tbuckley/cabot-search huggingface dataset:
Ischemia induces changes in the level of mRNAs coding for stress protein 71 and creatine kinase M.
Authors: H B Mehta, B K Popovich, W H Dillmann
Journal: Circulation Research (1988)

Hyperthermia, hypoxia, and other conditions induce the appearance of heat shock or stress proteins in cells. We have previously shown that in the ischemic dog myocardium the level of a messenger RNA (mRNA) coding for a protein with migration characteristics similar to heat shock/stress protein 71 increases. Using a human heat-shock protein (hHSP) 70 genomic clone and anti-HSP70 antibodies as probes, we demonstrate in this report that heart stress protein (SP) 71 mRNA and its translational products (71 kDa polypeptides) are members of the stress protein family. In rabbit hearts, the ischemia-induced mRNAs translate into three isoforms with different isoelectric points (6.0, 6.1, and 6.15), in contrast to dog heart mRNA that translates into a protein with a pI of 5.8. The levels of SP71 mRNA in the dog and rabbit ischemic myocardium increased by sixfold and 18-fold, respectively. In the same samples, the levels of creatine kinase M mRNA decreased by about 40%, whereas those of myosin heavy chain mRNA remain unaltered. Our comparative analysis of three different mRNAs indicates that ischemia manifests its effects by differentially changing the levels of specific mRNAs coding for proteins with separate and distinct roles in the cell.
Decreased in vitro anticoagulant potency of Rivaroxaban and Apixaban in plasma from patients with cirrhosis
Authors: Wilma Potze, Jelle Adelmeijer, Ton Lisman
Journal: Hepatology (2014)

Potential conflict of interest: Nothing to report. To the Editor: There is increasing interest in treatment and prevention of cirrhotic portal vein thrombosis (PVT) with anticoagulant drugs.1 Two recent reports in Hepatology suggested efficacy and safety of new‐generation oral anticoagulant drugs (the direct factor Xa inhibitors, Rivaroxaban and Apixaban) in treatment of PVT in patients with compensated cirrhosis.2 These new drugs have practical advantages over traditional anticoagulants.4 We recently showed altered in vitro potency of different anticoagulant drugs in patients with cirrhosis, compared to patients with intact liver function.5 A theoretical risk for excessive anticoagulation when using these drugs in patients with cirrhosis and concomitant alterations in their hemostatic system exists. We previously demonstrated a decreased in vitro anticoagulant effect of Rivaroxaban in patients with cirrhosis. Using thrombomodulin‐modified thrombin generation testing, we examined the in vitro anticoagulant potency of Apixaban, which we compared to the anticoagulant potency of Rivaroxaban. This study protocol was approved by the medical ethical committee of the University Medical Center Groningen (Groningen, The Netherlands), and written informed consent was obtained from each subject before inclusion in the study. We added vehicle, 25 ng/mL of Apixaban, or 50 ng/mL of Rivaroxaban to plasma samples of 11 healthy individuals and 14 patients with cirrhosis (9 patients with Child B cirrhosis and 5 with Child C cirrhosis). We performed thrombin generation tests in the presence of thrombomodulin and calculated the percentual decrease in total thrombin generation by the two anticoagulant drugs, as described previously.5 Whereas a fixed dose of the drugs decreased total thrombin generation in healthy volunteers by 55 ± 6% (Rivaroxaban, mean ± standard deviation) and 51 ± 4% (Apixaban), the mean decrease in thrombin generation in patients was significantly lower (30 ± 9% for Rivaroxaban, P < 0.0001 [t test]; 32 ± 10% for Apixaban, P < 0.0001). In conclusion, the in vitro anticoagulant potency of Apixaban is substantially reduced in patients with moderate and advanced cirrhosis, similar to the reduced potency of Rivaroxaban, which we previously reported. These results suggest that anticoagulant treatment with these direct factor Xa inhibitors will likely not result in overanticoagulation, with a potentially increased bleeding risk, provided drug levels remain in the target range. Careful monitoring of drug levels, for example, by anti‐Xa testing,6 may be required.
Multiple stenting in a patient with a high-grade malignant hilar biliary stricture: endoscopic four-branched partial stent-in-stent deployment of metallic stents
Authors: H. Kawamoto, K. Tsutsumi, M. Fujii, R. Harada, H. Kato, K. Hirao, N. Kurihara, T. Nakanishi, O. Mizuno, E. Ishida, T. Ogawa, H. Fukatsu, K. Sakaguchi
Journal: Endoscopy (2007)

Palliative therapy, such as biliary stenting, is often required before chemotherapy in patients with cholangiocellular carcinoma, who often have a hilar biliary stricture. In addition, chemotherapy itself puts patients at a higher risk of cholangitis. Drainage of both hepatic lobes is more advantageous than drainage of a single lobe alone, to avoid the development of cholangitis in the other lobe [1] [2], but the deployment of multiple stents in a hilar biliary stricture is technically demanding. We report here the endoscopic four-branched partial stent-in-stent deployment of metallic stents in a patient with a Bismuth type IV hilar biliary stricture.
A recombined allele of the lipase gene CEL and its pseudogene CELP confers susceptibility to chronic pancreatitis
Authors: Karianne Fjeld, Frank Ulrich Weiss, Denise Lasher, Jonas Rosendahl, Jian-Min Chen, Bente B Johansson, Holger Kirsten, Claudia Ruffert, Emmanuelle Masson, Solrun J Steine, Peter Bugert, Miriam Cnop, Robert Grützmann, Julia Mayerle, Joachim Mössner, Monika Ringdal, Hans-Ulrich Schulz, Matthias Sendler, Peter Simon, Paweł Sztromwasser, Janniche Torsvik, Markus Scholz, Erling Tjora, Claude Férec, Heiko Witt, Markus M Lerch, Pål R Njølstad, Stefan Johansson, Anders Molven
Journal: Nature Genetics (2015)
Extradural and Intrathoracic Lipoma-Reply
Authors: Herbert C. Maier
Journal: JAMA (1962)

<h3>To the Editor:—</h3> In reference to the letter by Dr. Irwin Perlmutter commenting on my article "Extradural and Intrathoracic Lipoma Causing Spinal Cord Compression," I am in complete agreement that immediate decompression of the spinal cord is indicated for paresis, irrespective of whether the compression is thought to be due to a benign or malignant lesion such as neuroblastoma. The purpose of reporting the article was to illustrate the fact that a case which might appear to have an extensive malignant process may actually be far more favorable than anticipated. Hence the reason for attempting decompression, even in the face of apparently very unfavorable preoperative findings.
Protein tyrosine kinase 6 (PTK6): a new/potential therapy target in breast cancer?.
Authors: M Aubele, AK Walch, H Braselmann, N Ludyga, MJ Atkinson, B Luber, G Auer, JM Bartlett
Journal: Cancer Research (2009)

Abstract Abstract #3073 Background: Elevated expression of the cytoplasmic tyrosine kinase PTK6 (breast tumor kinase, BRK) occurs in approximately two-thirds of primary breast tumors, where it is implicated in EGF receptor-dependent signaling and epithelial tumorigenesis. The role of PTK6 in breast cancer development and prognosis is unclear, its function in-vivo remains undefined.&amp;#x2028; Material and Methods: We performed a retrospective study of PTK6 expression in 426 archival breast cancer samples from patients with long term (≥240 months) follow up. Immunohistochemical analysis of the following proteins was determined: PTK6, all 4 HER receptors, Sam68 (a substrate of PTK6), and the signalling proteins MAP kinase (MAPK), phosphorylated MAPK (P-MAPK), and PTEN. Correlations between markers were determined, and the prognostic value of parameters by univariate and multivariate survival analysis. We compared PTK6 gene copy number with the protein expression levels using FISH analysis.&amp;#x2028; Results: The disease-free survival of patients ( ≥240 months) was positively correlated with PTK6 protein expression, and was inversely correlated with nodal status and tumor size (p≤0.01). A time dependence for the prognostic value of key markers was evident, with HER2/neu only showing prognostic significance at early time points (60 months).&amp;#x2028; PTK6 expression in tumor tissue significantly correlated with the expression of PTEN, MAPK, P-MAPK, and Sam68 (p≤0.05). To investigate whether these correlations may be due to molecular interactions, we used the T47D cell line for immunoprecipitation and Western Blot analysis. Co-precipitation-type protein-protein interactions could be demonstrated between PTK6 and MAPK, P-MAPK, HER2/neu, HER3, HER4, PTEN, and Sam68.&amp;#x2028; Quantitative analysis revealed an increased PTK6 gene copy number in 75% of the tumors. Polysomy of chromosome 20 was responsible for most cases (47%) whilst gene amplifications were less frequent (28%).&amp;#x2028; Discussion: We show that PTK6 protein expression is of significant prognostic value in predicting the long term outcome of breast carcinomas. Further, several potential binding partners were identified, indicating the involvement of PTK6 in three main signal transduction pathways.&amp;#x2028; Supported by: Deutsche Krebshilfe # 10379 / EU LSHC-CT-2004-503426. Citation Information: Cancer Res 2009;69(2 Suppl):Abstract nr 3073.
<i>RYR2</i> and <i>CASQ2</i> Mutations in Patients Suffering From Catecholaminergic Polymorphic Ventricular Tachycardia
Authors: Hadas Lahat, Elon Pras, Michael Eldar
Journal: Circulation (2003)

To the Editor:Catecholamine-induced polymorphic ventricular tachycardia (CPVT) is characterized by episodes of syncope, seizures, or sudden death in response to physical activity or emotional stress.The two modes of inheritance that have been described are autosomal dominant 1 and autosomal recessive. 2Mutations in the ryanodine receptor 2 gene (RYR2), which encodes a cardiac sarcoplasmic reticulum Ca 2ϩ release channel, were shown to cause the autosomal dominant form of the disease. 3 Recently, Priori et al 4 reported on clinical and molecular characterization of 30 probands with catecholaminergic polymorphic ventricular tachycardia and their 118 family members.A mutation screening of the RYR2 gene identified mutations in only 14 of 30 probands and in 9 family members.Our group has recently described a missense mutation in a highly conserved region of the calsequestrin 2 gene (CASQ2) as the potential cause of the autosomal recessive form of CPVT. 5 The CASQ2 protein serves as the major Ca 2ϩ reservoir within the sarcoplasmic reticulum of cardiac myocytes and is part of a protein complex that contains the ryanodine receptor.The mutation converts a negatively charged aspartic acid into a positively charged histidine in a highly negatively charged domain and is likely to exert its deleterious effect by disrupting Ca 2ϩ binding.It is possible that at least some of the nongenotyped CPVT probands described by Priori et al 4 may carry mutations in the CASQ2 gene.Lack of family history in part of the probands' affected families may suggest a recessive inheritance, increasing the likelihood that some of them harbor mutations in a common gene.We suggest that a full genetic evaluation of CPVT patients should include mutation screening for both known genes, RYR2 and CASQ2.
How to contain respiratory syncytial virus
Authors: Phil Gunby
Journal: JAMA (1980)

For nearly 25 years respiratory syncytial virus has been known to cause outbreaks of acute, occasionally fatal respiratory infection in humans. Less clear is how this paramyxovirus spreads. The two most popular hypotheses are transmission by direct contact or airborne spread or both. Newly reported research supports the first idea and modifies the second. Caroline B. Hall, MD, associate professor of pediatrics and medicine, University of Rochester Medical Center, reports that this virus seems to be spread by "self-inoculation of the eyes or nose after touching contaminated surfaces" or by aerosols from coughing, sneezing, or perhaps simply exhaling. However, during airborne spread, the virus apparently requires a droplet so large that it rarely travels beyond 180 cm. Hall and R. Gordon Douglas, Jr, MD, professor of medicine at the university and head of the Division of Infectious Diseases, presented a report on the subject at a joint meeting of the
An Exacerbation of SLE After Visiting a Tanning Salon
Authors: Robert S. Stern
Journal: JAMA (1986)

To the Editor.—  The public's desire to achieve a tan is reflected in the proliferation of commercial tanning salons. For example, in the 1980 Boston Yellow Pages there were no listings for tanning salons. By 1983, there were 24 such listings, and by 1985 there were 58. In its 1985 Yellow Pages advertisement, the largest of the tanning salon chains in Boston states that it provides a guaranteed tan in six visits, and is safer than the sun. Our patient's experience, and experimental findings, provide increasing evidence that exposure to ultraviolet light in the A range (UVA) in tanning salons is harmful and can be especially dangerous to certain patients.  Report of a Case.—  A 30-year-old woman was referred for evaluation of a rash of approximately two weeks' duration. After several years of intermittent polyarthralgias, a diagnosis of systemic lupus erythematosus (SLE) was finally made in January 1984. At this
A unique property of a plasma proteoglycan, the C1q inhibitor. An anticoagulant state resulting from its binding to fibrinogen.
Authors: D K Galanakis, B Ghebrehiwet
Journal: Journal of Clinical Investigation (1994)

The C1q inhibitor, C1qI, an approximately 30-kD circulating chondroitin-4 sulfate proteoglycan, displayed concentration-dependent prolongation of plasma and fibrinogen solution clotting times. Under factor XIIIa catalyzed cross-linking conditions and maximum C1qI concentrations, minor amounts of clot formed displaying complete gamma-gamma dimer formation but virtually no alpha-polymer formation. The anticoagulant effect was undiminished by its binding to C1q, by increased ionic strength, and by CaCl2, but was abolished by incubation of C1qI with chondroitinase ABC. 125I-labeled C1qI bound to immobilized fibrinogen, fibrin monomer, fibrinogen plasmic fragments D1 and E, and fibrin polymers. Occupancy on the E domain required uncleaved fibrinopeptides together with another structure(s), and it did not decrease binding of thrombin to fibrinogen. Occupancy on the D domain did not decrease the fibrinogen binding to fibrin monomer. We conclude that the E domain occupancy impaired fibrinopeptide cleavage, and occupancy on the D domain impaired polymerization, both steric hindrance effects. C1qI binding to fibrinogen explains at least in part the well-known fibrin(ogen) presence in immune complex-related lesions, and the fibrinogen presence in vascular basement membranes and atheromata. We postulate that fibrin binding by resident basement membrane proteoglycans provides dense anchoring of thrombus, substantially enhancing its hemostatic function.
ON THE DEVELOPMENT OF THE CAUSAL TREATMENT OF TUBERCULOSIS.
Authors: EDWIN KLEBS
Journal: JAMA (1897)

I will not state in this paper the whole history of this question, which at its first commencement excited so much enthusiasm, and later caused so much disappointment to all concerned. As one of the few observers, having published detailed reports on the question ("On the Causal Treatment of Tuberculosis," Hamburg-Leipzig, 1894), I may be justified in expressing my regret that so many of the works on this subject, mostly in Germany, are written in the obscure and abbreviated style possibly appropriate for "vorläufige Mittheilungen," but not for definite scientific work. Robert Koch, in his first paper on "Tuberculin" (1890), showed the effects of this substance on tuberculous rabbits, but never gave later detailed accounts of his experiments. Everyone wishing to work on the subject was therefore obliged to find his way in the dark. Indeed, the preparation of tuberculin was not published for a long time afterward. Finding that
Pain of Myocardial Infarction Reproduced by Precordial Palpation
Authors: D. J. Bauman
Journal: JAMA (1979)

<h3>To the Editor.—</h3> Precise reproduction of a patient's chest pain by chest wall palpation is usually interpreted by physicians as a strong argument against an ischemic origin for the pain. Although this is undoubtedly generally true, a patient recently seen at our institution illustrates that it is not invariably so. <h3>Report of a Case.—</h3> A 48-year-old man was admitted to the Salt Lake Veterans Medical Center on Nov 23, 1978. He had been awakened that morning by severe, dull, aching anterior chest pain that radiated down both arms. He was unresponsive to eight nitroglycerin tablets. The pain persisted for five hours before being completely relieved by 16 mg of morphine sulfate administered in increments intravenously at the time of admission to thecoronary care unit. Serial ECGs (Figure) and enzyme studies (Table) were interpreted to be diagnostic of an acute anterior wall myocardial infarction. When his condition was evaluated two
Early Recurrences of Atrial Fibrillation After Electrical Cardioversion: A Result of Fibrillation-Induced Electrical Remodeling of the Atria?
Authors: Robert G Tieleman, Isabelle C Van Gelder, Harry J.G.M Crijns, Pieter J De Kam, Maarten P Van Den Berg, Jaap Haaksma, Hanneke J Van Der Woude, Maurits A Allessie
Journal: Journal of the American College of Cardiology (1998)
AMERICAN HYGIENE.CHAIRMAN'S ADDRESS BEFORE THE SECTION ON HYGIENE AND SANITARY SCIENCE, AT THE FIFTY-SIXTH ANNUAL SESSION OF THE AMERICAN MEDICAL ASSOCIATION, PORTLAND, ORE., JULY 11-14, 1905.
Authors: JOHN S. FULTON
Journal: JAMA (1905)

The same Scripture which forbids a man to think of himself more highly than he ought to think, warns also against the opposite sin, bidding him think soberly, according as God has dealt to every man the measure of faith. Applying to the duty of this hour the rule and measure of scientific faith which has been dealt to me, I desire to consider soberly the office of this Section as a member, first, of the body medical, and afterward of that greater body in which the profession itself is a member—the body politic. If I confess no surprise that a majority of the members of the American Medical Association see in this Section no very distinguished merit, I imply no disparagement of the past history of the Section, nor any want of intelligence on the part of those who think less highly than I of the capabilities of this
(16) Recessive dystrophic epidermolysis bullosa?
Authors: A. Cattell, E. Waddington
Journal: British Journal of Dermatology (1973)

Journal Article (16) Recessive dystrophic epidermolysis bullosa? Get access A. Cattell, A. Cattell Department of Dermatology, University Hospital of Wales, Cardiff Search for other works by this author on: Oxford Academic Google Scholar E. Waddington E. Waddington Department of Dermatology, University Hospital of Wales, Cardiff Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 89, Issue s9, 1 July 1973, Pages 67–71, https://doi.org/10.1111/j.1365-2133.1973.tb03449.x Published: 01 July 1973
A 61-year-old man with pain in antecubital fossa after an elbow hyperextension injury
Authors: J Waterhouse, C R King, P Chin, B B Forster
Journal: British Journal of Sports Medicine (2009)

A 61-year-old, right-hand dominant man was brought to the emergency department (ED) after catching a heavy object in his left arm and causing a hyperextension injury to his left elbow. He developed acute onset of pain localised to the antecubital fossa. Three days after the injury, …
Isolated Blast Crisis in CNS in a Patient With Chronic Myelogenous Leukemia Maintaining Major Cytogenetic Response After Imatinib
Authors: Hyun Jung Kim, Chul Won Jung, Kihyun Kim, Jin Seok Ahn, Won Seog Kim, Kwan Park, Young Hye Ko, Won Ki Kang, Keunchil Park
Journal: Journal of Clinical Oncology (2006)

apparently unrelated histiocytic condition, Langerhans histiocytosis with hemophagocytosis, is well-described in this setting. 9 In addition, there are only a few rare case reports describing splenic involvement by SHML, and in these cases there was extranodal involvement of adjacent tissues as well, which was not observed in this case. 10,11 The rapid clinical improvement in our patient after splenectomy suggests that there may be therapeutic benefit from early surgical intervention in this setting.Unfortunately, 3 months later she progressed to acute undifferentiated myeloid leukemia, which proved refractory to multiple chemotherapy regimens including several experimental protocols, and she died 11 months after splenectomy without ever achieving clinical remission.More generally, marked splenomegaly is quite uncommon in MDS, and should prompt further diagnostic evaluation before being attributed to the underlying myeloid disorder.
Multiple Insular Necrosis of Skin and Subjacent Tissues
Authors: H. S. Renshaw
Journal: BMJ (1894)

NECROSIS OF SKIN.[JU NE 9, 189.case SeemS to )ave maInde its first a*)pearance (exclu(ding tlev bulli shle pr'eviously hlad oii lioh: feet) oi thdese surfa-tes.Amonig otlherplanis of treaulmenr, s,)me parts iffecte(ld wer a.treated pertectly dry, with starch or flour powdered on, but witlh no better effect than those treated with soothing lotions.Curiously enough, another case of pemphigus was under my .. -I Zv' 11 1 care at the same time as the one I have previously described.This was in a married lady, about 35 years of age.Two or thlree bulla' made their appearance on the shin, coming on Iith cold, aniid febrile symiiptomiis.'h'liey werez irritable anid l)ainful.T)ihe bulle dried up, aniid the skin peeled off after about tlhree weeks, anid ino othfers lhave since -appeared.The patient was sutfIring at the time froiim neuralgia, anid was iI "I ge(nerally weakly coiiditionI.MULTIPl.E INSULAR NECROSIS OF SKIN AND SUBJACENT TISSUES.
Is Self-Monitoring of Blood Glucose Appropriate for All Type 2 Diabetic Patients?
Authors: Wendy A. Davis, David G. Bruce, Timothy M.E. Davis
Journal: Diabetes Care (2006)

OBJECTIVE—We sought to determine whether self-monitoring of blood glucose (SMBG) is associated with better glycemic control in type 2 diabetes. RESEARCH DESIGN AND METHODS—We used cross-sectional and longitudinal data from type 2 diabetic participants in the observational, community-based Fremantle Diabetes Study (FDS) who reported SMBG status at study entry (n = 1,286) and annual reviews over 5 years (n = 531). RESULTS—At study entry, 70% of patients performed SMBG, with a median of four tests per week (interquartile range two to seven). Patients with shorter diabetes duration; who were attending diabetes education, diabetes-related clinics, or medical specialists; who were taking insulin with or without oral hypoglycemic agents (OHAs); and who were self-reporting hypoglycemic events were more likely to use SMBG. Both cross-sectional and longitudinal FDS data showed that HbA1c (A1C) was not significantly different between SMBG users and nonusers, either overall or within diabetes treatment groups (diet, OHAs, and insulin with or without OHAs). There was also no independent cross-sectional relationship between A1C and SMBG frequency. The average annual societal cost of using SMBG (in year 2000 Australian dollars [A$], excluding glucometers) was A$162 per type 2 diabetic patient or A$51 million when projected to the Australian diagnosed type 2 diabetic population. CONCLUSIONS—Neither SMBG testing nor its frequency was associated with glycemic benefit in type 2 diabetic patients regardless of treatment. Our data did not include methods of SMBG delivery and application, factors that require further assessment in the evaluation of SMBG utility in non–insulin-treated type 2 diabetes. SMBG may be still of value in the identification and prevention of hypoglycemia and in dose adjustment in insulin-treated patients.