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The foregut, located at the front of the digestive tract, serves a vital role in insects by storing and grinding food into small particles. The innermost layer of the foregut known as the chitinous intima, comes into direct contact with the food and acts as a protective barrier against abrasive particles. Knickkopf (Knk) is required for chitin organization in the chitinous exoskeleton, tracheae and wings. Despite its significance, little is known about the biological function of Knk in the foregut. In this study, we found that LmKnk was stably expressed in the foregut, and highly expressed before molting in Locusta migratoria. To ascertain the biological function of LmKnk in the foregut, we synthesized specific double‐stranded LmKnk (dsLmKnk) and injected it into locusts. Our findings showed a significant decrease in the foregut size, along with reduced food intake and accumulation of residues in the foregut after dsLmKnk injection. Morphological observations revealed that newly formed intima became thinner and lacked chitin lamella. Furthermore, fluorescence immunohistochemistry revealed that LmKnk was located in the apical region of new intima and epithelial cells. Taken together, this study provides insights into the biological function of LmKnk in the foregut, and identifies the potential target gene for exploring biological pest management strategies. [ABSTRACT FROM AUTHOR]

Cerebrovascular alterations in acute bacterial meningitis significantly contribute to adverse patient outcomes, with reported complication rates ranging from 10% to 29%. Focal alterations in arterial lumens, leading to vasoconstriction, are common in cerebral ischemic and inflammatory conditions, such as bacterial meningitis, presenting neurological complications, such as seizures, brain swelling, hydrocephalus, hearing loss and ischemic or hemorrhagic brain damage. The observed arterial narrowing during meningitis is attributed to diverse factors, including direct encroachment by inflammatory exudate, vascular wall edema, vasospasm, and vasculitis due to cellular infiltration and vessel remodeling. Early‐stage constriction might result from a watery exudate's encroachment, whereas persistent inflammation leads to thicker exudates, attracting inflammatory cells and inducing arteriopathic growth factor synthesis. This process promotes structural modifications in the vessel wall, progressing from subintimal infiltration to organic intimal thickening, culminating in vasculitis and the risk of cerebral ischemia. Accordingly, this review seeks to more clearly delineate the intricate relationship between subarachnoid space inflammation and acute and chronic vessel wall remodeling during bacterial meningitis. Conceivably, understanding this pathological process holds promise in unveiling potential treatment avenues to improve patient outcomes, and reduced morbidity and mortality associated with cerebrovascular complications during bacterial meningitis. [ABSTRACT FROM AUTHOR]

Chunkun Yang,1,* Qinwei Zhu,2,* Yanbo Chen,3,* Kui Ji,2 Shuanghong Li,2 Qian Wu,1 Qingquan Pan,2 Jun Li1 1Department of Cardiology, Guang’anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, People’s Republic of China; 2Department of Emergency, Weifang Hospital of Traditional Chinese Medicine, Weifang, Shandong, People’s Republic of China; 3Department of Arrhythmia, Weifang People’s Hospital, Weifang, Shandong, People’s Republic of China*These authors contributed equally to this workThese authors contributed equally to this workCorrespondence: Jun Li, Email gamyylj@163.comAbstract: Cardiovascular diseases (CVDs) are the most common cause of death worldwide and has been the focus of research in the medical community. Curcumin is a polyphenolic compound extracted from the root of turmeric. Curcumin has been shown to have a variety of pharmacological properties over the past decades. Curcumin can significantly protect cardiomyocyte injury after ischemia and hypoxia, inhibit myocardial hypertrophy and fibrosis, improve ventricular remodeling, reduce drug-induced myocardial injury, improve diabetic cardiomyopathy(DCM), alleviate vascular endothelial dysfunction, inhibit foam cell formation, and reduce vascular smooth muscle cells(VSMCs) proliferation. Clinical studies have shown that curcumin has a protective effect on blood vessels. Toxicological studies have shown that curcumin is safe. But high doses of curcumin also have some side effects, such as liver damage and defects in embryonic heart development. This article reviews the mechanism of curcumin intervention on CVDs in recent years, in order to provide reference for the development of new drugs in the future.Keywords: curcumin, intima, endothelial cells, vascular smooth muscle cell, cardiovascular diseases, inflammation, apoptosis

Introduction. There is a growing number of people over 60 years old and consequently a growing number of elderly and senile patients with varicose veins globally. These patients have involutive changes that occur in the body, and therefore they need a special and personalized approach to examination and treatment. Aim. Study and evaluate age-related and varicose disease-related structural changes in the inner lining of the large subcutaneous vein. Materials and methods. 135 fragments of the large subcutaneous vein were examined, 55 of which belonged to deceased people who had no venous disease, 80 operated patients with varicose veins. There are 4 age groups: young, middle, elderly and senile. Histological, morphometric and electron microscopic examination was performed. Results and discussions. The study showed that involutive changes are characterized by a decrease in the number of endothelial cells along the inner perimeter and their flattening, loosening and edema of the subendothelial stroma in persons over 75 years of age. In varicose veins, morphological changes progress with increasing patient age and disease duration. In young and middle-aged people with varicose veins, endotheliocytes flatten, protrude into the lumen of the vessel, collapse, areas of endothelial atrophy appear along the perimeter, signs of myoelastofibrosis appear, as indicated by an increase in the volume fraction of intima due to connective-woven structures. In patients over 60 years of age, endothelial desquamation is more evident in intimacy, the preserved cells are destructively changed, the volume fraction of intima significantly decreases, which corresponds to the signs of intima sclerosis. Conclusions. Under normal conditions in senile age, the volume fraction is significantly reduced compared to the middle age group (p < 0.005). In case of varicose veins, structural changes, both qualitative and quantitative, progress against the background of involutive changes and disease duration, which aggravates endothelial dysfunction.

Mechanical properties of living cells play a crucial role in a wide range of biological functions and pathologies, including atherosclerosis. We used low-stress Scanning Ion-Conductance Microscopy (SICM) correlated with confocal imaging and demonstrated the topographical changes and mechanical properties alterations in EA.hy926 and THP-1 exposed to LDL extracted from CVD patients' blood samples. We show that the cells stiffened in the presence of LDL, which also triggered caveolae formation. Endothelial cells accumulated less cholesterol in the form of lipid droplets in comparison to THP-1 cells based on fluorescence intensity data and biochemical analysis; however, the effect on Young's modulus is higher. The cell stiffness is closely connected to the distribution of lipid droplets along the z-axis. In conclusion, we show that the sensitivity of endothelial cells to LDL is higher compared to that of THP-1, triggering changes in the cytoskeleton and membrane stiffness which may result in the increased permeability of the intima layer due to loss of intercellular connections and adhesion. [ABSTRACT FROM AUTHOR]

Introduction: Clinical verification of rheumatoid vasculitis (RV) persists as a mid‐to‐late diagnosis with medical imaging or biopsy. Early and subclinical presentations of RV, in particular, can remain underdiagnosed in the absence of adequate diagnostic testing. In this study, the research demonstrated the precursory changes for RV in patients with rheumatoid arthritis (RA) using non‐invasive ultrasound imaging of a peripheral vessel. Method: Six participants were recruited: three participants with (RA) and three age‐ and gender‐matched healthy controls. All participants completed a Foot Health Survey Questionnaire (FHSQ), and participants with RA completed a Rheumatoid Arthritis Disease Activity Index‐5 (RADAI‐5). Bilateral B‐mode and Doppler ultrasound of the dorsalis pedis artery (DPA) was performed. The degree of inflammation, lumen and artery diameters, lumen diameter‐to‐artery diameter ratio and peak systolic velocity in the proximal DPA were compared between the two groups. Results: The mean RADAI‐5 score (5.4 ± 0.8 out of 10) indicated moderate disease activity amongst participants with RA. Inflammation was observed in the DPA wall in all participants with RA, compared to no inflammation observed in the control group (Friedmans two‐way analysis: χ2 = 15.733, P = 0.003). Differences between groups for inflammation, lumen diameter and lumen diameter‐to‐artery diameter ratio were found (P < 0.034), without differences for artery diameter and peak systolic velocity (P > 0.605). DPA wall inflammation did not correlate with FHSQ scores (r = −0.770, P = 0.073). Conclusion: Despite moderate RA disease activity, this is the first study to demonstrate the use of ultrasound to observe inflammation in small vessel disease. Our findings suggest ultrasound imaging may be a viable screening tool to demonstrate arterial wall inflammation, indicating the precursory changes of RV. [ABSTRACT FROM AUTHOR]

Atherosclerosis is driven by intimal arterial macrophages accumulating cholesterol. Atherosclerosis also predominantly occurs in areas consisting of proinflammatory arterial endothelial cells. At time of writing, there are no available clinical treatments that precisely remove excess cholesterol from lipid-laden intimal arterial macrophages. Delivery of anti-miR-33a-5p to macrophages has been shown to increase apoAI-mediated cholesterol efflux via ABCA1 upregulation but delivering transgenes to intimal arterial macrophages is challenging due to endothelial cell barrier integrity. In this study, we aimed to test whether lipoparticles targeting proinflammatory endothelial cells can participate in endothelial cell-derived exosome exploitation to facilitate exosome-mediated transgene delivery to macrophages. We constructed lipoparticles that precisely target the proinflammatory endothelium and contain a plasmid that expresses XMOTIF-tagged anti-miR-33a-5p (LP-pXMoAntimiR33a5p), as XMOTIF-tagged small RNA demonstrates the capacity to be selectively shuttled into exosomes. The cultured cells used in our study were immortalized mouse aortic endothelial cells (iMAECs) and RAW 264.7 macrophages. From our results, we observed a significant decrease in miR-33a-5p expression in macrophages treated with exosomes released basolaterally by LPS-challenged iMAECs incubated with LP-pXMoAntimiR33a5p when compared to control macrophages. This decrease in miR-33a-5p expression in the treated macrophages caused ABCA1 upregulation as determined by a significant increase in ABCA1 protein expression in the treated macrophages when compared to the macrophage control group. The increase in ABCA1 protein also simulated ABCA1-dependent cholesterol efflux in treated macrophages—as we observed a significant increase in apoAI-mediated cholesterol efflux—when compared to the control group of macrophages. Based on these findings, strategies that involve combining proinflammatory-targeting lipoparticles and exploitation of endothelial cell-derived exosomes appear to be promising approaches for delivering atheroprotective transgenes to lipid-laden arterial intimal macrophages.

Objective·To explore the feasibility of fluorinated decellularized rabbit aorta as a small artificial blood vessel for tissue engineering.Methods·The obtained rabbit aorta was decellularized in combination with Triton X-100, sodium deoxycholate (SD), sodium dodecyl sulfate (SDS), DNAse, and RNAse. Hematoxylin-eosin staining (H-E staining), Masson staining and Verhoff-von Gieson staining were performed in the decellularized group and undecellularized group, respectively. The effect of decellularization was identified by field emission scanning electron microscope, and the morphological changes of decellularized blood vessels were observed. The decellularized rabbit aorta was used as the arterialized artificial small vessel scaffold, and the decellularized small vessel intima was modified with liquid perfluorocarbons coating to prepare a new type of artificial small vessel. The characteristic groups of the artificial small vessel were qualitatively and quantitatively determined. The dissipation time of liquid on the inner surface of the vessel and the flow of liquid on the surface of the vessel tilted at 45° were observed to analyze the hydrophobicity of the vessel. The blood vessels in the decellularized group and the fluorinated group were implanted with platelet-rich plasma, incubated, and observed under an electron microscope to evaluate the antiplatelet aggregation in vitro. The balloon pressure pump was connected to the aorta of the undecellularized group, decellularized group and fluoride group for bursting pressure test.Results·Histological observation of blood vessels showed that the combination could effectively remove cells while retaining collagen and elastic fibers, and there was no damage to the intima under the electron microscope. There was no significant difference in the pressure blasting test among the three groups. In the hydrophobicity experiment, the retention time of water droplets on the membrane of the fluorinated group was over 5 min, and no obvious water marks were left on the 45° inclined plate. In the platelet adhesion test, intimal aggregation activated platelets in the decellularized group, while they were inhibited in the fluorinated group.Conclusion·The decellularized blood vessels have good mechanical properties and physical stability by combined decellularization, and the fluorinated coating makes the blood vessels have good anticoagulant and biocompatibility.

Background: Carotid intima media thickness (CIMT) and carotid plaque can predict premature coronary heart disease (PCAD) in patients hospitalized due to coronary artery disease or undergoing therapeutic interventions. This study aimed to determine the relationship between intima media thickness and carotid plaque characteristics with the incidence and severity of premature coronary artery disease. Materials and Methods: The current study was an analytical cross-sectional study conducted on patients referred to Imam Hossein Hospital in 2021-2022 who underwent coronary angiography. Patients were classified into two groups with coronary artery involvement and the group without evidence of significant coronary involvement. Then the data of patients, such as sex, age, risk factors of cardiovascular diseases, and clinical history of individuals, were collected through interviews and aspects related to carotid intima media thickness and plaque formation through a specialized review of reports. Results: A total of 59 women (%59) and 41 men (%41) participated in this study. The mean age was 51.50±9.54. The results of this study showed that there was a direct (positive) and significant correlation between carotid intima media thickness factors, including right and left carotid intima-media thickness, right and left carotid intima media thickness scores, and the number of carotid plaques with increasing severity of coronary artery involvement (P-values<0.05). There was a statistically significant correlation between carotid plaque number and severity of coronary artery disease (P-value<0.05). Conclusion: CIMT has a significant correlation with PCAD, and in patients at risk of PCAD, measurement of CIMT was a suitable method. [ABSTRACT FROM AUTHOR]

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The risk factors that are the most significant for the development of most cardiovascular diseases are arterial hypertension (AH), type 2 diabetes (DM), and inflammation. However, for the development of aortic aneurysms, DM is not one of them. Our study aimed to evaluate the difference between inflammatory infiltration in three individual layers of the ascending aortic aneurysm within diabetic and hypertensive patients. Forty-five patients aged 36 to 80 were divided into a group with diabetic patients without AH (group DM, N=8) and hypertensive patients without DM (group AH, N=37). For the histological analysis, aortic aneurysms were stained with hematoxylin eosin and Movat. We used immunochemical methods to detect pro- (M1), anti-inflammatory (M2) macrophages, T-helper, T-killer cells, B cells, and plasma cells. Statistical analysis was done by independent-samples Kruskal-Wallis test adjusted by Bonferroni correction for multiple tests (P

In patients with an ascending aorta aneurysm, restructuring of all its layers and, first of all, the intima and media was revealed. The thickness of the intima was 79.3±63.1 μm in patients with aortic diameter <55 mm (group Ao<55) and 162.7±177.4 μm (p<0.05) in patients with aortic diameter ⩾55 mm (Ao⩾55 group), the thickness of the aortic media was 1184.0±198.2 and 1144.3±288.4 μm, respectively. In patients of the Ao<55 group, aortic dilatation was accompanied by compensatory thickening of the inner and middle layers of the aorta. In the Ao⩾55 group, thinning of the aortic media, fragmentation of elastic fibers, and its cystic degeneration were revealed. c-kit+ Stem cells were detected in the subendothelium of the thickened intima of the dilated ascending aorta. The appearance of c-kit+ cells correlated with intimal remodeling and its colonization with CD34+ and CD44+ myofibroblast-like cells. [ABSTRACT FROM AUTHOR]

Pulmonary vascular remodeling is the critical structural alteration and pathological feature in pulmonary hypertension (PH) and involves changes in the intima, media and adventitia. Pulmonary vascular remodeling consists of the proliferation and phenotypic transformation of pulmonary artery endothelial cells (PAECs) and pulmonary artery smooth muscle cells (PASMCs) of the middle membranous pulmonary artery, as well as complex interactions involving external layer pulmonary artery fibroblasts (PAFs) and extracellular matrix (ECM). Inflammatory mechanisms, apoptosis and other factors in the vascular wall are influenced by different mechanisms that likely act in concert to drive disease progression. This article reviews these pathological changes and highlights some pathogenetic mechanisms involved in the remodeling process. [ABSTRACT FROM AUTHOR]

The synovium is a loose connective tissue that separates the intra-articular (IA) joint compartments of all diarthrodial joints from the systemic circulation. It can be divided into two layers: the intima, a thin and cell-dense layer atop a more heterogeneous subintima, composed of collagen and various cell types. The subintima contains penetrating capillaries and lymphatic vessels that rapidly clear injected drugs from the joint space which may vary not only with drug size and charge but also with the microstructure and composition of the intima and subintima of the synovium. Prior work has measured the mechanical properties and solute diffusivities in the synovium of porcine, bovine, and human joints. Here, we measured the Young's moduli of synovium from smaller joints of the rat knee, as well as pig and human, using atomic force microscopy (AFM). The format for AFM enabled testing of intima and subintimal regions of synovium in all three species. The Young's moduli of the subintimal regions were similar across all three species (1-1.5 kPa). Furthermore, there was little evidence of differences in Young's moduli between synovium from the intima and subintima in each species. A general similarity of data from AFM testing with moduli measured with bulk testing of pig and human synovium suggests that AFM can be useful to measure the mechanical properties of smaller joint synovium and spatial variations in stiffness with depth. Enzymatic digestion of synovium tissue from the pig was also performed with findings of lower moduli values following treatment with chondroitinase ABC but not collagenase. Although the molecular composition of the synovium is not yet fully characterized and may vary across species, these findings suggest that noncollagenous species contribute to AFM-measured properties in synovium. These are some of the first data to measure mechanical properties in small joint synovium and will be useful in models studying IA drug clearances in joints with pathology and following treatment.

ObjectiveIn our latest research, we have demonstrated that the recipient parasylvian cortical arteries (PSCAs) with hemodynamic sources from the middle cerebral artery (M-PSCAs) has a higher risk of postoperative cerebral hyperperfusion (CHP) syndrome than those from non-M-PSCAs in adult moyamoya disease (MMD) patient. However, whether there are differences between M-PSCAs and non-M-PSCAs in vascular specimens characteristics has not been studied. In this study, we further investigate the vascular specimen of recipient PSCAs by histological and immunohistochemical methods.Methods50 vascular specimens of recipient PSCAs were obtained from 50 adult MMD patients during the combined bypass surgeries in our departments of Zhongnan hospital. 4 recipient PSCAs samples were also obtained in the same way from the middle cerebral artery occlusion patients. The samples were received the pathological sectioning, hematoxylin and eosin staining, and immunohistochemistry, then the vascular wall thickness, matrix metalloproteinase-9 (MMP-9) and hypoxia-inducing factor-1α (HIF-1α) were analyzed.ResultsM-PSCAs adult MMD patients had a thinner intima than non-M-PSCAs in the recipient PSCAs specimens. In recipient non-M-PSCAs vascular specimens, the immunoreactivity indicating HIF-1α and matrix metalloproteinase-9 (MMP-9) was significantly higher than M-PSCAs groups. The logistic regression analyses showed that the M-PSCAs was an independent risk factor of postoperative cerebral hyperperfusion (CHP) syndrome (OR 6.235, 95% CI1.018-38.170, P = 0.048) in MMD.ConclusionOur results indicate that M-PSCAs adult MMD patients had thinner intima than non-MCAs adult MMD patients in the PSCAs. More importantly, HIF-1α and MMP-9 were overexpressed in non-M-PSCAs vascular specimens.

BackgroundType A aortic dissections (TAAD) are devastating aortic complications. Patients with Marfan syndrome, a bicuspid aortic valve or a thoracic aortic aneurysm have an increased risk to develop a TAAD. These predisposing conditions are characterized by a histologically thin intimal layer and hardly any atherosclerosis. Little is known about the susceptibility for atherosclerosis in patients with a type A aortic dissection.ObjectiveWe aim to systematically describe atherosclerotic lesions in TAAD patients.Materials and methodsA total of 51 patients with a TAAD (mean age 62.5 ± 10.8 years, 49% females) and 17 control patients (mean age 63 ± 5.5 years, 53% females) were included in this study. Cardiovascular risk factors were assessed clinically. All sections were stained with Movat pentachrome and hematoxylin eosin. Plaque morphology was classified according to the modified AHA classification scheme proposed by Virmani et al.ResultsIn the TAAD group thirty-seven percent were overweight (BMI > 25). Diabetes and peripheral arterial disease were not present in any of the patients. Fifty-nine percent of the patients had a history of hypertension. The intima in TAAD patients was significantly thinner as compared to the control group (mean thickness 143 ± 126.5 μm versus 193 ± 132 μm, p < 0.023). Seven TAAD patients had a normal intima without any form of adaptive or pathological thickening. Twenty-three TAAD patients demonstrated adaptive intimal thickening. Fourteen had an intimal xanthoma, also known as fatty streaks. A minority of 7 TAAD patients had progressive atherosclerotic lesions, 4 of which demonstrated pathological intimal thickening, 3 patients showed early fibroatheroma, late fibroatheroma and thin cap fibroatheroma. In the control group the majority of the patients exhibited progressive atherosclerotic lesions: three pathologic intimal thickening, two early fibroatheroma, six late fibroatheroma, one healed rupture and two fibrotic calcified plaque.DiscussionThis study shows that TAAD patients hardly exhibit any form of progressive atherosclerosis. The majority of TAAD patients showcase non-progressive intimal lesions, whereas the control group mostly demonstrated progressive intimal atherosclerotic lesions. Findings are independent of age, sex, or the presence of (a history of) hypertension.

Objective: To find out how common subclinical atherosclerosis is in psoriasis patients. Study Design: Descriptive cross-sectional study Place and Duration of Study: Dermatology unit of Fauji Foundation, Rawalpindi Pakistan, from Jan 2020 to Jun 2020. Methodology: After receiving informed consent, 314 cases that met the selection criteria were enrolled. Psoriasis was diagnosed depending on physical examination the family history of patients. Ultrasonography high-resolution B mode was opted to assess carotid atherosclerosis (Xario color Doppler probe frequency 5 to 7mHZ.). If the (IMT) was less than 0.9mm, it was regarded normal; values greater than 0.9mm were termed thickened intima, while digits greater than 1.5mm were considered atherosclerotic plaque. SPSS version 21.0 was used for data analysis. Results: Age of patients was from 18 to 70 years old, with a Mean±SD (44.00 ±12.12) years. Males made up 47(15%) of the population, while females made up 267(85%). There were 33(10.5%) smokers and 281(89.5%) non-smokers. The mean IMT was 0.84±0.61, with 0.1mm and 2.05mm as the minimum and maximum, respectively. Subclinical atherosclerosis was found in 96 patients (30.6%) (p

BACKGROUND: Aging is accompanied by a progressive decline in the structure and function of multiple organs. The structure and function of arterial vessels are impaired during the aging process. OBJECTIVE: To observe the effect of aging on the ultrastructure of arterial wall. METHODS: Five adult Sprague-Dawley rats and five aged Sprague-Dawley rats were selected. The common iliac artery of the rats was taken under anesthesia and fixed in glutaraldehyde, and the ultrasonography of the intima and media of the common iliac artery was observed using a transmission electron microscope. RESULTS AND CONCLUSION: The connection between endothelial cells of the common iliac artery in adult rats was normal, while there was a relatively large gap between endothelial cells of the common iliac artery in aged rats. Smooth muscle cells of the common iliac artery in adult rats exhibited a contractile phenotype, and there were many elastic fibers in the extracellular matrix; in aged rats, smooth muscle cells presented with a synthetic phenotype, and the number of collagen fibers in the common iliac artery was significantly increased. Dead endothelial cells and smooth muscle cells, characterized by chromatin degradation and cell lysis, were observed in the common iliac artery of aged rats, whilst no cell death was observed in adult rats. These findings indicate that the intima of the common iliac artery is thickened, smooth muscle cells present with a synthetic phenotype, the number of elastic fibers is reduced and the number of collagen fibers is increased in aged rats compared with adult rats. [ABSTRACT FROM AUTHOR]

Intima-media thickness is a known subclinical radiologic marker of the early manifestations of atherosclerotic disease. It is the thickness of the vessel wall, most often the carotid artery. Intima-media thickness is measured on conventional US manually or automatically. Other measurement techniques include radiofrequency US. Because there is variation in its measurement, especially in children, several recommendations have been set to increase the measurement's validity and comparability among studies. Despite these recommendations, several pitfalls should be avoided, and quality control should be performed to avoid erroneous interpretation. This article summarizes current literature in relation to the clinical applications for intima-media thickness measurement in children with known risk factors such as obesity, liver steatosis, hypercholesterolemia, diabetes, hypertension, systemic inflammatory diseases, cancer survival, kidney and liver transplant, and sickle cell disease or beta thalassemia major. Most potential indications for intima-media thickness measurement remain in the research domain and should be interpreted combined with other markers. The objective of diagnosing an increased intima-media thickness is to start a multidisciplinary treatment approach to prevent disease progression and its sequelae in adulthood. [ABSTRACT FROM AUTHOR]

The existence of residual stresses in unloaded arteries has long been known. However, their efect is often neglected in experimental studies. Using a recently developed modelling framework, we aimed to investigate the role of residual stresses in the mechanical behaviour of the tri-layered wall of the pig thoracic aorta. The mechanical behaviour of the intact wall and isolated layers of n = 3 pig thoracic aortas was investigated via uniaxial tensile testing. After modelling the layer-specific mechanical data using a hyperelastic strain energy function, the layer-specifc deformations in the unloaded vessel were estimated so that the mechanical response of the computationally assembled tri-layered fat wall would match that measured experimentally. Physiological tension--infation of the cylindrical trilayered vessel was then simulated, analysing changes in the distribution of stresses in the three layers when neglecting residual stresses. In the tri-layered model with residual stresses, layers exhibited comparable stresses throughout the physiological range of pressure. At 100 mmHg, intimal, medial, and adventitial circumferential load bearings were 16 ± 3%, 59 ± 4%, and 25 ± 2%, respectively. Adventitial stifening at high pressures produced a shift in load bearing from the media to the adventitia. When neglecting residual stresses, in vivo stresses were highest at the intima and lowest at the adventitia. Consequently, the intimal and adventitial load bearings, 23 ± 2% and 18 ± 3% at 100 mmHg, were comparable at all pressures. Residual stresses play a crucial role in arterial mechanics guaranteeing a uniform distribution of stresses through the wall thickness. Neglecting these leads to incorrect interpretation of the layers' role in arterial mechanics. [ABSTRACT FROM AUTHOR]

Recent researches on COVID 19 has been extended to analyze the various morphological and anatomical changes in a patient's body due to the invasion of the virus. These latest studies have concluded that there happens a high rise in the viscosity of the blood in a COVID 19 patient, supported by the extensive analysis of the clinical data. In the present paper, a mathematical model in the form of a differential equation system has been proposed to disclose the various changes that occur in the flow across the stenosis of an arterial segment. The consequences of the hyperviscosity of blood on the blood flow characteristics in a stenosed artery are analyzed by solving the model using a finite element method (FEM) solver. A laminar flow coupled with solid mechanics through the Fluid-Structure Interaction (FSI) interface has been studied using an Arbitrary Lagrangian-Eulerian (ALE) method. For the first time, the mathematical model was used to analyze the hyper-viscous flow condition in COVID 19 patients. The present research is mainly based on the numerous clinical reports enlisting the various morphological, hematological, and rheological changes in the blood.

There is a great progress in understanding the cellular and molecular aspects of atherosclerosis, which is one of the leading causes of death. Yet, there are questions regarding the cellular and metabolic mechanisms that lead to atherogenesis. Among the many factors that influence this process, food plays a significant role. Among other factors that play a paramount role in atherogensis are alterations of the transport of food in enterocytes, oxysterols, development of an atherogenic serum, endothelial damage, accumulation of foam cells within the vessel wall, lysosome-ER transport, and hypertension. Here, we discuss the contribution of secretion, transcytosis, endocytosis of chylomicrons, low-density lipoproteins (LDL), very LDL, and high-density lipoproteins to atherogenesis.

Objectives: Salivary dysfunction, such as reduced salivary flow and an altered salivary composition, is caused by several diseases, medical conditions, and medications. The purpose of the present study was to clarify the relationship between hypertension and morphological changes in the submandibular glands. Materials and methods: An epidemiological study was conducted to elucidate the relationship between hypertension and dry mouth. The effects of hypertension on morphological changes and the intima thickness of arteries in the submandibular glands were histopathologically investigated. Results: Among 1933 subjects in the epidemiological study, 155 (8.0%) had dry mouth. A multivariate analysis revealed that dry mouth correlated with age (p < 0.001), sex (p < 0.001), and hypertension (p < 0.05). No significant differences were observed in the size of the submandibular glands between patients with or without hypertension. The average area of acinar cells was smaller in patients with than in those without hypertension (0.366 ± 0.153 vs. 0.465 ± 0.178, p < 0.05). The arteriosclerotic index was significantly higher in patients with than in those without hypertension (0.304 ± 0.034 vs 0.475 ± 0.053, p < 0.05). Conclusions: Hypertension may contribute to the degeneration of the submandibular glands by decreasing the number of acinar cells and promoting fatty infiltration and stenosis of the arteries. Clinical relevance: There may be a correlation between hypertension and the degeneration of the submandibular glands by decreasing the number of acinar cells and promoting fatty infiltration and stenosis of the arteries. [ABSTRACT FROM AUTHOR]

Although medical image segmentation field is regarded as one of most established fields, still fully automatic segmentation to extract target object with high accuracy from intravascular ultrasound (IVUS) is very active area of research. In this paper, we propose a fully automatic morphological approach using Bezier curve in interpolating the boundaries of intima/adventitia of the vessel from IVUS with careful binarization algorithms. In experiment with 800 IVUS images, the proposed method is as good as fuzzy C-means based approach in comparison with human expert’s result with 84.4% satisfaction and better than other morphological method in all performance indices of curve fitting with 97.02% in accuracy and 58.19% in precision. [ABSTRACT FROM AUTHOR]

The sources of vascularization of the kidneys of five polar owl carcasses were studied by filling the vessels with self-hardening plastic Belokril through the femoral artery. High-grade oil paints were added to the monomer to give the vessels the desired color. After the injection, the carcasses were placed in a high concentration caustic soda solution for three days. The resulting corrosion impression was washed under warm water and dried. It was identified that in the lumbar trunk, the main vessel was the descending aorta, from which extra- and intraorganic arteries departed for vascularizing the kidneys. Extraorganic arteries included external and internal iliac, sciatic and middle sacral arteries. Intraorganic arteries included cranial, middle, and caudal renal arteries. Inside the parenchyma of each lobe of the kidney, intraorganic arteries branched in the main type of caudomedial, dorsomedial and lateromedial directions and were subdivided into segmental, interlobular and perilobular arteries and intralobular capillaries. An asymmetry in the branching of the renal arteries was observed. During histological examination, we noted that the renal arteries were lined with endothelium on the inner side and the intima contained endotheliocytes with oval nuclei. Under the endothelial layer were loose collagen fibers running along the middle shell. There was no loose connective tissue between the inner and middle shells, so the subendothelial layer was very weak and there was no internal elastic membrane. The muscle membrane was well developed, with collagen and elastic fibers located between the muscle fibers. The outer shell was represented by loose connective tissue with the presence of arterial and venous vessels. The collagen fibers had a slightly convoluted course. [ABSTRACT FROM AUTHOR]

The aim of this study was to evaluate the features of pulmonary histopathological changes in cases of trisomy 18 complicated with congenital heart disease and pulmonary arterial hypertension. Twenty‐eight patients with trisomy 18 underwent open lung biopsy at the time of primary operation in our hospital between 2008 and 2019. We compared these histopathological findings with those from previously described groups without trisomy 18. Mean age at primary cardiac surgery was 37 days (range, 9–69 days). According to the Heath‐Edwards (HE) classification, 1, 8, 12, and 5 patients were graded as 0, 1, 2, and 3, respectively, whereas 2 patients were not classifiable due to medial defects in the small pulmonary arteries (MD). Four (14.3%) and 13 (46.4%) patients presented with MD and hypoplasia of the small pulmonary arteries (HS). Fifteen (53.6%) and 21 (75.0%) patients presented with alveolar hypoplasia (AH) and alveolar wall thickening (AT). MD, HS, and AH in trisomy 18 were present frequently, differing significantly from previous reports. These findings might be associated with congenital inadequate development of vessels and alveoli in the lung, contributing to a high risk of PAH in trisomy 18. [ABSTRACT FROM AUTHOR]

Connexins (Cxs) form gap junctions for intercellular exchange of inorganic ions and messenger molecules. In the kidney, Cxs play essential roles within its compartments, but data on the precise cellular localization and cell type-related function of their isoforms are scarce. We tested whether Cx43 distribution is restricted to vascular and interstitial cells and whether medullary fibroblasts express Cx43 to coordinate profibrotic signaling. Confocal immunofluorescence techniques, ultrastructural labeling, and functional experiments in cell culture were performed. Cx43 was chiefly expressed in the vasculature but was absent from tubular epithelia. All arterial, arteriolar, and lymphatic endothelia showed continuous Cx43 signal along their borders. In the inner medulla, only the interstitium showed Cx43 signals, which were assigned to fibroblasts and their processes. Cultured Cx43- expressing medullary fibroblasts served to study the role of gap junctions in a profibrotic context. In a dye spreading assay, Cx43-sensitive diffusion of Lucifer yellow was dependent on gap junctional passage. The addition of transforming growth factorb1 (5 ng/mL for 48 h) activated Cx43 biosynthesis and caused Cx43-sensitive transformation of the fibroblasts into a myofibroblast phenotype. This suggested that Cx43 gap junctional channels enable the coordination of profibrotic signaling between cells of the medullary interstitium. In summary, we demonstrate the presence of Cx43-expressing gap junctions within the two major renal compartments, the vasculature and interstitium. Endothelial Cx43 likely provides functions of an earlier-defined "electrical syncytium" within the vascular wall. Additionally, Cx43 facilitates profibrotic signaling between medullary interstitial fibroblasts. [ABSTRACT FROM AUTHOR]

With the move towards simulation based microsurgical training and emphasis on the declining usage of animal models, there is a need for an objective method to evaluate microvascular anastomosis in a non-living, simulated microsurgical training environment. Our aim was to create a validated assessment tool to evaluate the intimal surface of the end product to measure skills acquisition. The intimal surface of 200 anastomoses from 23 candidates and 2 experts were assessed using ImageJ to measure 4 parameters: 1) distance between the distal insertion points, 2) distance between the proximal insertion points, 3) length of sutures placed, 4) number of axes. Using these parameters, a 9-component scoring system was produced based on the hypothesis of the ideal anastomosis having equidistance between the above parameters. The scoring system was devised based on population performance to give a maximum score of 100. The EPIA tool demonstrated its ability to differentiate between seniority from undergraduate to expert. Furthermore, predictive validity was shown by demonstrating skill acquisition between day 3 and 5 of the microsurgery course. The EPIA tool is a valid and feasible method to assess and provide feedback regarding the end product as an adjunct to current scoring systems in simulated microsurgery. [ABSTRACT FROM AUTHOR]

The etiology of polyarteritis nodosa (PAN) and localized PAN, including cutaneous arteritis (CA), remains unknown; however, initial endothelial damage has been implicated. The intima of the vasculitis lesions is predominantly infiltrated by innate-like bystander-activated CD8 T cells, in addition to the macrophages. Macrophages are among the major inflammatory cells involved in innate immunity and are classified into M1 and M2 subtypes. M1-type macrophages kill pathogens and cause inflammation, while M2-type macrophages promote the repair of tissues. Macrophage subtypes infiltrating in PAN and localized PAN vasculitis lesions have not yet been investigated. Innate immune response to a triggering factor on the endothelial cell surface may initiate CA pathogenesis. Thus, many M1-type macrophages may infiltrate in the intima during early CA. We assessed this hypothesis by immunohistochemical observation of macrophage phenotypes and polarization. Twenty-seven skin biopsy specimens from patients with CA were retrieved. Based on histology, we classified CA into four phases. The phenotypes of infiltrating macrophages in CA were evaluated by immunohistochemistry using antibodies against Iba-1, a pan-macrophage marker, and CD163, an M2-type macrophage marker. Our results showed that the ratio of CD163-positive M2-type macrophages to Iba1-positive macrophages was lower in the intima in the early stage of CA than in the later stage. In the media to adventitia, there was no significant difference in the ratios between these stages. These findings indicate that innate immunity is involved in the intima in the early stage of CA, suggesting that a trigger for CA might exist in endothelial cells. [ABSTRACT FROM AUTHOR]

Atherosclerosis is a chronic inflammatory disease of arteries and it affects the structure and function of all three layers of the coronary artery wall. Current theories suggest that the dysfunction of endothelial cells is one of the initial steps in the development of atherosclerosis. The view that the tunica intima normally consists of a single layer of endothelial cells attached to the subendothelial layer and internal elastic membrane has been questioned in recent years. The structure of intima changes with age and it becomes multilayered due to migration of smooth muscle cells from the media to intima. At this stage, the migration and proliferation of smooth muscle cells do not cause pathological changes in the intima. The multilayering of intima is classically considered to be an important stage in the development of atherosclerosis, but in fact atherosclerotic plaques develop only focally due to the interplay of various processes that involve the resident and invading inflammatory cells. The tunica media consists of multiple layers of smooth muscle cells that produce the extracellular matrix, and this layer normally does not contain microvessels. During the development of atherosclerosis, the microvessels from the tunica adventitia or from the lumen may penetrate thickened media to provide nutrition and oxygenation. According to some theories, the endothelial dysfunction of these nutritive vessels may significantly contribute to the atherosclerosis of coronary arteries. The adventitia contains fibroblasts, progenitor cells, immune cells, microvessels, and adrenergic nerves. The degree of inflammatory cell infiltration into the adventitia, which can lead to the formation of tertiary lymphoid organs, correlates with the severity of atherosclerotic plaques. Coronary arteries are surrounded by perivascular adipose tissue that also participates in the atherosclerotic process.

Vascular smooth muscle cells (VSMCs) constitute the major cells in the media layer of arteries, and are critical to maintain the integrity of the arterial wall. They participate in arterial wall remodeling, and play important roles in atherosclerosis throughout all stages of the disease. Studies demonstrate that VSMCs can adopt numerous phenotypes depending on inputs from endothelial cells (ECs) of the intima, resident cells of the adventitia, circulating immune cells, hormones, and plasma lipoproteins. This plasticity allows them to perform multiple tasks in physiology and disease. In this minireview, we focus on a previously underappreciated activity of VSMCs, i.e., their impact on atherosclerosis immunity via formation of artery tertiary lymphoid organs (ATLOs).

IVUS is an intra-operative imaging modality that facilitates observing and appraising the vessel wall structure of the human coronary arteries. IVUS is regularly used to locate the atherosclerosis lesions in the coronary arteries. Auto-segmentation of the vessel structure is important to detect the disorder of coronary artery. In this paper, we propose a simple strategy to extract Intima/Adventitia area effectively using fuzzy binarization from intravascular images. The proposed method apply fuzzy binarization to find the adventitia but apply average binarization to locate the intima since they have different homogeneity of pixel intensity comparing with the environment. In this paper, we demonstrate an effective auto-segmentation method for detecting the interior/exterior of the vessel walls by differentiating the fuzzy binarization result and average binarization result from IVUS image. Important statistics such as Intima-Media Thickness (IMT) or volume of a target area can be easily computed from result. [ABSTRACT FROM AUTHOR]

Les sarcomes cardiaques primitifs sont des tumeurs malignes rares de pronostic sombre. À travers l'observation d'un jeune patient hospitalisé pour une poussée d'insuffisance cardiaque révélant un sarcome intimal primitif de l'oreillette gauche, nous exposons les principales modalités diagnostiques et thérapeutiques de ces tumeurs ainsi que leur pronostic. Primitive intimal sarcoma is a rare malignant cardiac tumor. Through the observation of a 41-year-old man who presented with an acute heart failure revealing a left atrial intimal sarcoma, we discuss different diagnostic and therapeutic modalities. [ABSTRACT FROM AUTHOR]

Background: The aim of this study is to describe the morphology, morphometry and ultrastructure of segments of the thoracic and abdominal aorta portions in Chinchilla lanigera. Thickness measurements of the tunica intima and media complex of the aorta were taken.Materials and Methods: In all observed specimens, the thickness values for the tunica intima and media complex of the cranial thoracic aorta were significantly higher (mean: 702.19 μm) when compared to the values of other analysed aortic segments (means: 354.18 μm; 243.55 μm). Complex statistical methods were used to assess the differences between various aortic segments.Results and Conclusions: The components of the vessel walls show variations in structure and thickness, presumably due to an adaptation to functional demand. [ABSTRACT FROM AUTHOR]

Vascular smooth muscle cells (VSMCs) constitute the major cells in the media layer of arteries, and are critical to maintain the integrity of the arterial wall. They participate in arterial wall remodeling, and play important roles in atherosclerosis throughout all stages of the disease. Studies demonstrate that VSMCs can adopt numerous phenotypes depending on inputs from endothelial cells (ECs) of the intima, resident cells of the adventitia, circulating immune cells, hormones, and plasma lipoproteins. This plasticity allows them to perform multiple tasks in physiology and disease. In this minireview, we focus on a previously underappreciated activity of VSMCs, i.e., their impact on atherosclerosis immunity via formation of artery tertiary lymphoid organs (ATLOs). [ABSTRACT FROM AUTHOR]

Background: Implantation of a retrievable vena cava filter (VCF) is an effective method for preventing pulmonary embolism. Retrieval of filters, however, may be difficult due to intimal hyperplasia and inflammation in the cava wall. The transcription factor nuclear factor-kappaB (NF-κB) plays an important role in regulation of numerous genes participating in the inflammatory and proliferative responses of cells. The present study was to determine whether VCF implantation resulted in activation of NF-κB in the venous neointima.Methods: Filters were placed in vena cava (VC) in four swine for 30 days and then removed. Intimal specimens adhering to the filter struts were analyzed with reference to normal VC tissues. Immunohistochemical analyses were used to assess the NF-κB subunits p65 and p50 and the phosphorylated inhibitor of κB-α (phosphor-IκB-α) in the tissues. NF-κB DNA-binding activity was measured with enzyme-linked immunosorbent assay.Results: As compared to normal VC tissues, the intimal tissues contained higher percentages of cell nucleus-located p65 and p50, and NF-κB DNA-binding activity. Elevated immunoreactivities of p65, p50 and phosphor-IκB-α were also present in the intima.Conclusion: The present study demonstrates for the first time that VCF implantation caused NF-κB activation in neointima. We further demonstrate the activation is at least partly due to phosphorylation of IκB-α. Our data suggest that NF-κB activation would significantly contribute to development of intimal hyperplasia and inflammation in filter-inserted vena cava walls. NF-κB might be a therapeutic target for inhibiting filter-induced neointima and improving filter retrieval. [ABSTRACT FROM AUTHOR]

Phylogenetically late intima of elastic arteries has no proteins for transportation of non-ligand oxidized low density lipoproteins (LDL) adsorbed on the matrix to resident macrophages. Phylogenetically early cells realize the reaction of extracellular digestion by secreting the proteolytic enzymes metalloproteases in the matrix. They hydrolyze matrix proteoglycans, adsorbed and non-ligand LDL, absorb detritis, and terminate hydrolysis of the most hydrophobic polyenic cholesterol esters (poly-CE) in lysosomes. Smooth muscle cells migrate from arterial media, change their phenotype from contractile to synthetic and produce in situ de novo matrix proteoglycans. Elastic arterial wall consists of three layers: a) endothelial monolayer, b) intima + media (smooth muscle cells) and b) adventitia. It seems reasonable to define functional differences between phylogenetically early resident macrophages and phylogenetically late monocytes-macrophages. They may be associated with scavenger receptors, CD36 translocase activity, production of acid hydrolases for poly-CE or realization of the biological reaction of extracellular digestion. We suppose that atheromatous masses are formed in the matrix of arterial intima but not in lysosomes when the ability of monocytes-macrophages to provide endocytosis of non-ligand LDL from the matrix is limited. If atheromatosis is a syndrome caused by intracellular deficiency of essential polyenic fatty acids (PFA), intimal atheromatosis is associated with partial utilization of excess PFA in the matrix of elastic arteria. At late stages of phylogenesis the intima formed from smooth muscle cells of the media.

Coronary artery dissection (CAD) is the intimal tearing of the coronary arterial wall and can be iatrogenic, spontaneous, or traumatic in origin. CAD is a rare but challenging condition that can cause significant hemodynamic compromise. Management strategies for CAD, such as the use of mechanical circulatory support devices, are available in the clinical setting. However, the incidence, etiology, and optimal management of CAD are not well-defined, emphasizing the need for adequate animal models in preclinical studies. Large animal models provide the human-like conditions necessary for testing and development of potential treatment strategies. In this chapter, we describe a method for the creation of a CAD swine model., (© 2024. The Author(s), under exclusive license to Springer Science+Business Media, LLC, part of Springer Nature.)