Vessel Wall Thickness Research Articles

Postgenomic and structural changes in the myocardia of Wistar rats fed a high-salt diet

The relationship between dietary sodium, hypertension, and cardiovascular injury is far from clear. One of the important links in this process can be microRNAs that have the ability to modulate gene expression at the post-transcriptional level. However, their role in this process has not been fully studied. In addition, further studies require the identification of structural changes in the myocardium in conditions of long-term consumption of a high-salt diet. The aim of the study was to evaluate the expression levels of nuclear transcription factor κB (NFκB), microRNA (miRNA)-21 and structural changes in the myocardium during long-term consumption of a diet containing 8% (high) sodium chloride in Wistar rats. Material and methods. 20 Wistar rats with initial body weight 280.5±42.7 g were divided into two equal groups. The high salt (HS) group received 8% NaCl in the diet, the control (NS) group received the standard diet (0.34% NaCl). After 4 months, systolic blood pressure was measured in rats using the cuff method on the tail; the myocardial mass index was assessed after dissection; histological and electron microscopic examination of the myocardium was performed, and the expression levels of miRNA-21 and NFκB in the myocardium were determined. Results and discussion. Consumption of a diet high in sodium chloride for 4 months did not significantly affect the level of systolic blood pressure in normotensive Wistar rats, but led to an increase in myocardial mass index by 25.0% (p<0.05). In the HS group, hypertrophy of cardiomyocytes and an increase in the wall thickness of arterial vessels were revealed. The area of perivascular fibrosis in rats of the HS-group was almost 1.8 fold higher than in the NS-group. In animals of HS-group, the relative levels of expression of NFκB (more than 2 times) and miRNA-21 (almost 6 times) increased compared with the control. It can be assumed that the negative impact on the cardiovascular system of high-salt diets is partially realized through NFκB-associated signaling pathways and miRNA-21 activation. Conclusion. In Wistar rats, long-term use of a high-salt diet results in myocardial remodeling that is not associated with changes in blood pressure. At the same time, the adverse effects of high salt intake on the myocardium are mediated, in particular, by postgenomic mechanisms, namely an increase in the expression levels of NFκB and microRNA-21.

Effects of atorvastatin in suppressing pulmonary vascular remodeling in rats with chronic obstructive pulmonary disease

ObjectiveTo investigate the effects of atorvastatin calcium on pulmonary vascular remodeling, the authors explored the regulatory mechanism of Histone Deacetylation Enzyme-2 (HDAC2) in rats with Chronic Obstructive Pulmonary Disease (COPD), and provided a new direction for drug treatment in the progression of vascular remodeling. MethodsEighteen female SD rats were randomly divided into control (Group S1), COPD (Group S2), and atorvastatin calcium + COPD (Group S3) groups. A COPD rat model was established by passive smoking and intratracheal injection of Lipopolysaccharide (LPS). Haematoxylin and eosin staining and Victoria Blue + Van Gibson staining were used to observe pathological changes in the lung tissue. The pulmonary vascular inflammation score was calculated, and the degree of pulmonary vascular remodeling was evaluated. The ratio of Muscular Arteries in lung tissue (MA%), the ratio of the vessel Wall Area to the vessel total area (WA%), and the ratio of the vessel Wall Thickness to the vascular outer diameter (WT%) were measured using imaging software. The expression of HDAC2 was measured using western blotting, ELISA (Enzyme-Linked Immunosorbent Assay), and qPCR (Real-time PCR). ResultsCompared with the control group, the degree of pulmonary vascular inflammation and pulmonary vascular remodeling increased in rats with COPD. The WT%, WA%, and lung inflammation scores increased significantly; the expression of HDAC2 and HDAC2mRNA in the serum and lung tissue decreased, and the level of Vascular Endothelial Growth Factor (VEGF) in the lung tissues increased (p < 0.05). Compared with the COPD group, the lung tissues from rats in the atorvastatin group had fewer inflammatory cells, and the vascular pathological changes were significantly relieved. The WT%, WA%, and lung inflammation scores decreased significantly; the expression of HDAC2 and HDAC2mRNA in the serum and lung tissues increased, and the level of VEGF in the lung tissues decreased (p < 0.05). ConclusionThe present study revealed that atorvastatin calcium could regulate the contents and expression of HDAC2 in serum and lung tissues and inhibit the production of VEGF, thereby regulating pulmonary vascular remodeling in a rat model with COPD.

Endovenous radiofrequency ablation using a new bipolar electrode in a canine model: a new endovenous radiofrequency electrode.

This study aimed to determine the effectiveness and safety of a newly developed endovenous radiofrequency (RF) catheter compared with that of the existing RF catheter in a canine model. Seven dogs underwent ablation using 1 control catheter (ClosureFAST, CF; Covidien) and 1 experimental catheter (VENISTAR, VS; STARmed Co., Ltd.) in the femoral and cephalic veins. The ablated vein was evaluated macroscopically (2,3,5-triphenyltetrazolium chloride staining, TTC), microscopically (hematoxylin and eosin staining), and ultrasonographically. Vessel injury score was used to evaluate the ablating effect objectively. Veins from 1 dog were evaluated on the day of ablation, while in the remaining 6 dogs, the ablated veins were evaluated 2 weeks later. A total of 23 veins (CF, 11 veins; VS, 12 veins) were ablated in 7 dogs. Non-TTC-stained vein wall areas were identified in all ablated veins. No significant difference was observed in the mean vessel injury score (2.54 ± 1.16 vs. 2.42 ± 1.13, P = 0.656) and the mean vessel wall thickness (0.32 ± 0.03 mm vs. 0.31 ± 0.05 mm, P = 0.212) between CF and VS. There was no blood flow in all veins ablated with VS, whereas there was remaining blood flow in 1 vein ablated with CF. Perivenous complication was not observed. Endovenous RF ablation using a newly developed VS RF catheter seems to provide comparable occlusion rate and degree of vein wall injury without perivenous adverse events compared to the most commonly used RF catheter (CF).

Mixed epithelial and stromal tumor of the kidney: A retrospective clinicopathological evaluation

ObjectiveMixed epithelial and stromal tumor of the kidney (MESTK) is a rare renal tumor for which there is limited clinical case experience. The aim of this study was to investigate the clinicopathological features, imaging manifestations, immunohistochemical phenotype, diagnosis, and differential diagnosis of MESTK. MethodsWe systematically evaluated the clinicopathological characteristics of 13 patients diagnosed with MESTK from 2016 to 2022. ResultsThere were 12 female cases and 1 male case, and their age ranged from 24 to 62 (mean age 47 years). The tumor was located in the left kidney in 11 patients. Seven of these patients were located in the upper pole of the left kidney. The mean diameter of the tumor was 4.6 cm (range 1.3–8.6 cm), and the main body of the tumor was mainly located in the medulla or medulla. In 7 cases, the tumors were clearly outlined, 4 cases had clear but irregular borders, and in 3 cases, the masses broke through the renal capsule but did not invade the surrounding organs. All tumors had varying proportions of cystic and solid components. In most tumors, the epithelial cell component was predominant. Among the epithelial components, we observed a predominance of large cysts. Small cysts and tubular structures were also seen; the least common were papillary structures. The most common types of lining epithelium were flat and cuboidal. The cell cytoplasm was predominantly eosinophilic with hyaline degeneration. The tumor cells were composed of different proportions of sparse hypocellular areas and dense hypercellular areas between these cells. In most cases, the cellular stroma had an ovarian-like appearance. It is characterized histologically by mature adipocytes, thick-walled blood vessels, and chronic inflammatory cells. Calcification and collagenization were seen in a few cases. In all female patients, estrogen and progesterone receptors in the interstitial component were almost always positively expressed. In male patients, all interstitial components showed locally positive expression of androgens. ConclusionMESTK had unique characteristics with complex and variable lesion shapes. There was a high degree of overlap with cystic kidney cancer, and the rate of missed and misdiagnosis was extremely high. The diagnosis could not be confirmed by preoperative imaging. The final diagnosis depended on pathomorphology.

Research Progress of Steels for Nuclear Reactor Pressure Vessels.

The nuclear reactor pressure vessel is an important component of a nuclear power plant. It has been used in harsh environments such as high temperature, high pressure, neutron irradiation, thermal aging, corrosion and fatigue for a long time, which puts forward higher standards for the performance requirements for nuclear pressure vessel steel. Based on the characteristics of large size and wall thickness of the nuclear pressure vessel, combined with its performance requirements, this work studies the problems of forging technology, mechanical properties, irradiation damage, corrosion failure, thermal aging behavior and fatigue properties, and summarizes the research progress of nuclear pressure vessel materials. The influencing factors of microstructures evolution and mechanism of mechanical properties change of nuclear pressure vessel steel are analyzed in this work. The mechanical properties before and after irradiation are compared, and the influence mechanisms of irradiation hardening and embrittlement are also summarized. Although the stainless steel will be surfacing on the inner wall of nuclear pressure vessel to prevent corrosion, long-term operation may cause aging or deterioration of stainless steel, resulting in corrosion caused by the contact between the primary circuit water environment and the nuclear pressure vessel steel. Therefore, the corrosion behavior of nuclear pressure vessels materials is also summarized in detail. Meanwhile, the evolution mechanism of the microstructure of nuclear pressure vessel materials under thermal aging conditions is analyzed, and the mechanisms affecting the mechanical properties are also described. In addition, the influence mechanisms of internal and external factors on the fatigue properties, fatigue crack initiation and fatigue crack propagation of nuclear pressure vessel steel are analyzed in detail from different perspectives. Finally, the development direction and further research contents of nuclear pressure vessel materials are prospected in order to improve the service life and ensure safe service in harsh environment.

TNF Signaling Is Required for Castration-Induced Vascular Damage Preceding Prostate Cancer Regression.

The mainstay treatment for locally advanced, recurrent, or metastatic prostate cancer (PrCa) is androgen deprivation therapy (ADT). ADT causes prostate cancers to shrink in volume, or regress, by inducing epithelial tumor cell apoptosis. In normal, non-neoplastic murine prostate, androgen deprivation via castration induces prostate gland regression that is dependent on TNF signaling. In addition to this direct mechanism of action, castration has also been implicated in an indirect mechanism of prostate epithelial cell death, which has been described as vascular regression. The initiating event is endothelial cell apoptosis and/or increased vascular permeability. This subsequently leads to reduced blood flow and perfusion, and then hypoxia, which may enhance epithelial cell apoptosis. Castration-induced vascular regression has been observed in both normal and neoplastic prostates. We used photoacoustic, power Doppler, and contrast-enhanced ultrasound imaging, and CD31 immunohistochemical staining of the microvasculature to assess vascular integrity in the period immediately following castration, enabling us to test the role of TNF signaling in vascular regression. In two mouse models of androgen-responsive prostate cancer, TNF signaling blockade using a soluble TNFR2 ligand trap reversed the functional aspects of vascular regression as well as structural changes in the microvasculature, including reduced vessel wall thickness, cross-sectional area, and vessel perimeter length. These results demonstrate that TNF signaling is required for vascular regression, most likely by inducing endothelial cell apoptosis and increasing vessel permeability. Since TNF is also the critical death receptor ligand for prostate epithelial cells, we propose that TNF is a multi-purpose, comprehensive signal within the prostate cancer microenvironment that mediates prostate cancer regression following androgen deprivation.

Effects of Heavy Metal Stress on Physiology, Hydraulics, and Anatomy of Three Desert Plants in the Jinchang Mining Area, China.

The physiological mechanisms and phytoremediation effects of three kinds of native quinoa in a desert mining area were studied. We used two different types of local soils (native soil and tailing soil) to analyze the changes in the heavy metal content, leaf physiology, photosynthetic parameters, stem hydraulics, and anatomical characteristics of potted quinoa. The results show that the chlorophyll content, photosynthetic rate, stomatal conductance, and transpiration rate of Kochia scoparia were decreased, but intercellular CO2 concentration (Ci) was increased under heavy metal stress, and the net photosynthetic rate (Pn) was decreased due to non-stomatal limitation. The gas exchange of Chenopodium glaucum and Atriplex centralasiatica showed a decrease in Pn, stomatal conductance (Gs), and transpiration rate (E) due to stomatal limitation. The three species showed a similar change in heavy metal content; they all showed elevated hydraulic parameters, decreased vessel density, and significantly thickened vessel walls under heavy metal stress. Physiological indicators such as proline content and activity of superoxide dismutase (SOD) and peroxidase (POD) increased, but the content of malondialdehyde (MDA) and glutathione (GSH), as well as catalase (CAT) activity, decreased in these three plants. Therefore, it can be concluded that these three species of quinoa, possibly the most dominant 30 desert plants in the region, showed a good adaptability and accumulation capacity under the pressure of heavy metal stress, and these plants can be good candidates for tailings remediation in the Jinchang desert mining area.

Material-based modeling of cavatappi artificial muscles

Soft actuators show much promise for use in bioinspired and biomimetic robotics as they share many similarities with actuation systems found in nature. Twisted and coiled actuators are soft actuators that have been shown to outperform many metrics of biological muscles, leading researchers to derive actuation models for future control and implementation. Although models have been proposed for twisted and coiled carbon nanotubes and polymer fibers, cavatappi artificial muscles—a novel twisted and coiled fluidic soft actuator—have not been modeled yet. This work establishes a framework for modeling cavatappi using the thick-wall pressure vessel stress analysis and the spring theory. The presented model uses the mechanical properties of the precursor drawn material used for fabrication, initial twist (internal fiber angle), muscle geometry, and internal pressure to predict the artificial muscles contraction under different external loads. The model predictions agree with the experimental results for cavatappi of different internal fiber angles and load conditions. Given their potential implementation in bioinspired applications, our model can help better design, optimize, and control the actuation response of cavatappi.

Ulinastatin ameliorates preeclampsia induced by N(gamma)-nitro-l-arginine methyl ester in a rat model via inhibition of the systemic and placental inflammatory response.

The pathogenesis of preeclampsia (PE) is associated with inflammation and endothelial damage. Ulinastatin (UTI) mainly inhibits proteolytic activity and significantly reduces the release of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) from macrophages. It also ameliorates vascular endothelial damage in pathological conditions. Hence, we investigated the effects of UTI in a rat model of PE induced using N(gamma)-nitro-l-arginine methyl ester (L-NAME). Although inducing PE in a rat model, 5000 U/kg of UTI were injected daily. Systolic blood pressure (SBP) and protein levels in the urine were measured. Renal function, and serum concentrations of TNF-α, IL-6, placental growth factor (PLGF), and von Willebrand factor (vWF) were evaluated. The number and weight of live fetuses as well as the weight of placentas were measured. Placentas were collected for western blot and pathological analysis. UTI slightly ameliorated proteinuria and the increases in SBP, blood urea nitrogen (BUN), and serum creatinine. Furthermore, UTI improved serum and placental protein expression levels of TNF-α, IL-6, vWF, and PLGF. Pathological analysis revealed that vascular density and blood flow perfusion was enhanced, vessel wall thickening and neutrophil infiltration were diminished, and the weight and number of live fetuses as well as the weight of the placentas were improved with UTI. Preventive use of UTI in the PE rat model induced by L-NAME partially alleviated hypertension, proteinuria, and impaired renal function; improved fetal growth restriction; diminished vascular endothelial injury; and ameliorated placental vasculogenesis abnormality and malperfusion by inhibiting the systemic and placental inflammatory response, suggesting that UTI is a potential drug for PE prevention or treatment.

Adrenal Hemangioma Presenting as an Incidentaloma Clinically Suspicious for Malignancy

Abstract Introduction/Objective Adrenal hemangiomas are rare, benign and non-functioning tumors. Clinical diagnosis can be challenging given that the presentation is usually vague and lesions are often found incidentally during diagnostic imaging performed for other reasons. Methods/Case Report We report a case of a 67-year-old man with history of hypertension, hyperlipidemia, and anemia, arthralgia and joint swelling with unexplained weight loss, which prompted imaging studies. Computed tomography (CT) scan revealed a 5.4 cm mass involving the left adrenal gland. The patient had no clinical manifestations of adrenal medullary or cortical hyperfunction. Biochemical testing performed included urine and plasma metanephrines and aldosterone/renin ratio, which yielded results within normal range. The patient was taking prednisone for hand and ankle swelling, precluding assessment for Cushing’s syndrome. Given the size of the lesion, the possibility of malignancy was considered. The patient elected for a left adrenalectomy. Gross examination revealed a 4.9 cm mass, weighing 54 grams, with a tan-brown, congested cut surface and a thin rim of residual normal appearing adrenal gland parenchyma. Histologic examination of the surgical specimen showed an enlarged adrenal gland predominantly replaced by hemorrhage with foci of thick and thin walled vessels with areas of intermingled adrenocortical elements at the periphery. A diagnosis of adrenal hemangioma was made. Results (if a Case Study enter NA) NA. Conclusion Adrenal hemangioma should be considered in the differential diagnosis of adrenal tumors. Surgical resection is the mainstay of treatment for a large, isolated adrenal mass to exclude malignancy and prevent retroperitoneal hemorrhage.

Elastotic Mass-Forming Lesion of the Omentum; A New Pathological Entity

Abstract Introduction/Objective Elastotic lesions are rare benign mass-forming entity. Although, few reports of mucosal and submucosal elastotic lesions have been previously described, localization of these lesions in the omentum is not previously described in the literature. Methods/Case Report We report a case of 60-year-old man with medical history of obesity, hypertension, diabetes mellitus, and a remote abdominal surgery in 1980s who presented to the emergency room complaining of abrupt severe constant epigastric pain that started few hours before. The pain was not relieved by antiacid or analgesic medications. CT of the abdomen showed multiple distended fluid-filled loops of small bowel in mid abdomen with infiltrative changes of mesentery. A diagnosis of small bowel obstruction was made, and patient proceed to have an exploratory laparotomy. During the procedure, extensive adhesions between small bowel and omentum and small bowel obstruction due to a phytobezoar were noted for which he underwent lysis of adhesion, excision of thickened omentum, and enterotomy for removal of significant food bezoar. Grossly, the omentum has multiple chalky tan-gray masses ranging between 1.2 and 1.0 cm in greatest dimension surrounded by indurated fatty tissue. Microscopically, multiple hypocellular foci are seen that are composed almost entirely of truncated elastic fibers, with sparse delicate bands of collagen and scattered prominent thick-walled vessels. Elastic stain highlights these elastic fibers while trichrome stains the elastic fibers pale gray in contrast to the bright blue color of the collagen fibers. Mucicarmine, and Congo red are negative. Patient tolerated the procedure well however, postoperatively he had local wound infection leading to prolonged skin dehiscence. Results (if a Case Study enter NA) NA. Conclusion Elastotic mass-forming lesions in the omentum is a new entity that has not been described before in this location that can clinically manifest with signs and symptoms of bowel obstruction. We suggested the name of elastomatosis omentum.

Abstract 14065: Functional and Structural Alterations in Stress-Related Neural Networks Implicated in Atherosclerosis

Introduction: While a link between chronic stress and cardiovascular disease (CVD) is well established, the neurocircuit alterations underlying this association remain unclear. We leveraged advanced multimodal imaging to gain insights into neurocircuit alterations that associate with atherosclerosis. Methods: Individuals with posttraumatic stress disorder (PTSD), trauma-exposed controls without PTSD (TC), and healthy controls (HC) were prospectively enrolled. Participants underwent whole-body 18 F-fluorodeoxyglucose positron emission tomography/magnetic resonance (FDG-PET/MR) imaging. Stress-related neural network activity (SNNA) was assessed on PET as amygdala metabolic activity relative to regulatory (ventromedial prefrontal cortex [vmPFC]) activity. The structural integrity of the uncinate fasciculus, the major white matter tract connecting the amygdala to vmPFC, was assessed using diffusion tensor imaging (DTI). Atherosclerotic burden was assessed on MR as vessel normalized wall index and standard deviation (SD) of vessel wall thickness. Results: Of 91 participants (24 PTSD, 42 TC, 24 HC), 57% were female, and the median age was 37 years. Compared to controls, individuals with PTSD had higher SNNA (Fig 1A) and lower uncinate fasciculus integrity (Fig 1B). SNNA and uncinate fasciculus integrity were negatively correlated (r = - 0.30, p=0.008). Those with PTSD had higher ascending aorta normalized wall indices (p=0.018, adjusted for Framingham risk score). Notably, the SD of carotid wall thickness correlated positively with SNNA and negatively with uncinate fasciculus integrity (Fig 1C &amp; D). Conclusion: These findings suggest that increases in the amygdala relative to vmPFC metabolic activity or disruptions of their structural interconnections may potentiate atherosclerosis. Interventions targeting this stress-related neural network may reduce adverse brain-heart interactions and related cardiovascular disease burden.

Investigation of Serum Angiotensin-Converting Enzyme (ACE) Concentration and ACE Gene Polymorphism in Patients With SARS-CoV-2 Pneumonia Admitted to the Emergency Department.

Background This study seeks to investigate the distribution of the angiotensin-converting enzyme (ACE) gene polymorphism and serum levels in patients with viral pneumonia and predict which polymorphism will lead to severe progression of the disease. Methodology The serum ACE levels and ACE gene polymorphisms were successfully evaluated with respect to subsequent viral pneumonia using records of 100 patients with viral pneumonia and 100 healthy controls. Results ACE serum concentration was statistically significantly elevated. ACE serum concentration with a cut-off value of ≥5,256.05 pg/mL had 85.3% sensitivity and 83.2% selectivity. In addition, patients with ACE genotype D/D were 0.08 times more likely to manifest severe lung involvement than those with I/I, and patients with the I/D genotype were 0.02 times more likely than their counterparts with I/I. The computed tomography findings of the patients revealed that ACE serum concentration was significantly effective in discriminating between mild and moderate-to-severe lung involvement. No significant difference was observed between the blood parameters and ACE genotype distributions. Conclusions I/D polymorphism likely affects the expression of the ACE gene and/or the function of the angiotensin I converting enzyme. The D/D genotype is associated with vessel wall thickness and higher blood pressure. Strong evidence was found between D/D and I/D genotypes in the patient cohort concerning genotypes and ACE serum concentration. Further analysis showed that ACE serum levels were more elevated in the D/D genotype compared to the I/D genotype in the patient cohort.

PSUN57 Noninvasive Assessment of the Coronary Artery Vessel Wall in Cushing's Syndrome Patients using 3-T Magnetic Resonance Imaging: Evidence for Increased Atherosclerosis Compared to Risk Matched Controls

Abstract Background Hypercortisolism due to Cushing's Disease (CD), Ectopic ACTH Syndrome (EAS), adrenal adenoma (AA), or Cyclical Cushing's Syndrome (cCS) is associated with increased cardiovascular morbidity and mortality. The mechanism(s) by which hypercortisolism increases coronary artery atherosclerosis is not understood. We previously used Multidetector computerized tomographic coronary angiography (MDCT) to demonstrate significantly increased noncalcified plaque volume in CS patients. Time-Resolved Phase-Sensitive Dual Inversion Recovery technique (TRAPD-3T) magnetic resonance imaging (MRI) is a recently developed noninvasive tool to examine vessel wall thickness (VWT) of coronary arteries. We postulated that TRAPD MRI might be used as an independent biomarker of coronary artery disease burden in CS. Methods 29 CS patients (AA: 1, CD: 14, EAS: 12, cCS: 2) and 29 age, gender, BMI and Framingham score-matched control patients (CPts) underwent TRAPD-3T MRI of the proximal right coronary artery vessel wall thickness. Prior to MRI, 25 CS patients were untreated and 3 were treated. Vessel wall thickness was measured as the average distance between inner and outer boundaries of the vessel wall. Vessel wall thickness variation was calculated as the standard deviation of these measurements. Circularity was the ratio of the mean thickness over the variation in measurement. The larger the circularity ratio, the more consistent the vessel wall thickness and the less eccentric the blood vessel. All measurements given as mean ± SD. Paired t-tests were used to compare the groups. Results Compared to control subjects, CS patients had significantly higher values for coronary VWT (CS: 1.38 ± 0.19mm, CPts: 1.27 ± 0.15mm; p &amp;lt; 0.015) and VWT variation (CS: 0.19 ± 0.072mm, CPts: 0.14 ± 0.045mm; p &amp;lt;0.002). By contrast, control patients had significantly higher vessel wall circularity compared to CS patients (CS: 9.58 ± 2.65mm, CPts: 8.05 ± 2.65mm; p&amp;lt;0.03). CS pts had less vessel wall circularity, thus increased eccentricity, indicating more advanced atherosclerosis. The degree of hypercortisolism was not associated with Framingham risk score, VWT, variability, or circularity. There was also no significant difference in VWT, variability, or circularity between males and females with hypercortisolism. Conclusion The finding of more advanced atherosclerosis in CS patients compared to age-matched controls suggests that excess cortisol may directly or indirectly promote atherosclerotic plaque formation. Adequate treatment of cardiovascular risk factors along with treatment of underlying hypercortisolism is essential to reducing morbidity and mortality. The TRAPD MR technique has promise as a non-invasive and radiation-free technique to monitor CAD and its prevention/treatment in these patients during and after treatment. Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.

Cell contractility and Focal Adhesion Kinase control circumferential arterial stiffness.

Arterial stiffening is a hallmark of aging and cardiovascular disease. While it is well established that vascular smooth muscle cells (SMCs) contribute to arterial stiffness by synthesizing and remodeling the arterial extracellular matrix, the direct contributions of SMC contractility and mechanosensors to arterial stiffness, and particularly the arterial response to pressure, remain less well understood despite being a long-standing question of biomedical importance. Here, we have examined this issue by combining use of pressure myography of intact carotid arteries, pharmacologic inhibition of contractility, and genetic deletion of SMC focal adhesion kinase (FAK). Biaxial inflation-extension tests performed at physiological pressures showed that acute inhibition of cell contractility with blebbistatin or EGTA altered vessel geometry and preferentially reduced circumferential, as opposed to axial, arterial stiffness in wild-type mice. Similarly, genetic deletion of SMC FAK, which attenuated arterial contraction to KCl, reduced vessel wall thickness and circumferential arterial stiffness in response to pressure while having minimal effect on axial mechanics. Moreover, these effects of FAK deletion were lost by treating arteries with blebbistatin or by inhibiting myosln light chain kinase. The expression of arterial fibrillar collagens, the integrity of arterial elastin, or markers of SMC differentiation were not affected by deletion of SMC FAK. Our results connect cell contractility and SMC FAK to the regulation of arterial wall thickness and directionally-specific arterial stiffening.

Diosmin and its glycocalyx restorative and anti-inflammatory effects on injured blood vessels.

The endothelium, a crucial homeostatic organ, regulates vascular permeability and tone. Under physiological conditions, endothelial stimulation induces vasodilator endothelial nitric oxide (eNO) release and prevents adhesion molecule accessibility and leukocyte adhesion and migration into vessel walls. Endothelium dysfunction is a principal event in cardiovascular disorders, including atherosclerosis. Minimal attention is given to an important endothelial cell structure, the endothelial glycocalyx (GCX), a negatively charged heterogeneous polysaccharide that serves as a protective covering for endothelial cells and enables endothelial cells to transduce mechanical stimuli into various biological and chemical activities. Endothelial GCX shedding thus plays a role in endothelial dysfunction, for example by increasing vascular permeability and decreasing vessel tone. Consequently, there is increasing interest in developing therapies that focus on GCX repair to limit downstream endothelium dysfunction and prevent further downstream cardiovascular events. Here, we present diosmin (3',5,7-trihydroxy-4'-methoxyflavone-7-rhamnoglucoside), a flavone glycoside of diosmetin, which downregulates adhesive molecule expression, decreases inflammation and capillary permeability, and upregulates eNO expression. Due to these pleiotropic effects of diosmin on the vasculature, a possible unidentified mechanism of action is through GCX restoration. We hypothesize that diosmin positively affects GCX integrity along with GCX-related endothelial functions. Our hypothesis was tested in a partial ligation left carotid artery (LCA) mouse model, where the right carotid artery was the control for each mouse. Diosmin (50 mg/kg) was administered daily for 7 days, 72h after ligation. Within the ligated mice LCAs, diosmin treatment elevated the activated eNO synthase level, inhibited inflammatory cell uptake, decreased vessel wall thickness, increased vessel diameter, and increased GCX coverage of the vessel wall. ELISA showed a decrease in hyaluronan concentration in plasma samples of diosmin-treated mice, signifying reduced GCX shedding. In summary, diosmin supported endothelial GCX integrity, to which we attribute diosmin's preservation of endothelial function as indicated by attenuated expression of inflammatory factors and restored vascular tone.

HIGH RISK PREGNANCY WITH POOR FETAL OUTCOME- IS PLACENTA THE REAL CULPRIT ?.

Background: In high risk pregnancies with poor fetal outcome careful examination of placenta along with microscopic study may frequently point to the cause of perinatal death. So we have planned a prospective observational study was to illustrate the gross and microscopic changes in placenta in certain normal and abnormal pregnancies and to analyses the relationship of placental pathology with fetal outcome. A p Methods: rospective study of 100 deliveries at a tertiary teaching hospital in India. Each placenta was studied macroscopically in labour room and sent for microscopic examination. The study included placentas of normal pregnancies and those with high-risk pregnancies. Microscopically placentas were studied for vessel wall thickening, infarction, villitis, chorioangiosis, calcication and intervillous hemorrhage. The outcome variables were studied in each histological group and compared with the normal group using Ψ2 test for homogeneity. For cell frequencies less than 5, Fischer Exact Test was used. Vess Results: el wall thickening was demonstrated in 51% patients. Infarcts were demonstrated in 14%. Placental abnormalities Conclusions: like vessel wall thickening, and infarction is associated with abnormal fetal and neonatal outcome.

Enhanced gaseous hydrogen solubility in ferritic and martensitic steels at low temperatures

Metals that are exposed to high pressure hydrogen gas may undergo detrimental failure by embrittlement. Understanding the mechanisms and driving forces of hydrogen absorption on the surface of metals is crucial for avoiding hydrogen embrittlement. In this study, the effect of stress-enhanced gaseous hydrogen uptake in bulk metals is investigated in detail. For that purpose, a generalized form of Sievert's law is derived from thermodynamic potentials considering the effect of microstructural trapping sites and multiaxial stresses. This new equation is parametrized and verified using experimental data for carbon steels, which were charged under gaseous hydrogen atmosphere at pressures up to 1000 bar. The role of microstructural trapping sites on the parameter identification is critically discussed. Finally, the parametrized equation is applied to calculate the stress-enhanced hydrogen solubility of thin-walled pipelines and thick-walled pressure vessels during service.

Simulation Analysis of Delamination Damage for the Thick-Walled Composite-Overwrapped Pressure Vessels.

In order to verify the delamination damage occurring in thick-walled composite-overwrapped pressure vessels, firstly, for composite delamination damage, a composite laminate model was established. Model I and model II delamination failure processes of composite structures were simulated and verified based on a tiebreak contact algorithm for different mesh sizes, respectively, and the approximate equivalent results were achieved by correcting the inter-ply strength. Then, for in-plane damage to composite materials, the elastic–plastic process was verified by selecting a progressive damage model, with quasistatic nonlinear tensile shear of sample specimens as an example. Further, under the purpose of generality and simplicity, the location of the first occurrence of delamination failure was simulated and analyzed with the tiebreak contact algorithm and a reasonable mesh size, using quasistatic loading of a thick composite-overwrapped pressure vessel cylindrical section as an example. The results showed that delamination occurred at approximately the center, which is in general agreement with the experimentally observed phenomenon. On this basis, the locations of the first significant delamination phenomena in composite-overwrapped vessels under three different ratios of plus or minus 45-degree layup angles were predicted. Finally, the differences in structural strength between the single laying methods and the combined laying method were compared. The results showed that the ratio of 50% had a higher modulus value than a pure 0° ply, but too large a ratio was detrimental to the improvement of structural properties.

Comparative Morphological, Anatomical and Physiological Analyses Explain the Difference of Wounding-Induced Agarwood Formation between Ordinary Agarwood Nongrafted Plants and Five Grafted Qi-Nan Clones (Aquilaria sinensis)

Agarwood is the dark resinous heartwood of injured ordinary Aquilaria sinensis (OA). Recently, some new clones of A. sinensis (Qi-Nan) that intensively produce high-quality agarwood were selected and cultivated by grafted clonal seedlings. However, very little is known about their agarwood formation mechanism, and it is unclear whether the current method of distinguishing Qi-Nan from OA by observing its leaf apparent morphology is scientifically reliable. In this study, the differences between OA and Qi-Nan clones in agarwood formation and their correlation with morphological, anatomical and physiological characteristics were investigated in two types of A. sinensis trees. After the mechanical injury, agarwood yield and essential oil content in agarwood of Qi-Nan were significantly higher than that of OA. There was no significant difference in leaf shape parameters between Qi-Nan and OA, but Qi-Nan showed higher specific leaf weight, total leaf chlorophyll, leaf nitrogen content and net photosynthetic rate. A xylem anatomical analysis showed that Qi-Nan had significantly smaller vessel wall thickness, greater ray cell wall thickness and larger interxylary phloem area than OA. Moreover, Qi-Nan had a greater consumption of non-structural carbohydrates than OA. Agarwood yield and oil content in agarwood showed significantly positive correlations with leaf photosynthetic capacity, the wall thickness of xylem ray cell, interxylary phloem area, starch utilization rate of trees, and a significantly negative correlation with the wall thickness of xylem vessel of trees. In brief, Qi-Nan has a stronger photosynthetic basis to supply more carbon sources, a more efficient xylem structural basis for agarwood production and a higher carbon source utilization rate, leading to a higher agarwood yield and oil content. It is not reliable to distinguish Qi-Nan from OA simply by observing leaf apparent morphology.