tbuckley/cabot-search huggingface dataset:
Delivery of Therapeutic Nanoshells to Hypoxic Areas of Tumors Using a Cellular Trojan Horse.
Authors: M. Choi, R. Bardhan, S. Badve, H. Nakshatri, N. Halas, S. Clare
Journal: Cancer Research (2009)

Abstract Background: The goal of this project is to develop a novel and innovative delivery system for anti-tumor therapeutics which circumvents the impediments to efficient delivery that are present in a solid malignancy. Malformed blood vessels, elevated interstitial pressure, and large transport distances in a tumor, individually or in concert limit or thwart the diffusion of oxygen, glucose and soluble therapeutics. This results in hypoxia, necrosis, and makes regions of the tumor inaccessible to otherwise efficacious therapies. In addition, hypoxia exerts a selective pressure on tumor cells in that only those with an aggressive phenotype are able to survive hypoxia; these cells may be the source of subsequent local recurrence and distant metastasis.Monocytes/macrophages respond to intratumoral hypoxia and necrosis and are recruited by a chemoattractant gradient. Our strategy is to take advantage of the recruitment of monocytes/macrophages by a tumor, and of the monocytes/macrophages innate phagocytosis ability in order to load them with nanoshells, and thereby to create a Trojan horse. This study was designed to determine if monocytes/macrophage loaded with gold-silica nanoshells would respond to the chemoattractant gradient and become tumor associated macrophages. Nanoshells can convert absorbed light into thermal energy, which can be utilized for photothermal ablation. Therefore, our xenograft model system was utilized also to test whether malignant epithelial cells can be successfully be treated by thermal ablation of neighboring macrophages.Materials and Methods: A human breast tumor xenograft, and a separate metastatic brain tumor xenograft were established in nude mice. Monocytes were isolated from human whole blood and loaded with nanoshells. The nanoshells were conjugated with a near-infrared dye. The loaded macrophages were injected via the tail vein into the systemic circulation of the mice. The tumors were imaged by fluorescence imaging and magnetic resonance imaging before and after irradiation with a near-infrared laser (0.5 W, 5mm spot size) for varying lengths of time.Results: The in vivo delivery of the macrophages loaded with nanoshells to the human xenograft tumors was verified. Significant uptake of loaded macrophages in tumor was observed at 24 hours after injection. Uptake was also observed in the lungs, liver and spleen. An increase of ∼ 30°C at the tumor skin was noted following 90 seconds of irradiation of the orthotopic tumor.Discussion: Nanoshell-loaded macrophages respond to the presence of an orthotopic breast tumor and to breast cells metastatic to the brain, exit the circulation and accumulate in the rim of hypoxic cells surrounding necrosis. Photothermal ablation of the tumor cells infiltrated by this innovative therapeutic delivery method produces a targeted therapy in that it targets the tumor hypoxia. Citation Information: Cancer Res 2009;69(24 Suppl):Abstract nr 6113.
Criticism of the Bassini Operation and its Modifications
Authors: G. B. Mair
Journal: BMJ (1945)

The dihydrofolate reductase of <i>Escherichia coli</i> is rapidly and irreversibly inactivated in the presence of the proteolytic enzyme Pronase. However, the reductase is almost completely protected when dihydrofolate, NADP, NADPH, or <i>N</i><sup>5</sup>-formyltetrahydrofolate are present at saturating concentrations. NAD, NADH, 2-amino-4-hydroxy-6hydroxymethyl dihydropteridine, <i>p</i>-aminobenzoylglutamate, amid glutamate were all ineffective in this regard. On the other hand, NAD did not accelerate the inactivation of <i>E. coli</i> dihydrofolate reductase by Pronase. Certain small-molecule, heterocyclic inhibitors of dihydrofolate reductase were also excellent protective agents when added at 30 times the concentration needed for 50% inhibition of the reductase. Surprisingly, at this same concentration certain other inhibitors with equal or better capacity for binding to the reductase failed to show any protective activity. The structural requirements for protection were explored, and some possible implications of the findings are discussed.
Postoperative Synergistic Gangrene
Authors: David S. de Jongh
Journal: JAMA (1967)

POSTOPERATIVE synergistic gangrene, a spreading, infectious gangrene of skin and subcutaneous tissues, usually begins around retention sutures after abdominal operations. It is caused by an anhemolytic, microaerophilic<i>Streptococcus</i>in synergism with other organisms. A deep ulcer with gangrenous margins develops and may reach tremendous proportions. Although systemic symptoms tend to be minimal, the ulcer is painful. Even before the introduction of antibiotic therapy, this lesion was unusual. Vier,<sup>1</sup>in 1940, stated that the average surgeon observed only one or two cases during his lifetime. Although synergistic gangrene was described by several authors<sup>2,3</sup>before 1956, no publication dealing with this infection was found in the American medical literature from that time to the present (January 1966). The case reported here is significant in that the presence of a microaerophilic<i>Streptococcus</i>cultured from the abdominal wound was not recognized as the primary agent in the infection, and the patient was
Giant-Cell Arteritis Presenting as Mondor Disease
Authors: Emmanuel J. Diamantopoulos
Journal: Annals of Internal Medicine (1999)

Letters5 January 1999Giant-Cell Arteritis Presenting as Mondor DiseaseEmmanuel J. Diamantopoulos, MD, Georgia Yfanti, MD, and Emmanual Andreadis, MDEmmanuel J. Diamantopoulos, MDSearch for more papers by this author, Georgia Yfanti, MDSearch for more papers by this author, and Emmanual Andreadis, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-130-1-199901050-00027 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:Mondor disease is an uncommon condition characterized by thrombophlebitis of the chest veins. It is usually associated with breast cancer. We describe a 68-year-old woman who had had fever, headaches, myalgias, and night sweats for 2 months. On hospital admission she was febrile and pale. Physical examination did not reveal any abnormal signs. Laboratory evaluation revealed anemia, leukocytosis, thrombocytosis, elevated erythrocyte sedimentation rate, abnormal liver function test results, elevated serum γ-globulin levels, and acute phase reactant proteins.During hospitalization, the patient developed painful longitudinal subcutaneous hard cords in the upper outer quadrant of both breasts. The clinical ...References1. Mondor H. Tronculite sous-cutaneé subaigue de la paroi thoracique antero-láterale. Mém Acad Chir (Paris). 1939;65:1271-8. Google Scholar2. Bartolo M, Bartolo M, Amoroso A, Bonomo L. La malattia di Mondor. Osservazioni su 22 casi. Recenti Prog Med. 1993;84:737-41. MedlineGoogle Scholar3. Catania S, Zurrida S, Veronesi P, Galimberti V, Bono A, Pluchinotta A. Mondor's disease and breast cancer. Cancer. 1992;69:2267-70. CrossrefMedlineGoogle Scholar4. Susmano A, Roseman D, Haber MH. Giant cell arteritis of the breast. Arch Intern Med. 1990;150:900. CrossrefMedlineGoogle Scholar Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByMondor's Disease: A Review of the LiteratureScalp vein thrombosis mimicking giant cell arteritis relapseThromboses veineuses superficielles céphaliques satellites d’une artérite temporale de Horton, une manifestation exceptionnelleCordón indurado en la pared torácica anteriorEnfermedad de Mondor en un varónMondor's Disease and Polymyalgia Rheumatica: A Case ReportDiseases of the Blood Vessels 5 January 1999Volume 130, Issue 1Page: 78-79KeywordsAcute phase proteinsArteriesBiopsyBreast cancerFeversSystemic diseasesThoraxThrombocytosisTrauma surgeryVeins Issue Published: 5 January 1999 CopyrightCopyright © 1999 by American College of Physicians. All Rights Reserved.PDF DownloadLoading ...
Epidermal Electronics: Capacitive Epidermal Electronics for Electrically Safe, Long‐Term Electrophysiological Measurements (Adv. Healthcare Mater. 5/2014)
Authors: Jae‐Woong Jeong, Min Ku Kim, Huanyu Cheng, Woon‐Hong Yeo, Xian Huang, Yuhao Liu, Yihui Zhang, Yonggang Huang, John A. Rogers
Journal: Advanced Healthcare Materials (2014)

On page 642, integration of capacitive sensing capabilities to ultra-thin, soft, and elastic electronics enable robust electrophysiological signal measurements through electrical coupling between tissues and electrodes, mediated by an intervening dielectric layer. The capacitive skin electronics shown by John A. Rogers and co-workers are reusable, electrically safe, and minimally sensitive to motion artifacts. The presented device provides levels of fidelity in ECG, EMG, and EOG recordings comparable to those of standard gel electrodes.
The Prevalence of Rheumatoid Arthritis
Authors: JOHN B. O'SULLIVAN
Journal: Annals of Internal Medicine (1972)

In 1964 the prevalence of rheumatoid arthritis in the population of Sudbury was 3.8% for women and 1.3% for men by ARA criteria. By New York criteria the prevalence rate in the same population was 0.5% for women and 0.1% for men. Follow-up examinations performed through 3 to 5 years after the initial population study indicate that the New York criteria identify persons whose disease remains clinically meaningful and, as such, indicate the frequency of rheumatoid arthritis to be about 2 to 3 cases per 1000. On the other hand, the large number of Sudbury residents who reported a previous episode of pain in 3 or more joints but had no clinical signs at the time of this study raises the interesting possibility that rheumatoid arthritis exists more frequently as a benign, nondeforming condition.
RESPONSES - Re: Trends in Reported Incidence of Primary Malignant Brain Tumors in Children in the United States
Authors: M. A. Smith
Journal: JNCI Journal of the National Cancer Institute (1999)

I read with some concern the editorial by Black (1) for the article written by Smith et al. (2) reporting on the trends in reported incidence of primary malignant brain tumors in children in the United States.In their article, Smith et al. (2) offer fairly complex statistical arguments that purport to show no increase in the incidence of primary brain tumors in children.The authors (1,2) argue that the increased incidence relates to improved diagnostic techniques.I believe that they overlooked two critical points.Malignant brain tumors of childhood are not silent diseases.If indeed there was an increased sensitivity to diagnosis made in 1984, certainly in the subsequent 10-year interval, those cases that may have been missed would have become clinically evident.This point was not made by either the editorial or the article.Secondly, there is a diminishing, albeit very slight, mortality, and this may be attributable to the considerable improvements that have been made in neurosurgical techniques during this period.The fact that the mortality has not diminished further argues for an increasing incidence.The Journal highlighted the article by Smith et al. by having an editorial written that states that we would be better off not seeking reasons for this increasing incidence and rather that we should place our efforts elsewhere.This emphasis is all the more troubling to me, since this article appeared in the popular media, in both newspapers and television.
A previously unidentified MECP2 open reading frame defines a new protein isoform relevant to Rett syndrome
Authors: Gevork N Mnatzakanian, Hannes Lohi, Iulia Munteanu, Simon E Alfred, Takahiro Yamada, Patrick J M MacLeod, Julie R Jones, Stephen W Scherer, N Carolyn Schanen, Michael J Friez, John B Vincent, Berge A Minassian
Journal: Nature Genetics (2004)
Effects of therapy with cholestyramine on progression of coronary arteriosclerosis: results of the NHLBI Type II Coronary Intervention Study.
Authors: J F Brensike, R I Levy, S F Kelsey, E R Passamani, J M Richardson, I K Loh, N J Stone, R F Aldrich, J W Battaglini, D J Moriarty
Journal: Circulation (1984)

In the National Heart, Lung and Blood Institute Type II Coronary Intervention Study, patients with Type II hyperlipoproteinemia and coronary artery disease (CAD) were placed on a low-fat, low-cholesterol diet and then were randomly allocated to receive either 6 g cholestyramine four times daily or placebo. This double-blind study evaluated the effects of cholestyramine on the progression of CAD as assessed by angiography. Diet alone reduced the low-density lipoprotein cholesterol 6% in both groups. After randomization, low-density lipoprotein cholesterol decreased another 5% in the placebo group and 26% in the cholestyramine-treated group. Coronary angiography was performed in 116 patients before and after 5 years of treatment. CAD progressed in 49% (28 of 57) of the placebo-treated patients vs 32% (19 of 59) of the cholestyramine-treated patients (p less than .05). When only definite progression was considered, 35% (20 of 57) of the placebo-treated patients vs 25% (15 of 59) of the cholestyramine-treated patients exhibited definite progression; the difference was not statistically significant. However, when this analysis was performed with adjustment for baseline inequalities of risk factors, effect of treatment was more pronounced. Of lesions causing 50% or greater stenosis at baseline, 33% of placebo-treated and 12% of cholestyramine-treated patients manifested lesion progression (p less than .05). Similar analyses with other end points (percent of baseline lesions that progressed, lesions that progressed to occlusion, lesions that regressed, size of lesion change, and all cardiovascular end points) all favored the cholestyramine-treated group, but were not statistically significant. Thus, although the sample size does not allow a definitive conclusion to be drawn, this study suggests that cholestyramine treatment retards the rate of progression of CAD in patients with Type II hyperlipoproteinemia.
Sulfisoxazole-induced thrombocytopenic purpura. Immunologic mechanism as cause
Authors: H. E. Hamilton
Journal: JAMA (1978)

During treatment of brucellosis with sulfisoxazole, tetracycline, and streptomycin sulfate, severe thrombocytopenic purpura developed in a young farmer. Verification for an immune mechanism was provided by clinical challenge with a small dose of sulfisoxazole that caused recurrence of thrombocytopenia and by serologic laboratory test results that detected a serum factor causing platelet agglutination requiring the presence of sulfisoxazole. The original antigenic stimulation was considered to come from drinking cows' milk contaminated with sulfonamide drugs. Cross-reactivity with some other sulfonamide drugs was demonstrated. (<i>JAMA</i>239:2586-2587, 1978)
Phosphatidylinositol metabolism in hypertrophic rat heart.
Authors: H Kawaguchi, H Sano, K Iizuka, H Okada, T Kudo, K Kageyama, S Muramoto, T Murakami, H Okamoto, N Mochizuki
Journal: Circulation Research (1993)

The accumulation of inositol 1,4,5-trisphosphate (IP3) after hormonal stimulation has a physiological role, possibly by alteration of Ca2+ levels in cardiac myocyte. However, this accumulation has not been studied under pathophysiological conditions. In this report, we examine phosphatidylinositol metabolism during cellular response to norepinephrine in pressure-overloaded hypertrophic rat heart. After stimulation with norepinephrine, the accumulations of IP3 and diacylglyceride significantly increased in isolated myocytes from stroke-prone spontaneously hypertensive rat (SHRSP) heart, indicating phosphatidylinositol-specific phospholipase C activity increased in SHRSP heart cells. Protein kinase C activity was also enhanced in SHRSP, with a marked increase in particulate activity. We determined the intracellular calcium concentration and found it to be higher in SHRSP than in Wistar-Kyoto (WKY) rats at 30-40 weeks of age. Ca2+ influx was also elevated in SHRSP stimulated by norepinephrine. In SHRSP heart, cytosolic Ca2+ concentration may rise quickly in response to some stimuli, such as alpha 1-adrenergic stimulation, which is shown to be one of the pathways that increases cytosolic Ca2+ levels in hypertrophied rat heart. These data suggest that a part of the phosphatidylinositol-turnover pathway, such as the phosphatidylinositol 4,5-bisphosphate-IP3-Ca2+ pathway or the diacylglyceride-protein kinase C pathway, may play an important role in the development of hypertrophy in SHRSP heart.
To Bring Consumers to the Table, Simplify the Review
Authors: Mark D. Smith, Maribeth Shannon
Journal: JAMA Internal Medicine (2013)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Internal Medicine HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Internal Medicine journal
Comprehensive Molecular Analyses of Lung Adenocarcinoma with Regard to the Epidermal Growth Factor Receptor, K-ras, MET, and Hepatocyte Growth Factor Status
Authors: Takamitsu Onitsuka, Hidetaka Uramoto, Kenji Ono, Mitsuhiro Takenoyama, Takeshi Hanagiri, Tsunehiro Oyama, Hiroto Izumi, Kimitoshi Kohno, Kosei Yasumoto
Journal: Journal of Thoracic Oncology (2010)
Impotence: science and sciencibility
Authors: V. Deacon, P. Snaith
Journal: BMJ (1986)

Cyanosis attributable to right to left shunt in the carcinoid syndrome SIR,-Dr G W Stewart and colleagues (1 March, p 589) described an interesting case of pronounced arterial hypoxaemia in a patient with the carcinoid syndrome.In the absence ofpulmonary metastases they attributed the hypoxaemia to intrapulmonary shunting through microscopic arteriovenous fistulas.The data presented, however, do not exclude an alternative explanation-right to left shunting through a patent foramen ovale.Although right to left shunting through the foramen ovale is well recognised in patients with pulmonary hypertension,'"3 it may also occur in the presence of normal pulmonary artery and right heart pressures, apparently as a result of reduced right atrial compliance.4Thus though mean left atrial pressure may exceed mean right atrial pressure, during atrial filling right atrial pressure rises disproportionately, causing phasic shunting across the interatrial septum.Right atrial compliance
Death of the teaching autopsy: Autopsy is a success story in Cuba
Authors: A. Espinosa-Brito
Journal: BMJ (2004)

EDITOR—Advances in sophisticated antemortem diagnostic methods may have reduced the value of autopsy.1 The percentage of deaths without clinical-pathological concordance has not decreased despite modern diagnostic technologies.2 Indeed, in certain cases these new methods have misled the diagnosis, partly because of doctors' excessive confidence in them.

Ours is the main provincial hospital for adult patients with …
Angina With “Normal” Coronary Arteries
Authors: Raffaele Bugiardini, C. Noel Bairey Merz
Journal: JAMA (2005)

Many women with angina are told that they have no significant heart disease following demonstration of normal or near-normal coronary arteries and are offered no specific treatment beyond reassurance.MEDLINE and the Cochrane Database of Systematic Reviews were searched from their start dates until June 2004 for analysis using specific key words including diagnosis and therapy of angina with normal angiography and angina with normal coronary arteries. Reference lists of published articles and data of meeting presentations were also consulted.Normal or nonobstructive coronary disease at angiography is not uncommon and occurs in 10% of women presenting with ST-segment elevation myocardial infarction compared with 6% in men. Patients with evidence of myocardial ischemia or myocardial infarction and nonobstructive atherosclerotic disease of the coronary arteries are more likely to be women and nonwhite. Symptoms are often indistinguishable from those with obstructive coronary artery disease. The prognosis of patients with unstable angina and nonobstructive atherosclerotic coronary artery disease is not benign and includes a 2% risk of death or myocardial infarction at 30 days of follow-up. Recent work has shown that at least 20% of women with normal or nonobstructive angiography have myocardial ischemia, likely due to atherosclerosis-related endothelial dysfunction, which itself is associated with an increased risk of later adverse cardiac events and development of frank future obstructive disease. Randomized placebo-controlled studies have demonstrated that tricyclic antidepressants, beta-blockers, angiotensin-converting enzyme inhibitors, L-arginine, statins, and exercise may relieve symptoms, vascular dysfunction, or both; however, longer-term studies evaluating cardiac event rates need to be performed.Patients with chest pain and normal or nonobstructive coronary angiograms are predominantly women, and many have a prognosis that is not as benign as commonly thought. Assessment of endothelial function may help identify patients at risk for future cardiac events. Therapy should be directed at symptom relief with tricyclic agents and beta-blockers, and aggressive antiatherosclerotic therapy with statins, angiotensin-converting enzyme inhibitors, or both should be applied when risk factors are present or prognostic risk is high. Large-scale randomized trials need to be conducted to determine optimal ways of preventing clinical events.