tbuckley/cabot-search huggingface dataset:
Surgical Bleeding: Handbook for Medicine, Surgery, and Specialties
Authors: Charles H. Fuller
Journal: JAMA (1967)

As the editors note in their preface this is an eclectic book, whose value lies in the presentation of authoritative approaches to the many and varied problems of surgical bleeding.  The medical profession has, in recent years, been deluged with treatises, monographs, and handbooks dedicated to this or that highly specialized problem in medical practice. All too often these minitexts are overly concise, overly ambitious, and overly wide of the intended mark. In short, they are often superfluous. The present volume most assuredly should not be classified with these others. It is, rather, a textbook, in the true sense, on the subject of surgical bleeding. That this subject is worthy of presentation in textbook fashion soon becomes apparent to the reader.  The editors have corralled 113 outstanding contributors who have compiled 71 chapters in over 500 pages. Seemingly every medical discipline relevant to the subject of surgical bleeding has been
Alimentary tract and pancreas. Stimulation of mucosal prostaglandin synthesis in human stomach and duodenum by antacid treatment.
Authors: G Preclik, E F Stange, K Gerber, G Fetzer, H Horn, H Ditschuneit
Journal: Gut (1989)

The effect of a low dose antacid treatment on mucosal prostaglandin metabolism was studied in 15 healthy volunteers. A daily dose of 46 mmol (= 138 mval) Al(OH)3 and 42 mmol (= 84 mval) Mg(OH)2 with a titrated in vitro neutralising capacity of 272 mval of H+ was given for three weeks. Total prostaglandin formation and the prostaglandin profile as well as the degradation of PGE2 were assayed by incubating homogenates of endoscopic biopsies from antral and duodenal mucosa with the precursor (14C)arachidonic acid. Total prostaglandin synthesis in antrum (623 (110) pmol/mg protein) and duodenum (432 (72) pmol/mg) was stimulated after three weeks administration of low dose antacids by 176% (p less than 0.05) and 154% (p less than 0.05), respectively. An untreated control group exhibited no significant changes. In contrast, the prostaglandin profile showed only a small increase of the prostacyclin metabolite 6-keto PGF1a (p less than 0.05) at the expense PGD2. PGE2 catabolism was unaffected. This enhanced activity of mucosal prostaglandin cyclooxygenase might represent one possible mechanism of action of a low dose antacid treatment.
Lactic Acidosis and Bicarbonate Therapy
Authors: Robert G. Narins, Jordan J. Cohen
Journal: Annals of Internal Medicine (1987)

Letters and Corrections1 November 1987Lactic Acidosis and Bicarbonate TherapyROBERT G. NARINS, M.D., JORDAN J. COHEN, M.D.ROBERT G. NARINS, M.D.Search for more papers by this author, JORDAN J. COHEN, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-107-5-785_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: In his recent letter (1), critical of our support (2) for bicarbonate therapy of keto and lactic acidosis, Hollander straddles the horns of an uncomfortable dilemma. On the one hand, he agrees that acidemia can be lethal, but he decries its correction with bicarbonate. Space limitations precluded our discussing in detail the major shortcomings of published experimental models of lactic acidosis. We maintained that animals undergoing differing degrees of evisceration while receiving cardiotoxins or being rendered acutely and severely hypoxic hardly duplicated commonly occurring human forms of the disorder. The increased cardiac output of the hypoxic model...References1. HOLLANDER R. Lactic acidosis and bicarbonate therapy [Letter]. Ann Intern Med. 1987;107:116-7. LinkGoogle Scholar2. NARINSCOHEN RJ. Bicarbonate therapy for organic acidosis: the case for its continued use. Ann Intern Med. 1987;106:615-8. LinkGoogle Scholar3. MADIAS N. Lactic acidosis. Kidney Int. 1986;29:752-74. CrossrefMedlineGoogle Scholar4. ARIEFFPARKLEACH ARW. Pathophysiology of experimental lactic acidosis in dogs. Am J Physiol. 1980;239:F135-42. MedlineGoogle Scholar5. GRAFLEACHARIEFF HWA. Metabolic effects of sodium bicarbonate in hypoxic lactic acidosis in dogs. Am J Physiol. 1985;249:F630-5. MedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byThe Pathophysiology of Hypoglycemia and Lactic Acidosis in Malaria 1 November 1987Volume 107, Issue 5Page: 785-786KeywordsBicarbonatesCardiac outputLactic acidosis Issue Published: 1 November 1987 PDF downloadLoading ...
EXPERIMENTAL CONGENITAL TOXOPLASMOSIS
Authors: David Cowen, Abner Wolf
Journal: The Journal of Experimental Medicine (1950)

A study has been made of congenital toxoplasmosis in the offspring of mice infected with Toxoplasma by the vaginal route during pregnancy. Some of the young mice were retarded in postnatal development, and some became ill or died in the 2nd to 4th weeks of life while the majority remained symptom-free in spite of the presence of toxoplasmic lesions of varying degrees of severity. Congenital toxoplasmosis developed only in offspring whose mothers had been infected on the 7th to 9th day of pregnancy. Infection of the offspring without active toxoplasmosis in the mother was not observed. The highest incidence of congenital infection (57.6 per cent) was obtained by giving 2 vaginal instillations of Toxoplasma-infected mouse brain on the 8th and 9th days of pregnancy. Mice infected before the 7th day developed placental toxoplasmosis but rarely delivered viable young. When the mother was infected after the 9th day, the offspring were normal. When congenital toxoplasmosis occurred in a litter, a majority or all of the individual offspring were usually infected. Although pathologic changes were not present in the suckling mice at birth, and did not appear before the 9th postnatal day, reasons are stated for excluding the possibility of postnatal contact or milk-borne infection. It cannot be assumed from the experimental disease that the vagina is a portal of entry of Toxoplasma in human congenital toxoplasmosis. Any route of infection leading to a maternal parasitemia during pregnancy might result in toxoplasmosis of the placenta and transmission of the disease to the offspring before birth. Unlike the restricted time interval effective in the mouse, there is a long period during the later months of pregnancy in the human being in which transplacental passage of the infection may occur. When transmission to the fetus takes place shortly before parturition, evidence of disease in the human infant, as in the mouse, may not become manifest until several weeks postpartum, and the prenatal origin of the infection may not be apparent. When the fetus becomes infected well before parturition, symptoms of congenital toxoplasmosis may be present at birth. The asymptomatic character of the infection in many of the young mice would appear to have a counterpart in certain instances of human congenital toxoplasmosis.
The mTORC1 inhibitor everolimus has antitumor activity in vitro and produces tumor responses in patients with relapsed T-cell lymphoma
Authors: Thomas E. Witzig, Craig Reeder, Jing Jing Han, Betsy LaPlant, Mary Stenson, Han W. Tun, William Macon, Stephen M. Ansell, Thomas M. Habermann, David J. Inwards, Ivana N. Micallef, Patrick B. Johnston, Luis F. Porrata, Joseph P. Colgan, Svetomir Markovic, Grzegorz S. Nowakowski, Mamta Gupta
Journal: Blood (2015)
Abstract A23: Cell autonomous and nonautonomous activities of heat shock factor 1 support tumor initiation, progression, and metastasis
Authors: Ruth Scherz-Shouval, Sandro Santagata, Martina Koeva, Luke Whitesell, Susan Lindquist
Journal: Cancer Research (2013)

Abstract The heat-shock response is a powerful transcriptional program which acts genome-wide, not only to restore the normal protein folding through the induction of heat shock proteins (HSP), but to re-shape global cellular pathways controlling survival, growth and metabolism. In mammals, this response is regulated primarily by the Heat Shock Factor 1 (HSF1) transcription factor. We have previously shown that HSF1 plays a fundamental role in tumorigenesis, by promoting the survival and malignance of tumor cells, both in tissue culture and in mouse models of cancer [1]. Recently we demonstrated that HSF1 exerts its role by activating a unique transcriptional program in the cancer cells, that is distinct from the one activated during heat shock [2]. In breast cancer and several other types of carcinoma, we found that high HSF1 protein levels and activation of the HSF1-dependent transcriptional program are associated with poor clinical outcome [3]. Here we show that HSF1 is activated not only in the tumor cells, but also in the stromal cells infiltrating the tumor. Examining human patient samples, we find immunohistochemical evidence for activation of HSF1 in the stroma. Using mouse xenograft models and in vitro co-culture we show that HSF1 in the stroma supports tumor cell growth. Finally, expression profiling and analysis of the DNA binding pattern of HSF1 in tumors and in cell culture indicates that stromal HSF1 supports tumorigenesis by activating a unique, stroma-specific transcriptional program. Taken together, our data suggests that HSF1 acts in the cancer cells and in the stroma to activate distinct, yet complimentary transcriptional programs that will facilitate tumor initiation, progression and metastasis. References 1. Dai, C., et al., Heat shock factor 1 is a powerful multifaceted modifier of carcinogenesis. Cell, 2007. 130(6): p. 1005-18. 2. Mendillo, M.L., et al., HSF1 drives a transcriptional program distinct from heat shock to support highly malignant human cancers. Cell, 2012. 150(3): p. 549-62. 3. Santagata, S., et al., High levels of nuclear heat-shock factor 1 (HSF1) are associated with poor prognosis in breast cancer. Proc Natl Acad Sci U S A, 2011. 108(45): p. 18378-83. Citation Format: Ruth Scherz-Shouval, Sandro Santagata, Martina Koeva, Luke Whitesell, Susan Lindquist. Cell autonomous and nonautonomous activities of heat shock factor 1 support tumor initiation, progression, and metastasis. [abstract]. In: Proceedings of the AACR Special Conference on Tumor Invasion and Metastasis; Jan 20-23, 2013; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2013;73(3 Suppl):Abstract nr A23.
MICROVASCULAR OBSTRUCTION AND INTRAMYOCARDIAL HEMORRHAGE DETECTED ON CMR AS PREDICTORS FOR MACE AND LEFT VENTRICLE ADVERSE REMODELLING. A META-ANALYSIS OF PROSPECTIVE STUDIES
Authors: Romero Jorge, Florentino Lupercio, David Goodman, Jared Liebelt, Mario Garcia
Journal: Journal of the American College of Cardiology (2014)
Renal Adenocarcinoma: Long Survival
Authors: Ramon Leiguarda, Luis Jost, Mario Turin, Boris Elsner
Journal: Annals of Internal Medicine (1973)

Letters, Comments, and Corrections1 February 1973Renal Adenocarcinoma: Long SurvivalRAMON LEIGUARDA, M.D., LUIS JOST, M.D., MARIO TURIN, M.D., BORIS ELSNER, M.D.RAMON LEIGUARDA, M.D.Search for more papers by this author, LUIS JOST, M.D.Search for more papers by this author, MARIO TURIN, M.D.Search for more papers by this author, BORIS ELSNER, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-78-2-311_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: Adenocarcinoma of the kidney is rare in infancy and childhood, less than 50 cases being reported in the literature (1, 2). We have seen a patient who presented with pulmonary metastasis 15 years after nephrectomy. Such a long interval before the appearance of metastatic disease has not been previously described for childhood renal cell carcinoma.A 13-year-old white girl had a left nephrectomy for adenocarcinoma of the kidney. The tumor was large and showed a clear cell pattern histologically. Blood vessel invasion or lymph node metastasis were not found in the resected specimen. The patient had careful...References1. DEHNERLEESTMAPRICE LJE: Renal cell carcinoma in children: a clinicopathologic study of 15 cases and review of the literature. J Pediatr 76:358-368, 1970 CrossrefMedlineGoogle Scholar2. PALMAKENNYMURPHY LGG: Childhood renal carcinoma. Cancer 26:1321-1324, 1970 CrossrefMedlineGoogle Scholar3. TAKÁTSCSAPÓ LZ: Death from renal carcinoma 37 years after its original recognition. Cancer 19:1172-1176, 1966 CrossrefMedlineGoogle Scholar4. WILMORE L: Intracerebral metastatic hypernephroma appearing 17 years postnephrectomy. Mo Med 66:883-884, 1969 MedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Department of Clinical Pathology Center of Medical Education and Clinical Investigation Buenos Aires Argentina PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByRecurrent renal cell carcinoma after 45 yearsTerapia Chirurgica E Ormonale Nel Carcinoma Del Rene: Risultati a DistanzaRenal Cell Carcinoma: Long-Term Survival and Late Recurrence 1 February 1973Volume 78, Issue 2Page: 311-312KeywordsAdenocarcinomaBlood vesselsKidneysLymph nodesNephrectomyRenal cell carcinomaRenal diseases Issue Published: 1 February 1973 PDF DownloadLoading ...
Maximal aerobic power measurement in runners and swimmers.
Authors: I. Corry, N. Powers
Journal: British Journal of Sports Medicine (1982)

Five cross-country runners and five competitive swimmers performed a pulling exercise with elastic shock cords and a treadmill run to exhaustion. The mean VO2 max related to lean body mass of the runners was significantly higher than the swimmers on the treadmill (p less than 0.05) while, on the pulling test, the mean VO2 max of the swimmers was significantly higher than the runners (p less 0.01). The maximum heart rates achieved pulling were 95% of the running maximum by runners and 96% by swimmers with no significant difference between them. Their mean oxygen pulse was almost the same for maximal running but the swimmers had a significantly higher oxygen pulse than the runners for maximal pulling (p less than 0.01). The swimmers could reach about 79% of their running VO2 max by pulling while the runners used 53% of their running VO2 max.
578 HEPATITIS B VIRUS INDUCES INTERLEUKIN-8 PRODUCTION WHICH IN TURN INHIBITS INTERFERON- ALFA ANTIVIRAL ACTIVITY IN HEPATOMA CELL LINES
Authors: T. Pollicino, L. Bellinghieri, G. Raffa, A. Restuccia, D. Teti, G. Raimondo
Journal: Journal of Hepatology (2009)
Clinical Evaluation of Left Ventricular Pressures in Myocardial Infarction
Authors: WILLIAM W. PARMLEY, GEORGE DIAMOND, HARUO TOMODA, JAMES S. FORRESTER, H. J. C. SWAN
Journal: Circulation (1972)

Left venitricular pressures were obtained in 14 patients with acute myocardial infarction, of whom seven survived. Calculated contractile element velocity (V CE ), left ventricular end-diastolic pressure, and maximum dp/dt were compared with other hemodynamic measurements of LV function. V CE at 5 mm Hg (V CE5 ) was calculated according to the Maxwell three-component model of muscle and used as an index of overall contractile state. There was considerable overlap between survivors and nonsurvivors in the levels of V CE5 , LVEDP, cardiac index, heart rate, and systemic vascular resistance. There was a reasonably good separation between survivors and nonsurvivors with measurements of mean arterial pressure, maximum LV dp/dt, mean isovolumic Δp/Δt, and stroke work. Changes in V CE5 were no more sensitive after five inotropic interventions than ventricular function curves in monitoring changes in conitractile state. It is concluded that LV pressure measurements in acute myocardial infarction offer little further clinical information of importance beyond that which can be obtained from measurements of pulmonary capillary wedge pressure, arterial pressure, and cardiac output.
Evaluation of Viral and Mammalian Promoters for Use in Gene Delivery to Salivary Glands
Authors: Changyu Zheng, Bruce J. Baum
Journal: Molecular Therapy (2005)

To optimize vectors for salivary gland gene transfer, we screened viral [cytomegalovirus (CMV; human immediate early), Rous sarcoma virus (RSV), simian virus 40, and Moloney murine leukemia virus long terminal repeat] and mammalian [elongation factor 1alpha (EF1alpha), cytokeratin 18 (K18), cytokeratin 19 (K19), kallikrein (Kall), and amylase (AMY), all human, and rat aquaporin-5 (rAQP5), and derivative elements] promoters driving luciferase activity in vitro and in vivo. In adenoviral vectors, the CMV promoter showed highest activity, with the EF1alpha and RSV promoters slightly less powerful, in rat submandibular glands (SMGs). The K18 2.5-kb, K19 3.0-kb, and rAQP5 0.4-kb and Kall promoters had intermediate activity, while the AMY promoter exhibited lowest activity. To localize transgene expression, enhanced green fluorescence protein was used. The CMV, RSV, EF1alpha, K18 2.5-kb, K19 3.0-kb, rAQP5 0.4-kb, and AMY promoters were not cell-type specific in SMGs; however, the Kall promoter was primarily active in ductal cells. These data will facilitate optimal expression cassette design for salivary gland gene transfer.
PL-02 * NOTCH-MEDIATED SUPPRESSION OF MULTICILIATE DIFFERENTIATION PROMOTES CHOROID PLEXUS TUMOR INITIATION FROM EPITHELIAL PROGENITOR IN RESPONSE TO Shh SIGNALS
Authors: L. Li, K. Picotte, J. Ohli, U. Schuller, H. Zhao
Journal: Neuro-Oncology (2014)

Choroid plexus (CP) tumors are intraventricular papillary neoplasms mainly found in children. While CP papilloma is a benign tumor, CP carcinoma is malignant and associated with poor prognosis. Though previous studies implicate Notch signaling in CP tumorigenesis, the developmental origin and mechanisms of Notch-induced CP tumors remain unclear. We used the Rosa26-NICD1 strain to express the intracellular domain of Notch 1 (NICD1) using Cre-loxP technologies. Hindbrain CP targeted for NICD1 expression developed abnormal growth consistent with CP papilloma. While Notch-induced CP tumor cells expressed CP markers Lmx1a and Otx2, the expression of Aquaporin 1 (AQP1), marker for differentiated CP epithelium, was absent. Embryonic studies showed that CP tumor arises during development and exhibit properties similar to those of CP epithelial progenitors. However, unlike progenitor cells, tumor cells fail to exit the cell cycle and differentiate into mature CP epithelium. Gene expression studies revealed increased expression of Gli1 and N-Myc, effectors of the Sonic Hedgehog (Shh) pathway, in both Notch-induced CP tumors and human CP tumors, suggesting the role of Shh signaling in CP tumors. Conversely, Shh treatment stimulated the proliferation of Notch-induced CP tumor cells. Vertebrate Shh signaling is uniquely dependent on primary cilium. Unlike differentiated CP epithelial cells with small tufts of primary cilia on their apical surface, Notch-induced CP tumor cells only possess solitary primary cilium. Further analysis revealed reduced expression of Foxj1 and Mcidas, crucial regulators of multiciliate differentiation, in tumor cells. Together, these results indicate that Notch-induced CP tumor arises from CP epithelial progenitors during development but lack terminal differentiation; and Notch pathway activation in tumor cells suppresses multiciliate differentiation, thereby allowing Shh-driven proliferation. Our studies demonstrate that Notch and Shh pathways converge on primary cilium to drive CP tumor formation, Shh pathway is a potential therapeutic target for Notch-induced CP tumors.
Visceral Leishmaniasis in Southern Sudan
Authors: Jill Seaman
Journal: Annals of Internal Medicine (1997)

Letters15 February 1997Visceral Leishmaniasis in Southern SudanJill Seaman, MD, Alec J. Mercer, MSc, and Barbara L. Herwaldt, MD, MPHJill Seaman, MDMedecins Sans Frontieres-Holland, Amsterdam, the NetherlandsCenters for Disease Control and Prevention, Atlanta, GA 30341-3724Search for more papers by this author, Alec J. Mercer, MScMedecins Sans Frontieres-Holland, Amsterdam, the NetherlandsCenters for Disease Control and Prevention, Atlanta, GA 30341-3724Search for more papers by this author, and Barbara L. Herwaldt, MD, MPHMedecins Sans Frontieres-Holland, Amsterdam, the NetherlandsCenters for Disease Control and Prevention, Atlanta, GA 30341-3724Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-126-4-199702150-00019 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail IN RESPONSE:Regarding Dr. Nishioka's first concern, we doubt that we substantially overestimated the importance of older age as a risk factor for death. Sudanese staff estimated the ages of patients and commonly considered factors in addition to physical appearance (for example, for a woman, the ages and number of her children and the timing of her marriage [that is, menarche] with respect to a political or military event).In our multivariable analysis of the risk for death among adults, we avoided making assumptions about the relation between age and death by treating age as a series of independent binary ... Author, Article, and Disclosure InformationAffiliations: Medecins Sans Frontieres-Holland, Amsterdam, the NetherlandsCenters for Disease Control and Prevention, Atlanta, GA 30341-3724 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 15 February 1997Volume 126, Issue 4Page: 332KeywordsAnemiaHemoglobinHemorrhageLeishmaniasisMedical risk factorsMenarcheNeutropeniaNeutrophilsResearch laboratoriesRisk ratio Issue Published: 15 February 1997 Copyright & PermissionsCopyright © 1997 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
1087-133 Assessment of ventricular untwisting recoil velocity by doppler tissue echocardiography: An index of relaxation time constant
Authors: Yuichi Notomi, Takahiro Shiota, Zoran B Popovic, Hirotsugu Yamada, Maureen G Martin-Miklovic, Dimitri G Deserranno, Don W Wallick, Neil L Greenberg, Mario J Garcia, James D Thomas
Journal: Journal of the American College of Cardiology (2004)
TCT-45 Impact of Ischemic Post-Conditioning on Infarct Size and Clinical Outcomes in Primary Percutaneous Coronary Intervention: A Meta-analysis of 26 Randomized Controlled Trials
Authors: Alok Saurav, Ajay K. Kaja, Vimal Kandasamy, Manu Kaushik, Michael DelCore, Aryan Mooss, Michael D. White, Mark Woodruff
Journal: Journal of the American College of Cardiology (2014)
PERFORMANCE CHARACTERISTICS OF THE PICKER PCD CAMERA: IMPACT OF CRYSTAL THICKNESS ON SINGLE PHOTON IMAGING
Authors: L J Daley, O Cooper, D Rich, G Freedman, J S Seibyl, C K Ng, H M Dey
Journal: Clinical Nuclear Medicine (1998)

Daley, L J; Cooper, O; Rich, D; Freedman, G; Seibyl, J S; Ng, C K; Dey, H M Author Information
Marcia Angell and the<i>Journal</i>
Authors: Edward W. Campion, Gregory D. Curfman, Robert S. Schwartz, Robert Steinbrook, Robert D. Utiger
Journal: New England Journal of Medicine (2000)

Marcia Angell, a superb editor, has an instinct for the best in medical writing and an exceptional talent for quickly grasping the core of a manuscript, whatever its topic. In judging a submitted article, she consistently stresses rigor of experimental design, clarity of analysis, and above all, credibility. In her own writing, she brings to the profession and the public clear thinking about matters of substance. Angell's distinctive editorials for the Journal speak for the rights of patients and voice concern about encroachments on clinical practice and academic medicine by outside influences. She is a staunch advocate of the highest . . .