gebhart/patrepeval huggingface dataset:
Effects of feeding antibiotic-free creep feed supplemented with oligofructose, probiotics or synbiotics to suckling piglets increases the preweaning weight gain and composition of intestinal microbiota (2005)

The objective of this study was to determine whether feeding an antibiotic-free creep feed supplemented with either oligofructose, probiotics or synbiotics to suckling piglets influences growth performance, the gut microflora, gut morphology and hematological traits at weaning. Twenty sows with 10 piglets each were randomly assigned to one of four treatments. The treatments consisted of a control (antibiotic-free) diet, 0.2% oligofructose (OF), 0.3% probiotics or 0.5% synbiotics (mixture of 0.2% OF+0.3% probiotics). Piglets were offered the diet ad libitum from 7 d after birth until one day after weaning (21 d of age). At the day after weaning, blood samples were collected from the jugular vein to determine the immune response. Digesta samples of the ileum and colon were collected to determine the microbial composition. Tissue segments from the duodenum and ileum were collected for morphometric measurements of the small intestine. The average daily weight gain was significantly higher for piglets fed the OF or synbiotics diet compared with the pigs fed the control diet. The hematological traits (the concentration of lymphocytes and neutrophils in whole blood) were not affected by the diet. Piglets fed the OF, probiotics or synbiotics diet had a significantly decreased number of total coliform bacteria in the colon. Feeding OF, probiotics or synbiotics significantly increased the population of bifidobacteria in the ileum compared to the control. In the colon, the probiotics and synbiotics diet significantly increased the number of bifidobacteria compared with the control diet. The results of this experiment showed that supplementation of oligofructose or synbiotics to an antibiotic-free creep feed during the preweaning period affected gut microbial population and performance of piglets.
Angiogenic factors in multiple myeloma: higher levels in bone marrow than in peripheral blood. (2000)

In all the patients, the concentration of each angiogenic factor was higher in bone marrow than in peripheral blood. Mean values of the three angiogenic factors in BM or in PB were lower in stage I than stage II-III. One patient with extramedullary solitary myeloma had high levels of VEGF and bFGF but this increase was not found in the other 6 patients with extramedullary disease when compared with patients without extramedullary disease. VEGF and bFGF did not correlate with each other while HGF showed a weak correlation with VEGF and a stronger one with bFGF. Moreover, VEGF correlated with features of disease activity, such as C-reactive protein, and 2-microglobulin, while both bFGF and HGF showed an inverse correlation with albumin level. No correlation was found between VEGF, bFGF and HGF levels and age, M protein level, osteolytic lesions, or percentage of BM plasma cells. Since angiogenic factors may be released by normal cells in response to hypoxia, we also evaluated erythropoietin (EPO) levels (which correlate with the hypoxic stimulus) both in PB and BM plasma of these patients but none of the measured angiogenic factors correlated with EPO levels. Interpretation and Conclusions. Several soluble factors may play a role in the angiogenic activity described in MM but their contribution to the progression of disease may be different. The finding of higher levels of these factors in BM than in PB might indicate that the bone marrow environment is their major source. Concentrations of angiogenic factors parallel the activity of disease and are independent of the hypoxic stimulus.
Protein modification and replicative senescence of WI‐38 human embryonic fibroblasts (2010)

Oxidized proteins as well as proteins modified by the lipid peroxidation product 4-hydroxy-2-nonenal (HNE) and by glycation (AGE) have been shown to accumulate with aging in vivo and during replicative senescence in vitro. To better understand the mechanisms by which these damaged proteins build up and potentially affect cellular function during replicative senescence of WI-38 fibroblasts, proteins targeted by these modifications have been identified using a bidimensional gel electrophoresis-based proteomic approach coupled with immunodetection of HNE-, AGE-modified and carbonylated proteins. Thirty-seven proteins targeted for either one of these modifications were identified by mass spectrometry and are involved in different cellular functions such as protein quality control, energy metabolism and cytoskeleton. Almost half of the identified proteins were found to be mitochondrial, which reflects a preferential accumulation of damaged proteins within the mitochondria during cellular senescence. Accumulation of AGE-modified proteins could be explained by the senescence-associated decreased activity of glyoxalase-I, the major enzyme involved in the detoxification of the glycating agents methylglyoxal and glyoxal, in both cytosol and mitochondria. This finding suggests a role of detoxification systems in the age-related build-up of damaged proteins. Moreover, the oxidized protein repair system methionine sulfoxide reductase was more affected in the mitochondria than in the cytosol during cellular senescence. Finally, in contrast to the proteasome, the activity of which is decreased in senescent fibroblasts, the mitochondrial matrix ATP-stimulated Lon-like proteolytic activity is increased in senescent cells but does not seem to be sufficient to cope with the increased load of modified mitochondrial proteins.
( 111 ) INDIUM-CAPROMAB PENDETIDE UNEXPECTEDLY LOCALIZES TO RENAL CELL CARCINOMA (1999)

No AccessJournal of UrologyClinical Urology: Case Reports1 Feb 1999(111) INDIUM-CAPROMAB PENDETIDE UNEXPECTEDLY LOCALIZES TO RENAL CELL CARCINOMA ELI K. MICHAELS, MICHAEL BLEND, and JUAN CARLOS QUINTANA ELI K. MICHAELSELI K. MICHAELS More articles by this author , MICHAEL BLENDMICHAEL BLEND More articles by this author , and JUAN CARLOS QUINTANAJUAN CARLOS QUINTANA More articles by this author View All Author Informationhttps://doi.org/10.1016/S0022-5347(01)61960-8AboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail "(111) INDIUM-CAPROMAB PENDETIDE UNEXPECTEDLY LOCALIZES TO RENAL CELL CARCINOMA." The Journal of Urology, 161(2), pp. 597–598 References 1 : The detection of metastatic prostate cancer with simultaneous dual isotope SPECT images. RSNA. ORG/EJ.September 11, 1997; vol. 1. Google Scholar 2 : Risk of genitourinary malignancies after cancer of the prostate. Cancer1988; 61: 396. Google Scholar 3 : Monoclonal antibodies to the extracellular domain of prostate-specific membrane antigen also react with tumor vascular endothelium. Cancer Res.1997; 9: 3629. Google Scholar From the Departments of Urology and Radiology, Section of Nuclear Medicine, University of Illinois at Chicago, Chicago, IllinoisSupported by a grant from the Cytogen Corporation.© 1999 by American Urological Association, Inc.FiguresReferencesRelatedDetailsCited bySCOTT D, HALKAR R, FISCHER A, GALT J and CLARKE H (2018) FALSE-POSITIVE 111INDIUM CAPROMAB PENDETIDE SCAN DUE TO BENIGN MYELOLIPOMAJournal of Urology, VOL. 165, NO. 3, (910-911), Online publication date: 1-Mar-2001. Volume 161Issue 2February 1999Page: 597-598 Advertisement Copyright & Permissions© 1999 by American Urological Association, Inc.MetricsAuthor Information ELI K. MICHAELS More articles by this author MICHAEL BLEND More articles by this author JUAN CARLOS QUINTANA More articles by this author Expand All Advertisement PDF downloadLoading ...
Obstructive Sleep Apnea in Extremely Overweight Adolescents undergoing Bariatric Surgery (2005)

Abstract Objectives : To determine the prevalence of obstructive sleep apnea (OSA) in extremely overweight adolescents and to examine the effect of significant weight loss on OSA severity. Research Methods and Procedures : We reviewed the anthropometric and polysomnographic data on all extremely overweight adolescents who underwent laparoscopic Roux en Y gastric bypass surgery at Cincinnati Children's Hospital Medical Center from July 2001 to September 2004. Repeat polysomnograms were performed after significant weight loss. Comparisons were made between pre‐ and postoperative polysomnographic data. Results : Nineteen of 34 patients (55%) who underwent bariatric surgery were diagnosed with OSA. Subsequent to surgery, 10 of these patients returned for follow‐up polysomnographic testing. After significant weight loss (mean, 58 kg), OSA severity markedly decreased in all patients (median apnea‐hypopnea index at baseline vs. after weight loss, 9.1 vs. 0.65). Discussion : Our study indicated that OSA was highly prevalent in extremely overweight adolescents meeting eligibility criteria for bariatric surgery. The significant weight loss after gastric bypass was associated with a marked reduction in OSA severity.
Synergistically Anti-metastatic Effect of 5-Flourouracil on Colorectal Cancer Cells via Calcium-mediated Focal Adhesion Kinase Proteolysis (2017)

Calcium supplementation represents a method of enhancing the potency of existing antitumor agents such as 5-FU, augmenting their clinical effectiveness.
Identification of N-sulphated disaccharide units in heparin-like polysaccharides (1979)

1. Preparations of heparin and heparan sulphate were degraded with HNO2. The resulting disaccharides were isolated by gel chromatography, reduced with either NaBH4 or NaB3H4 and were then fractionated into non-sulphated, monosulphated and disulphated species by ion-exchange chromatography or by paper electrophoresis. The non-sulphated disaccharides were separated into two, and the monosulphated disaccharides into three, components by paper chromatography. 2. The uronic acid moieties of the various non- and mono-sulphated disaccharides were identified by means of radioactive labels selectively introduced into uronic acid residues (3H and 14C in D-glucuronic acid, 14C only in L-iduronic acid units) during biosynthesis of the polysaccharide starting material. Labelled uronic acids were also identified by paper chromatography, after liberation from disaccharides by acid hydrolysis or by glucuronidase digestion. Similar procedures, applied to disaccharides treated with NaB3H4, indicated 2,5-anhydro-D-mannitol as reducing terminal unit. On the basis of these results, and the known positions and configurations of the glycosidic linkages in heparin, the two non-sulphated disaccharides were identified as 4-O-(beta-D-glucopyranosyluronic acid)-2,5-anhydro-D-mannitol and 4-O-(alpha-L-idopyranosyluronic acid)-2,5-anhydro-D-mannitol. 3. The three monosulphated [1-3H]anhydromannitol-labelled disaccharides were subjected to Smith degradation or to digestion with homogenates of human skin fibroblasts, and the products were analysed by paper electrophoresis. The results, along with the 1H n.m.r. spectra of the corresponding unlabelled disaccharides, permitted the allocation of O-sulphate groups to various positions in the disaccharides. These were thus identified as 4-O-(beta-D-glucopyranosyl-uronic acid)-2,5-anhydro-D-mannitol 6-sulphate, 4-O-(alpha-L-idopyranosyluronic acid)-2,5-anhydro-D-mannitol 6-sulphate and 4-O-(alpha-L-idopyranosyluronic acid 2-sulphate)-2,5-anhydro-D-mannitol. The last-mentioned disaccharide was found to be a poor substrate for the iduronate sulphatase of human skin fibroblasts, as compared with the disulphated species, 4-O-(alpha-L-idopyranosyluronic acid 2-sulphate)-2,5-anhydro-D-mannitol 6-sulphate. 4. The identified [1-3H]anhydromannitol-labelled disaccharides were used as reference standards in a study of the disaccharide composition of heparins and heparan sulphates. Low N-sulphate contents, most pronounced in the heparin sulphates, were associated with high ratios of mono-O-sulphated/di-O-sulphated (N-sulphated) disaccharide units, and in addition, with relatively large amounts of 2-sulphated L-iduronic acid residues bound to C-4 of N-sulpho-D-glucosamine units lacking O-sulphate substituents.
Transgenic Mouse Models for Cardiac Dysfunction by a Specific Gene Manipulation (2005)

The sarcoplasmic reticulum Ca2+ ATPase (SERCA) plays a pivotal role in calcium cycling and the beat-to-beat function of the heart. Recent studies have shown that decreased expression and activity of SERCA are associated with end-stage heart failure in humans and in experimental animal models of heart failure. There has been considerable controversy over whether a decrease in SERCA level is a cause or effect of hypertrophy. To address directly whether alterations in SERCA levels modify calcium homeostasis and heart function, we have chosen to alter the SERCA protein expression genetically using transgenic and gene-targeted knockout mouse technology. This chapter describes the methodology for generation of mouse models that overexpress different SERCA isoforms and a SERCA2 knockout mouse model with decreased SERCA levels.
Development of a conditional bioluminescent transplant model for TPM3-ALK-induced tumorigenesis as a tool to validate ALK-dependent cancer targeted therapy (2007)

Overexpression and activation of TPM3-ALK tyrosine kinase fusion protein is a causal oncogenic event in the development of Anaplastic Large Cell Lymphoma and Inflammatory Myofibroblastic ALK-positive tumors. Thus, the development of ALK specific tyrosine kinase inhibitors is a current therapeutic challenge. Animal models are essential to assess, in vivo, the efficiency of ALK-oncogene inhibitors and to identify new and/or additional therapeutic targets in the ALK tumorigenesis pathway. Using the tetracycline system to allow conditional and concomitant TPM3-ALK and luciferase expression, we have developed a unique transplant model for bioluminescent TPM3-ALK-induced fibroblastic tumors in athymic nude mice. The reversible TPM3-ALK expression allowed us to demonstrate that this oncogene is essential for the tumor growth and its maintenance. In addition, we showed that this model could be used to precisely assess tumor growth inhibition upon ALK chemical inactivation. As proof of principle, we used the general tyrosine kinase inhibitor herbimycin A to inhibit ALK oncoprotein activity. As expected, herbimycin A treatment reduced tumor growth as assessed both by tumor volume measurement and bioluminescent imaging. We conclude that this transplant model for TPM3-ALK-induced tumors represents a valuable tool not only to accurately and rapidly evaluate in vivo ALK-targeted therapies but also to gain insight into the mechanism of ALK-positive tumor development.
Enterococcus faecalis Acetoacetyl-Coenzyme A Thiolase/3-Hydroxy-3-Methylglutaryl-Coenzyme A Reductase, a Dual-Function Protein of Isopentenyl Diphosphate Biosynthesis (2002)

Many bacteria employ the nonmevalonate pathway for synthesis of isopentenyl diphosphate, the monomer unit for isoprenoid biosynthesis. However, gram-positive cocci exclusively use the mevalonate pathway, which is essential for their growth (E. I. Wilding et al., J. Bacteriol. 182:4319-4327, 2000). Enzymes of the mevalonate pathway are thus potential targets for drug intervention. Uniquely, the enterococci possess a single open reading frame, mvaE, that appears to encode two enzymes of the mevalonate pathway, acetoacetyl-coenzyme A thiolase and 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. Western blotting revealed that the mvaE gene product is a single polypeptide in Enterococcus faecalis, Enterococcus faecium, and Enterococcus hirae. The mvaE gene was cloned from E. faecalis and was expressed with an N-terminal His tag in Escherichia coli. The gene product was then purified by nickel affinity chromatography. As predicted, the 86.5-kDa mvaE gene product catalyzed both the acetoacetyl-CoA thiolase and HMG-CoA reductase reactions. Temperature optima, DeltaH(a) and K(m) values, and pH optima were determined for both activities. Kinetic studies of acetoacetyl-CoA thiolase implicated a ping-pong mechanism. CoA acted as an inhibitor competitive with acetyl-CoA. A millimolar K(i) for a statin drug confirmed that E. faecalis HMG-CoA reductase is a class II enzyme. The oxidoreductant was NADP(H). A role for an active-site histidine during the first redox step of the HMG-CoA, reductase reaction was suggested by the ability of diethylpyrocarbonate to block formation of mevalonate from HMG-CoA, but not from mevaldehyde. Sequence comparisons with other HMG-CoA reductases suggest that the essential active-site histidine is His756. The mvaE gene product represents the first example of an HMG-CoA reductase fused to another enzyme.
MELOE-1 is a new antigen overexpressed in melanomas and involved in adoptive T cell transfer efficiency (2008)

A cytotoxic T lymphocyte (CTL) clone was derived from a tumor-infiltrating lymphocyte (TIL) population infused to a melanoma patient who remained relapse free for 10 yr after this adoptive transfer. This clone recognized all melanoma cell lines tested and, to a lower extent, melanocytes, in the context of human histocompatibility leukocyte antigen A2 (HLA-A2), but it did not recognize other tumor cell types. The gene coding for the antigen recognized by this clone was identified by the screening of a melanoma complementary DNA expression library. This antigen is overexpressed in melanomas, compared with other cancer cell lines and healthy tissues, and was thus called melanoma-overexpressed antigen (meloe). Remarkably, the structure of meloe was unusual, with multiple short open reading frames (ORFs). The peptide recognized by the CTL clone was encoded by one of these ORFs, called MELOE-1. Using a specific HLA-A2/peptide tetramer, we showed a correlation between the infusion of TILs containing MELOE-1-specific T cells and relapse prevention in HLA-A2 patients. Indeed, 5 out of 9 patients who did not relapse were infused with TILs that contained MELOE-1-specific T cells, whereas 0 out of the 21 patients who relapsed was infused with such TIL-containing lymphocytes. Overall, our results suggest that this new antigen is involved in immunosurveillance and, thus, represents an attractive target for immunotherapy protocols of melanoma.
User Independent Gaze Estimation by Exploiting Similarity Measures in the Eye Pair Appearance Eigenspace (2014)

The design of gaze-based computer interfaces has been an active research area for over 40 years. One challenge of using gaze detectors is the repetitive calibration process required to adjust the parameters of the systems, and the constrained conditions imposed on the user for robust gaze estimation. We envision user-independent gaze detectors that do not require calibration, or any cooperation from the user. Toward this goal, we investigate an appearance-based approach, where we estimate the eigenspace for the gaze using principal component analysis (PCA). The projections are used as features of regression models that estimate the screen's coordinates. As expected, the performance of the approach decreases when the models are trained without data from the target user (i.e., user-independent condition). This study proposes an appealing training approach to bridge the gap in performance between user-dependent and user-independent conditions. Using the projections onto the eigenspace, the scheme identifies samples in training set that are similar to the testing images. We build the sample covariance matrix and the regression models only with these samples. We consider either similar frames or data from subjects with similar eye appearance. The promising results suggest that the proposed training approach is a feasible and convenient scheme for gaze-based multimodal interfaces.
A Kalman Filter-Based Update Scheme for Road Following (1996)

We propose a new approach for vision based road following. The approach is tailored to a well structured highway environment with lane markers. Lane markers are detected and used for dynamic update of: (i) the lateral position and orientation of the vehicle with respect to the lane markers, (ii) the estimated road curvature, and (iii) the camera parameters (height and inclination angle) in the presence of car vibration and changes in road slope. For that purpose we model the road and hence the shape of the lane markers as quadric curves. The identification of these curves is done in a 3D reference coordinate system attached to the vehicle, rather than a 3D coordinate system attached to the road. This approach allows an unified description/estimation of the road and the vehicle parameters. 1
Multi-shot Person Re-Identification Using Part Appearance Mixture (2017)

Appearance based person re-identification in real-world video surveillance systems is a challenging problem for many reasons, including ineptness of existing low level features under significant viewpoint, illumination, or camera characteristic changes to robustly describe a person's appearance. One approach to handle appearance variability is to learn similarity metrics or ranking functions to implicitly model appearance transformation between cameras for each camera pair, or group, in the system. The alternative, that this paper follows, is the more fundamental approach of improving appearance descriptors, called signatures, to cater for high appearance variance and occlusions. The novel signature representation for multi-shot person reidentification presented in this paper uses multiple appearance models, each describing appearance as a probability distribution of a low-level feature for a certain portion of individual's body. Combined with metric learning, rank-1 recognition rates of 92:5% and 79:5% are achieved on PRID2011 [12] and iLIDS-VID [34] datasets, respectively.
Thrombospondin-1 antagonizes nitric oxide-stimulated vascular smooth muscle cell responses (2006)

In the presence of NO, thrombospondin-1 is converted from a weak stimulator to a potent inhibitor of VSMC responses. Both exogenous and endogenous thrombospondin-1 inhibit NO signaling in VSMC. This activity is mediated by the type 1 repeats and utilizes the same CD36-dependent cGMP signaling pathway in endothelial and VSMC.
Molecular cloning of HEK, the gene encoding a receptor tyrosine kinase expressed by human lymphoid tumor cell lines. (1992)

We describe the molecular cloning of a receptor tyrosine kinase from a cell line (LK63) derived from a case of human pre-B-cell leukemia. We have previously shown that a monoclonal antibody (IIIA4) raised against LK63 recognized a glycosylated, cell-surface 135-kDa molecule (HEK), which displayed tyrosine kinase activity in vitro. The HEK protein was purified by using a IIIA4 antibody column and both N-terminal and internal amino acid sequences were obtained. A 51-mer degenerate oligonucleotide based on the internal amino acid sequence was used to screen an LK63-derived lambda gt10 cDNA library under low-stringency hybridization conditions. One clone of 2.5 kilobases (kb) was isolated and characterized and used to rescreen the library under more-stringent hybridization conditions. A 4.5-kb clone containing the entire HEK coding region was isolated and its complete DNA sequence was determined. The 4.5-kb insert was subcloned into the expression vector CDM8 and transfected into COS cells. COS cells transfected with the sense HEK/CDM8 construct stained specifically with the IIIA4 antibody, thereby confirming that the antigen recognized by the IIIA4 antibody and the expressed protein product of the HEK cDNA clone were identical. DNA sequence analysis revealed that HEK is a newly discovered member of the EPH/ELK family of receptor tyrosine kinases. Northern blot analysis of a number of cell lines demonstrated the expression of 5.5- to 6.0-kb HEK transcripts in LK63 and the T-cell lines JM and HSB-2. Southern blot analysis of DNA from LK63 suggested that the HEK gene was neither amplified nor rearranged in the LK63 tumor.