白癜风伴矮小、耳聋、视力下降一例

报道1例白癜风伴矮小、耳聋、视力下降。患者,男,6岁,出生时即出现黄疸,1岁时发现发育延迟,4岁时出现听力减退,5岁时诊断为矮小,同年发生右上臂白斑。全外显子测序发现PTPRQ基因突变。皮肤科检查：右上臂屈侧多片色素减退斑。诊断：白癜风合并矮小、耳聋、视力下降。     

2006年国外皮肤病治疗回顾

本文回顾2006年部分国外皮肤性病期刊关于皮肤病治疗的报道,其中大部分为个案报道,对幼年透明纤维瘤病、硬化性黏液水肿、Rothmann-Makai综合征等18种皮肤病的治疗情况进行了介绍.     

HPLC法测定红花微乳中羟基红花黄色素A的含量

目的:建立HPLC法测定红花微乳中羟基红花黄色素A的含量。方法:采用色谱柱:Diamonsil C18(2)5μm,250mm×4.6mm;流动相:甲醇-0.4%的磷酸水溶液(三乙胺调至pH=3.3)为30∶70;检测波长:402nm;柱温:室温。结果:羟基红花黄色素A在0.3128～3.128μg的范围内呈良好的线性关系(r=0.9990)。结论:本测定方法快捷,简便,准确,重现性好。     

和血祛风冲剂对类风湿关节炎大鼠细胞因子的影响

目的：通过对大鼠福氏完全佐剂性关节炎动物模型进行观察,探讨和血祛风冲剂对该动物模型细胞因子的影响。方法：观察和血祛风冲剂不同剂量组与寒湿痹冲剂对大鼠福氏完全佐剂性关节炎动物模型白介素1（IL－1）、肿瘤坏死因子α（TNF－α）、类风湿因子（RF)、免疫球蛋白G、A、M（IgG,IgA,IgM)进行观察。结果;和血祛风冲剂各剂量组及寒湿痹冲剂均有消肿作用,均楫IL-1、TNF－α、RF、IgG水平,对IgG抑制作用前者优于后者。结论：和血祛风冲剂治疗类风湿关节炎的机理 可能是抑制炎性细胞因子及免疫球蛋白的水平。     

Effect of Brazilian green propolis on the production of reactive oxygen species by stimulated neutrophils

The activity of a crude ethanol extract of green propolis and its fractions obtained by partition with hexane, chloroform and n-butanol was assessed on luminol- and lucigenin- enhanced chemiluminescence (CL) produced by rabbit neutrophils (PMNs) stimulated with particles of serum-opsonized zymosan (OZ). The total production of reactive oxygen species (ROS) by PMNs was measured by the luminol-enhanced CL (LumCL) assay and the production of the superoxide anion (O2*-) by the lucigenin-enhanced CL (LucCL) assay. All evaluated propolis samples had inhibitory effect on the LumCL and LucCL, which was concentration dependent. The n-butanol and chloroform fractions displayed the highest inhibitory effect on the LumCL produced by PMNs stimulated with OZ, in comparison with both the ethanol extract and the hexane fraction. Besides, the hexane fraction was the one which presented the highest effect for the LucCL assay. Some isolated compounds from both n-butanol and chloroform fractions were also assessed, including kaempferide, isosakuranetin, aromadendrine-4'-methyl-ether and 3-prenyl-p-coumaric acid. Kaempferide presented the highest inhibitory effect on the LumCL in comparison with the other compounds. Moreover, under the conditions assessed, the studied green propolis samples and isolated compounds were not toxic to the rabbit PMNs.     

Aquaporin-4 gene disruption in mice protects against impaired retinal function and cell death after ischemia

PURPOSE: Water channel aquaporin (AQP)-4 is expressed in Muller cells in retina, which are similar to astroglial cells in the central nervous system, where AQP4 deletion protects against cytotoxic brain edema after cerebral ischemia. A transient ischemia-reperfusion model was used to determine whether AQP4 deletion in mice protects the retina. METHODS: Retinal function and morphology were assessed in wild-type versus AQP4-deficient mice after ischemic damage produced by a 45- to 60-minute elevation of intraocular pressure to 120 mm Hg. Retinal function was assessed by electroretinography, and retinal structure by light microscopy. Extracellular space (ECS) size in fluorescently stained retinal slices was assessed by fluorescence recovery after photobleaching. RESULTS: Retinal function and cell survival were significantly improved in AQP4-deficient mice in both inbred (C57/bl6) and outbred (CD1) genetic backgrounds. By electroretinography, b-wave amplitude was reduced by 75% to 83% at 1 to 4 days after ischemia in wild-type mice versus 48% to 51% in AQP4-null CD1 mice. Reductions were 53% to 72% versus <34% in C57/bl6 mice. Retinal structure and cell count were preserved in AQP4-null mice, particularly in the inner nuclear and plexiform layers of the retina, where Müller cells are concentrated. At 4 days after ischemia, inner retinal thickness was thinned by 43% in wild-type mice versus 11% in AQP4-null mice. Several mechanisms for retinal protection were investigated, including ECS expansion, reduced early swelling, and altered Kir4.1 K(+) channel expression. CONCLUSIONS: AQP4 deletion in mice is neuroprotective in a transient ischemia model of retinal injury, suggesting the possible use of AQP4 inhibitors in retinal vascular occlusive and ischemic diseases.     

剖宫产术中妇科肿瘤的处理

妊娠期合并肿瘤发病率虽然不高,但却是重要的临床问题。不少良性肿瘤如子宫肌瘤及卵巢良性肿瘤常可与妊娠同在。妊娠合并恶性妇科肿瘤临床少见,主要是宫颈癌、卵巢癌等[1]。由于妊娠对肿瘤可能存在影响,而肿瘤对妊娠、胎儿以及分娩均存在影响,且肿瘤的治疗对妊娠也存在影响。因     

miR-320-3p 调控脂肪细胞分化的研究

目的探讨miR-320-3p 对脂肪细胞分化的影响。方法分离并培养小鼠骨髓间充质干细胞（MSCs）,并对其进行脂肪细胞诱导分化3 d,用qRT-PCR 检测miR-320-3p 在成脂分化过程中的表达水平。在骨髓基质细胞系 ST2 中转染miR-320-3p,对其进行成脂方向诱导分化,用油红O 染色和qRT-PCR 检测miR-320-3p 对ST2 成脂分化的影响。结果MSCs 向脂肪细胞分化过程中miR-320-3p 表达增加（P < 0.01）;与转染阴性对照NC mimics 相比,ST2 细胞转染miR-320-3p mimics 后油红O 染色显示脂肪细胞明显增多,脂肪细胞特异性转录因子过氧化物酶体增殖物激活受体γ(PPARγ)、CCAAT 增强子结合蛋白α（C/EBPα）和脂肪细胞脂肪酸结合蛋白4（FABP4）基因表达显著升高,差异有统计学意义（P < 0.05）。结论miR-320-3p 可促进ST2 向脂肪细胞分化。     

青藤碱的药理作用——Ⅴ.对防御性条件反射活动的影响

青藤碱具有多种中枢作用,研究青藤碱对条件反射活动的影响,对进一步分析青藤碱的中枢作用机制是有意义的.因此本文就青藤碱对小白鼠和猫的防御性条件反射的影响进行观察.(一)对小白鼠防御运动性条件反射的影响仿胥彬防御运动性条件反射木箱,以强风鸣声作阳性条件刺激,弱风鸣声作分化条件刺激.从给予强风鸣声至跑到木箱对侧的间隔时间,称为条件反射潜伏期.给药后给阳性条件刺激10秒钟动物不跑到木箱对侧称为条件反射消失,从弱风鸣声响后10秒内跑到木箱对侧称为分化抑制解除;当条件反射消失后接着给直流电作非条件刺激,刺激持续时间不超过10秒,如动物不跑到木箱对侧称为非条件反射消失.当条件反射形成后再进行分化,阳性和分化抑制性条件反射巩固和反射潜伏期基本稳定后进行实验.     

Microstructure and Friction Properties of CoCrFeMnNiTix High-Entropy Alloy Coating by Laser Cladding

To enhance the friction and wear properties of 40Cr steel’s surface, CoCrFeMnNi high-entropy alloy (HEA) coatings with various Ti contents were prepared using laser cladding. X-ray diffraction (XRD), scanning electron microscopy (SEM), and energy dispersive spectroscopy (EDS) were used to characterize the phase composition, microstructure, and chemical composition of the samples. The findings demonstrated that the CoCrFeMnNiTi_x HEA coatings formed a single FCC phase. Fe₂Ti, Ni₃Ti, and Co₂Ti intermetallic compounds were discovered in the coatings when the molar ratio of Ti content was greater than 0.5. The EDS findings indicated that Cr and Co/Ni/Ti were primarily enriched in the dendrite and interdendrite, respectively. Ti addition can effectively enhance the coating’s mechanical properties. The hardness test findings showed that when the molar ratio of Ti was 0.75, the coating’s microhardness was 511 HV0.5, which was 1.9 times the hardness of the 40Cr (256 HV0.5) substrate and 1.46 times the hardness of the CrCrFeMnNi HEA coating (348 HV0.5). The friction and wear findings demonstrated that the addition of Ti can substantially reduce the coating’s friction coefficient and wear rate. The coating’s wear resistance was the best when the molar ratio of Ti was 0.75, the friction coefficient was 0.296, and the wear amount was 0.001 g. SEM and 3D morphology test results demonstrated that the coating’s wear mechanism changed from adhesive wear and abrasive wear to fatigue wear and abrasive wear with the increase in Ti content.