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  1. Oct 2022
  2. Sep 2022
    1. Can copyright vest in an AI? The primary objective of intellectual property law is to protect the rights of the creators of intellectual property.10 Copyright laws specifically aim to: (i) promote creativity and encourage authors, composers, artists and designers to create original works by affording them the exclusive right to exploit such work for monetary gain for a limited period; and (ii) protect the creators of the original works from unauthorised reproduction or exploitation of those works.

      Can copyright vest in an AI?

      The primary objective of intellectual property law is to protect the rights of the creators of intellectual property.10 Copyright laws specifically aim to: (i) promote creativity and encourage authors, composers, artists and designers to create original works by affording them the exclusive right to exploit such work for monetary gain for a limited period; and (ii) protect the creators of the original works from unauthorised reproduction or exploitation of those works.

    1. To my knowledge, conferring copyright in works generated by artificial intelligence has never been specifically prohibited. However, there are indications that the laws of many countries are not amenable to non-human copyright. In the United States, for example, the Copyright Office has declared that it will “register an original work of authorship, provided that the work was created by a human being.” This stance flows from case law (e.g. Feist Publications v Rural Telephone Service Company, Inc. 499 U.S. 340 (1991)) which specifies that copyright law only protects “the fruits of intellectual labor” that “are founded in the creative powers of the mind.” Similarly, in a recent Australian case (Acohs Pty Ltd v Ucorp Pty Ltd), a court declared that a work generated with the intervention of a computer could not be protected by copyright because it was not produced by a human.

      To my knowledge, conferring copyright in works generated by artificial intelligence has never been specifically prohibited. However, there are indications that the laws of many countries are not amenable to non-human copyright. In the United States, for example, the Copyright Office has declared that it will “register an original work of authorship, provided that the work was created by a human being.” This stance flows from case law (e.g. Feist Publications v Rural Telephone Service Company, Inc. 499 U.S. 340 (1991)) which specifies that copyright law only protects “the fruits of intellectual labor” that “are founded in the creative powers of the mind.” Similarly, in a recent Australian case (Acohs Pty Ltd v Ucorp Pty Ltd), a court declared that a work generated with the intervention of a computer could not be protected by copyright because it was not produced by a human.

    1. With the advent of AI software, computers — not monkeys — will potentially create millions of original works that may then be protected by copyright, under current law, for more than 100 years.

      With the advent of AI software, computers — not monkeys — will potentially create millions of original works that may then be protected by copyright, under current law, for more than 100 years.

    1. Jul 3, 2016 — Effective contingency planning addresses the causes and consequences of EHR unavailability, and involves processes and preparations that can ...

      Contingency Planning - HealthIT.govhttps://www.healthit.gov › files › safer › guides PDF Jul 3, 2016 — Effective contingency planning addresses the causes and consequences of EHR unavailability, and involves processes and preparations that can ...

  3. Aug 2022
    1. Developmental cell death eliminates half of the neurons initially generated in the mammalian brain, and occurs perinatally in many species. It is possible that the timing of neuronal cell death is developmentally programmed, and only coincidentally associated with birth. Alternatively, birth may play a role in shaping cell death. To test these competing hypotheses, we experimentally advanced or delayed birth by 1 d in mice (within the normal range of gestation for the species) and examined effects on the temporal pattern and magnitude (amount) of neuronal cell death, using immunohistochemical detection of activated caspase-3 as a cell death marker. In order to detect effects of subtle changes in birth timing, we focused on brain areas that exhibit sharp postnatal peaks in cell death. We find that advancing birth advances peak cell death, supporting the hypothesis that birth triggers cell death. However, a delay of birth does not delay cell death. Thus, birth can advance cell death, but if postponed, a developmental program governs. Advancing or delaying birth also caused region-specific changes in the overall magnitude of cell death. Our findings shed light on the long-standing question of what controls the timing and magnitude of developmental neuronal cell death, and position birth as an orchestrator of brain development. Because humans across the world now routinely alter birth timing, these findings may have implications for current obstetric practices.
    1. This means that neurons in small children are prepared to commit suicide through apoptosis if they are not used. In the case of a crisis, such as lack of oxygen, the apoptosis program starts up and the cells die and disappear. Instead of being treated with adult drugs, newborn infants must be given treatment specifically designed for them, but research on newborn infants involves many special difficulties and unique infant medicines with low-frequency use are not interesting for pharmaceutical companies.
    1. Neuronal cell death occurs extensively during development and pathology, where it is especially important because of the limited capacity of adult neurons to proliferate or be replaced. The concept of cell death used to be simple as there were just two or three types, so we just had to work out which type was involved in our particular pathology and then block it. However, we now know that there are at least a dozen ways for neurons to die, that blocking a particular mechanism of cell death may not prevent the cell from dying, and that non-neuronal cells also contribute to neuronal death. We review here the mechanisms of neuronal death by intrinsic and extrinsic apoptosis, oncosis, necroptosis, parthanatos, ferroptosis, sarmoptosis, autophagic cell death, autosis, autolysis, paraptosis, pyroptosis, phagoptosis, and mitochondrial permeability transition. We next explore the mechanisms of neuronal death during development, and those induced by axotomy, aberrant cell-cycle reentry, glutamate (excitoxicity and oxytosis), loss of connected neurons, aggregated proteins and the unfolded protein response, oxidants, inflammation, and microglia. We then reassess which forms of cell death occur in stroke and Alzheimer’s disease, two of the most important pathologies involving neuronal cell death. We also discuss why it has been so difficult to pinpoint the type of neuronal death involved, if and why the mechanism of neuronal death matters, the molecular overlap and interplay between death subroutines, and the therapeutic implications of these multiple overlapping forms of neuronal death.
    1. 5-Hydroxytryptophan (5-HTP), a precursor of serotonin, is therapeutically used for several psychiatric disorders such as anxiety and depression in the clinic. However, severe side effects, including abnormal mental functions, behavioral disturbances and intolerance are associated with this treatment. 5-HTP-induced elevation of plasma and brain serotonin levels may affect blood-brain barrier (BBB) breakdown, edema formation and regional cerebral blood flow (CBF) disturbances. Breakdown of BBB to serum proteins leads to vasogenic brain edema formation and cellular injuries. However, 5-HTP-neurotoxicity is still not well known. In this investigations 5-HTP induced elevation of endogenous plasma and brain serotonin levels and its effect on BBB breakdown, edema formation neuronal injuries was examined in a rat model. Furthermore, potential role of oxidative stress and nitric oxide (NO) was evaluated. In addition, several neurochemical agents such as p-CPA (5-HT synthesis inhibitor) indomethacin (prostaglandin synthase inhibitor), diazepam (ant stress drug), cyproheptadine, ketanserin (5-HT2 receptor antagonists) and vinblastine (inhibitor of microtubule function) were examined on 5-HT neurotoxicity. Our observations suggest that 4 h after 5-HTP administrations, the endogenous serotonin levels increased by fourfold (150 mg/kg) in the plasma and brain associated with profound hyperthermia (+ 3.86 ± 0.24 °C, oxidative stress and NO upregulation. Breakdown of the BBB to Evans blue albumin (EBA) in 8 brain regions and to [131]Iodine in 14 brain regions was observed. The CBF exhibited marked reduction in all the brain regions examined. Brain edema and cellular injuries are present in the areas associated with BBB disruption. Drug treatments reduced the BBB breakdown, edema formation NO production and brain pathology. These observations are the first to point out that 5-HTP-neurotoxicity caused by BBB breakdown, edema formation and NO production is instrumental in causing adverse mental and behavioral abnormalities, not reported earlier.View chapterPurchase bookRead full chapterURL: https://www.sciencedirect.com/science/article/pii/S007477421930025X
    1. L-tryptophan Availability and Brain Serotonergic Activity In serotonergic neurons Trp serves as the precursor for 5-HT. The 5-HT metabolic pathway is initiated by Trp being hydroxylated to the intermediate 5-hydroxytryptophan (5-HTP), which is subsequently decarboxylated to become 5-HT. Tissue levels of 5-HTP are usually low since this substance is rapidly decaroxylated by the enzyme aromatic amino acid decarboxylase [for review see (21)]. Thus, the rate limiting step in the biosynthesis of 5-HT is the hydroxylation of Trp which is catalyzed by the enzyme tryptophan hydroxylase (TPH) (Figure 1). This enzyme is specific for 5-HT producing cells, however, it is present in two different isoforms, TPH1 and TPH2 [reviewed in (22, 23)].

      5-htp metabolic pathwayIn serotonergic neurons Trp serves as the precursor for 5-HT. The 5-HT metabolic pathway is initiated by Trp being hydroxylated to the intermediate 5-hydroxytryptophan (5-HTP), which is subsequently decarboxylated to become 5-HT.

    1. The potential for digital technology to support learners in this process was highlighted in the studies reviewed, but commonly learners lacked the competence to use digital technologies for educational purposes. Learners often required support, especially with the planning and reviewing aspects of self-directed learning, as well as guidance regarding how digital technologies can be used effectively for educational purposes. Importantly, studies that focus on understanding the facilitation of self-directed learning in childhood education are seldom. Further studies on self-directed learning in childhood education are vital – given that this is a fundamental competence for preparing our youth to deal with work and life in our rapidly changing world.

      Learners often required support, especially with the planning and reviewing aspects of self-directed learning, as well as guidance regarding how digital technologies can be used effectively for educational purposes. Importantly, studies that ..

  4. Jul 2022
    1. by V Raghupathi · 2020 · Cited by 78 — Some evidence suggests that education is strongly linked to health determinants such as preventative care [9]. Education helps promote and ...benefits of education on healthnegative effects of education on healthimpact of education on health pdfimpact of education on lifehealth and educationhow does education affect mental healthPeople also search for
    1. Dec 13, 2021 — I want to talk about how open source has in the most cases, been turned into exploitation by the biggest organisations in the world.exploiting meaningwhat is an exploit in computer securityit exploit definition owaspexploit vs vulnerabilityexploit in cyber security exampletypes of exploitsPeople also search for
    1. Jun 6, 2018 — Microsoft's $7.5 billion acquisition of GitHub is a perfect illustration of how value is ascribed differently in Silicon Valley than in the ...github microsoft acquisitionwhy did microsoft buy githubwhy did microsoft buy github redditmicrosoft github strategygithub revenuewho owned github before microsoftPeople also search for

      Jun 6, 2018 — Microsoft's $7.5 billion acquisition of GitHub is a perfect illustration of how value is ascribed differently in Silicon Valley than in the ...

  5. Jun 2022
    1. FAANG is an acronym of five major technology stocks that include Facebook (now Meta), Amazon, Apple, Netflix, and Google (now Alphabet). Jim Cramer coined the term in 2013 while giving accolades to the companies for being the dominant companies in their niches.
    1. That means many investors already have at least some exposure to them. Because the heavy weighting of FAANG stocks in indexes such as the S&P 500 gives them an outsize impact on the broader stock market, it’s worthwhile for investors to learn a bit more about them.
    1. In finance, “FAANG” is an acronym that refers to the stocks of five prominent American technology companies: Meta (META) (formerly known as Facebook), Amazon (AMZN), Apple (AAPL), Netflix (NFLX); and Alphabet (GOOG) (formerly known as Google).