Advancements in novel neurotechnologies, such as brain computer interfaces (BCI) and neuromodulatory devices such as deep brain stimulators (DBS), will have profound implications for society and human rights. While these technologies are improving the diagnosis and treatment of mental and neurological diseases, they can also alter individual agency and estrange those using neurotechnologies from their sense of self, challenging basic notions of what it means to be human. As an international coalition of interdisciplinary scholars and practitioners, we examine these challenges and make recommendations to mitigate negative consequences that could arise from the unregulated development or application of novel neurotechnologies. We explore potential ethical challenges in four key areas: identity and agency, privacy, bias, and enhancement. To address them, we propose (1) democratic and inclusive summits to establish globally-coordinated ethical and societal guidelines for neurotechnology development and application, (2) new measures, including “Neurorights,” for data privacy, security, and consent to empower neurotechnology users’ control over their data, (3) new methods of identifying and preventing bias, and (4) the adoption of public guidelines for safe and equitable distribution of neurotechnological devices.
Arteriosclerotic and nonarteriosclerotic rats were treated with carbon tetrachloride (CCL4) to induce cirrhosis of the liver. Massive myocardial infarction was then induced in intact and CCL4-treated animals. During acute necrosis (Days 1 thru 3), animals were killed at 4, 8, 12 and 24 h on Days 1 and 2, and during myocardial repair on Days 4, 5 and 8. During the induction of cirrhosis, animals developed polydypsia, polyuria, and hyperglycemia; during myocardial infarction, the arteriosclerotic + cirrhotic animals developed severe and persistent congestive heart failure, i.e., hydrothorax. Adrenal and thymus gland weights and corticosterone levels indicated that cirrhosis per se increased pituitary--adrenal activity, particularly in arteriosclerotic animals. Enzyme levels of SGOT and SGPT demonstrated severe hepatic damage due to cirrhosis and acute myocardial infarction. Blood triglycerides and cholesterol responded abnormally in cirrhotic animals during acute myocardial ischemia due to their entrapment within hepatic cells. The cirrhotic animals manifested poor myocardial repair with persistent foci of necrosis, calcification, and a high incidence of large, occlusive, atrial thrombi. It is suggested that cirrhosis interferes with lipid metabolism and adrenal steroid conjugation leading to abnormal levels of mineralocorticoids which favor congestive heart failure, poor myocardial repair, and atrial thrombosis. 相似文献
Intact and ovariectomized, non-arteriosclerotic female rats and arteriosclerotic, breeder female rats were subjected to myocardial infarction by the administration of 2 subcutaneous injections, 24 hr apart, of the beta-adrenergic stimulator, isoproterenol. The animals were sacrificed at regular hourly intervals following each injection and then on days 4, 6, 8, 10, 12, and 16 thereafter. Measurement of serum insulin and free fatty acids (FFA) demonstrated a blunted response in these metabolic parameters in the case of the ovariectomized virgin rats. The non-arteriosclerotic, intact virgin rats exhibited dynamic changes in serum insulin, glucose, FFA and corticosterone (Cmpd. B) following both isoproterenol injections, whereas the arteriosclerotic breeder rats manifested elevated levels of these parameters on Day 1, but did not display any increases in serum levels, except for FFA, following the second isoproterenol injection on Day 2. In spite of the hormonal alterations brought about by the gonadectomy and their differing metabolic response, the ovariectomized females did not have a mortality rate significantly different from the intact females. Thus, the presence or absence of ovarian estrogens seemingly does not affect the progress of an isoproterenol-induced myocardial infarction. 相似文献
The speed and scale of the COVID-19 pandemic has highlighted the limits of current health systems and the potential promise of non-establishment research such as “DIY” research. We consider one example of how DIY research is responding to the pandemic, discuss the challenges faced by DIY research more generally, and suggest that a “trust architecture” should be developed now to contribute to successful future DIY efforts. 相似文献