Vessel Lumen Research Articles

Transcriptome-based WGCNA reveals the molecular regulation of xylem plasticity in acclimation to drought and rewatering in mulberry

Xylem plasticity is important for trees to coordinate hydraulic efficiency and safety under changing soil water availability. However, the physiological and transcriptional regulations of cambium on xylem plasticity are not well understood. In this study, mulberry saplings of drought-resistant Wubu and drought-susceptible Zhongshen1 were subjected to moderate or severe drought stresses for 21 days and subsequently rewatered for 12 days. The anatomical, physiological and transcriptional responses in wood and cambium were analyzed. Most parameters were not affected significantly under moderate drought for both cultivars. Severe drought led to decreased vessel lumen diameter and increased vessel frequency, increased starch and hemicellulose in wood of both cultivars. Notably, increased soluble sugars and lignin were detected only in wood of Wubu. In cambial zone, levels of starch, glucose, fructose, mannose and cytokinin were decreased in both cultivars, whereas soluble sugars were increased in Wubu but deceased in Zhongshen1. RNA-sequencing identified 1824 and 2471 differentially expressed genes in Wubu and Zhongshen1 under severe drought, respectively. These responses were partially recovered after rewatering. Weighted gene correlation network analysis identified modules of co-expressed genes correlated with the anatomical and physiological traits of wood and cambium, with the turquoise and green modules most strongly correlated with traits under drought or rewatering. These modules were enriched in gene ontology terms related to cell division, cytoskeleton organization, cell wall modification, dark respiration, vesicle transport and protein metabolism. Detailed gene expression patterns indicate that reprogramming of cambium activity was relatively similar in both cultivars, but at different scales. These findings provide important insights into the physiological and molecular mechanisms underlying xylem plasticity based on cambium and offer valuable references for breeding drought-resistant mulberry and other woody species in light of future drier climate scenarios.

Comparison of the Effect of Delay Phenomenon and Quercetin Application on the Viability of Dorsal Skin Island Flaps in Rats: An Experimental Study.

Surgical delay is any surgical intervention performed 7-14 days before flap elevation, separating part of flap from its vascular bed and aiming to decrease flap necrosis. However, delay surgery needs to be planned and performed as a separate surgical operation. Quercetin is a flavonoid with anti-inflammatory, and vasodilator effects. This study compares the effects of quercetin and surgical delay on flap survival. The study included 32 male Wistar rats divided into four groups: control group (group 1), surgical delay group (group 2), quercetin group (group 3), and both surgical delay and quercetin group (group 4). All dorsal skin island flaps were elevated based on deep circumflex iliac artery and 7 days were selected as waiting period after flap elevation, 50 mg/kg (0.5 mL) intraperitoneal quercetin administration period, and surgical delay period. Macroscopically flap necrosis rates were calculated and histopathological examination was performed to evaluate number of vessels, vessel lumen diameters, inflammation, epidermal damage, and dermal fibrosis scores. All rats were euthanized. Flap necrosis rates, inflammation, epidermal damage, and dermal fibrosis scores of group 3 and 4 were found to be lower than group 1 and 2 (P < 0.05). Vascular lumen diameter of group 2, 3, and 4 were found to be higher than group 1 (P < 0.05) but no statistically significant difference was found for this parameter between group 2, 3, and 4 (P > 0.05). The number of vessels were found to be higher in group 2, group 3, and group 4 compared with group 1, but this difference was not to be found statistically significant (P = 0.534). This study shows that quercetin application is more effective in reducing flap necrosis rates and anti-inflammatory effect than surgical delay and also has superior effect in terms of vasodilation.

Cerebral vascular malformations: pathogenesis and therapy.

Cerebral vascular malformations (CVMs), particularly cerebral cavernous malformations and cerebral arteriovenous malformations, pose significant neurological challenges due to their complex etiologies and clinical implications. Traditionally viewed as congenital conditions with structural abnormalities, CVMs have been treated primarily through resection, embolization, and stereotactic radiosurgery. While these approaches offer some efficacy, they often pose risks to neurological integrity due to their invasive nature. Advances in next-generation sequencing, particularly high-depth whole-exome sequencing and bioinformatics, have facilitated the identification of gene variants from neurosurgically resected CVMs samples. These advancements have deepened our understanding of CVM pathogenesis. Somatic mutations in key mechanistic pathways have been identified as causative factors, leading to a paradigm shift in CVM treatment. Additionally, recent progress in noninvasive and minimally invasive techniques, including gene imaging genomics, liquid biopsy, or endovascular biopsies (endovascular sampling of blood vessel lumens), has enabled the identification of gene variants associated with CVMs. These methods, in conjunction with clinical data, offer potential for early detection, dynamic monitoring, and targeted therapies that could be used as monotherapy or adjuncts to surgery. This review highlights advancements in CVM pathogenesis and precision therapies, outlining the future potential of precision medicine in CVM management.

Unveiling the Clinical and Imaging Signatures of Intravascular Lymphoma of the Central Nervous System: A Multicentric Cohort Study.

Intravascular lymphoma is a rare subtype of B-cell lymphoma characterized by a clonal proliferation restricted to the lumen of small vessels. Over 50% of patients exhibit central nervous system (CNS) involvement, but diagnosis is often delayed due to the lack of distinctive features. We aimed to identify key phenotypic features for early diagnosis of intravascular lymphoma with CNS involvement through an in-depth cohort study. We built up a multicenter retrospective cohort of 17 patients recruited in collaboration with the French Expert Network for Oculo-Cerebral Lymphomas (LOC network), and retrospectively analyzed data from medical records. In this cohort, 15 of 17 (88%) patients developed focal neurological episodes, often fluctuating and/or recurrent, with a sudden onset in 68% of episodes, suggesting a vascular origin. Rapid cognitive deterioration occurred in 15 of 17 (88%) patients, psychiatric manifestations in 8 of 17 (47%), and "B signs" in 14 of 17 (82%). Brain MRI showed polymorphic FLAIR hyperintensities in 14 of 16 (87%) patients, and DWI-positive lesions in 13 of 16 (81%) of patients, which accumulated over time and had unusual characteristics for ischemic lesions (progressive growth, persistent DWI-hyperintensity over 1 month, surrounded by a wider FLAIR hyperintensity). Early-onset inflammatory syndrome, and elevated lactate dehydrogenase (LDH) levels were observed in over 90% of cases. Mild and inconsistent meningitis contrasted with a nearly-constant hyperproteinorachia. An increased interleukin 10/6 ratio over 0,7 was found in 4 of 7 (57%) patients, and skin biopsy led to a pathological diagnosis in 3 of 6 (50%) patients. The results of this study highlight "red flags" that could help accelerate the diagnosis of intravascular lymphoma involving the CNS. ANN NEUROL 2024.

Post-traumatic stress disorder: Cerebral and extracerebral processing of traumatic memories and treatment strategies

Post-traumatic stress disorder (PTSD) is a severe neuropsychiatric condition characterized by anxiety-related symptoms, including intrusive memories. However, the exact anatomic location of traumatic memories remains unclear. Traumatic imagery may involve the amygdala and posterior cingulate cortex, rather than the hippocampus. Besides the central nervous system, cells and even proteins can process information and store memories. For instance, &gt;36% of cardiac transplant recipients inherit donor personality traits, emphasizing that tissues can store and recall memories. Moreover, physical therapists mention &amp;ldquo;musculofascial memories,&amp;rdquo; that is, the ability of muscles and fascia to retain the memory of past injuries and adapt their function accordingly. Immune cells record previous infections, demonstrating the broader perspective of memory storage in the body. At the cellular level, psychological stress induces premature cellular senescence, a survival program characterized by proliferation arrest; resistance to apoptosis; and a toxic secretome known as the senescence-associated secretory phenotype (SASP). SASP contains brain-derived neurotropic factor (BDNF), a neurotrophin linked to fear memory that is frequently elevated in the peripheral blood of patients with PTSD. Endothelial cells (ECs), the tiles paving the lumen of large and small vessels, age earlier than other cells in patients with severe mental illness, including PTSD. Senescent ECs release SASP directly into the systemic circulation, spreading senescence throughout the body. In this narrative review, we hypothesize that ECs store traumatic memories and SASP-associated BDNF activates traumatic imagery. We also discuss membrane lipid replacement, mitochondrial transplantation and transfer, and several natural and synthetic compounds that may counteract endothelial senescence and SASP.

Advancements in imaging of intracranial atherosclerotic disease: beyond the arterial lumen to the vessel wall.

Intracranial atherosclerotic disease (ICAD) significantly increases the risk of ischemic stroke. It involves the accumulation of plaque within arterial wallsandnarrowing or blockage of blood vessel lumens. Accurate imaging is crucial for the diagnosis and management of ICAD at both acute and chronic stages. However, imaging the small, tortuous intracranial arterial walls amidstcomplex structures is challenging. Clinicians have employed diverse approaches to improve imaging quality, with a particular emphasis on optimizing the acquisition ofimages using newtechniques, enhancing spatial and temporal resolution of images, and refining post-processing techniques. ICAD imaging has evolved from depicting lumen stenosis to assessing blood flow reserve and identifying plaque components. Advanced techniques such as fractional flowreserve (FFR), high-resolution vessel wall magnetic resonance (VW-MR), optical coherence tomography (OCT), and radial wall strain (RWS) now allow direct visualization offlow impairment, vulnerable plaques, and blood flow strainto plaque, aiding in the selection of high-risk strokepatients for intervention. This article reviews the progression of imaging modalities from lumen stenosis to vessel wall pathology and compares their diagnostic value forrisk stratification in ICAD patients.

Senolysis potentiates endothelial progenitor cell adhesion to and integration into the brain vasculature

BackgroundOne of the most severe consequences of ageing is cognitive decline, which is associated with dysfunction of the brain microvasculature. Thus, repairing the brain vasculature could result in healthier brain function.MethodsTo better understand the potential beneficial effect of endothelial progenitor cells (EPCs) in vascular repair, we studied the adhesion and integration of EPCs using the early embryonic mouse aorta–gonad–mesonephros – MAgEC 10.5 endothelial cell line. The EPC interaction with brain microvasculature was monitored ex vivo and in vivo using epifluorescence, laser confocal and two-photon microscopy in healthy young and old animals. The effects of senolysis, EPC activation and ischaemia (two-vessel occlusion model) were analysed in BALB/c and FVB/Ant: TgCAG-yfp_sb #27 mice.ResultsMAgEC 10.5 cells rapidly adhered to brain microvasculature and some differentiated into mature endothelial cells (ECs). MAgEC 10.5-derived endothelial cells integrated into microvessels, established tight junctions and co-formed vessel lumens with pre-existing ECs within five days. Adhesion and integration were much weaker in aged mice, but were increased by depleting senescent cells using abt-263 or dasatinib plus quercetin. Furthermore, MAgEC 10.5 cell adhesion to and integration into brain vessels were increased by ischaemia and by pre-activating EPCs with TNFα.ConclusionsCombining progenitor cell therapy with senolytic therapy and the prior activation of EPCs are promising for improving EPC adhesion to and integration into the cerebral vasculature and could help rejuvenate the ageing brain.

Effect of Vessel Attenuation, VMI Level, and Reconstruction Kernel on Pericoronary Adipose Tissue Attenuation for EID CT and PCD CT: An Ex Vivo Porcine Heart Study.

BACKGROUND. Pericoronary adipose tissue (PCAT) attenuation and the fat attenuation index (FAI) may serve as markers of inflammation and the risk of adverse cardiac events. However, standardization of relevant CT acquisition and reconstruction parameters is lacking. OBJECTIVE. The purpose of this study was to investigate the influence of vessel attenuation, the virtual monoenergetic image (VMI) level, and the reconstruction kernel on PCAT attenuation and FAI by use of energy-integrating detector (EID) and photon-counting detector (PCD) CT systems in an ex vivo porcine heart model. METHODS. The right coronary artery (RCA) of a porcine heart was injected with saline or varying contrast medium dilutions to achieve vessel attenuation ranging from 0 to 1000 HU. After each injection, the heart was sequentially scanned by EID CT at 120 kVp and PCD CT at 140 kVp at a constant CTDIvol of 10 mGy. For EID CT, polychromatic images were reconstructed with a Qr40 kernel. For PCD CT, VMIs (obtained at 40-80 keV in 10-keV increments) were reconstructed with Qr40, Bv40, and Bv56 kernels. ROIs were placed to measure RCA and PCAT attenuation. FAI was determined using software; histogram analysis was performed to assess voxel attenuation in the volumes of interest for FAI calculation. RESULTS. Correlations were observed between attenuation in the RCA and attenuation in the adjacent PCAT (r = 0.3-1.0) and between vessel attenuation and the FAI (r = -0.9 to 1.0). For PCAT attenuation and the FAI, these associations became progressively weaker when progressively sharper kernels were used. For increasing vessel attenuation on EID CT and for increasing VMI level on PCD CT, FAI histograms showed right shifts in peak attenuation values; the percentage of histogram voxels that met the threshold range for inclusion in FAI calculation was 9-38% for EID CT and 6-39% for PCD CT at VMI levels of 70-80 keV. For PCD CT, use of sharper kernels was associated with left shifts in peak attenuation values and greater percentages of voxels within the threshold range for inclusion in FAI calculation. CONCLUSION. PCAT attenuation and the FAI are influenced by vessel lumen attenuation, the VMI level, and the reconstruction kernel. A minority of pericoronary voxels contribute to FAI measurements for polychromatic EID CT and for PCD CT at high VMI levels. CLINICAL IMPACT. These findings may help standardize acquisition and reconstruction parameters for PCAT attenuation and FAI measurements.

A High-Fidelity Computational Model for Predicting Blood Cell Trafficking and 3D Capillary Hemodynamics in Retinal Microvascular Networks.

To present a first principle-based, high-fidelity computational model for predicting full three-dimensional (3D) and time-resolved retinal microvascular hemodynamics taking into consideration the flow and deformation of individual blood cells. The computational model is a 3D fluid-structure interaction model based on combined finite volume/finite element/immersed-boundary methods. Three in silico microvascular networks are built from high-resolution in vivo motion contrast images of the superficial capillary plexus in the parafoveal region of the human retina. The maximum tissue area represented in the model is approximately 500 × 500 µm2, and vessel lumen diameters ranged from 5.5 to 25 µm covering capillaries, arterioles, and venules. Blood is modeled as a suspension of individual blood cells, namely, erythrocytes (RBC), leukocytes (WBC), and platelets in plasma. An accurate and detailed biophysical modeling of each blood cell and their flow-induced deformation is considered. A physiological, pulsatile boundary condition corresponding to an average cardiac cycle of 0.9 second is used. Detailed quantitative data and analysis of 3D retinal microvascular hemodynamics are presented, and their relationship to RBC flow dynamics is illustrated. Blood velocity is shown to have temporal oscillations superimposed on the background pulsatile variation, which arise because of the way RBCs partition at vascular junctions, causing repeated clogging and unclogging of vessels. Temporal variations in RBC velocity and hematocrit are anti-correlated in a given vessel, but their time-averaged distributions are positively correlated across the network. Whole blood velocity is 65% to 85% of RBC velocity, with the discrepancy related to the formation of an RBC-free region, adjacent to the vascular endothelium and typically 0.8 to 1.8 µm thick. The 3D velocity and RBC concentration profiles are shown to be oppositely skewed with respect to each other, because of the way that RBCs "hug" the apex of each bifurcation. RBC deformation is predicted to have biphasic behavior with respect to vessel diameter, with minimal cell length for vessels approximately 7 µm in diameter. The wall shear stress (WSS) exhibits a strongly 3D distribution with local regions of high value and gradient spanning a range of 10 to 80 dyn/cm2. WSS is highest where there is faster flow, greater curvature of the vessel wall, capillary bifurcations, and at locations of RBC crowding and associated thinning of the cell-free layer. This study highlights the usefulness of high-fidelity cell-resolved modeling to obtain accurate and detailed 3D, time-resolved retinal hemodynamic parameters that are not readily available through noninvasive imaging approaches. The results presented are expected to complement and enhance the interpretation of in vivo data, as well as open new avenues to study retinal hemodynamics in health and disease.

High-Resolution Vessel Wall Imaging in Primary CNS Vasculitis: A Case Series

High-resolution vessel wall imaging (HRVWI) is a relatively new technique in which vessel walls can be imaged suppressing the cerebrospinal fluid and blood signals. If there is inflammation of the vessel wall (vasculitis) it will show contrast enhancement. This is the only modality which is available to study vessel walls. All angiography techniques including Magnetic Resonance Angiography(MRA), Contrast computerized tomography angiography (CT -Angiography), and digital subtraction angiography (DSA) shows only the state of the lumen of the blood vessel. Involvement of blood vessels in Central Nervous system (CNS) can occur in systemic vasculitis (like microscopic polyangiitis, Polyarteritis nodosa, etc) where there is evidence of other organ involvement or primary CNS vasculitis (PCNSV) in which only involvement of the brain and spinal cord occurs. PCNSV is a rare disease and till now only the brain biopsy is the gold standard for definitive diagnosis. Brain biopsy is an invasive procedure, not always available, and many patients don’t give consent for the procedure. HRWVI can complement the angiography in the diagnosis of CNS vasculitis, especially PCNSV. Here we describe a case series of 4 cases of CNS vasculitis (3 cases of possible PCNSV and one vasculitic moya- moya syndrome) who had presented with stroke, All had abnormal Cerebrospinal fluid (CSF) and HRVWI showed contrast enhancement of the vessel wall indicating the possibility of vasculitis. In two cases, there was involvement of medium-sized arteries (middle cerebral artery), one patient had unilateral internal carotid artery (ICA) involvement and one had bilateral supra- clinoid stenosis of ICA associated with hyperthyroidism (vasculitic Moyamoya syndrome).

Variation in functional traits among different mycorrhizal types and life history stages of temperate broadleaf tree species

Exploring the variation in functional traits in plants from different perspectives not only helps reveal the adaptation of plants to their environment but also reflects the ecological strategies of plants. In this study, three species of arbuscular mycorrhizal (AM) trees and three species of ectomycorrhizal (EM) trees were selected in the Heilongjiang Liangshui National Nature Reserve. To investigate the similarities and differences between the functional traits of the two mycorrhizal types of trees at different life history stages, hydraulic traits, anatomical traits, leaf functional traits, and stoichiometry of each species were measured at different life history stages. Traits such as mean vessel area, hydraulic weighted vessel diameter and nitrogen content appeared to be relatively important traits in this study, and all traits were more strongly correlated in AM trees. The sapwood-specific hydraulic conductivity, leaf-specific hydraulic conductivity, vessel density, vessel lumen fraction, nitrogen content and phosphorus content of EM species were significantly higher than those of AM species, while the total vessel area, mean vessel area, hydraulic weighted vessel diameter and density of primary leaf veins of EM species were significantly lower than those of AM species. The leaf mass per area and leaf dry matter content of saplings were significantly lower than those of juvenile trees and adult trees. Most of the trait variation interspecific and intraspecific, and the variability of hydraulic and anatomical traits such as sapwood-specific hydraulic conductivity, leaf-specific hydraulic conductivity, vessel density and total vessel area was relatively large. Leaf dry matter content, hydraulic weighted vessel diameter, vessel density and the vessel lumen fraction contributed significantly to whole branch hydraulic conductivity. It is evident that plastic adjustment and synergistic variation in functional traits are important mechanisms by which plants with different mycorrhizal types and at different life history stages can adapt to different environments.

Coronary Artery Vasculitis and Encasement: Multimodality Imaging Findings and Mimics.

Coronary artery vasculitis (CAV) and coronary artery encasement are rarely diagnosed conditions that are important diagnostic considerations, particularly in patients with acute coronary syndrome without traditional cardiovascular risk factors or systemic illness. Vasculitis refers to inflammation of the blood vessel walls, which can be primary or secondary. This process should be distinguished from neoplastic involvement of the coronary arteries, termed coronary artery encasement. Prospective diagnosis of these diseases is challenging, often requiring multidisciplinary workup with careful attention to clinical presentation and multiorgan findings. While CAV and coronary artery encasement can be indistinguishable at coronary CT angiography, certain imaging features help order the differential diagnosis. CAV should be considered when there is smooth wall thickening that is circumferential and/or continuous. A diagnosis of coronary artery encasement is favored when there is irregular or nodular wall thickening that is eccentric to the vessel lumen. Epicardial fat stranding may also appear more extensive compared with CAV. Potential mimics of CAV include atherosclerosis, acute plaque rupture, coronary artery aneurysm, and spontaneous coronary artery dissection. Detection and diagnosis of CAV may help avoid complications related to accelerated atherosclerosis and infarction. Radiologists should be familiar with the range of pathologic conditions that can affect the coronary arteries beyond atherosclerosis as they may be the first to raise such diagnostic possibilities, guiding next steps in patient workup and management. ©RSNA, 2024 Supplemental material is available for this article.

Modulatory potentials of nitric oxide in obesity-induced endothelial dysfunction

Obesity is caused by a significant increase in adipose tissue due to excessive caloric intake that exceeds energy expenditure. Obesity has emerged as a significant public health issue in both poor resource and economic developed nations, owing to its increased incidence and links to chronic diseases, such osteoarthritis, hypertension, non-alcoholic fatty liver disease (NAFLD), and cardiovascular diseases (CVDs). It is believed that uncoupled eNOS, nicotinamide adenine dinucleotide phosphate (NADPH) oxidases, xanthine oxidase, lipoxygenase, cyclooxygenase, microsomal P-450 enzymes, and pro-oxidant heme molecules are responsible for the drastic decrease in NO production and the relative increase in reactive oxygen species (ROS) secretion, which are considered as the molecular mechanisms associated with obesity-induced endothelial dysfunction. Vascular endothelium defines a monolayer of cells, which lies between the vascular smooth muscle cells (VSMCs) and the vessel lumen. It performs a number of protective actions facilitated by the release of nitric oxide (NO), a soluble gas that is generated in endothelial cells by the amino acid L-arginine through the action of endothelial nitric oxide synthase (eNOS). The maintenance of vascular homeostasis is facilitated by various biological actions of NO, such as modulation of vascular dilator tone, control of local cell growth, and protection of the endothelium from the harmful effects of cellular components in blood circulation, while maintaining normal endothelial functions. Decreased peripheral arterial endothelium-dependent dilation (EDD) in response to mechanical (intravascular shear) or chemical (acetylcholine) stimuli suggests that decreased NO bioavailability has been recognised as major molecular mechanisms associated with the progress and development of obesity-induced endothelial dysfunction. In this review, the modulatory effects of NO in obesity-induced endothelial dysfunction will be discussed.

Vascular smooth muscle cells can be circumferentially aligned inside a channel using tunable gelatin microribbons

The gold standard to measure arterial health is vasodilation in response to nitric oxide (NO). Vasodilation is generally measured via pressure myography of arteries isolated from animal models. However, animal arteries can be difficult to obtain and may have limited relevance to human physiology. It is, therefore, critical to engineer human cell-based arterial models capable of contraction. Vascular smooth muscle cells (SMCs) must be circumferentially aligned around the vessel lumen to contract the vessel, which is challenging to achieve in a soft blood vessel model. In this study, we used gelatin microribbons to circumferentially align SMCs inside a hydrogel channel. To accomplish this, we created tunable gelatin microribbons of varying stiffnesses and thicknesses and assessed how SMCs aligned along them. We then wrapped soft, thick microribbons around a needle and encapsulated them in a gelatin methacryloyl hydrogel, forming a microribbon-lined channel. Finally, we seeded SMCs inside the channel and showed that they adhered best to fibronectin and circumferentially aligned in response to the microribbons. Together, these data show that tunable gelatin microribbons can be used to circumferentially align SMCs inside a channel. This technique can be used to create a human artery-on-a-chip to assess vasodilation via pressure myography, as well as to align other cell types for 3D in vitro models.

Wood Anatomical and Demographic Similarities Between Self-Standing Liana and Tree Seedlings in Tropical Dry Forests of Colombia.

Canopy lianas differ considerably from trees in terms of wood anatomical structure, and they are suggested to have a demographic advantage-faster growth and higher survival-than trees. However, it remains unclear whether these anatomical and demographic differences persist at the seedling stage, when most liana species are self-standing and, consequently, might be ecologically similar to trees. We assessed how self-standing liana and tree seedlings differ in relation to wood anatomy, growth, and survival. We measured 12 wood traits and monitored seedling growth and survival over one year for 10 self-supporting liana and 10 tree seedling species from three tropical dry forests in Colombia. Liana and tree seedlings exhibited similar survival rates and wood anatomies for traits related to water storage and mechanical support. Yet, for traits associated with water transport, liana seedlings showed greater variability in vessel lumen size, while tree seedlings had higher vessel density. Also, the liana relative growth rate was significantly higher than for trees. These results indicate that, while self-supporting liana and tree seedlings are anatomically similar in terms of mechanical support and water storage-likely contributing to their similar survival rates-liana seedlings have a growth advantage, possibly due to more efficient water transport. These findings suggest that the well-documented anatomical and demographic differences between adult lianas and trees may depend on the liana's developmental stage, with more efficient water transport emerging as a key trait from early stages.

Brain-to-blood transport of fluorescein in vitro

Investigating blood-brain barrier (BBB) dysfunction has become a pre-clinical and clinical research focus as it accompanies many neurological disorders. Nevertheless, knowledge of how diagnostic BBB tracers cross the endothelium from blood-to-brain or vice versa often remains incomplete. In particular, brain-to-blood transport (efflux) may reduce tracer extravasation of intravascularly (i.v.) applied tracers. Conversely, impaired efflux could mimic phenotypic extravasation. Both processes would affect conclusions on BBB properties primarily attributed to blood-to-brain leakage. Here, we specifically investigated efflux of fluorescent BBB tracers, focusing on the most common non-toxic marker, sodium fluorescein, which is applicable in patients. We used acute neocortical slices from mice and applied fluorescein, sulforhodamine-B, rhodamine-123, FITC dextran to the artificial cerebrospinal fluid. Anionic low molecular weight (MW) fluorescein and sulforhodamine-B, but not ~ 10-fold larger FITC-dextran and cationic low MW rhodamine-123, showed efflux into the lumen of blood vessels. Our data suggest that fluorescein efflux depends on organic anion transporter polypeptides (Oatp) rather than P-glycoprotein. Furthermore, sodium-potassium ATPase inhibition and incomplete oxygen-glucose deprivation (OGD, 20% O2) reduced fluorescein efflux, while complete OGD (0% O2) abolished efflux. We provide evidence for active efflux of fluorescein in vitro. Impaired efflux of fluorescein could thus contribute to the frequently observed BBB dysfunction in neuropathologies in addition to blood-to-brain leakage.

A Retrospective Observational Study Examining Physical Activity Among Adults in the United States With Angina or Coronary Heart Disease.

Coronary heart disease (CHD) involves inadequate blood supply to the myocardium by the coronary arteries due to the formation of atherosclerotic plaque in the vessel lumen. It has a complex etiopathogenesis. Physical activity (PA) and exercise lead to vascular remodeling and improved endothelial function, which, in turn, improves the arterial blood supply to the myocardium. The study aims to determine the prevalence of self-reported PA among CHD patients in the United States based on demographic, socioeconomic, and healthcare access variables for the year 2021. The data for the study on CHD were extracted using the Behavioral Risk Factor Surveillance System (BRFSS) Web-Enabled Analysis Tool database of the U.S. The control variables used broadly include demographics, socioeconomic, and healthcare access. In 2021, 433,615 people in the USA participated in the BRFSS study. Among them, 22,819 self-identified as having angina or CHD. In the past month, 62.2% of participants with the disease were involved in PA, and 37.8% were not. Among participants without angina or CHD, 76.5% were involved, and 23.5% were not involved in PA in the past month. This study highlights the need for specific interventions to overcome obstacles preventing PA among CHD patients.

Pericyte ablation causes hypoactivity and reactive gliosis in adult mice

Capillary pericytes are important regulators of cerebral blood flow, blood–brain barrier integrity and neuroinflammation, but can become lost or dysfunctional in disease. The consequences of pericyte loss or dysfunction is extremely difficult to discern when it forms one component of a complex disease process. To evaluate this directly, we examined the effect of adult pericyte loss on mouse voluntary movement and motor function, and physiological responses such as hypoxia, blood–brain barrier (BBB) integrity and glial reactivity. Tamoxifen delivery to Pdgfrβ-CreERT2:: Rosa26-DTA transgenic mice was titrated to produce a dose-dependent ablation of pericytes in vivo. 100mg/kg of tamoxifen ablated approximately half of all brain pericytes, while two consecutive daily doses of 300mg/kg tamoxifen ablated >80% of brain pericytes. In the open field test, mice with ∼50% pericyte loss spent more time immobile and travelled half the distance of control mice. Mice with >80% pericyte ablation also slipped more frequently while performing the beam walk task. Our histopathological analyses of the brain revealed that blood vessel density was unchanged, but vessel lumen width was increased. Pericyte-ablated mice also exhibited: mild BBB disruption; increased neuronal hypoxia; astrogliosis and increased IBA1+ immunoreactivity, suggestive of microgliosis and/or macrophage infiltration. Our results highlight the importance of pericytes in the brain, as pericyte loss can directly compromise brain health and induce behavioural alterations in mice.

The possibilities of using adaptive optics in modern ophthalmology

Until recently, the assessment of individual retinal cells was possible only with the help of histological examination, since such retinal imaging methods as scanning laser ophthalmoscopy and optical coherence tomography had low resolution to obtain images of structures at the cellular level, which was mainly due to aberrations caused by the optics of the eye. Adaptive optics technology has improved the performance of optical systems by correcting optical wavefront aberrations. Adaptive optics allows noninvasively visualizing the retina at the microscopic level in vivo, providing the opportunity to analyze individual structures such as photoreceptors, blood vessels, nerve fibers, ganglion cells and a lattice plate. Adaptive optics imaging in patients with diabetic retinopathy makes it possible to accurately determine the spatial distribution of cones, a decrease in which is associated with the presence of diabetic retinopathy and an increase in the severity of the disease. The detection of differences in cone distribution density between the control group and patients with diabetes mellitus without clinical signs of diabetic retinopathy may contribute to its early diagnosis, as well as a deeper understanding of the consequences of changes in the photoreceptor apparatus. Adaptive optics imaging methods are able to identify disorders of photoreceptor cells and assess the degree of progression of age-related macular degeneration, which definitely expands diagnostic capabilities at the early stages of its detection. Assessment of the condition of nerve fiber bundles through the use of Adaptive optics helps to identify changes associated with glaucoma, and also provides the ability to visualize details that cannot be evaluated using optical coherence tomography. Adaptive optics imaging allows you to directly measure the wall of retinal vessels and the diameter of their lumen. The ratio of wall thickness to vessel lumen and the cross-sectional area of the vessel wall directly reflect the remodeling process and can be used for the purpose of early diagnosis and monitoring of hypertension.

CAUSES OF PAIN IN THE MUSCLES OF THE LOWER EXTREMITIES IN CHILDREN WITH CEREBRAL PALSY

A high level of muscle spasticity in children with cerebral palsy is one of the causes of degenerative and dystrophic changes in tissues. Against the background of high spasticity, there is a violation of blood flow in the vessels of the lower extremities, which leads to changes in subfascial pressure and the formation of primary pain syndromes. The analysis of the literature shows the need to study the issues related to the mechanism of formation of changes in the muscles and determine the primary causes of pain. Objective. Тo study the mechanism of changes in the muscles of the lower extremities, as well as the primary causes of pain syndrome. Methods. The analysed indicators were obtained during the treatment of 40 patients with cerebral palsy, who were divided into 3 groups depending on the muscle tone disorder. Clinical and instrumental methods were used to examine patients. The data obtained were statistically processed with the determination of M ± m, the coefficient of reliability according to Student’s criteria. Results. According to the results of the study, high spasticity leads to impaired blood flow and increased subfascial pressure in the musculofascial sheaths. There is an inverse correlation between the increase in subfascial pressure, the diameter of the vessel lumen and blood flow velocity. This is one of the causes of degenerative and denervation changes in muscles and fascia. It was proved that the occurrence of primary pain in the lower extremities is caused by various etiological causes: tissue ischemia; increased subfascial pressure; narrowing of pathologically significant anatomical areas in which nerves lie; degenerative and dystrophic changes in the joints. Conclusions. The study found that the cause of changes in the muscles and fascia is a violation of blood flow, a change in subfascial pressure in the musculofascial cases of the lower extremities. The occurrence of pain in the lower extremities in children with cerebral palsy is multifactorial in nature and consists of myofascial, articular, and tunnel syndromes.