tbuckley/cabot-search huggingface dataset:
Secondary Hyperparathyroidism in Chronic Renal Failure
Authors: James W. Johnson
Journal: JAMA (1971)

Parathyroid function was assessed by radioimmunoassay of parathyroid hormone concentration (PTH) in 11 patients undergoing hemodialysis prior to and following renal homotransplantation (RHT). Seven patients had elevated plasma PTH levels prior to RHT, and in six of these PTH secretion was decreased by artificially induced hypercalcemia. One month after RHT, PTH was undetectable or had decreased in ten. Transient spontaneous hypercalcemia occurred in six of the 11 after RHT and appeared to be influenced by factors other than PTH. In all instances, the sequelae of secondary hyperparathyroidism regressed spontaneously.
Presentation of the Henry Jacob Bigelow Gold Medal
Authors: Donald Munro
Journal: New England Journal of Medicine (1947)

THE occasion of this meeting of the Boston Surgical Society is for the presentation of the Henry Jacob Bigelow Gold Medal. Tradition and custom, however, have decreed that some scientific contribution shall be made at every meeting of the Society. In consequence, the distinguished surgeon who will receive the Bigelow Medal, Dr. Frank H. Lahey, has been asked to present a paper. We are fortunate in that he has chosen thyroid surgery as his subject. He is well known to all in this audience and needs no further introduction. I have the honor of presenting Dr. Frank H. Lahey.(Dr. . . .
Nitric oxide inhibits viral replication in murine myocarditis.
Authors: C J Lowenstein, S L Hill, A Lafond-Walker, J Wu, G Allen, M Landavere, N R Rose, A Herskowitz
Journal: Journal of Clinical Investigation (1996)

Nitric oxide (NO) is a radical molecule that not only serves as a vasodilator and neurotransmitter but also acts as a cytotoxic effector molecule of the immune system. The inducible enzyme making NO, inducible NO synthase (iNOS), is transcriptionally activated by IFN-gamma and TNF-alpha, cytokines which are produced during viral infection. We show that iNOS is induced in mice infected with the Coxsackie B3 virus. Macrophages expressing iNOS are identified in the hearts and spleens of infected animals with an antibody raised against iNOS. Infected mice have increased titers of virus and a higher mortality when fed NOS inhibitors. Thus, viral infection induces iNOS in vivo, and NO inhibits viral replication. NO is a novel, nonspecific immune defense against viruses in vivo.
Evaluation of eight and a half years of neonatal screening for haemoglobinopathies in Birmingham
Authors: P. D Griffiths, J. R Mann, P. J Darbyshire, A. Green
Journal: BMJ (1988)

A pilot neonatal screening programme for haemoglobinopathies linked with screening for phenylketonuria and congenital hypothyroidism was reviewed. During 1978 to December 1986 137 000 neonates were tested. There were improvements in the detection rate and accuracy of diagnosis for homozygotes and mixed heterozygotes, mainly associated with the introduction of citrate agarose gel electrophoresis as a follow up procedure on all specimens showing any abnormality on the initial cellulose acetate electrophoresis. We recommend that the programme is continued on a service basis.
Diagnostic value of synovial fluid microscopy: a reassessment and rationalisation.
Authors: A J Freemont, J Denton, A Chuck, P J Holt, M Davies
Journal: Annals of the Rheumatic Diseases (1991)

This study is in two parts. In the first synovial fluid from 1892 patients with 14 different arthropathies was examined microscopically. Crystals of different types were identified and the disease distribution of these and various cell types, including several not previously reported in synovial fluid, have been described. These features have been used to derive a series of microscopic diagnostic criteria for each arthropathy. The criteria have been used in the second part of the study to examine synovial fluids from 200 patients without knowledge of any clinical diagnosis. Cytological and clinical diagnoses were compared at the end of the study. Matching diagnoses were made in 71 (35.5%) and a short list of differential diagnoses (based on cytological criteria), which included the clinical diagnosis, was made in a further 43 (21.5%). Of the rest, 63 (31.5%) were correctly described as inflammatory or non-inflammatory and in five (2.5%) no diagnosis could be made. Only in seven cases (3.5%) was an inaccurate (false positive) cytological diagnosis made. The results indicate that synovial fluid microscopy is a potentially more important diagnostic screening test in rheumatological and orthopaedic practice than it would at first appear from published reports.
Secreted Antiviral Entry Inhibitory (SAVE) Peptides for Gene Therapy of HIV Infection
Authors: Lisa Egerer, Andreas Volk, Joerg Kahle, Janine Kimpel, Frances Brauer, Felix G Hermann, Dorothee von Laer
Journal: Molecular Therapy (2011)

Gene therapeutic strategies for human immunodeficiency virus type 1 (HIV-1) infection could potentially overcome the limitations of standard antiretroviral drug therapy (ART). However, in none of the clinical gene therapy trials published to date, therapeutic levels of genetic protection have been achieved in the target cell population for HIV-1. To improve systemic antiviral efficacy, C peptides, which are efficient inhibitors of HIV-1 entry, were engineered for high-level secretion by genetically modified cells. The size restrictions for efficient peptide export through the secretory pathway were overcome by expressing the C peptides as concatemers, which were processed into monomers by furin protease cleavage. These secreted antiviral entry inhibitory (SAVE) peptides mediated a substantial protective bystander effect on neighboring nonmodified cells, thus suppressing virus replication even if only a small fraction of cells was genetically modified. Accordingly, these SAVE peptides may provide a strong benefit to AIDS patients in future, and, if applied by direct in vivo gene delivery, could present an effective alternative to antiretroviral drug regimen. Gene therapeutic strategies for human immunodeficiency virus type 1 (HIV-1) infection could potentially overcome the limitations of standard antiretroviral drug therapy (ART). However, in none of the clinical gene therapy trials published to date, therapeutic levels of genetic protection have been achieved in the target cell population for HIV-1. To improve systemic antiviral efficacy, C peptides, which are efficient inhibitors of HIV-1 entry, were engineered for high-level secretion by genetically modified cells. The size restrictions for efficient peptide export through the secretory pathway were overcome by expressing the C peptides as concatemers, which were processed into monomers by furin protease cleavage. These secreted antiviral entry inhibitory (SAVE) peptides mediated a substantial protective bystander effect on neighboring nonmodified cells, thus suppressing virus replication even if only a small fraction of cells was genetically modified. Accordingly, these SAVE peptides may provide a strong benefit to AIDS patients in future, and, if applied by direct in vivo gene delivery, could present an effective alternative to antiretroviral drug regimen.
Dysgammaglobulinaemia complicated by disseminated measles.
Authors: H Mawhinney, I V Allen, J M Beare, J M Bridges, J H Connolly, M Haire, N C Nevin, D W Neill, J R Hobbs
Journal: BMJ (1971)

We report the case of a boy with dysgammaglobulinaemia who died with giant ccll pneumonia and disseminated measles seven weeks after receiving live attenuated measles vaccine.Case Report From tbe age of 6 weeks the patient had frequent infections asso- ciated with a rash on the face, scalp, and limbs.He was given three doses of triple antigen (diphtheria, pertussis, and tetanus) and oral live attenuated poliomyelitis vaccine; the third dose at the age of 8 months.Fifty-six days later live attenuated measles vaccine was given.One week later he developed a pyrexial illness with a skin rash.There was no known contact with measles.An elder brother had a similar illness when 2 days old and died at 7 months with staphylococcal bronchopneumonia, a cervical abscess, and boils on neck.
Is Calcium a Mediator of Infarct Size Reduction With Preconditioning in Canine Myocardium?
Authors: Karin Przyklenk, Katsuya Hata, Robert A. Kloner
Journal: Circulation (1997)

The cellular mechanisms by which brief episodes of ischemia protect or "precondition" the heart and limit infarct size caused by a later period of sustained coronary artery occlusion remain unresolved. We propose that calcium may be an important mediator in eliciting this cardioprotection.To test this hypothesis, anesthetized dogs received a 15-minute intracoronary infusion of 20 mmol/L CaCl2 or saline before undergoing 1 hour of coronary occlusion and 4 hours of reperfusion (protocol 1). Collateral blood flow during occlusion was measured with radiolabeled microspheres, area at risk of infarction (AR) was delineated by injection of blue dye, and area of necrosis (AN) was determined by tetrazolium staining. AN/AR was reduced from 20+/-5% in the saline-treated controls to 9+/-3% in CaCl2-treated dogs (P<.05). Additional animals underwent 10 minutes of preconditioning ischemia or a comparable waiting period before the 1-hour test occlusion (protocol 2). Administration of 5-(N,N-dimethyl)-amiloride (an inhibitor of calcium influx via Na+-H+ and Na+-Ca2+ exchange) before the preconditioning stimulus attenuated the protective effect of ischemic preconditioning: AN/AR was 12+/-1%, larger than the value of 4+/-1% observed in preconditioned dogs that received saline (P<.05) and comparable to the values of 12+/-3% and 14+/-3% seen in saline- and dimethylamiloride-treated controls.Brief intracoronary infusion of CaCl2 mimicked, whereas treatment with dimethylamiloride blocked, infarct size reduction with preconditioning, thereby implicating calcium as a mediator of preconditioning in this canine model.
Involvement of Interferon Regulatory Factor 1 and S100C/A11 in Growth Inhibition by Transforming Growth Factor β1 in Human Hepatocellular Carcinoma Cells
Authors: Masahiro Miyazaki, Masakiyo Sakaguchi, Ichiro Akiyama, Yoshihiko Sakaguchi, Seishi Nagamori, Nam-ho Huh
Journal: Cancer Research (2004)

Abstract Growth inhibition by transforming growth factor (TGF)-β1 has been attributed to the induction of cyclin-dependent kinase inhibitors, among which p21/Waf1 plays a major role in many biological contexts. In the present study, two new intracellular mediators for the induction of p21/Waf1 by TGF-β1 were identified in a human hepatocellular carcinoma cell line (JHH-5) expressing mutant-type p53. After addition of TGF-β1 to JHH-5 cells, a marked increase of the p21/Waf1 expression preceded the inhibition of DNA synthesis. Expression of IFN regulatory factor (IRF)-1, a known transacting factor for p21/Waf1 promoter, was elevated just before or in parallel with the increase of p21/Waf1. Transduction of antisense IRF-1 inhibited the increase in p21/Waf1 in JHH-5 cells treated with TGF-β1 and partially released the cells from the growth arrest by TGF-β1. Expression of S100C/A11, a member of the Ca2+-binding S100 protein family, also markedly increased after addition of TGF-β1. S100C/A11 protein was translocated to and accumulated in nuclei of TGF-β1-treated JHH-5 cells, where p21/Waf1 was concomitantly accumulated. When a recombinant S100C/A11 protein was introduced into nuclei of JHH-5 cells, DNA synthesis was markedly inhibited in a dose-dependent manner in the absence of TGF-β1. Prior transfection of p21/Waf1-targeted small interfering RNA efficiently blocked decrease of DNA synthesis in JHH-5 cells caused by TAT-S100C/A11 or TGF-β1 and markedly inhibited expression of p21/Waf1 protein in the cells. These results indicate that IRF-1 and S100C/A11 mediate growth inhibition by TGF-β1 via induction of p21/Waf1.
Attitudes to venereal disease in a permissive society.
Authors: A S Wigfield
Journal: BMJ (1971)

The subject of permissiveness is charged with emotion, and it is difficult to know what one's attitude should be.Excessive virtue as the goal of a puritanical outlook is as undesirable as it is unattainable, and we may doubt how much former family influence, so sadly lacking today, we would like to see return.We do not want parental tyranny, though some of us would relish more filial piety.We welcome a reduction in sexual hypocrisy though moderation born of tolerance seems to have been carried to excess, and in its wake comes the greatest upsurge of venereal disease the world has probably ever known.David Reubenl says: "In spite of the shrill denials of the professional moralists, it is obvious that human beings are designed to copulate."This would appear obvious in spite of David Reuben.So are bulls designed to copulate.Again he says: "The decency leagues are trying to deprive others of the reasonable use of their sexual organs," a statement for which no evidence is forthcoming and indeed is so far from the truth as to deprive itself of rational interpretation.There is nonsense and common sense uttered in both camps, but one wonders whether Reuben's "reasonable use" applies equally to "repro- sex," "love sex," and "fun sex."What is one's reaction to be when a wife's fun sex becomes reprosex by miscalculation, especially when pursued independently of her husband, or she becomes infected?The sexually permissive section of society shows little but ignorance, indifference, or contempt for the venereal diseases.We venereologists wonder what can be done to contain them as they threaten to get out of hand.We wonder how high our graphs will climb.
Cost of preventing variceal rebleeding with transjugular intrahepatic portal systemic shunt and distal splenorenal shunt
Authors: Thomas D. Boyer, J. Michael Henderson, Adrienne M. Heerey, Susana Arrigain, Vicky Konig, Jason Connor, Kareem Abu-Elmagd, John Galloway, Layton F. Rikkers, Lennox Jeffers
Journal: Journal of Hepatology (2007)
Abstract 3413: A genetic analysis of splicing in neuroblastoma identifies opposing functions for FUBP1 splice variants in MYC regulation
Authors: Justin Chen, Christopher S. Hackett, Shile Zhang, Young K. Song, Annette Molinaro, David A. Quigley, Allan Balmain, William C. Gustafson, Terry A. Van Dyke, Pui-Yan Kwok, Javed Khan, William A. Weiss
Journal: Cancer Research (2014)

Abstract Neuroblastoma, a tumor of the peripheral neural crest, is the most common cancer of infancy and the most common extracranial solid tumor of childhood. Large scale sequencing efforts have identified recurrent mutations in only a handful of genes in a minority of patients, but these efforts have so far focused on the exome, limiting identification of mutations leading to changes in alternative splicing. Regulation of alternative splicing is a critical and tightly regulated cellular function involving a complex interplay between cis-acting sequences on the pre-mRNA transcript and accessory trans-acting splicing factors. To elucidate genetic control of splicing, we used a splicing quantitative trait loci (sQTL) analysis in a backcrossed mouse model of neuroblastoma. We utilized Affymetrix Exon Arrays to profile mRNA expression at the exon level for superior cervical ganglia and cerebella (n=102) which we coupled with genotypes at 350 SNP and microsattlelite locations. With whole-genome sequencing data available for the inbred parental strains, our approach provided us with localized sequences for each individual mouse. In addition to identifying novel candidate trans-acting splicing factors, these sQTL identify novel candidate intronic regulatory sequences critical for splicing and reveal strain-specific splicing events leading to functional consequences in neuroblastoma. Among these, we show that a subtle splicing event within FUBP1 modulates levels of the MYC oncoprotein in human neuroblastoma-derived cell lines and correlates with outcome in children with neuroblastoma. Citation Format: Justin Chen, Christopher S. Hackett, Shile Zhang, Young K. Song, Annette Molinaro, David A. Quigley, Allan Balmain, William C. Gustafson, Terry A. Van Dyke, Pui-Yan Kwok, Javed Khan, William A. Weiss. A genetic analysis of splicing in neuroblastoma identifies opposing functions for FUBP1 splice variants in MYC regulation. [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 3413. doi:10.1158/1538-7445.AM2014-3413
Abstract 386: Differential roles of uPAR in peritoneal ovarian carcinomatosis: the inflammatory link
Authors: Neveen A. Said, Nada Al-Hassan, Vessela S. Ivanova, Viqar Syed, Kouros Motamed
Journal: Cancer Research (2012)

Abstract Epithelial Ovarian cancer is the 4th leading cause of death from gynecologic malignancies in the United States. More than 75% of patients are diagnosed at late stages, with the solid tumor masses growing either as peritoneal implants, or floating within the ascitic fluid, a condition known as “peritoneal ovarian carcinomatosis (POC)”. Despite aggressive surgical treatment “debulking” recurrence, with acquired chemo- and radio-resistance are frequent with poor 5-year survival rate. Efforts to improve survival rates are hindered by suboptimal compliance with strategies that can detect, and effectively treat ovarian cancer in its early stages. A number of factors have been implicated as mediators POC, including integrins, growth factors, and proteases. The urokinase plasminogen activator receptor (uPAR) which is multifunctional receptor involved in a myriad of tumor cell processes, including invasion, ECM remodeling, adhesion, migration, angiogenesis, and metastasis. However the role of uPAR in modulating the inflammatory ovarian cancer microenvironment is still elusive. To define the potential pro-inflammatory role of uPAR in ovarian cancer, first, we characterized its expression in human ovarian cancer tissue microarray and found the expression of tumor as well as stromal uPAR is significantly upregulated as a function of tumor grade and stage. Second, using a syngeneic murine model of POC injecting ID8 cells intraperitoneally in uPAR knockout mice, we found that genetic ablation of uPAR restrained tumor take, peritoneal implants and prolonged the survival of uPAR knockout mice compared to their wild type counterparts. Ascitic fluid accumulation was significantly decreased in uPAR knockout mice with significantly lower levels of soluble pro-inflammatory cytokines/chemokines and bioactive lipids (8-isoprostane and PGE2) compared to the wildtypes. In addition, absence of uPAR was associated with decreased tumor infiltrating and associated macrophages. Third, in vitro mechanistic studies revealed that both OvCa cell- and macrophage-uPAR contributed to OvCa cell invasiveness and secretion of inflammatory mediators. In summary, our studies indicated that uPAR plays a significant role in ovarian cancer cell-macrophage crosstalk and contributes to the inflammatory ovarian cancer microenvironment. This provides a rationale for targeting the uPAR with either specific neutralizing antibodies or targeting its downstream inflammatory effectors in patients with ovarian cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 386. doi:1538-7445.AM2012-386
Transient Myocardial Damage Secondary to Extravasation of Contrast Material during Left Ventricular Angiocardiography
Authors: CHUICHI KAWAI, WALTER H. ABELMANN
Journal: Circulation (1964)

In a patient with moderate valvular aortic stenosis transient myocardial injury resulted from extravasation of contrast material into the posterolateral wall of the left ventricle during selective left ventricular cineangiocardiography via the transseptal approach. The patient developed anterior upper chest pain, runs of idioventricular rhythm followed by spontaneous return to sinus rhythm with elevated ST segments, and increase in serum transaminase levels. Lack of previous reports of transient myocardial damage secondary to extravasation of contrast material, increased possibility of such accidents with increased use of selective left ventricular angiocardiography, and possible preventive methods were emphasized.
A Multiplexed Serum Biomarker Immunoassay Panel Discriminates Clinical Lung Cancer Patients from High-Risk Individuals Found to be Cancer-Free by CT Screening
Authors: William L. Bigbee, Vanathi Gopalakrishnan, Joel L. Weissfeld, David O. Wilson, Sanja Dacic, Anna E. Lokshin, Jill M. Siegfried
Journal: Journal of Thoracic Oncology (2012)
Post-traumatic Neurosis: From Railway Spine to the Whiplash
Authors: Lawrence K. Richards
Journal: JAMA (1983)

This is a terrific little book. It is a scholarly literature review spanning over 200 years (intensively, almost 150 years), which is enjoyable reading because of the author's excellent use of the English language and historical, exciting evolutionary perspectives. There are a few photographs, illustrations, tables, and graphs, which are expertly used to augment the text. After a stimulating introduction and the recounting of a 1776 case history, the author begins a systematic description of the literature regarding spinal and head injuries of the CNS. The author's sufficiently objective view presents the reader with the historical progression of the medicolegal debate: is post-traumatic neurosis a meaningful reality or a disguise for the malingerer? In sequence, the contributors and their work appear, names ranging from the famous to the modest. Some are associated with neurology, neurosurgery, and psychiatry, others with surgery, basic science, and other areas of medicine. In chapter 3,
Attachment and chemotaxis of melanocytes after ultraviolet irradiation in vitro
Authors: M. Neitmann, M. Alexander, J. Brinckmann, P. Schlenke, M. Tronnier
Journal: British Journal of Dermatology (1999)

Journal Article Attachment and chemotaxis of melanocytes after ultraviolet irradiation in vitro Get access M. Neitmann, M. Neitmann Departments of Dermatology and Search for other works by this author on: Oxford Academic Google Scholar M. Alexander, M. Alexander Departments of Dermatology and Search for other works by this author on: Oxford Academic Google Scholar J. Brinckmann, J. Brinckmann Departments of Dermatology and Search for other works by this author on: Oxford Academic Google Scholar P. Schlenke, P. Schlenke Immunology, Medical University of Lübeck, Ratzeburger Allee 160, 23538 Lübeck, Germany Search for other works by this author on: Oxford Academic Google Scholar M. Tronnier M. Tronnier Departments of Dermatology and Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 141, Issue 5, 1 November 1999, Pages 794–801, https://doi.org/10.1046/j.1365-2133.1999.03151.x Published: 01 November 1999
Trimethylamine-N-Oxide, a Metabolite Associated with Atherosclerosis, Exhibits Complex Genetic and Dietary Regulation
Authors: Brian J. Bennett, Thomas Q. de Aguiar Vallim, Zeneng Wang, Diana M. Shih, Yonghong Meng, Jill Gregory, Hooman Allayee, Richard Lee, Mark Graham, Rosanne Crooke, Peter A. Edwards, Stanley L. Hazen, Aldons J. Lusis
Journal: Cell Metabolism (2013)
Critical Review of Recent Work on Ventricular Diastolic Suction
Authors: GERHARD A. BRECHER
Journal: Circulation Research (1958)

Unequivocal evidence in favor of the concept that a ventricular diastolic vis a fronte contributes to ventricular filling has been established only in the following conditions: a. When the ventricle contains an abnormally small residual volume (rat, dog, turtle) b. When the ventricle contains a more nearly normal, residual volume due to ejection against the resistance of a fluid column (dog, turtle). The quantitative contribution of the ventricular vis a fronte to ventricular filling at various residual volumes and various levels of cardiac activity is still unknown. The physiological significance of diastolic suction for the return flow of blood can therefore not yet he evaluated.