tbuckley/cabot-search huggingface dataset:
Differential regulation of thrombospondin-1 and fibronectin by angiotensin II receptor subtypes in cultured endothelial cells
Authors: Jens W Fischer, Monika Stoll, Alfred W.A Hahn, Thomas Unger
Journal: Cardiovascular Research (2001)

Angiotensin II (ANG II) can modulate cellular proliferation in various cell types via AT(1) and AT(2) receptors. In the present study, we investigated the effect of the angiotensin AT(1) and AT(2) receptors on DNA-synthesis as well as on the expression of the extracellular matrix (ECM) components, thrombospondin-1 (TSP-1) and fibronectin (FN) in endothelial cells (EC).The experiments were performed in microvascular EC derived from rat heart (CEC) and macrovascular EC derived from bovine aorta (BAEC). The experiments were performed in cells of the second and third passage and the expression of AT(1) and AT(2) receptors was verified by binding studies, Northern analysis or RT-PCR. Quiescent rat CEC and BAEC were stimulated to proliferate by the addition of 25 ng/ml bFGF, while ANG II (10(-7) M) and the selective ANG II receptor antagonists, Losartan (10(-5) M) and PD123177 (10(-6) M) or the AT(2) agonist, CGP42112A (10(-7) M) were added 16 h later.ANG II induced a dose-dependent decrease of DNA-synthesis in BAEC measured by [3H]-thymidine incorporation. This inhibitory effect of ANG II was prevented by the addition of the AT(2) receptor antagonist PD123177 (10(-6) M), demonstrating, that the inhibition of DNA synthesis is mediated by the AT(2) receptor. In the presence of Losartan, stimulation of both, CEC and BAEC, with ANG II resulted in a marked increase of TSP-1 mRNA levels, which was maximal between 3 and 6 h in rat CEC and after 9 h in BAEC. In addition, TSP-1 was clearly induced by the AT(2) agonist CGP42112A. In contrast, blockade of the AT(2) receptor by the selective AT(2) antagonist, PD123177 (10(-6) M), resulted in a pronounced down regulation of FN mRNA 9 h after the stimulation.The present results suggest that the ANG II receptor subtype AT(2) mediates growth inhibition in macrovascular EC similar to what has been shown before in microvascular rat EC and that AT(2) receptors mediates remodeling of the endothelial ECM by upregulation of TSP-1 expression in both macro- and micro-vascular endothelial cells.
Acute Quadriplegia in Acromegaly
Authors: Ken Tanigawa, Shunichi Yamashita, Shigenobu Nagataki
Journal: Annals of Internal Medicine (1992)

Letters1 July 1992Acute Quadriplegia in AcromegalyKen Tanigawa, MD, Shunichi Yamashita, MD, Shigenobu Nagataki, MDKen Tanigawa, MDSearch for more papers by this author, Shunichi Yamashita, MDSearch for more papers by this author, Shigenobu Nagataki, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-117-1-94_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the Editors: The pathophysiology of acromegaly has been well-reviewed (1). Although enlargement is observed in soft tissue and cartilage, it is variable in bone, with a few reports of involvement of the cervical spine (2-5). We report a case of a 52-year-old Japanese man admitted for the chief symptoms of hand numbness and gait disturbance, which gradually progressed over a 2-year period to paresthesia of the hands and gait disturbance.Physical examination and laboratory investigations showed the classic stigmata of acromegaly. On neurologic examination, there was decreased strength of the flexor carpi muscles of the right hand, hypesthesia of...References1. Melmed S. Acromegaly. N Engl J Med. 1990;322:966-77. CrossrefMedlineGoogle Scholar2. Gelman M. Cauda equina compression in acromegaly. Radiology. 1974;112:3547-60. CrossrefGoogle Scholar3. EpsteinWhelanBenjamin NMV. Acromegaly and spinal stenosis. J Neurosurg. 1982;56:145-7. CrossrefMedlineGoogle Scholar4. ParikhIyerEliasGwinup MKAG. Spinal stenosis in acromegaly. Spine. 1987;12:627-8. CrossrefMedlineGoogle Scholar5. DiamondNeryPosen TLS. Spinal and peripheral bone mineral densities in acromegaly: the effect of excess growth hormone and hypogonadism. Ann Intern Med. 1989;11:567-73. LinkGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: Ken Tanigawa, MD; Shunichi Yamashita, MD; Shigenobu Nagataki, MDAffiliations: Nagasaki University School of Medicine Sakamoto Nagasaki 852 Japan PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byA 1 July 1992Volume 117, Issue 1Page: 94-95KeywordsAcromegalyBoneCartilageHand strengthMusclesResearch laboratoriesSoft tissuesSpine ePublished: 1 December 2008 Issue Published: 1 July 1992 PDF downloadLoading ...
SKIN RASHES FOLLOWING THE ADMINISTRATION OF ATOPHAN
Authors: JOHN PHILLIPS
Journal: JAMA (1913)

During the past two years atophan has been used extensively in the treatment of gout, arthritis of different forms and neuritis. Its use has also been recommended in migraine, sciatica, lumbago, iritis, episcleritis, otosclerosis, pyorrhea alveolaris, eczema and urticaria. The purpose of this paper is to call attention to the occurrence of various skin rashes—purpura, urticaria and scarlatiniform eruptions—caused by the administration of atophan as exemplified in the cases reported herewith.  REPORT OF CASES  CASE 1.  —Man, aged 56, who for twelve years had suffered from the polyarticular form of arthritis deformans, was first given atophan in July, 1911, 7½ grains being administered four times daily. Ten days later a purpuric eruption appeared over the anterior surface of the lower extremities, extending from the knee down to the dorsum of the foot. The lesions were in the form of numerous small petechiae. The medicine was discontinued and in
Abstract 4368: Vitamin E and the green tea active agent EGCG suppress radiation-induced carcinogenesis by different molecular mechanisms
Authors: Marc S. Mendonca, Anthony Borgman, Helen Chin-Sinex, Ryan Dhaemers
Journal: Cancer Research (2010)

Abstract Treatment induced secondary malignancies after successful radiation and/or chemotherapy cure of primary tumors is a growing area of concern. The identification of chemopreventive compounds that reduce radiation-induced secondary malignancy but are both nontoxic and tolerated with long-term use is a critical need. We investigated the chemopreventive potential and mechanism of action of Vitamin E and EGCG (the active agent in green tea) with the human CGL1 radiation neoplastic transformation assay. The molecularly characterized CGL1 assay allows both alterations of the quantitative neoplastic transformation as well the potential underlying molecular processes of the chemoprevention to be determined. We found long-term treatment with 15 microM EGCG or 50 microM Vitamin E beginning 72 hours after 7 Gy irradiation, significantly reduce radiation-induced neoplastic transformation frequency by a factor of 2.3. We determined that Vit E suppressed radiation-induced carcinogenesis by the induction of a p53 and pro-apoptotic Bax dependent apoptosis in the progeny of the irradiated cells. In addition, we demonstrated that EGCG does not reduce radiation-induced carcinogenesis by increased apoptosis, but rather by the onset of p16 dependent senescence in the irradiated CGL1 progeny. Vit E and EGCG are excellent candidate nontoxic chemopreventive agents for radiation-induced carcinogenesis that work by two distinct molecular mechanisms. We propose that this information should also aid in the development of next generation chemopreventive compounds. These studies were supported by a grant from the DOD awarded to MSM. 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 4368.
General Medical Council rejects complaint brought by a member
Authors: C. Dyer
Journal: BMJ (2002)

The General Medical Council has rejected a complaint by one of its own members that two hospital consultants were guilty of serious professional misconduct in criticising her. She said that they made “derogatory and denigratory comments” about her in email responses to a BMJ news story published last year (2001;322: 1565).

The email letters were posted on the BMJ 's website, and are reproduced in the letters section of the BMJ today.

Council member Jennifer Colman accused Paul Diggory, consultant in elderly care medicine at Mayday University Hospital, Croydon, and Wendy Franks, consultant ophthalmologist at Moorfields Eye Hospital, London, of misconduct for …
Influenza Vaccine in Renal Disease
Authors: Gary R. Noble
Journal: JAMA (1978)

Recommendations<sup>1,2</sup>that patients with chronic renal disease should be given influenza vaccine annually are based on three premises: (1) patients with renal failure have a higher than normal mortality following influenza infection; (2) influenza vaccine may reduce morbidity and mortality in these patients; (3) the vaccine does not cause a substantial reduction in their renal function nor does it increase the risk of organ rejection in patients with renal allografts. The first premise is supported by the observations of Eickhoff et al,<sup>3</sup>who found that during the Asian influenza epidemic of 1957, more deaths from chronic nephritis or cardiovascular renal disease were reported than were expected from projections based on mortality in preceding years. There is also some suggestion of increased risk of renal allograft rejection following influenza A or B infection.<sup>4,5</sup>The mechanisms by which influenza infection may cause increased mortality and the precise degree of risk
To Buy or Not to Buy
Authors: Gerard Anderson, Earl Steinberg
Journal: New England Journal of Medicine (1984)

With the passage of the Medicare prospective-payment legislation1 and issuance of the subsequent regulations,2 hospital administrators (and to a lesser degree, physicians) have focused their attention on the question whether the current payment rales for diagnosis-related groups (DRGs) are sufficient to cover the costs of caring for patients with the technological arsenal that is already in place in hospitals. Considerably less attention has been directed at the impact the recent legislation may have on the rate at which hospitals will be able to acquire new diagnostic and therapeutic technology.The new payment system is predicated on a belief that under . . .
Do We Need the Overtube for Push-Enteroscopy?
Authors: C. Benz, R. Jakobs, J. F. Riemann
Journal: Endoscopy (2001)

Background and Aims: Push-enteroscopy is well established in many gastroenterological departments. There is no agreement about whether the use of an overtube is helpful to optimize the depth of insertion. In this prospective and randomized study we investigated the effect of the overtube for push-type enteroscopy.
Persistence of Contractile Behaviour in Acutely Ischaemic Myocardium
Authors: W. B. Hood, V. H. Covelli, W. H. Abelmann, J. C. Norman
Journal: Cardiovascular Research (1969)

Experiments were performed in pigs and dogs which showed that myocardium rendered acutely ischaemic by occluding the left anterior descending coronary artery nonetheless maintained contractile behaviour. The ischaemic myocardium responded to both positive and negative inotropic agents, and, despite aneurysmal dilatation during systole, was less distensible than at necropsy. These effects could be quantitated by application of force-velocity relationships.
Circulating chemokine (C-X-C Motif) receptor 5+CD4+ T cells benefit hepatitis B e antigen seroconversion through IL-21 in patients with chronic hepatitis B virus infection
Authors: Yongyin Li, Shiwu Ma, Libo Tang, Yun Li, Wei Wang, Xuan Huang, Qintao Lai, Mingxia Zhang, Jian Sun, Chris Kafai Li, William G.H. Abbott, Nikolai V. Naoumov, Yu Zhang, Jinlin Hou
Journal: Hepatology (2013)

Given the clinical significance of hepatitis B e antigen (HBeAg) seroconversion in chronic hepatitis B virus (HBV) infection, it is critical to elucidate the mechanisms regulating this process. In the present study, we found that the frequency of circulating chemokine (C-X-C motif) receptor 5 (CXCR5)(+) CD4(+) T cells was higher in patients who had achieved HBeAg seroconversion in both cross-sectional (P < 0.001) and longitudinal (P = 0.009) studies. These cells were able to produce a significantly higher level of intracellular interleukin 21 (IL-21) after stimulation with HBV peptides in patients with telbivudine-induced HBeAg seroconversion (P = 0.007). Furthermore, sorted CXCR5(+) CD4(+) T cells from HBeAg seroconverters boosted a higher frequency of antibody against hepatitis B e antigen (anti-HBe)-secreting B cells in coculture assay (P = 0.011). Of note, the increase in frequency of anti-HBe-secreting B cells was abrogated by soluble recombinant IL-21 receptor-Fc chimera (P = 0.027), whereas exogenous recombinant IL-21 enhanced this effect (P = 0.043). Additionally, circulating CXCR5(+) CD4(+) T cells shared similar phenotypic markers, and were positively correlated in frequency with, splenic follicular T helper cells.Circulating CXCR5(+) CD4(+) T cells, by producing IL-21, may have a significant role in facilitating HBeAg seroconversion in patients with chronic HBV infection.
Therapy of Hyponatremia
Authors: Robert G. Narins
Journal: New England Journal of Medicine (1986)

Worsening weakness, lethargy, and nausea merge with progressive headache and obtundation to culminate in generalized seizures, coma, and ultimately death. This noxious sequence describes equally well the effects of worsening hyponatremia or hypernatremia and underscores the importance of the central nervous system in syndromes of disordered water balance. In two contributions to this issue, Arieff1 and Sterns and his colleagues2 describe 23 patients with hyponatremia who had fatal or permanently crippling central nervous system effects. Unfortunately, the authors leave unsettled whether it was the severity of the hyponatremia or its speed of correction that caused these neuropathologic complications. Were their . . .
Toxicogenomics in risk assessment: an overview of an HESI collaborative research program.
Authors: William Pennie, Syril D Pettit, Peter G Lord
Journal: Environmental Health Perspectives (2004)

The value of genomic approaches in hypothesis generation is being realized as a tool for understanding toxicity and consequently contributing to an assessment of drug and chemical safety. In 1999 the membership of the International Life Sciences Institute Health and Environmental Sciences Institute formed a committee to develop a collaborative scientific program to address issues, challenges, and opportunities afforded by the emerging field of toxicogenomics. Experts and advisors from academia and government laboratories participate on the committee, along with approximately 30 corporate member organizations from the pharmaceutical, agrochemical, chemical, and consumer products industries. The committee has designed, conducted, and analyzed numerous toxicogenomic experiments within the broad fields of hepatotoxicity, nephrotoxicity, and genotoxicity. The considerable body of data generated by these programs has been instrumental in increasing understanding of sources of biological and technical variability in the alignment of toxicant-induced transcription changes with the accepted mechanism of action of these agents and the challenges in the consistent analysis and sharing of the voluminous data sets generated by these approaches. Recognizing the importance of standardized microarray data formats and public repository databases as the mechanism by which microarray data can be compared and interpreted by the scientific community, the committee has partnered with the European Bioinformatics Institute to develop a database to house the data generated by its collaborative research.
Disrupted working body schema of the trunk in people with back pain
Authors: H Bray, G L Moseley
Journal: British Journal of Sports Medicine (2009)

Background To test whether working body schema of the trunk is disrupted in people with back pain using a motor imagery task in which one decides whether a pictured model has their trunk rotated to the left or to the right. The authors hypothesised that chronic back pain is associated with reduced accuracy of left/right trunk rotation judgements. Methods 21 Patients with back pain and 14 controls completed two tasks, each involving two trials of 40 images: a left/right hand judgement task, which was used as a control task, and the left/right trunk rotation judgement task. Two (task) × three (group: bilateral back pain, unilateral back pain and control) analyses of variance were undertaken on mean response time and accuracy. Results Response time was similar across participants and tasks (NS). Accuracy was not. The patients with bilateral back pain made more mistakes on the left/right trunk rotation task than patients with unilateral back pain, who in turn made more mistakes on that task than the controls (body part × group interaction; p&lt;0.001). The mean (95% CI) accuracy for left/right trunk rotation judgements was 53.4% (44.5% to 62.3%) for the patients with bilateral back pain, 67.2% (60.2% to 74.1%) for the patients with unilateral back pain and 87% (75% to 98%) for the control participants. This pattern was not observed on the left/right-hand judgement task, on which all three groups made correct judgements about 83% of the time (NS). Discussion Chronic back pain is associated with disruption of the working body schema of the trunk. This might be an important contributor to motor control abnormalities seen in this population.
Extensive Neuronal Differentiation of Human Neural Stem Cell Grafts in Adult Rat Spinal Cord
Authors: Jun Yan, Leyan Xu, Annie M Welsh, Glen Hatfield, Thomas Hazel, Karl Johe, Vassilis E Koliatsos
Journal: PLoS Medicine (2007)

Effective treatments for degenerative and traumatic diseases of the nervous system are not currently available. The support or replacement of injured neurons with neural grafts, already an established approach in experimental therapeutics, has been recently invigorated with the addition of neural and embryonic stem-derived precursors as inexhaustible, self-propagating alternatives to fetal tissues. The adult spinal cord, i.e., the site of common devastating injuries and motor neuron disease, has been an especially challenging target for stem cell therapies. In most cases, neural stem cell (NSC) transplants have shown either poor differentiation or a preferential choice of glial lineages.In the present investigation, we grafted NSCs from human fetal spinal cord grown in monolayer into the lumbar cord of normal or injured adult nude rats and observed large-scale differentiation of these cells into neurons that formed axons and synapses and established extensive contacts with host motor neurons. Spinal cord microenvironment appeared to influence fate choice, with centrally located cells taking on a predominant neuronal path, and cells located under the pia membrane persisting as NSCs or presenting with astrocytic phenotypes. Slightly fewer than one-tenth of grafted neurons differentiated into oligodendrocytes. The presence of lesions increased the frequency of astrocytic phenotypes in the white matter.NSC grafts can show substantial neuronal differentiation in the normal and injured adult spinal cord with good potential of integration into host neural circuits. In view of recent similar findings from other laboratories, the extent of neuronal differentiation observed here disputes the notion of a spinal cord that is constitutively unfavorable to neuronal repair. Restoration of spinal cord circuitry in traumatic and degenerative diseases may be more realistic than previously thought, although major challenges remain, especially with respect to the establishment of neuromuscular connections.
Gastric Hyperplasia and Increased Proliferative Responses of Lymphocytes in Mice Lacking the COOH-terminal Ankyrin Domain of NF-κB2
Authors: Hideaki Ishikawa, Daniel Carrasco, Estefania Claudio, Rolf-Peter Ryseck, Rodrigo Bravo
Journal: The Journal of Experimental Medicine (1997)

The nfkb2 gene encodes the p100 precursor which produces the p52 protein after proteolytic cleavage of its COOH-terminal domain. Although the p52 product can act as an alternative subunit of NF-kappaB, the p100 precursor is believed to function as an inhibitor of Rel/NF-kappaB activity by cytoplasmic retention of Rel/NF-kappaB complexes, like other members of the IkappaB family. However, the physiological relevance of the p100 precursor as an IkappaB molecule has not been understood. To assess the role of the precursor in vivo, we generated, by gene targeting, mice lacking p100 but still containing a functional p52 protein. Mice with a homozygous deletion of the COOH-terminal ankyrin repeats of NF-kappaB2 (p100(-/-)) had marked gastric hyperplasia, resulting in early postnatal death. p100(-/-) animals also presented histopathological alterations of hematopoietic tissues, enlarged lymph nodes, increased lymphocyte proliferation in response to several stimuli, and enhanced cytokine production in activated T cells. Dramatic induction of nuclear kappaB-binding activity composed of p52-containing complexes was found in all tissues examined and also in stimulated lymphocytes. Thus, the p100 precursor is essential for the proper regulation of p52-containing Rel/NF-kappaB complexes in various cell types and its absence cannot be efficiently compensated for by other IkappaB proteins.
A Randomized Assessment of the Incremental Role of Ablation of Complex Fractionated Atrial Electrograms After Antral Pulmonary Vein Isolation for Long-Lasting Persistent Atrial Fibrillation
Authors: Hakan Oral, Aman Chugh, Kentaro Yoshida, Jean F. Sarrazin, Michael Kuhne, Thomas Crawford, Nagib Chalfoun, Darryl Wells, Warangkna Boonyapisit, Srikar Veerareddy, Sreedhar Billakanty, Wai S. Wong, Eric Good, Krit Jongnarangsin, Frank Pelosi, Frank Bogun, Fred Morady
Journal: Journal of the American College of Cardiology (2009)
Nitrofurantoin cytotoxicity. In vitro assessment of risk based on glutathione metabolism.
Authors: S P Spielberg, G B Gordon
Journal: Journal of Clinical Investigation (1981)

Nitrofurantoin, a commonly used urinary tract antiseptic, has been associated with idiosyncratic pulmonary and hepatic damage. We have used human lymphocytes in vitro to explore the biochemical basis of susceptibility to nitrofurantoin toxicity. The drug itself did not damage the cells as assessed by trypan blue dye exclusion. In the presence of a mouse hepatic microsomal drug-activating system, however, nitrofurantoin metabolites produced dose dependent toxicity to the lymphocytes. Inhibition of the enzyme epoxide hydrolase did not enhance toxicity; the metabolite thus does not appear to be a furan epoxide. Binding of reactive metabolites to cell macromolecules may lead directly to cell death, or in vivo, by acting as haptens to secondary immunologic responses. The metabolite caused a dose-dependent depletion of lymphocyte glutathione content. Cells from a patient with glutathione synthetase deficiency showed markedly enhanced nitrofurantoin toxicity. The findings suggest that glutathione plays a major role in protecting cells from nitrofurantoin-induced damage, and that studies of lymphocyte toxicity and glutathione metabolism in patients experiencing idiosyncratic reactions to nitrofurantoin may lead to elucidation of the biochemical and genetic basis of drug susceptibility.