tbuckley/cabot-search huggingface dataset:
The studies of PLGA nanoparticles loading atorvastatin calcium for oral administration in vitro and in vivo
Authors: Zhenbao Li, Wenhui Tao, Dong Zhang, Chunnuan Wu, Binbin Song, Shang Wang, Tianyang Wang, Mingming Hu, Xiaohong Liu, Yongjun Wang, Yinghua Sun, Jin Sun
Journal: Asian Journal of Pharmaceutical Sciences (2016)

A biodegradable poly(lactic-co-glycolic acid) loading atorvastatin calcium (AC) nanoparticles (AC-PLGA-NPs) were prepared by probe ultrasonication and evaporation method aiming at improving the oral bioavailability of AC. The effects of experimental parameters, including stabilizer species, stabilizer concentration and pH of aqueous phase, on particle size were also evaluated. The resultant nanoparticles were in spherical shape with an average diameter of 174.7 nm and a narrow particle size distribution. And the drug loading and encapsulation efficiency were about 8% and 71%, respectively. The particle size and polydispersion were almost unchanged in 10 days. The release curves of AC-PLGA-NPs in vitro displaying sustained release characteristics indicated that its release mechanisms were matrix erosion and diffusion. The pharmacokinetic study in vivo revealed that the Cmax and AUC0-∞ of AC-PLGA-NPs in rats were nearly 3.7-fold and 4.7-fold higher than that of pure atorvastatin calcium suspension. Our results demonstrated that the delivery of AC-PLGA-NPs could be a promising approach for the oral delivery of AC for enhanced bioavailability.
Precision Health Outcomes Require Precise Patient Identification
Authors: Julie A. Freischlag, Michelle M. Silva
Journal: JAMA Surgery (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 Surgery HomeNew OnlineCurrent IssueFor Authors Podcast 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 Surgery journal
Association of single-nucleotide polymorphism (SNP) in the 5-alpha-reductase gene (SRD5A2) with increased prevalence of metabolic syndrome in chemotherapy-treated testicular cancer (TC) survivors.
Authors: H. Boer, C. Meijer, J. D. Dijck-Brouwer, I. P. Kema, J. D. Lefrandt, N. Zwart, H. M. Boezen, A. J. Smit, J. A. Gietema
Journal: Journal of Clinical Oncology (2011)

4564 Background: The metabolic syndrome is more prevalent in chemotherapy (CT)-treated TC survivors in comparison with controls. Polymorphisms in the androgen receptor (AR) gene and in SRD5A2 are involved in altered androgen sensitivity, which in turn could result in the metabolic syndrome. We investigated whether a SNP in SRD5A2 and number of CAG repeats in the AR gene were associated with metabolic and cardiovascular status in TC survivors. Methods: TC survivors treated with cisplatin CT were cross-sectionally evaluated for development of cardiovascular risk factors (173 TC survivors; median age 37 yrs [range 19-59], median follow-up of 5 yrs [range 3-20]). Prevalence of metabolic syndrome (criteria AHA/NHBLI), hormonal status and vascular status (intima media thickness of the carotid artery [IMT]) were examined. SNP rs523349 (V89L) in SRD5A2 and CAG repeat numbers in the AR gene were tested against cardiovascular profile. Results: Number of CAG repeats in the AR gene was not associated with any of cardiovascular parameters. Metabolic syndrome was more prevalent in patients heterozygote or homozygote variant for rs523349 in SRD5A2compared to wild types (table). Mean IMT and urinary albumin excretion were higher in the group heterozygote or homozygote variant for rs523349. Conclusions: Metabolic syndrome in TC survivors develops more frequently in patients with a SNP (rs523349) in the gene encoding 5-alpha-reductase. These survivors have more signs of vascular damage. Altered androgen sensitivity appears to be involved in the development of adverse metabolic and subsequent vascular changes in TC survivors and is a target for intervention. Mean (sd)/Median (range)/N (%) SRD5A2 gene Wild-type (VV) (n=91) Variant (VL/LL) (n=82) P* SNP rs523349 (V89L) Age yrs 37 (19-59) 37 (23-56) 0.39 Follow-up yrs 4.9 (3-20) 5.5 (3-20) 0.23 Metabolic syndrome 17 (19%) 27 (33%) 0.032 Body mass index kg/m2 25.3 (3.6) 25.5 (4.3) 0.71 IMT mean mm 0.57 (0.12) 0.62 (0.12) 0.026 Creatinine clearance mL/min 122 (30.8) 124 (35.5) 0.66 Albumin excretion mg/24h 3.1 (0.1-615) 5.6 (0.1-158) 0.017 * Chi2-test, t-test or MW-test used when appropriate.
Surveillance de la coqueluche en Suisse, 1992 à 1997 – épidémie importante en 1994. Que nous réserve l’avenir ?
Authors: H. C. Matter
Journal: Eurosurveillance (1999)

Les cas de coqueluche sont recenses depuis juin 1991 par le Reseau Suisse de Surveillance Sentinelle (Swiss Sentinel Surveillance Network, SSSN). Ce reseau est charge de controler les tendances de la coqueluche en Suisse et d’evaluer la politique vaccinale actuelle (1,2). Le reseau Sentinelle est compose d’un echantillon d’environ 200 medecins volontaires (generalistes, specialistes en medecine interne, et pediatres du secteur prive). Chaque semaine, ils declarent les donnees de morbidite au Bureau Federal Suisse de Sante Publique (Swiss Federal Office of Public Health, SFOPH). Les medecins participants representent environ 3,5% de tous les medecins de moins de 65 ans dans chacune des trois specialites en Suisse.
Abstract 3659: High-Mobility Group Box 1 Restores Cardiac Dysfunction after Myocardial Infarction in Transgenic Mice
Authors: Tatsuro Kitahara, Yasuchika Takeishi, Tetsuro Shishido, Satoshi Suzuki, Shigehiko Kato, Toshiki Sasaki, Olga Bilim, Mitsunori Ishino, Isao Kubota
Journal: Circulation (2008)

High-mobility group box 1 (HMGB1) is a nuclear DNA-binding protein and is released from necrotic cells, inducing inflammatory responses and promoting tissue repair and angiogenesis. To test the hypothesis that HMGB1 enhances angiogenesis and restores cardiac dysfunction after myocardial infarction, we generated transgenic mouse with cardiac specific overexpression of HMGB1 (HMGB1-Tg) using α-myosin heavy chain (MHC) promoter. The left anterior descending coronary artery was ligated in HMGB1-Tg and wild-type littermate (Wt) mice. After coronary artery ligation, HMGB1 was released into circulation from the necrotic cardiomyocytes of HMGB1 overexpressing hearts. The size of myocardial infarction was smaller in HMGB1-Tg than in Wt mice (figure ). Echocardiography and cardiac catheterization demonstrated that cardiac remodeling and dysfunction after myocardial infarction were prevented in HMGB1-Tg mice compared to Wt mice. Furthermore, survival rate after myocardial infarction in HMGB1-Tg mice was higher than that in Wt mice (figure ). Immunohistochemical staining revealed that capillary and arteriole formations after myocardial infarction were enhanced in HMGB1-Tg mice. We demonstrated the first in vivo evidence that HMGB1 enhances angiogenesis, restores cardiac dysfunction, and improves survival after myocardial infarction. These results may provide a novel therapeutic approach for left ventricular dysfunction after myocardial infarction.
P0596 : Association of hepatitis E virus and cryoglobulinemia
Authors: S. Pischke, S. Polywka, J.H. Schirmer, F. Haag, M. Sterneck, M. Luetgehetmann, C. Iking-Konert, W. Dammermann, S. Lueth, F. Moosig, A.W. Lohse
Journal: Journal of Hepatology (2015)
Abstract 3932: Using Sleeping Beauty transposon mutagenesis to identify CRC driver genes
Authors: Zhubo Wei, Haruna Takeda, Neal G. Copeland, Nancy A. Jenkins
Journal: Cancer Research (2015)

Abstract In order to better understand the initiation and development of colorectal cancer (CRC), Sleeping Beauty (SB) transposon mutagenesis screens were performed in mice with mutations in genes that play important roles in differen stages of CRC. Functional validation assays, including invasion assay and xenograft assay, were carried out for the candidate genes that were selected by their potentials in tumor progression and/or human CRC. We identified six genes driving malignant tumor progression, and a new human CRC tumor suppressor gene, ZNF292, that may also function in other types of cancer. More detailed investigations are being done for those identified genes, including experiments using knockout mice. Our study provides a resource for the development of new CRC therapies. Citation Format: Zhubo Wei, Haruna Takeda, Neal G. Copeland, Nancy A. Jenkins. Using Sleeping Beauty transposon mutagenesis to identify CRC driver genes. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 3932. doi:10.1158/1538-7445.AM2015-3932
Activating TCR Signaling to Thwart T-ALL
Authors: François Lemonnier, Tak W. Mak
Journal: Cancer Discovery (2016)

Abstract Summary: Thymic negative selection is a process that aims to eliminate autoreactive T cells by inducing the apoptosis of thymocytes expressing a T-cell receptor (TCR) with high affinity for self-MHC. In this issue, Trinquand and colleagues demonstrate that TCR engagement or anti-CD3 stimulation of TCR-expressing T acute lymphoblastic leukemia cells results in their apoptosis. This cell death is reminiscent of thymic negative selection and has the potential for therapeutic exploitation. Cancer Discov; 6(9); 946–8. ©2016 AACR. See related article by Trinquand et al., p. 972.
Cost of Antihyperglycemic Medications in the United States
Authors: Carlos Alatorre, Eric H. Schultz, David R. Nelson
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
NCI Launches Large Study of Breast Cancer Genetics in Black Women
Authors: Jennifer Abbasi
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 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
Residual Gastric Volume and Risk of Ventilator-Associated Pneumonia
Authors: Gunnar Elke, Daren Heyland
Journal: JAMA (2013)

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
Bortezomib in a myelodysplastic cell line: A gene expression study
Authors: S. Galimberti, H. Savli, M. Canestraro, M. Canestraro, G. A. Palumbo, B. Nagy, F. Di Raimondo, M. Petrini
Journal: Journal of Clinical Oncology (2008)

18018 Background: NF-kB has been reported to be constitutively activated in P39 cell line (a myelomonocytic cell line) and in MDS cases with higher risk of transformation. Another gene whose expression levels have been reported to play a relevant prognostic role in MDS is WT1. Two NF-kB binding sites within the WT1 promoter have been reported; thus, we decided to assess if a compound able to inactivate NF-kB would be also able to down-regulate the WT1 expression. Finally, we performed microarray and real-time quantitative PCR assays for understanding the molecular pathways more significantly affected by this treatment. Methods: For gene expression studies, samples were hybridized on Whole Human Genome Microarray (Agilent). The genes identified as de-regulated by bortezomib were then analyzed for network and gene ontology by Ingenuity Pathway Analysis software. Results have been confirmed by using the TaqMan Low Density Array Human Apoptosis Panel. Results: Bortezomib inactivated NF-kB, and exerted an anti-proliferative and pro-apoptotic effect by blocking cell cycle in the G2 phase. It increased the release of reactive oxygen species and down-regulated the WT1 expression. In the untreated P39, 84 of the 93 genes involved in the apoptosis pathway and represented in the Taqman Low-Density Arrays were expressed. After 12h-treatment, bortezomib up-regulated DIABLO and NFKBIB, (a NF-kB inhibitor), and down-regulated NF-kB1, NF-kB2, and BIRC1, an anti- apoptotic gene. Moreover, microarray assays showed that the PPAR, P53, IL6, IL2, hypoxia, Huntington’s disease, TLR and cell cycle were the pathways more significantly modified. Among down-regulated genes, JUN, HSP70 and HSP90 would be relevant. Indeed, high levels of HSPs have been reported to negatively condition the overall survival of patients with high-risk MDS. Other genes down-regulated were CREBBP, PMAIP1, SPP1, and some adhesion molecules, such as ICAM1. Even reduction of integrins could be a relevant effect exerted by the proteasome inhibitor, because higher serum levels of ICAM1 have been reported to be associated with high-risk MDS and to negatively condition the survival. Conclusions: These results suggest the possible use of proteasome inhibitors in treatment of high-risk MDS. In vivo trials will be useful to confirm this hypothesis. No significant financial relationships to disclose.
Bone Marrow Mesenchymal Stromal Cells Regulate the Metabolism of H2O2 In Human Leukemic Cells.
Authors: Christine Vignon, Marie-Thérèse Georget, Yves Levern, Elfi Ducrocq, Marie-Christine Bernard, Marie-Hélène Estienne, Dominique Kerboeuf, Philippe Rosset, Emmanuel Gyan, Christian Binet, Jorge Domenech, Fabrice Gouilleux, Olivier Herault
Journal: Blood (2010)
A Small-Molecule Antagonist of HIF2α Is Efficacious in Preclinical Models of Renal Cell Carcinoma
Authors: Eli M. Wallace, James P. Rizzi, Guangzhou Han, Paul M. Wehn, Zhaodan Cao, Xinlin Du, Tzuling Cheng, Robert M. Czerwinski, Darryl D. Dixon, Barry S. Goggin, Jonas A. Grina, Megan M. Halfmann, Melissa A. Maddie, Sarah R. Olive, Stephen T. Schlachter, Huiling Tan, Bin Wang, Keshi Wang, Shanhai Xie, Rui Xu, Hanbiao Yang, John A. Josey
Journal: Cancer Research (2016)

Abstract More than 90% of clear cell renal cell carcinomas (ccRCC) exhibit inactivation of the von Hippel–Lindau (pVHL) tumor suppressor, establishing it as the major underlying cause of this malignancy. pVHL inactivation results in stabilization of the hypoxia-inducible transcription factors, HIF1α and HIF2α, leading to expression of a genetic program essential for the initiation and progression of ccRCC. Herein, we describe the potent, selective, and orally active small-molecule inhibitor PT2385 as a specific antagonist of HIF2α that allosterically blocks its dimerization with the HIF1α/2α transcriptional dimerization partner ARNT/HIF1β. PT2385 inhibited the expression of HIF2α-dependent genes, including VEGF-A, PAI-1, and cyclin D1 in ccRCC cell lines and tumor xenografts. Treatment of tumor-bearing mice with PT2385 caused dramatic tumor regressions, validating HIF2α as a pivotal oncogenic driver in ccRCC. Notably, unlike other anticancer agents that inhibit VEGF receptor signaling, PT2385 exhibited no adverse effect on cardiovascular performance. Thus, PT2385 represents a novel class of therapeutics for the treatment of RCC with potent preclincal efficacy as well as improved tolerability relative to current agents that target the VEGF pathway. Cancer Res; 76(18); 5491–500. ©2016 AACR.
A single-arm, phase II, multicenter trial of sunitinib (SU) in locally advanced or metastatic pheochromocytoma/paraganglioma (PC/PG): Updated interim results.
Authors: Raya Leibowitz-Amit, Anthony M. Joshua, Shereen Ezzat, Isabelle Bourdeau, Harold Olney, Sjoukje Oosting, Jo-An Seah, Joseph D. Ruether, Soo Chin, Sylvia L. Asa, Monika K Krzyzanowska, Jennifer J. Knox
Journal: Journal of Clinical Oncology (2014)

e15621 Background: Metastatic PC/PG is rare, may be sporadic or have a genetic basis. Treatment remains challenging in the absence of well-controlled randomized trials. The HIF-VEGF axis has been implicated in PC/PG when associated with germ-line VHL or SDH mutations, and case reports suggest clinical activity of SU in this setting. We aim to prospectively evaluate radiological and biochemical response to SU in PC/PG and assess its toxicity profile. Methods: This is an ongoing single-arm, phase-II, multi-center, investigator-initiated clinical trial, enrolling patients (pts) with metastatic/unresectable malignant PG or PC with ECOG PS 0-2, evidence of radiological or biochemical progression or disease-related symptoms and no previous biological treatment. Following blood pressure stabilization all pts receive 50 mg SU daily for 4/6 week cycle, and are assessed for response by imaging and urine metanephrines, catecholamines or serum chromogranin A q12 weeks until disease progression, unacceptable toxicity or withdrawal. Up to 28 response-evaluable pts will be enrolled in two stages. Using response hypotheses of H0 < 5 % and Ha> 20%, activity of the drug would have been rejected following accrual of 14 pts if no responses were seen. Results: From May 2009 to December 2013, 14 pts enrolled in 3 academic hospitals (Canada and the Netherlands). Median age at SU start was 48 yrs (range 17-68 yrs) and median treatment duration was 9 cycles (range 2-40). SU was generally tolerable in PG/PC pts, with the overall known toxicity profile. Toxicity-related dose reductions were mandated in 9/14 (65%). The interim radiological RR is 21%, and a subjective clinical benefit was observed in 50% of symptomatic pts. The biochemical RR of 67% exceeds the radiological RR, consistent with the recognized impact of SU on tyrosine hydroxylase, the rate-limiting enzyme in catecholamine synthesis. Conclusions: This trial surpassed the pre-specified futility stopping rule with the current documented responses on SU and is ongoing. Clinical trial information: NCT00843037. Response type Total evaluable Response; N (%) Clinical 6 3 (50) Biochemical 12 8 (67) Radiological 14 PR: 3 (21)* SD: 10 (72) PD: 1 (7) * one PR was unconfirmed.