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At least 1,315 records · Page 73Linked to original sources
PubMed2002

PCB sources, transformations, and contributions in recent Fox River, Wisconsin sediments determined from receptor modeling.

The PCB contamination in lower Fox River sediments was investigated in order to identify possible PCB sources, contributions, and transformations, using two receptor models. Congener specific sediment PCB data from sites immediately upstream of DePere dam to Green Bay that had been gathered for the Green Bay/Fox River Mass Balance Study, were used in this analysis. The first receptor model is a self training factor analysis (FA) model with non-negative constraints that was applied to identify the PCB sources and significant congener patterns. The second is a chemical mass balance model (CMB) in which published Aroclor sources, inferred from our FA model, were used to apportion these Aroclors to each sample. The FA model indicated two significant factors, the major one being Aroclor 1242 and the other, a profile dominated by low chlorinated congeners, indicating a possible PCB alteration profile. This profile had significant contributions to samples at or around sites with total PCB concentrations higher than 50 ppm, indicating a potential anaerobic dechlorination activity. It was also deduced from the FA model that very small contributions of more highly chlorinated Aroclors may be present in the system. The results from the CMB model confirmed that the system is dominated by Aroclor 1242. Its average contribution was 95%, with small amounts of Aroclor 1254 (2%) and 1260 (1%). Two of the samples, located in the vicinity of point sources, showed high contributions of Aroclor 1016 by the CMB model. This is interpreted as an altered Aroclor profile resembling the less chlorinated Aroclor 1016. Contributions obtained form the CMB and FA models show similar patterns.

Bacteria, Anaerobic↗
PubMed1986

Human cutaneous nevi transplanted onto nude mice: a model for the study of the lesional steps in tumor progression.

Normal human cutaneous nevi were transplanted to the skin of nude mice and some of the grafts were treated topically with 7,12-dimethylbenz[a]anthracene (DMBA, 1.6 mumol weekly). Histologically proven human skin was present in 22 grafts. In the 9 untreated control grafts, the tendency of nevic cells to form nests and the number of nevomelanocytes decreased with time; the melanocytic cells showed no signs of hypertrophy or atypia. In most of the 14 specimens treated with DMBA, the nevomelanocytes showed distinct signs of hypertrophy. The cells were enlarged and often dendritic and were filled with melanin granules for which the transfer to keratinocytes appeared to be blocked. The nevomelanocytes of 4 of the 9 specimens treated with DMBA for greater than or equal to 82 days (9-16 DMBA applications), showed atypical enlarged nuclei with mitotic figures. Since atypia is one criterion for identifying precursors of transformed cells, the model of human nevi grafted onto nude mouse skin may be useful for studying the various steps involved in the progression of benign melanocytic nevi to malignant melanoma.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed2002

Serial analysis of gene expression in normal p53 null mammary epithelium.

Much evidence has accumulated implicating the p53 gene as of importance in breast carcinogenesis. However, much still remains to be uncovered on the specific downstream pathways influenced by this important activator/repressor of transcription. This study investigated the effects of a p53 null genotype on the transcriptome of 'normal' mouse mammary epithelium using a unique in vivo model of preneoplastic transformation. We used SAGE for the comparative analysis of p53 wild type (wt) and null mammary epithelium unexposed and exposed to hormonal stimulation. Analysis of the hormone exposed samples provided a comprehensive view of the dramatic changes in gene expression as consequence of the functional differentiation of the mammary epithelium in an in vivo system. We detected the dysregulation in p53(null) epithelium of <1% of the transcriptome. Changes in expression affected not only known p53 target genes, but also several unexpected genes such as Expi (Wdnm1), Cyp1b1, Gelsolin, Ramp2 and class I MHC genes. The dysregulation of specific genes and their potential use as preneoplastic markers was further validated using an independent model of premalignant mammary outgrowth lines. This is the first study to examine the transcriptome of very early stages of preneoplastic progression in an in vivo model that mimics human breast cancer.

Animals↗
PubMedDate not supplied

Computer simulation of ventricular wall motion using the finite element method.

To investigate how changes in the mechanical characteristics of the myocardium caused by cardiac diseases affect ventricular wall motion, a new computer program to simulate wall motion using the finite element method has been developed. A simple two-dimensional finite element model of the left ventricle is designed with an idealized tension-length curve applied to each element. Pathological changes in the ischemic process are induced in a certain portion of the model to make it possible to evaluate the relationship between the type and degree of changes and abnormal ventricular wall motion (i.e., hypokinesis, akinesis, and dyskinesis). Assumption of plastic deformation at the affected site of the model reproduced the genesis of a ventricular aneurysm. The model is then transformed into a three-dimensional wire frame structure, and the results can viewed from any perspective. These simulations enable the semiquantitative comprehension of cardiac wall motion without need for complicated physiological experiments and may be applied to human cardiac motion in combination with data obtained from cardiac scintigraphy, echocardiography, ventriculography, or cine-CT.

Computer Simulation↗
PubMed2006

[Effects of Jianpi Qinghua Recipe on oxygen radicals and transforming growth factor beta1 in renal tissue in a rat model of chronic renal failure with hyperlipidemia].

OBJECTIVE: To evaluate the effects of Jianpi Qinghua Recipe (JPQHR) on oxygen radicals and transforming growth factor beta1 (TGFbeta1) in renal tissue in a rat model of chronic renal failure with hyperlipidemia. METHODS: Chronic renal failure with hyperlipidemia was induced in rats in untreated group and JPQHR-treated group by 5/6 nephrectomy and high fat diet. Then the rats in these two groups were fed distilled water and JPQHR respectively for eight weeks. The rats in normal control group received no specific interventions. After eight weeks of treatment, the levels of 24 h urine protein (Upr), blood urea nitrogen (BUN) and serum creatinine (Cr), cholesterol (Ch), triglycerides (TG), high-density lipoprotein (HDL) and low-density lipoprotein (LDL) of rats in these three groups were examined. The activity of superoxide dismutase (SOD), contents of malondialdehyde (MDA) and non-esterified fatty acids (NEFA) and expression level of TGFbeta1 mRNA in renal tissue of rats in each groups were also determined. RESULTS: The levels of 24 Upr, BUN and serum Cr, Ch, TG and LDL in the JPQHR-treated group were significantly lower than those in the untreated group. The contents of MDA and NEFA and the expression level of TGFbeta1 mRNA in the JPQHR-treated group were also significantly lower than those in the untreated group, while the activity of SOD was significantly increased in the JPQHR-treated group as compared with that in the untreated group. CONCLUSION: The results indicate that JPQHR can improve the renal function of rats with chronic renal failure and hyperlipidemia by regulating lipid metabolism, maintaining balance between prooxidants and antioxidants and reducing expression of TGFbeta1 mRNA in renal tissue.

Animals↗
PubMed1994

A long-half-life and fibrin-specific form of tissue plasminogen activator in rabbit models of embolic stroke and peripheral bleeding.

BACKGROUND AND PURPOSE: We compared the activity of a new long-half-life, fibrin-specific tissue-type plasminogen activator (TPA) variant with that of wild-type TPA in rabbit models of embolic stroke and peripheral bleeding. METHODS: In the embolic stroke model. TPA-induced clot lysis is followed by continuous monitoring of a radiolabeled clot lodged in the middle cerebral artery. Twenty-four hours after embolization and treatment with either thrombolytic agent or excipient, the brains are removed, fixed, and evaluated for cerebral hemorrhage. In a parallel template bleeding time experiment, the effects of equipotent doses of the two TPA molecules were measured. RESULTS: Infusion of wild-type TPA or bolus administration of the TPA variant resulted in dose-dependent clot lysis. The TPA variant was found to be an order of magnitude more potent than wild-type TPA on a milligram-per-kilogram basis. Unlike wild-type TPA, the variant caused less systemic activation of plasminogen (P < .05) and fewer hemorrhagic transformations in this model (P < .05). The TPA variant did not extend template bleeding times. CONCLUSIONS: These findings show that by combining increased fibrin specificity with decreased plasma clearance, it is possible to produce a thrombolytic agent that is more convenient and more potent than wild-tpe TPA. At the same time the significant reduction in hemorrhagic conversions may be attributable to the conservation of systemic plasminogen seen with this molecule.

Animals↗
PubMed1994

Modeling three-dimensional velocity-to-position transformation in oculomotor control.

1. A considerable amount of attention has been devoted to understanding the velocity-position transformation that takes place in the control of eye movements in three dimensions. Much of the work has focused on the idea that rotations in three dimensions do not commute and that a "multiplicative quaternion model" of velocity-position integration is necessary to explain eye movements in three dimensions. Our study has indicated that this approach is not consistent with the physiology of the types of signals necessary to rotate the eyes. 2. We developed a three-dimensional dynamical system model for movement of the eye within its surrounding orbital tissue. The main point of the model is that the eye muscles generate torque to rotate the eye. When the eye reaches an orientation such that the restoring torque of the orbital tissue counterbalances the torque applied by the muscles, a unique equilibrium point is reached. The trajectory of the eye to reach equilibrium may follow any path, depending on the starting eye orientation and eye velocity. However, according to Euler's theorem, the equilibrium reached is equivalent to a rotation about a fixed axis through some angle from a primary orientation. This represents the shortest path that the eye could take from the primary orientation in reaching equilibrium. Consequently, it is also the shortest path for returning the eye to the primary orientation. Thus the restoring torque developed by the tissue surrounding the eye was approximated as proportional to the product of this angle and a unit vector along this axis. The relationship between orientation and restoring torque gives a unique torque-orientation relationship. 3. Once the appropriate torque-orientation relationship for eye rotation is established the velocity-position integrator can be modeled as a dynamical system that is a direct extension of the one-dimensional velocity-position integrator. The linear combination of the integrator state and a direct pathway signal is converted to a torque signal that activates the muscles to rotate the eyes. Therefore the output of the integrator is related to a torque signal that positions the eyes. It is not an eye orientation signal. The applied torque signal drives the eye to an equilibrium orientation such that the restoring torque equals the applied torque but in the opposite direction. The eye orientation reached at equilibrium is determined by the unique torque-orientation relation. Because torque signals are vectors, they commute.(ABSTRACT TRUNCATED AT 400 WORDS)

Abducens Nerve↗
PubMed1994

Evolutionary relationships and functional conservation among vertebrate Max-associated proteins: the zebra fish homolog of Mxi1.

In mammals, current evidence supports the view that Myc-responsive activities are regulated in part through an intracellular balance between levels of transcriptionally-active Myc/Max heterodimers and those of transcriptionally-inert Max/Max, Mad/Max and Mxi1/Max complexes. To gain insight into the roles of Mad and Mxi1 in cellular growth and differentiation and to fortify key structure-function relationships from an evolutionary standpoint, low stringency hybridization screens were used to identify potential homologs of these Max-associated proteins in the zebra fish genome. A single class of cDNA clones that cross-hybridized both to human mad and mxi1 probes was shown to encode a putative protein with significantly greater homology to mammalian Mxi1 than to Mad, particularly in the basic and helix-loop-helix (bHLH) regions. The high degree of structural relatedness between vertebrate Mxi1 proteins apparent in molecular modelling studies was consistent with the findings that the HLH/leucine zipper (LZ) region of zMxi1 exhibited the same profile of dimerization specificities as its mammalian counterpart in the two-hybrid system and that zmxi1 could, like human mxi1 (Lahoz et al., 1994), suppress the oncogenic potential of mouse c-myc in a mammalian cell. Finally, a comparison of steady-state zc-myc and zmxi1 mRNA levels during zebra fish embryogenesis demonstrated (i) high levels of zc-myc relative to zmxi1 mRNA during initiation of organogenesis, a period characterized by intense growth and active differentiation and (ii) rising levels of zmxi1 mRNA during progression towards the terminally differentiated state. These contrasting patterns of developmental expression together with the capacity of zmxi1 to repress myc-induced transformation support a model for the regulation, by Max-associated proteins, of Myc functions in the control of normal cell development and neoplastic growth.

Amino Acid Sequence↗
PubMed1989

Analysis of drug penetration through the skin by the two-layer skin model.

A diffusion model for the skin penetration of drug in the finite-dose system was developed considering the skin to be composed of two layers, the outermost layer (stratum corneum) and the lower layer (viable epidermis and dermis). Based on this skin model, the Laplace transforms of the equations for the drug amounts in the receptor, the vehicle, and the skin were derived. The penetration profiles of 6-mercaptopurine (6-MP) through the intact and stripped guinea pig skin were obtained from in vitro diffusion experiments. The computer fitting of those profiles to the Laplace-transformed equations by a nonlinear least-squares program based on a fast inverse Laplace transform algorithm [MULTI-(FILT)] gave parameters such as diffusion coefficients of 6-MP and thicknesses of both layers. The mean transit time (MTT) for each diffusion process was defined based on statistical moment concept and calculated using the obtained parameters. Under the present condition, the process to move from the vehicle to the stratum corneum is demonstrated to have the longest mean time in overall processes of 6-MP penetration.

Animals↗
PubMed2006

Use of Ras-transformed human ovarian surface epithelial cells as a model for studying ovarian cancer.

The Ras gene family has been implicated in the development of many human epithelial cancers. Mutations in K-ras or its downstream mediator BRAF have been detected in about two thirds of low-grade serous carcinomas and borderline serous tumors; mutations in K-ras are also often present in benign and invasive mucinous ovarian cancers. Although the oncogenic allele H-ras(V12) is present in only approximately 6% of ovarian cancers, physiologically activated H-ras protein is commonly detected in human ovarian cancer, presumably because of an increase in upstream signals from tyrosine kinase growth factor receptors such as Her-2/neu, despite the lack of a Ras mutation. The mechanisms by which ras oncogenes transform human epithelial cells are not clear. The methods described here are what we use to culture human ovarian surface epithelial cells, to immortalize those cells, and to transform the immortalized cells with oncogenic H-ras or K-ras. These Ras-transformed human ovarian surface epithelial cells form tumors in nude mice and recapitulate many features of human ovarian cancer, thus providing an excellent model system for studying the initiation and progression of human ovarian cancer.

Animals↗
PubMed1993

ECG data compression by modeling.

The paper presents a novel algorithm for data compression of single lead electrocardiogram (ECG) data. The method is based on parametric modeling of the discrete cosine transformed ECG signal. Improved high frequency reconstruction is achieved by separately modeling the low and the high frequency regions of the transformed signal. Differential pulse code modulation is applied on the model parameters to obtain a further increase in the compression. Compression ratios up to 1:40 were achieved without significant distortion.

Algorithms↗
PubMed1999

Requirement of type III TGF-beta receptor for endocardial cell transformation in the heart.

Transforming growth factor-beta (TGF-beta) signaling is mediated by a complex of type I (TBRI) and type II (TBRII) receptors. The type III receptor (TBRIII) lacks a recognizable signaling domain and has no clearly defined role in TGF-beta signaling. Cardiac endothelial cells that undergo epithelial-mesenchymal transformation express TBRIII, and here TBRIII-specific antisera were found to inhibit mesenchyme formation and migration in atrioventricular cushion explants. Misexpression of TBRIII in nontransforming ventricular endothelial cells conferred transformation in response to TGF-beta2. These results support a model where TBRIII localizes transformation in the heart and plays an essential, nonredundant role in TGF-beta signaling.

Animals↗
PubMed1988

Cooperative transforming activities of ras, myc, and src viral oncogenes in nonestablished rat adrenocortical cells.

Early-passage rat adrenocortical cells were infected with Kirsten murine sarcoma virus and MMCV mouse myc virus, two retroviruses carrying the v-Ki-ras and v-myc oncogenes, respectively. Efficient morphological transformation required coinfection with the two viruses, was dependent on the presence of high serum concentrations, and was not immediately accompanied by growth in soft agar. The doubly infected cells coordinately acquired the capacity for anchorage- and serum-independent growth during passage in culture. The appearance of such highly transformed cells was correlated with the emergence of a dominant clone, as suggested by an analysis of retrovirus integration sites. These results indicate that the concerted expression of v-Ki-ras and v-myc could induce rapid morphological transformation of nonestablished adrenocortical cells but that an additional genetic or epigenetic event was required to permit full transformation by these two oncogenes. In contrast, v-src, introduced by retrovirus infection in conjunction with v-myc, rapidly induced serum- and anchorage-independent growth. Therefore, the p60v-src protein-tyrosine kinase, unlike p21v-ras, is apparently not restricted in the induction of a highly transformed phenotype in adrenocortical cells. This system provides an in vitro model for the progressive transformation of epithelial cells by dominantly acting oncogenes.

Adrenal Cortex↗
PubMed1994

Regulation of normal and transformed tracheobronchial epithelial cell proliferation by autocrine growth factors.

Several peptide growth factors have been identified as autocrine regulators of normal tracheobronchial epithelial cells, including the transforming growth factors alpha and beta. Using in vitro tissue culture models of multistep neoplastic transformation as well as cell lines derived from human bronchogenic tumors, a significant number of growth factors have been found to function as autocrine factors for neoplastic tracheobronchial cells as well. In several instances, the regulation of the autocrine pathway is disrupted in neoplastic tracheobroncial cells compared with their normal counterparts. These results indicate that there are multiple aberrations in growth factor pathways occurring in tracheobronchial epithelial cells during progression to the neoplastic phenotype.

Animals↗
PubMed1992

ECG data compression by modeling.

This paper presents a novel algorithm for data compression of single lead Electrocardiogram (ECG) data. The method is based on Parametric modeling of the Discrete Cosine Transformed ECG signal. Improved high frequency reconstruction is achieved by separately modeling the low and the high frequency regions of the transformed signal. Differential Pulse Code Modulation is applied on the model parameters to obtain a further increase in the compression. Compression ratios up to 1:40 were achieved without significant distortion.

Algorithms↗
PubMed1995

Populations with constant immigration.

"We consider a Leslie-type model of a one-sex (female) population of natives with constant immigration. The fertility and mortality schedule of the natives may be below or above replacement level. Immigrants retain their fertility and mortality, their children adopt the fertility and mortality of the natives. It is shown how this model may be written in a homogeneous form (without additive term) with a Leslie-type matrix. Reproductive values of individuals in each age group are discussed in terms of a left eigenvector of this matrix. The homogeneous form of our projection model permits the transformation into a Markov chain with transient and recurrent states. The Markov chain is the basis for the definition of genealogies, which incorporate immigration. It is shown that genealogies describe the life histories of individuals in a population with immigration. We calculate absorption times of the Markov chain and relate them to genealogies. This extends the theory originally designed for closed populations to populations with immigration." (SUMMARY IN FRE)

Demography↗
PubMed1993

Expression of c-fos and c-myc protooncogenes in an immortalized hepatocyte line harbouring SV40 T antigen and hGH as transgenes.

A clonal hepatocyte line (FMH-202-2), derived from livers of fetal transgenic mice harbouring human growth hormone (hGH) and SV40 T antigen as transgenes, was used in the investigation of protooncogene expression involved in liver-specific growth control and/or in hepatocellular transformation. In this model system, representing an immortalized, yet untransformed phenotype, the transgenes hGH and SV40 T antigen were expressed constitutively. The c-fos protooncogene was induced by incubation with insulin, epidermal growth factor (EGF) and insulin-like growth factor (IGF-I) in a transient manner comparable to its expression in primary murine hepatocytes. Elucidation of second messenger mechanisms demonstrated that c-fos induction by hepatotrophic growth factors was not mediated by protein kinase C. In contrast to primary hepatocytes, the c-myc protooncogene exhibited a constitutive expression pattern which was independent of growth factor stimulation. These results indicate that apart from hGH and SV40 T antigen, c-myc may play a role in cellular immortalization, but that constitutive expression of these genes, even in combined coexpression, does not suffice to induce the transformed phenotype.

Animals↗