模拟酸雨胁迫对马尾松和杉木幼苗土壤呼吸的影响

利用LI-8100测定模拟酸雨不同处理下(pH2.5、4.0和5.6)盆栽马尾松(Pinus Massoniana)和杉木幼苗(Cunninghamia lanceolata)的土壤呼吸速率及土壤温度、含水量,研究酸雨对其土壤呼吸的影响.结果表明:模拟酸雨喷淋下马尾松和杉木土壤pH值呈现下降的趋势且下降幅度同酸雨酸度呈现正相关性;马尾松和杉木各个处理下土壤呼吸速率季节变化显著,且同地下10cm土壤温度季节变化趋势一致,pH2.5处理下的土壤呼吸速率平均值分别为1.79μmol · m-2 · s-1和1.12μmol · m-2 · s-1,比对照组(pH5.6)土壤呼吸速率平均值1.57μmol · m-2 · s-1和1.54μmol · m-2 · s-1分别高14%和低39%;马尾松和杉木各个处理下土壤呼吸速率同10cm土壤温度之间均呈现显著的指数关系(P<0.001),与5cm土壤含水量之间相关性不明确;在P=0.05水平上进行多元回归分析,可以得到土壤呼吸速率同土壤温度和含水量的综合拟合方程,和单因素(温度、含水量)拟合相比能够更好地解释土壤呼吸的变化情况;马尾松和杉木在pH2.5和4.0处理下的土壤呼吸温度系数Q10值分别为1.36、2.01和1.51、2 25,同对照组1.14和1.58相比,均有明显差异,且两者Q10值的变化呈先增大后减小的趋势.这证明酸雨是影响马尾松和杉木土壤CO2通量的一个重要因素.     

Isolation of sulfite reductase variants of a commercial wine yeast with significantly reduced hydrogen sulfide production

The production of hydrogen sulfide (H₂S) during fermentation is a common and significant problem in the global wine industry as it imparts undesirable off-flavors at low concentrations. The yeast Saccharomyces cerevisiae plays a crucial role in the production of volatile sulfur compounds in wine. In this respect, H₂S is a necessary intermediate in the assimilation of sulfur by yeast through the sulfate reduction sequence with the key enzyme being sulfite reductase. In this study, we used a classical mutagenesis method to develop and isolate a series of strains, derived from a commercial diploid wine yeast (PDM), which showed a drastic reduction in H₂S production in both synthetic and grape juice fermentations. Specific mutations in the MET10 and MET5 genes, which encode the catalytic α- and β-subunits of the sulfite reductase enzyme, respectively, were identified in six of the isolated strains. Fermentations with these strains indicated that, in comparison with the parent strain, H₂S production was reduced by 50–99%, depending on the strain. Further analysis of the wines made with the selected strains indicated that basic chemical parameters were similar to the parent strain except for total sulfite production, which was much higher in some of the mutant strains.     

Hydration, structure, and molecular interactions in the headgroup region of dioleoylphosphatidylcholine bilayers: an electron spin resonance study

The relationship between bilayer hydration and the dynamic structure of headgroups and interbilayer water in multilamellar vesicles is investigated by electron spin resonance methods. Temperature variations of the order parameter of a headgroup spin label DPP-Tempo in DOPC in excess water and partially dehydrated (10 wt % water) show a cusp-like pattern around the main phase transition, Tc. This pattern is similar to those of temperature variations of the quadrupolar splitting of interbilayer D2O in PC and PE bilayers previously measured by 2H NMR, indicating that the ordering of the headgroup and the interbilayer water are correlated. The cusp-like pattern of these and other physical properties around Tc are suggestive of quasicritical fluctuations. Also, an increase (a decrease) in ordering of DPP-Tempo is correlated with water moving out of (into) interbilayer region into (from) the bulk water phase near the freezing point, Tf. Addition of cholesterol lowers Tf, which remains the point of increasing headgroup ordering. Using the small water-soluble spin probe 4-PT, it is shown that the ordering of interbilayer water increases with bilayer dehydration. It is suggested that increased ordering in the interbilayer region, implying a lowering of entropy, will itself lead to further dehydration of the interbilayer region until its lowered pressure resists further flow, i.e., an osmotic phenomenon.     

Oxidative stress and inflammation in cerebral cavernous malformation disease pathogenesis: Two sides of the same coin

Cerebral Cavernous Malformation (CCM) is a vascular disease of proven genetic origin, which may arise sporadically or is inherited as an autosomal dominant condition with incomplete penetrance and highly variable expressivity. CCM lesions exhibit a range of different phenotypes, including wide inter-individual differences in lesion number, size, and susceptibility to intracerebral hemorrhage (ICH). Lesions may remain asymptomatic or result in pathological conditions of various type and severity at any age, with symptoms ranging from recurrent headaches to severe neurological deficits, seizures, and stroke. To date there are no direct therapeutic approaches for CCM disease besides the surgical removal of accessible lesions. Novel pharmacological strategies are particularly needed to limit disease progression and severity and prevent de novo formation of CCM lesions in susceptible individuals.Useful insights into innovative approaches for CCM disease prevention and treatment are emerging from a growing understanding of the biological functions of the three known CCM proteins, CCM1/KRIT1, CCM2 and CCM3/PDCD10. In particular, accumulating evidence indicates that these proteins play major roles in distinct signaling pathways, including those involved in cellular responses to oxidative stress, inflammation and angiogenesis, pointing to pathophysiological mechanisms whereby the function of CCM proteins may be relevant in preventing vascular dysfunctions triggered by these events. Indeed, emerging findings demonstrate that the pleiotropic roles of CCM proteins reflect their critical capacity to modulate the fine-tuned crosstalk between redox signaling and autophagy that govern cell homeostasis and stress responses, providing a novel mechanistic scenario that reconciles both the multiple signaling pathways linked to CCM proteins and the distinct therapeutic approaches proposed so far. In addition, recent studies in CCM patient cohorts suggest that genetic susceptibility factors related to differences in vascular sensitivity to oxidative stress and inflammation contribute to inter-individual differences in CCM disease susceptibility and severity.This review discusses recent progress into the understanding of the molecular basis and mechanisms of CCM disease pathogenesis, with specific emphasis on the potential contribution of altered cell responses to oxidative stress and inflammatory events occurring locally in the microvascular environment, and consequent implications for the development of novel, safe, and effective preventive and therapeutic strategies.     

Opposing roles of IL-10 in acute bacterial infection

Interleukin-10 (IL-10) is recognized as an anti-inflammatory cytokine that downmodulates inflammatory immune responses at multiple levels. In innate cells, production of this cytokine is usually triggered after pathogen recognition receptor (PRR) engagement by pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patters (DAMPs), as well as by other soluble factors. Importantly, IL-10 is frequently secreted during acute bacterial infections and has been described to play a key role in infection resolution, although its effects can significantly vary depending on the infecting bacterium. While the production of IL-10 might favor host survival in some cases, it may also result harmful for the host in other circumstances, as it can prevent appropriate bacterial clearance. In this review we discuss the role of IL-10 in bacterial clearance and propose that this cytokine is required to recover from infection caused by extracellular or highly pro-inflammatory bacteria. Altogether, we propose that IL-10 drives excessive suppression of the immune response upon infection with intracellular bacteria or in non-inflammatory bacterial infections, which ultimately favors bacterial persistence and dissemination within the host. Thus, the nature of the bacterium causing infection is an important factor that needs to be taken into account when considering new immunotherapies that consist on the modulation of inflammation, such as IL-10. Indeed, induction of this cytokine may significantly improve the host’s immune response to certain bacteria when antibiotics are not completely effective.     

A molecular analysis of matrix remodeling and angiogenesis during long bone development

The replacement of cartilage by bone is the net result of genetic programs that control chondrocyte differentiation, matrix degradation, and bone formation. Disruptions in the rate, timing, or duration of chondrocyte proliferation and differentiation result in shortened, misshapen skeletal elements. In the majority of these skeletal disruptions, vascular invasion of the elements is also perturbed. Our hypothesis is that the processes involved in endochondral ossification are synchronized via the vasculature. The purpose of this study was to examine carefully the events of vascular invasion and matrix degradation in the context of chondrocyte differentiation and bone formation. Here, we have produced a ‘molecular map’ of the initial vascularization of the developing skeleton that provides a framework in which to interpret a wide range of fetal skeletal malformations, disruptions, and dysplasias.     

高产辅酶Q10结构类似物抗性突变株的选育

以土壤杆菌(Agrobacteriumsp.)TLY-4为出发菌株,采用70%致死剂量的NTG进行诱变处理,通过筛选抗辅酶Q10结构类似物维生素K3突变株,定向选育到了两株辅酶Q10高产突变株,编号为R-122和R-015,其摇瓶发酵72h时的辅酶Q10产量分别为57.3 mg/L和59.9 mg/L,较出发菌株提高了35.7%和41.6%。通过连续传代实验,表明突变株高产辅酶Q10的遗传性状稳定。实验以有机溶剂DMF和吐温-80共同增溶的方法,解决了维生素K3在培养基中易析出的问题,并确定了平板培养基中维生素K3的最小抑菌浓度为0.15 mg/mL。     

辅酶Q10联合金凤丸对体外授精-胚胎移植患者卵巢功能及子宫内膜容受性的影响

目的:探讨辅酶Q10联合金凤丸对体外授精-胚胎移植患者卵巢功能及子宫内膜容受性的影响。方法:选择2017年7月～2017年10月接诊的185例体外授精-胚胎移植患者进行研究,通过随机数表法将其分为观察组(n=95)和对照组(n=90)。对照组采用金凤丸进行治疗,观察组在对照组的基础上加用辅酶Q10进行治疗。治疗后,比较两组血清卵泡刺激素(FSH)、促黄体生成素(LH)、睾酮(T)、雌二醇(E_2)、胰岛素(INS)、子宫内膜厚度、孕激素(P)水平、获卵数、受精率及妊娠率。结果:治疗后,两组患者血清FSH、LH、T、E_2、INS水平均较治疗前明显下降,且观察组以上指标水平均显著低于对照组(P0.05);两组患者子宫内膜厚度和血清P水平均较治疗前明显升高,且观察组以上指标均显著高于对照组(P0.05);两组患者获卵数无明显差异,观察组患者受精率、妊娠率均显著高于对照组(P0.05)。结论:辅酶Q10联合金凤丸可明显增加子宫内膜厚度,提高妊娠率。