Pressure-dependent effect of shock waves on rat brain: induction of neuronal apoptosis mediated by a caspase-dependent pathway

2007 ◽  
Vol 106 (4) ◽  
pp. 667-676 ◽  
Author(s):  
Kaoruko Kato ◽  
Miki Fujimura ◽  
Atsuhiro Nakagawa ◽  
Atsushi Saito ◽  
Tomohiro Ohki ◽  
...  
Keyword(s):  
Shock Wave ◽  
Brain Injury ◽  
Shock Waves ◽  
Caspase 3 ◽  
Wave Exposure ◽  
Histological Changes ◽  
Dependent Effect ◽  
Wave Induced ◽  
Dependent Pathway ◽  
Active Caspase

Object Shock waves have been experimentally applied to various neurosurgical treatments including fragmentation of cerebral emboli, perforation of cyst walls or tissue, and delivery of drugs into cells. Nevertheless, the application of shock waves to clinical neurosurgery remains challenging because the threshold for shock wave–induced brain injury has not been determined. The authors investigated the pressure-dependent effect of shock waves on histological changes of rat brain, focusing especially on apoptosis. Methods Adult male rats were exposed to a single shot of shock waves (produced by silver azide explosion) at over-pressures of 1 or 10 MPa after craniotomy. Histological changes were evaluated sequentially by H & E staining and terminal deoxynucleotidyl transferase–mediated deoxyuridine triphosphate nick-end labeling (TUNEL). The expression of active caspase-3 and the effect of the nonselective caspase inhibitor N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (Z-VAD-FMK) were examined to evaluate the contribution of a caspase-dependent pathway to shock wave–induced brain injury. High-overpressure (> 10 MPa) shock wave exposure resulted in contusional hemorrhage associated with a significant increase in TUNEL-positive neurons exhibiting chromatin condensation, nuclear segmentation, and apoptotic bodies. The maximum increase was seen at 24 hours after shock wave application. Low-overpressure (1 MPa) shock wave exposure resulted in spindle-shaped changes in neurons and elongation of nuclei without marked neuronal injury. The administration of Z-VAD-FMK significantly reduced the number of TUNEL-positive cells observed 24 hours after high-overpressure shock wave exposure (p < 0.01). A significant increase in the cytosolic expression of active caspase-3 was evident 24 hours after high-overpressure shock wave application; this increase was prevented by Z-VAD-FMK administration. Double immunofluorescence staining showed that TUNEL-positive cells were exclusively neurons. Conclusions The threshold for shock wave–induced brain injury is speculated to be under 1 MPa, a level that is lower than the threshold for other organs. High-overpressure shock wave exposure results in brain injury, including neuronal apoptosis mediated by a caspase-dependent pathway. This is the first report in which the pressure-dependent effect of shock wave on the histological characteristics of brain tissue is demonstrated.

A Multi-Scale Finite Element Model for Shock Wave-Induced Axonal Brain Injury

2008 ◽  
Author(s):  
M. Sotudeh-Chafi ◽  
N. Abolfathi ◽  
A. Nick ◽  
V. Dirisala ◽  
G. Karami ◽  
...  
Keyword(s):  
Shock Wave ◽  
Brain Injury ◽  
Shock Waves ◽  
Brain Tissue ◽  
Scale Model ◽  
Micro Scale ◽  
Multi Scale ◽  
Injury Criteria ◽  
Wave Induced ◽  
The Brain

Traumatic brain injuries (TBIs) involve a significant portion of human injuries resulting from a wide range of civilian accidents as well as many military scenarios. Axonal damage is one of the most common and important pathologic features of traumatic brain injury. Axons become brittle when exposed to rapid deformations associated with brain trauma. Accordingly, rapid stretch of axons can damage the axonal cytoskeleton, resulting in a loss of elasticity and impairment of axoplasmic transport. Subsequent swelling of the axon occurs in discrete bulb formations or in elongated varicosities that accumulate organelles. Ultimately, swollen axons may become disconnected [1]. The shock waves generated by a blast, subject all the organs in the head to displacement, shearing and tearing forces. The brain is especially vulnerable to these forces — the fronts of compressed air waves cause rapid forward or backward movements of the head, so that the brain rattles against the inside of the skull. This can cause subdural hemorrhage and contusions. The forces exerted on the brain by shock waves are known to damage axons in the affected areas. This axonal damage begins within minutes of injury, and can continue for hours or days following the injury [2]. Shock waves are also known to damage the brain at the subcellular level, but exactly how remains unclear. Kato et al., [3] described the effects of a small controlled explosion on rats’ brain tissue. They found that high pressure shock waves led to contusions and hemorrhage in both cortical and subcortical brain regions. Based on their result, the threshold for shock wave-induced brain injury is speculated to be under 1 MPa. This is the first report to demonstrate the pressure-dependent effect of shock wave on the histological characteristics of brain tissue. An important step in understanding the primary blast injury mechanism due to explosion is to translate the global head loads to the loading conditions, and consequently damage, of the cells at the local level and to project cell level and tissue level injury criteria towards the level of the head. In order to reach this aim, we have developed a multi-scale non-linear finite element modeling to bridge the micro- and macroscopic scales and establish the connection between microstructure and effective behavior of brain tissue to develop acceptable injury threshold. Part of this effort has been focused on measuring the shock waves created from a blast, and studying the response of the brain model of a human head exposed to such an environment. The Arbitrary Lagrangian Eulerian (ALE) and Fluid/Solid Interactions (FSI) formulation have been used to model the brain-blast interactions. Another part has gone into developing a validated fiber-matrix based micro-scale model of a brain tissue to reproduce the effective response and to capturing local details of the tissue’s deformations causing axonal injury. The micro-model of the axon and matrix is characterized by a transversely isotropic viscoelastic material and the material model is formulated for numerical implementation. Model parameters are fit to experimental frequency response of the storage and loss modulus data obtained and determined using a genetic algorithm (GA) optimizing method. The results from macro-scale model are used in the micro-scale brain tissue to study the effective behavior of this tissue under injury-based loadings. The research involves the development of a tool providing a better understanding of the mechanical behavior of the brain tissue against blast loads and a rational multi-scale approach for driving injury criteria.

Nanobubbles, cavitation, shock waves and traumatic brain injury

2016 ◽  
Vol 18 (48) ◽  
pp. 32638-32652 ◽  
Author(s):  
Upendra Adhikari ◽  
Ardeshir Goliaei ◽  
Max L. Berkowitz
Keyword(s):  
Shock Wave ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Shock Waves ◽  
Tight Junction ◽  
Blood Brain Barrier ◽  
Neurological Complications ◽  
Tight Junction Proteins ◽  
Wave Induced ◽  
Junction Proteins

Shock wave induced cavitation denaturates blood–brain barrier tight junction proteins; this may result in various neurological complications.

scholarly journals Ultrafast ignition with relativistic shock waves induced by high power lasers

2014 ◽  
Vol 2 ◽  
Author(s):  
Shalom Eliezer ◽  
Noaz Nissim ◽  
Shirly Vinikman Pinhasi ◽  
Erez Raicher ◽  
José Maria Martinez Val
Keyword(s):  
Shock Wave ◽  
Shock Waves ◽  
Radiation Pressure ◽  
Ponderomotive Force ◽  
Relativistic Hydrodynamics ◽  
Pressure Shock ◽  
Compression Pressure ◽  
High Power Lasers ◽  
Relativistic Shock ◽  
Wave Induced

Abstract In this paper we consider laser intensities greater than $\def \xmlpi #1{}\def \mathsfbi #1{\boldsymbol {\mathsf {#1}}}\let \le =\leqslant \let \leq =\leqslant \let \ge =\geqslant \let \geq =\geqslant \def \Pr {\mathit {Pr}}\def \Fr {\mathit {Fr}}\def \Rey {\mathit {Re}}10^{16}\ \mathrm{W\ cm}^{-2}$ where the ablation pressure is negligible in comparison with the radiation pressure. The radiation pressure is caused by the ponderomotive force acting mainly on the electrons that are separated from the ions to create a double layer (DL). This DL is accelerated into the target, like a piston that pushes the matter in such a way that a shock wave is created. Here we discuss two novel ideas. Firstly, the transition domain between the relativistic and non-relativistic laser-induced shock waves. Our solution is based on relativistic hydrodynamics also for the above transition domain. The relativistic shock wave parameters, such as compression, pressure, shock wave and particle flow velocities, sound velocity and rarefaction wave velocity in the compressed target, and temperature are calculated. Secondly, we would like to use this transition domain for shock-wave-induced ultrafast ignition of a pre-compressed target. The laser parameters for these purposes are calculated and the main advantages of this scheme are described. If this scheme is successful a new source of energy in large quantities may become feasible.

Underwater shock wave induced by pulsed discharge on water

2021 ◽  
Author(s):  
Tomohiro Furusato ◽  
Mitsuru Sasaki ◽  
Yoshinobu Matsuda ◽  
Takahiko Yamashita
Keyword(s):  
Biological Sciences ◽  
Shock Wave ◽  
Shock Waves ◽  
Surface Discharge ◽  
Underwater Shock Wave ◽  
Mean Velocity ◽  
Combined Action ◽  
Underwater Shock ◽  
The Mean ◽  
Wave Induced

Abstract Plasmas on liquids have provided significant applications in material, environmental, and biological sciences. The mechanisms of these chemical reactions in liquids have been primarily discussed by the plasma–liquid interactions and convection by an electrohydrodynamic flow. Although shock waves play a significant role in the radical formation, agitation, and cell destruction, not much information is available on underwater shock waves induced by the surface discharge on water. In this study, an underwater shock wave generated by the pulsed surface discharge on water using the laser shadowgraph method has been demonstrated. The results reveal that the shock wave generated by the discharge on water was transmitted into the water. The mean velocity of the shock wave reached 1.7 km/s. The results indicate that the surface discharge accelerates the reaction in the water by the combined action of the underwater shock wave and the plasma reaction at the air–water interface. The results are expected to aid in the understanding the mechanisms of existing applications, such as decomposition, synthesis, and sterilization.

Shock-wave induced instability in internal explosion dynamics

2005 ◽  
Vol 109 (1101) ◽  
pp. 537-556 ◽  
Author(s):  
A. Bagabir ◽  
D. Drikakis
Keyword(s):  
Shock Wave ◽  
Wave Propagation ◽  
Shock Waves ◽  
Symmetry Breaking ◽  
Flow Instability ◽  
Shock Wave Propagation ◽  
Vortical Flow ◽  
Density Region ◽  
Riemann Solvers ◽  
Wave Induced

Abstract The paper presents an investigation of flow instabilities occurring in shock-wave propagation and interaction with the walls of an enclosure. The shock-wave propagation is studied in connection with perturbed and unperturbed cylindrical blasts, initially placed in the centre of the enclosure, as well as for three different blast intensities corresponding to Mach numbers Ms = 2, 5 and 10. The instability is manifested by a symmetry-breaking of the flow even for the case of an initially perfectly-symmetric blast. It is shown that the symmetry-breaking initiates around the centre of the enclosure as a result of the interaction of the shock waves reflected from the walls, with the low-density region in the centre of the explosion. The instability leads to fast attenuation of the shock waves, especially for smaller initial blast intensities. The computations reveal that the vortical flow structures arising from the multiple shock reflections and flow instability are Mach number dependent. The existence of perturbations of large amplitude in the initial condition strengthens the instability and has significant effects on the instantaneous wall pressure distributions. The computational investigation has been performed using high-resolution Riemann solvers for the gas dynamic equations.

Shock wave-induced brain injury in rat: Novel traumatic brain injury animal model

2008 ◽  
pp. 421-424 ◽  
Author(s):  
Atsuhiro Nakagawa ◽  
Miki Fujimura ◽  
Kaoruko Kato ◽  
Hironobu Okuyama ◽  
Tokitada Hashimoto ◽  
...  
Keyword(s):  
Shock Wave ◽  
Traumatic Brain Injury ◽  
Animal Model ◽  
Brain Injury ◽  
Wave Induced

scholarly journals Z-Guggulsterone Induces Apoptosis in Gastric Cancer Cells through the Intrinsic Mitochondria-Dependent Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-6
Author(s):  
Ruxi Lv ◽  
Min Zhu ◽  
Kun Chen ◽  
Haitao Xie ◽  
Hongxia Bai ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Protein Expression ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Bax Protein ◽  
Tnf Α ◽  
Dependent Pathway ◽  
Tgf Β1 ◽  
Active Caspase

Background. To study the effects of z-guggulsterone on gastric cancer cell apoptosis and the mechanism related. Materials and Methods. Human gastric tumor SGC-7901 cells and GES-1 normal epithelial cells were treated with z-guggulsterone (0–75 μM) for 24 h. MTT assay was applied to evaluate cell proliferation. Flow cytometry and Hoechst staining were used to assess cell apoptosis. Western blotting was applied to evaluate FXR, small heterodimer partner (SHP), Bcl-2, and Bax protein expression. ELISA was applied to gain the levels of active caspase-3 and the contents of TNF-α, TGF-β1, and VEGF. Results. The expression levels of FXR and SHP were higher in tumor cells than in normal epithelial cells. Inhibition of FXR signaling with z-guggulsterone dose-dependently inhibited SGC-7901 cell proliferation and promoted SGC-7901 cell apoptosis. Bcl-2 protein expression was significantly decreased, and active caspase-3 and Bax protein expression was increased in SGC-7901 cells incubated with z-guggulsterone. The content of TNF-α was significantly increased, and the contents of VEGF and TGF-β1 were decreased in SGC-7901 cells incubated with z-guggulsterone. Conclusions. Inhibition of FXR signaling with z-guggulsterone induced anticancer effects in SGC-7901 cells by decreasing cell proliferation and promoting apoptosis. Z-guggulsterone induced cell apoptosis through the mitochondria-dependent pathway.

Shock-wave-induced nucleation leading to crystallization in water

2019 ◽  
Vol 52 (5) ◽  
pp. 1016-1021 ◽  
Author(s):  
A. Sivakumar ◽  
S. A. Martin Britto Dhas
Keyword(s):  
Shock Wave ◽  
Shock Waves ◽  
Water Samples ◽  
Sea Water ◽  
X Ray Diffraction ◽  
Spectroscopy Analysis ◽  
X Ray ◽  
Wave Induced ◽  
The Impact ◽  
Induced Crystallization

It is well known that super-cooled materials can be crystallized under the application of shock waves. This is the first report describing crystallization from unsaturated liquids. Shock-wave-induced crystallization of salts from environmental ground and sea water samples is explored. A table-top pressure-driven shock tube is utilized so as to produce the required shock waves of Mach numbers 1.1, 1.2, 1.4, 2.2 and 4.7. The demonstration comprises a train of acoustic shock pulses applied to the water samples. As a consequence of the impact of the shock waves, the colourless water becomes turbid, following which tiny crystallites are precipitated at the bottom of the vessel after a few minutes. The obtained precipitate is subjected to powder X-ray diffraction and energy-dispersive X-ray spectroscopy analysis to confirm the nature of the settled particles and the elements present in them, respectively. From the observed results, it is concluded that shock-wave-induced crystallization in water provides an alternative method for removing dissolved salts from both ground and sea water samples.

scholarly journals Time-Course of the Effects of QSYQ in Promoting Heart Function in Ameroid Constrictor-Induced Myocardial Ischemia Pigs

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
Qi Qiu ◽  
Yang Lin ◽  
Cheng Xiao ◽  
Chun Li ◽  
Yong Wang ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Time Course ◽  
Caspase 3 ◽  
Heart Function ◽  
Cardiac Injury ◽  
Myocardial Tissue ◽  
Therapeutic Effects ◽  
Ang Ii ◽  
Histological Changes ◽  
Active Caspase

We aim to investigate the therapeutic effects of QSYQ on a pig myocardial ischemia (MI) model and to determine its mechanism of action. The MI model was induced by Ameroid constriction of the left anterior descending coronary (LAD) in Ba-Ma miniature pigs. Four groups were created: model group, digoxin group, QSYQ group, and sham-operated group. Heart function, Ang II, CGMP, TXB2, BNP, and cTnT were evaluated before (3 weeks after operation: 0 weeks) and at 2, 4, and 8 weeks after drug administration. After 8 weeks of administration, the pigs were sacrificed for cardiac injury measurements. Pigs with MI showed obvious histological changes, including BNP, cTnT, Ang II, CGRP, TXB2, and ET, deregulated heart function, and increased levels of apoptotic cells in myocardial tissue. Treatment with QSYQ improved cardiac remodeling by counteracting those events. The administration of QSYQ was accompanied by a restoration of heart function and of the levels of Ang II, CGRP, TXB2, ET BNP, and cTnT. In addition, QSYQ attenuated administration, reduced the apoptosis, and decreased the level of TNF-αand active caspase-3. In conclusion, administration of QSYQ could attenuate Ameroid constrictor induced myocardial ischemia, and TNF-αand active caspase-3 seemed to be the critical potential target of QSYQ.

scholarly journals Dual Vulnerability of TDP-43 to Calpain and Caspase-3 Proteolysis after Neurotoxic Conditions and Traumatic Brain Injury

2014 ◽  
Vol 34 (9) ◽  
pp. 1444-1452 ◽  
Author(s):  
Zhihui Yang ◽  
Fan Lin ◽  
Claudia S Robertson ◽  
Kevin KW Wang
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Caspase 3 ◽  
Chronic Traumatic Encephalopathy ◽  
Prior History ◽  
Mouse Cortex ◽  
History Of ◽  
Fragmentation Patterns ◽  
Wave Induced

Transactivation response DNA-binding protein 43 (TDP-43) proteinopathy has recently been reported in chronic traumatic encephalopathy, a neurodegenerative condition linked to prior history of traumatic brain injury (TBI). While TDP-43 appears to be vulnerable to proteolytic modifications under neurodegenerative conditions, the mechanism underlying the contribution of TDP-43 to the pathogenesis of TBI remains unknown. In this study, we first mapped out the calpain or caspase-3 TDP-43 fragmentation patterns by in vitro protease digestion. Concurrently, in cultured cerebrocortical neurons subjected to cell death challenges, we identified distinct TDP-43 breakdown products (BDPs) of 35, 33, and 12kDa that were indicative of dual calpain/caspase attack. Cerebrocortical culture incubated with calpain and caspase-fragmented TDP-43 resulted in neuronal injury. Furthermore, increased TDP-43 BDPs as well as redistributed TDP-43 from the nucleus to the cytoplasm were observed in the mouse cortex in two TBI models: controlled cortical impact injury and overpressure blast-wave-induced brain injury. Finally, TDP-43 and its 35 kDa fragment levels were also elevated in the cerebrospinal fluid (CSF) of severe TBI patients. This is the first evidence that TDP-43 might be involved in acute neuroinjury and TBI pathology, and that TDP-43 and its fragments may have biomarker utilities in TBI patients.

Sign in / Sign up

Export Citation Format

Share Document