Sensors for chemicals based on electrically conductive immiscible HIPS/TPU blends containing carbon black

Carbon Black (CB)-containing immiscible polymer blends based on high-impact polystyrene/thermoplastic polyurethane (HIPS/TPU) were studied as sensing materials for an homologous series of alcohols, including, methanol, ethanol and 1-propanol. The studied immiscible blend was designed to exhibit a double-continuity structure i.e., the CB particles form chain-like network structures within the TPU phase, which forms a continuous phase within the HIPS matrix. Extruded HIPS/TPU/CB filaments produced by a capillary rheometer process at various shear rate levels were used for the sensing experiments. All filaments displayed a selective resistance changes upon exposure to the various alcohols combined with reproducibility and recovery behaviour. An attempt is made to identify the dominant mechanisms controlling the sensing process in a CB-containing immiscible polymer blend characterized by a double-continuity structure. The distinct structure and composition of the HIPS/TPU interphase region were found to have a crucial role in the sensing mechanism, determining the selectivity of the filaments toward the studied alcohols. Additionally, the sensing performance of HIPS/TPU/CB system is compared to recent results for TPU/CB compounds, polypropylene/TPU/CB and HIPS/ethylene vinyl acetate/CB immiscible polymer blends.     

Significance of DNA ploidy in the treatment of T1 glottic carcinoma

OBJECTIVE: To assess the role of DNA ploidy as a predictor of radioresistance in T1 glottic carcinoma. DESIGN: Case-control study. Flow cytometric DNA ploidy measurements were performed on formalin-fixed paraffin-embedded tumor specimens from 15 patients with T1 glottic laryngeal carcinomas in whom radiotherapy had failed and from a matched group of 15 patients in whom an identical radiotherapy regimen was curative. Analysis of DNA content was performed blind to outcome of treatment. SETTING: Academic tertiary referral medical center. PARTICIPANTS: Thirty patients with clinically staged T1, N0, M0 glottic carcinoma. INTERVENTION: All patients received radiation to the larynx through opposed lateral ports at a total dose of 64 to 70 Gy. RESULTS: Ten diploid and five aneuploid histograms were found in the resistant group, and six diploid and nine aneuploid histograms were found in the radiosensitive group. This difference was not statistically significant. A trend toward a higher relapse rate after radiotherapy (62.5%) among patients with diploid tumor compared with those with aneuploid tumor (35.7%) was noted. CONCLUSIONS: DNA ploidy did not predict response to radiotherapy in patients with T1 glottic cancer, probably because of the small number of patients. A trend toward lower risk of local recurrence after radiotherapy in aneuploid tumors was noted. A larger prospective study is needed to assess the value of DNA ploidy in the treatment of early laryngeal cancer.     

Constitutive overexpression of Cu/Zn superoxide dismutase exacerbates kainic acid-induced apoptosis of transgenic-Cu/Zn superoxide dismutase neurons

Cu/Zn superoxide dismutase (Cu/Zn SOD) is a key enzyme in the metabolism of oxygen free radicals. The gene resides on chromosome 21 and is overexpressed in patients with Down syndrome. Cultured neurons of transgenic Cu/Zn SOD (Tg-Cu/Zn SOD) mice with elevated activity of Cu/Zn SOD were used to determine whether constitutive overexpression of Cu/Zn SOD creates an indigenous oxidative stress that predisposes the Tg-Cu/Zn SOD neurons to added insults. Neurons from three independently derived Tg-Cu/Zn SOD strains showed higher susceptibility than nontransgenic neurons to kainic acid (KA)-mediated excitotoxicity, reflected by an earlier onset and enhanced apoptotic cell death. This higher susceptibility of transgenic neurons to KA-mediated apoptosis was associated with a chronic prooxidant state that was manifested by reduced levels of cellular glutathione and altered [Ca2+]i homeostasis. The data are compatible with the thesis that overexpression of Cu/Zn SOD creates chronic oxidative stress in the transgenic neurons, which exacerbates their susceptibility to additional insults such as KA-mediated excitotoxicity.     

Genetic influences on job satisfaction: A reply to Cropanzano and James.

Responds to the points made by R. Cropanzano and K. James (see record 1991-00462-001) concerning the article by R. D. Arvey et al (1989). The authors acknowledge that the Arvey et al study is based on a single design, makes use of a small and special sample, and, as such, is vulnerable to threats of internal and external validity. Nevertheless, after providing a more comprehensive conceptual and empirical context for the study, and after reviewing a number of the issues raised by Cropanzano and James, the authors conclude that it is not premature to accept the idea that work attitudes are partially genetically influenced. Indeed, the authors use behavioral genetic theory, together with data gathered in the Arvey et al study, to make specific point predictions regarding the outcomes of an array of studies that easily can be undertaken. Finally, the authors acknowledge that the comments and issues raised by Cropanzano and James, along with the interchange, can offer directions for future research in this important area. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Personality similarity in twins reared apart and together.

We administered the Multidimensional Personality Questionnaire (MPQ) to 217 monozygotic and 114 dizygotic reared-together adult twin pairs and 44 monozygotic reared-apart adult twin pairs. A four-parameter biometric model (incorporating genetic, additive versus nonadditive, shared family-environment, and unshared environment components) and five reduced models were fitted through maximum-likelihood techniques to data obtained with the 11 primary MPQ scales and its 3 higher order scales. Solely environmental models did not fit any of the scales. Although the other reduced models, including the simple additive model, did fit many of the scales, only the full model provided a satisfactory fit for all scales. Heritabilities estimated by the full model ranged from .39 to .58. Consistent with previous reports, but contrary to widely held beliefs, the overall contribution of a common family-environment component was small and negligible for all but 2 of the 14 personality measures. Evidence of significant nonadditive genetic effects, possibly emergenic (epistatic) in nature, was obtained for 3 of the measures. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

X-linked juvenile retinoschisis: localization between (DXS1195, DXS418) and AFM291wf5 on a single YAC

We studied 17 pedigrees with 108 affected males with X-linked juvenile retinoschisis (RS; McKusick No. 31270) and have analyzed all of the known polymorphic markers in the RS region of Xp22.1-p22.2 between DXS987 and DXS41. By haplotype analyses we found 7 individuals who showed crossovers in this interval surrounding RS. We previously reported AFM291wf5 as the centromeric boundary, and this remains unchanged in the present study. A new recombination was identified on the telomeric side at (DXS1195, DXS418). Our data support the locus order Xpter--(DXS987, DXS207, DXS1053, DXS43)--(DXS1195, DXS418)--(RS, DXS257, DXS999)--(AFM291wf5, DXS443)--DXS1052--(DXS1226, DXS274, DXS41)--Xcen; loci grouped in parentheses could not be mutually ordered by our genetic data. Physical mapping has indicated a distance of at most 900-1,000 kb between (DXS1195, DXS418) and AFM291wf5. No recombination was observed between RS and DXS257 which lies in our new interval of interest, but one critical individual was not informative with this marker. Our data now define the smallest RS inclusion interval. This interval is contained on a single YAC from which we have identified expressed sequences as candidate genes for RS.     

Amyloidogenic Properties of Peptides Derived from the VHL Tumor Suppressor Protein

The von Hippel-Lindau tumor suppressor protein (pVHL) is involved in maintaining cellular oxygen homeostasis through the regulated degradation of HIF-α. The intrinsically disordered nature of pVHL makes it prone to aggregation that impairs its function, and this is further aggravated in mutant versions of the protein, thus promoting tumor development. By using in silico analysis, we predicted six peptide fragments from pVHL to be amyloidogenic. This was verified for two of the peptides by biophysical approaches, which demonstrated self-assembly and formation of β-sheet-rich aggregates, which, under transmission electron microscopy, atomic force microscopy, and X-ray diffraction, displayed typical fibrillar amyloid characteristics. These motifs may serve as proxies for exploring the nature of pVHL aggregation.     

Methods development for epidemiologic investigations of the health effects of prolonged ozone exposure. Part II. An approach to retrospective estimation of lifetime ozone exposure using a questionnaire and ambient monitoring data (California sites)

An extensive body of data supports a relation between acute exposures to ambient ozone and the occurrence of various acute respiratory symptoms and changes in measures of lung function. In contrast, relatively few data are available on the human health effects that result from long-term exposure to ambient ozone, Current efforts to study long-term ozone-related health effects are limited by the methods available for ascertaining lifetime exposures to ozone. The present feasibility study was undertaken as part of the Health Effects Institute's Environmental Epidemiology Planning Project (Health Effects Institute 1994) to (1) determine whether, in the context of an epidemiologic study, reliable estimates can be obtained for lifetime exposures to ozone by combining estimates from lifetime residential histories, typical activity patterns during life, and residence-specific ambient ozone monitoring data; (2) identify the minimum data required to produce reliable estimates of lifetime exposure; and (3) analyze the relations between various estimates of lifetime ozone exposure and measures of lung function. A convenience sample of 175 first-year students at the University of California, Berkeley, who lived all of their lives in selected areas of California (the Los Angeles Basin or the San Francisco Bay Area), were studied on two occasions (test and retest or test sessions 1 and 2), five to seven days apart. Residential and lifestyle data were obtained from a questionnaire: residence-based ambient ozone exposure values were assigned by interpolation of ambient ozone monitoring data to residential locations. Estimated lifetime exposure was based on average ozone levels between 10 a.m. and 6 p.m. and hours of exposure to ozone concentrations greater than 60 parts per billion (ppb). "Effective" lifetime exposure to ozone was based on a weighted average of estimated time spent in different ambient ozone environments as determined by different combinations of activity data. Pulmonary function was evaluated with flows and volumes from maximum expiratory flow-volume curves and slope of phase III of the single-breath nitrogen washout (SBNW) curves. Although the test-retest reliability of the residential history was acceptably high only for first and second residences, most of the unreliability for other residences came from residences occupied for relatively short durations. Therefore, the test-retest reliability of estimated lifetime exposure to ozone was high, with intraclass correlations greater than 0.90 for all approaches evaluated. Multiple, linear regression analyses showed a consistently negative relation between estimates of lifetime exposure to ozone and flows that reflect the physiology of pulmonary small airways. No relation was observed between lifetime ozone exposure and forced expiratory volume or the slope of phase III, and the relation between lifetime exposure and forced expiratory volume in one second was inconsistent. The results of the flow measures were unaffected by the method used to estimate lifetime exposure and gave effect estimates that were nearly identical. The data from this study indicate that useful and reproducible estimates of lifetime ozone exposure can be obtained in epidemiologic studies by using a residential history. However, the total burden of ozone to which the subjects were exposed cannot be determined accurately from such data. Nonetheless, the estimates so obtained appear to be associated with alterations in pulmonary function that are consistent with the predicted site of maximum effect of ozone in the human lung.