益生菌与宿主疾病关系的研究进展

人类肠道中含有的多种微生物,称为肠道菌群,它们对宿主的健康起着至关重要的作用。肠道菌群的组成包括细菌、病毒和真核生物,已经被证明与宿主健康有密切的联系,尤其是其中的益生菌。益生菌通过多种途径发挥作用,包括与宿主微生物的相互作用、抵御病原菌的定殖、改善肠道屏障功能、调节免疫功能、产生相关代谢产物,在宿主的代谢、免疫和神经系统中发挥有益作用。综述益生菌的作用机制,讨论了近年来益生菌应用临床研究实例以更好地理解其对疾病风险和健康可持续性的贡献,将为新的治疗干预和疾病预防策略提供参考。     

植物干细胞培养研究进展

植物干细胞位于分生组织,是处于未分化状态的细胞,液泡化程度低,具有较高的线粒体活性,遗传稳定,具有很强的自我更新和再生能力。植物干细胞培养在下游制药和功能性食品以及化妆品行业具有广泛的应用潜质。文中综述了植物干细胞的基本培养技术、鉴别技术,为该领域的深入研究提供参考。     

A cost–benefit analysis of the environmental taxation policy in China: A frontier analysis‐based environmentally extended input–output optimization method

China's high‐speed economic development and reliance on overconsumption of natural resources have led to serious environmental pollution. Environmental taxation is seen as an effective economic tool to help mitigate air pollution. In order to assess the effects of different scenarios of environmental taxation policies, we propose a frontier‐based environmentally extended input–output optimization model with explicit emission abatement sectors to reflect the inputs and benefits of abatement. Frontier analysis ensures policy scenarios are assessed under the same technical efficiency benchmark, while input–output analysis depicts the wide range of economic transactions among sectors of an economy. Four scenarios are considered in this study, which are increasing specific tax rates of SO₂, NO_x, and soot and dust separately and increasing all three tax rates simultaneously. Our estimation results show that: raising tax rates of SO₂, NO_x, and soot and dust simultaneously would have the highest emission reduction effects, with the SO₂ tax rate making the greatest contribution to emission reduction. Raising the soot and dust tax rate is the most environmentally friendly strategy due to its highest abatement to welfare through avoided health costs. The combination of frontier analysis and input–output analysis provides policy makers a comprehensive and sectoral approach to assess costs and benefits of environmental taxation.     

Barbronia weberi (Clitellata,Hirudinida, Salifidae) has ovary cords of the Erpobdella type

The organization of the ovaries in representative of the Salifidae (Hirudinida, Erpobdelliformes) was studied at the ultrastructural level for the first time. Like in other leeches, the ovaries of Barbronia weberi are composed of an outer envelope (i.e., an ovisac made up of two coelomic epithelia, muscle cells, and connective tissue) and several internal units, which are broadly similar to the ovary cords found in representatives of the Erpobdellidae. There are usually 6–8 ovary cords that are twisted or cambered with a narrow apical part and a broader, irregularly shaped distal end in each ovisac of B. weberi. Each ovary cord is built from somatic and germ‐line cells and the latter tend to form multicellular cysts that are equipped with a central cytoplasmic core (cytophore). There are two morphologically different subpopulations of germ‐line cells: oocytes and more numerous nurse cells. Growing oocytes form protuberances on the ovary cord surface and eventually detach from the cord and float freely in the ovisac lumen, whereas the other components of germ‐line cysts (i.e., nurse cells and cytophore) degenerate. It should be pointed out that there is a prominent gradient of germ‐cell development along the long axis of the cord. The somatic cells form the ovary cord envelope (the so‐called spongiosa cells) and also penetrate the spaces between germ‐line cells. Both kinds of the somatic cells, that is, those forming the cord envelope and the somatic cells that are associated with oocytes (follicular cells) have a well‐developed system of intercellular channels. Additionally, one prominent somatic cell, the apical cell, was found at the apical tip of each ovary cord. Because the aforementioned features of ovary cords found in B. weberi are very similar (with a few minor exceptions) to the ovary cords that have been described in Erpobdella octoculata and E. johanssoni, we propose the term “ovary cords of the Erpobdella type” for them. Our results support a close phylogenetic relationship between Salifidae and Erpobdellidae. J. Morphol. 275:479–488, 2014. © 2013 Wiley Periodicals, Inc.     

CD36 initiates the secretory phenotype during the establishment of cellular senescence

Cellular senescence is a unique cell fate characterized by stable proliferative arrest and the extensive production and secretion of various inflammatory proteins, a phenomenon known as the senescence‐associated secretory phenotype (SASP). The molecular mechanisms responsible for generating a SASP in response to senescent stimuli remain largely obscure. Here, using unbiased gene expression profiling, we discover that the scavenger receptor CD36 is rapidly upregulated in multiple cell types in response to replicative, oncogenic, and chemical senescent stimuli. Moreover, ectopic CD36 expression in dividing mammalian cells is sufficient to initiate the production of a large subset of the known SASP components via activation of canonical Src–p38–NF‐κB signaling, resulting in the onset of a full senescent state. The secretome is further shown to be ligand‐dependent, as amyloid‐beta (Aβ) is sufficient to drive CD36‐dependent NF‐κB and SASP activation. Finally, loss‐of‐function experiments revealed a strict requirement for CD36 in secretory molecule production during conventional senescence reprogramming. Taken together, these results uncover the Aβ–CD36–NF‐κB signaling axis as an important regulator of the senescent cell fate via induction of the SASP.     

Novel miR-sc4 regulates the proliferation and migration of Schwann cells by targeting Cdk5r1

Clinical and experimental studies have shown an association between intracellular free Zn²⁺ ([Zn²⁺]_i)-dyshomeostasis and cardiac dysfunction besides [Ca²⁺]_i-dyshomeostasis. Since [Zn²⁺]_i-homeostasis is regulated through Zn²⁺-transporters depending on their subcellular distributions, one can hypothesize that any imbalance in Zn²⁺-homeostasis via alteration in Zn²⁺-transporters may be associated with the induction of ER stress and apoptosis in hypertrophic heart. We used a transverse aortic constriction (TAC) model to induce hypertrophy in young male rat heart. We confirmed the development of hypertrophy with a high ratio of heart to body weight and cardiomyocyte capacitance. The expression levels of ER stress markers GRP78, CHOP/Gadd153, and calnexin are significantly high in TAC-group in comparison to those of controls (SHAM-group). Additionally, we detected high expression levels of apoptotic status marker proteins such as the serine kinase GSK-3β, Bax-to-Bcl-2 ratio, and PUMA in TAC-group in comparison to SHAM-group. The ratios of phospho-Akt to Akt and phospho-NFκB to the NFκB are significantly higher in TAC-group than in SHAM-group. Furthermore, we observed markedly increased phospho-PKCα and PKCα levels in TAC-group. We, also for the first time, determined significantly increased ZIP7, ZIP14, and ZnT8 expressions along with decreased ZIP8 and ZnT7 levels in the heart tissue from TAC-group in comparison to SHAM-group. Furthermore, a roughly calculated total expression level of ZIPs responsible for Zn²⁺-influx into the cytosol (increased about twofold) can be also responsible for the markedly increased [Zn²⁺]_i detected in hypertrophic cardiomyocytes. Taking into consideration the role of increased [Zn²⁺]_i via decreased ER-[Zn²⁺] in the induction of ER stress in cardiomyocytes, our present data suggest that differential changes in the expression levels of Zn²⁺-transporters can underlie mechanical dysfunction, in part due to the induction of ER stress and apoptosis in hypertrophic heart via increased [Zn²⁺]_i- besides [Ca²⁺]_i-dyshomeostasis.     

GPR54 deficiency reduces the Treg population and aggravates experimental autoimmune encephalomyelitis in mice

GPR54 is highly expressed in the central nervous system and plays a crucial role in pubertal development. However, GRP54 is also expressed in the immune system, implying possible immunoregulatory functions. Here we investigated the role of GPR54 in T cell and immune tolerance. GPR54 deficiency led to an enlarged thymus, an increased number of thymocytes, and altered thymic micro-architecture starting around puberty, indicating GPR54 function in T-cell development through its regulatory effect on the gonadal system. However, flow cytometry revealed a significant reduction in the peripheral regulatory T cell population and a moderate decrease in CD4 single-positive thymocytes in prepubertal Gpr54~(-/-) mice. These phenotypes were confirmed in chimeric mice with GPR54 deficient bone marrow-derived cells. In addition, we found elevated T cell activation in peripheral and thymic T cells in Gpr54~(-/-) mice. When intact mice were immunized with myelin oligodendrocyte glycoprotein, a more severe experimental autoimmune encephalomyelitis(EAE) developed in the Gpr54~(-/-) mice. Interestingly, aggravated EAE disease was also manifested in castrated and bone marrow chimeric Gpr54~(-/-) mice compared to the respective wild-type control,suggesting a defect in self-tolerance resulting from GPR54 deletion through a mechanism that bypassed sex hormones. These findings demonstrate a novel role for GPR54 in regulating self-tolerant immunity in a sex hormone independent manner.