tbuckley/cabot-search huggingface dataset:
It May Be Time to Abandon Urine Tests for Bladder Cancer
Authors: Joseph J. Fantony, Brant A. Inman
Journal: Journal of the National Comprehensive Cancer Network (2015)

Bladder cancer is the second most common malignancy of the genitourinary tract and fifth most common malignancy overall in the United States. 1 The current standard for diagnosis and surveillance of bladder cancer includes a combination of cystoscopy and urine cytology. 2The propensity of bladder cancer for recurrence leads to a need for frequent monitoring, making bladder cancer currently the most expensive per-patient malignancy to treat in the United States. 3hese points, along with the discomfort, anxiety, and morbidity of frequent cystoscopy have led to much effort in developing alternative, less-invasive methods for bladder surveillance. 4In this commentary, we suggest that no advancement in noninvasive testing has occurred in recent years capable of altering the current endoscopic surveillance scheme.We further argue that the poor performance, marginal clinical utility, and potential harm of the currently available urine tests make them inadequate for regular clinical use.
Functionalized biocompatible WO3 nanoparticles for triggered and targeted in vitro and in vivo photothermal therapy
Authors: Shazid Md. Sharker, Sung Min Kim, Jung Eun Lee, Kyung Ho Choi, Gyojic Shin, Sangkug Lee, Kang Dae Lee, Ji Hoon Jeong, Haeshin Lee, Sung Young Park
Journal: Journal of Controlled Release (2015)
CD49d Is The Strongest Flow Cytometry-Based Predictor Of Overall Survival In Chronic Lymphocytic Leukemia
Authors: Pietro Bulian, Tait D Shanafelt, Chris Fegan, Antonella Zucchetto, Lilla Cro, Holger Nuckel, Luca Baldini, Antonina Kurtova, Alessandra Ferrajoli, Jan A. Burger, Gianluca Gaidano, Giovanni Del Poeta, Chris Pepper, Davide Rossi, Valter Gattei
Journal: Blood (2013)
Demographic Prevalence of Class III Obesity—Reply
Authors: Lin Yang, Graham A. Colditz
Journal: JAMA Internal Medicine (2015)

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No Accumulation of Transposable Elements in Asexual Arthropods
Authors: Jens Bast, Ina Schaefer, Tanja Schwander, Mark Maraun, Stefan Scheu, Ken Kraaijeveld
Journal: Molecular Biology and Evolution (2015)

Transposable elements (TEs) and other repetitive DNA can accumulate in the absence of recombination, a process contributing to the degeneration of Y-chromosomes and other nonrecombining genome portions. A similar accumulation of repetitive DNA is expected for asexually reproducing species, given their entire genome is effectively nonrecombining. We tested this expectation by comparing the whole-genome TE loads of five asexual arthropod lineages and their sexual relatives, including asexual and sexual lineages of crustaceans (Daphnia water fleas), insects (Leptopilina wasps), and mites (Oribatida). Surprisingly, there was no evidence for increased TE load in genomes of asexual as compared to sexual lineages, neither for all classes of repetitive elements combined nor for specific TE families. Our study therefore suggests that nonrecombining genomes do not accumulate TEs like nonrecombining genomic regions of sexual lineages. Even if a slight but undetected increase of TEs were caused by asexual reproduction, it appears to be negligible compared to variance between species caused by processes unrelated to reproductive mode. It remains to be determined if molecular mechanisms underlying genome regulation in asexuals hamper TE activity. Alternatively, the differences in TE dynamics between nonrecombining genomes in asexual lineages versus nonrecombining genome portions in sexual species might stem from selection for benign TEs in asexual lineages because of the lack of genetic conflict between TEs and their hosts and/or because asexual lineages may only arise from sexual ancestors with particularly low TE loads.
Injured sensory neuron–derived CSF1 induces microglial proliferation and DAP12-dependent pain
Authors: Zhonghui Guan, Julia A Kuhn, Xidao Wang, Bradley Colquitt, Carlos Solorzano, Smitha Vaman, Andrew K Guan, Zoe Evans-Reinsch, Joao Braz, Marshall Devor, Sherry L Abboud-Werner, Lewis L Lanier, Stavros Lomvardas, Allan I Basbaum
Journal: Nature Neuroscience (2015)
Apremilast, an oral phosphodiesterase 4 inhibitor, in patients with difficult-to-treat nail and scalp psoriasis: Results of 2 phase III randomized, controlled trials (ESTEEM 1 and ESTEEM 2)
Authors: Phoebe Rich, Melinda Gooderham, Hervé Bachelez, Joana Goncalves, Robert M. Day, Rongdean Chen, Jeffrey Crowley
Journal: Journal of the American Academy of Dermatology (2015)

In the phase III double-blind Efficacy and Safety Trial Evaluating the Effects of Apremilast in Psoriasis (ESTEEM) 1 and 2, apremilast, an oral phosphodiesterase 4 inhibitor, demonstrated efficacy in moderate to severe psoriasis.We sought to evaluate efficacy of apremilast in nail/scalp psoriasis in ESTEEM 1 and 2.A total of 1255 patients were randomized (2:1) to apremilast 30 mg twice daily or placebo. At week 16, placebo patients switched to apremilast through week 32, followed by a randomized withdrawal phase to week 52. A priori efficacy analyses included patients with nail (target nail Nail Psoriasis Severity Index score ≥1) and moderate to very severe scalp (Scalp Physician Global Assessment score ≥3) psoriasis at baseline.At baseline, 66.1% and 64.7% of patients had nail psoriasis; 66.7% and 65.5% had moderate to very severe scalp psoriasis in ESTEEM 1 and 2. At week 16, apremilast produced greater improvements in Nail Psoriasis Severity Index score versus placebo; mean percent change: -22.5% versus +6.5% (ESTEEM 1; P < .0001) and -29.0% versus -7.1% (ESTEEM 2; P = .0052). At week 16, apremilast produced greater NAPSI-50 response (50% reduction from baseline in target nail Nail Psoriasis Severity Index score) versus placebo (both studies P < .0001) and ScPGA response (Scalp Physician Global Assessment score 0 or 1) versus placebo (both studies P < .0001). Improvements were generally maintained over 52 weeks in patients with Psoriasis Area and Severity Index response at week 32.Baseline randomization was not stratified for nail/scalp psoriasis.Apremilast reduces the severity of nail/scalp psoriasis.
Multilocus Inherited Neoplasia Alleles Syndrome
Authors: James Whitworth, Anne-Bine Skytte, Lone Sunde, Derek H. Lim, Mark J. Arends, Lisa Happerfield, Ian M. Frayling, Rick van Minkelen, Emma R. Woodward, Marc D. Tischkowitz, Eamonn R. Maher
Journal: JAMA Oncology (2015)

Mendelian causes of inherited cancer susceptibility are mostly rare and characterized by variable expression and incomplete penetrance. Phenotypic variability may result from a range of causes including locus heterogeneity, allelic heterogeneity, genetic and environmental modifier effects, or chance. Another potential cause is the presence of 2 or more inherited cancer predisposition alleles in the same individual. Although the frequency of such occurrences might be predicted to be low, such cases have probably been underascertained because standard clinical practice has been to test candidate inherited cancer genes sequentially until a pathogenic mutation is detected. However, recent advances in next-generation sequencing technologies now provide the opportunity to perform simultaneous parallel testing of large numbers of inherited cancer genes. Herein we provide examples of patients who harbor pathogenic mutations in multiple inherited cancer genes and review previously published examples to illustrate the complex genotype-phenotype relationships in these cases. We suggest that clinicians should proactively consider the likelihood of this phenomenon (referred to herein as multilocus inherited neoplasia alleles syndrome [MINAS]) in patients with unusual inherited cancer syndrome phenotypes. To facilitate the clinical management of novel cases of MINAS, we have established a database to collect information on what is likely to be an increasingly recognized cohort of such individuals.
True costs are different from those given in paper
Authors: N R Waugh
Journal: BMJ (1996)

EDITOR,—I believe that there are problems with the costing used in J P O'Hare and colleagues' study of the effect of adding retinal photography to screening for diabetic retinopathy.1

Firstly, no detail of the method is given. The figure of £12.50 for the cost of adding photography first appears in the discussion, and it would be useful to know what it includes (for example, labour, materials, capital for camera and van).

Secondly, the cost per patient whose sight is saved is based on dividing the extra cost of adding …
Re: Grace L. Lu-Yao, Peter C. Albertsen, Dirk F. Moore, Yong Lin, Robert S. DiPaola, Siu-Long Yao. Fifteen-year Outcomes Following Conservative Management Among Men aged 65 Years or Older with Localized Prostate Cancer. Eur Urol 2015;68:805–11
Authors: Michael Froehner, Rainer Koch, Manfred P. Wirth
Journal: European Urology (2015)
Hyperbranched–hyperbranched polymeric nanoassembly to mediate controllable co-delivery of siRNA and drug for synergistic tumor therapy
Authors: Hui-Zhen Jia, Wei Zhang, Jun-Yi Zhu, Bin Yang, Si Chen, Gang Chen, Yi-Fang Zhao, Jun Feng, Xian-Zheng Zhang
Journal: Journal of Controlled Release (2015)
High-Density Genetic Mapping Identifies New Susceptibility Variants in Sarcoidosis Phenotypes and Shows Genomic-driven Phenotypic Differences
Authors: Natalia V. Rivera, Marcus Ronninger, Klementy Shchetynsky, Andre Franke, Markus M. Nöthen, Joachim Müller-Quernheim, Stefan Schreiber, Indra Adrianto, Bekir Karakaya, Coline H. M. van Moorsel, Zdenka Navratilova, Vitezslav Kolek, Benjamin A. Rybicki, Michael C. Iannuzzi, Martin Petrek, Jan C. Grutters, Courtney Montgomery, Annegret Fischer, Anders Eklund, Leonid Padyukov, Johan Grunewald
Journal: American Journal of Respiratory and Critical Care Medicine (2015)

Sarcoidosis is a multisystem disease of unknown cause. Löfgren's syndrome (LS) is a characteristic subgroup of sarcoidosis that is associated with a good prognosis in sarcoidosis. However, little is known about its genetic architecture or its broader phenotype, non-LS sarcoidosis.To address the genetic architecture of sarcoidosis phenotypes, LS and non-LS.An association study in a white Swedish cohort of 384 LS, 664 non-LS, and 2,086 control subjects, totaling 3,134 subjects using a fine-mapping genotyping platform was conducted. Replication was performed in four independent cohorts, three of white European descent (Germany, n = 4,975; the Netherlands, n = 613; and Czech Republic, n = 521), and one of black African descent (United States, n = 1,657), totaling 7,766 subjects.A total of 727 LS-associated variants expanding throughout the extended major histocompatibility complex (MHC) region and 68 non-LS-associated variants located in the MHC class II region were identified and confirmed. A shared overlap between LS and non-LS defined by 17 variants located in the MHC class II region was found. Outside the MHC region, two LS-associated loci, in ADCY3 and between CSMD1 and MCPH1, were observed and replicated.Comprehensive and integrative analyses of genetics, transcription, and pathway modeling on LS and non-LS indicates that these sarcoidosis phenotypes have different genetic susceptibility, genomic distributions, and cellular activities, suggesting distinct molecular mechanisms in pathways related to immune response with a common region.
Ibrutinib versus temsirolimus in patients with relapsed or refractory mantle-cell lymphoma: an international, randomised, open-label, phase 3 study
Authors: Martin Dreyling, Wojciech Jurczak, Mats Jerkeman, Rodrigo Santucci Silva, Chiara Rusconi, Marek Trneny, Fritz Offner, Dolores Caballero, Cristina Joao, Mathias Witzens-Harig, Georg Hess, Isabelle Bence-Bruckler, Seok-Goo Cho, John Bothos, Jenna D Goldberg, Christopher Enny, Shana Traina, Sriram Balasubramanian, Nibedita Bandyopadhyay, Steven Sun, Jessica Vermeulen, Aleksandra Rizo, Simon Rule
Journal: The Lancet (2015)
MDGA2 is a novel tumour suppressor cooperating with DMAP1 in gastric cancer and is associated with disease outcome
Authors: Kunning Wang, Qiaoyi Liang, Xiaoxing Li, Ho Tsoi, Jingwan Zhang, Hua Wang, Minnie Y Y Go, Philip W Y Chiu, Enders K W Ng, Joseph J Y Sung, Jun Yu
Journal: Gut (2015)

<h3>Background</h3> Using the promoter methylation assay, we have shown that MDGA2 (MAM domain containing glycosylphosphatidylinositol anchor 2) is preferentially methylated in gastric cancer. We analysed its biological effects and prognostic significance in gastric cancer. <h3>Methods</h3> MDGA2 methylation status was evaluated by combined bisulfite restriction analysis and bisulfite genomic sequencing. The effects of MDGA2 re-expression or knockdown on cell proliferation, apoptosis and the cell cycle were determined. MDGA2 interacting protein was identified by mass spectrometry and MDGA2-related cancer pathways by reporter activity and PCR array analyses. The clinical impact of MDGA2 was assessed in 218 patients with gastric cancer. <h3>Results</h3> MDGA2 was commonly silenced in gastric cancer cells (10/11) and primary gastric cancers due to promoter hypermethylation. MDGA2 significantly inhibited cell proliferation by causing G1–S cell cycle arrest and inducing cell apoptosis in vitro, and suppressed xenograft tumour growth in both subcutaneous and orthotopic xenograft mouse models (both p&lt;0.001). The anti-tumorigenic effect of MDGA2 was mediated through direct stabilising of DNA methyltransferase 1 associated protein 1 (DMAP1), which played a tumour suppressive role in gastric cancer. This interaction activated their downstream key elements of p53/p21 signalling cascades. Moreover, promoter methylation of MDGA2 was detected in 62.4% (136/218) of gastric cancers. Multivariate analysis showed that patients with MDGA2 hypermethylation had a significantly decreased survival (p=0.005). Kaplan–Meier survival curves showed that MDGA2 hypermethylation was significantly associated with shortened survival in patients with early gastric cancer. <h3>Conclusions</h3> MDGA2 is a critical tumour suppressor in gastric carcinogenesis; its hypermethylation is an independent prognostic factor in patients with gastric cancer.
Concomitant Retrograde Coronary Venous Infusion of Basic Fibroblast Growth Factor Enhances Engraftment and Differentiation of Bone Marrow Mesenchymal Stem Cells for Cardiac Repair after Myocardial Infarction
Authors: Xiao Wang, Lei Zhen, Huangtai Miao, Qiwei Sun, Ya Yang, Bin Que, Edmundo Patricio Lopes Lao, Xingxin Wu, Hongmei Ren, Shutian Shi, Wayne B. Lau, Xinliang Ma, Changsheng Ma, Shaoping Nie
Journal: Theranostics (2015)

Aim: Basic fibroblast growth factor (bFGF) increases the migration and viability of bone marrow mesenchymal stem cells (MSCs) in vitro.Retrograde coronary venous infusion can provide both increased regional bFGF concentrations and homogeneous cell dissemination.We determined whether retrograde delivery of bFGF enhances the potency of transplanted MSCs for cardiac repair in a canine infarct model.Methods and Results: Under hypoxic conditions, cellular migration was significantly increased in MSCs co-cultured with bFGF compared to vascular endothelial growth factor or insulin-like growth factor, and bFGF promoted MSCs differentiation into a cardiomyocyte phenotype.A canine infarct model was employed by coronary ligation.One week later, animals were subjected to retrograde infusion of combination bFGF (200ng/mL) and MSCs (1×10 8 cells) (n=5), MSCs (1×10 8 cells, n=5), bFGF (200ng/mL, n=5), or placebo (phosphate-buffered saline, n=3).Four weeks after infusion, only the bFGF+MSCs therapy exhibited significantly increased left ventricular ejection fraction (LVEF) by echocardiography (p<0.01 vs pre-infusion), and the treatment effect (delta LVEF) was greater in the bFGF+MSCs group compared to saline (7.43±1.51%versus -10.07±2.94%;p<0.001).Morphologic analysis revealed an increased infarct wall thickness in the bFGF+MSCs group compared to all others (p<0.05),accompanied by increased vascular density and reduced apoptosis.Immunofluorescence demonstrated increased cell engraftment and enhanced vascular differentiation in the bFGF+MSCs group compared to MSCs alone (p<0.05).Conclusions: Retrograde coronary venous bFGF infusion augments engraftment and differentiation capacity of transplanted MSCs, recovering cardiac function and preventing adverse remodeling.This novel combined treatment and delivery method is a promising strategy for cardiac repair after ischemic injury.
Diversity and combinations of infectious agents in 38 adults with an infection-triggered reactive haemophagocytic syndrome: a multicenter study
Authors: N. Lerolle, M. Laanani, S. Rivière, L. Galicier, P. Coppo, J.-L. Meynard, J.-M. Molina, E. Azoulay, C. Aumont, C. Marzac, L. Fardet, O. Lambotte
Journal: Clinical Microbiology and Infection (2015)
Akt signal transduction pathway is a target of diindolylmethane and indole-3-carbinol in thyroid cancer
Authors: Yuangen Chen, Kiranmayi Tadi, Badithe T. Ashok, Yushan Chang, Stimsom Schantz, Steven Schaefer, Augustine Moscatello, Raj K. Tiwari
Journal: Cancer Research (2005)

Proc Amer Assoc Cancer Res, Volume 46, 2005

2460 

Compounds in cruciferous vegetables such as indole-3-carbinol (I3C) have a significant role in prevention of many different cancers. However, the anti-proliferative activity of these compounds in thyroid cancer has not been documented. We have been studying the anti-thyroid cancer (CaT) activity of indole-3-carbinol (I3C) and its acid catalyzed dimer, diindolylmethane (DIM) using four different cell lines representing papillary cancer (8505-C and B-CPAP) and follicular carcinoma of the thyroid (ML-1 and CGTHW-1). Cell survival and IC50 values were calculated using the XTT assay and the Trypan Blue exclusion test. Apoptosis was measured by ELISA and protein levels were estimated by western blotting. Both I3C and DIM showed significant anti-CaT effects. I3C had IC50 values that ranged between 100-500 μM, whereas, the IC50 values for DIM were significantly lower between 10-100 μM. The anti-proliferative effect observed with I3C and DIM was due to induction of apoptosis; however, apoptosis induced by DIM was greater than that seen with I3C. Microscopic examination of primary culture of cells from a goiter nodule revealed a significant reduction in the number of DIM and I3C treated cells accompanied by morphological changes. The effects of I3C and DIM on signal transduction pathways were investigated as possible targets for the observed anti-cancer effect. Western blot analysis revealed that the Akt signal transduction pathway is a target of both I3C and DIM. PI3-K and p-Akt were markedly down regulated in ML-1, CGTHW-1 and B-CPAP. The results clearly indicate that DIM has a higher anti-proliferative activity compared to I3C. Based on these data we have initiated a human clinical trial to examine the distribution and retention of DIM in thyroid tissues.
Post-Transplant Diabetes Mellitus: Causes, Treatment, and Impact on Outcomes
Authors: Vijay Shivaswamy, Brian Boerner, Jennifer Larsen
Journal: Endocrine Reviews (2015)

Abstract Post-transplant diabetes mellitus (PTDM) is a frequent consequence of solid organ transplantation. PTDM has been associated with greater mortality and increased infections in different transplant groups using different diagnostic criteria. An international consensus panel recommended a consistent set of guidelines in 2003 based on American Diabetes Association glucose criteria but did not exclude the immediate post-transplant hospitalization when many patients receive large doses of corticosteroids. Greater glucose monitoring during all hospitalizations has revealed significant glucose intolerance in the majority of recipients immediately after transplant. As a result, the international consensus panel reviewed its earlier guidelines and recommended delaying screening and diagnosis of PTDM until the recipient is on stable doses of immunosuppression after discharge from initial transplant hospitalization. The group cautioned that whereas hemoglobin A1C has been adopted as a diagnostic criterion by many, it is not reliable as the sole diabetes screening method during the first year after transplant. Risk factors for PTDM include many of the immunosuppressant medications themselves as well as those for type 2 diabetes. The provider managing diabetes and associated dyslipidemia and hypertension after transplant must be careful of the greater risk for drug-drug interactions and infections with immunosuppressant medications. Treatment goals and therapies must consider the greater risk for fluctuating and reduced kidney function, which can cause hypoglycemia. Research is actively focused on strategies to prevent PTDM, but until strategies are found, it is imperative that immunosuppression regimens are chosen based on their evidence to prolong graft survival, not to avoid PTDM.