tbuckley/cabot-search huggingface dataset:
HISTOCHEMICAL CHANGES IN LYMPHOCYTES DURING THE PRODUCTION OF ANTIBODIES IN LYMPH NODES OF RABBITS
Authors: T. N. Harris, Susanna Harris
Journal: The Journal of Experimental Medicine (1949)

Following the injection of various antigenic and non-antigenic materials into the foot-pads of rabbits, the draining (popliteal) lymph nodes were removed on successive days and studied histologically, chemically, and serologically. On the 2nd day after injection of antigen, nucleoli and cytoplasmic granules and crescents stained with pyronine began to appear. They were found first in somewhat altered reticulum cells, later in transitional forms, then in young lymphocytes, and finally in more mature lymphocytes. The identity of this pyronine-stained material as ribonucleic acid was demonstrated by specific digestion with protease-free ribonuclease. The concentration of ribonucleic acid was determined in aqueous extracts of the lymph nodes. It was observed that the concentration had risen to more than twice its normal value by the 2nd to 5th day following the injection of antigens into the foot, and then it declined. The peak of this change occurred at or slightly before the appearance of the maximal concentration of antibodies in the same node. Non-antigenic materials, when injected into the foot, did not give rise to an increase in the ribonucleic acid content of the lymph node. The concentration of desoxyribonucleic acid was constant in all lymph nodes, within the limits of experimental variation.
Reactive Hyperreninemia in Renovascular Hypertension After Angiotensin Blockade with Saralasin or Converting Enzyme Inhibitor
Authors: DAVID B. CASE
Journal: Annals of Internal Medicine (1979)

Baseline plasma renin activity and responses to saralasin and converting enzyme inhibitor SQ 20881 (teprotide) in 47 untreated patients with surgically correctable renovascular hypertension were compared to those in 100 patients with high- and normal-renin essential hypertensioopn. All 32 renovascular patients on normal sodium intake had high renin-sodium profiles and renin values ≥ 5 ng angiotensin l/mL·h, as compared to 20 of 64 with essential hypertension. Diagnostic discrimination was greatly enhanced by infusion of saralasin or SQ 20881, which elicited marked reactive hyperreninemia in 31 of 32 renovascular patients but in only two of 64 with essential hypertension. Reactive hyperreninemia appeared to be more a specific test for renovascular hypertension than depressor responses. Prior dietary sodium depletion abolished this specificity. The results suggest that after initial screening with renin measurements, testing with angiotensin blocking agents may be a useful secondary screening procedure for more invasive and definitive procedures.
Topical Tazarotene for the Treatment of Ectropion in Ichthyosis
Authors: Brittany G. Craiglow, Keith A. Choate, Leonard M. Milstone
Journal: JAMA Dermatology (2013)

Importance: Ectropion is a complication of certain subtypes of ichthyosis and is often associated with substantial medical and cosmetic consequences.At present there is no standard of care for the treatment of ectropion in this population.Retinoids cause dyshesion and thinning of stratum corneum, thereby reducing hyperkeratosis that likely underlies ectropion in patients with ichthyosis.As such, retinoids provide a potential effective treatment for ectropion in this group of patients.Observation: We describe a patient with recessive ichthyosis for whom daily application of topical tazarotene produced rapid and persistent improvement of bilateral lower eyelid ectropion without adverse effects.
FINE PARTICLE AIR POLLUTION IS A POTENTIAL TRIGGER FOR STEMI BUT NOT NON-STEMI
Authors: Blake Gardner, David Q. Rich, Suresh Kulandhaisamy, Michael Topf, Kelly Thevenet-Morisson, Cathleen Kane, Mark Frampton, Wojciech Zareba, Mark Utell, Frederick Ling
Journal: Journal of the American College of Cardiology (2013)
Reversible Cardiomyopathy Associated with Sunitinib and Sorafenib
Authors: Imran Uraizee, Susan Cheng, Javid Moslehi
Journal: New England Journal of Medicine (2011)

To the Editor: Tyrosine kinase inhibitors with potent properties against vascular endothelial growth factor (VEGF) signaling pathway (VSP inhibitors) are effective antitumor agents in metastatic renal-cell carcinoma and are now increasingly used in the treatment of other tumors.1 Although VSP inhibitors have been associated with cardiomyopathy, the nature of this side effect is unclear. We report two cases of severe symptomatic, yet reversible, cardiomyopathy after VSP inhibitor therapy. A 46-year-old woman with metastatic gastrointestinal stromal tumor was started on sunitinib therapy after unsuccessful treatment with imatinib. She tolerated sunitinib well for 2 years at a dose of 25 mg once . . .
Psychological and Allergic Aspects of Asthma
Authors: M. Coleman Harris
Journal: JAMA (1965)

This book is essentially  reprint of articles, some of which were written almost 20 years ago. At least one of the authors (Dr. Bret Ratner) has long been dead, and two ( Herbert Herxheimer and Dennis Leigh) reside and practice in England. It may well be that some of the other authors are no longer living, or if they are alive, reside in countries outside of the United States. There is no information whatsoever about any of the authors, in the body of the book, the editor's preface, or even on the dust jacket!  The focus of the book is described as having a more historical nature, with one of its major objectives to stimulate research on the psychosocial implications of asthma, which will meet the vigorous methodological conditions possible in the laboratory setting. It is extremely doubtful that this publication will achieve such  goal. Many, if not most,
Role of angiotensin II in dietary modulation of rat late distal tubule bicarbonate flux in vivo.
Authors: D Z Levine, M Iacovitti, S Buckman, K D Burns
Journal: Journal of Clinical Investigation (1996)

We have reported that overnight fasting stimulates bicarbonate reabsorption (JtCo2) in rat distal tubules. The present in vivo microperfusion studies evaluated the hypothesis that endogenous angiotensin II (AII) mediates this response. Rat late distal (LD) tubules were perfused at 8 nl/min in vivo with a hypotonic solution containing 28 mM bicarbonate. In overnight-fasted rats, LD JtCO2 was significantly higher than in normally fed rats (50 +/- 4 vs. 16 +/- 6 pmol/min.mm, P < 0.05). When overnight-fasted rats were salt-loaded, JtCO2 fell significantly (38 +/- 3 pmol/min.mm, P < 0.05). Conversely, in fed rats ingesting a zero-salt diet, JtCO2 increased three-fold (45 +/- 5 pmol/min.mm, P < 0.05). Enalaprilat infusion (0.25 micrograms/kg body wt, intravenously), in these zero-salt and overnight-fasted rats, reduced LD JtCO2 values to normal. Further, infusion of losartan (5 mg/kg body wt, intravenously), the specific AII AT1 receptor blocker, reduced JtCO2 in overnight-fasted rats by two-thirds (16 +/- 4 pmol/min.mm, P < 0.05). Finally, we perfused 10(-11) M AII intraluminally with and without 10(-6) M losartan: AII increased JtCO2 to 45 +/- 6 pmol/min.mm, equal to the zero-salt flux. This was completely abrogated by simultaneous losartan perfusion. Therefore, these results suggest that AII is an in vivo stimulator of late distal tubule bicarbonate reabsorption.
Epidermolysis bullosa acquisita-like eruption with anticollagen VII autoantibodies induced by<scp>d</scp>-penicillamine in Wilson disease
Authors: S. Ingen-Housz-Oro, S. Grootenboer-Mignot, N. Ortonne, S. Nahon, J. Horvath, C. Bernardeschi, E. Laffitte, C. André, S. Chollet-Martin, P. Wolkenstein, O. Chosidow
Journal: British Journal of Dermatology (2014)

Funding sources: no external funding. Conflicts of interest: none declared. P.W. and O.C. contributed equally to this paper. Dear Editor, d‐penicillamine may induce several cutaneous adverse events, the most frequent being elastosis perforans serpiginosa (EPS) and pemphigus vulgaris.1 Cases of epidermolysis bullosa acquisita (EBA)‐like reactions have been rarely described and not immunologically confirmed.2 Here, we report two family‐related cases of EBA‐like reaction and hypothesize that d‐penicillamine could induce anticollagen VII autoimmunity. A woman and her brother in their thirties, whose parents were first cousins, were referred for haemorrhagic blisters and skin fragility on their elbows and knees. Ten years earlier, they had had a diagnosis of Wilson disease. Both patients had a Kaiser‐Fleischer ring without organomegaly, neurological or psychiatric disturbance. The ATP‐7B gene was not mutated in either patient. Both patients began d‐penicillamine treatment at the same time after the diagnosis. In the woman (Fig. 1a,b) and her brother (Fig. 1c,d), skin examination showed skin fragility, ecchymotic macules, atrophic scars and milia on the extensions of elbows and knees. Histology showed dermal haemorrhagic suffusion, abnormal elastic fibres and no inflammatory infiltrates under a normal epidermis (Fig. 2a). Orcein staining confirmed abnormal elastic fibres with a characteristic ‘lumpy‐bumpy’ aspect (Fig. 2b,c). The same aspect of elastic fibres was seen in nonlesional skin (data not shown). Direct immunofluorescence results were negative for both cases, as were indirect immunofluorescence results for rat oesophagus, human skin and salt‐split human skin as substrates. Immunoblot analysis of placental extracts3 from the woman showed a strong band of 145 kDa and a weaker band of 290 kDa corresponding to the molecular weight of the NC1 (carboxyl‐terminal noncollagen 1) domain and full protein of collagen VII, respectively. Extracts from the brother revealed a weaker band of 145 kDa (Fig. 2d). Collagen VII enzyme‐linked immunosorbent assay (ELISA) with recombinant human NC1 and NC2 domains (MBL, Nagoya, Japan) gave negative results for both cases. Vitamin C and blood and urine porphyrin levels were normal. The woman and her brother shared HLA antigens A02, B40, DQB1*04 and DRB1*08.
484 PREDICTORS OF SUSTAINED VIROLOGIC RESPONSE AMONG GENOTYPE 1 PREVIOUS NON-RESPONDERS AND RELAPSERS TO PEGINTERFERON/RIBAVIRIN WHEN RE-TREATED WITH BOCEPREVIR PLUS PEGINTERFERON ALFA-2B/RIBAVIRIN
Authors: S. Zeuzem, J.M. Vierling, R. Esteban, A.L. Gibas, S. Pol, N. Boparai, M. Burroughs, C.A. Brass, J.K. Albrecht, F. Poordad
Journal: Journal of Hepatology (2011)
Distinct clustering of symptomatic burden among myeloproliferative neoplasm patients: retrospective assessment in 1470 patients
Authors: Holly L. Geyer, Robyn M. Scherber, Amylou C. Dueck, Jean-Jacques Kiladjian, Zhijian Xiao, Stefanie Slot, Sonja Zweegman, Federico Sackmann, Ana Kerguelen Fuentes, Dolores Hernández-Maraver, Konstanze Döhner, Claire N. Harrison, Deepti Radia, Pablo Muxi, Carlos Besses, Francisco Cervantes, Peter L. Johansson, Bjorn Andreasson, Alessandro Rambaldi, Tiziano Barbui, Alessandro M. Vannucchi, Francesco Passamonti, Jan Samuelsson, Gunnar Birgegard, Ruben A. Mesa
Journal: Blood (2014)
GW25-e5168 Impaired Post-Transcriptional Regulation of RyR2 by microRNA-106b-25 Cluster Promotes Atrial Fibrillation
Authors: Na Li, David Y. Chiang, Niels Voigt, James F. Martin, Dobromir Dobrev, Xander H.T. Wehrens
Journal: Journal of the American College of Cardiology (2014)
Paralytic Ileus Following Use of Banthine during Gastrointestinal Bleeding
Authors: C. G. Gunn, Max S. Allen
Journal: New England Journal of Medicine (1954)

PARALYTIC ileus may occur in many situations.However, it is uncommon in patients with gastrointestinal hemorrhage unless shock, electrolyte imbalance, peritonitis or obstruction is present.In the 5 cases presented below, paralytic ileus followed the administration of Banthine or pro-Banthine during treatment for gastrointestinal hemorrhage. This sequela of Banthine therapy has not been observed in this hospital unless frank hemorrhage into the bowel has been present. Three of the patients had peptic ulcers, 1 had esophageal varices, and 1 had lymphosarcoma infiltrating the stomach.Case ReportsCase 1. F.M., a 65-year-old man, was admitted to the hospital because of weakness . . .
Stimulation of the calcium-sensing receptor stabilizes the podocyte cytoskeleton, improves cell survival, and reduces toxin-induced glomerulosclerosis
Authors: Jun Oh, Julia Beckmann, Jacek Bloch, Verena Hettgen, Julian Mueller, Li Li, Meike Hoemme, Marie-Luise Gross, Roland Penzel, Peter Mundel, Franz Schaefer, Claus P. Schmitt
Journal: Kidney International (2011)
Fatal Phenformin-Associated Lactic Acidosis
Authors: Jonathan Rosand
Journal: Annals of Internal Medicine (1997)

Letters15 July 1997Fatal Phenformin-Associated Lactic AcidosisJonathan Rosand, MD, Jonathan W. Friedberg, MD, and Jane M. Yang, MDJonathan Rosand, MDMassachusetts General Hospital; Boston. MA 02114, Jonathan W. Friedberg, MDMassachusetts General Hospital; Boston. MA 02114, and Jane M. Yang, MDMassachusetts General Hospital; Boston. MA 02114Author, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-127-2-199707150-00034 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:The popularity of metformin has renewed interest in biguanide hypoglycemic agents. The association between phenformin and fatal lactic acidosis, particularly in patients with renal failure, led to the withdrawal of phenformin from the U.S. market in 1977 [1]. We describe a patient who recently died of phenformin-associated lactic acidosis.A 64-year-old Haitian woman with diabetes, hypertension, and consequent renal insufficiency presented with profound lactic acidosis (pH, 7.15; bicarbonate level <5.0 mmol/L; lactic acid level, 54.5 mmol/L). She had been hospitalized on four previous occasions for unexplained severe lactic acidosis. After recovery from such an episode, muscle biopsy ...References1. Misbin RI. Phenformin-associated lactic acidosis: pathogenesis and treatment. Ann Intern Med. 1977; 87:591-5. Google Scholar2. Reznik-Schuller HM, Reuber MD. Ultrastructure of liver tumors induced in F344 rats by methapyrilene. J Environ Pathol Toxicol Oncol. 1986; 7:181-96. Google Scholar3. Bailey CJ, Turner RC. Metformin. N Engl J Med. 1996; 334:574-9. Google Scholar Author, Article, and Disclosure InformationAffiliations: Massachusetts General Hospital; Boston. MA 02114 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byFrom old to new — Repurposing drugs to target mitochondrial energy metabolism in cancerThe Surprising Effect of Phenformin on Cutaneous Darkening and Characterization of Its Underlying Mechanism by a Forward Chemical Genetics ApproachReview of Biguanide (Metformin) ToxicitySynergistic Anti-Cancer Effect of Phenformin and OxamateMetformin: an old but still the best treatment for type 2 diabetesReview: Metformin: Potential benefits and use in chronic kidney diseaseInsulin, glucagon, and hypoglycemic drugs 15 July 1997Volume 127, Issue 2Page: 170KeywordsAutopsyBicarbonatesDehydrogenasesElectron microscopyHepatocytesLactic acidosisMitochondriaPyruvateRenal failureSodium Issue Published: 15 July 1997 Copyright & PermissionsCopyright © 1997 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
ACUTE AND CHRONIC CARIES AND NECROSIS OF THE MASTOID; PACHYMENINGITIS EXTERNA; EPIDURAL ABSCESS.
Authors: HERMAN KNAPP
Journal: JAMA (1898)

Of all the ear diseases, I know none that are, on the one hand, so important and dangerous, and on the other, so gratifying and manageable as the group comprehended in the title of this communication. If left alone they prove fatal in a large percentage of cases; if treated understandingly, they nearly all recover. The grippe has made us familiar with acute mastoid caries. In the first or second week of an attack of acute otitis media there is intense pain in ear and head; tympanic membrane red and bulging; in a few days otorrhea, with or without paracentesis of the drumhead; relief of pain for a few days, then return of it with tenderness and swelling of the mastoid, membrana tympani bulging in upper-posterior part, slight fever, loss of appetite, headache, mental depression; hearing greatly impaired. The further course varies greatly. The discharge may be free for a
PREDICTORS OF INAPPROPRIATE IMPLANTABLE CARDIOVERTER-DEFIBRILLATOR DISCHARGES
Authors: John N. Catanzaro, Amgad Makaryus, John Makaryus, Cristina Sison, Christos Vavasis, David Donaldson, Erik Altman, Stuart Beldner, Ram Jadonath
Journal: Journal of the American College of Cardiology (2011)
Inhibition of prostacyclin and thromboxane A2 generation by low-dose aspirin at the site of plug formation in man in vivo.
Authors: P A Kyrle, H G Eichler, U Jäger, K Lechner
Journal: Circulation (1987)

In a double-blind placebo-controlled crossover study, we investigated in seven healthy male volunteers the effect of a low-dose aspirin regimen (35 mg acetylsalicylate per day for 7 days) on the formation of thromboxane A2 (TxA2) and prostacyclin (PGI2) in blood emerging from a standardized injury of the microvasculature made to determine skin bleeding time. When subjects were treated with placebo, there was rapid and substantial generation of TxA2 and PGI2 at the site of platelet-vessel wall interaction within the first 2 min after vascular injury. This was reflected by a greater than 100-fold and greater than 10-fold increase in thromboxane B2 (TxB2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) in blood obtained from incisions made to determine bleeding time as compared with the corresponding plasma values. Low-dose aspirin caused a significant inhibition of both TxA2 and PGI2 generation in blood sampled from the skin incisions, represented by a 85% and 92% and 81% and 84% inhibition of TxB2 and 6-keto-PGF1 alpha, respectively, as compared with controls. We therefore conclude that rapid activation of both platelet prostaglandin metabolism and vascular PGI2 biosynthesis occurs at the site of platelet-vessel wall interaction, and low-dose aspirin results in a significant inhibition of both platelet and vascular cyclooxygenase activity. Thus, our data fail to confirm the concept of a differential effect of low-dose aspirin on platelet and vascular prostaglandin synthesis in man in vivo.
Abstract 2613: Racial/Ethnic specific polygenic models of breast cancer risk
Authors: Venetta Thomas, Zhi Liu, Sathish K. Srinivasan, Ren-Hua Chung, Eden Martin, Edward A. Levine, Rita I. Freimanis, Jennifer J. Hu
Journal: Cancer Research (2012)

Abstract Breast cancer is the most frequently diagnosed cancer and the second leading cause of cancer death in American women. Earlier family linkage studies have identified high-penetrance breast cancer genes, such as BRCA1, BRCA2, and TP53. Moreover, genes involved in DNA repair, such as CHEK2, ATM, BRIP and PALB2, have been associated with moderate breast cancer risk. Recent Genome-wide Association Studies (GWAS) have identified multiple single nucleotide polymorphisms (SNPs) associated with breast cancer risk. We evaluated whether breast cancer risk is associated with multiple SNPs in DNA damage signaling and repair and immune and inflammatory responses in addition to SNPs identified from GWAS. We hypothesize that targeting critical candidate pathways may yield important information regarding SNP-SNP interactions in breast cancer risk. We selected SNPs from DNA damage signaling and cell cycle control, base excision repair, nucleotide excision repair, double-strand break repair, mismatch repair, and immune and inflammatory responses. We have genotype results of 3,754 SNPs in 910 controls (763 Whites and 147 African Americans) and 793 breast cancer cases (667 Whites and 116 African Americans). 16.2% and 20.6% of controls and cases (respectively) had a first degree relative with breast cancer. 48% and 55.7% of the controls and cases (respectively) had their first child before or at the age of 24. 40.5% and 42.2% of the controls and cases (respectively) had a history of smoking. Our study results suggest that 6 SNPs were associated with breast cancer risk in Whites: (1) 2 SNPs from GWAS - rs3817198 in LSP1 (p&amp;lt;0.001) and rs3803662 in TNRC9 (p&amp;lt;0.001); (2) 2 SNPs from inflammation - rs1801157 in SDF-1 (p&amp;lt;0.001) and rs12720356 in Tyk2 (p&amp;lt;0.001) and (3) 2 SNPs from DNA repair and apoptosis - rs2992 in CHAF1A (p&amp;lt;0.0001) and rs2231301 in BCL2l2 (p&amp;lt;0.001). Only 1 SNP, rs1990760 in IFIH1 (p&amp;lt;0.01) was associated with breast cancer risk in African Americans. The IFIH1 gene was previously linked to Type 1 diabetes but not in cancer risk. There was significant trend in breast cancer risk with increasing numbers of risk genotypes for rs3817198, rs3803662, rs1801157, rs12720356, rs2992, and rs2231301 (p test for trend &amp;lt;0.0001) in Whites after adjustment for potential confounders. Our results suggest that multiple SNPs contribute to breast cancer risk in a racial/ethnic specific manner and larger studies are warranted to further evaluate our findings. More importantly, functional analysis is under way to corroborate the association of multiple SNPs with breast cancer risk. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 2613. doi:1538-7445.AM2012-2613
OUTCOMES OF TEMPORARY INTERRUPTIONS OF RIVAROXABAN OR WARFARIN IN PATIENTS WITH ATRIAL FIBRILLATION IN THE ROCKET AF TRIAL
Authors: Matthew W. Sherwood, Anne Hellkamp, Manesh Patel, Jonathan Piccini, Yuliya Lokhnygina, James Douketis, Richard Becker, Kenneth Mahaffey, Keith Fox, Robert Califf
Journal: Journal of the American College of Cardiology (2013)