tbuckley/cabot-search huggingface dataset:
S160 The effect of shift work on serial peak expiratory flow measurements used to diagnose occupational asthma
Authors: V. C. Moore, M. S. Jaakkola, C. B. S. G. Burge, C. F. A. Pantin, A. S. Robertson, P. S. Burge
Journal: Thorax (2010)

We investigated the effects of shift work on Peak Expiratory Flow (PEF) measurements used for diagnosing occupational asthma (OA). In a clinic database of workers investigated for OA, 123 workers with OA and 69 workers without OA had PEF records containing &gt;1 shift pattern with ≥4 days on each shift. The OA definition was based on Oasys-2 score &gt;2.51 and the non-OA on an alternative clinical diagnosis and Oasys-2 score &lt;2.51. Records not fulfilling the minimum data quantity for the Area Between Curves (ABC) PEF score, or containing respiratory infections, changes in asthma treatment or different exposures on each shift were excluded. The mean ABC score, mean PEF diurnal variation (DV) on workdays and cross-shift PEF changes were calculated for each shift. The ABC score of the OA workers was lower on nights (p=0.028) and afternoons (p=0.020) compared to day shifts, without significant differences in diurnal variation. There was statistically significant difference between day and night shift cross-shift changes (p&lt;0.001), larger changes being observed in nights. The sensitivity and specificity of the ABC score was 79% and 99% for day shifts, 83% and 98% for nights and 72% and 96% for afternoon shifts. The sensitivity of increased DV on work days compared to rest days was 76% for day shifts, 78% for nights and 70% for afternoons, specificities being 26%, 48% and 42%, respectively. PEF changes between work and rest show small differences with shift types. The ABC score has high sensitivity and specificity for all three shifts; differences in DV have high sensitivity, but low specificity when using a cut-off point of &gt;0% for the difference between work and rest day DV.
Abstract 1291: Identification of penfluridol as potential treatment for pancreatic cancer cells.
Authors: Wenwen Chien, Kian Leong Lee, Qiaoyang Sun, Peer Wuensche, Makoto Sudo, Lorenz Poellinger, Jeffrey W. Tyner, Henry Yang, H. Phillip Koeffler
Journal: Cancer Research (2013)

Abstract Tyrosine kinase inhibitors (TKIs) have provided promising anti-cancer activities, but intrinsic or acquired resistance to these drugs is a major problem. To overcome this resistance, we have used microarray analysis to identify a signature of intrinsic drug resistance in human pancreatic cancer cells, and applied this gene expression profile to silico drug screening for potential drugs for pancreatic cancer therapy. The potency of dasatinib (a multiple family TKI) was assessed against a panel of 14 human pancreatic cancer cell lines. This drug is undergoing clinical trials for pancreatic cancers. Nine of fourteen pancreatic cell lines were growth inhibited by dasatinib. Three dasatinib-resistant (MiaPaCa2, Panc1, SU8686) and three -sensitive (Panc0504, Panc1005, Panc0403) pancreatic cancer cell lines were used in microarray analysis to compare the gene expression profiles. A total of 598 genes were differentially expressed in dasatinib-resistant cell lines compared to the sensitive cell lines. To discover therapeutic drugs that sensitize pancreatic cancer cells to dasatinib, we performed in silico drug screening using the Connectivity Map database (CMAP). The gene signature induced by thioridazine in CMAP showed a “glove in hand” pattern to that found in dasatinib-resistant versus -sensitive pancreatic cancer cell lines. Thioridazine belongs to the phenothiazine family including chlorpromazine, perphenazine, penfluridol, and pimethixene. Each was examined. Assays of cell proliferaton, cell cycle, and Annexin V showed that each was effective at inhibiting the cell cycle and inducing apoptosis. Penfluridol (a calcium channel inhibitor) was the most potent against both the dasatinib-resistant and -sensitive pancreatic cancer cell lines. Drug combination studies of penfluridol and either dasatinib or gemcitabine (FDA-approved for pancreatic cancer) showed synergistic enhancement of cytotoxicity. Mechanistic investigations suggested that multiple signaling pathways were suppressed by penfluridol. These studies suggest a potential novel class of drugs for treatment of pancreatic cancers. Citation Format: Wenwen Chien, Kian Leong Lee, Qiaoyang Sun, Peer Wuensche, Makoto Sudo, Lorenz Poellinger, Jeffrey W. Tyner, Henry Yang, H. Phillip Koeffler. Identification of penfluridol as potential treatment for pancreatic cancer cells. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1291. doi:10.1158/1538-7445.AM2013-1291
Comprehensive genomic profiling of anal squamous cell carcinoma reveals distinct genomically defined classes
Authors: J.H. Chung, E. Sanford, A. Johnson, S.J. Klempner, A.B. Schrock, N.A. Palma, R.L. Erlich, G.M. Frampton, Z.R. Chalmers, J. Vergilio, D.A. Rubinson, J.X. Sun, J. Chmielecki, R. Yelensky, J.H. Suh, D. Lipson, T.J. George, J.A. Elvin, P.J. Stephens, V.A. Miller, J.S. Ross, S.M. Ali
Journal: Annals of Oncology (2016)
Abstract 5409: Cancer immunosuppression: The role of human leukocyte antigen G expression
Authors: Robert L. Elliott, Xian P. Jiang, Jeffery T. Phillips, Jonathan F. Head
Journal: Cancer Research (2012)

Abstract Human leukocyte antigen G (HLA-G) is an immunotolerant nonclassical major histocompatibility complex class Ib molecule. During pregnancy it is expressed by trophoblastic placental cells to protect the fetus from maternal alloreactivity. HLA-G is involved in cancer immune evasion and is overexpressed by many tumors. Reverse transcription-polymerase chain reaction and immunohistochemistry were used to examine HLA-G expression in human normal breast and breast cancer cell lines, and human normal breast and breast cancer tissues. Reverse transcription-polymerase chain reaction confirmed that normal epithelial MCF-12A cells had no HLA-G mRNA, but cancer cell lines MCF-7, T47D, and MDA-MB-231 and NCI/Adr-Res had various levels of HLA-G mRNA expression. Thirty-eight breast cancers and 12 normal breast tissues were examined by immunohistochemistry. Fifty-eight percent (22/38) of cancers had medium to strong staining for HLA-G, whereas only 8% (1/12) of normal breast tissues had medium to strong staining, and the difference was statistically significant (p&amp;lt;0.05). HLA-G staining was found in the cytoplasm and membranes of cancer cells. In conclusion breast cancer cells overexpress HLA-G mRNA and protein, which probably contributes to immune evasion and treatment resistance. We believe HLA-G should be monitored in breast and other epithelial cancers as it may be both a prognostic indicator and a therapeutic target. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 5409. doi:1538-7445.AM2012-5409
THE RELATIONSHIP BETWEEN RESTING HEART RATE AND PEAK VO2: A COMPARISON OF ATRIAL FIBRILLATION AND SINUS RHYTHM
Authors: Yuko Kato, Shinya Suzuki, Hiroaki Semba, Hiroto Kano, Shunsuke Matsuno, Hideaki Takai, Takayuki Otsuka, Tokuhisa Uejima, Yuji Oikawa, Kazuyuki Nagashima, Hajime Kirigaya, Koichi Sagara, Takashi Kunihara, Junji Yajima, Hitoshi Sawada, Tadanori Aizawa, Takeshi Yamashita
Journal: Journal of the American College of Cardiology (2016)
Abstract 277: Genetic re-programming of the acute myeloid leukemia cell line HL-60
Authors: Michael Roberts, David Bittner, Sarah Brnich, Bryan Conner, Carla Cox, Julia Filiberti, Michael Grant, Michael Mansuy, Jeffrey Forrester
Journal: Cancer Research (2011)

Abstract HL-60 cells represent an established line of human acute myeloid leukemia cells that can be induced to differentiate along several distinct myeloid lineages. Phorbol esters activate a signaling network, which includes the protein kinase C (PKC) signaling pathway, causing the leukemia cells to differentiate into macrophage-like cells. As the leukemia genetic program is converted to the macrophage program, the cells exit the cell cycle, undergo morphological changes, become adherent, display other macrophage properties, and ultimately initiate apoptosis. This study provides a detailed DNA microarray analysis of the genetic network of the leukemia cell during first 24 hours post-induction of differentiation. Approximately 1,000 genes were identified that exhibit significant changes in mRNA levels from the leukemia expression profile. A cluster analysis was performed to group these genes by their pattern of expression resulting in a collection of distinct expression profiles. Expression levels of selected genes within each cluster were validated by real time PCR. Among the most significant changes observed were dramatic increases in the expression of CCL chemokine family genes and a variety of transcription factor genes including members of the AP-1 and NF-κB families. Expression level changes in genes involved in cell cycle progression (ex. MYC and p21) were also observed along with genes involved in the regulation of apoptosis (ex. BCL2A1, TNF, IER2 and OLR1). Functional analysis at the protein level using the electrophoretic mobility shift assay (EMSA), western blotting and immunofluorescence imaging will also be presented. This study provides a comprehensive view of the re-programming events that occur in phorbol ester induced macrophage differentiation of HL-60 cells with regard to the inflammatory response, cell cycle exit, differentiation and initiation of apoptosis. 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 277. doi:10.1158/1538-7445.AM2011-277
DYNAMIC DISTURBANCES IN THE HANDWRITING OF PSYCHOTICS
Authors: THEA STEIN LEWINSON
Journal: American Journal of Psychiatry (1940)

1. The handwriting of psychotic patients show definite characteristics. 2. The basic disturbance in the psychotic handwriting is expressed by the drastic disturbance in the dynamic relationship. 3. The fundamental dynamic disturbance finds different modifications in the handwriting of the schizophrenic, the paranoid and the manic-depressive patients. 4. These different modifications are characterized by an emphasized disturbance in one of the graphic spheres: a. The dimension of breadth in schizophrenic writings. b. The dimension of depth in paranoid writings. c. The dynamic relationship implicating the dimension of height in manic-depressive condition writings.
Scintigraphic Evaluation of Metastatic Osteosarcoma The Importance of SPECT Bone Scintigraphy and Correlative Imaging
Authors: JOSÉ E. RIVERA-RODRÍGUEZ
Journal: Clinical Nuclear Medicine (1997)

A 31-year-old man with a history of osteosarcoma and prior resection of the left distal femur had an acute onset of hemoptysis. Planar skeletal scintigraphy with Tc-99m MDP showed an area of increased uptake in the region of the posterior left 8th rib, suspicious for a metastatic lesion. Chest x-ray showed a pulmonary nodule in the left lower lobe. Rib x-rays showed no metastases. Because the patient was scheduled for a thoracotomy to remove the lung lesion, original plans called for removal of the left eight posterior rib as well. Repeat bone scintigraphy, this time using SPECT, clearly showed that the lesion identified on planar imaging was indeed in the pulmonary parenchyma and not in the rib, representing"shine through." This case shows the importance of correlative imaging as well as SPECT bone scintigraphy when findings on the planar study are not clear, and it may affect the patient's surgical management.
Review of 13 cases of Capgras syndrome
Authors: R Kiriakos, J Ananth
Journal: American Journal of Psychiatry (1980)

The authors describe 13 psychotic patients who had Capgras syndrome. Only 4 patients had evidence of organicity. The authors conclude that Capgras syndrome occurs equally in functional psychosis and in the presence of organicity and recommend that the presence or absence of organicity be determined in every patient with Capgras syndrome.
Abstract 3285: Synergistic anticancer effects of resveratrol and clofarabine in malignant mesothelioma cells.
Authors: David M. Lee, Yoon-Jin Lee, Jae-Hyuk Im, Seong-Youn Won, Hae-Seon Nam, Sang-Han Lee
Journal: Cancer Research (2013)

Abstract Malignant mesothelioma is highly resistant to apoptosis. Hence, new strategies to enhance the apoptotic signal and overcome resistance to therapeutic drugs are necessary to improve the therapeutic efficacy of malignant mesothelioma. Here, we investigated the effects of the combined treatment of various phytochemicals as a chemo-potentiator in combination with the chemotherapeutic agent clofarabine in malignant mesothelioma MSTO-211H cells and normal mesothelial Met-5A cells. Treatment with resveratrol in combination with clofarabine at a subtoxic concentration produced a synergistic antiproliferative effect and induced apoptotic cell death, as evidenced by increased subG1 peak on flow cytometric analysis, chromatin condensation and nuclear fragmentation on DAPI staining, and DNA laddering on agarose gel electrophoresis, in MSTO-211H cells, but not in Met-5A cells. In MSTO-211H cells, endogenous expression of the transcription factors Nrf2 and Sp1 proteins, several Nrf2 and Sp1-regulated gene products (HO-1, c-Met, and cyclin D1), and Akt phosphorylation, were effectively suppressed by the combined treatment of clofarabine and resveratrol. Furthermore, the nuclear accumulations of Nrf2 and Sp1 were inhibited by the combination treatment. In combination with clofarabine, the ability of resveratrol to increase the contents of the phosphorylated p53 and the apoptotic molecules, PARP and cleaved caspase 3, was also evident in a time- and dose-dependent experiment. Taken together, the data provide evidence that the synergistic antiproliferative effect of resveratrol and clofarabine is linked to simultaneous suppression of multi-target molecules, such as Nrf2, Sp1, and Akt activities, and suggest that this combination may have therapeutic value in treatment of malignant mesothelioma. Citation Format: David M. Lee, Yoon-Jin Lee, Jae-Hyuk Im, Seong-Youn Won, Hae-Seon Nam, Sang-Han Lee. Synergistic anticancer effects of resveratrol and clofarabine in malignant mesothelioma cells. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 3285. doi:10.1158/1538-7445.AM2013-3285
Abstract 2773: HSP90 inhibitors target KRAS mutant human tumors through degradation of STK33
Authors: Ninel Azoitei, Christopher M. Hoffmann, Jana M. Ellegast, Claudia R. Ball, Kerstin Obermayer, Ulrike Gößele, Britta Koch, Katrin Faber, Felicitas Genze, Mark Schrader, Hans A. Kestler, Hartmut Döhner, Gabriela Chiosis, Hanno Glimm, Stefan Fröhling, Claudia Scholl
Journal: Cancer Research (2012)

Abstract Mutations in the KRAS proto-oncogene occur in ∼30% of human cancers and are particularly prevalent in adenocarcinomas of the pancreas, lung, and colon. Previous efforts to develop drugs that directly inhibit the activity of mutant KRAS have not met with success. We have recently shown that cancer cells driven by mutant KRAS require expression of the serine/threonine kinase STK33 for their viability and proliferation, supporting STK33 as a context-dependent therapeutic target. However, specific strategies for interfering with the critical functions of STK33, which remain to be elucidated, are not yet available. Using a mass spectrometry-based screen for STK33 protein interaction partners, we report that the HSP90/CDC37 chaperone complex and BAG2, a member of the BAG family of molecular chaperone regulators, bind to and stabilize STK33 in human cancer cells. Pharmacologic inhibition of HSP90, using structurally divergent small molecules currently in clinical development, induced proteasome-mediated degradation of STK33 in human cancer cells of various tissue origin in vitro and in vivo, and triggered apoptosis preferentially in KRAS mutant cells in an STK33-dependent manner. Furthermore, HSP90 inhibitor treatment impaired sphere formation and viability of primary human colon cancer-initiating cells harboring mutant KRAS. Similar to HSP90 inhibition, short hairpin RNA-mediated suppression of BAG2 depleted STK33, whereas BAG2 overexpression rescued STK33 protein levels in the presence of HSP90 inhibitors, resulting in diminished apoptosis in KRAS mutant cancer cells. These findings (1) provide mechanistic insight into the activity of HSP90 inhibitors in KRAS mutant cancer cells, (2) indicate that the enhanced requirement for STK33 can be exploited to target mutant KRAS-driven tumors, (3) identify STK33 depletion through HSP90 inhibition as a biomarker-guided therapeutic strategy with immediate translational potential, and (4) point to BAG2 as a candidate cancer drug target. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 2773. doi:1538-7445.AM2012-2773
Nurses' pay award will not help recruitment
Authors: L. Beecham
Journal: BMJ (1998)

Leaders of Britain's 500 000 nurses, midwives, and health visitors say that the phasing of a 3.8% award, which is below inflation, will only deepen the current recruitment crisis.

The government's decision to phase the recommendation of the nurses' review body means that from 1 December the minimum salary for a staff nurse will be £14 …
S132 Chronic Bronchitis, Pulmonary Function, and Occupational Exposure in Framingham Heart Study
Authors: SY Liao, X Lin, DC Christiani
Journal: Thorax (2012)

<h3>Introduction</h3> Occupational exposure to dust, gases and fumes has been associated with chronic airway disease or poor lung function in several workforce based studies. However, workforce studies may underestimate such associations because of healthy worker effect confounding bias. We conducted a community-based study that used a more generalised populations of individuals and less susceptible to healthy worker effect. We investigated the associations between the self-reported occupational exposure and chronic bronchitis, as well as pulmonary function testing. <h3>Methods</h3> The study population is the Third-Generation cohort from Framingham Heart Study with a total of 3,894 participants. We used participants’ examination of FEV1, FEV1/FVC, chronic bronchitis (based on self reported symptoms) as outcomes. Occupational exposure was assessed by self-reported exposure to vapours, gas, dust, or fumes at work. Gender, age, height, pack-years, and smoking status were used as covariates in our analysis. We used linear mixed effect models for continuous outcomes and generalised estimating equations for dichotomous outcomes due to the family structure. <h3>Results</h3> There are 1,745 participants reporting occupational exposure at work and 2,149 participants reporting no occupational exposure. The association of occupational exposure on the FEV1 and FEV1/FVC was not significant in this cohort. However, self-reported occupational exposure was associated with a risk of chronic bronchitis after controlling for covariates (OR 1.55, 95% CI 1.19 to 2.01). Current smoking was associated with a greater risk of chronic bronchitis after controlling for covariates (OR 3.20, 95% CI 2.37 to 4.32). Those with combined occupational and smoking exposure had a 5 fold increased risk of chronic bronchitis compared those with neither occupational nor smoking exposure. <h3>Conclusions</h3> Occupational exposure is significantly associated with chronic bronchitis. In addition to preventing smoking exposure, preventive strategies should be taken by clinicians and health policy-makers to reduce occupational exposures in workplace.
Introduction: Emerging Areas of Research Reported during the CDC National Conference on Pfiesteria: From Biology to Public Health
Authors: Carol Rubin, Michael A. McGeehin, Adrianne K. Holmes, Lorraine Backer, Gene Burreson, Marie C. Earley, David Griffith, Ronald Levine, Wayne Litaker, Joanne Mei, Luke Naeher, Larry Needham, Edward Noga, Mark Poli, Helen Schurz Rogers
Journal: Environmental Health Perspectives (2001)
SP0024 Comorbidity in Rheumatic Diseases
Authors: J. Askling
Journal: Annals of the Rheumatic Diseases (2013)

<h3></h3> Successful minimization of the consequences of co-morbidities in RA is a multi-step process that requires and understanding of: (i) which these major co-morbidities are, (ii) which their typical manifestations are, (iii) how the risk for each of these conditions may be assessed, (iv) how the presence of these morbidities may be diagnosed, (v) which the main risk factors for the development of these disease are, (vi) which interventions are effective in preventing onset of these diseases, (vii) what interventions may be used to treat these diseases, (viii) which care-provider should ideally be responsible for which part of the surveillance, prevention, and treatment of these conditions. The aim of this presentation will be to discuss items (i) through (viii) for those co-morbidities that occur in RA, either because of the RA itself, its treatment, or for other reasons. Finally, we will discuss how this might be implemented in a busy everyday clinical rheumatology practice. <h3>Disclosure of Interest</h3> None Declared