Educationally deficient adults : their education and training needs /

Reprint of the 1964 ed. published by McGraw-Hill. N. Y.

Feasibility of developing training programs designed to improve deficient driver factors. Volume I: a review of existing data bases and recommendations for future data collection. Final report.

National Highway Traffic Safety Administration, Washington, D.C.

Feasibility of developing training programs designed to improve deficient driver factors. Volume II: identifying accident avoidance behaviors: a guide for accident investigators. Final report.

National Highway Traffic Safety Administration, Washington, D.C.

Deficient generalized Fibonacci maximum path graphs /

"UILU-ENG 78 1739."

A Grammar of the Greek language : originally composed for the College-school at Gloucester, in which it has been the editor's design to reject what, in the most improved editions of Camden, is redundant, to supply what is deficient, to reduce to order what is intricate and confused, and to consign to an appendix what is not requisite to be got by heart /

Mode of access: Internet.

Technology of cellulose ethers; a theoretical and practical treatise on the origin, history, chemistry, manufacture, technical application and analysis of the etherified celluloses and carbohydrate carboxylate ehters (esterified cellulose ethers, etherified organic cellulose esters) ...

Paged continuously.

Lipid and carbohydrate based adjuvant/carriers in immunology

This review discusses various issues regarding vaccines:what are they and how they work, safety aspects, the role of adjuvants and carriers in vaccination, synthetic peptides as immunogens, and new technologies for vaccine development and delivery including the identification of novel adjuvants for mucosal vaccine delivery. There has been a recent increase of interest, in the use of lipids and carbohydrates as adjuvants, and so a particular emphasis is placed on adjuvants derived from lipids or carbohydrates, or from both. Copyright (C) 2003 European Peptide Society and John Wiley Sons, Ltd.

Functional analysis of neurotransmission at β2-laminin deficient terminals

beta2-Laminin is important for the formation of neuromuscular junctions in vertebrates. Previously, we have inactivated the gene that encodes for beta2-laminin in mice and observed predominantly prejunctional structural defects. In this study, we have used both intra- and extracellular recording methods to investigate evoked neurotransmission in beta2-laminin-deficient mice, from postnatal day 8 (P8) through to day 18(P18). Our results confirmed that there was a decrease in the frequency of spontaneous release, but no change in the postjunctional response to such release. Analysis of evoked neurotransmission showed an increase in the frequency of stimuli that failed to elicit an evoked postjunctional response in the mutants compared to litter mate controls, resulting in a 50% reduction in mean quantal content at mutant terminals. Compared to littermate controls, beta2-laminin-deficient terminals showed greater synaptic depression when subjected to high frequency stimulation. Furthermore, the paired pulse ratio of the first two stimuli was significantly lower in beta2-laminin mutant terminals. Statistical analysis of the binomial parameters of release showed that the decrease in quantal content was due to a decrease in the number of release sites without any significant change in the average probability of release. This suggestion was supported by the observation of fewer synaptic vesicle protein 2 (SV2)-positive varicosities in beta2-laminin-deficient terminals and by ultrastructural observations showing smaller terminal profiles and increased Schwann cell invasion in beta2-laminin mutants; the differences between beta2-laminin mutants and wild-type mice were the same at both P8 and P18. From these results we conclude that beta2-laminin plays a role in the early structural development of the neuromuscular junction. We also suggest that transmitter release activity may act as a deterrent to Schwarm cell invasion in the absence of beta2-laminin.

Effects of phytase supplementation of phosphorus-adequate, lysine-deficient, wheat-based diets on growth performance of weaner pigs

The effects of microbial phytase supplementation of phosphorus-adequate, wheat-based diets with available lysine : energy density ratios ranging from 0.75 to 0.90 g available lysine/MJ DE on growth performance of weaner pigs were investigated in 3 studies. In the first study, increasing levels of dietary phytate depressed growth rates (P<0.08) and efficiency of feed conversion (P<0.01) and phytase supplementation enhanced growth rates (P<0.05) and tended to improve feed efficiency (P<0.15). There were no significant interactions between dietary phytate and phytase inclusion to support the hypothesis that dietary substrate levels of phytate govern responses to phytase. However, in this and other studies, percentage increases in efficiency of feed conversion generated by phytase were positively correlated to dietary phytate concentrations to a significant extent (P<0.005), so it is possible that dietary substrate levels are of importance to the magnitude of responses following phytase supplementation. Diets with 3 levels of protein, expressed as 0.80, 0.85, and 0.90 g available lysine/MJ DE, were offered to pigs without and with phytase in the second study. Protein/amino acid levels or lysine : energy density ratios did not influence growth performance, which was not expected. However, phytase tended to increase growth rates (P<0.08) and improved feed efficiency (P<0.01). Although it is believed that phytase may have a positive influence on protein utilisation, this was not demonstrated in this experiment. In the third study, the simultaneous inclusion of phytase and xylanase feed enzymes in wheat-based weaner diets did not increase growth performance responses in comparison with phytase alone. Individually, phytase improved feed efficiency (P<0.05) and numerically increased growth rates (P<0.25). Although responses in growth performance of weaner pigs following phytase supplementation lacked consistency, they were generally positive and indicative of anti-nutritive properties of phytate that are unrelated to P availability. That these positive responses were observed in diets with suboptimal available lysine : energy density ratios is consistent with the possibility that phytate has a negative influence on protein utilisation, which is ameliorated by phytase. However, these antinutritive effects and their underlying mechanisms need to be better defined if full advantage of the potential protein-sparing effects of microbial phytase is to be taken.

Effect of carbohydrate supplementation on walking performance in peripheral arterial disease: A preliminary physiologic study

Objective: In this preliminary study we tested the effect of short-term carbohydrate supplementation on carbohydrate oxidation and walking performance in peripheral arterial disease. Methods: Eleven patients with peripheral arterial disease and intermittent claudication and 8 healthy control subjects completed several weeks of baseline exercise testing, then were given supplementation for 3 days with a carbohydrate solution and placebo. Maximal walking time was assessed with a graded treadmill test. Carbohydrate oxidation during a submaximal phase of this test was measured with indirect calorimetry. At the end of baseline testing a biopsy specimen was taken from the gastrocnemius muscle, and the active fraction of pyruvate dehydrogenase complex activity was determined. Results: Carbohydrate supplementation resulted in a significant increase in body weight and carbohydrate oxidation during exercise in patients with intermittent claudication and control subjects. Maximal walking time decreased by 3% in control subjects, whereas it increased by 6% in patients with intermittent claudication (group X treatment interaction, P < .05). There was a wide range of performance responses to carbohydrate supplementation among patients with claudication (-3%-37%). This effect was greater in poorer performers, and was negatively correlated (P < .05) with muscle pyruvate dehydrogenase complex activity. Conclusion: Preliminary data suggest that carbohydrate oxidation during exercise might contribute to exercise intolerance in more dysfunctional patients with intermittent claudication and that carbohydrate supplementation might be an effective therapeutic intervention in these patients.

Distinct cis-elements in the Asparagus officinalis asparagine synthetase promoter respond to carbohydrate and senescence signals

The Asparagus officinalis L. asparagine (Asn) synthetase (AS) promoter was analysed for elements responding to carbohydrate and senescence signals. Transgenic Arabidopsis thaliana L. plants containing deletion constructs of the –1958 bp AS promoter linked to the β-glucuronidase (GUS) reporter gene (AS::GUS) were analysed by measuring GUS specific activity. Inclusion of sucrose (Suc), glucose (Glc) or fructose (Fru) in plant media repressed levels of GUS activity in –1958AS::GUS plants, regardless of the light environment, with increases in GUS found 1 d after incubation on Suc-lacking media. Hexokinase is likely to be involved in the signal pathway, as Suc, Glc, Fru, 2-deoxy-d-glucose and mannose were more effective repressors than 3-O-methylglucose, and the hexokinase inhibitor mannoheptulose reduced repression. Plants containing AS::GUS constructs with deletions that reduced the promoter to less than –405 bp did not show low sugar induction. AS::GUS activity was significantly higher in excised leaves induced to senesce by dark storage for 24 h, compared to fresh leaves, for lines containing at least –640 bp of the AS promoter but not those with –523 bp or smaller promoter fragments. Fusion of the –640 to –523 bp region to a –381AS::GUS construct generated a promoter that retained senescence induction but lacked low sugar induction. Alignment of this region to the 33-bp senescence-related sequence of the Arabidopsis and Brassica napus L. SAG12 promoters identified the sequence TTGCACG as being conserved in all the promoters, and which may be an important senescence-responsive element.

Abolition of valproate-derived choleresis in the Mrp2 transporter-deficient rat

Valproic acid (VPA) is a major therapeutic agent in the treatment of epilepsy and other neurological disorders. It is metabolized in humans and rats primarily along two pathways: direct glucuronidation to yield the acyl glucuronide (VPA-G) and beta-oxidation. We have shown much earlier in the Sprague-Dawley rat that i.v. administration of sodium valproate (NaVPA) caused a marked choleresis ( mean of 3.3 times basal bile flow after doses of 150 mg/kg), ascribed to the passive osmotic flow of bile water following excretion of VPA-G across the canalicular membrane. Active biliary pumping of anionic drug conjugates across the canalicular membrane is now believed to be attributable to transporter proteins, in particular Mrp2, which is deficient in the TR- ( a mutant Wistar) rat. In the present study, normal Wistar and Mrp2-deficient TR- rats were dosed i.v. with NaVPA at 150 mg/kg. In the Wistar rats, there was a peak choleretic effect of about 3.2 times basal bile flow, occurring at about 30 to 45 min postdose ( as seen previously with Sprague-Dawley rats). In TR- rats given the same i.v. dose, there was no evidence of postdose choleresis. The choleresis was correlated with the excretion of VPA-G into bile. In Wistar rats, 62.8 +/- 7.7% of the NaVPA dose was excreted in bile as VPA-G, whereas in TR- rats, only 2.0 +/- 0.6% of the same dose was excreted as VPA-G in bile ( with partial compensatory excretion of VPA-G in urine). This study underlines the functional ( bile flow) consequences of biliary transport of xenobiotic conjugated metabolites.

GLUT4 overexpression or deficiency in adipocytes of transgenic mice alters the composition of GLUT4 vesicles and the subcellular localization of GLUT4 and insulin-responsive aminopeptidase

The majority of GLUT4 is sequestered in unique intracellular vesicles in the absence of insulin. Upon insulin stimulation GLUT4 vesicles translocate to, and fuse with, the plasma membrane. To determine the effect of GLUT4 content on the distribution and subcellular trafficking of GLUT4 and other vesicle proteins, adipocytes of adipose-specific, GLUT4-deficient (aP2-GLUT4-/-) mice and adipose-specific, GLUT4-overexpressing (aP2GLUT4- Tg) mice were studied. GLUT4 amount was reduced by 80 - 95% in aP2-GLUT4-/- adipocytes and increased similar to10-fold in aP2-GLUT4-Tg adipocytes compared with controls. Insulin-responsive aminopeptidase ( IRAP) protein amount was decreased 35% in aP2-GLUT4-/- adipocytes and increased 45% in aP2-GLUT4-Tg adipocytes. VAMP2 protein was also decreased by 60% in aP2-GLUT4-/- adipocytes and increased 2-fold in aP2GLUT4- Tg adipocytes. IRAP and VAMP2 mRNA levels were unaffected in aP2-GLUT4-Tg, suggesting that overexpression of GLUT4 affects IRAP and VAMP2 protein stability. The amount and subcellular distribution of syntaxin4, SNAP23, Munc-18c, and GLUT1 were unchanged in either aP2-GLUT4-/- or aP2-GLUT4-Tg adipocytes, but transferrin receptor was partially redistributed to the plasma membrane in aP2-GLUT4-Tg adipocytes. Immunogold electron microscopy revealed that overexpression of GLUT4 in adipocytes increased the number of GLUT4 molecules per vesicle nearly 2-fold and the number of GLUT4 and IRAP-containing vesicles per cell 3-fold. In addition, the proportion of cellular GLUT4 and IRAP at the plasma membrane in unstimulated aP2-GLUT4-Tg adipocytes was increased 4- and 2-fold, respectively, suggesting that sequestration of GLUT4 and IRAP is saturable. Our results show that GLUT4 overexpression or deficiency affects the amount of other GLUT4-vesicle proteins including IRAP and VAMP2 and that GLUT4 sequestration is saturable.

Dietary carbohydrate source affects glucose concentrations, insulin secretion, and food intake in overweight cats

This study was undertaken to assess the impact of dietary carbohydrate source on food intake, body composition, glucose tolerance, insulin sensitivity, and glucose and insulin concentrations in overweight and obese cats with reduced insulin sensitivity. Sixteen overweight and obese cats were divided into two groups and randomly allocated one of two extruded diets formulated to contain similar starch content (33%) from different cereal sources (sorghum and corn versus rice). Meal response, glucose tolerance and insulin sensitivity tests were performed before and after a 6-week weight-maintenance phase and after an additional 8-week free-access feeding phase. Dual energy x-ray absorptiometry (DEXA)-derived body composition was determined in each cat before the study and after each test phase. Food intake was measured daily and body weight measured twice weekly for the duration of the study. When compared with the sorghum/corn-based diet, cats fed the rice-based diet consumed more energy and gained more weight in response to free-access feeding. Cats fed the rice-based diet also tended to have higher glucose concentrations and insulin secretion in response to a glucose load or a test meal. We conclude that a sorghum and corn blend is a superior carbohydrate source than rice for overweight cats with glucose intolerance and reduced insulin sensitivity. Such a diet may help to minimize overeating and additional weight gain, and may also reduce the risk of developing type 2 diabetes mellitus. (C) 2004 Elsevier Inc. All rights reserved.

Axonal regeneration and lack of astrocytic gliosis in EphA4-deficient mice

Spinal cord injury usually results in permanent paralysis because of lack of regrowth of damaged neurons. Here we demonstrate that adult mice lacking EphA4 (-/-), a molecule essential for correct guidance of spinal cord axons during development, exhibit axonal regeneration and functional recovery after spinal cord hemisection. Anterograde and retrograde tracing showed that axons from multiple pathways, including corticospinal and rubrospinal tracts, crossed the lesion site. EphA4 -/- mice recovered stride length, the ability to walk on and climb a grid, and the ability to grasp with the affected hindpaw within 1-3 months of injury. EphA4 expression was upregulated on astrocytes at the lesion site in wild-type mice, whereas astrocytic gliosis and the glial scar were greatly reduced in lesioned EphA4-/- spinal cords. EphA4 -/- astrocytes failed to respond to the inflammatory cytokines, interferon-gamma or leukemia inhibitory factor, in vitro. Neurons grown on wild-type astrocytes extended shorter neurites than on EphA4 -/- astrocytes, but longer neurites when the astrocyte EphA4 was blocked by monomeric EphrinA5-Fc. Thus, EphA4 regulates two important features of spinal cord injury, axonal inhibition, and astrocytic gliosis.