China
Africa
Explore chapters and articles related to this topic
Artificial Intelligence Applications in Genetic Disease/Syndrome Diagnosis
Published in P. Kaliraj, T. Devi, Artificial Intelligence Theory, Models, and Applications, 2021
The CNN-enabled smoker’s thoracic CT helps in identifying their mortality rate as well as acute respiratory distress (ARD) (González et al., 2018). The disease that affects the air sac/interstitium of the lung called infiltrative lung disease was also diagnosed with CNN (Walsh et al., 2016). CNN was given exercises to distinguish the disease of the lung affecting the interstitium called fibrotic lung disease from reports of the CT scans (Walsh et al., 2018). Algorithms designed by Prevedello et al. (2017) andChen et al. (2016) with AI used CT information for the identification of cerebral hemorrhage and cerebral edema, respectively. Similarly, CT used by SVM estimated the possibility of occurrence of a cerebral hemorrhage in ischemic stroke patients in post thrombolytic therapy (Bentley et al., 2014).
Organotin Compounds
Published in Fina P. Kaloyanova, Mostafa A. El Batawi, Human Toxicology of Pesticides, 2019
Fina P. Kaloyanova, Mostafa A. El Batawi
Although inhalatory and dermal exposure do not reportedly produce severe cerebral edema and death, ingestion of diethyltin diodide dissolved in linoleic acid (used for treatment of furunculosis) produced 210 intoxications with 110 deaths.8 The symptoms were cerebral edema, severe headache, nausea, vomiting, visual disturbances, and blindness in 33% of the cases. Ophthalmoscopy discovered papilledema and papillary stasis. Psychological disturbances, meningeal irritation, and other central nervous system symptoms were reported as well.7
Circulating markers of intestinal barrier injury and inflammation following exertion in hypobaric hypoxia
Published in European Journal of Sport Science, 2023
Zachary J. McKenna, Bryanne N. Bellovary, Jeremy B. Ducharme, Michael R. Deyhle, Andrew D. Wells, Zachary J. Fennel, Jonathan W. Specht, Jonathan M. Houck, Trevor J. Mayschak, Christine M. Mermier
Each year, more than 40 million people visit high altitude areas (> 2500 m), and an estimated 140 million people have a permanent residence above 2500 m (Tremblay & Ainslie, 2021). The decreased barometric pressure and reductions in the partial pressures of inspired oxygen at high altitudes can have a host of physiological consequences including significant impacts on morbidity and mortality (Burtscher, 2014). High altitude illnesses vary from mild to life-threatening and often present in the form of acute mountain sickness (AMS), high-altitude cerebral edema (HACE), and high-altitude pulmonary edema (HAPE). The most common of these is AMS which has an estimated prevalence between 20% and 60% for those traveling to high altitudes (Meier et al., 2017). AMS develops following rapid high-altitude ascent and includes a variety of nonspecific symptoms such as headache, nausea, dizziness, fatigue, and insomnia. In addition, gastrointestinal (GI) distress (e.g. anorexia, nausea, diarrhea, or vomiting) is one of the most commonly reported AMS symptoms with an estimated incidence of 80% amongst people suffering from the illness (Anand et al., 2006). The pathophysiology of AMS is currently unknown, though one prevailing theory is related to dysfunction within the central nervous system (Imray et al., 2010). However, given the high incidence of GI symptoms associated with high altitude exposures, we speculate that the GI system may contribute to the development of AMS as well as other high-altitude associated GI complications (i.e. peptic ulcers (Fruehauf et al., 2020) and GI bleeding (Wu et al., 2007)).
A Cu(II) complex: treatment activity on intracerebral hemorrhage via inhibiting inflammatory response in vascular endothelial cells
Published in Inorganic and Nano-Metal Chemistry, 2021
Jing Liu, Hong-Wei Zhao, Yong-Pan Tian, Yu Yang, Ji-Xiang Wu
Intracerebral hemorrhage (ICH) can cause the brain edema or even neuronal death, inducing a strong oxidative stress response, an inflammatory response, and a large number of inflammatory cell infiltration, resulting in severe damage to the blood-brain barrier.[1] Current research shows that patients with cerebral hemorrhage continue to bleed after the onset of the disease, and this phenomenon will lead to further deterioration of the early condition. Various active substances released by hematoma have a destructive effect, which will lead to changes in certain local cerebral blood flow, cerebral edema, damage to the blood-brain barrier, and toxic damage to brain cells.[2,3] In addition, the inflammatory cytokine interleukin-6 and brain tumor necrosis factor-α also play an important role in the pathophysiology of cerebral hemorrhage. Therefore, intervention in the transformation of the role of inflammatory cytokines may become a new method for the treatment of cerebral hemorrhage.
Simulating cerebral edema and delayed fatality after traumatic brain injury using triphasic swelling biomechanics
Published in Traffic Injury Prevention, 2019
Andrew V. Basilio, Peng Xu, Yukou Takahashi, Toshiyuki Yanaoka, Hisaki Sugaya, Gerard A. Ateshian, Barclay Morrison
Traumatic brain injury (TBI) is a major contributor of mortality and morbidity after motor vehicle crashes (MVCs). In 2013, 21.5% of TBI-related hospitalizations were attributed to MVCs (Taylor et al. 2017). In the quest to reduce the societal costs of MVCs, finite element (FE) models have contributed to our understanding of injury causation as well as aided in the design of improved safety systems for both occupants and vulnerable road users. A family of FE models has been developed by the Global Human Body Models Consortium (GHBMC) that includes structures of the entire human body, including a detailed mesh of the head and brain. The GHBMC model has been validated at both the component and whole-model levels to support its biofidelic, dynamic response (Arun et al. 2015). The current use of FE models in the automotive industry focuses on predicting stress and strain during the accident itself to predict primary injury; contemporary models have not been used to simulate delayed brain swelling from edema that occurs after the impact on the time-scale of hours to days. Over 70% of severe TBI patients (GCS ≤ 8) experience cerebral edema leading to increased intracranial pressure (ICP), and elevated ICP is highly associated with poor outcome and increased mortality (Balestreri et al. 2006). By simulating cerebral edema, it may be possible to improve prediction of mortality during this sub-acute phase to inform the design of novel safety systems.