tbuckley/cabot-search huggingface dataset:
Wnt-signalling pathways and microRNAs network in carcinogenesis: experimental and bioinformatics approaches
Authors: Emenike K. Onyido, Eloise Sweeney, Abdolrahman Shams Nateri
Journal: Molecular Cancer (2016)

Over the past few years, microRNAs (miRNAs) have not only emerged as integral regulators of gene expression at the post-transcriptional level but also respond to signalling molecules to affect cell function(s). miRNAs crosstalk with a variety of the key cellular signalling networks such as Wnt, transforming growth factor-β and Notch, control stem cell activity in maintaining tissue homeostasis, while if dysregulated contributes to the initiation and progression of cancer. Herein, we overview the molecular mechanism(s) underlying the crosstalk between Wnt-signalling components (canonical and non-canonical) and miRNAs, as well as changes in the miRNA/Wnt-signalling components observed in the different forms of cancer. Furthermore, the fundamental understanding of miRNA-mediated regulation of Wnt-signalling pathway and vice versa has been significantly improved by high-throughput genomics and bioinformatics technologies. Whilst, these approaches have identified a number of specific miRNA(s) that function as oncogenes or tumour suppressors, additional analyses will be necessary to fully unravel the links among conserved cellular signalling pathways and miRNAs and their potential associated components in cancer, thereby creating therapeutic avenues against tumours. Hence, we also discuss the current challenges associated with Wnt-signalling/miRNAs complex and the analysis using the biomedical experimental and bioinformatics approaches.
Tramadol Abuse and Dependence Among Physicians
Authors: Edgar H Adams, Richard C Dart, Janet S Knisely, Sidney H Schnoll
Journal: JAMA (2005)

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
P0674 : Clinically approved T-type calcium channel inhibitors prevent hepatitis C virus (HCV) membrane fusion in a genotype-dependent manner
Authors: P.M. Perin, S. Haid, R. Brown, K. Schulze, C.C. Colpitts, C. Zeilinger, M. von Schaewen, B. Heller, K. Vercauteren, E. Luxenburger, Y. Andonyadis, F. Vondran, A. Kirschning, L.M. Schang, R. Müller, C.A. Guzman, L. Kaderali, G. Randall, P. Meuleman, A. Ploss, T. Pietschmann
Journal: Journal of Hepatology (2015)
Uncontrolled Complement Activation and the Resulting Chronic Hemolysis As Measured by LDH Serum Level At Diagnosis As Predictor of Thrombotic Complications and Mortality in a Large Cohort of Patients with Paroxysmal Nocturnal Hemoglobinuria (PNH),
Authors: Jong Wook Lee, Jun Ho Jang, Jin Seok Kim, Sung-Soo Yoon, Je-Hwan Lee, Yeo-Kyeoung Kim, Deog-Yeon Jo, Jooseop Chung, Sang Kyun Sohn
Journal: Blood (2011)
Physician Participation in Assisted Suicide
Authors: David Orentlicher
Journal: JAMA (1989)

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
Vigilance still needed to contain Africa’s yellow fever outbreak, says WHO
Authors: Anne Gulland
Journal: BMJ (2016)

Continued vigilance is needed to ensure that the yellow fever outbreak in central Africa is contained, the World Health Organization (WHO) has said.

WHO’s emergency committee for yellow fever met for the second time on 31 August and reiterated its previous decision that the outbreak in Angola and the Democratic Republic of Congo (DRC) was a “serious public health event, which warrants continued national action and international support.” 

The committee said, however, that it did not constitute a public health emergency of international concern.

In a news conference, Oyewale Tomori, chair of the emergency committee and professor of virology at Redeemer’s University in Nigeria, said, “Although the …
The number of privately treated tuberculosis cases in India: an estimation from drug sales data
Authors: Nimalan Arinaminpathy, Deepak Batra, Sunil Khaparde, Thongsuanmung Vualnam, Nilesh Maheshwari, Lokesh Sharma, Sreenivas A Nair, Puneet Dewan
Journal: The Lancet Infectious Diseases (2016)

Understanding the amount of tuberculosis managed by the private sector in India is crucial to understanding the true burden of the disease in the country, and thus globally. In the absence of quality surveillance data on privately treated patients, commercial drug sales data offer an empirical foundation for disease burden estimation.We used a large, nationally representative commercial dataset on sales of 189 anti-tuberculosis products available in India to calculate the amount of anti-tuberculosis treatment in the private sector in 2013-14. We corrected estimates using validation studies that audited prescriptions against tuberculosis diagnosis, and estimated uncertainty using Monte Carlo simulation. To address implications for numbers of patients with tuberculosis, we explored varying assumptions for average duration of tuberculosis treatment and accuracy of private diagnosis.There were 17·793 million patient-months (95% credible interval 16·709 million to 19·841 million) of anti-tuberculosis treatment in the private sector in 2014, twice as many as the public sector. If 40-60% of private-sector tuberculosis diagnoses are correct, and if private-sector tuberculosis treatment lasts on average 2-6 months, this implies that 1·19-5·34 million tuberculosis cases were treated in the private sector in 2014 alone. The midpoint of these ranges yields an estimate of 2·2 million cases, two to three times higher than currently assumed.India's private sector is treating an enormous number of patients for tuberculosis, appreciably higher than has been previously recognised. Accordingly, there is a re-doubled need to address this burden and to strengthen surveillance. Tuberculosis burden estimates in India and worldwide require revision.Bill & Melinda Gates Foundation.
Calcium/Calmodulin‐Dependent Kinase IV Facilitates the Recruitment of Interleukin‐17–Producing Cells to Target Organs Through the CCR6/CCL20 Axis in Th17 Cell–Driven Inflammatory Diseases
Authors: Tomohiro Koga, Kotaro Otomo, Masayuki Mizui, Nobuya Yoshida, Masataka Umeda, Kunihiro Ichinose, Atsushi Kawakami, George C. Tsokos
Journal: Arthritis & Rheumatology (2016)

The recruitment of interleukin-17 (IL-17)-producing T helper (Th17) cells to inflammatory sites has been implicated in the development of organ damage in inflammatory and autoimmune diseases including systemic lupus erythematosus (SLE). To define the mechanism of calcium/calmodulin-dependent kinase IV (CaMKIV) activation of Th17 cell recruitment to target tissues, we performed anti-glomerular basement membrane antibody-induced glomerulonephritis (AIGN) experiments in mice and studied samples from patients with SLE.We induced experimental AIGN in CaMKIV-sufficient or CaMKIV-deficient mice and compared histology, Th17 cell-related chemokine expression, and numbers of IL-17-producing cells in kidneys. We also evaluated the efficacy of the CaMKIV inhibitor KN-93 in AIGN-induced kidney disease. The expression of CCR6 in memory CD4+ T cells before AIGN induction was analyzed by flow cytometry. We investigated the correlation between CCR6 expression in peripheral blood and the severity of glomerulonephritis in patients with SLE.CaMKIV-deficient mice displayed less glomerular injury after induction of AIGN. Kidney infiltration by IL-17-producing CD4+ T cells along with CCR6 and CCL20 expression were significantly decreased in CaMKIV-deficient mice. Similarly, treatment of mice with KN-93 improved clinical and pathologic outcomes. Expression and function of CCR6 in peripheral blood memory CD4+ T cells was decreased in CaMKIV-deficient mice. Expression of CCR6 correlated positively with severity of organ damage in SLE patients.CaMKIV inhibition represents a novel therapeutic strategy for treatment of Th17 cell-mediated tissue damage in inflammatory diseases.
18F-FDG PET/CT Demonstrating Malignant Degeneration of a Uterine Fibroid
Authors: Punit Sharma
Journal: Clinical Nuclear Medicine (2016)

Whereas benign leiomyoma of the uterus (fibroid) is very common, malignant degeneration of such fibroids to leiomyosarcoma is rare. Anatomical imaging with CT or MRI cannot differentiate between larger leiomyoma and leiomyosarcoma. Imaging with 18F-FDG PET/CT can be helpful in differentiating the two. High-grade 18F-FDG uptake in uterine fibroids is suspected and warrants surgical excision for further evaluation. We present such as case of a 42-year-old premenopausal woman where 18F-FDG PET/CT helped in making the diagnosis of malignant degeneration of uterine fibroid.
Patient Expectancy as a Mediator of Placebo Effects in Antidepressant Clinical Trials
Authors: Bret R. Rutherford, Melanie M. Wall, Patrick J. Brown, Tse-Hwei Choo, Tor D. Wager, Bradley S. Peterson, Sarah Chung, Irving Kirsch, Steven P. Roose
Journal: American Journal of Psychiatry (2016)

Objective: Causes of placebo effects in antidepressant trials have been inferred from observational studies and meta-analyses, but their mechanisms have not been directly established. The goal of this study was to examine in a prospective, randomized controlled trial whether patient expectancy mediates placebo effects in antidepressant studies. Method: Adult outpatients with major depressive disorder were randomly assigned to open or placebo-controlled citalopram treatment. Following measurement of pre- and postrandomization expectancy, participants were treated with citalopram or placebo for 8 weeks. Independent samples t tests determined whether patient expectancy differed between the open and placebo-controlled groups, and mixed-effects models assessed group effects on Hamilton Depression Rating Scale (HAM-D) scores over time while controlling for treatment assignment. Finally, mediation analyses tested whether between-group differences in patient expectancy mediated the group effect on HAM-D scores. Results: Postrandomization expectancy scores were significantly higher in the open group (mean=12.1 [SD=2.1]) compared with the placebo-controlled group (mean=11.0 [SD=2.0]). Mixed-effects modeling revealed a significant week-by-group interaction, indicating that HAM-D scores for citalopram-treated participants declined at a faster rate in the open group compared with the placebo-controlled group. Patient expectations postrandomization partially mediated group effects on week 8 HAM-D. Conclusions: Patient expectancy is a significant mediator of placebo effects in antidepressant trials. Expectancy-related interventions should be investigated as a means of controlling placebo responses in antidepressant clinical trials and improving patient outcome in clinical treatment.
Phase III study (MONET1) of motesanib plus carboplatin/paclitaxel (C/P) in patients with advanced nonsquamous non-small cell lung cancer (NSCLC): Asian subgroup analysis.
Authors: Yukito Ichinose, Kaoru Kubota, Giorgio Scagliotti, David R. Spigel, Joo-Hang Kim, Tetsu Shinkai, Koji Takeda, Sang-We Kim, Te-Chun Hsia, Rubi Li, Beatrice Tiangco, Stephen Yau, Wan-Teck Lim, Bin Yao, Yong Jiang Hei, Keunchil Park
Journal: Journal of Clinical Oncology (2012)

7549 Background: MONET1 evaluated overall survival (OS) in patients (pts) with nonsquamous NSCLC receiving motesanib (an oral VEGFR 1, 2 and 3, PDGFR and Kit inhibitor) plus C/P compared with pts receiving placebo plus C/P. Analysis of the total population (N=1090) showed that motesanib + C/P did not significantly improve OS vs C/P alone (primary endpoint). Here we present results of a subgroup analysis of Asian pts. Methods: Asian pts (Japan, S. Korea, Philippines, Hong Kong, Taiwan, Singapore) with stage IIIB/IV or recurrent nonsquamous NSCLC and no prior systemic therapy for advanced NSCLC were analysed. Pts were randomized to up to six 3-wk cycles of C (AUC 6 mg/mL·min) and P (200 mg/m 2 ) with either motesanib 125 mg QD (Arm A) or placebo QD (Arm B) orally continuously. Results: 227 Asian pts (incl. 106 Japanese pts) with nonsquamous NSCLC were randomized (Arm A/B, n=110/117); 198 had adenocarcinoma (n=97/101). Median age was 60 y (range 30–78); 80% had stage IV disease. At the time of analysis, 139 pts had died (118 pts with adenocarcinoma). Pts received a median of 164 days of motesanib vs 125 days of placebo (vs 106 and 126 days in non-Asian pts). Median follow-up was 63 wks. Efficacy results are shown in the table. Motesanib/placebo-related AEs were seen in 94/74% of pts respectively; Gr ≥3 related AEs in 48/22%. Most common emergent AEs were (Arm A/B) alopecia (78/76%), diarrhea (63/33%), and nausea (55/43%); gallbladder disorders (Gr 1–2) were seen in 9/2% of pts. Gr ≥3 AEs more frequent in Arm A vs B included neutropenia (36/22%) and hypertension (13/3%). Emergent Gr 5 events were seen in (Arm A/B) 5/4% vs 16/11% in non-Asian pts. Conclusions: In contrast to non-Asian pts, in the subgroup of Asian pts with advanced nonsquamous NSCLC, motesanib plus C/P treatment was associated with increased OS, PFS, and objective response rates (ORR) compared with C/P alone, with no excess of treatment-related mortality. [Table: see text]
Anomalous expression of GATA factors underlies the loss of Disabled-2 expression and ovarian tumorigenesis
Authors: Malgorzata E. Rula, Callinice D. Capo-Chichi, Isabelle H. Roland, Cynthia Cohen, Thomas C. Hamilton, Andrew K. Godwin, Xiang-Xi Xu
Journal: Cancer Research (2004)

4187   Disabled-2 (Dab2) is a candidate ovarian tumor suppressor involved in organization and surface positioning of ovarian surface epithelial cells. Dab2 expression is lost in 85% of epithelial ovarian carcinomas analyzed. Here, we found that anomalous expression of GATA factors underlies the loss of Dab2 expression. GATA-4 and GATA-6 are expressed strongly and are localized in the nucleus in ovarian surface epithelial cells in tissues or primary cell cultures. By immunohistochemistry, we found that 82% of the 50 tumors analyzed had lost GATA-6 function, either by a complete absence of expression or the cytoplasmic mislocalization. The frequent loss of GATA-6 was also confirmed in a panel of ovarian surface epithelial and tumor cell lines. The loss of GATA-6 correlates with the loss of Disabled-2, collagen IV, and laminin, markers for epithelial cell types. Repression of GATA-6 by siRNA approach in cultured cells leads to the loss of Disabled-2 and laminin expression. However, restoration of GATA-4 and GATA-6 expression is not able to induce expression of endogenous Dab2 in tumor cells, suggesting that the loss of GATA factors and dedifferentiation are irreversible processes. Additionally, Dab2 promoter activity in primary and tumor cell lines does not correlate with Dab2 expression in the cells, suggesting the loss of GATA-6 may influence Dab2 gene expression at a chromatin level. We propose that alterations of GATA transcription factor expression and aberrant nucleocytoplasmic localization may contribute to the anomalous epithelial dedifferentiation and tumorigenicity of the ovarian surface epithelial cells.
Quality Improvement Organizations and Hospital Care
Authors: Jonathan R Sugarman, Greg A Baumgardner
Journal: JAMA (2005)

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
2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia: Executive Summary
Authors: Richard L. Page, José A. Joglar, Mary A. Caldwell, Hugh Calkins, Jamie B. Conti, Barbara J. Deal, N.A. Mark Estes, Michael E. Field, Zachary D. Goldberger, Stephen C. Hammill, Julia H. Indik, Bruce D. Lindsay, Brian Olshansky, Andrea M. Russo, Win-Kuang Shen, Cynthia M. Tracy, Sana M. Al-Khatib
Journal: Circulation (2015)
ClaPD (Clarithromycin/[Biaxin®], Pomalidomide, Dexamethasone) Therapy in Relapsed or Refractory Multiple Myeloma
Authors: Tomer M Mark, Melissa Rodriguez, Manan Shah, Ryann Quinn, Jessica Campbell, Ramsey Abdullah, Roger N Pearse, Faiza Zafar, Karen Pekle, Patrice Mignott, David Jayabalan, Scott A Ely, Morton Coleman, Selina Chen-Kiang, Ruben Niesvizky
Journal: Blood (2011)
Survival and Proliferation of Neural Progenitor–Derived Glioblastomas Under Hypoxic Stress is Controlled by a CXCL12/CXCR4 Autocrine-Positive Feedback Mechanism
Authors: Anda-Alexandra Calinescu, Viveka Nand Yadav, Erica Carballo, Padma Kadiyala, Dustin Tran, Daniel B. Zamler, Robert Doherty, Maithreyi Srikanth, Pedro Ricardo Lowenstein, Maria Graciela Castro
Journal: Clinical Cancer Research (2016)

Purpose: One likely cause of treatment failure in glioblastoma is the persistence of glioma stem-like cells (GSLCs) which are highly resistant to therapies currently employed. We found that CXCL12 has highest expression in glioma cells derived from neural progenitor cells (NPC). The development and molecular signature of NPC-derived glioblastomas were analyzed and the therapeutic effect of blocking CXCL12 was tested.Experimental Design: Tumors were induced by injecting DNA into the lateral ventricle of neonatal mice, using the Sleeping Beauty transposase method. Histology and expression of GSLC markers were analyzed during disease progression. Survival upon treatment with pharmacologic (plerixafor) or genetic inhibition of CXCR4 was analyzed. Primary neurospheres were generated and analyzed for proliferation, apoptosis, and expression of proteins regulating survival and cell-cycle progression.Results: Tumors induced from NPCs display histologic features of human glioblastoma and express markers of GSLC. In vivo, inhibiting the CXCL12/CXCR4 signaling axis results in increased survival of tumor-bearing animals. In vitro, CXCR4 blockade induces apoptosis and inhibits cell-cycle progression, downregulates molecules regulating survival and proliferation, and also blocks the hypoxic induction of HIF-1α and CXCL12. Exogenous administration of CXCL12 rescues the drug-induced decrease in proliferation.Conclusions: This study demonstrates that the CXCL12/CXCR4 axis operates in glioblastoma cells under hypoxic stress via an autocrine-positive feedback mechanism, which promotes survival and cell-cycle progression. Our study brings new mechanistic insight and encourages further exploration of the use of drugs blocking CXCL12 as adjuvant agents to target hypoxia-induced glioblastoma progression, prevent resistance to treatment, and recurrence of the disease. Clin Cancer Res; 23(5); 1250-62. ©2016 AACR.
Noninvasive Tremor Treatment
Authors: Rebecca Voelker
Journal: JAMA (2016)

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
Microvascular invasion in hepatocellular carcinoma is defined by tumor characteristics and aberrant angiogenesis in peritumoral tissue
Authors: Hironori Kusano, Jing Han, Marian Bulthuis, Peter J. Zwiers, Koert P. de Jong, Hirohisa Yano, Grietje Molema, Annette S. Gouw
Journal: Hepatology (2013)