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目的通过建立完全性睡眠剥夺的幼鼠模型,探讨短期完全性睡眠剥夺对幼鼠体温调节及生长的影响。方法2005-01-03将上海交通大学附属新华医院儿科研究所12只出生后3周刚断奶的雄性幼鼠,随机分为试验组和对照组。采用小站台水环境的方法对幼鼠进行48h的睡眠剥夺。睡眠剥夺前、24h及48h后,分别进行体温、体重及进食量的监测,并计算日能耗,睡眠剥夺结束后处死幼鼠并对重要脏器进行称量。结果实验结果表明48h睡眠剥夺后,两组幼鼠体温均出现随时间变化特点,在睡眠剥夺24h后增高,48h后出现体温下降;睡眠剥夺后试验组幼鼠体重明显低于对照组,而试验组的进食量在48h后明显多于对照组;在日能量消耗的比较中,试验组在24h睡眠剥夺后的能耗明显高于对照组;睡眠剥夺48h后各器官重量仅双肺重量与体重的比值在两组间存在差异。结论幼鼠完全性睡眠剥夺的早期即出现体温显著下降,较早显现体温调节中枢的失衡,并且体格发育受到显著影响。     

间歇性缺氧诱导SD幼鼠遗尿模型的实验研究

目的 利用间歇性缺氧诱导幼年Sprague-Dawley幼鼠,探索建立遗尿模型可行性.方法 20 d雄性SD鼠24只,体重(45±4.7)g,随机分成间歇性缺氧组和对照组,各12只.实验组行间歇性缺氧4周,对照组暴露于空气,于1、2、3、4周及停止缺氧后1周监测.监测内容:①两组幼鼠清醒和睡眠脑电图;②睡眠遗尿及觉醒功能;③清醒排尿次数及性状.结果 ①两组幼鼠睡眠期和清醒期脑电图差异明显,无病理性波形出现;②间歇性缺氧组12只幼鼠因觉醒功能障碍,均发生遗尿,缺氧停止,遗尿消失;对照组觉醒功能正常,0例遗尿(P＜0.05);③第3、4周,间歇性缺氧组清醒排尿次数高于对照组(P＜0.05),有间歇性排尿.结论 SD幼鼠间歇性缺氧后因觉醒障碍发生遗尿,且伴有排尿次数增多和间歇性排尿等症状,符合遗尿儿童临床特征,故利用间歇性缺氧诱导SD幼鼠,建立动物模型基本可行.     

慢性疼痛对幼鼠学习记忆行为及海马Bcl-2 mRNA、脑源性生长因子mRNA的影响

目的观察弗氏完全佐剂(CFA)引起的慢性疼痛对幼鼠空间学习记忆行为及海马Bcl-2mRNA、脑源性生长因子(BDNF)mRNA基因表达的影响,探讨慢性疼痛对幼鼠空间学习记忆能力的影响及作用机制。方法新生SD大鼠60只,随机分为疼痛组和对照组,每组30只。在幼鼠出生后2天,疼痛组左足底皮下注射CFA20μl,对照组注射0·9%生理盐水20μl。分别在出生后10天和21天,每组各取10只处死取海马,采用半定量逆转录聚合酶链反应(RT-PCR)技术检测海马Bcl-2mRNA、BDNFmRNA表达的变化。出生后21天,每组剩余的10只进行Morris水迷宫实验。结果Morris水迷宫实验中,疼痛组幼鼠寻找隐蔽平台的潜伏期较对照组延长(P<0·05);在空间探索实验中,疼痛组幼鼠在平台所在象限游泳的时间和路径比例,均小于对照组(P<0·05)。两组可视平台实验的潜伏期差异无统计学意义(P>0·05)。在出生后10天,疼痛组海马Bcl-2mRNA和BDNFmRNA的表达均小于对照组(P<0·05);在出生后21天,疼痛组与对照组比较差异均无统计学意义。结论CFA引起的慢性疼痛可使幼鼠空间学习记忆能力下降,海马Bcl-2mRNA、BDNFmRNA的改变可能参与了慢性疼痛影响幼鼠学习记忆的机制。     

IUGR大鼠胰岛素样生长因子与小肠及体格发育关系的研究

目的：生后早期的生长主要受营养的调控,营养物质-胰岛素-胰岛素样生长因子(IGF)轴在胎儿宫内发育迟缓(IUGR)生长追赶及胃肠发育中起着重要的作用,而胃肠发育又与营养物质的吸收、生长追赶关系密切。目前国内有关IUGR出生时小肠发育状况报道甚少,且仅限于IUGR出生时胃肠形态结构的观察。该研究探讨生后早期不同蛋白质和热卡水平的营养干预如何调控IGF系统及影响IUGR大鼠的小肠发育和体格生长追赶,并追踪至成年期。方法：采用孕母饥饿法建立IUGR模型。64只IUGR新生鼠随机分为4组：IUGR正常饮食组(SC组),饮食中蛋白含量20%;IUGR高蛋白组(SH组),饮食中蛋白含量占30%;IUGR低蛋白组(SL组),饮食中蛋白含量为10%;IUGR高热卡组(SA组),饮食中热卡较其它组高20%。16只正常新生鼠为正常对照组(C组)予以正常饮食。幼鼠3周断乳后继续予原饮食模式1周,第4周起各组均予正常饮食喂养。分别于出生时及生后第4周、12周测定各组大鼠的血清IGF-1、胰岛素生长因子结合蛋白-3(IGFBP-3)浓度及体重、身长和小肠重量、长度。结果：IUGR大鼠虽然宫内营养不良,但SH组及SA组呈快速小肠发育和体格生长追赶伴IGFs水平明显升高,其中4周时SH组IGFs水平显著高于其余各组(P0.05)。SL组4周和8周的体重、身长、小肠长度和重量均低于其它4组(P0.05)。结论：4周时血清IGF-1是反映生长追赶的灵敏指标,与小肠和体格的生长追赶呈正相关,至成年期这种相关性消失。     

早期营养干预对宫内生长迟缓大鼠胰岛素样生长因子和小肠发育及生长追赶的影响

目的　探讨早期营养干预对宫内生长迟缓 (IUGR)幼鼠血清胰岛素样生长因子 (IGF)和小肠发育及生长追赶的影响。方法　将 2 4只IUGR新生雌鼠和 8只正常新生雌鼠随机分为 4组 :IUGR模型组 ,IUGR低蛋白组 ,IUGR高蛋白组 ,正常对照组。于生后 4周时检测各组大鼠血清IGF1、胰岛素样生长因子结合蛋白 3(IGFBP3)浓度、体重、身长和小肠重量、长度及肠黏膜组织结构变化。结果　 4周时IUGR高蛋白组血IGF1、IGFBP3和小肠黏膜绒毛高度、吸收表面积均显著高于对照组和IUGR模型组 (P <0 .0 5或P <0 .0 1) ;小肠重量、长度和体重、身长与对照组比较无显著性差异 (P均 >0 .0 5 )。结论　生后头 4周予高蛋白饮食早期营养干预IUGR幼鼠 ,可通过促进小肠发育达到满意的体格生长追赶。血清IGF1是反映生长追赶的灵敏指标     

早期营养干预对宫内生长迟缓大鼠小肠发育及体格生长的影响(英文)

目的：了解出生后早期营养干预对宫内生长迟缓 (IUGR)大鼠体格、小肠发育的影响。方法：生后 4周内每周分别测量正常大鼠正常饮食组 (CC) ,IUGR正常饮食组 (IC)、低蛋白饮食组 (IL)及高蛋白饮食组(IH)大鼠体重、身长。并于出生时及第 3,4周测量其小肠长度、重量及肠粘膜双糖酶 (乳糖酶、麦芽糖酶、蔗糖酶 )活力。结果：①IUGR鼠出生时体重、身长、小肠长度及重量均显著小于正常鼠 (P <0 .0 5 ) ;乳糖酶、麦芽糖酶活力高于正常组 (P <0 .0 5 )。②IL组身长、体重、小肠重量及长度生后初 4周均落后于CC ,IC和IH组 (P <0 .0 5 ) ;IH组体格、小肠追赶生长迅速 ,4周时体重与CC组比较差异无显著性 (P >0 .0 5 )。③ 3周时IL ,IH组乳糖酶活力高于CC组 (P <0 .0 5 ) ;4周时IL组蔗糖酶活力小于CC组 (P <0 .0 5 )。结论：生后早期营养干预对IU GR大鼠早期体格追赶生长、小肠发育有重要的影响。     

出生时重量指数与小于胎龄儿预后的关系

按出生时重量指数将211例小于胎龄儿分为低重量指数组、正常组及高重量指数3组,随访新生儿期疾病及生后40周时体格及智能发育情况。结果低重量指数组新生儿窒息、新生儿肺炎及新生儿死亡明显高于其它两组,生后40周时身高、体重、智能评分也高于其它两组,提出分析SGA的预后,既要考虑出生体重,也要考虑体重和身高的综合影响。     

肥胖幼鼠脂肪组织vaspin与胰岛素敏感性的关系

目的：探讨幼年肥胖Sprague-Dawlely（SD）大鼠脂肪组织vaspin含量与胰岛素敏感性的关系。方法：断乳3周SD大鼠24只,随机分为高脂饮食组和普通饮食组,每组12只。成功建模后,测定各组体重、腹围。禁食12 h 后取内眦静脉血测定空腹血糖（FPG）、空腹胰岛素（FINS）;再腹腔注射50%葡萄糖（2 g/kg）,于注射后60 min、120 min再次取内眦静脉血测定各时间点血糖（BG）及胰岛素（INS）。幼鼠处死后将内脏脂肪组织称重。酶联免疫吸附法测定各组幼鼠内脏脂肪组织中vaspin的含量,并对vaspin表达量与各体格测量指标及胰岛素敏感性评价指标进行相关性分析。结果：高脂饮食组大鼠的体重、腹围、内脏脂肪重量、FPG、FINS、120 min INS、vaspin、胰岛素抵抗指数（HOMA-IR）、胰岛素分泌指数（HOMA-β）均高于普通饮食组（P<0.05）,高脂饮食组胰岛素敏感指数（ISI）明显低于普通饮食组（P<0.01）。Vaspin含量与肝脏重量、内脏脂肪重量、腹围、120 min INS、FPG、FINS、HOMA-IR、HOMA-β呈正相关（P<0.05）,而与ISI呈负相关（P<0.05）。结论：幼年肥胖SD大鼠胰岛素抵抗状态与vaspin高水平表达有关,推测vaspin是一种增加胰岛素敏感性、促进胰岛β细胞分泌胰岛素和改善糖耐量的脂肪细胞因子,可能参与了胰岛素抵抗、糖代谢紊乱状态的形成。     

PI3K/Akt 信号通路对新生大鼠缺氧缺血性脑损伤后学习记忆能力的影响

目的：研究PI3K/Akt 信号通路抑制剂 wortmannin 对新生大鼠缺氧缺血性脑损伤（HIBD）后远期学习记忆及认知功能的影响。方法：于制备新生大鼠左脑 HIBD 模型前 30 min,应用脑立体定位仪定位大鼠左侧海马区,注射wortmannin 2 μL,同时建立 HIBD+DMSO 组、HIBD模型组、假手术组及空白对照组。于大鼠 28 日龄时用 Morris水迷宫试验检测各组大鼠的学习记忆能力。结果：随游泳次数增加各组大鼠逃避潜伏期（EL）时间均有不同程度缩短;从第 2 天开始,HIBD+wortmannin 组EL明显长于假手术组和空白对照组 (t=2.637,P=0.023;t=3.585,P=0.003),且随着时间的延长差距逐渐扩大。到第 4 天和第8天时,HIBD+wortmannin 组EL值明显长于其他4组(P<0.05; P<0.01)。而在空间探索试验撤去平台后 120 s 内,HIBD+DMSO组和 HIBD 组的穿越平台次数低于假手术组和空白对照组（P<0.05）,HIBD+wortmannin组的穿越平台次数低于 DMSO+HIBD 组和 HIBD组（P<0.05）, 同时亦明显低于假手术组和空白对照组（P<0.01）。结论：抑制PI3K/Akt信号通路可加重大鼠认知功能障碍,从而影响远期的学习记忆及认知功能。     

0～12个月婴儿体格及精神发育监测与相关因素探讨

目的了解婴儿期体格及精神发育水平和速度,探讨不同喂养方式和出生体重对婴儿发育的影响.方法监测578名婴儿体格及精神发育情况,并对婴儿喂养方式进行调查.结果婴儿体格生长水平和速度低于全国平均水平;3、6个月和12个月精神发育异常检出率分别为1.21%、1.03%和1.33%;完全母乳喂养组婴儿除体重高于混合喂养和人工喂养组外(P＜0.05),其他均无差异;低出生体重婴儿体格、智力发育落后于正常出生体重和巨大儿.结论我市婴儿体格发育水平低于全国平均水平,智力发育异常率与全国接近,喂养方式不再是影响城区婴儿生长发育的主要因素,出生体重对婴儿体格和智力发育均有影响.     

长沙市学龄儿童睡眠不足对智力结构的影响

目的：探讨小学生睡眠不足对智力发育的影响,为有效干预提供科学理论依据。方法：2009 年 6 月至 2010 年 4 月,在长沙市4 个行政区分层随机抽取4所小学10~11岁5年级小学生316名进行调研,了解其不同程度的睡眠不足在中国韦氏儿童智力量表测验上反映的智力结构特点。结果：收回有效问卷286份,应答率90.5%,其中睡眠时间正常（夜间睡眠时间≥8 h,对照组）106人,睡眠不足180人（夜间睡眠时间<8 h,睡眠不足组）。睡眠不足组各项分测验、言语智商、操作智商和总智商得分均显著低于对照组（P<0.05）,语言理解因子和记忆/注意因子得分亦显著低于对照组（P<0.05）。与对照组比较,中度睡眠不足亚组语言智商、总智商及语言理解因子、记忆/注意因子得分降低（P<0.05）;重度睡眠不足亚组各项得分均降低（P<0.05）。睡眠不足组及中度和重度睡眠不足亚组儿童中智力不平衡者的比例显著高于对照组（P<0.05）。结论：睡眠不足对小学生智力发育有不良影响,尤其是对言语智商发育的影响较大,主要发生于中、重度睡眠不足的小学生。     

Influence of 24-hour sleep deprivation on respiration in lambs

The aim of this study was first to examine the effects of 24-h sleep deprivation on apnea index and duration in lambs. The effects on sleep architecture and sigh and swallowing indices were also studied. The impact of postnatal maturation on all measured variables was assessed by studying two different age groups. Twelve lambs (six aged 1-2 d and six aged 23-24 d on the day of surgery) were chronically instrumented for polysomnographic recordings including sleep state assessment, nasal flow, diaphragm electromyogram, and glottal constrictor muscle electromyogram. Two recordings, one control and one after 24-h sleep deprivation, were performed in all lambs. Results show that the effects of sleep deprivation predominate in rapid eye movement sleep in the younger group, with increased rapid eye movement sleep proportion and apnea, sigh, and swallowing index. Our results in lambs suggest that the consequences of sleep deprivation upon respiration are predominant early after birth. Although the potential relationship of these observations to neonatal apneas and sudden infant death syndrome has yet to be defined, awareness of the effects of sleep deprivation is important for neonatal care.     

癫(癎)诱发后CB1受体在睡眠剥夺大鼠海马表达的研究

目的探讨癫痫诱发后大麻素CB1受体在睡眠剥夺大鼠海马的表达变化及其意义。方法50只Sprague-Dawley大鼠随机分为癫痫诱发前和癫痫诱发后2组，每组25只。每组大鼠又随机分为空白对照组（CC），环境对照组（TC）和睡眠剥夺1d、3d、5d组（SD1d、SD3d、SD5d）。用改良多平台睡眠剥夺法建立快速眼球运动（REM）睡眠剥夺模型，戊四氮诱发癫痫。应用RT-PCR方法检测癫痫诱发前后大麻素CB1受体mRNA表达，并电镜观察其海马的超微结构改变。结果SD1d组神经元轻度固缩，染色质轻度边聚，SD3d组神经元凋亡，SD5d组超微结构改变基本同SD3d组。癫痫诱发后发现CC组与TC组大鼠无抽搐，CB1受体mRNA表达较癫痫诱发前明显升高（P〈0．01）。SD1d、SD3d、SD5d组大鼠抽搐严重，CB1受体mRNA表达与癫痫诱发前相比差异无统计学意义（P〉0．05）。结论睡眠剥夺能够造成神经元凋亡，影响大麻素CB1受体mRNA表达。大麻素CB1受体表达增高可能是一种自身稳定调节的保护机制，能抑制癫痫发作。     

Long-term sleep disturbances in children: A cause of neuronal loss

Short-term sleep loss is known to cause temporary difficulties in cognition, behaviour and health but the effects of persistent sleep deprivation on brain development have received little or no attention. Yet, severe sleep disorders that last for years are common in children especially when they have neurodevelopmental disabilities. There is increasing evidence that chronic sleep loss can lead to neuronal and cognitive loss in children although this is generally unrecognized by the medical profession and the public. Without the restorative functions of sleep due to total sleep deprivation, death is inevitable within a few weeks. Chronic sleep disturbances at any age deprive children of healthy environmental exposure which is a prerequisite for cognitive growth more so during critical developmental periods. Sleep loss adversely effects pineal melatonin production which causes disturbance of circadian physiology of cells, organs, neurochemicals, neuroprotective and other metabolic functions. Through various mechanisms sleep loss causes widespread deterioration of neuronal functions, memory and learning, gene expression, neurogenesis and numerous other changes which cause decline in cognition, behaviour and health. When these changes are long-standing, excessive cellular stress develops which may result in widespread neuronal loss. In this review, for the first time, recent research advances obtained from various fields of sleep medicine are integrated in order to show that untreated chronic sleep disorders may lead to impaired brain development, neuronal damage and permanent loss of developmental potentials. Further research is urgently needed because these findings have major implications for the treatment of sleep disorders.     

Feasibility and behavioral effects of an at-home multi-night sleep restriction protocol for adolescents

Background: Sleep deprivation is common among adolescents and has been associated with adverse behavioral and educational outcomes. However, it is difficult to draw strong causal conclusions because of a dearth of experimental sleep research. In part, this appears related to methodological challenges when working with this population. This study tested the feasibility and behavioral effects of a multi‐night, at‐home experimental sleep restriction protocol in a sample of adolescents. Methods: Twenty healthy adolescents aged 13.9–16.9 years were enrolled in a three‐week sleep manipulation protocol using a counterbalanced cross‐over experimental design. The protocol included a baseline week, followed in random order by a short sleep week (Monday–Friday nights limited to 6.5 hours time in bed) and an extended sleep week (10 hours lights‐out time in bed Monday–Friday nights). Sleep was monitored via self‐report and objective actigraphy. These were reviewed with participants and parents on the Saturdays at the end of each week, when parents and participants also completed behavior rating questionnaires. Results: One participant dropped out of the study, but each of the remaining 19 displayed markedly less sleep in the short sleep condition than the extended sleep condition (average nightly gap ～2.5 hours). Data also reflected indirect effects of sleep deprivation that are consistent with an increase in homeostatic sleep drive. Compared to the extended sleep week, parents during the short sleep week reported that the participants displayed significantly greater problems with sleepiness, attention, oppositionality/irritability, behavior regulation, and metacognition. Participant self‐report results were similar, though less robust. Conclusions: A multi‐night, at‐home sleep manipulation protocol for use with adolescents is indeed feasible. This study also provided the first experimental evidence that chronic sleep restriction during adolescence is causally related to a wide range of behavioral deficits.     

Prevention and treatment of sleep deprivation among emergency physicians

Emergency physicians commonly experience sleep deprivation because of the need to work shifts during evening and late night hours. The negative effects of this problem are compounded by job stress and traditional methods of scheduling work shifts. Sleep deprivation may be reduced by schedules designed to lessen interference with normal sleep patterns and circadian rhythms. Pharmacological treatments for sleep deprivation exist in the form of alertness-enhancing agents, caffeine and modafinil. Sleep-promoting agents may also help treat the problem by helping physicians to sleep during daytime hours. Minimizing sleep deprivation may help prevent job burnout and prolong the length of an emergency physician's career.     

Double trouble? The effects of sleep deprivation and chronotype on adolescent affect

Background: Two understudied risk factors that have been linked to emotional difficulties in adolescence are chronotype and sleep deprivation. This study extended past research by using an experimental design to investigate the role of sleep deprivation and chronotype on emotion in adolescents. It was hypothesized that sleep deprivation and an evening chronotype would be associated with decreased positive affect (PA), increased negative affect (NA), and lower positivity ratios. Methods: Forty‐seven healthy adolescents (aged 10–15 for girls, 11–16 for boys) participated in a sleep deprivation and a rested condition. A subsample of 24 adolescents was selected on the basis of extreme morningness or eveningness scores (based on outer quartiles of scores on the Children’s Morningness‐Eveningness Preferences Scale). PA and NA were measured using the Positive and Negative Affect Schedule for Children, and positivity ratios were calculated by dividing PA by NA. Results: Participants reported less positive affect and lower positivity ratios when sleep deprived, relative to when rested. Evening chronotypes reported less positive affect and lower positivity ratios than morning chronotypes in both rested and sleep deprivation conditions. Conclusions: These findings extend previous research by suggesting that adolescents are adversely impacted by sleep deprivation, and that an evening chronotype might serve as a useful marker of emotional vulnerability. Early intervention and prevention strategies can focus on improving sleep and on using chronotherapy principles to reduce eveningness.     

Spontaneous non-nutritive sucking in continuously fed infants

In order to investigate the effects of a deprivation of the nutritive sucking (NS) on the activity of non-nutritive sucking (NNS), we examined 8 infants (ages 1-13 months) continuously fed by intracaval catheter. They had no NS experience at all from birth. Eight age-matched normally fed infants served as controls. The infants were examined for a full 24-h period by polygraphic recordings and behavioural observation. The amount of NNS was computed for the whole 24-h period and separately for each behavioural state (waking, quiet sleep, paradoxical sleep and ambiguous sleep). All the continuously fed infants showed a typical pattern of NNS. There were no differences in amount of NNS between continuously fed and control infants in any behavioural state. These results suggest that NS does not contribute to the long term maintenance of the NNS activity.     

Sleep habits and height at ages 5 to 11.

Shorter durations of slow wave sleep and lower growth hormone responses have been reported in children with short stature caused by psychosocial deprivation. We investigated whether lower total sleep duration was associated with shorter stature in a sample of children taking part in the National Study of Health and Growth. Parental responses to a self administered questionnaire were used to estimate usual times for going to sleep at night and usual times for waking in the morning for 5145 children aged 5 to 11 years of age. After adjusting for the effects of other variables known to be associated with height, it was shown that there was a weak negative association between sleep duration and height. It is concluded that variation in sleep duration between children is unlikely to have an important influence on growth.