积极、消极情感在社区老年高血压患者疾病感知与健康促进行为之间的双重中介作用

目的 探讨社区老年高血压患者疾病感知和健康促进行为的关系及积极、消极情感在两者之间的中介作用。方法 采用疾病感知问卷简化版(BIPQ)、老年人健康促进行为量表(GHP),积极、消极情感量表(PANAS)对2021年12月至2022年2月广州市3家社区卫生服务中心和1家三甲医院的高血压门诊就诊的240例老年高血压患者进行横断面调查。构建结构方程模型,并采用Bootstrap抽样法对模型进行验证。结果 社区老年高血压患者疾病感知总分为(24.74±4.45)分,健康促进行为总分为(71.78±8.70)分,积极情感总分为(20.15±3.55)分,消极情感总分为(12.16±3.11)分。相关分析显示,疾病感知、消极情感与健康促进行为呈负相关(P<0.01);积极情感与健康促进行为呈正相关(P<0.01);疾病感知与消极情感呈正相关(P<0.01),而与积极情感呈负相关(P<0.01)。双重中介结构方程模型显示：拟合优度检验(χ²/df)=1.641、近似残差均方根(RMSEA)=0.054、比较拟合指数(CFI)=0.961。积极、消极情感在...     

Preponderance of β- over α-adrenoceptors in mediating the positive inotropic effect of phenylephrine in the ferret ventricular myocardium

Summary [³H]prazosin bound to the membrane fraction derived from the ferret ventricular muscle with high affinity in a saturable manner (K _d = 0.25 nmol/l and B _max = 27 fmol/mg protein in the right ventricle). [³H]CGP-12177, a -adrenoceptor ligand, bound to the membrane fraction with a _{K d} value of 0.29 nmol/l and a B _max of 42 fmol/mg protein. In the isolated ferret papillary muscle driven at 1 Hz at 37°C, phenylephrine elicited a concentration-dependent positive intropic effect. The maximal effect of phenylephrine was comparable to that of isoprenaline. Prazosin (0.3 ol/l) shifted the concentration-response curve for phenylephrine slightly but significantly to the right, the maximal response being unaffected. In contrast, bupranolol (0.3 gmol/l) shifted the curve for phenylephrine markedly downwards: the maximal response was depressed significantly to 40% and the curve became less steep. In the presence of prazosin and bupranolol the curve was shifted to the right, being essentially parallel to the control curve. These results indicate that in the ferret ventricular myocardium both - and -adrenoceptors mediate the positive inotropic effect of phenylephrine. The extent of contribution of the two classes of adrenoceptor is quite different from that in other mammalian species. In the ferret heart, -adrenoceptors predominate over -adrenoceptors in mediating the positive inotropic effect of phenylephrine, although the number of -adrenoceptors is not especially high when compared with other species. Send offprint requests to M. Endoh at the above address     

Anti-cholinergic effect of verapamil on the muscarinic acetylcholine receptor-gated K+ channel in isolated guinea-pig atrial myocytes

Summary Effects of verapamil on the acetylcholine (ACh)-induced K⁺ current were examined in single atrial cells, using the tight-seal whole-cell clamp technique. The pipette solution contained guanosine-5-triphosphate (GTP) or guanosine-5-O-(3-thiotriphosphate) (GTP-S, a non-hydrolysable GTP analogue). In GTP-loaded cells, ACh induced a specific K⁺ current, which is known to be mediated by pertussis toxin-sensitive GTP-binding (G) proteins. Verapamil (0.1–100 M) depressed the ACh-induced K⁺ current in a concentration-dependent fashion. In GTP-S-loaded cells, the K⁺ current remained persistently after wash-out of ACh, probably due to irreversible activation of G proteins by GTP-S. Verapamil (0.1–100 M) also depressed the intracellular GTP-S-induced K⁺ current. However, the magnitude of verapamil-depression of the K⁺ current in GTP-S-loaded cells was significantly smaller than that in GTP-loaded cells at concentrations between 1 and 10 M of the drug. From these results, it is suggested that verapamil may block not only the function of muscarinic ACh receptors but also of G proteins and/or the K⁺ channel itself and thereby depress the ACh-induced K⁺ current in isolated atrial myocytes.Supported by grants from the Ministry of Education, Science and Culture of Japan and the Research Program on Ca Signal Control Send offprint requests to Y. Kurachi at the above address     

Low plasma glutamine in combination with high glutamate levels indicate risk for loss of body cell mass in healthy individuals: the effect of N-acetyl-cysteine

Skeletal muscle catabolism, low plasma glutamine, and high venous glutamate levels are common among patients with cancer or human immunodeficiency virus infection. In addition, a high glycolytic activity is commonly found in muscle tissue of cachectic cancer patients, suggesting insufficient mitochondrial energy metabolism. We therefore investigated (a) whether an anaerobic physical exercise program causes similar changes in plasma amino acid levels, and (b) whether low plasma glutamine or high glutamate levels are risk factors for loss of body cell mass (BCM) in healthy human subjects, i.e., in the absence of a tumor or virus infection. Longitudinal measurements from healthy subjects over longer periods suggest that the age-related loss of BCM occur mainly during episodes with high venous glutamate levels, indicative of decreased muscular transport activity for glutamate. A significant increase in venous glutamate levels from 25 to about 40 M was seen after a program of anaerobic physical exercise. This was associated with changes in T lymphocyte numbers. Under these conditions persons with low baseline levels of plasma glutamine, arginine, and cystine levels also showed a loss of BCM. This loss of BCM was correlated not only with the amino acid levels at baseline examination, but also with an increase in plasma glutamine, arginine, and cystine levels during the observation period, suggesting that a loss of BCM in healthy individuals terminates itself by adjusting these amino acids to higher levels that stabilize BCM. To test a possible regulatory role of cysteine in this context we determined the effect of N-acetyl-cysteine on BCM in a group of subjects with relatively low glutamine levels. The placebo group of this study showed a loss of BCM and an increase in body fat, suggesting that body protein had been converted into other forms of chemical energy. The decrease in mean BCM/body fat ratios was prevented by N-acetyl-cysteine, indicating that cysteine indeed plays a regulatory role in the physiological control of BCM.Abbreviations BCM Body cell mass - HIV Human immunodeficiency virus type 1 - NAC N-Acetyl-cysteine     

Antimicrobial effect of radiation of ionized plasma

Department of Experimental Surgery, Interfaculty Laboratory Complex, and Department of Clinical Laboratory Diagnosis, Postgraduate Medical Faculty, N. I. Pirogov Second Moscow Medical Institute. (Presented by Academician of the Academy of Medical Sciences of the USSR V. V. Kupriyanov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 110, No. 10, pp. 413–145, October, 1990.     

Protective effect of thymidine against cytostatic action of cyclic-AMP in mammalian cell cultures

Under the influence of 1 mM cyclic-adenosine-3,5-monophosphate (cyclic-AMP) the degree of survival and rate of reproduction of Chinese hamster cells in culture were reduced to 27 and 42% of the control level, respectively. Addition of 0.02 mM thymidine along with the cyclic-AMP almost completely abolished the cytostatic effect of the latter. Thymidine also prevented the cytostatic effect of noncyclic 5-AMP, but did not affect death of the cells due to the action of dibutyryl cyclic-AMP and theophylline. Thymidine did not prevent the inhibitory action of cyclic-AMP on a mutant line of mouse cells deficient in thymidine kinase. It is concluded that, in the concentrations used, the cytostatic action of exogenous cyclic-AMP on mammalian cells is the result of its splitting to 5-AMP in the culture medium, and that it acts by blocking one of the stages of TMP biosynthesis.Department of Genetics and Plant Breeding, Faculty of Biology, M. V. Lomonosov Moscow University. (Presented by Academician S. E. Severin.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 80, No. 7, pp. 93–95, July, 1975.     

拟除虫菊酯浸泡大网孔门窗帘毒杀侵入实验小屋蚊虫的研究

本研究采用牛房实验小屋，加装不透光百叶窗和透光门廊，从而全面观察药帘对侵入实验小屋蚊虫毒杀情况，包括蚊虫入屋前接触药帘时和屋内蚊虫外逸出屋外后的死亡情况。结果表明，澳氰菊酯、二氯苯醚菊酯毒效强和持效长，浸泡门窗帘后６个月１８次试验，对侵入屋内蚊虫毒杀，平均死亡率分别为８９．４％和９０．６％。两药对入屋内蚊虫的吸血率均没有明显减少，可能与诱饵动物的吸引力有关。二氯苯醚菊酯有明显驱避作用，其减少蚊虫入屋率，按蚊为７０．６％，库蚊为７５．２％均没有明显减少，阿蚊却没有效应。     

Charcot-Marie-Tooth phenotype produced by a duplicated PMP22 gene as part of a 17P trisomy-translocation to the X chromosome

The Charcot-Mane-Tooth disease type 1A (CMTlA) phenotype is most often associated with a 1.5 megabase (mb), tandem duplication of chromosome 17 band p12 (17˜12). The prevailing hypothesis is that the demyelinating neuropathy results from a dosage effect of the peripheral myelin protein gene PMP22 which is included within this duplication. We present a patient with clinical and electrophysiological features ofCMTlA in whom an extra PMP22 gene resulted from a rare unbalanced translocation of 17p to the X chromosome. This finding further supports the hypothesis of gene dosage as the basis for CMTlA. More-over, this case highlights the importance of fluorescence in siiu hybridization (FISH) as an alternative molecular technique in the diagnosis of CMTlA.     

Reversal of toxic and non-toxic effects of digoxin by digoxin-specific fab fragments in isolated human ventricular myocardium

Summary The time course of the reversal of toxic and nontoxic effects of digoxin by digoxin-specific antibody fragments (Fab) was measured in isolated human ventricular myocardium. A concentration of 2×10^–6 mol/l digoxin was used to produce positive inotropy followed by mechanical signs of toxicity. After addition of a 1.5-fold higher molar concentration of digoxin-specific Fab, signs of toxicity disappeared within 30 min and digoxin-induced force of contraction decayed with a monoexponential time course with a half-life of 52 min. This rate of decay was almost identical to that observed for the dissociation of the digoxin-(Na⁺+K⁺)-ATPase complex in human heart cell membranes. It is concluded that (a) digoxin-specific Fab are capable of completely removing digoxin from its binding sites, (b) the maximal rate of removal of digitalis glycosides from the (Na⁺+K⁺)-ATPase is limited by the dissociation rate constant, and (c) there is a close correlation between the degree of binding of digitalis glycosides to the (Na⁺+K⁺)-ATPase and the increase in force of contraction.Abbreviation Fab Fragment antibody binding (digitalis antidote)     

Atrial fibrillation: a new explanation of the old phenomenon

We propose a new mechanism of atrial fibrillation basing on the results of 30 series of acute experiments on anesthetized cats. In brief, combination of two or more arrhythmogenic factors shortens the interval between the inward and outward ionic currents in cardiomyocytes to a critical value. Under these conditions repolarization of cardiomyocyte membrane reaches the excitation threshold before complete inactivation of the depolarizing currents. This inevitably results in autoexcitation of myocytes (or extrasystole), that in turn promotes repolarization. Once occurred, autoexcitation turns into self-triggering activity resembling tachyarrhythmia paroxysm.