酿酒酵母生长代谢影响因素的测定

以酿酒酵母为研究对象,通过单一变量控制,分别观察一定梯度的外界条件（温度,pH值,培养基,钙离子浓度及酒精浓度）对酵母生长和发酵的影响,探讨微生物生长代谢的规律性。结果表明,温度,酸碱度,培养基浓度,钙离子及酒精浓度是酵母生长代谢的重要影响因素。酵母最佳生长条件是：温度30℃,初始pH值为5,麦汁培养基浓度为11°BX,钙离子浓度为0.14 g.L-1,酒精浓度为1%;而酵母最适代谢条件略有不同,初始pH值为6,钙离子浓度为0.07 g.L-1,酒精浓度为0%。     

Klotho基因在骨质疏松大鼠模型中的表达

研究了卵巢摘除致雌性大鼠骨质疏松过程中Klotho基因表达的变化,探讨雌激素缺失引起骨质疏松发生的可能分子机制.摘除卵巢并喂以特殊饲料致大鼠骨质疏松后,分别测定骨质疏松组和对照组大鼠血清中的钙浓度与碱性磷酸酶含量,X射线法检测两组大鼠股骨密度,实时荧光定量PCR评估两组大鼠肾脏组织中Klotho基因的表达量.结果显示,与对照组相比,卵巢摘除后大鼠血钙浓度降低,碱性磷酸酶含量升高,骨密度减少,同时肾脏组织中Klotho基因表达显著下调.提示Klotho基因的下调及其对相关信号传导通路的影响可能是雌激素缺失导致骨质疏松的分子机制之一.     

围产期奶牛饲喂阴离子盐对血液钙磷浓度、尿液pH值、产奶量及产后健康状况的影响

选择15头中国荷斯坦经产奶牛按配对试验设计研究了在围产期（产前3周至分娩）饲喂阴离子盐添加剂对奶牛血液钙磷离子浓度、尿液pH值、产奶量及产后健康状况的影响。试验处理为添加阴离子盐的试验1组（50g／d）、试验2组（100g／d）和对照组（0g／d）。结果表明：阴离子盐饲粮显著提高了奶牛产前产后的血清钙离子浓度（P〈0．05），但两试验组之间差异不显著；对血磷浓度影响不显著，血钙与血磷间互作效应不显著（P〉0．05）。试验组尿液pH值显著降低（P〈0．05），试验1组pH约降低了0．6，试验2组pH约降低了1．0，但两试验组之间差异不显著（P〉0．05）；对产奶量没有显著影响（P〉0．05）。对产后疾病的预防效果比较明显，胎衣不下率试验1组降低了20％，试验2组降低了40％；产后瘫痪发病率试验1组降低了40％，试验2组降低了60％；乳房水肿发病率试验1组降低20％，试验2组降低了20％。围产期奶牛饲喂阴离子盐能够显著提高血钙浓度，降低尿液pH值和有效预防产后代谢疾病，对产奶量影响不显著。     

SBR工艺过程中出水pH值中长期变化情况分析

针对SBR工艺出水pH值,利用模拟污水和生活污水,通过检测SBR工艺进出水pH值,分析SBR工艺在较长时间内的进出水pH数值变化.研究表明,SBR工艺处理高质量浓度污水时,进水偏酸性时,经SBR工艺处理后出水偏碱性.SBR工艺处理低质量浓度生活污水或模拟污水,进水偏酸性时,出水则偏向碱性;进水偏碱性时,则出水偏向酸性.上述结论所涉及的原理各不相同,同时不随工艺参数的调整而发生改变.     

免疫初乳对大鼠血液某些生理指标和激素水平的影响

24只健康成年SD大鼠,雌雄对半,随机分成对照组(C组)、普通初乳组(NC组)、免疫初乳组(IC组),每组8只.NC和IC组每天分别灌服普通初乳和免疫初乳(1 mL/100 g体重),C组灌服生理盐水.连续6 d.在第6天观察了灌胃免疫初乳后大鼠血液某些生理指标和激素水平的变化,探讨免疫初乳在参与机体生理活动和内分泌功能活动过程中的作用.结果显示,在整个实验期内,IC组大鼠血液中性粒细胞显著高于C、NC组;NC和IC组大鼠血浆中Ins水平极显著高于对照组;IC组大鼠T3水平显著高于对照组;然而,在整个实验期,大鼠血浆T4、IL-2水平各组间无显著差异.提示免疫初乳可提高正常机体非特异性免疫功能,促进机体代谢激素的分泌,但对细胞免疫没有明显效应.     

Ca2+选择性电极制作及在分析测定中应用

以PVC为电极膜,二癸基磷酸钙为电活性物质,研究了钙离子选择性电极的制作方法.该电极在钙离子浓度10-1～10-5mol/L范围内电极电势符合Nernst方程,检出下限为10-6mol/L,适宜pH范围为4～9.在一定浓度范围内钙离子选择性电极可代替原子吸收光谱法和容量法进行土壤及水样品中钙含量测定,回收率87.7%～90.5%.     

植酸自组装膜对Q235钢在氯化钠溶液中的缓蚀作用

从植物中提取的植酸作金属缓蚀剂对环境保护具有重要意义.采用失重法、扫描电子显微镜和X射线能谱研究了植酸对Q235钢在NaCl溶液中的缓蚀行为以及影响因素.失重实验结果表明,不同pH值植酸对Q235钢的缓蚀效果明显不同,在酸性条件下植酸加速Q235钢的腐蚀,在中性及碱性条件下,植酸对Q235钢的腐蚀具有明显的抑制作用.中性或碱性条件下,NaCl溶液中植酸对Q235钢缓蚀效率随植酸浓度的增加而增加,植酸浓度达0.5%以上时,缓蚀效率高达90%以上.扫描电镜结果表明,植酸处理后的Q235钢表面生成膜在不同pH下明显不同,碱性条件下的生成膜明显好于酸性条件下的生成膜.     

三峡库区紫色土坡耕地氮磷径流特征研究

在三峡库区主要土壤类型(紫色土)、坡度(5°、25°)、种植模式(柑桔-牧草)上建立径流池,旨在研究自然环境条件下土壤氮磷径流特点.结果表明径流水的总氮平均浓度在5°坡度时明显高于25°坡度,径流水的总氮和总磷浓度在25°坡度变化幅度大于5°坡度.坡度平缓时,径流水的总氮和总磷浓度明显呈正态分布.5°坡度氮径流量和磷径流率呈显著性正相关,25°坡度径流水的总氮量和总磷量呈显著性正相关.5°坡度径流水的总磷量与土壤全磷含量呈显著性负相关,曲线模拟成S形曲线.相同坡度条件下,径流水的总氮量、土壤氮径流量明显高于径流水的总磷量和土壤磷径流量,但土壤氮和磷的径流率接近.     

三丁基锡暴露对褐菖鲉碱性磷酸酶活性的影响

研究了在实验室条件下,腹腔注射不同浓度(1.9、9.6、19.3、193 μg/kg)的三丁基锡(tributyltin,TBT)对褐菖鲉肝脏、肾脏和脾脏碱性磷酸酶[alkaline phosphatase (AKP)]活性的影响.研究结果表明,在7 d的曝污实验中,低剂量的TBT对碱性磷酸酶活性主要产生诱导作用,碱性磷酸酶活性随着TBT浓度的增大呈现先增大后减小的钟形曲线.这提示TBT暴露会影响褐菖鲉正常的代谢及其免疫功能.     

疏水性聚酯薄膜的制备及表面形貌分析

利用NaOH溶液化学刻蚀聚酯薄膜成功制得疏水性薄膜.研究了聚酯在碱性溶液中发生水解反应时外界条件对刻蚀结果的影响规律,分析了外界化学条件引起表面微观物理形貌的变化及其所对应的表面特性.结果表明,薄膜经pH为12的碱液在40℃下超声刻蚀5 min左右,并用无水乙醇浸泡,可达到与水接触角120°以上的疏水效果.     

Voltage-dependent InsP3-insensitive calcium channels in membranes of pancreatic endoplasmic reticulum vesicles.

Stimulus-secretion coupling in exocrine glands involves Ca2+ release from intracellular stores. In endoplasmic reticulum vesicle preparations from rat exocrine pancreas, an inositol 1,4,5-trisphosphate(InsP3)-sensitive, as well as an InsP3-insensitive, Ca2+ pool has been characterized. But Ca2+ channels in the endoplasmic reticulum of rat exocrine pancreas have not been demonstrated at the level of single-channel current. We have now used the patch-clamp technique on endoplasmic reticulum vesicles fused by means of the dehydration-rehydration method. In excised patches, single Ba2(+)- and Ca2(+)-selective channels were recorded. The channel activity was markedly voltage-dependent. Caffeine increased channel open-state probability, whereas ruthenium red and Cd2+ blocked single-channel currents. Ryanodine, nifedipine and heparin had no effect on channel activity. The channel activity was not dependent on the free Ca2+ concentration, the presence of InsP3, or pH. We conclude that this calcium channel mediates Ca2+ release from an intracellular store through an InsP3-insensitive mechanism.     

Protective role of a novel human erythrocyte-derived depressing factor on blood vessels in rats

The protective role of a human erythrocyte-derived depressing factor (EDDF) on blood vessels was evaluated. The experiments were carried out on 25male Wistar rats aged 6-8 weeks, which were divided into control (n = 8), calcium overload (n = 8) and NG-L-nitro-arginine hypertensive model groups (L-NNA,n = 9), respectively. The isolated vascular ring perfusion assay, two-photon laser scanning fluorescence microscopy (TPM) and transmitted electron microscope were used to examine the effect of EDDF on vascular function and ultrastructure. Results showed that the contractile response of calcium overload rats and L-NNA rats to phenylephrine (PE) was significantly enhanced compared with that of the control (P < 0.05), and EDDF (10-3 g @mL-1) remarkably decreased the vascular contractile response of control's and calcium overload rats (P < 0.05),while EDDF had no effect on that of L-NNA rats. EDDF also alleviated the ultrastructural lesion of aorta VSMC in calcium overload rats by easing the abnormal in the nucleus, mitochondrion and other organell. It is concluded that EDDF could efficiently protect blood vessels against injury by influencing Ca2+ transport and ameliorating the lesion of VSMC, and further supported the hypothesis that the NO-cGMP pathway might contribute to the vasodilation and partially antihypertensive mechanism of EDDF.``     

Ebselen 抑制 ONOO~- 对神经元[Ca~(2+)]_i 的影响

Ｆｕｒａ－２显微荧光测钙技术研究发现,过氧亚硝基阴离子（ＯＮＯＯ－）作用于ＭＮ９Ｄ细胞,数ｓ内即可导致其胞内游离钙离子浓度（［Ｃａ２＋］ｉ）的急剧升高．胞外液换为无钙液或向胞外液中加入硝苯吡啶（Ｎｉｆｅｄｉｐ－ｉｎｅ）、二硫苏糖醇（ＤＴＴ）均可抑制ＯＮＯＯ－对［Ｃａ２＋］ｉ的影响,提示Ｌ－型钙通道的激活是ＯＮＯＯ－引起［Ｃａ２＋］ｉ升高的主要原因,ＯＮＯＯ－的这种作用可能与其氧化特性有关．Ｅｂｓｅｌｅｎ（２－苯基－１,２－苯并异硒唑－３（２Ｈ）酮）明显抑制ＯＮＯＯ－对［Ｃａ２＋］ｉ的影响,并且存在一定的剂量效应关系．     

无熟料高炉矿渣水泥的物料配比与性能的关系

研究了Ca(OH)_2、硬石膏及少量可溶性钙盐(甲酸钙、乙酸钙等)复合对高炉矿渣活性的激发作用及物料配比与性能的关系。结果表明:Ca(OH)_2与硬石膏复合对矿渣活性有一定的激发效果,可溶性钙盐的加入降低了水泥的pH值,进一步激发了矿渣的活性,乙酸钙(Ca(CH_2COOH)_2)的激发效果好于甲酸钙(Ca(COOH)_2);在矿渣掺量为80%,Ca(OH)_2掺量15%,硬石膏掺量5%,外加1.0%Ca(CH_2COOH)_2生产出的无熟料水泥28 d抗压强度达54.6 MPa;Ca(COOH)_2与硬石膏促进高炉矿渣水化的主要水化产物为钙矾石和C-S-H凝胶。     

两种金属离子[Ca~(2+),Mg~(2+)]——螯合剂缓冲体系中自由[Ca~(2+)]的计算

在一种金属离子[Ca2+ ]及两种金属离子[Ca2+ ,Mg2+ ]螯合剂缓冲体系中总[Ca2+ ]t 的计算工作基础上,进行了含有两种金属离子[Ca2+ ,Mg2+ ]——螯合剂缓冲体系中自由钙[Ca2+ ]的计算研究.特别是利用微机给出了简单计算公式,编制了计算程序;并给出部分常用数据.只要在所需pH 值、温度、[EDTA]t 或[EGTA]t 浓度条件下,根据实验要求,由[Ca2+ ]t 和[Mg2+ ]t 就可以求出自由[Ca2+ ].     

STIM1 is a Ca2+ sensor that activates CRAC channels and migrates from the Ca2+ store to the plasma membrane

As the sole Ca2+ entry mechanism in a variety of non-excitable cells, store-operated calcium (SOC) influx is important in Ca2+ signalling and many other cellular processes. A calcium-release-activated calcium (CRAC) channel in T lymphocytes is the best-characterized SOC influx channel and is essential to the immune response, sustained activity of CRAC channels being required for gene expression and proliferation. The molecular identity and the gating mechanism of SOC and CRAC channels have remained elusive. Previously we identified Stim and the mammalian homologue STIM1 as essential components of CRAC channel activation in Drosophila S2 cells and human T lymphocytes. Here we show that the expression of EF-hand mutants of Stim or STIM1 activates CRAC channels constitutively without changing Ca2+ store content. By immunofluorescence, EM localization and surface biotinylation we show that STIM1 migrates from endoplasmic-reticulum-like sites to the plasma membrane upon depletion of the Ca2+ store. We propose that STIM1 functions as the missing link between Ca2+ store depletion and SOC influx, serving as a Ca2+ sensor that translocates upon store depletion to the plasma membrane to activate CRAC channels.     

Recruitment of cytosolic proteins to a secretory granule membrane depends on Ca2+-calmodulin

An increase in free calcium triggers catecholamine secretion from chromaffin cells and calmodulin is strongly implicated as the intracellular Ca2+ receptor. In our recent studies of calmodulin action in the chromaffin cell, micromolar Ca2+ concentrations resulted in calmodulin and cytosolic proteins becoming bound to the chromaffin granule membranes. We now report that calmodulin is bound with high affinity to granule membrane proteins of molecular weights (Mrs) 25,000 and 22,000 (25K and 22K) at low Ca2+ (less than 10(-8) M) and to proteins with Mrs 69K and 50K at high Ca2+ (greater than 1 microM). Other cytosolic components (Mrs 70K, 36K, 34K and 32K) require calmodulin for their interfraction with membrane. These proteins separately bound to calmodulin-Sepharose at high Ca2+ concentrations. Although the functions of these adrenal proteins have not been established, the 34K and 32K Mr components co-migrate with clathrin light chains isolated from medullary coated vesicles and the Mr 34K components from both sources share the same one-dimensional peptide map. These interactions were observed at micromolar Ca2+ levels at 'intracellular' conditions of pH and ionic strength and would be expected to occur during secretion from the chromaffin cell.     

Coordination of agonist-induced Ca2+-signalling patterns by NAADP in pancreatic acinar cells

Many hormones and neurotransmitters evoke Ca2+ release from intracellular stores, often triggering agonist-specific signatures of intracellular Ca2+ concentration. Inositol trisphosphate (InsP3) and cyclic adenosine 5'-diphosphate-ribose (cADPR) are established Ca2+-mobilizing messengers that activate Ca2+ release through intracellular InsP3 and ryanodine receptors, respectively. However, in pancreatic acinar cells, neither messenger can explain the complex pattern of Ca2+ signals triggered by the secretory hormone cholecystokinin (CCK). We show here that the Ca2+-mobilizing molecule nicotinic acid adenine dinucleotide phosphate (NAADP), an endogenous metabolite of beta-NADP, triggers a Ca2+ response that varies from short-lasting Ca2+ spikes to a complex mixture of short-lasting (1-2s) and long-lasting (0.2-1 min) Ca2+ spikes. Cells were significantly more sensitive to NAADP than to either cADPR or InsP3, whereas higher concentrations of NAADP selectively inactivated CCK-evoked Ca2+ signals in pancreatic acinar cells, indicating that NAADP may function as an intracellular messenger in mammalian cells.     

A functional correlate for the dihydropyridine binding site in rat brain

Calcium channels, controlling the influx of extracellular Ca2+ and hence neurotransmitter release, exist in the brain. However, drugs classed as calcium antagonists and which inhibit Ca2+ entry through voltage-activated Ca2+ channels in heart and smooth muscle, seem not to affect any aspect of neuronal function in the brain at pharmacologically relevant concentrations. Yet the dihydropyridine calcium antagonists (for example, nitrendipine) bind stereospecifically with high affinity to a recognition site on brain-cell membranes thought to represent the Ca2+ channel and consequently, the physiological relevance of these sites has been questioned. However, activation of voltage-dependent Ca2+ channels can increase cytoplasmic Ca2+ and neurotransmitter release in neuronal tissue. We show here that Bay K8644, a dihydropyridine Ca2+-channel activator, can augment K+-stimulated release of serotonin from rat frontal cortex slices and that these effects can be antagonized by low concentrations of calcium antagonists. As 3H-dihydropyridine binding to cortical membrane preparations resembles the binding in heart and smooth muscle where there are good functional correlates we conclude that the dihydropyridine binding sites in the brain represent functional Ca2+ channels that can be unmasked under certain circumstances.