tbuckley/cabot-search huggingface dataset:
A Prospective Study of Cholesterol, Apolipoproteins, and the Risk of Myocardial Infarction
Authors: Meir J. Stampfer, Frank M. Sacks, Simonetta Salvini, Walter C. Willett, Charles H. Hennekens
Journal: New England Journal of Medicine (1991)

The independent contributions of subfractions of high-density lipoprotein (HDL) cholesterol (HDL2 and HDL3) and apolipoproteins in predicting the risk of myocardial infarction are unclear. Prospective data are sparse, but HDL2 is widely believed to be a more important predictor than HDL3.
Ending Deaths from Famine -- The Opportunity in Somalia
Authors: Robert W. Kates
Journal: New England Journal of Medicine (1993)

As we witnessed the starvation, disease, and dying in Somalia, it was surely difficult to remember that Somalia was the site of the greatest triumph of 20th-century international public health. There, in October 1977, Ali Maow Maalin, a 23-year-old cook in the town of Merca, was identified as having “the world's last endemic case of smallpox”1. Now, more than 15 years later, Somalia may again prove to be a turning point in the much longer and larger human struggle to end deaths from famine. To understand that opportunity amid all the pain and suffering requires a sense of that . . .
167P: Efficacy of EGFR-TKIs for lung squamous carcinomas harboring EGFR mutation: A multicenter study and pooled analysis of published reports
Authors: Y. Liu, Y. Zhang, L. Zhang, B. Liu, X. Zhou, Y. Li, L. Zhou, Y. Gong, Y. Wang, Y. Lu
Journal: Journal of Thoracic Oncology (2016)
A Simple Method for Quantitative Urine Culture
Authors: Stephen N. Cohen, Edward H. Kass
Journal: New England Journal of Medicine (1967)

ONE of the major impediments to widespread screening for the presence of bacteriuria is the absence of a simple and inexpensive method that is also reliable. Chemical tests presently available, as well as cultural methods of proved validity, have failed to meet these demands, and have not been as widely accepted as might be desired.1 2 3 4 5 6 7 8 9 Recently, Guttmann and Naylor10 described a simple method for cultivation of bacteria from the urine, using an ordinary glass microscopical slide that had been coated with appropriate culture medium. The simplicity of this method and its comparability to standard colony-counting technics were of sufficient appeal . . .
Outcome after PORT in ypN2 or R1/R2 versus no PORT in ypN0 Stage III-N2 NSCLC after Induction Chemotherapy and Resection
Authors: Charlotte Billiet, Stéphanie Peeters, Herbert Decaluwé, Johan Vansteenkiste, Christophe Dooms, Christophe M. Deroose, Marc Hendrikx, Paul De Leyn, Paul Bulens, Rezaul Karim, Cécile Le Péchoux, Jeroen Mebis, Dirk De Ruysscher
Journal: Journal of Thoracic Oncology (2016)
Multiple Sclerosis Cerebrospinal Fluid Produces Myelin Lesions in Tadpole Optic Nerves
Authors: Takeshi Tabira, Henry deF. Webster, Shirley H. Wray
Journal: New England Journal of Medicine (1976)

To investigate the myelinotoxicity of cerebropsinal fluid in multiple sclerosis, we used an in vivo model of the myelinated central-nervous-system tract of tadpoles for quantitative double-blind tests of 46 cerebrospinal-fluid samples. Groups of xenopus tadpoles were injected with cerebrospinal fluid near the optic nerve. Forty-eight hours later, whole mounts of optic nerves were prepared, and a differential interference microscope was used to count myelin lesions. Cerebrospinal-fluid samples from 60 per cent of the patients with an acute attack of definite multiple sclerosis had myelinotoxic activity. This activity correlated best with the severity and duration of the disease, rather than with gamma-globulin or total protein concentrations. Activity was negative in 85 per cent of cerebrospinal-fluid samples from a control group with other neurologic diseases. This assay is a useful method for investigating myelinotoxic factors of cerebrospinal fluid in patients with multiple sclerosis, but was not helpful diagnostically.
Restriction spectrum imaging predicts response to bevacizumab in patients with high-grade glioma
Authors: Carrie R. McDonald, Rachel L. Delfanti, Anitha P. Krishnan, Kelly M. Leyden, Jona A. Hattangadi-Gluth, Tyler M. Seibert, Roshan Karunamuni, Pia Elbe, Joshua M. Kuperman, Hauke Bartsch, David E. Piccioni, Nathan S. White, Anders M. Dale, Nikdokht Farid
Journal: Neuro-Oncology (2016)

Diffusion-weighted imaging has shown initial promise for evaluating response to bevacizumab in patients with high-grade glioma (HGG). However, it is well recognized that the apparent diffusion coefficient (ADC) is influenced by bevacizumab-induced reductions in edema, which may limit its prognostic value. We demonstrate that an advanced diffusion-weighted imaging technique, restriction spectrum imaging (RSI), improves the evaluation of response to bevacizumab because unlike ADC, RSI is not affected by resolution of edema. RSI and ADC maps were analyzed for 40 patients with HGG prior to and following initiation of bevacizumab. Volumes of interest were drawn for regions of contrast enhancement (CE) and fluid attenuated inversion recovery (FLAIR) hyperintensity and histogram percentiles within volumes of interest were calculated for ADC 10th percentile (ADC-CE10%, ADC-FLAIR10%) and for RSI 90th percentile (RSI-CE90%, RSI-FLAIR90%). Cox proportional hazard models were used to evaluate the relationship between imaging parameters, progression-free survival (PFS), and overall survival (OS). An increase in RSI-FLAIR90% following bevacizumab was the strongest predictor of poor PFS (P= .016) and OS (P= .004), whereas decreases in ADC-FLAIR10% showed a weaker association with OS only (P= .041). Within the CE region, increases in RSI-CE90% alone were associated with poorer OS. Correlational analysis revealed that decreases in FLAIR volume were associated with decreases in ADC-FLAIR10%, but not with changes in RSI-FLAIR90%. RSI is less influenced by changes in edema, conferring an advantage of RSI over ADC for evaluating response to anti-angiogenic therapy in patients with HGG.
Spontaneous Release of Interleukin-2 by Lung T Lymphocytes in Active Pulmonary Sarcoidosis
Authors: Paula Pinkston, Peter B. Bitterman, Ronald G. Crystal
Journal: New England Journal of Medicine (1983)

We investigated the possible role of interleukin-2, a T-cell product that stimulates the clonal increase of responsive T lymphocytes, in the pathogenesis of pulmonary sarcoidosis. We obtained mononuclear effector cells from the lungs of 10 patients with sarcoidosis and high-intensity alveolitis, 17 patients with sarcoidosis and low-intensity alveolitis, 3 patients with idiopathic pulmonary fibrosis, and 10 normal controls. Lung cells from the group with sarcoidosis and low-intensity alveolitis, from the group with idiopathic pulmonary fibrosis, and from the controls produced insignificant amounts of interleukin-2. However, lung cells from 9 of 10 patients with sarcoidosis and high-intensity alveolitis spontaneously released interleukin-2, and in a proportion that correlated with the proportion of T cells in the lung washings (P less than 0.01). Blood T cells from the same patients did not release interleukin-2. To determine whether release of interleukin-2 by the lung T cells had a biologic effect in vivo, we measured T-lymphocyte replication in the lungs of patients and controls. The lung T lymphocytes replicated at a rate that was several times higher in the patients with sarcoidosis and high-intensity alveolitis than in the other patient groups or the controls (P less than 0.01). These observations suggest that the release of interleukin-2 by lung T cells has a central role in increasing the numbers of lung T cells in active pulmonary sarcoidosis.
The Treatment of Idiopathic Thrombocytopenia with Vinblastine-Loaded Platelets
Authors: Yeon S. Ahn, John J. Byrnes, William J. Harrington, Marilyn L. Cayer, David S. Smith, Dennis E. Brunskill, Lorraine M. Pall
Journal: New England Journal of Medicine (1978)

We devised a method to enhance delivery of vinblastine to macrophages, the cells believed to be responsible for platelet destruction in idiopathic thrombocytopenic purpura. Our strategy was based on the ability of platelets to bind vinca alkaloids such as vinblastine. Platelets were incubated with an excess of vinblastine, concentrated and then, after excess alkaloid had been removed, given to 11 patients with idiopathic thrombocytopenia refractory to other treatment (including intravenous injections of vinca alkaloids). Platelet antibodies in the patients' plasma led to ingestion of the vinca-laden platelets by macrophages. There were six complete remissions, three partial remissions and two failures. Side effects in a few patients, reversible but annoying, were minimized as technics were refined. We conclude that in patients with idiopathic thrombocytopenia refractory to all other measures, including the use of vinca alkaloids, platelet-vinca complex may be effective.
Jacob, Monod, the Lac Operon, and the PaJaMa Experiment—Gene Expression Circuitry Changing the Face of Cancer Research
Authors: Stephen B. Baylin
Journal: Cancer Research (2016)

Visit the Cancer Research 75th Anniversary [timeline][1].

See related article by Pitot and Heidelberger, [Cancer Res 1963;23:1694–700][2] .

It is a virtually universal rule in science that if we step back to reflect upon a field currently viewed as extremely dynamic and novel, we find ourselves
Mercury Poisoning and Its Treatment with<scp>n</scp>-Acetyl-<scp>d,l</scp>-Penicillamine
Authors: R. A. Pieter Kark, David C. Poskanzer, John D. Bullock, George Boylen
Journal: New England Journal of Medicine (1971)

Abstract Severe chronic elemental mercury poisoning produced in a factory worker the signs usually attributed to organic mercury poisoning. Since it is known that the converse occurs, the two types...
Compliance and persistency with imatinib
Authors: W. Feng, H. Henk, S. Thomas, J. Baladi, A. Hatfield, G. A. Goldberg, J. Cortes
Journal: Journal of Clinical Oncology (2006)

6038 Background: Imatinib is an oral therapy with efficacy in chronic myelogenous leukemia (CML) and gastrointestinal stromal tumors (GIST). Optimal dosing and adherence to treatment is critical to achieve the best clinical outcomes. This study examined compliance and persistency with imatinib and identified the clinical and patient characteristics related to compliance. Methods: Claims data from a US health plan were used to identify imatinib-treated patients from 6/1/01–3/31/04 who had continuous pharmacy and medical benefits in the 3 months prior and 12 months following initiation of imatinib therapy, and a diagnosis of CML or GIST (ICD-9-CM 205.1, 205.10, or 205.11 for CML; 159.0, 159.8, or 159.9 for GIST). Compliance was defined by medication possession ratio (MPR = total days supply of imatinib in the first year divided by 365). Persistency was defined as failure to refill imatinib within 30 days from the run-out date of the prior prescription. Multivariate analyses were used to identify key factors associated with compliance. Results: Total 878 imatinib-treated patients were identified of whom 413 had at least 15 months’ continuous eligibility. Sixty-nine percent (n = 286) were diagnosed with CML, 8% (n = 34) with GIST, and 23% (n = 93) with neither. Results are presented for CML and GIST patients. The average age was 51 and 58% were males. The average starting daily dose was 424 mg, with 80% (n = 255) initiating on 400 mg daily. The mean MPR was 76%. Overall, 28% patients discontinued imatinib for at least 30 consecutive days during the 1-year follow up period. Multivariate analyses indicated MPR improved with age until age 51 and then deteriorated (p &lt; 0.001) but at a diminishing rate, decreased as the number of medications increased (p &lt; 0.001), and was lower in women (p = 0.005) and patients with more cancer complications (p &lt; 0.001). In addition, women were more likely to discontinue than men (OR = 2.08; p = 0.003). Conclusions: Compliance to imatinib was about 75% with 30% of patients interrupting therapy for at least 30 consecutive days in the first year. It has been found that interruption of imatinib therapy may lead to rapid tumor progression in GIST (PASCO05 Le Cesne #9031). Not having patients take the correct doses on a regular basis may lead to sub therapeutical clinical outcomes. [Table: see text]
1330: Brigatinib efficacy and safety in patients (Pts) with anaplastic lymphoma kinase (ALK)-positive (ALK+) non-small cell lung cancer (NSCLC) in a phase 1/2 trial
Authors: R. Rosell, S.N. Gettinger, L.A. Bazhenova, C.J. Langer, R. Salgia, A.T. Shaw, N.I. Narasimhan, D.J. Dorer, D. Kerstein, D.R. Camidge
Journal: Journal of Thoracic Oncology (2016)
Abstract 2505: Therapeutic efficacy of the ZVex™ and GLAAS™ platforms in a B16-F10/hCAIX melanoma mouse model
Authors: David J. Campbell, Rebecca S. Reeves, Patrick A. Flynn, Scott H. Robbins, Peter Berglund, Jan H. ter Meulen
Journal: Cancer Research (2015)

Abstract ZVex™ and GLAAS™ are two dendritic-cell (DC) targeting platform technologies designed to enhance immune responses through the in vivo induction of antigen specific CD8 and CD4 T-cells, respectively. ZVex™ is a lentiviral vector pseudotyped with a modified Sindbis virus envelope engineered to deliver tumor antigen-encoding nucleic acids to dendritic cells in vivo. GLAAS™(Glucopyranosyl Lipid A Adjuvant System) activates DC by binding to the TLR-4 receptor and inducing strong Th1 type CD4 responses against co-delivered recombinant proteins. Currently both platform technologies are being investigated in phase I clinical trials in cancer patients. Human carbonic anhydrase 9 (hCAIX) is a tumor-associated transmembrane antigen that is over-expressed on various cancer cell types. We mapped hCAIX specific, multi-functional CD8 and CD4 T-cell epitopes within the extracellular and transmembrane regions of the protein for the mouse haplotype H-2b by intracellular cytokine staining. Mice lethally challenged s.c. on the flank with a B16-F10 tumor cell line expressing the hCAIX protein (designated BC.12) fully controlled large tumors (&amp;gt;100 mm2) when therapeutically immunized (subcutaneously at the base of tail) with ZVex™ encoding hCAIX or the recombinant hCAIX protein with GLAAS™ (either s.c. or i.m.). In both models, tumor control was dose-dependent. Additionally, the presence of a strong transmembrane H-2b restricted CD8 T-cell epitope was required for tumor control and regression. hCAIX-specific CD8 T-cell responses were detectable as far out as day 67 post challenge in mice displaying full regression of tumor. These results demonstrate proof of concept for ZVex™ and GLAAS™ platform technologies in an aggressive murine melanoma model. Citation Format: David J. Campbell, Rebecca S. Reeves, Patrick A. Flynn, Scott H. Robbins, Peter Berglund, Jan H. ter Meulen. Therapeutic efficacy of the ZVex™ and GLAAS™ platforms in a B16-F10/hCAIX melanoma mouse model. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 2505. doi:10.1158/1538-7445.AM2015-2505
Prenatal Diagnosis of α-Thalassemia
Authors: Yuet Wai Kan, Mitchell S. Golbus, Andree M. Dozy
Journal: New England Journal of Medicine (1976)

The technic of DNA-DNA hybridization was used for prenatal diagnosis of a pregnancy at risk for homozygous alpha-thalassemia. Fibroblasts were cultured from amniotic fluid, and the number of alpha-globin genes in the DNA was quantified by hybridization with radioactive DNA complementary to alpha-globin mRNA sequences. As compared to control studies of DNA from patients with alpha-thalassemia syndromes and from unaffected subjects, the results indicated that the fetus had alpha-thalassemia-1. The diagnosis was confirmed by umbilical-cord blood studies.
Case 32-1986
Authors: Richard C. Cabot, Robert E. Scully, Eugene J. Mark, Betty U. McNeely, Rose H. Goldman, Eugene J. Mark
Journal: New England Journal of Medicine (1986)

Presentation of CaseA 74-year-old man was admitted to the hospital because of pulmonary hypertension.Seven years earlier he entered another hospital after a dog bite. Examination revealed inspiratory wheezes, an increased anteroposterior diameter of the thorax, digital clubbing, and possible cyanosis. An x-ray film of the chest was reported to show increased markings at both lung bases and decreased markings in the upper lobes. The patient denied dyspnea at that time and reportedly felt well until two years later, when he was exposed to the fumes of a mixture of household ammonia and chlorine bleach, followed by severe dyspnea . . .
Increased Production of Prostaglandin D2 in Patients with Systemic Mastocytosis
Authors: L. Jackson Roberts, Brian J. Sweetman, Robert A. Lewis, K. Frank Austen, John A. Oates
Journal: New England Journal of Medicine (1980)

SYSTEMIC mastocytosis is a disorder of unknown origin, characterized by abnormal proliferation of tissue mast cells involving various organs and associated with a variety of clinical symptoms and signs.1 Episodic attacks of flushing, frequently accompanied by hypotension and tachycardia, are a predominant manifestation of systemic mastocytosis, which at times can result in life-threatening shock.Although the symptoms of mastocytosis have generally been attributed to the release of histamine from mast cells, only partial amelioration of symptoms has been described in the few isolated case reports on the effects of histamine-antagonist therapy of this disorder.2 , 3 After the recent demonstration that combined . . .
Gait Disorders in the Elderly
Authors: L Sudarsky
Journal: New England Journal of Medicine (1990)

DISTURBANCES of gait are common in the elderly and can be disabling. In one population-based study, 15 percent of the subjects over 60 years of age had some abnormality of gait.1 The prevalence of gait disturbances may be considerably higher among very old persons, those in the ninth decade and beyond. In a study of the functional status of a cohort of 79-year-olds in Göteborg, Sweden, one in four was found to use mechanical aids for walking.2 None of the subjects could comfortably walk at 1.4 m per second, a pace considered by the Swedish government to be the norm . . .
Ventricular Arrhythmias in Patients with Hypertensive Left Ventricular Hypertrophy
Authors: James M. McLenachan, Esther Henderson, Karen I. Morris, Henry J. Dargie
Journal: New England Journal of Medicine (1987)

In patients with hypertension, a pattern of left ventricular hypertrophy on the electrocardiogram is associated with a risk of sudden death in excess of the risk attributable to hypertension alone. We therefore investigated the frequency of complex ventricular arrhythmias by means of 48-hour ambulatory electrocardiographic monitoring in 100 treated hypertensive patients, of whom 50 had electrocardiographic evidence of left ventricular hypertrophy and 50 did not, and in 50 normotensive controls. The groups were matched for age, sex, and smoking habits, and the two hypertensive groups were matched for blood-pressure levels before and after antihypertensive therapy. Nonsustained ventricular tachycardia, defined as ≥3 complexes at a rate ≤120 beats per minute, occurred in 14 (28 percent) of the 50 patients with an electro-cardiographic pattern of left ventricular hypertrophy, in 4 (8 percent) of the 50 patients without hypertrophy (P<0.05), and in 1 (2 percent) of the control subjects. Eight of the 50 patients (16 percent) with hypertrophy had episodes of nonsustained ventricular tachycardia longer than 5 complexes, whereas no patients without hypertrophy and no controls had such episodes. The group with nonsustained ventricular tachycardia was characterized by a high left ventricular mass on echocardiography and a high prevalence of ST-T abnormalities on electrocardiography. Ventricular tachycardia was not closely related to blood-pressure levels, nor was it associated with diuretic therapy or hypokalemia. The clinical importance of these arrhythmias is uncertain. Nevertheless, our data suggest that complex ventricular arrhythmias occur commonly in hypertensive patients with left ventricular hypertrophy and may contribute to the higher incidence of sudden death in these patients. (N Engl J Med 1987; 317:787–92.)
Difference between Endothelium-Dependent Relaxation in Arterial and in Venous Coronary Bypass Grafts
Authors: Thomas F. Lüscher, Dennis Diederich, Robert Siebenmann, Kurt Lehmann, Peter Stulz, Ludwig von Segesser, Zhihong Yang, Marko Turina, Erich Grädel, Erika Weber, Fritz R. Bühler
Journal: New England Journal of Medicine (1988)

Both the internal mammary artery and the saphenous vein are used to construct coronary-artery bypass grafts. We hypothesized that the release or production of endothelium-derived relaxing factor, which regulates blood flow and inhibits platelet function, may differ in venous and arterial grafts. We therefore studied endothelium-dependent relaxation in internal mammary arteries, internal mammary veins, and saphenous veins obtained from 58 patients undergoing coronary bypass surgery. Vascular rings with and without endothelium were suspended in organ chambers, and isometric tension was recorded. Acetylcholine (10–8 to 10–4 M), thrombin (1 U per milliliter), and adenosine diphosphate (10–7 to 10–4 M) evoked potent endothelium-dependent relaxation in the mammary artery but weak response in the saphenous vein (P<0.005; n = 6 to 27). In the mammary artery, relaxation was greatest in response to acetylcholine (86±4 percent reduction in norepinephrine-induced tension), followed by thrombin (44±7 percent) and adenosine diphosphate (39±8 percent). In the saphenous and mammary veins, relaxation was less than 25 percent. Relaxation was unaffected by indomethacin but was inhibited by methylene blue and hemoglobin (P<0.005 and 0.01, respectively), which suggests that endothelium-derived relaxing factor was the mediator. Endothelium-independent relaxation in response to sodium nitroprusside was similar in arteries and veins. We conclude that endothelium-dependent relaxation is greater in the mammary artery than in the saphenous vein. The possibility that this contributes to the higher patency rate among arterial grafts than among venous grafts will require further study. (N Engl J Med 1988; 319: 462–7.)
Decreased Coronary Reserve
Authors: Melvin L. Marcus, Donald B. Doty, Loren F. Hiratzka, Creighton B. Wright, Charles L. Eastham
Journal: New England Journal of Medicine (1982)

The pathogenesis of angina pectoris in patients with aortic stenosis and normal coronary arteries remains uncertain. Using a specially designed Doppler probe, we measured the maximal velocity of coronary blood flow in the left-anterior descending coronary artery at the time of elective open-heart surgery in 14 patients with aortic stenosis and left ventricular hypertrophy (13 had angina) and in 8 controls without left ventricular hypertrophy. The ratio of peak velocity of coronary blood flow, after a 20-second occlusion, to resting velocity was decreased by more than 50 per cent (P<0.05) in the patients with aortic stenosis. In 7 of the patients this ratio was decreased by more than 75 per cent. Studies of the velocity of coronary blood flow in vessels perfusing the right ventricle in these patients showed only mild abnormalities. These data demostrate a selective and marked decrease in coronary reserve to the hypertrophied left ventricle in patients with severe aortic stenosis. The impairment in coronary reserve is probably an important contributor to the pathogenesis of angina pectoris in these patients. (N Engl J Med. 1982; 307: 1362–7.)