紫外线辐射增加对生物的影响

因大气臭氧层的破坏引起了地表紫外线－Ｂ（ＵＶ－Ｂ）辐射增加,从而导致对各种生物产生不良影响。过量的ＵＶ－Ｂ辐射能增加人类患皮肤癌及白内障等多种疾病的机会,改变自然界某些昆虫的生活习性。同时,ＵＶ－Ｂ辐射还能抑制和破坏许多陆生和水生植物的生长,引起全球生态平衡的改变和作用生产的下降。     

江苏、安徽的禽致病性大肠杆菌

禽致病性大肠杆菌(Avian Pathogenic Escherichia coli,APEC)司引起禽类的多种疾病,是目前严重危害养禽业的传染病之一[1-2].APEC有复杂的血清型和广谱的耐药性,严重制约了该病的有效防控.最近的研究表明APEC能引起包括人在内的哺乳动物发病,提示APEC可能是人畜共患病的潜在病原体.因此,对APEC分子流行病学的研究,为进一步开展对该病的防控提供参考.     

微型杀手 超级细菌

俗话说，软的怕硬的，硬的怕不要命的。如果某种生物有一个金刚不坏之身，岂不是更令人发指。不是危言耸听，就有这么一个恐怖分子令人类束手无措，因为它不仅能引起多种疾病，更关键的是，几乎所有的抗生素都无法把它消灭，它就是“超级细菌”。     

微型杀手 超级细菌

俗话说，软的怕硬的，硬的怕不要命的。如果某种生物有一个金刚不坏之身，岂不是更令人发指。不是危言耸听，就有这么一个恐怖分子令人类束手无措，因为它不仅能引起多种疾病，更关键的是，几乎所有的抗生素都无法把它消灭，它就是“超级细菌”。     

拟诺卡氏菌属放线菌研究进展

拟诺卡氏菌属是一个经典的丝状放线菌类群,在近十余年来获得了快速发展,目前已合格发表42个种、2个亚种。该菌群在土壤环境,尤其是天然高盐碱土样生境中广泛分布,同时从海洋、人居环境、临床样本、堆肥等生境中也能分离到。拟诺卡氏菌不仅能合成抗生素、酶抑制剂、生物表面活性剂等多种结构新颖的活性物质,而且还能产生多种具有潜在工业用途的酶,因此近年来引起了国内外学者的广泛关注。本文综述了拟诺卡氏菌分类学、生态分布与适应机制、代谢产物及遗传转化的研究进展,并对其研究趋势做了分析。     

瞳孔光反应系统的空间分布式神经网络模型

为模拟刺激光空间分布变化引起瞳孔反应的实验现象,本文建立了空间分布式神经网络瞳孔模型。它是在瞳孔双通道模型基础上,借鉴Ｃａｎｎｏｎ－Ｒｏｂｉｎｓｏｎ的Ｏｃｕｌｏｍｏｔｏｒ模型的双层网络结构和视网膜的镶嵌式特点,经空间延括而成。空间各部位信号经第一层神经元处理得到对应各部位的线性ＤＣ和非线性ＡＣ输出,在第二层神经元进行空间综合,再经第三层神经元复合去控制效应器官虹膜肌的反应。该分布式部位机制模型能解释多种瞳孔实验现象。     

生物传感器的应用研究进展

生物传感器是一门由生物、化学、物理、医学、电子技术等多种学科互相渗透成长起来的高新技术 ,是一种将生物感应元件的专一性与一个能够产生和待测物浓度成比例的信号传导器结合起来的分析装置。由于其具有选择性好、灵敏度高、分析速度快、成本低、能在复杂体系中进行在线连续监测的特点 ,已在生物、医学、环境监测、食品、医药、及军事医学等领域显示出广阔的应用前景 ,引起了世界各国的极大关注。综述了生物传感器的基本原理、分类、特点及在环境监测、食品分析、生物医学和军事上的应用 ,并对其发展前景进行了展望。     

抗菌肽对细菌杀伤作用的分子机制

抗菌肽是一类新型的抗菌物质,从最低等的生物病毒、细菌到高等的动植物都有广泛分布. 以往的研究主要集中于抗菌肽对细菌细胞膜的作用机制,已经构建了三种作用模式. 但近几年的研究表明,很多抗菌肽都能有效地穿过细菌的细胞膜,直接与胞内分子相互作用,并不引起膜的破裂. 抗菌肽根据其结构特点有着多种杀菌穿膜的机制,其后分别与胞内的靶分子如核酸,蛋白质,信号转导通路等互相作用,最终实现对细菌的杀伤作用.     

海洋污损生物数据管理系统的设计与构建

固着或栖息在船舶和人工设施水下部位的海洋污损生物, 会对人们的涉海活动产生不利影响, 其群落的形成和发展过程与温度、盐度、深度、季节、海域、浸海时间、离岸距离和附着基类型等多种因素密切相关。为便于系统分析和综合处理各海区污损生物资料, 理清各要素之间的内在关系, 需要一个能将上述因子与生物群落参数有机地结合起来的数据平台, 将分散、零星的资料予以归纳整合并通过网络共享, 以更好地为生产实践和科学研究服务。本研究采用Internet技术, 应用ASP.NET框架和MySQL数据库, 使用MS Visual Studio 2013设计并开发了服务端部署在Windows 7或Windows Server 2008 R2 (推荐)操作系统上的海洋污损生物数据管理系统, 实现了基于网络的海洋污损生物数据集成、储存与管理, 可完成来源不同、时相变化和海区多样的污损生物数据资料的集成与储存, 能通过单一或多种组合条件进行查询和检索, 并可根据用户的需要导出多种格式的检索结果报表。该系统具备操作简便、方便网络共享、易于升级更新和开拓新功能等特点, 能有效满足科研、生产和管理部门的需要。     

限制进食可以延长寿命

限制饮食，即减少40％。60％的食物摄入而不出现营养不良的情况下，可以明显延长多种生物，甚至包括灵长类动物的寿命。但是引起这种效应的分子机制一直不清楚。最新研究结果表明能够调节多种基因表达的转录因子、进化保守蛋白PHA-4和SKN-1在这个过程中扮演重要角色。     

In vivo and in vitro activation of alveolar macrophages by recombinant interferon-gamma

In vivo administration of recombinant interferon-gamma (rIFN-gamma) was previously shown to result in activation of the microbicidal activities of peritoneal macrophages (PM phi). Because macrophages at different anatomical sites vary in their functional capacities, we considered it of interest to determine whether administration of murine rIFN-gamma, either in vitro or in vivo, can enhance the microbicidal activity of resident alveolar macrophages (AM phi) and to compare the effects of rIFN-gamma on AM phi and PM phi. After incubation in vitro with rIFN-gamma, the antimicrobial activities of both murine AM phi and PM phi were enhanced, as assessed by their ability to inhibit replication of the intracellular parasite, Toxoplasma gondii. This effect was dose dependent for AM phi over a range of 0.1 to 1 U/ml and for PM phi over a range of 0.5 to 1000 U/ml. In this assay, the minimum dosage required for in vitro activation of AM phi was one-half that required for activation of PM phi, suggesting a greater sensitivity of AM phi to the in vitro activity of rIFN-gamma. Macrophages from both anatomical sites were also activated when rIFN-gamma was administered in vivo. This effect was dose dependent over a range of 10(3) to 10(5) U/mouse. Freshly harvested AM phi and PM phi from mice injected 24 hr earlier with 10(4) U rIFN-gamma by either the i.v. or i.p. routes markedly inhibited intracellular multiplication of Toxoplasma. In contrast, AM phi and PM phi from control mice permitted fourfold to ninefold increases in numbers of intracellular Toxoplasma. The anti-toxoplasma activity of AM phi and PM phi gradually diminished over a period of 3 days when assayed at successive 24 hr periods after a single i.v. injection of rIFN-gamma. At 3 days after injection, a substantial loss of anti-toxoplasma activity was observed with PM phi as compared with controls; residual anti-toxoplasma activity was still demonstrable in AM phi at 3 days. These results demonstrate that in vitro as well as in vivo treatment with rIFN-gamma confers on AM phi an enhanced antimicrobial activity. These findings provide a rationale for evaluating rIFN-gamma in the treatment of pulmonary infections, especially those due to opportunistic pathogens against which AM phi play a major role in host defense.     

cAMP activates Na+/H+ antiporter in murine macrophages

The role of cAMP in activating the Na+/H+ antiporter in murine macrophage (M phi) system was investigated. Incubation of PU5-1.8 macrophage tumour cells, peritoneal M phi and bone marrow derived macrophages (BMDM phi s) with dibutyryl-cAMP (db-cAMP) or cholera toxin (CT) led to an increase in intracellular pH (pHi). The magnitudes of these responses differed markedly in the three cell types, BMDM phi s being the most sensitive, PU5-1.8 cells the least so. These cells also differed in their responses to inhibitors of Na+/H+ exchange. In PU5-1.8 cells, the db-cAMP- or CT-triggered intracellular alkalinization was abolished by amiloride treatment which, however, was ineffective in BMDM phi s. The chemotactic peptide, N-formyl-methionyl-leucyl-phenylalanine (FMLP), also caused a significant increase in cytoplasmic pH. However, its action was apparently not mediated by cAMP. The significance of these observations is discussed.     

荧光活性染料DiO标记腹腔巨噬细胞的示踪与应用研究

目的 以细胞膜绿色荧光活性染料DiO （DiOC18（3））标记腹腔巨噬细胞（peritoneal macrophage）,探讨在巨噬细胞消失反应（macrophage disappearance reaction,MDR）中腹腔巨噬细胞的示踪研究。方法 DiO标记腹腔巨噬细胞,过继移植给C57BL/6小鼠;以脂多糖（lipopolysaccharide,LPS）诱导体内MDR。采用荧光显微镜和流式细胞术检测DiO标记的腹腔巨噬细胞数量及荧光强度;分离收集小鼠的各组织,进行冰冻切片,检测DiO标记的腹腔巨噬细胞分布情况。结果 荧光显微镜和流式细胞仪观察发现,腹腔注射LPS能显著降低腹腔中DiO标记的腹腔巨噬细胞数量及荧光强度。在MDR过程中消失的腹腔巨噬细胞,通过冰冻切片发现在肝脏、胸腺及脾脏中有分布。结论 DiO标记对腹腔巨噬细胞的存活无影响且能长效保持荧光,是一种安全、有效的示踪腹腔巨噬细胞分布的技术手段。     

Mercury chloride effects on the function and cellular integrity of sea bass (Dicentrarchus labrax) head kidney macrophages

The objective of this work was to study mercury chloride effects on the function and integrity of sea bass (Dicentrarchus labrax) head kidney macrophages (S-HKM), and to evaluate the response of HgCl2-exposed cells to macrophage activating factor(s) (MAF) produced by sea bass head kidney leukocytes. There was considerable variability in the effects of HgCl2 on the production of reactive oxygen species (ROS) by S-HKM. When incubated with HgCl2, cells from five out of nine fish tested showed a decrease in ROS production as compared to cells incubated with medium alone. In those cultures, MAF addition prevented the mercury chloride-induced decrease in ROS production. In other S-HKM cultures isolated from different fish, mercury chloride abrogated the up-regulating effect of MAF on the respiratory burst. MAF activation of the phagocytic activity of S-HKM was also impaired by HgCl2 addition. Mercury chloride induced apoptosis in S-HKM cultures and MAF addition prevented this effect.     

Mechanisms of cholinesterase inhibition by inorganic mercury

The poorly known mechanism of inhibition of cholinesterases by inorganic mercury (HgCl2) has been studied with a view to using these enzymes as biomarkers or as biological components of biosensors to survey polluted areas. The inhibition of a variety of cholinesterases by HgCl2 was investigated by kinetic studies, X-ray crystallography, and dynamic light scattering. Our results show that when a free sensitive sulfhydryl group is present in the enzyme, as in Torpedo californica acetylcholinesterase, inhibition is irreversible and follows pseudo-first-order kinetics that are completed within 1 h in the micromolar range. When the free sulfhydryl group is not sensitive to mercury (Drosophila melanogaster acetylcholinesterase and human butyrylcholinesterase) or is otherwise absent (Electrophorus electricus acetylcholinesterase), then inhibition occurs in the millimolar range. Inhibition follows a slow binding model, with successive binding of two mercury ions to the enzyme surface. Binding of mercury ions has several consequences: reversible inhibition, enzyme denaturation, and protein aggregation, protecting the enzyme from denaturation. Mercury-induced inactivation of cholinesterases is thus a rather complex process. Our results indicate that among the various cholinesterases that we have studied, only Torpedo californica acetylcholinesterase is suitable for mercury detection using biosensors, and that a careful study of cholinesterase inhibition in a species is a prerequisite before using it as a biomarker to survey mercury in the environment.     

Suppressive effect of delta 9-tetrahydrocannabinol in vitro on phagocytosis by murine macrophages

Incubation of normal mouse peritoneal cells consisting of over 90% phagocytizing macrophages with delta 9-tetrahydrocannabinol (THC) resulted in a inhibition of phagocytic function. The THC in a dose-related manner suppressed the percentage of macrophages per culture which ingested yeast and the average number of yeast particles ingested by the phagocytizing macrophages. The vehicle used to suspend the THC in vitro, i.e., DMSO, had no detectable effect on macrophage function. Suppression of phagocytosis with no effects on viability or cell number occurred with doses of 10 micrograms or less THC per milliliter culture medium. Measurable suppression also occurred after 24- to 48-hr treatment of the macrophages with the THC. This compound had little if any detectable effect on phagocytosis when added directly to the cultures shortly before testing for phagocytosis. Further studies concerning the effects of THC on macrophage function appear warranted.     

Role of macrophages in the host response to Lewis lung peritoneal carcinomatosis

Lewis lung (3LL) peritoneal carcinomatosis elicits a complex host response in the peritoneal compartment. The response was delayed, showing few inflammatory cells through day 6 after lethal challenge with 3LL cells. Responses began in about half the mice on day 7 and had appeared in all mice by day 11. On day 7, some mice still showed no detectable 3LL growth in the peritoneal lavage fluid, and no differences in the peritoneal cell populations as compared with the control group. Other tumor-bearing mice, however, had evidence of 3LL cells and hemorrhagic ascites in the peritoneal compartment, with increased numbers of peritoneal macrophages (PM) and polymorphonuclear neutrophils (PMN). By day 11, all tumor-bearing mice had 3LL growth and hemorrhagic ascites. On days 7–11, there was a major influx of macrophages with a later influx of PMN between days 11 and 14. Two distinct PM populations were detected on day 7 in mice that showed detectable 3LL peritoneal carcinomatosis: resident PM, which did not express the Mac-2 antigen, and recruited PM, which were Mac-2⁺. At least some resident PM remained in the peritoneal compartment through day 14. Analysis of the kinetics of the cytotoxic capabilities of PM from tumor-bearing mice showed that by day 7 macrophages were able to kill the B16 melanoma tumor target, but not the 3LL target. The PM, however, were able to be activated further to kill the 3LL target by treatment in vitro with lipopolysaccharide and interferon . No inhibition of PM tumoricidal activity could detected in the peritoneal wash of tumor-bearing mice. A lack of activation of PM from 3LL tumor-bearing mice may be involved in progression of peritoneal carcinomatosis.     

Diminished protein kinase C-activated arachidonate metabolism accompanies rat macrophage differentiation in the lung

Alveolar macrophages (AM) differ from other macrophage (m phi) populations in their profile of eicosanoids synthesized from arachidonic acid (AA)3. Little information is available regarding possible differences in the regulation of AA metabolism among various m phi populations. In our study, we compared the ability of cultured resident rat AM and peritoneal m phi (PM) to release and metabolize AA in response to exogenous activators of protein kinase C (PKC). When stimulated with PMA, prelabeled PM released free [3H]AA in a dose-dependent manner over the concentration range 1 to 100 nM. As assessed by HPLC, PMA-stimulated PM metabolized AA to a variety of predominantly cyclooxygenase products. The dose-dependent synthesis of PGE2 by unlabeled PM stimulated with PMA was confirmed using RIA. The ability of PMA to trigger AA release and metabolism in PM was a function of its capacity to activate PKC, as indicated by the following: 1) an additional activator of PKC, oleoyl acetylglycerol, also triggered PM AA metabolism, whereas phorbol didecanoate, which lacks the ability to activate PKC, did not; 2) two structurally unrelated inhibitors of PKC activation (staurosporine and sphinganine) both abrogated PMA induced AA release in PM; and 3) pretreatment for 18 h with high dose PMA (used to deplete cellular PKC), but not phorbol didecanoate, rendered PM refractory to subsequent PMA stimulation of AA release. In contrast to PM, AM cultured in identical fashion failed to release or metabolize AA in response to either PMA or oleoyl acetylglycerol. PM and AM were also compared for their ability to release extracellular superoxide anion in response to PMA; once again, PM exhibited significantly greater release than did AM. Inasmuch as this unresponsiveness to activation of PKC distinguishes AM from other m phi populations, we conclude that it is a unique consequence of m phi differentiation in the lung. Moreover, because both AA metabolism and the respiratory burst are affected, this refractoriness appears to reflect a defect at some proximal level in PKC-mediated signaling.     

Metabololipidomic and proteomic profiling reveals aberrant macrophage activation and interrelated immunomodulatory mediator release during aging

Macrophages adapt distinct pro-inflammatory (M1-like) and pro-resolving (M2-like) phenotypes with specific tasks in the immune response and tissue homeostasis. Altered macrophage responses with age are causative for unresolved inflammation, so-called inflammaging, and lead to higher infection susceptibility with unfavorable progression. Here, we reveal molecular determinants of age-related changes in phenotypic functions of murine peritoneal macrophages (PM) by employing comprehensive mass spectrometry-based proteomics (4746 protein groups) and metabololipidomics (>40 lipid mediators). Divergent expression of various macrophage-specific marker proteins and signaling pathways indicates aberrant PM phenotypes in old mice which detrimentally impact their capabilities to release immunomodulatory chemokines and cytokines. We show that aging strikingly compromises the polarization process of macrophages to adapt either pro-inflammatory or pro-resolving phenotypes, thereby yielding aberrant and afunctional macrophage subtypes that cannot be readily assigned to either a typical M1 or M2 phenotype. In particular, the phenotypic adaptation of the bacteria-challenged metabololipidome in macrophages related to inflammation is severely limited by age, which persists across ex vivo polarization towards M1 and M2a macrophages. Our results establish distinct age-associated PM phenotypes outside of the simplified M1 and M2 dichotomy and challenge the dogma of increased pro-inflammatory macrophage pre-activation due to aging by revealing maladaptive functions throughout all phases of inflammation, including resolution.     

Dietary fats affect macrophage-mediated cytotoxicity towards tumour cells

In the present study, the effects of feeding mice diets of different fatty acid compositions on the production of TNF-alpha and nitric oxide by lipopolysaccharide-stimulated peritoneal macrophages and on macrophage-mediated cytotoxicity towards L929 and P815 cells were investigated. C57Bl6 mice were fed on a low-fat (LF) diet or on high-fat diets (21% fat by weight), which included coconut oil (CO), olive oil (OO), safflower oil (SO) or fish oil (FO) as the principal fat source. The fatty acid composition of the macrophages was markedly influenced by that of the diet fed. Lipopolysaccharide (LPS)-stimulated macrophages from FO-fed mice showed significantly lower production (up to 80%) of PGE2 than those from mice fed on each of the other diets. There was a significant positive linear correlation between the proportion of arachidonic acid in macrophage lipids and the ability of macrophages, to produce PGE2. Lipopolysaccharide-stimulated TNF-alpha production by macrophages decreased with increasing unsaturated fatty acid content of the diet (i.e. FO < SO < OO < CO < LF). Macrophages from FO-fed mice showed significantly lower production of TNF-alpha than those from mice fed on each of the other diets. Nitrite production was highest for LPS-stimulated macrophages from mice fed on the LF diet. Macrophages from FO-fed mice showed significantly higher production of nitrite than those from mice fed on the OO and SO diets. Compared with feeding the LF diet, feeding the CO, OO or SO diets significantly decreased macrophage- mediated killing of P815 cells (killed by nitric oxide). Fish oil feeding did not alter killing of P815 cells by macrophages, compared with feeding the LF diet; killing of P815 cells was greater after FO feeding than after feeding the other high fat diets. Compared with feeding the LF diet, feeding the OO or SO diets significantly decreased macrophage-mediated killing of L929 cells (killed by TNF). Coconut oil or FO feeding did not alter killing of L929 cells by macrophages, compared with feeding the LF diet. It is concluded that the type of fat in the diet affects macrophage composition and alters the ability of macrophages to produce cytotoxic and immunoregulatory mediators and to kill target tumour cells.