The vascular morphology and in vivo muscle temperatures of thresher sharks (Alopiidae)

2011 ◽  
Vol 272 (11) ◽  
pp. 1353-1364 ◽  
Author(s):  
James C. Patterson ◽  
Chugey A. Sepulveda ◽  
Diego Bernal
2021 ◽  
Vol 23 (Supplement_6) ◽  
pp. vi230-vi230
Author(s):  
Sadaf Soloukey ◽  
Luuk Verhoef ◽  
Frits Mastik ◽  
Bastian Generowicz ◽  
Eelke Bos ◽  
...  

Abstract BACKGROUND Neurosurgical practice still relies heavily on pre-operatively acquired images to guide tumor resections, a practice which comes with inherent pitfalls such as registration inaccuracy due to brain shift, and lack of real-time functional or morphological feedback. Here we describe functional Ultrasound (fUS) as a new high-resolution, depth-resolved, MRI/CT-registered imaging technique able to detect functional regions and vascular morphology during awake and anesthesized tumor resections. MATERIALS AND METHODS fUS relies on high-frame-rate (HFR) ultrasound, making the technique sensitive to very small motions caused by vascular dynamics (µDoppler) and allowing measurements of changes in cerebral blood volume (CBV) with micrometer-millisecond precision. This opens up the possibility to 1) detect functional response, as CBV-changes reflect changes in metabolism of activated neurons through neurovascular coupling, and 2) visualize in-vivo vascular morphology of pathological and healthy tissue with high resolution at unprecedented depths. During a range of anesthetized and awake neurosurgical procedures we acquired vascular and functional images of brain and spinal cord using conventional ultrasound probes connected to a research acquisition system. Building on Brainlab’s Intra-Operative Navigation modules, we co-registered our intra-operative Power Doppler Images (PDIs) to patient-registered MRI/CT-data in real-time. RESULTS During meningioma and glioma resections, our co-registered PDIs revealed fUS’ ability to visualize the tumor’s feeding vessels and vascular borders in real-time, with a level of detail unprecedented by conventional MRI-sequences. During awake resections, fUS was able to detect distinct, ESM-confirmed functional areas as activated during conventional motor and language tasks. In all cases, images were acquired with micrometer-millisecond (300 µm, 1.5–2.0 ms) precision at imaging depths exceeding 5 cm. CONCLUSION fUS is a new real-time, high-resolution and depth-resolved imaging technique, combining favorable imaging specifications with characteristics such as mobility and ease of use which are uniquely beneficial for a potential image-guided neurosurgical tool.


2018 ◽  
Vol 27 (11) ◽  
pp. 1280-1286 ◽  
Author(s):  
Nathalie De Carvalho ◽  
Julia Welzel ◽  
Sandra Schuh ◽  
Lotte Themstrup ◽  
Martina Ulrich ◽  
...  

2011 ◽  
Vol 40 (1) ◽  
pp. 18-32 ◽  
Author(s):  
Per Lindblom ◽  
Anna-Lena Berg ◽  
Hui Zhang ◽  
Rolf Westerberg ◽  
Jonathan Tugwood ◽  
...  

Tesaglitazar was developed as a dual peroxisome proliferator–activated receptor (PPARα/γ). To support the clinical program, a hamster carcinogenicity study was performed. The only neoplastic findings possibly related to treatment with tesaglitazar were low incidences of hemangioma and hemangiosarcoma in the liver of male animals. A high-power, two-year investigative study with interim necropsies was performed to further elucidate these findings. Treatment with tesaglitazar resulted in changes typical for exaggerated PPARα pharmacology in rodents, such as hepatocellular hypertrophy and hepatocellular carcinoma, but not an increased frequency of hemangiosarcomas. At the highest dose level, there was an increased incidence of sinusoidal dilatation and hemangiomas. No increased endothelial cell (EC) proliferation was detected in vivo, which was confirmed by in vitro administration to ECs. Immunohistochemistry and gene expression analyses indicated increased cellular stress and vascular endothelial growth factor (VEGF) expression in the liver, which may have contributed to the sinusoidal dilatation. A two-fold increase in the level of circulating VEGF was detected in the hamster at all dose levels, whereas no effect on VEGF was observed in patients treated with tesaglitazar. In conclusion, investigations have demonstrated that tesaglitazar does not produce hemangiosarcomas in hamster despite a slight effect on vascular morphology in the liver.


2007 ◽  
Vol 292 (1) ◽  
pp. R440-R446 ◽  
Author(s):  
John N. Lorenz ◽  
Lois J. Arend ◽  
Rachel Robitz ◽  
Richard J. Paul ◽  
A. John MacLennan

There is growing evidence that sphingosine 1-phosphate (S1P) plays an important role in regulating the development, morphology, and function of the cardiovascular system. There is little data, however, regarding the relative contribution of endogenous S1P and its cognate receptors (referred to as S1P1–5) to cardiovascular homeostasis. We used S1P2 receptor knockout mice (S1P2−/−) to evaluate the role of S1P2 in heart and vascular function. There were no significant differences in blood pressure between wild-type and S1P2−/− mice, measured in awake mice. Cardiac function, evaluated in situ by using a Millar catheter, was also not different in S1P2−/− mice under baseline or stimulated conditions. In vivo analysis of vascular function by flowmetry revealed decreases in mesenteric and renal resistance in S1P2−/− mice, especially during vasoconstriction with phenylephrine. In intact aortic rings, the concentration-force relations for both KCl and phenylephrine were right shifted in S1P2−/− mice, whereas the maximal isometric forces were not different. By contrast, in deendothelialized rings the concentration-force relations were not different but the maximal force was significantly greater in S1P2−/− aorta. Histologically, there were no apparent differences in vascular morphology. These data suggest that the S1P2 receptor plays an important role in the function of the vasculature and is an important mediator of normal hemodynamics. This is mediated, at least in part, through an effect on the endothelium, but direct effects on vascular smooth muscle cannot be ruled out and require further investigation.


2017 ◽  
Vol 372 (1720) ◽  
pp. 20150522 ◽  
Author(s):  
Katie Bentley ◽  
Shilpa Chakravartula

The process of new blood vessel growth (angiogenesis) is highly dynamic, involving complex coordination of multiple cell types. Though the process must carefully unfold over time to generate functional, well-adapted branching networks, we seldom hear about the time-based properties of angiogenesis, despite timing being central to other areas of biology. Here, we present a novel, time-based formulation of endothelial cell behaviour during angiogenesis and discuss a flurry of our recent, integrated in silico/in vivo studies, put in context to the wider literature, which demonstrate that tissue conditions can locally adapt the timing of collective cell behaviours/decisions to grow different vascular network architectures. A growing array of seemingly unrelated ‘temporal regulators’ have recently been uncovered, including tissue derived factors (e.g. semaphorins or the high levels of VEGF found in cancer) and cellular processes (e.g. asymmetric cell division or filopodia extension) that act to alter the speed of cellular decisions to migrate. We will argue that ‘temporal adaptation’ provides a novel account of organ/disease-specific vascular morphology and reveals ‘timing’ as a new target for therapeutics. We therefore propose and explain a conceptual shift towards a ‘temporal adaptation’ perspective in vascular biology, and indeed other areas of biology where timing remains elusive. This article is part of the themed issue ‘Systems morphodynamics: understanding the development of tissue hardware’.


2019 ◽  
Vol 5 (2) ◽  
pp. 22 ◽  
Author(s):  
Enrico Mazzuca ◽  
Andrea Aliverti ◽  
Giuseppe Miserocchi

The balance of lung extravascular water depends upon the control of blood flow in the alveolar distribution vessels that feed downstream two districts placed in parallel, the corner vessels and the alveolar septal network. The occurrence of an edemagenic condition appears critical as an increase in extravascular water endangers the thinness of the air–blood barrier, thus negatively affecting the diffusive capacity of the lung. We exposed anesthetized rabbits to an edemagenic factor (12% hypoxia) for 120 min and followed by in vivo imaging the micro-vascular morphology through a “pleural window” using a stereo microscope at a magnification of 15× (resolution of 7.2 μm). We measured the change in diameter of distribution vessels (50–200 μm) and corner vessels (<50 μm). On average, hypoxia caused a significant decrease in diameter of both smaller distribution vessels (about ~50%) and corner vessels (about ~25%) at 30 min. After 120 min, reperfusion occurred. Regional differences in perivascular interstitial volume were observed and could be correlated with differences in blood flow control. To understand such difference, we modelled imaged alveolar capillary units, obtained by Voronoi method, integrating microvascular pressure parameters with capillary filtration. Results of the analysis suggested that at 120 min, alveolar blood flow was diverted to the corner vessels in larger alveoli, which were found also to undergo a greater filtration indicating greater proneness to develop lung edema.


2001 ◽  
Vol 45 (2) ◽  
pp. 311-322 ◽  
Author(s):  
Alejandro F. Frangi ◽  
Wiro J. Niessen ◽  
Paul J. Nederkoorn ◽  
Jeannette Bakker ◽  
Willem P.Th.M. Mali ◽  
...  

Biomedicines ◽  
2021 ◽  
Vol 9 (10) ◽  
pp. 1430
Author(s):  
Océane Campion ◽  
Jessica Thevenard Devy ◽  
Clotilde Billottet ◽  
Christophe Schneider ◽  
Nicolas Etique ◽  
...  

Background: LRP-1 is a multifunctional scavenger receptor belonging to the LDLR family. Due to its capacity to control pericellular levels of various growth factors and proteases, LRP-1 plays a crucial role in membrane proteome dynamics, which appears decisive for tumor progression. Methods: LRP-1 involvement in a TNBC model was assessed using an RNA interference strategy in MDA-MB-231 cells. In vivo, tumorigenic and angiogenic effects of LRP-1-repressed cells were evaluated using an orthotopic xenograft model and two angiogenic assays (Matrigel® plugs, CAM). DCE-MRI, FMT, and IHC were used to complete a tumor longitudinal follow-up and obtain morphological and functional vascular information. In vitro, HUVECs’ angiogenic potential was evaluated using a tumor secretome, subjected to a proteomic analysis to highlight LRP-1-dependant signaling pathways. Results: LRP-1 repression in MDA-MB-231 tumors led to a 60% growth delay because of, inter alia, morphological and functional vascular differences, confirmed by angiogenic models. In vitro, the LRP-1-repressed cells secretome restrained HUVECs’ angiogenic capabilities. A proteomics analysis revealed that LRP-1 supports tumor growth and angiogenesis by regulating TGF-β signaling and plasminogen/plasmin system. Conclusions: LRP-1, by its wide spectrum of interactions, emerges as an important matricellular player in the control of cancer-signaling events such as angiogenesis, by supporting tumor vascular morphology and functionality.


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