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Grace X. Ma Steve Shive Yin Tan Wanzhen Gao Joanne Rhee Micah Park Jaesool Kim Jamil I. Toubbeh 《Cancer epidemiology》2009,33(5):381-386
Background: Despite evidence of a decline in both incidence and prevalence of colorectal cancer nationwide, it remains the second most commonly diagnosed cancer and the third highest cause of mortality among Asian Americans, including Korean Americans. This community-based and theoretically guided study evaluated a culturally appropriate intervention program that included a bilingual cancer educational program among Korean Americans including information on CRC risks, counseling to address psychosocial and access barriers, and patient navigation assistance. Methods: A two-group quasi-experimental design with baseline and post-intervention assessment and a 12-month follow-up on screening was used in the study. Korean Americans (N = 167) were enrolled from six Korean churches. The intervention group received culturally appropriate intervention program addressing accessibility and psychosocial barriers, and navigation assistance for screening. The control group received general health education that included cancer-related health issues and screening. Results: There was a significant difference (p < 0.05) between the post-intervention and control groups in awareness of CRC risk factors. There was also a significant improvement in the pre–post across HBM measures in the intervention group for perceived susceptibility (p < 0.05) and benefits and barriers to screening (p < 0.001). At baseline, 13% of participants in the intervention group and 10% in control group reported having had a CRC cancer screening test in the previous year. At the 12-month post-intervention follow-up, 77.4% of participants in the intervention group had obtained screening compared to 10.8% in the control group. Conclusion: While health disparities result from numerous factors, a culturally appropriate and church-based intervention can be highly effective in increasing knowledge of and access to, and in reducing barriers to CRC screening among underserved Koreans. 相似文献
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MARTIN CLÉMENT CAROLINE CHAMBERLAND JACQUELINE PÉRODIN RICHARD LEDUC GAÉTAN GUILLEMETTE EMANUEL ESCHER 《Journal of receptor and signal transduction research》2013,33(5-6):417-433
Several models of activation mechanisms were proposed for G protein-coupled receptors (GPCRs), yet no direct methods exist for their elucidation. The availability of constitutively active mutants has given an opportunity to study active receptor conformations within acceptable limits using models such as the angiotensin II type 1 (AT1)1 receptor mutant N111G-hAT1 which displays an important constitutive activity. Recently, by using methionine proximity assay, we showed for the hAT1 receptor that TMD III, VI, and VII form the ligand-binding pocket of the C-terminal amino acid of an antagonistic AngII analogue. In the present contribution, we investigated whether the same residues would also constitute the ligand-binding contacts in constitutively activated mutant (CAM) receptors. For this purpose, the same Met mutagenesis strategy was carried out on the N111G double mutants. Analysis of 43 receptors mutants in the N111G-hAT1 series, photolabeled and CNBr digested, showed that there were only subtle structural changes between the wt-receptor and its constitutively active form. 相似文献
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MORAIS PAULO AMORIM ANTÓNIO VIEIRA DA SILVA CLÁUDIA RIBEIRO TERESA COSTA SANTOS JORGE AFONSO COSTA HELOÍSA 《Journal of genetics》2015,94(3):509-512
Journal of Genetics - 相似文献
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Emile CL. Marnette Harm Houweling Herman Van Dam Jan Willem Erisman 《Biogeochemistry》1993,23(2):119-144
The chemical composition of surface waters of two Dutch moorland pools and of incident precipitation, was monitored from 1982
to 1990. For this period, sulfur and water budgets were calculated using a hydrochemical model developed for well-mixed non-stratifying
lakes. Total atmospheric deposition of S decreased significantly after 1986 at both locations. A model describing the sulfur
budget in terms of input, output and reduction/oxidation processes predicted a fast decrease of pool water SO4
2− concentrations after a decrease of atmospheric input. However, SO4
2− concentrations in the surface water was lowered only slightly or remained constant. Apparently a source within the lake caused
the unexpectedly high SO4
2− concentrations. The possible supply of SO4
2− from the sediment through regulation by (K-)Al-SO4 containing minerals or desorption of SO4
2− from positively charged surfaces in the sediment was evaluated. Solubility calculations of pore water with respect to alunite,
basaluminite and jurbanite indicated that SO4
2− concentration was not regulated by these minerals. It is suggested here (1) that desorption of SO4
2− from peaty sediments may account for the estimated SO4
2− supply provided that the adsorption complex is periodically recharged by partial oxidation of the upper bottom sediments
and (2) that because of exposure of a part of the pool bottom to the atmosphere during dry summers and subsequent oxidation
of reduced S, the amount of SO4
2− may be provided which complements the decreasing depositional SO4
2− input. In future research these two mechanisms need to be investigated. 相似文献
7.
GUILLAUME TCHERKEZ RUDI SCHÄUFELE SALVADOR NOGUÉS CLÉMENT PIEL ARNOUD BOOM GARY LANIGAN CÉCILE BARBAROUX CATARINA MATA SLIMAN ELHANI DEBBIE HEMMING CHRISTINA MAGUAS DAN YAKIR FRANZ W. BADECK HOWARD GRIFFITHS HANS SCHNYDER JALEH GHASHGHAIE 《Plant, cell & environment》2010,33(6):900-913
While there is currently intense effort to examine the 13C signal of CO2 evolved in the dark, less is known on the isotope composition of day‐respired CO2. This lack of knowledge stems from technical difficulties to measure the pure respiratory isotopic signal: day respiration is mixed up with photorespiration, and there is no obvious way to separate photosynthetic fractionation (pure ci/ca effect) from respiratory effect (production of CO2 with a different δ13C value from that of net‐fixed CO2) at the ecosystem level. Here, we took advantage of new simple equations, and applied them to sunflower canopies grown under low and high [CO2]. We show that whole mesocosm‐respired CO2 is slightly 13C depleted in the light at the mesocosm level (by 0.2–0.8‰), while it is slightly 13C enriched in darkness (by 1.5–3.2‰). The turnover of the respiratory carbon pool after labelling appears similar in the light and in the dark, and accordingly, a hierarchical clustering analysis shows a close correlation between the 13C abundance in day‐ and night‐evolved CO2. We conclude that the carbon source for respiration is similar in the dark and in the light, but the metabolic pathways associated with CO2 production may change, thereby explaining the different 12C/13C respiratory fractionations in the light and in the dark. 相似文献
8.
Michael CW Chan Renee WY Chan Wendy CL Yu Carol CC Ho WH Chui CK Lo Kit M Yuen Yi Guan John M Nicholls JS Malik Peiris 《Respiratory research》2009,10(1):102
Background
Highly pathogenic avian influenza (HPAI) H5N1 virus is entrenched in poultry in Asia and Africa and continues to infect humans zoonotically causing acute respiratory disease syndrome and death. There is evidence that the virus may sometimes spread beyond respiratory tract to cause disseminated infection. The primary target cell for HPAI H5N1 virus in human lung is the alveolar epithelial cell. Alveolar epithelium and its adjacent lung microvascular endothelium form host barriers to the initiation of infection and dissemination of influenza H5N1 infection in humans. These are polarized cells and the polarity of influenza virus entry and egress as well as the secretion of cytokines and chemokines from the virus infected cells are likely to be central to the pathogenesis of human H5N1 disease.Aim
To study influenza A (H5N1) virus replication and host innate immune responses in polarized primary human alveolar epithelial cells and lung microvascular endothelial cells and its relevance to the pathogenesis of human H5N1 disease.Methods
We use an in vitro model of polarized primary human alveolar epithelial cells and lung microvascular endothelial cells grown in transwell culture inserts to compare infection with influenza A subtype H1N1 and H5N1 viruses via the apical or basolateral surfaces.Results
We demonstrate that both influenza H1N1 and H5N1 viruses efficiently infect alveolar epithelial cells from both apical and basolateral surface of the epithelium but release of newly formed virus is mainly from the apical side of the epithelium. In contrast, influenza H5N1 virus, but not H1N1 virus, efficiently infected polarized microvascular endothelial cells from both apical and basolateral aspects. This provides a mechanistic explanation for how H5N1 virus may infect the lung from systemic circulation. Epidemiological evidence has implicated ingestion of virus-contaminated foods as the source of infection in some instances and our data suggests that viremia, secondary to, for example, gastro-intestinal infection, can potentially lead to infection of the lung. HPAI H5N1 virus was a more potent inducer of cytokines (e.g. IP-10, RANTES, IL-6) in comparison to H1N1 virus in alveolar epithelial cells, and these virus-induced chemokines were secreted onto both the apical and basolateral aspects of the polarized alveolar epithelium.Conclusion
The predilection of viruses for different routes of entry and egress from the infected cell is important in understanding the pathogenesis of influenza H5N1 infection and may help unravel the pathogenesis of human H5N1 disease. 相似文献9.
T G Forsthuber C L Shive W Wienhold K de Graaf E G Spack R Sublett A Melms J Kort M K Racke R Weissert 《Journal of immunology (Baltimore, Md. : 1950)》2001,167(12):7119-7125
Myelin oligodendrocyte glycoprotein (MOG) is an Ag present in the myelin sheath of the CNS thought to be targeted by the autoimmune T cell response in multiple sclerosis (MS). In this study, we have for the first time characterized the T cell epitopes of human MOG restricted by HLA-DR4 (DRB1*0401), an MHC class II allele associated with MS in a subpopulation of patients. Using MHC binding algorithms, we have predicted MOG peptide binding to HLA-DR4 (DRB1*0401) and subsequently defined the in vivo T cell reactivity to overlapping MOG peptides by testing HLA-DR4 (DRB1*0401) transgenic mice immunized with recombinant human (rh)MOG. The data indicated that MOG peptide 97-108 (core 99-107, FFRDHSYQE) was the immunodominant HLA-DR4-restricted T cell epitope in vivo. This peptide has a high in vitro binding affinity for HLA-DR4 (DRB1*0401) and upon immunization induced severe experimental autoimmune encephalomyelitis in the HLA-DR4 transgenic mice. Interestingly, the same peptide was presented by human B cells expressing HLA-DR4 (DRB1*0401), suggesting a role for the identified MOG epitopes in the pathogenesis of human MS. 相似文献
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