ABSTRACT
BACKGROUND: Studies examining the potential association between cooking oil and frailty risk in older adults have produced conflicting outcomes. Therefore, our objective was to explore the relationship between cooking oil (vegetable and animal fat oils), changes in oil usage, and the risk of frailty in older adults. METHODS: We included 4,838 participants aged ≥ 65 years without frailty (frailty index < 0.25) from the 2011 wave of the Chinese Longitudinal Healthy Longevity Survey. Follow-up occurred in the 2014 and 2018 waves. Cox proportional hazard models were utilized to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) to examine the association between cooking oil and frailty. Additionally, we evaluated the effect of switching cooking oil on frailty during the follow-up period. RESULTS: During a median follow-up of 3.0 (2.8-6.9) years, 1,348 individuals (27.9%) developed frailty. Compared to those using vegetable oil, users of animal fat oil had a lower risk of frailty (HR = 0.72, 95% CI: 0.61-0.85). Participants who switched from vegetable oil to animal fat oil, as well as those consistently using animal fat oil, had lower risks of frailty with HRs of 0.70 (0.52-0.95) and 0.63 (0.51-0.77) respectively, compared to those who consistently used vegetable oil. Conversely, individuals who switched from animal fat oil to vegetable oil experienced an increased risk of frailty (HR: 1.41, 95% CI: 1.01-1.97). CONCLUSIONS: The utilization of animal fat oil in cooking exhibited a reduced frailty risk among older adults. Conversely, transitioning from animal fat oil to vegetable oil may elevate the risk. These findings propose that substituting vegetable oil with animal fat oil in the diet may safeguard against frailty.
Subject(s)
Cooking , Frailty , Humans , Aged , Male , Female , Frailty/epidemiology , Frailty/prevention & control , Cooking/methods , Cohort Studies , China/epidemiology , Frail Elderly , Aged, 80 and over , Longitudinal Studies , Incidence , Plant Oils , Proportional Hazards ModelsABSTRACT
The underlying mechanisms of arterial remodeling (AR) remain unclear. Studies have indicated that decellularized scaffolds stimulate the differentiation of fibroblasts into myofibroblasts and promote the accumulation of the extracellular matrix (ECM). In the present study, the impact of ECM changes following AR on vascular smooth muscle cell (VSMC) phenotypes was investigated. VSMCs were co-cultured with normal or calcified decellularized arterial scaffolds. The expression levels of α-smooth muscle actin (α-SMA) and osteopontin (OPN) were measured at 2, 5, 10, 15 and 21 days following the establishment of the co-culture systems. The expression of α-SMA in the normal co-culture group was significantly increased compared with that in the calcified arterial decellularized scaffold co-culture group (P<0.05 and P<0.001). In addition, the expression of OPN in the AR co-culture group was significantly increased compared with the normal co-culture group (P<0.05 and P<0.001). To conclude, the calcified decellularized arterial scaffolds impact VSMC transformation by downregulating α-SMA expression and upregulating OPN expression (P<0.001). To the best of our knowledge, the present study is the first study that co-cultured VSMCs with normal or calcified decellularized arterial scaffolds.
ABSTRACT
OBJECTIVE: To analyze the positive predictive value of large artery occlusion and clinical prognosis in acute ischemic stroke patients with total anterior circulation infarct (TACI) who underwent endovascular treatment in the absence of multimodal CT angiography or CT perfusion. METHODS: The inclusion criteria for the acute ischemic stroke patients to receive endovascular treatment were as the follows: the Oxfordshire Community Stroke Project classification was TACI, Alberta Stroke Program Early Computed Tomography Score (ASPECTS) ≥ 6, National Institutes of Health stroke scale (NIHSS) score ≥8, and less than 4.5 hours since stroke onset. The endovascular treatment was performed on patients who met the inclusion criteria. The endovascular treatment included intra-arterial thrombolysis, mechanical treatments, or both. A retrospective analysis was performed on all eligible acute ischemic stroke patients who underwent endovascular treatment from January 1, 2015 to December 31, 2015. RESULTS: A total of 17 patients met the inclusion criteria and underwent endovascular treatment. The median age was 76 years (range, 59-88 years). 12 patients (70.6%) were diagnosed with atrial fibrillation. 16 patients were diagnosed with large artery occlusion by digital subtraction angiography, and the positive predictive value was 94.1%. 16 patients (94.1%) had recanalization (TICI Grade 3); 12 patients (70.6%) had a modified Rankin Scale score of 0-2, and 1 patient (5.9%) died 90 days after treatment. CONCLUSIONS: In the absence of multimodal CT, endovascular treatment might be beneficial to patients with TACI acute ischemic stroke within 4.5 hours of stroke onset, who had NIHSS score of 8 or greater and ASPECTS of 6 or greater. These inclusion criteria have a high positive predictive value for anterior circulation large artery occlusion.
Subject(s)
Brain Infarction/therapy , Endovascular Procedures , Aged , Aged, 80 and over , Brain Infarction/mortality , Female , Humans , Male , Middle Aged , Prognosis , Retrospective Studies , Severity of Illness Index , Time Factors , Treatment OutcomeABSTRACT
Nontraumatic spontaneous rupture of a bronchial artery aneurysm is rarely seen. In this report, we described such a phenomenon in a patient induced by usage of anticoagulant agent. The patient had no antecedent history of trauma, hypertension, or apparent aortic pathology. The patient who had been taking low-molecular-weight heparin and warfarin to treat deep vein thrombosis complained of a sudden upper abdomen pain with shortness of breath and hypoxemia. The patient was diagnosed and treated for an acute hemomediastinum caused by a ruptured bronchial artery aneurysm. If the patient had continued to take the anticoagulant antithrombotic drugs, it may cause a more virulent bleeding. Taken together, CT angiography is a useful diagnosis tool for patients with sudden chest pain and abdominal pain, and rare cause should be considered.
ABSTRACT
OBJECTIVES: To study whether Clopidogrel-Aspirin combined treatment for high risk transient ischaemic attack (TIA) or minor stroke results in increased number of lesions associated with anti-thrombotic cerebral haemorrhage or cerebral micro-bleeds (CMB) than aspirin alone treatment. METHODS: The patients recruited in CHANCE test in our hospital participated in this study. We made a comparison between treatments Aspirin-Clopidogrel combined group and the Aspirin alone group in the numbers of CMB and subsequent cerebral haemorrhages. In addition, we analysed the association between the increased numbers of CMB and subsequent intracerebral haemorrhages. All 129 patients with high risk TIA with microbleeds or minor stroke within 24âhours after the onset (average age 65.9 ± 9.3, 48.7% were male patients) were divided randomly into two groups: (1) 67 patients were given combination therapy with clopidogrel and aspirin (clopidogrel at an initial dose of 300âmg, then 75âmg per day for 90âdays, plus aspirin at a dose of 75âmg per day for the first 21âdays);(2) the rest patients were given aspirin treatment (75âmg per day for 90âdays). All participants received open-label aspirin at a clinician-determined dose of 75-300âmg on the first day. RESULTS: The CMB were found in 52.7% of all patients in both groups. There was no siginificant difference between the Aspirin group and the Aspirin-clopidogrel treated group, though the latter showed some slight increase in CMB (Odds ratios (OR) = 1.16, 95% confidence intervals (CI) = 0.54-2.47, P = 0.71). But the numbers of CMB were remarkably associated with the number of primary existing CMB (OR = 6.46, 95%CI 2.57-16.23, P < 0.001), especially that of primary existing CMB ≥ 3.In addition, the increasing numbers of CMB associated with primary CMB lesions, which located in corticosubcortical area (CSC) (OR = 4.69, 95%CI 1.51-14.53, P = 0.007). CONCLUSIONS: For the treatment of high-risk TIA or minor stroke patients, the clopidogrel-aspirin treatment did not increase the number of CMB than Aspirin alone. It appears that the extent of CMB was associated with the extent of existing CMB occurred in previous stroke, which was mostly located in cortical, subcortical zone.
Subject(s)
Aspirin/adverse effects , Cerebral Hemorrhage/prevention & control , Ischemic Attack, Transient/prevention & control , Platelet Aggregation Inhibitors/adverse effects , Stroke/prevention & control , Ticlopidine/analogs & derivatives , Aged , Cerebral Cortex/blood supply , Clopidogrel , Drug Therapy, Combination/adverse effects , Female , Humans , Male , Middle Aged , Risk Factors , Ticlopidine/adverse effects , Treatment OutcomeABSTRACT
Vascular calcification significantly affects the health of the elderly. Increasing evidence proved that vascular calcification is an actively regulated osteogenic process. The osteochondrocytic differentiation of mesenchymal stem cells (MSCs) is a significant step of osteogenic processes. The Wnt pathways has been identified as contributing to the regulation of osteogenic mineralization during development and disease. However, it remains unknown whether these MSCs in the vascular calcification differentiate into normal vascular smooth muscle cells (VSMCs) in vivo in order to treat damaged vascular tissue or into calcified VSMCs to aggravate calcification correlated to the Wnt pathways. Thus, it is necessary to analyze the mechanisms of MSC differentiation in detail. In the present study a cellcell coculturing in vitro system was used to observe MSCs that directly interact with normal or calcified VSMCs during calcification and to investigate the gene expression of the Wnt pathways during the process. Direct cocultures were established by seeding two different cell types, VSMCs or calcified VSMCs, or a mixture of both at ratios of 5,000:5,000 cells/1.7 cm2 onto either gelatincoated 1.7cm2 chamber slides for immunohistochemical analysis or gelatincoated 75cm2 tissue culture flasks for protein or RNA isolation. Osteoblastic differentiation was evaluated by examining the cell morphology and assessing the activity of alkaline phosphatase in the cell lysates by alkaline phosphatase staining. Additionally, the mRNA expression levels of the genes encoding for proteins involved in the Wnt signaling proteins, Wnt5A, LRP6, Ror2, cJunNterminal kinase and ßcatenin, were assessed in each group. The present study demonstrated that Wnts are expressed in the progress of differentiation of MSCs during calcification. MSCs can differentiate into different cell phenotypes when there is direct cellcell contact with VSMCs or calcified VSMCs, and the Wnt5a/Ror2 signaling pathway may be associated with the determination of differentiation of MSCs in this process.
Subject(s)
Bone Marrow Cells/cytology , Mesenchymal Stem Cells/cytology , Vascular Calcification , Wnt Proteins/metabolism , Animals , Cell Differentiation , Cells, Cultured , Coculture Techniques , Humans , JNK Mitogen-Activated Protein Kinases/genetics , JNK Mitogen-Activated Protein Kinases/metabolism , Low Density Lipoprotein Receptor-Related Protein-6/genetics , Low Density Lipoprotein Receptor-Related Protein-6/metabolism , Male , Mesenchymal Stem Cells/metabolism , Myocytes, Smooth Muscle/cytology , Myocytes, Smooth Muscle/metabolism , RNA, Messenger/metabolism , Rats , Receptor Tyrosine Kinase-like Orphan Receptors/genetics , Receptor Tyrosine Kinase-like Orphan Receptors/metabolism , Wnt Proteins/genetics , Wnt Signaling Pathway , Wnt-5a Protein , beta Catenin/genetics , beta Catenin/metabolismABSTRACT
OBJECTIVE: Vascular calcification is a common pathobiological process which occurs among the elder population and in patients with diabetes and chronic kidney disease. Osteoprotegerin, a secreted glycoprotein that regulates bone mass, has recently emerged as an important regulator of the development of vascular calcification. However, the mechanism is not fully understood. The purpose of this study is to explore novel signaling mechanisms of osteoprotegerin in the osteoblastic differentiation in rat aortic vascular smooth muscle cells (VSMCs). METHODS AND RESULTS: VSMCs were isolated from thoracic aorta of Sprague Dawley rats. Osteoblastic differentiation of VSMCs was induced by an osteogenic medium. We confirmed by Von Kossa staining and direct cellular calcium measurement that mineralization was significantly increased in VSMCs cultured in osteogenic medium; consistent with an enhanced alkaline phosphatase activity. This osteoblastic differentiation in VSMCs was significantly reduced by the addition of osteoprotegerin in a dose responsive manner. Moreover, we identified, by real-time qPCR and western blotting, that expression of Notch1 and RBP-Jκ were significantly up-regulated in VSMCs cultured in osteogenic medium at both the mRNA and protein levels, these effects were dose-dependently abolished by the treatment of osteoprotegerin. Furthermore, we identified that Msx2, a downstream target of the Notch1/RBP-Jκ signaling, was markedly down-regulated by the treatment of osteoprotegerin. CONCLUSION: Osteoprotegerin inhibits vascular calcification through the down regulation of the Notch1-RBP-Jκ signaling pathway.
Subject(s)
Homeodomain Proteins/metabolism , Immunoglobulin J Recombination Signal Sequence-Binding Protein/metabolism , Muscle, Smooth, Vascular/metabolism , Myocytes, Smooth Muscle/metabolism , Osteoprotegerin/pharmacology , Receptor, Notch1/metabolism , Signal Transduction/drug effects , Vascular Calcification/drug therapy , Alkaline Phosphatase/metabolism , Animals , Male , Myocytes, Smooth Muscle/cytology , Osteoblasts/cytology , Osteoblasts/drug effects , RatsABSTRACT
Cardiovascular disease and osteoporosis are major causes of mortality in the elderly. Alendronate, a bisphosphonate, is widely used in the treatment of osteoporosis and may be used to inhibit vascular calcification. However, its mechanisms are not completely understood. The present study aimed to explore novel signaling mechanisms behind the action of alendronate in the osteoblastic differentiation of rat aortic vascular smooth muscle cells (VSMCs). The osteoblastic differentiation of VSMCs was induced by an osteogenic medium. Using von Kossa staining and direct cellular calcium content determination, mineralization was found to be significantly increased in VSMCs induced with osteogenic medium, consistent with an enhanced alkaline phosphatase activity. Osteoblastic differentiation in VSMCs was significantly reduced by the action of alendronate in a dosedependent manner. In addition, the expression of Notch1 and RBPJκ was significantly upregulated in VSMCs cultured with osteogenic medium at the mRNA and protein levels. The effects of Notch1RBPJκ were inhibited by treatment with alendronate in a dosedependent manner. In summary, results of the current study indicate that alendronate inhibits vascular calcification through downregulation of the Notch1RBPJκ signaling pathway.
Subject(s)
Alendronate/pharmacology , Cell Differentiation/physiology , Immunoglobulin J Recombination Signal Sequence-Binding Protein/metabolism , Muscle, Smooth, Vascular/cytology , Myocytes, Smooth Muscle/cytology , Osteogenesis/drug effects , Receptor, Notch1/metabolism , Signal Transduction/drug effects , Alkaline Phosphatase/metabolism , Animals , Calcium/metabolism , Gene Expression Regulation/drug effects , Homeodomain Proteins/genetics , Homeodomain Proteins/metabolism , Male , Myocytes, Smooth Muscle/drug effects , Myocytes, Smooth Muscle/metabolism , Myocytes, Smooth Muscle/pathology , Osteogenesis/genetics , Rats , Vascular Calcification/metabolismABSTRACT
Accumulating evidence have demonstrated that mesenchymal stem cells (MSCs) are involved in the initiation and progression of various vascular diseases. Canonical Wnt signaling controls the fate of MSCs, and plays an important role in vascular calcification. However, vascular calcification can be inhibited by the non-canonical Wnt signaling pathway Wnt5a/Ror2. This study aimed to investigate whether the Wnt5a/Ror2 pathway is associated with determination of the differentiation fate of MSCs in vascular calcification. Direct co-cultures were established by seeding smooth muscle cells (SMCs) or calcified SMCs and MSCs together at ratios of SMCs or calcified SMCs 15x104; SMCs or calcified SMCs 5x104: MSCs 10x104, SMCs or calcified SMCs 10x104: MSCs 5x104. Osteosynthesis-inducing medium (OS) was added to the culture medium in the groups of MSCs with non-calcified SMCs. Cells were cultured for nine days. Osteoblastic differentiation was evaluated by cell morphology and the activity of alkaline phosphatase (ALP) in cell lysates and ALP staining. Furthermore, we investigated the inhibition of Wnt signaling, and observed that the members of the non-canonical signaling pathway Wnt5a/Ror2 were expressed in each group. Additionally, MSCs cultured in culture media with OS did not differentiate into an osteoblast phenotype when in direct contact with non-calcified SMCs, irrespective of the number of MSCs. However, an osteoblast phenotype was observed when MSCs were cultured in media without OS differentiation towards direct contact with calcified SMCs, and the levels of osteoblastic markers had a direct correlation with the number of MSCs. Of note, the Wnt5a protein was associated with the levels of calcification, thus, although rarely detected in non-calcification, Ror2 mRNA in the non-calcified groups was significantly higher compared to that in the calcified groups. Therefore, the Wnt5a/Ror2 pathway is associated with determination of the differentiation fate of bone marrow mesenchymal stem cells in vascular calcification.