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71.
Grip strength changes over 27yr in Japanese-American men 总被引:3,自引:0,他引:3
Rantanen T.; Masaki K.; Foley D.; Izmirlian G.; White L.; Guralnik J. M. 《Journal of applied physiology》1998,85(6):2047-2053
The aim of thisstudy was to describe changes in grip strength over a follow-up periodof ~27 yr and to study the associations of rate of strength declinewith weight change and chronic conditions. The data are from theHonolulu Heart Program, a prospective population-based studyestablished in 1965. Participants at exam1 were 8,006 men (ages 45-68 yr) who were ofJapanese ancestry and living in Hawaii. At follow-up, 3,741 men (agerange, 71-96 yr) participated. Those who died before the follow-upshowed significantly lower grip-strength values at baseline than didthe survivors. The average annualized strength change among thesurvivors was 1.0%. Steeper decline (>1.5%/yr) wasassociated with older age at baseline, greater weight decrease, andchronic conditions such as stroke, diabetes, arthritis, coronary heartdisease, and chronic obstructive pulmonary disease. The risk factorsfor having very low hand-grip strength at follow-up, here termedgrip-strength disability (21 kg, the lowest 10th percentile), werelargely same as those for steep strength decline. However, theage-adjusted correlation between baseline and follow-up strength wasstrong (r = 0.557, P < 0.001); i.e., those who showedgreater grip strength at baseline were also likely to do so 27 yrlater. Consequently, those in the lowest grip-strength tertile atbaseline had about eight times greater risk of grip-strength disabilitythan those in the highest tertile because of their lower reserve ofstrength. In old age, maintenance of optimal body mass may help preventsteep strength decrease and poor absolute strength. 相似文献
72.
Douglas E. Foley 《Anthropology & education quarterly》1999,30(4):488-490
Ethnic Identity and Power. Cultural Contexts of Political Action in School and Society. Yali Zou and Enrique T. Trueba. eds. Albany: State University of New York Press, 1998. 452 pp. 相似文献
73.
74.
Scrub typhus is a potentially fatal mite-borne febrile illness, primarily of the Asia-Pacific Rim. With an endemic area greater than 13 million km2 and millions of people at risk, scrub typhus remains an underreported, often misdiagnosed febrile illness. A comprehensive, updatable map of the true distribution of cases has been lacking, and therefore the true risk of disease within the very large endemic area remains unknown. The purpose of this study was to establish a database and map to track human scrub typhus. An online search using PubMed and the United States Armed Forces Pest Management Board Literature Retrieval System was performed to identify articles describing human scrub typhus cases both within and outside the traditionally accepted endemic regions. Using World Health Organization guidelines, stringent criteria were used to establish diagnoses for inclusion in the database. The preliminary screening of 181 scrub typhus publications yielded 145 publications that met the case criterion, 267 case records, and 13 serosurvey records that could be georeferenced, describing 13,739 probable or confirmed human cases in 28 countries. A map service has been established within VectorMap (www.vectormap.org) to explore the role that relative location of vectors, hosts, and the pathogen play in the transmission of mite-borne scrub typhus. The online display of scrub typhus cases in VectorMap illustrates their presence and provides an up-to-date geographic distribution of proven scrub typhus cases. 相似文献
75.
Robert J. Yamulla Eric G. Kane Alexandra E. Moody Kristin A. Politi Nicole E. Lock Andrew V. A. Foley David M. Roberts 《Genetics》2014,197(4):1285-1302
The Wnt pathway is a conserved signal transduction pathway that contributes to normal development and adult homeostasis, but is also misregulated in human diseases such as cancer. The tumor suppressor adenomatous polyposis coli (APC) is an essential negative regulator of Wnt signaling inactivated in >80% of colorectal cancers. APC participates in a multiprotein “destruction complex” that targets the proto-oncogene β-catenin for ubiquitin-mediated proteolysis; however, the mechanistic role of APC in the destruction complex remains unknown. Several models of APC function have recently been proposed, many of which have emphasized the importance of phosphorylation of high-affinity β-catenin-binding sites [20-amino-acid repeats (20Rs)] on APC. Here we test these models by generating a Drosophila APC2 mutant lacking all β-catenin-binding 20Rs and performing functional studies in human colon cancer cell lines and Drosophila embryos. Our results are inconsistent with current models, as we find that β-catenin binding to the 20Rs of APC is not required for destruction complex activity. In addition, we generate an APC2 mutant lacking all β-catenin-binding sites (including the 15Rs) and find that a direct β-catenin/APC interaction is also not essential for β-catenin destruction, although it increases destruction complex efficiency in certain developmental contexts. Overall, our findings support a model whereby β-catenin-binding sites on APC do not provide a critical mechanistic function per se, but rather dock β-catenin in the destruction complex to increase the efficiency of β-catenin destruction. Furthermore, in Drosophila embryos expressing some APC2 mutant transgenes we observe a separation of β-catenin destruction and Wg/Wnt signaling outputs and suggest that cytoplasmic retention of β-catenin likely accounts for this difference. 相似文献
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77.
Melanie J. Edwards Ian R. Wallis William J. Foley 《Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology》2010,180(2):247-257
We fed common brushtail possums artificial diets containing a buffer and the plant secondary metabolite (PSM), orcinol, to
test the hypothesis that organic acids, common products of PSM metabolism, limit feeding by common brushtail possums (Trichosurus vulpecula). We introduced several diets containing orcinol and a buffer (urinary alkalising agent) over a course of three experiments.
A diet containing 2% orcinol (wet matter) caused possums to reduce their food intake immediately, but feeding returned to
normal 1–2 days later. Even though possums excreted strongly acidic urine (pH 5.1) and had perturbed nitrogen metabolism,
they maintained their food intake and body mass until the experiment terminated 9 days after the introduction of orcinol.
Possums ate 52% less when the basal diet contained 4% orcinol. As expected, the acid loads caused a change in the composition
of urinary nitrogen with possums excreting more ammonium than urea and a large amount of unidentified nitrogenous material.
Supplementing the diet containing orcinol with buffer neutralised the metabolic acid load and partly restored normal nitrogen
metabolism, but did not restore feeding. Also, animals eating orcinol excreted normal amounts of 3-methylhistidine, indicating
no increase in muscle protein catabolism. This suggests that a limitation to the rate of detoxification or toxicosis, rather
than acid loads, limits the ingestion of acid-inducing PSMs. 相似文献
78.
Tumor necrosis factor alpha (TNF-α) signals through NF-κB, JNK, and caspase modules to drive physiological responses that range from inflammation to apoptosis. The balance between the individual modules determines the nature of the response, and deregulated TNF signaling has been implicated in numerous pathological conditions. We used a quantitative high-throughput RNA interference assay to probe the entire complement of human kinases and phosphatases for gene products that tilt the balance of TNF signal transduction in favor of cell death or cell viability. Of all gene products tested, loss of hexokinase 1 resulted in the greatest elevations in TNF-dependent death. In secondary assays, we demonstrated that hexokinase 1 does not alter TNF-dependent activation of NF-κB or JNK modules. Instead, hexokinase 1 modifies the induction of caspase-driven cell death. Specifically, we showed that hexokinase 1 inhibits the formation of active, pro-apoptotic caspases in response to extrinsic inducers of apoptosis. These data are the first loss-of-function reports to examine the involvement of hexokinase 1 in the transduction of cell death signals and indicate that hexokinases are critical determinants of the viability of cells in response to extrinsic apoptotic cues. 相似文献
79.
80.
Anne Marie McLaughlin Muhammad Farooq Maria B Donnelly Kieran Foley 《BMC anesthesiology》2010,10(1):1-5