Computational modeling investigation of pulsed high peak power microwaves and the potential for traumatic brain injury.
Ontology highlight
ABSTRACT:
SUBMITTER: Dagro AM
PROVIDER: S-EPMC8555891 | biostudies-literature | 2021 Oct
REPOSITORIES: biostudies-literature
Publications
Computational modeling investigation of pulsed high peak power microwaves and the potential for traumatic brain injury.
Dagro Amy M AM Wilkerson Justin W JW Thomas Thaddeus P TP Kalinosky Benjamin T BT Payne Jason A JA
Science advances 20211029 44
When considering safety standards for human exposure to radiofrequency (RF) and microwave energy, the dominant concerns pertain to a thermal effect. However, in the case of high-power pulsed RF/microwave energy, a rapid thermal expansion can lead to stress waves within the body. In this study, a computational model is used to estimate the temperature profile in the human brain resulting from exposure to various RF/microwave incident field parameters. The temperatures are subsequently used to sim ...[more]
Similar Datasets
Project description:Blast traumatic brain injury is ubiquitous in modern military conflict with significant morbidity and mortality. Yet the mechanism by which blast overpressure waves cause specific intracranial injury in humans remains unclear. Reviewing of both the clinical experience of neurointensivists and neurosurgeons who treated service members exposed to blast have revealed a pattern of injury to cerebral blood vessels, manifested as subarachnoid hemorrhage, pseudoaneurysm, and early diffuse cerebral edema. Additionally, a seminal neuropathologic case series of victims of blast traumatic brain injury (TBI) showed unique astroglial scarring patterns at the following tissue interfaces: subpial glial plate, perivascular, periventricular, and cerebral gray-white interface. The uniting feature of both the clinical and neuropathologic findings in blast TBI is the co-location of injury to material interfaces, be it solid-fluid or solid-solid interface. This motivates the hypothesis that blast TBI is an injury at the intracranial mechanical interfaces. In order to investigate the intracranial interface dynamics, we performed a novel set of computational simulations using a model human head simplified but containing models of gyri, sulci, cerebrospinal fluid (CSF), ventricles, and vasculature with high spatial resolution of the mechanical interfaces. Simulations were performed within a hybrid Eulerian-Lagrangian simulation suite (CTH coupled via Zapotec to Sierra Mechanics). Because of the large computational meshes, simulations required high performance computing resources. Twenty simulations were performed across multiple exposure scenarios-overpressures of 150, 250, and 500 kPa with 1 ms overpressure durations-for multiple blast exposures (front blast, side blast, and wall blast) across large variations in material model parameters (brain shear properties, skull elastic moduli). All simulations predict fluid cavitation within CSF (where intracerebral vasculature reside) with cavitation occurring deep and diffusely into cerebral sulci. These cavitation events are adjacent to high interface strain rates at the subpial glial plate. Larger overpressure simulations (250 and 500kPa) demonstrated intraventricular cavitation-also associated with adjacent high periventricular strain rates. Additionally, models of embedded intraparenchymal vascular structures-with diameters as small as 0.6 mm-predicted intravascular cavitation with adjacent high perivascular strain rates. The co-location of local maxima of strain rates near several of the regions that appear to be preferentially damaged in blast TBI (vascular structures, subpial glial plate, perivascular regions, and periventricular regions) suggest that intracranial interface dynamics may be important in understanding how blast overpressures leads to intracranial injury.
| S-EPMC8173077 | biostudies-literature
Project description:High-power microwaves are used to inhibit electronics of threatening military or civilian vehicles. This work aims to assess health hazards of high-power microwaves and helps to define hazard threshold levels of modulated radiofrequency exposures such as those emitted by the first generations of mobile phones. Rats were exposed to the highest possible field levels, under single acute or repetitive exposures for eight weeks. Intense microwave electric fields at 1 MV m-1 of nanoseconds duration were applied from two sources at different carrier frequencies of 10 and 3.7 GHz. The repetition rate was 100 pps, and the duration of train pulses lasted from 10 s to twice 8 min. The effects on the central nervous system were evaluated, by labelling brain inflammation marker GFAP and by performing different behavioural tests: rotarod, T-maze, beam-walking, open-field, and avoidance test. Long-time survival was measured in animals repeatedly exposed, and anatomopathological analysis was performed on animals sacrificed at two years of life or earlier in case of precocious death. Control groups were sham exposed. Few effects were observed on behaviour. With acute exposure, an avoidance reflex was shown at very high thermal level (22 W kg-1); GFAP was increased some days after exposure. Most importantly, with repeated exposures, survival time was 4-months shorter in the exposed group, with eleven animals exhibiting a large sub-cutaneous tumour, compared to two in the sham group. A residual X-ray exposure was also present in the beam (0.8 Gy), which is probably not a bias for the observed result. High power microwaves below thermal level in average, can increase cancer prevalence and decrease survival time in rats, without clear effects on behaviour. The parameters of this effect need to be further explored, and a more precise dosimetry to be performed.
| S-EPMC7141660 | biostudies-literature
Project description:Traumatic brain injury (TBI) is a head injury that disrupts the normal brain structure and function. TBI has been extensively studied using various in vitro and in vivo models. Most of the studies have been done with rodent models, which may respond differently to TBI than human nerve cells. Taking advantage of the recent development of cerebral organoids (COs) derived from human induced pluripotent stem cells (iPSCs), which resemble the architecture of specific human brain regions, here, we adapted the controlled cortical impact (CCI) model to induce TBI in human COs as a novel in vitro platform. To adapt the CCI procedure into COs, we have developed a phantom brain matrix, matching the mechanical characteristics of the brain, altogether with an empty mouse skull as a platform to allow the use of the stereotactic CCI equipment on COs. After the CCI procedure, COs were histologically prepared to evaluate neurons and astrocyte populations using the microtubule-associated protein 2 (MAP2) and the glial fibrillary acidic protein (GFAP). Moreover, a marker of metabolic response, the neuron-specific enolase (NSE), and cellular death using cleaved caspase 3 were also analyzed. Our results show that human COs recapitulate the primary pathological changes of TBI, including metabolic alterations related to neuronal damage, neuronal loss, and astrogliosis. This novel approach using human COs to model TBI in vitro holds great potential and opens new alternatives for understanding brain abnormalities produced by TBI, and for the development and testing of new therapeutic approaches.
| S-EPMC8534257 | biostudies-literature
Project description:ObjectiveTraumatic brain injury (TBI) is a heterogeneous disease with multiple neurological deficits that evolve over time. It is also associated with an increased incidence of neurodegenerative diseases. Accordingly, clinicians need better tools to predict a patient's long-term prognosis.MethodsDiffusion-weighted and anatomical MRI data were collected from 17 adolescents (mean age = 15y8mo) with moderate-to-severe TBI and 19 healthy controls. Using a network diffusion model (NDM), we examined the effect of progressive deafferentation and gray matter thinning in young TBI patients. Moreover, using a novel automated inference method, we identified several injury epicenters in order to determine the neural degenerative patterns in each TBI patient.ResultsWe were able to identify the subject-specific patterns of degeneration in each patient. In particular, the hippocampus, temporal cortices, and striatum were frequently found to be the epicenters of degeneration across the TBI patients. Orthogonal transformation of the predicted degeneration, using principal component analysis, identified distinct spatial components in the temporal-hippocampal network and the cortico-striatal network, confirming the vulnerability of these networks to injury. The NDM model, best predictive of the degeneration, was significantly correlated with time since injury, indicating that NDM can potentially capture the pathological progression in the chronic phase of TBI.InterpretationThese findings suggest that network spread may help explain patterns of distant gray matter thinning, which would be consistent with Wallerian degeneration of the white matter connections (i.e., "diaschisis") from diffuse axonal injuries and multifocal contusive injuries, and the neurodegenerative patterns of abnormal protein aggregation and transmission, which are hallmarks of brain changes in TBI. NDM approaches could provide highly subject-specific biomarkers relevant for disease monitoring and personalized therapies in TBI.
| S-EPMC7086000 | biostudies-literature
Project description:Traumatic brain injury can lead to the neurodegenerative disease chronic traumatic encephalopathy. This condition has a clear neuropathological definition but the relationship between the initial head impact and the pattern of progressive brain pathology is poorly understood. We test the hypothesis that mechanical strain and strain rate are greatest in sulci, where neuropathology is prominently seen in chronic traumatic encephalopathy, and whether human neuroimaging observations converge with computational predictions. Three distinct types of injury were simulated. Chronic traumatic encephalopathy can occur after sporting injuries, so we studied a helmet-to-helmet impact in an American football game. In addition, we investigated an occipital head impact due to a fall from ground level and a helmeted head impact in a road traffic accident involving a motorcycle and a car. A high fidelity 3D computational model of brain injury biomechanics was developed and the contours of strain and strain rate at the grey matter-white matter boundary were mapped. Diffusion tensor imaging abnormalities in a cohort of 97 traumatic brain injury patients were also mapped at the grey matter-white matter boundary. Fifty-one healthy subjects served as controls. The computational models predicted large strain most prominent at the depths of sulci. The volume fraction of sulcal regions exceeding brain injury thresholds were significantly larger than that of gyral regions. Strain and strain rates were highest for the road traffic accident and sporting injury. Strain was greater in the sulci for all injury types, but strain rate was greater only in the road traffic and sporting injuries. Diffusion tensor imaging showed converging imaging abnormalities within sulcal regions with a significant decrease in fractional anisotropy in the patient group compared to controls within the sulci. Our results show that brain tissue deformation induced by head impact loading is greatest in sulcal locations, where pathology in cases of chronic traumatic encephalopathy is observed. In addition, the nature of initial head loading can have a significant influence on the magnitude and pattern of injury. Clarifying this relationship is key to understanding the long-term effects of head impacts and improving protective strategies, such as helmet design.
| S-EPMC5278309 | biostudies-literature
Project description:Microwave (MW) radiation is increasingly being used for several biological applications. Many investigations have focused on understanding the potential influences of pulsed MW irradiation on biological solutions. The current study aimed to investigate the effects of 3.5 GHz pulsed MW radiation-irradiated liquid solutions on the survival of human cancer and normal cells. Different physiological solutions such as phosphate buffer saline, deionized water, and Dulbecco's modified Eagle medium (DMEM) for cell culture growth were irradiated with pulsed MW radiation (45 shots with the energy of 1 mJ/shot). We then evaluated physiological effects such as cell viability, metabolic activity, mitochondrial membrane potential, cell cycle, and cell death in cells treated with MW-irradiated biological solutions. As MW irradiation with power density ~ 12 kW/cm2 mainly induces reactive nitrogen oxygen species in deionized water, it altered the cell cycle, membrane potential, and cell death rates in U373MG cells due to its high electric field ~ 11 kV/cm in water. Interestingly, MW-irradiated cell culture medium and phosphate-buffered saline did not alter the cellular viability and metabolic energy of cancer and normal cells without affecting the expression of genes responsible for cell death. Taken together, MW-irradiated water can alter cellular physiology noticeably, whereas irradiated media and buffered saline solutions induce negligible or irrelevant changes that do not affect cellular health.
| S-EPMC8055702 | biostudies-literature
Project description:BackgroundTraumatic brain injury (TBI) often precipitates a cascade of neurophysiological alterations, impacting structures such as the optic nerve and ocular motor system. However, the literature lacks expansive investigations into the longitudinal changes in the optic chiasm and its relationship with the clinical recovery of visual processing. This study aimed to scrutinize longitudinal changes in optic chiasm volume (OCV) and establish the relationship of OCV with process speed index at 12 months post-injury. Process speed index is derived from Wechsler Adult Intelligence Scale IV.MethodsThorough cross-sectional and longitudinal analyses were executed, involving 42 patients with moderate to severe TBI and 35 healthy controls. OCV was acquired at 3, 6, and 12 months post-injury using T1-weighted images. OCV of healthy controls and that of patients with TBI at 3, 6, and 12 months post-injury were compared using a Mann-Whitney U test. A multiple linear regression model was constructed to assess the association between OCV and PSI and to predict PSI at 12 months post-injury using OCV at 3 months post-injury.ResultsOCV of patients with TBI was significantly larger compared to healthy controls, persisting from 3 to 12 months post-injury (p < 0.05). This increased OCV negatively correlated with PSI at 12 months post-injury, indicating that larger OCV sizes were associated with decreased PSI (p = 0.031). Furthermore, the multiple linear regression model was significant in predicting PSI at 12 months post-injury utilizing OCV at 3 months post-injury (p = 0.024).ConclusionFor the first time, this study elucidates the increased OCV and the significant association between OCV in sub-chronic stage and PSI at 12 months post-injury, potentially providing clinicians with a tool for anticipatory cognitive rehabilitation strategies following TBI.
| S-EPMC11437778 | biostudies-literature
Project description:Prognostic assessment in traumatic brain injury (TBI) is embedded deeply in clinical care. Considering the limitations of current prognostic indicators, there is increasing interest in understanding the role of new biomarkers, and in finding other prognostic indicators of long-term outcomes following TBI. New prognostic indicators may result in the development of more accurate prediction models that could be useful for both risk stratification and clinical decision making. We aimed to review methodological issues and provide tentative guidelines for prognostic research in TBI. Prognostic factor research focuses on the role of a specific patient or disease-related characteristic in relation to outcome. Typically, univariable relations of the prognostic factor are studied, followed by analyses adjusting for other variables related to the outcome. Following existing guidelines, we emphasize the importance of transparent reporting of patient and specimen characteristics, study design, clinical end-points, and statistical analysis. Prognostic model research considers combinations of predictors, with challenges for model specification, estimation, evaluation, validation, and presentation. We highlight modern approaches and opportunities related to missing values, exploration of non-linear effects, and assessing between-study heterogeneity. Prognostic research in TBI can be improved if key methodological principles are adhered to and when research is performed in collaboration among multiple centers to ensure generalizability.
| S-EPMC8403181 | biostudies-literature
Project description:Traumatic brain injury (TBI) has historically been viewed as a primarily male problem, since men are more likely to experience a TBI because of more frequent participation in activities that increase risk of head injuries. This male bias is also reflected in preclinical research where mostly male animals have been used in basic and translational science. However, with an aging population in which TBI incidence is increasingly sex-independent due to falls, and increasing female participation in high-risk activities, the attention to potential sex differences in TBI responses and outcomes will become more important. These considerations are especially relevant in designing preclinical animal models of TBI that are more predictive of human responses and outcomes. This review characterizes sex differences following TBI with a special emphasis on the contribution of the female sex hormones, progesterone and estrogen, to these differences. This information is potentially important in developing and customizing TBI treatments.
| S-EPMC6139061 | biostudies-literature
Project description:IntroductionTraumatic brain injury (TBI) is a leading cause of death and disability in children, but data on the longitudinal healthcare and financial needs of pediatric patients is limited in scope and duration. We sought to describe and predict these metrics following acute inpatient treatment for TBI.MethodsChildren surviving their initial inpatient treatment for TBI were identified from Optum's deidentified Clinformatics® Data Mart Database (2007-2018). Treatment cost, healthcare utilization, and future inpatient readmission were stratified by follow-up intervals, type of claim, and injury severity. Both TBI-related and non-TBI related future cost and healthcare utilization were explored using linear mixed models. Acute inpatient healthcare utilization metrics were analyzed and used to predict future treatment cost and healthcare demands using linear regression models.ResultsAmong 7,400 patients, the majority suffered a mild TBI (50.2%). For patients with at least one-year follow-up (67.7%), patients accrued an average of 28.7 claims and $27,199 in costs, with 693 (13.8%) readmitted for TBI or non-TBI related causes. Severe TBI patients had a greater likelihood of readmission. Initial hospitalization length of stay and discharge disposition other than home were significant positive predictors of healthcare and financial utilization at one-and five-years follow-up. Linear mixed models demonstrated that pediatric TBI patients would accrue 21.1 claims and $25,203 in cost in the first year, and 9.4 claims and $4,147 in costs every additional year, with no significant differences based on initial injury severity.DiscussionPediatric TBI patients require long-term healthcare and financial resources regardless of injury severity. Our cumulative findings provide essential information to clinicians, caretakers, researchers, advocates, and policymakers to better shape standards, expectations, and management of care following TBI.
| S-EPMC11638116 | biostudies-literature