弥漫性轴索损伤病人的护理

弥漫性轴索损伤 (DAI) ,在脑损伤中发生率高 ,病死率高 ,占脑外伤死亡病人总数的 3 5 %。全部DAI病人中植物生存率为 15 % ,重残 14 % [1] 。为了降低病死率 ,提高病人的生存质量 ,现将 1999年 1月— 2 0 0 2年 1月我院收治的 5 5例DAI昏迷病人的护理体会总结如下。1　临床资料　　本组 5 5例 ,男 3 8例 ,女 17例 ,年龄 6岁～ 68岁 ,平均 40 .9岁。格拉斯哥 (GLS)计分均 <8分 ,其中评分为 3分～ 5分的特重型病人 3 2例。致伤原因 :车祸 44例 ,高处坠落 8例 ,打击伤 3例。 5 5例病人中有 17例因合并颅内血肿而行开颅手术 ,其他病人为保…     

刺鼠信号蛋白对自体移植皮片中酪氨酸酶的活性影响

目的 检测刺鼠信号蛋白对自体移植皮片中酪氨酸酶的活性影响,进一步认识自体移植皮片过度色素沉着的原因。方法 建立过度色素沉着的自体移植皮片的动物模型；利用免疫组织化学方法分别检测刺鼠信号蛋白作用前后自体移植皮片中酪氨酸酶的表达,并与对照治疗组及正常皮肤相比较。结果 酪氨酸酶的表达定位于表皮基底部黑色素细胞的胞浆,在大部分组织中呈阳性表达,经刺鼠信号蛋白作用后酪氨酸酶在自体移植皮片中的表达明显减少,与在其他各对照组中的表达差异有极显著意义（P＜0.01）。结论 刺鼠信号蛋白在自体移植皮片中能竞争性拮抗α-MSH的黑色素合成,使皮片着色能力降低,从而证明皮片移植后表皮细胞中α-MSH的表达上调是皮片呈过度色素沉着的重要原因。     

Foot Polydactyly and Polysyndactyly: Genetic Implications in Two Families

The purpose of this study was to determine the genetic characteristics of foot polydactyly and identify its inheritance pattern by analyzing familial pedigree. Five cases from 2 Korean families were studied: 1 is a family whose members have been affected for 4 generations and the other for 2 generations. Using peripheral blood samples, we performed chromosomal analysis using the banding technique with Giemsa stain and karyotyping. We investigated the shape and structure of 46 chromosomes, looking for translation, deletion, inversion, ring chromosome, and isochromosome abnormalities. All peripheral blood samples demonstrated no chromosomal abnormalities, though the genetic nature of foot polydactyly and a new genetic locus was identified recently by other studies. Familial pedigree analysis suggested that polydactyly was inherited as an autosomal dominant trait in the first family. The mode of inheritance for the second family could not be determined due to an insufficient number of family members. The result of this study brought us to the conclusion that, while genetic factors play a major role in polydactyly, other factors may contribute to its occurrence.     

中西医结合治疗小儿急性肾小球肾炎临床观察

急性肾小球肾炎为临床常见病，多发于少年儿童，男性多见。西医除对症处理外，无特效药物，中药治疗本病可明显缩短病程。笔者自2003年1月至2006年1月用清热利湿解毒汤治疗急性肾小球肾炎60例取得确切疗效，现报道如下。     

腹腔镜肝切除术患者的护理

笔者报道腹腔镜肝切除术患者的护理。术前进行心理护理和呼吸训练；术后注意早期活动，加强腹腔镜CO2气腹后的观察、护理，做好皮下气肿、胆漏、出血、高碳酸血症和下肢静脉血栓等术后并发症的观察及护理。认为周到细致的护理是手术成功的重要保证。     

Changes in CSF neurotransmitters in infantile spasms

Cerebrospinal fluid (CSF) from 7 patients with infantile spasms (mean age: 6.7 months) was collected before and after treatment with adrenocorticotropic hormone (ACTH). The concentration of neurotransmitter metabolites was analyzed using high-performance liquid chromatography and compared to the metabolite concentration in the CSF from 7 age-matched controls (mean age: 6.1 months). Pretreatment levels of CSF 5-hydroxyindoleacetic acid (5-HIAA), homovanillic acid, 3-methoxy-4-hydroxyphenyl glycol (MHPG), and kynurenine were significantly lower in infantile spasm patients compared to controls. Following treatment, marked increases in 5-HIAA and decreases in kynurenine levels were observed in the CSF of the 5 infants whose seizures were eliminated or reduced by ACTH. In the 2 nonresponders 5-HIAA levels decreased. The level of MHPG was reduced slightly in 5 infants, including the 2 nonresponders, and was increased in 2 responders. CSF homovanillic acid levels increased in 4 infantile spasm infants and decreased in 3 following ACTH. These data demonstrate that the presence of seizures in infantile spasms is associated with a significant decrease in serotonergic activity and that elimination of seizures by ACTH is accompanied by increased serotonin turnover. The simultaneous increase of 5-HIAA and decrease of kynurenine, an alternate metabolite of tryptophan, suggests an underlying disturbance of tryptophan metabolism in infantile spasms. The possibility that elimination of seizures by ACTH may be related to decreased production of certain kynurenine metabolites, particularly quinolinic acid, is discussed.     

Conventional and experimental drug therapy in myelofibrosis with myeloid metaplasia

Myelofibrosis with myeloid metaplasia (MMM) is currently classified as a classic (ie, BCR-ABL-negative) myeloproliferative disorder characterized by anemia, multiorgan extramedullary hematopoiesis, constitutional symptoms, and premature death from either leukemic transformation or other disease complications. Stem cell transplantation can be curative, but many patients either are not appropriate candidates or do not choose to accept the significant risks associated with transplantation. Current pharmacologic therapy has been beneficial mainly in terms of palliating disease-associated cytopenias, constitutional symptoms, splenomegaly, and other organ damage from excess myeloproliferation. Novel treatment strategies are under investigation, including targeted inhibition of JAK2^V617F, the activating tyrosine kinase point mutation present in about half of patients with MMM. In this article, we review both the old and new pharmacologic options for MMM.