gebhart/patrepeval huggingface dataset:
Expression of retrovirally transduced genes in primary cultures of adult rat hepatocytes. (1987)

Differentiated primary rat hepatocyte cultures have been infected with retroviral vectors expressing human hypoxanthine/guanine phosphoribosyltransferase or the transposon Tn5 neomycin-resistance gene. Expression of the markers was detected only after infection of the cells during a short period of cell replication and transient dedifferentiation from days 1 to 5 of culture. Provirus integrated during that period remains fully expressed during the entire subsequent stationary period of culture up to at least 25 days. Selection with the neomycin analogue G418 of cells infected with the neomycin vector led to the appearance of cells with hepatocyte morphology in which newly synthesized albumin was detectable by immunoprecipitation, indicating successful infection of hepatocytes.
Peroxisomal Proliferation Protects from β-Amyloid Neurodegeneration (2005)

Alzheimer disease is a neurodegenerative process that leads to severe cognitive impairment as a consequence of selective death of neuronal populations. The molecular pathogenesis of Alzheimer disease involves the participation of the beta-amyloid peptide (Abeta) and oxidative stress. We report here that peroxisomal proliferation attenuated Abeta-dependent toxicity in hippocampal neurons. Pretreatment with Wy-14.463 (Wy), a peroxisome proliferator, prevent the neuronal cell death and neuritic network loss induced by the Abeta peptide. Moreover, the hippocampal neurons treated with this compound, showed an increase in the number of peroxisomes, with a concomitant increase in catalase activity. Additionally, we evaluate the Wy protective effect on beta-catenin levels, production of intracellular reactive oxygen species, cytoplasmic calcium uptake, and mitochondrial potential in hippocampal neurons exposed to H(2) O(2) and Abeta peptide. Results show that the peroxisomal proliferation prevents beta-catenin degradation, reactive oxygen species production, cytoplasmic calcium increase, and changes in mitochondrial viability. Our data suggest, for the first time, a direct link between peroxisomal proliferation and neuroprotection from Abeta-induced degenerative changes.
The pathogenesis of HIV-1 infection (2001)

Epidemiologists have long established beyond all reasonable doubt that infection by the human immunodeficiency virus type 1 (HIV-1) leads to the acquired immune deficiency syndrome (AIDS). Natural history cohorts have demonstrated that the median time from infection to development of AIDS is approximately 12 years, and that this long duration is broadly similar in all populations infected by HIV-1, in all risk groups, in all ethnic groups and in all geographical areas. These epidemiological observations suggest that HIV-1 causes AIDS largely independently of human major histocompatibility complex (MHC) and HIV-1 sequence polymorphisms, as great diversity of both these factors exist world-wide. This is not to say that HLA and HIV diversity do not affect the natural history of HIV disease, but these observations support a common mechanism of HIV-1 pathogenesis which is largely independent of human and viral diversity.
Association of loss of heterozygosity on chromosome 17p with high platelet-derived growth factor alpha receptor expression in human malignant gliomas. (1996)

The aim of this study was to examine platelet-derived growth factor alpha receptor (PDGFR-alpha) expression in gliomas of various degrees of malignancy and to correlate the findings with genetic alterations present in the same tumor samples. We analyzed 83 tumors by in situ hybridization using a PDGFR-alpha cRNA probe. Increased PDGFR-alpha mRNA expression was observed in astrocytic tumors of all stages of malignancy, although the highest levels were found in glioblastoma multiforme. To evaluate the frequency of PDGFR-alpha gene amplification, differential PCR requiring less DNA than Southern analysis was used with fluorescence-labeled primers corresponding to the kinase insert region of the PDGFR-alpha. Only 7 of 43 glioblastomas and none of the other tumors tested showed amplification of the PDGFR-alpha gene, suggesting that a mechanism other than gene amplification is responsible for the overexpression of PDGFR-alpha in glial brain tumors. Comparison of the in situ hybridization data with genetic alterations in the same tumor material showed a significant correlation of loss of heterozygosity on chromosome 17p (Fisher's exact, P < 0.0002) with high expression levels of PDGFR-alpha. Because that was the case in both low- and high-grade astrocytomas, our data imply that PDGFR-alpha is actively involved in tumor cell proliferation in early and late stages of glioma development. The association of PDGFR-alpha expression with a distinct subset of glioblastomas characterized by loss of heterozygosity 17p further supports the differentiation of these tumors into molecular variants.
The Australian National Database of Spoken Language (2002)

The Australian National Database of Spoken Language is a collaborative project involving four active institutions and the explicit support of a wide cross-section of the speech science and technology community in Australia. The novel collaborative structure and procedures for selecting speakers, the material recorded, the recording environment, and subsequent annotation and descriptive procedures are described. A summary of the overall goals and the current status of the project are given.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>
Biofilms as Complex Differentiated Communities (2002)

Prokaryotic biofilms that predominate in a diverse range of ecosystems are often composed of highly structured multispecies communities. Within these communities metabolic activities are integrated, and developmental sequences, not unlike those of multicellular organisms, can be detected. These structural adaptations and interrelationships are made possible by the expression of sets of genes that result in phenotypes that differ profoundly from those of planktonically grown cells of the same species. Molecular and microscopic evidence suggest the existence of a succession of de facto biofilm phenotypes. We submit that complex cell-cell interactions within prokaryotic communities are an ancient characteristic, the development of which was facilitated by the localization of cells at surfaces. In addition to spatial localization, surfaces may have provided the protective niche in which attached cells could create a localized homeostatic environment. In a holistic sense both biofilm and planktonic phenotypes may be viewed as integrated components of prokaryote life.
Active contours without edges (2001)

We propose a new model for active contours to detect objects in a given image, based on techniques of curve evolution, Mumford-Shah (1989) functional for segmentation and level sets. Our model can detect objects whose boundaries are not necessarily defined by the gradient. We minimize an energy which can be seen as a particular case of the minimal partition problem. In the level set formulation, the problem becomes a "mean-curvature flow"-like evolving the active contour, which will stop on the desired boundary. However, the stopping term does not depend on the gradient of the image, as in the classical active contour models, but is instead related to a particular segmentation of the image. We give a numerical algorithm using finite differences. Finally, we present various experimental results and in particular some examples for which the classical snakes methods based on the gradient are not applicable. Also, the initial curve can be anywhere in the image, and interior contours are automatically detected.
Biological validation of a linear regression mathematical model of gene expression and radiation response (2007)

3803 Background: In a previous study we showed that a multivariate linear regression model of gene expression and radiation response (as measured by survival fraction at 2Gy, SF2) predicted cellular radiosensitivity and identified at least one novel protein (RbAp48) mechanistically involved in radiation response. The model predicted that three additional known genes (rgs-19, r5pia and topo1) could be involved in regulating radiation response. In this study, we continue the biological testing of the multivariate linear regression model. Methods: The details of the multivariate linear regression model of gene expression and radioresponse in a 35 cell line database have been published previously (1).RGS-19 (Flag -tag) and R5PIA were transfected into MDA-MB231 and MALME-3M cell lines respectively, using Lipofectamine2000 reagent (Invitrogen). Overexpression of both RGS-19 and R5PIA were confirmed by western blot. Cell survival after 2, 4 6,and 8 Gy radiation were determined by the clonogenic assay. RbAp48 siRNA (100 nM) designed by Dharmacon’s SMARTpool technology or a pool of 4 negative controls siRNA (100 nM) was transfected into HCT116 colon cancer cell lines following the DharmaFECT transfection protocol (Dharmacon). Knockdown of RbAp48 was verified 72 hours after transfection, by Western Blot. Results: The model predicted that overexpression of RGS-19 and R5PIA should lead to radiosensitization while downregulation of RbAp48 should lead to radioresistance. Indeed, overexpression of RGS-19 resulted in radiosensitization of MDA-MB231 breast cancer cell lines (SF2, Empty Vector: 0.50 ± 0.06 vs. RGS19 plasmid: 0.35 ± 0.06, n=3, p=0.01) (SF8 value, Empty Vector: 0.096 ± 0.053 and RGS19 plasmid: 0.068 ± 0.06, n=3, p=0.06). In contrast, overexpression of R5PIA had no effects on radiosensitivity of SKMEL28 cancer cell lines as measured by SF2 (Empty Vector: 0.64 ± 0.10 and R5PIA plasmid: 0.68 ± 0.09, n=4). Additionally downregulation of RbAp48 resulted in radiation resistance of HCT-116 (SF2, control siRNA: 0.26 ± 0.04, RbAp48 siRNA: 0.37 ± 0.03, n=6) (SF8 control siRNA: 0.00275 ± 0.0002, RbAp48 siRNA: 0.00575 ± 0.0004, n=6), also consistent with the predictions of the model. Conclusions: These data further confirm the biological validity of the mathematical algorithm applied to this genomic analysis. Two of the three genes tested affected radiation response as predicted by the model. A third gene (top1) is currently a target for radiosensitization in clinical use. References 1. Torres-Roca JF, Eschrich S, Zhao H, Bloom G, Sung J, McCarthy S, Cantor AB, Scuto A, Li C, Zhang S, Jove R, Yeatman T. (2005) Cancer Res 65:7169-76
Warfarin in the Prevention of Stroke Associated with Nonrheumatic Atrial Fibrillation (1992)

Low-intensity anticoagulation with warfarin prevented cerebral infarction in patients with nonrheumatic atrial fibrillation without producing an excess risk of major hemorrhage. This benefit extended to patients over 70 years of age.
Two-Dimensional Crystallization of Histidine-Tagged, HIV-1 Reverse Transcriptase Promoted by a Novel Nickel-Chelating Lipid (1994)

Recombinant proteins containing a short stretch of contiguous histidine residues (approximately 6) ("a His-tag") can be specifically bound to N-nitrilotriacetic-acid-chelated nickel ions, providing a convenient general method for their purification. A lipid derivatized with a nickel-chelating head group may provide a general approach to two-dimensional crystallization of the His-tagged proteins, using the lipid layer technique. We have designed a synthetic phospholipid that carries a chelated nickel ion (Ni-NTA-DOPE). His-tagged recombinant HIV-1 reverse transcriptase (HIV-RT) bound specifically to lipid layers containing Ni-NTA-DOPE and formed crystals within minutes from a dilute protein solution. Two-dimensional crystals preserved in negative stain diffracted strongly to approximately 21 A. The projection map computed from averaged Fourier transforms revealed a structure similar in size and shape to a selected projection view of the 3-D structure that was previously determined for HIV-RT by X-ray crystallography.
AICAR Administration Causes an Apparent Enhancement of Muscle and Liver Insulin Action in Insulin-Resistant High-Fat-Fed Rats (2002)

Exercise improves insulin sensitivity. As AMP-activated protein kinase (AMPK) plays an important role in muscle metabolism during exercise, we investigated the effects of the AMPK activator 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR) on insulin action in insulin-resistant high-fat-fed (HF) rats. Rats received a subcutaneous injection of 250 mg/kg AICAR (HF-AIC) or saline (HF-Con). The next day, euglycemic-hyperinsulinemic clamp studies were performed. Glucose infusion rate during the clamp was enhanced (50%) in HF-AIC compared with HF-Con rats. Insulin-stimulated glucose uptake was improved in white but not in red quadriceps, whereas glycogen synthesis was improved in both red and white quadriceps of HF-AIC rats. HF-AIC rats also showed increased insulin suppressibility of hepatic glucose output (HGO). AICAR-induced responses in both liver and muscle were accompanied by reduced malonyl-CoA content. Clamp HGO correlated closely with hepatic triglyceride content (r = 0.67, P < 0.01). Thus, a single dose of AICAR leads to an apparent enhancement in whole-body, muscle, and liver insulin action in HF rats that extends beyond the expected time of AMPK activation. Whether altered tissue lipid metabolism mediates AICAR effects on insulin action remains to be determined. Follow-up studies suggest that at least some of the post-AICAR insulin-enhancing effects also occur in normal rats. Independent of this, the results suggest that pharmacological activation of AMPK may have potential in treating insulin-resistant states and type 2 diabetes.
Peptides and Hormesis (2003)

The article provides a broad assessment of the occurrence of hormetic-like biphasic dose-response relationships by over 30 peptides representing many major peptide classes. These peptide-induced biphasic dose responses were observed to occur in a extensive range of tissues, affecting an diverse range of biological endpoints. Despite diversity of peptides, models and endpoints, the quantitative features of the biphasic dose responses are remarkably similar with respect to the amplitude and width of the stimulatory response. These findings strongly suggest that hormetic-like biphasic dose responses represent a broadly generalizable biological phenomenon.
Content-aware image and video resizing based on frequency domain analysis (2011)

An adaptive image and video resizing algorithm based on the frequency domain analysis is proposed in this work. Given an image, we first construct an importance map by combining the gradient and the saliency information. We partition the image into several strips so that each strip contains pixels of similar importance levels. We model the distortion, which is caused by scaling a strip, in the frequency domain. Then, we scale each strip adaptively to minimize the overall distortion of the whole image. Moreover, we extend the proposed algorithm for video resizing. We add the motion term to construct the importance map, and suppress excessive parameter variations to achieve jitter-free video resizing. Simulation results show that the proposed algorithm provides higher quality resizing results than conventional algorithms, although it requires lower computational complexity.
Value of the P-wave signal-averaged ECG for predicting atrial fibrillation after cardiac surgery. (1993)

The P-wave duration recorded with the SAECG is a potent, accurate, and independent predictor of AF after cardiac surgery.
C-Terminal Substitution of HBV Core Proteins with Those from DHBV Reveals That Arginine-Rich 167RRRSQSPRR175 Domain Is Critical for HBV Replication (2012)

To investigate the contributions of carboxyl-terminal nucleic acid binding domain of HBV core (C) protein for hepatitis B virus (HBV) replication, chimeric HBV C proteins were generated by substituting varying lengths of the carboxyl-terminus of duck hepatitis B virus (DHBV) C protein for the corresponding regions of HBV C protein. All chimeric C proteins formed core particles. A chimeric C protein with 221-262 amino acids of DHBV C protein, in place of 146-185 amino acids of the HBV C protein, supported HBV pregenomic RNA (pgRNA) encapsidation and DNA synthesis: 40% amino acid sequence identity or 45% homology in the nucleic-acid binding domain of HBV C protein was sufficient for pgRNA encapsidation and DNA synthesis, although we predominantly detected spliced DNA. A chimeric C protein with 221-241 and 251-262 amino acids of DHBV C, in place of HBV C 146-166 and 176-185 amino acids, respectively, could rescue full-length DNA synthesis. However, a reciprocal C chimera with 242-250 of DHBV C ((242)RAGSPLPRS(250)) introduced in place of 167-175 of HBV C ((167)RRRSQSPRR(175)) significantly decreased pgRNA encapsidation and DNA synthesis, and full-length DNA was not detected, demonstrating that the arginine-rich (167)RRRSQSPRR(175) domain may be critical for efficient viral replication. Five amino acids differing between viral species (underlined above) were tested for replication rescue; R169 and R175 were found to be important.
Involvement of Suppressor of Cytokine Signaling-3 as a Mediator of the Inhibitory Effects of IL-10 on Lipopolysaccharide-Induced Macrophage Activation (2002)

Previous studies have shown that IL-10 can induce the expression of the suppressor of cytokine signaling 3 (SOCS-3) mRNA in human monocytes and neutrophils, suggesting that the capacity of IL-10 to inhibit the expression of LPS-inducible proinflammatory genes may depend on SOCS-3 induction. However, no direct experimental evidence has been provided to support such hypothesis. Herein, we show that stable transfection of SOCS-3 into the mouse macrophage cell line J774 resulted in an inhibition of NO, TNF-alpha, IL-6, and GM-CSF secretion in response to LPS at levels similar to those exerted by IL-10 in LPS-stimulated wild-type J774. Constitutive SOCS-3 expression also down-regulated the mRNA expression of inducible NO synthase and IL-6 and impaired the production of TNF-alpha, mainly at a post-transcriptional level. In addition, SOCS-3-transfected cells displayed a constitutive expression of the IL-1R antagonist gene, consistent with the observation that IL-10 enhances IL-1R antagonist mRNA in LPS-stimulated wild-type cells. Furthermore, in peritoneal macrophages harvested from mice carrying heterozygous disruption of the SOCS-3 gene, IL-10 was less effective in repressing LPS-stimulated TNF-alpha and NO production. Taken together, our data show that SOCS-3 inhibits LPS-induced macrophage activation, strongly supporting the idea that it plays a role in the molecular mechanism by which IL-10 down-modulates the effector functions of LPS-activated macrophages. Finally, we show that forced expression of SOCS-3 significantly suppresses the ability of IL-10 to trigger tyrosine phosphorylation of STAT3. Therefore, SOCS-3 functions both as an LPS signal inhibitor and as a negative feedback regulator of IL-10/STAT3 signaling.
Evaluation of Gene Expression Profiles in Thyroid Nodule Biopsy Material to Diagnose Thyroid Cancer (2008)

We developed a procedure of molecular diagnosis of benign vs. malignant tumors applicable to the material collected by FNAB. The molecular test complied with a preclinical validation stage; it must be now evaluated on ultrasound-guided FNAB in a large-scale prospective study.
Wave-number-based assessment of the doubly asymptotic approximation. I. Frequency domain wet surface impedance (2000)

The doubly asymptotic approximation (DAA) is a canonical relationship for the interaction between surface normal velocity and pressure. Its validity for a slender hemicapped cylinder is examined by formulating a frequency domain version of DAA using the global basis functions employed in the wave-number-based formulation of the surface variational principle [K. Wu and J. H. Ginsberg, ASME J. Vib. Acoust. 120, 392-400 (1998)]. The wet surface impedance matrix, which relates the spectral representation of normal velocity to a corresponding representation of pressure, is obtained according to a second-order version of DAA and according to the surface variational principle. Comparison and interpretation of the results reveals that DAA fails to account for highlights associated with transition from supersonic to subsonic surface waves as the surface wavelength decreases with frequency held constant.
Serum Total Cholesterol, Apolipoprotein E {FC12}e4 Allele, and Alzheimer’s Disease (1998)

The epsilon 4 allele of the apolipoprotein E (apoE) is associated with Alzheimer's disease (AD) and also with elevated serum total cholesterol and low-density lipoprotein levels. However, the interrelationships between apoE genotype, plasma cholesterol levels and AD risk have been studied very little. We examined the possible role of serum total cholesterol in the pathogenesis of AD in a population-based sample of 444 men, aged 70-89 years, who were survivors of the Finnish cohorts of the Seven Countries Study. Previous high serum cholesterol level (mean level > or = 6.5 mmol/l) was a significant predictor of the prevalence of AD (odds ratio = 3.1; 95% confidence interval = 1.2, 8.5) after controlling for age and the presence of apoE epsilon 4 allele. In men who subsequently developed AD the cholesterol level decreased before the clinical manifestations of AD. We conclude that high serum total cholesterol may be an independent risk factor for AD and some of the effect of the apoE epsilon 4 allele on risk of AD might be mediated through high serum cholesterol.
Mitral valve prolapse in a case of Marfan syndrome with congenital cardiac disease, chronic obstructive pulmonary disease and schizophrenia. (1995)

Mitral valve prolapse (MVP) is a common pathological finding in several inherited connective-tissue diseases among which the Marfan syndrome. In the literature several cases of Marfan syndrome characterized by schizophrenia, chronic obstructive pulmonary disease and severe mitral regurgitation due to a MVP have been reported. Our case of MVP was observed in a patient with Marfan syndrome with its characteristic musculoskeletal disorders associated with congenital cardiac disease, severe chronic obstructive pulmonary disease and schizophrenia. According to the latest genetic studies, Marfan syndrome seems to result from genetic mutations in an extracellular matrix glycoprotein, fibrillin. Authors believe that MVP represents only one of several pathological alterations which may be seen in the Marfan syndrome, as expression of a more generalized genetic disorder.