Young Brain(年輕的大腦)到底是什麼？
Young Brain 年輕的大腦 - Despite the high incidence of brain injuries in children, we have yet to fully understand the unique vulnerability of a young brain to an injury and key determinants of long-term recovery. [1] Highlights • A longitudinal fixel-based analysis in young brain-injured patients. [2] This is thought to be largely because evolutionary-dependent stimuli are necessary for the appropriate postnatal development of the young brain, an effect sometimes termed the “experience-expectant brain,” with parents providing the necessary input for normative synaptic connections to develop and appropriate neuronal survival to occur. [3] 05) ratios, respectively, in old compared to young brains. [4] However, this activational state may generate substantial toxicity in the young brain after TBI that is partially due to developmentally regulated inadequate antioxidant reserves. [5] ST-NSCs divide rapidly to generate neurons and deplete in the young brain. [6] In brain age prediction models, this correlation can manifest as an overprediction of the age of young brains and an underprediction for elderly ones. [7] Our findings indicated that impairment in the translational regulation of mRNA via N6-methyladenosine methylation is a potential mechanism underlying the effects of anesthesia on neural development in the young brain. [8] Of course, the stories must have entertained me, but their ideas of ef ciency made a major impression on my young brain. [9] Moreover, clasmatodendrosis, an underrecognized astrogliopathy, was found to be significantly increased in the aged brain, but not in the young brain. [10] Systemic administration of anti-VCAM1 antibody or genetic ablation of Vcam1 in BECs counteracts the detrimental effects of plasma from aged individuals on young brains and reverses aging aspects, including microglial reactivity and cognitive deficits, in the brains of aged mice. [11] Additionally, the histology of elderly brains differs from that of young brains. [12] This study demonstrates that stroke causes functional impairment in the hippocampus and recovery of behavioral and synaptic function is more robust in the young brain. [13] ST-NSC divide rapidly to generate neurons and deplete in the young brain. [14] Specifically, infusion of the serum protein albumin into the young brain (mimicking BBB leakiness) induced astrocytic TGFβ signaling and an aged brain phenotype including aberrant electrocorticographic activity, vulnerability to seizures, and cognitive impairment. [15] In summary, while no single variable can alone accurately predict the manifestation of social behavior problems after TBI during early childhood, an increased understanding of how both injury and environmental factors can influence social outcomes provides a useful framework for the development of more effective rehabilitation strategies aiming to optimize recovery for young brain‐injured patients. [16] The effect of age is organ-specific, and the young brain is more permissive for breast cancer metastasis. [17] BACKGROUND Preclinical investigations of the effects of general anesthesia on the young brain show differences in vulnerability of males and females to anesthetic exposure at different times during development. [18] There are critical developmental trajectories in the young brain, whereby injury can lead to long term functional abnormalities. [19] Using biological and synthetic scaffolds to mimic the stiffness of young brains, we find that isolated aged OPCs cultured on these scaffolds are molecularly and functionally rejuvenated. [20] The more prominent psychotic features in younger adults may reflect greater susceptibility of the young brain to exogenous psychosis. [21] These techniques allowed for separation of the twins at an early age and harnessed the regenerative capacity of their young brains. [22] Expressing IGF2b induced divisions in young brains but resulted in incomplete divisions in old brains, stressing the role of cell-intrinsic processes in stem cell behavior. [23] Fluoxetine is the antidepressant with the most favourable benefit:risk ratio profile to treat adolescent depression, but the neural mechanisms underlying antidepressant drugs in the young brain are still poorly understood. [24] We draw the important caveat that relatively little is known about influencing leadership in young brains making this a fertile and exciting, if challenging, area for leader development research. [25] However, although the young brain is presumed to be especially sensitive to environmental influence, to our knowledge only two studies have examined parenting quality with infants as it relates to indicators of brain development, and both were cross-sectional. [26] Specifically, the degree of connectivity of each activated node in the aged brains was significantly lower than those seen in the young brain, and multivariate analyses of all derived network metrics showed distinct clusters of these metrics in young vs. [27] Creative thinking is associated with connectivity between the default and executive control networks in the young brain. [28] The donor was a young brain-dead, male patient from a hospital, 30 minutes away. [29] Conclusion: The type and size of the pre/perinatal lesion in left hemisphere could affect the natural potential of the young brain for reorganization and therefore the clinical outcome. [30] , environmental sounds) is processed and organized in the young brain. [31] We report the first LT recipient who received a whole liver graft from a young brain-dead donor affected with HHT to introduce a broader concept in this field of medicine in which HHT is usually a primary etiology for liver transplant [1–3]. [32]儘管兒童腦損傷的發病率很高，但我們尚未完全了解年輕大腦對損傷的獨特脆弱性以及長期恢復的關鍵決定因素。 [1] 亮點 • 對年輕腦損傷患者的基於縱向固定器的分析。 [2] 這被認為主要是因為進化依賴的刺激對於年輕大腦的適當出生後發育是必要的，這種效應有時被稱為“預期體驗大腦”，父母為規範突觸連接的發育和適當的神經元提供必要的輸入。生存發生。 [3] 05) 分別在老年人與年輕大腦中的比率。 [4] 然而，這種激活狀態可能會在 TBI 後的年輕大腦中產生大量毒性，部分原因是發育調節的抗氧化劑儲備不足。 [5] ST-NSC 迅速分裂以產生神經元並在年輕大腦中耗盡。 [6] 在大腦年齡預測模型中，這種相關性可以表現為對年輕大腦年齡的過度預測和對老年人大腦年齡的低估。 [7] 我們的研究結果表明，通過 N6-甲基腺苷甲基化對 mRNA 翻譯調節的損害是麻醉對年輕大腦神經發育影響的潛在機制。 [8] 當然，這些故事一定讓我很開心，但他們關於效率的想法給我年輕的大腦留下了深刻的印象。 [9] 此外，人們發現在老年大腦中，一種未被充分認識的星形膠質細胞增生症（clasmatodendrosis）顯著增加，而在年輕大腦中則沒有。 [10] 在 BEC 中系統性施用抗 VCAM1 抗體或基因消融 Vcam1 可抵消老年人血漿對年輕大腦的有害影響，並逆轉老年小鼠大腦中的衰老方面，包括小膠質細胞反應性和認知缺陷。 [11] 此外，老年大腦的組織學與年輕大腦的不同。 [12] 這項研究表明，中風會導致海馬體功能障礙，並且行為和突觸功能的恢復在年輕大腦中更為穩健。 [13] ST-NSC 迅速分裂以產生神經元並在年輕大腦中耗盡。 [14] 具體而言，將血清蛋白白蛋白注入年輕大腦（模擬 BBB 滲漏）可誘導星形膠質細胞 TGFβ 信號傳導和老年大腦表型，包括異常的皮層電活動、癲癇發作和認知障礙。 [15] 總之，雖然沒有單一變量可以單獨準確預測兒童早期 TBI 後社會行為問題的表現，但對傷害和環境因素如何影響社會結果的深入了解為製定更有效的康復策略提供了有用的框架，旨在優化年輕腦損傷患者的康復。 [16] 年齡的影響是器官特異性的，年輕的大腦更容易發生乳腺癌轉移。 [17] 背景 全身麻醉對年輕大腦影響的臨床前研究表明，男性和女性在發育過程中的不同時間對麻醉暴露的易感性存在差異。 [18] 在年輕的大腦中有關鍵的發育軌跡，因此損傷會導致長期的功能異常。 [19] 使用生物和合成支架來模擬年輕大腦的剛度，我們發現在這些支架上培養的分離的老化 OPC 在分子和功能上都恢復了活力。 [20] 年輕人中更突出的精神病特徵可能反映了年輕大腦對外源性精神病的更大易感性。 [21] 這些技術允許雙胞胎在很小的時候就分開，並利用了他們年輕大腦的再生能力。 [22] 表達 IGF2b 在年輕大腦中誘導分裂，但在老腦中導致不完全分裂，強調細胞內在過程在幹細胞行為中的作用。 [23] 氟西汀是治療青少年抑鬱症最有利的抗抑鬱藥：風險比概況，但抗抑鬱藥在年輕大腦中的神經機制仍然知之甚少。 [24] 我們提出一個重要的警告，即對影響年輕大腦的領導力知之甚少，這使得它成為領導者發展研究的一個肥沃而令人興奮的領域，即使具有挑戰性。 [25] 然而，儘管年輕的大腦被認為對環境影響特別敏感，但據我們所知，只有兩項研究檢查了嬰兒的育兒質量，因為它與大腦發育指標有關，而且都是橫斷面的。 [26] 具體來說，老年大腦中每個激活節點的連接程度顯著低於年輕大腦中的連接程度，並且對所有派生網絡指標的多變量分析顯示，這些指標在年輕與年輕大腦中具有不同的集群。 [27] 創造性思維與年輕大腦中默認和執行控製網絡之間的連接有關。 [28] 捐贈者是一名年輕的腦死亡男性患者，距離一家醫院有 30 分鐘的路程。 [29] 結論：左半球產前/圍產期病變的類型和大小會影響年輕大腦的自然重組潛力，從而影響臨床結果。 [30] ，環境聲音）在年輕的大腦中進行處理和組織。 [31] 我們報告了第一個接受 HHT 影響的年輕腦死亡供體的全肝移植的 LT 受者，以在該醫學領域引入一個更廣泛的概念，其中 HHT 通常是肝移植的主要病因 [1-3]。 [32]