20 research outputs found
Recommended from our members
Juvenile social relationships reflect adult patterns of behavior in wild geladas
Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/113724/1/ajp22443.pd
Pedunculated pulmonary parenchymal leiomyoma associated with hypertrophicosteoarthropathy: case report.
International Recommendations for Training Future Toxicologic Pathologists Participating in Regulatory-Type, Nonclinical Toxicity Studies*
The International Federation of Societies of Toxicologic Pathologists (IFSTP) proposes a
common global framework for training future toxicologic pathologists who will support
regulatory-type nonclinical toxicology studies. Trainees optimally should undertake a
scientific curriculum of at least 5 years at an accredited institution leading to a
clinical degree (veterinary medicine or medicine). Trainees should then obtain 4 or more
years of intensive pathology practice during a residency and/or on-the-job
“apprenticeship,” at least 2 years of which must be focused on regulatory-type toxicologic
pathology topics. Possession of a recognized pathology qualification (i.e., certification)
is highly recommended. A non-clinical pathway (e.g., a graduate degree in medical biology
or pathology) may be possible if medically trained pathologists are scarce, but this
option is not optimal. Regular, lifelong continuing education (peer review of nonclinical
studies, professional meetings, reading, short courses) will be necessary to maintain and
enhance one’s understanding of current toxicologic pathology knowledge, skills, and tools.
This framework should provide a rigorous yet flexible way to reliably train future
toxicologic pathologists to generate, interpret, integrate, and communicate data in
regulatory-type, nonclinical toxicology studies
Influence of taste disorders on dietary behaviors in cancer patients under chemotherapy
<p>Abstract</p> <p>Objectives</p> <p>To determine the relationship between energy and nutrient consumption with chemosensory changes in cancer patients under chemotherapy.</p> <p>Methods</p> <p>We carried out a cross-sectional study, enrolling 60 subjects. Cases were defined as patients with cancer diagnosis after their second chemotherapy cycle (n = 30), and controls were subjects without cancer (n = 30). Subjective changes of taste during treatment were assessed. Food consumption habits were obtained with a food frequency questionnaire validated for Mexican population. Five different concentrations of three basic flavors --sweet (sucrose), bitter (urea), and a novel basic taste, umami (sodium glutamate)-- were used to measure detection thresholds and recognition thresholds (RT). We determine differences between energy and nutrient consumption in cases and controls and their association with taste DT and RT.</p> <p>Results</p> <p>No demographic differences were found between groups. Cases showed higher sweet DT (6.4 vs. 4.4 μmol/ml; p = 0.03) and a higher bitter RT (100 vs. 95 μmol/ml; <it>p </it>= 0.04) than controls. Cases with sweet DT above the median showed significant lower daily energy (2,043 vs.1,586 kcal; p = 0.02), proteins (81.4 vs. 54 g/day; <it>p </it>= 0.01), carbohydrates (246 vs.192 g/day; <it>p </it>= 0.05), and zinc consumption (19 vs.11 mg/day; <it>p </it>= 0.01) compared to cases without sweet DT alteration. Cases with sweet DT and RT above median were associated with lower completion of energy requirements and consequent weight loss. There was no association between flavors DT or RT and nutrient ingestion in the control group.</p> <p>Conclusion</p> <p>Changes of sweet DT and bitter RT in cancer patients under chemotherapy treatment were associated with lower energy and nutrient ingestion. Taste detection and recognition thresholds disorders could be important factors in malnutrition development on patients with cancer under chemotherapy treatment.</p
Bibliographie critique
Dreyfus Simone, Vignes Daniel-Henri, Debbasch Charles, Montero José Perez, Barale Jean, Castriotta G., Fischer Georges, Langrod Georges, F. R., Latournerie Marie-Aimée, G. G., O. F. Bibliographie critique. In: Annuaire français de droit international, volume 6, 1960. pp. 1135-1162
Bibliographie critique
Dreyfus Simone, Vignes Daniel-Henri, Debbasch Charles, Montero José Perez, Barale Jean, Castriotta G., Fischer Georges, Langrod Georges, F. R., Latournerie Marie-Aimée, G. G., O. F. Bibliographie critique. In: Annuaire français de droit international, volume 6, 1960. pp. 1135-1162
Autophagy plays a critical role in the degradation of active RHOA, the control of cell cytokinesis, and genomic stability.
International audienceDegradation of signaling proteins is one of the most powerful tumor-suppressive mechanisms by which a cell can control its own growth. Here, we identify RHOA as the molecular target by which autophagy maintains genomic stability. Specifically, inhibition of autophagosome degradation by the loss of the v-ATPase a3 (TCIRG1) subunit is sufficient to induce aneuploidy. Underlying this phenotype, active RHOA is sequestered via p62 (SQSTM1) within autolysosomes and fails to localize to the plasma membrane or to the spindle midbody. Conversely, inhibition of autophagosome formation by ATG5 shRNA dramatically increases localization of active RHOA at the midbody, followed by diffusion to the flanking zones. As a result, all of the approaches we examined that compromise autophagy (irrespective of the defect: autophagosome formation, sequestration, or degradation) drive cytokinesis failure, multinucleation, and aneuploidy, processes that directly have an impact upon cancer progression. Consistently, we report a positive correlation between autophagy defects and the higher expression of RHOA in human lung carcinoma. We therefore propose that autophagy may act, in part, as a safeguard mechanism that degrades and thereby maintains the appropriate level of active RHOA at the midbody for faithful completion of cytokinesis and genome inheritance