邻近皮瓣修复面部皮肤缺损

目的 探讨邻近皮瓣修复面部皮肤缺损的应用效果。方法 162例面部病变切除后皮肤缺损患者，其中先天性色素痣63例，基底细胞癌28例，鳞状细胞癌6例，其他皮肤病变65例。均采用邻近皮瓣即时修复，其中菱形皮瓣57例、双叶皮瓣8例，A-T皮瓣23例、V-Y皮瓣13例、Z成形术23例、推进皮瓣27例、鼻状皮瓣11例。结果 162例皮瓣存活良好，手术切口1期愈合，存活后皮瓣颜色与邻近部位无明显差异，术后无眼睑、眉毛、鼻梁及口角牵扯歪钭，术后3个月切口不显露。结论 邻近皮瓣是修复面部较大皮肤缺损的良好方法，手术外观效果好。     

益气活血方对气虚血瘀证脑缺血再灌注损伤大鼠Fas、FasL蛋白表达的影响

目的：探讨益气活血方对气虚血瘀证局灶性脑缺血再灌注损伤大鼠Fas、FasL蛋白表达的影响。方法：采用气虚血瘀证局灶性脑缺血再灌注损伤大鼠模型，用线栓法阻塞大鼠大脑中动脉复制局部脑缺血再灌注模型，缺血2h后再灌注l，3，7d。用免疫组化染色法分别检测缺血皮质Fas、FasL蛋白表达。结果：与模型组比较。益气活血方组Fas、FasL蛋白表达显降低。结论：益气活血方可能通过抑制Fas、FasL蛋白表达，减轻气虚血瘀证局灶性脑缺血再灌注损伤。     

云南省600例0~5岁儿童维生素A缺乏调查

目的:了解云南省城乡0~5岁儿童维生素A营养状况及影响因素。方法:省、地、县随机整群抽取600例儿童,采用微量荧光光度法检测VitA含量。结果:VitA缺乏发生率16·17%,地、县明显高于省会城市;0岁儿童明显高于其他年龄组;腹泻儿童明显高于正常儿童;VitA缺乏的影响因素:近1周内进食鸡蛋、奶类制品、鱼虾类、肝类、黄绿色蔬菜、鱼肝油等食物有利于维生素A的吸收,急性呼吸道感染、发烧与维生素A缺乏发生率差异不明显。结论:维生素A缺乏发生率城市明显低于农村地、县两级,说明维生素A缺乏防治工作重点在农村,特别是0岁儿童,防治的主要措施是采取合理膳食,均衡营养,控制腹泻流行。     

补碘对7～12岁轻度碘缺乏病儿童脑功能及生长、发育的影响

通过半年对３５名７～１２岁轻度碘缺乏病儿童进行补碘，并与同龄、同地的正常儿童和缺碘未补碘儿童进行比较，以观察补碘对儿童脑功能及生长发育的影响。结果发现：①补碘可使儿童碘营养状况恢复正常，尿碘值由（８３．２±３．５）μｇ／Ｌ上升到（１６２．２±１．６）μｇ／Ｌ，血清Ｔ４、ＦＴ４Ｉ和ｒＴ３：也与正常儿童一致而与未补碘儿童有显著性差异（Ｐ＜０．０５）．②轻度碘缺乏病儿童智商低于正常儿童（Ｐ＜０．０１），补碘在一定程度上改善其智商水平。③轻度碘缺乏病及补碘未能明显影响儿童的生长发育，可能与儿童总营养水平较差有关。     

Diminished effect of etidronate in vitamin D deficient osteopenic postmenopausal women

Objective: The effects of vitamin D deficiency in osteopenic postmenopausal women treated with intermittent cyclical etidronate have been studied. Bone mass and biochemical parameters as bone markers were measured before and after one year of therapy with intermittent cyclical etidronate. Results: In 30 patients without vitamin D deficiency, bone mass in the lumbal spine and femoral neck was significantly increased compared to 28 vitamin D deficient patients. After cyclical intermittent etidronate therapy, serum osteocalcin and PTH were significantly increased in the vitamin D deficient patients, whereas in non-vitamin D deficient patients they did not change. Conclusion: It is worthwhile measuring serum vitamin D before starting etidronate therapy and, in case of deficiency, to give vitamin D. Received: 6 April 1995/Accepted in revised form: 23 April 1996     

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     

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)