tbuckley/cabot-search huggingface dataset:
Insulin Receptor Substrate-1 Regulates the Transformed Phenotype of BT-20 Human Mammary Cancer Cells
Authors: Ozlem Dalmizrak, An Wu, Jia Chen, Hongzhi Sun, Fransiscus E. Utama, Diana Zambelli, Thai H. Tran, Hallgeir Rui, Renato Baserga
Journal: Cancer Research (2007)

Abstract Although originating from a human breast cancer, BT-20 cells do not form colonies in soft agar. BT-20 cells do not express insulin receptor substrate-1 (IRS-1), which is known to promote both normal and abnormal growth and to inhibit differentiation. Stable expression of IRS-1 confers to BT-20 cells the ability to form colonies in soft agar. BT-20 cells form tumors in xenografts in mice, but the size of tumors is twice as large when the cells express IRS-1. The increased transformed phenotype is characterized by occupancy of the rDNA and cyclin D1 promoters by IRS-1 and the activation of the cyclin D1, c-myc, and rDNA promoters. In addition, the retinoblastoma protein, which is detectable in the rDNA promoter of quiescent BT-20/IRS-1 cells, is replaced by IRS-1 after insulin-like growth factor-I stimulation. Our results indicate that in BT-20 human mammary cancer cells, expression of IRS-1 activates promoters involved in cell growth and cell proliferation, resulting in a more transformed phenotype. Targeting of IRS-1 could be effective in inhibiting the proliferation of mammary cancer cells. [Cancer Res 2007;67(5):2124–30]
ω-3 Fatty acid–based lipid infusion in patients with chronic plaque psoriasis: Results of a double-blind, randomized, placebo-controlled, multicenter trial
Authors: Peter Mayser, Ulrich Mrowietz, Peter Arenberger, Pavel Bartak, Jozef Buchvald, Enno Christophers, Stefania Jablonska, Werner Salmhofer, Wolf-Bernhard Schill, Hans-Joachim Krämer, Ewald Schlotzer, Konstantin Mayer, Werner Seeger, Friedrich Grimminger
Journal: Journal of the American Academy of Dermatology (1998)
Correlation of In Vivo Delayed-Type Hypersensitivity with In Vitro Lymphocyte Transformation in Sarcoidosis.
Authors: O. P. Sharma
Journal: Annals of Internal Medicine (1970)

Meeting Abstracts1 May 1970Correlation of In Vivo Delayed-Type Hypersensitivity with In Vitro Lymphocyte Transformation in Sarcoidosis.O. P. Sharma, M.D., R.A. Fox, D. G. JamesO. P. Sharma, M.D.Search for more papers by this author, R.A. FoxSearch for more papers by this author, D. G. JamesSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-72-5-811_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe cardinal immunological defect in sarcoidosis is depression of delayed-type hypersensitivity which is readily demonstrated by skin tests using tuberculin, Candida albicans, or the chemical dinitrochlorobenzene (DNCB). It is also known that in vitro culture of lymphocytes from sarcoidosis patients fail to undergo blastic transformation in response to phytohemagglutinin (PHA).Induction of in vivo dinitrochlorobenzene sensitisation has been correlated with in vitro cultured lymphocyte transformation in 21 patients with histologically confirmed sarcoidosis and an equal number of matched control subjects. Failure to sensitise with DNCB was noted in 71% of sarcoidosis patients and 14% of controls. Poor lymphocyte transformation occurred... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: London England PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited bySome Aspects of Sarcoidosis 1 May 1970Volume 72, Issue 5Page: 811-811KeywordsCandida albicansHypersensitivityLymphocytesPhytohemagglutininsSarcoidosisSkin testsTuberculin Issue Published: 1 May 1970 PDF downloadLoading ...
Cancer Risk After Hip Replacement With Metal Implants: a Population-Based Cohort Study in Sweden
Authors: O. Nyren, J. K. McLaughlin, G. Gridley, A. Ekbom, O. Johnell, J. F. Fraumeni, H.-O. Adami
Journal: JNCI Journal of the National Cancer Institute (1995)

Joint replacement with metal implants has been the standard procedure for surgical treatment of irreversible degeneration of hip and knee joints for more than two decades. However, reports of local malignancy after joint replacement and experimental studies that suggest a carcinogenic action of metal ions and polymethylmethacrylate (an acrylic compound used to stabilize the implant in the host) have raised concern about the possible long-term risks associated with metal implants.Our aim was to study cancer risk in a Swedish cohort of patients who had hip replacement surgery during the period 1965 through 1983.We studied the risk of cancer in a cohort of 39 154 patients (14 869 men and 24 285 women), identified in the nationwide Swedish Inpatient Register with at least one hip replacement during the period 1965 through 1983. The patients were followed through 1989 by means of record linkage to the Swedish Cancer Register. The cohort contributed a total of 327 922 person-years at risk. Standardized incidence ratios (SIRs) were computed using age-, sex-, and period-specific incidence rates derived from the entire Swedish population.The overall relative risk of cancer was increased by only 3%. Bone cancer--the focus of previous concerns--occurred in six cases versus 4.3 expected, and connective tissue cancer occurred in 28 cases versus 25.9 expected. Increased risks were observed for kidney cancer (SIR = 1.31; 95% confidence interval [CI] = 1.13-1.51), prostate cancer (SIR = 1.13; 95% CI = 1.04-1.22), and melanoma (SIR = 1.23; 95% CI = 1.00-1.50). The relative risk of gastric cancer steadily declined with increasing follow-up time, in both men and women (SIR = 0.58; 95% CI = 0.39-0.84 more than 10 years after hip replacement).In this study, the largest study to date to evaluate hip replacement and subsequent cancer risk, the overall cancer risk appears to be negligible from a public health perspective, and our results have not produced any strong evidence against the continued use of these devices. Nevertheless, the small but statistically significant increases in kidney and prostate cancers and the decrease in gastric cancer deserve further study.
Do Readers and Peer Reviewers Agree on Manuscript Quality?
Authors: Amy C. Justice, Jesse A. Berlin, Suzanne W. Fletcher, Robert H. Fletcher, Steven N. Goodman
Journal: JAMA (1994)

To study readers' judgments of manuscript quality and the degree to which readers agreed with peer reviewers.Cross-sectional study.Annals of Internal Medicine.One hundred thirteen consecutive manuscripts reporting original research and selected for publication. Each of two manuscript versions (one before and one after revision) was judged by two readers, randomly sampled from those who said (based on the title) that they would read the article; one peer reviewer (peer), chosen in the usual way for Annals; and one expert in clinical research methods (expert). Each judge completed an instrument that included a 10-point subjective summary grade of manuscript quality.Agreement on the 10-point summary grade of manuscript quality between reader-expert, reader-peer, and reader-reader.Readers and peers gave high grades (77% and 73% gave a grade of 5 or better, respectively), while experts were more critical (52% gave a grade of 5 or better; P < .0001). Agreement was relatively high among judge groups (in all cases, > 69%) but agreement beyond chance was poor (kappa < 0.04). One third of readers (33%) thought that the manuscript had little relevance to their work.Readers, like most peer reviewers, are generally satisfied with the quality of manuscripts but would like research articles to be more relevant to their clinical practice.
Dementia: A Global Approach
Authors: Mugdha Thakur
Journal: JAMA (2011)

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
Nurse-Physician Communications in the Hospital
Authors: Luther P. Christman
Journal: JAMA (1965)

Today the staff members of hospitals are becoming keenly aware of difficulties in communication among themselves and the effect these difficulties have on patient care. Because staffs must continually cope with frustrating communication problems, many undesirable emotional overtones usually arise which in turn intensify the problems. In most hospitals there is little or no organizational means by which clarification of such communication problems may take place. Many hazards to patient care exist which could be eliminated if the communication difficulties could be reduced qualitatively as well as quantitively. What are the obstacles to the type of communication that facilitates organizing for the best kind of clinical care? What are the consequences when the communicative process is not adequate to this end? One does not need to be an expert to observe that the unlimited demands being placed on two of the nation's scarce health resources, physicians and nurses, greatly contribute
Prophylactic Surgery to Reduce the Risk of Gynecologic Cancers in the Lynch Syndrome
Authors: Kathleen M. Schmeler, Henry T. Lynch, Lee-may Chen, Mark F. Munsell, Pamela T. Soliman, Mary Beth Clark, Molly S. Daniels, Kristin G. White, Stephanie G. Boyd-Rogers, Peggy G. Conrad, Kathleen Y. Yang, Mary M. Rubin, Charlotte C. Sun, Brian M. Slomovitz, David M. Gershenson, Karen H. Lu
Journal: New England Journal of Medicine (2006)

Women with the Lynch syndrome (hereditary nonpolyposis colorectal cancer) have a 40 to 60 percent lifetime risk of endometrial cancer and a 10 to 12 percent lifetime risk of ovarian cancer. The benefit of prophylactic gynecologic surgery for women with this syndrome has been uncertain. We designed this study to determine the reduction in the risk of gynecologic cancers associated with prophylactic hysterectomy and bilateral salpingo-oophorectomy in women with the Lynch syndrome.Three hundred fifteen women with documented germ-line mutations associated with the Lynch syndrome were identified. Women who had undergone prophylactic hysterectomy (61 women) and women who had undergone prophylactic bilateral salpingo-oophorectomy (47 women) were matched with mutation-positive women who had not undergone the procedure in question (210 women for the analysis of endometrial cancer and 223 for the analysis of ovarian cancer). Women who had undergone prophylactic surgery and their matched controls were followed from the date of the surgery until the occurrence of cancer or until the data were censored at the time of the last follow-up visit.There were no occurrences of endometrial, ovarian, or primary peritoneal cancer among the women who had undergone prophylactic surgery. Endometrial cancer was diagnosed in 69 women in the control group (33 percent), for an incidence density of 0.045 per woman-year, yielding a prevented fraction (the proportion of potential new cancers prevented) of 100 percent (95 percent confidence interval, 90 to 100 percent). Ovarian cancer was diagnosed in 12 women in the control group (5 percent), for an incidence density of 0.005 per woman-year, yielding a prevented fraction of 100 percent (95 percent confidence interval, -62 to 100 percent).These findings suggest that prophylactic hysterectomy with bilateral salpingo-oophorectomy is an effective strategy for preventing endometrial and ovarian cancer in women with the Lynch syndrome.
Glass fiber dissolution in simulated lung fluid and measures needed to improve consistency and correspondence to in vivo dissolution.
Authors: S M Mattson
Journal: Environmental Health Perspectives (1994)

The dissolution of a range of glass fibers including commercial glass and mineral wools has been studied using a modification of Gamble's solution in a flow system at pH 7.4 and 37 degrees C. Dissolution has been followed by weight loss, effluent analysis, and morphology change of fibers and bulk glass. Flow per glass surface area can strongly affect both dissolution rate and morphology due to the effect of the dissolution process on the fluid. Effluent pH is shown to be a guide for choice of optimum flow/area conditions. These conditions provide measurable concentrations of dissolved glass in the effluent while maintaining their concentrations below the point at which they significantly affect the dissolution process. SiO2 and Al2O3 vary widely in the extent to which they are involved in the leaching process, which removes alkalis, alkaline earths, and B2O3. This makes analysis of a single component in the effluent unsuitable as a means of comparing the dissolution rates of a wide range of compositions.
Abstract 3174: The host genomic environment of the provirus determines the abundance of BLV-infected clones
Authors: Nicolas Gillet, Alix de Brogniez, Nathalie Renotte, Geronimo Gutierrez, Irene Alvarez, Karina Trono, Luc Willems
Journal: Cancer Research (2014)

Abstract Human T-lymphotropic Virus 1 (HTLV-1) induces a persistent infection that remains generally asymptomatic. Nevertheless, in a small proportion of individuals and after a long latency, HTLV-1 infection leads to leukemia or lymphoma. Onset of clinical manifestations correlates with a persistently elevated number of infected cells. Because the vast majority of cells are infected at early stages, primary infection is a crucial period for HTLV-1 persistence and pathogenesis. Since HTLV-1 is transmitted through breast feeding and because systematic population screenings are rare, there is a lack of available samples at early infection. Therefore, we addressed this question in a closely related animal model by inoculating cows with Bovine Leukemia Virus (BLV). Initial BLV provirus insertion is not random but occurs nearby transcribed genomic regions (genes and CpG islands). This pattern of integration is highly similar to the observed pattern in HTLV-1 in vitro experiments. Later on, the proportion of clone carrying a provirus in transcribed regions decreases to reach levels comparable to those observed in asymptomatic HTLV-1 carriers. The negative selection against BLV clones carrying a provirus nearby transcribed regions is more efficient in animals that will subsequently present low proviral load set point. Finally, like for HTLV-1 infected people, the abundance of the BLV infected clones correlates with the integration of the provirus in transcribed regions. These observations highlight the high similarities between BLV and HTLV-1 clonality and suggest a key role exerted by the host immune system during primary infection. Citation Format: Nicolas Gillet, Alix de Brogniez, Nathalie Renotte, Geronimo Gutierrez, Irene Alvarez, Karina Trono, Luc Willems. The host genomic environment of the provirus determines the abundance of BLV-infected clones. [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 3174. doi:10.1158/1538-7445.AM2014-3174
Increasing the accuracy of peanut allergy diagnosis by using Ara h 2
Authors: Thanh D. Dang, Mimi Tang, Sharon Choo, Paul V. Licciardi, Jennifer J. Koplin, Pamela E. Martin, Tina Tan, Lyle C. Gurrin, Anne-Louise Ponsonby, Dean Tey, Marnie Robinson, Shyamali C. Dharmage, Katrina J. Allen
Journal: Journal of Allergy and Clinical Immunology (2012)

Measurement of whole peanut-specific IgE (sIgE) is often used to confirm sensitization but does not reliably predict allergy. Ara h 2 is the dominant peanut allergen detected in 90% to 100% of patients with peanut allergy and could help improve diagnosis.We sought to determine whether Ara h 2 testing might improve the accuracy of diagnosing peanut allergy and therefore circumvent the need for an oral food challenge (OFC).Infants from the population-based HealthNuts study underwent skin prick tests to determine peanut sensitization and subsequently underwent a peanut OFC to confirm allergy status. In a stratified random sample of 200 infants (100 with peanut allergy and 100 with peanut tolerance), whole peanut sIgE and Ara h 2 sIgE levels were quantified by using fluorescence enzyme immunoassay.By using the previously published 95% positive predictive value of 15 kU(A)/L for whole peanut sIgE, a corresponding specificity of 98% (95% CI, 93% to 100%) was found in this study cohort. At the equivalent specificity of 98%, the sensitivity of Ara h 2 sIgE is 60% (95% CI, 50% to 70%), correctly identifying 60% of subjects with true peanut allergy compared with only 26% correctly identified by using whole peanut sIgE. We report that when using a combined approach of plasma sIgE testing for whole peanut followed by Ara h 2 for the diagnosis of peanut allergy, the number of OFCs required is reduced by almost two thirds.Ara h 2 plasma sIgE test levels provide higher diagnostic accuracy than whole peanut plasma sIgE levels and could be considered a new diagnostic tool to distinguish peanut allergy from peanut tolerance, which might reduce the need for an OFC.
Acquired Aplastic Anemia
Authors: Neal S. Young
Journal: JAMA (1999)

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 Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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) 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
Abstract 4864: Tumor promoting role of NF-kappa B in the glioma environment
Authors: Aneta Kwiatkowska, Mohan Sobana Nandhu, Mariano Sebastian Viapiano
Journal: Cancer Research (2014)

Abstract Introduction: Gliomas are the most common primary malignant brain tumors. Their characteristic features are extensive growth and lack of the clear borders due to diffuse invasion of surrounding tissue. Invasive glioma cells have been shown to interact through soluble signals with other cells in the neural microenvironment, which is normally highly inhibitory to cell motility. This communication changes the behavior of the tumor microenvironment to become permissive and facilitate tumor invasion. Here, we investigated the role of NFκB signaling in the glioma microenvironment and demonstrate that activation of NFκB in neural cells is critical for tumor growth and invasion. Methodology: We analyzed the growth and invasion of malignant gliomas using an NFκB-deficient mouse model (RelA(p65)-/- TNFR1-/-). Since p65-/- mice do not survive to adulthood, mouse glioma cells were implanted in p65+/- mice (which have significantly reduced NFκB activity) or their control littermates. Organotypic cultures of p65-/- brain slices and cultures of p65-/- neonatal astrocytes were used to assess the role of active NFκB signaling in astroglia on tumor invasion. Results: Using the mouse glioma cell line GL261 (poorly invasive) we observed significantly reduced tumor volume in NFκB -deficient mice compared to wild-type littermates. Further studies using mouse glioma stem-like cells Mut4 (highly invasive; GFAP-Cre: Nf1loxP/+ Trp53-/+ PTENloxP/+; Alcantara-Llaguno et al., Cancer Cell, 2009) demonstrated reduction both in tumor size and extent of invasion in the NFκB-deficient microenvironment. Importantly, immunohistochemical analysis demonstrated significantly reduced number of protoplasmic GFAP- positive astrocytes surrounding the tumors in p65+/- brains. Further analysis in brain slice cultures showed that invasion of glioblastoma cells was highly reduced through p65+/- tissue. Moreover, p65+/- astrocytes exhibited significantly reduced responses towards glioma cells, including reduced invasion through Matrigel in response to signals released by GL261 cells. Conclusions: Our results strongly suggest that NFκB signaling may be involved in the recruitment or activation of reactive astrocytes surrounding the invasive borders of gliomas. This activation is likely necessary for enhanced tumor invasion through brain tissue. Our results highlight the relevance of the astroglial compartment as a collateral target that should be considered in future strategies targeting brain tumor invasion. Citation Format: Aneta Kwiatkowska, Mohan Sobana Nandhu, Mariano Sebastian Viapiano. Tumor promoting role of NF-kappa B in the glioma environment. [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 4864. doi:10.1158/1538-7445.AM2014-4864