erlotinib. [5] The expression of integrins β1 and α5 was also observed in a refractory tumor sample from a lung cancer patient treated with erlotinib. Together, we will present our novel concept that integrinβ1/Src/Akt pathway represents a novel a bypass effector pathway for the acquisition of resistance to EGFR-TKIs. Citation Format: Mayumi Ono, Rina Kanda, Kosuke Watari, Akihiko Kawahara, Masayoshi Kage, Hidetaka Uramoto, Michihiko Kuwano. The Integrinβ1/Src/Akt-driven bypass signaling pathway contributes to Erlotinib resistance in lung cancer. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr LB-220. doi:10.1158/1538-7445.AM2013-LB-220
Large-scale genotoxicity assessments in the marine environment.
Authors: J E Hose
Journal: Environmental Health Perspectives (1994)

There are a number of techniques for detecting genotoxicity in the marine environment, and many are applicable to large-scale field assessments. Certain tests can be used to evaluate responses in target organisms in situ while others utilize surrogate organisms exposed to field samples in short-term laboratory bioassays. Genotoxicity endpoints appear distinct from traditional toxicity endpoints, but some have chemical or ecotoxicologic correlates. One versatile end point, the frequency of anaphase aberrations, has been used in several large marine assessments to evaluate genotoxicity in the New York Bight, in sediment from San Francisco Bay, and following the Exxon Valdez oil spill.
Tessa Louise Whitton
Authors: Stephen Hill
Journal: BMJ (2007)

<h3>Background and objectives</h3> Cancer survival is improving along with an increase in the potential for adverse kidney effects from antineoplastic treatments or nephrectomy. We sought to describe recent trends in the incidence of kidney failure related to antineoplastic treatments and urinary tract cancers and evaluate patient survival and kidney transplantation access. <h3>Design, setting, participants, &amp; measurements</h3> We used the French Renal Epidemiology and Information Network registry to identify patients with kidney failure related to antineoplastic treatments or urinary tract cancer from 2003 to 2015. We identified 287 and 1157 cases with nephrotoxin- and urinary tract cancer–related kidney failure, respectively. The main study outcomes were death and kidney transplantation. After matching cases to two to ten controls (<i>n</i>=11,678) with other kidney failure causes for age, sex, year of dialysis initiation, and diabetes status, we estimated subdistribution hazard ratios (SHR) of each outcome separately for patients with and without active malignancy. <h3>Results</h3> The mean age- and sex-adjusted incidence of nephrotoxin-related kidney failure was 0.43 (95% CI, 0.38 to 0.49) per million inhabitants and 1.80 (95% CI, 1.68 to 1.90) for urinary tract cancer–related kidney failure; they increased significantly by 5% and 2% annually, respectively, during 2006–2015. Compared with matched controls, age-, sex-, and comorbidity-adjusted SHRs for mortality in patients with nephrotoxin-related kidney failure were 4.2 (95% CI, 3.2 to 5.5) and 1.4 (95% CI, 1.0 to 2.0) for those with and without active malignancy, respectively; for those with urinary tract cancer, SHRs were 2.0 (95% CI, 1.7 to 2.2) and 1.1 (95% CI, 0.9 to 1.2). The corresponding SHRs for transplant wait-listing were 0.19 (95% CI, 0.11 to 0.32) and 0.62 (95% CI, 0.43 to 0.88) for nephrotoxin-related kidney failure cases and 0.28 (95% CI, 0.21 to 0.37) and 0.47 (95% CI, 0.36 to 0.60) for urinary tract cancer cases. Once on the waiting list, access to transplantation did not differ significantly between cases and controls. <h3>Conclusions</h3> Cancer-related kidney failure is slowly but steadily increasing. Mortality does not appear to be increased among patients without active malignancy at dialysis start, but their access to kidney transplant remains limited.
960-85 Implantation of a Single-Lead Unipolar Transvenous Cardioverter/Defibrillatior (ICD) Under Local Anesthesia
Authors: Günter Stix, Anahit Anvari, Martin Grabenwoger, Susanne Asenbaum, Zeynep Türel, Gerald Maurer, Herwig Schmidinger
Journal: Journal of the American College of Cardiology (1995)
Abstract 2535: Regulation of Chk1 by the mTOR pathway is essential for cancer cells to complete DNA replication in response to replication stress
Authors: Changxian Shen, Greicy H. Goto, Duane J. Oswald, Hakan Cam, Raushan Kurmasheva, Katsumi Kitagawa, Peter J. Houghton
Journal: Cancer Research (2012)

Abstract Oncogenic signaling leads to DNA replication stress, DNA damage and consequently DNA damage response (DDR), a barrier for tumorigenesis. For survival and proliferation, cancer cells must overcome this oncogene-induced DDR, but the molecular mechanism by which this is achieved is largely unknown. Here we report that the mTOR pathway prevents either spontaneous or drug induced DNA damage by sustaining ATR-Chk1 checkpoint in pediatric rhabdomyosarcoma (RMS) both in vivo and in vitro. Pharmacological inhibition of mTOR signaling by the selective TOR kinase inhibitor AZD8055 lead to spontaneous DNA damage and apoptosis as demonstrated by the induction of H2AX phosphorylation and PARP1 cleavage both in cell culture and tumor xenografts of RMS. Treatment RMS Rh30 cells with AZD8055 enhanced hydroxyurea induced H2AX phosphorylation and attenuated ATR-Chk1 checkpoint activation, as shown by decreased levels of phospho-Chk1(S345). We further found that mTOR signaling controls CHK1 expression at the transcriptional level via enhancing the activity of cyclin dependent kinases (CDKs). Consistent with its essential role for cells to survive DNA replication stress, siRNA-mediated knockdown of Chk1, or inhibition of Chk1 function by a Chk1 kinase inhibitor resulted in H2AX phosphorylation, while ectopic increase of Chk1 attenuated the DNA damage induced by mTOR kinase inhibition. Most importantly, the mTOR kinase inhibitor prevented the slow S-phase progression following DNA replication stress, which was accompanied with a decrease of Chk1 protein levels and phospho-Chk1(S345). Our data suggest that the TORC1/TORC2 pathway promotes RMS tumorigenesis by enhancing the cell survival functions of the ATR-Chk1 checkpoint in response to DNA replication stress. Our findings discovered an important unexpected functional linkage between TOR signaling and the ATR-Chk1 checkpoint signaling cascade and may impact targeting these two prominent cancer cell signaling pathways. Supported by CA77776. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 2535. doi:1538-7445.AM2012-2535
A Gene Signature Predicting for Survival in Suboptimally Debulked Patients with Ovarian Cancer
Authors: Tomas Bonome, Douglas A. Levine, Joanna Shih, Mike Randonovich, Cindy A. Pise-Masison, Faina Bogomolniy, Laurent Ozbun, John Brady, J. Carl Barrett, Jeff Boyd, Michael J. Birrer
Journal: Cancer Research (2008)

Abstract Despite the existence of morphologically indistinguishable disease, patients with advanced ovarian tumors display a broad range of survival end points. We hypothesize that gene expression profiling can identify a prognostic signature accounting for these distinct clinical outcomes. To resolve survival-associated loci, gene expression profiling was completed for an extensive set of 185 (90 optimal/95 suboptimal) primary ovarian tumors using the Affymetrix human U133A microarray. Cox regression analysis identified probe sets associated with survival in optimally and suboptimally debulked tumor sets at a P value of &amp;lt;0.01. Leave-one-out cross-validation was applied to each tumor cohort and confirmed by a permutation test. External validation was conducted by applying the gene signature to a publicly available array database of expression profiles of advanced stage suboptimally debulked tumors. The prognostic signature successfully classified the tumors according to survival for suboptimally (P = 0.0179) but not optimally debulked (P = 0.144) patients. The suboptimal gene signature was validated using the independent set of tumors (odds ratio, 8.75; P = 0.0146). To elucidate signaling events amenable to therapeutic intervention in suboptimally debulked patients, pathway analysis was completed for the top 57 survival-associated probe sets. For suboptimally debulked patients, confirmation of the predictive gene signature supports the existence of a clinically relevant predictor, as well as the possibility of novel therapeutic opportunities. Ultimately, the prognostic classifier defined for suboptimally debulked tumors may aid in the classification and enhancement of patient outcome for this high-risk population. [Cancer Res 2008;68(13):5478–86]
Current Posttraumatic Stress Disorder and Cardiovascular Disease Risk Factors in Dutch Resistance Veterans from World War II
Authors: Paul R.J. Falger, Wybrand Op den Velde, Johannes E. Hovens, Erik G.W. Schouten, Johannes H.M. De Groen, Hans Van Duijn
Journal: Psychotherapy and Psychosomatics (1992)

The extraordinary trauma experienced by Resistance veterans from World War II (WWII) and other veterans may be associated with an increased incidence of posttraumatic stress disorder (PTSD) and somatic morbidity, including cardiovascular disease (CVD). This study explored some relationships between current PTSD and CVD risk factors in 147 male Dutch WW II Resistance veterans. They were compared to 65 same-aged male patients with a recent myocardial infarction and 79 surgical patients. Of these subjects, WW II Resistance veterans scored highest on CVD risk factors (i.e., angina pectoris, type A behavior, life stressors, and vital exhaustion), except smoking. Fifty-six percent of these veterans were currently suffering from PTSD. They reported CVD risk factors, in particular type A behavior and vital exhaustion, more often than veterans without PTSD; they also reported more premorbid adverse living conditions. These data suggest that early sensitization to environmental stressors may be associated with a high prevalence of current PTSD and excess CVD risk factors in subjects exposed to extraordinary war-time trauma and that this may lead to vital exhaustion.
α <sub>2</sub> -Antiplasmin Causes Thrombi to Resist Fibrinolysis Induced by Tissue Plasminogen Activator in Experimental Pulmonary Embolism
Authors: Anjum N. Butte, Aiilyan K. Houng, Ik-Kyung Jang, Guy L. Reed
Journal: Circulation (1997)

Background In patients with pulmonary embolism, thrombi resist fibrinolysis induced by plasminogen activators. Because the molecular basis of this thrombus resistance is poorly understood, we used a potent inhibitor to examine the potential role of α 2 -antiplasmin (α2AP) in experimental pulmonary embolism. Methods and Results Lysis of experimental pulmonary emboli was measured 4 hours after embolization in anesthetized ferrets. All animals received heparin (100 U/kg). Five experimental groups were studied: (1) no recombinant tissue plasminogen activator (rTPA); (2) rTPA at 1 mg/kg; (3) rTPA at 2 mg/kg; (4) rTPA at 1 mg/kg plus a control monoclonal antibody (MAb); and (5) rTPA at 1 mg/kg plus an α2AP inhibitor (MAb 77A3). In comparison with ferrets receiving no rTPA (15.6±10.5% lysis, mean±SD), rTPA–treated groups showed significantly greater lysis ( P &lt;.01). Animals treated with rTPA and α2AP inhibitor (56.2±4.7% lysis) showed significantly greater lysis than all other treatment groups, including ferrets treated with the same dose of rTPA alone (38.5±6.3%, P &lt;.01), with twice the rTPA dose alone (45.0±6.5%, P &lt;.05), or with a control MAb (35.2±4.6%, P &lt;.01). The combination of rTPA treatment and α2AP inhibition caused no consumption of fibrinogen. Conclusions Inhibition of α2AP significantly amplified the lysis of experimental pulmonary emboli by rTPA without increasing fibrinogen consumption. These results suggest that α2AP may play an important role in thrombus resistance in patients with venous thromboembolism.
Effect of continuous hemofiltration on hemodynamics, lung inflammation and pulmonary edema in a canine model of acute lung injury
Authors: Xiao Su, Chunxue Bai, Qunying Hong, Duming Zhu, Lixian He, Jianping Wu, Feng Ding, Xiaohui Fang, Michael A. Matthay
Journal: Intensive Care Medicine (2003)