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Le Touquet – Paris-Plage, France

Bigot E.,Biochemistry | Bataille R.,Anti Cancer Center Rene Gauducheau | Patrice T.,Cancer Photobiology
Journal of Photochemistry and Photobiology B: Biology | Year: 2012

Photodynamic therapy (PDT) generates singlet oxygen ( 1O 2) and Reactive Oxygen Species (ROS) that are counteracted by patient's defenses. As cancer treatments are among the most important PDT applications the aim of this pilot study was to determine whether the serum of cancer patients produces more or less secondary ROS or peroxides after a photoreaction as compared to healthy persons. Fifty-three volunteers and 105 cancer patients were recruited. The capacity of 1O 2 or secondary oxidant production was found to be increased in 6 healthy donors and 36 cancer patients (23/69 women and 13/31 men p < 0.007 and p < 0.04) with a mean value of 1.52 as compared to 1.29 in the healthy subjects (p < 0.05) when considering values higher than the normal range (norm = 1 ± 10%) or 1.1 vs. 0.85 (p < 0.01) in the whole cohort. This increase correlated with a poor prognosis, TNM and SBR classification. Serum 1O 2 deactivation capacity was impaired and secondary ROS were more produced during cancer progression. Although it is currently unclear whether this is the cause or effect of cancer, this finding may hold interest as a potential marker of cancer severity. It would also support the interest of PDT as an adjuvant for cancer treatment, even for aggressive tumors particularly when associated to surgery for bulk removal. © 2011 Elsevier B.V. All rights reserved.

Obesity and gestational diabetes mellitus continue to increase worldwide and span the spectrum of age, race, ethnicity, and socioeconomic status. Alarmingly, 1 in 10 infants and toddlers is obese, and 1 in 5 youths is both obese and at risk formetabolic syndrome prior to puberty. The mechanisms underlying how poor maternal health imparts risk for future metabolic disease in the offspring are beginning to emerge in deeply phenotyped human and nonhuman primate models. Maternal diet and obesity impact fuels, hormones, and inflammation with powerful effects on fetal metabolic systems. These are accompanied by persistent changes in the infant microbiome and epigenome and in offspring behavior. These results suggest that gestational and lactational dietary exposures are driving health risks in the next generation. Whether maternal diet can prevent changes in the womb to alter infant life-course disease risk is still unknown. Controlled, mechanistic studies to identify interventions are sorely needed for a healthier next generation. ©2015 by the American Diabetes Association.

Guerin P.,Institute du Thorax | Bigot E.,Biochemistry | Patrice T.,Photobiologie des Cancers
Journal of Thrombosis and Thrombolysis | Year: 2013

Blood flow arrest and reperfusion during myocardial infarction (MI) cause myocyte and endothelium injury through oxidative stress and inflammation, both of which involve Reactive Oxygen Species (ROS) and peroxides that consume antioxidant defenses. The aim of this study was to determine whether serum from the occluded coronary vessel has impaired anti-oxidative defenses as compared to serum from aortic blood or from the periphery of healthy controls. Forty-seven patients (44 men) were included for study. Inclusion criteria were chest pain, ST elevation, and cardiac troponin increase. A photoreaction producing a standardized amount of singlet oxygen (1O2), an excited form of oxygen, was performed in serum samples obtained during primary percutaneous coronary intervention (PCI). Immediately after laser light delivery to 5 % sera containing 5 μg/mL rose bengal, dichloro-dihydro-fluorescein (DCFH) was added and its post-oxidation transformation into the fluorescent DCF, was recorded. At least 5 h after the start of symptoms, the mean secondary ROS production after 1O2 delivery was increased in coronary sera (p < 0.001), but in aortic blood remained similar to that of healthy controls. The peak troponin value correlated with DCF fluorescence throughout the interval between symptoms onset and PCI. A high fluorescence was associated with a higher risk of MACE. These results show that oxidants secondary to 1O2 are increased in occluded vessels during AMI in parallel to c-troponin, demonstrating that antioxidants are consumed. A O 2 increase during reperfusion would thus extend the damage resulting from IDM necrosis. The effect of conditioning during PCI could be studied using the described method. © 2012 Springer Science+Business Media, LLC.

Grasshopper communities were sampled in three associated habitats of the Central Basin of Tennesee: cedar glades, xeric limestone prairies, and cedar hardwood forest. Twenty-five grasshopper species were collected across all three habitats. Eleven species were found in the cedar glades, 12 species were collected in the xeric limestone prairies, and six species were collected from the cedar-hardwood forests. A Principal Component Analysis of the resulting species lists indicated that grasshopper community composition differed significantly between each habitat. Four new state records for Tennessee were documented during this survey. An annotated species list is presented.

Wang S.-S.,University of Texas Southwestern Medical Center | Wang S.-S.,University of Texas at Dallas | Gu Y.-F.,University of Texas Southwestern Medical Center | Gu Y.-F.,University of Texas at Dallas | And 17 more authors.
Proceedings of the National Academy of Sciences of the United States of America | Year: 2014

Why different species are predisposed to different tumor spectra is not well understood. In particular, whether the physical location of tumor suppressor genes relative to one another influences tumor predisposition is unknown. Renal cancer presents a unique opportunity to explore this question. Renal cell carcinoma (RCC) of clearcell type (ccRCC), the most common type, begins with an intragenic mutation in the von Hippel-Lindau (VHL) gene and loss of 3p (where VHL is located). Chromosome 3p harbors several additional tumor suppressor genes, including BRCA1-associated protein-1 (BAP1). In the mouse, Vhl is on a different chromosome than Bap1. Thus, whereas loss of 3p in humans simultaneously deletes one copy of BAP1, loss of heterozygosity in the corresponding Vhl region in the mouse would not affect Bap1. To test the role of BAP1 in ccRCC development, we generated mice deficient for either Vhl or Vhl together with one allele of Bap1 in nephron progenitor cells. Six2- Cre;VhlF/F;Bap1F/+ mice developed ccRCC, but Six2-Cre;VhlF/F mice did not. Kidneys from Six2-Cre;VhlF/F;Bap1F/+ mice resembled kidneys from humans with VHL syndrome, containing multiple lesions spanning from benign cysts to cystic and solid RCC. Although the tumors were small, they showed nuclear atypia and exhibited features of human ccRCC. These results provide an explanation for why VHL heterozygous humans, but not mice, develop ccRCC. They also explain why a mouse model of ccRCC has been lacking. More broadly, our data suggest that differences in tumor predisposition across species may be explained, at least in part, by differences in the location of two-hit tumor suppressor genes across the genome.

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