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51.
Expression of intercellular adhesion molecules in human saphenous veins: effects of inflammatory cytokines and neointima formation in culture 总被引:12,自引:0,他引:12
Atherosclerosis causes occlusions in as many as 50% of human saphenous vein coronary artery bypass grafts. Monocyte infiltration is an early step in saphenous vein-graft atherosclerosis, however, comparatively little is known of its underlying mechanisms. As a first approach, we sought to define the occurrence, location and regulation of leukocyte adhesion molecules in human saphenous vein before and after surgical preparation for grafting, during neointima formation in culture and on stimulation with inflammatory cytokines. We compared the distribution of intercellular adhesion molecule (ICAM-1), vascular cell adhesion molecule (VCAM-1) and platelet endothelial cell adhesion molecule (PECAM-1 or CD-31) in endothelial cells and smooth muscle cells (SMCs), using immunocytochemistry. ICAM-1 was expressed on endothelial cells before culture and on both endothelial cells and medial or neointimal SMCs after culturing vein for 14 days in 30% foetal bovine serum or after culturing for 24 h with TNF-alpha. Relative tissue levels of ICAM-1 measured by Western blotting were significantly elevated by culturing freshly-isolated (0.02+/-0.01 to 0.18+/-0.03) and surgically-prepared (0.02+/-0.01 to 0.14+/-0.03; n=6) veins or following TNF-alpha treatment of surgically-prepared veins (0.04+/-0.01 to 0.32+/-0.11, n=7). VCAM-1 was undetectable before or after culturing but was strongly upregulated on endothelial cells by incubation with the cytokines TNF-alpha, IL-1alpha or interferon-gamma. PECAM-1 was expressed constitutively on endothelial cells. We conclude that human saphenous vein expresses several adhesion molecules capable of mediating monocyte migration. The increased expression of ICAM-1 in SMC after culturing or cytokine treatment and of VCAM-1 in endothelial cells suggests that interactions with beta1 and beta2 integrins are important pathways for stimulated monocyte ingress into human saphenous vein grafts. 相似文献
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Amy J. Mathers Nicole Stoesser Anna E. Sheppard Louise Pankhurst Adam Giess Anthony J. Yeh Xavier Didelot Stephen D. Turner Robert Sebra Andrew Kasarskis Tim Peto Derrick Crook Costi D. Sifri 《Antimicrobial agents and chemotherapy》2015,59(3):1656-1663
The global emergence of Klebsiella pneumoniae carbapenemase-producing K. pneumoniae (KPC-Kp) multilocus sequence type ST258 is widely recognized. Less is known about the molecular and epidemiological details of non-ST258 K. pneumoniae in the setting of an outbreak mediated by an endemic plasmid. We describe the interplay of blaKPC plasmids and K. pneumoniae strains and their relationship to the location of acquisition in a U.S. health care institution. Whole-genome sequencing (WGS) analysis was applied to KPC-Kp clinical isolates collected from a single institution over 5 years following the introduction of blaKPC in August 2007, as well as two plasmid transformants. KPC-Kp from 37 patients yielded 16 distinct sequence types (STs). Two novel conjugative blaKPC plasmids (pKPC_UVA01 and pKPC_UVA02), carried by the hospital index case, accounted for the presence of blaKPC in 21/37 (57%) subsequent cases. Thirteen (35%) isolates represented an emergent lineage, ST941, which contained pKPC_UVA01 in 5/13 (38%) and pKPC_UVA02 in 6/13 (46%) cases. Seven (19%) isolates were the epidemic KPC-Kp strain, ST258, mostly imported from elsewhere and not carrying pKPC_UVA01 or pKPC_UVA02. Using WGS-based analysis of clinical isolates and plasmid transformants, we demonstrate the unexpected dispersal of blaKPC to many non-ST258 lineages in a hospital through spread of at least two novel blaKPC plasmids. In contrast, ST258 KPC-Kp was imported into the institution on numerous occasions, with other blaKPC plasmid vectors and without sustained transmission. Instead, a newly recognized KPC-Kp strain, ST941, became associated with both novel blaKPC plasmids and spread locally, making it a future candidate for clinical persistence and dissemination. 相似文献
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Xingjia Wu BS Stephanie Alberico BS Edward Saidu BS Sazzadur Rahman Khan PhD Shijun Zheng PhD Rebecca Romero BS Hyun Sik Chae PhD Sheng Li PhD Amane Mochizuki PhD Juanita Anders PhD 《Wound repair and regeneration》2015,23(1):104-114
A major complication for diabetic patients is chronic wounds due to impaired wound healing. It is well documented that visible red wavelengths can accelerate wound healing in diabetic animal models and patients. In vitro and in vivo diabetic models were used to investigate the effects of organic light emitting diode (OLED) irradiation on cellular function and cutaneous wound healing. Human dermal fibroblasts were cultured in hyperglycemic medium (glucose concentration 180 mM) and irradiated with an OLED (623 nm wavelength peak, range from 560 to 770 nm, power density 7 or 10 mW/cm2 at 0.2, 1, or 5 J/cm2). The OLED significantly increased total adenosine triphosphate concentration, metabolic activity, and cell proliferation compared with untreated controls in most parameters tested. For the in vivo experiment, OLED and laser (635 ± 5 nm wavelength) treatments (10 mW/cm2, 5 J/cm2 daily for a total of seven consecutive days) for cutaneous wound healing were compared using a genetic, diabetic rat model. Both treatments had significantly higher percentage of wound closure on day 6 postinjury and higher total histological scores on day 13 postinjury compared with control. No statistical difference was found between the two treatments. OLED irradiation significantly increased fibroblast growth factor‐2 expression at 36‐hour postinjury and enhanced macrophage activation during initial stages of wound healing. In conclusion, the OLED and laser had comparative effects on enhancing diabetic wound healing. 相似文献
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Sandeep Toot Juanita Hoe Ritchard Ledgerd Karen Burnell Mike Devine Martin Orrell 《Aging & mental health》2013,17(3):328-335
The aims of this study were to identify which factors may lead to crisis for people with dementia and their carers and identify interventions these individuals believe could help in crisis. Qualitative study using focus groups to compare the perspectives of people with dementia, family carers and healthcare professionals on causes of crises and crisis interventions. To help in a crisis, people with dementia were favourable towards support from family and friends, access to mobile phones and home adaptations to reduce risks. Carers were keen on assistive technology and home adaptation. Both carers and staff valued carer training and education, care plans and well-coordinated care. Staff were the only group emphasizing more intensive interventions such as emergency home respite and extended hours services. In terms of causes of crises, people with dementia focused on risks and hazards in their home, whereas family carers emphasized carer stress and their own mental health problems. Staff, in contrast were concerned about problems with service organization and coordination leading to crises. Physical problems were less commonly identified as causes of crises but when they did occur they had a major impact. Practical interventions such as home adaptations, assistive technology, education and training for family carers, and flexible home care services were highly valued by service users and their families during times of crisis and may help prevent hospital admissions. Specialist home care was highly valued by all groups. 相似文献
56.
Maggie C.Y. Ng Richa Saxena Jiang Li Nicholette D. Palmer Latchezar Dimitrov Jianzhao Xu Laura J. Rasmussen-Torvik Joseph M. Zmuda David S. Siscovick Sanjay R. Patel Errol D. Crook Mario Sims Yii-Der I. Chen Alain G. Bertoni Mingyao Li Struan F.A. Grant Josée Dupuis James B. Meigs Bruce M. Psaty James S. Pankow Carl D. Langefeld Barry I. Freedman Jerome I. Rotter James G. Wilson Donald W. Bowden 《Diabetes》2013,62(3):965-976
Type 2 diabetes (T2D) disproportionally affects African Americans (AfA) but, to date, genetic variants identified from genome-wide association studies (GWAS) are primarily from European and Asian populations. We examined the single nucleotide polymorphism (SNP) and locus transferability of 40 reported T2D loci in six AfA GWAS consisting of 2,806 T2D case subjects with or without end-stage renal disease and 4,265 control subjects from the Candidate Gene Association Resource Plus Study. Our results revealed that seven index SNPs at the TCF7L2, KLF14, KCNQ1, ADCY5, CDKAL1, JAZF1, and GCKR loci were significantly associated with T2D (P < 0.05). The strongest association was observed at TCF7L2 rs7903146 (odds ratio [OR] 1.30; P = 6.86 × 10−8). Locus-wide analysis demonstrated significant associations (Pemp < 0.05) at regional best SNPs in the TCF7L2, KLF14, and HMGA2 loci as well as suggestive signals in KCNQ1 after correction for the effective number of SNPs at each locus. Of these loci, the regional best SNPs were in differential linkage disequilibrium (LD) with the index and adjacent SNPs. Our findings suggest that some loci discovered in prior reports affect T2D susceptibility in AfA with similar effect sizes. The reduced and differential LD pattern in AfA compared with European and Asian populations may facilitate fine mapping of causal variants at loci shared across populations.Type 2 diabetes (T2D) is a major public health problem affecting 25.8 million people in the U.S. (1). Marked racial differences in its prevalence have been observed, with African American (AfA) adults >40 years of age having nearly twofold higher prevalence than European Americans (27.1 and 15.5%, respectively) (2). In addition to socioeconomic and behavioral risk factors, genetic factors are likely contributors to T2D risk in AfA (3).Genome-wide association studies (GWAS) for T2D and related traits have successfully identified >50 loci with common genetic variants associated with T2D risk in primarily European-descent populations (4–14) and more recently in East and South Asians (15–21). The reported index single nucleotide polymorphisms (SNPs) at these loci have been replicated in multiple populations (22–24) but less successfully in AfA (25–27). Although differences in environment and lack of study power may partly account for the lack of transferability across ethnicities, differences in linkage disequilibrium (LD) patterns, effect sizes, and risk allele frequency also likely impact the replication of index SNPs. Although the long-range LD in European populations allows for the identification of T2D loci using less dense markers, causal variants are not distinguishable from other nearby SNPs in high LD. This issue prompts the need to examine T2D loci in other populations with different allelic and LD architecture, which may help fine mapping of the underlying functional variants (28).We performed a comprehensive evaluation of the LD region of T2D loci reported in European and Asian GWAS in a meta-analysis of six AfA GWAS. By testing the index and nearby SNPs, we evaluated the transferability of the previously reported loci for T2D association in AfA. We demonstrated that the reduced and differential LD structure in AfA facilitated fine mapping of regions potentially harboring causal variants at some T2D loci. 相似文献
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Yong Liu Jun-Jie ChenNicolas Crook Rong YuXue-Wen Xu Ying Cen 《Burns : journal of the International Society for Burn Injuries》2013