Functional Casein-Poly saccharide Conjugates Prepared by Controlled Dry Heating

Casein was conjugated with dextran and galactomannan in a controlled dry state at a relative humidity of 79% and at 60°C for 24 hr. The covalent attachment of polysaccharides to casein was confirmed by SDS-PAGE and HPLC. The emulsifying activity of the casein-dextran and casein-galactomannan conjugates was 1.5 times higher than that of casein. The emulsion stability of the casein-dextran and casein-galactomannan conjugates was 10 times higher than that of casein. The improvement in these emulsifying properties reached a steady state when the conjugation of casein with polysaccharide was done for 24 hr in a controlled dry state, suggesting the rapid formation of conjugates through a Maillard reaction in the case of casein. Compared to commercial emulsifiers, the casein-polysaccharide conjugates showed better emulsifying properties in acidic and high-salt concentration systems.     

Prostaglandins may play a signal-coupling role during phagocytosis in Amoeba proteus

Summary Phagocytosis in Amoeba proteus can be induced with prostaglandins (PG). In addition, arachidonic acid (the fatty acid precursor to the PG-2 series) also induces phagocytosis. The induction of phagocytosis with arachidonic acid can be partially inhibited by the cyclooxygenase inhibitor indomethacin. Phagocytosis in the amoeba can also be induced with the chemotactic peptide N-formylmethionyl-leucylphenylalanine (NFMLP). The peptide presumably induces phagocytosis by interacting with receptors on the amoeba surface, which may initiate the release of arachidonic acid from membrane lipids. NFMLP-induced phagocytosis can also be partially inhibited by indomethacin. It is suggested that PG's or biochemically related substances may play a signal-coupling role during phagocytosis in the amoeba.     

Liposome-mediated labeling of adrenocorticotropin fragments parallels their biological activity

To test our hypothesis that specific interactions of ACTH peptides with model lipid membranes reflect the biological importance of similar interactions on target cells, we investigated the liposome-mediated labeling of ACTH fragments with the extremely hydrophobic photolabel, 3-trifluoromethyl-3-(m-[125I]iodophenyl)diazirine. Correlations were found between the labeling rates and the agonistic and antagonistic potencies of the peptides for in vitro steroidogenesis and inhibition of a synaptosomal protein kinase. A model for the cross-reactivity between ACTH and opioid peptides is discussed.     

Effects of Dopaminergic Drugs on Cerebellar Prostaglandin Concentrations

Abstract: Previous data indicate that the injection of dopaminergic drugs induces changes in cerebellar 3',5'-guanosine monophosphate (cGMP) content. Accordingly, we have investigated the effects of haloperidol, sulpiride, or apomorphine on cerebellar prostaglandin (PG) concentration, a parameter related to cGMP content. Results obtained show that dopamine receptor blocking agents, such as haloperidol and sulpiride, significantly decrease cerebellar PGE₂ and PGF_2α concentrations, while opposite changes are induced by apomorphine, a dopamine receptor agonist.     

Stimulation of Phospholipase A2 and Secretion of Catecholamines from Brain Synaptosomes by Potassium and A23187

Abstract: Potassium depolarization of rat brain synaptosomes (containing incorporated l-acyl-2-[¹⁴C]arachidonyl-phosphatidylcholine) stimulated endogenous phospholipase A₁ (EC 3.1.1.32) and A₂ (EC 3.1.1.4), as determined by the formation of [¹⁴C]lysophosphatidylcholine, [¹⁴C]arachidonate, and [¹⁴C]prostaglandins, and also stimulated the secretion of [³H]catecholamines. The phospholipase A₂ stimulation, dependent on calcium, was elicited in resting synaptosomes by A23187 and was demonstrated with incorporated 1-acyl-2-[^l4C]oleoyl-phosphatidylcholine but not with incorporated [^I4C]phosphatidylethanolamine or [^l4C]phosphatidylserine. Inhibitors of phospholipase A₂ [p-bromophenacylbromide (10 μM), trifluoperazine (3 μM), and quinacrine (3 μM) reduced the potassium-stimulated [³H]catecholamine release from synaptosomes to 78, 39. and 55%, respectively, of depolarized controls. The addition of lysophosphatidylcholine increased the release of [³H]norepinephrine to levels observed with potassium depolarization, whereas lysophosphatidylethanolamine, lysophosphatidylserine, and sodium dodecyl sulfate were much less effective. Potassium stimulation of synaptosomes increased the endogenous levels of free arachidonic acid and prostaglandins E₂ and F_2α. Indomethacin and aspirin decreased the amounts of prostaglandins formed, allowed the accumulation of free arachidonic acid, and diminished the potassium-stimulated release of [³H]dopamine. p-Bromophenacylbromide inhibited the formation of prostaglandin F_2α. Addition of prostaglandin E₂ inhibited, whereas prostaglandin F_2α enhanced the release of [³H]norepinephrine. These results suggest that calcium influx induced by synaptosomal depolarization activates endogenous phospholipase A₂, with subsequent formation of lysophosphatidylcholine and prostaglandins, both of which may modulate neurosecretion.     

Vasoactive Intestinal Peptide and Forskolin Stimulate Interleukin 6 Production by Rat Cortical Astrocytes in Culture via a Cyclic AMP-Dependent, Prostaglandin-Independent Mechanism

Abstract: In this study we analyzed the involvement of the cyclic AMP (cAMP)-protein kinase A system in the regulation of interleukin 6 production by cultured cortical astrocytes. Vasoactive intestinal peptide strongly increased, in a dose-dependent manner, interleukin 6 production. This effect was reduced when protein kinase A was blocked by KT-5720; it was not affected by calphostin C, a protein kinase C inhibitor. Forskolin caused a concentration-dependent increase in interleukin 6 release that was also inhibited by KT-5720. Because prostaglandins are believed to play a role in interleukin 6 production, we tried to determine whether the stimulatory effects of vasoactive intestinal peptide and forskolin on cytokine release might be mediated by stimulation of prostaglandin production in cortical astrocytes. Vasoactive intestinal peptide did not increase the production of either prostaglandin E₂ or F_2α. Conversely, forskolin concentration-dependently stimulated the production of both prostaglandins, an effect that was blocked by indomethacin. Indomethacin did not affect either vasoactive intestinal peptide- or forskolin-stimulated interleukin 6 production. To exclude the possibility that prostaglandins participate in interleukin 6 production induced by forskolin, we tested prostaglandins E₂ and F_2α. The former was completely ineffective in eliciting the cytokine production, whereas prostaglandin F_2α slightly increased interleukin 6 production only at the highest concentrations. 8-Bromo-cAMP and dibutyryl-cAMP stimulated interleukin 6 production to a lesser extent than vasoactive intestinal peptide and forskolin. In conclusion, we provide evidence that vasoactive intestinal peptide increases interleukin 6 production by astrocytes through the stimulation of the cAMP-protein kinase A pathway, an effect that is reproduced by cAMP analogues. In addition, we point out that prostaglandins are not involved in vasoactive intestinal peptide- and forskolin-mediated induction of interleukin 6 production in cultured astrocytes.     

纵坑切梢小蠹蛀梢期空间分布

在昆明地区,纵坑切梢小蠹(Tomicus piniperda)成虫蛀梢多集中在蛀干木附近。 种群密度以蛀干木为中心向周围呈指数递减,散布半径约30m。在蛀梢过程中,该种群逐渐向新区扩张。在树冠内,纵坑切梢小蠹主要分布在4-10轮枝上。第7轮枝虫口百分率最高。6-7轮枝受害率最大。 树冠上层受害较其下层严重。从树冠水平层次考察,树冠外层虫量相对集中,约为树冠中、内层虫量之和。 树冠内层虫量最少。纵坑切梢小蠹在树冠内的种群分布系由梢径、种群密度、蛀梢行为、降落方式、光照等因素综合影响的结果。     

10CM短柱快速分离3-MH的实验研究

本研究在改进后短程序基础上,对氨基酸分离柱进行了改进。改进后的分离柱长为10cm。比原来20cm长柱分离3—MH的时间缩短了近1/2。实验所得的(回收率为97.59%,分离度0.89±0.02。变异系数1.17)这些指标较国外用其它方法所得的结果有良好的相关性。多次测定结果说明长柱与短柱比较无明显差异。证明了短柱对3—MH含量无影响。这一改进所建立的方法大大地缩短了样品的分析时间,节约了大量进口试剂,开展这方面的工作将有利益提高严重烧伤、创伤后蛋白质代谢和营养学等方面的研究水平。     

Prostaglandin H Synthetase-Mediated Metabolism of Dopamine: Implication for Parkinson's Disease

Abstract: Differences in prostaglandin H synthetase (PHS) activity in the substantia nigra of age- and post-mortem interval-matched parkinsonian, Alzheimer's, and normal control brain tissue were assessed. Prostaglandin E₂ (PGE₂, an index of PHS activity) was higher in substantia nigra of parkinsonian brain tissue than Alzheimer's or control tissue. Incubation of substantia nigra slices with arachidonic acid (AA) increased PGE₂ synthesis. Dopamine stimulated PHS synthesis of PGE₂. [³H]Dopamine was activated by PHS to electrophilic intermediate(s) that covalently bound to DNA, microtubulin protein, bovine serum albumin, and sulfhydryl reagents. When AA was replaced by hydrogen peroxide, PHS/H₂O₂-supported binding proceeded at rates similar to those observed with PHS/AA. Indomethacin and aspirin inhibited AA-mediated cooxidation of dopamine but not H₂O₂-mediated metabolism. PHS-mediated metabolism of dopamine was not affected by monoamine oxidase inhibitors. Substrate requirements and effects of specific inhibitors suggest cooxidation of dopamine is mediated by the hydroperoxidase activity of PHS. ³²P-postlabeling was used to detect dopamine-DNA adducts. PHS/AA activation of dopamine in the presence of DNA resulted in the formation of five dopamine-DNA adducts, i.e., 23, 43, 114, 70, and 270 amol/µg DNA. DNA adduct formation was PHS, AA, and dopamine dependent. PHS catalyzed cooxidation of dopamine in dopaminergic neuronal degeneration is discussed.     

Action of vasoactive intestinal peptide (VIP) on amphibian adrenocortical function,in vitro

Vasoactive intestinal peptide (VIP) is located in chromaffin cells of the frog adrenal gland and is able to stimulate corticosteroid secretion in amphibians. In the present study we have investigated the possible involvement of prostaglandins, microfilaments and calcium in the mechanism of action of VIP on frog adrenocortical tissue. Rana ridibunda interrenal dice were perifused with amphibian culture medium for more than 10 hours. Corticosterone and aldosterone concentrations were measured in the effluent perifusate using sensitive and specific radioimmunoassay methods. In the presence of indomethacin (5 μM), a specific blocker of prostaglandin biosynthesis, the spontaneous secretion of corticosteroids was markedly reduced (80%) but the stimulatory effect of VIP was not altered. The administration of the microfilament disrupting agent cytochalasin B (50 μM) inhibited both spontaneous and VIP-induced corticosteroid secretion. In the absence of calcium, the spontaneous level of corticosteroid was reduced to about 60% but VIP was still able to stimulate corticosteroid secretion. From these data we conclude that the integrity of the cytoskeleton is required for the secretory response of adrenocortical cells to VIP, whereas neither prostaglandins nor calcium are involved in VIP-induced adrenocortical stimulation.