tbuckley/cabot-search huggingface dataset:
CD8+ T-cell responses to adeno-associated virus capsid in humans
Authors: Federico Mingozzi, Marcela V Maus, Daniel J Hui, Denise E Sabatino, Samuel L Murphy, John E J Rasko, Margaret V Ragni, Catherine S Manno, Jurg Sommer, Haiyan Jiang, Glenn F Pierce, Hildegund C J Ertl, Katherine A High
Journal: Nature Medicine (2007)
A Clinician’s Guide to Dermatologic Differential Diagnosis, vol 1: The Text A Clinician’s Guide to Dermatologic Differential Diagnosis, vol 2: The Atlas
Authors: Lawrence Charles Parish
Journal: JAMA (2007)

These 2 volumes, comprising text and extensive bibliographies in volume 1 and color images in volume 2, represent an enormous undertaking. They feature 284 dermatologic entities illustrated by 4000 figures and together weigh approximately 14 lb.
The Insulin Controversy
Authors: ROMESH KHARDORI
Journal: Annals of Internal Medicine (1980)

Letters1 February 1980The Insulin ControversyROMESH KHARDORI, M.B., M.D.ROMESH KHARDORI, M.B., M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-92-2-267_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: In his editorial note "New Light on the Insulin Controversy," Hudson (1) has done a remarkable job in placing matters in the right perspective. His account lacks, however, mention of Zuelzer, who had successfully prepared an extract of pancreas that had considerably reduced glycosuria when administered intravenously into a pancreatectomized dog. He had also tried his extract on eight hospitalized patients in 1908 and observed some improvement in all, with striking results in two. In fact in 1912 the Hoechst Company acquired Zuelzer's patent in a contract and agreed to pay him 6000 marks plus a portion...References1. HUDSON R. New light on the insulin controversy. Ann Intern Med. 1979;91:311-2. Editorial. LinkGoogle Scholar2. MURRAY I. The search for insulin. Scott Med J 1969;14:286-93. CrossrefMedlineGoogle Scholar3. PAULESCO N. Recherche sur le role du pancreas dans assiucitation nutritive. Arch Int Physiol. 1921; 17:85. Google Scholar4. BANTING F and BEST C. The internal secretion of pancreas. J Lab Clin Med. 1922;7:251. Google Scholar5. PAVEL I. Report presented at VII International Diabetes Federation Meeting at Buenos Aires, Argentina, 1970: Quoted from: BAJAJ JS, ed. Insulin and Metabolism. Bombay: Publications of the Diabetic Association of India; 1972:35-48. Google Scholar6. SCOTT E. On influence of intravenous injections of an extract of the pancreas on experimental diabetes. Am J Physiol. 1912;29:306. CrossrefGoogle Scholar1. STEVENSON L. Sir Frederick Banting. Toronto: Ryerson Press; 1946. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: ROMESH KHARDORI, M.B., M.D.Affiliations: Good Samaritan Hospital and Medical Center Portland, OR 97210 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 February 1980Volume 92, Issue 2_Part_1Page: 267-268KeywordsInsulinPancreas ePublished: 1 December 2008 Issue Published: 1 February 1980 PDF downloadLoading ...
Abstract P5-11-05: Overexpression of girdin in nucleus indicates poor disease-free survival in ER-positive breast cancer
Authors: W-T Peng, X Hu, L Yao, Y-Z Jiang, K-D Yu, Z-M Shao
Journal: Cancer Research (2013)

Abstract Background Girdin is identified as a novel modulator of the PI3K-Akt signaling pathway in regulating neurons integration during neurogenesis process. Recently, several studies demonstrated that Girdin and its phosphorylation type (p-Girdin) were also involved in tumor metastasis and angiogenesis. However, the clinical implications of Girdin and p-Girdin in breast cancer remain unclear. In this study, we detected the expression pattern of p-Girdin (Ser1416) and Girdin in breast cancer to uncover the association between p-Girdin/Girdin status and clinicopathological parameters like estrogen receptor (ER), progestogen receptor (PR), and human epidermal growth factor receptor 2 (Her2), etc. Methods This study included 250 patients who were histologically confirmed as invasive ductal breast cancer and underwent mastectomy in the Department of Breast Surgery in Shanghai Cancer Center during 2001 to 2006. We performed immunohistochemistry of p-Girdin/Girdin on tissue microarrays constructed from above specimens. Results We observed that Girdin was mainly located in the cytoplasm of mammary epithelial carcinoma cells (195/248, 78.63%) while p-Girdin was mainly located in the nucleus (160/250, 64.00%). However, Girdin/p-Girdin was also weakly expressed in the nucleus/cytoplasm (77/248, 31.05% for Girdin and 193/250, 77.2% for p-Girdin). By the Chi-square test, we found that Girdin in the nucleus (GN) was positively associated with ER status (P = 0.012); Girdin in the cytoplasm (GC) was positively associated with ER (P = 0.004), PR (P = 0.028), and Her2 status (P = 0.004); p-Girdin in the cytoplasm (pGC) was positively associated with PR status (P = 0.001) and negatively associated with tumor size (P = 0.025). However, no significant association was observed between p-Girdin in the nucleus (pGN) and other parameters. Using Kaplan-Meier method, we disclosed a trend that GN indicated poor disease-free survival (DFS) in ER-positive breast cancer (P = 0.075). After adjusted for histological grade and tumor size, multivariate cox regression analysis confirmed this trend (HR = 3.051, 95% CI: 1.137-8.191, P = 0.027). Furthermore, GC was prone to associating with poor DFS, especially in stage II (P = 0.079) and grade III (P = 0.058) patients. Conclusions Our work reveals, for the first time, that the location and expression pattern of both Girdin and p-Girdin (Ser1416) in breast cancer, suggesting that p-Girdin/Girdin are associated with ER, PR and Her2 status. In addition, Girdin in the nucleus is associated with poor DFS in ER-positive breast cancer. Citation Information: Cancer Res 2013;73(24 Suppl): Abstract nr P5-11-05.
TREATMENT OF AMEBIASIS
Authors: William M. James
Journal: JAMA (1934)

<h3>To the Editor:—</h3> There is a communication inThe Journal, Dec. 2, 1933, pages 1819-1820, signed by Dr. J. C. Geiger and others, with respect to the various drugs used in the treatment of human amebiasis due to infestation with Endamoeba histolytica. In this, reference is made on page 1820, column 2, paragraphs 2 and 4, to the use of "bismuth subcarbonate in massive doses" in the treatment of this infestation, and a paper by the late Dr. W. E. Deeks and myself in the<i>American Journal of Tropical Medicine</i>(<b>5</b>:97 [March] 1925) is mentioned. Kindly permit me to correct an error here. It is bismuth subnitrate, not the subcarbonate, that was first used in this manner by Dr. Deeks. I do not have at hand this copy of the<i>American Journal of Tropical Medicine</i>, and my supply of reprints has been exhausted. I am referring, however, to the
Training More Generalists
Authors: Jeremiah A. Barondess
Journal: Annals of Internal Medicine (1994)

Letters1 January 1994Training More GeneralistsJeremiah A. Barondess, MDJeremiah A. Barondess, MDNew York Academy of Medicine; New York, NY 10029Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-120-1-199401010-00032 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail IN RESPONSE:I appreciate the responses of Drs. Robinson and Greenberg. The primary issues are and will remain the quality and coherence of the care received by our patients and the impact of fragmented, technology-intensive care that characterizes our present system.Internal medicine, once the most popular specialty choice of medical graduates, has undergone an amazing slide in its popularity, a decline that does not appear to have ended. The repayment of debts incurred during the educational process, while obviously important, is not the primary reason for this remarkable change. The erosion of the intellectual content and clinical challenges of ... Author, Article, and Disclosure InformationAffiliations: New York Academy of Medicine; New York, NY 10029 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byPrimary Care as Form or Content? 1 January 1994Volume 120, Issue 1Page: 92-93KeywordsGraduate medical educationSub-specialty care ePublished: 15 August 2000 Issue Published: 1 January 1994 Copyright & PermissionsCopyright © 1994 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Immune-mediated hepatitis drives low-level fusion between hepatocytes and adult bone marrow cells
Authors: Marc H. Dahlke, Roberto Loi, Alessandra Warren, Lauren Holz, Felix C. Popp, Daniel J. Weiss, Pompiliu Piso, David G. Bowen, Geoffrey W. McCaughan, Hans J. Schlitt, Patrick Bertolino
Journal: Journal of Hepatology (2005)
Abstract 4795: CCK2R marks gastric antral stem cell and mediates antral carcinogenesis
Authors: Hayakawa Yoku, Guanchun Jin, Hongshan Wang, Xiaowei Chen, Christoph B. Westphalen, Samuel Asfaha, Daniel L. Worthley, Bernhard Renz, Hiroshi Ariyama, Zinaida A. Dubeykovskaya, Yoshihiro Takemoto, Ashlesha Mulay, Yagnesh Tailor, Duan Chen, Sureshkumar Muthupalani, James G. Fox, Shigeo Takaishi, Timothy C. Wang
Journal: Cancer Research (2014)

Abstract Gastrin is a hormone that binds to the CCK2 receptor and promotes proximal gastric cancer, but inhibits distal gastric cancer development. However, the precise roles of the CCK2 receptor, and its alternative ligand, progastrin, in gastric carcinogenesis have not been clarified. In this study, we found that progastrin accelerated antral proliferation and carcinogenesis through CCK2R+ antral stem cell expansion, using mouse gastric cancer models and transgenic mice lines including human progastrin-overexpressing (hGAS) mice, CCK2R knockout mice, Lgr5-CreERT-IRES-GFP knockin mice, and newly generated CCK2R-BAC-CreERT mice. Progastrin promoted gastric antral cancer development induced by MNU and/or H. felis. During carcinogenesis, progastrin increased the expression of Lgr5 and gland fission in response to the chemical carcinogen MNU. Genetic ablation of CCK2R diminished these progastrin-mediated effects. In vitro 3D culture experiments revealed that progastrin, but not amidated gastrin, significantly increased gastric organoid formation and growth in Noggin-free condition, effects that were ablated by a CCK2R inhibitor YF-476 or CCK2R gene deletion. In the antrum, CCK2R was expressed in an Lgr5low cell population that displayed stemness, which could be enhanced by progastrin. In the presence of progastrin, Lgr5lowCCK2R+ cells interconverted to Lgr5hi cells. Finally, we generated a new BAC-transgenic CCK2R-CreERT murine line, and lineage tracing experiments showed that CCK2R+ cells, which reside slightly above the base of the antrum, contained long-lived stem cells in vivo and in vitro. Chemical inhibition of CCK2R attenuated progastrin-dependent cancer development in mice. In conclusion, CCK2R labels Lgr5low antral stem cells that can be activated and expanded by progastrin. These findings may help the understanding of the underlying mechanism in gastric stem cell regulation by a CCK2R signal. Citation Format: Hayakawa Yoku, Guanchun Jin, Hongshan Wang, Xiaowei Chen, Christoph B. Westphalen, Samuel Asfaha, Daniel L. Worthley, Bernhard Renz, Hiroshi Ariyama, Zinaida A. Dubeykovskaya, Yoshihiro Takemoto, Ashlesha Mulay, Yagnesh Tailor, Duan Chen, Sureshkumar Muthupalani, James G. Fox, Shigeo Takaishi, Timothy C. Wang. CCK2R marks gastric antral stem cell and mediates antral carcinogenesis. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 4795. doi:10.1158/1538-7445.AM2014-4795
Cessation of Gout Following Portacaval Shunt
Authors: Aaron M. Lefkovits
Journal: JAMA (1968)

A portacaval shunt was required when cirrhosis of the liver and, subsequently, bleeding from esophageal varices developed in a 67-year-old man who had chronic tophaceous gout of at least 11 years' duration with frequent episodes of acute gouty arthritis. Since the shunt procedure, the patient has had no acute gouty arthritic attacks and has remained normouricemic without treatment.
Leukotrienes in Acute Lung Injury
Authors: James A. Frank, Michael A. Matthay
Journal: American Journal of Respiratory and Critical Care Medicine (2005)

A rapidly growing body of literature has begun to clarify the role of plasma membrane-derived mediators, including metabolites of arachidonic acid, sphingomyelin, lysophospholipid, ceramide, and platelet-activating factor (PAF), in the pathogenesis of acute lung injury.For example, PAF causes increased permeability pulmonary edema by inducing ceramide synthesis and cyclooxygenase activity (1).Endothelial barrier integrity is maintained in experimental ventilator-induced lung injury (VILI) by sphingosine-1 phosphate (2).Injurious ventilation increases lung phospholipase A2 activity, a major source of arachidonic acid release from the plasma membrane (3).The 5-lipoxygenase (5-LO) metabolite leukotriene (LT) D4 increases alveolar epithelial sodium transport by increasing sodium potassium ATPase activity and membrane abundance of the transporter (4).Although the precise mechanisms by which these interrelated pathways affect the balance of forces responsible for edema formation in acute lung injury have not been entirely resolved, it is clear that these lipid mediators play a larger role in lung endothelial and alveolar epithelial barrier function than previously recognized.Twenty years ago, it was reported that patients with acute lung injury had markedly elevated levels of LTs in pulmonary edema fluid compared with control patients with hydrostatic pulmonary edema, although the role of the LTs in the pathogenesis of lung injury was not clear at that time (5).In this issue of the Journal, Caironi and colleagues (pp.334-343) provide new information on the role of 5-LO metabolites in acute lung injury resulting from sustained high Vt ventilation (6).These studies were designed to determine the contribution of impaired hypoxic pulmonary vasoconstriction (HPV) to hypoxemia resulting from VILI and to determine the wider role of LTs in the pathogenesis of VILI.Vasoconstriction is the normal pulmonary vascular response to hypoxemia and results in the redirection of blood flow to areas with greater ventilation.This intrinsic vascular response is in part mediated through LTs.Using mice that lack 5-LO, these investigators found that ventilation with high Vt for 6 hours resulted in an impaired vasoconstriction response via a 5-LO-dependent pathway.HPV was measured as the change in pulmonary vascular resistance in response to occlusion of the left mainstem bronchus.Interestingly, impaired HPV was detected despite normal arterial oxygen partial pressures before the hypoxic challenge.Normal pulmonary vasoconstriction was preserved by pretreatment with LT inhibitors and was restored by infusion of angiotensin II.In separate studies, high Vt ventilation for up to 10 hours resulted in increased alveolar epithelial permeability, elevated bronchoalveolar lavage levels of cysteinyl LTs (LTC4, LTD4, LTE4), and an influx of neutrophils into the airspaces.Importantly, 5-LO-deficient mice had better preservation of alveolar
IL13 Receptor α2 Signaling Requires a Scaffold Protein, FAM120A, to Activate the FAK and PI3K Pathways in Colon Cancer Metastasis
Authors: Rubén A. Bartolomé, Irene García-Palmero, Sofía Torres, María López-Lucendo, Irina V. Balyasnikova, J. Ignacio Casal
Journal: Cancer Research (2015)

IL13 signaling through its receptor IL13Rα2 plays a critical role in colon cancer invasion and liver metastasis, but the mechanistic features of this process are obscure. In this study, we identified a scaffold protein, FAM120A (C9ORF10), as a signaling partner in this process. FAM120A was overexpressed in human colon cancer cell lines and 55% of human colon cancer specimens. IL13Rα2-FAM120A coimmunoprecipitation experiments revealed further signaling network associations that could regulate the activity of IL13Rα2, including FAK, SRC, PI3K, G-protein-coupled receptors, and TRAIL receptors. In addition, FAM120A associated with kinesins and motor proteins involved in cargo movement along microtubules. IL13Rα2-triggered activation of the FAK and PI3K/AKT/mTOR pathways was mediated by FAM120A, which also recruited PI3K and functioned as a scaffold protein to enable phosphorylation and activation of PI3K by Src family kinases. FAM120A silencing abolished IL13-induced cell migration, invasion, and survival. Finally, antibody blockade of IL13Rα2 or FAM120A silencing precluded liver colonization in nude mice or metastasis. In conclusion, we identified FAM120A in the IL13/IL13Rα2 signaling pathway as a key mediator of invasion and liver metastasis in colon cancer.
The Diagnosis of Cytomegalovirus Retinitis
Authors: Jeffrey N. Bloom
Journal: Annals of Internal Medicine (1988)

Immunosuppressed patients are at risk for developing cytomegalovirus retinitis. This disorder is the most common cause of vision loss in patients with the acquired immunodeficiency syndrome (AIDS). Cytomegalovirus retinitis is probably the result of hematogenous spread of the virus to the retina after systemic reactivation of a latent cytomegalovirus infection. Although the ophthalmic infection may initially be asymptomatic, the retinal necrosis it produces may result in both loss of visual field and decreased visual acuity. Routine screening of these patients is required for early diagnosis. The retinitis is detected with ophthalmoscopy as either a perivascular yellow-white retinal lesion frequently associated with retinal hemorrhage or as a focal white granular infiltrate, often without hemorrhage. Both lesions enlarge in a progressively expanding "brushfire" pattern. The diagnosis of cytomegalovirus retinitis, as well as the evaluation of its response to therapy, is determined primarily by clinical criteria. Serial retinal photography is an objective method to assess the changing appearance of these lesions. Ganciclovir and foscarnet are investigational antiviral drugs that appear to be effective in treating cytomegalovirus retinitis. However, maintenance therapy with these medications is required after initial treatment because the disease often relapses. The combined expertise of the internist and the ophthalmologist is needed to diagnose and treat these patients.
Effects of oral propranolol on left ventricular size and performance during exercise and acute pressure loading.
Authors: M H Crawford, J Lindenfeld, R A O'Rourke
Journal: Circulation (1980)

Oral propranolol (160 mg/day) was administered to 19 normal subjects for 2 weeks. Echocardiograms were performed at rest, during graded supine bicycle exercise in 10 subjects and during acute pressure loading with intravenous phenylephrine in the remaining nine subjects. Resting heart rate on propranolol decreased compared with control (52 +/- 8 vs 63 +/- 10 beats/min; p less than 0.001), as did systolic blood pressure (99 +/- 9 vs 107 +/- 9 mm Hg; p less than 0.01). Left ventricular end-diastolic dimension was slightly enlarged (48.3 +/- 4.2 vs 47.1 +/- 3.6 mm, p = 0.05), but percent dimensional shortening was unchanged (37 +/- 4 vs 38 +/- 5%). At each stage during supine bicycle exercise, heart rate was slower, blood pressure lower, left ventricular dimensions were larger and percent dimensional shortening was reduced on propranolol by an analysis of variance. In contrast, during acute pressure loading, while the heart rate response to increased blood pressure was blocked by atropine, there was no significant difference in left ventricle size and performance compared with control. We conclude that prolonged oral propranolol therapy has little, if any, intrinsic effect on myocardial performance in normal subjects. Its major action on the heart is competitive inhibition of beta-adrenergic tone, which is most manifest during conditions associated with increased sympathetic tone, such as exercise.
In searching for a good substitute of a complex compositum index to differentiate HCV-related chronic active hepatitis (CAH) from liver cirrhosis
Authors: G. Tarantino, P. Conca, A. Ceriello, G. Gagliardi, P. Sorrention, P. Ragucci, A. Gentile, D. Capone, V. Basile
Journal: Journal of Hepatology (2000)
The nuclear deubiquitinase BAP1 is commonly inactivated by somatic mutations and 3p21.1 losses in malignant pleural mesothelioma
Authors: Matthew Bott, Marie Brevet, Barry S Taylor, Shigeki Shimizu, Tatsuo Ito, Lu Wang, Jenette Creaney, Richard A Lake, Maureen F Zakowski, Boris Reva, Chris Sander, Robert Delsite, Simon Powell, Qin Zhou, Ronglai Shen, Adam Olshen, Valerie Rusch, Marc Ladanyi
Journal: Nature Genetics (2011)
Competition in Health Care
Authors: Jay A. Winsten
Journal: New England Journal of Medicine (1981)

WE are rapidly approaching the point at which modern medicine can offer more than society can afford. New approaches are required to decide how much of our limited resources can be devoted to medical care. Such decisions may be made centrally, by government, or decentrally, through consumers' aggregate demand in a medical marketplace.Interest in the latter, "consumer-choice," approach has been on the ascendancy over the past two years, stimulated by a small but influential cadre of senators, congressmen, and academics.1 2 3 4 5 6 7 8 9 Advocates see a revitalized medical marketplace in which health-care providers and insurers actively compete for consumers' business on the . . .
Alzheimer’s disease and insulin resistance: translating basic science into clinical applications
Authors: Fernanda G. De Felice
Journal: Journal of Clinical Investigation (2013)

Alzheimer's disease (AD) and diabetes are currently considered among the top threats to human health worldwide. Intriguingly, a connection between these diseases has been established during the past decade, since insulin resistance, a hallmark of type 2 diabetes, also develops in Alzheimer brains. In this article, the molecular and cellular mechanisms underlying defective brain insulin signaling in AD are discussed, with emphasis on evidence that Alzheimer's and diabetes share common inflammatory signaling pathways. I put forward here a hypothesis on how a cross-talk between peripheral tissues and the brain might influence the development of AD, and highlight important unanswered questions in the field. Furthermore, I discuss a rational basis for the use of antidiabetic agents as novel and potentially effective therapeutics in AD.
Decline and Rise of Psychoanalysis
Authors: Jacob Swartz
Journal: JAMA (1974)

To the Editor.—  From its historic beginnings to the present day, psychoanalysis has had to deal with views such as those of J. H. Conn in  Decline of Psychoanalysis (228:711, 1974). As a psychoanalyst and as chairman of the Committee on Public Information of the American Psychoanalytic Association, I have had occasion to respond to misconceptions about psychoanalysis on a number of occasions. Conn published similar comments on  Rise and Decline of Psychoanalysis in Psychiatric Opinion (10:34-38, 1973). My response at that time is, again, appropriate.  First, let me present some facts that should help raise some questions about what Conn sees as a decline. The American Psychoanalytic Association is the largest organization of psychoanalysts in the United States, with a membership of 2,050 psychoanalysts, 32 affiliated societies, and 23 training centers all over the country. In addition, there are some 800 psychoanalysts-in-training and some 600 who are