Coupled atmosphere–mixed layer ocean response to ocean heat flux convergence along the Kuroshio Current Extension

Author Posting. © The Author(s), 2010. This is the author's version of the work. It is posted here by permission of Springer for personal use, not for redistribution. The definitive version was published in Climate Dynamics 36 (2011): 2295-2312, doi:10.1007/s00382-010-0764-8.The winter response of the coupled atmosphere-ocean mixed layer system to anomalous geostrophic ocean heat flux convergence in the Kuroshio Extension is investigated by means of experiments with an atmospheric general circulation model coupled to an entraining ocean mixed layer model in the extra-tropics. The direct response consists of positive SST anomalies along the Kuroshio Extension and a baroclinic (low-level trough and upper-level ridge) circulation anomaly over the North Pacific. The low-level component of this atmospheric circulation response is weaker in the case without coupling to an extratropical ocean mixed layer, especially in late winter. The inclusion of an interactive mixed layer in the tropics modifies the direct coupled atmospheric response due to a northward displacement of the Pacific Inter-Tropical Convergence Zone which drives an equivalent barotropic anomalous ridge over the North Pacific. Although the tropically-driven component of the North Pacific atmospheric circulation response is comparable to the direct response in terms of sea level pressure amplitude, it is less important in terms of wind stress curl amplitude due to the mitigating effect of the relatively broad spatial scale of the tropically-forced atmospheric teleconnection.We gratefully acknowledge financial support from NOAA’s Office of Global Programs (grant to C. Deser and Y.-O. Kwon). Y.-O. Kwon is also supported through the Claudia Heyman Fellowship of the WHOI Ocean Climate Change Institute

Molecular, cellular and physiological characterization of the cancer cachexia-inducing C26 colon carcinoma in mouse

BACKGROUND: The majority of cancer patients experience dramatic weight loss, due to cachexia and consisting of skeletal muscle and fat tissue wasting. Cachexia is a negative prognostic factor, interferes with therapy and worsens the patients' quality of life by affecting muscle function. Mice bearing ectopically-implanted C26 colon carcinoma are widely used as an experimental model of cancer cachexia. As part of the search for novel clinical and basic research applications for this experimental model, we characterized novel cellular and molecular features of C26-bearing mice. METHODS: A fragment of C26 tumor was subcutaneously grafted in isogenic BALB/c mice. The mass growth and proliferation rate of the tumor were analyzed. Histological and cytofluorometric analyses were used to assess cell death, ploidy and differentiation of the tumor cells. The main features of skeletal muscle atrophy, which were highlighted by immunohistochemical and electron microscopy analyses, correlated with biochemical alterations. Muscle force and resistance to fatigue were measured and analyzed as major functional deficits of the cachectic musculature. RESULTS: We found that the C26 tumor, ectopically implanted in mice, is an undifferentiated carcinoma, which should be referred to as such and not as adenocarcinoma, a common misconception. The C26 tumor displays aneuploidy and histological features typical of transformed cells, incorporates BrdU and induces severe weight loss in the host, which is largely caused by muscle wasting. The latter appears to be due to proteasome-mediated protein degradation, which disrupts the sarcomeric structure and muscle fiber-extracellular matrix interactions. A pivotal functional deficit of cachectic muscle consists in increased fatigability, while the reported loss of tetanic force is not statistically significant following normalization for decreased muscle fiber size. CONCLUSIONS: We conclude, on the basis of the definition of cachexia, that ectopically-implanted C26 carcinoma represents a well standardized experimental model for research on cancer cachexia. We wish to point out that scientists using the C26 model to study cancer and those using the same model to study cachexia may be unaware of each other's works because they use different keywords; we present strategies to eliminate this gap and discuss the benefits of such an exchange of knowledge