tbuckley/cabot-search huggingface dataset:
P240 Does a relationship exist between serum albumin and lactate with the length of stay in patients admitted with community acquired pneumonia?
Authors: AT Sahal, J Das
Journal: Thorax (2013)

<h3>Introduction</h3> Previous studies have shown that high lactate and CURB65 scores are associated with increased mortality and morbidity in patients with community acquired pneumonia (CAP). We attempted to investigate a simple way to identify those patients who are likely to have prolonged hospital admission from CAP by using different biomarker. <h3>Method</h3> We included first 50 patients who were diagnosed to have CAP by respiratory physicians on admission at Russell’s Hall hospital, Dudley in December 2012. We calculated CURB scores and measured their lactate level, serum albumin and white cells count on admission. We also monitored their albumin levels throughout the admission. We then examined the association between these factors and LOS using Spearman9s rank correlation coefficient (RS). <h3>Results</h3> There was no mortality from CAP in our study population. Mean length of stay was 7 days (1–41). There was positive correlation between CURB65 and LOS (Rs = 0.41, p = 0.003). We did not observe any statistically significant correlation between the lactate level, albumin level or white cell count on admission and the LOS. Interestingly, we noticed that there was a statistically significant negative correlation with the day 3–5 albumin level with LOS (Rs = -0.522, p = 0.000627). <h3>Conclusions</h3> Our study suggests that low albumin on day 3–5 increases hospital LOS therefore it could be postulated that early nutritional intervention to keep higher level of albumin might decrease length of stay. We also believe that combing admission CURB65 and day 3 albumin will give us better tool to predict LOS but prospective study is needed to evaluate these findings further.
Abstract 3058: <i>ADAMTS9</i> inhibits angiogenesis and induces apoptosis in nasopharyngeal carcinoma
Authors: Hong Lok Lung, Paulisally Hau Yi Lo, Arthur Kwok Leung Cheung, Suneel S. Apte, Maria Li Lung
Journal: Cancer Research (2010)

Abstract Background and aims: A disintegrin-like and metalloprotease with thrombospondin type 1 motif 9 (ADAMTS9), a gene mapping to 3p14.2, has been shown to be silenced by promoter hypermethylation in nasopharyngeal carcinoma (NPC). The ADAMTS family consists of 19 secretion protein members consisting of a disintegrin domain, metalloproteinase domain, and different numbers of thrombospondin type 1 motifs. ADAMTS9 encodes a member of a large family of 19 metalloproteases involved in maturation of precursor proteins, extracellular matrix remodeling, cell migration, and inhibition of angiogenesis. Although the related matrix metalloproteases and ADAM proteases have been clearly implicated in tumor progression and angiogenesis, the role of ADAMTS proteases in cancer is less clearly defined. In the present study, we investigated the in vivo and in vitro functional roles of ADAMTS9 in angiogenesis of NPC. Methods: To examine the antigiogenic activity of ADAMTS9 in NPC, the in vivo gel plug and in vitro tube formation assays were performed using a tetracycline-regulated expression vector in the present study. Results: Here we show that when incubated with conditional media from the ADAMTS9 stable transfectant, the human umbilical vein endothelial cells (HUVEC) showed a dramatic decrease of tube formation ability. When the gel plugs used for the in vivo angiogenesis in the above section were stained with H&amp;E, we observed that the numbers of apoptotic cells in the ADAMTS9 stable transfectant were dramatically increased. The numbers of apoptotic cells were also increased when growing in the absence of serum. Conclusions: Taken together, these studies indicate that ADAMTS9 is an important candidate tumor suppressor gene in NPC, which might mediate its tumor suppressive effects through the anti-angiogenic and pro-apoptotic mechanisms. 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 3058.
Abstract 3057: The serine protease inhibitor, elafin, exhibits novel tumor suppressor functions in the context of breast cancer
Authors: Joseph A. Caruso, Kelly K. Hunt, Khandan Keyomarsi
Journal: Cancer Research (2010)

Abstract Serine proteases and their inhibitors have an established role in cancer progression, invasion, and metastasis. Elafin is an endogenously expressed inhibitor of human neutrophil elastase. In mammary epithelial cells elafin is highly expressed; however in breast cancer it is transcripitionally downregulated. We hypothesize that the loss of elafin is critical to the development of the malignant phenotype in breast cancer. In human mammary epithelial cells (HMECs) and breast cancer cell lines, the regulation and activity of elafin is dependent on the critical tumor suppressor retinoblastoma (Rb). Elafin is dramatically upregulated in quiescent HMECs following growth factor deprivation. This upregulation is characterized by an Rb dependent increase in elafin stability and cytoplasmic accumulation. Knockdown of elafin by shRNA in HMECs causes them to be refractory to growth factor deprivation induced quiescence; suggesting that elafin upregulation is a key regulator of cellular quiescence. Overexpression of elafin by adenovirus in both HMECs and breast cancer cell lines lacking Rb causes caspase-3 dependent, apoptotic cell death. Additionally, adenoviral elafin causes Rb-dependent cell cycle arrest in tumor cells with functional Rb. The Rb pathway is lost or inactivated in the majority of cancers. The design of a therapeutic strategy capable of specifically targeting tumor cells with Rb inactivation may prove to have significant utility in the treatment of cancer. The data summarized here demonstrates that overexpression of elafin is cytostatic in Rb-positive breast cancer cells and cytotoxic in Rb-negative breast cancer cells expressing caspase 3; suggesting that elafin could be engineered into a therapeutic modality in the treatment of breast 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 3057.
Stat Bite: Accredited Mammography units
Authors: M. McKinney, L. Fintor
Journal: JNCI Journal of the National Cancer Institute (1991)

Stat BiteAccredited Mammography units Get access Martha McKinney, Ph.D, Martha McKinney, Ph.D Search for other works by this author on: Oxford Academic PubMed Google Scholar Lou Fintor Lou Fintor Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 83, Issue 18, 18 September 1991, Page 1283, https://doi.org/10.1093/jnci/83.18.1283 Published: 18 September 1991
P884 DONOR/RECIPIENT GENDER MISMATCH MODIFIES THE IMPACT OF DONOR AGE ON GRAFT SURVIVAL FOLLOWING LIVER TRANSPLANTATION
Authors: D. Bitetto, S. Pecere, M. Gambato, A. Ferrarese, L. Pasulo, M.G. Lucà, E. Poli, S. Ginanni Corradini, U. Baccarani, P. Burra, P. Toniutto, S. Fagiuoli
Journal: Journal of Hepatology (2014)
Abstract 5613: Enhanced treatment of lung metastasis of triple negative breast cancer by doxorubicin-mitomycin C co-loaded polymer lipid nanoparticles.
Authors: Preethy Prasad, Ping Cai, Andrew Rauth, Xiao Wu
Journal: Cancer Research (2013)

Abstract Background: Treatment of triple negative breast cancer (TNBC) is a big challenge due to its aggressiveness, metastases, lack of therapeutic target and receptor proteins. Our laboratory has developed doxorubicin (Dox) -mitomycin C (MMC) co-loaded stealth polymer lipid hybrid nanoparticles (DMsPLN) and demonstrated their anti-cancer synergy in vitro and high efficacy in vivo. The purpose of this study is to evaluate the biodistribution, in vivo efficacy and safety of DMsPLN in a lung metastatic human TNBC model. Method: Lung metastasis of breast tumor was established using MDA-MB 231-luc-D3H2LN, a luciferase expressing cell line that was derived from spontaneous lymph node metastasis. The cells were injected via tail vein to develop lung metastasis in SCID mice. The biodistribution and tumor accumulation of the nanoparticles were examined by whole animal optical imaging using near infrared fluorescence labeled nanoparticles. The efficacy and systemic toxicity of DMsPLN were evaluated against clinically used doxorubicin (Dox). DMsPLN and free Dox solution were administered intravenously at various equivalent Dox doses. The tumor burden was monitored weekly by bioluminescence imaging. The size and number of tumor nodules in the lungs were examined at different time points and the systemic toxicity was monitored by repeated measurement of body weight. Results: A lung metastatic breast tumor model was successfully developed using the MDA-MB 231-luc-D3H2LN which allowed for non-destructive monitoring of tumor growth and metastases using bioluminescence imaging. Whole animal imaging demonstrated the accumulation of the fluorescent nanoparticles in the lung metastatic site. Treatment with free Dox (10 mg/kg) resulted in severe total body weight loss over 20% which is ruled as a toxic endpoint. However, the DMsPLN (10 mg/kg equivalent Dox dose) group did not show any systemic toxicity. Treatment with DMsPLN at various Dox doses resulted in a reduction in tumor burden compared to the saline and Dox-treated groups. Citation Format: Preethy Prasad, Ping Cai, Andrew Rauth, Xiao Wu. Enhanced treatment of lung metastasis of triple negative breast cancer by doxorubicin-mitomycin C co-loaded polymer lipid nanoparticles. [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 5613. doi:10.1158/1538-7445.AM2013-5613 Note: This abstract was not presented at the AACR Annual Meeting 2013 because the presenter was unable to attend.
Rapid Radiation of Canaries (Genus Serinus)
Authors: A. Arnaiz-Villena, M. Alvarez-Tejado, V. Ruiz-del-Valle, C. Garcia-de-la-Torre, P. Varela, M. J. Recio, S. Ferre, J. Martinez-Laso
Journal: Molecular Biology and Evolution (1999)

Mitochondrial cytochrome b (mit cyt b) DNA from 20 out of 37 extant canaries (genus Serinus) has been sequenced from living specimens photographed around the world. Phylogenetic analysis has consistently resulted in the same groupings of birds, which have generally been related to geographical proximity. The fossil registry of chicken and pheasant and its divergence time have been used to calibrate the molecular clock; mit cyt b DNA dendrograms suggest that the Serinus bird lineage appeared in the Miocene (9 MYA), a time when the Mediterranean Sea was closing its western and eastern oceanic connections. Pleistocene glaciations (starting 2 MYA) may have only been important in the subspeciation and isolation of birds in the Northern and Southern hemispheres around the world, and not only in North America, where it has already been described. The European-isolated Serinus citrinella (Citril finch) is not a canary but rather a true goldfinch. Only about 4% average nucleotide divergence is found among the different Serinus species; this suggests a remarkably rapid radiation when compared to other passerine (songbird) genera radiations. In addition, reproductive barriers are observed between closely related species but not between other more distant ones. Finally, a tentative classification for the genus Serinus species is put forward.
Abstract 4361: Retinoblastoma (RB) genomic progression analysis using Tissue Microarrays (TMA) comprising 121 RB patient tumors
Authors: Crystal N. D'Silva, Maisa Yoshimoto, Renato Natalino, Fernando Soares, Celia Antoneli, Karina Ribeiro, William Halliday, Brenda L. Gallie, Jeremy A. Squire
Journal: Cancer Research (2010)

Abstract Retinoblastoma is the second most common childhood intraocular malignancy and development of the tumor is initiated by bi-allelic loss of the RB1 gene. Bi-allelic RB1 loss may not always directly lead to malignant retinoblastoma, rather other genetic changes are likely involved. Subsequent mutational events, specifically gain and loss of chromosomal regions harboring key oncogenes and tumor suppressor genes, appear to underlie the progression of precursor lesions such as retinoma to retinoblastoma. Research thus far has implicated several cytogenetic aberrations in this sequence of molecular events, the two most recurrent and notable being the augmented copy number status of KIF14 and MDM4 on 1q and of DEK and E2F3 on 6p. A small subset of retinoblastoma also exhibits high-level amplification of the MYCN gene on chromosome 2p. KIF14, MDM4, DEK, E2F3 and MYCN have been widely characterized as oncogenes in a variety of cancers. The functional roles of the proteins encoded by these genes would also confer tumor cells manifesting these genomic changes with a selective survival and proliferative advantage. Our project is testing the hypothesis that 1q and 6p gain and 2p amplification - defined by extra copies of KIF14 and MDM4, DEK and E2F3 and MYCN respectively - are associated with clinical parameters of progression. The study comprises formalin-fixed paraffin-embedded fluorescence in situ hybridization (FFPE-FISH) analysis of pre-constructed tissue microarrays comprising 121 patient tumours, in order to determine the genomic copy number status of the five aforementioned genes. Results show 1q gain (3-10 copies) in 102/121 (84%), 6p gain in 115/121 (95%), MYCN gain in 14/121 (12%) and MYCN amplification (&amp;gt;10 copies) in 16/121 (14%) patient tumors. Assessment of potential correlations between the copy number status of these genes and clinical variables of disease progression include patient age, pathology at the time of diagnosis, optic nerve invasion, choroid involvement, laterality of the disease, number of tumor foci present at the time of diagnosis and histopathological parameters. To our knowledge, there has been no recent study associating genomic change of these five genes with clinical parameters of progression in a sample size of statistical significance. The large cohort and consequent statistical power of our results will facilitate a better understanding of the biological role of these genes in the progression from retinoma to retinoblastoma. 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 4361.
Abstract 3846: Pleiotrophin in the tumor microenvironment induces expression of VEGFR2 on macrophages and promotes an anti-inflammatory phenotype
Authors: Kristi D. Lynn, Christina L. Roland, Sean P. Dineen, Laura A. Sullivan, Rolf A. Brekken
Journal: Cancer Research (2010)

Abstract Macrophages are an abundant immune cell in the tumor microenvironment that contribute to tumor growth and metastasis. Macrophage recruitment into tumors is mediated by multiple cytokines, including vascular endothelial growth factor-A (VEGF). We are interested in investigating the effects of VEGF inhibition on macrophages and other stromal cells within the tumor. We demonstrated recently that macrophages (systemic and tumor associated) in tumor-bearing animals express VEGFR2 in contrast to macrophages from non tumor-bearing animals. Furthermore, we found that selective inhibition of VEGFR2 inhibits macrophage infiltration into tumors in vivo. These results demonstrate that when VEGFR2 is expressed on macrophages it is the dominant receptor driving VEGF-induced migration in vitro and in vivo. Additionally, we found that the cytokine pleiotrophin (PTN) is sufficient to induce VEGFR2 expression on macrophages. PTN is expressed by many human breast cancer cells (e.g., MDA-MB-231) and the majority of human primary breast tumors. However, the connection between PTN and macrophage phenotype is still unexplored. Macrophages can be divided into two functional sub-types: M1 or classically activated macrophages and M2 or alternatively activated macrophages. M1 macrophages are powerful effector cells that produce pro-inflammatory cytokines and are capable of destroying tumor cells. In contrast, M2 macrophages inhibit the inflammatory response and promote tumor growth and angiogenesis. We employed the MMTV-PyMT transgenic, spontaneous breast cancer model to characterize PTN expression, immune cell infiltration, and immune cell function during the course of tumor progression. We found that PTN levels correlate with VEGFR2+ macrophage and M2 macrophage levels, which all peak during the transition from hyperplasia to early malignancy. Whereas, MDSC and Treg levels as well as levels of the anti-inflammatory cytokines IL-10 and IL-1β peak during the early carcinoma stage. We identified that PTN not only induces VEGFR2 expression by macrophages but also promotes an M2 phenotype in vitro. In addition, we have evidence that VEGF can modulate the level of PTN expression through VEGFR1. These results suggest a mechanism through which anti-VEGF therapy modulates PTN and M2 macrophage levels in vivo. Based on these observations, we hypothesize that PTN is a critical cytokine involved in breast tumor progression through promotion of a VEGFR2+, M2 macrophage phenotype in the tumor microenvironment. 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 3846.
SAT0391 Does dynamic contrast-enhanced mri provide better separation of active early rheumatoid arthritis patients and healthy controls than conventional MRI?:
Authors: M.B. Axelsen, B.J. Ejbjerg, M.L. Hetland, K. Hørslev-Petersen, U.B. Lauridsen, O. Majgaard, M. Boesen, O. Kubassova, H. Bliddal, M. Østergaard
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Objectives</h3> To identify the MRI parameter that best separates healthy controls from early RA patients. Patterns of enhancement from conventional MRI and dynamic contrast enhanced (DCE)-MRI of healthy controls and of early RA patients with active disease undergoing treatment were compared. <h3>Methods</h3> Conventional and DCE-MRI of the wrist and the 2nd-5th metacarpophalangeal (MCP) joints was performed once in 26 healthy controls, age 47.5 (24-64) years (median (range)), and before and after 6 and 12 months of DMARD treatment in 14 early RA patients (age 39 (26-63) years; disease duration &lt;6 months), using a 1.0T Siemens Impact whole body MRI unit (Siemens, Erlangen, Germany). DCE-MRI was obtained in 1 preselected coronal slice covering the wrist and the 2nd-5th MCP-joints. The dynamic sequences were analyzed using Dynamika v. 4.2 (Image Analysis Ltd., Leeds, UK): Regions of interest were drawn delineating the individual joints. The number of enhancing voxels (Nvoxel), the average initial rate of enhancement (IRE, %/s), the average maximal enhancement (ME), MExNvoxel and IRExNvoxel were calculated for the combined examined areas (wrist and 2nd-5th MCP-joint). The conventional contrast-enhanced MR-images were evaluated by the OMERACT RA MRI (RAMRIS) synovitis score. <h3>Results</h3> 16 of 26 (61.5%) healthy controls and 13 of 14 (92.9%) RA patients at baseline showed enhancement (Number of enhancing voxels (Nvoxel) median 3 and 362, respectively). Healthy controls values were lower than baseline RA values for all parameters (Mann-Whitney, all p&lt;0.001 (except for ME p=0.003)), Table 1. At baseline only 1 patient had a baseline RAMRIS below the 95th percentile of the controls, the numbers were 3 for Nvoxel, MExNvoxel and IRExNvoxel and 9 and 10 for IRE and ME, respectively. RAMRIS, Nvoxel, IRExNvoxel (trend) but not IRE, ME, and MExNvoxel decreased from baseline to 6 months after start of treatment (Wilcoxon signed rank test, p=0.003, 0.038, 0.050, 0.26, 0.374, and 0.051). <h3>Conclusions</h3> RAMRIS synovitis scoring of conventional contrast-enhanced MRI and, to a lesser extent 1 slice DCE-MRI analysis of number of enhancing voxels, best discriminated early RA patients from healthy controls. Both parameters decreased during treatment, ie. showed sensitivity to change. <h3>Disclosure of Interest</h3> M. B. Axelsen Grant/Research support from: Abbott, B. Ejbjerg: None Declared, M. Hetland: None Declared, K. Hørslev-Petersen Grant/Research support from: Abbott, U. Lauridsen: None Declared, O. Majgaard: None Declared, M. Boesen Consultant for: Image Analysis, O. Kubassova Shareholder of: and director of Image Analysis, H. Bliddal Grant/Research support from: Abbott, M. Østergaard Grant/Research support from: Abbott
156 HEPATITIS C RECURRENCE AFTER LIVER TRANSPLANTATION: MAINTENANCE THERAPY WITH PEGYLATED INTERFERON IN NONRESPONDERS TO STANDARD THERAPY SLOWS THE DISEASE PROGRESSION AND IMPROVES SURVIVAL
Authors: G. Crespo, I. García-Juárez, Z. Mariño, M.-C. Londoño, S. Lens, J.A. Carrión, M. Navasa, X. Forns
Journal: Journal of Hepatology (2013)
Case 12-2009
Authors: Steven D. Brass, Eric E. Smith, Joseph F. Arboleda-Velasquez, William A. Copen, Matthew P. Frosch
Journal: New England Journal of Medicine (2009)

A 46-year-old man presented to this hospital with migraine headache, a 4-year history of neurologic events resulting in aphasia and hemiparesis, and a family history of two similarly affected brothers. Neuroimaging studies showed white-matter and deep gray-matter abnormalities. A diagnostic test was performed.