A Survey of Air-to-Ground Propagation Channel Modeling for Unmanned Aerial Vehicles

In recent years, there has been a dramatic increase in the use of unmanned aerial vehicles (UAVs), particularly for small UAVs, due to their affordable prices, ease of availability, and ease of operability. Existing and future applications of UAVs include remote surveillance and monitoring, relief operations, package delivery, and communication backhaul infrastructure. Additionally, UAVs are envisioned as an important component of 5G wireless technology and beyond. The unique application scenarios for UAVs necessitate accurate air-to-ground (AG) propagation channel models for designing and evaluating UAV communication links for control/non-payload as well as payload data transmissions. These AG propagation models have not been investigated in detail when compared to terrestrial propagation models. In this paper, a comprehensive survey is provided on available AG channel measurement campaigns, large and small scale fading channel models, their limitations, and future research directions for UAV communication scenarios

Deficiency of Vasodilator-Stimulated Phosphoprotein (VASP) Increases Blood-Brain-Barrier Damage and Edema Formation after Ischemic Stroke in Mice

Background: Stroke-induced brain edema formation is a frequent cause of secondary infarct growth and deterioration of neurological function. The molecular mechanisms underlying edema formation after stroke are largely unknown. Vasodilator-stimulated phosphoprotein (VASP) is an important regulator of actin dynamics and stabilizes endothelial barriers through interaction with cell-cell contacts and focal adhesion sites. Hypoxia has been shown to foster vascular leakage by downregulation of VASP in vitro but the significance of VASP for regulating vascular permeability in the hypoxic brain in vivo awaits clarification. Methodology/Principal Findings: Focal cerebral ischemia was induced in Vasp2/2 mice and wild-type (WT) littermates by transient middle cerebral artery occlusion (tMCAO). Evan’s Blue tracer was applied to visualize the extent of blood-brainbarrier (BBB) damage. Brain edema formation and infarct volumes were calculated from 2,3,5-triphenyltetrazolium chloride (TTC)-stained brain slices. Both mouse groups were carefully controlled for anatomical and physiological parameters relevant for edema formation and stroke outcome. BBB damage (p,0.05) and edema volumes (1.7 mm360.5 mm3 versus 0.8 mm360.4 mm3; p,0.0001) were significantly enhanced in Vasp2/2 mice compared to controls on day 1 after tMCAO. This was accompanied by a significant increase in infarct size (56.1 mm3617.3 mm3 versus 39.3 mm3610.7 mm3, respectively; p,0.01) and a non significant trend (p.0.05) towards worse neurological outcomes. Conclusion: Our study identifies VASP as critical regulator of BBB maintenance during acute ischemic stroke. Therapeutic modulation of VASP or VASP-dependent signalling pathways could become a novel strategy to combat excessive edema formation in ischemic brain damage

CNS targets of adipokines

This is the author accepted manuscript. The final version is available from American Physiological Society via the DOI in this record.Our understanding of adipose tissue as an endocrine organ has been transformed over the last twenty years. During this time a number of adipocyte-derived factors or adipokines have been identified. This paper will review evidence for how adipokines acting via the central nervous system (CNS) regulate normal physiology and disease pathology. The reported CNS-mediated effects of adipokines are varied and include the regulation of energy homeostasis, autonomic nervous system activity, the reproductive axis, neurodevelopment, cardiovascular function, and cognition. Due to the wealth of information available and the diversity of their known functions, the archetypal adipokines leptin and adiponectin will be the focused on extensively. Other adipokines with established CNS actions will also be discussed. Due to the difficulties associated with studying CNS function on a molecular level in humans, the majority of our knowledge, and as such the studies described in this paper, comes from work in experimental animal models; however, where possible the relevant data from human studies are also highlighted

Effects of short-term denervation and subsequent reinnervation on motor endplates and the soleus muscle in the rat

The rat sciatic nerve was locally frozen, and changes in the nerve, motor endplates, and the soleus muscle were examined for up to 6 weeks by light and electron microscopy. The wet weights of denervated soleus muscles compared with contralateral values progressively declined to a minimum at 2 weeks after injury (60.7±2.5%) and began to reverse following 3 weeks. The sciatic nerve thoroughly degenerated after freezing. However, numerous regenerated myelinated and thin nerve fibers were observed at 3 weeks. They were considerably enlarged but still smaller than normal counterparts at 6 weeks postoperatively. Nerve terminals containing synaptic vesicles of endplates disappeared at day 1 and mostly reappeared at 3 weeks (about 700f the endplates). All endplates examined were reinnervated at 4, 5, and 6 weeks. On the other hand, postsynaptic folds of muscle fibers seemed to be only slightly influenced by denervation or reinnervation. Ultrastructural alterations of myofibrils, in particular the loss of register, immediately appeared after denervation, spread progressively, peaked at 2 weeks, ameliorated following reinnervation, and became significantly normalized at 6 weeks after freezing. The proportion of type II fibers in the soleus muscle similary showed an increase and a decrease with a short delay in response to denervation and reinnervation, respectively. This study clearly demonstrated that the nerve supply affects the ultrastructural integrity of skeletal muscles. In addition, changes in the endplates and the soleus muscle evaluated in this study after short-term denervation are largely reversible following reinnervation

Injury and repair of the soleus muscle after electrical stimulation of the sciatic nerve in the rat

To study injury and subsequent changes in skeletal muscles, the rat sciatic nerve was electrically stimulated at 50 Hz and muscle contraction was induced for 30 min. Muscle damage was classified into five types (hypercontraction, hyperstretching, Z band disorders, misalignment of myofilament and regions of scarce myofilaments) by electron microscopy and quantified by ultrastructural assessment. After electrical nerve stimulation, the percentages of the injured areas of the soleus muscle were 18.8 ± 15.8% (mean ± SD) at O h, 9.7 ± 1.0 0x1.3f1c4p-890t 6 h, 22.0 ± 23.6 0x0p+0t 12 h, 13.1 ± 3.2 0x0p+0t 24 h, 4.9 ± 6.0 0x0p+0t 3 days and 0.5 ± 0.4 0x0p+0t 7 days. At 0 h, the vast majority of ultrastructural alterations were sarcomere hypercontraction. At 6 h, hypercontraction was not recognizable and sarcomere hyperstretching and Z band disarrangement constituted the major findings. At 12 h, when the injury reaehed its maximum, myofilament disorganization and hyperstretching were predominant. At 24 h or afterwards, the injury began to decrease and recovered to almost normal conditions by 7 days. There were very few necrotic muscle fibers in all specimens. It is considered that the muscle lesions in the present study were reversible, and recovered through changes in various types of sarcomere alterations. Z band streaming and free ribosomes were frequently found at 12 and 24 h, which may indicate repair processes rather than newly formed lesions

Comparison of the sarcomere alterations after muscle contraction and tension loading in the rat soleus muscle.

Muscle contraction induced by 30 min of continuous nerve stimulation at 50 Hz resulted in sarcomere changes of the soleus muscle in the rat in our previous study. To further investigate the cause of sarcomere alterations, the sciatic nerve was electrically stimulated intermittently for 30 min. Nerve stimulation was also conducted after cutting the tendons of the soleus, gastrocnemius and plantaris muscles in order to prevent imposing tension on these muscles as a result to their own contractions. In addition, the muscles were pulled by weights via their tendons to load high tension for 30 min without nerve stimulation. Sarcomere alterations immediately after treatments were quantified by electron microscopy. The percentages of aberrant sarcomere areas of the soleus muscle were 25.7 ± 16.4% (mean ± SD) in the group of intermittent nerve stimulation with intact tendons and 21.1 ± 35.4% in the group of tenotomy and continuous nerve stimulation, which were roughly equal to or more severe than the group of continuous nerve stimulation with intact tendons (18.8 ± 15.8%) in our previous study. Sarcomere alterations consisted mainly of hypercontraction in these groups. Almost all sarcomere changes in the tension-loaded (pulled) soleus muscles were scarce myofilaments (1.7 ± 1.0% by 600 g; 4.5 ± 2.9% by 1200 g), and hypercontraction was not observed. These findings indicate that neither high tension nor a decrease of muscle blood flow during continuous contraction seems to be the primary cause of sarcomere alterations in the present study. There are probably other causes that produce aberrant sarcomeres