The mechanism of skeletal muscle myosin ATPase. Interaction of myosin active center with ATP and with ADP

The kinetics of the fluorescence enhancement and the transient release of H+ caused by the binding of ADP to the active center of myosin has been compared to that caused by myosin-ATP interaction. The results show that both the time courses of the fluorescence enhancement and the transient H+ release caused by ADP binding, like that caused by ATP hydrolysis in the initial burst, are monophasic exponential processes. The fact that the rates of these two processes are also equal suggests that they both reflect the same mechanistic event in the mechanism of ADP binding. The kinetics of ADP binding as measured by the fluorescence enhancement and the H+ release is different from that of ATP. This is in agreement with our previous finding that the enhancement of fluorescence and the transient release of H+, in the case of ATP, reflect the initial burst of ATP hydrolysis, whereas in the case of ADP, they represent a conformational change in the myosin-ADP complex. The magnitude of the H+ transient caused by the initial burst is approximately equal to that caused by ADP binding. The amplitude of the fluorescence enhancement caused by ADP binding is equal to one-third of that caused by the initial burst.     

Kinetic studies of fructokinase I of pea seeds

Fructokinase I of pea seeds has been purified to homogeneity and the enzyme shown to be monomeric, with a molecular weight of 72,000 +/- 4000. The reaction mechanism was investigated by means of initial velocity studies. Both substrates inhibited the enzyme; the inhibition caused by MgATP was linear-uncompetitive with respect to fructose whereas that caused by D-fructose was hyperbolic-noncompetitive against MgATP. The product D-fructose 6-phosphate caused hyperbolic-noncompetitive inhibition with respect to both substrates. MgADP caused noncompetitive inhibition, which gave intercept and slope replots that were linear with D-fructose but hyperbolic with MgATP. Free Mg2+ caused linear-uncompetitive inhibition when either substrate was varied. L-Sorbose and beta, gamma-methyleneadenosine 5'-triphosphate were used as analogs of D-fructose and MgATP, respectively. Inhibition experiments using these compounds indicated that substrate addition was steady-state ordered, with MgATP adding first. The product inhibition experiments were found to be consistent with a steady-state random release of products. The substrate inhibition caused by MgATP was most likely due to the formation of an enzyme-MgATP-product dead-end complex, whereas that caused by D-fructose was due to alternative pathways in the reaction mechanism. The inhibition caused by Mg2+ can be explained in terms of a dead-end complex with either a central complex or an enzyme-product complex.     

Effect of pH on pulmonary vascular tone, reactivity, and arachidonate metabolism

We studied the effects of perfusate pH on pulmonary vascular tone, reactivity, and thromboxane and prostacyclin synthesis in isolated buffer-perfused rabbit lungs. Extracellular acidosis did not affect base-line vascular tone, but alkalosis had a biphasic effect. Increasing the perfusate pH from 7.40 to 7.65 caused vasodilation, whereas raising pH to 7.70-8.10 caused vasoconstriction. Removing calcium (Ca2+) from the perfusate completely prevented the vasoconstriction caused by alkalosis. Perfusate pH strikingly affected pulmonary vascular reactivity. Acidosis inhibited the vasoconstriction caused by thromboxane and potassium chloride (KCl) but did not affect the response to angiotensin II. Alkalosis, in contrast, augmented the vasoconstriction caused by thromboxane and angiotensin II but reduced the vasoconstriction caused by KCl. Changes in pH also altered thromboxane and prostacyclin synthesis after the infusion of exogenous arachidonic acid (AA) or the endogenous release of AA by the lipid peroxide tert-butyl hydroperoxide.     

Adrenergic influence on rat plasma concentrations of tyrosine and tryptophan

Isoprenaline given to rats in doses between 0.08 and 10 mg/kg intraperitoneally caused a significant decrease in plasma concentrations of tyrosine and tryptophan. Low doses of adrenaline (0.04 ? 0.16 mg/kg, intraperitoneally) caused a 30 per cent decrease in plasma concentrations of tyrosine, while high doses (0.63 ? 1.25 mg/kg, intraperitoneally) caused an increase in plasma tyrosine to nearly 200 per cent of the controls. High doses of noradrenaline (0.63 ? 2.5 mg/kg, intraperitoneally) caused a similar increase in plasma tyrosine concentration. The decrease in plasma amino acids caused by these catecholamines is inhibited by propranolol, suggesting that this effect is mediated via adrenergic β-receptors, while the increasing effect is inhibited by phenoxybenzamine, which suggests that this effect is caused by an α-adrenergic mechanism.     

Pharmacological modification of pulmonary vascular injury: possible role of cAMP

Experiments were designed to test the hypothesis that drugs which increase adenosine 3',5'-cyclic monophosphate (cAMP) in the lung would prevent the pulmonary hypertension and the increase in vascular permeability caused by the infusion of the oxidant lipid peroxide, tert-butyl hydroperoxide (t-bu-OOH), in isolated rabbit lungs perfused with Krebs-Henseleit buffer. Pretreatment with indomethacin or verapamil was also studied, since these drugs block the increase in pulmonary arterial pressure caused by t-bu-OOH. Indomethacin or verapamil prevented the pulmonary hypertension but did not prevent the increase in permeability caused by t-bu-OOH. Consequently, indomethacin or verapamil treatment partially reduced the gain in lung weight caused by t-bu-OOH. In contrast, pretreatment with isoproterenol, prostaglandin E1, or a cAMP analogue not only prevented the pulmonary hypertension but also inhibited the increase in vascular permeability caused by t-bu-OOH. Consequently, these drugs completely blocked the gain in lung weight caused by t-bu-OOH. Posttreatment with aminophylline or the cAMP analogue also significantly reduced the gain in lung weight caused by t-bu-OOH. These results indicate that pharmacological therapy can reduce the pulmonary hypertension and the increase in vascular permeability caused by the infusion of a lipid hydroperoxide. Since isoproterenol, aminophylline, prostaglandin E1, and a cAMP analogue all had similar effects, the results suggest that the likely common mechanism for their protective effect is an increase in cAMP.     

高压蒸汽灭菌对钛合金内植入物的疲劳的影响

分析了制约骨折手术成功的因素,一是钛合金内植人物经受长期反复高压蒸汽灭菌造成材料疲劳引起断裂;二是AO手术的引起应力集中和疲劳断裂。提出了发展骨内固定植入物的建议。     

Multiple fatal mycetism caused byAmanita virosa in Mexico

Mushroom poisonings caused by amatoxins are mostly lethal. Information about mycetisms caused by white species ofAmanita is scarce. The present paper describes a case of mushroom poisoning caused byA. virosa. A prolongated latency period (6–10 hours), followed by cholera-like, improvement and visceral complication phases confirmed the amatoxin poisoning. The consumption of about 3 pounds of the toadstool by seven persons caused the death of five. Two patients survive the ingestion.     

小叶榕不同提取物的主要药效学研究

为研究小叶榕不同提取部位的镇咳、抗炎作用,采用氨水致咳小鼠动物模型、枸橼酸致咳豚鼠动物模型来评价小叶榕不同提取部位的镇咳作用;采用二甲苯滴耳廓致肿胀的小鼠动物模型、大鼠棉球肉芽肿动物模型来评价小叶榕不同提取部位的抗炎作用。结果表明:小叶榕醇沉不溶物能延长小鼠和豚鼠的咳嗽潜伏期,但不能减少咳嗽次数,小叶榕水提物、水提醇沉溶解物、大孔吸附树脂吸附洗脱物能延长小鼠和豚鼠的咳嗽潜伏期,并能减少咳嗽次数,其中水提醇沉溶解物镇咳作用最强;小叶榕醇沉不溶物不能减轻二甲苯引起的小鼠耳廓肿胀的程度,能减轻大鼠棉球肉芽肿足跖肿胀的程度,但效果不明显,小叶榕水提物、水提醇沉溶解物、大孔吸附树脂吸附洗脱物均能明显减轻二甲苯引起的小鼠耳廓肿胀的程度,并能明显减轻大鼠棉球肉芽肿足跖肿胀的程度。这表明国产小叶榕不同提取部位具有明显的镇咳、抗炎作用。     

Effect of two long acting injectable progestogens on lactation in the human.

The effects of Depoprovera and Deladroxone were studied in humans, on certain milk components as well as on the growth of the nursed infants. Both drugs caused reduction in milk yield. Both drugs caused an increase in the concentration of milk total proteins, however. Depoprovera caused an increase while Deladroxone caused a decrease in the total amount of milk proteins per feed. Depoprovera showed no effect while Deladroxone caused an increase in the concentration of milk lipids; however, both drugs caused reduction in the total amount of milk lipids per feed. Both drugs showed no effect on the concentration of milk lactose, but caused reduction in the total amount of milk lactose per feed. The percentage increase in weight of nursed infants was decreased by Depoprovera, but not affected by Deladroxone.     

Inhibitory action of auxin on root elongation not mediated by ethylene

The inhibitory effects of indole-3-acetic acid (IAA) and 1-aminocyclopropane-1-carboxylic acid (ACC) on elongation growth of pea (Pisum sativum L.) seedling roots were investigated in relation to the effects of these compounds on ethylene production by the root tips. When added to the growth solution both compounds caused a progressively increasing inhibition of growth within the concentration range of 0.01 to 1 micromolar. However, only ACC increased ethylene production in root tips excised from the treated seedlings after 24 hours. High auxin concentrations caused a transitory increase of ethylene production during a few hours in the beginning of the treatment period, but even in 1 micromolar IAA this increase was too low to have any appreciable effect on growth. ACC, but not IAA, caused growth curvatures, typical of ethylene treatment, in the root tips. IAA caused conspicuous swelling of the root tips while ACC did not. Cobalt and silver ions reversed the growth inhibitory effects induced by ACC but did not counteract the inhibition of elongation or swelling caused by IAA. The growth effects caused by the ACC treatments were obviously due to ethylene production. We found no evidence to indicate that the growth inhibition or swelling caused by IAA is mediated by ethylene. It is concluded that the inhibitory action of IAA on root growth is caused by this auxin per se.     

新疆额河河谷林区景观格局对杨树植食性昆虫危害的影响

开展森林景观格局与植食性昆虫危害关系的研究,是构建景观生态安全格局和实现有害生物生态调控的重要理论依据。在额河河谷林区开展实地调查获取杨树植食性昆虫危害数据,基于遥感数据提取景观格局相关指数,使用线性混合效应模型（Linear Mixed-Effects Models）分别从景观水平和景观类型水平上分析了林区景观格局与林地、耕地、草地和荒地的景观格局对两种植食性昆虫危害的影响。结果表明在额河河谷林区中,景观破碎化是造成两种植食性昆虫危害加重的关键,但食叶率和潜叶蛾虫口密度对景观格局的响应不完全一致;景观水平下,景观丰富度和景观连接度越高,食叶率越高,平均斑块面积与潜叶蛾虫口密度呈显著负相关;景观类型水平下,林地的斑块数量越多,额河河谷林区受到的植食性昆虫危害越严重,耕地面积的增加导致潜叶蛾虫口密度上升,荒地的景观凝聚力指数和草地的平均斑块分维数与食叶率呈显著正相关。因此在优化景观格局时,合理规划景观组成并减少景观破碎化有助于维持经济发展和生态保护的平衡,促进森林的可持续发展。     

腹腔镜胃癌根治术中转开腹的原因分析

目的:分析腹腔镜胃癌根治术中转开腹手术的原因。方法:回顾性分析2011年1月~2013年1月300例采用腹腔镜行胃癌根治手术患者的资料,总结分析其中11例行中转开腹手术的原因。结果:因腹腔内出血中转4例,腹内脏器损伤2例,腹腔严重粘连3例,气腹造成难以控制的高碳酸血症1例,器械损伤1例。结论:腹腔镜胃癌根治术具有创伤小、恢复快、住院时间短、患者易接受等优点,但也存在一定的中转开腹手术率,主要与患者原因、术者原因和器械原因有关。     

Fluctuations and regulation of wheat-bulb fly populations at Rothamsted

Four populations of the wheat-bulb fly studied at Rothamsted incurred substantial and regulatory losses of larvae caused by food shortage. The following hypothesis is proposed to explain population changes of the fly. Fluctuations caused by weather are stabilized by density-dependent larval mortality caused by food shortage. The effect of weather is, however, pervasive as it also affects food shortage by influencing the number of shoots available to larvae.     

Onychomycosis by <Emphasis Type="Italic">Scytalidium dimidiatum</Emphasis> in green tea leaf pluckers: report of two cases

Two cases of onychomycosis in green tea leaf pluckers caused by Scytalidium dimidiatum, a dematiaceous non-dermatophytic mold has been desribed. Onychomycosis caused by Scytalidium dimidiatum is clinically indistinguishable from that caused by dermatophytes and responds poorly to antifungals. The clinical presentations in the cases were of distal subungual type with associated melanonychia involving thumbnails. These cases have unique importance, because besides disfigurement, this has adversely affected the livelihood of the patient and poor response to antifungal dissuaded them from treatment compliance. To the best of our knowledge, this is the first report of onychomycosis caused by Scytalidium dimidiatum in green tea leaf pluckers.     

红色毛癣菌和枝孢样枝孢霉混合感染导致银屑病患者甲真菌病1例

目的报道1例银屑病患者出现红色毛癣菌和枝孢样枝孢霉混合感染导致的甲真菌病。方法报告病例,对甲标本进行真菌镜检和培养,对病原菌进行形态学及分子生物学鉴定。结果该病例经临床、真菌镜检和真菌培养鉴定,确诊为红色毛癣菌和枝孢样枝孢霉导致的甲真菌病。病原菌通过菌落和显微镜下形态特征结合rRNA内转录间隔区序列分析证实。结论通过形态学及分子生物学鉴定,证实为真菌红色毛癣菌和枝孢样枝孢霉混合感染导致的甲真菌病。     

A Comparison of Some Metabolic Effects of N-Methylaspartate Stereoisomers,Glutamate and Depolarization: A Multinuclear MRS Study

Exposure of guinea pig brain slices to low concentrations (10 M) of NMDA caused decreases in PCr and ATP within 30 min, with a slower decrease in NAA and increase in lactate, both detectable after 1 h. Exposure to NMDA for over 1 h or at higher concentrations caused further increases in lactate and decreases in NAA, with no further change in PCr or ATP. The L-isomer, NMLA, and the racemic mixture, NMDLA, caused similar changes in lactate and NAA, but both produced greater decreases in the energy state than NMDA, similar to those caused by prolonged exposure to glutamate. MK-801 prevented the changes in the energy state caused by NMDA, but not those caused by NMLA or by glutamate. The results are compared to previous studies on depolarization and discussed in terms of the role of the NMDA sub-type of glutamate receptor in the excitotoxic hypothesis of neuronal degeneration.     

复杂易位遗传效应的探讨—附一例罕见复杂易位核型

本报道一例罕见复杂易位核型：46,XX,t(1;14;10)。并到往资料,探讨和分析复杂易位和一般平衡易位对表型及生育的遗传效应。结果显示,一般易位导致智能低下和多发畸形的频率各为3.57%,复杂易位所致智能低下频率为21.73%, 多发畸形的频率为17.39%。提示复杂2易位所致智能低下和畸形频率明显高于一般易位。     

Role of an oxidative stress in the macrophage dysfunction caused by erythrophagocytosis

A phagocytic challenge with immunoglobulin G (IgG)-coated erythrocytes (EIgGs) has been shown to cause a subsequent depression of macrophage respiratory burst capacity and phagocytic function. The present study evaluated the hypothesis that this macrophage dysfunction is caused by an oxidative stress. An oxidative stress induced by ferric ammonium citrate (FAC) plus cumene hydroperoxide (CHP) caused a depression of macrophage function that was attenuated by antioxidants and iron chelators. In contrast, the same antioxidants and iron chelators did not alter changes caused by a challenge with EIgGs. EIgG challenge caused an increase in lipid peroxidation but failed to deplete glutathione (GSH) or decrease the activity of glyceraldehyde-3-phosphate dehydrogenase (GA-3-PD), suggesting that there was only a slight oxidative stress. Inhibition of the Fc gamma receptor (Fc gammaR) stimulated respiratory burst by removing calcium during the challenge did not attenuate the changes caused by an EIgG challenge. A phagocytic challenge with nonerythrocyte particles, IgG-coated beads (BIgGs), did not depress the respiratory burst capacity but did depress phagocytic function. Fc gammaR expression was depressed following a phagocytic challenge but not an oxidative stress. Thus, an oxidative stress can depress macrophage function, but the dysfunction caused by a phagocytic challenge with EIgGs involves Fc gammaR depletion and the erythrocyte contents rather than an oxidative stress.     

Wing pathology of white-nose syndrome in bats suggests life-threatening disruption of physiology

White-nose syndrome (WNS) is causing unprecedented declines in several species of North American bats. The characteristic lesions of WNS are caused by the fungus Geomyces destructans, which erodes and replaces the living skin of bats while they hibernate. It is unknown how this infection kills the bats. We review here the unique physiological importance of wings to hibernating bats in relation to the damage caused by G. destructans and propose that mortality is caused by catastrophic disruption of wing-dependent physiological functions. Mechanisms of disease associated with G. destructans seem specific to hibernating bats and are most analogous to disease caused by chytrid fungus in amphibians.     

Two frameshift mutations in the cystic fibrosis gene

Cystic fibrosis (CF) is a recessive disease caused by mutations in the CF transmembrane conductance regulator (CFTR) gene. We have identified in exon 7 two frameshift mutations, one caused by a two-nucleotide insertion and the other caused by a one-nucleotide deletion; these mutations--CF1154insTC and CF1213delT, respectively, are predicted to shift the reading frame of the protein and to introduce UAA(ochre) termination codons at residues 369 and 368.