Effects of marathon running on running economy and kinematics

The present study was designed to investigate interactions between running economy and mechanics before, during, and after an individually run marathon. Seven experienced triathletes performed a 5-min submaximal running test on a treadmill at an individual constant marathon speed. Heart rate was monitored and the expired respiratory gas was analyzed. Blood samples were drawn to analyze serum creatine kinase activity (S-CK), skeletal troponin I (sTnI), and blood lactate (B-La). A video analysis was performed (200 frames · s⁻¹) to investigate running mechanics. A kinematic arm was used to determine the external work of each subject. The results of the present study demonstrate that after the marathon, a standardized 5-min submaximal running test resulted in an increase in oxygen consumption, ventilation, and heart rate (P < 0.05), with a simultaneous decrease in the oxygen difference (%) between inspired and expired air, and respiratory exchange ratio (P < 0.05). B-La did not change during the marathon, while sTnI and S-CK values increased (P < 0.05), peaking 2 h and 2 days after the marathon, respectively. With regard to the running kinematics, a minor increase in stride frequency and a similar decrease in stride length were observed (P < 0.01). These results demonstrate clearly that weakened running economy cannot be explained by changes in running mechanics. Therefore, it is suggested that the increased physiological loading is due to several mechanisms: increased utilization of fat as an energy substrate, increased demands of body temperature regulation, and possible muscle damage. Accepted: 20 March 2000     

DNA damage in cytologically normal urothelial cells of patients with a history of urothelial cell carcinoma

In order to determine if patients with a history of previous urothelial cell carcinoma (UCC) but with current normal urinary cytology have DNA damage in urothelial cells, the single-cell gel electrophoresis (comet) assay was conducted with cells obtained by urinary bladder washings from 44 patients (28 with a history of previous UCC). Increased DNA damage was observed in cytologically "normal" urothelial cells of patients with a history of UCC when compared with referents with no similar history and after correcting the data for smoking status and age (P < 0.018). Increased DNA damage also correlated with the highest tumor grade, irrespective of time or course of the disease after clinical intervention (Kendall tau correlation, 0.37, P = 0.016). Moreover, aneuploidy, as assessed by DNA content ratio (DCR; 75th/25th percentile of total DNA fluorescence of 50 comets/patient) was unaltered by smoking status, but increased with UCC grade: 1.39 +/- 0.12 (median +/- 95% confidence interval; referents); 1.43 +/- 0.11 (Grade I UCC; P = 0.264, against referents); 1.49 +/- 0.16 (Grade II UCC; P = 0.057); 1.57 +/- 0.16 (Grade III UCC; P = 0.003). Micronucleated urothelial cells (MNC) were also scored on Giemsa-stained routine cytological smears and were found not to correlate with DNA damage or DCR. MNC frequencies were higher for patients with a history of UCC and/or smoking than referents with neither history, but there was no statistical difference between groups. Taken together, these results suggest that the normal-appearing urothelium of patients resected for UCC still harbor genetically unstable cells.     

Heavy-ion-induced mutations in the gpt delta transgenic mouse: comparison of mutation spectra induced by heavy-ion,X-ray,and gamma-ray radiation

Heavy-ion radiation accounts for the major component of absorbed cosmic radiation and is thus regarded as a significant risk during long-term manned space missions. To evaluate the genetic damage induced by heavy particle radiation, gpt delta transgenic mice were exposed to carbon particle irradiation and the induced mutations were compared with those induced by reference radiations, i.e., X-rays and gamma-rays. In the transgenic mouse model, deletions and point mutations were individually identified as Spi(-) and gpt mutations, respectively. Two days after 10 Gy of whole-body irradiation, the mutant frequencies (MFs) of Spi(-) and gpt were determined. Carbon particle irradiation significantly increased Spi(-) MF in the liver, spleen, and kidney but not in the testis, suggesting an organ-specific induction of mutations by heavy-ion irradiation. In the liver, the potency of inducing Spi(-) mutation was highest for carbon particles (3.3-fold increase) followed by X-rays (2.1-fold increase) and gamma-rays (1.3-fold increase), while the potency of inducing gpt mutations was highest for gamma-rays (3.3-fold increase) followed by X-rays (2.1-fold increase) and carbon particles (1.6-fold increase). DNA sequence analysis revealed that carbon particles induced deletions that were mainly more than 1,000 base pairs in size, whereas gamma-rays induced deletions of less than 100 base pairs and base substitutions. X-rays induced various-sized deletions and base substitutions. These results suggest that heavy-ion beam irradiation is effective at inducing deletions via DNA double-strand breaks but less effective than X-ray and gamma-ray irradiation at producing oxidative DNA damage by free radicals.     

Transfection of Lepidopteran insect cells with Baculovirus DNA

Summary Several protocols are presented for preparation and transfection of Baculovirus and plasmid DNAs into Lepidopteran insect cells using the calcium-phosphate co-precipitation technique. Important parameters for optimum efficiency include the inherent susceptibility of the recipient cell line for transfection, and the method of preparation of viral and plasmid DNAs. The protocols presented provide reproducible high efficiencies for transfection of several Lepidopteran cell lines.     

Proctolin-related material in the mouse brain as revealed by immunohistochemistry

By use of a specific antiserum against the insect peptide proctolin we were able to identify proctolin-immunoreactive neurons in the mouse brain. These nerve cells belong to the nuc. mesencephalicus n. trigemini. Furthermore, the antiserum stained very few nerve fibers with varicosities in the immediate neighborhood of the roof of the third ventricle. The chemical identity of the immunoreactive material with genuine proctolin remains to be elucidated.     

内隐记忆的研究证据及临床意义

内隐记忆 (ｉｍｐｌｉｃｉｔｍｅｍｏｒｙ)一词最初由Ｇｒａｆ与Ｓｃｈａｃｔｅｒ于 1985年提出 ,指对特定的过去经验进行有意识或外显的回忆测验中表现出来的对先前获得信息的无意识提取 ,也就是说 ,在有意或无意间获得的信息、技能或习惯 ,虽不能有意识地回忆和再认 ,但会影响类似作业的成效和行为的有效性。这一概念的提出扩大了记忆研究的内涵 ,因此迅速成为记忆研究的热点之一。目前内隐记忆的研究在测量方法与理论解释方面都取得了一些进展 ,大量证据表明它与外显记忆存在质的不同 ,是一个相对独立的记忆系统。不过现存的问题也很多 ,…     

金属硫蛋白对培养神经细胞迟发性损伤的作用和一氧化氮的表达

本文以新生大鼠原代培养皮质神经元为实验材料，造成迟发性神经元损伤模型．在不同时程内，测试培养液中的细胞乳酸脱氢酶漏出量和用还原型尼克酰胺腺嘌呤二核着苷酸脱氢酶染色反应，观察培养细胞中一氧化氮合酶的表达水平．结果表明，缺血组在缺血与再灌流中，细胞乳酸脱氢酶漏出量明显高于对照组，差异显著（Ｐ＜０．００１）．一氧化氮合酶阳性神经元数量在缺血组的缺血时即明显高于对照组（Ｐ＜０．０１），再灌流后一氧化氮合酶表达仍然强烈，与对照组相比有显著差异（Ｐ＜０．０１）．当损伤细胞再灌流时，同时加入金属硫蛋白后，显示一氧化氮合酶表达减弱，和缺血组相比有显著差异（Ｐ＜０．０５～０．００１），细胞乳酸脱氢酶漏出量在再灌流后的早期近似于对照组．结合文献和本实验结果提示：在迟发性神经元损伤形成过程中一氧化氮起着重要作用；金属硫蛋白对脑缺血后迟发性神经元损伤有一定保护作用，是一种细胞保护剂，可望用于临床，控制缺血再灌流损伤。     

HSP70在米非司酮引产胎儿肝、肾、脑组织中的表达

目的对米非司酮引产胎儿肝、肾、脑组织进行热休克蛋白70的检测,探讨米非司酮对胎儿损伤的可能性.方法米非司酮引产胎儿17例,水囊引产胎儿5例, 采用免疫组化方法,检测HSP70在胎儿肝肾脑组织中的表达.结果实验组中HSP70均呈阳性表达,且有不同程度的表达,对照组均呈阴性表达.结论米非司酮可不同程度造成胎儿肝、肾、脑组织损伤.     

Short term status epilepticus in rats causes specific behavioral impairments related to substantia nigra necrosis

Summary Status epilepticus (SE) was induced for 40 min by flurothyl in well oxygenated rats. This insult resulted in selective destruction of up to 65% of the substantia nigra pars reticulata. We investigated the short and long term behavioral effects of this damage. No deficits were observed in sensorimotor reactivity, locomotor coordination, spontaneous or apomorphine-stimulated locomotor activity in the rats with induced epilepsy. However, these rats exhibited a long-lasting enhancement of amphetamine-stimulated locomotor activity. We propose that this selective impairment is caused by the necrosis of the pars reticulata. This damage might lead to deficient regulation either of mesostriatal dopamine neurons innervating nc. accumbens, or of neurons in the mesencephalic reticular formation mediating the locomotor response initiated in the nc. accumbens.