Concentration Polarization of High-Density Lipoprotein and Its Relation with Shear Stress in an In Vitro Model

The purpose of this study was to determine the concentration polarization of high-density lipoprotein (HDL) at the surface of the carotid artery under conditions of steady flow and to establish its relationship with shear stress using an in vitro vascular simulation model of carotid bifurcation. Shear stress, HDL concentration at the surface, and the ratio of HDL concentration at the surface to concentration in bulk flow were measured at different locations within the model under high-speed (1.451 m/s) and low-speed (0.559 m/s) flow. HDL showed concentration polarization at the surface of the carotid artery model, particularly in the internal carotid artery sinus. With decreasing flow velocity, the shear stress at the surface also decreased, and HDL concentration polarization increased. The concentration polarization of HDL was negatively and strongly correlated with shear stress at both low- (r = −0.872, P < .001) and high-speed flow (r = −0.592, P = .0018)

Relationship between Concentration Difference of Different Density Lipoproteins and Shear Stress in Atherosclerosis

Previous research has observed concentration polarization in LDL and HDL in the arterial system. However, there is no report that links this concentration polarization to the development of vascular atherosclerosis (AS). Therefore, the purpose of this study is to establish the relationship between concentration difference of LDL and HDL and shear stress using a carotid bifurcation vascular model. PTFE was employed to create the carotid bifurcation model. Endothelial cells were coated on the inner wall of the graft. In a recirculation system, HDL and LDL concentration were measured under two different ICA flow velocities at 5 different locations within our model. We report the following: (1) LDL and HDL concentration difference was observed in both high flow and low flow environments; (2) the degree of LDL and HDL concentration polarization varied depending of high flow and low flow environment; (3) absolute values of concentration difference between LDL and HDL at the inner wall surface decreased with the increase in shear stress when shear stress was more than 1.5 Pa. This variation trend would be more pronounced if shear stress were less than 0.5 Pa. Our study suggests that under the action of shear stress, concentration differences of LDL or HDL create a disturbance in the balance of atherogenic factors and anti-As factors, resulting in the occurrence of AS

Y: Concentration polarization of high-density lipoprotein and its relation with shear stress in an in vitro model

The purpose of this study was to determine the concentration polarization of high-density lipoprotein (HDL) at the surface of the carotid artery under conditions of steady flow and to establish its relationship with shear stress using an in vitro vascular simulation model of carotid bifurcation. Shear stress, HDL concentration at the surface, and the ratio of HDL concentration at the surface to concentration in bulk flow were measured at different locations within the model under high-speed (1.451 m/s) and low-speed (0.559 m/s) flow. HDL showed concentration polarization at the surface of the carotid artery model, particularly in the internal carotid artery sinus. With decreasing flow velocity, the shear stress at the surface also decreased, and HDL concentration polarization increased. The concentration polarization of HDL was negatively and strongly correlated with shear stress at both low-(r = −0.872, P &lt; .001) and high-speed flow (r = −0.592, P = .0018)

Sustained therapeutic perfusion outside transplanted sites in chronic myocardial infarction after stem cell transplantation

International audienceThis study aimed at comparing long-term variations in the perfusion of chronic myocardial infarction (MI) areas after local injections of autologous bone marrow stem cells (BMSCs). 14 coronary ligated rats with transmural chronic MI (4 months) were used: a control group (n = 7) versus a treated group (n = 7) in which (111)In labeled-BMSCs were directly engrafted on MI areas. By using (111)In/(99m)Tc SPECT and Sestamibi gated-SPECT,. left ventricle perfusion and function were monitored in all animals by serial (99m)Tc-Sestamibi pinhole gated-SPECT over a period of 6 months. Post-therapeutic myocardial perfusion improved as early as 48 h following injection in the 2 groups. This benefice was sustained during the 6-month follow-up in the non-engrafted MI-areas from treated rats (at 6-months: +10 ± 5 %), whereas the engrafted ones, as well as the MI areas from control rats, exhibited progressive deterioration over time (at 6-months: -9 ± 10 % and -5 ± 3 %, respectively). Perfusion enhancement of the chronic MI areas treated by BMSCs transplantation is: (1) marked in the following days, presumably because of an unspecific inflammatory reaction, and (2) sustained over the long term but only outside the sites of cell engraftment, suggesting a distant paracrine effect of transplanted cells

The Effect of Dexmedetomidine on Cognitive Function and Protein Expression of Aβ, p-Tau, and PSD95 after Extracorporeal Circulation Operation in Aged Rats

Postoperative cognitive dysfunction (POCD) is a kind of serious neurologic complications and dexmedetomidine has a certain effect on POCD. However, functional mechanism of dexmedetomidine on POCD still remains unclear, so the research mainly studied the effect of dexmedetomidine on cognitive function and protein expression in hippocampus and prefrontal cortex cerebrospinal fluid after extracorporeal circulation operation in aged rats. We Found that, compared with POCD group, the cognitive function was improved in POCD + Dex group. We speculate that dexmedetomidine could improve the cognitive function after extracorporeal circulation operation in aged rats and Aβ, p-Tau, and PSD95 protein might have contributed to this favorable outcome

Table2_Construction of a ferroptosis scoring system and identification of LINC01572 as a novel ferroptosis suppressor in lung adenocarcinoma.DOCX

Background: Ferroptosis is a novel process of programmed cell death driven by excessive lipid peroxidation that is associated with the development of lung adenocarcinoma. N6-methyladenosine (m6a) modification of multiple genes is involved in regulating the ferroptosis process, while the predictive value of N6-methyladenosine- and ferroptosis-associated lncRNA (FMRlncRNA) in the prognosis of patients remains with LUAD remains unknown.Methods: Unsupervised cluster algorithm was applied to generate subcluster in LUAD according to ferroptosis-associated lncRNA. Stepwise Cox analysis and LASSO algorithm were applied to develop a prognostic model. Cellular location was detected by single-cell analysis. Also, we conducted Gene set enrichment analysis (GSEA) enrichment, immune microenvironment and drug sensitivity analysis. In addition, the expression and function of the LINC01572 were investigated by several in vitro experiments including qRT-PCR, cell viability assays and ferroptosis assays.Results: A novel ferroptosis-associated lncRNAs-based molecular subtype containing two subclusters were determined in LUAD. Then, we successfully created a risk model according to five ferroptosis-associated lncRNAs (LINC00472, MBNL1-AS1, LINC01572, ZFPM2-AS1, and TMPO-AS1). Our nominated model had good stability and predictive function. The expression patterns of five ferroptosis-associated lncRNAs were confirmed by polymerase chain reaction (PCR) in LUAD cell lines. Knockdown of LINC01572 significantly inhibited cell viability and induced ferroptosis in LUAD cell lines.Conclusion: Our data provided a risk score system based on ferroptosis-associated lncRNAs with prognostic value in LUAD. Moreover, LINC01572 may serve as a novel ferroptosis suppressor in LUAD.</p

Table1_Construction of a ferroptosis scoring system and identification of LINC01572 as a novel ferroptosis suppressor in lung adenocarcinoma.DOCX

Background: Ferroptosis is a novel process of programmed cell death driven by excessive lipid peroxidation that is associated with the development of lung adenocarcinoma. N6-methyladenosine (m6a) modification of multiple genes is involved in regulating the ferroptosis process, while the predictive value of N6-methyladenosine- and ferroptosis-associated lncRNA (FMRlncRNA) in the prognosis of patients remains with LUAD remains unknown.Methods: Unsupervised cluster algorithm was applied to generate subcluster in LUAD according to ferroptosis-associated lncRNA. Stepwise Cox analysis and LASSO algorithm were applied to develop a prognostic model. Cellular location was detected by single-cell analysis. Also, we conducted Gene set enrichment analysis (GSEA) enrichment, immune microenvironment and drug sensitivity analysis. In addition, the expression and function of the LINC01572 were investigated by several in vitro experiments including qRT-PCR, cell viability assays and ferroptosis assays.Results: A novel ferroptosis-associated lncRNAs-based molecular subtype containing two subclusters were determined in LUAD. Then, we successfully created a risk model according to five ferroptosis-associated lncRNAs (LINC00472, MBNL1-AS1, LINC01572, ZFPM2-AS1, and TMPO-AS1). Our nominated model had good stability and predictive function. The expression patterns of five ferroptosis-associated lncRNAs were confirmed by polymerase chain reaction (PCR) in LUAD cell lines. Knockdown of LINC01572 significantly inhibited cell viability and induced ferroptosis in LUAD cell lines.Conclusion: Our data provided a risk score system based on ferroptosis-associated lncRNAs with prognostic value in LUAD. Moreover, LINC01572 may serve as a novel ferroptosis suppressor in LUAD.</p