New stand magnifiers do not meet rated levels of performance

A new range of stand magnifiers has been released by the COIL company in the United Kingdom. Examination of these magnifiers reveals that they fail to deliver the rated magnifications labelled prominently on the appliances, as a result of the manufacturer's conformance with the requirements of the German DIN standard and the use of back vertex power (F'_v) rather than equivalent dioptric power (F_m) of the magnifier. In this study we provide information on the optometric parameters of these new stand magnifiers that will assist the more accurate specification of improvements in vision expected from their use.     

儿茶酚-邻-甲基转移酶基因多态性与强迫症

目的：探索儿茶酚-邻-甲基转移酶(COMT)基因多态性同强迫症临床特征的关系。方法：采用聚合酶链反应扩增技术与限制性片段长度多态(PCR-RFLP)测定120例强迫症(OCD)患者和130例健康对照者的基因型；根据Yale-Brown强迫量表评分将强迫症划分亚型。结果：强迫症患者COMT基因型与等位基因分布与健康对照者之间无显著差异；强迫行为组与强迫思想组的COMT基因型分布存在差异；G／A基因型多见于强迫行为组。结论：COMT基因多态可能对强迫症的发病没有直接的作用，但G／A基因型可能对症状是否表现为强迫动作有一定的影响。     

EVOKED POTENTIALS OF OBSESSIVE-COMPULSIVE DISORDER： STATE OR TRAIT MARKER

Objective To investigate the status of evoked potentials in obsessive-compulsive disorder(OCD). Methods Evoked potentials P300, auditory brainstem response (ABR) and visual evoked potential ( VEP) were recorded from 35 OCD patients and 28 normal controls (NC) with a Nicolet Spirit Instrument. 23 of the OCD patients were followed up after 5 months with the same markers. Results Compared with NC, OCD patients showed decreased P3 of P300 amplitude (OCD group 3. 5 ±1. 6μv vs. NC group 5.9 ±2. 1μv, P <0. 01), delayed V latency (6.4±0. 4ms vs. 5. 5 ±0. 3ms, P <0. 01) and increased V amplitude(0. 35±0. 1μv vs. 0. 16 ±0.09μv, P <0. 05) of ABR and delayed P2 of VEP latency (199±39ms vs. 183±28ms, P <0. 05). The follow-up measures of evoked potentials suggested that decreased P3 of P300 amplitude and delayed P2 of VEP latency might be state markers of OCD, while decreased V amplitude and delayed V of ABR latency might be trait markers of OCD. Conclusion The changes of P300 and VEP are related to clini     

流式细胞光度术在鼻咽癌上皮样细胞株细胞周期动力学研究中的应用

本实验应用流式细胞光度术研究鼻咽癌上皮样细胞株（ＣＮＥ）的细胞周期动力学。结果发现ＣＮＥ细胞仍保持原代细胞的ＤＮＡ含量水平（超三倍体和亚四倍体），随着细胞接种时间的延长细胞周期中Ｇ０／Ｇ１时相细胞的百分数逐渐升高，而Ｓ％和Ｇ２＋Ｍ％则逐渐降低。该项研究还发现随着孵育时间的延长，细胞周期中各时相细胞的运动均逐渐延缓，其中以Ｇ０／Ｇ１和Ｇ２＋Ｍ时相细胞的运动减慢较为明显。     

Graves病的发病与社会心理因素

对１０７例甲状腺机能亢进症患者和９１名正常人采用艾森克个性问卷及自编社会环境的调查显示：４６．９４％的患者起病前有负性生活事件发生，个性特征甲亢组神经不稳定型及掩饰性评分显著高于正常组，有显著性差异，此结果提示甲亢患者存在明显个性缺陷和负性生活事件，这些因素可作为甲亢发病的一种诱因。     

成年男性舌下神经在舌根部的定位研究

目的:探讨成年男性舌根部舌下神经解剖走行特点,指导临床舌根部射频温控减容术治疗阻塞性睡眠呼吸暂停低通气综合征(OSAHS)时针形电极刺入舌根部的部位及深度,以避免损伤舌下神经。方法:选择10具成年男性的舌标本,定型后在冰冻状态下作冠状切面,通过计算机图像处理与测量系统行舌下神经定位测量,并进行相关的统计学分析。结果:(1)两侧舌下神经呈对称性分布。(2)成年男性舌下神经舌内部分的主干(本实验为舌盲孔前后15mm范围内)其垂直向解剖走行基本恒定,距舌表面(22.21±2.22)mm;水平向走行中,舌盲孔后一般位于舌中内(近中线侧)(28.61±2.66)％处,舌肓孔前为(21.89±1.93)％处。结论:本实验为舌根部射频温控减容术治疗OSAHS提供了一个相对安全的范围:在不超过(22.21±2.22)mm深度且舌盲孔后避开中内(近中线侧)(28.61±2.66)％区域、舌盲孔前避开中(内近中线侧)(21.89±1.93)％区域,基本不会损伤舌下神经。     

手法复位石膏外固定治疗Barton骨折

Barton骨折是桡骨远端背侧、掌侧缘骨折,合并腕的半脱位,是一种较少见的关节内骨折。自1998年以来对21例Barton骨折患者采用闭合手法整复、石膏夹板外固定治疗,经随访观察,疗效满意。     

对比因素对儿童分辨物体细节能力的影响

目的观察对比因素对儿童分辨物体细节能力的影响,了解儿童对比视力的状况。方法使用对比视力表,测量53名裸眼视力≥5.0的正常儿童92%,52%,30%对比水平处的对比视力。结果儿童的对比视力随对比度的降低而显著下降,对比度与视力之间存在显著相关;左、右眼的对比视力差异无统计学意义;男性和女性的对比视力差异无统计学意义。结论低对比的学习环境会增加儿童视觉负荷,在防治学生近视过程中应引起重视。     

Quantitation of muscle glycogen synthesis in normal subjects and subjects with non-insulin-dependent diabetes by 13C nuclear magnetic resonance spectroscopy

To examine the extent to which the defect in insulin action in subjects with non-insulin-dependent diabetes mellitus (NIDDM) can be accounted for by impairment of muscle glycogen synthesis, we performed combined hyperglycemic-hyperinsulinemic clamp studies with [13C]glucose in five subjects with NIDDM and in six age- and weight-matched healthy subjects. The rate of incorporation of intravenously infused [1-13C]glucose into muscle glycogen was measured directly in the gastrocnemius muscle by means of a nuclear magnetic resonance (NMR) spectrometer with a 15.5-minute time resolution and a 13C surface coil. The steady-state plasma concentrations of insulin (approximately 400 pmol per liter) and glucose (approximately 10 mmol per liter) were similar in both study groups. The mean (+/- SE) rate of glycogen synthesis, as determined by 13C NMR, was 78 +/- 28 and 183 +/- 39 mumol-glucosyl units per kilogram of muscle tissue (wet weight) per minute in the diabetic and normal subjects, respectively (P less than 0.05). The mean glucose uptake was markedly reduced in the diabetic (30 +/- 4 mumol per kilogram per minute) as compared with the normal subjects (51 +/- 3 mumol per kilogram per minute; P less than 0.005). The mean rate of nonoxidative glucose metabolism was 22 +/- 4 mumol per kilogram per minute in the diabetic subjects and 42 +/- 4 mumol per kilogram per minute in the normal subjects (P less than 0.005). When these rates are extrapolated to apply to the whole body, the synthesis of muscle glycogen would account for most of the total-body glucose uptake and all of the nonoxidative glucose metabolism in both normal and diabetic subjects. We conclude that muscle glycogen synthesis is the principal pathway of glucose disposal in both normal and diabetic subjects and that defects in muscle glycogen synthesis have a dominant role in the insulin resistance that occurs in persons with NIDDM.     

Creutzfeldt-Jakob disease (CJD) with a mutation at codon 148 of prion protein gene: relationship with sporadic CJD

Creutzfeldt-Jakob disease (CJD), the most common human prion disease, includes sporadic (s) and familial (f) forms. Regardless of etiology, both forms are thought to share the pathogenic mechanism whereby the cellular prion protein (PrP(C)) converts into its pathogenic isoform (PrP(Sc)). While PrP(C) conversion is thought to be random in sCJD, conversion in fCJD is facilitated by the congenital presence of mutated PrP. Differences in PrP genotype (PRNP) and in conversion circumstances lead to PrP(Sc) with distinct characteristics that elicit different disease phenotypes. Here, we describe a case of fCJD with a substitution of histidine (H) for arginine (R) at codon 148 (R148H) and heterozygosity of the methionine/valine (M/V) polymorphic codon 129, with the 129M allele coupled with the mutation. The disease phenotype and all major characteristics of PrP(Sc) of fCJD(R148H) were virtually indistinguishable from those of sCJDMV2, which has features different from those of any other sCJD. Therefore, despite the differences in etiology, PRNP, and conversion process, the two forms of PrP(Sc) had similar characteristics. Furthermore, comparison of fCJD(R148H) with a recently reported case carrying R148H and homozygosity at codon 129 suggests that codon 129 coupled with the mutation as well as that located on the normal allele can modify major phenotypic and PrP(Sc) features of fCJD(R148H).