tbuckley/cabot-search huggingface dataset:
Diagnosis and Localization in Primary Aldosteronism
Authors: Richard Horton, Ethyl Finck
Journal: Annals of Internal Medicine (1972)

Aldosterone in peripheral and adrenal vein plasma was measured in 21 patients highly suspect for primary aldosteronism. Peripheral and adrenal vein aldosterone levels were measured by a sensitive, accurate radioimmunoassay. Base-line and postfludrocortisone plasma aldosterone values were elevated in all patients while they were supine, with values ranging above normal to very high levels. Adrenal venograms were done in sixteen patients, and a positive radiologic interpretation was made in three fourths. The adrenalvein aldosterone values, however, were diagnostic in all patients. Primary aldosteronism, due to an adenoma, was shown by high levels of aldosterone on the side of the lesion and much lower levels, usually approaching peripheral, on the unaffected side. Aldosteronism due to bilateral hyperplasia appears to be associated with symmetrically elevated levels. These studies suggest that adrenal vein analysis of aldosterone is the most important part of the venogram procedure for localization and diagnosis in primary aldosteronism.
Identification of distinct C3b and C4b recognition sites in the human C3b/C4b receptor (CR1, CD35) by deletion mutagenesis.
Authors: L B Klickstein, T J Bartow, V Miletic, L D Rabson, J A Smith, D T Fearon
Journal: The Journal of Experimental Medicine (1988)

Complementary DNA clones encoding the NH2-terminal region of human CR1 have been isolated and sequenced. The deduced complete amino acid sequence of the F allotype of human CR1 contains 2,039 residues, including a 41-residue signal peptide, an extracellular domain of 1,930 residues, a 25-amino acid transmembrane domain, and a 43-amino acid cytoplasmic region. The extracellular domain is composed exclusively of 30 short consensus repeats (SCRs), characteristic of the family of C3/C4-binding proteins. The 28 NH2-terminal SCRs are organized as four long homologous repeats (LHRs) of seven SCRs each. The newly sequenced LHR, LHR-A, is 61% identical to LHR-B in the NH2-terminal two SCRs and greater than 99% identical in the COOH-terminal five SCRs. Eight cDNA clones were spliced to form a single construct, piABCD, that contained the entire CR1 coding sequence downstream of a cytomegalovirus promoter. COS cells transfected with piABCD transiently expressed recombinant CR1 that comigrated with the F allotype of erythrocyte CR1 on SDS-PAGE and that mediated rosette formation with sheep erythrocytes bearing C4b and C3b. Recombinant CR1 also had factor I-cofactor activity for cleavage of C3(ma). Analyses of six deletion mutants expressed in COS cells indicated that the NH2-terminal two SCRs of LHR-A contained a site determining C4 specificity and the NH2-terminal two SCRs of LHR-B and -C each had a site determining C3 specificity. The presence of these three distinct sites in CR1 may enable the receptor to interact multivalently with C4b/C3b and C3b/C3b complexes generated during activation of the classical and alternative pathways.
Specific identification of fibrin(ogen) degradation products in plasma and serum using blotting and peroxidase labeled antiserum
Authors: Anna B. Proietti, Maura McGuire, William Bell
Journal: American Journal of Hematology (1990)

Abstract We describe a method for identifying fibrinogen and fibrin split products using electrophoresis on agarose gel with sodium dodecyl sulfate (SDS) followed by blotting in nitrocellulose paper. Detection of these derivatives after blotting is accomplished with per‐oxidase‐conjugated rather than by isotopically labeled antibodies. This technique can detect diverse fibrinogen derivatives produced in vivo or in vitro by the combined action of thrombin, plasmin, and factor XIII. This methodology is applicable to plasma, serum, and other body fluids including urine and ascitic fluid. This sensitive and specific assay, distinguishing the products of cross‐linked fibrin from those of fibrinogen and detecting fibrin polymers in plasma, can be achieved without the use of radioactivity.
Increase in Food Protein consumed during Milk and Egg Open Food Challenges are not associated with increase in failures.
Authors: S.A. Lowe, J.E. Conner, L.A. Crandall, C.M. Lee, M.B. Ho, M.B. Feuling, C.L. Sova, M. Vasudev
Journal: Journal of Allergy and Clinical Immunology (2012)
Abstract 5200: MicroRNA-634 induces caspase-dependent apoptosis by targeting anti-apopotic and mitochondria-related genes in human cancer cells
Authors: Naoto Fujiwara, Jun Inoue, Tatsuyuki Kawano, Ken-ichi Kozaki, Johji Inazawa
Journal: Cancer Research (2014)

Abstract MicroRNAs (miRNAs) are endogenous small non-coding RNAs composed of 20∼25 base pairs that can negatively regulate gene expression by interfering with the translation of target transcripts. Since it has been known that some miRNAs function as tumor suppressors (TS) and their expression levels are often down-regulated in cancer, TS-miRNAs are expected to be therapeutic agents for cancer therapy. Thus, we conducted function-based screening using a miRNA library, and identified several TS-miRNAs, including miR-152, miR-218, miR-596. Recently, we identified miR-634 as a new TS-miRNA, which induced cell death with mitochondrial dysfunction and caspase activation. The expression analysis and the target-prediction program revealed miR-634 might directly target genes related with anti-apoptosis and mitochondrial function. Importantly, this miRNA was frequently down-regulated in primary tumor samples of esophageal squamous cell carcinoma (ESCC), compared with that in corresponding normal tissues. Furthermore, the combination therapy of miR-634 and cisplatin was effective to ESCC cell line in vitro and in vivo. Thus, these findings suggest that miR-634 may be useful as a potential therapeutic agent of ESCC. Citation Format: Naoto Fujiwara, Jun Inoue, Tatsuyuki Kawano, Ken-ichi Kozaki, Johji Inazawa. MicroRNA-634 induces caspase-dependent apoptosis by targeting anti-apopotic and mitochondria-related genes in human cancer cells. [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 5200. doi:10.1158/1538-7445.AM2014-5200
Adenoma of the Islands of Langerhans
Authors: Herbert A. Perkins, Jane F. Desforges, Charles G. Guttas
Journal: New England Journal of Medicine (1950)

ALTHOUGH the diagnosis of spontaneous hypoglycemia, once considered, is easy enough to prove, the determination of its etiology may be difficult. The case presented below made it evident that the recent literature on the subject is to some extent misleading and that as a result there are certain misconceptions in the interpretation of the findings in such cases.Case ReportA 45-year-old married Jewish refugee was admitted to the hospital on July 22, 1948, complaining of "falling out spells" of 1 1/2 years' duration. She had been well until one evening in January, 1947, when, while she was sitting in . . .
Exploration of human, rat, and rabbit embryonic cardiomyocytes suggests K-channel block as a common teratogenic mechanism
Authors: Christian Danielsson, Johan Brask, Anna-Carin Sköld, Rami Genead, Agneta Andersson, Ulf Andersson, Kenneth Stockling, Rickard Pehrson, Karl-Henrik Grinnemo, Sajjad Salari, Heike Hellmold, Bengt Danielsson, Christer Sylvén, Fredrik Elinder
Journal: Cardiovascular Research (2012)

Several drugs blocking the rapidly activating potassium (K(r)) channel cause malformations (including cardiac defects) and embryonic death in animal teratology studies. In humans, these drugs have an established risk for acquired long-QT syndrome and arrhythmia. Recently, associations between cardiac defects and spontaneous abortions have been reported for drugs widely used in pregnancy (e.g. antidepressants), with long-QT syndrome risk. To investigate whether a common embryonic adverse-effect mechanism exists in the human, rat, and rabbit embryos, we made a comparative study of embryonic cardiomyocytes from all three species.Patch-clamp and quantitative-mRNA measurements of K(r) and slowly activating K (K(s)) channels were performed on human, rat, and rabbit primary cardiomyocytes and cardiac samples from different embryo-foetal stages. The K(r) channel was present when the heart started to beat in all species, but was, in contrast to human and rabbit, lost in rats in late organogenesis. The specific K(r)-channel blocker E-4031 prolonged the action potential in a species- and development-dependent fashion, consistent with the observed K(r)-channel expression pattern and reported sensitive periods of developmental toxicity. E-4031 also increased the QT interval and induced 2:1 atrio-ventricular block in multi-electrode array electrographic recordings of rat embryos. The K(s) channel was expressed in human and rat throughout the embryo-foetal period but not in rabbit.This first comparison of mRNA expression, potassium currents, and action-potential characteristics, with and without a specific K(r)-channel blocker in human, rat, and rabbit embryos provides evidence of K(r)-channel inhibition as a common mechanism for embryonic malformations and death.
Testicular neoplasia in cryptorchid boys at primary surgery: case series
Authors: D. Cortes, J. Visfeldt, H. Moller, J. Thorup
Journal: BMJ (1999)

Cryptorchidism is associated with testicular cancer; the lifetime risk of 2-3% is about four times higher than in the general population.1 2 Some groups of cryptorchid patients may have an especially high risk of testicular cancer.3 Testicular carcinoma in situ is a well described histological pattern that precedes germ cell tumours.1 4 We investigated whether it is possible at primary surgery to identify cryptorchid boys who have testicular neoplasia and therefore are at high risk of testicular cancer.

We examined 1535 consecutive specimens of testicular tissue that were obtained from undescended testes at surgery for cryptorchidism in 1249 boys between 1971 and 1998. Previous reports have described 1026 of the biopsies in detail.2 4 No patient had fallopian tubes or a uterus.

The table shows the total occurrence of testicular neoplasia at surgery for cryptorchidism. There was one case …
Influenza virus immunization. Antibody response and adverse effects in children with renal disease
Authors: K. J. Sheth
Journal: JAMA (1978)

Before and four weeks after immunization with a single 0.5-ml dose of influenza virus vaccine, sera from 36 children with renal diseases were tested for serum hemagglutinating-inhibiting antibody (HAI) titers to A/New Jersey/76, A/Victoria/75, and A/Port Chalmers/73. Before immunization, 1:40 HI antibodies to A/New Jersey were noted in one child only, to A/Victoria in ten children (27%), and to A/Port Chalmers in 25/34 children (68%). Serum HAI titers increased fourfold or more (P less than .01) in 31/36 children (86%) after immunization. Neither the type of the renal disease nor therapy with prednisone had any effect on the rise of serum HAI titers (P less than .05). Of the seven children with preimmunization proteinuria, four had a transient rise in protein levels following immunization. None required an increased prednisone dose for exacerbation of nephrotic syndrome. Children with chronic renal problems should be protected against influenza.
Benzodiazepines in hepatic encephalopathy: sleeping with the enemy
Authors: S DASARATHY, K D MULLEN
Journal: Gut (1998)

See article on page861 

This issue of the journal contains an article on the sometimes controversial area of the pathogenesis of hepatic encephalopathy (see page 861). There is little consensus in the field but most accept that failure of hepatic clearance of toxic compounds originating in the gut causes hepatic encephalopathy. Most evidence suggests that ammonia is the key gut derived toxin mediating hepatic encephalopathy.1 Initially there was doubt whether ammonia was truly present in blood in vivo. Once this issue was resolved, many studies were undertaken to establish whether the level of hyperammonaemia correlated with the clinical severity of hepatic encephalopathy. The result of these efforts has largely been negative. To quote Stahl’s classic study published in 1963, “A considerable overlap still persists amongst the ammonia values of the different degrees of coma.”2 Other gut derived compounds have been proposed as possible mediators of hepatic encephalopathy and include gamma amino butyric acid and benzodiazepines.3 These benzodiazepines refer to a group of largely lipophillic compounds of low molecular weight, which bind to specific benzodiazepine receptors. Since the discovery of central nervous system (CNS) benzodiazepine receptors in 1977, a vigorous search has been made to identify endogenous ligands that bind to these receptors.4 5Unlike the analogous situation with opiate receptors where endogenously synthesised ligands were identified (for example, endorphins and enkephalins) the benzodiazepine receptor ligands may be xenobiotic in origin. That is, these receptors exist in mammalian brain because of exposure to natural benzodiazepines present in food or generated in the gut.6-8 The endogenous benzodiazepine hypothesis should probably therefore be renamed the “natural benzodiazepine hypothesis” unless subsequently evidence of endogenous synthesis of these compounds becomes available.

The natural benzodiazepine hypothesis simply states that hepatic encephalopathy may arise in a proportion of patients as a …
Assessment of 24,25(OH)2D levels does not support FGF23-mediated catabolism of vitamin D metabolites
Authors: Bing Dai, Valentin David, Hala M. Alshayeb, Arif Showkat, Geeta Gyamlani, Ronald L. Horst, Barry M. Wall, L. Darryl Quarles
Journal: Kidney International (2012)

Progressive elevations of fibroblastic growth factor 23 (FGF23) in chronic kidney disease may reduce serum 25-hydroxyvitamin D (25(OH)) and 1,25-dihydroxyvitamin D (1,25(OH)(2)D) levels, via stimulation of 24-hydroxylase (Cyp24a1)-mediated catabolism of these vitamin D metabolites. To test this possibility, we measured serum concentrations of 24,25-dihydroxyvitamin D (24,25(OH)(2)D), a product of Cyp24a1 hydroxylation of 25(OH)D, in the Col4a3 knockout mouse, a model of Alport syndrome-derived chronic kidney disease, and in patients with chronic kidney disease of variable severity. There was an inverse correlation between serum FGF23 and both 25(OH)D and 1,25(OH)(2)D in the mouse model, but no significant relationship was observed in the cross-sectional patient cohort. The FGF23-dependent increase in Cyp24a1 mRNA expression in the mouse kidneys was consistent with the possibility that FGF23 induces vitamin D catabolism. There was, however, a reduction in serum 24,25(OH)(2)D levels, rather than the expected elevation, in both the mice and patients with chronic kidney disease. Low 25(OH)D and elevated FGF23 and parathyroid hormone levels were correlated with the reduced serum 24,25(OH)(2)D concentrations of these patients. Thus, we failed to find support for FGF23-mediated catabolism of vitamin D metabolites in chronic kidney disease assessed by 24,25(OH)(2)D levels.
A novel ligand in lymphocyte-mediated cytotoxicity: expression of the beta subunit of H+ transporting ATP synthase on the surface of tumor cell lines.
Authors: B Das, M O Mondragon, M Sadeghian, V B Hatcher, A J Norin
Journal: The Journal of Experimental Medicine (1994)

Extracellular adenosine triphosphate (eATP) has been suggested to play a role in lymphocyte-induced tumor destruction. We now provide evidence that a protein responsible for ATP synthesis in mitochondria may also play a physiologic role in major histocompatibility complex-independent, lymphocyte-mediated cytotoxicity. A 51.5-kD protein (p51.5) bearing structural and immunologic characteristics of the beta subunit of H+ transporting ATP synthase (E.C. 3.6.1.34, beta-H+ATPase, published molecular mass of 51.6 kD) was detected on the plasma membrane of three different human tumor cell lines studied. NH2-terminal amino acid sequence analysis of purified p51.5 from K562 tumor cells revealed 100% homology of 16 residues identified in the first 21 positions to the known sequence of human mitochondrial beta-H+ ATPase. Antibody directed against a 21-mer peptide in the ATP binding region of beta-H+ ATPase (anti-beta) reacted with only one band on Western blots of whole tumor extracts and tumor membrane extracts suggesting that the antiserum reacts with a single species of protein. Anti-beta reacted with the cell membranes of tumor cells as determined by fluorescence-activated flow cytometry and immunoprecipitated a 51.5-kD protein from surface-labeled neoplastic cells (but not human erythrocytes and lymphocytes). Purified p51.5 bound to human lymphocytes and inhibited natural killer (NK) cell-mediated cytotoxicity. Furthermore, anti-beta treatment of the K562 and A549 tumor cell lines inhibited NK (by &amp;gt; 95%) and interleukin 2-activated killer (LAK) cell (by 75%) cytotoxicity, respectively. Soluble p51.5 upon binding to lymphocytes retained its reactivity to anti-beta suggesting that the ATP binding domain and the lymphocyte-receptor binding domain reside in distinct regions of the ligand. These results suggest that beta-H+ ATPase or a nearly identical molecule is an important ligand in the effector phase (rather than the recognition phase) of a cytolytic pathway used by naive NK and LAK cells.
Pasteur and Modern Science
Authors: Ian M. Smith
Journal: JAMA (1962)

How are we to find apprentices to follow in our footsteps? How can we win in the competition for the top minds? How can we explain to the young the excitement, the achievements, the inner satisfactions of biology and medicine? This 150-page paperback by Rene Dubos is a book to be presented to high school graduating classes by county medical societies to help in recruiting medical students. It conveys the supreme pleasure of science and medicine—pleasure without satiation. Can Louis Pasteur's career be analyzed, or are all the conclusions exceptions to the usual course? Pasteur obeyed very few of the rules for being successful. He obviously would have failed his class in social adjustment. He was unsmiling, passionately argumentative, an aggressive showman, and an almost isolated worker with few collaborators. At every step in his life he chose to take a stand against the odds, often at the cost of
Mechanisms of nondisjunction induction in drosophila oocytes.
Authors: B Leigh
Journal: Environmental Health Perspectives (1979)

Quantitative and qualitative studies on the induction of no-disjunction and related phenomena can be carried out using the germ cells of Drosophila. X-Irradiation breaks chromosomes and cold-shock disrupts spindles, these two treatments producing different spectra of nondisjunction in oocytes.
Environmental, lifestyle, and familial/ethnic factors associated with myeloproliferative neoplasms
Authors: Lesley A. Anderson, Andrew S. Duncombe, Maria Hughes, Moyra E. Mills, Jessica C. Wilson, Mary F. McMullin
Journal: American Journal of Hematology (2011)

Myeloproliferative neoplasms (MPNs) are characterized by overproduction of mature functional blood cells and are often associated with an acquired genetic mutation of Janus Kinase 2(V617F). The etiology of MPNs remains unknown. The aim of this article was to review and collate all known published data investigating environmental and lifestyle factors associated with MPNs. Medline, Embase, PubMed, Cochrane, and Web of Science were systematically searched using terms for MPNs and observational study designs to identify studies investigating the risk factors for MPNs published before March 2010. Of 9,156 articles identified, 19 met the selection criteria. Although the studies exhibited heterogeneity, in case definitions, study design, and risk factors investigated, several themes emerged. A strong association was found with Jewish descent, and with a family history of MPNs. Autoimmune conditions, specifically Crohn's disease, were more common in patients with MPNs. Certain occupational groups were significantly associated with MPNs including occupations with potential exposure to benzene and/or petroleum. Blood donation was associated with an increased risk of polycythemia vera specifically. The vast heterogeneity in studies identified as part of this review suggests that large scale systematic assessment of etiological factors associated with MPNs is warranted.
IFN-γ response and IL-8 plasma levels in neonates with respiratory syncytial virus bronchiolitis
Authors: C. Schultz, N. Richter, J.C. Möller, P. Bucsky
Journal: European Respiratory Journal (2001)

IFN-c response and IL-8 plasma levels in neonates with respiratory syncytial virus bronchiolitisTo the Editors:In a recent article published in the European Respiratory Journal, BONT et al.[1] presented data on systemic cytokine responses in hospitalized ventilated and nonventilated infants with respiratory syncytial virus (RSV) bronchiolitis.Their main findings were a lower production of interferon-c (IFN-c) and elevated plasma levels of interleukin (IL)-8 in ventilated patients.They concluded from their data that a depressed lymphocyte function and elevated IL-8 plasma levels are markers of severe RSV bronchiolitis in infants requiring ventilation.
ENCEPHALOMYELITIS OF MICE
Authors: Max Theiler, Sven Gard
Journal: The Journal of Experimental Medicine (1940)

1. The two strains of virus named GD VII and FA, respectively, accidentally discovered during experiments with yellow fever, have been shown to be immunologically related to each other, as well as to the virus of mouse encephalomyelitis. 2. Infection of the central nervous system can be produced with both strains by intracerebral, intranasal, or intraperitoneal inoculations. The cardinal symptom produced by the GD VII strain of virus by all three methods of inoculation is a flaccid paralysis of the limbs. The symptoms produced by the FA strain are referable to lesions of the brain when infection is produced by intracerebral and intranasal inoculation. Following intraperitoneal inoculation of the FA strain of virus, however, a flaccid paralysis is usually produced. 3. By the use of graded collodion membranes the particle size of the virus of mouse encephalomyelitis has been shown to be from 9 to 13 mmicro 4. The stability of the virus at different hydrogen ion concentrations has been tested. It has been found that there are two optima of stability, one at about pH 8.0 and the other at pH 3.3. 5. The virus is readily inactivated at 37 degrees C. by 1 per cent hydrogen peroxide. 6. Of organic solvents tested, ether had no action, whereas ethyl alcohol in 20 per cent concentration almost completely inactivated the virus after 45 minutes in the cold. 7. The virus can be precipitated by means of ammonium sulfate. 8. With increasing age mice acquire a relative resistance to the virus. 9. Immunity to a subsequent intracerebral inoculation can be produced by intraperitoneal, as well as intranasal, administrations of relatively large amounts of virus. 10. Mice infected by the intracerebral inoculation of a relatively avirulent virus acquire a high degree of immunity to a subsequent inoculation of a highly virulent strain. 11. The course of infection in mice following intracerebral, intranasal, and intraperitoneal inoculation of the FA strain of virus has been studied.
Metastatic meningioma of the lung.
Authors: J L Aumann, J M van den Bosch, J R Elbers, S J Wagenaar
Journal: Thorax (1986)

A difficult diagnostic problem may be caused by the presence of multiple pulmonary nodules on a chest radiograph.The differential diagnosis includes infection, primary or meta- static tumour (benign or malignant), and the expression of systemic disease such as rheumatoid arthritis and sarcoid- osis.This case report describes a patient with multiple lung tumours considered to be due to metastatic meningioma.Case report