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  • Hindawi Limited  (8)
  • 1
    In: BioMed Research International, Hindawi Limited, Vol. 2017 ( 2017), p. 1-9
    Abstract: Objective . This study mainly aimed to explore the association between brain-derived neurotropic factor (BDNF) Val66Met polymorphism and posttraumatic stress disorder (PTSD) among flood survivors in China. Methods . Individuals who experienced the 1998 Dongting Lake flood in Southeast Huarong, China, were enrolled in this study. Qualified health personnel carried out face-to-face interviews with participants. PTSD was identified using PTSD Checklist-Civilian version (PCL-C). Blood samples were collected from the participants to extract DNA for genotyping. Results . A total of 175 participants were enrolled in this study. The prevalence of PTSD among flood survivors at 17-year follow-up was 16.0% (28/175). Individuals with PTSD were more likely to be female, experience at least three flood-related stressors, experience at least three postflood stressors, and carry the Met than those without PTSD. Compared with Val/Val homozygotes, Met carriers had higher scores of PCL-C (mean ± standard error: 23.60 ± 7.23 versus 27.1 9 ± 9 . 48 , P 〈 0.05 ). Multivariable logistic regression analysis indicated that Met carriers (aOR = 4.76, 95% CI = 1.02–22.15, P 〈 0.05 ) were more likely to develop PTSD than Val/Val homozygotes. Conclusions . Met carriers for BDNF rs6265 are at higher risk of developing PTSD and also exhibit more severe PTSD symptoms than Val/Val homozygotes among flood survivors in China.
    Type of Medium: Online Resource
    ISSN: 2314-6133 , 2314-6141
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2017
    detail.hit.zdb_id: 2698540-8
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  • 2
    In: Journal of Diabetes Research, Hindawi Limited, Vol. 2015 ( 2015), p. 1-9
    Abstract: The aim of this study was to evaluate the associations between chronic smoking and insulin resistance and β -cell function in Chinese men without diabetes. A total of 1,568 participants were recruited by multistage sampling. Using homeostatic model assessment (HOMA), geometric means of insulin resistance (HOMA-IR) and β -cell function (HOMA- β ) with 95% confidence interval (CI) were calculated by general linear model. Odds ratios (ORs) with 95% CI were estimated to evaluate the associations between smoking status and insulin resistance and β -cell deficiency under a logistic regression model. Current smokers had higher levels of 2 h glucose (6.66 versus 6.48 mmol/L) for oral glucose tolerance test and lower levels of fasting insulin (5.68 versus 6.03 mU/L) than never smokers. The adjusted means for HOMA- β (%) were 54.86 in current smokers and 58.81 in never smokers ( P = 0.0257 ). Current smoking was associated with β -cell deficiency (OR 1.29, 95% CI 1.01–1.64) compared to never smoking. The β -cell function gradually decreased with increasing smoking intensity ( P trend = 0.0026 ), and the differences were statistically significant when the pack-year of smoking was 20 or above. No association was observed between smoking status and HOMA-IR. Our study suggested that chronic smoking may dose-dependently suppress insulin secretion in Chinese men.
    Type of Medium: Online Resource
    ISSN: 2314-6745 , 2314-6753
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2015
    detail.hit.zdb_id: 2711897-6
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  • 3
    Online Resource
    Online Resource
    Hindawi Limited ; 2022
    In:  Computational and Mathematical Methods in Medicine Vol. 2022 ( 2022-4-5), p. 1-8
    In: Computational and Mathematical Methods in Medicine, Hindawi Limited, Vol. 2022 ( 2022-4-5), p. 1-8
    Abstract: In order to analyze the effect of postoperative nursing for bones and joints, this paper combines the intelligent medical Internet of Things technology to construct a postoperative nursing system for bones and joints and conducts research on postoperative nursing methods for bones and joints. Moreover, this paper realizes the integration of “voice data + video data + software data” and the integration of “wired network + RFID sensor network + WIFI wireless network.” In this paper, this paper constructs an intelligent medical IoT nursing analysis system, combines actual cases to analyze the effect of postoperative nursing of bones and joints, and selects an intelligent IoT system and statistical software SPSS23.0 to complete statistical processing.
    Type of Medium: Online Resource
    ISSN: 1748-6718 , 1748-670X
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2022
    detail.hit.zdb_id: 2256917-0
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  • 4
    In: Oxidative Medicine and Cellular Longevity, Hindawi Limited, Vol. 2019 ( 2019-05-09), p. 1-19
    Abstract: Ribosome biogenesis is a crucial biological process related to cell proliferation, redox balance, and muscle contractility. Aortic smooth muscle cells (ASMCs) show inhibition of proliferation and apoptosis, along with high levels of oxidative stress in aortic dissection (AD). Theoretically, ribosome biogenesis should be enhanced in the ASMCs at its proliferative state but suppressed during apoptosis and oxidative stress. However, the exact status and role of ribosome biogenesis in AD are unknown. We therefore analyzed the expression levels of BOP1, a component of the PeBoW complex which is crucial to ribosome biogenesis, in AD patients and a murine AD model and its influence on the ASMCs. BOP1 was downregulated in the aortic tissues of AD patients compared to healthy donors. In addition, overexpression of BOP1 in human aortic smooth muscle cells (HASMCs) inhibited apoptosis and accumulation of p53 under hypoxic conditions, while knockdown of BOP1 decreased the protein synthesis rate and motility of HASMCs. The RNA polymerase I inhibitor cx-5461 induced apoptosis, ROS production, and proliferative inhibition in the HASMCs, which was partly attenuated by p53 knockout. Furthermore, cx-5461 aggravated the severity of AD in vivo , but a p53-/- background extended the life-span and lowered AD incidence in the mice. Taken together, decreased ribosome biogenesis in ASMCs resulting in p53-dependent proliferative inhibition, oxidative stress, and apoptosis is one of the underlying mechanisms of AD.
    Type of Medium: Online Resource
    ISSN: 1942-0900 , 1942-0994
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2019
    detail.hit.zdb_id: 2455981-7
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  • 5
    Online Resource
    Online Resource
    Hindawi Limited ; 2021
    In:  International Journal of Optics Vol. 2021 ( 2021-9-4), p. 1-9
    In: International Journal of Optics, Hindawi Limited, Vol. 2021 ( 2021-9-4), p. 1-9
    Abstract: The selective control of photoassociation of Yb2 is investigated in theory. Based on ab initio to rationalize Franck–Condon filtering, the optimal target states of photoassociation have been obtained. The corresponding vibrational transitions from X1Σ+g to the excited state (A1Σu+, B1Πu, C1Σu+, and D1Πu) are v ′  = 23, 50, 55, and 0, respectively. By using quantum wave packet dynamic methods, we calculated the yields with time evaluation for the selected target states. The projections of time-dependent wave functions of initial states on the target vibrational eigenstates reflected the synthetic yields of Yb2. For target A1Σu+, we used Gaussian pulse to make the yield of v ′  = 23 up to 97% at 725 fs. After a laser pulse, the positive chirp promoted the yield of vibrational states to increase, but the negative chirp inhibited its decrease. For the D1Πu state, when laser intensity is 1.0 × 1014 W/cm2, the purity and yield of target state v ′  = 0 reached the maximum at 1350 fs. That is to say, changing the laser parameters and pulse shapes could control the photochemical reaction along our desired direction. These conditions will provide an important reference and suggest a scheme for a feasible photoassociation of further experimental and theoretical research studies. Current study may promote an important step toward the realization of highly accurate quantum manipulation and material synthesis.
    Type of Medium: Online Resource
    ISSN: 1687-9392 , 1687-9384
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2021
    detail.hit.zdb_id: 2583298-0
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  • 6
    In: Oxidative Medicine and Cellular Longevity, Hindawi Limited, Vol. 2022 ( 2022-10-7), p. 1-24
    Abstract: Hypoxic pulmonary hypertension (HPH) is a progressive cardiopulmonary system disease characterized by pulmonary vascular remodeling. Its occurrence and progression are closely related to oxidative stress. Lycopene, extracted from red vegetables and fruits, exhibits a particularly high antioxidant capacity that is beneficial for cardiovascular diseases. Nevertheless, the role and mechanism of lycopene in HPH remain unknown. Here, we found that lycopene reversed the elevated right ventricular systolic pressure (RVSP), right ventricular hypertrophy, and pulmonary vascular remodeling induced by hypoxia in rats. In vitro, lycopene caused lower proliferation and migration of PASMCs, with higher apoptosis. Consistent with the antiproliferative result of lycopene on hypoxic PASMCs, the hippo signaling pathway associated with cell growth was activated. Furthermore, lycopene reduced malondialdehyde (MDA) levels and enhanced superoxide dismutase (SOD) activity in the lungs and serum of rats under hypoxia conditions. The expression of NOX4 in the lungs was also significantly decreased. Hypoxic PASMCs subjected to lycopene showed decreased reactive oxygen species (ROS) production and NOX4 expression. Importantly, lycopene repressed HIF-1α expression both in the lungs and PASMCs in response to hypoxia in the absence of a significant change of HIF-1α mRNA. Compared with 2ME2 (a HIF-1α inhibitor) alone treatment, lycopene treatment did not significantly change PASMC proliferation, NOX4 expression, and ROS production after 2ME2 blocked HIF-1α, suggesting the inhibitory effect of lycopene on HIF-1α-NOX4-ROS axis and the targeted effect on HIF-1α. After CHX blocked protein synthesis, lycopene promoted the protein degradation of HIF-1α. MG-132, a proteasome inhibitor, notably reversed the decrease in HIF-1α protein level induced by lycopene in response to hypoxia. Therefore, lycopene suppressed hypoxia-induced oxidative stress through HIF-1α-NOX4-ROS axis, thereby alleviating HPH. Our findings will provide a new research direction for clinical HPH therapies.
    Type of Medium: Online Resource
    ISSN: 1942-0994 , 1942-0900
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2022
    detail.hit.zdb_id: 2455981-7
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  • 7
    In: BioMed Research International, Hindawi Limited, Vol. 2018 ( 2018-11-27), p. 1-7
    Abstract: Objectives . AQP7 and AQP9 represent glycerol channel in adipose tissue and liver and have been associated with metabolic diseases. We aimed to investigate the associations between genetic variants in AQP7 and AQP9 genes and the risk of type 2 diabetes (T2DM) in Chinese population. Methods . Blood samples were drawn from 400 T2DM patients and 400 age- and gender-matched controls. Genomic DNA was extracted by proteinase K digestion and phenol–chloroform extraction. Genotyping of 5 single nucleotide polymorphisms (SNPs) in AQP7 (rs2989924, rs3758269, and rs62542743) and AQP9 (rs57139208, rs16939881) was performed by the polymerase chain reaction assay with TaqMan probes. Results . The subjects with rs2989924 GA+AA genotypes had 1.47-fold increased risk of T2DM (odds ratio [OR] 1.47, 95% confidence interval [CI] 1.06-2.04), compared to those with GG genotype, and this association remained significant after adjustment for covariates (OR 1.66, 95% CI 1.07-2.57). When compared with rs3758269 CC genotype, the subjects with CT+TT genotypes had 45% decreased T2DM risk after multivariate adjustment (OR 0.55, 95% CI 0.35-0.85). The associations were evident in elder and overweight subjects and those with central obesity. No association was observed between AQP9 SNPs and T2DM risk. Conclusions . AQP7 SNP rs2989924 and rs3758269 were associated with T2DM risk in Chinese Han population.
    Type of Medium: Online Resource
    ISSN: 2314-6133 , 2314-6141
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2018
    detail.hit.zdb_id: 2698540-8
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  • 8
    In: Mediators of Inflammation, Hindawi Limited, Vol. 2022 ( 2022-6-20), p. 1-13
    Abstract: Nonalcoholic steatohepatitis (NASH) is the common liver disease characterized by hepatic steatosis, inflammation, and fibrosis; there are no approved drugs to treat this disease because of incomplete understanding of pathophysiological mechanisms of NASH. Milk fat globule-epidermal growth factor-factor 8 (MFG-E8), a multifunctional glycoprotein, has shown anti-inflammation and antifibrosis. Here, MFG-E8 was shown to play a key role in NASH progression. Using methionine and choline deficient (MCD) diet-fed mice, we found MFG-E8 knockout exacerbated hepatic damage and steatosis as indicated by increased plasma transaminases activities and hepatic histopathologic change, higher hepatic triglycerides (TGs), and lipid accumulation. Moreover, liver fibrosis and inflammation elicited by MCD were aggravated in MFG-E8 knockout mice. Mechanistically, MFG-E8 knockout facilitated activation of hepatic toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-κB) signaling pathway in MCD-fed mice. In vitro experiment, the TLR4 specific antagonist TAK-242 rescued palmitic acid- (PA-) primed lipid formation and inflammation in MFG-E8 knockout primary murine hepatocytes. These findings indicated that MFG-E8 is involved in the progression of NASH and the possible mechanism by which MFG-E8 knockout exacerbated NASH in mice is associated with activation of the TLR4/NF-κB signaling pathway.
    Type of Medium: Online Resource
    ISSN: 1466-1861 , 0962-9351
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2022
    detail.hit.zdb_id: 2008065-7
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