tbuckley/cabot-search huggingface dataset:
Abstract 4930: A commensal relationship between tumor cell subpopulations promotes collective invasion.
Authors: Gray Pearson, Amanda Prechtl, Jill Westcott, Tuyen Dang, Erin Maine
Journal: Cancer Research (2013)

Abstract The invasion of tumor cells out of ductal epithelium is a poorly understood process that dramatically increases the odds of patient death. We have defined a new non cell-autonomous control mechanism for neoplastic invasion that trigger tumors to switch from a benign to a malignant stage of growth. Using high resolution live-imaging and functional studies we show that an epigenetically distinct and autonomously invasive subpopulation of tumor cells induces the invasion of a large bulk population of autonomously noninvasive tumor cells by adopting migratory principles observed during sprouting angiogenesis. The molecular dissection of this cooperative interaction revealed a new “invasion signature” of 29 genes that is distinct from traditional epithelial-to-mesenchymal transition markers. Patients expressing this invasion signature had a worse clinical outcome, which suggests that this commensal relationship between tumor cell subpopulations contributes to tumor progression. Functional analysis showed that multiple components of the invasion signature were specifically required for the cooperative induction of invasion, but not cell motility, thus revealing new roles for these genes as non-cell autonomous regulators of invasion. These results are of broad interest because they are the first demonstration of a commensal relationship between tumor cell subpopulations during the induction of invasion. Further, these findings establish a mechanistic underpinning that obviates the notion that the exclusive role of heterogeneity in tumors is to act as a source for unique traits that can be selected for and expanded to improve the cell autonomous fitness of neoplastic cell populations. Thus, our results support a paradigm shift towards identifying both the cell autonomous and the non cell-autonomous regulatory mechanisms of cell biological processes within heterogeneous tumors to understand neoplastic progression and develop new intervention modalities. Citation Format: Gray Pearson, Amanda Prechtl, Jill Westcott, Tuyen Dang, Erin Maine. A commensal relationship between tumor cell subpopulations promotes collective invasion. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 4930. doi:10.1158/1538-7445.AM2013-4930 Note: This abstract was not presented at the AACR Annual Meeting 2013 because the presenter was unable to attend.
Influenza Anti-Neuraminidase: The Second Best Antibody
Authors: Walter R. Dowdle
Journal: New England Journal of Medicine (1972)

The influenza virus is composed of four major structural proteins: the nucleoprotein and the membrane protein, which are located internally, and the hemagglutinin and the neuraminidase, which are located externally.1 The infected host may respond immunologically by producing antibodies to all four proteins. Since antibodies to the internal proteins appear to offer no protective advantage, our attention is directed largely toward the two external proteins.The hemagglutinin and the neuraminidase are morphologically and antigenically distinct structures on the surface of the virus. Both may independently undergo antigenic mutation. These facts have led to the institution of a completely new system . . .
Abstract 4501: Diverse microtubule stabilizers cause differential expression of mitotic kinases leading to distinct centrosomal and mitotic defects.
Authors: Cristina C. Rohena, Jiangnan Peng, Tyler A. Johnson, Phillip Crews, Susan L. Mooberry
Journal: Cancer Research (2013)

Abstract Microtubule stabilizers are some of the most useful and successful drugs used to treat adult solid tumors. However, the molecular events responsible for their antimitotic actions are not yet fully understood. In this study we evaluated the mitotic defects and signaling events initiated by three structurally and biologically different microtubule stabilizers; taccalonolide AJ, laulimalide/fijianolide B and paclitaxel. These microtubule stabilizers cause the formation of aberrant, but morphologically distinct mitotic spindles leading to the hypothesis that they initiate distinct mitotic signaling events. Each microtubule stabilizer caused different patterns of expression of key mitotic signaling proteins. Taccalonolide AJ caused centrosome separation failure to a much greater extent than paclitaxel or laulimalide. Taccalonolide AJ is also unique in that it was the only stabilizer to cause centrosome disjunction failure. These observations were consistent with the different defects in expression and activation of Plk1 and Eg5 caused by each stabilizer. Localization studies revealed that TPX2 and Aurora A are associated with each spindle aster formed by each stabilizer, which suggests a common mechanism of aster formation. However, taccalonolide AJ was the only stabilizer evaluated that caused pericentrin accumulation on every spindle aster. Pericentrin's localization to every spindle aster could facilitate the maintenance and stability of the highly focused asters formed by taccalonolide AJ. Laulimalide and paclitaxel caused completely different patterns of expression and activation of these proteins, as well as phenotypically different spindle phenotypes. Elucidating how chemically distinct microtubule stabilizers disturb mitotic signaling could identify key proteins involved in controlling sensitivity and resistance to the antimitotic actions of these agents. Citation Format: Cristina C. Rohena, Jiangnan Peng, Tyler A. Johnson, Phillip Crews, Susan L. Mooberry. Diverse microtubule stabilizers cause differential expression of mitotic kinases leading to distinct centrosomal and mitotic defects. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 4501. doi:10.1158/1538-7445.AM2013-4501
Mannose-binding lectin deficiency confers risk for bacterial infections in a large Hungarian cohort of patients with liver cirrhosis
Authors: Istvan Altorjay, Zsuzsanna Vitalis, Istvan Tornai, Karoly Palatka, Sandor Kacska, Gyula Farkas, Miklos Udvardy, Jolan Harsfalvi, Tamas Dinya, Peter Orosz, Bela Lombay, Gabriella Par, Alajos Par, Timea Csak, Janos Osztovits, Ferenc Szalay, Antal Csepregi, Peter Laszlo Lakatos, Maria Papp
Journal: Journal of Hepatology (2010)
Increased incidence of anti-LKM in a consecutive sample of HCV patients from central Greece: A preliminary study
Authors: G.N. Dalekos, E. Makri, S. Loges, P. Obermayer-Straub, Th. Tsikrikas, K. Zachou, G. Papadamou, M.P. Manns
Journal: Journal of Hepatology (2000)
Adaptive differentiation of murine lymphocytes. II. The thymic microenvironment does not restrict the cooperative partner cell preference of helper T cells differentiating in F1 leads to F1 thymic chimeras.
Authors: D H Katz, L R Katz, C A Bogowitz, B J Skidmore
Journal: The Journal of Experimental Medicine (1979)

The cooperating preference of helper T cells originating from F1 bone marrow, but differentiating in adult thymectomized, lethally irradiated F1 recipients reconstituted with either f1 or homozygous parental thymus grafts was investigated. Cooperating preference was assayed by determining the levels of helper activity provided by antigen-primed T cells derived from such thymic chimeras for hapten-primed B lymphocytes obtained from conventional F1 or parental donors in adoptive secondary antibody responses in vivo. The results of these analyses revealed a tendency of helper T cells derived from parental thymic chimeras to provide better help for B cells of the same parental type corresponding to the origin of the thymus graft than for the opposite parent. Such preference was, however, only marginal and rarely were differences in levels of helper activity provided to the respective parental types statistically significant. Moreover, this marginal preference, when observed, pertained only to responses of the IgG class; no concordant preference in providing helper activity for IgE antibody responses was observed even with the same populations of thymic chimera helper T cells. Finally, in no instance was there any evidence of restriction in the classical sense of presence versus absence of help as we have routinely observed in all of our previous studies concerning genetic restrictions of T-B-cell cooperative interactions. Although the basis for differences in the studies reported here when compared to observations made in cytotoxic T-lymphocyte systems is unclear, and could reflect genuine mechanistic requirements concerning what directs H-2 restrictions in helper T cells and cytotoxic T lymphocytes, respectively, it is also possible that we are placing too much faith in our interpretations of data obtained in bone marrow chimera systems than is perhaps justified by the potentially great fragility of such systems.
Abstract 1445: Thyroid hormone receptor represses microRNA-130b to enhance cell metastasis
Authors: Yang Hsiang Lin, Meng-Han Wu, Yung-Hsin Yeh, Angel Chao, Kwang-Huei Lin
Journal: Cancer Research (2014)

Abstract Thyroid hormone (T3) and its receptor (TR) are involved in cell growth and cancer progression. Although deregulation of miRNA expression has been detected in many tumor types, the mechanisms underlying functional impairment and specific involvement of miRNA in tumor metastasis remain unclear. We proposed that deregulation of specific miRNAs and target gene expressions mediated by T3/TR constitute critical steps of cancer progression. In the current study, we demonstrated that T3/TR negatively regulates microRNA-130b (miR-130b) expression, both in vitro and in vivo. Overexpression of miR-130b markedly inhibited cell migration and invasion in vitro and in vivo, which was mediated via suppression of interferon regulatory factor 1 (IRF1). Cell migration ability was promoted by T3, but partially suppressed upon miR-130b overexpression. Furthermore, miR-130b suppressed the expression of epithelial-mesenchymal transition (EMT)-related genes, matrix metalloproteinase (MMP)-9, p-AKT and p-signal transducer and activator of transcription (STAT)-3. Notably, miR-130b was downregulated in hepatoma samples and inversely correlated with TR and IRF1. Our data collectively highlight a novel pathway interlinking T3/TR, miR-130b, EMT-related genes, MMP9, p-AKT and p-STAT3 cascade that regulates the motility and invasion of hepatoma cells. Thus, miR-130b activation may be a useful strategy for cancer treatment in metastatic HCC. Citation Format: Yang Hsiang Lin, Meng-Han Wu, Yung-Hsin Yeh, Angel Chao, Kwang-Huei Lin. Thyroid hormone receptor represses microRNA-130b to enhance cell metastasis. [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 1445. doi:10.1158/1538-7445.AM2014-1445
On the virtues of going all the way
Authors: Shimon Edelman, Elise M. Breen
Journal: Behavioral and Brain Sciences (1999)

Representational systems need to use symbols as internal stand-ins for distal quantities and events. Barsalou's ideas go a long way towards making the symbol system theory of representation more appealing, by delegating one critical part of the representational burden – dealing with the constituents of compound structures – to image-like entities. The target article, however, leaves the other critical component of any symbol system theory – the compositional ability to bind the constituents together – underspecified. We point out that the binding problem can be alleviated if a perceptual symbol system is made to rely on image-like entities not only for grounding the constituent symbols, but also for composing these into structures.
Medical Physiology and Biophysics
Authors: Roderick E. Darby
Journal: JAMA (1961)

The title of this new edition of what was formerly<i>Howell's Textbook of Physiology</i>is appropriate, because physiology is becoming progressively more closely associated with the other basic sciences. Over 20 authors (physiologists, biophysicists, anatomists, biologists, biochemists, and physicians) contributed to this volume. The sections on the physiology of reproduction and the endocrine system have been extensively revised; many chapters have been rewritten; and two chapters, one on the biophysics of the cell membrane and one on the neurophysiology of emotion and motivation, have been added. The three chapters which deal with nutrition and energy transformations in muscle and nerve cells have been omitted. More pathological physiology is presented in this edition whenever a clinical entity better explains a physiological concept or mechanism. Many new diagrams and graphs have been added. This is an excellent basic textbook of physiology for medical students. It also serves as a reliable, current reference
Downregulation of male-specific cytochrome P450s 2C11 and 3A2 in bile duct–ligated male rats: Importance to reduced hepatic content of cytochrome P450 in cholestasis
Authors: Jiezhong Chen, Michael Murray, Christopher Liddle, Xing-Mai Jiang, Geoffrey C. Farrell
Journal: Hepatology (1995)

The effects of bile duct ligation (BDL) on the activity and content of individual hepatic mixed-function oxidases (MFOs) was examined. Five days after BDL, hepatic microsomal total cytochrome P450 (CYP) content and NADPH-cytochrome P450-reductase (P450-reductase) activity were reduced to 56% and 57% of control, respectively. MFO activities attributable to the sexually undifferentiated CYPs 1A, 2A1, 2C6, and 2E1 were decreased to 32% to 52% of control, but the activities of two male sex-specific CYPs, 2C11 and 3A2, were reduced to a significantly greater extent (P < .05). The microsomal contents of CYP proteins 2C6 and 2E1 were decreased after BDL to 61% and 63% of control, whereas 2C11 and 3A2 proteins were 21% and 45% of control. Corresponding reductions of the messenger RNA (mRNA) species for CYP 2C11 (9% of control) and 3A2 (37%) were detected, whereas there was no reduction of 2C6 mRNA. These findings are consistent with downregulation of the CYP 2C11 and 3A2 genes. Nuclear run-on studies performed 3 days after BDL showed that there was a generalized impairment of gene transcription after BDL, but a disproportionate reduction in transcription of CYPs 2C11 and 3A2. A possible explanation for downregulation of CYP 2C11 and 3A2 was provided by the observation that serum estradiol concentrations were threefold greater in BDL male rats, while serum testosterone was reduced; estradiol is known to downregulate CYPs 2C11 and 3A2. It is concluded that male sex-specific CYP enzymes are decreased to a greater extent than other microsomal proteins in BDL male rats.(ABSTRACT TRUNCATED AT 250 WORDS)
Racial differences in mortality among elderly patients hospitalized with heart failure
Authors: Saif S. Rathore, JoAnne M. Foody, Yongfei Wang, Grace L. Smith, Jeph Herrin, Frederick A. Masoudi, Diana L. Ordin, Edward L. Havranek, Harlan M. Krumholz
Journal: Journal of the American College of Cardiology (2003)
Hypothermia from Erythromycin
Authors: Bjørnar Hassel
Journal: Annals of Internal Medicine (1991)

Letters1 July 1991Hypothermia from ErythromycinBjørnar Hassel, MDBjørnar Hassel, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-115-1-69_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the Editors: Hypothermia in association with antibiotic therapy has never been reported in the medical literature. I report two cases of hypothermia that occurred during erythromycin treatment.A 3-year-old boy with atopic eczema and mild, untreated bronchial asthma developed purulent bronchitis and a rectal temperature of 39.5 °C. He received erythromycin, 100 mg four times a day in an oral solution. After the third dose, he became increasingly somnolent and unresponsive; his skin became pale, cold, and clammy, and his muscles became slack. Respiration was unaffected. Rectal temperature was 34.3 °C. He had not received any medication other than... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Norwegian Defence Research Establishment N-2007 Kjeller Norway PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByHypothermia from a two‐component mixture comprising Amoxicillin and SulbactamHypothermia from AzithromycinPenicillins, cephalosporins, and tetracyclinesThrombotic thrombocytopenic purpura due to rifampicin.Parotitis due to nicardipine.Acute hypothermia due to penicillin. 1 July 1991Volume 115, Issue 1Page: 69-70KeywordsAntibioticsAsthmaBronchitisEczemaErythromycinHypothermiaMusclesRespirationTemperature Issue Published: 1 July 1991 PDF DownloadLoading ...
Immune Mechanisms In Graves' Disease
Authors: KENNETH D. BURMAN, JAMES R. BAKER
Journal: Endocrine Reviews (1985)

GRAVES' DISEASE is an autoimmune disorder characterized by the presence of stimulatory anti-TSH receptor antibodies which are thought to act via the TSH receptor to increase iodide uptake and cyclic AMP (cAMP), in turn, resulting in T3 and T4 production and secretion (1–7). There have been many clinical articles published summarizing the clinical and laboratory manifestations of Graves' disease (1–7) and excellent reviews of "Autoimmune Thyroid Disease" by Weetman and McGregor (2) and of "Endocrine Ophthalmopathy" by Jacobson and Gorman (8) have been published recently. The purpose of the present review is to discuss in detail the known and suspected immunologic mechanisms which are important in mediating or aggravating Graves' disease and its associated clinical findings. This review will emphasize that our present understanding of normal immune mechanisms of antibody formation, in addition to our comprehension of the perturbations leading to Graves' disease, is inadequate.
Hypertension in Cushing's Syndrome
Authors: Henry Mannix
Journal: JAMA (1962)

The majority of patients with Cushing's syndrome have hypertension as one of the important findings. There also may be a deficit in cholesterol metabolism, but the mechanism is not altogether clear. Although Cushing's syndrome has been treated with an agent that inhibits cholesterol biosynthesis, it is felt at the present time that surgery is the preferred treatment—first, because the mortality is very low; second, because 25 per cent of cases are due to tumors; and finally, because the long-term atherogenic effects of these inhibitors are not known.
Reversible Septal Perfusion Abnormality in a Patient with Left Bundle Branch Block on TI-201 SPECT Imaging at Rest
Authors: MOHAN MAKHIJA, MICHAEL DISIGLIO
Journal: Clinical Nuclear Medicine (1992)

Reversible septa1 perfusion abnormalities mimicking stress-induced ischemia have been reported in patients who have left bundle branch block (LBBB) but no coronary artery disease observed on TI-201 SPECT imaging or planar imaging at exercise stress. Normal TI-201 imaging results have been reported in patients with LBBB and no acute myocardial infarction. Findings consistent with anteroseptal myocardial infarction in the absence of coronary artery disease have been reported in patients with LBBB on resting studies with potassium-43 or rubidium81, but not with TI-201 SPECT imaging. The authors describe a patient with LBBB and no infarction, mimicking myocardial infarction of the septum on TI-201 SPECT
Immunologic behavior of lymphocytes in experimental viral myocarditis: significance of T lymphocytes in the severity of myocarditis and silent myocarditis in BALB/c-nu/nu mice.
Authors: C Kishimoto, K Kuribayashi, T Masuda, N Tomioka, C Kawai
Journal: Circulation (1985)

To clarify the immune mechanism in myocarditis, we examined by immunofluorescence techniques the serial changes in percentages of T and B lymphocytes in the heart, spleen, and peripheral blood of DBA/2 mice inoculated with encephalomyocarditis (EMC) virus (experiment I). B cells were demonstrated by staining with fluorescein isothiocyanate (FITC)-labeled rabbit antimouse immunoglobulin (Ig). T cells were demonstrated with rat anti-Thy1.2 monoclonal antibody plus FITC-labeled antimouse Ig. There was a marked decrease in T cells in peripheral blood and a moderate decrease in the cells in the spleen on day 14. There were no significant changes in B cells in peripheral blood or spleen throughout the entire period and T cells accounted for approximately 80% of the cells in the myocardium on days 7 and 14. To confirm the involvement of T cells in the development of myocarditis, we also carried out studies in which BALB/c-nu/nu mice (group 1, n = 58), BALB/c-nu/+ mice (group 2, n = 54), and BALB/c-nu/nu mice injected with 5 X 10(7) spleen cells from BALB/c-nu/+ mice (group 3, n = 50) were inoculated with EMC virus (experiment II). Four mice from each of the three groups were killed on day 6 for virologic studies. In experiment II, there were no significant differences in the incidence of myocarditis among the three groups. Virus titrations of the heart and serum neutralizing antibody titers did not show any significant differences between the three groups on days 6 and 16.(ABSTRACT TRUNCATED AT 250 WORDS)
Work of a nurse in a health centre treatment room
Authors: P. N. Dixon
Journal: BMJ (1969)

In six months there were 1,704 attendances at the treatment room of a small health centre. The attendance rate for the population registered with the health centre doctors was 448 per 1,000 patients per year. Females between 15 and 44 years and males under 15 had the highest attendance rates. There were 256 casual attenders, 58 (23%) of whom were referred to a doctor or hospital for further advice or treatment. It is suggested that in a health centre treatment room about six hours of nursing time a week for every 1,000 patients is required, and that a case can be made out for some of the routine work of casualty departments being done in health centres.