Endogenous inhibitor of prostaglandin synthetase.

Mammalian serum and plasma contain an endogenous inhibitor of prostaglandin synthetase (EIPS). Human plasma fractions rich in EIPS show anti-inflammatory activity in vivo. In rats, glucocorticoids raise EIPS activity of plasma and serum. These findings suggest the existence of a natural mechanism of controlling prostaglandin synthesis, possibly related to corticosteroid action.     

Glucocorticoid hormones inhibit DNA synthesis and enhance interferon production in human lymphoid cell line

Although buffy coat leukocytes have been the prime source of human interferon, cells of the Burkitt lymphoma line Namalwa are increasingly used for the large scale production of interferon. On induction with Sendai virus or Newcastle disease virus, Namalwa cells produce a substantial quantity of interferon which contains predominantly the leukocyte antigenic species and minor amounts of fibroblast-type interferon. We have recently demonstrated that inducers of erythropoietic differentiation in Friend cells are able to enhance interferon synthesis in Namalwa cells when added to cultures larger than or equal to 24 h before interferon induction by Sendai virus. The most potent compounds, n-butyrate, stimulated interferon production about 30-fold and has also been independelty described by others. All active compounds inhibited DNA synthesis in Namalwa cells and the extent of inhibition apparently paralleled the stimulatory potency of the respective compound. Induction of differentiation of Friend cells can be antagonised by various steroid hormones, which by themselves have no measurable effects on these cells. In contrast, we report here that glucocorticoid hormones inhibit DNA synthesis in Namalwa cells and augment Sendai virus-induced interferon synthesis.     

Genetic hypertension in rats is accompanied by a defect in renal prostaglandin catabolism.

Noradrenaline releases prostaglandins in the kidney, and in rats these augment rather than reduce vasoconstriction produced by the amine. Homogenates of kidneys of New Zealand rats inbred for hypertension exhibit lower prostaglandin inactivation by 15-hydroxydehydrogenase than controls. At the same time, augmentation of noradrenaline vasoconstriction by the released prostaglandin is exaggerated. This biochemical defect could be the inherited abnormality primarily responsible for the development of hypertension in these animals.     

Bacteriophages inhibit degradation of abnormal proteins in E. coli.

On infection of Escherichia coli cells by bacteriophages T4, T5 or T7, the degradation of E. coli protein fragments and abnormal proteins is inhibited. Normal E. coli proteins, however, continue to be degraded at their usual rates. T4 early proteins (s) is needed to inhibit the turnover of abnormal proteins in T4-infected E. coli cells.     

Enkephalins presynaptically inhibit cholinergic transmission in sympathetic ganglia.

Recent biochemical and immunohistochemical studies have shown that the opioid peptides, enkephalins, occur in nerve terminals and cell bodies in mammalian sympathetic ganglia1-3. Opiates and enkephalins are thought to inhibit synaptic transmission in the peripheral nervous tissues as well as in the central nervous system4-12. The mechanisms of the opiate actions, however, are not entirely clear; both pre- and postsynaptic sites of action have been proposed7-9,11,12. As acetylcholine is known to be the major neurotransmitter in the autonomic ganglia and as the mechanism of synaptic transmission is well clarified13, analysis of the peptide action could be more easily but equally usefully carried out in the peripheral synapses than in central synapses. We now report that enkephalins presynaptically inhibit cholinergic transmission in sympathetic ganglia.     

Thromboxane molecules do not adopt the prostaglandin hairpin conformation.

The hairpin conformational hypothesis has been proposed to rationalise much of the structure-activity and receptor-binding data which have accumulated for the prostaglandin (PG) hormones. The hairpin conformation, thought to be necessary for PG activity, requires that the alpha- and omega-chains of the molecule be extended and in parallel alignment, separated by a van der Waals contact distance for the full length of the chains, with the ends of the chains approximately 5.5 A apart. The similarity between the structures of the thromboxanes (TXs) and the PGs suggests that the profile of activity of TXs, like that of PGs, centres on subtle conformational variation of the hairpin geometry. Thromboxane B2 (TXB2) is a stable hydrolysis product of a highly reactive, short-lived intermediate, thromboxane A2 (TXA2), which is formed from the prostaglandin endoperoxide (PGH2) as indicated in Fig. 1. An examination of molecular models of TXA2 and TXB2 suggests that the structural differences between the ring moieties may have much less influence in altering the side-chain conformation of TXs than do substitutents on the relatively more flexible cyclopentane ring of a PG molecule. We report here the first diffraction analysis of a thromboxane structure and note that the molecular conformation is not hairpin shaped.     

根霉Rhizopus sp.TC1产酶条件的研究

根据要因实验原则,选择影响因子较大的因素进行实验,初步研究了根霉Rhizopussp.TC1的产酶条件.经实验确定优化产酶条件为:稻草∶麸皮=1∶1;固液比=1∶3;接种量9 mL种子液/100 g湿基;温度28℃,在此条件下发酵96 h,FPA和CMC酶活分别达到17.8 IU/g、187.0 IU/g,较优化前的12.3 IU/g、131.6 IU/g分别提高了45%和42%.