Effects of sympathetic stimulation on ventricular refractory periods in cats with acute coronary artery ligation

Summary Ventricular refractory periods shorten in the ischemic area following acute coronary artery ligation. Subsequent bilateral sympathetic nerve stimulation reduces disparity in refractory periods across normal, border (peri-ischemic) and ischemic areas.This work was supported by NIH Research Grants HL 19044 and HL 21735, NIH Biomedical Research Support Grant DRR No. S07-05363 and a Grant-in-Aid from the American Heart Association, Florida Affiliate, Broward County Chapter. Dr Gaide is the recipient of NIH New Investigator Research Award HL 27680.     

Sexual receptivity of the female and insemination power of the male Culex pipiens autogenicus (Diptera, Culicidae). The cases of strict monogamy and occasional polygamy]

Females of Culex pipiens autogenicus generally have two refractory periods: post-emergence refractory period (during the first 48 hrs. after emergence) and post-insemination refractory period. Males of Culex pipiens autogenicus can inseminate 2 to 3 females. After the 4th insemination he can no longer completely fulfill his reproductory role. Therefore the female can inseminated by another male.     

Brain glycogen following experimental cerebral ischemia in gerbils (Meriones unguiculatus)

Summary Cortical glycogen levels decreased after both 1 and 3 h of unilateral ischemia. After 1 h of recirculation, the levels of glycogen were restored to control values in both groups. Subsequently, glycogen increased above normal levels after 1 week of recirculation in the 1 h ischemic groups, and after 5 h in the 3 h ischemic group. Thus, the onset of the excess glycogen accumulation appears to be dependent on the intensity of the ischemic insult.     

Calcium activity and post-ischemic suppression of protein synthesis

Increase in intracellular calcium concentration is a prominent feature of ischemia and has been considered a major factor in the initiation of ischemic pathology, which involves inhibition of protein synthesis. A reduction of calcium ion activity during and immediately after in vitro ischemia did not prevent inhibition of protein synthesis in hippocampae slices. When slices were overloaded with calcium by NMDA receptor activation or by the calcium ionophore A23187, no significant inhibition of protein synthesis was observed. We conclude that calcium overload plays only a limited role in ischemic inhibition of protein synthesis.     

急性脑梗死超早期静脉溶栓治疗24例疗效报告

急性缺血性脑血管病起病6h内,脑血管造影发现70～80％的病人,在出现症状的区域内,脑血管有血栓性或狭窄性病变^[1]。所以在急性脑梗死（ACI）超早期,用能溶解血栓及栓子的药物,使阻塞的血管再通,从而挽救缺血的脑组织,是近年达成的共识。本文对2005年10月～2007年12月,对发病6h内的（ACI）患者予以尿激酶（UK）静脉溶栓治疗进行了研究。     

LIM domain only 4 protein promotes granulocyte colony-stimulating factor-induced signaling in neurons

Granulocyte colony-stimulating factor (GCSF) is currently in clinical trials to treat neurodegenerative diseases and stroke. Here, we tested whether LIM domain only 4 protein (LMO4), a hypoxia-inducible gene that protects neurons from ischemic injury, could modulate the neuroprotective effect of GCSF. We showed that GCSF treatment acetylates and phosphorylates Stat3, activates expression of a Stat3-dependent anti-apoptotic gene, p27, and increases neuron survival from ischemic injury. LMO4 participates in Stat3 signaling in hepatocytes and associates with histone deacetylase 2 (HDAC2) in cancer cells. In the absence of LMO4, GCSF fails to rescue neurons from ischemic insults. In wild-type neurons, inhibition of HDAC promoted Stat3 acetylation and the antiapoptotic effect of GCSF. In LMO4 null cortical neurons, expression of wild-type but not HDAC-interaction-deficient LMO4 restored GCSF-induced Stat3 acetylation and p27 expression. Thus, our results indicate that LMO4 enhances GCSF-induced Stat3 signaling in neurons, in part by sequestering HDAC.     

微生物技术在固体矿产资源开发中的应用

本文总结了国内外生物湿法冶金技术在低品位硫化铜矿、难处理金矿以及其他固体矿产资源中的研究现状,指出了存在的问题,并提出了未来的发展方向。     

Consequences of acute ischemia for the electrical and mechanical function of the ventricular myocardium. A brief review

Reduction or interruption of the blood supply to the myocardium leads to marked disturbances of electrical and mechanical function within a few seconds. Electrical dysfunction is characterized by an initial depolarization of the resting membrane, and a decrease of the amplitude, the upstroke velocity and the duration of the action potential. Both depolarization and depression of the action potential are closely associated with intracellular metabolic acidosis. After this initial phase, electrical cell-to-cell uncoupling develops, probably as a consequence of increased cytosolic free [Ca++]. Mechanical dysfunction is characterized by a dissociation of the initial decrease of active force development from the subsequent ischemic contracture. Active force development in acute ischemia is inhibited by the accumulation of ischemic metabolic products (H+, inorganic phosphate (Pi), Mg++) but not by a marked decrease of [ATP]. The subsequent ischemic contracture is probably initiated by release of Ca++ from intracellular stores. This release causes rapid consumption of ATP and the development of rigor within 1-2 minutes.     

δ-Opioid receptors protect from anoxic disruption of Na+ homeostasis via Na+ channel regulation

Hypoxic/ischemic disruption of ionic homeostasis is a critical trigger of neuronal injury/death in the brain. There is, however, no promising strategy against such pathophysiologic change to protect the brain from hypoxic/ischemic injury. Here, we present a novel finding that activation of δ-opioid receptors (DOR) reduced anoxic Na⁺ influx in the mouse cortex, which was completely blocked by DOR antagonism with naltrindole. Furthermore, we co-expressed DOR and Na⁺ channels in Xenopus oocytes and showed that DOR expression and activation indeed play an inhibitory role in Na⁺ channel regulation by decreasing the amplitude of sodium currents and increasing activation threshold of Na⁺ channels. Our results suggest that DOR protects from anoxic disruption of Na⁺ homeostasis via Na⁺ channel regulation. These data may potentially have significant impacts on understanding the intrinsic mechanism of neuronal responses to stress and provide clues for better solutions of hypoxic/ischemic encephalopathy, and for the exploration of acupuncture mechanism since acupuncture activates opioid system.     

Selective effects of gonadal steroids on the response of peripheral serotonin receptors

The maximal contraction provoked by serotonin (5-HT) in isolated stomach strips of adult rats, a functional index for peripheral 5-HT receptors, was sexually differentiated, androgen-sensitive, and estrogen refractory. This is at variance with the reported sensitivity of central 5-HT receptors to estrogen.     

Season-dependent effects of melatonin on testes and fur color in mountain hares (Lepus timidus L.)

Melatonin was administered in 3 seasons to adult male mountain hares (Lepus timidus L.) kept in long or short photoperiods. Melatonin and short photoperiods induced testis regression and fur whitening in summer and autumn but not in winter. Both treatments combined seemed to provoke an advanced onset of the refractory period.     

Selective effects of gonadal steroids on the response of peripheral serotonin receptors

Summary The maximal contraction provoked by serotonin (5-HT) in isolated stomach strips of adult rats, a functional index for peripheral 5-HT receptors, was sexually differentiated, androgen-sensitive, and estrogen refractory. This is at variance with the reported sensitivity of central 5-HT receptors to estrogen.     

Die Beeinflussbarkeit der Tiegelschen Kontraktur durch Änderungen der extracellulären Calciumkonzentration

Summary 1. The occurrence of Tiegel's contractures in phasic and tonic muscles is significantly influenced by the extracellular calcium concentration. 2. Muscles of both types show only small and short aftercontractures after preceding treatment with calciumfree Ringer's solution and become refractory to repeated stimuli while in the relaxed state. 3. Muscles of both types, however, which have been pretreated with calcium-rich Ringer's solution, show strong and long-lasting after-contractures and become refractory to repeated stimuli while in a state of maximal contracture. 4. The possible explanations for this different behaviour are briefly discussed and it is assumed that calcium ions have several sites of action within the muscle cell.     

Neuroprotection against hypoxia/ischemia: δ-opioid receptor-mediated cellular/molecular events

Hypoxic/ischemic injury remains the most dreaded cause of neurological disability and mortality. Despite the humbling experiences due to lack of promising therapy, our understanding of the complex cascades underlying the neuronal insult has led to advances in basic science research. One of the most noteworthy has been the effect of opioid receptors, especially the delta-opioid receptor (DOR), on hypoxic/ischemic neurons. Our recent studies, and those of others worldwide, present strong evidence that sheds light on DOR-mediated neuroprotection in the brain, especially in the cortex. The mechanisms of DOR neuroprotection are broadly categorized as: (1) stabilization of the ionic homeostasis, (2) inhibition of excitatory transmitter release, (3) attenuation of disrupted neuronal transmission, (4) increase in antioxidant capacity, (5) regulation of intracellular pathways—inhibition of apoptotic signals and activation of pro-survival signaling, (6) regulation of specific gene and protein expression, and (7) up-regulation of endogenous opioid release and/or DOR expression. Depending upon the severity and duration of hypoxic/ischemic insult, the release of endogenous opioids and DOR expression are regulated in response to the stress, and DOR signaling acts at multiple levels to confer neuronal tolerance to harmful insult. The phenomenon of DOR neuroprotection offers a potential clue for a promising target that may have significant clinical implications in our quest for neurotherapeutics.     

Evidence that endogenous vasopressin plays a protective role in circulatory shock. Role for reticuloendothelial system using Brattleboro rats

Summary Experiments performed on male Wistar, Long Evans and Brattleboro rats indicate that the latter strain of animals, lacking vasopressin in their posterior pituitaries, are extremely sensitive to hemorrhagic and bowel ischemic shock. Mild forms of both hemorrhagic and bowel ischemic shock, as produced in Wistar on Long Evans rats, results in marked hypotension, hemoconcentration and blockade of the reticuloendothelial system (RES) in Brattleboro animals of similar sex, age and weight. These direct findings indicate that release of endogenous vasopressin in shock syndromes may be critical in maintenance of circulatory homeostasis and RES function.Supported in part by NIH Grant Nos HL-18002 and HL-18015 and NIDA Grant No. DA-02339. The author would like to acknowledge the excellent technical assistance provided by Y. Waldemar, J. Gargani and R. W. Burton.     

Etude des variations nycthémérales de la filtration glomérulaire chez le rat

Summary Parallel variations in plasma and urine variations of endogenous urea and creatinine level in the rat during 4 consecutive 6-h-long periods permit to evidence urea and creatinine clearance diurnal variations with very significant increase in the 2 nightly periods. The signification of this very large nightly glomerular filtration increase is discussed.     

Massive striatal dopamine release in acute cerebral ischemia in rats

Summary Extracellular dopamine, 3,4-dihydroxyphenylacetic acid (DOPAC) and cerebral blood flow were simultaneously determined using in vivo brain dialysis and a hydrogen clearance method in the striatum of spontaneously hypertensive rats during ischemia and after recirculation. Massive striatal dopamine release was demonstrated in acutely induced ischemic brain.     

NADPH oxidases as therapeutic targets in ischemic stroke

Reactive oxygen species (ROS) act physiologically as signaling molecules. In pathological conditions, such as ischemic stroke, ROS are released in excessive amounts and upon reperfusion exceed the body's antioxidant detoxifying capacity. This process leads to brain tissue damage during reoxygenation. Consequently, antioxidant strategies have long been suggested as a therapy for experimental stroke, but clinical trials have not yet been able to promote the translation of this concept into patient treatment regimens. As an evolution of this concept, recent studies have targeted the sources of ROS generation-rather than ROS themselves. In this context, NADPH oxidases have been identified as important generators of ROS in the cerebral vasculature under both physiological conditions in general and during ischemia/reoxygenation in particular. Inhibition of NADPH oxidases or genetic deletion of certain NADPH oxidase isoforms has been found to considerably reduce ischemic injury in experimental stroke. This review focuses on recent advances in the understanding of NADPH oxidase-mediated tissue injury in the cerebral vasculature, particularly at the level of the blood-brain barrier, and highlights promising inhibitory strategies that target the NADPH oxidases.     

Hepatic blood flow in acute myocardial ischemia

Hepatic blood flow was monitored in cats during myocardial ischemia (MI). Increased plasma CPK activity, the S-T segment of the electrocardiogram, and hepatic flow was reduced by 5 h to 40% of control. The results suggest that MI can influence organs distant from the original ischemic episode.     

Jahreszeitliche Schwankungen der Blutgerinnung beim Hunde

Summary The blood coagulation in dogs was investigated from December 1954 to August 1956. The one-stage-method ofQuick showed no important changes, while the recalcification time was longer during the warm periods in summer as compared with the previous and following periods. In cases of prolonged recalcification time, there was found to be an increased amount of heparin in blood.