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Although traumatic brain injury (TBI) occurs in a very short time, the biological consequence of a TBI, such as Alzheimer's disease, may last a lifetime. To date, effective interventions are not available to improve recovery from a TBI. Herein we aimed to ascertain whether recovery of neurosurgical high-frequency irreversible electroporation (HFIRE) injury in brain tissues can be accelerated by 7,8-dihydroxyflavone (7,8-DHF). The HFIRE injury was induced in the right parietal cortex of 8 adult healthy and neurologically intact male dogs. Two weeks before HFIRE injury, each dog was administered orally with or without 7,8-DHF (30 mg/kg) once daily for consecutive 2 weeks (n = 4 for each group). The values of blood-brain barrier (BBB) disruption, brain edema, and cerebral infarction volumes were measured. The concentrations of beta-amyloid, interleukin-1β, interleukin-6 and tumor necrosis factor-α in the cerebrospinal fluid were measured biochemically. The BBB disruption, brain edema, infarction volumes, and maximal cross-section area caused by HFIRE injury in canine brain were significantly attenuated by 7,8-DHF therapy (P < 0.0001). Additionally, 7,8-DHF significantly reduced the HFIRE-induced cerebral overproduction of beta-amyloid and proinflammatory cytokines in the cerebrospinal fluid (P < 0.0001) in dogs with HFIRE. Recovery of neurosurgical HFIRE injury in canine brain tissues can be accelerated by 7,8-DHT via ameliorating BBB disruption as well as cerebral overproduction of both beta-amyloid and proinflammatory cytokines. [ABSTRACT FROM AUTHOR]

Heat stroke is characterized by hyperthermia, systemic inflammation, and multiple organ failure including arterial hypotension. This definition can be fulfilled by a rat model of heat stroke used in the present study. Anesthetized animals were exposed to heat exposure (43 °C for 70 min) and then returned to room temperature (26 °C) for recovery. One hour before heat exposure, an intraperitoneal dose of quercetin (30 mg/kg) or vehicle (normal saline 1 ml/kg) was administered to the experimental groups of rats. Additional injection was administered immediately after the onset of heat stroke. Immediately after the onset of heat stroke. Vehicle-treated rats displayed (i) hyperthermia; (ii) suppressed left ventricular function; (iii) decreased contents of cardiac total antioxiant capacity (e.g., superoxide dismutase, glutathione peroxidase, catalase); (iv) increased contents of cardiac oxidative capacity malondialdehyde and thiobarbituric acid reactive substances; (v) increased cardiac levels of pro-inflammatory cytokines tumor necrosis factor-α and interleukin-6; and (vi) decreased cardiac levels of an anti-inflammatory cytokine interleukin 10. Histopathologic and survival observation provided supportive evidence for biochemical analyses. These heat stroke reactions all can be significantly attenuated by quercetin therapy. Our data suggest that quercetin therapy might improve outcomes of heat stroke in rats by attenuating excessive hyperthermia as well as myocardial injury. The protective effects of quercetin could be attributed to anti-lipid peroxidative, anti-oxidant, and anti-inflammatory properties. [ABSTRACT FROM AUTHOR]

Abstract: The quality of ultrasonic images is usually influenced by speckle noises and the temporal decorrelation of the speckle patterns. Most traditional motion estimation algorithms are not suitable for speckle tracking in medical ultrasonic images which usually have a low signal-to-noise ratio (SNR). This paper proposes a new motion estimation algorithm that is designed for assessing the dense velocity fields of soft tissue motion in a sequence of ultrasonic B-mode images. We design a hierarchical maximum a posteriori estimator together with an adaptive feature weighted mechanism to estimate the motion field from an ultrasonic image sequence. The proposed method was compared with several existing motion estimation methods via a series of experiments with synthetic speckle image sequences. Performance was also tested on in vivo ultrasonic images. The experimental results show that motion can be assessed with better accuracy than other methods for synthetic speckle images and a good correspondence with clinicians’ observations has also been achieved for clinical ultrasonic images. [Copyright &y& Elsevier]

• Heat stress induces hyperthermia, hypotension, cardiac injury and lethality. • Myricetin preconditioning significantly attenuates these heat stroke reactions. • The beneficial effects of myricetin are significantly abolished by heat shock protein 72 antiody. Heat stroke-induced mortality is rising across the globe. So, the design of prophylactic and/or therapeutic modalities for heat stroke is pressing need. The common plant derived flavonoid exhibits strong anti-oxidant and anti-inflammatory activities; however, its effects in heat stroke remain unknown. The study aimed to investigate the cardioprotective effects of myricetin on heat stroke induced acute myocardial injury as well as lethality in rats and to explore the underlying mechanisms. Myocardial injury was induced by subjecting the anesthetized rats to a high ambient temperature of 43 °C for 70 min. An intragastrical dose of myricetin (5−25 mg/kg body weight) was given to rats once per day for one week prior to the start of heat stress. Heat shock protein 72 antibodies was given intraperitoneally to rats 24 h before the start of heat stress. Myocardial injury severity was estimated by determing myocardial damage scores, myocardial injury indicators, myocardial oxidative and inflammatory factors. Western blot analysis was used for cardiac expression of heat shock protein (HSP)72. Significant (P < 0.05) up-regulation of HSP-72 after chronic administration of myricetin coincided with significant (P < 0.05) reduction in hyperthermia, hypotension, cardiac inflammatory and oxidative damage and lethality. Inhibition of HSP-72 showed a significant (P < 0.05) reversal in the cardiaprotection as well as survival. Our results indicate that myricetin diminishes myocardial injury as well as lethality in heat stroke by up-regulating HSP-72 and show promise as a novel prevention therapeutic for heat stroke. [ABSTRACT FROM AUTHOR]

A self-assembled mesoporous silica sphere templating process was developed to create hierarchical continuous porous coral reef like N-doped carbon nanostructures on stainless steel meshes as bifunctional electrodes for ultrahigh performance lithium ion based energy storage devices. The lithium ion capacitors (LICs) assembled from using the electrode as both the cathode and anode, exhibited a high energy density of 145 Wh kg−1 at a power density of 1.4 kW kg−1 and maintained an energy density of 58 Wh kg−1 under an ultrahigh power density of 27.3 kW kg−1, outperforming most of the state-of-the-art LICs. • Hierarchical porous N-doped carbon nanostructure on stainless steel mesh as anode. • Bifunctional electrodes for ultrahigh performance lithium ion batteries/capacitors. • Li ion capacitors deliver 145 Wh kg−1 at 1.4 kW kg−1 and 58 Wh kg−1 at 27.3 kW kg−1. • Excellent cycling stability with 85% capacity retention after 5000 cycle operations. A self-assembled mesoporous silica sphere templating process was developed to create hierarchical continuous porous coral reef like N-doped carbon nanostructures on stainless steel meshes as bifunctional electrodes for ultrahigh performance lithium ion based energy storage devices. The coral reef like carbon nanostructure achieved a high specific surface area of 1229 m2 g−1 and a large specific pore volume of 2.21 cm3 g−1, without application of chemical activations. The electrode, when serving as an anode for lithium ion batteries (LIB) or lithium ion capacitors (LIC), delivered an ultrahigh specific capacity of 2058 mAh g−1 at 0.2 A g−1. If used as a cathode for LICs, it generated a high specific capacity of 125 mAh g−1 at 0.1 A g−1. The LICs assembled from using the electrode as both the cathode and anode, exhibited a high energy density of 145 Wh kg−1 at a power density of 1.4 kW kg−1 and maintained an energy density of 58 Wh kg−1 under an ultrahigh power density of 27.3 kW kg−1, among the top tie of the state-of-the-art LICs. The cycling stability of the LIC was outstanding with a 85% capacity retention after 5000 cycle operations at 5 A g−1. The hierarchical continuous porous coral reef like N-doped carbonaceous nanostructure provides micropores as micro-reservoirs of Li ions for local and fast Li ion intercalation/de-intercalation, edge N-doping for additional redox pseudo-capacitances, and large pore volumes to accommodate the volume expansion/shrinkage at the charge/discharge cycles and to offer fast mass transfer path for electrolyte ions, altogether leading to the successful applications as bifunctional electrodes for Li ion based energy storage devices. [ABSTRACT FROM AUTHOR]

7,8-Dihydroxyflavone (DHF) mimicks the physiological action of brain-derived neurotrophic factor (BDNF). Since local BDNF delivery to the injured spinal cord enhanced diaphragmatic respiratory function, we aimed to ascertain whether DHF might have similar beneficial effects after Brown-Sequard Syndrome in a rat model of spinal cord lateral hemisection (HX) at the 9th thoracic (T9) vertebral level. Three sets of adult female rats were included: sham+vehicle group, T9HX+vehicle group and T9HX+DHF group. On the day of surgery, HX+DHF group received DHF (5 mg/kg) while HX+vehicle group received vehicle. Neurobehavioral function, morphology of motor neurons innervating the tibialis anterior muscle and the transmission in descending motor pathways were evaluated. Adult female rats received T9 HX had paralysis and loss of proprioception on the same side as the injury and loss of pain and temperature on the opposite side. We found that, in this model of Brown-Sequard syndrome, reduced cord dendritic arbor complexity, reduced cord motoneuron numbers, enlarged cord lesion volumes, reduced motor evoked potentials, and cord astrogliosis and microgliosis were noted after T9HX. All of the above-mentioned disorders showed recovery by Day 28 after surgery. Therapy with DHF significantly accelerated the electrophysiological, histological and functional recovery in these T9HX animals. Our data provide a biological basis for DHF as a neurotherapeutic agent to improve recovery after a Brown-Sequard syndrome. Such an effect may be mediated by synaptic plasticity and glia-mediated inflammation in the spared lumbar motoneuron pools to a T9HX. • Spinal cord hemisection induced Brown-Sequard syndrome in rats. • Spinal cord injury altered spinal pyramidal neuron structures. • Spinal cord injury reduced motor evoked potentials and gliosis. • 7,8-Dihydroxyflavone protected against spinal cord injury-induced complications. [ABSTRACT FROM AUTHOR]

We first explore whether aircraft noise (AN) induces cognitive deficit via inducing oxidative damage in multiple vital organs including intestines, hearts and hippocampus tissues. Second, we explore whether the AN-induced cognitive deficits and inflammatory and oxidative damage to multiple organs can be alleviated by Astaxanthin (AX) pretreatment. Cognitive deficits were induced by subjecting the mice to AN 2 h daily for 7 consecutive days. An intragastrical dose of AX emulsifier (at the dose of daily feed intake [6 g] of a mouse three times weekly) was given to mice for consecutive 8 weeks prior to the start of AN. Cognitive functions were evaluated by using passive avoidance apparatus, Y-maze, Morris water maze and novel recognition test. Intestinal permeability was determined by measuring the intestinal clearance of fluorescein-isothiocyante. Evans Blue extravasation assay was used to measure the permeability of blood-brain-barrier. Inflammatory and oxidative damage to multiple organs were determined by measuring several pro-inflammatory cytokines and oxidative stress indicators in intestines; hearts and hippocampus. Mice treated with AN displayed exacerbated stress reactions, cognitive deficits, gut barrier hyperpermeability, increased upload of lipopolysaccharide translocation, systemic pro-inflammatory cytokines overproduction, blood-brain-barrier hyperpermeability, hippocampal neuroinflammation and increased levels of oxidative stress indicators in intestine, heart and hippocampus. All of the above-mentioned disorders caused by AN were significantly (P < 0.05) reversed by AX. Our data indicate that AX pretreatment alleviates cognitive deficits in aircraft noised mice by attenuating inflammatory and oxidative damage to intestines, hearts and hippocampal tissues. [ABSTRACT FROM AUTHOR]

To our knowledge, little evidence is available about effects of aircraft noise (AN), a non-chemical stressor, on cognitive function. Again, it is unknown whether or not the heat stress (HS)-induced cognitive deficits can be exacerbated by AN. The adult male mice were assigned to four groups: group 1 mice exposed to non-HS (24–26 °C 2 h daily for 4 consecutive days) and white noise (WN) (2 h daily for 4 consecutive days), group 2 mice exposed to WN and HS (32–34 °C 2 h daily for 4 consecutive days), group 3 mice exposed to AN and non-HS (2 h daily for 4 consecutive days) and group 4 mice exposed to AN and HS (2 h daily for consecutive 4 days). Cognitive function were determined by passive avoidance, Y-maze, Morris water maze, and novel object recognition tests. Gut barrier and blood-brain-barrier (BBB) permeability, upload of lipopolysaccharide (LPS) translocation, systemic and central inflammation, and stress reactions were examined. Heat stressed mice displayed both increased stress reactions and learning and memory loss. Heat stress also caused gut barrier hyperpermeability, increased upload of LPS translocation, systemic inflammation, BBB disruption and hippocampal neuroinflammation. Aircraft noise stressed mice did not display systemic inflammation but caused gut barrier hyperpermeability, increased upload of LPS translocation, increased stress reactions, BBB disruption, hippocampal neuroinflammation and cognitive deficits. Aircraft noise exposure further exacerbated the heat stress-induced cognitive deficits and its complications. Our data suggest that AN, like HS, causes cognitive impairments via similar mechanisms in male mice. [Display omitted] • Heat or aircraft noise induced learning and memory loss in mice. • Heat-induced cognitive deficits can be potentiated by aircraft noise. • Heat or aircraft noise induced gut barrier and blood-brain-barrier disruption and neuroinflammation. • Hypothalamic-pituitary-adrenal axis responses were stimulated by heat or aircraft noise. [ABSTRACT FROM AUTHOR]