tbuckley/cabot-search huggingface dataset:
THE PARASITIC THEORY OF CANCER
Authors: H. G. Plimmer
Journal: BMJ (1903)

CANCER. 15I I occupations, cancer houses, and many others can only be settled after statistical and other investigations have be'en made and checked and cross-checked, controlled and re- controlled by each other.Such investigations are-beyond the means and powers of individual science workers or of- medical institutions, and need to be undertaken by an organized body with relays of workers and sufficient funds at its command to provide for the uninterrupted pursuit of the inquiries.Katz, of Hamburg, whom I have' previously quoted, re- mnarked: " It is to be deplored that Cohnheim's doctrine has so long found an extended acceptance, for the further deve- lopment of cancer research would have, through it, no value.A standstill would result from the fatalism which underlies this theory.The same may be said with regard to Ribbert's theory, which, though of far later date than Cohnheim's, is in pursuit and continuation of it."But a theory, if it has the evidence of truth, must be ninutely and impartially examined, even though it seems to 1ead to a conclusion which we might wish to esape.There is, however, no occasion for so pessimistic a view as that of Katz.The "tumour-germ" theory, at least does this: it convinces us of the local origin of cancer, and of the positive curability of it if removed quite early and com- plOtely.Of course, it does not guarantee one against the for- mation of another malignant new growth, any more than the uepair of a broken bone guarantees one against the occurrence of another fracture.It should also encourage the early and more frequent removal even of benign growths.Future researches may reveal a method whereby a special inhibitory influence may be brought to bear upon the cells of the "tumour matrix," on the lines tried by Foulerton; or a restraining, even a strangulating, effect upon the tumour cells by the tumour matrix may be produced, as suggested by Marshall.But in any case, we can reasonably hope and expect that the organized researches now commenced by the Colleges will in time yield much information as to how to pre- vent cancer by teaching us what are the real agencies which stimulate it into existence.In bringing these remarks to a conclusion I will borrow the description recently given by Mrs. Crawford of the mind of the late M. Thiers.and apply it to the theory founded by Durante and Cohnheim."It has search-light luminosity.Like radium, it keeps burning brightly, without consuming itself.";And, I would add, it will not only remain active and brilliant to the end, but it will, I believe, shed more and more light on the etiology of canoer with every fresh addi- tion made to the science of embryology and to our knowledge of tumours.
Abstract A79: Genome-wide RNAi screen for tetraploid-specific lethality in cancer cells
Authors: Taruho S. Kuroda, Regina K. Dagher, David Pellman
Journal: Cancer Research (2009)

Abstract Cancer cells are often genetically unstable, resulting in aneuploid genomes. The consequences of aneuploidy are poorly understood, but have been suggested to play roles in tumor aggressiveness, chemotherapy resistance, and metastasis. One important route to an aneuploid genome may be through doubling of the genome, leading to unstable tetraploid cells. Many cell division errors are ultimately manifest as a failure of cytokinesis. Especially in cells defective in p53 function, tetraploid cells proliferate, but generate both high rates of whole chromosome aneuploidy and defects in the maintenance of chromosome structural integrity. Our laboratory has demonstrated that, in p53-primary cells, tetraploidy promotes tumor development and the resulting tumors display markedly abnormal genomes (Fujiwara T. et al. Nature 2005, 437: 1043). It is now known that several human cancer-mutations — e.g. Rb loss or loss of the adenomatous polyposis coli tumor suppressor — also predispose cytokinesis failure and tetraploidy. These findings highlight a need to understand in detail the physiological changes that accompany tetraploidy. To gain a comprehensive understanding of physiological alterations associated with tetraploidy in cancer cells, we have established tetraploid cell lines derived from a near diploid human colorectal cancer cell line HCT116. Using these paired tetraploid and diploid cell lines, we have performed a genome-wide RNAi screen to identify genes whose knock down selectively affect the viability of either diploids or tetraploid cells. We are currently validating the result of our ploidy-specific lethality screen and we would like to update our progress at this conference. Citation Information: Cancer Res 2009;69(23 Suppl):A79.
Abstract 4752: Cortactin and coronin 1B cooperate to promote tumor cell invasion in head and neck squamous cell carcinoma
Authors: Elyse L. Walk, Hong Wu, Marileila V. Garcia, James E. Bear, Scott A. Weed
Journal: Cancer Research (2011)

Abstract Amplification of chromosome 11q13 in head and neck squamous cell carcinoma (HNSCC) is a common occurrence associated with poor patient prognosis. Within the core amplified region is the gene that encodes cortactin (CTTN), a filamentous (F)- actin binding protein and Src kinase substrate that stabilizes Arp2/3-F-actin branchpoints in dynamic cortical F-actin structures. CTTN amplification results in increased lymph node metastases and decreased survival rates in HNSCC patients. CTTN amplification in HNSCC cell lines enhances tumor cell motility and invasion. Chromosomal regions of varying length flanking the core 11q13 amplicon are often amplified in HNSCC, and contain several genes with the potential to cooperate with CTTN in regulating actin dynamics. One of these genes within the 11q13 region outside of the core amplicon is CORO1B (coronin 1B), an actin-binding protein that antagonizes cortactin function by promoting the breakdown of cortactin-stabilized Arp2/3-F-actin branches, resulting in impaired cell motility. Here we show that coronin 1B is a potential mediator of HNSCC invasion. CORO1B amplification and overexpression occurs in a subset of HNSCC patients with CTTN amplification. Coronin 1B localizes with cortactin within HNSCC invadopodia, ventral membranous protrusions responsible for degrading extracellular matrix to facilitate loco-regional invasion and extracapsular spread. RNAi-mediated coronin 1B knockdown decreases the number of invadopodia per cell, enhances cell spreading and reduces extracellular matrix degradation. These results collectively point to a potential role for coronin 1B in regulating HNSCC tumor cell invasion through modulating cortactin activity and invadopodia function. Our data also support a potential diagnostic function for CORO1B amplification in denoting a previously unidentified HNSCC subset that may display increased invasiveness in cases containing 11q13 amplification. 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 4752. doi:10.1158/1538-7445.AM2011-4752
QRS DURATION AND LEFT VENTRICULAR EJECTION FRACTION IN NON ST SEGMENT ELEVATION MYOCARDIAL INFARCTION
Authors: Mahek Kishor Shah, Vikas Bhalla, Chinualumogu Nwakile, Toni Anne De Venecia, Shantanu Patil, Karla Curet, Obiora Maludum, Gregg Pressman, Vincent Figueredo
Journal: Journal of the American College of Cardiology (2015)
Factors in the Mortality and Morbidity Associated with Surgical Treatment of Cerebrovascular Insufficiency
Authors: J. H. C. RANSON, A. M. IMPARATO, R. H. CLAUSS, G. E. REED, W. K. HASS
Journal: Circulation (1969)

The mortality and morbidity associated with 267 surgical procedures for cerebrovascular insufficiency carried out over a 5-year period are reviewed. Patients with marked intracranial arterial disease on angiogram, with completed strokes, over 70 years old or who required continuous nursing care are identified as the highest surgical risks. The introduction of monitoring of the oxygen saturation of lateral sinus venous blood has reduced the incidence of intra-operative new neurological deficit during general anesthesia from 9.1 to 4.4%. Episodes of hypotension occurred in 27% of patients but were associated with 48% of grave complications. The occurrence of hypotension is related to diabetes, preoperative hypertension, and to the extent of the operative procedure. Evidence is presented that hypotension is due to abnormal circulatory reflexes and may best be prevented by careful maintenance of intravascular volume.
Provision of Health Services
Authors: Russel V. Lee
Journal: New England Journal of Medicine (1967)

HEALTH services are unlike any other needs of man in a number of significant ways. In the first place there is really no upper limit to what may be furnished. It is easy to determine how much food and how much housing are needed. But the level at which the provision of health services should stop cannot be specified because there is now demonstrable benefit from increasing the available services even beyond one's wildest dreams. For instance, it might be well if every man, woman and child had a complete, annual physical examination with all the usual laboratory procedures. That . . .
Extended Duration of DH–JH Rearrangement in Immunoglobulin Heavy Chain Transgenic Mice: Implications for Regulation of Allelic Exclusion
Authors: Yung Chang, Melvin J. Bosma, Gayle C. Bosma
Journal: The Journal of Experimental Medicine (1999)

Here we show that suppression of VH–DJH rearrangement in mice bearing a μ heavy (H) chain transgene (μ-tg mice) is associated with an extended period of DH–JH rearrangement, the first step of Immunoglobulin H chain gene rearrangement. Whereas DH–JH rearrangement is normally initiated and completed at the pro-B cell stage, in μ-tg mice it continues beyond this stage and occurs most frequently at the small (late) pre-B stage. Despite ongoing DH–JH rearrangement in late pre-B cells of μ-tg mice, VH–DJH rearrangement is not detectable in these cells. We infer that the lack of VH–DJH rearrangement primarily reflects tg-induced acceleration of B cell differentiation past the stage at which rearrangement of VH elements is permissible. In support of this inference, we find that the normal representation of early B lineage subsets is markedly altered in μ-tg mice. We suggest that the effect of a productive VH–DJH rearrangement at an endogenous H chain allele may be similar to that of a μ-tg; i.e., cells that make a productive VH–DJH rearrangement on the first attempt rapidly progress to a developmental stage that precludes VH–DJH rearrangement at the other allele (allelic exclusion).
Demonstration of Excessive Metabolic Activity of Thoracic and Abdominal Muscles on FDG-PET in Patients With Chronic Obstructive Pulmonary Disease
Authors: Aysel Aydin, Marc Hickeson, Jian Q. Yu, Hongming Zhuang, Abass Alavi
Journal: Clinical Nuclear Medicine (2005)

Purpose: The purpose of this study was to determine if an FDG-PET study was able to visualize muscle uptake of the chest and abdomen in patients with chronic obstructive pulmonary disease (COPD). Methods: This study included 25 patients with COPD and 25 patients without COPD who had undergone a FDG-PET study. The nonattenuation-corrected images were used to determine the degree of FDG uptake in the intercostals, subscapular, abdominal rectus, and abdominal oblique muscles. The intensity of uptake in the muscles was rated on a 4-point grading scale with 1 being less, 2 the same, 3 slightly more, and 4 markedly more intense than the sternum. Results: Thirteen patients with COPD demonstrated FDG activity in the intercostal muscles that was equal to or greater than the sternum and the tracer was demonstrated predominantly in the inferolateral chest wall (n = 8), the entire lateral chest wall (n = 2), the posteroinferior chest wall (n = 2), and the entire chest wall (n = 1). In all 13 patients with COPD who demonstrated FDG activity in the abdominal oblique muscles, the site of muscle activity was predominantly in the anteroinferior abdominal wall (n = 8), the lateral wall (n = 4), and the anterior wall (n = 1). In patients without known COPD, the frequency and intensity of uptake in the muscles were less than those with the disease. Conclusion: This study demonstrates the ability of FDG-PET imaging to assess muscle function in respiratory disorders and may prove to be of some value in further characterizing this disorder.
Real-time Three-dimensional Echocardiography for Determining Right Ventricular Stroke Volume in an Animal Model of Chronic Right Ventricular Volume Overload
Authors: Takahiro Shiota, Michael Jones, Masahide Chikada, Craig E. Fleishman, John B. Castellucci, Bruno Cotter, Anthony N. DeMaria, Olaf T. von Ramm, Joseph Kisslo, Thomas Ryan, David J. Sahn
Journal: Circulation (1998)

Background —The lack of a suitable noninvasive method for assessing right ventricular (RV) volume and function has been a major deficiency of two-dimensional (2D) echocardiography. The aim of our animal study was to test a new real-time three-dimensional (3D) echo imaging system for evaluating RV stroke volumes. Methods and Results —Three to 6 months before hemodynamic and 3D ultrasonic study, the pulmonary valve was excised from 6 sheep (31 to 59 kg) to induce RV volume overload. At the subsequent session, a total of 14 different steady-state hemodynamic conditions were studied. Electromagnetic (EM) flow probes were used for obtaining aortic and pulmonic flows. A unique phased-array volumetric 3D imaging system developed at the Duke University Center for Emerging Cardiovascular Technology was used for ultrasonic imaging. Real-time volumetric images of the RV were digitally stored, and RV stroke volumes were determined by use of parallel slices of the 3D RV data set and subtraction of end-systolic cavity volumes from end-diastolic cavity volumes. Multiple regression analyses showed a good correlation and agreement between the EM-obtained RV stroke volumes (range, 16 to 42 mL/beat) and those obtained by the new real-time 3D method ( r =0.80; mean difference, −2.7±6.4 mL/beat). Conclusions —The real-time 3D system provided good estimation of strictly quantified reference RV stroke volumes, suggesting an important application of this new 3D method.
Hemodynamics and coronary blood flow during exercise after coronary artery bypass grafting with internal mammary arteries in children with Kawasaki disease.
Authors: K Kawachi, S Kitamura, T Seki, R Morita, T Kawata, J Hasegawa, Y Kameda
Journal: Circulation (1991)

Saphenous vein grafts (SVG) and internal mammary artery (IMA) grafts have been used for coronary artery bypass grafting. In adult patients with bypass grafting for atherosclerotic coronary artery disease, IMA grafts have been reported to have long-term patency; however, results are conflicting on whether the graft is sufficient to meet increased myocardial oxygen demand during exercise. There have been no studies on hemodynamics and blood flow during exercise after bypass grafting with IMA in pediatric patients with Kawasaki disease.We studied 17 pediatric patients with Kawasaki disease (average age, 7.5 +/- 3.1 years), who underwent coronary artery bypass grafting with the IMA. The average number of coronary artery bypass grafts was 2.1 +/- 0.7/patient. For all patients, the left IMA was anastomosed to the left anterior descending coronary artery; for eight patients, the right IMA was also anastomosed to the right coronary artery. In addition, 11 SVGs were used. The postoperative patency rates after 1 month were 100% with the IMA graft and 91% with SVG. One year after the operation, the patency rates were 100% with IMA and 50% with SVG. Hemodynamics during exercise were measured with a bicycle ergometer, and coronary sinus blood flow was measured by the continuous thermodilution method in six patients. The relation between delta LVEDP (the difference between left ventricular end-diastolic pressure at rest and during exercise) and delta SVI (the difference between the stroke volume index at rest and during exercise) was analyzed. Four of six patients had reduced cardiac function before operation (delta LVEDP, positive; delta SVI, negative). However, after the operation, all patients demonstrated improvements in cardiac function during exercise (delta LVEDP, positive; delta SVI, positive). Coronary sinus flow per left ventricular mass increased after operation from 70 +/- 46 to 87 +/- 56 ml/min at rest (p less than 0.05) and from 139 +/- 118 to 183 +/- 150 ml/min during exercise (p less than 0.05).In conclusion, this study reveals improvements in both hemodynamics and coronary blood flow during exercise after coronary artery bypass grafting with IMA grafts in pediatric patients with Kawasaki disease.
The new religion: screening at your parish church
Authors: C. Warlow
Journal: BMJ (2009)

Unusually for me, I went to church. On a Monday. Not to ask forgiveness or to sing a hymn, or to be instructed from the pulpit, but to be screened. After all, if Liverpool Anglican Cathedral can be a venue for corporate dinners, why not a mere church for health (disease) screening? 

A vascular screening company had come to town after leafleting many of my neighbours with the message that “four out of five people who suffered a stroke had no apparent warning signs.” I imagine they meant transient ischaemic attacks. In fact four out of five people with a stroke have and are generally known to have one or more vascular risk factors, such as hypertension or atrial fibrillation (not signs maybe, but certainly prognostic signposts). But we mustn’t let awkward facts get in the way of marketing, particularly not to the “worried wealthy” of Edinburgh.

So, without revealing my interest in stroke prevention for the past 30 years, I signed on, paid £152 (€170; $230), and turned up at church, along with other older people who didn’t look as healthy as me. (I thought I had better hide my cycle helmet.) First up was aortic aneurysm screening with …
Breast Cancer: Treatment Differences and Survival-Reply
Authors: A. Lee-Feldstein, H. Anton-Culver, P. J. Feldstein
Journal: JAMA (1994)

<h3>In Reply.</h3> —Our study included breast cancer patients diagnosed from 1984 through 1990. For HMO hospitals, estimated 5-year survival was 67.0% (SE, 5.3%) for localized disease and 49.5% (SE, 9.2%) for regional disease. Dr Amster and colleagues report figures for Kaiser Southern California breast cancer patients diagnosed from 1987 through 1992. Because this period varies from ours, patient groups treated at Kaiser hospitals would differ in our respective studies. Our article reports significantly worse survival for patients with localized disease treated at HMO hospitals (including Kaiser hospitals) compared with those treated at small community hospitals, particularly among patients treated before 1988. Amster et al present no data to refute this result. Since there is a time trend toward better survival in HMO hospitals in the later part of our study period (Table) and assuming that this trend continues after 1990, one would expect better survival from 1987 through 1992 among Kaiser's
FLT3-regulated antigens as targets for leukemia-reactive cytotoxic T lymphocytes
Authors: B Brackertz, H Conrad, J Daniel, B Kast, H Krönig, D H Busch, J Adamski, C Peschel, H Bernhard
Journal: Blood Cancer Journal (2011)

The FMS-like tyrosine kinase 3 (FLT3) is highly expressed in acute myeloid leukemia (AML). Internal tandem duplications (ITD) of the juxtamembrane domain lead to the constitutive activation of the FLT3 kinase inducing the activation of multiple genes, which may result in the expression of leukemia-associated antigens (LAAs). We analyzed the regulation of LAA in FLT3-wild-type (WT)- and FLT3-ITD(+) myeloid cells to identify potential targets for antigen-specific immunotherapy for AML patients. Antigens, such as PR-3, RHAMM, Survivin, WT-1 and PRAME, were upregulated by constitutively active FLT3-ITD as well as FLT3-WT activated by FLT3 ligand (FL). Cytotoxic T-cell (CTL) clones against PR-3, RHAMM, Survivin and an AML-directed CTL clone recognized AML cell lines and primary AML blasts expressing FLT3-ITD, as well as FLT3-WT(+) myeloid dendritic cells in the presence of FL. Downregulation of FLT3 led to the abolishment of CTL recognition. Comparing our findings concerning LAA upregulation by the FLT3 kinase with those already made for the Bcr-Abl kinase, we found analogies in the LAA expression pattern. Antigens upregulated by both FLT3 and Bcr-Abl may be promising targets for the development of immunotherapeutical approaches against myeloid leukemia of different origin.
A randomized trial of intravenous heparin in conjunction with anistreplase (anisoylated plasminogen streptokinase activator complex) in acute myocardial infarction: The Duke University clinical cardiology study (DUCCS) 1
Authors: Christopher M O'Connor, Roderick Meese, Robert Carney, Jack Smith, Eric Conn, John Burks, Carl Hartman, Steve Roark, Neal Shadoff, Maurice Heard, Brant Mittler, Gary Collins, Frank Navetta, Jeff Leimberger, Kerry Lee, Robert M Califf
Journal: Journal of the American College of Cardiology (1994)
β-Cell Function in Severely Obese Type 2 Diabetic Patients
Authors: Stefania Camastra, Melania Manco, Andrea Mari, Aldo V. Greco, Silvia Frascerra, Geltrude Mingrone, Ele Ferrannini
Journal: Diabetes Care (2007)

Bariatric surgery in severely obese diabetic patients can restore glucose tolerance (1). Malabsorptive bariatric surgery (e.g., bilio-pancreatic diversion [BPD]) in nondiabetic subjects induces an improvement in insulin sensitivity that is greater than predicted by weight loss (2,3); such an effect can be demonstrated early after surgery (4). Impaired β-cell function is the main determinant of glucose intolerance, and modeling of C-peptide responses to graded glucose infusions (5) or oral glucose administration (6) makes it possible to estimate key dynamic parameters of β-cell function such as β-cell glucose sensitivity. The impact of bariatric surgery on β-cell function in diabetic subjects has been investigated using the intravenous glucose tolerance test (7). This test, however, can misjudge β-cell function as compared with more physiological challenges (such as the oral glucose tolerance test or mixed meals) because it explores only one specific aspect of islet function, namely the acute insulin discharge in response to a sudden maximal increment in plasma glucose concentrations (8). Recently, we have applied C-peptide–based modeling to reconstruct insulin secretion and β-cell function during a 24-h multiple-meal test (9). Here, we adopted this approach to analyze the long-term effects of BPD on glucose metabolism in morbidly obese patients with type 2 diabetes.

We studied 10 morbidly obese (mean ± SE BMI 49.5 ± 2.9 kg/m2), non–insulin-treated type 2 diabetic patients (3 men and 7 women) (age 50 ± 2 years) whose weight had been stable (±2 kg) for the preceding 6 months. Oral antidiabetic drugs were discontinued 1 week before the baseline studies. The study protocol was approved by the local ethics committee, and all subjects provided informed written consent to participate.

Following the baseline studies, patients underwent BPD, consisting of a partial gastrectomy with a distal Roux-en-Y reconstruction (2), and were restudied 24 ± 2 months postsurgery. …