tbuckley/cabot-search huggingface dataset:
Drowning: A Seasonal Disease
Authors: Robert H. Moser
Journal: JAMA (1974)

The blaze of summer is upon us with all its attendant joys and woes. Despite the charm of warmth and sun after the dreary winter, I am always reminded of a tragedy that occurred one sun-swept day in June, a few years back. I recounted this incident once before,<sup>1</sup>but it bears repetition before a larger audience. One brisk Sunday morning, three teaching sisters of the Third Order of St. Francis were exploring the sea cliffs on an isolated beach on the south shore of Maui. It was a high-surf day and waves charged into the<i>pali</i>in a spectacular show of spray and sound. The youngest, more adventurous sister, a 29-year-old teacher, scrambled down the rocky surface to a vantage point about six feet above the sea. Suddenly a giant wave swept in, engulfed her, and carried her out into the rough water of the cove. One of
IS STRESS MYOCARDIAL PERFUSION IMAGING WITH REGADENOSON, A NEW PHARMACOLOGIC STRESS AGENT, SAFE IN ORTHOTOPIC HEART TRANSPLANT PATIENTS? FIRST REPORT OF REGADENOSON, A SELECTIVE A2A RECEPTOR AGONIST IN THE HEART TRANSPLANT POPULATION
Authors: Joao L. Cavalcante, Mouaz Al-Mallah, Cristina Tita, David Lanfear, Celeste Williams, Barbara Czerska, Karthikeyan Ananthasubramanian
Journal: Journal of the American College of Cardiology (2010)
Urination and fluid intake.
Authors: E C Ashby
Journal: BMJ (1993)

ED1TOR,-MY editorial on retinopathy of pre- maturity mentioned antioxidants in general, both regarding aetiology and prevention.Several anti- oxidant mechanisms have certainly been described previously,' but owing to restriction of space vitamin E was the only antioxidant specifically mentioned in the editorial.I agree that trans- ferrin also is very interesting.Further research concerning the relation of iron and transferrin concentrations in extremely premature children and development of retinopathy of prematurity, as well as the possible preventive effects of transferrin on retinopathy ofprematurity, will be welcomed.
Heparanase: A Critical Determinant of Breast Cancer Metastasis to Brain.
Authors: D. Marchetti, L. Zhang
Journal: Cancer Research (2009)

Abstract Identification of mechanisms responsible for brain-metastatic breast cancer (BMBC) is imperative for the development of novel therapies. Heparanase (HPSE) is the only functional mammalian endoglycosidase degrading heparan sulfate (HS), the main polysaccharide component of growth factor - binding cell surface and extracellular matrix proteoglycans. HPSE relevance in cancer invasion and metastasis has been established. HPSE overexpression correlates with cancer metastasis, tumor vascularity, and the reduced post-operative survival of cancer patients, making it a promising target for anti-cancer therapeutics.Her-2 is a member of the epidermal growth factor receptor (EGFR) family; Her-2 overexpression and EGFR positivity are key characteristics of BMBC. EGFR is important for Her-2 signaling via Her-2/EGFR heterodimer formation. However, mechanisms linking Her-2 function and pathways to precise targets and BMBC onset have not been investigated.We hypothesize that Her-2/EGFR activation augments BMBC by inducing HPSE. We examined HPSE expression, intracellular trafficking, and activity in human Her-2 expressing BMBC models. We demonstrate that: 1) HPSE is expressed in human BMBC cells and expression is augmented according to their metastatic propensities (231parental &amp;gt; 231Br &amp;gt; 231Br2 &amp;gt; 231Br3); 2) EGF induces HPSE expression and nucleolar localization in Her-2 expressing BMBC cells in a dose- and time-dependent fashion; 3) DNA Topoisomerase I (Topo I) is a HPSE target in nucleoli; and 4) HPSE affects Topo I activity and function. Topo I is essential for transcription, and abnormal levels of the enzyme have been observed in a variety of tumors, including brain tumors.These novel findings are relevant to BMBC mechanisms. HPSE – Her-2 interactions will be elucidated to decipher how Her-2 signaling regulates HPSE functionality and mechanistic linkages between these two oncogenic proteins in BMBC cell lines and pre-clinical models. Citation Information: Cancer Res 2009;69(24 Suppl):Abstract nr 6156.
Toxicity beyond the Lung: Connecting PM <sub>2.5</sub> , Inflammation, and Diabetes
Authors: Carol Potera
Journal: Environmental Health Perspectives (2013)

Toxicity beyond the LungConnecting PM 2.5 , Inflammation, and Diabetes Exposure to fine particulate matter (PM 2.5 ) has been associated with increased risk of heart disease, 1 insulin resistance (IR), 2 and diabetes, 3 all conditions that are characterized by inflammation. 4Experimental data suggest a high-fat diet 2 may exacerbate the health effects of inhaled PM 2.5 ; obese people also appear to be at increased risk. 1 In this issue of EHP, investigators tease out some of the complex cellular mechanisms that could explain how PM 2.5 may work with a high-fat diet to cause IR. 5 Some of the authors previously reported that mice breathing PM 2.5 and eating a high-fat diet developed IR, systemic inflammation, and increased abdominal fat, compared with mice eating the same diet but breathing filtered air. 2 For the current study, the investigators focused on CCR2, a protein that recruits innate immune cells to insulin-sensitive tissues such as visceral fat and the liver, where it induces the inflammation characteristically seen in animal models of obesity and type 2 diabetes. 6They compared wild-type mice that produce CCR2 with "knockout" (CCR2 -/-) mice that don't.All the mice were fed a high-fat diet and then for 17 weeks were exposed to either filtered air or air containing 117 µg/m 3 of PM 2.5 .Among the key findings, PM 2.5 exposure was associated with increased IR and increased levels of liver lipids in the wild-type mice.The elevated liver lipids resulted from a rise in SREBP-1c activity 5 ; this protein helps regulate fatty acid synthesis. 7In contrast, liver lipid levels and SREBP-1c activity in CCR2 -/-mice were equivalent whether the mice were exposed to PM 2.5 or breathing filtered air. 5 IR is also characterized by abnormal insulin signaling through the AKT pathway.Reduced phosphorylation of this enzyme is associated with inflammation. 8The researchers found that phosphorylation of AKT was reduced in wild-type mice exposed to PM 2.5 but unchanged in CCR2 -/-mice.PM 2.5 exposure also was associated with higher levels of inflammatory F4/80 macrophages in visceral fat stores, but only in wild-type mice. 5he important message in all these findings is that PM 2.5 recruits inflammatory cells via CCR2-dependent mechanisms."This mechanism directly ties a known inflammatory mechanism in the pathogenesis of type 2 diabetes to exposure to environmental air
Mass Spectrometric Analyses of Organophosphate Insecticide Oxon Protein Adducts
Authors: Charles M. Thompson, John M. Prins, Kathleen M. George
Journal: Environmental Health Perspectives (2009)

Organophosphate (OP) insecticides continue to be used to control insect pests. Acute and chronic exposures to OP insecticides have been documented to cause adverse health effects, but few OP-adducted proteins have been correlated with these illnesses at the molecular level. Our aim was to review the literature covering the current state of the art in mass spectrometry (MS) used to identify OP protein biomarkers.We identified general and specific research reports related to OP insecticides, OP toxicity, OP structure, and protein MS by searching PubMed and Chemical Abstracts for articles published before December 2008.A number of OP-based insecticides share common structural elements that result in predictable OP-protein adducts. The resultant OP-protein adducts show an increase in molecular mass that can be identified by MS and correlated with the OP agent. Customized OP-containing probes have also been used to tag and identify protein targets that can be identified by MS.MS is a useful and emerging tool for the identification of proteins that are modified by activated organophosphate insecticides. MS can characterize the structure of the OP adduct and also the specific amino acid residue that forms the key bond with the OP. Each protein that is modified in a unique way by an OP represents a unique molecular biomarker that with further research can lead to new correlations with exposure.
Hyperosmolality related to propylene glycol in an infant treated with enoximone infusion.
Authors: I Huggon, I James, D Macrae
Journal: BMJ (1990)

TABLE v-Numbers (percentages) ofelderly people in the various age groups who died in 1976, 1980, and 1984 and who spent 30 days or more, 90 days or more, or all oftheirfinalyear oflife in hospital
Bone marrow necrosis in two patients with acute promyelocytic leukemia during treatment with all‐trans retinoic acid
Authors: Steven A. Limentani, Judith O. Pretell, David Potter, Jon S. Dubois, Philip R. Daoust, Paul S. Spieler, Kenneth B. Miller
Journal: American Journal of Hematology (1994)

Abstract All‐trans retinoic acid has been used for the treatment of acute promyelocytic leukemia (APL) with encouraging results. However, it has recently been associated with a number of potentially serious complications including the retinoic acid syndrome. We describe two patients with APL who were begun on all‐trans retinoic acid therapy (45 mg/m 2 ), but who developed leukocytosis which was treated with hydroxyurea. Both patients demonstrated clinical and laboratory findings of disseminated intravascular coagulation, massive cell lysis manifested by marked increases in serum lactic dehydrogenase, and rapid clinical deterioration. Both patients developed bone marrow necrosis within viable, non‐infarcted bone trabeculae. We postulate that the development of bone marrow necrosis in these two patients was not a chance occurrence. Rather, the specific combination of cytotoxic and differentiating agents used in these patients (hydroxyurea with all‐trans retinoic acid) caused massive cell lysis and death. The absence of bone marrow necrosis in the setting of induction therapy for APL both with and without all‐trans retinoic acid therapy suggests that the addition of hydroxyurea was critical to the development of marrow necrosis. We, therefore, recommend caution in the use of hydroxyurea and all‐trans retinoic acid in the treatment of APL. © 1994 Wiley‐Liss, Inc.
What happens to papers rejected by the BMJ on ethical grounds
Authors: N A Pace, M. Owen, S. Schroter
Journal: BMJ (2008)

The paper rejected by the BMJ but subsequently published by the Journal of Paediatrics and Child Health raises a further issue.1 What happens to those papers that the BMJ committee rejected?

After permission we reviewed the committee’s minutes and documentation for the period 2004-5 and identified six papers rejected on …
Elevated aflatoxin exposure and increased risk of hepatocellular carcinoma
Authors: Chien-Jen Chen, Li-Yu Wang, Sheng-Nan Lu, Mei-Huei Wu, San-Lin You, Yu-Jing Zhang, Lian-Wen Wang, Regina M Santella
Journal: Hepatology (1996)

To elucidate the importance of aflatoxin in the etiology of hepatocellular carcinoma (HCC), a community–based cohort study combined with molecular dosimetry of aflatoxin exposure was performed in the Penghu Islets where the HCC mortality rate is highest in Taiwan. A total of 6,487 residents aged 30 to 65 years were recruited in the two– stage screening survey and underwent regular follow–up examination. Among 33 newly diagnosed HCC cases, 31 (94%) were chronic hepatitis B surface antigen (HBsAg) carriers and 3 (9%) were positive for antibodies against hepatitis C virus (HCV). Among 20 HCC patients and 86 matched healthy controls whose serum samples were tested for aflatoxin B1 (AFB1)–albumin adducts by competitive enzyme–linked immunosorbant assay (ELISA), 13 (65%) HCC patients and 32 (37%) matched controls were seropositive, showing a statistically significant multivariate–adjusted odds ratio of 5.5 with a 95% confidence interval of 1.2 to 24.5. The results imply the elevated risk of HCC among Penghu residents may be attributable to their heavy exposure to aflatoxins and high HBsAg carrier rate.
SPONTANEOUS DETACHMENT OF THE RETINA
Authors: A. W. Ormond
Journal: BMJ (1930)

BR[IISH fold of omiientumii with' the o-al body ill one piece, and pre- se,r-ed.thnem for future study.Tlhree vear-s later (1889) a womiian was admitted under myicare in the Middlesex Hospital w-itlh signs of intra- pelvic bleedinig.I-promiiptly operated, anid found a mtiovable body as big as a walniut with a smootlh cav-ity at onie pole, and at oniee recogniized its similarity to the famliliar uterinie miiole.The effuse(d blood anid clot were collected, anid the operation comiipleted.I theni wa1..slhed the clot in a glass vessel with a gentle stream of wvater from a tap.Suddenly I saw the head of an embryo rise to the surface in a gentle swirl.This clinched the evidence-I lhad found a tuibaCl mioleThe lnamiie soon biecamie currlenit in gynaecological literatture.Wlhenl nio embry-vo is forthcomiing the l)resellce of chorionic villi in the mole is niow accepted tas evidence of tubal g,estatioll.T'hiis lectuire wa;lsopenied witlh a recital of the Blood Trail.Let imie ead b e-rlin(lidng voU tlhat imleni who mnake orlminal observations are often obdurl-ate in acceptinig the dis-moreries of their contemiporaries.hllarvey: discoveredI the circuilationi of the blood, but did not believ-e in the existence of the lacteals descr-ibed by Aselli (1622).The (lisco-erv of, the lymphatic system waas second( onily in ilmiportance to tha-t of the circulation of the 1b1o0o1.Baerfounid the human ov-um, btut wotuld not accept the idea; tliat the sperimatozQon iniitiates development, in the ovtumii.We miay believe that the tail of the spermatozoon led to the discovery, " since things in motion sooner catcl the eve thani wlhat not stirs."L,awson Tait, in hiis vigorouis Ingleby Lecture (1886) on P)elvic Haeimiatocele, inisisted that the blood came fr-om the sae of ani eetopic pregnianicy.He niot only ridiculed mylV dis- (overy of tlhe tubal miiole, but warned teachers of midwi'ifery ag-aini,st mi1y transcenidental nlotions relatinig to tubal ail)Ortioll.To-day1 a tubal nmole is (is fu ilil0'a to a gly~ecoloq1i.stas a pa plea.tea to a in idtife.
Correction: Dosage of Thioguanine
Authors: SEWA LEGHA
Journal: Annals of Internal Medicine (1975)

Comments and Correction1 February 1975Correction: Dosage of ThioguanineSEWA LEGHA, M.D.SEWA LEGHA, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-82-2-288 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: In the letter "Hyperphosphatemia and Hypocalcemia in Myeloproliferative Disorder" (Ann Intern Med81:119-120, 1974), the dose of thioguanine was published as 25 mg/kg body weight. The correct dose is 2 to 3 mg/kg body weight · day.... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Investigational Drug Branch National Cancer Institute Bethesda, Maryland 20014 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 February 1975Volume 82, Issue 2Page: 288-288KeywordsBody weightHypocalcemiaMyeloproliferative disordersThioguanine ePublished: 1 December 2008 Issue Published: 1 February 1975 PDF downloadLoading ...
Alpha adrenergic-mediated accumulation of calcium in reperfused myocardium.
Authors: A D Sharma, J E Saffitz, B I Lee, B E Sobel, P B Corr
Journal: Journal of Clinical Investigation (1983)

Reperfusion of ischemic myocardium is associated with increases in total myocardial calcium (Ca+2), which may influence the ultimate extent of ischemic damage as well as the development of arrhythmias. Since reperfusion is also associated with enhanced alpha-adrenergic responsivity, this study was performed to determine the potential interactions between alpha-adrenergic receptors and myocardial calcium during reperfusion. Cats were subjected to 35 min of left anterior descending coronary artery occlusion and 10 min of reperfusion. Total myocardial calcium was measured by atomic absorption spectrometry. Intracellular calcium was calculated from measurements of extracellular space [( 3H]inulin). In control animals with reperfusion, total calcium increased from 0.32 +/- 0.03 to 0.65 +/- 0.05 mmol/100 g dry tissue (P less than 0.0001), while intracellular calcium increased from 0.15 +/- 0.03 to 0.40 +/- 0.05 mmol/100 g dry tissue (P less than 0.001). Pretreatment with the alpha-adrenergic blocking agents phentolamine or prazosin prevented the increase in total and intracellular calcium. Phentolamine and the aqueous soluble alpha 1-adrenergic antagonist BE-2254 administered as late as 2 min before reperfusion similarly attenuated the increase in tissue calcium. Although administration of BE-2254 2 min before reperfusion failed to block the reperfusion-induced increase in extracellular space, the increase in calculated intracellular calcium was prevented. beta-Adrenergic blockade with propranolol partially attenuated but did not prevent an increase in total tissue calcium. Labetalol, a combined alpha- and beta-adrenergic blocking agent completely blocked the increase in tissue calcium during reperfusion. Additional experiments performed after 70 min of ischemia with reperfusion demonstrated a 49% attenuation of the increase in tissue calcium with alpha-adrenergic blockade. Electron microscopy with pyroantimonate and x-ray microprobe analysis demonstrated a large increase in calcium precipitate in mitochondria after reperfusion in untreated animals. Though alpha-adrenergic blockade prevented the calcium deposition in mitochondria, other criteria of ischemia persisted. Thus, alpha-adrenergic blockade specifically prevents the increase in intracellular calcium during reperfusion in reversibly injured tissue, independent of alterations in extracellular space and tissue water.
Molecular characterization of a cross-reactive Juniperus oxycedrus pollen allergen, Jun o 2: A novel calcium-binding allergen☆☆☆★
Authors: Raffaella Tinghino, Bianca Barletta, Sabrina Palumbo, Claudia Afferni, Patrizia Iacovacci, Adriano Mari, Gabriella Di Felice, Carlo Pini
Journal: Journal of Allergy and Clinical Immunology (1998)
Cross-reacting antibodies in coeliac disease?
Authors: K E A LUNDIN
Journal: Gut (1999)

See article on page 168 

Most patients with coeliac disease have antibodies to wheat gliadin, reticulin, and endomysium. In 1997 a seminal paper showed that at least a substantial fraction of anti-endomysial antibodies (EMA) recognises the endogenous enzyme tissue transglutaminase (tTG).1 However, antibodies recognising other antigens can also be found and in this issue (see page 168) Krupickova and colleagues attempt to characterise these antibodies.

Anti-gliadin antibodies (AGA) were isolated from coeliac serum samples using (semi)purified α-gliadin as the substrate. These antibodies were tested for specificity using a synthetic α-gliadin peptide competition assay. This important study is the first of its kind. An interesting finding is that the antibody responses are directed towards a limited set of epitopes. These epitopes do not overlap with peptides recognised by small intestinal HLA-DQ restricted T cells,2 3 but our current knowledge is too limited to …
Levels of Alanine Aminotransferase Confound Use of Transient Elastography to Diagnose Fibrosis in Patients With Chronic Hepatitis C Virus Infection
Authors: Elliot B. Tapper, Eric B. Cohen, Keyur Patel, Bruce Bacon, Stuart Gordon, Eric Lawitz, David Nelson, Imad A. Nasser, Tracy Challies, Nezam Afdhal
Journal: Clinical Gastroenterology and Hepatology (2012)
Abstract 2298: Cell-specific effects of BRafV600E expression disrupt gliogenesis and lead to astrocytoma formation.
Authors: Robin G. Lerner, Yuichiro Ihara, Brian Reichholf, Dian Qu, Sista Sugiarto, Amelie Griveau, David James, Martin McMahon, Claudia Petritsch
Journal: Cancer Research (2013)

Abstract Within the adult mammalian brain the asymmetric distribution of cell-fate determinants during mitosis maintains a balance between differentiated and self-renewing cells. We have previously shown that disruption of asymmetric divisions in oligodendrocyte progenitor cells (OPC) causes cells to aberrantly self-renew and fail to differentiate, giving rise to oligodendroglioma (Sugiarto et al. Cancer Cell; 2011; 20; 320-40). Here we proposed to address whether asymmetric divisions are also disrupted in precursors of malignant astrocytoma, a highly aggressive and therapy resistant type of glioma. The constitutively active BRaf mutant BRafV600E is mutated in a subset of malignant astrocytoma alongside deletion of Cdkn2a, and can transform NSCs into astrocytoma precursors (Huillard et al. PNAS; 2012; 109; 8710-5). We used BRafCA mice (Dankort et al. Genes Dev. 2007; 21; 379-84) with Cre recombinase-activated expression of BRafV600E and deletion of Ink4a/Arf to generate an in situ model of NSC-derived malignant astrocytoma. In vivo studies to assess asymmetric division and related defects were complemented by studies of BRafV600E expressing, Ink4a/Arf-deleted neurosphere cells in cell-based assays of asymmetric division, self-renewal and differentiation. Our results provide unprecedented evidence that BRafV600E, although uniformly expressed in NSC and their progeny, disrupts asymmetric divisions in a cell-type specific manner. NSCs continue to divide asymmetrically but their progeny, including OPC, divide more symmetrically and exhibit defects in differentiation and proliferation. These defects are reversible with BRafV600E-specific inhibitor PLX4720, and are associated with increased expression of the mitotic kinase polo-like kinase 1, increased pERK and decreased pAKT. These data describe a mechanism by which NSC-targeted expression of BRafV600E may generate numerous subpopulations of tumor cells with distinct characteristics. This heterogeneity may mirror that seen in malignant astrocytoma, which has often been associated with high incidence of therapy resistance (Burger et al. Cancer. 1985; 56; 1106-11). Citation Format: Robin G. Lerner, Yuichiro Ihara, Brian Reichholf, Dian Qu, Sista Sugiarto, Amelie Griveau, David James, Martin McMahon, Claudia Petritsch. Cell-specific effects of BRafV600E expression disrupt gliogenesis and lead to astrocytoma formation. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 2298. doi:10.1158/1538-7445.AM2013-2298
No evidence of transfer of fluoride from plasma to breast milk.
Authors: J Ekstrand, L O Boreus, P de Chateau
Journal: BMJ (1981)

the catheter, howevcr, it can be relocated at anv time by repeating the procedure described above.The figure shows a side-opening catheter, but the results we obtained with a catheter having a single hole at the tip appear to be the same.a c d Four stages of fluid bridge (flow) test: (a) catheter is passed up into bladder, (b) bladder neck is located, (c) test position is selected, (d) bladder neck opens during cough.Conversion: SI to traditional units-Fluoride: 1 1mol/lI 19 ng/ml.