tbuckley/cabot-search huggingface dataset:
Abstract 5219: MicroRNA-874 impedes angiogenesis in non-small cell lung cancer
Authors: Chandramu Chetty, Dilip R. Maddirela, Venkateswara R. Gogineni, Subramanyam Chittivelu, Jasti S. Rao, Bhagavatula Moorthy
Journal: Cancer Research (2014)

Abstract MicroRNAs (miRs) are short (20-24nt) non-coding RNAs that are involved in post-transcriptional regulation of gene expression in eukaryotes by affecting both the stability and translation of mRNAs. MicroRNAs play crucial roles in normal biological processes and are commonly dysregulated in human diseases. Thus far, miRs have been shown to act as either tumor suppressor genes or oncogenes in driving critical gene expression pathways in cancer stem cells in a wide range of human malignancies, including non-small cell lung cancer (NSCLC).We previously found that miR-874 could suppress tumor growth and metastasis of NSCLC. Since angiogenesis is important for tumor growth and metastasis, in this study, we further investigated the possible roles of miR-874 in tumor angiogenesis. Attenuation of miR-874 expression in histological sections of NSCLC tumors and the CD133 positive population of NSCLC cells (NSCLC-initiating cells; NSCLC-ICs), as compared to its normal counterparts, was observed by in situ hybridization and real time quantitative PCR, respectively. Tumor-conditioned medium from NSCLC-ICs induced significantly high levels of endothelial cell capillary network and neovascularization in vivo; whereas, re-expression of miR-874 in NSCLC-ICs inhibited this capillary network formation ability by suppressing the protein levels of VEGF, Stat3, MMP-2, uPA and PI3K. Further, miR-874-treatment decreased in vivo angiogenesis and pre-established orthotopic tumor growth in nude mice as compared to mock- and control-miR-treatments. Immunohistochemical analysis revealed a significant decrease in the expression of VEGF, Stat3 and microvessel density (CD31 levels) in xenograft tumor sections from miR-874-treated mice. In conclusion, our study highlights the possible anti-angiogenic role of miR-874 in NSCLC-initiating cells and presents a new, hopeful therapeutic target and prognostic marker for NSCLC. Citation Format: Chandramu Chetty, Dilip R. Maddirela, Venkateswara R. Gogineni, Subramanyam Chittivelu, Jasti S. Rao, Bhagavatula Moorthy. MicroRNA-874 impedes angiogenesis in non-small cell lung cancer. [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 5219. doi:10.1158/1538-7445.AM2014-5219
Abstract 4242: Effects of dual inhibition of EGFR and Aurora A kinase in a lung cancer model
Authors: Tetyana Bagnyukova, Xiaofan Pan, Jiping Zhang, Brian Egleston, Igor Astsaturov, Erica Golemis, Hossein Borghaei
Journal: Cancer Research (2014)

Abstract Lung cancer is the leading cause of cancer related death in the US. Patients with advanced disease generally have a poor prognosis with a median survival of around 10 to 12 months with standard chemotherapy. Astsaturov and colleagues (2010) employed a synthetic lethal screening method and have reported that the combined inhibition of the EGFR and Aurora A kinase pathways had synergistic effect on cancer cell viability in head and neck and colon cancer cell lines suggesting a potential benefit of such combination therapy in patients. Our study aims to examine the effects of combination of erlotinib (E), an EGFR small-molecule inhibitor, and Alisertib (MLN8237, A), an inhibitor of Aurora A kinase, in lung cancer models. Treatment of two human NSCLC cell lines, A549 and H322M, with E+A showed synergistic activity in vitro. These cell lines were chosen for the xenografts studies in CB17 SCID mice. After tumors reached a volume of 100 mm3, mice were treated with E+A for three weeks. The xenografts were sensitive to growth inhibition by E (10 mg/kg/day) and A (20 mg/kg/twice daily) alone and the combination had an additive effect. In order to understand early cell signaling events in tumors treated with these agents we repeated the xenograft experiment by treating mice with a one time dosing of each drug alone and in combination. Three tumors per group were collected at 0 , 6 , 24 , or 48 hours after treatment and a panel of signaling molecules downstream of the EGFR and Aurora A kinase pathways were examined by Western blot. These included EGFR/pEGFR; HER2; HER3; MEK/pMEK; ERK/pERK; Src/pSrc and Akt/pAkt among others. Our results suggest that combined inhibition of both pathways in lung cancer cell lines and xenografts can lead to a reduced proliferative index as indicated by quantitative changes in these proteins and that this combination might be effective as a treatment strategy. A clinical trial with this combination is in progress at our center. Citation Format: Tetyana Bagnyukova, Xiaofan Pan, Jiping Zhang, Brian Egleston, Igor Astsaturov, Erica Golemis, Hossein Borghaei. Effects of dual inhibition of EGFR and Aurora A kinase in a lung cancer model. [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 4242. doi:10.1158/1538-7445.AM2014-4242
Molecular Chaperone GRP94 Binds to the Fanconi Anemia Group C Protein and Regulates Its Intracellular Expression
Authors: Taizo Hoshino, Jianxiang Wang, Marcel P. Devetten, Nobuhisa Iwata, Sachiko Kajigaya, Robert J. Wise, Johnson M. Liu, Hagop Youssoufian
Journal: Blood (1998)
Abstract 5051: Alteration of Atherogenic Lipoproteins by Statin Therapy in Patients With Diabetes in a Large Pooled Clinical Trial Database
Authors: Christie M Ballantyne, Philip J Barter, Stephen J Nicholls, Valerie A Cain, Joel S Raichlen
Journal: Circulation (2008)

Reducing LDL-C to current goals may still leave an excess of atherogenic lipoproteins as reflected in apolipoprotein (Apo) B levels. Apo B provides a measure of atherogenic particles in blood, a predictor of CHD events. Patients with diabetes mellitus (DM) are at increased CHD risk and warrant intensive therapy. Recent joint ADA and ACCF guidelines recommend reducing Apo B to &lt;90 mg/dL in high-risk patients and optionally to &lt;80 mg/dL in those at very high risk. We examined the effect of statin therapy on the relationship between these Apo B targets and LDL-C and non-high-density lipoprotein cholesterol (non-HDL-C) in high-risk patients with and without DM. A pooled analysis of data in the rosuvastatin clinical development program was used to identify 12,269 high CHD risk patients who were examined at baseline and after therapy with rosuvastatin, atorvastatin or simvastatin. Apo B was compared with LDL-C and non-HDL-C both at baseline and on therapy using linear regression. At baseline, Apo B target of 90 mg/dL in DM was equivalent to LDL-C of 115 mg/dL and non-HDL-C of 139.8 mg/dL, which was slightly higher than for non-DM (Table ). Achieving Apo B of 90 mg/dL or 80 mg/dL required much more aggressive LDL-C and non-HDL-C goals on statin therapy. Of note, this effect and resultant targets were very similar in DM and non-DM. Achieving with statin therapy Apo B of 90 mg/dL in high-risk patients requires LDL-C target of ~80 mg/dL and non-HDL-C target of ~108 mg/dL. The on-therapy LDL-C target (&lt;70 mg/dL) and non-HDL-C target (&lt;100 mg/dL) for very high risk patients correspond to Apo B target of 80 mg/dL. During statin therapy, Apo B correlated well with LDL-C (R 2 =0.77– 0.81) and very well with non-HDL-C (R 2 =0.88 – 0.90). Non-HDL-C may be a useful surrogate for direct Apo B measurement. High-risk DM and non-DM patients require lower LDL-C and non-HDL-C targets during statin therapy in order to reduce Apo B to the recommended level.
Estimating Deaths Due to Influenza and Respiratory Syncytial VirusEstimating Deaths Due to Influenza and Respiratory Syncytial Virus
Authors: Nigel J Gay, Nick J Andrews, Caroline L Trotter, W John Edmunds
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
Abstract MP30: Chronic Kidney Disease Progression and Risk of End-Stage Renal Disease: The Use of Change in Novel Kidney Filtration Markers
Authors: Casey M Rebholz, Kunihiro Matsushita, Elizabeth Selvin, Morgan E Grams, Josef Coresh
Journal: Circulation (2014)

Introduction: Chronic kidney disease (CKD) progression assessed by estimated GFR from creatinine (eGFR-Cr) is a risk factor for cardiovascular disease and end-stage renal disease (ESRD) and has been proposed as a surrogate endpoint for clinical trials. It is unclear if CKD progression assessed by change in different filtration markers has similar risk associations with ESRD. Hypothesis: We hypothesized that percent change in novel kidney filtration markers (β 2 -microglobulin and cystatin C) over a 6-year period would be independently associated with increased risk of ESRD during 15 years of follow-up, similar to the risk seen with change in eGFR-Cr. Methods: We conducted prospective analyses of the ARIC study (N=9,703). β 2 -microglobulin, cystatin C, and creatinine were measured at study visits 1 (1990-92) and 2 (1996-98). Incident ESRD (kidney dialysis or transplant) was defined as entry into the U.S. Renal Data System registry between study visit 2 and September 30, 2011. Cox proportional hazards regression was used to estimate the association between percent change in filtration marker and incident ESRD, adjusting for demographics, kidney disease risk factors, and 1 st measurement of the filtration marker. Results: During a median follow-up of 13.1 years, there were 142 incident ESRD cases. Median eGFR-Cr was 97.3 mL/min/1.73 m 2 at 1 st measurement and 89.0 mL/min/1.73 m 2 at 2 nd measurement. Percent change in eGFR-Cr was moderately correlated with percent change in the inverse of β 2 -microglobulin (r = 0.34) and the inverse of cystatin C (r = 0.36). Progression of CKD (10-25% and &gt;25% decline in filtration function) was associated with increased ESRD risk, with novel markers (β 2 -microglobulin, cystatin C) showing an association at least as strong as the creatinine and eGFR-Cr estimates (Table). Conclusions: CKD progression assessed using novel filtration markers is independently associated with ESRD risk, suggesting the potential utility of measuring change in β 2 -microglobulin and cystatin C in clinical trials.
Pediatricians Warned About Student Athletes' Risky Weight-Control Tactics
Authors: Bridget M Kuehn
Journal: JAMA (2006)

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
Abstract 891: Substandard Quality of ECG Monitoring in Current Clinical Practice: Preliminary Results of the Practical Use of the Latest Standards for Electrocardiography (PULSE) Trial
Authors: Marjorie Funk, Jeanine May, Kimberly Stephens, Chelsea Hoffman, Elisabeth Hurley, Catherine Winkler, Kristopher Fennie, Julie Gaither, Barbara Drew
Journal: Circulation (2009)
Drug company influence extends to nurses, pharmacists, and patient groups
Authors: Zosia Kmietowicz
Journal: BMJ (2004)

The influence of pharmaceutical companies extends far beyond doctors, with its authority growing among nurses and pharmacists as well as patient groups, MPs heard last week.

Speaking at the third public session of the House of Commons Health Committee's inquiry into the influence of the drug companies, Matt Griffiths, senior charge nurse and joint prescribing adviser at the Royal College of Nursing, told MPs how interest from pharmaceutical companies in nursing had increased since nurses gained the right to prescribe.

As well as sponsoring meetings for nurses, pharmaceutical companies were active in running educational “diploma” courses for nurses on conditions such as …
Leptin and Neutrophil‐Activating Peptide 2 Promote Mesenchymal Stem Cell Senescence Through Activation of the Phosphatidylinositol 3‐Kinase/Akt Pathway in Patients With Systemic Lupus Erythematosus
Authors: Haifeng Chen, Bingyu Shi, Xuebing Feng, Wei Kong, Weiwei Chen, Linyu Geng, Jinyun Chen, Rui Liu, Xia Li, WanJun Chen, Xiang Gao, Lingyun Sun
Journal: Arthritis & Rheumatology (2015)

Objective Mesenchymal stem cells (MSCs) derived from patients with systemic lupus erythematosus (SLE) exhibit enhanced senescence. Cellular senescence has been reported to be induced by several inflammatory cytokines, including interferon‐α (IFNα) and IFNγ, that are involved in the pathogenesis of SLE. We undertook this study to investigate whether the inflammatory environment in SLE could affect MSC senescence. Methods Cellular senescence was measured by staining of senescence‐associated β‐galactosidase and by expression of the cell cycle inhibitors p53 and p21. Eighty cytokines and chemokines in serum from healthy controls and patients with SLE were identified by cytokine antibody array. Results SLE serum promoted senescence of MSCs, which was reversed by the phosphatidylinositol 3‐kinase (PI3K)/Akt signaling inhibitor LY294002 but not by the JAK/STAT inhibitor AG490 and not by the MEK/ERK inhibitor PD98059. Cytokine antibody array analysis revealed that leptin and neutrophil‐activating peptide 2 (NAP‐2) were the 2 factors most significantly elevated in SLE serum compared with normal serum. Blockade of leptin or NAP‐2 in MSC cultures abolished SLE serum–induced senescence, while direct addition of these 2 factors could promote senescence in cultures of normal MSCs. Inhibition of PI3K/Akt signaling with LY294002 reduced leptin‐ and NAP‐2–induced senescence in MSCs. Conclusion Taken together, our data show that leptin and NAP‐2 act synergistically to promote MSC senescence through enhancement of the PI3K/Akt signaling pathway in SLE patients.
Supplemental Oxygen and Risk of Surgical Site Infection—Reply
Authors: Kane O. Pryor, Thomas J. Fahey, Cynthia A. Lien, Peter A. Goldstein
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
RORC1 Regulates Tumor-Promoting “Emergency” Granulo-Monocytopoiesis
Authors: Laura Strauss, Sabina Sangaletti, Francesca Maria Consonni, Gabor Szebeni, Sara Morlacchi, Maria Grazia Totaro, Chiara Porta, Achille Anselmo, Silvia Tartari, Andrea Doni, Francesco Zitelli, Claudio Tripodo, Mario P. Colombo, Antonio Sica
Journal: Cancer Cell (2015)
Differential Regulatory Role of Pituitary Adenylate Cyclase–Activating Polypeptide in the Serum‐Transfer Arthritis Model
Authors: Bálint Botz, Kata Bölcskei, László Kereskai, Miklós Kovács, Tamás Németh, Krisztián Szigeti, Ildikó Horváth, Domokos Máthé, Noémi Kovács, Hitoshi Hashimoto, Dóra Reglődi, János Szolcsányi, Erika Pintér, Attila Mócsai, Zsuzsanna Helyes
Journal: Arthritis & Rheumatology (2014)

Pituitary adenylate cyclase-activating polypeptide (PACAP) expressed in capsaicin-sensitive sensory neurons and immune cells has divergent functions in inflammatory and pain processes. This study was undertaken to investigate the involvement of PACAP in a mouse model of rheumatoid arthritis. Arthritis was induced in PACAP(-/-) and wild-type (PACAP(+/+) ) mice by K/BxN serum transfer. General features of the disease were investigated by semiquantitative scoring, plethysmometry, and histopathologic analysis. Mechano- and thermonociceptive thresholds and motor functions were also evaluated. Metabolic activity was assessed by positron emission tomography. Bone morphology was measured by in vivo micro-computed tomography, myeloperoxidase activity and superoxide production by bioluminescence imaging with luminol and lucigenin, respectively, and vascular permeability by fluorescent indocyanine green dye study. PACAP(+/+) mice developed notable joint swelling, reduced grasping ability, and mechanical (but not thermal) hyperalgesia after K/BxN serum transfer. In PACAP(-/-) mice clinical scores and edema were significantly reduced, and mechanical hyperalgesia and motor impairment were absent, throughout the 2-week period of observation. Metabolic activity and superoxide production increased in the tibiotarsal joints of wild-type mice but were significantly lower in PACAP(-/-) animals. Myeloperoxidase activity in the ankle joints of PACAP(-/-) mice was significantly reduced in the early phase of arthritis, but increased in the late phase. Synovial hyperplasia was also significantly increased, and progressive bone spur formation was observed in PACAP-deficient mice only. In PACAP-deficient mice with serum-transfer arthritis, joint swelling, vascular leakage, hyperalgesia, and early inflammatory cell accumulation are reduced; in the later phase of the disease, immune cell function and bone neoformation are increased. Elucidation of the underlying pathways of PACAP activity may open promising new avenues for development of therapy in inflammatory arthritis.
Does the WHO have a role in Europe?
Authors: M. McKee
Journal: BMJ (1998)

News p 1408 

In 1988 an observer could be forgiven for asking whether the World Health Organisation had any meaningful role in Europe. Indigenous malaria, the classic focus of international health action, had long been eradicated. Non-communicable diseases were increasing but were viewed largely as a matter for individual countries, which were believed to have the capacity to respond. There was little demand for international input into health sector reform because, although East and West pursued different ideologies, no scope existed for constructive dialogue between them. The WHO did support many valuable networks, but some were arguing that this role could be undertaken by the European Union.

So have things changed? The European region of the WHO covers the same geographical area as it did 10 years ago (though it is easy to forget that this extends from Reykjavik to Vladivostok), but the political environment has changed enormously, bringing huge implications for health in its wake. The most obvious manifestation …
La Tension Artérielle en Clinique, Sa Mesure, Sa Valeur Séméiologique.
Authors: L. Gallavardin
Journal: JAMA (1920)

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