Phase-Resolved Optical Coherence Elastography: An Insight into Tissue Displacement Estimation

Robust methods to compute tissue displacements in optical coherence elastography (OCE) data are paramount, as they play a significant role in the accuracy of tissue elastic properties estimation. In this study, the accuracy of different phase estimators was evaluated on simulated OCE data, where the displacements can be accurately set, and on real data. Displacement (∆d) estimates were computed from (i) the original interferogram data (Δφori) and two phase-invariant mathematical manipulations of the interferogram: (ii) its first-order derivative (Δφd) and (iii) its integral (Δφint). We observed a dependence of the phase difference estimation accuracy on the initial depth location of the scatterer and the magnitude of the tissue displacement. However, by combining the three phase-difference estimates (Δdav), the error in phase difference estimation could be minimized. By using Δdav, the median root-mean-square error associated with displacement prediction in simulated OCE data was reduced by 85% and 70% in data with and without noise, respectively, in relation to the traditional estimate. Furthermore, a modest improvement in the minimum detectable displacement in real OCE data was also observed, particularly in data with low signal-to-noise ratios. The feasibility of using Δdav to estimate agarose phantoms’ Young’s modulus is illustrated

Low-sodium diet induces atherogenesis regardless of lowering blood pressure in hypertensive hyperlipidemic mice.

This study investigated the influence of sodium restriction and antihypertensive drugs on atherogenesis utilizing hypertensive (H) low-density lipoprotein-receptor knockout mice treated or not with losartan (Los) or hydralazine (Hyd) and fed low-sodium (LS) or normal-sodium (NS) chow. Despite reducing the blood pressure (BP) of H-LS mice, the LS diet caused arterial lipid infiltration due to increased plasma total cholesterol (TC) and triglycerides (TG). Los and Hyd reduced the BP of H-LS mice, and Los effectively prevented arterial injury, likely by reducing plasma TG and nonesterified fatty acids. Aortic lipid infiltration was lower in Los-treated H-LS mice (H-LS+Los) than in normotensive (N)-LS and H-LS mice. Aortic angiotensin II type 1 (AT1) receptor content was greater in H-NS than H-LS mice and in H-LS+Hyd than H-LS+Los mice. Carboxymethyl-lysine (CML) and receptor for advanced glycation end products (RAGE) immunostaining was greater in H-LS than H-NS mice. CML and RAGE levels were lower in LS animals treated with antihypertensive drugs, and Hyd enhanced the AT1 receptor level. Hyd also increased the gene expression of F4/80 but not tumor necrosis factor-α, interleukin (IL)-1β, IL-6, IL-10, intercellular adhesion molecule-1 or cluster of differentiation 66. The novelty of the current study is that in a murine model of simultaneous hypertension and hyperlipidemia, the pleiotropic effect of chronic, severe sodium restriction elicited aortic damage even with reduced BP. These negative effects on the arterial wall were reduced by AT1 receptor antagonism, demonstrating the influence of angiotensin II in atherogenesis induced by a severely LS diet

Low-sodium diet induces atherogenesis regardless of lowering blood pressure in hypertensive hyperlipidemic mice - Fig 5

<p>Histomorphometric analysis of immunofluorescence-stained AT1 receptor (<b>A</b> segments I and II; <b>B</b> segments III and IV), and vascular injury quantified by a histomorphometric analysis of immunofluorescence-stained CML (<b>C</b> segments I and II; <b>D</b> segments III and IV) and RAGE (<b>E</b> segments I and II; <b>F</b> segments III and IV); data are represented as the mean percentage of the total positively stained area of the aortic arch cross-sections; n = 4 mice per group. ^a <i>P</i> < 0.05, hypertensive mice fed a normal-sodium diet (H-NS) <i>vs</i> hypertensive mice fed a low-sodium diet (H-LS), Mann Whitney test. ^b <i>P</i> < 0.05, Kruskal Wallis with Dunn’s post hoc test applied for comparisons among LS groups.</p

Representative examples of lipid infiltration visualized by oil red O staining of the intima and media layers of different aortic arch segments from animal groups consisting of hypertensive mice fed a normal-sodium diet (H-NS), normotensive mice fed a low-sodium diet (N-LS), hypertensive mice fed a low-sodium diet (H-LS), hypertensive mice fed a low-sodium diet and treated with losartan (H-LS+Los) and hypertensive mice fed a low-sodium diet and treated with hydralazine (H-LS+Hyd).

<p>Arrows indicate sites of aortic arch lipid infiltration. ADV = adventitia, MED = media, INT = intima (400×).</p

Gene expression (mRNA) of the AT1 receptor (<i>Agtr1</i>) and RAGE (<i>Ager</i>) in the mouse aortic arch.

<p>Data are expressed as relative mRNA units normalized to mouse β2M expression. Mann Whitney test was used for comparisons between hypertensive mice fed a normal-sodium (H-NS) diet and hypertensive mice fed a low-sodium (H-LS) diet. The Kruskal Wallis test with Dunn’s post hoc test was applied for comparisons among the LS groups; n ≥ 4 mice per group.</p

Phenotypic characteristics of normotensive (N) or hypertensive (H) LDLR KO mice fed either a normal-sodium (NS) or a low-sodium (LS) diet and treated or not with losartan (Los) or hydralazine (Hyd).

<p>Phenotypic characteristics of normotensive (N) or hypertensive (H) LDLR KO mice fed either a normal-sodium (NS) or a low-sodium (LS) diet and treated or not with losartan (Los) or hydralazine (Hyd).</p

Gene-specific RT-PCR primers.

<p>Gene-specific RT-PCR primers.</p

Univariate regression analysis of arterial lipid infiltration in N and H LDLR KO mice fed a NS or LS diet treated or not with an antihypertensive drug.

<p>Univariate regression analysis of arterial lipid infiltration in N and H LDLR KO mice fed a NS or LS diet treated or not with an antihypertensive drug.</p

Th17/Treg-Related Intracellular Signaling in Patients with Chronic Obstructive Pulmonary Disease: Comparison between Local and Systemic Responses

Th17/Treg imbalance plays a pivotal role in COPD development and progression. We aimed to assess Th17/Treg-related intracellular signaling at different COPD stages in local and systemic responses. Lung tissue and/or peripheral blood samples were collected and divided into non-obstructed (NOS), COPD stages I and II, and COPD stages III and IV groups. Gene expression of STAT3 and -5, RORγt, Foxp3, interleukin (IL)-6, -17, -10, and TGF-β was assessed by RT-qPCR. IL-6, -17, -10, and TGF-β levels were determined by ELISA. We observed increased STAT3, RORγt, Foxp3, IL-6, and TGF-β gene expression and IL-6 levels in the lungs of COPD I and II patients compared to those of NOS patients. Regarding the systemic response, we observed increased STAT3, RORγt, IL-6, and TGF-β gene expression in the COPD III and IV group and increased IL-6 levels in the COPD I and II group. STAT5 was increased in COPD III and IV patients, although there was a decrease in Foxp3 expression and IL-10 levels in the COPD I and II and COPD III and IV groups, respectively. We demonstrated that an increase in Th17 intracellular signaling in the lungs precedes this increase in the systemic response, whereas Treg intracellular signaling varies between the compartments analyzed in different COPD stages