UNILATERAL BRAIN DAMAGE AND BILATERAL SKIN CONDUCTANCE LEVELS IN HUMANS

Left and right, palmar and dorsal skin conductance levels (SCLs) were obtained from hospital controls, left hemisphere lesion Ss, right hemisphere lesion Ss, and diffuse or bilateral lesion Ss during several experimental conditions involving rest, passive auditory stimulation, motor reactions, and simple “perception”. The unilateral lesion groups generally displayed significantly higher palmar SCLs on the side contralateral to their lesion. Such “laterality” was not demonstrated in dorsal recordings or in the hospital controls or diffuse lesion group. These unilateral lesion groups had higher palmar SCLs during passive stimulation than during rest, motor, or perception phases. Results were discussed in terms of possible neural mechanisms underlying the phenomena.     

密质骨损伤机理的实验研究

用Ｉｎｓｔｒｏｎ试验机对新鲜夫股骨密质骨试样进行一维拉伸实验研究，利用实验结果对由平行粘弹性杆系统建立的密质骨损伤本构模型待定参数进行拟合，获得较高的相关系数和较好的显著性水平。     

Modulation of osteopontin in proteinuria-induced renal interstitial fibrosis

Proteinuria is associated with macrophage-dependent interstitial fibrosis (IF). Osteopontin (OPN), a macrophage chemoattractant, may be involved in the transition of proteinuria to IF but protective properties have also been reported. To elucidate whether OPN may be involved in the proteinuria-induced cascade of tubulointerstitial damage, renal expression of OPN was studied during the development of proteinuria-induced renal damage and during anti-proteinuric intervention with ACE inhibition (ACEi). First, the temporal relationships between proteinuria, interstitial OPN induction, and IF in adriamycin nephrosis (AN), a model of chronic proteinuria-induced renal damage, were studied. Second, the effect of anti-proteinuric treatment on OPN expression was investigated. The time course of OPN induction and markers of renal damage was studied in rats with unilateral AN at 6-week intervals until week 30. In a second study, a renal biopsy was taken 6 weeks after induction of bilateral AN; subsequently, rats were treated with ACEi until termination (week 12). In unilateral AN, proteinuria developed gradually and stabilized at week 10. In proteinuric kidneys, OPN expression was induced from week 12 onwards. Simultaneously, a progressive increase in interstitial macrophages, alpha-smooth muscle actin (alpha-SMA), collagen type III, and focal glomerulosclerosis (FGS) was observed. In bilateral AN, ACEi reduced proteinuria and OPN protein and stabilized fibrosis. In untreated animals, OPN mRNA increased, with stable OPN protein and fibrosis and increased FGS. Thus, in AN, development of proteinuria is followed by up-regulation of OPN along with markers of renal damage. The up-regulation of OPN is reversible by anti-proteinuric treatment without a corresponding reduction in fibrosis. Whereas these data are consistent with a role for OPN in the cascade of transition from proteinuria to fibrosis, intervention with ACEi showed that reduction of OPN does not attenuate established fibrosis.     

Hepatitis B surface antigen particles of subtypes adw and adr, and compound subtype (adwr) in symptom-free carriers in Japan.

Of sera from 1,878 Japanese blood donors who carried hepatitis B surface antigen (HBsAg), 420 were subtyped as adw (22.4%) and 1,443 as adr (76.8%); only 15 (0.8%) contained HBsAg of subtype ayw or ayr. Sera with HBsAg/adr had higher HBsAg titres than those with HBsAg/adw (geometric mean of haemagglutination titre: 10.1 +/- 2.4 vs. 9.7 +/- 2.4, p less than 0.01), and a higher prevalence of hepatitis B e antigen (24% vs. 13%, p less than 0.001). Carriers of HBsAg/adr progressively predominated over those of HBsAg/adw with increasing age. Of sera from 1,863 carriers of HBsAg/adw or HBsAg/adr, 182 (9.8%) contained HBsAg particles with both subtypic determinants in the w/r allele. The presence of w and r determinants on the same particles was ascertained by sandwiching them between monoclonal antibody with the specificity for w and that with the specificity for r. HBsAg particles of compound subtype (adwr) were found more often in sera with hepatitis B e antigen than those without it (145/403 [36.0%] vs. 37/1,460 [2.5%], p less than 0.001). Sera with HBsAg/adwr particles had HBsAg titres higher than those without them (12.4 +/- 1.9 vs. 9.7 +/- 2.3, p less than 0.001). HBsAg/adwr particles arise from phenotypic mixing of the S-gene product of wild-type virus and that of mutants with point mutations for subtypic changes. The results obtained indicated that HBV strains of subtype adr have a higher replicative activity than those of adw, and suggested that mutations in the S gene for subtypic changes would be associated with an active replication of hepatitis B virus.     

Antistressor effect of dalargin in rats with immobilization stress

Laboratory of Experimental Surgery, A. V. Vishnevskii Institute of Surgery, Academy of Medical Sciences of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR M. I. Kuzin.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 111, No. 6, pp. 617–619, June, 1991.     

耳穴静态电测量中的瞬变响应

耳穴电参数时变关系实验表明，在测量起始ｔ＜２τ时，因瞬变作用，电位Ｅ（ｔ）和压降Ｕ（ｔ）为瞬态响应，响应函数呈指数关系，特征参数为弛豫时间τ，τ≈ＲＣ；ｔ＞２τ时，为时变间期。电路分析给出数学描述，并与耳穴和模拟实验结果较相符。提示，时变特征应以ｔ＞２τ后提取，静态电测量时，采样应避开瞬变期，可提高准确性。该工作对正确鉴别时变性和特征提取，全面认识耳穴电特性具有重要意义。     

Analysis of 8-hydroxydeoxyguanosine 5'-monophosphate (8-OH-dGMP) as a reliable marker of cellular oxidative DNA damage after gamma-irradiation

In order to improve 8-hydroxyguanine (8-OH-Gua) detection in DNA, we digested isolated DNA with nuclease P1 and analyzed for 8-hydroxydeoxyguanosine 5'-monophosphate (8-OH-dGMP) using a high-performance liquid chromatography system equipped with an electrochemical detector (HPLC-ECD). The amount of 8-OH-Gua in the DNA was expressed as the ratio of 8-OH-dGMP to deoxycytidine monophosphate (dCMP). Using this analysis, the background level of 8-OH-Gua in DNA from human lung carcinoma cells (A549) was several-fold lower than that obtained by a previous method. A549 cells were exposed to 20-60 Gy of gamma-radiation and an increase in 8-OH-Gua concentration was observed with increasing gamma-ray dose (0.3 residues per 10(7) dCMP per Gy). Moreover, by an immunohistochemical procedure using a commercial FITC-kit, 8-OH-Gua was clearly detected in A549 cells and the fluorescence intensity of cells with oxidative DNA damage increased with the doses of gamma-irradiation. Using an endonuclease nicking assay, we also found that gamma-rays decreased 8-OH-Gua repair activity. The results indicate that 8-OH-dGMP is a useful and sensitive marker for estimating oxidative damage in DNA.     

Increase in ferric and ferrous iron in the rat hippocampus with time after kainate-induced excitotoxic injury

The present study aimed to elucidate the distribution of ferric and ferrous iron in the hippocampus after kainate-induced neuronal injury. A modified Perl's or Turnbull's blue histochemical stain was used to demonstrate Fe3+ and Fe2+ respectively. Very light staining for iron was observed in the hippocampus, in normal or saline-injected rats and 1-day post-kainate-injected rats. At 1 week postinjection, a number of Fe3+-positive, but very few Fe2+-positive, cells were present, in the degenerating CA fields. At 1 month postinjection, large numbers of Fe3+-positive glial cells, and some Fe2+-positive blood vessels, were observed. At 2 months postinjection, large numbers of Fe3+- and Fe2+-positive glial cells were present. The labeled cells had light and electron microscopic features of oligodendrocytes, and were double labeled with CNPase, a marker for oligodendrocytes. The observation of an increasing number of Fe3+- and Fe2+-positive cells in the degenerating hippocampus with time is consistent with the results of a nuclear microscopic study, in which an increasing amount of iron was detected in the degenerating hippocampus after kainate injection. In addition, the present study showed a shift in the oxidation state of the accumulated iron, with more cells becoming Fe2+ at a late stage. A possible consequence of the high amounts of Fe2+ in the hippocampus after kainate injection is that it could promote free radical damage in the lesioned areas.     

Enhanced sprouting of retinotectal fibers after early superior colliculus lesions in hamsters treated with gangliosides

Summary The effects of exogenous gangliosides on sprouting of optic tract axons was studied in hamsters which, after a right tectal lesion on the day after birth (P1), had an abnormal retinotectal projection from the left eye to the left superior colliculus (SC). Sprouting of these axons was induced by removing the competing input by right eye removal on postnatal day 9 (P9). Intraperitoneal G_M1, given daily and started on P9, significantly stimulated the sprouting response. This was demonstrated by Fink-Heimer silver staining of anterograde axonal degeneration three days after the left eye was removed on P36. Terminal fields in the left SC were, in average, twice as large compared to controls. An estimate of the total number of terminals (silver stained particles) revealed a value of 7.9×10⁶ for G_M1 and 3.2×10⁶ for control hamsters, respectively. Diencephalic structures which also receive collateral input from the sprouting optic tract did not show any alterations in the size of the terminal field due to G_M1-treatment, suggesting that, in vivo, gangliosides fail to initiate sprouting in areas that have not previously been denervated. Unexpectedly, G_M1-treated hamsters also had significantly smaller right SC damage and less left damage near the midline. Subsequent reanalysis of the data based on a lesion-matching procedure indicates that effects on reducing atrophy were independent of the G_M1-enhanced sprouting of retinofugal axons. These findings provide the first direct evidence that exogenous G_M1 stimulates lesion-induced axon sprouting in the mammalian brain.     

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