tbuckley/cabot-search huggingface dataset:
Pharmacological analysis of 5-hydroxytryptamine receptors in isolated intracranial and extracranial vessels of cat and man.
Authors: L Edvinsson, J E Hardebo, C Owman
Journal: Circulation Research (1978)

In intra-and extracranial arteries from cat and man (under conditions in which dilation was blocked), 5-hydroxytryptamine (5-HT) and D-lysergic acid diethylamide (LSD) produced a contraction at lower doses than that produced by tryptamine.Methysergide inhibited the S-HT-induced contraction of the extracranial arteries in a competitive manner.In intracranial arteries the inhibition comprised a reduction in slope and maximum of the log dose-response curves.The contractile effects of 5-HT on both types of arteries appear to be mediated by 5-HT receptors, but the receptors have different characteristics in the sense that the mode of antagonism by methysergide was different.The dissociation constant (Kg) and the corresponding pA 2 value (8.61 x 10 " M and 8.21, respectively) for the interaction between methysergide and 5-HT in extracranial arteries conform with that reported for other smooth muscle tissues.The dilator response was tested in arteries given an active tonic contraction with prostaglandin F 2(1 .Both 5-HT and tryptamine produced a dose-dependent dilation, 5-HT being the more potent.Neither methysergide nor LSD antagonized the response in a competitve manner whereas the two /3receptor antagonists, propranolol and 1-JV-isopropyl-p-nitrophenyl-ethanolamine (INPEA), caused a parallel shift of the log dose-response curves (tested for 5-HT).The mean values for Kg (pA 2 ) in the presence of propranolol were 1.93 x 10-" M (8.29) for the intracranial and 1.83 x 1 0 * M (8.50) for the extracranial vessels.Calculated pA, values with INPEA were 8.47 and 7.93, respectively.The mode of inhibition by the ^-antagonists suggests that the dilator effect of 5-HT is mediated by a receptor that may be the same as, or closely related to, the adrenergic fireceptor.
IMAGING OF ABDOMINAL INFECTION/INFLAMMATION WITH TC-99m-ALBUMIN COLLOID-WBCʼS.
Authors: C. S. Marcus, B. Shoji, J. A. Butler, P. L. Henneman, L. M. Yamanaka, M. R.P. Vivian, S. E. Wilson
Journal: Clinical Nuclear Medicine (1988)

Marcus, C. S.; Shoji, B.; Butler, J. A.; Henneman, P. L.; Yamanaka, L. M.; Vivian, M. R.P.; Wilson, S. E. Author Information
Multiple infections with helminths – whipworm, hookworm, and roundworm
Authors: Kunimitsu Inoue, Sotaro Ozaka, Kazuhisa Okamoto, Ryo Ogawa, Kazuhiro Mizukami, Tadayoshi Okimoto, Masaaki Kodama, Takashi Kobayashi, Yuki Eshita, Hideo Hasegawa, Kazunari Murakami
Journal: Endoscopy (2014)

An 84-year-old woman presented with dyspnea due to an exacerbation of chronic heart failure caused by severe anemia (hemoglobin 4.4 g/dL). Colonoscopy revealed a cloud of white worms moving among tarry stool in the cecum and ascending colon. The posterior portions of the worms were located in the colon lumen, while the anterior portions were firmly embedded in colon mucosa ([Fig. 1]). One of the parasites was removed with biopsy forceps and identified as a whipworm (Trichuris trichiura).
The Management of Hypertrophic Cardiomyopathy
Authors: Paolo Spirito, Christine E. Seidman, William J. McKenna, Barry J. Maron
Journal: New England Journal of Medicine (1997)

Hypertrophic cardiomyopathy is a complex cardiac disease with unique pathophysiologic characteristics and a great diversity of morphologic, functional, and clinical features.18 The heterogeneity of the disease is accentuated by the fact that it afflicts patients of all ages. During the past few years, technological developments in implantable defibrillators and pacemakers have provided new therapeutic options for patients with the disease.918 In addition, rapid advances in our knowledge of the molecular defects responsible for hypertrophic cardiomyopathy have deepened our understanding of the disorder and have suggested new approaches to the assessment of prognosis.1922 These recent developments, however, have . . .
Abstract 2078: PERK-mediated autophagy promotes Myc-induced transformation and tumorigenesis
Authors: Lori S. Hart, Tom Cunningham, Tatini Datta, Huayi Liu, Albert C. Koong, Serge Fuchs, J. Alan Diehl, Davide Ruggero, Constantinos Koumenis
Journal: Cancer Research (2011)

Abstract The Unfolded Protein Response (UPR) is a coordinated cellular homeostatic program initiated by the accumulation of unfolded or misfolded proteins in the endoplasmic reticulum (ER) lumen, with the ultimate fate of the cell depending on both the intensity and persistence of the stress. We have previously shown that tumor cell survival under hypoxic stress is dependent on the UPR kinase PERK, as the growth of PERK-null tumors is significantly inhibited in vivo. The transcription factor c-Myc, the target of chromosomal translocation and gene amplification during the development of many human cancers, upregulates genes involved in ribosome biogenesis and increases the rate of protein synthesis, therefore, we hypothesized the UPR is activated by c-Myc overexpression. Using in vitro and in vivo models of c-Myc expression, we demonstrate that c-Myc activates PERK-dependent phosphorylation of eIF2α and upregulates the downstream effectors, ATF4 and XBP1s. UPR activation contributes to cell survival during c-Myc induced transformation via the induction of autophagy, as measured by LC3 processing and p62 degradation. Inhibition of PERK dramatically reduces c-Myc induced transformation and tumor growth in nude mice. We are currently developing a lymphoma mouse model to test the strategy of PERK inhibition orthotopically. We have established a role for c-Myc in the cellular response to ER-stress and our results highlight a role for PERK inhibition in the treatment of malignancies characterized by c-Myc overexpression, such as lymphomas. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2078. doi:10.1158/1538-7445.AM2011-2078
Abstract 4093: miR-193b is an epigenetically regulated putative tumor suppressor in prostate cancer
Authors: Hanna E. Rauhala, Sanni E. Jalava, Jarkko Isotalo, Hazel Bracken, Saara Lehmusvaara, Hannu Oja, Teuvo L. Tammela, Tapio Visakorpi
Journal: Cancer Research (2010)

Abstract miRNAs have proven to be key regulators of gene expression and are differentially expressed in various diseases, including cancer. Our aim was to identify epigenetically dysregulated genes in prostate cancer. We performed miRNA expression profiling after relieving epigenetic modifications in six prostate cancer cell lines and non-malignant prostate epithelial cells. 38 miRNAs showed increased expression in any prostate cancer cell line after 5-aza-2′-deoxycytidine (5azadC) and trichostatin A (TSA) treatments. Six of these also had decreased expression in clinical prostate cancer samples compared to benign prostatic hyperplasia. Among these, miR-193b was methylated in 22Rv1 cell line at a CpG island ∼1kb upstream of the miRNA locus. Expressing miR-193b in 22Rv1 cells using pre-miR-193b oligonucleotides caused a significant growth reduction (p&amp;lt;0.001) resulting from a decrease of cells in S-phase of the cell cycle (p&amp;lt;0.01). In addition, the anchorage independent growth was partially inhibited in transiently miR-193b -expressing 22Rv1 cells (p&amp;lt;0.01). Altogether, our data suggest that miR-193b is an epigenetically silenced putative tumor suppressor in prostate cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 4093.
CLINICAL OUTCOMES OF MANUAL ASPIRATION THROMBECTOMY IN PATIENTS WITH ACUTE MYOCARDIAL INFARCTION: AN UPDATED META-ANALYSIS
Authors: Ashraf Mostafa, Alexandros Briasoulis, Luis Afonso, Ahmed Rashed, Mohan Palla, Ashok Kondur, Theodore Schreiber
Journal: Journal of the American College of Cardiology (2015)
Polydopamine-Based Surface Modification of Novel Nanoparticle-Aptamer Bioconjugates for<i> In Vivo</i> Breast Cancer Targeting and Enhanced Therapeutic Effects
Authors: Wei Tao, Xiaowei Zeng, Jun Wu, Xi Zhu, Xinghua Yu, Xudong Zhang, Jinxie Zhang, Gan Liu, Lin Mei
Journal: Theranostics (2016)

In this study, we reported a simple polydopamine (pD)-based surface modification method to prepare novel nanoparticle-aptamer bioconjugates (Apt-pD-DTX/NPs) for in vivo tumor targeting and enhanced therapeutic effects of breast cancer.With simple preparation procedures, the new functionalized Apt-pD-DTX/NPs could maximumly increase the local effective drug concentration on tumor sites, achieving enhanced treatment effectiveness and minimizing side effects.The dopamine polymerization and aptamer conjugation barely changed the characters of NPs.Both in vitro cell experiments (i.e.endocytosis of fluorescent NPs, in vitro cellular targeting and cytotoxicity assays) and in vivo animal studies (i.e. in vivo imaging, biodistribution and antitumor effects of NPs) demonstrated that the Apt-pD-DTX/NPs could achieve significantly high targeting efficiency and enhanced therapeutic effects compared with clinical Taxotere ® and NPs without functional modification.Above all, the Apt-pD-DTX/NPs showed great potential as a promising nanoformulation for in vivo breast cancer therapy and the construction of pD-modified NP-aptamer bioconjugates could be of great value in medical use.
Unilateral Pulmonary Edema Demonstrated with Tl-201 Imaging
Authors: MANUEL T. AMENDO, LYNNE B. KOSSOW, JOHN GHAZI
Journal: Clinical Nuclear Medicine (2002)

Clinical and scintigraphic findings are described in a patient in whom acute right-sided pulmonary edema developed during a treadmill exercise test. The patient’s SPECT Tl-201 stress images are reviewed along with the pertinent clinical history. The development of unilateral pulmonary edema during an exercise treadmill test was demonstrated with Tl-201 imaging.
EARLY AND LATE RE-OPENING AFTER PLACEMENT OF THE LARIAT APPENDAGE CLOSURE DEVICE: CLINICAL IMPLICATIONS
Authors: Carola Gianni, Luigi Di Biase, Douglas Gibson, Miguel Valderrabano, John Burkhardt, Rodney Horton, Chintan Trivedi, Rong Bai, Pasquale Santangeli, Sanghamitra Mohanty, Prasant Mohanty, Andrew Krumerman, Eugen Palma, Matthew Price, Andrea Natale
Journal: Journal of the American College of Cardiology (2015)
Abstract P6-06-02: UGT1A1*28 and Breast Cancer: Increased Risk for Gilbert's Syndrome Patients
Authors: ARF Francisco, DBD Gomes, MMT Souza, RR Martini, GAR Maciel, SK Ono-Nita, JCS Góes, EC. Baracat
Journal: Cancer Research (2010)

Abstract Introduction: Estrogens are essential for the initiation and development of breast cancer (BC). Among the enzymes involved in conjugation and inactivation of estrogens and its metabolites, there is the UDP-glucuronosyltransferase 1A1 (UGT1A1). Polymorphisms in the promoter region of the UGT1A1 gene are common in patients with Gilbert's syndrome (GS), reducing the enzyme activity by about 80%. Although considered benign, patients with Gilbert's Syndrome (GS) have lower activity of UGT1A1, which may lead to a higher risk for estrogen-dependent cancers, such as breast cancer (BC). Methods: Case control-study and meta-analysis. Setting: academic tertiary hospital in Brazil. Cases: Women with recently operated BC, no previous neoplasm or immunossuppression. Controls: Healthy women, older than 40 years old, mammography BIRADS 1 or 2 in the last 12 months, no previous neoplasm or immunossupression. Interventions: data collection; sequencing of the UGT1A1 gene. Literature search: PubMed, EMBASE, SciElo, hand search. Languages: English, German, Spanish, Portuguese. Studies: case-control studies, BC patients and healthy subjects, genetic diagnosis of GS. Results: From August 2008 to November 2009, 89 cases and 56 controls were enrolled. Patients were significantly older than controls (median 52 (46-64) vs 47 (43-50) y/o p=0.013), with comparable body mass index (median 27.55 vs 25.95 p=0.46), age at menarche (median 13 vs 13 p=0.68), age at menopause (median 48 vs 45, p=0.24), age at first full-term pregnancy (median 22 vs 23 p=o.46) and proportion of individuals with first degree-relatives with BC (22% vs 19%, p=0.68). The prevalence of GS was 19.1% in cases and 12.5% in controls (adjusted OR 1.65 CI95% 0.63-4.28 p=0.29), but the study was underpowered to detect differences smaller than 21%. The meta-analysis included 10 studies with 5815 BC patients and 8255 controls. There was a weak association between GS and BC (OR 1.13 CI95% 1.01-1.26 I2=2%), which was stronger for Caucasians (OR 1.14 CI95% 1.01-1,29 I2 = 20%), estrogen-receptor positive BC (OR 1.18 CI 95% 1.02-1.35 I2=0%) and individuals with a family history of BC (OR 1.4 CI95% 1.01-1.95 I2=0%). Conclusions: In our study, the polymorphism UGT1A1 *28/*28, present in most individuals with Gilbert's syndrome, was an important risk factor for developing breast cancer. Gilbert's syndrome, usually considered benign, may be a risk factor for breast cancer. There have been no studies evaluating the incidence of BC in patients with GS. Prospective studies with patients diagnosed with SG are needed to confirm this hypothesis and assess other patients subgroups. Citation Information: Cancer Res 2010;70(24 Suppl):Abstract nr P6-06-02.
S122 Sputum cytokine profiles in asthma and the impact of smoking-a factor analysis
Authors: M. Spears, C. Dewet, C. McSharry, R. Chaudhuri, I. Donnelly, L. Jolly, E. Cameron, N. C. Thomson
Journal: Thorax (2011)

<h3>Introduction</h3> Cigarette smokers with asthma have a distinct clinical phenotype from non-smokers with asthma. This may reflect altered airway inflammation although how cigarette smoking directs this is unclear. We employed exploratory factor analysis to examine the impact of smoking on airway inflammation. <h3>Methods</h3> 22 smokers (sm), 10 ex-smokers (ex-sm) and 21 never smokers (ns) with asthma performed spirometry, induced sputum and completed asthma control questionnaires pre and post an oral corticosteroid trial. Sputum fluid cytokines were quantified using a 25-plex bead system (Invitrogen, Paisley). Factor analysis was performed (SPSS V.17) using principal component analysis and Varimax rotation. Factors were identified according to; visual inspection of the scree plot, eigenvalues &gt;1.1, minimum of three cytokines loading &gt;0.4. Sequential removal of cytokines was performed in stages according to; moderate to strong (&gt;0.4) loadings, followed by requirement for ‘strong’ loading (&gt;0.6) to only one factor then removal of cytokines that reduced the reliability of the data set. In a final step cytokines with the lowest loadings were removed if a factor had &gt;3. <h3>Results</h3> The subjects were well matched except for higher asthma control questionnaires scores and inhaled corticosteroid dose in sm. Sm failed to demonstrate a lung function response to oral corticosteroids in contrast to nsm. No sputum cell differential differences were evident between smokers and non-smokers with asthma. A number of pre-steroid sputum cytokines were elevated in sm compared to nsm. The greatest difference present for interleukin 6 (sm 34.4 pg/ml (IQR 14.1, 72.4), nsm 8.1 pg/ml (4.4, 11.1), p&lt;0.001). Factor analysis of the pre-steroid cytokines demonstrated that three factors explained 90% of the variance in the data. Sequential processing revealed three cytokines per factor (Abstract S122 table 1). <h3>Discussion</h3> Sputum cytokine profiling of subjects with asthma with differing smoking histories reveals distinct groupings when examined by exploratory factor analysis providing insight into airway inflammation in asthma and the impact of smoking. Larger cohorts of patients with asthma should be examined to confirm these preliminary findings.
Abstract P5-04-02: DYRK2 regulates breast cancer invasion via Snail/E-cadherin pathway
Authors: R Mimoto, Y Imawari, M Kamio, K Kato, H Nogi, Y Toriumi, H Takeyama, K Yoshida, K Uchida
Journal: Cancer Research (2012)

Abstract Introduction: Epithelial-Mesenchymal Transition (EMT) is characterized by the loss of cellular adhesion molecule E-cadherin, and plays a fundamental role during early steps of breast cancer invasion. An important regulator of E-cadherin expression is Snail, a zinc finger transcriptional repressor. Snail is posphorylated by GSK3β and then degraded by βTrCP mediated ubiquitination. Here we found another kinase, DYRK2, regulates the stability of Snail. Knockdown of DYRK2 promoted the EMT and cancer invasion both in vitro and in vivo experiments. Methods: Cell lines: MCF-7 cells were transfected with pSuper vector (pSuper control) and pSuper shRNA DYRK2 (shRNA-DYRK2) with G418 to isolate stable cell lines. Immunoblotting: Expression of pertinent molecular markers was determined by western blotting. RT-PCR: RNA was extracted using TRIsure and 500 ng of total RNA was amplified using Primer Script One Step RT-PCR Kit Ver.2. Invasion assay: Various cancer cell lines were seeded on the top of the upper chamber with serum free medium while the bottom chambers were filled with medium containing 10% FBS. In vivo metastasis assay: Cells in PBS were injected into the left ventricle of 7-week-old female nude mice. Metastases to distant organs were confirmed by IVIS2000. Immunohistochemistry: We acquired paraffin-embedded tissue sections from primary breast tumor cores and from Jikei University of Medicine. Immunohistochemistry for DYRK2 was performed. Results: In MCF-7 cells, knockdown of DYRK2 increased Snail in the protein level but not in mRNA level. Upon DYRK2 knockdown, MG132 treatment had no effect on additional increase in Snail. DYRK2 knockdown decreased Snail ubiquitination. Stable DYRK2 depletion led to Snail accumulation and E-cadherin abrogation. Fibroblast marker, Vimentin, emerged in DYRK2 depleted cells. For further analysis, we carried out invasion assays. The invasion potential in DYRK2-depleted cells was substantially higher than that in control cells. In xenograft model, we used nude mice received intracardial injections of pSuper control or shRNA-DYRK2 cells. 6 weeks after injections, a significant increase in bone and lung metastasis was observed in shRNA-DYRK2 group. The patients with tumors expressed low DYRK2 showed significantly poor prognosis. Conclusion: In breast cancer cells, Snail is phosphorylated by DYRK2 and then acquires the ability to be ubiquitinated. In the absence of DYRK2, Snail is unable to be degraded by ubiquitin-proteasome machinery. Accumulation of Snail promotes EMT and cancer invasion, so low expression of DYRK2 leads to poor prognosis in breast cancer. Citation Information: Cancer Res 2012;72(24 Suppl):Abstract nr P5-04-02.
Abstract 1174: Mechanisms of Fn14 overexpression in invasive breast tumors
Authors: Joshua R. Niska, Amanda L. Willis, Pilar Ramos, Catherine M. Mancini, Julie E. Getz, Heather E. Cunliffe
Journal: Cancer Research (2010)

Abstract The fibroblast growth factor-inducible 14 (Fn14) signaling axis plays an important role in the regulation of breast cancer cell invasion. Breast tumors express Fn14 whereas normal mammary epithelium does not, and Fn14 expression correlates with poor prognostic indicators. The molecular mechanisms driving aberrant Fn14 expression in breast cancer have not yet been determined. This investigation aims to elucidate the mechanisms underlying Fn14 over-expression. Soluble tumor necrosis factor-like weak inducer of apoptosis (TWEAK), the cognate ligand for Fn14, was found to induce Fn14 expression in some breast cancer cell lines via a proposed autoregulatory mechanism. We also provide evidence to support the likelihood that membrane-bound TWEAK can stimulate Fn14 expression through adjacent tumor-cell interaction. EGF and a variety of other receptor tyrosine kinase ligands known to play a role in breast tumor progression stimulated de novo Fn14 expression in a panel of breast cancer cell lines. We therefore hypothesized that Fn14 expression may be induced by aberrant activation of the MAPK signaling pathway. Using an MCF7 model of TPA-mediated MAPK pathway activation and in vitro invasion using Matrigel-coated Transwell Boyden chambers, we observed TPA-mediated expression of Fn14 concomitant with a dramatic increase in cell invasion. Fn14 expression and invasion in this model were abrogated in the presence of U0126, a specific inhibitor of Mek1/2, implicating a role for MAPK signaling in regulation of Fn14 expression. From previously published microarray-based surveys of genomic aberrations in breast cancer, we also hypothesized that constitutive Fn14 expression may be due to Fn14 gene amplification. We performed fluorescence in situ hybridization analysis of 53 breast tumors and identified 15/53 (28%) tumors with additional copies of Fn14 relative to centromere 16. Fn14 was not amplified in normal breast epithelium or in Fn14-negative cell lines. We conclude that deregulation of Fn14 expression can occur through diverse molecular mechanisms associated with breast tumor progression. A more complete definition of the spectrum of molecular aberrations leading to induction of Fn14 expression in breast cancer requires further studies. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1174.
Hyperectasis of the Tympanic Membrane
Authors: Masafumi Ohki
Journal: New England Journal of Medicine (2013)

A 44-year-old woman with frequent bilateral ear fullness was given a diagnosis of atelectatic tympanic membranes several years ago. She was told to perform the Valsalva maneuver, which raises air pressure in the nasal cavity and aerates the middle ear through the eustachian tube.