tbuckley/cabot-search huggingface dataset:
Thromboembolic Complications in Myelomatosis
Authors: D. Catovsky, N. B. Ikoku, W. R. Pitney, D. A. G. Galton
Journal: BMJ (1970)

Fourteen cases of myelomatosis associated with major thromboembolic complications are reported. Six patients died of pulmonary embolism, seven had deep-vein thrombosis as a presenting symptom, and three had evidence of amyloidosis. A preliminary estimate of the incidence of thromboembolism based on 376 patients admitted so far to the Medical Research Council9s myelomatosis trial is about 3%, while pulmonary embolism accounted for about 3% of all deaths. Possibly a hypercoagulable state and the presence of amyloidosis may be important in the pathogenesis of this complication.
Gap junctions and the connexin protein family
Authors: G SOHL
Journal: Cardiovascular Research (2003)

Gap junctions (Gj) form conduits between adjacent cells that are composed of connexin (Cx) protein subunits and allow direct intercellular communication. To date, the connexin gene family comprises 20 members in the mouse and 21 members in the human genome, 19 of which can be grouped as sequence-orthologous pairs. The structure of connexin genes is relatively simple. An untranslated exon 1 is separated by an intron of different length from exon 2, containing the uninterrupted coding region and the 3'-untranslated region (3'-UTR). However, in some connexin genes, the untranslated regions and the reading frame are spliced. Among the known "cardiovascular" connexins, Cx37 and Cx40 were demonstrated to be functionally expressed in mouse and human endothelial cells and Cx40, Cx43 as well as Cx45 in cardiomyocytes of both species. Functional properties, like permeabilities, charge selectivity and unitary conductivity were investigated after directed expression of these connexins in cultured cell lines or paired Xenopus oocytes. Targeted deletion of their coding sequence in the mouse genome allowed study of the biological relevance of Cx37, Cx40, Cx43 and Cx45 with regard to cardiovascular morphology and function. After ablation of Cx37 or Cx40, mice were viable and could be used to study defects in the adult cardiovascular system but loss of Cx43 or Cx45 led to neonatal or embryonic lethality, respectively. Conditional and cell-type specific deletion of both connexins in the heart or blood vessels can help to overcome this obstacle. As yet only little is known about mutations in the human genes for Cx37, Cx40, Cx43 and Cx45. Thus, a profound comparison between human and mouse phenotypes is not yet possible.
Fibrinogen and Cardiovascular Risk
Authors: Ajay Anand
Journal: Annals of Internal Medicine (1993)

Letters15 December 1993Fibrinogen and Cardiovascular RiskAjay Anand, MDAjay Anand, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-119-12-199312150-00015 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:Drs. Ernst and Resch [1] present a comprehensive review of the role of fibrinogen as a cardiovascular risk factor. They delineate possible mechanisms by which fibrinogen may promote atherosclerosis and thrombosis. In one study [2] of fibrin gel network characteristics and plasma fibrinogen in patients who had a myocardial infarction before the age of 45 years, those with an increased plasma fibrinogen concentration had a lower fibrin gel porosity than either patients with normal plasma fibrinogen levels or controls. This suggests that a propensity to form tight, rigid, and space-filling fibrin network structures with small pores may ...References1. Ernst E, Resch KL. Fibrinogen as a cardiovascular risk factor: a meta-analysis and review of the literature. Ann Intern Med. 1993; 118:956-63. Google Scholar2. Fatah K, Hamsten A, Blomback B, Blomback M. Fibrin gel network characteristics and coronary heart disease: relations to plasma fibrinogen concentration, acute phase protein, serum lipoproteins and coronary atherosclerosis. Thromb Hemost. 1992; 68:130-5. Google Scholar3. Munkvad S, Nieuwenhuizen W, Jespersen J. Plasma HMW fibrinogen in patients with ischemic heart disease. Scand J Clin Lab Invest. 1990; 50:347-9. Google Scholar4. Eritsland J, Seljeflot I, Arnesen H, Smith P, Westvik AB. Effects of long-term treatment with warfarin on fibrinogen, FPA, TAT and d-dimer in patients with coronary artery disease. Thromb Res. 1992; 66:55-60. Google Scholar5. Engelberg H. Low-dose intermittent heparin therapy decreases plasma fibrinogen levels. Semin Thromb Hemost. 1991; 17(Suppl 2): 219-23. Google Scholar6. Banerjee AK, Pearson J, Gilliland EL, Goss D, Lewis JD, Stirling Y, et al. A six year prospective study of fibrinogen and other risk factors associated with mortality in stable claudicants. Thromb Haemost. 1992; 68:261-3. Google Scholar Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 15 December 1993Volume 119, Issue 12Page: 1222-1223KeywordsAspirinAttentionBlood plasmaFibrinFibrinogenMyocardial infarctionPathogenesisStable coronary artery diseaseSurgeryThrombosis Issue Published: 15 December 1993 Copyright & PermissionsCopyright © 1993 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Mutations in the COL4A5 gene in Alport syndrome: A possible mutation in primordial germ cells
Authors: Hitoshi Nakazato, Shinzaburo Hattori, Tadashi Ushijima, Toshinobu Matsuura, Yasushi Koitabashi, Tsuneo Takada, Kazuo Yoshioka, Fumio Endo, Ichiro Matsuda
Journal: Kidney International (1994)
Chronic doxorubicin induced cardiomyopathy in rabbits: mechanical, intracellular action potential, and adrenergic characteristics of the failing myocardium
Authors: H. Shenasa, A. Calderone, M. Vermeulen, P. Paradis, H. Stephens, R. Cardinal, J. d. Champlain, J. L Rouleau
Journal: Cardiovascular Research (1990)

Study objective – The aim was to assess myocardial, electrophysiological, and adrenergic changes caused by chronic administration of doxorubicin. Design – Doxorubicin induced cardiotoxicity was produced in three groups of rabbits by injecting doxorubicin 0.75 mg·kg−1 three times a week for 7, 9 and 11 weeks. There were 36 controls. All studies were conducted within 16 to 36 h after the last injection. Histological, mechanical, and action potential changes produced by doxorubicin were examined in vitro. The effects of doxorubicin on β adrenergic receptors and cyclic adenosine monophosphate (AMP) generation in myocardial membrane preparations were also evaluated. Experimental material – 145 New Zealand white rabbits, 2.4–2.7 kg, were used. After excision of the heart, a papillary muscle was used for mechanical studies, a portion of the septum for intracellular action potential studies, and the rest of the heart for histological or biochemical studies. Measurements and results – Histological studies showed widespread myocardial damage that became more severe as the cumulative doses increased. Right ventricular papillary muscles of doxorubicin treated rabbits had lower total tension (1.5 v 3.3 g·mm−2 for controls, p<0.05) and dT/dt, shorter contraction duration, and lower velocity of shortening than the control muscles under all loading conditions. The changes progressed as the cumulative doxorubicin dose increased. Action potential duration was shorter in the doxorubicin treated groups (ADD50 = 76 v 62 ms for controls, p<0.01), although resting action potential amplitude was normal. Tension-frequency response (6-36 stimuli·min−1) and response to increasing calcium concentrations (2.54–6.32 mM) were attenuated in the doxorubicin group. Percent change in tension and dT/dt in response to noradrenaline (50 μM), isoprenaline (20 μM), or dibutyryl cyclic AMP (40 mM), was increased in the doxorubicin group v controls (300–600% v 100–200% respectively), despite chronic increase in circulating catecholamines, depletion of myocardial catecholamines, and no change in β adrenergic receptor number or affinity. The apparent increase in β adrenergic responsiveness in the doxorubicin group may have been partly due to decreased basal cyclic AMP production (13 v 31 pMol·mg−1 protein·min−1, p<0.01), although maximum catecholamine stimulated cyclic AMP production was only mildly decreased (251 v 315 pMol·mg−1 protein·min−1, p<0.05). Conclusions – The subacute effects of chronic doxorubicin become progressively more marked as the cumulative dose increases, and there are significant differences in the myocardial characteristics between this chronic model and other models of heart failure. These differences may be related to the cytotoxic effects of doxorubicin on membranes and membrane bound enzymes.
DEFINITE AND PROBABLE STENT THROMBOSIS AFTER REVASCULARIZATION WITH EVEROLIMUS- AND SIROLIMUS-ELUTING STENTS. FROM THE SORT OUT IV TRIAL
Authors: Lisette Okkels Jensen, Per Thayssen, Michael Maeng, Hans-Henrik Tilsted, Anne Kaltoft, Knud Hansen, Evald Christiansen, Anders Junker, Jan Ravkilde, Leif Thuesen, Jens Lassen
Journal: Journal of the American College of Cardiology (2012)
Role of heme metabolism in AZT‐induced bone marrow toxicity
Authors: J. D. Lutton, A. Mathew, R. D. Levere, N. G. Abraham
Journal: American Journal of Hematology (1990)

Abstract We studied the effects of azidothymidine (AZT) on rat bone marrow heme metabolism and colony growth as determined by assays of granulocyte‐macrophage (CFU‐GM), erythroid (CFU‐E), burst‐forming erythroid (BFU‐E), and α‐aminolevulinic acid synthase (ALAS), the first enzyme in the heme pathway. In all cases, AZT (1–0.01 μM) was found to be toxic to bone marrow colony growth. When AZT was included in colony assays, 1 μM resulted in 98–100% inhibition, whereas lower concentrations (0.01 μM) inhibited growth by 58–76%. In addition, cultures from AZT‐treated animals had a marked reduction in colony growth as compared with sham controls. In most cases, hemin (10 −5 M) was found to overcome some of the colony inhibitory effects of AZT. Analysis of heme metabolism indicated that ALAS activity was reduced by 71% in bone marrow cells from treated animals. ALAS activity for control was 204 ± 33 pM ALA formed/4 ± 10 6 cells/hr, whereas ALAS activity from AZT‐treated animals was only 60 ± 3 pM ALA formed/4 ± 10 6 cells/hr. It is considered that AZT toxicity may be due in part to a depression in the pool of available heme, which is required for adequate hematopoiesis.
NM 283 has potent antiviral activity against genotype 1 chronic hepatitis C virus (HCV-1) infection in the chimpanzee
Authors: D.N. Standring, R. Lanford, T. Wright, R.T. Chung, V. Bichko, E. Cretton-Scott, X. Pan-Zhou, S. Bergelson, L. Qu, M. Tausek, E. Bridges, A. Moussa, R. Storer, C. Pierra, S. Benzaria, G. Gosselin, P. La Colla, J.P. Sommadossi
Journal: Journal of Hepatology (2003)
Role of Bone Scintigraphy in the Detection of Periostitis in Secondary Syphilis
Authors: KILLOL THAKORE, ALICE VIROSLAV, JOHN VANSANT
Journal: Clinical Nuclear Medicine (1994)

The authors report a case of a 35-year-old woman with secondary syphilis (rapid plasma reagin being positive at 1:64 dilution) and dermatologic manifestations of lues maligna (thick, crusted cutaneous plaques with erythematous borders showing mixed perivascular inflammatory infiltrates and areas of ulcerations) on punch biopsy. She presented with complaints of multiple skin sores, mild headache, and bilateral, nocturnal leg pain for 2 weeks, which was relieved by change in position of the extremities. The bone scan demonstrated multifocal bony involvement, without detectable radiographic abnormalities. Bone scintigraphy appears highly sensitive for the detection of skeletal lesions of secondary syphilis, which are radiographically undetectable and clinically asymptomatic. Bone scintigraphy should be an integral component of the initial work-up. The presence of bony lesions has significant clinical implications by potentially altering clinical management.
Rationale and efficacy of interleukin-1 targeting in Erdheim–Chester disease
Authors: Achille Aouba, Sophie Georgin-Lavialle, Christian Pagnoux, Nicolas Martin Silva, Amédée Renand, Françoise Galateau-Salle, Sophie Le Toquin, Henri Bensadoun, Frederique Larousserie, Stéphane Silvera, Nicole Provost, Sophie Candon, Raphaèle Seror, Mathilde de Menthon, Olivier Hermine, Loïc Guillevin, Boris Bienvenu
Journal: Blood (2010)
COX-2: a link between airway inflammation and disordered chloride secretion in cystic fibrosis?
Authors: A Clayton
Journal: Thorax (2006)

bronchodilator compared with a group receiving placebo. 9 By the end of the training programme, the duration of a constant work rate treadmill task was increased by 79% in patients receiving bronchodilator treatment compared with those receiving placebo.Finally, in this issue of Thorax, Peters et al report that 50% oxygen breathing acts synergistically with bronchodilator therapy (ipratropium bromide) to reduce hyperinflation and improve exercise tolerance in patients with COPD. 10 In a crossover study in 16 patients, the mean tolerance of a constant work rate increased by 57% and 31% when inhaling oxygen or receiving bronchodilator, respectively.The combination of oxygen and ipratropium increased exercise tolerance by an average of 87% over the control condition, demonstrating an approximately additive response.The mathematically inclined among us will note that only four of six possible permutations of these four interventions have so far been reported.The successful combinations of heliox with exercise training and of bronchodilators with heliox are waiting to be achieved.Further, can studies of the simultaneous application of three interventions be far behind?Four studies of this kind could be planned, the requirement being the necessity to prove the superiority of the exercise tolerance improvements in response to three interventions over that of three groups in which combinations of two of the three interventions are applied.Will we see the day when a study appears in which simultaneous application of all four of these physiological manoeuvres are combined to ameliorate exercise intolerance and are proved to be superior to three groups in which three of the four interventions are given?One can only dream.
Abstract SY13-03: Signal pathways in prostate cancer stem cells
Authors: Owen N. Witte
Journal: Cancer Research (2014)

Abstract New therapeutic strategies are needed to treat prostate cancer as it progresses to the castration resistant stage following treatment with drugs to reduce androgen production or interfere with androgen receptor function. Genetic analyses of DNA alterations and RNA expression show that multiple pathways can be involved in this cancer progression. An understanding of the cellular components needed to initiate prostate cancer and sustain it during the process of metastasis may help to elucidate new pathways for therapy. We have developed techniques to transform mouse and human benign prostate epithelial basal stem cells and define them as one cell of origin which can respond to multiple stimuli to produce cancers which are capable of maturing to more differentiated cell types including luminal, squamous and neuroendocrine phenotypes. Different subtypes of cells with the properties of cancer stem cells capable of transplantation of the cancer phenotype have been defined. Current work is focusing on the activation of specific kinase driven pathways to provide new targets for therapy in metastatic prostate cancer. We previously demonstrated that castration resistant prostate cancer (CRPC) tissues exhibit increased tyrosine phosphorylation, suggesting that enhanced tyrosine kinase activity may contribute to advanced disease. To identify specific kinase activation patterns in metastatic CRPC, we utilized phospho-tyrosine peptide enrichment and quantitative mass spectrometry using tissue from CRPC patients obtained at rapid autopsy. Evaluation of these rare metastatic CRPC samples for tyrosine phosphorylation and kinases revealed activated SRC, EGFR, RET, ALK, and other targets. Importantly, these kinase activation patterns exhibited intrapatient similarity and interpatient heterogeneity implying clonal origins of these lesions. To evaluate the function of these kinases in metastatic CRPC, we are analyzing their role during specific steps of the metastatic cascade. We hope our approach will improve an understanding of the mechanistic role of kinase activation in prostate cancer and identify promising therapeutic strategies targeting non-mutated kinases for metastatic CRPC. Citation Format: Owen N. Witte. Signal pathways in prostate cancer stem 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 SY13-03. doi:10.1158/1538-7445.AM2014-SY13-03
Staying Alive: A Family Memoir
Authors: A. Ardern-Jones
Journal: BMJ (2003)

This is a very brave book, and a good read for professionals caring for families with a high risk of breast cancer. This intimate family story explores the dynamics of a cancer (or precancer) diagnosis in not just one beloved relative but five women in a family: the author–who was found to have many individual primary sites of carcinoma in situ after prophylactic surgery–her mother, two aunts, and a cousin.
The hepatitis B virus X protein: The quest for a role in viral replication and pathogenesis
Authors: C Seeger
Journal: Hepatology (1997)

Although the biological importance of hepatitis B virus X protein (HBX) in the life cycle of hepatitis B virus has been well established, the cellular and molecular basis of its function remains largely undefined. Despite the association of multiple activities with HBX, none of them appear to provide a unifying hypothesis regarding the true biological function of HBX. Identification and characterization of cellular targets of HBX remain an essential goal in the elucidation of the molecular mechanisms of HBX. Using the Saccharomyces cerevisiae two-hybrid system, we have identified and characterized a novel subunit of the proteasome complex (XAPC7) that interacts specifically with HBX. We also showed that HBX binds specifically to XAPC7 in vitro. Mutagenesis studies have defined the domains of interaction to be critical for the function of HBX. Furthermore, overexpression of XAPC7 appeared to activate transcription by itself and antisense expression of XAPC7 was able to block transactivation by HBX. Therefore, the proteasome complex is possibly a functional target of HBX in cells.
CORTICOTROPIN, CORTISONE, AND HYDROCORTISONE IN TREATMENT OF OCULAR DISEASE
Authors: E. H. Steffensen
Journal: JAMA (1952)

The field of ophthalmology has witnessed widespread clinical trial of corticotropin (ACTH) and cortisone during the past two and one-half years, and the accumulated results of many investigators justify the use of these agents in the treatment of a variety of ocular diseases. When corticotropin was first available for clinical trial late in 1949, evidence had accumulated that suggested it might be of value in the treatment of certain eye diseases. For years ophthalmologists had been using fever therapy, usually in the form of intravenously injected, killed typhoid organisms, in the treatment of a number of ocular lesions. It has been pointed out that the benefits of fever therapy apparently are derived from an acceleration of mechanisms evoked in acute stress states. 1 Reaction to such stress depends upon the endogenous release of corticotropin, which in turn stimulates the adrenal cortex to liberate 11-oxycorticosteroids. Selye 2 and Albright 3 have
Overexpression of cyclin D mRNA distinguishes invasive and in situ breast carcinomas from non-malignant lesions
Authors: Debra Weinstat-Saslow, Maria J. Merino, Richard E. Manrow, Julia A. Lawrence, Ray F. Bluth, Karl D. Wittenbel, Jean F. Simpson, David L. Page, Patricia S. Steeg
Journal: Nature Medicine (1995)
Myths, Morbidity, and Mortality in Asthma
Authors: Robert P. McCombs
Journal: JAMA (1979)

Persistence of outmoded concepts or "myths" concerning the diagnosis and treatment of asthma probably is responsible for large economic losses, overutilization of hospital beds, and many preventable deaths. There have been many worthwhile studies refuting these myths, leading to the following conclusions: Asthma consists of much more than wheezing and in many cases must be treated long after wheezing stops. There is no convincing evidence relating the chronic pulmonary changes of asthma to the psyche. Modern methods of prescribing theophylline have not made it universally effective and safe. Intermittent postive-pressure breathing is rarely justified in asthma. Respiratory acidosis may be corrected only by improving alveolar ventilation. Corticosteroids are usually essential for control of severe asthma and may be used safely. Severe asthmatics need careful monitoring because sudden respiratory failure may occur.
Erosion of the Colon by a Long-Dwelling Peritoneal Dialysis Catheter
Authors: Larry C. Watson
Journal: JAMA (1980)

<h3>To the Editor.—</h3> Long-term peritoneal dialysis is a commonplace procedure for patients with chronic renal failure who are not candidates for transplantation or home dialysis. Although bowel perforation on insertion of the catheter is a well-recognized complication,<sup>1,2</sup>we know of no reported instance of erosion of bowel by a previously placed, long-dwelling Tenckhoff catheter. <h3>Report of a Case.—</h3> A 71-year-old man had a Tenckhoff catheter placed in the left lower quadrant of the abdomen nine months before admission. Because of glomerulonephritis-induced chronic renal failure, he underwent bimonthly peritoneal dialysis. He was not a candidate for home hemodialysis nor for transplantation. Examination of the abdomen demonstrated signs of peritoneal irritation, including rebound tenderness to palpation, involuntary muscle guarding, and tenderness to palpation in the left lower quadrant. Purulent peritoneal fluid from the Tenckhoff catheter yielded<i>Escherichia coli</i>and<i>Pseudomonas aeruginosa</i>on culture. The peritonitis apparently resolved with continued dialysis. Six
THE UTILITY OF APOLIPOPROTEIN A1, REMNANT LIPOPROTEINS, AND THE APOLIPOPROTEIN A1 REMNANT RATIO TO THE INCIDENCE OF CORONARY HEART DISEASE IN A PRIMARY PREVENTION COHORT OF AFRICAN AMERICANS OVERALL AND BY SEX: THE JACKSON HEART STUDY
Authors: Heidi Thomas May, John Nelson, Seth Lirette, Krishnaji Kulkarni, Jeffrey Anderson, Michael Griswold, Benjamin Horne, Adolfo Correa, J. Muhlestein
Journal: Journal of the American College of Cardiology (2014)
Liver enzyme abnormalities after insulin induced hypoglycaemic coma.
Authors: N G Soler, R Khardori
Journal: BMJ (1985)

non-registered osteopaths.In the third case this almost certainly resulted in acute vertebral body collapse.In the United Kingdom there has been a recent upsurge of interest in "alternative" treatment for spinal spondylotic disease.In 1984 a case was reported from the United States in which chiropractic manipulation exacerbated a myelopathy.'In the past 55 years there have been periodic reports of manipulation causing spinal problems with the most serious results affecting the cervical spine.2'5There are virtually no published scientific reports that document the beneficial effects of manipulative treatment, though where the spinal cord and its roots are near compression forced flexion and extension might compromise on a mechanical or vascular basis either acutely or insidiously with repeated manipulation.In the three cases reported patients were unwilling to give details of their treatment let alone complain.During the past 12 months of the five cases of "traumatic" subacute cervical cord compression that required surgery at the Maida Vale branch of the National Hospital for Nervous Diseases, three were caused by spinal manipulation.The medicolegal implications of doctor to osteopath referrals are self evident.1 Schmidley JW, Koch T. The noncerebrovascular complications of chiropractic manipulation.