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Additional Goal (additional + goal)
Selected AbstractsEffects of 17 ,-estradiol exposure on Xenopus laevis gonadal histopathologyENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 5 2010Jeffrey C. Wolf Abstract The natural estrogen 17 ,-estradiol (E2) is a potential environmental contaminant commonly employed as a positive control substance in bioassays involving estrogenic effects. The aquatic anuran Xenopus laevis is a frequent subject of reproductive endocrine disruptor research; however, histopathological investigations have tended to be less than comprehensive. Consequently, a study was designed to characterize gross and microscopic changes in the gonads of X. laevis as a result of E2 exposure. Additional goals of this study, which consisted of three separate experiments, included the standardization of diagnostic terminology and criteria, the validation of statistical methodology, and the establishment of a half maximal effective concentration (EC50) for E2 as defined by an approximately 50% conversion of presumptive genotypic males to phenotypic females. In the first experiment, frogs were exposed to nominal concentrations of 0, 0.2, 1.5, or 6.0,µg/L E2. From these experimental results and those of a subsequent range finding trial, the EC50 for E2 was determined to be approximately 0.2,µg/L. This E2 concentration was utilized in the other two experiments, which were performed at different facilities to confirm the reproducibility of results. Experiments were conducted according to Good Laboratory Practice guidelines, and the histopathologic evaluations were peer reviewed by an independent pathologist. Among the three trials, the histopathological findings that were strongly associated with E2-exposure (p,<,0.001 to 0.0001) included an increase in the proportion of phenotypic females, mixed sex, dilated testis tubules, dividing gonocytes in the testis, and dilated ovarian cavities in phenotypic ovaries. A comparison of the gross and microscopic evaluations suggested that some morphologic changes in the gonads may potentially be missed if studies rely entirely on macroscopic assessment. Environ. Toxicol. Chem. 2010;29:1091,1105. © 2010 SETAC [source] Diabetes, pre-diabetes and associated risks on Minnesota code-indicated major electrocardiogram abnormality among Chinese: a cross-sectional diabetic study in Fujian province, southeast ChinaOBESITY REVIEWS, Issue 4 2009L. Lin Summary The goal of this study was to determine the prevalence of diabetes mellitus (DM), impaired glucose regulation (IGR) and related metabolic disorders (overweight, obesity and hypertension) in a Chinese population (20,74 years old). An additional goal was to investigate the relationship between glucose metabolism and the Minnesota code-indicated major abnormal electrocardiogram (MA-ECG). There were 3960 individuals selected from urban and rural areas of Fujian, China from July 2007 to May 2008 by multistage-stratified sampling. Ultimately, data from 3208 subjects (20,74 years old) were analysed (including physical measurements, blood biochemical analysis, oral glucose tolerance test and 12-lead resting ECG). According to World Health Organization diagnostic criteria, the prevalence rates of DM and IGR were 9.51% (male, 10.08%; female, 9.14%) and 14.40% (male, 14.48%; female, 14.35%) respectively. Newly diagnosed DM was found in 53.44% of the diabetic subjects. Based on the 2000 China census, the age-standardized prevalence rates of DM and IGR were 7.19% (male, 7.74%; female, 6.61%) and 11.96 % (male, 12.35%; female, 11.56%) respectively. The age-standardized prevalence rates of DM and IGR in urban areas (7.74% and 12.97% respectively) were slightly but no significantly higher than in rural areas (6.67%, 10.86%). The prevalence rates of overweight, obesity and hypertension were 25.50%, 3.52% and 28.52% respectively (age- and sex- standardized rates: 23.69%, 3.02 % and 22.45 %). After adjusting for other confounding risk factors, multiple logistic regression analysis showed that DM and impaired glucose tolerance were independent risk factors for MA-ECG. Non-diabetic subjects with increased 30-min plasma glucose (PG) after an oral glucose load had a higher risk of MA-ECG after adjusting for other risk factors, especially in those with normal glucose tolerance but with 30-min PG , 7.8 mmol L,1 (odds ratio = 1.371 [1.055,1.780]). The prevalence rates of DM and IGR as well as other metabolic disorders have increased dramatically in the last decade in China, especially in rural areas, with many undiagnosed cases of DM. Even slightly elevated PG levels may predict early cardiovascular events. [source] UV-B-induced DNA damage and expression of defence genes under UV-B stress: tissue-specific molecular marker analysis in leavesPLANT CELL & ENVIRONMENT, Issue 9 2001G. Kalbin Abstract The aim of this study was to investigate the regulatory effect of ultraviolet-B (UV-B) radiation on a number of key stress response genes found in the epidermis and mesophyll of Pisum sativum L., Argenteum mutant. This mutant was chosen for the ease with which the entire epidermis can be removed from the mesophyll tissue. An additional goal was to explore the potential modifying effect of pre-acclimation of plants to UV-B radiation prior to exposure by UV-B during treatment. Results showed that mRNA accumulation was similar during acute short-term UV-B exposure for chalcone synthase (Chs) and short-chain alcohol dehydrogenase (SadA) in both epidermis and mesophyll. In contrast, the mRNA levels differed considerably between tissues for phenylalanine ammonia lyase, chalcone isomerase and lipid transfer protein. After 24 h incubation in visible light after cessation of UV-B exposure, the regulation of mRNA levels also differed between Chs and SadA, the former showing no expression in the epidermis and the latter none in the mesophyll. Acclimation to low UV-B levels before acute exposures resulted in delayed induction of Chs and SadA. Measurements of UV-B-induced cyclobutane pyrimidine dimers (CPDs) showed a greater formation in epidermis than in mesophyll. In addition, acclimation at low UV-B levels resulted in significantly higher basal levels of CPDs than in non-acclimated plants in both mesophyll and epidermis and also in increased damage in concomitant acute exposures. The lack of correlation between the number of CPDs and levels of transcripts for defence genes, indicates that DNA damage does not control transcription of these genes. [source] Association of cytokine gene polymorphisms in CWP and its severity in Turkish coal workersAMERICAN JOURNAL OF INDUSTRIAL MEDICINE, Issue 10 2008Ilker Ates PhD Abstract Background Cytokines appear to play a key role in some inflammatory reactions affecting the interactions among pro- and anti-inflammatory mechanisms that result in several diseases such as coal workers' pneumoconiosis (CWP). In this study, to determine the cytokine gene profiles of Turkish coal miners, we performed genotyping analysis to investigate the polymorphisms of CWP-related pro-inflammatory (TNFA, IL1A, IL1B, and IL6) and anti-inflammatory cytokines (IL-1RN and TGFB1). An additional goal was to observe whether these cytokine gene polymorphisms influence the development risk and severity of. Methods Genotyping was carried out by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique. Results TNFA (,238) gene polymorphism principally affected CWP development and severity (OR,=,3.47: 95% CI, 1.12,10.77 and OR,=,4.30: 95% CI, 1.25,14.74, respectively) and also risk of CWP (OR,=,3.79: 95% CI, 1.37,10.46). The TNFA (,308) variant was associated with a risk for the CWP severity (OR,=,2.84: 95% CI, 1.08,7.39). A protective effect of IL6 was found on the development (OR,=,0.48: 95% CI, 0.21,0.93) and severity of CWP (OR,=,0.37: 95% CI, 0.15,0.91). Conclusions We suggest that TNFA (,238) variant may be a risk factor in both development and the severity of CWP, while TNFA (,308) variant seems to be important only in disease severity. On the other hand, IL6 variant may have a protective effect on the development and disease severity. Am. J. Ind. Med. 51:741,747, 2008. Published 2008 Wiley-Liss, Inc. [source] | |||||||||||||