tbuckley/cabot-search huggingface dataset:
Spatial variation in incidence of nonmelanoma skin cancers
Authors: J. Verne
Journal: British Journal of Dermatology (2011)

Funding sources None. Conflicts of interest None declared. This paper by Carsin et al.1 in the current issue of BJD is the first to look at the important issues of geographical, urban/rural and socioeconomic variations in incidence of nonmelanoma skin cancers (NMSCs). As the authors note, NMSCs are the commonest cancers in white populations yet few cancer registries comprehensively record data on them. This has significantly hampered epidemiological study of these cancers which are rarely fatal, but because of their great number, impose a significant burden on both primary and secondary care services. Moreover, a clinically important proportion of patients will need extensive and cosmetically challenging surgery. The setting is ideal: a fairly homogeneous fair‐skinned population with a cancer registry which registers all NMSCs. The study is an ecological study which cannot provide definitive aetiological answers. However, it makes some interesting discoveries. A key finding is of a significant inverse association between deprivation and incidence which is stronger for basal cell carcinoma (BCC) than squamous cell carcinoma (SCC). Both BCC and SCC were more common in densely populated areas. These differences may reflect greater empowerment to access and greater ease of access to health services rather than an aetiological phenomenon, although the authors refer to data showing that both overseas travel and use of sunbeds are more common in residents of urban areas. Areas with a higher frequency of farmers were positively associated with SCC risk in males.
Abstract 18569: Inhibition of Prolyl Hydroxylase Stimulates Hif-mediated Sdf-1 Expression and CXCR4+ Cell Recruitment for Myocardial Repair
Authors: Santhosh Kumar Ghadge, Thi Van Pham, Moritz Messner, Maximilian Doppelhammer, Wolfgang-Michael Franz, Marc-Michael Zaruba
Journal: Circulation (2014)

Objective: Data from our lab indicate that stabilization of the cardiac SDF-1/CXCR4 axis preserves myocardial function and attenuates ischemic cardiomyopathy. However, HIF-1α dependent SDF-1 upregulation lasts only for 48-72 hours after MI limiting the targeting of stem cells to ischemic myocardium. To overcome this caveat, we aimed to activate SDF-1 expression by stabilization of HIF-1α through inhibition of prolyl hydroxylase with the ratio to augment CXCR4+ stem cell recruitment and stimulate myocardial repair. Methods: To evaluate the effects on HIF-1α mediated SDF-1 expression, genetically taggedSDF1-EGFP mice were subjected to optimal doses (80mg/kg i.p.) of the prolyl hydroxylase Inhibitor dimethyloxalylglycine (DMOG). To track the fate of CXCR4+ cells, genetically tagged CXCR4-EGFP BAC reporter mice were utilized. FACS and immunhistochemical analyses of CXCR4+ bone marrowm(BM), peripheral blood, and heart cells as well as infarct sizes were analyzed under normoxaemic and ischemic conditions with and without DMOG treatment. Results: SDF1-EGFP mice treated with DMOG showed robust induction of SDF-1 in the heart. SDF-1 upregulation after DMOG treatment was further confirmed by SDF-1 ELISA of heart lysates. FACS of transgenic CXCR4-EGFP BM and hearts revealed that CXCR4+ was most frequently expressed on CD11b+ monocytes, and to a less amount on angiogenic CD31+ , CD34+, c-kit+, and Flk1+ cells, as well as stem cell populations like ACC133+ and Lin-/c-kit+/Sca-1+. After myocardial ischemia these cell populations were highly upregulated. A subpopulation of CXCR4-EGFP+ cells co-expressed CD31 in capillaries. Treatment with DMOG revealed a robust upregulation of CXCR4+ cell populations in the ischemic heart, predominantly of angiogenic CXCR4+/CD11b+ monocytes. Further analysis showed that DMOG Treatment after 7 days leads particularly to upregulation of CD206+ subpopulation in infarcted hearts in favor of repair mechanisms characterized by reduced infarct sizes. Summary and Conclusion: Our data suggest that inhibition of prolyl hydroxylase may be a promising target for HIF-1a mediated SDF-1 activation to increase stem cell homing and myocardial repair.
Procyanidin B-2, extracted from apples, promotes hair growth: a laboratory study
Authors: A. Kamimura, T. Takahashi
Journal: British Journal of Dermatology (2002)

We have previously reported that several selective protein kinase C (PKC) inhibitors, including procyanidin B-2, promote hair epithelial cell growth and stimulate anagen induction.We discuss the hypothesis that the hair-growing activity of procyanidin B-2 is related to its downregulation or inhibition of translocation of PKC isozymes in hair epithelial cells.We examined the effect of procyanidin B-2 on the expression of PKC isozymes in cultured murine hair epithelial cells as well as PKC isozyme localization in murine dorsal skin at different stages in the hair cycle.We observed that procyanidin B-2 reduces the expression of PKC-alpha, -betaI, -betaII and -eta in cultured murine hair epithelial cells and also inhibits the translocation of these isozymes to the particulate fraction of hair epithelial cells. Our immunohistochemical analyses demonstrated that PKC-alpha, -betaI, -betaII and -eta are specifically expressed in the outer root sheaths of both anagen and telogen hair follicles. The hair matrix at the anagen stage showed no positive staining for these PKC isozymes. Moderate to intense staining for PKC-betaI and -betaII in the epidermis and hair follicles was observed in a telogen-specific manner; however, expression of PKC-alpha and -eta during the telogen stage was not conspicuous. Gö 6976, an inhibitor of calcium-dependent (conventional) PKC, proved to promote hair epithelial cell growth.These results suggest that PKC isozymes, especially PKC-betaI and -betaII, play an important role in hair cycle progression and that the hair-growing mechanisms of procyanidin B-2 are at least partially related to its downregulation of PKC isozymes or its inhibition of translocation of PKC isozymes to the particulate fraction of hair epithelial cells.
Report Highlights Barriers to Research on Firearms and Violence
Authors: Thomas B Cole
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
The association of functional polymorphisms in the aryl hydrocarbon receptor ( <i>AHR</i> ) gene with the risk of vitiligo in Han Chinese populations
Authors: X‐W. Wang, K. Li, S. Guo, H‐N. Qiang, L. Liu, P. Song, C. Wei, X‐L. Yi, Z. Jian, Q. Li, C‐Y. Li, T‐W. Gao
Journal: British Journal of Dermatology (2011)

Background Vitiligo is an acquired depigmentation disorder resulting from selective destruction of melanocytes. The aryl hydrocarbon receptor (AHR) is vital to the regulation of melanogenesis and melanocyte proliferation and differentiation through modulating the expressions of melanogenesis-related genes. AHR mutations may negatively affect AHR proteins and its target genes. Therefore, we hypothesized that AHR polymorphisms might be involved in vitiligo by impacting the transcriptional activities of related genes as mentioned above. Objectives To evaluate the potential association between AHR polymorphisms and vitiligo susceptibility. Methods We performed a hospital-based, case–control study of 1000 patients with vitiligo and 1000 vitiligo-free but age- and gender-matched controls. Two single nucleotide polymorphisms of the AHR gene (rs10249788 and rs2066853) were selected and genotyped using a polymerase chain reaction–restriction fragment length polymorphism method. Results A statistically significantly decreased risk of vitiligo was found to be associated with the TT and CT genotypes of rs10249788 [odds ratio (OR) 0·59, 95% confidence interval (CI) 0·38–0·93; P = 0·028 and OR 0·82, 95% CI 0·68–0·98; P = 0·032, respectively] as well as among subgroups: male, active, nonsegmental vitiligo, and onset age ≤ 20 years. Moreover, subjects with the combined (CT + TT)/GG genotype or T/G haplotype (rs10249788/rs2066853) showed a decreased risk for vitiligo (OR 0·57, 95% CI 0·37–0·87, P = 0·009 and OR 0·78, 95% CI 0·64–0·96, P = 0·033, respectively). Conclusions These results suggest that the T allele of rs10249788 located in the promoter of the AHR gene is associated with a protective effect on vitiligo in Han Chinese populations.
Abstract 17038: A Role of Invasive Left Ventriculography during Cardiac Catheterization for Predicting Incidence of Major Cardiovascular Events
Authors: Shingo Kuwata, Kihei Yoneyama, Kengo Suzuki, Masaki Izumo, Yuki Ishibashi, Eiji Takahashi, Takanobu Mitarai, Ryo Kamijima, Kohei Koyama, Yasuhiro Tanabe, Ken Kongoji, Tomoo Harada, Yoshihiro J Akashi
Journal: Circulation (2014)

Introduction: We have developed the new index of left ventricular longitudinal axis shortening (LAS) using contrast left ventriculography (LVG) during Cardiac Catheterization. Objective: The purpose of this study was to evaluate whether LAS provided additive prognostic information beyond traditional ejection fraction (EF). Methods: Nine hundred and ninety eight consecutive patients who had undergone conventional catheters based on clinical indications between 2009 and 2012 were followed retrospectively from our clinical chart. LAS was assessed from LVG (see Figure). Cox regression analysis was used to predict the endpoints of all-cause mortality and congestive heart failure (HF). Receiver operating characteristic curve analysis was used for the discrimination ability of LAS for event beyond traditional EF. Results: Sixty-two events were observed during the follow-up period for mean 3.1±1.1 years. In the adjusted model, the endpoints were associated with lower LAS (hazard ratio 0.89; 95% confidence interval 0.80 to 0.90 per 1% LAS increment, p=0.036) after adjustment for the Framingham risk score, history of myocardial infarction and HF, number of stenosis vessels, EF, left ventricular end-diastolic pressure and Log brain natriuretic peptide (BNP). LAS improved ROC area by 7% compared with EF, and LAS combined with EF and log BNP by 13% (see Figure). Conclusion: LAS by LVG can be a predictor of death and congestive HF and appears to be a better parameter than traditional EF in patients who underwent invasive coronary angiography for clinical indications.
A Diagnosis of the Metabolic Syndrome in Youth That Resolves by Adult Life Is Associated With a Normalization of High Carotid Intima-Media Thickness and Type 2 Diabetes Mellitus Risk
Authors: Costan G. Magnussen, Juha Koskinen, Markus Juonala, Wei Chen, Sathanur R. Srinivasan, Matthew A. Sabin, Russell Thomson, Michael D. Schmidt, Quoc Manh Nguyen, Ji-Hua Xu, Michael R. Skilton, Mika Kähönen, Tomi Laitinen, Leena Taittonen, Terho Lehtimäki, Tapani Rönnemaa, Jorma S.A. Viikari, Gerald S. Berenson, Olli T. Raitakari
Journal: Journal of the American College of Cardiology (2012)
Development of Leiomyomas in Female Rats with an Endocrine Imbalance
Authors: Carroll A. Pfeiffer
Journal: Cancer Research (1949)

Summary  Of 185 endocrine imbalance female rats, 16 survived over 3 years. Leiomyomas were present in 4 of these 16 animals. One animal had multiple tumors; 2 were located in the middle and lower third of the right cornu, and a third was near the cervical end of the left cornu. The other 3 animals had single tumors. In one of these the tumor was located in the right cornu. In the other 2 it was in the left cornu. It is believed that the chronic estrogen stimulation resulting from the endocrine imbalance increases the chance of smooth muscle tumor formation.
Epicardial electrogram of the right ventricular outflow tract in patients with the brugada syndrome
Authors: Satoshi Nagase, Kengo Fukushima Kusano, Hiroshi Morita, Yoshihisa Fujimoto, Mikio Kakishita, Kazufumi Nakamura, Tetsuro Emori, Hiromi Matsubara, Tohru Ohe
Journal: Journal of the American College of Cardiology (2002)
803. Functional Analysis of Various Gene Linkers Serving Proportional Coexpression of PET Marker and Therapeutic Genes
Authors: Alexandra Winkeler, Markus Hartung, Marc Slack, Andreas H. Jacobs
Journal: Molecular Therapy (2004)

Top of pageAbstract
Objective: To improve the overall level of gene expression of the second gene of interest in our universal HSV-1 amplicon vectors (Jacobs et al. 2003) using alternative gene linkers (eukaryotic IRES, 2A) and/or mutant HSV-1 thymidine kinase (tk39; Black et al. 1996).

Background: The gene expression cassette cdIREStkgfp (Jacobs et al. 2003) was originally engineered to assess for the proportionality of co-expression of the therapeutic E. coli cytosine deaminase gene, cd, and the HSV-1-tkgfp fusion gene (fusion of the herpes simplex virus type 1 thymidine kinase gene serving as PET-marker gene and the gene coding for green fluorescent protein, gfp, as a reporter gene for cell culture; Jacobs et al. 1999). Functional evaluation had shown an attenuation of the IRES-mediated expression of the second fusion gene compared to the expression of the gene at the 5'-primed end of the IRES-element.

Methods: First, the ECMV-derived IRES-element was replaced by an eucaryotic IRES-element (Ie; Chappell et al. 2000) as well as by the 2A-element of the food and mouth disease (FMD) virus (deFelipe et al. 1999). Thereafter, human Gli36dEGFR glioma cells (as well as BHK, Vero2-2, U87 cells) were infected with an MOI=1 of HSV-CITG, HSV-CIeTG or HSV-C2ATG, and relative GFP-expression was compared. 24 h after infection, a single cell analysis of relative GFP-expression was performed by means of the MPI-Tool imaging software (Jacobs et al. 2003). Second, the HSV-1-tk gene was replaced by the gene mutant HSV-1-tk39 showing a higher enzymatic efficiency than the wild type HSV-1-tk (Black et al. 1996). Gli36dEGFR cells were infected with an MOI=3 of HSV-CITG or HSV-CITk39G, and an MTT-assay was performed employing different concentrations of ganciclovir (0.01-10 g/ml).

Results: In cell culture, the relative level of TKGFP-expression mediated by HSV-CIeTG-and HSV-C2ATG-infection was 65.2+21.9% and 86.6+12.4%, respectively, compared to HSV-CITG infected cells. These data indicate a further attenuation- instead of the expected improvement- of expression of the second gene in all tested cell lines. In contrast, the exchange of wild type HSV-1-tk to its mutant tk39 showed a significant increase in protein activity (LD50 HSV-CITG: 2.7 g/ml GCV; LD50 HSV-CITk39G: 0.023 g/ml GCV).

Conclusion: No significant improvement of the expression of the second gene was achieved by replacing the ECMV-derived IRES-element with the alternative linkers, eukaryotic IRES and 2A-FMD, in all cell lines tested. However, an increasing activity of the second gene product with respect to its TK-activity could be achieved by replacing the wild type tk-gene with the tk39 mutant possessing a higher enzymatic efficiency.
Abstract P112: Association between sleep duration and serum lipid levels in an elderly Korean population: The Korean Urban and Rural Elderly (KURE) Study
Authors: Hansol Choi, Ju-Mi Lee, YooSik Youm, Yumie Rhee, Chang Oh Kim, Hyeon Chang Kim
Journal: Circulation (2014)

Importance: Sleep duration has been considered as a risk factor for cardiometabolic disease and mortality. Several studies suggest that sleep duration can influence the serum lipid levels, but the association remains unclear. Objective: The aim of present study is to assess the association of sleep duration with serum lipid levels in an elderly Korean population. Methods: The KURE study is a cohort study to investigate risk factors for major disorders of the elderly. This cross-sectional analysis was conducted among 926 participants (302 men and 624 women aged 64-87 years) who completed baseline health examination in 2012. Sleep duration was measured by the interviewer-assisted questionnaire. Habitual sleep time was calculated based on the response to the questions about hour of bedtime, hour of rising, and hours of nap during the passing year. Total cholesterol, triglyceride and high density lipoprotein (HDL) cholesterol concentrations in serum were measured from overnight fasting blood samples. Low density lipoprotein (LDL) cholesterol was calculated from total cholesterol, HDL cholesterol and triglyceride levels using Friedewald’s formula. Multiple linear regression models were conducted to examine whether sleep duration was associated with serum lipid levels. Results: Sleep duration was not significantly associated with total cholesterol (β=-0.154mg/dL per sleep hour, p =0.843), triglyceride (β=-1.000, p =0.506) and LDL cholesterol (β=0.678, p =0.339) after adjusting for age, sex, body mass index, systolic blood pressure, tobacco smoking, alcohol intake, physical activity, diabetes mellitus, myocardial infarction and stroke. However sleep duration was inversely associated with HDL cholesterol (β=-0.644, p =0.015) in fully adjusted model. In the sex-specific analysis, sleep duration was marginally associated with HDL cholesterol in men (β=-0.770, p =0.078) and significantly associated with HDL cholesterol in women (β=-0.685, p =0.037) after fully adjustment. Conclusions: Our findings suggest that longer sleep duration was associated with lower serum HDL cholesterol level in an elderly Korean population. Keywords: Sleep duration, lipids, HDL cholesterol, elderly
Abstract P314: Plasma Polyunsaturated Fatty Acids and Fish Oil Intake in Relation to Pulse Wave Velocity - The AGES Reykjavik Study
Authors: Ilse Reinders, Rachel A Murphy, Xiaoling Song, Gary F Mitchell, Marjolein Visser, Mary Frances Cotch, Melissa E Garcia, Lenore J Launer, Gudny Eiriksdottir, Vilmundur Gudnason, Tamara B Harris, Ingeborg A Brouwer
Journal: Circulation (2015)

Introduction: Higher intake and circulating polyunsaturated fatty acids (PUFAs) are associated with lower CVD risk. PUFAs might influence vascular health via reducing arterial stiffness, resulting in a better CVD risk profile, but investigations of this association in the general population are limited. Hypothesis: We assessed the hypothesis that higher levels of plasma phospholipid long chain n-3 PUFAs (eicosapentaenoic acid (EPA), docosapentaenoic acid (DPA), docosahexaenoic acid (DHA), alpha-linolenic acid (ALA)), and long chain n-6 PUFAs (linoleic acid (LA) and arachidonic acid (AA)) are associated with lower arterial stiffness. We also assessed the hypothesis that higher dietary intake of fish oil in early life (ages 14 to 19), mid-life (ages 40 to 50) and in old age (ages 69 to 96, study baseline) is associated with lower arterial stiffness. Methods: We used longitudinal data from a subgroup of AGES-Reykjavik Study participants (n=501, 75.0±4.96 years, 46% men), a population-based study of community...
Abstract B21: Chemoresistant bladder cancer cells induces epithelial mesenchymal transition
Authors: Jingchun Liu, Darryl T. Martin, Marcia A. Wheeler, Robert M. Weiss
Journal: Clinical Cancer Research (2015)

Abstract Although chemotherapeutic treatments are efficacious in a number of cancers, some cancer cells ultimately will become resistant to chemotherapy. It has been suggested that chronic chemotherapy-resistance is linked to the induction of epithelial mesenchymal transition (EMT). EMT is associated with increased tumor invasiveness, development of angiogenesis, and the development of drug resistance and is linked to more aggressive cancer. The objective of this study is to determine if a link exists between mitomycin C (MMC)-resistant RT-4 bladder cancer cells and the induction of EMT. EMT is a process where cells acquire molecular alterations characterized by loss of cell-cell adhesion, repression of E-cadherin expression, and increased cell mobility. Clinical studies have shown that as bladder cancer grade increases, tumors typically exhibit a decreased expression of E-cadherin, a cell-cell adhesion molecule. In addition, there is an increase in N-cadherin expression in muscle invasive bladder tumors. We have shown that MMC-resistant human RT-4 bladder cancer cells demonstrate a decrease in cell-cell adhesion, a higher invasion potential, and a higher CD44(+)/CD24(-) ratio (96.4%) compared to parental human RT-4 bladder cancer cells. In addition, the invasion capacity of MMC-resistant RT-4 bladder cancer cells was higher than that of parental cells. The MMC-resistant RT-4 bladder cancer cells expressed higher levels of N-cadherin and numerous apoptotic related proteins including pSTAT3, RAD17, Bcl-X and catalase. Using an exon array we showed that the MMC-resistant RT-4 bladder cancer cells up-regulate several EMT markers including vimentin (77 times), transforming growth factor -beta (27 times), and Zinc finger E-box-binding homeobox 1 (33 times) and down-regulate E-cadherin (71 times). In summary, in our MMC-resistant RT4 bladder cancer cells, EMT was activated, and there was an increase in apoptotic related proteins as well as an increase N-cadherin expression. Our data suggest a link between chemotherapy-resistant bladder cancer cells and EMT. Deactivating EMT and down-regulating apoptotic related proteins may offer a novel strategy for overcoming bladder cancer drug resistance. Citation Format: Jingchun Liu, Darryl T. Martin, Marcia A. Wheeler, Robert M. Weiss. Chemoresistant bladder cancer cells induces epithelial mesenchymal transition. [abstract]. In: Proceedings of the AACR Precision Medicine Series: Drug Sensitivity and Resistance: Improving Cancer Therapy; Jun 18-21, 2014; Orlando, FL. Philadelphia (PA): AACR; Clin Cancer Res 2015;21(4 Suppl): Abstract nr B21.