Vessel Plugs Research Articles

Reduced cleavage of von willebrand factor by ADAMTS13 is associated with microangiopathic acute kidney injury following trauma.

Acute kidney injury (AKI) is common after trauma, but contributory factors are incompletely understood. Increases in plasma von Willebrand Factor (vWF) with concurrent decreases in ADAMTS13 are associated with renal microvascular thrombosis in other disease states, but similar findings have not been shown in trauma. We hypothesized that molecular changes in circulating vWF and ADAMTS13 promote AKI following traumatic injury. VWF antigen, vWF multimer composition and ADAMTS13 levels were compared in plasma samples from 16 trauma patients with and without trauma-induced AKI, obtained from the Prehospital Air Medical Plasma (PAMPer) biorepository. Renal histopathology and function, vWF and ADAMTS13 levels were assessed in parallel in a murine model of polytrauma and haemorrhage. VWF antigen was higher in trauma patients when compared with healthy controls [314% (253–349) vs. 100% (87–117)] [median (IQR)], while ADAMTS13 activity was lower [36.0% (30.1–44.7) vs. 100.0% (83.1–121.0)]. Patients who developed AKI showed significantly higher levels of high molecular weight multimeric vWF at 72-h when compared with non-AKI counterparts [32.9% (30.4–35.3) vs. 27.8% (24.6–30.8)]. Murine plasma cystatin C and vWF were elevated postpolytrauma model in mice, with associated decreases in ADAMTS13, and immunohistologic analysis demonstrated renal injury with small vessel plugs positive for fibrinogen and vWF. Following traumatic injury, the vWF-ADAMTS13 axis shifted towards a prothrombotic state in both trauma patients and a murine model. We further demonstrated that vWF-containing, microangiopathic deposits were concurrently produced as the prothrombotic changes were sustained during the days following trauma, potentially contributing to AKI development.

Safety of transradial access compared to transfemoral access with hemostatic devices (vessel plugs and suture devices) after percutaneous coronary interventions: A systematic review and meta-analysis.

Comparing the safety of transradial access (TRA) and conventional hemostasis with transfemoral access (TFA) and vascular closure devices (vessel plugs and suture devices) in patients undergoing percutaneous coronary interventions. TRA for PCIs is associated with fewer bleeding and vascular complications compared with TFA. Vascular closure devices (VCD) are often used post TFA to establish early hemostasis and mitigate bleeding risk. However, the comparative efficacy of TRA and TFA with VCDs remains controversial. Electronic database were systematically searched for all pertinent studies from inception through January 2020. Randomized studies, registry data, and abstracts published in peer-reviewed indexed journals were included. The short-term outcomes: major bleeding, vascular complications, and closure device failure were evaluated. Random-effects model was used to pool individual study results. Twelve studies (8 observational, 4 randomized) including 7,961 patients (TRA: 3,121 patients, TFA and vessel plugs: 3,157 patients, TFA & suture devices: 1,683 patients) were included in the analysis. Major bleeding was significantly lower with TRA compared with TFA and vessel plugs (odds ratio [OR] 0.22, 95%CI 0.11-0.44, p < .00001) and TFA & suture devices (OR 0.12, 95%CI 0.05-0.28, p < .00001). Vascular complications were significantly lower with TRA compared to TFA and vessel plugs (OR 0.25, 95%CI 0.13-0.49, p < .0001) and TFA & suture devices (OR 0.13, 95%CI 0.04-0.41, p = 0.0005). Rates of closure device failure were lower for TRA compared to TFA & suture devices (OR 0.13, 95%CI 0.04-0.41, p = .0005), but similar to TFA & vessel plugs (OR 0.23, 95%CI 0.01-4.28, p = .33), although confidence intervals were wide. All analysis revealed a low to moderate level of heterogeneity. TRA with conventional hemostasis is safer than TFA with hemostasis via vessel plugs or suture devices and should be considered best practice.

First Extensive Microscopic Study of Butternut Defense Mechanisms Following Inoculation with the Canker Pathogen Ophiognomonia clavigignenti-juglandacearum Reveals Compartmentalization of Tissue Damage.

Ophiognomonia clavigignenti-juglandacearum endangers the survival of butternut (Juglans cinerea) throughout its native range. While screening for disease resistance, we found that artificial inoculations of 48 butternut seedlings with O. clavigignenti-juglandacearum induced the expression of external symptoms, but only after a period of dormancy. Before dormancy, compartmentalized tissues such as necrophylactic periderms (NPs) and xylem reaction zones (RZs) contributed to limiting pathogen invasion. Phenols were regularly detected in RZs, often in continuity with NPs during wound closure, and confocal microscopy revealed their presence in parenchyma cells, vessel plugs and cell walls. Vessels were blocked with tyloses and gels, particularly those present in RZs. Suberin was also detected in cells formed over the affected xylem by the callus at the inoculation point, in a few tylosis walls, and in longitudinal tubes that formed near NPs. Following dormancy, in all inoculated seedlings but one, defensive barriers were breached by O. clavigignenti-juglandacearum and then additional ones were produced in response to this new invasion. The results of this histopathological study indicate that trees inoculated in selection programs to test butternut canker resistance should go through at least one period of dormancy and that asymptomatic individuals should be dissected to better assess how they defend themselves against O. clavigignenti-juglandacearum.

TCT-849 Safety of Transradial Access compared to Transfemoral Access with Hemostatic Devices (Vessel Plugs, Suture Devices & Vascular Clips) after Percutaneous Coronary Interventions: A systematic review and meta analysis

Transradial access (TRA) is associated with fewer bleeding and vascular complications compared to transfemoral access (TFA). The use of vascular closure devices (VCD) to establish early hemostasis after TFA mitigates bleeding risk. However, data comparing TRA and TFA with VCD is limited. We aimed to

WHAT ARBORISTS HAVE TO KNOW ABOUT VESSEL PLUGS

Summary When the xylem of a broadleaved tree is injured, the tree produces vessel plugs (tyloses or gum) to isolate sound xylem from the outside world. Trees with durable heartwood and trees with macroporous vessels partly do this in advance, in bright heartwood no vessel plugs will be formed. This, and the dependence of vessel plug formation on xylem water content, energy resources and temperature, has consequences for tree care operations.

The Role of Intervessel Pits and Vessel Plugs in Determining Flow Pathways Through and Between Vessels in Sycamore (Acer pseudoplatanusL.)

It has previously been suggested from physical evidence that vessels in twigs of sycamore (Acer pseudoplatanus L.) are connected by small pores in intervessel pit membranes. From results obtained using a combination of physical techniques and electron microscopy it is clear that this is an oversimplification: almost all intervessel pit membranes are absent in sycamore twig and stem wood, yet physical tests still suggest that vessels are connected by pores smaller than pit apertures. Where these pores are is less certain. They may be in plugs observed to fill vessel lumens. They may possibly be in a small number of intact intervessel pit membranes in the terminal elements of vessels, but such membranes could not be found under the microscope. In either case, the results of physical tests suggest that vessels connected by membraneless intervessel pits must effectively end together at a particular point in the tree.

A study of progressive stages of discoloration and decay in Malus using scanning electron microscopy

Scanning electron microscopy has elucidated the roles of microorganisms during various stages of discoloration and decay in living apple trees Malussylvestris Mill. Disks were removed sequentially at 30-cm intervals up the tree from the bases of decayed trunks into clear sapwood from ten 20- to 30-year-old (Red Delicious) apple trees variously affected by internal decay. Evidence for a microbial succession and morphological changes in cell constituents was observed. Bacteria, yeasts, and other nonhymenomycetes (e.g., Cytospora spp.) appeared to be primary colonists of discolored tissues, which altered cell wall components, and degraded wound-initiated vessel plugs. Basidiomycetous hyphae were observed only in tissues where amorphous vessel deposits had been degraded by pioneer microorganisms. Associations of secondary bacteria and yeasts with wood-destroying hymenomycetes, indicating a mutualistic existence, were frequent. Decay was of the white rot type with numerous crystalline structures observed in regions of advanced decay.

Ultrastructure of wilt syndrome caused by Verticillium dahliae. V. Attempted localization of phenolic compounds in the vascular region

Ferric chloride has been used in an attempt to detect phenolic compounds at the ultrastructure level in the petioles of chrysanthemums and sunflowers infected with Verticillium dahliae. The fungus contains two types of cytoplasmic structures which stain very densely with ferric chloride; one is similar to a multivesicular body, the other solid and apparently spherical. In treated chrysanthemums, the ferric ion accumulates mainly in vessel plugs, in laminar arrays or localized diffuse deposits in the secondary walls of vessels, in vasicentric parenchyma cells, and the protective layer of parenchyma cells immediately adjacent to the vessels. In treated sunflowers the ferric ion accumulates mainly in vessel plugs, in the pectinaceous layers of the cell wall (i.e. middle lamella and primary cell walls), and in the vasicentric parenchyma cells. Differences in the pattern of phenolic deposition in the two hosts could account wholly or in part for differences in symptom expression.

Ultrastructure of wilt syndrome caused by Verticillium dahliae. III. Chronological symptom development in sunflower leaves

When sunflowers are infected by the vascular pathogen Verticillium dahliae, the first visible foliar symptom is the appearance of tiny chlorotic flecks. An attempt was made to determine the temporal order in which early ultrastructural changes leading to symptom expression occur. The evidence indicates that ultrastructural changes occur in the following order: (1) degradation of xylem vessel walls, (2) initiation of the necrotic band, (3) degeneration of the mesophyll tissue remote from the vein, and (4) degeneration of the phloem. The possible importance of xylem vessel plugs and of phenolic compounds to the initiation of symptom development is also discussed.

Ageing characteristics of wood of healthy and sandhill-declined Citrus sinensis

Cytological studies of starch, lipid, nuclei, dehydrogenases, and diaphorase activity in parenchyma of healthy and sandhill-declined trunk wood of Citrus sinensis 'Valencia' indicated that wood aged rapidly after a high metabolic activity near the cambium. Ethylene evolution and oxygen uptake were high in wood next to the cambium; ethylene was low in older wood and gas evolution was typical of older wood. Diseased wood contained less starch but more lipid than healthy wood. Lipid vessel plugs, caused by lipid leakage into vessels, and moisture content increased in wood as it aged. Characteristics of parenchyma cell ageing and wood color place it in the revised category of woods with a delayed, uncolored heartwood.

HISTOCHEMICAL STUDIES ON THE ALTERATION OF LIGNIN AND PECTIC SUBSTANCES IN WHITE ELM INFECTED BY CERATOCYSTIS ULMI

Histochemical tests were performed on sections from 3- and 4-year-old seedlings of white elm (Ulmus americana) artificially inoculated with Ceratocystis ulmi in studies on alteration of lignin and of pectic substances following infection. Results showed more intense reactions to tests for lignin and pectins in sections from diseased elms than in sections from healthy elms. Lignin and pectin positive materials were found in vessel plugs. It is suggested that these alterations of lignin and pectins result from the action on cell walls of pectolytic enzymes produced by the pathogen.