儿童精神分裂症的临床分析

目的 探讨儿童精神分裂症的临床特点及预后。方法 选择1990－2000年儿童期发病的精神分裂症患86例（儿童组），并随机选择成人精神分裂症94例（成人组），分别对两组患的一般情况、临床表现、治疗及预后等进行调查、分析。结果 儿童组家族史阳性率明显高于成人组（P＜0．01）；成人组自语、自笑明显多于儿童组（P＜0．05），嫉妒妄想未见于儿童组，其余临床表现、住院时间及预后则无明显差异。结论 儿童精神分裂症有自己的特点，但总体上与成人差别不大。     

药物自我处置和症状自我监控技能训练对预防精神分裂症复发的作用初探

目的探讨药物自我处置和症状自我监控技能训练对降低精神分裂症患者复发和提高其药物依从性的作用.方法将133例痊愈的精神分裂症患者随机分为技能训练组(以下简称训练组;66例)和对照组(67例).对训练组患者分组进行技能训练,共20周,两组均有64例完成1年随访.每月评定1次简明精神病量表(BPRS),每天以自制的监护人及患者药物依从性评分表进行评分;每2个月测定1次氯氮平血浓度.结果(1)入组时与随访末次评定差值的比较,训练组的BPRS总分[(3.3±13.7)分]、漏服药次数[(-0.9±3.0)次]、监护人药物依从性评分[(-53.0±31.2)分]和氯氮平血浓度[(85.5±44.8)ng/ml],均优于对照组,分别为[(-19.2±21.7)分]、[(-9.5±5.9)次]、[(26.5±24.3)分]和[(199.1±85.0)ng/ml],均P＜0.001;(2)训练组的复发率(12%)和再住院率(3%)低于对照组(分别为52%和38%;P＜0.001);(3)Kaplan-Meier生存分析显示,训练组的复发和再住院累计生存率优于对照组(复发的log-rankx2=25.62,再住院的log-rankx2=25.49,均P＜0.001).结论两种技能训练能降低精神分裂症患者的复发并提高其药物依从性.     

社区精神分裂症患者应用重返社会程式训练的一年随访研究

目的探讨重返社会技能训练程式对于社区精神分裂症患者康复的作用.方法将100例非急性期的社区精神分裂症患者随机分为技能训练组(以下简称训练组;50例,其中脱落5例)和对照组(50例,其中脱落2例).在药物治疗的同时,对训练组进行重返社会技能训练,对照组接受传统精神康复干预,对两组患者随访1年.采用阳性和阴性症状量表(PANSS)和Morning Side康复状态量表(MRSS),在干预前、随访第1,3,6,9,12个月时对患者进行评估;同时监测病情复发率、(再)住院率、(再)就业率.结果 (1)入组时与随访末次评分减分值的比较,训练组PANSS总分[(6.80±11.30)分]、阳性量表[(0.51±3.36)分]、阴性量表[(3.14±5.27)分]、一般精神病理量表[(3.14±5.11)分]和MRSS总分[(13.92±21.08)分]均优于对照组[分别为(-4.33±18.35)分、(-2.93±7.16)分、(-1.23±7.27)分、(-0.16±7.97)分和(-10.09±30.93)分],P＜0.05～0.01;(2)训练组的病情复发率(20%)和(再)住院率(2%)低于对照组(分别为40%和19%;P＜0.05);(3)训练组的(再)就业率(51%)高于对照组(23%;P＜0.01).结论在药物治疗的基础上,重返社会程式可以有效地帮助精神分裂症患者尽早地重返社会.     

少年儿童精神分裂症的预后及影响因素分析

目的探讨少年儿童精神分裂症的预后特点及影响预后的主要因素.方法以起病年龄≤16岁为少年儿童组,23～25岁为成人组,采用社会功能缺陷量表(ADSS)、日常生活能力量表(ADL)及自制一般调查表,以随访方式取得资料,采用t检验、x2检验及多因素回归统计分析.结果儿童预后良好率(64.1%)显著高于成人(44.0%),尤其在精细劳动及社会高级功能方面优于成人,经多因素回归分析,影响预后良好的主要因素有家庭社会关爱程度,首次住院疗效(痊愈及显进),急性起病,维持足够治疗时间,病期短.结论少年儿童精神分裂症总体预后较好,充分的家庭社会关爱,首次住院痊愈或显进疗效,急性起病,维持足够的治疗时间,病期较短者,预后更好.     

儿童期情感性精神障碍临床特点的对照研究

目的探讨儿童情感性精神障碍的临床特征.方法将54例符合中国精神疾病分类方案与诊断标准第2版修订本中情感性精神障碍、年龄≤16岁的患者(儿童少年组,以下简称儿少组),与随机抽取的同期住院的53例成年情感性精神障碍患者(成人组)的临床特征进行对照分析.结果儿少组缓慢起病者(50%)多于成人组(23%),发病次数[(3.3±4.2)次]多于成人组[(2.3±1.8)次;x2=6.11～9.05,P＜0.05];儿少组情感性精神障碍的核心症状与成人组无本质区别,其中在联想困难、疑病、自杀观念、自杀行为、疲乏、体重下降、食欲下降方面少于成人组(P＜0.01,P＜0.05),焦虑、激越和学习成绩下降多于成人组(P＜0.01);躁狂症精力充沛、精神运动性兴奋、社会功能受损少于成人组(P＜0.05,P＜0.01);儿少组的抑郁发作者有26%、躁狂发作有66%分别伴有行为问题;儿少组的幻听、牵连观念及怪异行为多于成人组(P＜0.05).结论儿童抑郁症和躁狂症伴有较多的行为问题;儿童与成人的情感性精神障碍可能是起病于不同年龄的同一疾病.     

儿童少年期精神分裂症临床特点

目的：探讨儿童少年期精神分裂症的临床特点。方法：将符合中国精神障碍分类与诊断标准第3版诊断标准的38例儿童少年期精神分裂症患者与随机抽取的同期住我院的52例成人精神分裂症患者进行临床特点的对照分析。结果：儿童组临床误诊率高，思维贫乏、非血统妄想、怪异行为、情感倒错明显多于成人组，而成人组幻听、嫉妒妄想、原发性妄想、焦虑抑郁明显多于儿童组；阳性症状与阴性症状量表(PANSS)评分儿童组一般精神病理分明显高于成人组，阳性症状分成人组明显高于儿童组。结论：儿童少年期精神分裂症有其自身临床特点。     

精神分裂症院内康复措施及其疗效的一年随访

目的　探讨院内康复措施对精神分裂症患者的作用。方法　将 12 4例精神分裂症住院患者随机分为措施干预组和对照组 ,每组各 6 2例。在抗精神病药治疗的同时 ,对干预组施以小组工作制、院内职业康复的两种技能训练 ,共 10周。出院后随访 1年。用简明精神病评定量表 (BPRS)、住院病人护士观察量表 (NOSIE 30 )、社会功能缺陷筛选量表 (SDSS)和就业率等进行评估。结果　 (1)与入组时比较 ,住院期间干预组NOSIE 30各因素的变化值从住院的第 2周开始至第 10周均优于对照组(均P <0 0 1) ,且增分和减分的幅度逐渐增大。 (2 )出院时点与随访最后时点评分差值的比较 ,干预组的SDSS分 [(4 0± 2 7)分 ]、NOSIE 30积极因素分 [(- 2 4 8± 4 9)分 ]和消极因素分 [(8 9± 3 6 )分 ]均显著优于对照组 [分别为 (- 3 9± 1 9)分、(5 2± 5 0 )分和 (- 19 5± 5 9)分 ;均P <0 0 1～P <0 0 0 1];(3)干预组的复发率 (10 %)、再住院率 (3%)和再就业率 (4 1%)皆优于对照组 (分别为 6 9%、5 6 %和 13%,P =0 0 0 0 )。结论　院内康复措施对控制精神分裂症患者的病情、提高社会功能和再就业率 ,以及降低复发率和再住院率具有重要的作用。     

儿童和成人抗N-甲基-D-天冬氨酸受体脑炎的临床特征

目的比较分析儿童和成人抗N-甲基-D-天冬氨酸(N-methyl-D-aspartate,NMDA)受体脑炎在临床表现、辅助检查及免疫治疗等方面的异同。方法纳入34例抗NMDA受体脑炎患者,收集其临床资料,按发病年龄和住院科室分为儿童组和成人组,并对治疗前、后和随访(6个月~24个月)后进行改良Rankin量表(modified Rankin Scale,m RS)评分评估功能恢复结局。结果经分析19例儿童和15例成人的临床资料,儿童组和成人组发生中枢性通气不足分别有1例和10例,成人组中枢性通气不足发生率比儿童组高(P0.05);儿童组和成人组并发继发性癫痫分别为1例和11例,并发癫痫持续状态分别为0例和5例,成人组并发继发性癫痫和癫痫持续状态比儿童组多见(P0.05)。常规脑电图检查中,儿童组中有16例检出"δ"波,成人组有1例,儿童组"δ"波检出率更高(P0.05)。成人组2例女性合并可疑卵巢畸胎瘤;儿童组无合并肿瘤情况。儿童组和成人组免疫治疗方案中最常使用大剂量甲强龙冲击治疗;儿童组(17例)使用静脉用丙种球蛋白冲击治疗比成人组(8例)多见(P0.05);儿童组和成人组使用血浆置换例数比和免疫抑制剂(环磷酰胺)例数比分别为(0:5)和(1:7),成人组使用血浆置换及免疫抑制剂更多见(P0.05)。儿童组和成人组发病至就诊的平均时间分别为(14.47±8.39)d和26d,确诊的平均时间分别为(25.42±14.36)d和(40.13±14.14)d,儿童组发病至就诊、确诊的平均时间短于成人组(P0.05);儿童组有5例住重症监护室(ICU),比成人组(10例)少(P0.05);出院时儿童组和成人组m RS评分分别为(2.26±1.56)分和(3.67±1.59)分,儿童组低于成人组(P0.05)。结论成人抗NMDA受体脑炎临床症状相对复杂,病情较重,短期预后相比儿童差。     

晚发精神分裂症患者局部脑血流及认知功能的研究

目的　探讨晚发精神分裂症患者局部脑血流 (rCBF)及认知功能损害的特点。方法　对2 1例首次发病年龄≥ 5 0岁的精神分裂症患者进行脑单光子发射计算机体层摄影术 (SPECT)检查 ,并采用阳性和阴性症状量表 (PANSS)、简易精神状态量表 (MMSE)、中国修订韦克斯勒成人智力量表、韦克斯勒记忆量表 (WMS)及威斯康星卡片分类测验等进行评定 ,经利培酮 [(2 7± 0 8)mg/d ,2次 /d]治疗 8周后 ,其中 11例患者 (PANSS减分率大于 2 5 % )再次完成上述测定。 2 0名正常人完成SPECT、MMSE及WMS测定。结果　 (1)治疗前患者组左额叶、左顶叶、双侧颞下、双侧基底节及右丘脑 (P <0 0 1)的放射性计数比值 (RAR)低于对照组 (P <0 0 5 ) ,且左额叶RAR (0 85± 0 11)低于右额叶(0 86± 0 10 ;P =0 0 13) ;其MMSE评分 (2 3 33± 4 10 )低于对照组 [(2 8 35± 1 6 3)分 ,P <0 0 1];WMS总分及其大部分测验项目分亦均低于对照组 (P <0 0 1或 0 0 5 )。 (2 )治疗后患者组仅MMSE分[(2 4 73± 4 4 5 )分 ]、WMS的定向因子分 [(3 82± 1 0 8)分 ]和背数因子分 [(5 0 0± 3 4 9)分 ]高于治疗前[分别为 (2 2 4 5± 3 98)分、(3 18± 1 0 8)分和 (2 6 4± 3 88)分 ;P <0 0 5 ],而各脑区rCBF及其余认知功能的变化均无显     

儿童与成人精神分裂症患者住院用药比较

对我院 2 0 0 0～ 2 0 0 2年儿童与成人住院精神分裂症患者应用抗精神病药情况进行比较分析。1　对象和方法为首次住本院精神分裂症患者 ,均符合中国精神疾病分类方案与诊断标准第 2版修订本诊断标准。儿童组 112例 ,男 6 0例 ,女 5 2例 ;住院年龄 7～ 14岁 ,平均 (12 7± 2 5 )岁 ;病程 0 3～ 5 7年 ,平均 (1 9± 1 0 )年 ;住院天数 7～ 188天 ,平均 (86± 35 )天。成人组 112例 ,男 6 8例 ,女 4 4例 ;住院年龄 2 3～ 4 6岁 ,平均 (2 8 2± 6 8)岁 ;病程 0 3～ 7 1年 ,平均(2 4± 1 2 )年 ;住院天数 5～ 2 0 1天 ,平均 (97± 38)天…     

Tau-induced neurodegeneration: mechanisms and targets

The accumulation of hyperphosphorylated tau is a common feature of several dementias. Tau is one of the brain microtubule-associated proteins. Here we discuss tau’s functions in microtubule assembly and stabilization and with regard to its interactions with other proteins. We describe and analyze important post-translational modifications: hyperphosphorylation, ubiquitination, glycation, glycosylation, nitration, polyamination, proteolysis, acetylation, and methylation. We discuss how these post-translational modifications can alter tau’s biological function. We analyze the role of mitochondrial health in neurodegeneration. We propose that microtubules could be a therapeutic target and review different approaches. Finally, we consider whether tau accumulation or its conformational change is related to tau-induced neurodegeneration, and propose a mechanism of neurodegeneration.     

The effect of risperidone on reward‐related brain activity is robust to drug‐induced vascular changes

Dopamine (DA) mediated brain activity is intimately linked to reward‐driven cerebral responses, while aberrant reward processing has been implicated in several psychiatric disorders. fMRI has been a valuable tool in understanding the mechanism by which DA modulators alter reward‐driven responses and how they may exert their therapeutic effect. However, the potential effects of a pharmacological compound on aspects of neurovascular coupling may cloud the interpretability of the BOLD contrast. Here, we assess the effects of risperidone on reward driven BOLD signals produced by reward anticipation and outcome, while attempting to control for potential drug effects on regional cerebral blood flow (CBF) and cerebrovascular reactivity (CVR). Healthy male volunteers (n = 21) each received a single oral dose of either 0.5 mg, 2 mg of risperidone or placebo in a double‐blind, placebo‐controlled, randomised, three‐period cross‐over study design. Participants underwent fMRI scanning while performing the widely used Monetary Incentive Delay (MID) task to assess drug impact on reward function. Measures of CBF (Arterial Spin Labelling) and breath‐hold challenge induced BOLD signal changes (as a proxy for CVR) were also acquired and included as covariates. Risperidone produced divergent, dose‐dependent effects on separate phases of reward processing, even after controlling for potential nonneuronal influences on the BOLD signal. These data suggest the D2 antagonist risperidone has a wide‐ranging influence on DA‐mediated reward function independent of nonneuronal factors. We also illustrate that assessment of potential vascular confounds on the BOLD signal may be advantageous when investigating CNS drug action and advocate for the inclusion of these additional measures into future study designs.     

星形胶质细胞对天冬氨酸特异性半胱氨酸蛋白酶介导β淀粉样蛋白早期突触毒性作用的影响

目的探讨星形胶质细胞(astrocyte,AS)对天冬氨酸特异性半胱氨酸蛋白酶(cysteinyl aspartate specific proteinase,caspase)介导β淀粉样蛋白(β-amyloid,Aβ)早期突触毒性作用的影响,以期为进一步研究与血管性痴呆(vascular dementia,Va D)的发病机制奠定基础。方法以原代培养大鼠海马纯神经元体系(NE-S)及混合培养体系(MIX-S,主要包含神经元及AS)为研究对象,各体系分为6组:对照组、caspase-8抑制剂组、caspase-9抑制剂组、Aβ处理组、caspase-8抑制剂预处理加Aβ组和caspase-9抑制剂预处理加Aβ组。免疫荧光检测各组近胞体10μm段树突中突触后密度蛋白(postsynaptic density-95,PSD95)表达量的变化。结果 1在NE-S与MIX-S中,与对照组相比,caspase-8抑制剂组、caspase-9抑制剂组PSD95的表达量均无明显差异,Aβ处理组PSD95的表达量均显著降低(P均0.001)。2在NE-S中,与Aβ处理组相比,caspase-9抑制剂预处理加Aβ组PSD95的表达量显著回升至对照组水平,caspase-8抑制剂预处理加Aβ组则无显著改变;在MIX-S中的结果则相反,即caspase-8抑制剂预处理加Aβ组PSD95的表达量显著回升至对照组水平,而caspase-9抑制剂预处理加Aβ组则无显著改变。3MIX-S与NE-S两种培养系统间相比较,对照组间及Aβ处理组间PSD95的表达量均无显著差异,而caspase-8抑制剂预处理加Aβ组间及caspase-9抑制剂预处理加Aβ组间PSD95的表达量差异有显著性。结论在Aβ早期突触毒性作用中,AS参与caspase-8介导的死亡受体通路激活过程,且参与抑制神经元的线粒体通路。     

Ultrastructure of non-myelinated neurons during energy deprivation

Summary This paper examines the neuropathology of oxygen-glucose deprivation uncomplicated by stagnant conditions. Rabbit vagus nerves were pulled into asmulti-compartment perfusion chamber, stimulated five times per second and deprived of energy by substituting nitrogen and deoxyglucose for oxygen and glucose in the Locke's perfusate. After incubation the compartments were perfused with gluteraldehyde solution, and the nerves were prepared for electron microscopy. Fixation in the compartments ensured precise cross and longitudinal sections which permitted quantitative comparisons. Although the action potentials ceased in 45 min, 1 h of energy deprivation did not significantly affect the ultrastructure. After 2 h of deprivation the axons were smaller and flattened and microtubules appeared packed together. In the smallest axons the microtubules were gone, the neurofilaments were compacted and the few mitochondria had a dense, homogenous appearance. By 4 h the shrinking was extreme, yet 8% were swollen much larger than any of the controls. Longitudinal views showed these balloned areas were greatly expanded regions of the smallest axons. Both tiny and huge regions were devoid of microtubules and the swollen axons contained expanded mitochondria.Calcium is indirectly implicated in the pathogenesis by the concurrence of mitochondrial alteration as the microtubules disappear coupled with the known role of mitochondria in calcium regulation and the reported effect of high calcium on microtubual dissociation. In is suggested that axons first shrink as osmotially active molecules are used or washed out. After a time without energy the mitochondria can no longer regulate the intracellular calcium, microtubules dissociate, and calcium-activated phospholipases create osmotically active molecules. Finally, high-amplitude, disruptive swelling occurs.Supported, in part, by a Grant-in-aid from the American Heart Association with funds contributed by the American Heart Association, Kansas Affiliate and by the University of Kansas Biomedical Sciences Support Grant RR0737     

Development of 18F-labeled radiotracers for neuroreceptor imaging with positron emission tomography

Positron emission tomography (PET) is an in vivo molecular imaging tool which is widely used in nuclear medicine for early diagnosis and treatment follow-up of many brain diseases. PET uses biomolecules as probes which are labeled with radionuclides of short half-lives, synthesized prior to the imaging studies. These probes are called radiotracers. Fluorine-18 is a radionuclide routinely used in the radiolabeling of neuroreceptor ligands for PET because of its favorable half-life of 109.8 min. The delivery of such radiotracers into the brain provides images of transport, metabolic, and neurotransmission processes on the molecular level. After a short introduction into the principles of PET, this review mainly focuses on the strategy of radiotracer development bridging from basic science to biomedical application. Successful radiotracer design as described here provides molecular probes which not only are useful for imaging of human brain diseases, but also allow molecular neuroreceptor imaging studies in various small-animal models of disease, including genetically-engineered animals. Furthermore, they provide a powerful tool for in vivo pharmacology during the process of pre-clinical drug development to identify new drug targets, to investigate pathophysiology, to discover potential drug candidates, and to evaluate the pharmacokinetics and pharmacodynamics of drugs in vivo.     

Norharman-induced motoric impairment in mice: neurodegeneration and glial activation in substantia nigra

Summary. The β-carboline norharman is present in cooked food and tobacco smoke and show structural resemblance to the neurotoxicant 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. C57BL/6 mice were injected subcutaneously with norharman (3 and 10 mg/kg) twice per day for five consecutive days. Eighteen hours after the last dose an increased expression of glial fibrillary acidic protein and fluoro-jade staining were demonstrated whereas the number of tyrosine hydroxylase positive cells were unchanged in the substantia nigra. Two weeks after the last treatment a decreased motor activity was observed whereas cognitive functions remained intact. In cultured PC12 cells norharman treatment induced mitochondrial dysfunction and increased the number of caspase-3 and TUNEL-positive cells. The results demonstrate that norharman induced apoptosis in cultured cells as well as early neurodegeneration, glial activation and sustained motor deficits in mice and suggest that exposure to norharman may contribute to idiopathic Parkinson’s disease.     

轻型缺血性卒中静脉溶栓后双重抗血小板疗效观察

目的 观察rt-PA静脉溶栓联合双重抗血小板治疗轻型缺血性卒中的有效性及安全性。 方法 以2013年12月-2016年12月在石家庄市第一医院连续住院治疗的轻型缺血性卒中患者为研究 对象,将其随机分为对照组、溶栓+单抗组和溶栓+双抗组。对照组不进行静脉溶栓,长期口服阿 司匹林（100 mg/d）抗血小板治疗;溶栓+单抗组在rt-PA静脉溶栓（0.9 mg/kg,最大剂量90 mg）基 础上长期单用阿司匹林（100 mg/d）抗血小板治疗;溶栓+双抗组在溶栓后单抗基础上加用氯吡格雷 （75 mg/d）双重抗血小板治疗,双抗治疗21 d后改为阿司匹林长期单抗治疗。随访3个月,有效性指标 为3个月时NIHSS 0～1分、Barthel指数（Barthel index,BI）95～100分和mRS 0～1分的比例,3个月时缺 血性卒中的复发率;安全性指标为治疗24 h出血转化和症状性出血转化的发生率。另外比较三组间 基线和3个月时血清hs-CRP和IL-6的水平差异。 结果 研究共纳入85例患者,对照组28例,溶栓+单抗组28例,溶栓+双抗组29例,全部患者均完 成3个月随访,无死亡患者。对照组、溶栓+单抗组和溶栓+双抗组3个月随访时NIHSS 0～1分比例分 别为46.43%、78.57%和93.10%,BI 95～100分比例分别为53.57%、82.14%和89.66%,mRS 0～1分 的比例分别为50.00%、82.14%和93.10%,三组上述有效性指标差异均有统计学意义,两两比较显 示,溶栓+双抗组高于溶栓+单抗组和对照组,溶栓+单抗组高于对照组,差异均有统计学意义;对 照组、溶栓+单抗组和溶栓+双抗组3个月时缺血性卒中复发率分别为32.14%、7.14%和3.45%,差异 有统计学意义。安全性指标方面,三组均无出血转化事件。对照组、溶栓+单抗组和溶栓+双抗组3 个月时的hs-CRP水平分别为11.92±3.58 mg/L、9.04±2.85 mg/L和6.04±2.65 mg/L,IL-6水平分别为 26.18±4.65 ng/L、16.11±6.93 ng/L和12.84±2.57 ng/L,三组上述炎症因子水平差异均有统计学意 义,其中溶栓+双抗组低于溶栓+单抗组和对照组,溶栓+单抗组低于对照组。 结论 对于急性轻型缺血性卒中患者,rt-PA静脉溶栓治疗后短期双重抗血小板治疗可显著改善患 者神经功能,降低炎症因子水平,降低复发率,且不增加出血风险。     

The ENIGMA‐Epilepsy working group: Mapping disease from large data sets

Epilepsy is a common and serious neurological disorder, with many different constituent conditions characterized by their electro clinical, imaging, and genetic features. MRI has been fundamental in advancing our understanding of brain processes in the epilepsies. Smaller‐scale studies have identified many interesting imaging phenomena, with implications both for understanding pathophysiology and improving clinical care. Through the infrastructure and concepts now well‐established by the ENIGMA Consortium, ENIGMA‐Epilepsy was established to strengthen epilepsy neuroscience by greatly increasing sample sizes, leveraging ideas and methods established in other ENIGMA projects, and generating a body of collaborating scientists and clinicians to drive forward robust research. Here we review published, current, and future projects, that include structural MRI, diffusion tensor imaging (DTI), and resting state functional MRI (rsfMRI), and that employ advanced methods including structural covariance, and event‐based modeling analysis. We explore age of onset‐ and duration‐related features, as well as phenomena‐specific work focusing on particular epilepsy syndromes or phenotypes, multimodal analyses focused on understanding the biology of disease progression, and deep learning approaches. We encourage groups who may be interested in participating to make contact to further grow and develop ENIGMA‐Epilepsy.     

缺血性卒中并发2型糖尿病患者颈动脉斑块内新生血管分布特点的超声造影研究

目的 应用超声造影观察缺血性卒中并发2型糖尿病患者颈动脉斑块内新生血管分布情况,明确其 斑块内新生血管分布特征。 方法 病例组选取因急性缺血性卒中住院的糖尿病患者40例（入组前未服用降糖药）,卒中同侧颈 动脉斑块形成;对照组为同期门诊就诊的颈动脉斑块形成患者,无卒中病史,性别及年龄匹配的非 糖尿病患者32例。两组患者行弓上计算机断层扫描血管造影（computed tomography angiography,CTA） 检查排除主动脉弓斑块及颅内动脉病变,排除卵圆孔未闭及心房颤动等。对所有患者均行常规超声 及超声造影检查。常规超声观察斑块厚度及内部回声,超声造影观察斑块增强情况,横切面多角度 观察,将超声造影结果分为近内膜处有增强（代表新生血管）及近内膜处无增强两种。 结果 两组患者颈动脉斑块厚度及回声情况差异无统计学意义。超声造影结果显示病例组颈动脉 斑块近内膜处增强者34例（85%）,对照组近内膜处增强12例（37.5%）,差异有统计学意义（χ 2=17.38, P＜0.01）。 结论 未服用降糖药的2型糖尿病并发急性缺血性卒中的患者颈动脉粥样硬化斑块内近内膜处新生 血管增生多于无糖尿病患者,提示血糖升高与颈动脉斑块内血管新生有关。     

The role of post-translational modifications of huntingtin in the pathogenesis of Huntington’s disease

Post-translational modifications are rapid, effective and reversible ways to regulate protein stability, localization, function, and their interactions with other molecules. Post-translational modifications usually occur as chemical modifications at amino acid residues, including SUMOylation, phosphorylation, palmitoylation, acetylation, etc. These complex biochemical modifications tightly regulate and control a variety of cellular processes. Several forms of post-translational modifications of huntingtin (Htt) have been described. These modifications affect Htt metabolism, protein-protein interactions and cellular toxicity. Cleavage and clearance of mutant Htt, and the interactions between mutant Htt and other cellular proteins are important biochemical events leading to Huntington’s disease (HD). Therefore, identifying signaling pathways of Htt modification and evaluating the significance of Htt modifications would lead to a better understanding of the normal function of wild-type Htt and the pathogenic mechanisms of mutant Htt.