1,771,637 research outputs found
The vanishing author in computer-generated works: a critical analysis of recent Australian case law
No full textAbstract
The use of software is ubiquitous in the creation of many copyright works, yet the requirement in copyright law that every work have a human author who engages in independent intellectual effort means that its use may prevent copyright subsistence. Several recent Australian cases have refocused attention on authorship as an essential criterion of copyright subsistence, and these cases suggest that much computer-produced output may be authorless and thus lack copyright protection. This article, the first in a two-part series, analyses how each case deals with the question of authorship of computer-produced works and why the use of software diminishes copyright protection for a significant number of computer-generated works. The article critiques the application of conventional notions of human authorship developed in the pre-computer age to modern productions and suggests alternative approaches to authorship that satisfy both the major objectives of copyright policy and the need to adapt to the computer age. The article argues that, without a broader judicial approach to authorship of computer-generated works, Parliament must remedy the lacuna in protection for these ‘authorless’ works. Possible solutions for reform are suggested. In a forthcoming article, the author comprehensively examines those reform proposals
MicroRNA-485-5p inhibits glioblastoma progression by suppressing E2F transcription factor 1 under cisplatin treatment
No full textCisplatin (CDDP) has been widely used for glioblastoma treatment. miR-485-5p and E2F transcription factor 1 (E2F1) dysfunction has been reported in glioblastoma. Nonetheless, whether CDDP affects glioblastoma progression via the miR-485-5p-E2F1 axis requires investigation. The expression of miR-485-5p and E2F1 was investigated by quantitative real-time polymerase chain reaction or western blotting in glioblastoma tissues and cell lines. The interaction between miR-485-5p and E2F1 was confirmed using a luciferase assay. The malignancy of glioblastoma was detected using Cell Counting Kit-8, bromodeoxyuridine (BrdU), cell adhesion, flow cytometry, and transwell assays. We identified miR-485-5p downregulation and E2F1 upregulation in glioblastoma, and miR-485-5p inhibited cell growth and elevated cell apoptosis in glioblastoma cells after CDDP treatment. Moreover, miR-485-5p targeting E2F1 repressed cell growth and improved cell apoptosis in glioblastoma cells after CDDP treatment. Our study revealed that CDDP retarded glioblastoma cell development via the miR-485-5p-E2F1 axis, which may be a new direction for glioblastoma therapy.</p
Participant 485 Community Conversations Interview
No full textIn this interview, Participant 485 shares about navigating the COVID-19 pandemic as the parent of an adult child with autism. The participant shares about their child's schooling situation and plans for community-based learning before the pandemic, and explains how the pandemic impacted these plans. They describe that their child seems content with the remote situation and that being at home has relieved a lot of their child's anxiety, but shares that they hope the school will convey health and vaccine information about staff before returning to in-person schooling.New Jersey Department of Healt
Additional file 2 of LINC01224 promotes colorectal cancer progression through targeting miR-485-5p/MYO6 axis
No full textAdditional file 2: Figure S2. Expression analysis of LINC01224, miR-485-5p and MYO6 in CRC patients. (A) GEPIA database showed the overall survival of COAD and READ patients (integrated from TCGA project) with High and Low LINC01224 level. (B) MYO6 level in COAD and READ was predicted via GEPIA with normalization to TCGA normal and GTEx data. Log2FC>1; p-value>0.01. (C, D) Relative miR-485-5p and MYO6 expression was determined via qPCR in CRC and normal control (NC) samples (n = 52). (E) StarBase 3.0 project analyzed the correlation among LINC01224, miR-485-5p and MYO6 levels in CRC patients (integrated from TCGA project). *P < 0.05
Resolución UNRN N°485/2009. Designa docente interina.
No full textFil: Universidad Nacional de Río Negro (U). Universidad Nacional de Río Negro. Río Negro, ArgentinaResolución UNRN N° 485/2009. Designa docente interina.fals
DataSheet_1_LncRNA MALAT1 mediates osteogenic differentiation in osteoporosis by regulating the miR-485-5p/WNT7B axis.zip
No full textIntroductionAccumulating evidence demonstrates that long non-coding RNAs (lncRNAs) are associated with the development of osteoporosis.MethodsThis study aimed to investigate the effects of MALAT1 on osteogenic differentiation and cell apoptosis in osteoporosis. MALAT1 level, detected by RT-qPCR, was downregulated in hindlimb unloading (HU) mice and simulated microgravity (MG)-treated MC3T3-E1 cells. Moreover, osteogenic differentiation-related factor (Bmp4, Col1a1, and Spp1) levels were measured by RT-qPCR and Western blot. ALP activity was detected, and ALP staining was performed. Cell apoptosis was assessed by flow cytometry.ResultsThe results revealed that MALAT1 upregulated the expression of Bmp4, Col1a1, and Spp1, and enhanced ALP activity. Knockdown of MALAT1 suppressed their expression and ALP activity, suggesting that MALAT1 promoted osteogenic differentiation. Additionally, MALAT1 inhibited apoptosis, increased Bax and caspase-3 levels, and decreased Bcl-2 level. However, knockdown of MALAT1 had opposite results. In MG cells, MALAT1 facilitated osteogenic differentiation and suppressed apoptosis. Furthermore, miR-485-5p was identified as a target of MALAT1, and WNT7B was verified as a target of miR-485-5p. Overexpression of miR-485-5p rescued the promotion of osteogenic differentiation and the inhibition of apoptosis induced by MALAT1. Knockdown of WNT7B abolished the facilitation of osteogenic differentiation and the suppression of apoptosis induced by downregulation of miR-485-5p.DiscussionIn conclusion, MALAT1 promoted osteogenic differentiation and inhibited cell apoptosis through the miR-485-5p/WNT7B axis, which suggested that MALAT1 is a potential target to alleviate osteoporosis.</p
DataSheet_2_LncRNA MALAT1 mediates osteogenic differentiation in osteoporosis by regulating the miR-485-5p/WNT7B axis.zip
No full textIntroductionAccumulating evidence demonstrates that long non-coding RNAs (lncRNAs) are associated with the development of osteoporosis.MethodsThis study aimed to investigate the effects of MALAT1 on osteogenic differentiation and cell apoptosis in osteoporosis. MALAT1 level, detected by RT-qPCR, was downregulated in hindlimb unloading (HU) mice and simulated microgravity (MG)-treated MC3T3-E1 cells. Moreover, osteogenic differentiation-related factor (Bmp4, Col1a1, and Spp1) levels were measured by RT-qPCR and Western blot. ALP activity was detected, and ALP staining was performed. Cell apoptosis was assessed by flow cytometry.ResultsThe results revealed that MALAT1 upregulated the expression of Bmp4, Col1a1, and Spp1, and enhanced ALP activity. Knockdown of MALAT1 suppressed their expression and ALP activity, suggesting that MALAT1 promoted osteogenic differentiation. Additionally, MALAT1 inhibited apoptosis, increased Bax and caspase-3 levels, and decreased Bcl-2 level. However, knockdown of MALAT1 had opposite results. In MG cells, MALAT1 facilitated osteogenic differentiation and suppressed apoptosis. Furthermore, miR-485-5p was identified as a target of MALAT1, and WNT7B was verified as a target of miR-485-5p. Overexpression of miR-485-5p rescued the promotion of osteogenic differentiation and the inhibition of apoptosis induced by MALAT1. Knockdown of WNT7B abolished the facilitation of osteogenic differentiation and the suppression of apoptosis induced by downregulation of miR-485-5p.DiscussionIn conclusion, MALAT1 promoted osteogenic differentiation and inhibited cell apoptosis through the miR-485-5p/WNT7B axis, which suggested that MALAT1 is a potential target to alleviate osteoporosis.</p
Additional file 3 of FAM83H-AS1/miR-485-5p/MEF2D axis facilitates proliferation, migration and invasion of hepatocellular carcinoma cells
No full textAdditional file 3: Fig. S3. (A) 10 potential mRNAs which combine with miR-485-5p were predicted through miRWalk database analysis ( http://mirwalk.umm.uni-heidelberg.de/ ). (B) TargetScan database ( http://www.targetscan.org/vert_72/ ) predicted the binding site between MEF2D and miR-485-5p.
Converter USB/RS 485
No full textThis thesis is describing problematic of realisation of converter from USB type media into the universal RS-485 bus which is mainly used for the industrial applications (author is using frequently as a device in order to enable communication between server and RFID devices). This thesis contains theoretical information, realisation of the device itself and assesment of reached targets
Converter USB/RS 485
No full textThis thesis is describing problematic of realisation of converter from USB type media into the universal RS-485 bus which is mainly used for the industrial applications (author is using frequently as a device in order to enable communication between server and RFID devices). This thesis contains theoretical information, realisation of the device itself and assesment of reached targets
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