tbuckley/cabot-search huggingface dataset:
Thrombospondin binds to monocytes-macrophages and mediates platelet-monocyte adhesion.
Authors: R L Silverstein, R L Nachman
Journal: Journal of Clinical Investigation (1987)

Thrombospondin (TSP) is a multifunctional platelet glycoprotein synthesized by a variety of cells in culture including monocytes and macrophages. We now report that 125I-TSP binds specifically, saturably, and reversibly to mouse peritoneal macrophages and to cells of the monocyte-like human cell line U937 with dissociation constants of 6.7-14.5 X 10(-8) M and 3-4 X 10(5) binding sites per cell. TSP mediates an adhesive interaction between thrombin-stimulated platelets and both U937 cells and human blood monocytes. Using a sensitive rosetting assay, we found that monocytes were not rosetted by resting platelets whereas greater than 90% were rosetted by thrombin-stimulated platelets. Monoclonal and polyclonal anti-TSP antibodies markedly inhibited rosetting as did TSP itself. Neither control antibodies nor heparin, fibronectin, fibrinogen, nor the fibronectin adhesion tetrapeptide Arg-Gly-Asp-Ser inhibited rosetting. TSP may thus serve as a molecular bridge linking activated platelets with monocytes at sites of early vascular injury. Such interaction may be of critical importance in the regulation of thrombosis and the initiation of atherosclerosis.
Acquired partial deletions of the long arm of chromosome 5 in hematologic disorders
Authors: Lawrence P. Wisniewski, Kurt Hirschhorn
Journal: American Journal of Hematology (1983)

Abstract We have analyzed the data on 105 patients reported with a deletion of part of the long arm of chromosome 5 in the presence of hematologic disease. The major conditions associated with this abnormality are refractory anemia, polycythemia vera, and acute myelogenous leukemia, as well as the occasional occurrence of several other problems.
Paraproteins and the Anion Gap
Authors: Robert G. Narins, Thomas Murray
Journal: Annals of Internal Medicine (1977)

Letters and Corrections1 July 1977Paraproteins and the Anion GapROBERT G. NARINS, M.D., THOMAS MURRAY, M.D.ROBERT G. NARINS, M.D.Search for more papers by this author, THOMAS MURRAY, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-87-1-117_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: The cationic nature of myeloma paraproteins has been well documented (1, 2). The principle of electroneutrality requires that an equal concentration of anions be present to offset these added protein cations. Chloride and bicarbonate are retained to provide the negative charges, and the resulting hyperchloremia lowers the anion gap [Na-(Cl + HCO3)]. In this formulation each meq/litre increase in cationic protein should cause an equal and reciprocal decrease in the anion gap.The technique of isoelectric focusing has shown that the paraprotein spike from each patient is composed of a group of protein bands with isoelectric points...References1. AWDEHWILLIAMSONASKONAS ZAB: One cell—one immunoglobulin. Biochem J 116:241-248, 1970 CrossrefMedlineGoogle Scholar2. MURRAYLONGNARINS TWR: Multiple myeloma and the anion gap. N Engl J Med 292:574-575, 1975 CrossrefMedlineGoogle Scholar3. FRICKSCHMIDKISTLER PJH: Hyponatremia associated with hyperproteinemia in multiple myeloma. Helv. Med Acta 33:317-329, 1967 MedlineGoogle Scholar4. FROHLICHADAMGOLBEY JWM: Decreased anion gap associated with monoclonal and pseudomonoclonal gammopathy. Can Med Assoc J 114:231-232, 1976 MedlineGoogle Scholar1. MURRAYLONGNARINS TWR: Multiple myeloma and the anion gap. N Engl J Med 292:574-575, 1975 CrossrefMedlineGoogle Scholar2. FRICKSCHMIDKISTLER PJH: Hyponatremia associated with hyperproteinemia in multiple myeloma. Helv Med Acta 33:317-329, 1967 MedlineGoogle Scholar3. EMMETTNARINS MR: Clinical use of the anion gap. Medicine (Baltimore) 56:38-54, 1977 CrossrefMedlineGoogle Scholar4. FROHLICHADAMGOLBEY JWM: Decreased anion gap associated with monoclonal and pseudomonoclonal gammopathy. Can Med Assoc J 114:231-232, 1976 MedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 July 1977Volume 87, Issue 1Page: 117-118KeywordsAnionsAttentionBicarbonatesCationsChloridesMyelomaProteins Issue Published: 1 July 1977 PDF DownloadLoading ...
Avoidance of ingestion of anti-inflammatory drugs in dyspepsia is confounding variable
Authors: P. J B Brown
Journal: BMJ (2001)

EDITOR—Langman et al in their paper on the effect of anti-inflammatory drugs on overall risk of common cancer describe a method using coded data from the general practice research database to support their hypothesis that anti-inflammatory drugs may protect against oesophageal and gastric cancer.1 The study reported the association between a reduction of coded cases of cancer of the …
Ciba Foundation Colloquia on Endocrinology. Volume 13: Human Pituitary Hormones
Authors: William W. Cleveland
Journal: JAMA (1961)

This colloquium held in Buenos Aires in 1959 consists of 15 papers on various phases of pituitary metabolism, followed by highly interesting discussions. Of major interest to the pediatrician, perhaps, are the studies involving the human growth hormone. Dr. Charles Read presented important results of measurement of the growth hormone in serum of normal and abnormal persons. Various aspects of the metabolic effects of the growth hormone were presented by several other authors. By and large, this volume reports technical data derived from basic research, yet throughout these papers are highly exciting suggestions of the important application of these findings to the problems of normal and abnormal pituitary effects on patients, and particularly on the growth and maturation of children. Ciba is to be commended again for the organization and presentation of such an excellent colloquium.
Pulmonary position cryopreserved homografts: Durability in ross and non-ross patients
Authors: Seda E. Selamet, Welton M. Gersony, Karen Altmann, David E. Solowiejczyk, Majid Alfayyad, Laura Bevilaqua, Chava Khan, Ehud Krongrad, Jan M. Quagebeur, Howard D. Apfel
Journal: Journal of the American College of Cardiology (2003)
Imatinib mesylate versus allogeneic hematopoietic stem cell transplantation for patients with chronic myelogenous leukemia in the accelerated phase
Authors: Qian Jiang, Lan-Ping Xu, Dai-Hong Liu, Kai-Yan Liu, Shan-Shan Chen, Bin Jiang, Hao Jiang, Huan Chen, Yu-Hong Chen, Wei Han, Xiao-Hui Zhang, Yu Wang, Ya-Zhen Qin, Yan-Rong Liu, Yue-Yun Lai, Xiao-Jun Huang
Journal: Blood (2011)
Assessment of simple methods of measuring intestinal transit times in children with gastroenteritis.
Authors: R H Higgs, R B Ellis-Pegler, H P Lambert
Journal: Gut (1975)

Intestinal transit times in children less than 3 years old with gastroenteritis were measured using carmine suspension and radioopaque pellets. Carmine transit times were short as expected in the acute illness, and lengthened on recovery to the values found in children without diarrhoea. Pellet transit times of the sick children were the same as those of controls without bowel disease. Solid markers may thus be misleading in acute diarrhoeal illness of childhood. Possible mechanisms are discussed.
Developmental neurotoxicity of chlorpyrifos: what is the vulnerable period?
Authors: Dan Qiao, Frederic J Seidler, Stephanie Padilla, Theodore A Slotkin
Journal: Environmental Health Perspectives (2002)

Previously, we found that exposure of neonatal rats to chlorpyrifos (CPF) produced brain cell damage and loss, with resultant abnormalities of synaptic development. We used the same biomarkers to examine prenatal CPF treatment so as to define the critical period of vulnerability. One group of pregnant rats received CPF (subcutaneous injections in dimethyl sulfoxide vehicle) on gestational days (GD) 17-20, a peak period of neurogenesis; a second group was treated on GD9-12, the period of neural tube formation. In the GD17-20 group, the threshold for a reduction in maternal weight gain was 5 mg/kg/day; at or below that dose, there was no evidence (GD21) of general fetotoxicity as assessed by the number of fetuses or fetal body and tissue weights. Above the threshold, there was brain sparing (reduced body weight with an increase in brain/body weight ratio) and a targeting of the liver (reduced liver/body weight). Indices of cell packing density (DNA per gram of tissue) and cell number (DNA content) similarly showed effects only on the liver; however, there were significant changes in the protein/DNA ratio, an index of cell size, in fetal brain regions at doses as low as 1 mg/kg, below the threshold for inhibition of fetal brain cholinesterase (2 mg/kg). Indices of cholinergic synaptic development showed significant CPF-induced defects but only at doses above the threshold for cholinesterase inhibition. With earlier CPF treatment (GD9-12), there was no evidence of general fetotoxicity or alterations of brain cell development at doses up to the threshold for maternal toxicity (5 mg/kg), assessed on GD17 and GD21; however, augmentation of cholinergic synaptic markers was detected at doses as low as 1 mg/kg. Compared with previous work on postnatal CPF exposure, the effects seen here required doses closer to the threshold for fetal weight loss; this implies a lower vulnerability in the fetal compared with the neonatal brain. Although delayed neurotoxic effects of prenatal CPF may emerge subsequently in development, our results are consistent with the preferential targeting of late developmental events such as gliogenesis, axonogenesis, and synaptogenesis.
Patient confidentiality in a time of care.data
Authors: J. Sheather, S. Brannan
Journal: BMJ (2013)

The benefits of unlocking patient data are enormous; hopefully the risks can be managed

The NHS is in the midst of an information revolution. Powers introduced by the Health and Social Care Act will enable the Health and Social Care Information Centre to extract large amounts of personal confidential data from GP medical records. These powers override the common law duty of confidentiality and the ordinary requirement to seek consent for disclosure, although patients have a right to object to their data being disclosed.

Any large scale use of sensitive personal data inevitably raises ethical concerns, and, unsurprisingly, the new powers have sparked controversy. Public confidence in large publicly held databases, and in the politicians who commission and control them, is scant. Trust between doctors and patients and consequently in the wider health service is predicated on the belief that, in all but exceptional circumstances, confidentiality will be respected. But the potential benefits arising from the proper use of medical data are too important to be ignored without exceptional reason. We therefore must be clear about what the changes involve and what the benefits might be.

The first use of the new powers is the care.data initiative, commissioned by NHS England. …
Prevention of Posttransfusion Hepatitis: Cost-effective or Not?
Authors: Frank L. Iber
Journal: JAMA (1981)

During the late 1950s, it became clear that posttransfusion hepatitis was contributing significantly to morbidity in all forms of treatment, requiring transfusion with many separate units of blood. This was and is particularly dramatic in cardiovascular surgery, when the hepatitis, with its incubation period of 30 to 70 days, becomes apparent long after the risky operation and immediate postoperative period. Attack rates of hepatitis after cardiovascular surgery ranged from 2% to as high as 20%, with at least one in 15 of these cases of hepatitis affecting future health. It also became clear that blood for transfusion from commercial suppliers was responsible for a higher incidence of hepatitis than blood from suppliers dependent on volunteer donors. At this point, in the early 1960s, it was apparent that elimination of payment for blood, as usually identified with the commercial suppliers, and the presumed expansion of volunteer procurement programs would lower the
Are the kinetics of technetium-99m methoxyisobutyl isonitrile affected by cell metabolism and viability?
Authors: R S Beanlands, F Dawood, W H Wen, P R McLaughlin, J Butany, G D'Amati, P P Liu
Journal: Circulation (1990)

To investigate the role of cell viability and metabolism on the myocardial kinetics of a new tracer, technetium-99m-methoxyisobutyl isonitrile (Tc-99m-MIBI), 250 microCi/l Tc-99m-MIBI was infused in isolated rat hearts under constant flow conditions. The hearts were studied after inducing irreversible damage by cytochrome c oxidase inhibitor sodium cyanide (n = 8) or sarcolemmal membrane detergent Triton X-100 (n = 8). The control hearts (n = 6) received no toxins. Mean Tc-99m-MIBI peak accumulation activity was significantly reduced after cyanide (51.1 +/- 44.2% of control, p less than 0.01) and Triton (13.8 +/- 2.7% of control, p less than 0.001) administration. Kinetic studies also showed marked reduction in accumulation rates and marked increase in clearance rates for cyanide (p less than 0.01) and Triton (p less than 0.01) groups compared with controls. Potential changes in regional flow distribution were assessed using microspheres. When peak accumulation activity was corrected for these changes, there remained significant differences between the groups. In the cyanide and Triton groups, irreversible cell injury was confirmed by creatine kinase and lactate dehydrogenase release, triphenyl tetrazolium chloride staining, and electron microscopy. All the cells were viable in the control group. We conclude that the accumulation and clearance kinetics of Tc-99m-MIBI are significantly affected by cell viability. Tc-99m-MIBI kinetics appear to be dependent on sarcolemmal integrity and to a lesser extent on aerobic metabolism.
IRRADIATED FOODS, RADIUM AND PHOSPHORUS
Authors: Alfred F. Hess
Journal: JAMA (1925)

ABSTRACT To  Editor: —In The Journal, July 25, appears a communication from Dr. Tomb, suggesting that  acquisition by foods of antirachitic potency as a result of irradiation  merely a stored-up form of radiant energy, and raising  question of whether  emanation or  phosphorescence of phosphorus may not also be antirachitic in action. In this connection I should like to call attention to  fact that in my preliminary communication to  American Pediatric Society, in June, 1924, on  activation of inert vegetable oil, it was reported that animals failed to be protected from rickets by feeding small amounts of radium bromid or by additions of minimal amounts of radium to linseed oil. The details of these experiments may be found in a later publication (J. Biol. Chem.62:301, 1924).The author further suggests that the action of phosphorus in rickets is worthy of modern
Real-Time 3-Dimensional Transesophageal Echocardiography in the Evaluation of Post-Operative Mitral Annuloplasty Ring and Prosthetic Valve Dehiscence
Authors: Itzhak Kronzon, Lissa Sugeng, Gila Perk, David Hirsh, Lynn Weinert, Miguel Angel Garcia Fernandez, Roberto M. Lang
Journal: Journal of the American College of Cardiology (2009)
Mitochondrial inhibitor as a new class of insulin sensitizer
Authors: Yong Zhang, Jianping Ye
Journal: Acta Pharmaceutica Sinica B (2012)

Insulin resistance is a major risk factor for type 2 diabetes. AMP-activated protein kinase (AMPK) is a drug target in the improvement of insulin sensitivity. Several insulin-sensitizing medicines are able to activate AMPK through inhibition of mitochondrial functions. These drugs, such as metformin and STZ, inhibit ATP synthesis in mitochondria to raise AMP/ATP ratio in the process of AMPK activation. However, chemicals that activate AMPK directly or by activating its upstream kinases have not been approved for treatment of type 2 diabetes in humans. In an early study, we reported that berberine inhibited oxygen consumption in mitochondria, and increased AMP/ATP ratio in cells. The observation suggests an indirect mechanism for AMPK activation by berberine. Berberine stimulates glycolysis for ATP production that offsets the cell toxicity after mitochondria inhibition. The study suggests that mitochondrial inhibition is an approach for AMPK activation. In this review article, literature is critically reviewed to interpret the role of mitochondria function in the mechanism of insulin resistance, which supports that mitochondria inhibitors represent a new class of AMPK activator. The inhibitors are promising candidates for insulin sensitizers. This review provides a guideline in search for small molecule AMPK activators in the drug discovery for type 2 diabetes.
THE LYMPHOCYTIC ORIGIN OF A PLASMA FACTOR RESPONSIBLE FOR HYPERSENSITIVITY IN VITRO OF TUBERCULIN TYPE
Authors: Joseph M. Miller, Cutting B. Favour
Journal: The Journal of Experimental Medicine (1951)

Methods are described for the evaluation in vitro of the effect of tuberculin on the leucocytes of peripheral blood. Washed leucocytes from a tuberculin sensitive host suspended in normal plasma are not lysed by tuberculin until after several hours of contact. Washed leucocytes from a tuberculin-sensitive host slowly release into normal plasma a factor which will cause the lysis of normal leucocytes exposed to tuberculin. Dialysis of normal plasma containing shed plasma factor causes the latter to precipitate with the euglobulins. Shed plasma factor can be recovered from normal plasma which has been incubated with lymphocytes from tuberculin-sensitive hosts. Suspensions of neutrophils do not yield shed plasma factor.
Chronic Renal Disease and Heavy use of Analgesics
Authors: Telfer B. Reynolds
Journal: JAMA (1963)

Eight patients with serious chronic renal disease and a long history of heavy use of analgesics containing phenacetin (acetophenetidin) arc described. Admitted acetophenetidin consumption ranged from 1 to 5 gm daily over many years with an ingestion pattern suggesting habituation or addiction. Chronic headache was the outstanding symptom. Findings included hyperazotemia, moderate to severe anemia, mild hypertension, minimal proteinuria, and minor abnormalities in the urinary sediment. Six patients had bacteriuria. Two had "secondary" renal tubular acidosis. Three died of uremia. Pathologic findings were severe papillary necrosis without extensive polymorphonuclear exudate, interstitial fibrosis with remarkable atrophy of tubules and peritubular capillaries in the medulla, focal areas of tubular atrophy in the cortex, and increase in round cells and fibrous tissue in the interstitium. These changes were felt to be unique, recognizable, and different from those caused by pyelonephritis alone.
Abstract LB-10: Defective nucleolar localization and dominant interfering properties of a parafibromin L95P missense mutant causing the hyperparathyroidism-jaw tumor syndrome
Authors: Leelamma P. Jacob, Jian Hua Zhang, Pradeep K. Dagur, William F. Simonds
Journal: Cancer Research (2010)

Abstract The hyperparathyroidism-jaw tumor syndrome (HPT-JT) is a familial cancer syndrome that results from germline loss-of-function mutation of HRPT2/CDC73, a putative tumor suppressor gene that encodes parafibromin, a component of the transcriptional regulatory PAF1 complex with homology to the yeast protein Cdc73p. The vast majority of HRPT2/CDC73 germline mutations identified have been truncation or frameshift mutations, and loss-of-function due to missense mutation is rare. We report here a kindred with HPT-JT due to a germline L95P missense mutation in parafibromin. The mutant parafibromin was studied in vitro to understand the basis of its presumed loss-of-function. When transfected in cultured cells the L95P mutant was expressed to a lower level than wild-type parafibromin, a difference that was not overcome by inhibition of the proteasome degradation pathway. The L95P mutant parafibromin retained the ability to assemble with endogenous PAF1 complex components as evidenced by co-immunoprecipitation. Analysis of subcellular localization showed that the L95P mutant was markedly deficient in nucleolar localization compared to the wild-type, an impairment likely resulting from disruption of a nucleolar localization signal immediately upstream of the L95P mutation. Transfection of the L95P parafibromin mutant, but not the wild type, increased HEK 293 cell survival and stimulated cell-cycle progression in NIH-3T3 cells, properties that appear to result from dominant interference with endogenous parafibromin signaling pathways. The simultaneous loss of nucleolar localization and acquisition of a growth stimulatory phenotype with the L95P mutation raise the possibility that parafibromin must interact with targets in the nucleolus to fully execute its tumor suppressor functions. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr LB-10.
Pim2 cooperates with PML-RARα to induce acute myeloid leukemia in a bone marrow transplantation model
Authors: Shuchi Agrawal-Singh, Steffen Koschmieder, Sandra Gelsing, Carol Stocking, Martin Stehling, Christian Thiede, Nils H. Thoennissen, Gabriele Köhler, Peter J. M. Valk, Ruud Delwel, Ken Mills, Nicole Bäumer, Lara Tickenbrock, Klaus Hansen, Wolfgang E. Berdel, Carsten Müller-Tidow, Hubert Serve
Journal: Blood (2010)
Onychomycosis: the development of a clinical diagnostic aid for toenail disease. Part I. Establishing discriminating historical and clinical features
Authors: C.L. Fletcher, R.J. Hay, N.C. Smeeton
Journal: British Journal of Dermatology (2004)

Journal Article Onychomycosis: the development of a clinical diagnostic aid for toenail disease. Part I. Establishing discriminating historical and clinical features Get access C.L. Fletcher, C.L. Fletcher St John's Institute of Dermatology, St Thomas' Hospital, London SE1 7EH *Department of Public Health Sciences, Guy's, King's and St Thomas' Schools of Medicine, Dentistry and Biomedical Sciences, London, U.K Dr C.L.Fletcher, Dermatology Department, Kingston Hospital, Galsworthy Road, Kingston‐upon‐Thames, Surrey KT2 7QB, U.K. E‐mail: clfletcher@doctors.org.uk Search for other works by this author on: Oxford Academic Google Scholar R.J. Hay, R.J. Hay St John's Institute of Dermatology, St Thomas' Hospital, London SE1 7EH *Department of Public Health Sciences, Guy's, King's and St Thomas' Schools of Medicine, Dentistry and Biomedical Sciences, London, U.K Search for other works by this author on: Oxford Academic Google Scholar N.C. Smeeton N.C. Smeeton St John's Institute of Dermatology, St Thomas' Hospital, London SE1 7EH *Department of Public Health Sciences, Guy's, King's and St Thomas' Schools of Medicine, Dentistry and Biomedical Sciences, London, U.K Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 150, Issue 4, 1 April 2004, Pages 701–705, https://doi.org/10.1111/j.0007-0963.2004.05871.x Published: 01 April 2004 Article history Accepted: 09 October 2003 Published: 01 April 2004