tbuckley/cabot-search huggingface dataset:
Intraoperative lymphatic mapping and sentinel lymph node dissection in breast cancer
Authors: E. C. Hsueh, N. Hansen, A. E. Giuliano
Journal: CA A Cancer Journal for Clinicians (2000)

Because the tumor status of the regional lymph nodes is the most important prognostic factor in patients with early-stage breast cancer, accurate histopathologic assessment of these nodes is essential for optimal management, including the selection of candidates for adjuvant systemic therapies. Intraoperative lymphatic mapping using a vital blue dye, with or without a radiocolloid, can identify the first axillary node to receive lymphatic drainage from a primary breast carcinoma. Focused histopathologic assessment of this sentinel node can be used to determine the tumor status of the entire axillary basin. The minimal morbidity and high accuracy of sentinel lymph node dissection (SLND) in breast cancer have been validated by multiple independent investigators, and the data suggest that this surgical technique may eventually replace complete lymph node dissection as the preferred axillary procedure for the management of early-stage disease. In experienced hands, SLND can be successfully performed in more than 90% of eligible breast cancer patients; the tumor status of the sentinel node accurately predicts the status of all axillary nodes in more than 95% of cases. This article reviews the current status, controversies, and future directions of SLND as a staging technique for patients with primary breast carcinoma.
Nonsense mutations affect C1 inhibitor messenger RNA levels in patients with type I hereditary angioneurotic edema.
Authors: D Frangi, M Cicardi, A Sica, F Colotta, A Agostoni, A E Davis
Journal: Journal of Clinical Investigation (1991)

Members of two unrelated families with type I hereditary angioneurotic edema (HANE) were found to have elevated levels of C1 inhibitor (C1INH) mRNA. DNA sequence analysis of PCR-amplified monocyte C1INH mRNA revealed normal and mutant transcripts, as expected in this disorder that occurs in heterozygous individuals. Single base mutations near the 3' end of the coding sequence were identified in affected members of each family. One mutation consisted of insertion of an adenosine at position 1304 which created a premature termination codon (TAA), whereas the second consisted of deletion of the thymidine at position 1298 which created a premature termination codon (TGA) 23 nucleotides downstream. These mutations are approximately 250 nucleotides upstream of the natural termination codon. Nuclear run-off experiments in one kindred revealed no difference in transcription rates of the C1INH gene between the patients and normals. C1INH mRNA half-life experiments were not technically feasible because of the prolonged half-life of the normal transcript. Dideoxynucleotide primer extension experiments allowed the differentiation of the normal and mutant transcripts. These studies showed that the mutant transcript was not decreased relative to the normal, and this therefore was at least partially responsible for the C1INH mRNA elevation. This elevation may be due to the decreased catabolism of the mutant transcript.
Preferential accumulation and export of high molecular weight FGF-2 by rat cardiac non-myocytes
Authors: Jon-Jon Santiago, Xin Ma, Leslie J. McNaughton, Barbara E. Nickel, Brian P. Bestvater, Liping Yu, Robert R. Fandrich, Thomas Netticadan, Elissavet Kardami
Journal: Cardiovascular Research (2010)

Fibroblast growth factor-2 (FGF-2), implicated in paracrine induction of cardiac hypertrophy, is translated as high molecular weight (Hi-FGF-2) and low molecular weight (Lo-FGF-2) isoforms. Paracrine activities are assigned to Lo-FGF-2, whereas Hi-FGF-2 is presumed to have nuclear functions. In this work, we re-examined the latter presumption by asking whether: cardiac non-myocytes (CNMs) accumulate and export Hi-FGF-2 in response to pro-hypertrophic [angiotensin II (Ang II)] stimuli; an unconventional secretory pathway requiring activated caspase-1 affects Hi-FGF2 export; and secreted Hi-FGF-2 is pro-hypertrophic. Using neonatal rat heart-derived cultures and immunoblotting, we show that CNMs accumulated over 90% Hi-FGF-2, at levels at least five-fold higher than cardiomyocytes (CMs). Pro-hypertrophic agents (Ang II, endothelin-1, and isoproterenol) up-regulated CNM-associated Hi-FGF-2. The Ang II effect was mediated by Ang II receptor-1 but not Ang II receptor-2 as it was blocked by losartan but not PD123319. CNM-derived Hi-FGF-2 was detected in two extracellular pools: in conditioned medium from Ang II-stimulated CNMs and in association with the cell surface/matrix, eluted with a gentle 2 M NaCl wash of the cell monolayer. Conditioned medium from Ang II-treated CNMs increased neonatal CM size, an effect prevented by anti-FGF-2-neutralizing antibodies. The caspase-1 inhibitor YVAD prevented the Ang II-induced release of Hi-FGF-2 to both extracellular pools. CNMs are major producers of Hi-FGF-2, up-regulated by hypertrophic stimuli and exported to the extracellular environment by a mechanism requiring caspase-1 activity, suggesting a link to the innate immune response. Hi-FGF-2 is likely to promote paracrine induction of myocyte hypertrophy in vivo.
Diseases of Man Acquired From His Pets.
Authors: Balideo Bisseru
Journal: Annals of Internal Medicine (1968)

The title of this book does not do justice to its contents.It is about much ^ore than man's pets.Such animals as centipedes, harvest mites, sharks and Jellyfish could hardly be called 'pets', although the author cites a fantastic list of creatures that have at one time or another been kept as pets.This book ls about those diseases of man where animals (all creatures included) play Sorrie part in their causation.This is a big field, covering the greater part ?f tropical medicine as well as all those diseases in temperate climates where anirnals and humans are involved.Vo1-3.No.
Effect of exercise and physiotherapy in aiding sputum expectoration in adults with cystic fibrosis.
Authors: W Salh, D Bilton, M Dodd, A K Webb
Journal: Thorax (1989)

The role of exercise in aiding sputum expectoration in patients with cystic fibrosis and the comparative roles of exercise and physiotherapy in sputum expectoration were assessed in two studies. In the first study 19 adult patients undertook a two month programme of home exercise using a cycle ergometer. In the 12 patients completing the study peak work capacity, maximum oxygen consumption, and maximum minute ventilation had increased significantly by the end of the exercise programme; the increase in daily sputum weight (from 24 to 37 g) was not significant (p = 0.055). In the second study (with 10 patients) more sputum was expectorated during and after physiotherapy than during and after exercise (9.8 v 4.0 g). Exercise may have a role in aiding sputum expectoration in patients with cystic fibrosis but should not be considered as a replacement for physiotherapy.
Characterization of Early Cytokine Responses and an Interleukin (IL)-6–dependent Pathway of Endogenous Glucocorticoid Induction during Murine Cytomegalovirus Infection
Authors: Melanie C. Ruzek, Andrew H. Miller, Steven M. Opal, Bradley D. Pearce, Christine A. Biron
Journal: The Journal of Experimental Medicine (1997)

Early infection with murine cytomegalovirus (MCMV) induces circulating levels of interleukin (IL)-12, interferon (IFN)-γ, and tumor necrosis factor (TNF). Studies presented here further characterize these responses by defining kinetics and extending evaluation to include IL-1, IL-6, and glucocorticoids. IL-12 p40, IFN-γ, TNF, IL-1α, and IL-6 were shown to be increased, but IL-1β was undetectable, in serum of MCMV-infected mice. The IL-12 p40, IFN-γ, TNF, and IL-6 responses were dramatic with peak levels reaching &amp;gt;150–10,000 pg/ml at 32–40 h after infection and rapidly declining thereafter. Glucocorticoid induction, peaking at 36 h and reaching 30-fold increases above control values, accompanied the cytokine responses. Mice with cytokine deficiencies or neutralized cytokine function demonstrated that IL-6 was the pivotal mediator of the glucocorticoid response, with IL-1 contributing to IL-6 production. The IL-6 requirement appeared to be specific for virus-type stimuli as the synthetic analogue of viral nucleic acid, polyinosinic-polycytidylic acid, also induced IL-6–dependent glucocorticoid release, but treatments with the bacterial product lipopolysaccharide and a non-immune physical restraint stressor elicited IL-6–independent responses. Collectively, the results identify IL-6 as a primary mediator of glucocorticoid induction, and elucidate specific pathways of interactions between immune and neuroendocrine systems during viral infection.
Prevalence of Metabolic Syndrome Associated with Body Burden Levels of Dioxin and Related Compounds among Japan’s General Population
Authors: Hirokazu Uemura, Kokichi Arisawa, Mineyoshi Hiyoshi, Atsushi Kitayama, Hidenobu Takami, Fusakazu Sawachika, Satoru Dakeshita, Kentaro Nii, Hiroshi Satoh, Yoshio Sumiyoshi, Kenji Morinaga, Kazunori Kodama, Taka-ichiro Suzuki, Masaki Nagai, Tsuguyoshi Suzuki
Journal: Environmental Health Perspectives (2008)

Environmental exposure to some persistent organic pollutants has been reported to be associated with a metabolic syndrome in the U.S. population.We evaluated the associations of body burden levels of dioxins and related compounds with the prevalence of metabolic syndrome among the general population in Japan.We conducted a cross-sectional study with 1,374 participants not occupationally exposed to these pollutants, living throughout Japan during 2002-2006. In fasting blood samples, we measured biochemical factors and determined lipid-adjusted concentrations of 10 polychlorinated dibenzo-p-dioxins (PCDDs), 7 polychlorinated dibenzofurans (PCDFs), and 12 dioxin-like poly-chlorinated biphenyls (DL-PCBs) all of which have toxic equivalency factors. We also performed a questionnaire survey.The toxic equivalents (TEQs) of PCDDs, PCDFs, and DL-PCBs and total TEQs had significant adjusted associations with metabolic syndrome, whether or not we excluded diabetic subjects. By analyzing each component of metabolic syndrome separately, the DL-PCB TEQs and total TEQs were associated with all components, and the odds ratios (ORs) in the highest quartile of DL-PCB TEQs in four of the five components were higher than those for PCDDs or PCDFs. We also found congener-specific associations with metabolic syndrome; in particular, the highest quartiles of PCB-126 and PCB-105 had adjusted ORs of 9.1 and 7.3, respectively.These results suggest that body burden levels of dioxins and related compounds, particularly those of DL-PCBs, are associated with metabolic syndrome. Of the components, high blood pressure, elevated triglycerides, and glucose intolerance were most closely associated with these pollutants.
“Paradoxical shrinkage” of coronary arterial wall may contribute to luminal narrowing in stable angina but not in acute myocardial infarction
Authors: A. Itch, T. Baba, S. Miyazaki, S. Daikoku, T. Matsumoto, I. Morii, H. Sumida, S. Yasuda, T. Noguchi, Y. Goto, H. Nonogi
Journal: Journal of the American College of Cardiology (1998)
Left ventricular load, arterial impedance and their interrelationship
Authors: M. I. M. NOBLE
Journal: Cardiovascular Research (1979)

Journal Article Left ventricular load, arterial impedance and their interrelationship Get access MARK I. M. NOBLE MARK I. M. NOBLE The Midhurst Medical Research Institute, Midhurst, Sussex GU29 0BL Search for other works by this author on: Oxford Academic PubMed Google Scholar Cardiovascular Research, Volume 13, Issue 4, April 1979, Pages 183–198, https://doi.org/10.1093/cvr/13.4.183 Published: 01 April 1979
Combination of Ponatinib with Hedgehog Antagonist Vismodegib for Therapy-Resistant BCR-ABL1–Positive Leukemia
Authors: Seiichiro Katagiri, Tetsuzo Tauchi, Seiichi Okabe, Yosuke Minami, Shinya Kimura, Taira Maekawa, Tomoki Naoe, Kazuma Ohyashiki
Journal: Clinical Cancer Research (2013)

Abstract Purpose: The Hedgehog signaling pathway is a key regulator of cell growth and differentiation during development. Whereas the Hedgehog pathway is inactive in most normal adult tissues, Hedgehog pathway reactivation has been implicated in the pathogenesis of several neoplasms including BCR-ABL1–positive leukemia. The clear link between the Hedgehog pathway and BCR-ABL1–positive leukemia led to an effort to identify small molecules to block the pathway. Experimental Design: We investigated the combined effects of vismodegib and ponatinib, a pan-ABL1 kinase inhibitor, in nonobese diabetic/severe-combined immunodeficiency (NOD/SCID) repopulating T315I BCR-ABL1–positive cells in vitro and in vivo. Results: We observed that combination with vismodegib and ponatinib helps to eliminate therapy-resistant NOD/SCID repopulating T315I BCR-ABL1–positive cells. The percentage of CD19-positive leukemia cells in peripheral blood was significantly lower in vismodegib + ponatinib–treated mice than that of the vehicle or ponatinib alone (P &amp;lt; 0.001). Spleen weights were also lower in vismodegib + ponatinib–treated mice than in ponatinib alone (P &amp;lt; 0.05). Overall tumor burden, as assessed by BCR-ABL mRNA from bone marrow cells, was significantly lower in vismodegib + ponatinib–treated mice than in ponatinib alone (P &amp;lt; 0.005). We also found that vismodegib significantly reduced BCR-ABL1–positive leukemia cell self-renewal in vitro as well as during serial transplantation in vivo. Conclusions: The combination with a Smo inhibitor and ABL1 tyrosine kinase inhibitors may help eliminate therapy-resistant T315I BCR-ABL1–positive leukemia cells. Our preclinical results indicate that vismodegib has potential as an important option for controlling minimal residual cells in BCR-ABL1–positive leukemia. Clin Cancer Res; 19(6); 1422–32. ©2012 AACR.
Diet and exercise orthogonally alter the gut microbiome and reveal independent associations with anxiety and cognition
Authors: Silvia S Kang, Patricio R Jeraldo, Aishe Kurti, Margret E Berg Miller, Marc D Cook, Keith Whitlock, Nigel Goldenfeld, Jeffrey A Woods, Bryan A White, Nicholas Chia, John D Fryer
Journal: Molecular Neurodegeneration (2014)

The ingestion of a high-fat diet (HFD) and the resulting obese state can exert a multitude of stressors on the individual including anxiety and cognitive dysfunction. Though many studies have shown that exercise can alleviate the negative consequences of a HFD using metabolic readouts such as insulin and glucose, a paucity of well-controlled rodent studies have been published on HFD and exercise interactions with regard to behavioral outcomes. This is a critical issue since some individuals assume that HFD-induced behavioral problems such as anxiety and cognitive dysfunction can simply be exercised away. To investigate this, we analyzed mice fed a normal diet (ND), ND with exercise, HFD diet, or HFD with exercise. We found that mice on a HFD had robust anxiety phenotypes but this was not rescued by exercise. Conversely, exercise increased cognitive abilities but this was not impacted by the HFD. Given the importance of the gut microbiome in shaping the host state, we used 16S rRNA hypervariable tag sequencing to profile our cohorts and found that HFD massively reshaped the gut microbial community in agreement with numerous published studies. However, exercise alone also caused massive shifts in the gut microbiome at nearly the same magnitude as diet but these changes were surprisingly orthogonal. Additionally, specific bacterial abundances were directly proportional to measures of anxiety or cognition. Thus, behavioral domains and the gut microbiome are both impacted by diet and exercise but in unrelated ways. These data have important implications for obesity research aimed at modifications of the gut microbiome and suggest that specific gut microbes could be used as a biomarker for anxiety or cognition or perhaps even targeted for therapy.
Resistance to FasL and tumor necrosis factor-related apoptosis-inducing ligand-mediated apoptosis in Sézary syndrome T-cells associated with impaired death receptor and FLICE-inhibitory protein expression
Authors: Emmanuel Contassot, Katrin Kerl, Stéphanie Roques, Ryan Shane, Olivier Gaide, Marc Dupuis, Alain H. Rook, Lars E. French
Journal: Blood (2008)
Amnesia and Competency To Stand Trial
Authors: DENNIS KOSON, AMES ROBEY
Journal: American Journal of Psychiatry (1973)

In case law, defendants suffering solely from amnesia who are otherwise competent to stand trial are generally found to be competent. However, temporary, treatable amnesia may warrant a finding of incompetency. The authors review current concepts of amnesia. They stress the need for the psychiatrist to understand the nature of amnesia so that he may assist the court in its adjudication of competency to stand trial.
EFFECT OF NESIRITIDE ON RENAL FUNCTION IN PATIENTS WITH DECOMPENSATED DIASTOLIC HEART FAILURE: COMPARISON OF PATIENTS WITH ISOLATED RIGHT VENTRICULAR FAILURE WITH PATIENTS WITH NORMAL RIGHT VENTRICULAR FUNCTION
Authors: Iosif Kelesidis, Wajeeha Saeed, Jeremy Mazurek, Ronak Chaudhari, Ronald Zolty
Journal: Journal of the American College of Cardiology (2011)
Complete replacement of serum by albumin, transferrin, and soybean lipid in cultures of lipopolysaccharide-reactive B lymphocytes.
Authors: N N Iscove, F Melchers
Journal: The Journal of Experimental Medicine (1978)

Albumin, transferrin, and lipids can replace serum entirely for support of LPS-stimulated murine B lymphocytes in culture. In the presence of these compounds, growth and maturation to IgM and IgG secretion, induced by lipopolysaccharide (LPS), occurs at the same or higher efficiency in serum-free conditions as in conventional serum-containing medium, even at relatively low cell concentrations. In contrast to the rapid disappearance of LPS reactivity in conventional serum-containing medium, responsiveness remains at initial levels in serum-free conditions for 2 days before slowly declining. Overall lymphocyte survival is also markedly prolonged. In the presence of thymus "filler" cells, the serum-free conditions permit growth of every LPS-responsive cell to a clone of Ig-secreting cells at dilutions as low as a single reactive B cell per culture. The results have several important implications. These include the establishment for the first time of transferrin as a requirement for B lymphocyte responses in culture, and the availability now of conditions for the assay isolation of cell products regulating lymphocyte function, free of interference from undefined serum components.
p21CIP-1/WAF-1 Induction Is Required to Inhibit Prostate Cancer Growth Elicited by Deficient Expression of the Wnt Inhibitor Dickkopf-1
Authors: Christopher L. Hall, Honglai Zhang, Shobun Baile, Mats Ljungman, Stuart Kuhstoss, Evan T. Keller
Journal: Cancer Research (2010)

Osteoblastic bone metastases are the most common metastases produced by human prostate cancers (PCa). Deregulated activity of Wnt growth factors resulting from overexpression of the Wnt inhibitor Dickkopf-1 (DKK-1) is known to contribute to formation of the osteoblastic component of PCa skeletal bone metastases. In this study, we report that DKK-1 knockdown in osteolytic human PCa cells unexpectedly delays the development of both soft tissue and osseous lesions. PCa cells deficient in DKK-1 expression did not increase canonical Wnt signaling in target osteoblast cell lines; however, DKK-1 knockdown PCa cells exhibited increased expression of the CDK inhibitor p21(CIP1/WAF1) and a 32% increase in G(1) arrest compared with control cells. Ablating p21(CIP1/WAF1) in PCa cells deficient in DKK-1 was sufficient to rescue tumor growth. Collectively, our findings demonstrate that DKK-1 overexpression supports tumor growth in part by restricting expression of p21(CIP1/WAF1) through a mechanism independent of canonical Wnt signaling.
Validation of the VISA-A questionnaire for Turkish language: the VISA-A-Tr study: Table 1
Authors: Yunus Dogramaci, Aydiner Kalaci, Nigar Kücükkübaş, Taceddin Inandı, Erdinc Esen, A Nedim Yanat
Journal: British Journal of Sports Medicine (2009)

Objectives To evaluate the validity and reliability of the Turkish version of the Victorian Institute of Sports Assessment-Achilles (VISA-A) questionnaire for patients with Achilles tendinopathy. Design Fifty-five patients with a diagnosis of Achilles tendinopathy and 55 healthy subjects were included in the study. VISA-A questionnaires were translated and culturally adapted into Turkish. The final Turkish version (VISA-A-Tr) was tested for reliability on healthy individuals and patients. Tests for internal consistency, validity and structure were performed on 55 patients. Results The VISA-A-Tr showed good test–retest reliability (Pearson's r=0.99, p&lt;0.001). The patients with Achilles tendinopathy had a significantly lower score (p&lt;0.001) than the healthy individuals. The VISA-A-Tr score correlated significantly with the Stanish tendon grading system (Spearman's r=−0.86; p&lt;0.001). Conclusion The VISA-A-Tr is a valid and reliable tool for evaluating the severity of Achilles tendinopathy.
Somatic reversion in dedicator of cytokinesis 8 immunodeficiency modulates disease phenotype
Authors: Huie Jing, Qian Zhang, Yu Zhang, Brenna J. Hill, Christopher G. Dove, Erwin W. Gelfand, T. Prescott Atkinson, Gulbu Uzel, Helen F. Matthews, Peter J. Mustillo, David B. Lewis, Fotini D. Kavadas, I. Celine Hanson, Ashish R. Kumar, Raif S. Geha, Daniel C. Douek, Steven M. Holland, Alexandra F. Freeman, Helen C. Su
Journal: Journal of Allergy and Clinical Immunology (2014)
The SIRT1/HIF2α Axis Drives Reductive Glutamine Metabolism under Chronic Acidosis and Alters Tumor Response to Therapy
Authors: Cyril Corbet, Nihed Draoui, Florence Polet, Adan Pinto, Xavier Drozak, Olivier Riant, Olivier Feron
Journal: Cancer Research (2014)

Abstract Extracellular tumor acidosis largely results from an exacerbated glycolytic flux in cancer and cancer-associated cells. Conversely, little is known about how tumor cells adapt their metabolism to acidosis. Here, we demonstrate that long-term exposure of cancer cells to acidic pH leads to a metabolic reprogramming toward glutamine metabolism. This switch is triggered by the need to reduce the production of protons from glycolysis and further maintained by the NAD+-dependent increase in SIRT1 deacetylase activity to ensure intracellular pH homeostasis. A consecutive increase in HIF2α activity promotes the expression of various transporters and enzymes supporting the reductive and oxidative glutamine metabolism, whereas a reduction in functional HIF1α expression consolidates the inhibition of glycolysis. Finally, in vitro and in vivo experiments document that acidosis accounts for a net increase in tumor sensitivity to inhibitors of SIRT1 and glutaminase GLS1. These findings highlight the influence that tumor acidosis and metabolism exert on each other. Cancer Res; 74(19); 5507–19. ©2014 AACR.