Evaluation of the Valine requirement of small-framed first cycle laying hens.

An experiment was conducted to evaluate the total Valine (Val) requirement of first cycle laying hens from 41 to 60 wk of age. A total of 270 Hy-line W-36 laying hens were randomly assigned to 6 treatments with 15 replicate groups of 3 birds for each experimental unit. A Val deficient basal diet was formulated with corn and peanut meal with analyzed Val, Lys and crude protein concentrations of 0.515, 0.875, and 13.38%, respectively. Synthetic L-Val was supplemented to the basal diet in 0.070% increments to generate experimental diets containing 0.515, 0.585, 0.655, 0.725, 0.795, and 0.865% Val respectively. A controlled feeding program was applied during the experiment resulting in approximately 95 g feed intake per hen per day. Linear broken line, quadratic broken line, quadratic polynomial and exponential models were used to estimate the Val requirement of the hens based on hen-housed egg production (HHEP), egg mass (EM), and feed conversion ratio (FCR). Hen-housed egg production ranged from 48.3 to 81.4%, dependent upon dietary concentration of Val. Val requirements estimated by linear broken line, quadratic broken line, quadratic polynomial and exponential models were reported. Using the linear broken line model, the Val requirement was highest for egg mass, 597.3 mg/d, followed by egg production, 591.9 mg/d and lowest for FCR, 500.5 mg/d.

Evaluation of the tryptophan requirement of small-framed first cycle laying hens.

An experiment was conducted to evaluate the total Trp requirement of first cycle laying hens from 41 to 60 wk of age. In total, 270 Hy-Line W36 laying hens were randomly allocated to six treatments with 15 replicate groups of three birds for each experimental unit. A Trp-deficient basal diet was formulated with corn, corn gluten meal, and soybean meal with determined Trp, Lys, and crude protein concentrations of 0.096%, 0.873%, and 15.0%, respectively. Synthetic L-Trp was supplemented to the basal diet in 0.020% increments to generate experimental diets containing 0.096%, 0.116%, 0.136%, 0.156%, 0.176%, and 0.196% Trp, respectively. Hens were provided a controlled amount of feed of approximately 95 g/d. The diet containing the lowest concentration of Trp resulted in reduced egg production and was halted at 45 wk of age due to low performance with all other dietary treatments reaching the conclusion of the experiment at 60 wk of age. Plasma serotonin responded to dietary Trp concentration, but was not a good candidate for Trp requirement estimation. Linear broken line, quadratic broken line, quadratic polynomial, and exponential models were used to estimate Trp requirement based on hen-housed egg production (HHEP), egg mass (EM), and feed conversion ratio (FCR). HHEP ranged from 50.7% to 81.0%, dependent upon dietary concentration of Trp. Tryptophan requirements estimated by linear broken line, quadratic broken line, quadratic polynomial, and exponential models were reported. Using the linear broken line model, Trp requirement was highest for EM, 155.8 mg/d, followed by egg production, 153.2 mg/d and lowest for FCR, 140.4 mg/d.

Inheritance of occlusal topography: a twin study.

AIM: This was to determine the relative contribution of genetic factors on the morphology of occlusal surfaces of mandibular primary first molars by employing the twin study model. METHODS: The occlusal morphology of mandibular primary first molar teeth from dental casts of 9 monozygotic (MZ) twin pairs and 12 dizygotic (DZ) twin pairs 4 to 7 years old, were digitized by contact-type three-dimensional (3D) scanner. To compare the similarity of occlusal morphology between twin sets, each twin pair of occlusal surfaces was superimposed to establish the best fit by using computerized least squared techniques. Heritability was computed using a variance component model, adjusted for age and gender. RESULTS: DZ pairs demonstrated a greater degree of occlusal morphology variance. The total amount of difference in surface overlap was 0.0508 mm (0.0018 (inches) for the MZ (n=18) sample and 0.095 mm (0.0034 inches) for the DZ (n=24) sample and were not statistically significant (p=0.2203). The transformed mean differences were not statistically significantly different (p=0.2203). Heritability estimates of occlusal surface areas for right and left mandibular primary first molars were 97.5% and 98.2% (p<0.0001), respectively. CONCLUSIONS: Occlusal morphology of DZ twin pairs was more variable than that of MZ twin pairs. Heritability estimates revealed that genetic factors strongly influence occlusal morphology of mandibular primary first molars.

Autologous hematopoietic stem cell transplantation for older patients with relapsed non-Hodgkin's lymphoma.

To evaluate autologous stem cell transplant (ASCT) in older patients with intermediate grade non-Hodgkin's lymphoma (NHL), the Mayo Clinic Rochester BMT database was reviewed for all patients 60 years of age and older who received ASCT for NHL between September 1995 and February 2003. Factors evaluated included treatment-related mortality (TRM), event-free survival (EFS) and overall survival (OS). Ninety-three patients were identified, including twenty-four (26%) over the age of 70 years. Treatment-related mortality (5.4%) was not significantly different when compared to a younger cohort (2.2%). At a median follow-up of 14 months (0.6-87.6 months), the estimated median survival is 25 months (95% confidence interval (CI) 12-38) in the older group compared to 56 months (95% CI 37-75) (P=0.037) in the younger group. The estimated 4-year EFS was 38% for the older group compared to 42% in the younger cohort (P=0.1). By multivariate analysis, the only factor found to influence survival in the older group was age-adjusted International Prognostic Index at relapse, 0-1 better than 2-3 (P=0.03). Autologous stem-cell transplant can be safely performed in patients 60 years or older with chemotherapy sensitive relapsed or first partial remission NHL. The outcome may not be different from that of younger patients in terms of TRM and EFS.

Absolute lymphocyte count recovery after induction chemotherapy predicts superior survival in acute myelogenous leukemia.

Absolute lymphocyte count (ALC) recovery postautologous stem cell transplantation is an independent predictor for survival in acute myelogenous leukemia (AML). The role of ALC recovery after induction chemotherapy (IC) in AML is unknown. We hypothesize that ALC recovery after IC has a direct impact on survival. We have now evaluated the impact of ALC recovery after IC on overall survival (OS) and leukemia-free survival (LFS) in 103 consecutive, newly diagnosed AML patients treated with standard IC and consolidation chemotherapy (CC) from 1998 to 2002. ALC recovery was studied at days 15 (ALC-15), 21 (ALC-21), 28 (ALC-28) after IC and before the first CC (ALC-CC). Superior OS and LFS at each time point were observed with an ALC-15, ALC-21, ALC-28, and ALC-CC > or = 500 cells/microl. Patients with an ALC > or = 500 cells/microl at all time points vs those who did not have superior OS and LFS (not reached vs 13 months, P<0.0001; and not reached vs 11 months, P<0.0001, respectively). Multivariate analysis demonstrated ALC > or = 500 cells/microl at all time points to be an independent prognostic factor for survival. Our data suggest a critical role of lymphocyte (immune) recovery on survival after IC in AML.

BldD is a direct regulator of key developmental genes in Streptomyces coelicolor A3(2).

BldD is a transcription factor required for aerial hyphae formation in the filamentous bacterium Streptomyces coelicolor. Three targets of BldD regulation were discovered by a number of means, including examination of bld gene interdependence, selective enrichment of chromosomal DNA fragments bound by BldD and searching the promoter regions of known developmental genes for matches to a previously characterized BldD binding site. The three BldD targets identified were the developmental sigma factor genes, whiG and bldN, and a previously uncharacterized gene, designated bdtA, encoding a putative transcription factor. In each target gene, the sequences bound by BldD were characterized by electrophoretic mobility shift and DNase I footprinting assays, and their alignment suggested AGTgA (n)m TCACc as a consensus BldD operator. The in vivo effect of mutation in bldD on the expression of these three target genes was assessed using S1 nuclease protection assays. In each case, target gene expression was upregulated during early colony development in the bldD background, suggesting that, in the wild type, BldD acts to repress premature expression of whiG, bldN and bdtA during vegetative growth.

The BldD protein from Streptomyces coelicolor is a DNA-binding protein.

Gel mobility shift assays with His-tagged BldD isolated from Escherichia coli have illustrated that BldD is capable of specifically recognizing its own promoter region. DNase I and hydroxyl radical footprinting assays have served to delimit the BldD binding site, revealing that BldD recognizes and binds to a site just upstream from, and overlapping with, the -10 region of the promoter. How BldD binds to its promoter and the effect this binding has on the expression of BldD are discussed.

Effect of 1,25-dihydroxycholecalciferol, cholecalciferol, and fluorescent lights on the development of tibial dyschondroplasia and rickets in broiler chickens.

Experiments were conducted to determine whether dietary 1,25-dihydroxycholecalciferol [1,25-(OH)2D3] will alleviate a cholecalciferol deficiency induced by low dietary cholecalciferol and no fluorescent lighting and to determine cholecalciferol requirements as influenced by fluorescent lighting or 1,25-(OH)2D3. In each study, nutritionally complete basal diets were fed to broiler cockerels from 1 to 16 d of age. Experiment 1 had a 2 x 2 x 2 factorial arrangement of treatments with 1,25-(OH)2D3 at 0 and 10 micrograms/kg, cholecalciferol at 2.75 and 27.5 micrograms/kg, and fluorescent lights on or off. Experiments 2 to 4 had four levels of dietary cholecalciferol (0, 5.0, 27.5, and 50.0 micrograms/kg) and fluorescent lights on or off (Experiment 2) or 1,25-(OH)2D3 at 0 and 10 micrograms/kg (Experiments 3 and 4). In Experiment 1, fluorescent lighting increased bone ash, and decreased the incidence and severity of rickets at 2.75 micrograms/kg cholecalciferol and 0 microgram/kg 1,25-(OH)2D3 and reduced the severity of TD at both levels of cholecalciferol and 0 microgram/kg 1,25-(OH)2D3. In all cases 1,25-(OH)2D3 improved bone ash. The metabolite also decreased the incidence and severity of TD at both cholecalciferol levels with lights off and decreased the incidence and severity of rickets at 2.75 micrograms/kg cholecalciferol and lights off. In the absence of fluorescent lighting and 1,25-(OH)2D3 27.5 micrograms/kg cholecalciferol reduced the incidence and severity of rickets to levels equivalent to those produced by either fluorescent lighting or 1,25-(OH)2D3 alone (Experiments 2, 3, and 4). However, even 50.0 micrograms/kg cholecalciferol was not as effective as fluorescent lights or 1,25-(OH)2D3 in reducing the incidence and severity of TD.

Effects of dietary calcium and 1,25-dihydroxycholecalciferol on the development of tibial dyschondroplasia in broilers during the starter and grower periods.

Two experiments were conducted to determine whether dietary 1,25-dihydroxycholecalciferol [1,25-(OH)2D3] can prevent tibial dyschondroplasia in broiler chickens throughout the growing period when withdrawn from the grower diet. The birds were reared in floor pens with pine shavings to 6 wk in Experiment 1 and 5 wk of age in Experiment 2. Calcium was fed at .65 or 1.00% and 1,25-(OH)2D3 was fed at 0 or 5 micrograms/kg to 3 wk of age. Half the birds consuming 1,25-(OH)2D3 were then fed 0 microgram/kg until the end of the experiments. The higher level of calcium decreased the incidences of tibial dyschondroplasia and severe lesions and increased bone ash. Dietary 1,25-(OH)2D3 increased bone ash at both levels of calcium at 3 wk and the end of the experiments when supplemented for the duration of the studies. When 1,25-(OH)2D3 was fed, tibial dyschondroplasia was reduced in Experiment 2 only at 3 wk. Tibial dyschondroplasia was decreased at 5 wk in Experiment 2 when .65% calcium was fed with or without 1,25-(OH)2D3 from 3 to 5 wk of age. There were no treatment effects on plasma calcium, dialyzable phosphorus, or 25-hydroxycholecalciferol. Plasma 1,25-(OH)2D3 was decreased at 3 and 5 wk in Experiment 2 when 1.00% calcium was fed. The results of Experiment 2 suggest that 1,25-(OH)2D3 can prevent tibial dyschondroplasia caused by inadequate calcium when fed for only 3 wk. The bone ash observed when 1.00% dietary calcium is fed is equal to that obtained when 5 micrograms/kg 1,25-(OH)2D3 is fed with .65% calcium for the entire growout period.

Effect of genetic strain, calcium, and feed withdrawal on growth, tibial dyschondroplasia, plasma 1,25-dihydroxycholecalciferol, and plasma 25-hydroxycholecalciferol in sixteen-day-old chickens.

Four experiments were conducted to study the effects of genetic strain, dietary Ca level, and feed withdrawal on growth, feed efficiency, tibia bone ash, tibial dyschondroplasia (TD), and plasma 1,25-dihydroxycholecalciferol [1,25(OH)2D3] and 25-hydroxycholecalciferol [25(OH)D3]. Experiment 1 used five strains and Experiments 2 to 4 used three broiler strains. A TD-inducing basal diet was used in each experiment. In Experiment 3, the birds were fed .60 or .95% dietary Ca, and in Experiment 4 the birds were fed the basal diet and were fed or deprived of feed for 8 h daily. In Experiment 1, Athens-Canadian Randombred and Single Comb White Leghorn chicks did not develop TD. In birds fed the basal diet alone, Peterson x Hubbard chicks had a significantly higher incidence of the most severe TD lesion than two other broiler strains in each experiment and were significantly lighter in BW in two of the four experiments. Of the three broiler strains, the incidence and average lesion score of TD was significantly higher in Peterson x Hubbard birds in Experiment 2 and was numerically highest in the other three experiments. In birds fed the basal diet, Peterson x Hubbard birds had significantly higher plasma 1,25(OH)2D3 in two of the four experiments. Both feed deprivation and .95% Ca increased bone ash and decreased the incidence and severity of TD. There were no significant differences in plasma 1,25(OH)2D3 among strains of birds deprived of feed or fed .95% Ca. In three of the four experiments, high plasma 1,25(OH)2D3 in Peterson x Hubbard birds was associated with an increase in the incidence and severity of TD.

Quantitative requirement for cholecalciferol in the absence of ultraviolet light.

Studies were conducted to determine the basic requirement of the bird for cholecalciferol in the absence of ultraviolet light by utilizing filter sleeves on fluorescent lights in the room and brooder. In Experiment 1, some pens were fitted with filter tubes and some lights were turned off. All the birds received a cholecalciferol-deficient diet. Birds with ultraviolet light excluded grew slowly, developed rickets (95%), had low plasma calcium, and low bone ash (27%); whereas birds exposed to the fluorescent light had normal growth and plasma calcium, slightly low bone ash (38%), and some rickets (12%). Experiments 2 and 3 were conducted to determine the amount of cholecalciferol that must be added to the diet under conditions in which ultraviolet light was excluded. In Experiment 2, the highest level of cholecalciferol fed was 400 ICU/kg. This level was not sufficient to permit the chickens to have weight gain or bone ash equal to the birds receiving the ultraviolet light. The birds receiving 400 ICU/kg of diet also had a 77% incidence of rickets compared with 20% for the birds receiving ultraviolet lights. In Experiment 3, when birds received 800 or 1,600 ICU/kg of cholecalciferol in the diet, they grew and were comparable to those receiving ultraviolet light for the criteria measured.

Effect of dietary calcium on tibial dyschondroplasia. Interaction with light, cholecalciferol, 1,25-dihydroxycholecalciferol, protein, and synthetic zeolite.

A series of experiments was conducted to investigate interactions of dietary calcium levels with ultraviolet light, cholecalciferol (D3), 1,25-dihydroxycholecalciferol [1,25-(OH)2D3], dietary protein, and a synthetic zeolite on the development of tibial dyschondroplasia in broilers. A basal diet low in calcium, high in phosphorus and chloride, and known to promote a high incidence of tibial dyschondroplasia was used. The chicks received ultraviolet radiation from fluorescent lights in addition to 1,100 ICU/kg (27.5 micrograms/kg) of D3 in the basal diet when these were not experimental variables. Regardless of whether the calcium level was low (.65%) or adequate (.95%), the incidence of tibial dyschondroplasia was significantly lower in chicks receiving ultraviolet radiation or dietary vitamin D3 levels well above the required amounts. The addition of 10 micrograms/kg of 1,25-(OH)2D3 to the diet when calcium levels varied from .45 to .95% resulted in a reduction in the incidence of tibial dyschondroplasia and increased tibial bone ash when dietary protein levels were 18 or 22%. The addition of 1% synthetic zeolite to the diet did not influence the incidence of tibial dyschondroplasia when the diet contained widely varying dietary calcium levels (.65 to 1.81%) and .73% phosphorus.

Studies to determine whether an interaction exists among boron, calcium, and cholecalciferol on the skeletal development of broiler chickens.

Two experiments were designed to determine the effect of dietary boron on broiler cockerels and four experiments were conducted to determine whether an interaction exists among dietary boron, cholecalciferol, and calcium. The parameters measured were weight gain, feed efficiency, tibia bone ash, rickets, tibial dyschondroplasia, and plasma minerals. All experiments were conducted with tibial dyschondroplasia-inducing basal diets fed to broiler cockerels from 1 to 16 days of age. Experiments 1 and 2 had four levels of dietary boron (0, 20, 40, and 80 mg/kg (Experiment 1) and 0, 5, 10, and 20 mg/kg (Experiment 2). Boron had no effect on weight gain, feed efficiency, or plasma minerals in either experiment. In Experiment 2, increasing levels of boron had no influence on tibial dyschondroplasia but did exert a quadratic effect on bone ash with 5 and 10 mg/kg boron increasing bone ash. In Experiment 1, bone ash and the incidence of tibial dyschondroplasia were unaffected, but the severity of tibial dyschondroplasia linearly increased by increasing boron levels. Experiments 3 to 6 had a 2 x 2 x 2 factorial arrangement of treatments with calcium at .65 and .90%, cholecalciferol at 110 and 1,100 ICU/kg, and boron at 0 and 40 mg/kg (Experiments 3 to 5) or 0 and 3 mg/kg (Experiment 6). The higher levels of calcium and cholecalciferol improved weight gain, decreased the incidence of rickets, and decreased the incidence and severity of tibial dyschondroplasia. Feeding cholecalciferol at 1,100 ICU/kg increased plasma calcium and plasma dialyzable phosphorus and decreased plasma magnesium. Calcium at .90% had no effect on plasma magnesium or plasma dialyzable phosphorus and increased plasma calcium only in Experiment 4. The only response to boron in Experiments 3 to 6 was a boron effect and a boron by cholecalciferol interaction on bone ash in Experiment 3, in which boron reduced bone ash at .65% calcium and 110 ICU/kg cholecalciferol. From these experiments, there is no indication that an interaction among boron, cholecalciferol, and calcium exists in broiler cockerels.

Comparison of the effects of synthetic and natural zeolite on laying hen and broiler chicken performance.

Three experiments were conducted to investigate the effect of zeolites on laying hens (Experiments 1 and 2) and broiler chickens (Experiment 3). Each experiment used corn and soybean meal-based practical diets. Experiment 1 was a 90-day trial and used 200 40-wk-old laying hens. The basal diet contained 2.75% calcium and .7% total phosphorus. The dietary treatments were the basal diet and the basal diet plus 1.5% synthetic zeolite (SZ; Ethacal). Experiment 2 was a 56-day trial and used 360 36-wk-old laying hens. The dietary treatments were .12, .22, .32, and .42% nonphytin phosphorus with and without 1.0% SZ and 1.0% natural zeolite (NZ; Zar-Min). All diets contained 3.5% calcium. Experiment 3 utilized 240 broiler cockerels from 1 to 16 days. The dietary treatments were two calcium levels (.65 and 1.0%) with and without 1.0% supplementary SZ and NZ. In Experiment 1, egg specific gravity was significantly increased with SZ supplementation. Egg weight and egg production were unaffected. Phytin phosphorus retention and plasma dialyzable phosphorus were significantly reduced by SZ. In Experiment 2, egg specific gravity was not affected by SZ or NZ. Egg weight, egg production, plasma dialyzable phosphorus, and the retention of phosphorus and phytin phosphorus were significantly reduced by SZ with the effect on egg weight and egg production being the most severe at the lower levels of dietary nonphytin phosphorus. Natural zeolite had no effect on egg weight, egg production, plasma calcium, plasma phosphorus, or on the retention of calcium, phosphorus, and phytin phosphorus. In Experiment 3, weight gain and percentage tibia bone ash were significantly reduced by SZ. The SZ had no effect on the incidence and severity of tibial dyschondroplasia. Weight gain, feed efficiency, and the incidence and severity of tibial dyschondroplasia were significantly reduced and the percentage bone ash significantly increased by 1.0% calcium. Natural zeolite significantly improved feed efficiency and had no effect on any other parameter measured.

Some effects of dietary aluminum and silicon on broiler chickens.

Experiments were conducted to determine whether dietary silicon will reduce the toxic effects of dietary aluminum on broiler chickens. The parameters measured were weight gain, feed efficiency, percentage bone ash, tibial dyschondroplasia, and the retention of calcium, phosphorus, and phytin phosphorus. Experiments 1 and 2 were conducted with casein and gelatin-based purified diets and Experiments 3 and 4 with corn and soybean meal-based practical diets. All experiments used day-old broiler cockerels and lasted 16 days. Aluminum significantly reduced weight gain, feed efficiency, and percentage bone ash in all four experiments. Aluminum supplementation reduced the incidence and severity of tibial dyschondroplasia, but this effect was associated with a reduction in weight gain. Increasing dietary aluminum reduced the retention of phosphorus and phytin phosphorus. Silicon did not alleviate the effects of aluminum toxicity on any of the parameters measured but did independently increase growth rate in Experiments 1 and 2, Supplementary dietary silicon does not appear to reduce aluminum toxicity in broiler chickens. Aluminum appears to exert its toxic effect on chickens by reducing the retention of phosphorus and phytin phosphorus.

Effect of dietary silicon on growth and skeletal development in chickens.

Experiments were conducted to determine the effect of supplementary dietary silicon on weight gain, feed efficiency, percent tibia bone ash and on the development of tibial dyschondroplasia in broiler chickens. Experiments 1 and 2 were conducted with casein/gelatin-based purified diets and Experiments 3 and 4 with corn/soy-based practical diets. All experiments used day-old broiler cockerels and lasted 16 d. Silicon supplementation (250 mg/kg) significantly decreased growth rate and the incidence and severity of tibial dyschondroplasia in Experiment 1 and had no effect on either parameter in Experiments 2-4. Dietary silicon supplementation significantly reduced feed efficiency in Experiments 1 and 3. Tibia bone ash was unaffected by dietary silicon supplementation in any of the experiments conducted. The results of the present studies indicate that dietary silicon supplementation has no effect on growth and skeletal development in broiler chickens.