外周损伤引起成年大鼠体感皮层的功能重组

为了了解外周神经损伤对体感皮层分域组构的影响,在成年大鼠上观察了切断坐骨神经(SC)前、即刻和切断后数周内后爪皮层代表区的改变。在盐酸氯胺酮麻醉下,用微电极记录后爪皮肤轻触刺激在对侧体感皮层工区诱发的多单位反应,得出后爪的皮层代表区图。在16例中,8例大鼠观察了切断SC的即时效应。结果表明,不但SC代表区丧失皮肤反应性,原隐神经(SA)代表区的皮肤反应性也明显下降或消失,同时神经元自发活动也明显减弱。另8例大鼠在切断后数周内做了1～3次重复测定。在最初几天,原SA代表区范围内多数记录点的皮肤反应性仍未恢复,但在原SC代表区内,一些记录点转而对SA皮肤轻触刺激起反应。在随后数周内SA代表区进行性地扩张,占领了大部分原SC代表区。这一结果说明成年大鼠外周神经损伤可导致体感皮层发生显著的重组改变。     

国产五种菊属植物的核型研究

本文对国产5种菊属植物的核型进行了研究,结果为:D. indicum 2n=2x=18=16m 2st,2n=4x=36=28m 6sm 2st;D. lavandulifolium 2n=2x=18=14m 4sm,2n=4x=36=28m 6sm 2st;D. lavandulifolium var.seticuspe 2n=2x=18=12m 6sm;D. chanetii 2n=4x=36=20m 14sm 2st,2n=6x=54=38m 14sm 2st;D. potentilloides2n=2x=18=14m 2sm 2st;D. vestitum 2n=6x=54=38m 16sm.核型分析的结果表明,本文所研究类群中出现的多倍体多为异源多倍体;根据对核型资料、形态特征及地理分布特点的综合分析,作者认为多倍化是菊属野生种进行的主要途径。     

烙铁头蛇毒纤维蛋白原溶酶研究 Ⅰ分离纯化及理化性质(英文)

通过DEAE-SephadexA-50,DEAE-SepharoseCL-6B,MonoQ （FPLC）三步离子交换柱层析,纯化得到一新的纤维蛋白原溶酶,在碱性聚丙烯酰胺凝胶电泳和SDS-聚丙烯酰胺凝胶电泳上均呈单一的蛋白带。分子量为2600,等电点pl4.7;它是一个糖蛋白,含糖量6.4%,其中中性糖0.3%,已糖胺4.9%,唾液酸1.2%。烙铁头蛇毒纤维蛋白原溶酶TMVFg由187个氨基酸组成,含有较高的酸性氨基酸,此外甘氨酸含量也较高。TMVFg热稳定性强,而酸不稳定,在280 nm处具有典型的蛋白吸收峰,在无离子水中紫外消光系数E0.1%/280 nm=1.558。纯化的TMVFg具有较强的精氨酸酯酶活力,对苯甲酰-L-精氨酸乙酯（BAEE）的Km值为1.4×10[-3]M。TMVFg的活性受苯甲基丹磺酰氟（PMSF）抑制;乙二胺四乙酸（EDTA）对活性无影响。TMVFg不能使纤维蛋白原凝固,但能水解纤维蛋白原α、β链。纤溶实验表明TMVFg具有激活纤溶作用。纯化的烙铁头蛇毒纤维蛋白原溶酶对酪蛋白无作用,无出血活性,因而与凝血酶样酶、出血毒素及β-纤维蛋白原溶酶（OUYANG et al.,1977）明显不同。     

心房钠泵因子对颈动脉窦压力感受器反射的易化作用

Effects of atriopeptin II (APII) on the carotid sinus baroreflex in anesthetized rats and on the sinus nerve afferent activity in the anesthetized rabbits were investigated. The results were as follows: (1) By perfusing the isolated left carotid sinus with APII (1 microgram/ml) in anesthetized rats (n = 10), the threshold pressure (TP) of the carotid baroreflex did not show any change, while the equilibrium pressure (EP), the saturation pressure (SP) and the operating range (OR) were decreased from 101 +/- 2.8 to 95 +/- 2.0 mmHg (P less than 0.05), 202 +/- 5.2 to 168 +/- 6.1 mmHg (P less than 0.001) and 128 +/- 5.5 to 93 +/- 6.3 mmHg (P less than 0.001), respectively. The function curve of the baroreflex was shifted to the left and downward with a peak slope (PS) increased during perfusing with APII. In contrast, by perfusing the carotid sinus with sodium nitroprusside (NP, 0.5 micrograms/ml), TP and EP remained unchanged, whereas SP and OR were increased from 188 +/- 6.4 to 218 +/- 6.0 mmHg (n = 6, P less than 0.01) and from 107 +/- 6.9 to 132 +/- 7.6 mmHg (P less than 0.05), respectively. The function curve of the baroreflex and its PS were not affected by NP. The sinus nerve afferent activity was quite stable with the perfusion of carotid sinus at constant intrasinus pressure (ISP) in the rabbits (n = 6) and increased during the elevation of ISP.(ABSTRACT TRUNCATED AT 250 WORDS)     

Evidence for age-related changes in pyridine nucleotide content of isolated rat islets

The purpose of this study was to document the effect of age on alpha-glycerophosphate activity and pyridine nucleotide concentration in pancreatic islets isolated from rats. In order to do this, islets were isolated from pancreases of 2 and 12 month-old rats, and measurements made of alpha-glycerophosphate activity and of NAD+ and NADH, determinations were made following incubation at both basal (5.6 mM) and elevated glucose concentrations (28 mM). The results indicated that islet alpha-glycerophosphate dehydrogenase activity was decreased (P less than 0.001) by approximately 50% in the older rats. This was associated with an increase in mean (+/- SEM) basal NADH content (pmol/microgram DNA) in 12 month-old (4.48 +/- 0.31) as compared to 2 month-old rats (2.73 +/- 0.49). Although mean (+/- SEM) basal NAD+ levels (pmol/microgram DNA) were the same in 2 and 12 month-old rats (29.4 +/- 2.5 and 30.8 +/- 2.8, respectively), NAD+ content following incubation at elevated levels of glucose declined (absolutely and relatively) to a significantly greater degree in the younger rats. The incremental rise in islet NADH concentration following incubation at the elevated glucose concentration was similar in the two groups, but the relative increase was only approximately half as great in islets from 12 month-old rats. These data indicate that the age-related decline in the activity of alpha-glycerophosphate dehydrogenase, the enzyme regulating the glycerophosphate shuttle system in 12 month-old rats, is associated with alterations in islet pyridine nucleotide composition.(ABSTRACT TRUNCATED AT 250 WORDS)     

Enzymatic down regulation with exercise in rat skeletal muscle

Maximal activities of rat skeletal muscle mitochondrial citrate synthase (CS), malate dehydrogenase (MDH), and alanine aminotransferase (ALT), as well as several other mitochondrial enzymes involved in various metabolic functions were significantly suppressed after a single bout of acute or exhaustive treadmill running. This enzymatic "down regulation" was maintained 24 and 48 h post exhaustion, especially in the untrained rats. Neither muscle cytosolic nor hepatic enzymes exhibited down regulation after exercise. Proteolysis was increased with exercise as assessed by the clearance of [3H]leucine previously incorporated into the proteins of the rats. Decreased CS, MDH, and ALT activities correlated with a significant loss of mitochondrial total protein sulfhydryl (r = 0.67, 0.68, 0.59, respectively, P less than 0.001) in untrained rats and both CS and MDH could be partially restored by incubation with dithiothreitol. Endurance-tested untrained and trained rats had significantly higher glutathione peroxidase (GPX) activity in both muscle mitochondria and cytosol which correlated significantly with endurance time (r = 0.70 and 0.74, respectively). It is concluded that enzymatic down regulation is not caused by proteolysis alone; i.e., peroxides and oxygen free radicals produced in prolonged exercise may alter the intramitochondrial redox state by oxidizing free thiols that may be required at active sites of these enzymes. Training may enhance the ability of the muscle to resist the toxic oxygen species by increasing GPX activity.     

Role of sulphated tyrosine residue in influencing the biologic activity of human cholecystokinin-33

To evaluate the role of the sulphated tyrosine residue in position 27 in human cholecystokinin-33, parallel bioassay of the sulphated form of human cholecystokinin-33 and the unsulphated form of human cholecystokinin-33 was performed on the pancreatic protein secretion. Both peptides increased the protein output in a dose-related manner. However, the sulphated form possessed a considerably higher activity than the sulphated form. The relative potency of the unsulphated human cholecystokinin-33 compared to that of the sulphated human cholecystokinin-33 (taken as 1.0) was 0.08. From the results, it was suggested that the sulphated tyrosine may play an important role in controlling the activity of the longer molecular forms as well as that of the smaller forms of cholecystokinin.     

Insulin induces activation and translocation of protein kinase FA (a multifunctional protein phosphatase activator) in human platelet

Protein kinase FA (an activator of the ATP.Mg-dependent multifunctional protein phosphatase) has been identified in both cytosol and plasma membrane isolated from human platelets. The FA activity in the cytosol is active whereas the FA activity in the membrane is inactive. Quantitative analysis further indicates that approximately 90% of total FA is present in the membrane whereas only 10% of FA is localized in the cytosol, suggesting that the inactive membrane-associated FA might be regulated. This notion has subsequently been demonstrated that exposure of platelets to physiological concentrations of insulin for only 1 min resulted in an increase in cytosolic FA activity to about 300% of control values in the absence of insulin and in a corresponding decrease in FA activity in the membrane. It is concluded that the molecular basis for insulin action on cellular metabolism may partly be mediated through the activation and translocation of protein kinase FA in the membrane. It is suggested that redistribution of protein kinase FA may represent a transmembrane signal of insulin.