The role of carotid plaque echogenicity in baroreflex sensitivity

ObjectiveThe baroreflex sensitivity is impaired in patients with carotid atherosclerosis. The purpose of our study was to assess the impact of carotid plaque echogenicity on the baroreflex function in patients with significant carotid atherosclerosis, who have not undergone carotid surgery.MethodSpontaneous baroreflex sensitivity (sBRS) was estimated in 45 patients with at least a severe carotid stenosis (70%-99%). sBRS calculation was performed noninvasively, with the spontaneous sequence method, based on indirectly estimated central blood pressures from radial recordings. This method failed in three patients due to poor-quality recordings, and eventually 42 patients were evaluated. After carotid duplex examination, carotid plaque echogenicity was graded from 1 to 4 according to Gray-Weale classification and the patients were divided into two groups: the echolucent group (grades 1 and 2) and the echogenic group (grades 3 and 4).ResultsSixteen patients (38%) and 26 patients (62%) were included in the echolucent and echogenic group, respectively. Diabetes mellitus was observed more frequently among echolucent plaques (χ2 = 8.0; P < .004), while those plaques were also more commonly symptomatic compared with echogenic atheromas (χ2 = 8.5; P < .003). Systolic arterial pressure, diastolic arterial pressure, and heart rate were similar in the two groups. Nevertheless, the mean value of baroreflex sensitivity was found to be significantly lower in the echogenic group (2.96 ms/mm Hg) compared with the echolucent one (5.0 ms/mm Hg), (F [1, 42] = 10.1; P < .003).ConclusionsThese findings suggest that echogenic plaques are associated with reduced baroreflex function compared with echolucent ones. Further investigation is warranted to define whether such an sBRS impairment could be responsible for cardiovascular morbidity associated with echogenic plaques

Serum Lp(a) Lipoprotein Levels in Patients with Atherosclerotic Occlusive Disease of the Lower Extremities

AbstractObjective to evaluate the association between Lp(a) lipoprotein levels, other serum lipids and the presence of lower limb atherosclerotic occlusive disease. Materials and methods angiographic findings in 36 patients were related to serum Lp(a). Total cholesterol, triglycerides, LDL-cholesterol, HDL-cholesterol and Lp(a) levels were compared with those of 73 age- and sex-matched healthy controls. Results atheromatous lesions were localised in the femoropopliteal (≈60%) and aortoiliac (≈40%) segments. The number of stenosed arteries was ≥2 and the range of stenosis severity was between 40% and 100%. There was a significant increase in serum Lp(a) (p= 0.000001) and a decrease in serum HDL (p= 0.000009) levels in patients compared to controls. No difference was observed in total cholesterol, LDL-cholesterol or triglyceride. However, the ratio of total cholesterol/HDL-cholesterol was significantly higher (p= 0.005) in patients. Conclusion a dyslipidaemic serum profile, characterised by increased Lp(a) levels and decreased HDL-cholesterol levels, is associated with atherosclerotic occlusive disease of the lower extremities

Computational modelling of epithelial cell monolayers during infection with Listeria monocytogenes

Intracellular bacterial infections alter the normal functionality of human host cells and tissues. Infection can also modify the mechanical properties of host cells, altering the mechanical equilibrium of tissues. In order to advance our understanding of host–pathogen interactions, simplified in vitro models are normally used. However, in vitro studies present certain limitations that can be alleviated by the use of computer-based models. As complementary tools these computational models, in conjunction with in vitro experiments, can enhance our understanding of the mechanisms of action underlying infection processes. In this work, we extend our previous computer-based model to simulate infection of epithelial cells with the intracellular bacterial pathogen Listeria monocytogenes. We found that forces generated by host cells play a regulatory role in the mechanobiological response to infection. After infection, in silico cells alter their mechanical properties in order to achieve a new mechanical equilibrium. The model pointed the key role of cell–cell and cell–extracellular matrix interactions in the mechanical competition of bacterial infection. The obtained results provide a more detailed description of cell and tissue responses to infection, and could help inform future studies focused on controlling bacterial dissemination and the outcome of infection processes. © 2022 The Author(s

Spatiotemporal characterization of endothelial cell motility and physical forces during exposure to Borrelia burgdorferi

Cell motility and biomechanics are critical in various (patho)physiological processes, including the regulation of vascular barrier integrity, which can be subverted by bacterial pathogens. Here, we present a protocol on how to expose endothelial cells (ECs) to vector-borne Borrelia burgdorferi (Bb) and characterize EC kinematics and dynamics during exposure to live or heat-inactivated Bb through traction force and monolayer stress microscopy. Modifications to this protocol may be necessary for studying how different cell types interact with Bb or other microorganisms

A Stiff Extracellular Matrix Favors the Mechanical Cell Competition that Leads to Extrusion of Bacterially-Infected Epithelial Cells

Cell competition refers to the mechanism whereby less fit cells (“losers”) are sensed and eliminated by more fit neighboring cells (“winners”) and arises during many processes including intracellular bacterial infection. Extracellular matrix (ECM) stiffness can regulate important cellular functions, such as motility, by modulating the physical forces that cells transduce and could thus modulate the output of cellular competitions. Herein, we employ a computational model to investigate the previously overlooked role of ECM stiffness in modulating the forceful extrusion of infected “loser” cells by uninfected “winner” cells. We find that increasing ECM stiffness promotes the collective squeezing and subsequent extrusion of infected cells due to differential cell displacements and cellular force generation. Moreover, we discover that an increase in the ratio of uninfected to infected cell stiffness as well as a smaller infection focus size, independently promote squeezing of infected cells, and this phenomenon is more prominent on stiffer compared to softer matrices. Our experimental findings validate the computational predictions by demonstrating increased collective cell extrusion on stiff matrices and glass as opposed to softer matrices, which is associated with decreased bacterial spread in the basal cell monolayer in vitro. Collectively, our results suggest that ECM stiffness plays a major role in modulating the competition between infected and uninfected cells, with stiffer matrices promoting this battle through differential modulation of cell mechanics between the two cell populations

Borrelia burgdorferi modulates the physical forces and immunity signaling in endothelial cells

Borrelia burgdorferi (Bb), a vector-borne bacterial pathogen and the causative agent of Lyme disease, can spread to distant tissues in the human host by traveling in and through monolayers of endothelial cells (ECs) lining the vasculature. To examine whether Bb alters the physical forces of ECs to promote its dissemination, we exposed ECs to Bb and observed a sharp and transient increase in EC traction and intercellular forces, followed by a prolonged decrease in EC motility and physical forces. All variables returned to baseline at 24 h after exposure. RNA sequencing analysis revealed an upregulation of innate immune signaling pathways during early but not late Bb exposure. Exposure of ECs to heat-inactivated Bb recapitulated only the early weakening of EC mechanotransduction. The differential responses to live versus heat-inactivated Bb indicate a tight interplay between innate immune signaling and physical forces in host ECs and suggest their active modulation by Bb

Mindfulness in schools: a health promotion approach to improving adolescent mental health.

Between 10 and 20% of adolescents worldwide experience a mental health problem within a given 12-month period. Mental health problems impact on an adolescent’s potential to live a fulfilling and productive life and lead to challenges such as stigma, isolation and discrimination. To address this need, in recent years, there has been growing interest into broad-based school-integrated health promotion interventions that seek to build resilience and augment protective factors in adolescents. Mindfulness-based interventions (MBIs) reflect one such approach that have been administered to adolescent populations in both resilience building and treatment contexts. This paper discusses the utility of school-based MBIs as an adolescent health promotion approach and makes recommendations for intervention design, delivery and evaluation. Emerging evidence indicates that school-integrated MBIs may be a cost-effective means of not only meeting government objectives relating to adolescent mental health, but also for improving the wellbeing of teachers and parents. Furthermore, there is growing evidence indicating that mindfulness can elicit improvements in student learning performance and general classroom behaviour. However, notwithstanding these beneficial properties, there remains a need to conduct large-scale empirical investigations that seek to evaluate the effectiveness of school-integrated MBIs at a regional or national level. A further challenge is the need to ensure that mindfulness instructors are able to impart to adolescents an experiential understanding of this ancient contemplative technique.N

Giant primary adrenal hydatid cyst presenting with arterial hypertension: a case report and review of the literature

<p>Abstract</p> <p>Introduction</p> <p>A primary hydatid cyst of the adrenal gland is still an exceptional localization. The adrenal gland is an uncommon site even in Morocco, where echinococcal disease is endemic.</p> <p>Case presentation</p> <p>We report the case of a 64-year-old Moroccan man who presented with the unusual symptom of arterial hypertension associated with left flank pain. Computed tomography showed a cystic mass of his left adrenal gland with daughter cysts filing the lesion (Type III). Despite his negative serology tests, the diagnosis of a hydatid cyst was confirmed on surgical examination. Our patient underwent surgical excision of his left adrenal gland with normalization of blood pressure. No recurrence has occurred after 36 months of follow-up.</p> <p>Conclusion</p> <p>There are two remarkable characteristics of this case report; the first is the unusual location of the cyst, the second is the association of an adrenal hydatid cyst with arterial hypertension, which has rarely been reported in the literature.</p

Long-term morphological and hormonal follow-up in a single unit on 115 patients with adrenal incidentalomas

We investigated the natural course of adrenal incidentalomas in 115 patients by means of a long-term endocrine and morphological (CT) follow-up protocol (median 4 year, range 1–7 year). At entry, we observed 61 subclinical hormonal alterations in 43 patients (mainly concerning the ACTH–cortisol axis), but confirmatory tests always excluded specific endocrine diseases. In all cases radiologic signs of benignity were present. Mean values of the hormones examined at last follow-up did not differ from those recorded at entry. However in individual patients several variations were observed. In particular, 57 endocrine alterations found in 43 patients (37.2%) were no longer confirmed at follow-up, while 35 new alterations in 31 patients (26.9%) appeared de novo. Only four alterations in three patients (2.6%) persisted. Confirmatory tests were always negative for specific endocrine diseases. No variation in mean mass size was found between values at entry (25.4±0.9 mm) and at follow-up (25.7±0.9 mm), although in 32 patients (27.8%) mass size actually increased, while in 24 patients (20.8%) it decreased. In no case were the variations in mass dimension associated with the appearance of radiological criteria of malignancy. Kaplan–Meier curves indicated that the cumulative risk for mass enlargement (65%) and for developing endocrine abnormalities (57%) over time was progressive up to 80 months and independent of haemodynamic and humoral basal characteristics. In conclusion, mass enlargement and the presence or occurrence over time of subclinical endocrine alterations are frequent and not correlated, can appear at any time, are not associated with any basal predictor and, finally, are not necessarily indicative of malignant transformation or of progression toward overt disease

The effects of endogenous and exogenous androgens on cardiovascular disease risk factors and progression

Cardiovascular disease incidence rates have long been known to significantly differ between the two sexes. Estrogens alone fail to explain this phenomenon, bringing an increasing amount of attention to the role of androgens. Contrary to what was initially hypothesized, androgens seem to have an overall cardioprotective effect, especially in men. Recent studies and published data continue to support this notion displaying a consistent inverse correlation with atherosclerosis progression and cardiovascular disease both in regressive and prospective study models. Clinical studies have also revealed what seems to be a differential androgenic effect on various cardiovascular risk factors between men and women. Further insight indicates that in order to avoid confusion it may be also preferable to separately examine the effects of endogenous androgen levels from exogenous testosterone administration, as well as discern the differential results of low to normal and supraphysiological administration doses. This review summarizes old and recent data according to the above distinctions, in an attempt to further our understanding of the role of androgens in cardiovascular disease