tbuckley/cabot-search huggingface dataset:
Genetic diversity of Streptococcus suis clinical isolates from pigs and humans in Italy (2003-2007)
Authors: M S Princivalli, C Palmieri, G Magi, C Vignaroli, A Manzin, A Camporese, S Barocci, C Magistrali, B Facinelli
Journal: Eurosurveillance (2009)

Streptococcus suis, a major porcine pathogen, is emerging as a zoonotic agent capable of causing severe invasive disease in humans exposed to pigs or pork products. S. suis infection is rare in industrialised countries and usually arises as sporadic cases, with meningitis the most common clinical presentation in humans. Recent reports of two cases of meningitis in Sardinia and north-eastern Italy prompted this first characterisation of Italian S. suis isolates. Fifty-nine S. suis strains, the two recent human strains and 57 swine clinical isolates collected between 2003 and 2007 from different Italian herds and regions, were tested for antimicrobial susceptibility, PCR-screened for virulence and antibiotic resistance genes, and subjected to molecular typing. Phenotypic and genotypic analysis demonstrated an overall high genetic diversity among isolates, the majority of which were resistant to macrolides (78%) and tetracyclines (90%). The erm(B), tet(O), mosaic tet(O/W/32/O), tet(W), and tet(M) genes were detected. The tet(O/W/32/O) gene, the most frequent tet gene after tet(O), had never been described in the genus Streptococcus before. In addition, a virulent cps2, erm(B) tet(O) clone, belonging to sequence type 1 (ST1) of the ST1 complex, was found to be prevalent and persistent in Italian swine herds. Finally, the two human isolates (both ST1) carrying cps2, erm(B) and tet(W) were seen to be closely related to each other.
TISSUE GLYCOPROTEINS IN RATS BEARING WALKER 256 CARCINOMA.
Authors: Macbeth Ra, Bekesi Jg
Journal: Cancer Research (1964)

Summary  In total, 137 rats have been sacrificed at intervals following the intramuscular implantation of Walker 256 carcinoma and the protein-bound hexosamines and  N -acetylneuraminic acid determined in a variety of tissues. The tumor itself contained relatively large amounts of these carbohydrates, and the muscle adjacent to the tumor contained amounts significantly in excess of those found in normal muscle. The most interesting observation, however, was the early elevation observed in the protein-bound hexosamines of liver.  These observations, coupled with previous observations on plasma glycoproteins under similar circumstances, have been interpreted as favoring the liver as the source, at least of the initial plasma glycoprotein elevation observed in malignant disease.
Abstract 9489: Clinical Impact of Integrated Backscatter Intravascular Ultrasound (IB-IVUS) Analysis for Predicting Coronary No-Reflow Phenomenon After Percutaneous Coronary Intervention
Authors: Hyuma Daidoji, Hiroki Takahashi, Yoichiro Otaki, Harutoshi Tamura, Takanori Arimoto, Tetsuro Shishido, Takehiko Miyashita, Takuya Miyamoto, Tetsu Watanabe, Isao Kubota
Journal: Circulation (2011)

Background and Aims Coronary no-reflow phenomenon after percutaneous coronary intervention (PCI) is associated with a poor prognosis. It is important to predict and prevent coronary no-reflow after PCI and to use distal protection device appropriately. Previous studies showed that integrated backscatter intravascular ultrasound (IB-IVUS) provided high diagnostic accuracy for tissue characterization of coronary plaques based on histology. The purpose of this study was to investigate the relationship between plaque components assessed by IB-IVUS and coronary no-reflow after PCI. Result The 177 lesions (acute coronary syndrome (ACS), n=69; non-ACS, n=108) in 168 consecutive patients (mean age 69 ± 11 years old) who received PCI using IB-IVUS were enrolled. No-reflow, including transient filter no-reflow by using distal protection device, was observed in 18 ACS lesion (26%) and 12 non-ACS lesion (11%). In both ACS and non-ACS patients, lipid volume at stent deployment lesion, lipid area at minimum lumen site (MLS) and percentage of lipid area (%Lipid) at MLS were significantly larger in no-reflow group compared with the normal-reflow group. A receiver operating characteristic (ROC) analysis was performed to assess lipid volume, lipid area at MLS and %Lipid at MLS to predict coronary no-reflow. In ACS patients, the cut-off values for lipid volume, lipid area at MLS and %Lipid at MLS were determined by ROC analysis as 97mm 3 , 7.2mm 2 and 62%, respectively. Otherwise, in non-ACS patients, the cut-off values for lipid volume, lipid area at MLS and %Lipid at MLS were determined as 93mm 3 , 6.1mm 2 and 64%, respectively. Conclusion Our present study suggests that lipid rich plaque assessed by IB-IVUS should be considered as one of important predictors of coronary no reflow after PCI. These cut-off values determined by present IB-IVUS study could improve our approach to coronary no reflow risk stratification in patients with coronary artery disease.
Lung cancer in England: Trends in survival over the duration of the national lung cancer audit
Authors: Aamir Khakwani, Helen Powell, Anna Rich, Richard Hubbard
Journal: European Respiratory Journal (2013)

The National Lung Cancer Audit (NLCA) was set up in 2003 to improve patient outcomes and the aim of our study is to evaluate survival change over the lifetime of the NLCA.

We used data from the NLCA to identify patients with NSCLC and stratified patients according to their performance status (PS) and stage of cancer. We used Cox regression to calculate the annual change in overall survival for patients diagnosed each year between 2004/2005 (combined to create an adequate comparator group) and 2010 and adjusted for patient features.

Our cohort consisted of 120,745 patients with NSCLC diagnosed between 1st Jan 2004 and 31st Dec 2010. Overall median survival did not change through the life time of the NLCA database (193 days in 2004/2005 and 182 days in 2010). By stratifying our cohort by the most important determinants of survival (PS and stage), we observed that the overall median survival for patients with good PS and stage improved overtime (adj HR 0.74 in 2010, 95%CI 0.68-0.82), while the survival for other groups remained the same.

![Figure][1] 



This survival advantage was accounted for by adjusting for surgical intervention.

Our results demonstrate that for patients with NSCLC who have good PS and early stage survival has improved over the last 6 years. Increasing surgical resection rates appeared to explain some of this improvement but chemotherapy and histological subtype did not appear to affect survival.

 [1]: pending:yes
Abstract 822: Genetically engineered mouse models of catastrophic pancreatic ductal adenocarcinoma
Authors: Takashi Yamaguchi, Sanae K. Ikehara, Hayao Nakanishi, Yuzuru Ikehara
Journal: Cancer Research (2015)

Abstract Carcinogenesis of pancreatic ductal adenocarcinoma (PDAC) has been well studied using genetically engineered mouse (GEM) models with abnormalities in activation of both RAS and E2 factor (E2F)-which is associated with the Rb-E2F pathway, and dysfunction of p53-which is associated with the transformed 3T3 cell double minute 2 (MDM2)-p53 pathway. Catastrophic progression of the malignancy is one of unique manifestation, which has not been recapitulated in the GEMs to study underlined mechanisms, while we have recently reported a new GEM developing PDAC to die in 3 weeks after birth due to the catastrophic progression [Yamaguchi T. et al, J Pathol. 2014; 234(2):228-138]. The GEM had the specific expression of SV40 tsA58 large T antigen (tsTAg) to inhibit p53 and Rb family molecules (Rb1, Rbl1 and Rbl2) on pancreas with the expression of oncogenic Kras (KrasG12D) by Pdx1 promoter-mediated Cre-loxP recombination. In this study, we sought to determine if the induced tsTAg on pancreatic epithelial cells with constitutive KrasG12D expression are enough to develop PDAC and catastrophic manifestation, by the generation of a new GEM based on Cre-loxP recombination and Tet-On system. In the GEM, KrasG12D constitutively expresses on pancreatic epithelial cells after the Cre-loxP recombination under the control Pdx1 promoter, while tsTAg expression can be regulated by Tet-On system after the recombination by Pdx1 promoter. Any of the mice did not developed PDAC within 6 month, but all of the mice developed PDAC by Dox administration in within 1 week and died by the progression of PDAC within 3 weeks after the start.The rapid progression and development of PDAC appeared to be associated with the stronger tsTAg expression depending on reverse tetracycline trans-activator. These results demonstrated that KrasG12D driven PDAC carcinogenesis was promoted by the presence of tsTAg expression, resulting in production of PDAC cells with aggressive growth. In conclusion, our established new mouse model can contribute to increase knowledge about catastrophic PDAC. Citation Format: Takashi Yamaguchi, Sanae K. Ikehara, Hayao Nakanishi, Yuzuru Ikehara. Genetically engineered mouse models of catastrophic pancreatic ductal adenocarcinoma. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 822. doi:10.1158/1538-7445.AM2015-822
Canonical Inflammasomes Drive IFN-γ to Prime Caspase-11 in Defense against a Cytosol-Invasive Bacterium
Authors: Youssef Aachoui, Yuji Kajiwara, Irina A. Leaf, Dat Mao, Jenny P.-Y. Ting, Jörn Coers, Alan Aderem, Joseph D. Buxbaum, Edward A. Miao
Journal: Cell Host & Microbe (2015)
An Ethical Debate: The role of ethics committees
Authors: I. Craft
Journal: BMJ (1995)

When in vitro fertilisation was being developed some 20 years ago I was convinced that future assisted conception units would need ethics committees to consider the more emotive types of fertility treatment that gamete permutation would allow. Now I am by no means so sure.

The first such ethics committee was set up by the Royal College of Obstetricians and Gynaecologists in 1982. Since then I have always worked alongside an ethics committee, although the Human Fertilisation and Embryology Act 1990 does not require fertility centres to have ethics committees for considering different types of clinical treatments.

So why am I so disillusioned about the role of ethics committees and how they function? The reason is simple—I am not sure that they are in the best interests of patients as I now believe that most ethics committees fail to focus on what their real role should be. Surely their role must be to decide if a proposed treatment is ethical or unethical—not whether a specific woman (or couple) should have her request voted on after a written anonymous submission by a clinician and an independent counsellor, as has been the practice of the committee at my centre.

Ethics committees generally have no personal knowledge of the individuals requesting treatment—unlike the clinician and counsellor—and quite often …
Treating liver fat and serum triglyceride levels in NAFLD, effects of PNPLA3 and TM6SF2 genotypes: Results from the WELCOME trial
Authors: Eleonora Scorletti, Annette L. West, Lokpal Bhatia, Samuel P. Hoile, Keith G. McCormick, Graham C. Burdge, Karen A. Lillycrop, Geraldine F. Clough, Philip C. Calder, Christopher D. Byrne
Journal: Journal of Hepatology (2015)
CAVVR,PVOを伴い重症心不全を呈したrt.isomerismに対する外科治療経験
Authors: 中山智尋, 中山雅人, 矢野洋, 伊藤敏明, 増本弘, 桜井浩司, 羽田野為夫, 長野美子, 河合悟
Journal: Circulation (2002)
Abstract #5513: WW domain-containing oxidoreductase mediates methotrexate-induced apoptosis in human squamous cell carcinoma
Authors: Li-Jin Hsu, Chi-Wen Tsai, Nan-Shan Chang
Journal: Cancer Research (2009)

Fragile WWOX gene encodes a candidate tumor suppressor WW domain-containing oxidoreductase (designated WWOX, FOR or WOX1). Overexpressed WOX1 induces apoptosis in numerous cancer cells and suppresses tumor growth both in vitro and in vivo. Previous study showed significant reduction of WOX1 and its family proteins in poorly differentiated cutaneous squamous cell carcinomas (SCC) without down-regulation of WWOX mRNA, indicating a translational blockade of WWOX mRNA to protein. In this study, we determined that MTX induced caspase activation and apoptotic death in SCC-15, but not SCC-9 cells, in both time- and dose-dependent manners. MTX-induced cell death was associated with increased mRNA and protein levels of WOX1 in MTX-susceptible SCC-15 cells. Transient expression of an siRNA construct targeting WOX1 or a dominant negative in SCC-15 cells suppressed MTX-mediated cell death. Conversely, overexpression of WOX1 in SCC-9 cells enhanced death induced by MTX. Together, MTX induces apoptosis in SCC cells by upregulating WOX1.   Citation Information:  In: Proc Am Assoc Cancer Res; 2009 Apr 18-22; Denver, CO. Philadelphia (PA): AACR; 2009. Abstract nr 5513.
Abstract 48: Long-Term Patterns in the Development of Multiple Cardiovascular Diseases: The Framingham Heart Study
Authors: Norrina B Allen, Hongyan Ning, John Wilkins, Daniel Levy, Donald Lloyd-Jones
Journal: Circulation (2015)

Background: Having a first CVD event increases the risk for subsequent events; however, the long-term patterns in the development and sequence of multiple CVDs, including stroke, myocardial infarction (MI) and chronic heart failure (CHF) are unknown. The aim of this study was to identify distinct long-term patterns in the order and timing of MI, stroke and CHF occurrence. Methods: We used publicly available data from the Framingham Heart Study (FHS). The occurrence of fatal/non-fatal MI, stroke and CHF were examined separately using discrete mixture modeling implemented in SAS (Proc Traj) to identify trajectory groups for the risk of each CVD event starting at age 30. We included both first and subsequent events. Clusters of disease specific trajectory groups were examined. Baseline demographics and risk factors were compared across clusters. Results: Among 5,079 participants (ppts) in FHS, we identified 8 unique patterns in the development of CVDs (see figure). The majority, 72.5%, of Framingham ppts experienced average age- related increases in the yearly risk for all three endpoints of MI, stroke and heart failure (Average Risk group) other groups experienced early or higher risks for specific CVDs including the High CHF Risk group (6% of ppts), Early CHF group (2%), High Stroke Risk group (9%), High CHF and Stroke Risk group (1%), High MI Risk group (4%), High MI and CHF Risk group (1%), Early CHF and MI Risk group (1%). Groups in which stroke and/or HF risk was elevated had higher prevalence of smoking and greater baseline BP levels; those groups at elevated risk of MI had higher total cholesterol levels and higher BMI. Conclusions: We identified distinct patterns in development and ordering of MI, stroke and CHF associated with diverse risk factor profiles. By understanding the life-course and likely sequence of CVD events related to distinct risk factor profiles, clinicians may be able to consider personalized prevention strategies with the highest likelihood of preventing first CVD events and reducing the overall burden of CVD.
Abstract MP50: Fat Distribution and Metabolic Health: Central and Lower Body Adipose Tissue Depots are Differentially Associated with Insulin Sensitivity in Parous and Nulliparous Caucasian and African American Women
Authors: Katherine H Ingram, Gary R Hunter, Barbara A Gower
Journal: Circulation (2015)

Parity and race individually affect the accumulation of visceral adipose tissue, but their combined influence on the relationship between fat distribution and insulin sensitivity is unknown. The purpose of this study is to test the influence of parity and race in the relationship between insulin sensitivity and the preference of central versus lower-body fat accumulation in overweight women.   METHODS:  In non-Hispanic white (white; n= 109, 56 parous) and African American (AA; n= 119, 58 parous) pre-menopausal women matched for age and BMI (age 34 ± 6.2; BMI = 27.5 ± 4.7), intra-abdominal adipose tissue (IAAT) via CT, regional and total body fat by DXA, insulin sensitivity (SI) calculated from minimal model, and cardiorespiratory fitness (VO 2max ) were assessed.   RESULTS:  Nulliparous women (NP) were younger (31.3 ± 6.5 vs 36.4 ± 5.1), had less IAAT (69.6 ± 31.4 vs 85.4 ± 30.3), and a higher VO 2max  (29.5 ± 4.0 vs 27.7 ± 3.6), but showed no difference in SI or leg fat compared to parous women. Stratified by race, white women were more insulin sensitive (3.5 ± 1.8 vs 2.5 ± 1.9 [x 10-4 min-1/(μIU/ml)]), had a higher VO 2max  (29.2±4.0 vs 27.6±3.6), and more IAAT (92.7±30.4 vs 65.1 ± 25.9) than AA women, but less leg fat (26.6 ± 3.7 vs 28.2 ± 3.1).  IAAT is negatively related to SI in NP (r= -.40, p 2max . Leg fat is positively related to SI in both NP (r= .45, p  .4, p  Multiple linear regression indicates that IAAT, age, leg fat, race, and VO 2max  are independent predictors of SI in NP. In parous women, only race achieved significance. IAAT, age, leg fat, and VO 2max  are predictors of SI in white NP, but not in white parous. Leg fat is the sole predictor of SI in AA NP, while none of the variables are significant in AA parous.   CONCLUSION:  These data demonstrate that the relationship between fat distribution and insulin sensitivity in overweight women varies as a result of race and reproductive history. In NP, the more insulin sensitive the individual is, the more fat accumulates in the legs and the less it accumulates in the abdomen. Race clearly influences these relationships. The SI/abdominal fat relationship is more pronounced in white women, while SI/leg fat predominates in AA. SI loses its strong association with abdominal obesity in white parous women and its association with leg fat in AA parous women. This dissociation suggests that both hepatic metabolism and fat distribution are altered by high hormones during pregnancy in both racial groups.
Prediction of Pulmonary Metastasis in Renal Cell Carcinoma Patients with Indeterminate Pulmonary Nodules
Authors: Mehrad Adibi, Patrick A Kenney, Arun Z Thomas, Leonardo D Borregales, Graciela M Nogueras-González, Xuemei Wang, Catherine E Devine, Jose A Karam, Christopher G Wood
Journal: European Urology (2015)
One‐Pot Fabrication of Dendritic NiO@carbon–nitrogen Dot Electrodes for Screening Blood Glucose Level in Diabetes
Authors: Naeem Akhtar, Sherif A. El‐Safty, Mamdouh E. Abdelsalam, Hiroshi Kawarada
Journal: Advanced Healthcare Materials (2015)

Selective and sensitive glucose sensors with fast response for screening diabetic blood level are demanded. In this paper, the one-pot nanoarchitecture of dendritic NiO@carbon-nitrogen (C-N) dots (designated as NCD) sphere-wrapping Ni foam electrodes are reported as an effective and sensitive glucose sensor in blood samples. In this construction design, the NCD sphere electrode with excessive surface defects, large fractions of catalytic active sites, high surface area, and mobility of electron transfer through the actively surface NCD sphere can massively enhance the electrocatalytic activity for nonenzymatic glucose detection in diabetic blood. This portable sensor enables highly sensitive recognition of glucose detection (≈0.01 × 10-6 m) over a wider linear range (≈0.005-12 × 10-3 m) with rapid response time of a few seconds. The key result is that the engineered NCD sphere electrodes function as simple, easy-to-use electrochemical sensing assays of glucose levels in diabetic blood patients with a wide range of precision or linearity, recyclability, and excellent selectivity, even in the presence of potentially interfering organic (ascorbic acid, uric acid, dopamine, lactose, maltose, and sucrose) and inorganic (NaCl, Na2 SO4 , KCl, and K2 SO4 ) species. The results demonstrate the potential for the electrochemical sensors to be used in preventing serious health problems associated with diabetes mismanagement.
Collagen receptors: α1β1 and α2β1 integrins may be involved in asthma pathogenesis
Authors: Joanna Zuk, Stanislawa Bazan-Socha, Jacek Zarychta, Paulina Solarz, Jacek Musial
Journal: European Respiratory Journal (2013)

Introduction:  Collagen I (and III) is a major component of extracellular matrix in lungs. We hypothesized that integrin collagen receptors: α1β1 and α2β1 may be involved in airway remodelling. Recently we have shown that α2β1 integrin is up-regulated on peripheral blood CD4 T cells in patients with mild to moderate persistent asthma, while α1β1 integrin was not.  Aims:  The aim of this study was to analyze expression of α1β1 and α2β1 integrin collagen receptors on blood T cells in patients with severe asthma and persistent airway obstruction and to correlate it with bronchial wall thickness measured by lung CT.  Methods:  In 31 severe asthma subjects with persistent airway obstruction and 40 mild to moderate asthmatics with normal spirometry expression of the integrin subunits: α1, α2, α4 and α5 was assessed by flow cytometry. Chest CT was performed in patients with airway obstruction to measure bronchial wall thickness.  Re  sults:  Studied groups differed in age and asthma duration. Expression of α1 subunit was significantly higher in the group of patients with airway obstruction; such difference was not observed for α2. Surprisingly, we found significant negative correlation between α2 expression on CD4+ and CD8+ T cells and bronchial wall thickness. In contrast, α4 and α5 subunits correlated positively.  Conclusions:  Increased expression of α1β1 integrin on blood T cells in severe asthma suggests its possible role in asthma pathology. On the other hand, airway remodeling is associated with decreased α2β1 expression on T lymphocytes. Significance of this finding requires further study.
Abstract 1991: Axl overexpression drives migration and invasion in colon cancer
Authors: Diana J. Uribe, Lidia Bosurgi, Nicola Gagliani, Leonel Joannas, Adam Watson, Jesse D. Martinez, Carla V. Rothlin, Sourav Ghosh
Journal: Cancer Research (2014)

Abstract Receptor tyrosine kinases (RTK) of the TAM family have been described as oncogenes. Axl and Mertk, two members of the TAM family, are also potent negative regulators of the inflammatory response. Inflammation is an enabling characteristic of cancer hallmarks and can promote tumorigenesis and tumor progression. Genetic ablation of Axl and Mertk in mice, results in heightened inflammation in the gut and increased susceptibility to inflammation-driven colon cancer (azoxymethane/dextran sodium sulfate treatment paradigm). We sought to understand the role of Axl and Mertk, individually, in colon cancer cells to identify the key TAM oncogene in this disease. Here we show that Axl, but not Mertk, was highly expressed and correlated with grade of metastatic colon cancer. Silencing Axl expression in RKO-AS45-1 and HCT116 colon cancer cells had no significant effect on proliferation and survival, but markedly decreased migration and invasion. R428, a selective Axl small molecule inhibitor, also drastically reduced migration in these colon cancer cell lines. Analyses of Axl knockout mice revealed that single, genetic ablation of this TAM RTK does not increase susceptibility to DSS-induced colitis, in contrast to that observed in Axl and Mertk double knockout mice. These results are consistent with a redundant function of Axl and Mer in the regulation of the inflammatory response. Our findings suggest that the selective targeting of Axl in colon cancer might disable the oncogenic function of TAM RTKs, while sparing the protective, anti-inflammatory function of this RTK family in this disease. Citation Format: Diana J. Uribe, Lidia Bosurgi, Nicola Gagliani, Leonel Joannas, Adam Watson, Jesse D. Martinez, Carla V. Rothlin, Sourav Ghosh. Axl overexpression drives migration and invasion in colon cancer. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 1991. doi:10.1158/1538-7445.AM2014-1991