方丝弓技术实施扩弓作用初探

本临床研究应用了直的双根钛镍丝扩弓法,主弓配合辅弓扩弓法,多loop弓丝牙弓前部扩弓法,改良多用弓技术,四眼簧扩弓器,快速扩弓螺旋器,用预成的略大于牙弓的弓丝扩弓和上下颌后牙交互牵引扩大牙弓,共8种方法.作者结合临床经验及体会,分析了各种扩弓方法的原理,提出了每种扩弓方法的适应症以及加力时应注意的事项.这些常用的扩弓方法,在临床上是行之有效的.既满足了临床扩弓的要求,也促进了方丝弓矫治技术的普及和开展.     

变形链球菌表面蛋白和葡糖基转移酶基因疫苗免疫防龋动物实验:体质量影响研究

目的 :了解变形链球菌基因疫苗单独及联合免疫对定菌鼠体质量的影响。方法 :2 8d龄Wistar大鼠 3 6只 ,随机分为pcDNA3 pac组、pcDNA3 gtfB组、pcDNA3 pac联合pcDNA3 gtfB组、变形链球菌灭活全菌阳性对照组、pcDNA3空载体阴性对照组和PBS液空白对照组 ,进行 3次双侧颌下腺腺周注射免疫 ,建立定菌鼠模型及诱龋实验 3个月 ,于实验开始和结束时测定体质量。结果 :基因疫苗免疫组体质量与 pcD NA3及PBS组无显著差异 (P >0 .0 5) ,而灭活全菌细胞免疫组体质量显著下降 (P <0 .0 1)。结论 :pcD NA3 gtfB和pcDNA3 pac对大鼠体质量无不良影响 ,较灭活全菌疫苗安全     

实验性He创伤对牙髓和牙周组织影响的研究

为了探讨Ｈｅ创伤持续时间与牙髓、牙周组织变化间的关系，作者对４４只大鼠的下颌磨牙制造了实验性Ｈｅ创伤，利用组织病理学和软射线的研究方法，观察不同实验期受创伤大鼠磨牙的牙髓、牙周组织变化，并与软射线片进行对照分析。结果表明，牙髓组织随Ｈｅ务时间延长而病变逐渐加重；牙周组织受到长期Ｈｅ创伤后呈现适应性变化，牙周组织焦吩一软射线片显示的牙周变化部位相应。本研究结果为Ｈｅ创伤性牙髓炎和根尖周炎的病因，病理     

Acrylamide exposure impairs blood-cerebrospinal fluid barrier function

Previous studies show that chronic acrylamide exposure leads to central and peripheral neu- ropathy. However, the underlying mechanisms remained unclear. In this study, we examined the permeability of the blood-cerebrospinal fluid barrier, and its ability to secrete transthyretin and transport leptin of rats exposed to acrylamide for 7, 14, 21 or 28 days. Transthyretin levels in cerebrospinal fluid began to decline on day 7 after acrylamide exposure. The sodium fluorescein level in cerebrospinal fluid was increased on day 14 after exposure. Evans blue concentration in cerebrospinal fluid was increased and the cerebrospinal fluid/serum leptin ratio was decreased on days 21 and 28 after exposure. In comparison, the cerebrospinal fluid/serum albumin ratio was increased on day 28 after exposure. Our findings show that acrylamide exposure damages the blood-cerebrospinal fluid barrier and impairs secretory and transport functions. These changes may underlie acrylamide-induced neurotoxicity.     

Potential risk of mitomycin Cat high concentrations on peripheral nerve structure

Although the local application of mitomycin C may prevent epidural adhesion after laminectomy, mitomycin C can induce neurotoxicity in optic and acoustic nerves at high concentrations. To determine the safe concentration range for mitomycin C, cotton pads soaked with mitomycin C at different concentrations(0.1, 0.3, 0.5, and 0.7 mg/mL) were immediately applied for 5 minutes to the operation area of rats that had undergone laminectomy at L1. Rat sciatic nerves, instead of dorsal nerves, were used in this study. The results showed that mitomycin C at 0.1–0.5 mg/mL did not damage the structure and function of the sciatic nerve, while at 0.7 mg/mL, mitomycin C significantly reduced the thickness of the sciatic nerve myelin sheath compared with lower concentrations, though no functional change was found. These experimental findings indicate that the local application of mitomycin C at low concentrations is safe to prevent scar adhesion following laminectomy, but that mitomycin C at high concentrations( 0.7 mg/mL) has potential safety risks to peripheral nerve structures.     

辛伐他汀对不稳定性心绞痛患者C反应蛋白的影响

目的:通过辛伐他汀对不稳定性心绞痛患者超敏C反应蛋白(HSCRP)的作用,探讨在急性冠脉综合征患者中应用他汀类药物的必要性。方法:共入选45例不稳定心绞痛患者,随机分为辛伐他汀组(观察组)和常规治疗组(对照组),两组均于入院后第二天及六周后抽血测定血脂(TC,TG,LDL-C,HDL-C)及C反应蛋白。结果:对照组六周后血脂及HS-CRP无明显变化(P>0.05),观察组六周后TC,TG及LDLC有下降(P<0.05),HDL-C有明显升高(P<0.01),HSCRP有明显下降(P<0.01)。结论:辛伐他汀除有很好的调脂作用外,还能有效地抑制急性冠脉综合征患者的炎症反应,早期应用可以抑制冠脉炎症反应。     

参芪柴芍枳附汤辅治代谢性心脑血管疾病疗效观察

目的:观察参芪柴芍枳附汤辅治心脑血管疾病的疗效。方法:150例分为4个治疗组及1个对照组各30例,4个治疗组分别为糖尿病(消渴)+冠心病(胸痹)、糖尿病(消渴)+椎基底动脉供血不足(眩晕)、糖尿病(消渴)+脑梗死(中风)、糖尿病(消渴)+抑郁症(郁证),对照组为糖尿病(消渴)。对照组根据指南予以常规西医治疗。治疗组在常规西医治疗基础上加用参芪柴芍枳附汤口服,疗程15天。结果:各治疗组空腹血糖控制、中医临床症状及西医疗效均优于对照组(P<0.05)。结论:参芪柴芍枳附汤能改善心脑血管疾病临床症状。     

Region‐specific impairments in striatal synaptic transmission and impaired instrumental learning in a mouse model of Angelman syndrome

Angelman syndrome (AS) is a neurodevelopmental disorder characterized by mental retardation and impaired speech. Because patients with this disorder often exhibit motor tremor and stereotypical behaviors, which are associated with basal ganglia pathology, we hypothesized that AS is accompanied by abnormal functioning of the striatum, the input nucleus of the basal ganglia. Using mutant mice with maternal deficiency of AS E6‐AP ubiquitin protein ligase Ube3a (Ube3a^m?/p+), we assessed the effects of Ube3a deficiency on instrumental conditioning, a striatum‐dependent task. We used whole‐cell patch‐clamp recording to measure glutamatergic transmission in the dorsomedial striatum (DMS) and dorsolateral striatum (DLS). Ube3a^m?/p+ mice were severely impaired in initial acquisition of lever pressing. Whereas the lever pressing of wild‐type controls was reduced by outcome devaluation and instrumental contingency reversal, the performance of Ube3a^m?/p+ mice were more habitual, impervious to changes in outcome value and action–outcome contingency. In the DMS, but not the DLS, Ube3a^m?/p+ mice showed reduced amplitude and frequency of miniature excitatory postsynaptic currents. These results show for the first time a selective deficit in instrumental conditioning in the Ube3a deficient mouse model, and suggest a specific impairment in glutmatergic transmission in the associative corticostriatal circuit in AS.     

Hyperbaric Oxygen Treatment Produces an Antinociceptive Response Phase and Inhibits Astrocyte Activation and Inflammatory Response in a Rat Model of Neuropathic Pain

Hyperbaric oxygen (HBO) treatment has been proven to be a promising candidate for protection of the nervous system after acute injury in animal models of neuropathic pain. The purposes of this study were to examine the antinociceptive response phase induced by HBO treatment in a model of neuropathic pain and to determine the dependence of the treatment's mechanism of alleviating neuropathic pain on the inhibition of spinal astrocyte activation. Neuropathic pain was induced in rats by chronic constriction injury of the sciatic nerve. Mechanical threshold and thermal latency were tested preoperatively and for 1 week postoperatively, four times daily at fixed time points. Methane dicarboxylic aldehyde (MDA) and superoxide dismutase (SOD) parameters were used as indices of oxidative stress response and tested before and after the treatment. The inflammatory cytokines interleukin (IL)-1β and IL-10 were assayed in the sciatic nerve were with enzyme-linked immunoassay. Glial fibrillary acidic protein activation in the spinal cord was evaluated immunohistochemically. The rats exhibited temporary allodynia immediately after HBO treatment completion. This transient allodynia was closely associated with changes in MDA and SOD levels. A single HBO treatment caused a short-acting antinociceptive response phase. Repetitive HBO treatment led to a long-acting antinociceptive response phase and inhibited astrocyte activation. These results indicated that HBO treatment played a dual role in the aggravation and alleviation of neuropathic pain, though the aggravated pain effect (transient allodynia) was far less pronounced than the antinociceptive phase. Astrocyte inhibition and anti-inflammation may contribute to the antinociceptive effect of HBO treatment after nerve injury.