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61.
An interaction between lysozyme and mucus glycoproteins. Implications for density-gradient separations. 下载免费PDF全文
1. Some mucus glycoproteins form soluble complexes with lysozyme at neutral pH values. 2. The extent of complex-formation was determined, by an ultracentrifugal difference method, for a range of glycoproteins covering the common blood-group specificities. 3. Interaction was strongest with those glycoproteins of blood-group Lea specificity; these were also richest in sialic acid. 4. Interaction diminished with increase of ionic strength, and was not detectable at I 0.50; however, an asialoglycoprotein was found to retain some activity. The interaction is accordingly primarily, but probably not exclusively, coulombic in origin. 5. The buoyant density of lysozyme in CsCl, CsBr, CsI and Cs2SO4 was determined; the values in the last three salts are anomalously high. This finding accounts for the previously noted difficulty of separating free protein from glycoproteins by single-stage centrifugation in CsBr. 6. Conditions for effective separation of glycoproteins from secretions containing lysozyme by density-gradient centrifugation are reported. 相似文献
62.
Derek Horton 《Carbohydrate research》1978,67(2):357-370
Addition of phenyl azide to 3,5-di-O-acetyl-6,7-dideoxy-1,2-O-isopropylidene-β-l-idio-hept-6-ynofuranose (1) and subsequent saponification gave a 4-substituted 1-phenyl-1,2,3-triazole derivative (3) whose optical rotatory dispersion (o.r.d.) curve was positive. The α-d-gluco analog (5) of 1 similarly gave the 5-epimer (7) of 3; its o.r.d. curve was negative. Both 3 and 7 were degraded to the known 1-phenyl-1,2,3-triazole-4-carboxaldehyde. Similarly, addition of 2,4,6-trimethylbenzonitrile N-oxide to 1 or 5 gave the corresponding, crystalline 3-mesitylisoxazoles as single products; 13C-n.m.r. spectroscopy was used to establish the orientation of addition. Related 3-mesitylisoxazoles (11 and 13) were obtained from 1,2:3,4-di-O-isopropylidene-d-glycero-α-d-galacto-oct-7-ynopyranose (10) and its l-glycero 6-epimer (12), respectively; 11 showed the expected, large levorotation, and the 6-epimer 13 was also levorotatory. Benzonitrile (N-phenyl)imine, prepared in situ from 1-(α-chlorobenzylidene)-2-phenylhydrazine and base, did not react with 10 (or its 6-epimer 12), but did react with the 6-keto analog to give a 5-substituted 1,3-diphenyl-1,2-diazole. 相似文献
63.
Methyl 2,3-O-benzylidene-6-deoxy-α-L-mannopyranoside (2) reacted with butyllithium to give a mixture of 1,5-anhydro-3-C-butyl-1,2,6-trideoxy-L-ribo-hex-1-enitol (3) and its L-arabino analogue (4), together with methyl 2,3,6-trideoxy-α-L-erythro-hex-2-enopyranoside (5). In contrast, the 4-O-methyl analogue (8) of 2 was converted by butyllithium into methyl 2,6-dideoxy-4-O-methyl-α-L-erythro-hexo-pyranosid-3-ulose (9), which was further characterized as its oxime 10. The 4-O-benzyl analogue of 8, obtained as two separate diastereoisomers (6 and 7) differing in configuration at C-2 of the dioxolane ring, gave a complex mixture of products on treatment with butyllithium. 相似文献
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—The convulsant action of methyldithiocarbazinate (MDTC), thiocarbohydrazide (TCH) and thiosemicarbazide (TSC) has been studied in mice. The relationship between dose and time to convulsions indicated that MDTC has a dual action and is more potent than TSC. Pretreatment of mice with pyridoxal phosphate (0.25 mmol/kg) protected against convulsions and death produced by low doses of MDTC or TCH, and low or high doses of TSC. Pretreatment with pyridoxine hydrochloride (0.25 mmol/kg) protected mice against TSC but not against TCH. It protected against low doses of MDTC (0.12 mmol/kg), but shortened the latency to convulsions after intermediate doses of MDTC (0.37 mmol/kg). Glutamate decarboxylase activity (GAD, EC 4.1.1.15) in whole brain homogenates from mice killed at the onset of seizures, was significantly reduced by all 3 drugs at all doses. This inhibition did not exceed 30% after any dose of TSC or TCH, but was 64% in mice killed 4 min after the injection of MDTC (0.98 mmol/kg). The addition of pyridoxal phosphate to brain homogenates abolished GAD inhibition after MDTC but not after TCH. In vitro brain GAD was 50% inhibited by 10−4m -MDTC, 18% by 10−4m -TSC and 8% by 10 −4m -TCH. Kinetic studies suggested that at low concentrations MDTC inhibits by competing with pyridoxal phosphate. At the onset of convulsions the cerebral content of pyridoxal phosphate was reduced after low or high doses of TSC (0.27 and 2.2 mmol/kg) and after high doses of MDTC (0.98 mmol/kg). All three drugs (at 10−5−10−4m ) inhibited pyridoxal phosphokinase (EC 2.7.1.35) in vitro. Short latency convulsions after MDTC (0.37–0.98 mmol/kg) very probably arise from inhibition of cerebral GAD, due to competition for coenzymic sites and/or unavailability of coenzyme. Long-latency convulsions after MDTC (0.12–0.37 mmol/kg) are comparable to those seen after TSC (0.27–2.2 mmol/kg) and may depend on a mechanism additional to inhibition of GAD. 相似文献
66.
In the clawed toadXenopus laevis, thymectomy at 7 days of age abrogates the phytohemagglutinin response of leukocytes and the mixed leukocyte reaction.A project grant from the Medical Research Council to Dr. J.D. Horton is gratefully acknowledged. 相似文献
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