Solubility of Tricalcium Citrate in Solutions of Variable Ionic Strength and in Milk Ultrafiltrates

Summary Solubility of tricalcium citrate has been determined at 21 and 95° C. by dissolution in water and by precipitation from supersaturated solutions containing various proportions of calcium to citrate and at pH 4.4 to 8.8. Solubility product in solutions at equilibrium varied with ionic strength, according to the relation pks = 17.63 − 10.84 μ , but was unaffected by variations in pH and temperature and by the presence of magnesium or phosphate ions. Milk ultrafiltrates were shown to be saturated with tricalcium citrate, i.e., the calculated pk s values agreed with the solubility product in all but two of the 15 samples tested, and composition of two ultrafiltrates was unaffected by agitation with crystals of tricalcium citrate

Geometric modeling with rational B-spline surfaces

Issued as Final report, Project no. E-25-67

Direct Analysis of Lactose in Milk and Serum

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Analysis for Citric Acid in Presence of Casein

Summary Factors affecting citric acid determination in the presence of casein were studied with the pyridine-acetic anhydride method. Although the opalescence in skimmilk tests affected results by only 2%, the turbidity introduced by solutions of isolated casein could cause gross overestimation. A pH above 12.3 in the test aliquot assured a clear reaction mixture with both skimmilk and casein solutions. It is, therefore, recommended that test aliquots containing casein should comprise sufficient alkali to insure a clear reaction. Acid casein required seven resuspensions in fresh washing solution at pH 4.5 for complete removal of occluded citrate, lactose, and calcium. Adsorption of citric acid by casein precipitated at the iso-electric point, or with trichloroacetic acid, was demonstrated and appears to account for the lower citrate concentration in acid sera, as compared to skimmilk. These results extend the conclusions of a previous paper

Direct determination of citric acid in milk with an improved pyridine-acetic anhydride method.

Summary The determination of citric acid with pyridine and acetic anhydride has been investigated at reaction temperatures from 17 to 60° C. The optimum proportions of pyridine, acetic anhydride, water, and acetic acid for maximum color intensity and stability are given for each temperature. The procedure has been modified to eliminate the violent nature of the reaction, even when the analysis is done at a reaction temperature of 60° C. Details of a method for the determination of 25–200 μ g. of citric acid, at a reaction temperature of 32° C., are presented. In comparison with previously published methods based on the reaction, the recommended technique results in improved sensitivity, stability, and reproducibility without requiring careful timing. The method has been successfully applied to the routine analysis of milk and milk products. Milk and serum can be analyzed directly, after suitable dilution. Corrections for the interference caused by fat in homogenized milk, and by trichloroacetic acid in T.C.A. serum, can be made easily. Results of direct analysis of milk were from 5 to 15% higher than those for the corresponding sera and are believed to represent the true values for the citric acid content of milk

Roles of Fgf4 and Fgf8 in limb bud initiation and outgrowth.

Journal ArticleAlthough numerous molecules required for limb bud formation have recently been identified, the molecular pathways that initiate this process and ensure that limb formation occurs at specific axial positions have yet to be fully elucidated. Based on experiments in the chick, Fgf8 expression in the intermediate mesoderm (IM) has been proposed to play a critical role in the initiation of limb bud outgrowth via restriction of Fgf10 expression to the appropriate region of the lateral plate mesoderm. Contrary to the outcome predicted by this model, ablation of Fgf8 expression in the intermediate mesoderm before limb bud initiation had no effect on initial limb bud outgrowth or on the formation of normal limbs. When their expression patterns were first elucidated, both Fgf4 and Fgf8 were proposed to mediate critical functions of the apical ectodermal ridge (AER), which is required for proper limb bud outgrowth. Although mice lacking Fgf4 in the AER have normal limbs, limb development is severely affected in Fgf8 mutants and certain skeletal elements are not produced. By creating mice lacking both Fgf4 and Fgf8 function in the forelimb AER, we show that limb bud mesenchyme fails to survive in the absence of both FGF family members. Thus, Fgf4 is responsible for the partial compensation of distal limb development in the absence of Fgf8. A prolonged period of increased apoptosis, beginning at 10 days of gestation in a proximal-dorsal region of the limb bud, leads to the elimination of enough mesenchymal cells to preclude formation of distal limb structures. Expression of Shh and Fgf10 is nearly abolished in double mutant limb buds. By using a CRE driver expressed in both forelimb and hindlimb ectoderm to inactivate Fgf4 and Fgf8, we have produced mice lacking all limbs, allowing a direct comparison of FGF requirements in the two locations

Structural Modeling of the Next Generation Space Telescope's Primary Mirror

In recent years, astronomical observations made with space telescopes have dramatically increased our understanding of the history of the universe. In particular, the cosmic Background Explorer (COBE) and the Hubble Space Telescope (HST) have yielded observations that cannot be achieved at ground-based observatories. We now have views of the universe before galaxies existed (from COBE) and views of young galaxies (from HST). But none of the existing observatories can provide views of the period in which the galaxies were born, about 100 million to one billion years after the "big bang". NASA expects the Next Generation Space Telescope (NGST) to fill this gap. An investigation into the structural modeling of the primary mirror of the NGST, its methodology and results are presented

Incomplete Release of Citrate During Acid Precipitation of Casein

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Duplication of the Hoxd11 gene causes alterations in the axial and appendicular skeleton of the mouse.

Journal ArticleThe Hox genes encode a group of transcription factors essential for proper development of the mouse. Targeted mutation of the Hoxd11 gene causes reduced male fertility, vertebral transformation, carpal bone fusions, and reductions in digit length. A duplication of the Hoxd11 gene was created with the expectation that the consequences of restricted overexpression in the appropriate cells would provide further insight into the function of the Hoxd11 gene product. Genetic assays demonstrated that two tandem copies of Hoxd11 were functionally indistinguishable from the normal two copies of the gene on separate chromosomes with respect to formation of the axial and appendicular skeleton. Extra copies of Hoxd11 caused an increase in the lengths of some bones of the forelimb autopod and a decrease in the number of lumbar vertebrae. Further, analysis of the Hoxd11 duplication demonstrated that the Hoxd11 protein can perform some functions supplied by its paralogue Hoxa11. For example, the defects in forelimb bones are corrected when extra copies of Hoxd11 are present in the Hoxa11 homozygous mutant background. Thus, it appears that Hoxd11 can quantitatively compensate for the absence of Hoxa11 protein, and therefore Hoxa11 and Hoxd11 are functionally equivalent in the zeugopod. However, extra copies of Hoxd11 did not improve male or female fertility in Hoxa11 mutants. Interestingly, the insertion of an additional Hoxd11 locus into the HoxD complex does not appear to affect the expression patterns of the neighboring Hoxd10, -d12, or -d13 genes

Decoding an olfactory mechanism of kin recognition and inbreeding avoidance in a primate

<p>Abstract</p> <p>Background</p> <p>Like other vertebrates, primates recognize their relatives, primarily to minimize inbreeding, but also to facilitate nepotism. Although associative, social learning is typically credited for discrimination of familiar kin, discrimination of unfamiliar kin remains unexplained. As sex-biased dispersal in long-lived species cannot consistently prevent encounters between unfamiliar kin, inbreeding remains a threat and mechanisms to avoid it beg explanation. Using a molecular approach that combined analyses of biochemical and microsatellite markers in 17 female and 19 male ring-tailed lemurs (<it>Lemur catta</it>), we describe odor-gene covariance to establish the feasibility of olfactory-mediated kin recognition.</p> <p>Results</p> <p>Despite derivation from different genital glands, labial and scrotal secretions shared about 170 of their respective 338 and 203 semiochemicals. In addition, these semiochemicals encoded information about genetic relatedness within and between the sexes. Although the sexes showed opposite seasonal patterns in signal complexity, the odor profiles of related individuals (whether same-sex or mixed-sex dyads) converged most strongly in the competitive breeding season. Thus, a strong, mutual olfactory signal of genetic relatedness appeared specifically when such information would be crucial for preventing inbreeding. That weaker signals of genetic relatedness might exist year round could provide a mechanism to explain nepotism between unfamiliar kin.</p> <p>Conclusion</p> <p>We suggest that signal convergence between the sexes may reflect strong selective pressures on kin recognition, whereas signal convergence within the sexes may arise as its by-product or function independently to prevent competition between unfamiliar relatives. The link between an individual's genome and its olfactory signals could be mediated by biosynthetic pathways producing polymorphic semiochemicals or by carrier proteins modifying the individual bouquet of olfactory cues. In conclusion, we unveil a possible olfactory mechanism of kin recognition that has specific relevance to understanding inbreeding avoidance and nepotistic behavior observed in free-ranging primates, and broader relevance to understanding the mechanisms of vertebrate olfactory communication.</p