tbuckley/cabot-search huggingface dataset:
Magnetic Resonance Imaging of the Fibrotic Kidney
Authors: Glen R. Morrell, Jeff L. Zhang, Vivian S. Lee
Journal: Journal of the American Society of Nephrology (2017)

Magnetic resonance imaging (MRI) has been used for many years for anatomic evaluation of the kidney. Recently developed methods attempt to go beyond anatomy to give information about the health and function of the kidneys. Several methods, including diffusion-weighted MRI, renal blood oxygen level–dependent MRI, renal MR elastography, and renal susceptibility imaging, show promise for providing unique insight into kidney function and severity of fibrosis. However, substantial limitations in accuracy and practicality limit the immediate clinical application of each method. Further development and improvement are necessary to achieve the ideal of a noninvasive image-based measure of renal fibrosis. Our brief review provides a short explanation of these emerging MRI methods and outlines the promising initial results obtained with each as well as current limitations and barriers to clinical implementation.
Abstract 10919: Contemporary Life Expectancy and Standardized Mortality of Adult Survivors With Congenital Heart Lesions
Authors: Jose M Oliver, Pastora Gallego, Ana E Gonzalez Garcia, Diego Garcia Hamilton, Raquel Yotti, Ignacio Ferreira Gonzalez, Francisco Fernandez Aviles
Journal: Circulation (2015)

Background: Survival beyond the age of 18 years in patients born with congenital heart disease (CHD) is now near 90% but contemporary estimates of outcome in adult survivors are lacking. Methods: In a prospective cohort of 3,334 adults with CHD followed up to 24 years in a single tertiary centre median age of survival (MAS) was estimated by computing left-truncated and right-censored Kaplan-Meier curves with age as time scale. Standardized mortality ratio (SMR) was also determined using one-sample log-rank test from age at diagnosis-, sex- and time of follow-up-adjusted death rates of general population in Spain. Patients were classified into 3 groups according to CHD complexity: I, simple (1,647); II, moderate (1,283); and III, severe (404). For mortality analysis, data provided by the Spanish national death index were used. Results: There were 1,688 males and 1,646 females. Median age at first examination was 22 years (IQR 18-39) and median follow-up time 10.6 years (1-18). At the end of the study 336 patients had died (prevalence 10%; annual incidence 0.89%). Estimated MAS was 78.0 years (95% CI 76-82) for group I; 72,1 years (68-78) for group II; and 51.1 years (48-53) for group III (p&lt;0.001). MAS was older than 75 years in all diagnostic categories in group I; between 60 and 75 years (moderate reduction) in subvalvular aortic stenosis, Ebstein anomaly, coarctation of the aorta, tetralogy of Fallot and complete transposition; and &lt; 60 years (severe reduction) in Eisenmenger syndrome, single ventricle, AV discordance and pulmonary atresia The SMR was 1.66 (1.4-2.5) for the group I; 3.27 (2.6-4.1) for the group II; and 20.4 (10-26) for the group III (p&lt;0.001 in all, compared to reference population). The SMRs for main individual diagnostic categories are shown in figure. Conclusion: Life expectancy for CHD adults is reduced proportionally to complexity of the heart defect. Data for individual diagnostic categories might be used as a prognostic index.
Rare adult presentation of fixed airways obstruction: remember aortic arch abnormalities
Authors: Juwhan Choi, Kyung Hoon Min, Sung Yong Lee, Kyung Ho Kang, Jae Jeong Shim
Journal: Thorax (2017)

A 47-year-old woman with a history of chronic cough presented with dyspnoea. She had no history of smoking, tuberculosis and cardiovascular disease. Physical examination revealed wheezing in both lungs. We started maintenance and reliever therapy for suggested bronchial asthma. However, symptoms did not improve, and she was hospitalised repeatedly. Chest X-ray showed a right-sided aortic arch. In the pulmonary function test, a fixed obstruction pattern was observed, and a bronchodilator response …
Differences in length of stay among hospitalized children with acute lymphoblastic leukemia
Authors: E. Tai, L. Richardson, J. Townsend, B. Steele
Journal: Journal of Clinical Oncology (2009)

10044 Background: Acute lymphoblastic leukemia (ALL) is the most common malignancy among children in the United States. While age, race, and clinical complications have been associated with longer length of stay (LOS) among children with cancer, it is unknown what factors are related to LOS among children with ALL. We examined differences in LOS among hospitalized children with ALL. Methods: We used 2000, 2003, and 2006 data from the Healthcare Cost and Utilization Project (HCUP) Kids’ Inpatient Database (KID) which contains pediatric discharges from community, non-rehabilitation hospitals. We used negative binomial regression to determine factors related to LOS. Results: We found the following factors related to greater LOS among hospitalized children with ALL: Non-Hispanic blacks vs. non-Hispanic whites (Rate Ratio (RR) = 1.06, CI:1.03–1.10), Hispanics vs. non-Hispanic whites (RR = 1.07, CI:1.04–1.10), age &lt; 1 year vs. age 1–5 years (RR = 1.93, CI:1.83–2.04), female vs. male (RR = 1.05, CI:1.03–1.07), lowest quartile of household income in patient's zip code vs. highest quartile (RR = 1.09, CI:1.06–1.12), Medicaid vs. private insurance (RR = 1.11, CI:1.09–1.14), children's hospital vs. non-children's (RR = 1.11, CI:1.08–1.14), Western region of United States vs. Northeast region (RR = 1.14, CI:1.11–1.17), emergency room admission vs. routine admission (RR = 1.23, CI:1.20–1.26), blood transfusion (RR = 1.64, CI:1.61–1.67), bone marrow transplant (RR = 7.64, CI:7.11–8.20), and neutropenia (RR = 1.22, CI:1.19–1.24). Conclusions: Race/ethnicity, age, sex, household income, insurance status, admission source, hospital type and region, transfusion, bone marrow transplant, and neutropenia were significantly associated with longer LOS. These factors may help identify children with ALL at risk for complications. Prophylactic treatment for clinical complications may reduce LOS. No significant financial relationships to disclose.
Effect of Dietary Cystine on the Development of Hepatic Tumors in Rats Fed &lt;italic&gt;p&lt;/italic&gt;-Dimethylaminoazobenzene (Butter Yellow)&lt;xref ref-type="fn" rid="fn1"&gt;1&lt;/xref&gt;
Authors: Julius White, Jesse E. Edwards
Journal: JNCI Journal of the National Cancer Institute (1942)

Journal Article Effect of Dietary Cystine on the Development of Hepatic Tumors in Rats Fed p-Dimethylaminoazobenzene (Butter Yellow) Get access Julius White, Julius White senior biochemist National Cancer Institute, National Institute of Health, United States Public Health Service Search for other works by this author on: Oxford Academic PubMed Google Scholar Jesse E. Edwards Jesse E. Edwards research fellow National Cancer Institute, National Institute of Health, United States Public Health Service Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 2, Issue 6, June 1942, Pages 535–538, https://doi.org/10.1093/jnci/2.6.535 Published: 01 June 1942
Histologic Changes in the Adrenal Glands of Tumor-Bearing Mice
Authors: Albert J. Dalton, Virginia B. Peters
Journal: JNCI Journal of the National Cancer Institute (1944)

Histologic Changes in the Adrenal Glands of Tumor-Bearing Mice Get access Albert J. Dalton, Albert J. Dalton senior cytologist National Cancer Institute, National Institute of Health, United States Public Health Service Search for other works by this author on: Oxford Academic PubMed Google Scholar Virginia B. Peters Virginia B. Peters laboratory technician National Cancer Institute, National Institute of Health, United States Public Health Service Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 5, Issue 2, October 1944, Pages 99–109, https://doi.org/10.1093/jnci/5.2.99 Published: 01 October 1944
PTH-011 Endoscopic mucosal resection (emr) vs. endoscopic submucosal dissection (esd)/hybrid in the management of large colorectal polyps: experience from a tertiary centre
Authors: J Lambert, J Scott, B Crooks, S Kurrimboccus, N Prasad, R Hammonds, R George
Journal: Endoscopy (2017)

<h3>Introduction</h3> In tertiary centres both EMR and ESD sometimes in combination with hybrid techniques are used in the treatment of polpys&gt;20 mm. EMR allows for removal of polyps confined to the mucosa often in a piecemeal fashion while ESD aims for enbloc resection for lesions extending into the submucosa. The most serious complications include bleeding and perforation. Over a 3 year period at a tertiary centre we aimed to assess complication and recurrence rates between these two modalities. <h3>Method</h3> Data was collected retrospectively collected over a 3 year period. All EMR/ESD were performed by three dedicated consultant endoscopists with over 10 years experience in performing level III and IV endoscopic resection. The endoscopy Unisoft database was interrogated to select all patients having EMR/ESD including screen-detected lesions. Lesions&lt;20 mm were excluded and all patients were assessed for length of hospital stay (LOS), recurrence and complication rates. The first follow-up endoscopic examination was performed at 3–6 months after initial endoscopic resection, and the second at 12–14 months post-EpMR <h3>Results</h3> 128 polyps were removed endoscopically from 125 patients (80 males) 64%. Mean age was 70 and mean polyp size 38 mm (range 20–101 mm). For low-grade dysplatic lesions histology confirmed 83 (64%) tubulo-villous adenomas (TVA) and 21 (16%) Tubulo-adenomas (TA). There were 11 (8.5%) adenocarcinomas, 7 (5.4%) and high-grade dysplastic lesions. All adenocarcinomas were eventually referred for surgical management. One large high-grade dysplastic lesion was referred for Trans-anal microscopic surgery (TEMS) after submucosal fibrosis and bleeding encountered during ESD. There were 6 (4.6%) inflammatory/hyperplastic lesions. Procedural bleeding was encountered in six patients, one patient had delayed bleeding. One patient had post-polypectomy pain syndrome. There were no perforations. No difference in complication rates was found between EMR and ESD. 12 month recurrence rate was 15/113 (13%). This was related to increasing size of polyps. All recurrences were managed endoscopically. LOS was between 0–24 hours in over 97% of patients. <h3>Conclusion</h3> In high volume centres EMR/ESD is safe with low complication and recurrence rates. <h3>Disclosure of Interest</h3> None Declared
YAP/TAZ regulates sprouting angiogenesis and vascular barrier maturation
Authors: Jongshin Kim, Yoo Hyung Kim, Jaeryung Kim, Do Young Park, Hosung Bae, Da-Hye Lee, Kyun Hoo Kim, Seon Pyo Hong, Seung Pil Jang, Yoshiaki Kubota, Young-Guen Kwon, Dae-Sik Lim, Gou Young Koh
Journal: Journal of Clinical Investigation (2017)

Angiogenesis is a multistep process that requires coordinated migration, proliferation, and junction formation of vascular endothelial cells (ECs) to form new vessel branches in response to growth stimuli. Major intracellular signaling pathways that regulate angiogenesis have been well elucidated, but key transcriptional regulators that mediate these signaling pathways and control EC behaviors are only beginning to be understood. Here, we show that YAP/TAZ, a transcriptional coactivator that acts as an end effector of Hippo signaling, is critical for sprouting angiogenesis and vascular barrier formation and maturation. In mice, endothelial-specific deletion of Yap/Taz led to blunted-end, aneurysm-like tip ECs with fewer and dysmorphic filopodia at the vascular front, a hyper-pruned vascular network, reduced and disarranged distributions of tight and adherens junction proteins, disrupted barrier integrity, subsequent hemorrhage in growing retina and brain vessels, and reduced pathological choroidal neovascularization. Mechanistically, YAP/TAZ activates actin cytoskeleton remodeling, an important component of filopodia formation and junction assembly. Moreover, YAP/TAZ coordinates EC proliferation and metabolic activity by upregulating MYC signaling. Overall, these results show that YAP/TAZ plays multifaceted roles for EC behaviors, proliferation, junction assembly, and metabolism in sprouting angiogenesis and barrier formation and maturation and could be a potential therapeutic target for treating neovascular diseases.
Drugs caused record number of deaths in England and Wales in 2016
Authors: Richard Hurley
Journal: BMJ (2017)

The number of deaths from drug poisoning reached record levels in England and Wales last year, official figures have shown.

The Office for National Statistics, which compiled the figures, said that drug poisoning caused a higher number of deaths to be registered in England and Wales in 2016 than in any year since 1993, when comparable figures started being collected.1

In total, 3744 people in England and Wales had their cause of death registered in 2016 as poisoning by legal or controlled drugs, 70 more than in 2015. Two thirds of these deaths (2593) followed drug misuse.

More than half (2038) of all drug poisoning deaths resulted from an opioid, such as heroin or morphine (1209). Methadone caused 413 …
Intraductal tubulopapillary neoplasm of the pancreas diagnosed by endoscopic ultrasonography-guided fine needle aspiration
Authors: Bojan Kovacevic, Patricia Latorre Añó, Anders Toxværd, Peter Vilmann, Evangelos Kalaitzakis
Journal: Endoscopy (2017)

A 68-year-old man with chronic alcohol-related pancreatitis and chronic nephropathy requiring dialysis was admitted to the hospital because of a 3-day history of upper abdominal pain. Laboratory tests revealed slightly elevated C-reactive protein with normal amylase and liver function test results. Computed tomography scan of the abdomen showed pancreatic calcifications and a cystic lesion in the head/neck of the pancreas. Subsequent endoscopic ultrasound (EUS) showed a multicystic lesion ([Fig. 1]) with a dilated main pancreatic duct and a suspected solid lesion ([Fig. 2]). EUS-guided fine needle aspiration (FNA) of the suspected solid lesion in the main pancreatic duct was performed. Histopathology showed tubulopapillary structures with cylindrical cells and low grade dysplasia ([Fig. 3], [Video 1]). There were no signs of mucin on periodic acid–Schiff and Alcian blue staining. On immunohistochemistry, the lesion was positive for CK7, CDX2 and MUC-1, and there was focal MUC6 reaction but only very few MUC5AC positive cells. The findings were consistent with an intraductal tubulopapillary neoplasm (ITPN). The patient was considered unfit for surgical treatment, and 6 months following the diagnosis he is alive without signs of disseminated disease.
Licence to kill senescent cells in idiopathic pulmonary fibrosis?
Authors: Arnaud A. Mailleux, Bruno Crestani
Journal: European Respiratory Journal (2017)

Idiopathic pulmonary fibrosis (IPF) is a rare chronic fibrotic pulmonary disease of unknown aetiology, which results in the progressive destruction of lung with a very poor median survival of 3 years after diagnosis. According to the current paradigm, IPF results from progressive alterations of alveolar epithelial cells leading to the recruitment of mesenchymal cells to the alveolar regions of the lung with secondary deposition of extracellular matrix, and destruction of the normal lung structure and physiology [1]. The anarchic epithelial repair observed in IPF is also accompanied by reactivation of signalling pathways involved in fetal lung development [2]. IPF develops in a genetically susceptible individual, and is promoted by interaction with environmental agents such as inhaled particles, tobacco smoke, inhaled pollutants, and viral and bacterial agents. Two drugs are currently available for the treatment of pulmonary fibrosis: pirfenidone, a small molecule that probably targets lung fibroblasts through multiple mechanisms; and nintedanib, a multitarget tyrosine kinase inhibitor [1]. Targeting senescent cells may prove useful in the future treatment of idiopathic pulmonary fibrosis <http://ow.ly/rHpn30dvsuP>
肝細胞癌の治療のためのミクロRNA治療薬の機能的送達のための酸化還元感受性,オリゴペプチド誘導,自己集合,および高効率(ROSE)システム【Powered by NICT】
Authors: Hu Qida, Wang Kai, Sun Xu, Li Yang, Fu Qihan, Liang Tingbo, Tang Guping
Journal: Biomaterials (2016)
SINGAPORE RUGBY UNION INJURY SURVEILLANCE: HOW DO WE COMPARE TO PREVIOUS FINDINGS IN RUGBY UNION AND DO WE NEED TO IMPROVE?
Authors: Dinesh Sirisena, Henderson Annie
Journal: British Journal of Sports Medicine (2017)

Background Rugby union is a full contact sport in which injuries are a commonplace occurrence. Despite its increasing popularity in South East Asia, the obvious differences in physical attributes of players and environment, there have not been any previous analyses of the injury data so far. Objectives To examine whether rugby union injury rates in Singapore are similar to those reported in other countries and to assess whether the current system of data collection is both accurate and efficient. Design A retrospective analysis of injury data collected from an injury audit conducted over the 2015/16 Rugby union season. Setting 2015/16 Singapore Rugby Union domestic league. Participants Players from 5 teams, with 15 adults (&gt;18 yrs) players from each team on the field at any one time for the duration of an 80 minute game. Interventions No interventions were implemented during this study. Main Outcome Measurements Total exposure and injury rates (per 1000 player h), and uptake of the current reporting system. Results Data from a total of 28 of 86 (32%) matches were reported, including a total of 558.6 player hours. Injury incidence (136.1 per 1000 player hours) was higher than previously reported, with muscle (50.1), concussion (21.5), shoulder (14.4), knee (12.6) and facial soft tissue (10.8) injuries being most common. Conclusions The high injury rate compared to previous studies in rugby union may have been biased by the low reporting rates. A reporting rate of 32% significantly limits the interpretation of the injury surveillance in Singapore. The low reporting rates may be due to an antiquated system of collecting the data and reporting injuries, but a newer system of reporting injuries is being developed.
Inhibition of macrophage activation and tumor growth in animals by DHMEQ, an NF-kappaB inhibitor
Authors: Eriko Suzuki, Gaku Matsumoto, Masakazu Toi, Kazuo Umezawa
Journal: Cancer Research (2005)

4685   [Introduction] Solid tumors are often associated with the presence of a large number of macrophages. These tumor-associated macrophages may enhance the growth of tumors, since activated macrophages secrete various growth factors and cytokines following activation of transcription factors such as NF-kappaB. Therefore, inhibition of macrophage activation may suppress tumor growth in animals. In the course of our search for NF-kappaB inhibitors, we have designed new ones of low molecular weight based on the structure of epoxyquinomicin C, a compound isolated from  Amicolatopsis . One of the designed compounds, dehydroxymethylepoxyquinomicin (DHMEQ), inhibited TNF-alpha-induced activation of NF-kappaB. In the present research we looked into the effect of DHMEQ on the macrophage activities such as nitrogen monoxide (NO) production, secretion of cytokines, and phagocytosis. We also examined the antitumor effect of DHMEQ on breast carcinomas in mice. [Experimental procedures] We employed cells of the mouse macrophage-like cell line RAW264.7. Cytokines secreted into culture medium were measured by specific enzyme-linked immunosorbent assays. Phagocytosis was visualized by use of fluorescently labeled  Escherichia coli  and microspheres. [Summary] DHMEQ inhibited the lipopolysaccharide (LPS)-induced NF-kappaB activation without inhibiting the degradation of IkappaB. It also inhibited the inducible NO synthase expression and NO production. DHMEQ was shown to inhibit LPS-induced secretion of interleukin-1beta (IL-1beta), IL-6, IL-10, IL-12, and TNF-alpha without any toxicity. Moreover, the drug inhibited LPS-induced phagocytosis of fluorescently labeled  Escherichia coli  or microspheres by RAW264.7 cells. It also inhibited IL-1beta-induced phagocytosis of  Escherichia coli,  and we obtained the first evidence for the involvement of NF-kappaB in the regulation of phagocytosis by use of this inhibitor. Finally, the intraperitoneal administration of DHMEQ suppressed the growth of breast carcinomas MDA-MB-231 and MCF-7 in SCID mice, again with no signs of toxicity. [Conclusions] DHMEQ inhibited NO production, cytokine secretion, and phagocytosis in mouse macrophage-like cells. It also inhibited the growth of breast carcinomas in mice without toxicity. Previously DHMEQ showed antitumor activity toward prostate carcinoma and other tumor models in animals. It is possible that inhibition of macrophage activation may have contributed to the inhibition of tumor growth in these tumor models.
Abstract #1254: Podoplanin is a novel antibody-based therapeutic target for glioblastoma
Authors: Yukinari Kato, Kazuhiko Mishima, Mika Kaneko, Michael Zalutsky, Chien-Tsun Kuan, Darell Bigner
Journal: Cancer Research (2009)

Podoplanin is a mucin-like transmembrane sialoglycoprotein that is known to be expressed on lymphatic endothelial cells and tumor-initiating cells (TICs). Podoplanin is also expressed in several tumors such as squamous cell carcinomas, mesothelioma, and testicular tumors, and is involved in cancer cell migration, invasion, and metastasis. Interaction between podoplanin and C-type lectin-like receptor-2 (CLEC-2) is reported to be critical for podoplanin-induced platelet aggregation and cancer metastasis. Recently, we showed upregulated expression of podoplanin in central nervous system (CNS) germinomas, but not in non-germinomatous germ cell tumors, except for parts of immature teratomas in limited numbers. Furthermore, we investigated the podoplanin expression in CNS astrocytic tumors. Podoplanin mRNA and protein expression were markedly higher in glioblastomas than in anaplastic astrocytomas, and were not detected in diffuse astrocytoma, suggesting that podoplanin expression might be associated with malignancy of astrocytic tumors. We recently produced a novel anti-podoplanin antibody, NZ-1 (rat IgG 2a ). In this study, the epitope of NZ-1 antibody was investigated using ELISA, Western blot, and flow cytometry with synthesized podoplanin peptides and deletion mutants of recombinant podoplanin. The epitope for NZ-1 is platelet aggregation-stimulating (PLAG) domain-2/3, which is critical for activity of podoplanin. We have shown that two GBM cell lines, LN319 and D397MG, highly express podoplanin and demonstrated the surface binding for NZ-1 in flow cytometry. We then determined the binding affinity of NZ-1 for podoplanin in BIAcore using podoplanin peptide and Scatchard analysis using podoplanin-positive cell lines. NZ-1 was radioiodinated with Iodogen, and immunoreactive fraction (IRF) was 76.4%. Using I 125 -NZ-1, the K D  was determined to be 8.9 x 10 -11  M in BIAcore, and 2.6 x 10 -9  M for LN319 cells and 9.8 x 10 -10  M for D397MG cells in Scatchard analysis. NZ-1 was also internalized into LN319 and D397MG cells. Taken together, we have shown that podoplanin a potential therapeutic target of glioblastoma for antibody-based therapy.   Citation Information:  In: Proc Am Assoc Cancer Res; 2009 Apr 18-22; Denver, CO. Philadelphia (PA): AACR; 2009. Abstract nr 1254.