Omentin protects against LPS-induced ARDS through suppressing pulmonary inflammation and promoting endothelial barrier via an Akt/eNOS-dependent mechanism

Acute respiratory distress syndrome (ARDS) is characterized by increased pulmonary inflammation and endothelial barrier permeability. Omentin has been shown to benefit obesity-related systemic vascular diseases; however, its effects on ARDS are unknown. In the present study, the level of circulating omentin in patients with ARDS was assessed to appraise its clinical significance in ARDS. Mice were subjected to systemic administration of adenoviral vector expressing omentin (Ad-omentin) and one-shot treatment of recombinant human omentin (rh-omentin) to examine omentin''s effects on lipopolysaccharide (LPS)-induced ARDS. Pulmonary endothelial cells (ECs) were treated with rh-omentin to further investigate its underlying mechanism. We found that a decreased level of circulating omentin negatively correlated with white blood cells and procalcitonin in patients with ARDS. Ad-omentin protected against LPS-induced ARDS by alleviating the pulmonary inflammatory response and endothelial barrier injury in mice, accompanied by Akt/eNOS pathway activation. Treatment of pulmonary ECs with rh-omentin attenuated inflammatory response and restored adherens junctions (AJs), and cytoskeleton organization promoted endothelial barrier after LPS insult. Moreover, the omentin-mediated enhancement of EC survival and differentiation was blocked by the Akt/eNOS pathway inactivation. Therapeutic rh-omentin treatment also effectively protected against LPS-induced ARDS via the Akt/eNOS pathway. Collectively, these data indicated that omentin protects against LPS-induced ARDS by suppressing inflammation and promoting the pulmonary endothelial barrier, at least partially, through an Akt/eNOS-dependent mechanism. Therapeutic strategies aiming to restore omentin levels may be valuable for the prevention or treatment of ARDS.Acute respiratory distress syndrome (ARDS) is a devastating condition with a 30–60% mortality rate.^{1, 2} Although the pathogenesis of ARDS is complex, the inflammatory response and endothelial barrier disruption play important roles in the development of ARDS.^{3, 4, 5} Therefore, in addition to conventional anti-inflammatory treatments, therapeutic strategies aim to restore pulmonary endothelial barrier integrity and function through regulating inter-endothelial AJs and the endothelial cytoskeleton to minimize protein leakage and leukocyte infiltration under ARDS conditions.^{6, 7}Obesity, especially visceral obesity, has clearly been shown to impair systemic vasculature and to lead to the initiation and progression of vascular disorders.^{8, 9, 10} Although different from the well-documented impacts of obesity on cardiovascular disease, the relationships between obesity and ARDS have not been well elucidated. Clinical and experimental data focused on pertinent physiological changes in obesity indicate that the obesity may alter ARDS pathogenesis by ‘priming'' the pulmonary endothelial barrier for insult and amplifying the early inflammatory response, thus lowering the threshold to initiate ARDS.^{11, 12} Contrary to conventional dogma, adipose tissue is now appreciated as an important endocrine tissue that secretes various bioactive molecules called adipokines, which contribute to the progression of diverse vascular diseases, including hypertension, cardiovascular disease and atherosclerosis.^{13, 14, 15, 16} Although ARDS is not a classified pulmonary vascular disease, it is a severe inflammatory lung condition with widespread pulmonary endothelial breakdown. Clinical evidence has indicated that the obesity might be an emerging risk factor for ARDS and that circulating adipokines levels are associated with the initiation and progression of ARDS.^{11, 12, 17, 18} Moreover, experimental studies have suggested that some anti-inflammatory adipokines, such as adiponectin and apelin, exert beneficial actions on ARDS.^{19, 20, 21}Omentin is an anti-inflammatory adipokine that is abundant in human visceral fat tissue.^{22, 23} Paradoxically, higher circulating omentin-1 levels are present in lean and healthy individuals compared with the obese and diabetic patients. Moreover, as a novel biomarker of endothelial dysfunction, reduced circulating omentin levels are related to the pathological mechanism of obesity-linked vascular disorders, including type 2 diabetes, atherosclerosis, hypertension and cardiovascular disease.^{24, 25, 26, 27, 28} Furthermore, experimental studies have found that omentin stimulates vasodilation in isolated blood vessels and suppresses cytokine-stimulated inflammation in endothelial cells (ECs).^{29, 30, 31} Thus, these data suggest that omentin may protect against obesity-related vascular complications through its anti-inflammatory and vascular-protective properties; however, little is known regarding its role in lung tissue. It was reported that decreased circulating omentin-1 levels could be regarded as an independent predictive marker for the obstructive sleep apnea syndrome and that omentin protects against pulmonary arterial hypertension through inhibiting vascular structure remodeling and abnormal contractile reactivity.^{32, 33, 34} However, to our knowledge, no study has assessed the impact of omentin on ARDS.Akt-related signaling pathways function as an endogenous negative feedback mechanism in response to the injurious stimulus. Our prior studies have demonstrated that Akt-related signaling contributes to protection against ARDS.^{35, 36} Moreover, omentin has been reported to exert anti-inflammatory, pro-survival and pro-angiogenic functions in various cells via an Akt-dependent mechanism.^{30, 31, 37, 38, 39, 40, 41, 42}Collectively, given that ARDS is ultimately an obesity-related disorder of vascular function and that omentin is a favorable pleiotropic adipokine capable of anti-inflammatory, pro-angiogenic and anti-apoptotic abilities; omentin may exert beneficial effects on ARDS. In the present study, we first aimed to appraise the clinical significance of omentin in ARDS and then specifically evaluated its impact on inflammation and the endothelial barrier. Furthermore, we mechanistically investigated the role of Akt-related signaling pathways in these effects induced by omentin in vivo and in vitro.     

A novel pathway of arsenate detoxification

Microorganisms have evolved various mechanisms to detoxify arsenic, an ubiquitous environmental toxin. Known mechanisms include arsenite efflux, arsenate reduction followed by arsenite efflux and arsenite methylation. In this issue, Chen et al. describe a novel mechanism for arsenate detoxification via synergistic interaction of glyceraldehyde‐3‐phosphate dehydrogenase (GAPDH) and a major facilitator superfamily protein (ArsJ). They propose that GAPDH catalyzes the formation of 1‐arseno‐3‐phosphoglycerate, which is then extruded out of the cell by ArsJ. The significance of this pathway and questions for further research are discussed.     

双斑蟋营养成分分析及评价

由于具有较好的营养价值以及较高的食物转化效率,食用昆虫特别是蟋蟀受到普遍关注。在双斑蟋（Gryllus bimaculatus,GB）营养成分测定的基础上,对比家蟋（Acheta domesticus,AD）和黑蟋（Gryllus testaceus,GT）的营养及含量,分析评价了双斑蟋的使用价值。结果显示：双斑蟋水分含量71.0%、粗蛋白含量58.60%（干重）、粗脂肪含量28.90%（干重）、粗纤维含量7.23%（干重）、灰分4.93%（干重）;蛋白含量与黑蟋相当而高于家蟋,粗脂肪和灰分含量要高于家蟋和黑蟋;双斑蟋含有17种氨基酸,总氨基酸含量51.03%（干重）,必需氨基酸含量24.76%（干重）、占总氨基酸的48.3%,氨基酸含量低于其他两种蟋蟀;双斑蟋中常量元素含量最高的为钾（6 416 mg/kg,干重）、含量最低的是钙（92 mg/kg,干重）,微量元素中锌含量较高（241 mg/kg,干重）;双斑蟋油脂中不饱和脂肪酸的相对含量为65.33%,以亚油酸（37.05%）和油酸（25.86%）为主、饱和脂肪酸以棕榈酸（25.44%）和硬脂酸（8.74%）为主。双斑蟋的脂肪酸组成、含量与家蟋相近,而与黑蟋的脂肪酸组成差别较大,三种蟋蟀中含量最高的饱和脂肪酸为棕榈酸,而含量最高的不饱和酸为亚油酸。结果表明,双斑蟋的必需氨基酸组成符合FAO/WHO推荐的氨基酸构成比例的蛋白条件,具有较高的营养价值和食用价值。     

Soil Respiration in Different Agricultural and Natural Ecosystems in an Arid Region

The variation of different ecosystems on the terrestrial carbon balance is predicted to be large. We investigated a typical arid region with widespread saline/alkaline soils, and evaluated soil respiration of different agricultural and natural ecosystems. Soil respiration for five ecosystems together with soil temperature, soil moisture, soil pH, soil electric conductivity and soil organic carbon content were investigated in the field. Comparing with the natural ecosystems, the mean seasonal soil respiration rates of the agricultural ecosystems were 96%–386% higher and agricultural ecosystems exhibited lower CO₂ absorption by the saline/alkaline soil. Soil temperature and moisture together explained 48%, 86%, 84%, 54% and 54% of the seasonal variations of soil respiration in the five ecosystems, respectively. There was a significant negative relationship between soil respiration and soil electrical conductivity, but a weak correlation between soil respiration and soil pH or soil organic carbon content. Our results showed that soil CO₂ emissions were significantly different among different agricultural and natural ecosystems, although we caution that this was an observational, not manipulative, study. Temperature at the soil surface and electric conductivity were the main driving factors of soil respiration across the five ecosystems. Care should be taken when converting native vegetation into cropland from the point of view of greenhouse gas emissions.     

氮磷肥配施对冬小麦灌浆期光合参数及产量的影响

在西北绿洲生态条件下, 实验设4个处理, 即165(N₁)和225 kg·hm^-2(N₂)2个氮素(纯氮)水平及105(P₁)和165 kg·hm^-2(P₂)2个磷素(P₂O₅)水平, 研究了氮磷肥配施对冬小麦(Triticum aestivum)品种临抗2号光合特性及产量的影响。结果表明, 低氮(165 kg·hm^-2)处理组的净光合速率(P_n)、气孔导度(G_s)及蒸腾速率(T_r)日变化均呈双峰曲线, 有光合“午休”现象; 高氮(225 kg·hm^-2)处理可减弱甚至使光合“午休”现象消失; 高磷(165 kg·hm^-2)和低磷(105 kg·hm^-2)处理对光合特性的影响差异不显著。N₂P₂具有最高的群体叶面积指数(LAI)、群体光合速率(CAP)、穗粒数、亩穗数、千粒重及产量, 且与N₁P₁和N₁P₂的差异均达显著水平, 与N₂P₁则无显著差异。但N₂P₂水分利用效率(WUE)低于N₂P₁, 显著高于N₁P₁和N₁P₂ (N₁P₁高于N₁P₂, 但无显著差异)。氮肥对光合“午休”的影响大于磷肥, 二者互作效应差异不显著。该实验条件下, 当N、P分别为225和105 kg·hm^-2时有利于提高冬小麦的光合速率及产量。     

Two Novel Mutations in Myosin Binding Protein C Slow Causing Distal Arthrogryposis Type 2 in Two Large Han Chinese Families May Suggest Important Functional Role of Immunoglobulin Domain C2

Distal arthrogryposes (DAs) are a group of disorders that mainly involve the distal parts of the limbs and at least ten different DAs have been described to date. DAs are mostly described as autosomal dominant disorders with variable expressivity and incomplete penetrance, but recently autosomal recessive pattern was reported in distal arthrogryposis type 5D. Mutations in the contractile genes are found in about 50% of all DA patients. Of these genes, mutations in the gene encoding myosin binding protein C slow MYBPC1 were recently identified in two families with distal arthrogryposis type 1B. Here, we described two large Chinese families with autosomal dominant distal arthrogryposis type 2(DA2) with incomplete penetrance and variable expressivity. Some unique overextension contractures of the lower limbs and some distinctive facial features were present in our DA2 pedigrees. We performed follow-up DNA sequencing after linkage mapping and first identified two novel MYBPC1 mutations (c.1075G>A [p.E359K] and c.956C>T [p.P319L]) responsible for these Chinese DA2 families of which one introduced by germline mosacism. Each mutation was found to cosegregate with the DA2 phenotype in each family but not in population controls. Both substitutions occur within C2 immunoglobulin domain, which together with C1 and the M motif constitute the binding site for the S2 subfragment of myosin. Our results expand the phenotypic spectrum of MYBPC1-related arthrogryposis multiplex congenita (AMC). We also proposed the possible molecular mechanisms that may underlie the pathogenesis of DA2 myopathy associated with these two substitutions in MYBPC1.     

Comparison of cold resistance physiological and biochemical features of four Herba Rhodiola seedlings under low temperature

To discuss the cold resistance performance of different Herba Rhodiolae and successfully transplant Herba Rhodiolae to the Gansu plateau area for nursing, domestication and planting, this paper systematically studies six physiological and biochemical features of Rhodiola kirilowii, Rhodiola algida, Rhodiola crenulata and Herba Rhodiolae that are closely associated with cold resistance features and concludes with the cold resistance capability of Rhodiola kirilowii. In the selected six main indexes of the Herba Rhodiolae, the POD, SOD and CAT activity and MDA and Pro content in the leaf are the main physiological and biochemical indexes to indicate the cold resistance performance of four Herba Rhodiolae seedlings and can be regarded as the preliminary indexes to assess the winter performance of Herba Rhodiolae. The research work will provide the theoretical basis for the wild variants of Herba Rhodiolae and GAPJ base construction.     

Exogenous EDDS modifies copper-induced various toxic responses in rice

Copper is a micronutrient required for living organisms, but is potentially toxic in excess. EDDS enhances the phytoextraction of many metals, but the underlying mechanism is fully unclear. Exposure of 200 μM Cu²⁺ for 3 days resulted in rice seedling growth inhibition, accompanied by a decrease in plasma membrane H⁺-ATPase activity, and an increase in relative electrolyte leakage ratios, indicating that maintaining of membrane structure integrity is crucial in acclimation of plants to heavy metal stress. In addition, the chlorophyll and carotenoid content was markedly decreased and the level of the mRNA of Cytochrome P450 gene, OsHMA9, the sulfate transporter gene, and the metallothionein-like protein gene was observed to increase in response to Cu stress. Cu treatment also induced a global epigenetic response which is associated with cell nucleus condensation. These physiological, genetic, and epigenetic responses of rice seedlings to excess copper were modified by the addition of EDDS, suggesting that the supply of EDDS in medium containing a high concentration of Cu ions could enhance plant tolerance potential to excess Cu toxicity through alleviating Cu-induced poisonous effects at various levels.