tbuckley/cabot-search huggingface dataset:
Violent Partners: A Breakthrough Plan for Ending the Cycle of Abuse
Authors: Linda G. Mills
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
Blood vessel characterization in human dermal wound repair and scarring
Authors: M. Valluru, N.J. Brown, S.S. Cross, M.W.R. Reed, C.A. Staton
Journal: British Journal of Dermatology (2011)

Journal Article Blood vessel characterization in human dermal wound repair and scarring Get access M. Valluru, M. Valluru Microcirculation Research Group, Academic Unit of Surgical Oncology Search for other works by this author on: Oxford Academic Google Scholar N.J. Brown, N.J. Brown Microcirculation Research Group, Academic Unit of Surgical Oncology Search for other works by this author on: Oxford Academic Google Scholar S.S. Cross, S.S. Cross Academic Unit of Pathology, Faculty of Medicine, Dentistry and Health, University of Sheffield, Sheffield S10 2RX, U.K. Search for other works by this author on: Oxford Academic Google Scholar M.W.R. Reed, M.W.R. Reed Microcirculation Research Group, Academic Unit of Surgical Oncology Search for other works by this author on: Oxford Academic Google Scholar C.A. Staton C.A. Staton Microcirculation Research Group, Academic Unit of Surgical Oncology Carolyn Staton. E‐mail: c.a.staton@shef.ac.uk Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 165, Issue 1, 1 July 2011, Pages 221–224, https://doi.org/10.1111/j.1365-2133.2011.10327.x Published: 01 July 2011
Researchers Identify Protein That Helps Tumor Cells Resist Cancer Drugs
Authors: Tracy Hampton
Journal: JAMA (2004)

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
A Meta-Analysis Of Hodgkin Lymphoma Reveals 19p13.3 (TCF3) As a Novel Susceptibility Loc
Authors: Wendy Cozen, Dalin Li, Maria Timofeeva, Arjan Diepstra, Dennis Hazelett, Manon Delahaye-Sourdeix, Christopher K. Edlund, Klaus Rostgaard, David J. Van Den Berg, Lude Franke, Karin Eckstrom Smedby, Sally L. Glaser, Harm-Jam Westra, Leslie L. Robison, Thomas M. Mack, Herve Ghesquieres, Amie E. Hwang, Alexandra Nieters, Silvia de Sanjosé, Victoria K. Cortessis, Tracy Lightfoot, Nikolaus Becker, Marc Maynadie, Lenka Foretova, Eve Roman, Yolanda Benavente, Bharat N. Nathwani, Bengt Glimelius, Anthony Staines, Paolo Boffetta, Brian K Link, L. A. Kiemeney, Stephen M Ansell, Smita Bhatia, Louise C Strong, Pilar Galan, Lars Vatten, Thomas M Habermann, Eric J. Duell, Annette Lake, Rianne Veenstra, Lydia Visser, Kevin Urayama, Dorothy Montgomery, Valerie Gaborieau, Lawrence Weiss, Graham Byrnes, Mark Lathrop, Hans-Olov Adami, Mads Melbye, James R Cerhan, Alice Gallagher, G. Malcolm Taylor, Susan L Slager, Paul Brennan, David V. Conti, Gerhard Coetzee, Kenan Onel, Ruth F. Jarrett, Henrik Hjalgrim, Anke Van Den Berg, James D. McKay
Journal: Blood (2013)
804. Expression of Green Fluorescent Protein Modifies the Antitumor Effect of Oncolytic HSV-1 Vectors
Authors: Yasushi Ino, Yoshinaga Saeki, E. Antonio Chiocca, Tomoki Todo
Journal: Molecular Therapy (2004)

Replication-competent, oncolytic herpes simplex virus type 1 (HSV-1) vectors are useful tools for cancer gene therapy. The virus genome is genetically engineered so that the vector selectively replicates in and destroys tumor cells while sparing the surrounding normal tissues. A marker gene is frequently used in order for replicating virus vectors to be easily detected. Green Fluorescent Protein (GFP) is now a popular marker, because it can be detected in living cells and also be used for selection. MGH-1 is a double-mutated HSV-1 with deletions in both copies of the γ34.5 gene and an insertion of the LacZ gene down-stream of the ICP6 promoter inactivating the ICP6 gene. Using this MGH-1 as a backbone and a bacterial artificial chromosome technology, we newly created multiple types of “armed” oncolytic HSV-1 vectors (vHSV series) in which the ICP6 and LacZ genes were replaced with the ICP6 promoter-driven GFP gene and a transgene cassette driven by the HSV IE4/5 promoter. Prior to testing “armed” oncolytic vectors, we compared the antitumor activity of vHSV-null, the control oncolytic vector expressing only the GFP marker, with that of MGH-1. The replication capability of vHSV-null in cultured Vero cells at a MOI of 0.01 was approximately 10 times lower than that of MGH-1. Despite decreased replication capability, vHSV-null showed slightly faster cytopathic effect than MGH-1 in Neuro2a murine neuroblastoma cells at MOI=0.1. A/J mice bearing bilateral subcutaneous Neuro2a tumors were used for in vivo evaluations. When vectors were inoculated directly into the left tumor at 2×106 plaque-forming units (days 0 and 3), vHSV-null was significantly more effective than MGH-1 for inhibiting the growth of inoculated tumors (p < 0.05). Contralateral non-inoculated tumors also tended to be smaller in vHSV-null-treated animals than MGH-1-treated animals although not statistically significant. Such difference in tumor growth inhibition was not observed in athymic mice, indicating that the greater antitumor activity of vHSV-null in vivo compared with MGH-1 is associated with T cell-mediated immune responses most likely due to expression of GFP. While this possible immunostimulatory effect by GFP may be beneficial to oncolytic virus therapy, a caution is needed to evaluate the antitumor activity of oncolytic HSV-1 vectors when the GFP gene is used as a marker for virus replication.
Genetic Family Affair
Authors: Rebecca Voelker
Journal: JAMA (1998)

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
Understanding RUNX3’s role in gastric epithelial cells by identifying its target genes
Authors: Koo Jason, Voon Dominic, Ito Yoshiaki
Journal: Clinical Cancer Research (2007)

C76   The focus of this study revolves around RUNX3 as a tumor suppressor in the gastric epithelial cells (Li  et al ., 2002). Previous studies in human and mouse had strongly indicated that the loss of functional RUNX3 either by gene silencing or protein mislocalization to cytoplasm is causally related to the genesis and progression of gastric cancer (Li  et al ., 2002; Ito K.  et al ., 2005). Although RUNX3 plays a role in the pathogenesis of gastric cancer, a prominent cause of death in Asia, little is known about the molecular functions of RUNX3 in the gastric epithelium. Hence we aim to understand the role of RUNX3 in maintaining homeostasis in normal gastric epithelium and in gastric carcinogenesis through the identification of direct RUNX3 target genes. This is done by two complementary approaches, namely genome-wide chromatin immunoprecipitation (ChIP) assay and cDNA microarray. ChIP was performed on a gastric epithelial cell line that expresses endogenous RUNX3. Recovered DNA enriched for RUNX3 binding sites will be analysed by Paired-End Ditag (PET) sequencing to identify sites of physical binding by endogenous RUNX3 (Wei CL  et al ., 2006). These data are then correlated to quantitative data generated from expression microarray studies in which RUNX3 is either transiently re-introduced or knockdown by RNAi in RUNX3-negative and -positve gastric epithelial cells, respectively. Preliminary results from these complementary studies will be presented.
NIH: Plan to Speed Biomedical Payoffs
Authors: Brian Vastag
Journal: JAMA (2003)

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
Suppression of tumor-cell COX-2 in hormone refractory prostate cancer causes G1 arrest, inhibition of tumor growth and enhances chemotherapy response
Authors: Balakrishna L. Lokeshwar, Devendra S. Dandekar
Journal: Cancer Research (2004)

Proc Amer Assoc Cancer Res, Volume 45, 2004

4880 

Introduction: Increased expression of the inducible, pro-inflammatory enzyme cyclooxygenase-2 (COX-2) is associated with cancer, but its role in h ormone r efractory p rostate c ancer (HRPC) is less clear and the direct involvement of tumor derived COX-2 is still lacking. We investigated the consequences of suppression of COX-2 by a silencing of tumor cell expression of COX-2, via Tetracycline-inducible antisense cDNA. Methods: Clones of PC-3ML cells, conditionally expressing COX-2 antisense, were created by transfecting PC-3ML cells with a plasmid containing Tetracycline-regulated COX-2 cDNA in antisense orientation (Tet-ON COX-2-Off). Commercial ELISA kits were used to assay COX-1 and COX-2 activity (prostaglandin-E2 (PGE2) production), apoptosis, IL-1β, IL-8, bFGF and VEGF-1 secretion. Cell cycle analysis was determined by flow cytometry. Invasive activity was determined in vitro bythe Matrigel invasion assay.Cytotoxicity of anticancer drugs was evaluated by by clonogenic and MTT assay. Tumor growth and response to antitumor drugs were evaluated in xenografts of PC-3ML or Tet-ON COX-2-Off tumor cells by measuring tumor volumes in athymic mice. Apoptotic cells in tumor sections were enumerated in explanted tumors by TUNELassay. Results: Suppression of tumor cell COX-2 expression by antisense cDNA(Tet-ON COX-2-Off clones) caused a significant decrease in COX-2 activity (87%) and ∼60% decrease in the COX-2 protein level as compared to PC-3ML cells. Cell-cycle arrest at G1 was observed in COX-2-OFF clones (+44%). Also, significant decreases in VEGF-1 (58%); bFGF-1 (30%) and IL-8 (80%) were observed in COX-2-OFF clones. The invasive activity of COX-2-Off cells decreased significantly (80%) as compared to PC-3ML cells. A 52% reduction in the tumor growth rate was observed in mice injected with COX-2-OFF cells as compared to the mice injected with PC-3ML cells. The incidence of apoptotic cells in COX-2-Off tumors was 8-fold higher than that of control. Treating mice bearing PC-3 COX-2OFF tumors, with Docetaxel (2.3 mg/kg, IP,3 x wk.) further slowed tumor growth by 93%. Conclusion: We provide a direct evidence for the involvement of COX-2 in HRPC tumor growth. Inhibition of tumor COX-2 activity significantly reduces tumor growth and increases the efficacy of established antitumor drugs, such as Docetaxel. Direct inhibition of tumor cell COX-2 activity promises to be of greater efficacy than that by systemic COX-2 inhbition,using COX-2 inhibitors. [Funded by NIH grant 2R01 CA 061038 and US Army Grant DAMD 179818526 (BLL)]



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Abstract 8: Mechanism of Pressure Transfer From the Thorax to the Cranium During Application of Negative Intrathoracic Pressure During Treatment of Hypovolemic Hypotension
Authors: Demetris Yannopoulos, Timothy Matsuura, Kostantinos Kotsifas, Scott McKnite, Anja Metzger, Craig Voss, Keith G Lurie
Journal: Circulation (2009)
The Therapeutic Alliance Predicts Outcomes of Cognitive Behavior Therapy but Not of Mindfulness-Based Cognitive Therapy for Depressive Symptoms
Authors: Evelien Snippe, Joke Fleer, K. Annika Tovote, Robbert Sanderman, Paul M.G. Emmelkamp, Maya J. Schroevers
Journal: Psychotherapy and Psychosomatics (2015)
277. Variability in Infectivity of Primary Cell Cultures of Human Brain Tumors with HSV-1 Amplicon Vectors
Authors: Maria A. Rueger, Alexandra Winkeler, Hrvoje Miletic, Christine Kaestle, Raphaela Richter, Gabriele Schneider, Juergen A. Hampl, Cornel Fraefel, Andreas H. Jacobs
Journal: Molecular Therapy (2004)

Background and Purpose. The discrepancy between successful experimental gene therapy protocols and limited clinical translation might – among other reasons – be due to the variability in infectivity and transgene expression in tumors from different patients using vectors. We investigated the variability in infectivity of cells derived from primary brain tumor samples from different patients using HSV-1 amplicons.
Spinal cord injury: a role for the psychiatrist
Authors: T D Stewart
Journal: American Journal of Psychiatry (1977)

The initial psychiatric evaluation of individuals with spinal cord injuries should focus on the patients' coping strategies; this information is an essential part of the treatment and rehabilitation plan. Psychiatrists can also work effectively with staff members in groups designed to ease the strain of working with severely disabled patients. Such patients may have psychiatric illnesses that are not secondary to the injury; careful selection of antidepressant or antipsychotic medication is essential. The author points out that the psychiatrist has much to offer in the treatment of individuals with spinal cord and other severely disabling injuries.
Gene expression signatures associated with protracted stromal responses to therapeutically relevant cytotoxic stimuli predict breast cancer chemoresponsiveness
Authors: Michael T.-L. Lee, Jimmy J.-M. Su, Chi-Rong Li, Patrick Y.-W. Chu, Ming-Sheng Liu, Jung-Hsien Chiang, Kelvin K.-C. Tsai, Kok-Tong Tan
Journal: Clinical Cancer Research (2010)

Abstract Systemic chemotherapy inflicts cytotoxic injuries on tumor cells and cells in the stromal compartment and their complex interplay may critically affect therapeutic response and outcome. Evidence has shown that gene expression profiles associated with reactive tumor stroma link to prognosis and treatment outcome in breast cancer; however, the specific stromal alterations underlying these associations await further exploration. We here show that breast carcinoma-associated fibroblasts (CAFs) responded to therapeutically relevant magnitudes of cytotoxic stimuli (TRCS) by engaging in a series of cytostatic and pro-death cell programs in a time-dependent manner. By interrogating clinical samples we found a considerable number of CAFs with similar characteristics in the stroma of breast cancer following neoadjuvant chemotherapy (NACT). Profiling the TRCS-induced transcriptomal changes of breast CAFs demonstrated that the genes involved in the protracted (day 3-7) instead of the early (day 1-3) responses were significantly associated with the responsiveness of breast cancer to NACT. To further substantiate this finding we prioritized gene markers and identified a 30-gene chemotherapy-associated stroma signature (CASS) that can predict pathological complete remission (pCR) of breast cancer following NACT with remarkable accuracy (overall accuracy 80%, P &amp;lt; 0.01). The CASS outperformed and complemented standard clinicopathological variables and existing gene expression signatures for the prediction of pCR in several independent data sets. Thus, by exploiting the distinct pathological role of the stromal cytotoxic responses we identified strong and robust predictive markers for the intrinsic chemosensitivity of breast cancer (Supported by NHRI CA-099-PP-19 and Department of Health of Taiwan H99-TD-C-111-004 to KKT).
Bats May Be SARS Reservoir
Authors: Tracy Hampton
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
Transthoracic fine-needle aspiration in the aetiological diagnosis of community-acquired pneumonia
Authors: S.S. Hernes, E. Hagen, S. Tofteland, N.T. Finsen, A. Christensen, C.G. Giske, C. Spindler, P.S. Bakke, B. Bjorvatn
Journal: Clinical Microbiology and Infection (2009)
Drug points: Bilateral anterior toxic optic neuropathy and the use of infliximab
Authors: M. P M ten Tusscher
Journal: BMJ (2003)

Three cases of bilateral optic neuropathy were reported recently to the Netherlands Pharmacovigilance Centre Lareb. Patient 1, a 54 year old man, had blurred vision 34 days after he was given a third dose of infliximab for rheumatoid arthritis. He was also taking leflunomide, prednisone, naproxen, diazepam, fluoxetine, famotidine, and metoprolol, and acetaminophen or codeine. He had 20/30 vision in both eyes. Fundoscopy showed severe disc swelling, and perimetry showed visual field defects, which were most extensive in both lower quadrants. Fluorescein angiography showed capillary dilation and vascular leakage in both optic nerve heads. The patient was treated with steroids, but his vision did not recover.

Patient 2, a woman aged 62, had blurred vision 40 days after her third infliximab infusion for rheumatoid arthritis. She was also taking atenolol, enalapril or hydrochlorothiazide, salicylic acid, terfenadine, and rofecoxib. Retinoscopy showed slight swelling of the optic disc in the …