用电化学检测器的高效液相色谱法测定血清及尿中速尿的含量

本文报告了用电化学检测器的高效液相色谱法测定血清及尿中速尿含量的方法。样品予处理方法:血清用乙腈除蛋白,尿用蒸馏水稀释50倍。采用作者合成的FD-Val-OH作为内标物。色谱条件为:反相柱,以含35%乙醇的5mmol/L四丁基铵水溶液为流动相(pH7.50),流速1.0ml/min;用电化学检测器,检测电压0.90V:速尿及内标物的保留时间分别为10和15min。通过计算速尿对内标物的峰高比求得速尿含量。血清及尿中的最低检测浓度分别为16和9ng/ml。标准曲线在0.25～5ng/μl(血清)、0.5～10ng/μl(尿)的浓度范围内呈线性关系。血清及尿中回收率分别为100.5%和100.6%。变异系数在4.6%以下。     

Intralesional steroid injection for the management of otohematoma

OBJECTIVES: To compare the therapeutic efficacies of aspiration plus intralesional steroid injection and aspiration plus pressure dressing for the management of otohematoma. STUDY DESIGN AND SETTING: Fifteen patients with otohematoma were treated by aspiration plus pressure dressing (the pressure dressing group) and 34 patients were treated with intralesional steroid injections followed by simple aspiration (the steroid injection group). RESULTS: Otohematoma resolved within four weeks in all 15 patients in the pressure dressing group, but eight of the 15 showed perichondrial thickening. The duration of treatment was shorter in the steroid injection group than in the pressure dressing group; 14 (41.2%) of the 34 recovered after the first injections and another 15 (44.1%) after the second, and the remaining 5 (14.7%) after the third without any complications. However, multiple steroid injections are needed due to a high early recurrence rate. CONCLUSION: Intralesional steroid injection is the treatment of choice for the management of otohematoma. The correction of causative use of a hard pillow, a helmet, and headphones is essential to prevent late recurrence.     

First Evidence of Okadaic Acid in <Emphasis Type="Italic">Mytilus galloprovincialis</Emphasis> Mussels,Collected in a Mediterranean Lagoon,Tunisia

Evidence of the presence of okadaic acid (OA) and its monthly fluctuations are reported for the first time in Mytilus galloprovincialis samples collected from June 2005 to May 2006 in the Bizerte Lagoon. All of the samples with the exception of those taken in August 2005 were found to be contaminated. The level of OA in mussels exceeded the regulatory limit of DSP toxins (16 μg OA/100 g mussel meat) within the European Union (2002) in only two cases: in January and February, 2006 with 31.85 ± 3.06, and 18.86 ± 1.88 μg OA/100 g mussel meat respectively. During the investigative period, potentially toxic dinoflagellates were observed. The results reported here, although based on limited sampling, demonstrate for the first time the existence of a risk to public health from diarrheic shellfish poisoning in cultivated bivalve mollusc in Tunisia.     

运动性横纹肌溶解症的诊治

运动性横纹肌溶解症是指运动后肌纤维崩解断裂导致肌细胞内容物释放入血引起的临床综合征,以肌痛、乏力、肌肉肿胀、深色尿及血中肌细胞内容物(特别是肌红蛋白和肌酸激酶)的含量增高为临床特征。严重的运动性横纹肌溶解症可并发急性肾衰竭、急性筋膜间室综合征、弥漫性血管内凝血及多器官功能障碍综合征,甚至危及生命。早期积极静脉补液、及时血液净化治疗可防止病情进一步发展。本病大多预后较好,如出现严重并发症死亡率明显升高。在军事训练及体育运动中应注意防治。     

Relaxation Effect of Synthetic Ceramide Analogues in Cat Esophageal Smooth Muscle Cells

Ceramide has emerged as a novel second messenger for intracellular signalling. It is produced from sphingomyelin and is involved in the control of cell differntiation, proliferation, and apoptosis. C₂-ceramide, short chain ceramide, plays a role in mediating contraction of cat esophageal smooth muscle cells. We examined the effect of synthesized ceramide analogues on the C₂-ceramide and ACh-induced contraction in esophageal smooth muscle cells isolated with collagenase. CY3523, CY3525, or CY3723 inhibited C₂-ceramide induced contraction, in a time dependent manne. Each analogue also inhibited the contraction in concentration dependent manners. CY 3523, CY 3525, and CY 3723 had no effect to the contraction induced by PMA. The inhibition with CY3523, CY3525 and CY3723 on the C₂-ceramide induced contraction was recovered by PMA. These analogues decreased the density of MAPK bands (p44/42 or p38) in the western blot. These results suggest that ceramide analogues can inhibit C₂-ceramide induced contraction via PKC and MAPK dependent pathway.     

The effect of a free-radical scavenger, N-2-mercaptopropionylglycine, on the survival of skin flaps

Oxygen free radicals may have an important role in tissue injury, which occurs on reperfusion of previously ischemic skin flaps. Therefore, therapy directed against the toxic effects of reactive oxygen species may protect skin flaps from ischemia/reperfusion injury. Various scavengers of oxygen free radicals have previously been reported to be effective in ameliorating ischemia/reperfusion injury. In the present study, N-2-mercaptopropionylglycine (MPG), a free-radical scavenger, was evaluated for its effectiveness in limiting the extent of necrosis resulting from ischemia/reperfusion injury in rat skin. Island skin flaps were elevated in the abdomen and groin based on an inferior epigastric neurovascular pedicle. The venous drainage from the flap was occluded for 7 hours, and reperfusion was established. The majority of flaps in the control group exhibited complete necrosis on Day 7 postoperatively. Treatment with systemic MPG (20 mg/kg of body weight) significantly improved flap survival from 22 to 71% (p less than 0.01) when administered at the time of reperfusion. However, MPG administered 1 hour after reperfusion did not influence the survival of the flaps. The results suggest that MPG may exert its beneficial effects on flap survival by scavenging oxygen free radicals formed at the time of reperfusion following prolonged ischemia.     

Effects of chronic ethanol ingestion and folate deficiency on the activity of 10-formyltetrahydrofolate dehydrogenase in rat liver

BACKGROUND: We recently observed that ethanol feeding impairs 10-formyltetrahydrofolate (10-FTHF) dehydrogenase (EC 1.5.1.6.) and 10-FTHF hydrolase activity in rats. In the present study, we explored the effects of folate deficiency or sufficiency combined with alcoholic intake on 10-FTHF and possible mechanisms by which chronic ethanol ingestion produces folate deficiency. METHODS: Sprague-Dawley rats were fed either folate-sufficient (FS) or folate-deficient (FD) diets; with or without ethanol (E) for four weeks. Hepatic 10-FTHF dehydrogenase and hydrolase activity, plasma folate and homocysteine were measured at baseline and after feeding experimental diets. RESULTS: Liver weight increased slightly with either folate deficiency or ethanol consumption. In rats fed the folate-sufficient diet with ethanol (FSE), plasma folate was decreased slightly (p<0.05) and plasma homocysteine elevated compared to rats fed the FS diet without ethanol. Ethanol did not affect plasma folate and plasma homocysteine in FD rats. Red-blood cell (RBC) folate was increased similarly in rats by ethanol feeding (FSE and FDE>FS and FD). Feeding folate deficient or ethanol (FSE, FD and FDE) diets depressed hepatic activities of 10-FTHF dehydrogenase, which catalyzes the oxidative deformylation of 10-FTHF to tetrahydrofolate (THF) and carbon dioxide. Rats consuming the FDE diet had the lowest enzyme activities of the experimental groups, implying that folate deficiency and ethanol consumption each affect enzyme activity. CONCLUSIONS: We confirm that ethanol decreases hepatic 10-FTHF dehydrogenase activity and show that this decrease occurs irrespective of folate status. This shows that modulation of 10-FTHF is one possible mechanism by which ethanol intake decreases folate status and affects one-carbon metabolism.