tbuckley/cabot-search huggingface dataset:
Neural Control of Behavior
Authors: David Bentley, Masakazu Konishi
Journal: Annual Review of Neuroscience (1978)

A major goal of neurobiology is to provide an understanding of animal behavior in
terms of the operation of the nervous system. Much of neurobiological research is
therefore concerned at some level with the control of behavior. We have restricted
our comments to attempts to relate a cellular level of neural analysis, involving
neurons whose physiology, morphology, and connectivity are relatively well known,
to fairly complete behavioral acts and to the overall organization of behavior.
Consequently, examples will be drawn almost entirely from work on invertebrate
nervous systems. Rather than review any single research area in detail, we hope to
focus on the nature of behavior as seen from a cellular level, and to identify emerging
principles and problems provided by this approach.
Ovarian Cancer
Authors: Vicki Seltzer
Journal: JAMA (1995)

<h3>Objective.</h3> —To provide physicians with a current consensus on screening, prevention, diagnosis, and treatment of ovarian cancer. <h3>Participants.</h3> —A nonfederal, nonadvocate, 14-member consensus panel representing the fields of gynecologic, medical, and radiation oncology, obstetrics/ gynecology, and biostatistics; 25 experts in obstetrics/gynecology and gynecologic, medical, and radiation oncology who presented data to the consensus panel; and a conference audience of approximately 500. <h3>Evidence.</h3> —The literature was searched through MEDLINE, and an extensive bibliography of references was produced for the panel and the conference audience. Experts prepared abstracts with relevant citations from the literature. Scientific evidence was given priority over clinical anecdotal experience. <h3>Consensus.</h3> —The panel, answering predefined consensus questions, developed their conclusions based on the scientific evidence presented in open forum and the scientific literature. <h3>Consensus Statement.</h3> —The panel composed a draft statement that was read in its entirety and circulated to the experts and the audience for comment. The panel resolved conflicting recommendations and released a revised statement at the end of the conference. The panel finalized the revisions within a few weeks after the conference. <h3>Conclusions.</h3> —There is no evidence available yet that the current screening modalities of CA-125 and transvaginal ultrasonography can be effectively used for widespread screening to reduce mortality from ovarian cancer nor that their use will result in decreased rather than increased morbidity and mortality. Women with stage IA grade 1 and stage IB grade 1 ovarian cancer do not require postoperative adjuvant therapy. Many remaining stage I patients do require chemotherapy. Subsets of stage I must be fully defined and ideal treatment determined. Women with stages II, III, and IV epithelial ovarian cancer (other than low malignant potential tumors) should receive postoperative chemotherapy. (<i>JAMA</i>. 1995;273:491-497)
Residential Radon Exposure and Lung Cancer Among Nonsmoking Women
Authors: M. C. R. Alavanja, R. C. Brownson, J. H. Lubin, E. Berger, J. Chang, J. D. Boice
Journal: JNCI Journal of the National Cancer Institute (1994)

Journal Article Residential Radon Exposure and Lung Cancer Among Nonsmoking Women Get access Michael C. R. Alavanja, Michael C. R. Alavanja 1Epidemiology and Biostatistics Program, Division of Cancer Prevention and Control, National Cancer InstituteBethesda, Md Correspondence to : Michael C. R. Alavanja, Dr.P.H., National Institutes of Health. EPN/543. Bethesda, MD 20892. Search for other works by this author on: Oxford Academic PubMed Google Scholar Ross C. Brownson, Ross C. Brownson 2Division of Chronic Disease Prevention and Health Promotion, Missouri Department of HealthColumbia Search for other works by this author on: Oxford Academic PubMed Google Scholar Jay H. Lubin, Jay H. Lubin 1Epidemiology and Biostatistics Program, Division of Cancer Prevention and Control, National Cancer InstituteBethesda, Md Search for other works by this author on: Oxford Academic PubMed Google Scholar Eric Berger, Eric Berger 3Information Management ServicesRockville, Md Search for other works by this author on: Oxford Academic PubMed Google Scholar Jian Chang, Jian Chang 2Division of Chronic Disease Prevention and Health Promotion, Missouri Department of HealthColumbia Search for other works by this author on: Oxford Academic PubMed Google Scholar John D. Boice, Jr. John D. Boice, Jr. 1Epidemiology and Biostatistics Program, Division of Cancer Prevention and Control, National Cancer InstituteBethesda, Md Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 86, Issue 24, 21 December 1994, Pages 1829–1837, https://doi.org/10.1093/jnci/86.24.1829 Published: 21 December 1994 Article history Received: 13 April 1994 Revision received: 23 August 1994 Accepted: 15 September 1994 Published: 21 December 1994
Nodal marginal zone lymphoma: gene expression and miRNA profiling identify diagnostic markers and potential therapeutic targets
Authors: Alberto J. Arribas, Yolanda Campos-Martín, Cristina Gómez-Abad, Patrocinio Algara, Margarita Sánchez-Beato, Maria S. Rodriguez-Pinilla, Santiago Montes-Moreno, Nerea Martinez, Javier Alves-Ferreira, Miguel A. Piris, Manuela Mollejo
Journal: Blood (2011)
Human Regulatory T Cells Control Xenogeneic Graft-versus-Host Disease Induced by Autologous T Cells in RAG2−/−γc−/− Immunodeficient Mice
Authors: Tuna Mutis, Rozemarijn S. van Rijn, Elles R. Simonetti, Tineke Aarts-Riemens, Maarten E. Emmelot, Louis van Bloois, Anton Martens, Leo F. Verdonck, Saskia B. Ebeling
Journal: Clinical Cancer Research (2006)

Abstract Purpose: Effective prevention of graft-versus-host disease (GvHD) is a major challenge to improve the safety of allogeneic stem cell transplantation for leukemia treatment. In murine transplantation models, administration of naturally occurring CD4+CD25+ regulatory T cells (Treg) can prevent GvHD. Toward understanding the role of human Treg in stem cell transplantation, we studied their capacity to modulate T-cell–dependent xenogeneic (x)-GvHD in a new model where x-GvHD is induced in RAG2−/−γc−/− mice by i.v. administration of human peripheral blood mononuclear cells (PBMC). Experimental Design: Human PBMC, depleted of or supplemented with autologous CD25+ Tregs, were administered in mice at different doses. The development of x-GvHD, in vivo expansion of human T cells, and secretion of human cytokines were monitored at weekly intervals. Results: Depletion of CD25+ cells from human PBMC significantly exacerbated x-GvHD and accelerated its lethality. In contrast, coadministration of Treg-enriched CD25+ cell fractions with autologous PBMC significantly reduced the lethality of x-GvHD. Treg administration significantly inhibited the explosive expansion of effector CD4+ and CD8+ T cells. Interestingly, protection from x-GvHD after Treg administration was associated with a significant increase in plasma levels of interleukin-10 and IFN-γ, suggesting the de novo development of TR1 cells. Conclusions: These results show, for the first time, the potent in vivo capacity of naturally occurring human Tregs to control GvHD-inducing autologous T cells, and indicate that this xenogeneic in vivo model may provide a suitable platform to further explore the in vivo mechanisms of T-cell down-regulation by naturally occurring human Tregs.
VARIATION IN THE GROUP-SPECIFIC CARBOHYDRATE OF GROUP A STREPTOCOCCI
Authors: Maclyn McCarty, Rebecca C. Lancefield
Journal: The Journal of Experimental Medicine (1955)

The phenomenon of apparent loss of group-specific carbohydrate in the course of mouse passage of group A streptococci has been subjected to further study, and several additional variants showing this property have been described. The loss of group reactivity is shown to be due to an alteration in the chemical structure and serological specificity of the cell wall carbohydrate. This alteration appears to be essentially the same in each of the variants available for study. The carbohydrate of the variant strains (V) contains the same two monosaccharide components as the group A carbohydrate (A), but they are present in different proportions. Precipitating sera reactive with V carbohydrate have been prepared, and the A and V carbohydrates have been compared by qualitative and quantitative precipitin analysis. A second type of variation has been encountered during mouse passage. This variation is characterized by the occurrence of a cell wall carbohydrate (I) intermediate in chemical and serological properties between the A and V carbohydrates. The I carbohydrate reacts with both A and V antisera and does not appear to be a simple mixture of A and V carbohydrate. Similarly, antisera against the intermediate strain contain antibodies reactive with both A and V carbohydrates, and evidence is presented indicating that in part this represents antibody with double specificity.
HB-EGF and PDGF Mediate Reciprocal Interactions of Carcinoma Cells with Cancer-Associated Fibroblasts to Support Progression of Uterine Cervical Cancers
Authors: Takuya Murata, Hiroto Mizushima, Ichino Chinen, Hiroki Moribe, Shigeo Yagi, Robert M. Hoffman, Tadashi Kimura, Kiyoshi Yoshino, Yutaka Ueda, Takayuki Enomoto, Eisuke Mekada
Journal: Cancer Research (2011)

Tumor stroma drives the growth and progression of cancers. A heparin-binding epidermal growth factor-like growth factor, HB-EGF, is an EGF receptor ligand that stimulates cell growth in an autocrine or paracrine fashion. While elevated expression of HB-EGF in cancer cells and its contribution to tumor progression are well documented, the effects of HB-EGF expression in the tumor stroma have not been clarified. Here, we show that HB-EGF is expressed in stromal fibroblasts where it promotes cancer cell proliferation. In uterine cervical cancers, HB-EGF was detected immunohistochemically in the stroma proximal to the cancer epithelium. Proliferation of cervical cancer cells in vitro was enhanced by coculture with fibroblasts isolated from tumor tissues of patients with cervical cancer. Inhibition of HB-EGF function or treatment with platelet-derived growth factor (PDGF) inhibitors abrogated cancer cell growth enhanced by cervical cancer-associated fibroblast (CCF) coculture. Furthermore, tumor formation in a mouse xenograft model was enhanced by cotransplantation of CCF or mouse embryonic fibroblasts, but not with embryonic fibroblasts from HB-EGF-deficient mice. Conversely, conditioned medium from cancer cells induced HB-EGF expression in CCF. Mechanistic investigations established that PDGF was the primary factor responsible. Together, our findings indicate that HB-EGF and PDGF reciprocally mediate the interaction of cancer cells with cancer-associated fibroblasts, promoting cancer cell proliferation in a paracrine manner that has implications for novel combinatorial cancer therapies.
Targeted therapy by combined inhibition of the RAF and mTOR kinases in malignant spindle cell neoplasm harboring the KIAA1549-BRAF fusion protein
Authors: Vivek Subbiah, Shannon N Westin, Kai Wang, Dejka Araujo, Wei-Lien Wang, Vincent A Miller, Jeffrey S Ross, Phillip J Stephens, Gary A Palmer, Siraj M Ali
Journal: Journal of Hematology & Oncology (2014)

Oncologic patients who are extreme responders to molecularly targeted therapy provide an important opportunity to better understand the biologic basis of response and, in turn, inform clinical decision making. Malignant neoplasms with an uncertain histologic and immunohistochemical characterization present challenges both on initial diagnostic workups and then later in management, as current treatment algorithms are based on a morphologic diagnosis. Herein, we report a case of a difficult to characterize sarcoma-like lesion for which genomic profiling with clinical next generation sequencing (NGS) identified the molecular underpinnings of arrested progression(stable disease) under combination targeted therapy within a phase I clinical trial. Genomic profiling with clinical next generation sequencing was performed on the FoundationOne™ platform (Foundation Medicine, Cambridge MA). Histopathology and immunohistochemical studies were performed in the Department of Pathology, MD Anderson Cancer Center (Houston, TX). Treatment was administered in the context of a phase I clinical trial ClinicalTrials.gov Identifier: (NCT01187199). The histology of the tumor was that of a spindle cell neoplasm, grade 2 by FNCLCC standards. Immunohistochemical staining was positive for S100 and CD34. Genomic profiling identified the following alterations: a KIAA1549-BRAF gene fusion resulting from a tandem duplication event, a homozygous deletion of PTEN, and frameshift insertion/deletions in CDKN2A A68fs*51, SUFU E283fs*3, and MAP3K1 N325fs*3. The patient had a 25% reduction in tumor (RECIST v1.1) following combination therapy consisting of sorafenib, temsirolimus, and bevazicumab within a phase I clinical trial. The patient responded to combination targeted therapy that fortuitously targeted KIAA1549-BRAF and PTEN loss within a spindle cell neoplasm, as revealed by genomic profiling based on NGS. This is the first report of a tumor driven by a KIAA1549-BRAF fusion responding to sorafenib-based combination therapy.
Screening for coeliac disease in patients fulfilling the Rome II criteria for irritable bowel syndrome in a secondary care hospital in The Netherlands: a prospective observational study
Authors: E.-J. van der Wouden, G F. Nelis, J. Vecht
Journal: Gut (2007)

Irritable bowel syndrome is the most commonly diagnosed gastrointestinal condition and affects a large proportion of the population in the West.1 Several guidelines suggest that in typical patients with no alarm symptoms or signs, apart from routine laboratory tests, no additional tests are necessary.2 Coeliac disease, however, may present with symptoms suggestive of irritable bowel disease.3 Several studies suggested that screening for coeliac disease in patients with symptoms suggestive of irritable bowel disease might be cost-effective.4–7 We, therefore, started to routinely screen patients with typical irritable bowel disease symptoms for coeliac disease using antiendomysial antibodies.

All patients referred to three doctors at the outpatient gastroenterology department of our hospital between November 2002 and …
Highly elastomeric poly(glycerol sebacate)-co-poly(ethylene glycol) amphiphilic block copolymers
Authors: Alpesh Patel, Akhilesh K. Gaharwar, Giorgio Iviglia, Hongbin Zhang, Shilpaa Mukundan, Silvia M. Mihaila, Danilo Demarchi, Ali Khademhosseini
Journal: Biomaterials (2013)
From individual cognition to populational culture
Authors: Krist Vaesen
Journal: Behavioral and Brain Sciences (2012)

In my response to the commentaries from a collection of esteemed researchers, I reassess and eventually find largely intact my claim that human tool use evidences higher social and non-social cognitive ability. Nonetheless, I concede that my examination of individual-level cognitive traits does not offer a full explanation of cumulative culture yet. For that, one needs to incorporate them into population-dynamic models of cultural evolution. I briefly describe my current and future work on this.
Thomas Bateman MD FLS 1778-1821
Authors: N.J. Levell
Journal: British Journal of Dermatology (2000)

Thomas Bateman was a physician to the Carey Street Public Dispensary with Robert Willan in the first decade of the nineteenth century when the latter was developing the classification that would act as a foundation for modern dermatology. Following Willan's death with his work still incomplete, Bateman published a book, as an abstract of Willan's full concept, which was probably the most influential dermatology text of the nineteenth century. This was the first classification of dermatology that precisely defined the terms used and fitted individual diseases into a single class, rather than considering different stages of the same disease as maladies that belonged in different classes. This was the first attempt to link treatment to the disease process rather than to the clinical appearances and thus represents the origin of modern scientific clinical dermatology.
The Central Executioner of Apoptosis: Multiple Connections between Protease Activation and Mitochondria in Fas/APO-1/CD95- and Ceramide-induced Apoptosis
Authors: Santos A. Susin, Naoufal Zamzami, Maria Castedo, Eric Daugas, Hong-Gang Wang, Stephan Geley, Florence Fassy, John C. Reed, Guido Kroemer
Journal: The Journal of Experimental Medicine (1997)

According to current understanding, cytoplasmic events including activation of protease cascades and mitochondrial permeability transition (PT) participate in the control of nuclear apoptosis. However, the relationship between protease activation and PT has remained elusive. When apoptosis is induced by cross-linking of the Fas/APO-1/CD95 receptor, activation of interleukin-1β converting enzyme (ICE; caspase 1) or ICE-like enzymes precedes the disruption of the mitochondrial inner transmembrane potential (ΔΨm). In contrast, cytosolic CPP32/ Yama/Apopain/caspase 3 activation, plasma membrane phosphatidyl serine exposure, and nuclear apoptosis only occur in cells in which the ΔΨm is fully disrupted. Transfection with the cowpox protease inhibitor crmA or culture in the presence of the synthetic ICE-specific inhibitor Ac-YVAD.cmk both prevent the ΔΨm collapse and subsequent apoptosis. Cytosols from anti-Fas–treated human lymphoma cells accumulate an activity that induces PT in isolated mitochondria in vitro and that is neutralized by crmA or Ac-YVAD.cmk. Recombinant purified ICE suffices to cause isolated mitochondria to undergo PT-like large amplitude swelling and to disrupt their ΔΨm. In addition, ICE-treated mitochondria release an apoptosis-inducing factor (AIF) that induces apoptotic changes (chromatin condensation and oligonucleosomal DNA fragmentation) in isolated nuclei in vitro. AIF is a protease (or protease activator) that can be inhibited by the broad spectrum apoptosis inhibitor Z-VAD.fmk and that causes the proteolytical activation of CPP32. Although Bcl-2 is a highly efficient inhibitor of mitochondrial alterations (large amplitude swelling + ΔΨm collapse + release of AIF) induced by prooxidants or cytosols from ceramide-treated cells, it has no effect on the ICE-induced mitochondrial PT and AIF release. These data connect a protease activation pathway with the mitochondrial phase of apoptosis regulation. In addition, they provide a plausible explanation of why Bcl-2 fails to interfere with Fas-triggered apoptosis in most cell types, yet prevents ceramide- and prooxidant-induced apoptosis.
Detection and identification of asbestos by microscopical dispersion staining
Authors: Walter C. McCrone
Journal: Environmental Health Perspectives (1974)

Asbestos fibers as small as 1 mum in diameter can be uniquely identified by light microscopy by employing dispersion staining methods. The technique described herein involves suspension of fibers in liquids of known refractive indices and observation of color display by means of a dispersion staining objective. Wavelengths or indices of refraction may be determined at right angles to and parallel to fiber axes. This method is rapid and sensitive for identification purposes.
Kidney dendritic cell activation is required for progression of renal disease in a mouse model of glomerular injury
Authors: Felix Heymann, Catherine Meyer-Schwesinger, Emma E. Hamilton-Williams, Linda Hammerich, Ulf Panzer, Sylvia Kaden, Susan E. Quaggin, Jürgen Floege, Hermann-Josef Gröne, Christian Kurts
Journal: Journal of Clinical Investigation (2009)

The progression of kidney disease to renal failure correlates with infiltration of mononuclear immune cells into the tubulointerstitium. These infiltrates contain macrophages, DCs, and T cells, but the role of each cell type in disease progression is unclear. To investigate the underlying immune mechanisms, we generated transgenic mice that selectively expressed the model antigens ovalbumin and hen egg lysozyme in glomerular podocytes (NOH mice). Coinjection of ovalbumin-specific transgenic CD8+ CTLs and CD4+ Th cells into NOH mice resulted in periglomerular mononuclear infiltrates and inflammation of parietal epithelial cells, similar to lesions frequently observed in human chronic glomerulonephritis. Repetitive T cell injections aggravated infiltration and caused progression to structural and functional kidney damage after 4 weeks. Mechanistic analysis revealed that DCs in renal lymph nodes constitutively cross-presented ovalbumin and activated CTLs. These CTLs released further ovalbumin for CTL activation in the lymph nodes and for simultaneous presentation to Th cells by distinct DC subsets residing in the kidney tubulointerstitium. Crosstalk between tubulointerstitial DCs and Th cells resulted in intrarenal cytokine and chemokine production and in recruitment of more CTLs, monocyte-derived DCs, and macrophages. The importance of DCs was established by the fact that DC depletion rapidly resolved established kidney immunopathology. These findings demonstrate that glomerular antigen-specific CTLs and Th cells can jointly induce renal immunopathology and identify kidney DCs as a mechanistic link between glomerular injury and the progression of kidney disease.
ADAR2-Dependent RNA Editing of AMPA Receptor Subunit GluR2 Determines Vulnerability of Neurons in Forebrain Ischemia
Authors: Peter L. Peng, Xiafen Zhong, Weihong Tu, Mangala M. Soundarapandian, Peter Molner, Dongya Zhu, Lorraine Lau, Shuhong Liu, Fang Liu, YouMing Lu
Journal: Neuron (2006)
CT findings before and after azithromycin treatment of chronic lung allograft dysfunction
Authors: Robin Vos, Pim de Jong, Bart Vanaudenaerde, Stijn Verleden, Dirk Van Raemdonck, Lieven Dupont, Walter De Wever, Johny Verschakelen, Geert Verleden
Journal: European Respiratory Journal (2011)

Introduction:  We aimed to describe imaging findings in patients with chronic lung allograft dysfunction/CLAD (either neutrophilic reversible allograft disorder/NRAD or fibrotic bronchiolitis obliterans syndrome/fBOS) before and after azithromycin treatment.   Methods:  A previously described cohort of 107 patients with CLAD treated with azithromycin for 3.1±1.9 years ( Vos et al. J Heart Lung Transplant 2010 ), was retrospectively analyzed for inspiration and end-exhalation thin-section computed tomography (CT) findings before and 6.9 (4.7-11.4) months after treatment. All CT scans were scored by one observer whose reproducibility of the score has previously been described in another cohort study ( de Jong et al. Thorax 2006 ).   Results:  Before treatment, NRAD patients displayed more often centrilobular changes (nodules and tree-in-bud, p=0.03) and tended to have higher centrilobular scores compared with fBOS patients (p=0.05). In NRAD, bronchus dilatation, mucous plugging, centrilobular abnormalities, airway wall thickening, consolidation, ground glass and air trapping all improved on average. The degree of improvement for all abnormalities was significantly different from the degree of change seen in fBOS, in whom only some abnormalities (i.e. mucous plugging, centrilobular abnormalities, airway wall thickening and ground glass opacities) improved on average, but bronchial dilatation, consolidation and air trapping worsened on average. The presence of pre-treatment centrilobular abnormalities significantly predicted response in FEV 1  to treatment (p=0.03).   Conclusions:  CT imaging may be of additional value in phenotyping CLAD and may predict response to azithromycin treatment.