tbuckley/cabot-search huggingface dataset:
CD44-Activated HER-2 Signalling in Tamoxifen Resistant Breast Cancer Cells Promotes a Migratory Phenotype.
Authors: B. Baruah, P. Barrett-Lee, C. Smith, R. Nicholson, S. Hiscox
Journal: Cancer Research (2009)

Abstract Background: Acquired endocrine resistance in breast cancer cells is accompanied by altered growth factor receptor signalling. In tamoxifen-resistant ('TamR') MCF7 cells, our microarray analysis has demonstrated elevated levels of CD44, a transmembrane glycoprotein known to interact with, and modulate the function of, a number of growth factor receptors including members of the erbB family and plays a major role in tumor metastasis. Here, we have explored the role of CD44 as a modulator of erbB activity in TamR cells.Methods: Western blotting and immunocytochemistry were used to investigate expression of CD44 together with the activity of erbB signalling pathways following stimulation of CD44 by its ligand, hyaluronan (HA), or stimulation with erbB ligands (heregulin β1) after knockdown of CD44 expression using siRNA. Immunofluorescence microscopy was used to determine association between CD44 and erbB family members. Cell migration was assessed by seeding cells onto fibronectin-coated microporous inserts for 24 hours and also by performing scratch wound assays. Cell proliferation was determined by WST assay in response to trastuzumab (0-100nM) ± HAResults: CD44 was found to be over-expressed in TamR cells where it co-localized with HER-2. Whilst stimulation of HER-2 with heregulin beta-1 promoted an increase in cell migration, heregulin action was significantly attenuated in the absence of CD44 using siRNA. Moreover, treatment of TamR cells with the natural CD44 ligand, HA, promoted HER-2 signalling through MAPK and an increase in cell migration. Furthermore, whilst TamR cells were sensitive to the growth-inhibitory effects of trastuzumab, these effects were diminished in the presence of HA.Conclusions: Overexpression of CD44 sensitizes tamoxifen-resistant cells to heregulin and HA, factors commonly found within the stromal environment, with a resultant increase in migratory behaviour. Interestingly, activation of CD44 by HA appears to suppress the effects of trastuzumab on cell proliferation. Thus, CD44 may prove a valuable therapeutic target in breast cancer that expresses HER-2 and CD44. Citation Information: Cancer Res 2009;69(24 Suppl):Abstract nr 5137.
Evidence for an essential role of reactive oxygen species in the genesis of late preconditioning against myocardial stunning in conscious pigs.
Authors: J Z Sun, X L Tang, S W Park, Y Qiu, J F Turrens, R Bolli
Journal: Journal of Clinical Investigation (1996)

Conscious pigs underwent a sequence of 10 2-min coronary occlusions, each separated by 2 min of reperfusion, for three consecutive days (days 1, 2, and 3). On day 1, pigs received an i.v. infusion of a combination of antioxidants (superoxide dismutase, catalase, and N-2 mercaptopropionyl glycine; group II, n = 9), nisoldipine (group III, n = 6), or vehicle (group I [controls], n = 9). In the control group, systolic wall thickening (WTh) in the ischemic-reperfused region on day 1 remained significantly depressed for 4 h after the 10th reperfusion, indicating myocardial "stunning." On days 2 and 3, however, the recovery of WTh improved markedly, so that the total deficit of WTh decreased by 53% on day 2 and 56% on day 3 compared with day 1 (P < 0.01), indicating the development of a powerful cardioprotective response (late preconditioning against stunning). In the anti-oxidant-treated group, the total deficit of WTh on day 1 was 54% less than in the control group (P < 0.01). On day 2, the total deficit of WTh was 85% greater than that observed on day 1 and similar to that observed on day 1 in the control group. On day 3, the total deficit of WTh was 58% less than that noted on day 2 (P < 0.01). In the nisoldipine-treated group, the total deficit of WTh on day 1 was 53% less than that noted in controls (P < 0.01). On days 2 and 3, the total deficit of WTh was similar to the corresponding values in the control group. These results demonstrate that: (a) in the conscious pig, antioxidant therapy completely blocks the development of late preconditioning against stunning, indicating that the production of reactive oxygen species (ROS) on day 1 is the mechanism whereby ischemia induces the protective response observed on day 2; (b) antioxidant therapy markedly attenuates myocardial stunning on day 1, indicating that ROS play an important pathogenetic role in postischemic dysfunction in the porcine heart despite the lack of xanthine oxidase; (c) although the administration of a calcium-channel antagonist (nisoldipine) is as effective as antioxidant therapy in attenuating myocardial stunning on day 1, it has no effect on late preconditioning on day 2, indicating that the ability of antioxidants to block late preconditioning is not a nonspecific result of the mitigation of postischemic dysfunction on day 1. Generation of ROS during reperfusion is generally viewed as a deleterious process. Our finding that ROS contribute to the genesis of myocardial stunning but, at the same time, trigger the development of late preconditioning against stunning supports a complex pathophysiological paradigm, in which ROS play an immediate injurious role (as mediators of stunning) followed by a useful function (as mediators of subsequent preconditioning).
"Bell's Palsy" Caused by Basal Cell Carcinoma
Authors: Mark May
Journal: JAMA (1972)

Facial palsy may represent a serious local or generalized disease process which should not be labeled Bell's palsy until all possible causes have been excluded. Evaluation of such a patient includes topographical diagnostic studies of the facial nerve, and complete otolaryngologic examination, as well as appropriate laboratory studies. Symptoms in a region of a previous tumor may represent residual tumor even when the clinical pattern is atypical, as in this case of invasive basal cell carcinoma.
Re-invigorating Japan's commitment to global health: challenges and opportunities
Authors: Rayden Llano, Sayako Kanamori, Osamu Kunii, Rintaro Mori, Teiji Takei, Hatoko Sasaki, Yasuhide Nakamura, Kiyoshi Kurokawa, Yu Hai, Lincoln Chen, Keizo Takemi, Kenji Shibuya
Journal: The Lancet (2011)
Middle East Unites Against Cancer
Authors: Rebecca Voelker
Journal: JAMA (1996)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Inflammasome-Mediated Disease Animal Models Reveal Roles for Innate but Not Adaptive Immunity
Authors: Susannah D. Brydges, James L. Mueller, Matthew D. McGeough, Carla A. Pena, Amirhossein Misaghi, Chhavi Gandhi, Chris D. Putnam, David L. Boyle, Gary S. Firestein, Anthony A. Horner, Pejman Soroosh, Wendy T. Watford, John J. O'Shea, Daniel L. Kastner, Hal M. Hoffman
Journal: Immunity (2009)
Endoscopic removal of a band ligation device from the esophagus
Authors: R. Pokharna, K. Saini
Journal: Endoscopy (2006)

Endoscopy is the method of choice for evaluating and managing most foreign bodies in the gastrointestinal tract, with a success rate of more than 95% [1]. Foreign-body removal is carried out with various types of retrieval equipment. We report here a rare case of foreign-body removal in which a band ligation device was retrieved from the esophagus using a simple technique.
Routine measurement of fibrinogen concentration. Fibrinogen may be just a marker.
Authors: R J Jay
Journal: BMJ (1993)

Data quoted by McGavock and colleagues are sometimes misleading.They quote relapse rates for peptic ulceration of 30% after bismuth chelate treatment.However, the references they quote indicated relapse rates of 61% and 47% in patients treated with bismuth chelate alone.45To obtain the quoted improved rates of relapse with, for example, bismuth chelate and tinidazole would incur additional net NHS costs of about C69 per patient for tinidazole.Such discrepancies in quoted data further weaken the conclusions of the paper.Consideration of crude prescribing figures without regard to morbidity data, secular trends, and emerging evidence of efficacy is an insecure foundation for the criticisms which the authors make of general practitioners in Northern Ireland and, by extension, the pharmaceutical industry.Neither general practitioners nor administrators should act on the conclusions drawn from such inadequate data.
Increased plasma interleukin-6 in cutaneous plasmacytoma: the effect of intralesional steroid therapy
Authors: T. YAMAMOTO, I. KATAYAMA, K. NISHIOKA
Journal: British Journal of Dermatology (1997)

Cutaneous plasmacytosis is a rare disorder without systemic plasma cell proliferation in organs other than the skin, with a possible malignant transformation. However, there are few effective therapies available. It has been reported that interleukin-6 (IL-6), which is a cytokine inducing B-cell differentiation to immunoglobulin-producing cells, plays a part in systemic plasmacytosis. In this study, we performed intralesional steroid therapy in the lesions of cutaneous plasmacytosis in three patients, which resulted in sufficient clinical effects. We demonstrated that before treatment, plasma IL-6 levels were significantly elevated in all the patients, and that levels were reduced in parallel with the clinical improvement after therapy. Immunohistochemistry revealed IL-6 protein expression on tumour cells in the lesional skin. Reverse transcription-polymerase chain reaction (RT-PCR) detected IL-6 mRNA in the lesional skin in all cases, levels of which were decreased after the effective intralesional steroid therapy, but which were unchanged after ineffective topical photochemotherapy (PUVA). Peripheral blood mononuclear cells from the patients produced significantly large quantities of IL-6 which were reduced by addition of steroid in vitro. These results suggest that the generation of IL-6 plays the key role in cutaneous plasmacytosis and that intralesional steroid therapy is effective in reducing the production of IL-6 in this disorder.
Medical Malpractice Expert Witnessing: Introductory Guide for Physicians and Medical Professionals
Authors: Alan G. Williams
Journal: JAMA (2008)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Prevention of intestinal obstruction reveals progressive neurodegeneration in mutant TDP-43 (A315T)mice
Authors: Sarah Herdewyn, Carla Cirillo, Ludo Van Den Bosch, Wim Robberecht, Pieter Vanden Berghe, Philip Van Damme
Journal: Molecular Neurodegeneration (2014)

Intraneuronal inclusions of TAR DNA-binding protein 43 (TDP-43) have been found in the majority of Amyotrophic Lateral Sclerosis (ALS) patients. Mutations in the gene encoding TDP-43 cause familial ALS. Transgenic mice expressing mutant TDP-43 with one such mutation (TDP-43 (A315T)) under control of the murine prion promoter develop motor symptoms, but their use is currently hampered by sudden death. We aimed to understand and overcome the cause of sudden death in TDP-43 (A315T) mice. Since intestinal obstruction was suspected to be the cause, intestinal motility of TDP-43 (A315T) mice was studied in an ex-vivo pellet propulsion assay. The effect on the enteric and motor phenotype was assessed, both in animals on normal chow or on a jellified fiber deprived diet, aimed at preventing intestinal obstruction.The frequency of the propulsive motor complexes was significantly reduced in the colon of TDP-43 (A315T) compared to non transgenic (NTG) mice. Immunohistochemistry revealed significant enlargement in size and reduction in number of the nitric oxide synthase (NOS) neurons in the myenteric plexus of TDP-43 (A315T) mice. Prevention of intestinal obstruction by jellified food abolished sudden death, allowing the motor phenotype to develop and slowly progress with a more pronounced degeneration of upper and lower motor axons. A downregulation of endogenous TDP-43 mRNA and protein levels was observed prior to neurodegeneration.TDP-43 (A315T) mice suffer from intestinal dysmotility due to degeneration of NOS neurons in the myenteric plexus. Feeding the mice jellified food prevents sudden death and allows the motor phenotype to progress.
Prospective Study of Restless Legs Syndrome and Coronary Heart Disease Among Women
Authors: Yanping Li, Arthur S. Walters, Stephanie E. Chiuve, Eric B. Rimm, John W. Winkelman, Xiang Gao
Journal: Circulation (2012)

Previous cross-sectional studies suggested a positive association between restless legs syndrome (RLS) and coronary heart disease (CHD). This observation was not confirmed by subsequent prospective studies. However, these prospective studies did not take into account the duration of RLS symptoms. Therefore, we prospectively examined whether RLS was associated with an increased risk of CHD in women who participated in the Nurses' Health Study, taking into account the duration of RLS symptoms.
Drugs causing fixed eruptions
Authors: Jagjit S. Pasricha
Journal: British Journal of Dermatology (1979)

Forty patients having fixed drug eruptions were subjected to provocation tests. Twelve patients failed to complete the provocation tests while in the remaining, the causative drugs were shown to be tetracyclines (6), analgin (metamizole) (6), oxyphenbutazone (5), phenobarbitone (4), sulphadiazine (3), sulphaphenazole (2), penicillin (1), suphadimethoxone (1), Saridon (1), sulphadimidine (1) and sulphamethoxypryridazine (1). There was evidence of cross-sensitivity between tetracycline and demethylchlortetracycline and also between exyphenbutazone and phenylbutazone, but not between different sulphonamides, In 2 cases, the minimum dose of the drug capable of reactivating the lesions was 100 mg of sulphadiazine and 50 mg of Saridon respectively.
TCT-631 Clinical Outcome of Patients With Complex Lesion Treated With Bioresorbable Vascular Scaffold; Single Center Experience
Authors: Katsumasa Sato, Azeem Latib, Vasileios F. Panoulas, Hiroyoshi Kawamoto, Tadashi Miyazaki, Toru Naganuma, Antonio Colombo
Journal: Journal of the American College of Cardiology (2014)
Induction of NFATc2 Expression by Interleukin 6 Promotes T Helper Type 2 Differentiation
Authors: Sean Diehl, Chi-Wing Chow, Linda Weiss, Alois Palmetshofer, Thomas Twardzik, Laura Rounds, Edgar Serfling, Roger J. Davis, Juan Anguita, Mercedes Rincón
Journal: The Journal of Experimental Medicine (2002)

Interleukin (IL)-6 is produced by professional antigen-presenting cells (APCs) such as B cells, macrophages, and dendritic cells. It has been previously shown that APC-derived IL-6 promotes the differentiation of naive CD4+ T cells into effector T helper type 2 (Th2) cells. Here, we have studied the molecular mechanism for IL-6–mediated Th2 differentiation. During the activation of CD4+ T cells, IL-6 induces the production of IL-4, which promotes the differentiation of these cells into effector Th2 cells. Regulation of IL-4 gene expression by IL-6 is mediated by nuclear factor of activated T cells (NFAT), as inhibition of NFAT prevents IL-6–driven IL-4 production and Th2 differentiation. IL-6 upregulates NFAT transcriptional activity by increasing the levels of NFATc2. The ability of IL-6 to promote Th2 differentiation is impaired in CD4+ T cells that lack NFATc2, demonstrating that NFATc2 is required for regulation of IL-4 gene expression by IL-6. Regulation of NFATc2 expression and NFAT transcriptional activity represents a novel pathway by which IL-6 can modulate gene expression.
Dual parameter flow cytometry studies in human lymphomas.
Authors: S E Shackney, K S Skramstad, R E Cunningham, D J Dugas, T L Lincoln, R J Lukes
Journal: Journal of Clinical Investigation (1980)

Dual parameter flow cytometry studies using Coulter volume and cell DNA content were carried out in monodisperse cell suspensions of 64 samples of human lymphoma, chronic lymphocytic leukemia, hairy cell leukemia, and benign lymphoid proliferations. Differences in mean Coulter volume among the lymphomas were due both to the intrinsic differences in mean G1 cell Coulter volume and to the presence of increased fractions of larger S and G2 cells, especially among the large B cell lymphomas. However, the relative contribution of large non-G1 cells to the overall population Coulter volume distribution was a relatively minor one; the presence of cells in S did not increase mean Coulter volume by more than 10%, even in samples with high S fractions. There was a good correlation between mean G1 cell Coulter volume and the log of the fraction of cells in S among the B cell lymphomas (r = 0.55). Evidence is presented that within individual samples, large cells proliferate more rapidly than small cells. This was seen in every case, both in the normal samples and in the lymphomas, and in the T cell lymphomas as well as in the B cell lymphomas. Aneuploidy was detected by flow cytometry in 11 cases; in 7 cases the aneuploid cell component could be analyzed separately from the diploid cell component on the basis of cell Coulter volume differences. The aneuploid components of diploid-aneuploid mixtures had higher S fractions than the diploid components in six of seven cases (0.16 +/- 0.04 [SE] vs. 0.08 +/- 0.02). These findings are considered in relation to the histopathological classification of the lymphomas, and in relation to the concept of clonal selection and clonal evolution of tumors.
PROPHYLAXIS OF DISEASES OF WOMEN.
Authors: DAVID W. BASHAM
Journal: JAMA (1898)

Since the science of hygiene is justly allowed to occupy so important a place in the literature of general medicine, I deem it a duty incumbent upon those engaged in gynecologic and obstetric practice to endeavor to elevate the prophylaxis of the diseases of women to the same exalted plane. Generally the average gynecologic essayist, disdaining to concern himself with the ordinary affairs upon which our clients so much need good and wise counsel, endeavors to elucidate his own or some fellow practitioner's method of extirpating the internal genitalia, or some part thereof, from the female pelvis. All of this is laudable, because it serves a beneficent purpose as concerns both mankind and the profession of medicine. But if it be noble and great to emancipate the human body from disease and suffering by the dexterous use of the scalpel, scissors, and sterilized catgut sutures, how much better is the
Abstract 842: Role of Galectin-3 in invasive and apoptotic properties of neuroblastoma cells.
Authors: Umadevi V. Wesley, Esat Resad, Robert J. Dempsey
Journal: Cancer Research (2013)

Abstract Background: Neuroblastoma (NB) is a childhood cancer derived from the neural crest stem cells. It generally progresses to an aggressive therapy resistant, fatal metastatic tumor. MYCN over-expression and amplification, and increased BDNF/TrkB signaling are used as signatures of high-risk NB. However, only about 25% of malignant tumors display these features. Thus, the identification of additional biomarkers and therapeutic targets is essential. Up-regulation of Galectin 3 (Gal-3), a multifunctional, carbohydrate binding cytokine has been extensively correlated with highly malignant behavior and poor prognosis of many cancers. However, the role of Gal-3 in NB is largely unknown. In this study, we investigated the expression pattern of Gal-3 in a panel of NB cell lines and examined whether silencing of Gal-3 expression by means of a siRNA approach decreases their invasive properties, and increases their sensitivity to pro-apoptotic chemotherapeutic drug, fenretinide (4-HPR), a synthetic retinoid derivative. Materials and Methods: We utilized RT-PCR gene expression analysis, RNA interference approaches, western blot and immunofluorescence analysis, scratch technique, transwell Boyden chamber migration assay, colony forming assay, and cytokine antibody array screening to address these studies. Results: Gal-3 expression is differentially regulated in TrkB-positive, MYCN-amplified (SMS-KCNR and SK-N-BE) and TrkB-negative, non-MYCN-amplified (SK-N-AS, SK-N-SH, and SH-SY5Y) NB cell lines. Gal-3 expression was significantly higher in SK-N-AS cells that are of glial sub-lineage. Gal-3 was expressed both in cytoplasm and membrane. On the other hand, Gal-3 expression was relatively lower in less invasive, non-tumorigenic SK-N-SH cells. Silencing of Gal-3 by a small-interfering RNA against Gal-3 (Gal-3-SiRNA) decreased the colony forming potential, in vitro migratory and angiogenic abilities of SK-N-AS cells. Pre-treatment with Gal-3 SiRNA increased the sensitivity of SK-N-AS cells to 4-HPR induced apoptosis. Furthermore, exogenous Gal-3 treatment in neuroblast like Neuro-2a cells resulted in the up-regulation of IL-6 and phosphorylation of the pro-survival molecule AKT. Discussion: Our data suggest that Gal-3 mediates migratory and invasive phenotype of non-MYCN amplified NB derived cells possibly via regulating the IL-6 signaling and Akt phosphorylation. Silencing of Gal-3 may be potentially useful to suppress the resistance of NB cells to apoptosis. Citation Format: Umadevi V. Wesley, Esat Resad, Robert J. Dempsey. Role of Galectin-3 in invasive and apoptotic properties of neuroblastoma cells. [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 842. doi:10.1158/1538-7445.AM2013-842