Immunochemical characterization of anti-H monoclonal antibodies obtained from a mouse immunized with human saliva

Three IgM class anti-H monoclonal antibodies (1E3, 1E5 and 3H1) were obtained from a BALB/c mouse immunized with human O type saliva. These antibodies were found to agglutinate red cells from O group and A and B subgroups but not from Bombay and para-Bombay individuals whose H antigen was barely detected by anti-H reagents. The agglutination reactions of these antibodies were inhibited by H antigens from human tissues. It was also demonstrated that both 1E3 and 3H1 reacted with H disaccharide (Fuc alpha 1-->2Gal beta), H type 1 (Fuc alpha 1-->2Gal beta 1-->3GlcNAc beta), H type 2 (Fuc alpha 1-->2Gal beta 1-->4GlcNAc beta), H type 3 (Fuc alpha 1-->2Gal beta 1-->3GalNAc alpha) and H type 4 (Fuc alpha 1-->2Gal beta 1-->3GalNAc beta) but not with Lea (Gal beta 1-->3[Fuc alpha 1-->4]GlcNAc beta), Leb (Fuc alpha 1-->2Gal beta 1-->3[Fuc alpha 1-->4]GlcNAc beta), X (Gal beta 1-->4[Fuc alpha-->3]GlcNAc beta) or Y (Fuc alpha 1-->2Gal beta 1-->4[Fuc alpha 1-->3]GlcNAc beta). On the other hand, 1E5 was found to react with H type 1, H type 2, Leb and Y. Because of the unique reactivities against various fucosyl linkages these monoclonal antibodies could be useful not only as anti-H reagents but also as reagents for the structural analysis of fucosylated glycoconjugates.     

Analysis of secretion and expression of platelet-derived growth factor in cultured endothelial cells from stroke-prone spontaneously hypertensive rat

1. We characterized the endothelial cell-derived growth factors of SHRSP and Wistar Kyoto rats (WKY), respectively and found that platelet-derived growth factor (PDGF)-B chain related growth factor constituted a major portion of the mitogenic activity of the conditioned media of endothelial cells from both animals. There were no remarkable qualitative differences between the endothelial cell-derived growth factors of SHRSP and WKY. 2. Northern analysis revealed that the expression of PDGF-B chain was 2-4-fold enhanced in cultured aortic endothelial cells of SHRSP. This enhanced expression of PDGF-B chain, which may be induced under chronic hypertensive conditions, is suggested to contribute to the increase in endothelial cell-derived growth factors reported in this animal.     

Uronic acid-containing glycosaminoglycans and keratan sulfate are present in the tectorial membrane of the inner ear: functional implications

The use of growth hormone (GH) as an anabolic agent is limited by its tendency to cause hyperglycemia and by its inability to reverse nitrogen wasting in some catabolic conditions. In a previous study comparing the anabolic actions of GH and IGF-I (insulin-like growth factor I), we observed that intravenous infusions of IGF-I (12 micrograms/kg ideal body wt [IBW]/h) attenuated nitrogen wasting to a degree comparable to GH given subcutaneously at a standard dose of 0.05 mg/kg IBW per d. IGF-I, however, had a tendency to cause hypoglycemia. In the present study, we treated seven calorically restricted (20 kcal/kg IBW per d) normal volunteers with a combination of GH and IGF-I (using the same doses as in the previous study) and compared its effects on anabolism and carbohydrate metabolism to treatment with IGF-I alone. The GH/IGF-I combination caused significantly greater nitrogen retention (262 +/- 43 mmol/d, mean +/- SD) compared to IGF-I alone (108 +/- 29 mmol/d; P < 0.001). GH/IGF-I treatment resulted in substantial urinary potassium conservation (34 +/- 3 mmol/d, mean +/- SE; P < 0.001), suggesting that most protein accretion occurred in muscle and connective tissue. GH attenuated the hypoglycemia induced by IGF-I as indicated by fewer hypoglycemic episodes and higher capillary blood glucose concentrations on GH/IGF-I (4.3 +/- 1.0 mmol/liter, mean +/- SD) compared to IGF-I alone (3.8 +/- 0.8 mmol/liter; P < 0.001). IGF-I caused a marked decline in C-peptide (1,165 +/- 341 pmol/liter; mean +/- SD) compared to the GH/IGF-I combination (2,280 +/- 612 pmol/liter; P < 0.001), suggesting maintenance of normal carbohydrate metabolism with the latter regimen. GH/IGF-I produced higher serum IGF-I concentrations (1,854 +/- 708 micrograms/liter; mean +/- SD) compared to IGF-I only treatment (1,092 +/- 503 micrograms/liter; P < 0.001). This observation was associated with increased concentrations of IGF binding protein 3 and acid-labile subunit on GH/IGF-I treatment and decreased concentrations on IGF-I alone. These results suggest that the combination of GH and IGF-I treatment is substantially more anabolic than either IGF-I or GH alone. GH/IGF-I treatment also attenuates the hypoglycemia caused by IGF-I alone. GH/IGF-I treatment could have important applications in diseases associated with catabolism.     

A behavioral analysis of effective teaching.

Characterizes classroom instruction (CRI) from a behavior analytic perspective. It is argued that effective teaching strategies also serve managerial functions through the development of stimulus control and the management of behavioral choice. The stimulus control properties of CRI are discussed, and research concerning the effects of antecedent events on children's academic performance is reviewed. A theory for predicting choices in behavior, known as matching theory, is presented that evolved out of experimental operant research. The characteristics of CRI that make it particularly suited to matching theory analysis are identified, and research applying matching theory to children's classroom behavior is reviewed. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Capillary electrophoretic determination of acetic acid and trifluoroacetic acid in synthetic peptide samples

Synthetic peptide samples may contain counter-ions such as acetate or trifluoroacetate as a result of their method of preparation. Furthermore, because acetic acid (HOAc) and trifluoroacetic acid (TFA) are frequently used reagents in peptide synthesis, these acids may be found in synthetic peptide samples as impurities. This paper describes a method validation to determine HOAc and TFA in synthetic peptide samples by capillary electrophoresis (CE) using an internal standard (I.S.) with indirect UV detection. Typical analytical parameters such as precision, linearity, accuracy, specificity, limit of detection and ruggedness were evaluated during the validation. In addition, the contents of HOAc and TFA in two synthetic opioid peptide samples, TIPP[psi] and Orphanin FQ, were determined using the validated method. A unique feature of the method is that it offers determination of both acids in a single assay using a common I.S. The method is very efficient because of relatively short electrophoretic migration times (typically 2 to 8 min) for the acids investigated. This paper also discusses the factors that affect precision in a CE assay.     

Vertebral artery trauma

The developmental consequences of paternal exposure to acrylamide (50 mg/kg i.p. for 5 days) were assessed in preimplantation embryos. There was a significant increase in the proportion of morphologically abnormal embryos after postmeiotic treatment during spermatogenesis (88.7% vs. 14.8% in control). Abnormal embryos had an average of 1.8 +/- 3.5 cells and > 80% had at least one fragmented nucleus. In addition, morphologically normal embryos were significantly delayed (34.3 +/- 12.8 cells per embryo vs. 57.6 +/- 15.7 in control, P < 0.001). Acrylamide caused 10- and 20-fold increases in frequencies of cells with micronuclei (MN) in morphologically normal and abnormal embryos, respectively (41 and 93 MN per 1,000 cells). Both centromere-negative (MN-) and centromere-positive (MN+) were induced. Nuclei of abnormal embryos were significantly larger (900 microm2 vs. 250 microm2) than controls. In addition, MN of abnormal embryos were larger than those of normal embryos (21.2 microm2 vs. 6.5 microm2, P < 0.01). Among control embryos, MN+ were significantly larger than MN- (P < 0.05). These findings suggest that the preimplantation embryo is a sensitive indicator of paternally transmitted effects on early development. Multiple mechanisms appear to be involved, including cytogenetic damage, proliferation arrest/delay, and fertilization failure. Future studies are needed to establish how induced cytological defects in preimplantation embryos contribute to birth defects and other postimplantation abnormalities.