Effect of varying prepartum dietary cation-anion difference and calcium concentration on postpartum mineral and metabolite status and milk production of multiparous cows.

Eighty-two multiparous Holstein cows were enrolled 28 d before expected calving and assigned to 1 of 4 dietary treatments in a randomized block design experiment with a 2 × 2 factorial arrangement of treatments to determine the effect of feeding a neutral or acidogenic diet varying in Ca concentration on prepartum and postpartum intake, blood mineral and metabolite concentrations, and postpartum milk production. Prepartum diets were formulated to provide a dietary cation-anion difference (DCAD) of -21 (negative, NEG) or -2 (neutral, NEU) mEq/100 g of dry matter with either 1.3% or 1.8% Ca. After calving, cows remained on trial through 63 d in milk (DIM) and were fed a common lactation diet. Urine pH was lower for NEG compared with NEU and tended to be lower for 1.8% Ca compared with 1.3% Ca. Fractional excretion of Ca and Mg in urine was greater for NEG than for NEU. Prepartum plasma bicarbonate was lower and P was higher for NEG compared with NEU. Prepartum plasma P and blood urea nitrogen to creatinine ratio was higher for 1.3% compared with 1.8% Ca. Postpartum, concentrations of plasma total protein, albumin, blood urea nitrogen, Mg, and ionized Mg (iMg) were higher and Na was lower for NEU compared with NEG. An interaction of DCAD and Ca was observed for plasma creatinine, which was highest for cows fed NEU and 1.3% Ca compared with all other treatments. Interactions of DCAD and DIM were observed for plasma bicarbonate and iMg. Bicarbonate was higher at 3 DIM and lower at 14 DIM for NEU compared with NEG. Concentrations of iMg were higher at 1, 2, and 14 DIM for NEU compared with NEG. Interactions of Ca and DIM were observed for plasma Ca, Cl, and anion gap. Compared with cows fed 1.5% Ca, those fed 1.3% Ca had lower Ca and anion gap and higher Cl at 1 DIM and lower Cl and higher anion gap at 14 DIM. No differences were observed in body weight or body condition score due to DCAD or Ca. Prepartum dry matter intake (DMI) was lower for NEG compared with NEU and lower for 1.8% compared with 1.3% Ca. Postpartum DMI was not different among treatments. An interaction was observed for DCAD and DIM due to higher milk yield after 45 DIM for NEG compared with NEU. No differences were observed in milk component percentage or yield among treatments. There was an interaction of DIM and Ca for milk urea concentrations, which were higher at 5 wk and lower at 6 wk for 1.3% Ca compared with 1.8% Ca. These results suggest that feeding NEG prepartum alters plasma and urine mineral concentrations compared with feeding NEU and supports increased milk yield after 45 DIM. Feeding 1.8% Ca prepartum only improved plasma Ca at 1 DIM. Feeding either NEG or 1.8% Ca reduced DMI prepartum compared with NEU or 1.3% Ca.

Short communication: Blood mineral and gas concentrations of calves born to cows fed prepartum diets differing in dietary cation-anion difference and calcium concentration.

Eighty-two multiparous Holstein cows were fed diets differing in dietary cation-anion difference (DCAD) and Ca concentrations in a randomized block design experiment beginning 4 wk before anticipated calving to determine the effects on colostrum yield and quality and acid-base balance and mineral status of newborn calves. Treatments were arranged as a 2 × 2 factorial to provide 2 DCAD [-22 mEq/100 g of dry matter (NEG) or -3 mEq/100 g of dry matter (NEU)] and 2 supplemental Ca concentrations (1.3 or 1.8% of dry matter). After calving, cows were milked within 2 to 8 h and colostrum yield was recorded. Calves were fed 200 g of IgG of a commercial colostrum replacer within 4 h of birth. No differences were observed in birth weight or dystocia score among treatments, which averaged 42.7 kg and 1.12, respectively. Colostrum yield was not different among treatments and averaged 8.75 kg. Colostrum quality, as measured using a Brix refractometer, was not affected by DCAD but was higher for 1.3% compared with 1.8% Ca: 21.58% and 19.87%, respectively. Colostrum IgG concentrations were higher for NEG compared with NEU and for 1.3% compared with 1.8% Ca. No differences were observed in concentrations of serum IgG, Ca, P, K, Cl, anion gap, or whole-blood pH, partial pressure of O2, or SO2 of calves among treatments. Serum Mg and lactate concentrations were higher and CO2 tended to be lower for calves born to cows fed 1.3% compared with 1.8% Ca. Interactions of DCAD and Ca were observed for serum Na and Cl, which were higher for NEU-1.3% Ca and NEG-1.8% Ca compared with NEU-1.8% Ca and NEG-1.3% Ca. Whole-blood partial pressure of CO2, and HCO3 exhibited an interaction of DCAD and Ca and tended to be lower for NEU-1.3% Ca and NEG-1.8% Ca compared with NEU-1.8% Ca and NEG-1.3% Ca. Results of this trial indicate that feeding prepartum diets with 1.8% compared with 1.3% supplemental Ca reduced colostrum quality and serum concentrations of Mg and lactate in calves immediately after birth. Feeding NEG supported higher colostrum IgG concentrations. Blood mineral concentrations and blood gas balance tended to differ, but the effects were not consistent across DCAD and Ca.

Discrimination in resolving systems. VI. Comparison of the diastereomers of deoxyephedrinium and ephedrinium 4'-fluoromandelates.

(-)-(R)-Deoxyephedrine forms poorly discriminating diastereomeric salts with 4'-fluoromandelic acid from 95% ethanol. Both less-soluble (L) (S)-4'-fluoromandelate and more-soluble (M) (R)-4'-fluoromandelate phases are monoclinic and unsolvated. Their solubility ratio (M/L) in 95% ethanol is only 1.2, which correlates with the similarity and small differences in their respective heats of fusion and fusion temperatures. The (R)-deoxyephedrinium and the related (1R;2S)-ephedrinium 4'-fluoromandelate systems show L-salts with higher ion-pair volumes and lower densities than their M-salts. (R)-Deoxyephedrinium salts have higher volumes than the comparable (1R;2S)-ephedrinium salts even though the resolving base (R)-deoxyephedrine lacks the benzylic hydroxy. In the solids, bilayered structures segregate polar and nonpolar molecular regions. The principle interionic interactions are hydrogen bonds between protonated secondary ammonium ions and carboxylates forming infinite chains with a six-atom repeating unit H-N(+)-H...O-C(-)-O [C(2)(2)(6)]. These are buttressed by mandelate hydroxy to carboxylate hydrogen bonds. Differing interactions between phenyl and 4'-fluorophenyl rings in the nonpolar layers of the salts correlate with the density and stability inversion.

The use of near-infrared reflectance spectroscopy to predict the moisture, nitrogen, calcium, total phosphorus, gross energy, and phytate phosphorus contents of broiler excreta.

One hundred forty-three broiler chick excreta samples were obtained from previous experiments dealing with phytate phosphorus utilization. The air-dried samples were ground in a Cyclotech 1093 sample mill and analyzed for the following: moisture, N, Ca, energy, total P, and phytate P. By chemical assay, the sample compositions were moisture: mean = 9.62, SD = 1.27% (range = 7.37-13.59); N: mean = 5.31, SD = 0.37% (range = 4.28 to 6.48); Ca: mean = 1.66, SD = 0.32% (range = 0.85 to 2.6); total P: mean = 1.13, SD = 0.28% (range = 0.66 to 1.75); gross energy: mean = 3,560, SD = 120 kcal/kg (range = 3,309 to 3,882); phytate P: mean = 0.63, SD = 0.17% (range = 0.32 to 0.97). The samples were scanned in a Feed & Forage Analyzer Model 5000 with near-infrared reflectance spectroscopy (NIRS)-2 Software. One hundred twenty-three samples were used to create the calibration curves (20 randomly selected samples were set aside for validating the calibration). The combination of math treatments and scatter corrections that provided the best standard error of cross validation (and its correlation coefficient) was chosen for the standard curves. The coefficients of determination (R2) were moisture, 0.96; N, 0.88; Ca, 0.84; total P, 0.91; gross energy, 0.86; and phytate P, 0.86. The standard errors of prediction were moisture, 0.342%; N, 0.193%; Ca, 0.143%; total P, 0.134%; gross energy, 74.66 kcal; and phytate P, 0.91%. We concluded that it is possible to predict the moisture, N, Ca, gross energy, total P, and phytate P in broiler excreta by using NIRS.

Mutations in the gene encoding tight junction claudin-14 cause autosomal recessive deafness DFNB29.

Tight junctions in the cochlear duct are thought to compartmentalize endolymph and provide structural support for the auditory neuroepithelium. The claudin family of genes is known to express protein components of tight junctions in other tissues. The essential function of one of these claudins in the inner ear was established by identifying mutations in CLDN14 that cause nonsyndromic recessive deafness DFNB29 in two large consanguineous Pakistani families. In situ hybridization and immunofluorescence studies demonstrated mouse claudin-14 expression in the sensory epithelium of the organ of Corti.

Dominant modifier DFNM1 suppresses recessive deafness DFNB26.

More than 50% of severe childhood deafness is genetically determined, approximately 70% of which occurs without other abnormalities and is thus termed nonsyndromic. So far, 30 nonsyndromic recessive deafness loci have been mapped and the defective genes at 6 loci, DFNB1, DFNB2, DFNB3, DFNB4, DFNB9 and DNFB21, have been identified, encoding connexin-26 (ref. 3), myosin VIIA (ref. 4), myosin XV (ref. 5), pendrin, otoferlin and alpha-tectorin, respectively. Here we map a new recessive nonsyndromic deafness locus, DFNB26, to a 1.5-cM interval of chromosome 4q31 in a consanguineous Pakistani family. A maximum lod score of 8.10 at theta=0 was obtained with D4S1610 when only the 8 affected individuals in this family were included in the calculation. There are seven unaffected family members who are also homozygous for the DFNB26-linked haplotype and thus are non-penetrant. A dominant modifier, DFNM1, that suppresses deafness in the 7 nonpenetrant individuals was mapped to a 5.6-cM region on chromosome 1q24 with a lod score of 4.31 at theta=0 for D1S2815.

OTOF encodes multiple long and short isoforms: genetic evidence that the long ones underlie recessive deafness DFNB9.

We have recently reported that OTOF underlies an autosomal recessive form of prelingual sensorineural deafness, DFNB9. The isolated 5-kb cDNA predicted a 1,230 amino acid (aa) C-terminus membrane-anchored cytosolic protein with three C2 domains. This protein belongs to a family of mammalian proteins sharing homology with the Caenorhabditis elegans fer-1. The two other known members of this family, dysferlin and myoferlin, both have six predicted C2 domains. By northern blot analysis, a 7-kb otoferlin mRNA could be detected in the human brain. We isolated the corresponding cDNA, which is expected to encode a 1,977-aa-long form of otoferlin with six C2 domains. A 7-kb cDNA derived from the murine orthologous gene, Otof, was also identified in the inner ear and the brain. The determination of the exon-intron structure of the human and murine genes showed that they are composed of 48 coding exons and extend approximately 90 kb and approximately 80 kb, respectively. Alternatively spliced transcripts could be detected that predict several long isoforms (six C2 domains) in humans and mice and short isoforms (three C2 domains) only in humans. Primers were designed to explore the first 19 OTOF exons, henceforth permitting exploration of the complete coding sequence of the gene in DFNB9 patients. In a southwestern Indian family affected by DFNB9, a mutation in the acceptor splice site of intron 8 was detected, which demonstrates that the long otoferlin isoforms are required for inner ear function.

A gene for recessive nonsyndromic sensorineural deafness (DFNB18) maps to the chromosomal region 11p14-p15.1 containing the Usher syndrome type 1C gene.

Autosomal recessive nonsyndromic sensorineural deafness segregating in a large consanguineous Indian family was mapped to chromosome 11p14-p15.1 defining a new locus, DFNB18. A maximum lod score of 4.4 at theta = 0 was obtained for the polymorphic micro-satellite marker D11S1888. Haplotype analysis localizes this gene between markers D11S1307 and D11S2368, which is approximately 1.6 cM and encompasses the region of Usher syndrome type 1C (USH1C). We postulate that DFNB18 and USH1C are allelic variants of the same gene.

A PAX3 polymorphism (T315K) in a family exhibiting Waardenburg Syndrome type 2.

Waardenburg Syndrome (WS) is an autosomal-dominant disorder phenotypically characterized by sensorineural hearing loss and pigmentary disturbances. Presence of dystopia canthorum is indicative of WS type 1 and results from defects in the PAX3 gene, whereas normally located medial canthi is characteristic of type 2 WS (WS2) and is associated with defects in the microphthalmia-associated transcription factor (MIFT) gene. Here a neutral polymorphism is reported in the PAX3 gene (T315K) in a family with WS2.

Diffusion and nucleation of gas in gel and some implications for the development of decompression procedures.

Attention is directed to certain incongruities among accepted diving procedures in order to emphasize the need for a more complete understanding of the interactions between the factors involved in diving and decompression and in the onset of decompression sickness. It is suggested that physiological responses derived from the effects of diffusion and nucleation of gas in tissue might be interpreted in terms of similar events in specimens of gelatin subjected to patterns of compression and decompression. A model for behavior of specimens in gel is developed and conformity with the results of a program of experimentation is demonstrated. With the insight provided by this model, a substantial analogy between important aspects of the behavior of gel and tissue is claimed and application of this model to the refinement and development of diving and decompression procedures is proposed.