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PubMed1989

Continuous increase in blood lactate concentration during different ramp exercise protocols.

The applicability of a continuous model description of the blood lactate concentration [( La-]) vs. O2 uptake (VO2) relationship was studied in nine healthy male volunteers during three different ramp exercise protocols. The work rate was increased at either 8, 15, or 50 W/min. The continuous model for [La-] = â + b exp(ĉVO2) was compared statistically with a previously proposed log-log transformation model for the [La-] and VO2 variables. It was found that the mean square error was significantly less for the continuous as opposed to the log-log model (P less than 0.01) by analysis of variance pooled across all three ramp slopes. The mean square errors from the individual ramp slopes were also significantly less for the continuous model by paired t test (P less than 0.05). It was observed that the major contributor to the increased error of the log-log model was at VO2's at or above the intersection point (lactate threshold) of the two linear log-transformed segments. The log-log transformation does not appear to relate to any physiological process. The lactate slope index, taken as the point where the slope of the relationship between [La-] and VO2 (i.e., d[La-]/dVO2) equaled 1, occurred at a mean VO2 of 2.25 and 2.37 l/min for the 15- and 8-W/min ramp slopes, respectively, but at 2.76 l/min for the 50-W/min ramp (P less than 0.05). It is concluded that [La-] increases as a continuous function with respect to VO2 across a wide range of ramp work rate slopes.

Adult↗
PubMed1988

Characterization of activated proto-oncogenes in chemically transformed Syrian hamster embryo cells.

The Syrian hamster embryo (SHE) cell transformation model has been used by many investigators to study the multistep process of neoplastic transformation induced by chemical carcinogens. In this study we have attempted to determine if activated proto-oncogenes are present in the transformed cells induced by a variety of chemical carcinogens. Twelve carcinogen-induced hamster cell lines, established by treatment of normal SHE cells with benzo[a]pyrene, diethylstilbestrol, or asbestos, were examined. One spontaneously transformed cell line (BHK-A) was also studied. Some of the cell lines were also tested for oncogene activation at the preneoplastic stage, before they acquired tumorigenic potential. DNAs from normal, preneoplastic, and neoplastic cells were tested by transfection into mouse NIH 3T3 cells, and morphologically transformed foci were scored on the contact-inhibited monolayer of 3T3 cells. The frequency of focus formation for normal SHE cell DNA was less than 0.0008 foci/microgram DNA, while approximately 40% (5 of 12) of the DNAs from carcinogen-induced, tumorigenic hamster cell lines induced foci at a frequency of greater than or equal to 0.012 foci/microgram DNA. The other seven carcinogen-induced cell lines and the BHK-A cells were negative (less than 0.002 foci/microgram DNA). When the DNAs from transformed foci induced by the five positive cell lines were retransfected into NIH 3T3 cells, the frequency of secondary foci of 3T3 cells was as much as 50-fold higher (1.34 foci/microgram DNA) than with the primary transfectants. DNAs from transformed foci or tumors derived from transformed foci were screened by Southern blot analyses with known oncogenes and with a hamster repetitive DNA probe for the presence of transfected hamster oncogenes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Retinoic acid enhancement of an early step in the transformation of mouse epidermal cells in vitro.

Retinoic acid has been reported to act as an inhibitor and as an enhancer of mouse skin carcinogenesis in vivo. However, no in vitro cell transformation model has been reported to be sensitive to both effects. In an attempt to provide such a model, the effect of retinoic acid on an early step in carcinogen-induced transformation of mouse epidermal cell line 271c was measured using a recently described assay. The step observed is altered response to extracellular Ca2+ as an epidermal terminal differentiation signal. In six out of twelve experiments retinoic acid increased the frequency of altered colonies resulting from treatment with three chemical carcinogens. The enhancement effect was stronger after DMBA treatment than MNNG or MCA, resulting in up to a 13.7-fold increase in the frequency of colonies exhibiting altered terminal differentiation (TF). On the other hand, up to a 10-fold decrease in TF was observed in other experiments. Both the enhancement and inhibitory effects were greater at the higher doses of retinoic acid tested in the range of 10(-10) - 10(-7) M. Variations in cloning efficiency or surviving colony density did not account for the effects on TF. Enhancement effects tended to be observed at lower doses of carcinogen, or in experiments in which TF resulting from treatment with carcinogen alone was in the lower range observed. However, the factors determining each effect have yet to be defined. The enhancement effect of retinoic acid was not merely suppression of the phenotypic endpoint of the in vitro assays, because treatment of carcinogen-altered cells with retinoic acid or TPA in vitro also enhanced their tumorigenicity in vivo compared to acetone controls. These findings suggest that studies of the determinants of retinoid activity should be a prerequisite to their use in chemoprevention.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1998

Protein structure analysis using the resonant recognition model and wavelet transforms.

An approach based on the resonant recognition model and the discrete wavelet transform is introduced here for characterising proteins' biological function. The protein sequence is converted into a numerical series by assigning the electron-ion interaction potential to each amino acid from N-terminal to C-terminal. A set of peaks is found after performing a wavelet transform onto a numerical series representing a group of homologous proteins. These peaks are related to protein structural and functional properties and named characteristic vector of that protein group. Further more, the amino acids contributing mostly to a protein's biological functions, the so-called 'hot spots' amino acids, are predicted by the continuous wavelet transform. It is found that the hot spots are clustered around the protein's cleft structure. The wavelets approach provides a novel methods for amino acid sequence analysis as well as an expansion for the newly established macromolecular interaction model: the resonant recognition model.

Amino Acid Sequence↗
PubMed2001

Inhibition of cellular transformation by berry extracts.

Recent studies have examined and demonstrated the potential cancer chemopreventive activity of freeze-dried berries including strawberries and black raspberries. Although ellagic acid, an abundant component in these berries, has been shown to inhibit carcinogenesis both in vivo and in vitro, several studies have reported that other compounds in the berries may also contribute to the observed inhibitory effect. In the present study, freeze-dried strawberries (Fragara ananassa, FA) or black raspberries (Rubus ursinus, RU) were extracted, partitioned and chromatographed into several fractions (FA-F001, FA-F003, FA-F004, FA-F005, FA-DM, FA-ME from strawberries and RU-F001, RU-F003, RU-F004, RU-F005, RU-DM, RU-ME from black raspberries). These extracts, along with ellagic acid, were analyzed for anti-transformation activity in the Syrian hamster embryo (SHE) cell transformation model. None of the extracts nor ellagic acid by themselves produced an increase in morphological transformation. For assessment of chemopreventive activity, SHE cells were treated with each agent and benzo[a]pyrene (B[a]P) for 7 days. Ellagic acid, FA-ME and RU-ME fractions produced a dose-dependent decrease in transformation compared with B[a]P treatment only, while other fractions failed to induce a significant decrease. Ellagic acid, FA-ME and RU-ME were further examined using a 24 h co-treatment with B[a]P or a 6 day treatment following 24 h with B[a]P. Ellagic acid showed inhibitory ability in both protocols. FA-ME and RU-ME significantly reduced B[a]P-induced transformation only when co-treated with B[a]P for 24 h. These results suggest that a methanol extract from strawberries and black raspberries may display chemopreventive activity. The possible mechanism by which these methanol fractions (FA-ME, RU-ME) inhibited cell transformation appear to involve interference of uptake, activation, detoxification of B[a]P and/or intervention of DNA binding and DNA repair.

Animals↗
PubMed1990

Activation of cellular oncogenes by chemical carcinogens in Syrian hamster embryo fibroblasts.

Carcinogen-induced point mutations resulting in activation of ras oncogenes have been demonstrated in various experimental systems such as skin carcinogenesis, mammary, and liver carcinogenesis. In many cases, the data support the conclusion that these point mutations are critical changes in the initiation of these tumors. The Syrian hamster embryo (SHE) cell transformation model system has been widely used to study the multistep process of chemically induced neoplastic transformation. Recent data suggest that activation of the Ha-ras gene via point mutation is one of the crucial events in the transformation of these cells. We have now cloned the c-Ha-ras proto-oncogene from SHE cDNA-libraries, and we have performed polymerase chain reaction and direct sequencing to analyze tumor cell lines induced by different chemical carcinogens for the presence of point mutations. No changes were detectable at codons 12, 13, 59, 61, and 117 or adjacent regions in tumor cell lines induced by diethylstilbestrol, asbestos, benzo(a)pyrene, trenbolone, or aflatoxin B1. Thus, it is not known whether point mutations in the Ha-ras proto-oncogene are essential for the acquisition of the neoplastic phenotype of SHE cells. Activation of other oncogenes or inactivation of tumor suppressor genes may be responsible for the neoplastic progression of these cells. However, in SHE cells neoplastically transformed by diethylstilbestrol or trenbolone, a significant elevation of the c-Ha-ras expression was observed. Enhanced expression of c-myc was detected in SHE cells transformed by benzo(a)pyrene or trenbolone.

Animals↗
PubMed1994

Transformational partnership for delivery of R.N. baccalaureate education: a service/education leadership model.

A transformational partnership model between a consortium of rural community hospitals and a private Christian university reflects a shared vision for R.N. baccalaureate degree completion. The model includes a community-wide system to promote and sustain accessible, high-quality education for the place-bound R.N. who desires to achieve a B.S.N. Stakeholders, experiencing the current climate of change in health care, benefit from this innovative service/education leadership model. The collaboration built on a commitment to common goals and shared resources seeks to prepare individuals who apply critical thinking to practice settings along with the continuum of care.

Christianity↗
PubMed2000

Estimation of regression parameters and the hazard function in transformed linear survival models.

An estimator of the regression parameters in a semiparametric transformed linear survival model is examined. This estimator consists of a single Newton-like update of the solution to a rank-based estimating equation from an initial consistent estimator. An automated penalized likelihood algorithm is proposed for estimating the optimal weight function for the estimating equations and the error hazard function that is needed in the variance estimator. In simulations, the estimated optimal weights are found to give reasonably efficient estimators of the regression parameters, and the variance estimators are found to perform well. The methodology is applied to an analysis of prognostic factors in non-Hodgkin's lymphoma.

Analysis of Variance↗
PubMed2006

Geometric stability of intracavitary pulsed dose rate brachytherapy monitored by in vivo rectal dosimetry.

BACKGROUND AND PURPOSE: To evaluate geometric stability of applicator and rectum during pulsed dose rate (PDR) intracavitary brachytherapy. PATIENTS AND METHODS: A total of 14 patients with cervical cancer (stages IIB-IVA) were analysed retrospectively. A dose of 10 Gy to point A was prescribed per brachytherapy session, and PDR was given with 1 Gy/pulse, 1 pulse/h, using a ring applicator (Varian). A rectal dosimeter consisting of five diodes spaced by 1.5 cm was routinely placed in the rectum. The diodes detected the progression of each pulse of radiation, as the stepping source was advanced through the applicator. A mathematical model has been developed for spatial analysis of the pattern of the dose readings. The model transforms dose measurement into a quantification of the geometric relationship between rectum diodes and applicator. RESULTS: The model could be used for all treatment sessions, and the relative positions of diodes and applicator were calculated for each pulse of radiation. The SD of displacements during the treatment was below 2.8mm in all directions for all patients. The mean SD in lateral, longitudinal and anterior-posterior directions were 1.2 +/- 0.7, 1.2 +/- 0.7 and 0.9 +/- 0.6 mm, respectively. The mean measurement uncertainty was below 0.8 +/- 0.5 mm in all directions. CONCLUSIONS: A new mathematical method has been developed, enabling us to quantitate and monitor relative positions of applicator and rectal diodes during a PDR treatment. The spatial relation between rectal dosimeter and applicator was very stable during extended PDR treatments suggesting that the geometric stability of PDR treatment is at the same level as the stability reported for HDR brachytherapy.

Algorithms↗
PubMed1999

JNK activation is required for JB6 cell transformation induced by tumor necrosis factor-alpha but not by 12-O-tetradecanoylphorbol-13-acetate.

Signal transduction via mitogen-activated protein kinase pathways plays a key role in a variety of cellular responses, including cell proliferation, differentiation, tumor promotion, and cell death. c-Jun N-terminal kinases (JNKs) are identified as members of the mitogen-activated protein kinase family and are known to phosphorylate and activate several transcription factors, including c-Jun, ATF, and Elk-1. However, the role of JNK activation in tumor promotion is not yet defined. Because previous studies have indicated that exposure of JB6 Cl 41 cells to either 12-O-tetradecanoylphorbol-13-acetate (TPA) or tumor necrosis factor-alpha (TNF-alpha) results in cell transformation, we investigated the role of JNKs in this biological process by using dominant negative JNK(1) and the cell transformation model JB6 Cl 41 cells. Incubation of Cl 41 cells with TNF-alpha led to cell transformation and activation of JNKs. Introduction of the dominant negative mutant of JNK(1) into JB6 Cl 41 cells specifically inhibited TNF-alpha-induced activation of JNKs, but not Erks and p38 kinases. Most importantly, expressing dominant negative mutant JNK(1) inhibited TNF-alpha-induced cell transformation but not TPA-induced cell transformation. Our results directly demonstrated for the first time that JNK activation is required for TNF-alpha- but not TPA-induced cell transformation.

Animals↗
PubMed1995

A spectral network model of pitch perception.

A model of pitch perception, called the spatial pitch network or SPINET model, is developed and analyzed. The model neurally instantiates ideas from the spectral pitch modeling literature and joins them to basic neural network signal processing designs to stimulate a broader range of perceptual pitch data than previous spectral models. The components of the model are interpreted as peripheral mechanical and neural processing stages, which are capable of being incorporated into a larger network architecture for separating multiple sound sources in the environment. The core of the new model transforms a spectral representation of an acoustic source into a spatial distribution of pitch strengths. The SPINET model uses a weighted "harmonic sieve" whereby the strength of activation of a given pitch depends upon a weighted sum of narrow regions around the harmonics of the nominal pitch value, and higher harmonics contribute less to a pitch than lower ones. Suitably chosen harmonic weighting functions enable computer simulations of pitch perception data involving mistuned components, shifted harmonics, and various types of continuous spectra including rippled noise. It is shown how the weighting functions produce the dominance region, how they lead to octave shifts of pitch in response to ambiguous stimuli, and how they lead to a pitch region in response to the octave-spaced Shepard tone complexes and Deutsch tritones without the use of attentional mechanisms to limit pitch choices. An on-center off-surround network in the model helps to produce noise suppression, partial masking, and edge pitch. Finally, it is shown how peripheral filtering and short-term energy measurements produce a model pitch estimate that is sensitive to certain component phase relationships.

Cochlea↗
PubMedDate not supplied

Epigenetic events during the process of cell transformation induced by carcinogens (review).

Recent studies clearly demonstrate that several environmental carcinogens lack the ability to initially induce genetic damage. In that view, multistage chemical carcinogenesis may be processed under the control of a variety of epigenetic events in addition to genotoxic impacts. The understanding of this mechanism as reviewed in this report requires knowledge of early changes induced by carcinogens in target cells, biochemical, biological and molecular reactions closely related to both sides of the growth equation: cell proliferation and programmed death. Among several cell transformation models, the most suitable for carcinogen detection and mechanistic study is the Syrian hamster embryo (SHE) cell transformation assay. This closely mimics the multistage carcinogenesis and we can examine, in a relatively short time (8 days), the mechanisms by which genotoxic and non-genotoxic agents may increase the frequency of cell transformation as a preneoplastic end-point. The mode of action of hundred of compounds, carcinogens and non-carcinogens, has been explored so far using one-stage and two-stage treatment protocols. In general, with the two-stage protocol, all carcinogens, irrespective of their genotoxic or non-genotoxic potential, give unambiguous positive results. Since perturbations of cell proliferation and death are considered essential events in the process of carcinogenesis, studies have been conducted on the dysregulation of two specific parameters, the induction of ornithine decarboxylase (ODC) an enzyme related to cell proliferation, and the apoptosis rate, when SHE cells are exposed to carcinogens. In one-stage treatment (5 h-24 h), only the promoter TPA induces ODC activity, while other carcinogens do not increase this activity. Using the two-stage exposure protocol (1 h xenobiotic/5 h TPA), all carcinogens both genotoxic and non-genotoxic, are able to stimulate ODC activity above the level obtained with TPA alone. Based on the two-stage treatment with carcinogens a close relationship can be obtained between the ODC superinduction and the increase of morphological cell transformation frequency. In cancer development, it is postulated that the inhibition of apoptosis may help altered cells to escape cell death and acquire a tumorigenic phenotype. Two-stage treatment carcinogen/TPA, effectively decreases the apoptotic rate. This is accompanied by an upregulation of the Bcl-2 oncoprotein, a well-known apoptotic inhibitor. However, treatment with a non-carcinogen phthalic anhydride, also inhibits apoptosis while it does not superinduce ODC activity. Although inhibition of apoptosis is not specific to the carcinogenic compound, both superinduction of ODC activity and inhibition of apoptosis via Bcl-2 upregulation may cooperate during the early stages of the carcinogenic process. In a long-term stage transformation assay, the rate of transformed colonies is relatively low (2-8%) bringing about the slow evolution of tumoral disease in humans and tumoral induction in rodents. This could be the consequence of the activation of various cellular repair mechanisms during the exposure time. Experimental data reported so far point out that genotoxic and non-genotoxic carcinogens, thought to be more active in the initiation or in the promotion stage, must share the same stage pathway leading to cancer development.

Animals↗
PubMed2005

On the concept of model structural error.

A consideration of model structural error leads to some particularly interesting tensions in the model calibration/conditioning process. In applying models we can usually only assess the total error on some output variable for which we have observations. This total error may arise due to input and boundary condition errors, model structural errors and error on the output observation itself (not only measurement error but also as a result of differences in meaning between what is modelled and what is measured). Statistical approaches to model uncertainty generally assume that the errors can be treated as an additive term on the (possibly transformed) model output. This allows for compensation of all the sources of error, as if the model predictions are correct and the total error can be treated as "measurement error." Model structural error is not easily evaluated within this framework. An alternative approach to put more emphasis on model evaluation and rejection is suggested. It is recognised that model success or failure within this framework will depend heavily on an assessment of both input data errors (the "perfect" model will not produce acceptable results if driven with poor input data) and effective observation error (including a consideration of the meaning of observed variables relative to those predicted by a model).

Environment↗
PubMed1989

On the mechanisms involved in the inhibitory and stimulating actions of transforming growth factor-beta on porcine testicular steroidogenesis: an in vitro study.

By using immature porcine Leydig cells cultured in defined medium as a model, transforming growth factor-beta (TGF beta) was shown to exert a dramatic inhibitory effect on their basal and human chorionic gonadotropin (hCG) (or 8-bromo-cyclic AMP) stimulated dehydroepiandrosterone secretion, in the presence or absence of saturating concentrations of exogenous (low density lipoprotein) cholesterol substrate. In contrast, TGF beta exerted both a stimulating and inhibitory effect on testosterone secretion: while hCG-stimulated testosterone secretion was enhanced by low doses of TGF beta (0.06-0.4 ng/ml, 48 h), it was decreased with higher concentrations of TGF beta (2.5-10 ng/ml, 48 h). The data obtained show that the inhibitory action of TGF beta on testicular steroidogenesis was related to a decrease in pregnenolone formation by affecting a step(s) distal to cyclic AMP formation but before cholesterol association with cytochrome P-450 side-chain cleavage. As for the stimulatory effect of TGF beta on testosterone formation, this was mainly related to an increase (about 2-fold) in 3 beta-hydroxysteroid dehydrogenase/isomerase activity (ED50 0.05 ng/ml, 2 X 10(-13) M). The results indicate that the (short-term) steroidogenic stimulatory action of luteinizing hormone (LH)/hCG is antagonized by high concentrations of TGF beta by decreasing pregnenolone formation while it is enhanced by the stimulating action of low concentrations of TGF beta exerted on 3 beta-hydroxy steroid dehydrogenase/isomerase activity.

Androgens↗
PubMed2003

A one-parameter neural activation to muscle activation model: estimating isometric joint moments from electromyograms.

Nonlinearities have been observed in the isometric EMG-force relationship. However, these are generally not included when using EMG-driven Hill-type muscle models that account for muscle activation dynamics. In this paper, we present a formulation for a one-parameter transformation model (i.e., A-model) that accounts for the type of physiological nonlinearities observed at low levels of force. The general shape for the curvilinear portion of the curve was based on phenomenological data reported by Woods and Bigland-Ritchie. The one-parameter A-model is easy to implement, and when used with an EMG-driven Hill-type model, was shown to provide a better fit of the measured joint moment. Optimization methods were used to determine the appropriate curvature of the relationship for each muscle, and thus introduced a degree of "tuning" to each subject.

Action Potentials↗
PubMed1994

Solubilization of lignin by the ruminal anaerobic fungus Neocallimastix patriciarum.

The ability of the ruminal anaerobic phycomycete Neocallimastix patriciarum to digest model lignin compounds and lignified structures in plant material was studied in batch culture. The fungus did not degrade or transform model lignin compounds that were representative of the predominant intermonomer linkages in lignin, nor did it solubilize acid detergent lignin that had been isolated from spear grass. In a stem fraction of sorghum, 33.6% of lignin was apparently solubilized by the fungus. Solubilization of ester- and either-linked phenolics accounted for 9.2% of the lignin released. The amounts of free phenolic acids detected in culture fluid were equivalent to the apparent loss of ester-linked phenolics from the sorghum substrate. However, the fungus was unable to cleave the ether bond in hydroxycinnamic acid bridges that cross-link lignin and polysaccharide. It is suggested that the majority of the solubilized lignin fraction was a lignin carbohydrate complex containing ether-linked hydroxycinnamic acids. The lignin carbohydrate complex was probably solubilized through dissolution of xylan in the lignin-xylan matrix rather than by lignin depolymerization.

Anaerobiosis↗
PubMed1989

Fate of 7,12-dimethylbenz(a)anthracene in the mouse mammary gland during initiation and promotion stages of carcinogenesis in vitro.

Metabolic conversion and distribution of the products of 7,12-dimethylbenz(a)anthracene (DMBA) were analyzed in the mouse mammary cell transformation model in organ culture. In order to determine the levels of uptake of DMBA, the glands were exposed to the transforming dosage of the procarcinogen (7.8 microM, 20 microCi/ml) for 24 h, and the level of uptake was determined to be 8 x 10(4) cpm/mg of tissue. Subsequently, the glands were incubated in DMBA-free medium, and distribution of the radioactivity in DNA and in the acid-insoluble materials was measured. Data showed that, in addition to the 24-h DMBA treatment period, the initiation stage extends for another 3 h when the incubation is continued in DMBA-free medium. A saturation level of uptake of [3H]DMBA into the whole gland was observed at 12 h, while DMBA was continually metabolized with the products being bound to DNA and to the acid-insoluble fractions throughout the entire incubation period with or without DMBA. The three major adducts identified were anti-DMBA-3,4-diol-1,2-epoxide (DMBADE):deoxyguanosine, syn-DMBADE:deoxyadenosine, and anti-DMBADE:deoxyadenosine. Qualitatively the adduct profiles remained similar. However, with the additional 3-h incubation in DMBA-free medium, the three major DMBA-DNA adducts increased slightly by 6.5 to 7.5%. Thus the total 27-h time period can be considered as the duration of the initiation stage in the DMBA-induced carcinogenesis of mouse mammary cells in organ culture. Therefore the subsequent 6-h incubation in DMBA-free medium may be considered as within the promotional stage, and at the same time period the levels of the three DNA adducts decreased significantly by 67.5 to 84.1% (P less than 0.001).

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1996

Application of in vitro cell transformation assays to predict the carcinogenic potential of chemicals.

Genotoxicity test batteries have become a standard fool for identifying chemicals that may have potential carcinogenic risk to humans. It is now apparent, however, that the use of genotoxicity batteries for assessing carcinogenic potential has limitations including an overall low specificity and a limited ability to detect carcinogens acting via 'nongenotoxic' mechanisms. In vitro cell transformation models, because they measure a chemical's ability to induce preneoplastic or neoplastic endpoints regardless of mechanism, may fulfil the current need for an in vitro biologically relevant model with increased predictiveness for determining carcinogenic potential. This review will focus on data demonstrating the similarities of chemically induced cell transformation in vitro to carcinogenesis in vivo. Furthermore, a growing database demonstrating a high overall correlation between cell transformation results with those of the rodent bioassay will also be discussed. Finally, the inclusion of cell transformation approaches for assessing the carcinogenic potential of chemicals relative to currently used genotoxicity batteries will be presented.

Animals↗