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1.
Ecotoxicol Environ Saf ; 276: 116308, 2024 May.
Article in English | MEDLINE | ID: mdl-38593496

ABSTRACT

BACKGROUND: Impact of outdoor and household air pollution on physical function remains unelucidated. This study examined the influence of various ambient particulate sizes (PM1, PM2.5, and PM10) and household fuel usage on physical function. METHODS: Data from the China Health and Retirement Longitudinal Study (CHARLS) spanning 2011 and 2015 were utilized. The physical functional score was computed by summing scores from four tests: grip strength, gait speed, chair stand test, and balance. Multivariate linear and linear mixed-effects models were used to explore the separate and combined effects of PM1, PM2.5, PM10 and household fuel use on physical function in the cross-sectional and longitudinal analyses, respectively, and to further observe the effects of fuel cleanup on physical function in the context of air pollution exposure. RESULTS: Both cross-sectional and longitudinal analyses revealed negative correlations between PM1 (ß = -0.044; 95% CI: -0.084, -0.004), PM2.5 (ß = -0.024; 95% CI: -0.046, -0.001), PM10 (ß = -0.041; 95% CI: -0.054, -0.029), and physical function, with a more pronounced impact observed for fine particulate matter (PM1). Cleaner fuel use was associated with enhanced physical function compared to solid fuels (ß = 0.143; 95% CI: 0.070, 0.216). The presence of air pollutants and use of solid fuels had a negative impact on physical function, while cleaner fuel usage mitigated the adverse effects of air pollutants, particularly in areas with high exposure. CONCLUSION: This study underscores the singular and combined detrimental effects of air pollutants and solid fuel usage on physical function. Addressing fine particulate matter, specifically PM1, and prioritizing efforts to improve household fuel cleanliness in regions with elevated air pollution levels are crucial for preventing physical disability.


Subject(s)
Air Pollutants , Air Pollution, Indoor , Particulate Matter , Particulate Matter/analysis , China , Humans , Cross-Sectional Studies , Longitudinal Studies , Middle Aged , Male , Air Pollutants/analysis , Air Pollution, Indoor/analysis , Air Pollution, Indoor/adverse effects , Female , Aged , Cohort Studies , Particle Size , Environmental Exposure , Cooking , Air Pollution/statistics & numerical data , Air Pollution/adverse effects
2.
Front Med (Lausanne) ; 11: 1367900, 2024.
Article in English | MEDLINE | ID: mdl-38500953

ABSTRACT

Purpose: We aimed to explore the effects of percutaneous coronary intervention (PCI) on the ophthalmic artery (OA) hemodynamics in patients with acute coronary syndrome (ACS). Methods: A total of 73 participants (Group0: healthy controls, Group1: Patients with ACS underwent PCI < 3 months, Group2: Patients with ACS underwent PCI ≥ 3 months) were enrolled. Computed tomographic angiography images were used to construct three-dimensional models of participants' OAs. Numerical simulations based on computational fluid dynamics were used to acquire hemodynamic parameters. Results: The angle between the OA and internal carotid artery in Group2 was significantly larger compared with Group0 and Group1 (P = 0.003 and P = 0.044). Hemodynamic simulation showed a significantly slower OA blood velocity in Group1 than in the control (P < 0.001) and Group2 (P = 0.033). Lower wall shear stress was found in Group1 than that in control (P = 0.040). Patients after PCI had a higher wall pressure than healthy controls (P = 0.012 and P = 0.004). Mass flow ratios were decreased in Group1 and Group2 (P = 0.021 and P = 0.002). The hemodynamic parameters of OA were correlated with several clinical indicators. Conclusions: The OA blood flow velocity of patients with ACS after PCI initially slowed down, which increased the risk of plaque formation, and then showed an increasing trend. There was a correlation between OA hemodynamic parameters and clinical indexes related to cardiac stress. Ischemia-reperfusion injury and changes in blood flow status after PCI may affect OA morphology and hemodynamics, leading to ocular lesions. Trial registration: ChiCTR2100050428.

3.
J Leukoc Biol ; 115(6): 1154-1164, 2024 May 29.
Article in English | MEDLINE | ID: mdl-38289832

ABSTRACT

YTHDC1 has been confirmed to mediate osteoporosis (OP) progression by regulating osteogenic differentiation. However, whether YTHDC1 mediates osteoclast differentiation and its molecular mechanism remains unclear. Quantitative real-time polymerase chain reaction and Western blot analysis were performed to detect the levels of YTHDC1, PTPN6, NFATc1, TRAP, RUNX2, alkaline phosphatase, and HUR. YTHDC1 knockout mice was constructed by CRISPR/Cas9 system, and the OP mice model was established by ovariectomy. Hematoxylin and eosin staining and micro-computed tomography were used to evaluate bone formation and bone mass. Mouse primary bone marrow macrophage cells were isolated and induced into osteoclasts. TRAP-positive cells were detected using TRAP staining. MeRIP-qPCR, RIP-qPCR assay, RNA affinity isolation assay, and co-immunoprecipitation assay were used to confirm the interactions among YTHDC1, PTPN6, and HUR. YTHDC1 expression was reduced and positively correlated with lumbar bone mineral density in OP patients. In the ovariectomy model of YTHDC1 knockout mice, bone formation was reduced, bone histomorphology was changed, and osteoclastic-related factor (NFATc1 and TRAP) levels were enhanced. Overexpression YTHDC1 inhibited osteoclast differentiation. YTHDC1 increased PTPN6 messenger RNA stability in an m6A-dependent manner. Moreover, YTHDC1 interacted with HUR to positively regulate PTPN6 expression. PTPN6 knockdown promoted osteoclast differentiation, and this effect was reversed by overexpressing HUR or YTHDC1. YTHDC1 was involved in regulating OP progression through inhibiting osteoclast differentiation by enhancing PTPN6 messenger RNA stability in an m6A-HUR-dependent manner.


Subject(s)
Cell Differentiation , Mice, Knockout , Osteoclasts , Osteoporosis , RNA Stability , RNA, Messenger , Animals , Osteoclasts/metabolism , Mice , Osteoporosis/pathology , Osteoporosis/genetics , Osteoporosis/metabolism , Female , RNA, Messenger/genetics , RNA, Messenger/metabolism , Humans , ELAV-Like Protein 1/metabolism , ELAV-Like Protein 1/genetics , Osteogenesis , Disease Models, Animal , Ovariectomy , Adenosine/analogs & derivatives
4.
Ying Yong Sheng Tai Xue Bao ; 33(6): 1518-1524, 2022 Jun.
Article in Chinese | MEDLINE | ID: mdl-35729128

ABSTRACT

With six Pinus sylvestris var. mongolica plantations (Huinan, Xifeng, Fujia, Zhanggutai, Naiman and Wulanaodu) along an aridity gradient in the Horqin sandy land, we examined the changes in non-structural carbohydrates (NSCs) and nitrogen (N) contents of current and one-year-old needles and twigs, to explore the carbon supply and demand status as well as the nutrient accumulation strategies of P. sylvestris var. mongolica under drought. The results showed that the contents of NSCs and soluble sugars in needles and twigs of P. sylvestris var. mongolica plantations significantly decreased with increasing aridity. From the most humid site (Huinan) to the most aridity site (Wulanaodu), the soluble sugar contents in current and one-year old needles of P. sylvestris var. mongolica decreased from 12.8% and 12.5% to 9.0% and 9.5%, respectively. The soluble sugar contents in current-year old twigs decreased from 15.6% to 9.2%. With increasing aridity, the starch contents in needles and twigs remained relatively stable, soluble sugars/starch ratio in current and one-year old needles decreased, the N contents in current and one-year old twigs significantly increased. The P. sylvestris var. mongolica plantations in the Horqin sandy land consumed soluble sugar storage under drought, resulting in a risk of mortality from 'carbon starvation'. P. sylvestris var. mongolica tended to maintain stable starch storage and accumulate N in twigs to cope with long-term drought stress.


Subject(s)
Pinus sylvestris , Pinus , Carbohydrates , Carbon , Nitrogen , Starch , Sugars
5.
Med Sci Monit ; 27: e929170, 2021 Apr 20.
Article in English | MEDLINE | ID: mdl-33875631

ABSTRACT

BACKGROUND Postmenopausal osteoporosis, a common disease among elderly women, is linked to estrogen deficiency, mechanical loading, and genotype. Circular RNAs (circRNAs) are formed through reverse splicing of the splice donor at the 3' end and the splice accepter at the 5' end in pre-mRNA and have been shown to be involved in the development of multiple diseases. Based on their high sequence conservation and stability, circRNAs may be useful biomarkers in different diseases. However, the roles of circRNAs in postmenopausal osteoporosis remain incompletely understood. MATERIAL AND METHODS Fifty-three postmenopausal women were assigned to either the postmenopausal osteoporosis group (n=28) or the control group (n=25). Reverse-transcriptase quantitative polymerase chain reaction (RT-qPCR) analysis was performed to determine the differential expression of circRNAs between the 2 groups. Receiver-operating characteristic (ROC) curve analysis was conducted to evaluate the clinical diagnostic value of circRNA. Prediction of the binding sites between circRNA and miRNAs was conducted using miRanda and RNAhybrid. The function of the circRNA in osteoclastogenesis was determined by circRNA overexpression followed by tartrate-resistant acid phosphatase staining and RT-qPCR analysis. RESULTS Among 4 circRNAs previously identified by RNA-sequencing analysis as differentially expressed in patients with postmenopausal osteoporosis, only hsa_circ_0021739 showed a significant difference in expression between the groups and was downregulated in patients with postmenopausal osteoporosis. The hsa_circ_0021739 expression level was determined to be correlated with the lumbar vertebra, femur, and forearm T-scores. Overexpression of hsa_circ_0021739 decreased the level of hsa-miR-502-5p and inhibited the differentiation of osteoclasts. CONCLUSIONS The circRNA hsa_circ_0021739 is a potential blood biomarker for postmenopausal osteoporosis. In addition, hsa-miR-502-5p is a likely target of hsa_circ_0021739, which acts to regulate the differentiation of osteoclasts.


Subject(s)
Leukocytes, Mononuclear/immunology , MicroRNAs/genetics , Osteoclasts/physiology , Osteoporosis, Postmenopausal/genetics , RNA, Circular/genetics , Aged , Biomarkers , Cell Differentiation , Cells, Cultured , Down-Regulation , Female , Humans , Osteoporosis, Postmenopausal/immunology , ROC Curve , Transcriptome
6.
Neural Regen Res ; 16(8): 1592-1597, 2021 Aug.
Article in English | MEDLINE | ID: mdl-33433489

ABSTRACT

Cerebrovascular endothelial dysfunction is involved in the progression of leukoaraiosis. Asymmetric dimethylarginine is a competitive inhibitor of nitric oxide, which is highly expressed in patients with leukoaraiosis. Dimethylarginine dimethylaminohydrolase (DDAH) is a hydrolytic enzyme that is primarily responsible for eliminating asymmetric dimethylarginine, and it plays a role in the pathogenesis of cardiovascular and cerebrovascular diseases. The DDAH2 subtype is expressed in organs rich in induced nitric oxide synthase, including the heart, the placenta, and the cerebral endothelium during cerebral ischemia, in the stress state, or under neurotoxicity. Overexpression of the DDAH2 gene can inhibit asymmetric dimethylarginine-induced peripheral circulating endothelial cell dysfunction. However, it is unknown whether this polymorphism regulates plasma asymmetric dimethylarginine levels in patients with leukoaraiosis. In this double-blind study, we recruited 46 patients with leukoaraiosis and 46 healthy, matched controls. Plasma asymmetric dimethylarginine levels were determined using enzyme-linked immunoassays. Genomic DNA was isolated from whole blood samples, and polymerase chain reaction, SmaI restriction enzyme digestion, restriction fragment length polymorphisms, and agarose electrophoresis were used to detect DDAH2 (-449 G/C) gene polymorphisms. The results revealed that 95.65% of leukoaraiosis patients had recessive genetic models (GG and CG), while 89.13% of healthy control subjects had dominant genetic models (CC and CG). There was a significant difference in the genotype composition ratio between leukoaraiosis patients and healthy controls (P = 0.0002). The frequency of G alleles in the leukoaraiosis patients (71.74%) was significantly higher than in healthy controls, whereas the frequency of C alleles was lower (χ2 = 13.9580, P = 0.0002). Furthermore, asymmetric dimethylarginine concentrations in subjects with the GG genotype were significantly higher than in subjects with the CG and CC genotypes (Kruskal-Wallis H = 24.5955, P < 0.0001). In addition, the GG genotype of DDAH2 (-449 G/C) was more common in patients with leukoaraiosis. These findings suggest that the G allele of DDAH2 (-449 G/C) is a risk factor for leukoaraiosis morbidity and is correlated with high levels of asymmetric dimethylarginine. This study was approved by the Institutional Ethics Committee of The 2nd Affiliated Hospital of Harbin Medical University of China (approval No. KY2016-177) on July 28, 2016.

7.
Medicine (Baltimore) ; 96(8): e6153, 2017 Feb.
Article in English | MEDLINE | ID: mdl-28225497

ABSTRACT

To investigate the risk factors for leukoaraiosis (LA) and the correlation between risk factors and LA.The study comprised 92 patients with diagnoses of LA (LA group) and 56 non-LA individuals (control group). Data were collected for the following: age, gender, fasting blood glucose, total cholesterol, triglyceride, high- and low-density lipoprotein cholesterol, uric acid, creatinine, and histories of smoking, hypertension, and diabetes. Levels of serum asymmetric dimethylarginine (ADMA) were detected by enzyme-linked immunosorbent assay.Univariate analysis showed statistical significance between the 2 groups in age, histories of hypertension and smoking, uric acid, creatinine, and levels of serum ADMA (P < 0.05). Binary logistic analysis showed that age (P < 0.0001), hypertension (P = 0.0101), and serum ADMA (P = 0.0206) were related to LA. Pearson correlation analysis showed that levels of serum ADMA correlated with uric acid (r = 0.184, P = 0.025) and creatinine (r = 0.169, P = 0.04).Age, hypertension, and levels of serum ADMA were independent risk factors for LA. Serum ADMA levels may be related to uric acid and creatinine.


Subject(s)
Leukoaraiosis/epidemiology , Age Factors , Aged , Arginine/analogs & derivatives , Arginine/blood , Blood Chemical Analysis , Enzyme-Linked Immunosorbent Assay , Factor Analysis, Statistical , Female , Humans , Leukoaraiosis/blood , Leukoaraiosis/diagnostic imaging , Logistic Models , Male , Middle Aged , Risk Factors
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