Young Rat(年輕的老鼠)到底是什麼？
Young Rat 年輕的老鼠 - Methods and Results: Here, we report that systemic administration of serum exosomes from young rats into aged ischemic rats improved short- and long-term functional outcomes after ischemic stroke and reduced synaptic loss. [1] Therefore, our objective was the targeted determination of the lysophospholipidome in young rats fed a standard (ST) or a cafeteria diet (CAF) and submitted to different training intensities to evaluate its potential as a biomarker of a detrimental lifestyle. [2] young rats; ii) a progressive alteration of white matter; iii) a significant reduction of evoked activity in aged animals. [3] Although relatively smaller compared with other sources of variation, there was a statistically significant interactive effect of harvest number and harvest season on SY, with highest SY when harvest occurred during the mid-season or late season in old ratoons and during the mid-season in the case of young ratoons. [4] Young rats exhibited increased expression of pro‐inflammatory cytokines during depletion and repopulation and maintenance of Iba‐1 levels despite reduced microglial number. [5] There was a decrease in cardioprotection in RIPC-subjected old rats in comparison to young rats along with a reduction in the myocardial levels of H2S, CBS, CSE, HIF-1α, and nuclear: cytoplasmic Nrf2 ratio. [6] In this study, miR-130a expression was markedly down-regulated in the hippocampal of aged rats companying with up-regulated expression of Ac-p53 and p21 when compared with young rats. [7] Whether this pathway leads to appetite suppression in young rats is not known. [8] Cholinergic and noradrenergic neuromodulation of the synaptic transmission from cortical layer 6 of the primary somatosensory cortex to neurons in the posteromedial thalamic nucleus (PoM) was studied using an in vitro slice preparation from young rats. [9] In conclusion, GM dysbiosis by transferring the feces from senile osteoporotic rats to young rats could induce osteoporosis. [10] In young rats aged 7–9 weeks, single sc dose of 3–300 nmol/kg AM833 induced a reduction of total and ionized calcium of 40–50% from baseline with lowest level around 12 hours after dosing. [11] The animal experiments demonstrated that a mixture of five isolates effectively hydrolyzed the casein and rice protein and prevented diarrhea in young rats. [12] Treatment of young rats with 1. [13] The effect of hWJ‐MSC injection on young rats is also unknown. [14] However, the tissue lactate/pyruvate ratio (L/P) was three times lower in old rats than in young rats. [15] The aim of this study was to evaluate the physiological and biochemical effects of functional foods: probiotics, prebiotics, and symbiotics in young rats exposed chronically to cigarette smoke. [16] The present study aimed to establish potential interactions between endogenous parathyroid hormone (PTH) and activation of the bone kynurenine (KYN) pathway in relation to bone turnover and strength in young rats after one month (CKD-1) and three months (CKD-3) of experimental CKD. [17] Here, we show that young rats fed ultra-processed food rich in fat and sugar suffer from growth retardation due to lesions in their tibial growth plates. [18] In general, effects in aged rats appeared similar to those in young rats, though less pronounced. [19] In addition, CR could regulate ET-1 expression by inhibiting the activation of NF-κB signaling and activation and induction in the expression of NF-E2-related factor 2 (Nrf2) and histone deacetylase and gene repressor sirtuin 1 (SIRT1), both of which play a central role in mitigating oxidative stress in young rats. [20] OBJECTIVE To investigate the effects of DUSP1 on the hippocampal injury of young rats with epilepsy (EP) through mediating ERK1/2 signaling pathway. [21] No signif i cant dif f erence was observed in young rats, but the indicators of the experimental group were 3. [22] Here we examined the efficacy of selective adenosine A2A receptor inhibitor SCH58261 to combat brain injury, particularly oligodendrocyte (OL) lineage cells, in young rats. [23] GM transplanted from young rats alleviated bone loss in aged rats with senile osteoporosis by improving gut microbiome composition and intestinal barrier function. [24] FN increased the relative number of mitochondria and peroxisomes in the hepatocytes of old, and did not affect their number in young rats. [25] Spectral analysis of heart-rate variability found that the use of rhythmic extreme cold exposures (RECE) with temperature regimens of (–120; –120; –120°С) and (–60; –120; –120°С) significantly increased the body’s adaptive capabilities in young rats due to the activation of their homeostatic regulatory systems. [26] In addition, the acute hypoxia tolerance of young rats was significantly higher than that of adult rats. [27] In young rats, LA may produce up-regulation of pro-survival genes. [28] It was shown that viscosity of hepatocyte plasma and mitochondrial membranes in young rats under optimal vital functions in the area of protein-lipid membrane contacts was significantly lower than in old rats. [29] Normal old rats (20 months) had faster lean mass loss despite greater myofiber regeneration (centronucleation) compared with the young rats (4 months). [30] Photo: Young rat and cat in front of black background. [31] Aging was associated with an increase in intima-to-media thickness, an increase in collagen content, higher caspase-12 mRNA levels, and immunoreactivity compared to young rats. [32] In summary, the mild increase in endogenous PTH, its anabolic PTH1R/ATF4 axis and PTH-dependent alterations in the bone RANKL/OPG system may be one of the possible mechanisms responsible for the favorable impact on bone growth, cross-sectional geometry and strength in young rats with experimental CKD. [33] This study investigated the consequences of ceftriaxone (CTX), an enhancer of glutamate transporter 1 expression, treatment on long-term synaptic potentiation (LTP) in the hippocampus of young rats. [34] Phytoecdysteroids, in particular 20-hydroxyecdysone (20E), increase protein synthesis in C2C12 skeletal muscle cells and muscle strength in young rats. [35] Altogether, our findings were consistent with PTNFL observed in a young rather than a truly paediatric patient. [36] Eight weeks following unilateral brachial plexus injury, sagittal plane shoulder and elbow angles were extracted from gait recordings of young rats (n=18), after which rats were sacrificed for bilateral muscle architecture measurements. [37] Aged rats exhibited a higher myogenic tone than young rats, and the tone was sensitive to the ET A antagonist, BQ-123, but insensitive to the ET B antagonist, BQ-788. [38] The anticipated mechanism of action was examined in young rats, while responses in the target group of elderly patients were evaluated in old rats. [39] In young rats, metabolic pathways were primarily downregulated in response to immobilization (post-synaptic blockade of neuromuscular transmission). [40] In this study, bone marrow MSCs were extracted from aged and young rats and analyzed using high-throughput sequencing and bioinformatics. [41] Here, we established a model detecting initial subtle cognitive changes by comparing the performance of moderately aged Oncins France Strain A Sprague Dawley rats with young rats in the Morris water maze (MWM) and the Open Field (OF) test. [42] We showed that GM1 lessens ketamine-induced apoptosis in the hippocampus and cortex of young rats by regulating the PI3K/AKT/GSK3β pathway. [43] Results Compared to the young rats, old rats displayed a marked reduction in the overall ANS fiber density, affecting both sympathetic and cholinergic compartments, as indicated by dopamine β-hydroxylase (dβh) and vesicular acetylcholine transporter (VaChT) immunohistochemical staining. [44] Aged and young rats underwent 1-h transient middle cerebral artery occlusion (MCAO) to produce cerebral ischemic injury. [45] Our results revealed that even though Rbm20 depletion promoted expression of larger titin isoform and reduced myocardial stiffness in young rats (3 months of age), the established DCM phenotype required more time to embellish. [46] This modification is physiologically higher in the young rat, potentially limiting the therapeutic potential of O-GlcNAc stimulation in young septic rats. [47] Background: The effects of swimming training associated with insulin treatment on the cortical bone health in young rats with severe type 1 diabetes remain unclear, although there is evidence of such effects on the cancellous bone. [48] Old rats had ∼14% shorter fascicle lengths than young rats, which was driven by a ∼10% reduction in SSN, with no difference in sarcomere length (∼4%). [49] ISO had a smaller inhibitory effect on young rats, and SEVO had a smaller inhibitory effect on aged rats. [50]方法和結果：在這裡，我們報告將年輕大鼠的血清外泌體全身給藥到老年缺血性大鼠中可改善缺血性中風後的短期和長期功能結果並減少突觸損失。 [1] 因此，我們的目標是有針對性地測定餵食標準（ST）或自助餐（CAF）並接受不同訓練強度的年輕大鼠的溶血磷脂組，以評估其作為有害生活方式的生物標誌物的潛力。 [2] 幼鼠； ii) 白質逐漸改變； iii) 顯著減少老年動物的誘發活動。 [3] 雖然與其他變異來源相比相對較小，但收穫數量和收穫季節對 SY 的交互影響具有統計學意義，在舊宿根的季節中期或後期收穫時以及在季節中期收穫時，SY 最高。年輕的再生根的情況。 [4] 儘管小膠質細胞數量減少，但年輕大鼠在消耗和再增殖和維持 Iba-1 水平期間表現出促炎細胞因子的表達增加。 [5] 與年輕大鼠相比，接受 RIPC 的老年大鼠的心臟保護作用降低，同時 H2S、CBS、CSE、HIF-1α 和核：細胞質 Nrf2 比率的心肌水平降低。 [6] 在這項研究中，與年輕大鼠相比，老年大鼠海馬中 miR-130a 的表達顯著下調，同時 Ac-p53 和 p21 的表達上調。 [7] 尚不清楚該途徑是否會導致幼鼠食慾抑制。 [8] 使用來自年輕大鼠的體外切片製劑研究了從初級體感皮層的皮質層 6 到後內側丘腦核 (PoM) 中神經元的突觸傳遞的膽鹼能和去甲腎上腺素能神經調節。 [9] 綜上所述，通過將老年骨質疏鬆大鼠的糞便轉移到年輕大鼠的糞便中，轉基因生物失調可誘發骨質疏鬆症。 [10] 在 7-9 週齡的年輕大鼠中，單次皮下劑量 3-300 nmol/kg AM833 誘導總鈣和離子鈣從基線減少 40-50%，給藥後 12 小時左右最低水平。 [11] 動物實驗表明，五種分離物的混合物可有效水解酪蛋白和大米蛋白並預防幼鼠腹瀉。 [12] 用 1. 處理幼鼠。 [13] hWJ-MSC 注射液對年輕大鼠的影響也是未知的。 [14] 然而，老年大鼠的組織乳酸/丙酮酸比率 (L/P) 比年輕大鼠低三倍。 [15] 本研究的目的是評估功能性食品的生理和生化作用：益生菌、益生元和共生元對長期接觸香煙煙霧的幼鼠的影響。 [16] 本研究旨在確定內源性甲狀旁腺激素 (PTH) 與骨犬尿氨酸 (KYN) 通路激活之間的潛在相互作用，這些相互作用與 1 個月 (CKD-1) 和 3 個月 (CKD-3) 後年輕大鼠的骨轉換和強度有關。 ) 的實驗性 CKD。 [17] 在這裡，我們展示了餵食富含脂肪和糖的超加工食品的幼鼠由於脛骨生長板的損傷而出現生長遲緩。 [18] 一般來說，老年大鼠的效果似乎與年輕大鼠相似，但不太明顯。 [19] 此外，CR 可以通過抑制 NF-κB 信號通路的激活和激活和誘導 NF-E2 相關因子 2 (Nrf2) 和組蛋白去乙酰化酶和基因阻遏物 sirtuin 1 (SIRT1) 的表達來調節 ET-1 的表達。其中在減輕年輕大鼠的氧化應激方面起著核心作用。 [20] 客觀的 探討DUSP1通過介導ERK1/2信號通路對癲癇(EP)幼鼠海馬損傷的影響。 [21] 幼鼠未見明顯差異，但實驗組各項指標為3。 [22] 在這裡，我們檢查了選擇性腺苷 A2A 受體抑製劑 SCH58261 在年輕大鼠中對抗腦損傷，特別是少突膠質細胞 (OL) 譜系細胞的功效。 [23] 從年輕大鼠身上移植的轉基因通過改善腸道微生物組組成和腸道屏障功能來減輕老年骨質疏鬆症大鼠的骨質流失。 [24] FN增加了老年大鼠肝細胞中線粒體和過氧化物酶體的相對數量，並且不影響它們在年輕大鼠中的數量。 [25] 心率變異性的光譜分析發現，使用溫度方案為（–120；–120；–120°С）和（–60；–120；–120°С）的有節奏的極冷暴露（RECE）顯著增加由於激活了體內平衡調節系統，年輕大鼠的身體適應能力。 [26] 此外，幼鼠對急性缺氧的耐受性明顯高於成年鼠。 [27] 在年輕大鼠中，LA 可能會產生促生存基因的上調。 [28] 結果表明，在蛋白質-脂質膜接觸區域處於最佳生命功能的年輕大鼠的肝細胞血漿和線粒體膜的粘度明顯低於老年大鼠。 [29] 與年輕大鼠（4 個月）相比，儘管肌纖維再生（中心核化）更大，但正常老年大鼠（20 個月）的瘦體重損失更快。 [30] 照片：黑色背景前的幼鼠和貓。 [31] 與年輕大鼠相比，衰老與內膜到中膜厚度增加、膠原蛋白含量增加、caspase-12 mRNA 水平升高和免疫反應性有關。 [32] 總之，內源性 PTH 的輕度增加、其合成代謝 PTH1R/ATF4 軸和骨 RANKL/OPG 系統中 PTH 依賴性改變可能是對骨生長、橫截面幾何形狀和強度產生有利影響的可能機制之一在患有實驗性 CKD 的年輕大鼠中。 [33] 本研究調查了頭孢曲松 (CTX)（一種穀氨酸轉運蛋白 1 表達增強劑）治療幼鼠海馬中長期突觸增強 (LTP) 的後果。 [34] 植物蛻皮激素，尤其是 20-羥基蛻皮激素 (20E)，可增加 C2C12 骨骼肌細胞中的蛋白質合成和年輕大鼠的肌肉力量。 [35] 總之，我們的研究結果與在年輕而不是真正的兒科患者中觀察到的 PTNFL 一致。 [36] 單側臂叢神經損傷後八週，從年輕大鼠 (n=18) 的步態記錄中提取矢狀平面肩部和肘部角度，然後處死大鼠進行雙側肌肉結構測量。 [37] 老年大鼠比年輕大鼠表現出更高的肌張力，並且張力對 ET A 拮抗劑 BQ-123 敏感，但對 ET B 拮抗劑 BQ-788 不敏感。 [38] 在年輕大鼠中檢查了預期的作用機制，而在老年大鼠中評估了老年患者目標組的反應。 [39] 在年輕大鼠中，代謝途徑主要響應於固定（神經肌肉傳遞的突觸後阻斷）而下調。 [40] 在這項研究中，從老年和年輕大鼠中提取骨髓 MSC，並使用高通量測序和生物信息學進行分析。 [41] 在這裡，我們建立了一個模型，通過比較中年 Oncins France Sprague Dawley 大鼠與年輕大鼠在 Morris 水迷宮 (MWM) 和開放場 (OF) 測試中的表現來檢測初始微妙的認知變化。 [42] 我們發現 GM1 通過調節 PI3K/AKT/GSK3β 通路來減輕氯胺酮誘導的年輕大鼠海馬和皮層細胞凋亡。 [43] 結果 與年輕大鼠相比，老年大鼠的總 ANS 纖維密度顯著降低，影響交感神經和膽鹼能區室，如多巴胺 β-羥化酶 (dβh) 和囊泡乙酰膽鹼轉運蛋白 (VaChT) 免疫組織化學染色所示。 [44] 老年和年輕大鼠經歷 1 小時短暫大腦中動脈閉塞 (MCAO) 以產生腦缺血性損傷。 [45] 我們的研究結果表明，儘管 Rbm20 消耗促進了年輕大鼠（3 個月大）中較大肌聯蛋白異構體的表達並降低了心肌僵硬度，但確定的 DCM 表型需要更多時間來修飾。 [46] 這種修飾在年輕大鼠中在生理上更高，可能會限制 O-GlcNAc 刺激對年輕膿毒症大鼠的治療潛力。 [47] 背景：與胰島素治療相關的游泳訓練對患有嚴重 1 型糖尿病的年輕大鼠皮質骨健康的影響仍不清楚，儘管有證據表明這種影響對鬆質骨有影響。 [48] 老年大鼠的肌束長度比年輕大鼠短 14%，這是由 SSN 減少 10% 驅動的，而肌節長度沒有差異（~4%）。 [49] ISO對年輕大鼠的抑製作用較小，SEVO對老年大鼠的抑製作用較小。 [50]
aged rats compared 老年大鼠比較
In this study, we found that sirtuin 6 (SIRT6) expression was downregulated in the aortae of aged rats compared with those of young rats. [1] The results indicated an increase in the levels of MDA and NO, and also a decline in the levels of GSH and TAC as well as a decrease in the SOD activity in the heart of aged rats compared with young rats. [2] This work was designed to study microscopically the structural changes in the kidney tissue of aged rats compared to young rats. [3]在這項研究中，我們發現與年輕大鼠相比，老年大鼠主動脈中的 sirtuin 6 (SIRT6) 表達下調。 [1] 結果表明，與年輕大鼠相比，老年大鼠心臟MDA和NO水平升高，GSH和TAC水平下降，SOD活性降低。 [2] nan [3]
Old Young Rat 老幼鼠
Materials and Methods Thirty male rats (Rattus norvegicus) were divided in three groups (n = 10 per group)—3-month-old young rats, 12-month-old middle-aged rats, and 18-months-old aged rats. [1] Experimental approach: Thirty-two eight-year-old young rats were classified into five groups, namely, young control, aged control, aged-curcumin, aged-exercise, and aged-curcumin-exercise co-treatment. [2] Two-month-old young rats were set as a reference. [3]材料與方法 30隻雄性大鼠（褐家鼠）被分成三組（每組n = 10只）——3個月大的年輕大鼠、12個月大的中年大鼠和18個月大的老年大鼠。 [1] 實驗方法：將32只8歲幼鼠分為5組，即幼齡對照組、老年對照組、老年薑黃素組、老年運動組和老年薑黃素運動聯合治療組。 [2] nan [3]
Male Young Rat 雄性幼鼠
Methods 130 Wistar male young rats were randomly divided into three groups: Group A (normal control group including 31 rats), group B (epilepsy group including 33 rats), group C (NGF group including 33 rats), group D (FPS-ZM1 group including 33 rats). [1] MATERIAL AND METHODS Pancreatic islets were isolated from male young rats. [2]方法 130只Wistar雄性幼鼠隨機分為3組：A組（正常對照組31只）、B組（癲癇組33只）、C組（NGF組33只）、D組（FPS-ZM1組包括 33 隻大鼠）。 [1] 材料與方法 從雄性幼鼠中分離胰島。 [2]