Mapping of ICD-O Tuples to OncoTree Codes Using SNOMED CT Post-Coordination.

Around 500,000 oncological diseases are diagnosed in Germany every year which are documented using the International Classification of Diseases for Oncology (ICD-O). Apart from this, another classification for oncology, OncoTree, is often used for the integration of new research findings in oncology. For this purpose, a semi-automatic mapping of ICD-O tuples to OncoTree codes was developed. The implementation uses a FHIR terminology server, pre-coordinated or post-coordinated SNOMED CT expressions, and subsumption testing. Various validations have been applied. The results were compared with reference data of scientific papers and manually evaluated by a senior pathologist, confirming the applicability of SNOMED CT in general and its post-coordinated expressions in particular as a viable intermediate mapping step. Resulting in an agreement of 84,00 % between the newly developed approach and the manual mapping, it becomes obvious that the present approach has the potential to be used in everyday medical practice.

Seasonal temperature compensation in the horse mussel, Modiolus modiolus: metabolic enzymes, oxidative stress and heat shock proteins.

Seasonal collections of the subtidal horse mussel, Modiolus modiolus, from a depth of 10 m were made at the Isles of Shoals, New Hampshire to assess changes in overall energetic demand, measured as respiration, the maximal activities of rate-limiting enzymes of intermediate metabolism, level of oxidative stress, and the expression of heat shock proteins (HSP). Weighted respiration rates of mussels from winter collections were significantly lower than summer rates but decreased by less than 20%. Specific activities of several rate-limiting enzymes were measured in mussels from the summer and winter collections at the temperature of collection and the reciprocal seasonal temperature (15 and 5 degrees C). Comparisons of these enzyme activities and the protein concentrations of hexokinase and citrate synthase show that a quantitative strategy is used to acclimatize to winter temperatures by these rate-limiting enzymes of intermediate metabolism. The activities and protein concentrations of the antioxidant enzyme, Cu/Zn superoxide dismutase (SOD) is seasonally indistinguishable while the concentration of HSP 70 was greater in winter than in summer samples. These results show that mussels seasonally compensate for decreases in temperature by increasing the concentration of rate-limiting metabolic enzymes while maintaining the same level of antioxidant protection in summer and winter consistent with high aerobic metabolism in both winter and summer. Lastly, the significantly greater concentrations of HSP70 in winter samples suggests that protein chaperone functions must be maintained while other seasonal adjustments to cold temperatures are occurring.

Exposure to ultraviolet radiation causes apoptosis in developing sea urchin embryos.

Laboratory exposures of embryos from the sea urchin Strongylocentrotus droebachiensis to ultraviolet B radiation (UV-B, 290-320 nm), equivalent to a depth of 1-3 m in the Gulf of Maine, resulted in significant damage to DNA measured as cyclobutane pyrimidine dimer formation. Cells with DNA damage caused by ultraviolet radiation (UVR, 290-400 nm) and oxidative stress can survive, but are often retained in the G1/S phase of the cell cycle to repair DNA as a result of the expression of cell cycle genes such as p53 and p21, and the subsequent inhibition of the activity of cyclin-dependent kinases such as cdc2; if DNA cannot be repaired it can lead to programmed cell death or apoptosis. Sea urchin embryos exposed to UV-B radiation exhibit significantly higher protein concentrations of the antioxidant enzyme superoxide dismutase, and the transcriptional activators p53 and p21. The downstream activator of the cell cycle, cdc2, showed significantly lower protein concentrations with exposure to increasingly shorter wavelengths of UVR. Decreases in cdc2 could have been caused directly by exposure to UV-B or as a result of downregulation via the p53, p21 cascade, or both. These cellular events lead to apoptosis, as shown by the significant increase in DNA strand breaks observed in the nuclei of developing embryos exposed to UVR using the TUNEL assay. Cellular death, and a decrease in sea urchin embryo survivorship, are caused by the indirect and direct effects of exposure to UVR that leads to apoptosis in these laboratory experiments.