| 61. |
- Sun, Ying, et al.
(författare)
-
Joint Exposure to Positive Affect, Life Satisfaction, Depressive Symptoms, and Neuroticism and Incident Type 2 Diabetes
- 2022
-
Ingår i: Journal of Clinical Endocrinology and Metabolism. - : The Endocrine Society. - 0021-972X .- 1945-7197. ; 107:8, s. E3186-E3193
-
Tidskriftsartikel (refereegranskat)abstract
- Context Whether the psychological wellbeing status could be a risk factor for type 2 diabetes is unclear. Objective We aimed to measure the association between combined psychological wellbeing factors and type 2 diabetes and investigate whether this association was modified by genetic predisposition. Methods Prospective cohort study from the UK Biobank. In total, 127 496 participants who completed a psychological wellbeing questionnaire and did not have type 2 diabetes at baseline (2006-2010) were included; among them, 88 584 (69.5%) were analyzed to determine their genetic predisposition. The main outcome measure was incident type 2 diabetes. Results During the median follow-up of 10.0 years, 2547 incident type 2 diabetes cases were documented. Moderate to extreme unhappiness, satisfaction score <= 3, presence of broad depression, and a neuroticism score >= 3 were all significantly and independently associated with an increased risk of diabetes. When considered as a combination indicator, compared with individuals in the highest quartile of the psychological wellbeing score, the fully adjusted hazard ratios (95% CI) of type 2 diabetes were 1.41 (1.21-1.65) in the third quartile, 1.45 (1.24-1.69) in the second quartile, and 1.73 (1.48-2.01) in the lowest quartile. In the stratified analysis, we observed significant interactions between age and physical activity, and type 2 diabetes (P-interaction < .001 and 0.049, respectively). However, there was no significant interaction between the psychological wellbeing score and genetic susceptibility to diabetes (P-interaction = .980). Conclusion Worse overall psychological wellbeing was associated with a significantly increased risk of type 2 diabetes in a dose-response fashion regardless of genetic predisposition.
|
|
| 62. |
- Sun, Ying, et al.
(författare)
-
Sweetened Beverages, Genetic Susceptibility, and Incident Atrial Fibrillation : A Prospective Cohort Study
- 2024
-
Ingår i: Circulation. - : American Heart Association. - 1941-3149 .- 1941-3084. ; 17:3
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: An association between sweetened beverages and several cardiometabolic diseases has been reported, but their association with atrial fibrillation (AF) is unclear. We aimed to investigate the associations between consumption of sugar-sweetened beverages (SSB), artificially sweetened beverages (ASB), and pure fruit juice (PJ) and risk of consumption with AF risk and further evaluate whether genetic susceptibility modifies these associations.METHODS:A total of 201 856 participants who were free of baseline AF, had genetic data available, and completed a 24-hour diet questionnaire were included. Cox proportional hazard models were used to estimate the hazard ratios (HRs) and 95% confidence intervals (CIs).RESULTS: During a median follow-up of 9.9 years, 9362 incident AF cases were documented. Compared with nonconsumers, individuals who consumed >2 L/wk of SSB or ASB had an increased risk of AF (HR, 1.10 [95% CI, 1.01-1.20] and HR, 1.20 [95% CI, 1.10-1.31]) in the multivariable-adjusted model. A negative association was observed between the consumption of ≤ 1 L/wk of PJ and the risk of AF (HR, 0.92 [95% CI, 0.87-0.97]). The highest HRs (95% CIs) of AF were observed for participants at high genetic risk who consumed >2 L/wk of ASB (HR, 3.51 [95% CI, 2.94-4.19]), and the lowest HR were observed for those at low genetic risk who consumed ≤ 1 L/wk of PJ (HR, 0.77 [95% CI, 0.65-0.92]). No significant interactions were observed between the consumption of SSB, ASB, or PJ and genetic predisposition to AF.CONCLUSIONS: Consumption of SSB and ASB at >2 L/wk was associated with an increased risk for AF. PJ consumption ≤ 1 L/wk was associated with a modestly lower risk for AF. The association between sweetened beverages and AF risk persisted after adjustment for genetic susceptibility to AF. This study does not demonstrate that consumption of SSB and ASB alters AF risk but rather that the consumption of SSB and ASB may predict AF risk beyond traditional risk factors.
|
|
| 63. |
- Wang, Baoyuan, et al.
(författare)
-
Fast ionic conduction in semiconductor CeO2-delta electrolyte fuel cells
- 2019
-
Ingår i: NPG ASIA MATERIALS. - : Nature Publishing Group. - 1884-4049 .- 1884-4057. ; 11:1
-
Tidskriftsartikel (refereegranskat)abstract
- Producing electrolytes with high ionic conductivity has been a critical challenge in the progressive development of solid oxide fuel cells (SOFCs) for practical applications. The conventional methodology uses the ion doping method to develop electrolyte materials, e.g., samarium-doped ceria (SDC) and yttrium-stabilized zirconia (YSZ), but challenges remain. In the present work, we introduce a logical design of non-stoichiometric CeO2-delta based on non-doped ceria with a focus on the surface properties of the particles. The CeO2-delta reached an ionic conductivity of 0.1 S/cm and was used as the electrolyte in a fuel cell, resulting in a remarkable power output of 660 mW/cm(2) at 550 degrees C. Scanning transmission electron microscopy (STEM) combined with electron energy-loss spectroscopy (EELS) clearly clarified that a surface buried layer on the order of a few nanometers was composed of Ce3+ on ceria particles to form a CeO2-delta@CeO2 core-shell heterostructure. The oxygen deficient layer on the surface provided ionic transport pathways. Simultaneously, band energy alignment is proposed to address the short circuiting issue. This work provides a simple and feasible methodology beyond common structural (bulk) doping to produce sufficient ionic conductivity. This work also demonstrates a new approach to progress from material fundamentals to an advanced low-temperature SOFC technology.
|
|
| 64. |
- Wang, Baoyuan, et al.
(författare)
-
Preparation and characterization of Sm and Ca co-doped ceria-La0.6Sr0.4Co0.2Fe0.8O3-delta semiconductor-ionic composites for electrolyte-layer-free fuel cells
- 2016
-
Ingår i: Journal of Materials Chemistry A. - : Royal Society of Chemistry. - 2050-7488 .- 2050-7496. ; 4:40, s. 15426-15436
-
Tidskriftsartikel (refereegranskat)abstract
- A series of Sm and Ca co-doped ceria, i.e. Ca0.04Ce0.96-xSmxO2-delta (x = 0, 0.09, 0.16, and 0.24) (SCDC), were synthesized by a co-precipitation method. Detailed morphology, composition, crystal structure and electrochemical properties of the prepared materials were characterized. The results revealed that Sm and Ca co-doping could enhance the ionic conductivity in comparison with that of single Ca-doped samples. The composition as Ca0.04Ce0.80Sm0.16O2-delta exhibited a highest ionic conductivity of 0.039 S cm(-1) at 600 degrees C in comparison with the rest of the series, and the optimal ionic conductivity can be interpreted by the coupling effect of oxygen vacancies and mismatch between the dopant ionic radius and critical radius. Composite formation between the semiconductor La0.6Sr0.4Co0.2Fe0.8O3-delta (LSCF) and the as-prepared SCDC contributed to a remarkable improvement in the ionic conductivity, an unexpectedly high ionic conductivity of 0.188 S cm(-1) was obtained for LSCF-SCDC composites at 600 degrees C, which was four times higher than that of pure SCDC. Using transmission electron microscopy and spectroscopy approaches, we detected an enrichment of oxygen in the LSCF-SCDC interface region and a depletion of oxygen vacancies in LSCF-SCDC and LSCF-LSCF grain boundaries was significantly mitigated, which resulted in the enhancement of ionic conductivity of semiconductor-ionic LSCF-SCDC composites. The electrolyte-layer-free fuel cell (EFFC) fabricated from the LSCF-SCDC semiconductor-ionic membrane demonstrated excellent performances, e.g. 814 mW cm(-2) at 550 degrees C for using the LSCF-Ca0.04Ce0.80Sm0.16O2-delta (SCDC2).
|
|
| 65. |
|
|
| 66. |
- Wang, Mojin, et al.
(författare)
-
A-Kinase Anchoring Proteins 10 Expression in Relation to 2073A/G Polymorphism and Tumor Progression in Patients with Colorectal Cancer
- 2013
-
Ingår i: Pathology and Oncology Research. - : Springer Verlag (Germany). - 1219-4956 .- 1532-2807. ; 19:3, s. 521-527
-
Tidskriftsartikel (refereegranskat)abstract
- The cAMP/PKA signalling events regulated by A-kinase anchoring proteins 10 (AKAP10) is involved in tumorigenesis. Previous study showed that AKAP10 polymorphism (2073 A/G, I646V) was associated with colorectal cancer risk. However, there was no literature reporting the role of AKAP10 in the pathogenesis of colorectal cancer. The aim of the study was to investigate the clinicopathologic significance of A-kinase anchoring proteins 10 (AKAP 10) expression and the relationship with its polymorphism in colorectal cancer. The expression of AKAP10 was determined by immunohistochemical staining (IHC) and western blot assay on colorectal cancer (n = 176), adenoma (n = 87) and distant normal mucosa (n = 72). 176 patients with colorectal cancer were genotyped for AKAP10 2073A/G polymorphism by TaqMan RT-PCR. We found that the positive expression rate of AKAP10 in colorectal cancer (59 %) was significantly higher than those in adenoma (39 %) and distant normal mucosa (42 %) (P = 0.004). There was no significant difference between adenoma and distant normal mucosa (P = 0.741). Positive AKAP10 staining was correlated with deeper tumor invasion (P < 0.001), lymph nodes metastasis (P = 0.022), advanced tumor stage (P < 0.001) and poorly differentiated degree (P = 0.003). Compared with AA genotype (52 %), positive expression of AKAP10 was significantly increased in colorectal cancer patients with the variant (AG+GG) genotypes (68 %, P = 0.033). It was concluded that AKAP10 may play an important role in the development and progression of colorectal cancer.
|
|
| 67. |
- Wang, Mo-Jin, et al.
(författare)
-
Downregulation of microRNA-124 is an independent prognostic factor in patients with colorectal cancer
- 2013
-
Ingår i: International Journal of Colorectal Disease. - : Springer Verlag (Germany). - 0179-1958 .- 1432-1262. ; 28:2, s. 183-189
-
Tidskriftsartikel (refereegranskat)abstract
- PurposeRecently, microRNA-124 (miR-124) has been demonstrated as a potential tumor suppressor in several types of cancers. However, the role of miR-124 in colorectal cancer remains unclear. This study was aimed at investigating the clinicopathological significance of miR-124 expression in colorectal cancer.MethodsQuantitative real-time PCR was used to analyze miR-124 expression in 96 colorectal cancers and individual-matched normal mucosa samples. The expression of miR-124 was assessed for associations with clinicopathological characteristics using chi-square test. The survival curves were calculated by the Kaplan–Meier method. The influence of each variable on survival was examined by the Cox multivariate regression analysis.ResultsThe miR-124 expression was significantly downregulated in colorectal cancer compared to normal mucosa (P = 0.001). In colorectal cancer, miR-124 decreased expression correlated significantly with the grade of differentiation (P = 0.021). Univariate survival analysis showed that the downregulated miR-124 was significantly correlated with worse prognosis, both in terms of overall survival (P = 0.017) and disease-free survival (DFS) (P = 0.014). Further, the downregulated miR-124 was demonstrated as a prognostic factor for overall survival (hazard ratio, HR = 4.634; 95 % confidence interval, CI, 1.731–12.404; P = 0.002) and DFS (HR = 4.533, 95 % CI 1.733–11.856, P = 0.002), independently of gender, age, location, maximum tumor size, depth of invasion, differentiation, and TNM stage.ConclusionsMiR-124 may play a certain role in the development of colorectal cancer. The downregulation expression of miR-124 is an independent prognostic factor in patients with colorectal cancer.
|
|
| 68. |
- Wang, Mojin, et al.
(författare)
-
The PKA RI alpha/A-kinase anchoring proteins 10 signaling pathway and the prognosis of colorectal cancer
- 2015
-
Ingår i: Journal of Gastroenterology and Hepatology. - : Wiley: 12 months. - 0815-9319 .- 1440-1746. ; 30:3, s. 496-503
-
Tidskriftsartikel (refereegranskat)abstract
- Background and AimPreviously study showed that the loss of the control of cAMP-dependent protein kinase A RI (PKA RI)/ A-kinase anchoring proteins 10 (AKAP10) signaling pathway initiate dysregulation of cellular healthy physiology leading to tumorigenesis. The aim of this study was to investigate the role of PKA RI/AKAP10 signaling pathway in colorectal cancer (CRC). MethodsThe AKAP10 expression at the mRNA and protein level have been analyzed in colon cancer cell lines, primary CRCs and matched normal mucosa samples, and compared in accordance with specific clinicopathological features of CRC. The correlation between expression of AKAP10 and PKA RI were also analyzed. ResultsCompared with HCT116 and SW480 cells, the AKAP10 was significantly upregulated in the colon cell line KM12C and its metastatic counterparts, KM12SM and KM12L4A. Moreover, the KM12SM and KM12L4A having high metastatic potentials displayed the elevated levels of AKAP10 compared with KM12C having poor metastatic potential. A notably higher level of AKAP10 expression was found in CRC tissues at both mRNA and protein levels. Increased expression of AKAP10 in CRC patients was positively associated with the depth of invasion and the grade of differentiation. Univariate survival analysis showed that the increased expression of AKAP10 was related to poorer survival. Cox multivariate regression analysis confirmed that AKAP10 was an independent predictor of the overall survival of CRC patients. PKA RI mRNA was also expressed at high levels in CRC. The correlation coefficient between mRNA expression of AKAP10 and PKA RI in CRC was 0.417. AKAP10mRNA overexpression was correlated significantly with PKA RI. ConclusionsOur data indicated that PKA RI/AKAP10 signaling pathway is associated with the progression and prognosis of CRC.
|
|
| 69. |
- Wang, Ningjian, et al.
(författare)
-
Acquired risk factors and incident atrial fibrillation according to age and genetic predisposition
- 2023
-
Ingår i: European Heart Journal. - : Oxford University Press. - 0195-668X .- 1522-9645. ; 44:47, s. 4982-4993
-
Tidskriftsartikel (refereegranskat)abstract
- Background and Aims: Atrial fibrillation (AF) is the most common sustained arrhythmia in adults. Investigations of risk factor profiles for AF according to age and genetic risk groups are essential to promote individualized strategies for the prevention and control of AF.Methods: A total of 409 661 participants (mean age, 56 years; 46% men) free of AF at baseline and with complete information about risk factors were included from the UK Biobank cohort. The hazard ratios and population-attributable risk (PAR) percentages of incident AF associated with 23 risk factors were examined, including 3 social factors, 7 health behaviours, 6 cardiometabolic factors, 6 clinical comorbidities, and the genetic risk score (GRS), across 3 age groups (40-49, 50-59, and 60-69 years) and 3 genetic risk groups (low, moderate, and high GRS).Results: After a follow-up of 5 027 587 person-years, 23 847 participants developed AF. Most cardiometabolic factors and clinical comorbidities showed a significant interaction with age, whereby the associations were generally strengthened in younger groups (Pinteraction < .002). However, only low LDL cholesterol, renal dysfunction, and cardiovascular disease showed a significant interaction with genetic risk, and the associations with these factors were stronger in lower genetic risk groups (Pinteraction < .002). Cardiometabolic factors consistently accounted for the largest number of incident AF cases across all age groups (PAR: 36.2%-38.9%) and genetic risk groups (34.0%-41.9%), with hypertension and overweight/obesity being the two leading modifiable factors. Health behaviours (PAR: 11.5% vs. 8.7%) and genetic risk factors (19.1% vs. 14.3%) contributed to more AF cases in the 40-49 years group than in the 60-69 years group, while the contribution of clinical comorbidities remained relatively stable across different age groups. The AF risk attributable to overall cardiometabolic factors (PAR: 41.9% in the low genetic risk group and 34.0% in the high genetic risk group) and clinical comorbidities (24.7% and 15.9%) decreased with increasing genetic risk. The impact of social factors on AF was relatively low across the groups by age and genetic risk.Conclusions: This study provided comprehensive information about age- and genetic predisposition-related risk factor profiles for AF in a cohort of UK adults. Prioritizing risk factors according to age and genetic risk stratifications may help to achieve precise and efficient prevention of AF.
|
|
| 70. |
- Wang, Ningjian, et al.
(författare)
-
Long-term night shift work is associated with the risk of atrial fibrillation and coronary heart disease
- 2021
-
Ingår i: European Heart Journal. - : Oxford University Press. - 0195-668X .- 1522-9645. ; 42:40, s. 4180-
-
Tidskriftsartikel (refereegranskat)abstract
- AimsThe aim of this study was to test whether current and past night shift work was associated with incident atrial fibrillation (AF) and whether this association was modified by genetic vulnerability. Its associations with coronary heart disease (CHD), stroke, and heart failure (HF) were measured as a secondary aim.Methods and resultsThis cohort study included 283657 participants in paid employment or self-employed without AF and 276009 participants free of CHD, stroke, and HF at baseline in the UK Biobank. Current and lifetime night shift work information was obtained. Cox proportional hazard models were used. Weighted genetic risk score for AF was calculated. During a median follow-up of 10.4years, 5777 incident AF cases were documented. From 'day workers', 'shift but never/rarely night shifts', and 'some night shifts' to 'usual/permanent night shifts', there was a significant increasing trend in the risk of incident AF (P for trend 0.013). Usual or permanent night shifts were associated with the highest risk [hazard ratio (HR) 1.16, 95% confidence interval (CI) 1.02-1.32]. Considering a person's lifetime work schedule and compared with shift workers never working nights, participants with a duration over 10years and an average 3-8 nights/month frequency of night shift work exposure possessed higher AF risk (HR 1.18, 95% CI 0.99-1.40 and HR 1.22, 95% CI 1.02-1.45, respectively). These associations between current and lifetime night shifts and AF were not modified by genetic predisposition to AF. Usual/permanent current night shifts, >= 10years and 3-8 nights/month of lifetime night shifts were significantly associated with a higher risk of incident CHD (HR 1.22, 95% CI 1.11-1.35, HR 1.37, 95% CI 1.20-1.58 and HR 1.35, 95% CI 1.18-1.55, respectively). These associations in stroke and HF were not significant.ConclusionBoth current and lifetime night shift exposures were associated with increased AF risk, regardless of genetic AF risk. Night shift exposure also increased the risk of CHD but not stroke or HF. Whether decreasing night shift work frequency and duration might represent another avenue to improve heart health during working life and beyond warrants further study.
|
|
