间歇性低氧适应的心脏保护

间歇性低氧（intermittent hypoxia,IH）是指一定时间间断地暴露于低氧环境,而其余时间处于常氧环境。IH是机体某种生理和病理状态下的低氧形式。研究表明：间歇性低氧适应（IHadaptation）,类似缺血预适应（ischemic preconditioning,IPC）和长期高原低氧适应（long-termhigh-altitude hypoxic adaptation,LHA）,具有明显的心脏保护作用,表现为增强心肌对缺血／再灌注损伤的耐受性、限制心肌梗死面积和形态学改变、抗细胞凋亡、促进缺血／再灌注心脏舒缩功能的恢复,以及抗心律失常。尽管IH对心脏的保护作用不容质疑,但其作用机制远未阐明。IH心脏保护作用可能涉及氧的运输、能量代谢、神经体液调节、抗氧化酶、应激蛋白、腺苷系统、ATP敏感钾通道、线粒体及其钙调控、一氧化氮和蛋白激酶等多方面机制,并受低氧处理方式、动物年龄和性别等因素影响。IH心脏保护持续时间明显长于IPC,而对机体的不良影响远小于LHA,具有潜在的应用价值。     

Reversal by naloxone of adaptation of rats to noxious stimuli.

Bradykinin, a potent pain-producing substance, injected into the common iliac artery of the rat produced flexor reflexes of the hind-limb. The bradykinin-induced response was reduced following the repetition of such noxious stimuli in some male Sprague-Dawley rats classified as the noxious-adaptable group, while the reduction of bradykinin-response did not occur in the majority of the same strain rats in the noxious-non-adaptable group. Naloxone in doses of 0.1 – 2.0 mg/kg restored the flexor reflexes to the noxious stimulation, in a dose dependent manner, in the former group; ED_{5 0} value being 0.61 mg/kg. On the other hand, naloxone in doses up to 5.0 mg/kg produced no hyperalgesic effect in the latter group. Thus, genetic variation in endogenous opioid systems has to be considered.     

On the potential strength and consequences for nonrandom gene flow caused by local adaptation in flowering time

Gene flow is generally considered a random process, that is the loci under consideration have no effect on dispersal success. Edelaar and Bolnick (Trends Ecol Evol, 27, 2012 659) recently argued that nonrandom gene flow could exert a significant evolutionary force. It can, for instance, ameliorate the maladaptive effects of immigration into locally adapted populations. I examined the potential strength for nonrandom gene flow for flowering time genes, a trait frequently found to be locally adapted. The idea is that plants that successfully export pollen into a locally adapted resident population will be a genetically biased subset of their natal population – they will have resident‐like flowering times. Reciprocally, recipients will be more migrant‐like than the resident population average. I quantified the potential for biased pollen exchange among three populations along a flowering time cline in Brassica rapa from southern California. A two‐generation line cross experiment demonstrated genetic variance in flowering time, both within and among populations. Calculations based on the variation in individual flowering schedules showed that resident plants with the most migrant‐like flowering times could expect to have up to 10 times more of the their flowers pollinated by immigrant pollen than the least migrant‐like. Further, the mean flowering time of the pollen exporters that have access to resident mates differs by up to 4 weeks from the mean in the exporters’ natal population. The data from these three populations suggest that the bias in gene flow for flowering time cuts the impact on the resident population by as much as half. This implies that when selection is divergent between populations, migrants with the highest mating success tend to be resident‐like in their flowering times, and so, fewer maladaptive alleles will be introduced into the locally adapting gene pool.     

Functional morphology of accessory circulatory organs in the legs of hemiptera

The circulatory organs in the legs of 32 heteropteran and 2 homopteran species were investigated by means of semithin serial sections. In all species, the leg hemocoel is divided by a thin diaphragm into 2 counter-rotating blood sinuses. This diaphragm twists about an angle of 90° immediately distal to the femoral-tibial joint, thereby forming a kind of chamber that is equipped with a valve flap. Apart from the investigated representatives of the Gerromorpha, a muscle is associated with this chamber. Rhythmic contractions of this muscle compress one sinus, thereby forcing hemolymph from the leg into the thorax. Simultaneously, the other sinus widens and hemolymph is sucked from the thorax into the leg. The “leg heart” muscle generally originates from the anteriodorsal wall of the tibia. Its point of insertion varies between different species. In most of the investigated Hemiptera, this muscle inserts at the tendon of the pretarsal flexor muscle. In others, both attachments are located at the tibial cuticle. This peculiarity and other anatomical facts indicate that in the evolution of these organs in the Hemiptera, one portion of the pretarsal flexor muscle has been recruited for the formation of the leg heart.     

An evolutionary treatment of the morphology and physiology of circulatory organs in insects

An overview from an evolutionary perspective is presented on the research of the past 2 decades on insect circulatory organs. Based on various functional morphology it is clear that the flow mode of the dorsal vessel ('heart') has changed during the evolution of hexapods. In all apterygotes and mayflies the flow is bidirectional. In most pterygote insects, however, it is unidirectional. In some endopterygote insects, the direction of the flow alternates. This is achieved by heartbeat reversal, which may have various physiological functions and is a derived condition that probably occurred several times during the course of insect evolution. Special attention is given to the hemolymph flow in body appendages. In ancestral hexapods, they are supplied by arteries, whereas circulation in appendages of higher insects is accomplished by accessory pulsatile organs. These auxiliary hearts are autonomous pumps and exhibit a great diversity in their functional morphology. They represent evolutionary innovations which evolved by recruitment of building blocks from various organ systems and were assembled into new functional units. Almost all pulsatile circulatory organs in insects investigated exhibit a myogenic automatism with a superimposed neuronal control. The neuroanatomy of insect circulatory organs has been investigated only in a small number of species but in considerable detail. Numerous potential peptidergic and a few aminergic mediators could be demonstrated by immunocytochemical and biochemical methods. The cardiotropic effectiveness of these mediators may vary among species and it can be stated that there is no uniform picture of the control of the various circulatory organs in insects. A possible explanation for the differences may lie in the different evolutionary origins of the muscular components. Furthermore, insect circulatory organs may represent important neurohemal releasing sites.     

Mechanism for enterohepatic injury caused by circulatory disturbance of hepatic vessels in the rat

We reported previously that a transient occlusion followed by reperfusion of the portal vein and the hepatic artery of the rat significantly decreased the transhepatic transport of a cholephilic compound, and that this decrease was prevented by pretreating animals with poly(styrene co-maleic acid butyl ester)-conjugated superoxide dismutase (SM-SOD). To elucidate the mechanism for oxidative injury of the liver and the site for the generation of superoxide radicals, the effect of a portosystemic bypass on the liver function was examined in the rat whose hepatic vessels were temporarily occluded. A portosystemic bypass inhibited the reperfusion-induced decrease in hepatic transport of bromosulfophthalein as effectively as did SM-SOD. Kinetic analysis using 125I-labeled albumin revealed that the permeability of the small intestine markedly increased after a transient occlusion. The increase in intestinal permeability was also inhibited either by SM-SOD or by the portosystemic bypass. Xanthine oxidase activity in portal plasma markedly increased during occlusion and reperfusion, while it remained within normal ranges in the bypassed group. Thus, superoxide radical, and/or its metabolite(s), might play a critical role in increasing the intestinal permeability and in the pathogenesis of reperfusion-induced liver injury.     

Activity labeling patterns in the medulla of Drosophila melanogaster caused by motion stimuli

Summary We quantitatively describe 2-deoxyglucose (2-DG) neuronal activity labeling patterns in the first and second visual neuropil regions of the Drosophila brain, the lamina and the medulla. Careful evaluation of activity patterns resulting from large-field motion stimulation shows that the stimulus-specific bands in the medulla correspond well to the layers found in a quantitative analysis of Golgi-impregnated columnar neurons. A systematic analysis of autoradiograms of different intensities reveals a hierarchy of labeling in the medulla. Under certain conditions, only neurons of the lamina are labeled. Their characteristic terminals in the medulla are used to differentiate among the involved lamina monopolar cell types. The 2-DG banding pattern in the medulla marks layers M1 and M5, the input layers of pathway p1 (the L1 pathway). Therefore, activity labeling of L1 by motion stimuli is very likely. More heavily labeled autoradiograms display activated cells also in layers M2, M9, and M10. The circuitry involved in the processing of motion information thus concentrates on pathways p1 and p2. Layers M4 and M6 of the distal medulla hardly display any label under the stimulus conditions used. The functional significance of selective activity in the medulla is discussed.     

Cleavage of calnexin caused by apoptotic stimuli: implication for the regulation of apoptosis

Calnexin is an endoplasmic reticulum (ER)-resident molecular chaperone that plays an essential role in the correct folding of membrane proteins. We found that calnexin is subjected to partial cleavage in apoptotic mouse cells. Both ER stress-inducing and ER stress-non-inducing apoptotic stimuli caused the cleavage of calnexin, indicating that this event does not always occur downstream of ER stress. The inhibition of caspases that target the amino acid sequence DXXD abrogated calnexin cleavage in apoptotic stimulus-treated cells. In addition, disruption of one of two DXXD sequences located in the cytoplasmic domain caused calnexin to escape cleavage during apoptosis. Furthermore, calnexin was cleaved in vitro by recombinant caspase-3 or caspase-7. Finally, the overexpression of a presumed cleavage product of calnexin partly inhibited apoptosis. These results collectively suggest that caspase-3 or caspase-7 cleaves calnexin, whose cleaved product leads to the attenuation of apoptosis.