铁缺乏时淋巴细胞增殖反应改变的实验研究

本研究采用体外细胞培养，３Ｈ－Ｔｄｒ掺入，原子吸收光谱分析等技术方法，观察了低浓度Ｆｅ－ｃｉｔ时淋巴细胞内铁浓度变化及经ＣｏｎＡ、ＰＨＡ诱导的细胞增殖反应能力改变，结果显示：铁缺乏时（第２、３、４组）ＳＩ降低，与正常组（第１组）比较相差非常显著（Ｐ＜０．０１），ＳＩ与细胞内铁浓度的变化呈显著正相关（Ｐ＜０．０５，ｒ１＝０．９４６６，ｒ２＝０．９３３９），说明铁缺乏时淋巴细胞增殖反应能力受抑。     

贫血患者血清红细胞生成素浓度的测定及临床意义

用小鼠胎肝细胞体外血浆凝块培养红系集落(Erythroid colong formig unit inculturc,E-CFUc)方法,以红细胞生成素(Erythropoietin,EPO)850323为标准试剂,测定正常人、贫血病人血清EPO浓度。实验用妊娠13～15d小鼠胎肝细胞。血清均经透析处理,培养液中加量最大不超过10％。EPO(850323)在培养液中浓度为2.5～100mU/ml。血清EPO(mU/ml)测定结果:28例正常人为48.O±17.7,12例再生障碍性贫血病人为946～>10000,1例巨幼细胞性贫血病人为500,1例缺铁性贫血病人为400和18例慢性肾功能衰竭病人则为94.2±87.6。结果表明:贫血病因对血清EPO浓度有影响。     

Benign intracranial hypertension and recombinant growth hormone therapy in Australia and New Zealand

Benign intracranial hypertension (BIH) is reported in three children from Australia and one from New Zealand, who were being treated with recombinant human growth hormone (rhGH). Three males and one female, aged between 10.5 and 14.2 y, developed intracranial hypertension within 2 weeks to 3 months of starting treatment. A national database, OZGROW, has been prospectively collecting data on all 3332 children treated with rhGH in Australia and New Zealand from January 1986 to 1996. The incidence of BIH in children treated with growth hormone (GH) is small, 1.2 per 1000 cases overall, but appears to be greater with biochemical GHD (<10IUml ^-1), i.e. 6.5/1000 (3 in 465 cases), relative risk 18.4, 95% confidence interval 1.9-176.1, than in all other children on the database. The incidence in patients with Turner's syndrome was 2.3/1000 (1 in 428 cases). No cases in patients with partial GHD (10–20 IUml ^-1) or chronic renal failure were identified. Possible causative mechanisms are discussed. The authors'practice is now to start GH replacement at less than the usual recommended dose of 14IUm-² week^-1 in those children considered to be at high risk of developing BIH. Ophthalmological evaluation is recommended for children before and during the first few months following commencement of rhGH therapy and is mandatory in the event of peripheral or facial oedema, persistent headaches, vomiting or visual symptoms. The absence of papilledema does not exclude the diagnosis.     

海南文昌汉族人群中两种葡萄糖-6-磷酸脱氢酶基因突变的研究

目的:分析海南文昌人群中葡萄糖-6-磷酸脱氢酶基因1376G→T、95A→G突变。方法:应用硝基四氮唑蓝定量法进行G6PD缺乏症的筛查,用等位基因特异PCR检测1376G→T、95A→G突变。结果:在358位海南文昌汉族人中,发现G6PD缺乏症患者20例,其中9例患者有1376G→T突变,3例患者有95A→G突变。结论:1376G→T、95A→G突变是文昌人群中常见的突变。     

Hypercalcemic hyperparathyroidism and hypophosphatemic osteomalacia complicating neurofibromatosis

Summary Neurofibromatosis is sometimes complicated by impaired renal tubular reabsorption of phosphate, hypophosphatemia, and osteomalacia. Hyperparathyroidism has also been reported in patients with neurofibromatosis. When hypercalcemia and elevated levels of parathyroid hormone are found in osteomalacia, however, it may be difficult to determine if the hyperparathyroidism was primary or tertiary. We describe a patient with neurofibromatosis, hypercalcemic hyperparathyroidism, hypophosphatemic osteomalacia, vitamin D deficiency, and clear-cell hyperplasia of all four parathyroid glands. Serial biomechanical, bone biopsy, and densitometric studies confirmed that treatment with ergocalciferol, calcium, and phosphate supplements significantly improved the osteomalacia but caused increased parathyroid overactivity. After subtotal parathyroidectomy, the parathyroid hormone concentration became normal and the bone mineral content increased at the spine and hip, but inappropriate phosphaturia persisted. The findings indicate that hyperparathyroidism, osteomalacia, and vitamin D deficiency adversely affect each other.     

Sideropenic Dysphagia综合征膜性蹼26例分析

目的 :研究SideropenicDysphagla (S -D)综合征膜性蹼产生的机制。方法 :回顾分析S -D综合征2 6例的临床资料。结果 :影像学检查显示膜性蹼在颈段食道前壁呈 2mm深的模样陷凹。血液学检查为缺铁性低血红蛋白性贫血改变。结论 :缺铁性贫血是S -D综合征的原因 ,铁剂治疗有效     

黑蔓不同部位微量元素的测定

为了了解吉林省长白县山区所产卫矛科雷公藤属植物黑蔓的药理作用,扩大它的药用部位和应用范围,我们从无机元素与中药药效有密切关系的角度出发,实验测出黑蔓含有Ba、Si、Cu、Fe、Zn、Sn、Co、Mn、Mg、Ca、Se等无机元素,本文重点对其中人体必需的微量元素Cu、Fe、Zn、Se作了定量分析。     

Neuro-toxic interaction in alcohol-treated,thiamine-deficient mice

Summary Groups of adult male mice were either fed a thiamine-deficient diet for 10 weeks and thereafter treated with ethanol by making them inhale vapourized cane spirit for 10 weeks, or given both treatments simultaneously. The brains of these mice were then searched for degeneration using both light and electron microscopy. No degenerating nerve cells were observed in any animal in the cerebral cortex, hippocampus, cerebellum, olfactory bulbs, midbrain or hindbrain. However, axon terminal degeneration was seen in the olfactory bulbs and deep cerebellar nuclei in mice given the combined treatment. No cerebellar degeneration was found and only little degeneration was present in the olfactory bulbs of mice given the two treatments at different times. Thus, the combined treatment of alcohol and thiamine deficiency produced more brain damage than the sum of that produced by the two treatments given separately. This represents the first experimental in vivo demonstration of a biochemical interaction between these two factors in alcohol-related brain damage. The findings of long-term animal treatment with models using thiamine antagonists are compared.Supported by the special Research Fund Programme of Monash University (Post-Doctoral Fellowship)     

昆明城区、大理农村7月～7岁儿童铁缺乏调查分析

目的 :了解昆明城区及大理农村 7月～ 7岁儿童目前的铁缺乏水平 ,进一步展开对儿童铁缺乏症的防治 ,降低儿童营养性缺铁性贫血的患病率 .方法 :采用抽样调查的方法对两地 7月～ 7岁儿童共 96 9名进行血清铁蛋白 (SF)、锌原卟啉 (ZPP)、血红蛋白 (Hb)实验室检查 .结果 :7月～ 7岁儿童的总铁缺乏检出率为 2 5 1% ,铁减少检出率为 19 0 % ,贫血患病率为 6 1% ;男女童患病率在 1岁以前差别较大 ,1岁以后差别不明显 ;各年龄组患病率以 7月～ 1岁组最高 ;早产儿、低出生体重儿童患病率相对较高 ;铁缺乏的儿童营养不良的患病率高于正常儿童 .结论 :儿童缺铁性贫血仍要引起重视 .在防治中要抓重点人群 ,除改变膳食结构和饮食习惯 ,对目标人群要适当补充铁剂预防     

再生障碍性贫血造血细胞Fas抗原表达与T淋巴细胞功能的研究

目的 研究造血细胞凋亡与T淋巴细胞免疫在再生障碍性贫血(再障，Aplastic anemia，AA)发病机制中的作用及两者相关性。方法 采用流式细胞仪测定40例AA患者和15例非血液、免疫系统疾病对照者骨髓单个核细胞(BMMNC)的总CD34^ 、CD34^ Fas^ 、CD34^ Fas^-、CD3^ 、CD8^ 、CD3^ 、CD3^ CD25^ 标记值。结果 (1)与对照组比较，AA组总CD34^ 细胞％明显减少而其Fas表达率(以占总CD34^ 细胞％为计)明显增高。(2)AA组CD34^ 细胞％数与其Fas抗原表达率无明显负相关。(3)AA组T细胞％明显增多，且以CD8^ 细胞和CD3^ CD25^ 细胞增多为主。(4)AA组CD34^ 细胞％数与其T细胞活化状态无显著负相关。(5)AA组CD34^ 细胞Fas表达率与其T细胞活化状态无显著正相关。结论 AA骨髓存在着造血细胞数量减少和T淋巴细胞亚群数量、功能的异常，造血细胞数量减少还可能与Fas以外途径诱导的凋亡过度有关。骨髓造血细胞凋亡过度可能有活化T淋巴细胞免疫以外的途径诱导Fas途径或活化T淋巴细胞可以通过Fas之外的途径诱导造血细胞凋亡。