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At least 433 records · Page 24Linked to original sources
PubMed1979

[Effect of post-emergence application of two herbicides to winter wheat on the soil microflora (author's transl)].

In a field experiment the herbicides U 46 PD-Fluid (dichlorprop salt) and Tribunil (methabenzthiazuron) were applied in April 1976 post-emergence to winter wheat cultivated in 3 different soils. After 4 days, 1, 2 and 3 months samples were taken from 0-5 and 5-10 cm depth of a loamy sand soil. Dehydrogenase activity and respiration were investigated. Microbial populations were counted after 4 days only. In all 3 soils decomposition of straw in 10 cm depth was estimated using nylon gauze bags. The application of U 46 DP-Fluid stimulated bacterial and algal but reduced fungal and actinomycete populations at 0-5 cm depth. About 10% increase in the dehydrogenase activity was recorded during the whole season. Soil respiration investigated immediate after taking samples was stimulated on the 4th day after herbicide application, but reduced after 3 months. Storage of the soil samples at 5 degrees C for 10 months showed similar or opposite results depending on the incubation method used. A somewhat increased decomposition of the straw was also observed in the loamy sand until June. The application of Tribunil at the same depth stimulated populations of actinomycetes and algae but did not affect the other microflora. Reduced dehydrogenase activity was observed during the dry month of June, but the same remained unchanged at the other time of sampling. In freshly drawn soil samples, reduced soil respiration was observed after 1 and 3 months and this remained unaltered at other times. The storage at 5 degrees C of the soil samples revealed inhibition only after 1 month and at the other times a stimulation or no influence could be observed and this was found to be dependent on the incubation method. Straw decomposition was not changed following the application of Tribunil. In 5-10 cm depth, however, the above mentioned trends were only scarcely observed.

2,4-Dichlorophenoxyacetic Acid↗
PubMed1976

In vitro studies of the genetically determined unresponsiveness to thymus-independent antigens in CBA/N mice.

The X-chromosome-linked B lymphocyte defect of CBA/N mice has been studied in vitro by comparing the ability of (CBA/N X DBA/2)F1 (X-/X- X X+/Y) male (X-/Y) and female (X-/X+) spleen cells to respond to the thymus-independent antigen DNP (or TNP)-AECM-Ficoll. (CBA/N X DBA/2)F1 male spleen cells failed to generate significant in vitro anti-TNP antibody responses to DNP- or TNP-AECM-Ficoll, in contrast to spleen cells from F1 female (X-/X+) mice which responded normally to these T-independent antigens. Spleen cells from male F1 mice responded almost as well as F1 female cells to the thymus-dependent antigen, TNP-sheep red blood cells (TNP-SRBC) in vitro. Adding F1 male cells to F1 female cells failed to reduce the response of the latter to DNP-AECM-Ficoll, suggesting that the inability of F1 male cells to respond was not due to active suppression. The response of F1 male spleen cells to TNP-SRBC was not impaired by adding high concentrations of TNP-AECM-Ficoll indicating that the mechanism of unresponsiveness was not tolerance induction in all TNP-specific precursors. Lymphocytes from F1 male mice were capable of forming anti-TNP antibody after stimulation with lipopolysaccharide (LPS) in high concentrations; DNP-AECM-Ficoll had no effect on this polyclonal response. B lymphocytes from mice bearing only the X-chromosome of the CBA/N strain thus display a profound defect in B cell activation. This functional defect may represent either an inability of the defective B cells to be activated by thymus-independent antigens or the absence of a sub-class of B cells which respond to thymus-independent antigens.

Animals↗
PubMedDate not supplied

Physiologic disposition and metabolism of an anti-ulcer agent, N-(2-diisopropylaminoethyl)-N-(4,6-dimethyl-2-pyridyl)-N',N'-dimethylurea, in rats, dogs, and monkeys.

14C-N-(2-Diisopropylaminoethyl)-N-(4,6-dimethyl-2-dimethyl- 2-pyridyl)-N',N'-dimethylurea (I) was administered orally to dogs and rats and to rhesus, African green, and squirrel monkeys. Radioactivity was excreted mainly in the urine (60-76%) of all species except the rat (25%). The plasma t1/2 of I in the dog was 0.8 hr. Five urinary metabolites were identified by TLC, GLC, GS/MS, and NMR spectrometry: N,N-dimethyl-N'-(2-diisopropylaminoethyl)-N'-(4-hydroxy-methyl-6-methyl-2-pyridyl)urea (II), N,N-dimethyl-N'-(2-diisopropylaminoethyl-N'-(4-methyl-6-hydroxymethyl-2-pyridyl )urea (III), N,N-dimethyl-N'-(2-isopropylaminoethyl)-N'-(4,6-dimethyl-2-pyridyl)urea (IV), N-methyl-N'-(2-diisopropylaminoethyl)-N'-(4,6-dimethyl-2-pyridyl)urea (V), and N-(2-diisopropylaminoethyl)-N-(4,6-dimethyl-2-pyridyl)urea (VI). II was a major urinary metabolite in dog and II and IV were major metabolites in the squirrel monkey. II was present in relatively high concentrations in testes and stomach tissues of dogs, but not rats, treated with I, a finding that may be related to species differences in toxicity observed with I in these species.

Animals↗
PubMed1984

Lysine residues, but not carbohydrates, are required for the regulatory function of H on the amplification C3 convertase of complement.

Lysine epsilon-amino groups of human factor H were selectively converted to guanidino groups by treatment with 0.1 M O-methylisourea at pH 10.4. Guanidination resulted in a dose-dependent decrease in the capacity of the regulatory protein to accelerate decay dissociation of P-stabilized amplification C3 convertase sites, to serve as a co-factor for cleavage of cell-bound C3b by I, and to compete for binding of 125I-untreated H to C3b. Modification of approximately 75% lysine epsilon-amino groups suppressed 97% of H functional activity. Biochemical analysis of native H demonstrated a total carbohydrate content of 18.5% (w/w) and the presence in the molecule of 11 biantennary oligosaccharidic chains of the N-acetyl-lactosaminic type. Total desialation of H by using Clostridium perfringens neuraminidase, and total deglycosylation of desialated H by using beta-endo-N-acetylglucosaminidase resulted in a 1.5- to 2-fold increase in H activity on a weight basis. Deglycosylation did not alter the capacity of H to discriminate between activating and nonactivating surfaces of the alternative pathway. Thus, lysine residues are important determinants of the binding capacity of H for cell-bound C3b, whereas the carbohydrate portion of the molecule is not required for the regulatory function of the protein on the amplification C3 convertase.

Acetylglucosamine↗
PubMed1983

Fluometuron.

Explore the source record for details and available documents.

Animals↗
PubMed1983

Inhibition of phorbol ester-mediated interleukin-2 production by cellular differentiating agents.

Lymphocyte proliferation induced by the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) is inhibited by agents known to induce differentiation in murine erythroleukemia cells and other cell lines. In the present study, we determined the cellular targets for the action of TPA among murine thymocyte subpopulations, the phase of blastogenesis that is activated by the tumor promoter, and the phase that is inhibited by the differentiating agents. Mouse thymocytes were fractionated into populations bearing receptors for peanut agglutinin (PNA; PNA-positive cells) and populations lacking such receptors (PNA-negative cells). TPA is comitogenic for lectin-treated, unfractionated thymocytes and PNA-negative thymocytes but not for PNA-positive thymocytes. PNA-negative cells, a minor population in unfractionated thymocytes, are therefore the cellular targets for the comitogenic activity of TPA. TPA induces the production of interleukin-2 (IL-2) in lectin-treated PNA-negative populations but not in PNA-positive cells. The differentiating agents inhibit TPA-mediated proliferation of unfractionated and PNA-negative, lectin-treated thymocytes. In contrast, IL-2-mediated proliferation of lectin-treated thymocyte subpopulations is resistant to inhibition by these agents. Inhibition appears to be related to decreased production of IL-2, since the differentiating agents inhibit IL-2 production by both PNA-negative thymocytes and by a human leukemic cell line.

Animals↗
PubMed1980

The measurement of apolipoprotein A-I in human plasma by electroimmunoassay.

A variable proportion of the total apolipoprotein A-I (apo A-I) present in plasma or high density lipoproteins (HDL) is normally detectable by immunochemical methods. This has been attributed to masking of some of the immunoreactive sites of apo A-I by lipid in the intact HDL particle. This difficulty has been circumvented by heating or delipidation. We find that exposure of plasma to concentrations of urea greater than about 7.0 M in the barbital buffer used to dilute plasma samples for estimation by electroimmunoassay enables the complete detection of Apo A-I, as judged by comparison with samples delipidated with tetramethylurea. The need for time-consuming heating or delipidation is avoided.

Adult↗
PubMed1982

[On the determination of chlorpropham, metobromuron and chlorbromuron residues in drugs of the 2. AB-DDR (author's transl)].

A method for analyzing drugs of the 2. AB-DDR for residues of chlorpropham, metobromuron and chlorbromuron is proposed. It is based on the detection of aniline derivatives resulting from alkaline hydrolysis. Herbicide concentrations greater than 0.25 mg/kg drug may be detected and semiquantitatively estimated by thin-layer chromatography. Smaller amounts of herbicide residues are detected gas chromatographically (using an electron attachment detector) after bromination of the hydrolysis products. The limits of detection are: chlorpropham, 0.006 mg/kg drug; chlorbromuron, 0.008 mg/kg drug; and metobromuron, 0.04 mg/kg drug. For impregnated drugs, the recovery rates lie between 82 and 102%. The herbicide residues are released to infusions at a varying extent, depending on the kinds of drugs used.

Chlorpropham↗
PubMed1980

Dietary and other factors affecting nitrosomethylurea (NMU) formation in the rat stomach.

Nitrosomethylurea (NMU) formation was measured radioactively in the stomach contents of rats fed 3H-methylurea and sodium nitrite, mostly in semi-synthetic diets. When methylurea and sodium nitrite were added to various diets, the NMU concentration, averaged over 1-4 hours after the food was presented, was 4.6 micrograms/kg stomach contents for low-protein, 2.7 for control semi-synthetic, 2.4 for high-fat, 1.26 for bran, 1.24 for high-protein and 0.54 for the commercial diet. With the low-protein diet, the amount of NMU after 1 hour was 36.6 micrograms, corresponding to 5.3% conversion of methylurea. The decrease in yield as protein content increased was attributed to buffering action and competition for nitrite by the protein, as well as to the effects of the latter on consistency. It may also be correlated with the observation that human gastric cancer is associated with high-starch low-protein diets. Nitrite in diet was more effective in producing NMU than the same nitrite concentration in drinking water, except with sodium nitrite concentrations less than or equal to 0.5 g/kg vehicle, where the position was reversed. Sodium ascorbate added to a semi-synthetic diet at a level of 2.9 g/kg inhibited NMU production by 50%.

Animals↗
PubMed1978

Interaction of urea and substituted ureas with polyglycine and certain proteins.

Isopiestic equilibration measurements were made on ten protein-denaturant systems involving polyglycine, egg albumin, collagen, horse heart myoglobin, and the denaturants urea, 1,3-dimethylurea, 1,1-dimethylurea, and thiourea. The hydration of the proteins in the absence of denaturants is a function of the water activity and it is believed that this accounts, at least in part, for the varying hydration values found in the literature. The relative binding of water and denaturant to unfolded proteins was found to be a reversible process for which an equilibrium constant can be calculated. It was further found that in most cases the protein binds denaturant preferentially to water even in aqueous systems.

Glycine↗