tbuckley/cabot-search huggingface dataset:
Risk Factors for Astigmatism in Preschool Children
Authors: Roberta McKean-Cowdin, Rohit Varma, Susan A. Cotter, Kristina Tarczy-Hornoch, Mark S. Borchert, Jesse H. Lin, Ge Wen, Stanley P. Azen, Mina Torres, James M. Tielsch, David S. Friedman, Michael X. Repka, Joanne Katz, Josephine Ibironke, Lydia Giordano
Journal: Ophthalmology (2011)
Abstract 1891: Mutations in polymerase ϵ as key molecular alteration of the novel ultramutator phenotype do not define a clinically distinct entity of colorectal cancer
Authors: Albrecht Stenzinger, Endris Volker, Nicole Pfarr, Roland Penzel, Lina Jansen, Esther Herpel, Wilfried Roth, Hendrik Bläker, Jenny Chang-Claude, Hermann Brenner, Michael Hoffmeister, Wilko Weichert
Journal: Cancer Research (2014)

Abstract Background: Recent molecular profiling studies reported a new class of ultramutated colorectal cancers (CRC), which are likely caused by exonuclease domain (END) mutations in DNA polymerase ϵ (POLE). However, data on the clinical implications of these biological findings as to whether these mutations in analogy to endometrial cancer define a unique CRC entity with distinct clinical outcome is entirely lacking. Methods: We performed Sanger sequencing of the POLE END in 431 well annotated microsatellite stable (MSS) CRCs of a population-based epidemiological case-control study (DACHS). Mutation data were correlated with major epidemiological, clinical, genetic and pathological parameters including overall and disease-specific survival. Results: In 373 out of 431 MSS CRC all exons of POLE END were analyzable. 47 mutations in the END of POLE were identifiable in 41 of these samples (11%). Besides already reported mutations affecting the codons 459, 411 and 286, we found many new mutations in exons 13 and 14 (corresponding to codons 411-491 of the END) as well as in exon 12 (corresponding to codons 268-301 of the END), which have not been reported yet. However, we found no associations of POLE END mutations with clinicopathological parameters, including sex, age, tumor location and tumor stage, CIMP, RAS and BRAF mutations. Survival analysis by cox regression revealed adjusted (for sex, age, tumor location and therapy) HRs of 1.38 and 1.44 for disease-specific and overall survival indicating slightly impaired survival of patients with mutations in POLE END, however, these differences were not statistically significant. This was also true for the subgroups of different exons, known/new, potentially damaging/non-damaging mutations and the type of mutation. Conclusions: In contrast to endometrial cancer, somatic POLE mutations do not appear to define a clinically strongly distinct disease entity in CRC. Citation Format: Albrecht Stenzinger, Endris Volker, Nicole Pfarr, Roland Penzel, Lina Jansen, Esther Herpel, Wilfried Roth, Hendrik Bläker, Jenny Chang-Claude, Hermann Brenner, Michael Hoffmeister, Wilko Weichert. Mutations in polymerase ϵ as key molecular alteration of the novel ultramutator phenotype do not define a clinically distinct entity of colorectal 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 1891. doi:10.1158/1538-7445.AM2014-1891
Reversal of virus-induced systemic shock and respiratory failure by blockade of the lymphotoxin pathway
Authors: Maryann T. Puglielli, Jeffrey L. Browning, Avery W. Brewer, Robert D. Schreiber, Wun-Ju Shieh, John D. Altman, M.B.A. Oldstone, Sherif R. Zaki, Rafi Ahmed
Journal: Nature Medicine (1999)
Novel Biomaterials for Human Health: Hemocompatible Polymeric Micro‐and Nanoparticles and Their Application in Biosensor
Authors: Chong Sun, Xiaobo Wang, Chun Mao, Jian Shen
Journal: Advanced Healthcare Materials (2014)

This chapter contains sections titled: Introduction Design and Preparation of Hemocompatible Polymeric Micro- and Nanoparticles The Biosafety and Hemocompatibility Evaluation System for Polymeric Micro- and Nanoparticles Construction of Biosensor for Direct Detection in Whole Blood Conclusion and Prospect
UTY gene codes for an HLA-B60–restricted human male-specific minor histocompatibility antigen involved in stem cell graft rejection: characterization of the critical polymorphic amino acid residues for T-cell recognition
Authors: Mario H. J. Vogt, Els Goulmy, Freke M. Kloosterboer, Els Blokland, Roel A. de Paus, Roel Willemze, J. H. Frederik Falkenburg
Journal: Blood (2000)
The gene encoding gigaxonin, a new member of the cytoskeletal BTB/kelch repeat family, is mutated in giant axonal neuropathy
Authors: Pascale Bomont, Laurent Cavalier, François Blondeau, Christiane Ben Hamida, Samir Belal, Meriem Tazir, Ercan Demir, Haluk Topaloglu, Rudolf Korinthenberg, Beyhan Tüysüz, Pierre Landrieu, Fayçal Hentati, Michel Koenig
Journal: Nature Genetics (2000)
AEG33783, a potent JNK pathway inhibitor with neuroprotective properties, selectively induces apoptosis in tumor cell lines
Authors: Stephen J. Morris, Christelle Pomiès, Guillaume Lévesque, Geneviève Doucet, Jon P. Durkin, John W. Gillard
Journal: Cancer Research (2005)

Proc Amer Assoc Cancer Res, Volume 46, 2005

2265 

AEG33783 is a pre-clinical neuroprotective agent, under development to rescue peripheral neurons from chemotherapy-induced toxicity. [AEG33783][1] antagonizes JNK signaling through modulation of heat-shock protein levels in primary sympathetic neuronal culture, leading to potent neuronal protection against oxaliplatin, vinblastine and in-vivo protection against cisplatin and paclitaxel-induced nerve conduction velocity changes. Because JNK signaling is implicated in the survival of tumor cells, and [AEG33783][1] is projected to be used to treat chemotherapy-induced peripheral neuropathies, we examined the effect of [AEG33783][1] on cancer cells alone and in combination with chemotherapy agents. In combination with various chemotherapy agents (paclitaxel, vinblastine, and cisplatin) in 72 hour, MTS-based 96 well cell viability assays, [AEG33783][1] did not protect MDA MB231 (breast), HCT116 (colorectal), H460 (lung), or DU145 (prostate) from dose-proportional killing. At all doses there was increased chemotherapy efficacy. In fact, significant stand-alone cytotoxicity of [AEG33783][1] on certain neuroblastoma cell lines was noted, with IC50’s in the high nanomolar range. Of particular interest, [AEG33783][1] potentiated the efficacy of melphalan five- fold against neuroblastoma cells and importantly was not toxic to the diploid human fibroblast line WI38, nor did it affect melphalan toxicity on fibroblasts . Further examination of [AEG33783][1] in clonogenic assays revealed IC50 values in the high nanomolar range against cell lines of breast, prostate, and colorectal origin. [AEG33783][1] is revealed as a novel compound that has pronounced anticancer effects in addition to potent neuroprotective ability.

 [1]: /lookup/external-ref?link_type=GENPEPT&access_num=AEG33783&atom=%2Fcanres%2F65%2F9_Supplement%2F532.1.atom
SUBACUTE (STREPTOCOCCUS VIRIDANS) ENDOCARDITIS; THE RÔLE OF TRAUMA IN THE LOCALIZATION OF VEGETATIONS
Authors: Joseph J. Furlong
Journal: Annals of Internal Medicine (1944)

Case Reports1 May 1944SUBACUTE (STREPTOCOCCUS VIRIDANS) ENDOCARDITIS; THE RÔLE OF TRAUMA IN THE LOCALIZATION OF VEGETATIONSJOSEPH J. FURLONGJOSEPH J. FURLONGAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-20-5-822 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe outstanding importance of preëxisting rheumatic valvular disease as a factor in the subsequent development of subacute bacterial endocarditis has been indicated by the high incidence of this lesion in published analyses of large series of cases. Thus Christian reported that 89 per cent of 150 patients at Peter Bent Brigham Hospital, and Middleton 81.6 per cent of 88 cases at Wisconsin General Hospital showed evidence of preëxisting rheumatic endocarditis. The reason for this intimate relationship has been variously attributed to altered tissue resistance in the damaged valve, changes in blood supply, a predilection of scar tissue to reinfection, or...Bibliography ABBOTT ME: Congenital heart disease, In BLUMER'S "Bedside diagnosis," 1928, W. B. Saunders Co., Philadelphia. Google Scholar BLUMER G: Subacute bacterial endocarditis, Medicine 1923, ii, 105. CrossrefGoogle Scholar BLUMGART H: Subacute bacterial endocarditis involving the right side of the heart, Med. Clin. N. Am., 1933, xvi, 881. Google Scholar CHRISTIAN H: Etiology of subacute bacterial endocarditis, Am. Jr. Med. Sci., 1941, cci, 34. Google Scholar KINSELLAMUETHER RRO: Experimental streptococcic endocarditis, Arch. Int. Med., 1938, lxii, 247. CrossrefGoogle Scholar LIBMAN E: Bacteria-free stage of bacterial endocarditis, Am. Jr. Med. Sci., 1913, cxlvi, 625. CrossrefGoogle Scholar MIDDLETONBURKE WSM: Subacute (Streptococcus viridans) endocarditis, Am. Jr. Med. Sci., 1939, cxcviii, 301. Google Scholar THAYER W: Bacterial endocarditis, Edinburgh Med. Jr., 1938, xxxviii, 237-307. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: MC U.S.N.R. Seattle, Washington*Received for publication April 16, 1942.From the Department of Medicine of the Marquette University Medical School. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byInfective endocarditis in heroin addictsAortic Valvular Bacterial Endocarditis in Tetralogy of Fallot Following Blalock AnastomosisDiscrete Subaortic Stenosis Complicated by Aortic Valvular RegurgitationRight-sided bacterial endocarditis and endarteritisBacterial Endocarditis in the Elderly 1 May 1944Volume 20, Issue 5Page: 822-826KeywordsBacterial diseasesBloodEndocarditisFactor analysisLesionsScarsStreptococcusValvular diseases ePublished: 1 December 2008 Issue Published: 1 May 1944 PDF downloadLoading ...
Abstract 3731: Luminescent cell health assays for tumor spheroid evaluation
Authors: Michael P. Valley, Kevin R. Kupcho, Chad A. Zimprich, Andrew L. Niles, James J. Cali, Jens M. Kelm, Wolfgang Moritz, Dan F. Lazar
Journal: Cancer Research (2014)

Abstract Microtissues produced in 3D cell culture are much more representative of actual living tissue compared to monolayers produced in 2D cell culture. In fact, in the area of oncology research, multicellular tumor spheroids are considered an excellent platform for testing drug delivery and efficacy. As the necessity for established 3D cell culture models rises, there is also a need for convenient assays that have been specifically demonstrated to be effective for use with 3D microtissues. The more complex architecture of 3D microtissues demands increased lytic effectiveness and reagent penetration, characteristics that are often only minor considerations for reagents designed for 2D cell culture. Here we report on a variety of bioluminescent and fluorescent cell-based assays applied to hanging-drop spheroids produced from HCT116 colon cancer cells. The first assay to be described is an ATP detection reagent for measuring cell viability. This reagent has both an improved formulation and an optimized assay protocol and has clear advantages over other viability assays. Other cell health assays will also be described, including reagents that measure cell death, apoptosis, mechanistic cytotoxicity, or reporter gene expression. These additional assays do not require a change in formulation, but do require new protocols in order to optimize their effectiveness when applied to 3D microtissues. As with their application to cells in 2D culture, these “add-mix-measure” reagents are robust and amenable to both low- and high-throughput applications. Citation Format: Michael P. Valley, Kevin R. Kupcho, Chad A. Zimprich, Andrew L. Niles, James J. Cali, Jens M. Kelm, Wolfgang Moritz, Dan F. Lazar. Luminescent cell health assays for tumor spheroid evaluation. [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 3731. doi:10.1158/1538-7445.AM2014-3731
758. A Histone Deacetylase Inhibitor Enhances Recombinant Adeno-Associated Virus-Mediated Gene Expression in Cancer Cells In Vitro and In Vivo
Authors: Takashi Okada, Tatsuya Nomoto, Yuhe Liu, Mayumi Iwata-Okada, Masafumi Takahashi, Kuniko Shimazaki, Takashi Matsushita, Hiroaki Mizukami, Akihiro Kume, Keiya Ozawa
Journal: Molecular Therapy (2004)

Background: The transduction of cancer cells using recombinant adeno-associated virus (rAAV) occurs with low efficiency, which limits its utility in cancer gene therapy. We have previously sought to enhance rAAV-mediated transduction of cancer cells by applying DNA-damaging stresses. An alternative technique to improve the rAAV-mediated transduction of tumor cells is enhancement at a transcription step. Treatment with a histone deacetylase (HDAC) inhibitor is known to recover the gene expression from a silenced rAAV genome that has been integrated into the host's genome. However, rAAV exists mostly as an extrachromosomal genome rather than as an integrated genome, and this extrachromosomal form is the primary source of gene expression. We examined whether the HDAC inhibitor could contribute to the enhanced transcription before integration occurs.
Brief Report: Etanercept Inhibits the Tumor Necrosis Factor α–Driven Shift of Th17 Lymphocytes Toward a Nonclassic Th1 Phenotype in Juvenile Idiopathic Arthritis
Authors: Laura Maggi, Rolando Cimaz, Manuela Capone, Veronica Santarlasci, Valentina Querci, Gabriele Simonini, Francesca Nencini, Francesco Liotta, Sergio Romagnani, Enrico Maggi, Francesco Annunziato, Lorenzo Cosmi
Journal: Arthritis & Rheumatology (2014)

To evaluate the effects of etanercept on the phenotype of CD4+ T helper lymphocytes from patients with juvenile idiopathic arthritis (JIA).We compared the proportions of various Th cell subsets in peripheral blood (PB) from etanercept-treated and untreated JIA patients. An in vitro study was performed on PB mononuclear cells (PBMCs) from 15 children with untreated JIA, in which we evaluated the proliferative response of these cells, as well as their cytokine production profile, in the presence of various stimuli with or without etanercept.We found lower proportions of CD4+ CD161+ (nonclassic) Th1 lymphocytes in the PB of patients treated with etanercept than in untreated patients. In vitro, etanercept inhibited the proliferative response induced by either polyclonal or recall antigen stimulation of PBMCs. Moreover, etanercept increased the proportion of CD4+CD161+ Th17/Th1 and Th17 cells in vitro while decreasing the proportions of nonclassic Th1 cell subsets, leaving CD4+CD161- (classic) Th1 cells unaffected. We also found that tumor necrosis factor α (TNFα) was able to induce transition of Th17 lymphocytes toward the nonclassic Th1 phenotype in vitro, probably due to the high expression of TNF receptor type II observed in Th17 cells.We have previously demonstrated the occurrence of a shifting of CD4+CD161+ Th17 cells to the nonclassic Th1 phenotype in children with JIA. The present findings suggest that etanercept can exert its disease-modifying action by interfering with this shifting.
A Novel Method for N-Terminal Acetylation Prediction
Authors: Ying Liu, Yuanlie Lin
Journal: Genomics Proteomics & Bioinformatics (2004)

The NetAcet method has been developed to make predictions of N-terminal acetylation sites, but more information of the data set could be utilized to improve the performance of the model. By employing a new way to extract patterns from sequences and using a sample balancing mechanism, we obtained a correlation coefficient of 0.85, and a sensitivity of 93% on an independent mammalian data set. A web server utilizing this method has been constructed and is available at http://166.111.24.5/acetylation.html.
Evidence based case report: Low back pain: which is the best way forward?
Authors: A. Samanta, J. Beardsley
Journal: BMJ (1999)

Mr A, a fit and healthy 62 year old, presented with a 10 year history of intermittent non-specific low back pain. He had been able to control his symptoms with several self help measures, including weight control, regular aerobic activity, a firm mattress, back mobilisation exercises, and a naturally positive attitude. He had an active lifestyle and travelled extensively, but his episodes of acute pain had become increasingly severe and frequent and were starting to interfere with his quality of life. Radiological examination showed degenerative changes in the lumbar spine, predominantly at L4 and L5. A review of Mr A's medical history and a clinical examination did not give rise to any suspicion that he might have a serious spinal abnormality or nerve root problems.

We considered the following clinical question. Which of the treatments available locally showed the best evidence of limiting acute attacks of low back pain in a patient with a history of chronic back pain?Our specific aim in Mr A's case was to obtain reliable information as quickly as possible so that we could immediately advise him of the best treatment option.

Our previous experience of reviewing published reports on chronic low back pain had shown that there are many types of treatment, both complementary and conventional. Since our experience is with conventional treatments, we confined our search to these. Four main treatments available locally were relevant to Mr A's condition: physiotherapy and exercise programmes; spinal manipulation; spinal steroid injections; and transcutaneous electrical nerve stimulation. We decided to research the evidence for these treatments and to look for any other evidence based treatments that might be relevant.

Previous searching of Medline and Embase had shown a profusion of reports on treating low back pain. On closer examination, however, many of these lacked …
Somatization: the under-recognized factor in nonspecific eczema. The Hordaland Health Study (HUSK)
Authors: M. Klokk, S. Stansfeld, S. Øverland, I. Wilhelmsen, K.G. Gotestam, S. Steinshamn, A. Mykletun
Journal: British Journal of Dermatology (2010)

Psychodermatology has focused primarily on depression and anxiety in eczema. Skin symptoms are listed among many others for the ICD-10 diagnosis of somatization disorder. Somatization (unexplained somatic symptoms) is highly prevalent in the general population, but its association with eczema is yet to be empirically investigated.We therefore explored the association between somatization and eczema by examining the extent of somatization in eczema compared with allergic rhinitis, and by examining if eczema was more strongly associated with somatization than with anxiety and depression. Finally, we aimed to examine the relationship between the site of eczema and somatization for individual somatic symptoms and for somatic symptoms as a whole.For this population-based cross-sectional study we employed data from the Hordaland Health Study (HUSK) with 15,225 participants aged 41-48 years. Information on nonspecific eczema, allergic rhinitis, somatization, anxiety, depression and other covariates was obtained by self-report.The association between nonspecific eczema and somatization was strong and followed a dose-response pattern, as did all somatic symptoms in our index of somatization when analysed separately. The association between nonspecific eczema and somatization was stronger than that between rhinitis and somatization, and also the association between nonspecific eczema and anxiety and depression. In multivariate models, somatization accounted for most of the association between nonspecific eczema and anxiety/depression. In contrast, the association between nonspecific eczema and somatization was robust for adjustment for anxiety/depression.Somatization was strongly associated with nonspecific eczema. This applies to a whole range of somatic symptoms constituting the construct of somatization. There is hardly any mention of somatization in leading dermatological journals, in contrast to anxiety and depression which are frequently reported in eczema. We speculate that this under-recognition of somatization in the dermatological literature may correspond to under-recognition of this factor also in clinical practice.
Abstract 3750: Targeting PD-L1 sensitizes head and neck squamous cell carcinoma to cisplatin
Authors: Peter Qiao, Shayanne A. Lajud, Danish A. Nagda, Nobuaki Tanaka, Alyssa Civantos, Bert W. O'Malley, Daqing Li
Journal: Cancer Research (2014)

Abstract Platinum-based chemotherapy agents such as Cisplatin (CDDP) are commonly used as first-line treatment for several types of human cancers including ovarian, lung, testicular, and head and neck squamous cell carcinomas (HNSCC). Unfortunately, CDDP monotherapy is often ineffective due to inherent or acquired tumor resistance to therapy, also known as chemoresistance. This contributes to a need for the administration of larger, more toxic doses, as well as failure of chemotherapy and tumor recurrence. Despite the clinical significance of chemoresistance, the mechanisms driving this phenomenon are not completely understood. Programmed cell death ligand 1 (PD-L1), a membrane-bound glycoprotein responsible for modulating the immunological response through the induction of T-Cell anergy and apoptosis, has been shown to be overexpressed in many cancers, including HNSCC. While PD-L1 overexpression has been directly related to the immunoevasion of cancer cells allowing for tumor progression, recent reports suggest that PD-L1 also plays an important role in the tumor response to doxorubicin-based chemotherapy independent of its immune function. The present study investigates the role of PD-L1 in response to CDDP in HNSCC. In vitro experiments were performed using four well-characterized human HNSCC cell lines. Quantitative polymerase chain reaction (qPCR) and western blot were conducted to determine the baseline and post-CDDP-treatment PD-L1 gene expression. The results demonstrated that PD-L1 mRNA transcription and protein expression are upregulated in response to CDDP, suggesting that PD-L1 is involved in the chemoresponse. Conversely, knockdown of PD-L1 using siRNA resulted in chemosensitization of HNSCC cells to CDDP. Together, these findings implicate PD-L1 in the CDDP-chemoresponse in HNSCC. In conclusion, we propose a role for PD-L1 that is distinct from the classic immunoevasion pathway. Our findings demonstrate that disruption of this protein leads to increased sensitivity of HNSCC cells to CDDP, suggesting a potential combination therapeutic strategy for patients with CDDP-resistant HNSCC. Citation Format: Peter Qiao, Shayanne A. Lajud, Danish A. Nagda, Nobuaki Tanaka, Alyssa Civantos, Bert W. O'Malley, Daqing Li. Targeting PD-L1 sensitizes head and neck squamous cell carcinoma to cisplatin. [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 3750. doi:10.1158/1538-7445.AM2014-3750