家庭方言环境对儿童语言发育的影响

目的 探究家庭方言环境对儿童语言发育的影响, 为探讨儿童语言障碍原因提供理论依据。方法 收集2015年11月-2019年9月于上海儿童医学中心发育行为儿科就诊并完成语言能力测试的儿童资料。共688名儿童, 年龄范围35.1~95.7个月;根据家庭方言环境分为普通话组(n=151), 方言组(n=537)。采用χ²检验和Mann-Whitney U检验分析两组儿童的语言能力差异。结果 普通话组和方言组儿童的年龄、性别构成以及语言障碍比例, 差异无统计学意义(P>0.05);语言正常和障碍儿童在整体语言、听力理解、语言表达、语义、句法5个维度上均不受方言环境影响(P>0.05)。结论 家庭方言环境不是儿童语言发育的危险因素, 语言暴露的质量与数量对儿童早期发展更为重要。     

某医学中心药师对民众用药安全教育的经验交流

为推广正确用药知识,提升民众用药安全核心能力,使药品发挥治疗效果并避免药品使用不当产生不良后果,台湾地区某一大型综合医院药剂科药师通过成立"正确用药教育资源中心",联合各级药学会、学校、社区、公共平台等资源,让医院药师走出医院,走进校园、社区、公共场所等,借助活动、宣传、科普教育等方式,2014-2015年共举办114场,参与人数达到14 140人次,活动满意度达98.5%。藉此模式除提升民众正确用药的核心能力,同时可建构用药安全网,并充分发挥医院药师的工作价值。     

Refrigerated storage of lyophilized and rehydrated, lyophilized human red cells

Human red cells (RBCs) were collected in CPDA-1 and then freeze-dried in lyoprotective solution. The lyophilized RBCs were then stored at -20 degrees C for 7 days. At the end of the storage period, the lyophilized RBCs were rehydrated and washed in dextrose saline. The washed, reconstituted, lyophilized RBCs were resuspended in final wash solutions of ADSOL, CPDA-1, or a special additive solution containing glucose, citrate, phosphate, adenine, and mannitol, and then they were stored at 4 degrees C for an additional 7 days. The main purpose of this study was to determine whether human RBCs can be lyophilized in such a manner that normal metabolic, rheologic, and cellular properties are maintained during rehydration and subsequent storage in standard blood bank preservative solutions. Our results show that reconstituted, lyophilized RBCs maintained levels of ATP, 2,3 DPG, lactate, and cellular properties that are equal to or better than those in control nonlyophilized RBCs stored for a comparable period in CPDA-1. Reconstituted, lyophilized RBCs stored at 4 degrees C after rehydration also show better maintenance of ATP, 2,3 DPG, and lactate than do control RBCs stored in the same preservative solutions for comparable periods.     

Decrease in bispectral index prior to cardiovascular collapse during Caesarean sections

We report a case of significant reduction in bispectral index (BIS) associated with suspected amniotic fluid embolism (AFE) that occurred prior to change in haemodynamic variables. The patient was a 29‐year‐old nulliparous, who was admitted for Caesarean section under general anaesthesia in the 33rd week of pregnancy. After the baby was born, the BIS value suddenly decreased to 0, with suppression ratio of 100. One minute later, saturation decreased abruptly to 85%, end‐tidal carbon dioxide (EtCO₂) decreased to 5 mmHg, peak inspiratory pressure increased to 35 cm H₂O, and non‐invasive blood pressure (BP) failed to obtain a reading. After administration of vasoactive drugs, the systolic BP was maintained at 100 mmHg or higher, the BIS value rose to 10–20, and the EtCO₂ increased to 24–33 mmHg. In this case, the BIS monitoring may provide an earlier warning of impending cardiovascular collapse in the case of AFE.     

Mechanism of cell wall penetration by viruses. II. Demonstration of cyclic permeability change accompanying virus infection of Escherichia coli B cells

The virus-induced leakage of host-cell constituents represents a true increase in cellular permeability rather than an unpeeling of cell surface components, since an intracellular enzyme participates in the leakage. All of the T-system bacteriophages exhibit this leakage. The leakage does not occur with salt concentrations which permit only reversible virus-cell attachment but no penetration. These facts support the idea that the reaction underlying cell leakage is a part of the invasive mechanism. With increasing multiplicity of T2 infection of young, fresh Escherichia coli B cells, progressively larger molecules leak out of the cell. Acid-soluble P³² appears in large amounts with single infection. Appreciable amounts of galactosidase enzyme and RNA do not leak until multiplicities of 5 to 30 are attained. Cellular DNA is not liberated unless sufficiently high multiplicities are used to cause the extensive cell destruction and clearing of the suspension characteristic of lysis-from-without. This progression is interpreted as an increase with T2 multiplicity in the maximum hole size produced in the cell membrane. Calculation shows that this increase in hole size must result from a spreading change in the character of the cell wall, rather than the coincidental juxtaposition of 2 or more viruses at adjacent attachment sites. T1 virus liberates less macromolecular constituents than T2 from E. coli B. The following experimental results constitute evidence that in the course of normal virus infection, a resealing reaction is rapidly instituted in the cell wall which reverses the effect of the original permeability increase, and renders the cell refractory to a second lytic reaction by a homologous virus: (a) Cell leakage induced by T2 virus in the course of normal infection markedly slows down or stops within a few minutes, even when only a small fraction of the material potentially available for leakage has been released, (b) Superinfection after 8 minutes at 37°C., of a cell previously infected with a homologous virus causes little or no appearance of a second leakage of cell constituents. This experiment also leads to the conclusion that the sealing reaction, like that which causes the leakage, also involves a disturbance which spreads over all or most of the cell wall. (c) If a multiple virus infection is allowed to occur at 0°C. and then the cells are placed in a 37°C. bath after completion of attachment, a much greater cell leakage results than if the entire course had occurred at 37°C., as would be expected if a resealing reaction comes into play at 37°C. within a time less than that required by the completion of attachment. The virus particles attaching secondarily at 37°C. are prevented from exercising their permeability-increasing effect by the sealing reaction of the virus which had penetrated first. Although a second homologous cell infection with T1 or T2 phages after a 37°C. incubation fails to yield a second leakage, a second heterologous infection always causes exacerbation of new leakage, which, especially if T1 has preceded T2, may be much greater than the sum of those produced individually by each virus in separate cell suspensions. This phenomenon may be the action responsible for the "depressor" effect which occurs when 2 unrelated viruses attack the same cell. The properties of the sealing phenomenon are such as to make it appear a logical candidate for the mechanism underlying the exclusion of a superinfecting phage from participating in reproductive processes in a cell previously infected with a homologous virus, since the DNA of the second virus would be unable to penetrate the new barrier. Experiments to test this hypothesis revealed that the DNA from such superinfecting virus is completely extractable from cells by washing in dilute buffer, whereas about 40 to 50 per cent of the attached DNA of virus which has invaded virgin cells remains bound to the cells. Most of the viral DNA which appears in the original supernatant when P³²-labelled T2 invades E. coli B in a multiplicity less than one, does not represent inert material but rather virus DNA which has been split, or split and hydrolyzed as a result of its interaction with the cells, as judged by the altered susceptibility to hydrolytic enzyme or to TCA precipitation. This suggests that 25 per cent or more of the virus DNA may be expendable, at least after the penetration stage of the infection cycle. Mg⁺⁺ which strongly depresses the amount of cell leakage attending T2 infection, does not prevent T2 penetration nor does it block the appearance of the exclusion reaction. Hence, if the initial leakage does mirror the lytic process by which a hole for the DNA injection is provided, the Mg⁺⁺ does not function by preventing this hole formation. Its effect would have to lie in prevention of the spreading lysis-potentiating reaction or in augmenting the sealing mechanism. A large number of independent lines of evidence indicate that the phenomenon of lysis-from-without exhibited by the T-even coliphages is the result of failure of the sealing mechanism to keep pace with the lytic reaction. This can result from an excess of infecting phages or inhibition of the cellular energy-liberating reaction required by the sealing mechanism. The complete parallelism between the development of refractoriness to lysis-from-without and development of refractoriness to the production of a new leakage from a homologous superinfection is especially convincing in this connection. It is proposed that the early phase of bacteriophage invasion involves the following steps: reversible electrostatic attachment; splitting of the viral DNA from its protein coat; initiation of a lytic reaction in the cell wall at the site of virus attachment; injection of the DNA through the hole so produced; a spreading disturbance over the cell surface which makes it momentarily more susceptible to the lytic reaction; sealing of the hole and a concommittant spread over the cell wall of a reaction making the cell refractory to initiation of a second lytic reaction. Na⁺, K⁺, and Mg⁺⁺ all behave differently in their effect on the leakage produced in the course of T2 invasion of E. coli.     

Methylprednisolone Inhibits the Expression of Glial Fibrillary Acidic Protein and Chondroitin Sulfate Proteoglycans in Reactivated Astrocytes

创伤后的神经胶质增生导致硫酸软骨素蛋白聚糖(CSPG)的显著表达,从而抑制轴突生长和再生。甲基强地松龙(MP),一种合成的糖皮质激素,在急性脊髓损伤(SCI)的治疗中有神经保护作用和抗炎效应。但是,MP对于CSPG在活性胶质细胞中的表达的作用尚不清楚。本文用a-氨基-3-羟基-5-甲基-4-异恶唑丙酸酯(AM-PA)诱导星形胶质细胞再活化,用环噻嗪模拟SCI的兴奋性中毒刺激。AMPA治疗后,星形胶质细胞再活化的标志物-胶质纤维酸性蛋白(GFAP)、CSPG神经聚糖和磷酸盐的表达都显著上调。AMPA治疗星形胶质细胞的条件培养液强烈抑制大鼠背根神经节中神经元的轴突生长,但这种作用能被MP的预处理所逆转。此外,MP下调成年SCI大鼠中GFAP和CSPG的表达,对抗RU486的糖皮质激素受体(GR)和GR si RNA能逆转MP对GFAP和神经聚糖表达的抑制作用。这些结果提示,MP能在兴奋性中毒损伤后通过GR介导的星形胶质细胞再活化下调和GSPG表达抑制来改善神经修复,促进轴突生长。