The origin of tetraradial symmetry in cnidarians

Serially arranged sets of eight septa‐like structures occur in the basal part of phosphatic tubes of Sphenothallus from the early Ordovician (early Floian) Fenxiang Formation in Hubei Province of China. They are similar in shape, location and number, to cusps in chitinous tubes of extant coronate scyphozoan polyps, which supports the widely accepted cnidarian affinity of this problematic fossil. However, unlike the recent Medusozoa, the tubes of Sphenothallus are flattened at later stages of development, showing biradial symmetry. Moreover, the septa (cusps) in Sphenothallus are obliquely arranged, which introduces a bilateral component to the tube symmetry. This makes Sphenothallus similar to the Early Cambrian Paiutitubulites, having similar septa but with even more apparent bilateral disposition. Biradial symmetry also characterizes the Early Cambrian tubular fossil Hexaconularia, showing a similarity to the conulariids. However, instead of being strictly tetraradial like conulariids, Hexaconularia shows hexaradial symmetry superimposed on the biradial one. A conulariid with a smooth test showing signs of the ‘origami’ plicated closure of the aperture found in the Fenxiang Formation supports the idea that tetraradial symmetry of conulariids resulted from geometrical constrains connected with this kind of closure. Its minute basal attachment surface makes it likely that the holdfasts characterizing Sphenothallus and advanced conulariids are secondary features. This concurs with the lack of any such holdfast in the earliest Cambrian Torellella, as well as in the possibly related Olivooides and Quadrapyrgites. Bilaterally arranged internal structures in polyps representing probably the oldest medusozoans support the suggestions based on developmental evidence that the ancestor of cnidarians also was a bilaterally symmetrical animal. This is one more example of fossil data that strictly fit the molecular phylogenetic evidence but not necessarily morphology‐based zoological interpretations.     

Role of airway surface liquid and submucosal glands in cystic fibrosis lung disease

Cysticfibrosis (CF) is caused by mutations in the CF transmembraneconductance regulator (CFTR) protein, an epithelial chloride channelexpressed in the airways, pancreas, testis, and other tissues. Acentral question is how defective CFTR function in CF leads to chroniclung infection and deterioration of lung function. Several mechanismshave been proposed to explain lung disease in CF, including abnormalairway surface liquid (ASL) properties, defective airway submucosalgland function, altered inflammatory response, defective organellaracidification, loss of CFTR regulation of plasma membrane iontransporters, and others. This review focuses on the physiology of theASL and submucosal glands with regard to their proposed role in CF lungdisease. Experimental evidence for defective ASL properties and glandfunction in CF is reviewed, and deficiencies in understanding ASL/glandphysiology are identified as areas for further investigation. New modelsystems and measurement technologies are being developed to makeprogress in establishing lung disease mechanisms in CF, which shouldfacilitate mechanism-based design of therapies for CF.

     

不同来源金槐槐米的红外光谱及芦丁含量的比较

金槐是广西特色中药材,具有止血凉血等功效。不同来源的金槐槐米质量具有一定区别,但生产中常将其看做同一类别,严重影响了以槐米为原料的药材质量。该研究以8个广西栽培金槐主流品种(金槐J2、金槐J3、金槐J4、金槐J5、金槐J6、金槐J7、金槐J8、金槐J9)和三种不同年限的野生金槐(20 a以下、20~30 a、30 a以上)槐米为材料,采用傅里叶红外光谱法和紫外分光光度法对其红外光谱特征及芦丁含量进行了测定。结果表明:(1)金槐J3和3个不同生长年限的野生金槐槐米颗粒较大。(2)栽培品种金槐槐米和野生金槐槐米化学成分类似,但化学成分含量存在一定差异。所测槐米样品芦丁含量在22.85%~36.78%之间,其顺序依次为20~30 a野生金槐 30 a以上野生金槐金槐J3金槐J6 20 a以下野生金槐金槐J2金槐J8金槐J4金槐J9金槐J5金槐J7,11种样品间存在极显著差异(P0.01)。(3)基于芦丁含量制定的质量分级标准中,20~30 a野生金槐符合一级标准,金槐J2、金槐J3、金槐J6、20 a以下野生金槐以及30 a以上野生金槐符合二级标准,金槐J4、金槐J5、金槐J7、金槐J8、金槐J9符合三级标准。(4)栽培金槐可作为野生金槐的替代品,金槐J3有效成分含量高、品相好,更适于工业提取芦丁和金槐茶等产品的研发。     

Bone marrow‐derived mesenchymal stem cells enhance autophagy via PI3K/AKT signalling to reduce the severity of ischaemia/reperfusion‐induced lung injury

Autophagy, a type II programmed cell death, is essential for cell survival under stress, e.g. lung injury, and bone marrow‐derived mesenchymal stem cells (BM‐MSCs) have great potential for cell therapy. However, the mechanisms underlying the BM‐MSC activation of autophagy to provide a therapeutic effect in ischaemia/reperfusion‐induced lung injury (IRI) remain unclear. Thus, we investigate the activation of autophagy in IRI following transplantation with BM‐MSCs. Seventy mice were pre‐treated with BM‐MSCs before they underwent lung IRI surgery in vivo. Human pulmonary micro‐vascular endothelial cells (HPMVECs) were pre‐conditioned with BM‐MSCs by oxygen‐glucose deprivation/reoxygenation (OGD) in vitro. Expression markers for autophagy and the phosphoinositide 3‐kinase/protein kinase B (PI3K/Akt) signalling pathway were analysed. In IRI‐treated mice, administration of BM‐MSCs significantly attenuated lung injury and inflammation, and increased the level of autophagy. In OGD‐treated HPMVECs, co‐culture with BM‐MSCs attenuated endothelial permeability by decreasing the level of cell death and enhanced autophagic activation. Moreover, administration of BM‐MSCs decreased the level of PI3K class I and p‐Akt while the expression of PI3K class III was increased. Finally, BM‐MSCs‐induced autophagic activity was prevented using the inhibitor LY294002. Administration of BM‐MSCs attenuated lung injury by improving the autophagy level via the PI3K/Akt signalling pathway. These findings provide further understanding of the mechanisms related to BM‐MSCs and will help to develop new cell‐based therapeutic strategies in lung injury.     

SAPAP3 regulates epileptic seizures involving GluN2A in post-synaptic densities

Aberrantly synchronized neuronal discharges in the brain lead to epilepsy, a devastating neurological disease whose pathogenesis and mechanism are unclear. SAPAP3, a cytoskeletal protein expressed at high levels in the postsynaptic density (PSD) of excitatory synapses, has been well studied in the striatum, but the role of SAPAP3 in epilepsy remains elusive. In this study, we sought to investigate the molecular, cellular, electrophysiological and behavioral consequences of SAPAP3 perturbations in the mouse hippocampus. We identified a significant increase in the SAPAP3 levels in patients with temporal lobe epilepsy (TLE) and in mouse models of epilepsy. In addition, behavioral studies showed that the downregulation of SAPAP3 by shRNA decreased the seizure severity and that the overexpression of SAPAP3 by recombinant SAPAP3 yielded the opposite effect. Moreover, SAPAP3 affected action potentials (APs), miniature excitatory postsynaptic currents (mEPSCs) and N-methyl-D-aspartate receptor (NMDAR)-mediated currents in the CA1 region, which indicated that SAPAP3 plays an important role in excitatory synaptic transmission. Additionally, the levels of the GluN2A protein, which is involved in synaptic function, were perturbed in the hippocampal PSD, and this perturbation was accompanied by ultrastructural morphological changes. These results revealed a previously unknown function of SAPAP3 in epileptogenesis and showed that SAPAP3 may represent a novel target for the treatment of epilepsy.Subject terms: Diagnostic markers, Epilepsy     

蕤核叶片化学成分的研究

通过对蕤核叶片化学成分进行定性检测,测出其含有蛋白质、氨基酸、多肽类、生物碱、糖类、黄酮类、有机酸、蒽醌类、酚类和鞣质、挥发油和皂甙这些物质。对不同叶位生物碱和黄酮类物质分布规律进行研究,发现随着叶位降低,两类物质含量呈现先增加后减小的规律,高含量部位分布于第三、四叶位。同时,随着叶位降低,不同叶位叶面积逐渐增加,变化差异显著。     

Anesthetic isoflurane increases phosphorylated tau levels mediated by caspase activation and Aβ generation

Anesthetic isoflurane has been shown to promote Alzheimer's disease (AD) neuropathogenesis by inducing caspase activation and accumulation of β-amyloid (Aβ). Phosphorylation of tau protein is another important feature of AD neuropathogenesis. However, the effects of isoflurane on phosphorylated tau levels remain largely to be determined. We therefore set out to determine whether isoflurane can increase phosphorylated tau levels. 5 to 8 month-old wild-type and AD transgenic mice [B6.Cg-Tg (APPswe, PSEN1dE9)85Dbo/J] were treated with 1.4% isoflurane for two hours. The mice brain tissues were harvested at six, 12 and 24 hours after the anesthesia. For the in vitro studies, primary neurons from wild-type and the AD transgenic mice were exposed to 2% isoflurane for six hours, and were harvested at the end of anesthesia. The harvested brain tissues and neurons were subjected to Western blot analysis by which the levels of phosphorylated tau protein at Serine 262 (Tau-PS262) were determined. Here we show that the isoflurane anesthesia increased Tau-PS262 levels in brain tissues and primary neurons from the wild-type and AD transgenic mice. Moreover, the isoflurane anesthesia may induce a greater increase in Tau-PS262 levels in primary neurons and brain tissues from the AD transgenic mice. Finally, caspase activation inhibitor Z-VAD and Aβ generation inhibitor L-685,458 attenuated the isoflurane-induced increases in Tau-PS262 levels. In conclusion, clinically relevant isoflurane anesthesia increases phosphorylated tau levels, which may result from the isoflurane-induced caspase activation and Aβ generation. These findings will promote more studies to determine the effects of anesthetics on tau phosphorylation.     

不同温度下云南松对纵坑切梢小蠹伴生菌的抗性变化

温度对云南松的抗性以及纵坑切梢小蠢伴生菌的生长和致病力有着重要的影响。温度变化将导致二者之间的对抗力量的变化：在温度低于10℃和高于30℃条件下,云南松的生理代谢、抗性以及伴生菌的生长都将受到抑制,但伴生菌受到的抑制作用更大,云南松的抗性相对增强;在15～30℃温度范围内。纵坑切梢小蠢伴生菌生长较快。云南松的抗性相对减弱。结果表明,在温度相对适中的条件下,纵坑切梢小蠢伴生菌的生长侵染力相对增强,而云南松的抗性相对减弱。     

Pleural surface fluorescence measurement of Na+ and Cl- transport across the air space-capillary barrier.

We developed a pleural surface fluorescence method to measure Na(+) and Cl(-) transport in perfused mouse lungs. The air space was filled with aqueous fluid containing membrane-impermeant fluorescent indicators of Cl(-) (lucigenin) or Na(+) (Sodium Green). After instillation of a Cl(-)-free solution into the air space, an increase in perfusate Cl(-) concentration from 0 to 30 mM produced a decrease in surface lucigenin fluorescence (6.5%/min) corresponding to Cl(-) influx of 1.0 mM/min. Cl(-) influx was increased to 2.1 +/- 0.3 mM/min by forskolin, and the increase was inhibited by glibenclamide. cAMP-stimulated Cl(-) influx was decreased by 57% in CFTR null mice. After instillation of a Na(+)-free solution into the air space, an increase in perfusate Na(+) concentration from 0 to 30 mM gave increased Sodium Green fluorescence (Na(+) influx of 1.2 mM/min), which increased approximately fivefold after cAMP agonists. Cl(-) and Na(+) transport were not affected in lungs from mice lacking aquaporins AQP1 or AQP5. Our results establish a pleural surface fluorescence method to measure unidirectional Cl(-) and Na(+) flux in intact lung and provide evidence for cAMP-stimulated transcellular Cl(-) and Na(+) transport.     

Low expression of ENC1 predicts a favorable prognosis in patients with ovarian cancer

Ectodermal-neural cortex 1 (ENC1) belongs to a member of the kelch family of genes. It is an actin-binding protein and plays a pivotal role in neuronal and adipocyte differentiation. Here, we found that lower expression of ENC1 in the ovarian cancer patients was associated with favorable prognosis. In addition, ENC1 was heterogeneously expressed in various ovarian cancer cells. The messenger RNA and protein expression levels of ENC1 in HO-8910PM and NIH:OVCAR-3 cells were obviously higher than that in the other types of ovarian cancer cells. Knockdown of ENC1 in HO-8910PM or NIH:OVCAR-3 cells could significantly increase the reactive oxygen species levels, resulting in inhibition of in vitro proliferation, migration, and invasion. Our findings suggest that decreasing expression of ENC1 may be a new approach that can be used for ovarian cancer treatment.