Cancer cells possess different isotopic enrichment: Isotopic induced functionalizations of normal DNA mutations leading to cancer.

Although the dynamics of telomeres during the life expectancy of normal cells has been extensively studied, there are still some unresolved issues regarding this research field. For example, the conditions required for telomere shortening leading to malignant transformations are not fully understood. In this work, we mass analyzed DNA of normal and cancer cells for comparing telomere isotopic compositions of white blood cells and cancer cells.

Wild Zebrafish Sentinels: Biological Monitoring of Site Differences Using Behavior and Morphology.

Environmental change poses a devastating risk to human and environmental health. Rapid assessment of water conditions is necessary for monitoring, evaluating, and addressing this global health danger. Sentinels or biological monitors can be deployed in the field using minimal resources to detect water quality changes in real time, quickly and cheaply.

Collective Behavior in Wild Zebrafish.

Anthropogenic change is expected to alter environments at alarming rates. To predict the impact of modified environments on social behavior, we must study the relationship between environmental features and collective behavior in a genetically tractable model, zebrafish (). Here, we conducted a field study to examine the relationship between salient environmental features and collective behavior in four populations of zebrafish.

Exposure to Spectracide® causes behavioral deficits in Drosophila melanogaster: Insights from locomotor analysis and molecular modeling.

This study was focused on gaining insights into the mechanism by which the herbicide- Spectracide®, induces oxidative stress and alters behavior in Drosophila melanogaster. Exposure to Spectracide® (50%) significantly (p < 0.05) reduced the negative geotaxis response, jumping behavior and dampened locomotor activity rhythm in adult flies compared to non-exposed flies.

ATF4 regulates arsenic trioxide-mediated NADPH oxidase, ER-mitochondrial crosstalk and apoptosis.

Arsenic is a mitochondrial toxin, and its derivatives, such as arsenic trioxide (ATO), can trigger endoplasmic reticulum (ER) and the associated unfolded protein response (UPR). Here, we show that arsenic induction of the UPR triggers ATF4, which is involved in regulating this ER-mitochondrial crosstalk that is important for the molecular pathogenesis of arsenic toxicity. Employing ATF4 and ATF4 MEFs, we show that ATO induces UPR and impairs mitochondrial integrity in ATF4 MEF cells which is largely ablated upon loss of ATF4.

Perturbations in dopamine synthesis lead to discrete physiological effects and impact oxidative stress response in Drosophila.

The impact of mutations in four essential genes involved in dopamine (DA) synthesis and transport on longevity, motor behavior, and resistance to oxidative stress was monitored in Drosophila melanogaster. The fly lines used for this study were: (i) a loss of function mutation in Catecholamines up (Catsup(26)), which is a negative regulator of the rate limiting enzyme for DA synthesis, (ii) a mutant for the gene pale (ple(2)) that encodes for the rate limiting enzyme tyrosine hydroxylase (TH), (iii) a mutant for the gene Punch (Pu(Z22)) that encodes guanosine triphosphate cyclohydrolase, required for TH activity, and (iv) a mutant in the vesicular monoamine transporter (VMAT(Δ14)), which is required for packaging of DA as vesicles inside DA neurons. Median lifespans of ple(2), Pu(Z22) and VMAT(Δ14) mutants were significantly decreased compared to Catsup(26) and wild type controls that did not significantly differ between each other.

Legacy of a pioneer African American educator.

Purpose: The purpose was to reconstruct the historical and legendary contribution of one exemplary African American physical education teacher educator who lived and worked in the Deep South prior to and immediately following the 1954 Brown v. Board of Education court case. The following questions guided data collection and analysis: To what extent was the participant marginalized in his profession and within the community? How were the participant's life experiences influenced by stereotype threat? To what degree did self-efficacy help mediate marginalization and stereotype threat?

Method: The participant in this study was Dr.

Interaction of maternal protein and carbon monoxide on pup mortality in mice: implications for global infant mortality.

Background: The United States Surgeon General declared 2005 as the "Year of Healthy Child." To improve the health of all children, we need to start before pregnancy, with their mothers. Unfortunately, protein deficiency in the diets of poor pregnant mothers in developing countries is widespread.

Gastroschisis is caused by the combination of carbon monoxide and protein-zinc deficiencies in mice.

Background: Gastroschisis is a rare congenital defect of the abdominal wall. Its occurrence is noted primarily in the offspring of young mothers who often smoke during pregnancy. The incidence of gastroschisis has been increasing in many countries in recent years.

Teratogenicity and developmental toxicity of carbon monoxide in protein-deficient mice.

Experiments were carried out to determine the teratogenicity and developmental toxicity of carbon monoxide (CO) in mice fed protein-deficient diets. Pregnant CD-1 mice were fed 27 (control), 16, 8, or 4% protein diets throughout gestation and each group was exposed to 0 (control), 65, 125, 250, or 500 ppm of CO from gestation days 8-18. The CO exposure was continuous except for daily watering, feeding or cage changing.

Additivity of protein deficiency and carbon monoxide on placental carboxyhemoglobin in mice.

Objectives: The purpose of the study was to estimate maternal and placental carboxyhemoglobin in protein-deficient and carbon monoxide-exposed mice.

Study Design: Pregnant CD-1 mice were placed on diets containing 27% (control), 16%, 8%, or 4% protein on gestation day 1. The dams were exposed to carbon monoxide concentrations of 0 (control), 65, 125, 250, or 500 ppm from gestation days 8 to 18.

Neonatal development altered by maternal sulfur dioxide exposure.

Sulfur dioxide (SO2) is one of the commonly encountered environmental contaminants. Experiments were carried out to test for neonatal behavioral alterations associated with maternal SO2 exposure. Pregnant CD-I mice were exposed to 0, 32, or 65 PPM SO2 in environmental chambers from gestation day 7 to 18 (plug = day 1).

Nitrogen dioxide exposure alters neonatal development.

Nitrogen dioxide (NO2) is one of the commonly encountered environmental contaminants. Experiments were carried out to test for neonatal behavioral alterations associated with prenatal NO2 exposure. Pregnant CD-1 mice were exposed in environmental chambers to 0, 22, or 45 ppm of NO2 in air from gestation day 7 to 18.