Subjects: Digital Publishing >> New Media submitted time 2023-10-08 Cooperative journals: 《中国传媒科技》
Abstract：人工智能已经成为世界未来发展的重要技术之一,并成为各国国家战略竞争的主要组成部分。中国、日本、韩国作为东亚国家,在人工智能的政策、人才和伦理、法律与社会问题方面进行了国家层面的布局与探索,积累了经验,查找了差距,为人工智能的发展提供了国际镜鉴。如何破解其存在的矛盾:人工智能人才的短缺,人工智能引发的伦理、法律和社会问题是科技与传媒领域亟待关注与研究的问题。
Subjects: Psychology >> Social Psychology submitted time 2023-03-28 Cooperative journals: 《心理科学进展》
Abstract： Sleep problems may induce fear-related mood disorders such as anxiety, post-traumatic stress disorder (PTSD), and phobias, among others. Studying the cognitive cognitive and neural mechanisms involved in the relationship between sleep problems and fear learning can help enhance the prediction, diagnosis, and treatment of fear-related mood disorders. Previous studies have shown that sleep deprivation affects fear acquisition mainly by inhibiting the activity of the ventral medial prefrontal cortex (vmPFC) and blocking its functional connections with the amygdala, resulting in impaired safe learning that fails to inhibit fear of threatening stimuli, thus enhancing fear acquisition. In contrast, sleep deprivation during the fear memory consolidation phase impairs the activity of the amygdala and hippocampus, thereby impairing fear memory. On the other hand, sleep deprivation during the extinction learning phase results in delayed activation of brain regions associated with extinction learning, which in turn impairs fear extinction memory. Further studies have reported that different stages of sleep have distinct effects on brain regions associated with fear learning; in particular, rapid eye movement (REM) sleep deprivation (insufficient) and complete sleep deprivation have similar effects on the cognitive and neural mechanisms of fear learning. Deprivation of REM sleep suppresses vmPFC activity, enhances amygdala activation, and thus enhances fear acquisition. In addition, reduced functional connectivity in the limbic cortex disrupts fear memory consolidation. Deprivation of REM sleep after extinction learning phase increases amygdala, insula, and dorsal anterior cingulate cortex (dACC) activity and diminishes mPFC, thereby impairing extinction memory. Therefore, after clinical treatment, quality of sleep, particularly REM sleep, should be ensured at night. In addition to reinforcing recently acquired memories, REM sleep is involved in integrating new information into existing knowledge structures, reorganizing these structures, and generalizing recently acquired memories; therefore, improving REM sleep can promote fading retention and generalization. In contrast, the slow-wave sleep (SWS) stage facilitates fear extinction learning through target memory reactivation, which allows the hippocampus to re-code threatening stimuli and accelerate the consolidation of new safety information in the amygdala. During the SWS stage, participants are not conscious and therefore do not have to directly face the threatening stimulus, thus avoiding some of the drawbacks of traditional extinction therapy applied during wakefulness for patients with fear-related mood disorders, such as anxiety disorders and (PTSD). Clinically relevant studies have found that individuals with insomnia also exhibit delayed activation of the fear extinction brain regions, with related activation occurring only during extinction recall. At the same time, individuals with insomnia have stronger learned fear which causes their insomnia and can easily develop into pathological anxiety or PTSD. Furthermore, sleep immediately following exposure therapy can optimize the therapeutic effect and may even promote extinction generalization; therefore, sleep should be used in combination with traditional exposure therapy. Future research should be conducted to further the study of the neural mechanisms by which sleep affects fear generalization and the effect of circadian rhythm disruption on fear extinction, as well as clarifying the problems in the translation of animal sleep studies to human sleep studies.
Subjects: Psychology >> Social Psychology submitted time 2023-03-28 Cooperative journals: 《心理科学进展》
Abstract： Typically developing (TD) infants show an inborn predisposition to pay attention to faces from birth—that TD infants detect more quickly and fixate longer on faces compared with objects. This innate facial attention bias steadily exists in different stimulus situations at different developmental stages, and shows a rapid growth tendency after a short-term decline between the 4th and 6th weeks in the first year of life.The short-term decline may reflect the inhibitory effect of the initial function from the cortical network on the innate sub-cortical system during the critical period wherein TD infants’ visual attention transit from sub-cortical control to cortical control. After this critical transition, with the gradually maturation of the function of the domain-general frontal-parietal attention control cortical network, TD infants’ ability to suppress interference information and selectively pay attention to specific visual targets gradually enhances. Therefore, the role of visual salience in TD infants’ visual attention patterns is gradually declining with increasing age. With the continuous accumulation of face visual experience, the gradually formed face-specific cortical network strengthens TD infants’ preferentially selective response to faces, the role of the social salience on TD infants’ visual attention patterns continues to increase with increasing age. The two factors mentioned before work together to promote facial attention bias in TD infants. Taking the developmental trajectory of TD infants’ facial attention bias as a reference, Autism Spectrum Disorder (ASD) infants possess an initial innate predisposition to facial attention, but they gradually deviate from the normal track during the critical period of facial cortex development, and ultimately exhibit facial attention impairments around 1 year old. After infancy, there exist still disputes with regard to whether ASD individuals show facial attention impairments in simple stimulus arrays, but they exhibit less facial attention in complex social scenes than TD individuals. This is probably due to the fact that congenital perceptual attention impairments cause ASD individuals not to flexibly switch their attention between different stimuli. They are more likely to “lock” or “fixate” their attention on non-social stimuli with more salient perceptual characteristics in the visual environment. At the same time, due to the abnormal function of the social reward system, ASD individuals fail to recognize the social reward value of faces and lack social motivation to pay attention on faces. As a result, the innate predisposition to pay attention to faces cannot be reinforced promptly. For ASD infants at a critical period of facial cortical development, these two impairments both cause atypical early visual perception learning, which reduce the input of facial visual experience and hinder the professional development of face-selective areas. As a result, in the allocation of visual attention resources in ASD individuals, the role of the visual salience fail to decrease with increasing age, while the role of the social salience fail to increase with increasing age. Future research should explore the origin of the congenital predisposition of facial attention in neonates by using genetic methods and near-infrared brain imaging technology, and systematically investigate the influence of perceptual and social characteristics on the development track of face attention in high-risk infants with ASD to identify the potential mechanism of facial attention impairments.
submitted time 2023-03-25 Cooperative journals: 《心理科学进展》
Abstract： Sleep problems may induce fear-related mood disorders such as anxiety, post-traumatic stress disorder (PTSD), and phobias, among others. Studying the cognitive cognitive and neural mechanisms involved in the relationship between sleep problems and fear learning can help enhance the prediction, diagnosis, and treatment of fear-related mood disorders. Previous studies have shown that sleep deprivation affects fear acquisition mainly by inhibiting the activity of the ventral medial prefrontal cortex (vmPFC) and blocking its functional connections with the amygdala, resulting in impaired safe learning that fails to inhibit fear of threatening stimuli, thus enhancing fear acquisition. In contrast, sleep deprivation during the fear memory consolidation phase impairs the activity of the amygdala and hippocampus, thereby impairing fear memory. On the other hand, sleep deprivation during the extinction learning phase results in delayed activation of brain regions associated with extinction learning, which in turn impairs fear extinction memory. Further studies have reported that different stages of sleep have distinct effects on brain regions associated with fear learning; in particular, rapid eye movement (REM) sleep deprivation (insufficient) and complete sleep deprivation have similar effects on the cognitive and neural mechanisms of fear learning. Deprivation of REM sleep suppresses vmPFC activity, enhances amygdala activation, and thus enhances fear acquisition. In addition, reduced functional connectivity in the limbic cortex disrupts fear memory consolidation. Deprivation of REM sleep after extinction learning phase increases amygdala, insula, and dorsal anterior cingulate cortex (dACC) activity and diminishes mPFC, thereby impairing extinction memory. Therefore, after clinical treatment, quality of sleep, particularly REM sleep, should be ensured at night. In addition to reinforcing recently acquired memories, REM sleep is involved in integrating new information into existing knowledge structures, reorganizing these structures, and generalizing recently acquired memories; therefore, improving REM sleep can promote fading retention and generalization. In contrast, the slow-wave sleep (SWS) stage facilitates fear extinction learning through target memory reactivation, which allows the hippocampus to re-code threatening stimuli and accelerate the consolidation of new safety information in the amygdala. During the SWS stage, participants are not conscious and therefore do not have to directly face the threatening stimulus, thus avoiding some of the drawbacks of traditional extinction therapy applied during wakefulness for patients with fear-related mood disorders, such as anxiety disorders and (PTSD). Clinically relevant studies have found that individuals with insomnia also exhibit delayed activation of the fear extinction brain regions, with related activation occurring only during extinction recall. At the same time, individuals with insomnia have stronger learned fear which causes their insomnia and can easily develop into pathological anxiety or PTSD. Furthermore, sleep immediately following exposure therapy can optimize the therapeutic effect and may even promote extinction generalization; therefore, sleep should be used in combination with traditional exposure therapy. Future research should be conducted to further the study of the neural mechanisms by which sleep affects fear generalization and the effect of circadian rhythm disruption on fear extinction, as well as clarifying the problems in the translation of animal sleep studies to human sleep studies.
Subjects: Biology >> Zoology submitted time 2018-12-25 Cooperative journals: 《动物营养学报》
Abstract：本研究旨在探究不同分子质量及不同浓度的壳聚糖对奶牛体外瘤胃发酵参数及甲烷排放的影响。试验选用3头体况相近、健康状况良好、装有永久性瘤胃瘘管的荷斯坦奶牛作为试验动物，用于瘤胃液的采集。试验选择分子质量分别为1 000、3 000和50 000 u的壳聚糖，每种分子质量的壳聚糖再分别以底物0.4%、0.8%及1.6%的浓度添加到底物中，共设9个试验组，另外设1组对照组（不添加壳聚糖），每组4个重复，共重复3个批次。体外发酵24 h后，测定产气量、甲烷产量及瘤胃发酵参数。结果表明：与对照组相比，添加壳聚糖可以使瘤胃发酵液氨态氮浓度显著降低（P<0.05），丙酸浓度显著升高（P<0.05），乙酸/丙酸显著降低(P<0.05)，促进瘤胃发酵模式的改变。浓度为1.6%、分子质量为50 000 u和浓度为0.8%、分子质量为50 000 u的壳聚糖在不影响干物质消化率的基础上使发酵液甲烷产量有降低趋势（P<0.10）。综上，在体外条件下，添加壳聚糖可以有效调节瘤胃微生物发酵状态，综合考虑，浓度为1.6%、分子质量为50 000 u的壳聚糖最为适宜。
Subjects: Biology >> Zoology submitted time 2018-12-24 Cooperative journals: 《动物营养学报》
Abstract：植物提取物是以植物为原料，用化学或者物理的方法，定向获取和浓集植物中的一种或多种有效成分，而不改变其有效成分结构形成的产品。近年来，植物提取物作为一种天然饲料添加剂得到了广泛的关注。植物提取物在反刍动物营养的研究与生产中应用也很广泛。本文结合国内外研究进展，主要从植物提取物对反刍动物的免疫反应、氧化应激以及胰岛素调节3个方面进行了综述。
Subjects: Biology >> Zoology submitted time 2018-12-24 Cooperative journals: 《动物营养学报》
Abstract：壳聚糖是甲壳素脱乙酰基得到一种天然活性产物，具有黏膜黏附力及带有正电荷等特性，可有效促进肠道吸收营养物质和乳腺上皮细胞的增殖和分化，进而对肠道和乳腺组织起到保护作用。饲粮中添加壳聚糖能改变奶牛瘤胃发酵模式和菌群结构，使瘤胃的甲烷产量下降，并可提高奶牛的生产性能和免疫功能。此外，壳聚糖还具有无耐药性、安全、无残留等优点，不仅对奶牛乳房炎的主要致病菌的生长有抑制作用，还可有效地提高乳房炎奶牛的抗氧化能力和促进炎症康复，使其在奶牛生产实践中具有广阔的应用前景。本文主要从壳聚糖在奶牛体内的生物学功能及在生产中的应用研究进展进行综述，对壳聚糖在奶牛生产实践中进一步的应用提供理论支持
Subjects: Biology >> Zoology submitted time 2018-12-24 Cooperative journals: 《动物营养学报》
Abstract：植物提取物不但具有调控反刍动物瘤胃发酵模式、提高氮存留率、减少甲烷排放等功能，而且因其低毒副作用及其所具有的天然性、营养性和生物活性等特性，已成为抗生素的理想替代品之一。本文综述了植物提取物对反刍动物瘤胃发酵调控作用及其机制的最新研究进展，以期对今后该领域的研究及产品研发提供参考依据。
Subjects: Biology >> Zoology submitted time 2018-12-20 Cooperative journals: 《动物营养学报》
Abstract：本研究旨在对北京市周边地区奶牛场的玉米青贮饲料中干物质（DM）和中性洗涤纤维（NDF）的瘤胃降解特性进行对比分析。以3头安装永久性瘤胃瘘管的健康荷斯坦奶牛为试验动物，通过尼龙袋法测定昌平区、延庆区和房山区3个区，每个区3个奶牛场的玉米青贮饲料中DM和NDF的72 h瘤胃降解率及瘤胃降解参数。结果显示：1）房山区奶牛场的玉米青贮饲料中DM含量平均值最高，但NDF和酸性洗涤纤维（ADF）含量的平均值最低，昌平区和延庆区的奶牛场DM含量平均值相近，延庆区奶牛场的ADF含量平均值最高，昌平区奶牛场的NDF含量平均值最高。2）昌平区2号奶牛场玉米青贮饲料的DM有效降解率最高，达到了38.47%；房山区3号奶牛场玉米青贮饲料的DM有效降解率最低，仅为28.91%；二者之间差异显著（P<0.05）。3）NDF的有效瘤胃降解率以延庆区1号奶牛场最高,达到了30.18%，而最低的房山区2号奶牛场只有19.63%，二者之间差异显著（P<0.05）。由此可见，北京市周边地区不同奶牛场的玉米青贮饲料在奶牛瘤胃中的降解特性差异较大，应根据奶牛不同生长发育及泌乳阶段的营养需要，结合实际营养成分，合理配比饲粮
Subjects: Biology >> Zoology submitted time 2018-12-20 Cooperative journals: 《动物营养学报》
Abstract：本试验旨在通过体外培养法研究葡萄籽原花青素对奶牛瘤胃发酵参数及微生物区系的影响。试验分为6组，以500 g精粗比为40∶60的全混合日粮为发酵底物，各组分别添加0（对照）、0.1、0.2、0.3、0.4、0.5 g/kg的葡萄籽原花青素。体外发酵24 h后，读取产气量及测定瘤胃发酵参数和微生物含量。结果表明，与对照组相比：1）添加0.4和0.5 g/kg的葡萄籽原花青素显著降低了发酵液丁酸和异戊酸的含量（P<0.05），而添加0.2 g/kg的葡萄籽原花青素显著提高了发酵液异丁酸的含量（P<0.05）；2）添加不同水平的葡萄籽原花青素均显著提高了发酵液pH（P<0.05）；3）添加不同水平的葡萄籽原花青素有减少体外发酵产气量的作用，其中0.3 g/kg组效果显著（P<0.05），而0.2 g/kg组显著降低了甲烷产量（P<0.05）；4）葡萄籽原花青素能显著降低了发酵液中的原虫（0.2、0.3、0.4、0.5 g/kg组）、甲烷菌（0.1、0.2、0.4、0.5 g/kg组）、溶纤维丁酸弧菌（0.2、0.3、0.4、0.5 g/kg组）和产琥珀酸丝状杆菌含量（0.1、0.3、0.4、0.5 g/kg组）（P<0.05）。由此可见，在奶牛瘤胃体外发酵液中添加葡萄籽原花青素改善了瘤胃发酵模式，显著影响了瘤胃微生物区系，显著降低了甲烷产量，0.2 g/kg的添加水平较为适宜。
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