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At least 919 records · Page 51Linked to original sources
PubMed2003

[Model function for population rhythm using wavelet transform].

Interindividual variability among a population induces some chronobiological analysis difficulties; to solve them we create a so called Model Function, which is associated to a biological rhythm. This model function is an image of a population and can be used directly for further studies. Its building has several steps: normalisation, wavelet transform, threshold application, summation of transforms and inverse wavelet transform. This algorithm is tested on activity rhythm of four inbred mouse strains: B, C, BC and CB; this has permitted to check that F1s have an heterotic effect and that this acrophasis indicates a B dominance. The Model Function permits to deal with some difficult problems, such as rhythm shape and position of a population acrophasis. Those elements are absolutely necessary in chronotherapy which needs the knowledge of maximum efficacy and toxicity hours.

Algorithms↗
PubMed1997

The genetic penetrance of the activated neu oncogene for the induction of mammary cancer in vivo.

Carcinogenesis is most often viewed as a multistage disease process. An exception to this was suggested for neu transformation of mammary cells in a transgenic model (Muller et al., 1988); however, this interpretation is controversial (Bouchard et al., 1989). In order to better define neu mammary transformation in vivo, we directly measured the genetic penetrance of the neu oncogene. Mammary cells in situ were infected with replication-defective retroviral vectors carrying the activated neu oncogene (pJRneu). A limiting dilution in vivo transplantation assay was used to measure the percentage of mammary clonogenic (stem-like) cells that stably and functionally integrated this vector. Based on this, the percentage of clonogens integrating and expressing neu that could progress to mammary carcinomas was quantified to estimate the penetrance of this gene in mammary carcinogenesis. The genetic penetrance of neu was 3.6% (95% confidence interval 2.2%-5.8%). This high degree of genetic penetrance is compatible with the observations that certain neu-transgenic mice develop a very great number of mammary carcinomas (Muller et al., 1988). However, whether these data are compatible with a single-step transformation model (100% penetrance) is uncertain and is discussed.

Animals↗
PubMed2005

Establishing a murine pancreatic cancer CaSm model: up-regulation of CaSm is required for the transformed phenotype of murine pancreatic adenocarcinoma.

We have recently shown that the cancer-associated Sm-like protein (CaSm) is overexpressed in human pancreatic adenocarcinoma (PC). However, the role of CaSm in the process of neoplastic transformation remains unclear. To define further the role of CaSm in PC transformation, we have established a murine model based on the murine pancreatic cancer cell lines Panc02 and Panc03. CaSm is overexpressed in the aggressive Panc02 cells and expressed at much lower levels in the more indolent Panc03 cells. Up-regulation of CaSm in Panc03 cells increased in vitro proliferation and anchorage-independent growth and promoted subcutaneous tumor establishment and growth in syngeneic mice. Conversely, adenoviral down-regulation of CaSm in Panc02 led to significant inhibition of cellular proliferation and anchorage-independent growth in vitro and complete abolition of tumor growth and metastasis in vivo. Up-regulation of CaSm in NIH3T3 resulted in loss of contact inhibition and increased soft agar colony formation in vitro. The requirement for CaSm overexpression for neoplastic transformation confirms the concept that CaSm is a critical oncogene and potential target for molecular intervention. Furthermore, establishment of the murine clinically relevant model of pancreatic metastases provides a framework for the generation of preclinical data to support the development of novel molecular therapies targeting CaSm.

Adenocarcinoma↗
PubMed2000

Atrial heart fibrillation modeling: a tool for adequate choice of signal processing functions.

Framingham Study showed that Atrial Fibrillation (AF) exposes the patient to an increased stroke risk and to low cardiac output. It is well known that the mechanism of Atrial Fibrillation is reentry. In order to facilitate AF's studies, we propose a deterministic model that can be used for cardiac signal characterization. The model is based on a linear combination of several "Atrial Flutter-like signals. We obtained AF-close aspects. To demonstrate its usefulness we performed a power spectrum transform (i.e. scalar Fast Fourier Transform) of this model. Thanks to the model we show that this transform cannot be used as is, and may induce errors in results interpretation. We also show based on the same example how to overcome the limitation with help of the model. We expect that this model will help in mathematical transforms relevance evaluation. This may lead to new findings in AF classification, and to improvement in patients' treatment, follow-up and survival.

Atrial Fibrillation↗
PubMed2004

Spatial transformations for eye-hand coordination.

Eye-hand coordination is complex because it involves the visual guidance of both the eyes and hands, while simultaneously using eye movements to optimize vision. Since only hand motion directly affects the external world, eye movements are the slave in this system. This eye-hand visuomotor system incorporates closed-loop visual feedback but here we focus on early feedforward mechanisms that allow primates to make spatially accurate reaches. First, we consider how the parietal cortex might store and update gaze-centered representations of reach targets during a sequence of gaze shifts and fixations. Recent evidence suggests that such representations might be compared with hand position signals within this early gaze-centered frame. However, the resulting motor error commands cannot be treated independently of their frame of origin or the frame of their destined motor command. Behavioral experiments show that the brain deals with the nonlinear aspects of such reference frame transformations, and incorporates internal models of the complex linkage geometry of the eye-head-shoulder system. These transformations are modeled as a series of vector displacement commands, rotated by eye and head orientation, and implemented between parietal and frontal cortex through efficient parallel neuronal architectures. Finally, we consider how this reach system might interact with the visually guided grasp system through both parallel and coordinated neural algorithms.

Animals↗
PubMed2002

AP-1, NF-kappa-B, and ERK activation thresholds for promotion of neoplastic transformation in the mouse epidermal JB6 model.

The promotion-sensitive mouse epidermal JB6 cells (clone 41) have been used to identify the tumor-promoting activity of various compounds. Because treatment by tumor promoters [12-O-tetradecanoylphorbol-13-acetate (TPA), epidermal growth factor (EGF), or tumor necrosis factor alpha (TNF-alpha)] transforms clone 41 cells to anchorage-independent and tumorigenic phenotypes, they are considered to be undergoing late-stage tumor promotion. Here we address the question of how much activation of transformation-relevant transcription factors [activator protein-1 (AP-1), ternary complex factors (TCFs), or nuclear factor kappa-B (NF-kappa-B)] is required for transformation response and how much tumor promoter produces significant risk of transformation. Stable transfectants harboring a reporter construct with an AP-1 response element, serum-response element (SRE), or NF-kappa-B response element were established. We examined the relationship between concentration of tumor promoters, key signaling events, and activation of the transcription factors. A concentration of > 0.2 nM TPA or 0.12 ng/mL (0.02 nM) EGF produced a significant increase in transformation response as well as in extracellular signal-regulated protein kinase (ERK), SRE, or AP-1 activation. Treatment with > 0.4 U/mL (2.35 pM) TNF-alpha increased NF-kappa-B activity and transformation response in a dose-dependent manner. However, transformation response decreased at > 33 U/mL TNF-alpha due to a cytotoxic response. These findings suggest that the signaling pathway leading to the activation of ERK, TCF, and AP-1 proteins constitutes a major factor determining the risk of tumor promotion by TPA or EGF. Cell toxicity in addition to NF-kappa-B activation should be considered in predicting TNF-alpha-induced transformation response.

Animals↗
PubMed1998

Phase transformation of a liposomal dispersion into a micellar solution induced by drug-loading.

PURPOSE: Loading a liposomal dispersion with drug may cause a phase transformation into a micellar solution. The present contribution presents a detailed physicochemical characterization and an overall model which describes transformation due to the properties of any drug. METHODS: Characterization of liposomal dispersions was obtained by photon correlation spectroscopy (PCS) and small angle X-ray scattering (SAXS). Microstructure of colloidal solutions was analysed by 31P-NMR and SAXS. RESULTS: At weight ratios of phospholipid to drug from 16:1 to 2:1, liposomal dispersions of milky-white appearance and a mean particle size of about 200 nm were obtained. From a ratio of phospholipid to drug of 1:1 downwards, the systems became nearly transparent. The particle size decreased to a value below 25 nm. SAXS also revealed the change of the colloids. Down to a ratio of phospholipid to drug of 2:1 the systems were described as bilayer-structured. At and below the ratio of 1:1, a mixed micelle was indicated. In the 31P-NMR spectra, the transformation is emphasized by both appearance and disappearance of signals. A model based on the theory of self-assembly is presented which explains the phase transformation due to drug amphiphilicity. CONCLUSIONS: We predict that the model presented will hold in general only due to the amphiphilic properties of the drug.

Colloids↗
PubMed2005

Modeling dynamic reciprocity: engineering three-dimensional culture models of breast architecture, function, and neoplastic transformation.

In order to understand why cancer develops as well as predict the outcome of pharmacological treatments, we need to model the structure and function of organs in culture so that our experimental manipulations occur under physiological contexts. This review traces the history of the development of a prototypic example, the three-dimensional (3D) model of the mammary gland acinus. We briefly describe the considerable information available on both normal mammary gland function and breast cancer generated by the current model and present future challenges that will require an increase in its complexity. We propose the need for engineered tissues that faithfully recapitulate their native structures to allow a greater understanding of tissue function, dysfunction, and potential therapeutic intervention.

Animals↗
PubMed2001

Bionic wavelet transform: a new time-frequency method based on an auditory model.

In this paper, a new adaptive wavelet transform, named bionic wavelet transform (BWT), is developed based on a model of the active auditory system. The most distinguishing characteristic of BWT is that its resolution in the time-frequency domain can be adaptively adjusted not only by the signal frequency but also by the signal instantaneous amplitude and its first-order differential. The automatically adjusted resolution, even in a fixed frequency along the time-axis, is achieved by introducing the active control of the auditory system into the wavelet transform (WT). Other properties of BWT include that: 1) BWT is a nonlinear transform that has high sensitivity and frequency selectivity; 2) BWT represents the signal with a concentrated energy distribution; and 3) the inverse BWT can reconstruct the original signal from its time-frequency representation. In order to compare these three properties between BWT and WT, experiments were conducted on both constructed signals and real speech signals. The results show that BWT performs better than WT in these three aspects, and that BWT is appropriate for speech signal processing, especially for cochlear implants.

Algorithms↗
PubMed2004

[The expression of transforming growth factor beta-1 in rat model of chronic obstructive pulmonary disease and the effects of early drugs intervention].

OBJECTIVE: To evaluate the expression of transforming growth factor beta-1(TGF-beta1) and the effects of early drugs intervention of chronic obstructive pulmonary disease(COPD) in rat model. METHODS: The COPD rat model (group B) was established by intratracheal instillation of lipopolysaccharide twice and daily exposure to cigarette smoking. Drug intervention groups received dongchongxiacao orally daily from the three days before the experiment (group C) and erythromycin by intraperitoneal injection since the third week (group D)and inhalation of budesonide since the forth week (group E). At the end of 10 weeks, all 40 rats including normal control (group A) were assessed for lung resistance (RL) and dynamic lung compliance (Cdyn). The expression of TGF-beta1 gene and protein were also observed by immunohistochemistry and semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR), respectively. RESULTS: The changes of pathology and pathophysiology in rat COPD model were similar to those of human COPD. There was a significant increase in the smooth muscle and collagen thickness in the airway wall of the group B in comparison with that of the group A. RL in group B was significantly higher than that in group A (P<0.01), while it was inhibited by early drugs intervention (P<0.01). Cdyn was decreased in group B as compared with that in group A, which was limited by erythromycin and budesonide intervention (P<0.01). The relative content for TGF-beta1 was significantly increased in the epithelial cells of the bronchi, endothelial cells of the pulmonary small vessel and alveolar macrophages of COPD group as compared with those of normal controls (P<0.01).The relative contents for TGF-beta1 in the epithelial of bronchi in group D and group E were significantly lower than that in group B, but not found in group C. There was no difference between group D and group E. There were statistical positive relationships between the RL and the relative content for TGF-beta1 in the bronchial epithelial cells, between the RL and the mRNA level of TGF-beta1 in the lung tissue (P<0.01 approximately 0.05). CONCLUSION: This rat COPD model could be helpful to obtain more information about airway remodeling. TGF-beta1 may play an important role during the process of airway remodeling, and could be influenced by early drugs intervention such as budesonide and erythromycin, which may imply their potency in the treatment of COPD. But there is not same phenomenon found in dongchongxiacao group.

Animals↗
PubMed2004

Roughness models for particle adhesion.

The effects of different surface roughness models on a previously developed van der Waals adhesion model were examined. The van der Waals adhesion model represented surface roughness with a distribution of hemispherical asperities. It was found that the constraints used to define the asperity distribution on the surface, which were determined from AFM scans, varied with scan size and thus were not constant for all surfaces examined. The greatest variation in these parameters occurred with materials that had large asperities or with materials where a large fraction of the surface was covered by asperities. These rough surfaces were modeled with fractals and also with a fast Fourier transform algorithm. When the model surfaces generated using the Fourier transforms are used in the adhesion model, the model accurately predicts the experimentally observed adhesion forces measured with the AFM.

Journal Article↗
PubMed2002

Including transformation products into the risk assessment for chemicals: the case of nonylphenol ethoxylate usage in Switzerland.

A method for applying the risk assessment approach using ratios of predicted environmental concentrations (PECs) and predicted no-effect concentrations (PNECs) to mixtures of parent compounds and their environmental transformation products is presented. Nonylphenol ethoxylates (NPnEOs) and a selection of their most relevant transformation products are investigated as a case study illustrating the method. The PEC values of NPnEO and its transformation products are calculated with a regional multimedia fate model including the transformation kinetics of the NPnEO degradation cascade. PNEC values are derived from a selection of toxicity data on NPnEO and its transformation products. The toxicity of the emerging mixture of NPnEO and its transformation products is then estimated under the assumption of concentration addition (similar mode of action). On this basis, PEC-to-PNEC ratios for the aquatic environment and the sediment are calculated for the individual components of the mixture and the mixture itself. For this purpose, average release rates of NPnEO and its transformation products from Swiss sewage treatment plants were used. While the PEC values of the individual components do not exceed the corresponding PNEC values, the risk quotient of the mixture in water is greater than 1. In sediment, the mixture does not exceed a risk quotient of 1. A combination of sensitivity and scenario analyses is employed to identify the upper and lower bounds of the results.

Animals↗
PubMed2006

Solid-state photodimerization kinetics of alpha-trans-cinnamic acid to alpha-truxillic acid studied via solid-state NMR.

The present work focuses on the topochemical photoconversion process in which alpha-trans-cinnamic acid becomes alpha-truxillic acid. This solid-state [2 + 2] cycloaddition reaction has previously been studied with X-ray diffraction, atomic force microscopy, and vibrational spectroscopy. However structural and kinetic details about the reaction are still debated. We present results from (13)C cross-polarization magic angle spinning solid-state NMR experiments that suggest that the Johnson, Mehl, Avrami, and Kolmogorov model of phase transformation kinetics can be applied to this system. The model elucidates parameters of the reaction, such as the nucleation rate, diffusion rate, and dimensionality of the reaction. From our data, it is concluded that this reaction follows one-dimensional growth with a decreasing nucleation rate.

Journal Article↗
PubMed2004

Intestinal tumor progression is associated with altered function of KLF5.

Krüppel-like transcription factors have been linked to cell growth regulation and tumorigenesis in a number of systems. In the intestinal epithelium, expression of KLF5 (IKLF/BTEB2) is limited to proliferating crypt cells, indicating a growth-promoting role. Consistent with this role, we demonstrate that expression of KLF5 in non-transformed intestinal epithelial cells (ileal IEC-18 and Immorto-Min Colon Epithelial (IMCE) cells) enhances colony formation, cyclin D1 transcription, and cell growth. However, in contrast to these effects in non-transformed cells, KLF5 reduced colony number, failed to enhance cyclin D1 transcription, and was negatively correlated with cell growth in colon cancer cell lines. The relationship between tumor progression and KLF5 was further investigated using Ras-mediated transformation of IEC-18 and IMCE cells as syngeneic models. Ras-transformation recapitulated differences in the effects of KLF5 on cell growth and cyclin D1 transcription, providing a direct link between intestinal tumor progression and altered function of KLF5. Ras-transformation also markedly down-regulated KLF5; further analysis indicated that reduced expression of KLF5 mRNA and destabilization of KLF5 protein occur in intestinal tumors. Reduced levels of KLF5 mRNA were also detected in APC(min) mouse and human familial adenomatous polyposis adenomas compared with normal crypt epithelium, indicating that down-regulation of KLF5 is an early event in intestinal tumorigenesis in vivo. Collectively, these data indicate that intestinal tumor progression is associated with a change in the growth-related functions of KLF5 and that intestinal tumors down-regulate KLF5 expression by multiple mechanisms.

Adenoma↗
PubMed1992

Cytotoxic T lymphocytes (CTL) against a transforming gene product select for transformed cells with point mutations within sequences encoding CTL recognition epitopes.

The 94-kD large tumor (T) antigen specified by simian virus 40 (SV40) is sufficient to induce cell transformation. T antigen contains four H-2Db-restricted cytotoxic T lymphocyte (CTL) recognition epitopes that are targets for CTL clones Y-1, Y-2, Y-3, and Y-5. These epitopes have been mapped to T antigen amino acids 207-215 (site I), 223-231 (sites II and III), and 489-497 (site V), respectively. Antigenic site loss variant cells that had lost one or more CTL recognition epitopes were previously selected by coculturing SV40-transformed H-2Db cells with the site-specific Db-restricted CTL clones. The genetic bases for T antigen CTL recognition epitope loss from the variant cells were identified by DNA amplification and direct sequencing of epitope-coding regions from variant cell DNAs. Cells selected for resistance to CTL clone Y-1 (K-1; K-1,4,5; K-3,1) carry deleted SV40 genomes lacking site I, II, and III coding sequences. Point mutations present within the site II/III coding region of Y-2-/Y-3-resistant cell lines specify the substitution of asparagine for lysine as T antigen amino acid 228 (K-2) or phenylalanine for tyrosine at position 230 (K-3). Point mutations identified within independently selected Y-5 resistant populations (K-5 and K-1,4,5) direct the substitution of isoleucine for asparagine at position 496 (K-5) or the substitution of phenylalanine for isoleucine at position 491 (K-1,4,5) of T antigen. Each substitution causes loss of the relevant CTL recognition epitope, apparently by compromising CTL T cell receptor recognition. These experiments identify specific amino acid changes within a transforming protein that facilitate transformed cell escape from site-specific CTL clones while allowing maintenance of cellular transformation. This experimental model system provides unique opportunities for studying mechanisms of transformed cell escape from active immunosurveillance in vivo, and for analysis of differential host immune responses to wild-type and mutant cell-transforming proteins.

Amino Acid Sequence↗
PubMed2006

Genetic parameters for calving rate and calf survival from linear, threshold, and logistic models in a multibreed beef cattle population.

Generalized mixed linear, threshold, and logistic sire models and Markov chain, Monte Carlo simulation procedures were used to estimate genetic parameters for calving rate and calf survival in a multibreed beef cattle population. Data were obtained from a 5-generation rotational crossbreeding study involving Angus, Brahman, Charolais, and Hereford (1969 to 1995). Gelbvieh and Simmental bulls sired terminal-cross calves from a sample of generation 5 cows. A total of 1,458 cows sired by 158 bulls had a mean calving rate of 78% based on 4,808 calving records. Ninety-one percent of 5,015 calves sired by 260 bulls survived to weaning. Mean heritability estimates and standard deviations for daughter calving rate from posterior distributions were 0.063 +/- 0.024, 0.150 +/- 0.049, and 0.130 +/- 0.047 for linear, threshold, and logistic models, respectively. For calf survival, mean heritability estimates and standard deviations from posterior distributions were 0.049 +/- 0.022, 0.160 +/- 0.058, and 0.190 +/- 0.078 from linear, threshold, and logistic models, respectively. When transformed to an underlying normal scale, linear sire, mixed model, heritability estimates were similar to threshold and logistic sire mixed model estimates. Posterior density distributions of estimated heritabilities from all models were normal. Spearman rank correlations between sire EPD across statistical models were greater than 0.97 for daughter calving rate and for calf survival. Sire EPD had similar ranges across statistical models for daughter calving rate and for calf survival.

Animals↗