tbuckley/cabot-search huggingface dataset:
Conjugation to antifibrin Fab' enhances fibrinolytic potency of single-chain urokinase plasminogen activator.
Authors: C Bode, M S Runge, S Schönermark, T Eberle, J B Newell, W Kübler, E Haber
Journal: Circulation (1990)

Single-chain urokinase plasminogen activator (scu-PA) that had been modified with N-succinimidyl-3-(2-pyridyldithio)propionate was covalently linked by disulfide bonds to the Fab' of a monoclonal antibody specific for the beta-chain of fibrin (antibody 59D8). scu-PA-59D8 Fab' conjugate was separated from free scu-PA and two-chain urokinase coupled to 59D8 Fab' by two-step affinity chromatography. First, the reaction mixture was chromatographed on a column containing Sepharose linked to the peptide that had been used as immunogen for antibody 59D8; scu-PA-59D8 Fab' conjugate and unconjugated 59D8 Fab' were retained but not unconjugated scu-PA. Then, the eluate from the peptide-Sepharose column was chromatographed on a column containing Sepharose linked to benzamidine, which acts as a ligand for two-chain urokinase. The molecular weight of the scu-PA-59D8 Fab' conjugate was approximately 100 kDa when electrophoresed on a nonreducing sodium dodecylsulfate-polyacrylamide gel. Enzymatic assay after purification revealed that more than 97% of the scu-PA present in the conjugate retained the single-chain form. The Fab' portion of the conjugate functioned in a manner indistinguishable from that of native antibody 59D8. In an in vitro assay for lysis of fibrin monomer, the fibrinolytic potency of scu-PA-59D8 Fab' was 33-fold more than that of tissue plasminogen activator (p less than 0.001), 230-fold more than that of unconjugated scu-PA (p less than 0.0001), and 420-fold more than that of urokinase (p less than 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)
Gastric mesh erosion after hiatoplasty for recurrent paraesophageal hernia
Authors: B. Rumstadt, G. Kähler, O. Mickisch, D. Schilling
Journal: Endoscopy (2008)

A 57-year-old man was treated for recurrent paraesophageal hernia by means of laparoscopic hiatal reinforcement using a 12 × 10-cm titanium-covered polypropylene mesh. He began to experience nonspecific epigastric abdominal discomfort 10 months later. An upper endoscopy revealed the presence of mesh at the gastroesophageal junction ([Fig. 1]), which was then removed endoscopically, using grasping forceps ([Fig. 2]). Since the procedure, the patient has been free of symptoms, with no signs of reflux disease for 12 months at the time of writing.
STUDIES ON THE MECHANISM OF THE LUPUS ERYTHEMATOSUS (L.E.) PHENOMENON*
Authors: Alan C. Aisenberg
Journal: Journal of Clinical Investigation (1959)

Since the original demonstration by Hargraves of the Feulgen positive nature of the lupus erythematosus (L.E.) cell (1), it has become increasingly evident that the specific nature of the L.E. phenomenon resides in the reaction of the cell nu- cleus with a gamma globulin-like protein from the L.E. patient's serum (2-8).Friou, Finch and Detre in particular (3, 4), and others (5, 6) have shown by means of the fluorescent antibody tech- nique of Coons and Kaplan (9) that there is nu- clear localization of serum gamma globulin of pa- tients with L.E.The present communication on the L.E. phe- nomenon is divided into two parts.The first part, utilizing L. E. tests done with isolated cell nuclei and purified L.E. gamma globulin, presents evi- dence for the participation of an accessory serum factor necessary for phagocytosis in the L.E. phenomenon.The second part contains quantita- tive studies with fluorescent-labeled L.E. gamma globulin which suggest that the L.E. factor is not identical in all patients, and that the L.E. factor may react with a protein of the cell nucleus. METHODS AND MATERIALSPreparation of gamma globulin and nuclei.Sera were obtained from normal controls and from clinically typi- cal cases of L.E.D. (lupus erythematosus disseminata) with strongly positive L.E. tests diagnosed on the wards of the Massachusetts General Hospital.Gamma globu- lin was prepared from these sera by ethanol fractiona- tion, employing a modification of Methods 6 and 10 of Cohn (10).
Increased Release of Arachidonic Acid and Eicosanoids in Iron-Overloaded Cardiomyocytes
Authors: Rafael Mattera, Gregory P. Stone, Nael Bahhur, Yuri A. Kuryshev
Journal: Circulation (2001)

Background —Patients with transfusional iron overload may develop a life-limiting cardiomyopathy. The sensitivity of lipid-metabolizing enzymes to peroxidative injury, as well as the reported effects of arachidonic acid (AA) and metabolites on cardiac rhythm, led us to hypothesize that iron-overloaded cardiomyocytes display alterations in the release of AA and prostaglandins. Methods and Results —Neonatal rat ventricular myocytes (NRVMs) cultured for 72 hours in the presence of 80 μg/mL ferric ammonium citrate displayed an increased rate of AA release, both under resting conditions and after stimulation with agonists such as [Sar 1 ]Ang II. Although iron treatment did not affect overall incorporation of [ 3 H]AA into NRVM phospholipids, it caused a 2-fold increase in the distribution of precursor in phosphatidylcholine species, with a proportional decrease in phosphatidylinositol, phosphatidylserine, and phosphatidylethanolamine. Increased release of AA in iron-overloaded NRVMs was reduced by the diacylglycerol lipase inhibitor RHC80267 but was largely insensitive to inhibitors of phospholipases A 2 and C. Iron-overloaded cardiomyocytes also displayed increased production of eicosanoids and induction of cyclooxygenase-2 after stimulation with interleukin-1α. Conclusions —Iron overload enhances AA release and incorporation of AA into phosphatidylcholine, as well as cyclooxygenase-2 induction and eicosanoid production, in NRVMs. The effects of AA and metabolites on cardiomyocyte rhythmicity suggest a causal connection between these signals and electromechanical alterations in iron-overload–induced cardiomyopathy.
What Makes Women Sick: Gender and the Political Economy of Health
Authors: E. Fee
Journal: BMJ (1995)

Lesley Doyal Macmillan, £11.99, pp 280 ISBN 0 333 54205 3

Lesley Doyal's book provides an excellent introduction to women's health issues in a social and economic context. Discussing a wide range of topics from abortion to venereal disease, from alcohol to violence, she shows how these problems can be fully comprehended only in relation to the broader social and economic problems of women around the world.

Many books and journal articles provide the newest data and the latest statistics on specific women's health issues. Doyal provides something different: a clear framework for …
Kidney Androgen-Regulated Protein Transgenic Mice Show Hypertension and Renal Alterations Mediated by Oxidative Stress
Authors: O. Tornavaca, G. Pascual, M.L. Barreiro, M.T. Grande, A. Carretero, M. Riera, E. Garcia-Arumi, B. Bardaji, M. González-Núñez, M.A. Montero, J.M. López-Novoa, A. Meseguer
Journal: Circulation (2009)

Background— Kidney androgen-regulated protein (KAP), a proximal tubule androgen-regulated gene, codes for a protein of unknown function. Methods and Results— To investigate the consequences of KAP overexpression in kidney, we produced KAP transgenic mice and performed microarray expression analyses in kidneys of control and transgenic males. Downregulation of the androgen-sensitive Cyp4A14 monooxygenase gene in KAP transgenic mice prompted us to analyze blood pressure levels, and we observed that transgenic mice were hypertensive. Inhibition of 20-hydroxyeicosatetraenoic acid synthesis by N -hydroxy- N ′-(4- n -butyl-2-methylphenyl) formamidine (HET0016) reduced the increased 20-hydroxyeicosatetraenoic acid levels in urine and normalized arterial pressure in transgenic mice, as did the NADPH oxidase inhibitor apocynin. Increased oxidative stress in transgenic mice was demonstrated by (1) enhanced excretion of urinary markers of oxidative stress, 8-iso-prostaglandin F2α, 8-hydroxydeoxyguanosine, and thiobarbituric acid–reacting substances; (2) augmented mitochondrial DNA damage and malondialdehyde levels in kidneys; and (3) diminished catalase and glutathione peroxidase activity in transgenic kidneys. Mice exhibited renal defects that included focal segmental glomerulosclerosis, proteinuria, glycosuria, and fibrosis. Conclusions— Taken together, these results indicate that KAP expression is critical for cardiovascular-renal homeostasis maintenance and that hypertension is associated with increased oxidative stress. This is the first report showing that overexpression of an androgen-regulated, proximal tubule–specific gene induces hypertension. These observations may shed light on the molecular pathophysiology of gender differences in the prevalence and severity of hypertension and chronic renal disease.
Discovery of 50-year-Old Naval Logbook May Aid Follow-Up Study of Radium-Exposed Veterans
Authors: Andrew A. Skolnick
Journal: JAMA (1996)

A LOGBOOK discovered during the renovation of an office in the Submarine Research Laboratory in New London, Conn, confirms that at least some of the US submariners and airmen given radium treatments in the 1940s were subjects in a radiation experiment. The US Department of Defense (DoD) has maintained that the thousands of members of the armed forces who received nasopharyngeal radium irradiation to prevent areotitis media were recipients of standard clinical practice. However, the logbook with 1611 names of submarine trainees who received nasopharyngeal radium irradiation or symptomatic or other treatments in 1944 and 1945 clearly identified the radiation treatment as "experimental." At least 732 of those servicemen received nasopharyngeal radium treatment. US Sen Joseph I. Lieberman (D, Conn) —a member of the Senate Armed Services Committee who has been urging the DoD to conduct a follow-up study of veterans treated with nasopharyngeal radium irradiation—says, "This logbook appears to
Left Ventricular Performance During Muscular Exercise in Patients with and without Cardiac Dysfunction
Authors: JOHN ROSS, JAMES H. GAULT, DEAN T. MASON, JOSEPH W. LINHART, EUGENE BRAUNWALD
Journal: Circulation (1966)

The LVEDP, cardiac output, and V o o2 were measured before and during supine muscular exercise in 38 patients. The normal pattern, established in seven patients without left ventricular dysfunction, consisted of an exercise factor [see Equation in PDF File], an LVEDP during exercise of less than 12 mm Hg, and little change or a decrease in LVEDP, which was accompanied in most instances by an increase in the stroke volume. In the majority of 31 patients with various cardiac lesions, but without valvular regurgitation, measurement of the LVEDP before and during exercise permitted the definition of normal or abnormal left ventricular function when the status of the left ventricle could not have been ascertained from other measurements. Thus, in most of the patients with mitral stenosis and abnormal resting hemodynamics, the pattern of left ventricular function during exercise was considered to be normal. Among the patients with aortic stenosis or left ventricular myocardial disease and elevated resting LVEDP, two types of abnormal performance of the left ventricle were identified. In some patients, an increase in LVEDP was accompanied by an increase in stroke volume, and this response was termed "abnormal left ventricular dynamics"; in the remaining patients, an increase in LVEDP and no change or a fall in stroke volume occurred and this response was termed "depressed left ventricular function." It is concluded that determination of the LVEDP before and during exercise adds importantly to measurements of the changes in cardiac output and O 2 consumption in characterizing left ventricular performance. The method employs standard catheterization techniques and appears to provide a practical and useful means for evaluating the functional status of the left ventricle in patients with and without myocardial dysfunction.
UV-induced squamous cell carcinoma - a role for antiapoptotic signalling pathways
Authors: P.M. Rodust, E. Stockfleth, C. Ulrich, M. Leverkus, J. Eberle
Journal: British Journal of Dermatology (2009)

Journal Article UV‐induced squamous cell carcinoma – a role for antiapoptotic signalling pathways Get access P.M. Rodust, P.M. Rodust Charité– Universitätsmedizin Berlin, Department of Dermatology and Allergy, HTCC Skin Cancer Center Charité, Charitéplatz 1, 10117 Berlin, Germany Search for other works by this author on: Oxford Academic Google Scholar E. Stockfleth, E. Stockfleth Charité– Universitätsmedizin Berlin, Department of Dermatology and Allergy, HTCC Skin Cancer Center Charité, Charitéplatz 1, 10117 Berlin, Germany Search for other works by this author on: Oxford Academic Google Scholar C. Ulrich, C. Ulrich Charité– Universitätsmedizin Berlin, Department of Dermatology and Allergy, HTCC Skin Cancer Center Charité, Charitéplatz 1, 10117 Berlin, Germany Search for other works by this author on: Oxford Academic Google Scholar M. Leverkus, M. Leverkus Otto‐von‐Guericke University Magdeburg, Department of Dermatology and Venereology, Laboratory of Experimental Dermatology, Leipziger Street 44, 39120 Magdeburg, Germany Search for other works by this author on: Oxford Academic Google Scholar J. Eberle J. Eberle Charité– Universitätsmedizin Berlin, Department of Dermatology and Allergy, HTCC Skin Cancer Center Charité, Charitéplatz 1, 10117 Berlin, Germany Jurgen Eberle. E‐mail: juergen.eberle@charite.de Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 161, Issue s3, 1 November 2009, Pages 107–115, https://doi.org/10.1111/j.1365-2133.2009.09458.x Published: 01 November 2009
Massive CAG Repeat Expansion and Somatic Instability in Maternally Transmitted Infantile Spinocerebellar Ataxia Type 7
Authors: Heather Trang, Sabrina Y. Stanley, Paul Thorner, Hannaneh Faghfoury, Andreas Schulze, Cynthia Hawkins, Christopher E. Pearson, Grace Yoon
Journal: JAMA Neurology (2014)

We report the first case to date of maternally transmitted infantile spinocerebellar ataxia type 7 (SCA7), in which a tract of (CAG)45 expands to lengths as large as (CAG)92-250.A 38-year-old woman with classic SCA7 (and a son, who died at age 3 years) had pronounced cerebellar atrophy and a renal biopsy specimen that showed focal segmental glomerulosclerosis with abnormal podocytes containing cytoplasmic inclusions. Polymerase chain reaction amplification across the SCA7 repeat tract assessed expansion levels in tissues of the affected son. High levels of somatic CAG instability were observed in blood, kidney, and skeletal muscle. This transmitted expansion is considerably larger than previously reported maternal transmission expansions of 5 to 10 gained repeats.We document the first intertissue CAG instability reported to date in patients with SCA7, similar to SCA7 mouse models. Infantile SCA7, which is often paternally transmitted, can rarely arise by maternal transmission, which has implications for diagnosis and counseling among families of patients with SCA7.
The Kidney in Liver Disease
Authors: Robert E. Cronin
Journal: JAMA (1983)

Deteriorating kidney function in the patient with cirrhosis and ascites, with few exceptions, is a signal that death is imminent. All physicians who care for such patients feel the frustration of knowing that the renal failure is functional, ie, the kidney would function normally if the liver were not sick. Although this book does not give the answer to this dilemma, it does pull the work and thought of the acknowledged experts in this area into one volume and updates our current level of understanding.  This second edition is a multiauthored review of selected aspects of normal and abnormal renal and hepatic physiology. Several of the authors have taken the opportunity to review in depth their previously published clinical and laboratory studies. The prologue, written by Dr Solomon Papper, gives a personal view of the development of interest in the hepatorenal syndrome. The other 31 chapters deal with a range
Multiple components of the A1 adenosine receptor-adenylate cyclase system are regulated in rat cerebral cortex by chronic caffeine ingestion.
Authors: V Ramkumar, J R Bumgarner, K A Jacobson, G L Stiles
Journal: Journal of Clinical Investigation (1988)

The effects of chronic caffeine on the A1 adenosine receptor-adenylate cyclase system of rat cerebral cortical membranes were studied. Caffeine treatment significantly increased the number of A1 adenosine receptors as determined with the A1 adenosine receptor antagonist radioligand [3H]xanthine amine congener (XAC). R-PIA (agonist) competition curves constructed with [3H]XAC were most appropriately described by a two affinity state model in control membranes with a KH of 2.1 +/- 0.8 and a KL of 404 +/- 330 nM with 50 +/- 4% of receptors in the high affinity state (%RH). In contrast, in membranes from treated animals, there was a marked shift towards the high affinity state. In three of seven animals all of the receptors were shifted to a unique high affinity state which was indistinguishable from the KH observed in membranes from control animals. In four of seven animals the %RH increased from 50 to 69% with KH and KL indistinguishable from the control values. Thus, the agonist specific high affinity form of the receptor was enhanced following caffeine treatment. Maximal inhibition of adenylate cyclase activity in cerebral cortical membranes by R-PIA (1 microM) was significantly increased by 28% following caffeine treatment, consistent with an increased coupling of receptor-Gi protein with adenylate cyclase. Importantly, the quantity of Gi (alpha i) in rat cerebral cortex, determined by pertussis toxin-mediated labeling, was also increased to 133% of control values by this treatment. Thus, multiple components and interactions of the A1 adenosine receptor-adenylate cyclase complex are regulated by caffeine. These changes are likely compensatory measures to offset blockade of A1 receptors in vivo by caffeine and lead to a sensitization of this inhibitory receptor system.
Laboratory and Clinical Studies during Prolonged Partial Extracorporeal Circulation Using the Bramson Membrane Lung
Authors: J. DONALD HILL, M. L. BRAMSON, ALVIN HACKEL, CEDROC W. DEAL, PEDRO A. SANCHEZ, JOHN J. OSBORN, FRANK GERBODE
Journal: Circulation (1968)

The survival rate, electrolyte changes, hematological changes, arterial gas analysis, and pulmonary compliances in 14 prolonged venovenous perfusions with the Bramson membrane oxygenator are presented. The Bramson membrane oxygenator functioned efficiently. There were two deaths in the series, neither attributable to the perfusion. Arterial gas studies and pulmonary compliance studies indicated no measurable detrimental effect on the lungs. Platelet counts decreased and white blood cell counts increased during perfusion. A clinical prolonged veno-venous perfusion is reported.
Measles: Regaining Control
Authors: Roger M. Barkin
Journal: JAMA (1975)

Seven years after forecasts that measles would be eradicated, and nearly 12 years after the licensure of an effective live-virus measles vaccine, the United States continues to be plagued by the threat of epidemic measles.<sup>1</sup>In spite of early progress following the licensure of measles vaccine in 1963, a resurgence of measles began in 1969. In 1971, more than 75,000 cases were reported, after a 1968 total of 22,231 cases. The sharp upward trend in 1969 followed the redirection of federal funds into an intensive rubella immunization program and the 1971 reversal came when federal funds were reinstated (Figure). By the end of 1974, we will finally have regained the level of control first achieved in 1968. Epidemiologically, the emphasis on vaccine control programs for preschool and elementary school children has been reflected by the fact that these age groups have the largest decreases in attack rates. Although age-specific
Endoscopic Removal of an Obstructing Duodenal Duplication Cyst
Authors: P. Dave, J. Romeu, S. Clary, B. Rybak, J. Messer
Journal: Endoscopy (1984)

Duplications are congenital lesions, spherical or tubular in shape and composed of a muscular wall with a gastrointestinal lining. They may be found at any level from the mouth to the anus, and are usually intimately attached to some portion of the gastrointestinal tract (1, 2). The endoscopic removal of both primary duodenal polyps and prolapsing antral polyps which cause outlet obstruction has been previously described. We report a case of a symptomatic duplication cyst of the apex of the duodenal bulb, which was removed endoscopically. A patient with outlet obstruction symptoms due to a duplication cyst of the duodenal apex is described. Complete cessation of symptoms followed endoscopic removal of the cyst.
Biochemical and morphological changes in myocardium during coronary occlusion and reperfusion in canine hearts: effects of propranolol on myocardial damage
Authors: T. OGAWA, S. SUGIYAMA, N. HIEDA, T. ITO, T. SATAKE, T. OZAWA
Journal: Cardiovascular Research (1989)

To clarify the mechanism of irreversible myocardial damage, we studied the relationship between ischaemic mitochondrial dysfunction and leakage of lysosomal enzymes, and the effects of propranolol on myocardial damage. Open chest anaesthetised dogs were divided into six groups: 30 min occlusion of the left anterior coronary artery (LAD); 2 h LAD occlusion; 2 h LAD occlusion after premedication with 0.3 mg·kg−1 propranolol; 30 min LAD occlusion/1 h reperfusion; 2 h LAD occlusion/1 h reperfusion; and 2 h LAD occlusion/1 h reperfusion after propranolol premedication. After occlusion or reperfusion, heart mitochondria were prepared from normal and occluded or reperfused areas, and mitochondrial function (rate of oxygen consumption in State III, and respiratory control index) was measured polarographically. Myocardial tissue was fractionated and activities of lysosomal enzymes (N-acetyl-β-glucosaminidase and β-glucuronidase) were measured. Electron microscopic studies were performed. Thirty min occlusion induced mitochondrial dysfunction without leakage of lysosomal enzymes. Reperfusion for 1 h reversed these changes. However occlusion for 2 h induced mitochondrial dysfunction associated with the leakage of lysosomal enzymes, and mitochondrial dysfunction was not reversed by 1 h reperfusion. Propranolol reduced mitochondrial dysfunction after 2 h occlusion and prevented leakage of lysosomal enzymes. Mitochondrial function was fairly well maintained after 1 h reperfusion in dogs premedicated with propranolol. Structural changes in mitochondria were observed in the 2 h occlusion/1 h reperfusion group, and were reduced by premedication with propranolol. These results suggest that irreversible injury of ischaemic mitochondria is closely linked with instability of lysosomal membranes, and that propranolol prevented irreversible myocardial mitochondrial dysfunction.