Establishment and characterization of antigen-presenting cell lines (XS series) derived from newborn mouse epidermis.
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Animals↗
Biomedical subjects
S Xu
Publications and source records attributed to S Xu.
Vaccination of sheep against Schistosoma japonicum with either glutathione S-transferase, keyhole limpet haemocyanin or the freeze/thaw schistosomula/BCG vaccine.
The protective potential of glutathione S-transferase (GST), keyhole limpet haemocyanin (KLH) and the freeze/thaw (F/T) schistosomula/BCG vaccine was evaluated against Schistosoma japonicum in the natural sheep host. Groups of ten sheep each were vaccinated as follows: Group I: 2 x F/T 30,000 schistosomula+BCG 3 x 10(8) organisms, with a 2 week interval between vaccinations (F/T 'Low'). Group II: 3 x F/T 20,000 schistosomula+BCG 3 x 10(8), with 4 week interval (F/T 'High'). Group III: 2 x GST 0.24 mg+FCA (Freund's complete adjuvant) with 2 week interval (GST 'Low'). Group IV: 3 x GST 0.24 mg+FCA, with 4 week interval (GST 'High'). Group V: 2 x KLH 1.0 mg in phosphate-buffered saline (PBS), with 2 week interval (KLH 'Low'). Group VI: 3 x KLH 1.0 mg in PBS, with 4 week interval (KLH 'High'). Group VII: control (not vaccinated). Specific antibody, detected by GST-enzyme-linked immunosorbent assay (ELISA) and KLH-ELISA on the day after the last vaccination and 1, 2 and 3 weeks post-challenge, was found in all GST- or KLH-vaccinated groups. The same was found in F/T schistosomula-vaccinated groups against crude adult worm antigen (AWA). In Western blotting all GST-vaccinated sera recognized 26 kDa and 28 kDa bands on the challenge day and at 3 and 11 weeks post-challenge. Mean faecal egg counts between Weeks 6 and 10 post-challenge were reduced in a statistically significant way at five time points in the four groups, i.e. 83.38% (P < 0.005) in Group II, 49.29% (P < 0.025) in Group III, 47.9% (P < 0.05) and 71.15% (P < 0.01) in Group IV, 52.0% (P < 0.025) and 66.38% (P < 0.025) in Group VI. On autopsy and perfusion 1 week after the last faecal count, adult worm reductions were obtained of 40.36% (P < 0.05) in Group I, 37.26% (P < 0.025) in Group II, 24.73% (not significant) in Group III, 35.93% (P < 0.025) in Group IV, 27.46% (P < 0.05) in Group V and 33.81% (P < 0.01) in Group VI. Mean tissue egg densities were also reduced significantly in Groups III, IV and VI, especially in Group IV vaccinated animals. Mean liver egg granuloma diameters of the vaccinated groups were found to be less than those of the controls but there was no statistical significance.(ABSTRACT TRUNCATED AT 400 WORDS)
Animals↗
Role of nitric oxide and acetylcholine in neocortical hyperemia elicited by basal forebrain stimulation: evidence for an involvement of endothelial nitric oxide.
We examined the role of acetylcholine and nitric oxide in the increases in cerebrocortical blood flow elicited by stimulation of a region of the basal forebrain from which the major cholinergic projection to the cerebral cortex originates. In halothane-anesthetized rats a 3 x 3 mm area of the parietal cortex was exposed and the site was superfused with Ringer (37 degrees C; pH 7.3-7). Cortical blood flow was monitored at the site of superfusion by laser-Doppler flowmetry. The basal forebrain was stimulated electrically (100 microA; 50 Hz) and stimulated sites were histologically verified at the end of the experiment. With Ringer superfusion (n = 8), basal forebrain stimulation increased neocortical flow by 185 +/- 9% (mean +/- S.E.M.). The flow increase was attenuated (-38 +/- 6%; n = 5) by superfusion with the muscarinic cholinergic antagonist atropine (100 microM). Superfusion with atropine plus the nicotinic antagonist mecamylamine (100 microM) did not attenuate the response further (P > 0.05 from atropine alone; n = 6). Superfusion with the nitric oxide synthase inhibitor nitro-L-arginine, but not with the inactive isomer nitro-D-arginine (n = 6), attenuated the vasodilation in a dose-dependent fashion (-43 +/- 4% at 1 mM; n = 7) and reduced nitric oxide synthase catalytic activity at the site of superfusion by 95 +/- 4%. Co-application of nitro-L-arginine and atropine did not attenuate the vasodilation further (P > 0.05 from nitro-L-arginine alone; n = 6). Administration of the somewhat selective inhibitor of neuronal nitric oxide synthase 7-nitroindazole (50 mg/kg, i.p.) attenuated the increases in flow produced by topical application of N-methyl-D-aspartate (40 microM; n = 5) or by hypercapnia (n = 7), but did not affect the vasodilation produced by basal forebrain stimulation (n = 5) and by topical application of acetylcholine (10 microM; n = 5). 7-nitroindazole reduced constitutive nitric oxide synthase enzymatic activity in forebrain by 72 +/- 3% (n = 8). The data suggest that the neocortical vasodilation elicited by basal forebrain stimulation is, in part, mediated by local release of acetylcholine which, in turn, leads to increased nitric oxide synthesis in endothelial cells.
Acetylcholine↗
Age-related CNS disorder and early death in transgenic FVB/N mice overexpressing Alzheimer amyloid precursor proteins.
Transgenic FVB/N mice overexpressing human (Hu) or mouse (Mo) Alzheimer amyloid precursor protein (APP695) die early and develop a CNS disorder that includes neophobia and impaired spatial alternation, with diminished glucose utilization and astrogliosis mainly in the cerebrum. Age at onset of neophobia and age at death decrease with increasing levels of brain APP. HuAPP transgenes induce death much earlier than MoAPP transgenes expressed at similar levels. No extracellular amyloid was detected, indicating that some deleterious processes related to APP overexpression are dissociated from formation of amyloid. A similar clinical syndrome occurs spontaneously in approximately 20% of nontransgenic mice when they reach mid- to late-adult life, suggesting that APP overexpression may accelerate a naturally occurring age-related CNS disorder in FVB/N mice.
Aging↗
Tissue IGFBP-3 proteolysis: contrasting pathophysiology to that in the circulation.
Endogenous IGFBP-3 has been examined in the circulation and in four different extravascular fluids in normal healthy adults and in patients with psoriasis or arthritis. In all of these cases there was no apparent increase of IGFBP-3 protease activity in the circulation. In contrast, endogenous IGFBP-3 from normal skin interstititial fluid and synovial fluid from healthy adults was found to be predominantly in the 29 kDa proteolytically modified form. This indicated that in these extravascular fluids in normal healthy adults a protease was active which was similar, if not identical, to that found in the circulation in pregnancy and other conditions. This was confirmed by the fragmentation of recombinant IGFBP-3 when incubated with these fluids. When the skin interstitial fluid or synovial fluid were taken from abnormal tissues (psoriasis in the former and osteoarthritis or rheumatoid arthritis in the latter) there was a considerable reduction in the amount of endogenous IGFBP-3 in the 'clipped' form and a reduction in the protease activity. In psoriatic lesions, this reduction in IGFBP-3 protease activity was shown to be due to the presence of an inhibitor in the interstitial fluid but not in the circulation. In both peritoneal and follicular fluid, the ratio of intact to fragmented IGFBP-3 appeared to relate to the oestrogen status. In peritoneal fluid there was a decrease in intact IGFBP-3 during the late proliferative/early secretory phase of the endometrial cycle. In the ovary there was an increase in the amount of fragmented IGFBP-3 in the follicular fluid from the dominant follicle in comparison with atretic follicles from the same ovary. There is normally little proteo-lysis of IGFBP-3 in the circulation but this increases in many conditions where there is increased metabolic activity. The same enzyme(s) appear to be active in many extravascular fluids but under very different regulation. The activity in these extravascular fluids is normally high but can be decreased with local tissue inflammation; this decrease appears to be mediated by the induction of a local inhibitor.
Adult↗
Dissociation of mouse cardiac transplant rejection and donor alloantigen-specific T cell responsiveness.
Mouse hearts transplanted into MHC disparate donors are usually rejected 1 week after placement. It is widely accepted that alloantigen-reactive helper T lymphocytes (HTL) and cytotoxic T lymphocytes (CTL) are the key mediators of acute allograft rejection. This report demonstrates that the presence or absence of 'traditional' graft-reactive HTL and CTL is not necessarily related to allograft survival. In these studies, donor/recipient combinations disparate only at MHC or only at minor histocompatibility (mH) loci were employed. Allograft survival was monitored, donor-reactive IL-2 (interleukin-2) producing HTL and CTL were quantified by modified limiting dilution analysis, and serum levels of cytolytic alloantibody were determined. C57BL/10 hearts (H-2b) transplanted into B10.BR (H-2k) recipients (full MHC disparity) enjoyed prolonged survival despite massive infiltration of the allograft by donor-reactive HTL and CTL. IgM, but not IgG, donor-reactive alloantibody was present in the sera of these mice. Hence, traditional IL-2 producing HTL and CTL were not capable of mediating acute graft rejection, nor of providing help for alloantibody isotype switching in this MHC disparate combination. In contrast, C3H/HeN (H-2k) hearts transplanted into B10.BR (H-2k) recipients (mH disparity only) were acutely rejected. Donor-reactive HTL and CTL were rare or not detectable in these recipients, and cytolytic alloantibody was not detectable. Similar observations were made when B10.BR hearts were transplanted into C3H/HeN recipients. Interestingly, treatment of recipients with anti-CD4 monoclonal antibody prevented rejection of mH disparate allografts. Therefore, CD4+ T cells were required for rejection of mH disparate allografts, but this process was independent of detectable IL-2 production or CTL function. Hence, the significance of monitoring 'traditional' T cell functions should be questioned in certain donor/recipient combinations.
Animals↗
Inducible nitric oxide synthase gene expression in brain following cerebral ischemia.
Cerebral ischemia is followed by a local inflammatory response that is thought to participate in the extension of the tissue damage occurring in the postischemic period. However, the mechanisms whereby the inflammation contributes to the progression of the damage have not been fully elucidated. In models of inflammation, expression of the inducible isoform of nitric oxide synthase (iNOS) is responsible for cytotoxicity through the production of large amounts of nitric oxide (NO). In this study, therefore, we sought to establish whether iNOS is expressed in the ischemic brain. Rats were killed 6 h to 7 days after occlusion of the middle cerebral artery. iNOS expression in the ischemic area was determined by reverse-transcription polymerase chain reaction. Porphobilinogen deaminase mRNA was detected in the same sample and used for normalization. In the ischemic brain, there was expression of iNOS mRNA that began at 12 h, peaked at 48 h, and returned to baseline at 7 days (n = 3/time point). iNOS mRNA expression paralleled the time course of induction of iNOS catalytic activity, determined by the citrulline assay (17.4 +/- 4.4 pmol citrulline/micrograms protein/min at 48 h; mean +/- SD; n = 5 per time point). iNOS immunoreactivity was seen in neutrophils at 48-96 h after ischemia. The data provide molecular, biochemical, and immunocytochemical evidence of iNOS induction following focal cerebral ischemia. These findings, in concert with our recent demonstration that inhibition of iNOS reduces infarct volume in the same stroke model, indicate that NO production may play an important pathogenic role in the progression of the tissue damage that follows cerebral ischemia.
Amino Acid Oxidoreductases↗
Time dependence of effect of nitric oxide synthase inhibition on cerebral ischemic damage.
Nitric oxide, a potent vasodilator and an inhibitor of platelet aggregation, may be beneficial in the early stages of focal cerebral ischemia as it may facilitate collateral blood flow to the ischemic territory. Accordingly, the effect of inhibition of nitric oxide synthesis on cerebral ischemic damage may vary depending on the timing of the inhibition relative to the induction of ischemia. We therefore studied the time course of the effect of nitric oxide synthesis inhibition on focal cerebral ischemic damage. The middle cerebral artery was permanently occluded in spontaneously hypertensive rats and the nitric oxide synthase (NOS) inhibitor nitro-L-arginine methyl ester (L-NAME) was administered systemically (3 mg/kg) < 5 min or 2, 3, or 6 h later. Arterial pressure, rectal temperature, plasma glucose, and hematocrit were monitored. Infarct volume was determined on thionin-stained sections 24 h after induction of ischemia. NOS activity was determined in cerebellum from the conversion of L-[3H]arginine to L-[3H]citrulline. Administration of L-NAME < 5 min after arterial occlusion increased the infarct volume by 23 +/- 14% (mean +/- SD; p < 0.05, analysis of variance), while administration of L-NAME at 2 or 6 h did not affect the size of the infarct (p > 0.05). L-NAME administration 3 h after induction of ischemia reduced neocortical infarct size by 14 +/- 11% (p < 0.05). L-NAME decreased cerebellar NOS activity comparably in all groups (range 16-25%). We conclude that the effects of inhibition of nitric oxide synthesis on focal cerebral ischemic damage are time dependent.(ABSTRACT TRUNCATED AT 250 WORDS)
Amino Acid Oxidoreductases↗
A random model approach to interval mapping of quantitative trait loci.
Mapping quantitative trait loci in outbred populations is important because many populations of organisms are noninbred. Unfortunately, information about the genetic architecture of the trait may not be available in outbred populations. Thus, the allelic effects of genes can not be estimated with ease. In addition, under linkage equilibrium, marker genotypes provide no information about the genotype of a QTL (our terminology for a single quantitative trait locus is QTL while multiple loci are referred to as QTLs). To circumvent this problem, an interval mapping procedure based on a random model approach is described. Under a random model, instead of estimating the effects, segregating variances of QTLs are estimated by a maximum likelihood method. Estimation of the variance component of a QTL depends on the proportion of genes identical-by-descent (IBD) shared by relatives at the locus, which is predicted by the IBD of two markers flanking the QTL. The marker IBD shared by two relatives are inferred from the observed marker genotypes. The procedure offers an advantage over the regression interval mapping in terms of high power and small estimation errors and provides flexibility for large sibships, irregular pedigree relationships and incorporation of common environmental and fixed effects.
Alleles↗
A comment on the simple regression method for interval mapping.
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Chromosome Mapping↗
Identity and functional properties of novel skin-derived fibroblast lines (NS series) that support the growth of epidermal-derived dendritic cell lines.
We have established recently a series of unique cell lines (NS series) from dispase-separated mouse epidermis that promote the growth of epidermal-derived antigen-presenting cell lines (XS series). The purposes of this study were to determine the identity of NS cells and to characterize their functional properties. NS cells were distinguishable from leukocytes by the lack of typical surface markers and by the failure to respond to leukocyte growth factors. Despite their epidermal derivation, NS cells were distinct from keratinocytes by the absence of cytokeratins. On the other hand, NS cells were indistinguishable from lines of dermal fibroblasts by their a) morphology, b) surface phenotype, and c) intracellular deposits of type I collagen. Growth of the XS antigen-presenting lines has been promoted by co-culturing with gamma-irradiated NS cells, and this activity could be replaced with NS cell-conditioned media alone, but not with paraformaldehyde-fixed NS cells. Each clone derived from the NS01 line secreted XS cell-growth-promoting activity, and this activity was blocked by monoclonal antibodies against colony-stimulating factor-1 receptors. Dermal fibroblasts also promoted the growth of XS cells in a colony-stimulating factor-1-dependent manner. By contrast, culture supernatants from other cell lines derived from skin (e.g., Pam 212 keratinocytes, 7-17 dendritic epidermal T cells, or XS lines) failed to promote XS cell growth. These results indicate that NS cells belong to the fibroblast lineage and that they share the intrinsic property to secrete large amounts of colony-stimulating factor-1 with dermal fibroblasts. Dermal cells may support the growth of skin-associated antigen-presenting cells in vivo.
Animals↗
Phenotypic and functional heterogeneity among murine epidermal-derived dendritic cell clones.
We have established recently long-term dendritic cell lines from the epidermis of newborn BALB/c mice. These lines, termed XS series, resembled epidermal resident Langerhans cells or their progenitors in terms of surface phenotype, antigen-presenting capacity, and growth factor requirement. We examined in this study the degree of clonal heterogeneity among XS cells with respect to each of these features. Twelve stable clones were established by limiting dilution microculture from 8-10-week-old cultures of the XS52 or XS20 line. Despite the uniform expression of CD45, these clones varied substantially in their expression of Ia, B7-1, and B7-2 molecules. They also varied significantly in their relative efficiency in activating T cells. Finally, remarkable clone-to-clone heterogeneity was also observed in their growth factor responsiveness; some clones responded equally well to granulocyte macrophage-colony-stimulating factor-1, whereas others responded preferentially to one or the other of these factors. We propose that the observed clonal heterogeneity in XS cells reflects possible heterogeneity in the state of maturation and mitotic potential among the starting populations, i.e., skin-associated dendritic cells in newborn mice.
Animals↗
Determination of HLA class II alleles by genotyping in a Manchu population in the northern part of China and its relationship with Han and Japanese populations.
The genetic polymorphism of the HLA class II loci was investigated in a Manchu population resident in the northern part of China and compared with those of other Asian populations including Japanese and Han. In 8 DQA1 alleles, the most frequent allele was DQA1*03 with the gene frequency of 25.5%. Of 15 DQB1 alleles tested, 11 were observed and the most common allele was DQB1*0301 with the gene frequency of 24.5%. Among 19 DPB1 alleles, 11 were detected and DPB1*0501 (43.8%) was the most frequent allele as observed in other Asian populations such as Japanese, Chinese and Korean. Of 43 DRB1 alleles tested, 21 were detected and DRB1*0901 (14.0%), *1501 (11.0%), *1201 (11.0%), *07 (9.0%) and *1401 (9.0%) were highly predominant and account for the high frequencies of DR9, DR2, DR5, DR7 and DR6. In the DRB3 gene (DR52), DRB3*0202 (18.0%) was the most frequent. With respect to the DRB4 gene (DR53), the gene frequency of DRB4*0101 was 35.0%. Of 3 DRB5 alleles detected, DRB5*0101 (11.0%) was highly predominant. Comparison of HLA class II allele frequencies in Manchu with those in Japanese and Han Chinese populations (South & North) detected some significant differences and genetic divergence between these Oriental populations. The dendrogram constructed by the neighbor-joining (NJ) method based on the allele frequencies of DQA1, DQB1, DPB1 and DRB1 of 10 representative populations over the world suggested that Manchu is the closest, but at the same genetic distance to both Northern and Southern Han Chinese.
Alleles↗
Hydrogen peroxide mediates UV-induced impairment of antigen presentation in a murine epidermal-derived dendritic cell line.
Ultraviolet-B (290-320 nm) radiation is known to impair the antigen-presenting cell (APC) function of Langerhans cells (LC), skin-specific members of the dendritic cell (DC) family. We sought to address mechanisms of this effect, focusing on the role played by hydrogen peroxide. For this purpose, we used a newly established murine DC line, XS52, which resembles epidermal LC in several respects. The APC capacity of XS52 cells, using two different CD4+ T cell clones as responders, was inhibited significantly (> 50%) by exposure to UV radiation (unfiltered FS20 sunlamps) at relatively small fluences (50-100 J/m2). Ultraviolet radiation also inhibited growth factor-dependent proliferation of XS52 cells. On the other hand, cell surface phenotype was relatively well preserved after irradiation; expression levels of B7-1 and B7-2 were reduced slightly, while other molecules (e.g. Ia, CD54, CD11a and CD18) were not affected. With respect to the role played by hydrogen peroxide, pretreatment with purified catalase (900 U/ mL) prevented UV-induced inhibition of APC function. Short-term exposure to 3 mM H2O2 or t-butyl H2O2 mimicked UV radiation by inhibiting APC function. Finally, intrinsic catalase activity was substantially lower in XS52 cells compared with Pam 212 keratinocytes. These results indicate that the generation of hydrogen peroxide alone is sufficient to produce some, but not all, of the deleterious effects of UV radiation on DC derived from the skin.
Animals↗
Roles of URE2 and GLN3 in the proline utilization pathway in Saccharomyces cerevisiae.
The yeast Saccharomyces cerevisiae can use alternative nitrogen sources such as arginine, urea, allantoin, gamma-aminobutyrate, or proline when preferred nitrogen sources like glutamine, asparagine, or ammonium ions are unavailable in the environment. Utilization of alternative nitrogen sources requires the relief of nitrogen repression and induction of specific permeases and enzymes. The products of the GLN3 and URE2 genes are required for the appropriate transcription of many genes in alternative nitrogen assimilatory pathways. GLN3 appears to activate their transcription when good nitrogen sources are unavailable, and URE2 appears to repress their transcription when alternative nitrogen sources are not needed. The participation of nitrogen repression and the regulators GLN3 and URE2 in the proline utilization pathway was evaluated in this study. Comparison of PUT gene expression in cells grown in repressing or derepressing nitrogen sources, in the absence of the inducer proline, indicated that both PUT1 and PUT2 are regulated by nitrogen repression, although the effect on PUT2 is comparatively small. Recessive mutations in URE2 elevated expression of the PUT1 and PUT2 genes 5- to 10-fold when cells were grown on a nitrogen-repressing medium. Although PUT3, the proline utilization pathway transcriptional activator, is absolutely required for growth on proline as the sole nitrogen source, a put3 ure2 strain had somewhat elevated PUT gene expression, suggesting an effect of the ure2 mutation in the absence of the PUT3 product. PUT1 and PUT2 gene expression did not require the GLN3 activator protein for expression under either repressing or derepressing conditions. Therefore, regulation of the PUT genes by URE2 does not require a functional GLN3 protein. The effect of the ure2 mutation on the PUT genes is not due to increased internal proline levels. URE2 repression appears to be limited to nitrogen assimilatory systems and does not affect genes involved in carbon, inositol, or phosphate metabolism or in mating-type control and sporulation.
1-Pyrroline-5-Carboxylate Dehydrogenase↗
Autosomal dominant retinitis pigmentosa locus on chromosome 19q in a Japanese family.
A large four generation Japanese family was studied, in which autosomal dominant retinitis pigmentosa (ADRP) of very variable expression was segregating. Positive lod scores with maxima between 1.557-5.118 at theta = 0.00, strongly suggestive of linkage, were obtained for KLK, D19S180, D19S418, and D19S254 on chromosome 19q. Recently, an ADRP locus has been mapped to the same region in a British family, in which, again, several members subjectively had no clinical evidence of the disease although they had both an affected parent and an affected child.
Adolescent↗
Insulin-like growth factors (IGFs) and IGF-binding proteins in human skin interstitial fluid.
Despite extensive investigation of the insulin-like growth factor (IGF)/IGF-binding protein (IGFBP) system in the circulation and body fluids, there is no information on this in interstitial fluid. We have compared the IGF/IGFBP system in the circulation with that in fluid obtained from blisters artificially raised by negative pressure in 10 healthy volunteers. IGFBP-1, -2, -3, and -4 were all found in blister fluid, but in concentrations much lower than those in matched serum. The IGF-I, IGF-II, and IGFBP-3 levels measured by RIA were 18%, 14%, and 16% of those in serum, respectively. Fast protein liquid chromoatography showed that both IGF-I and IGFBP-3 in 150- and 50-kilodalton complexes were approximately 13% and 37%, respectively, of the corresponding peaks found in matched serum. Compared to that in serum, the IGFBP-3 in the blister fluid was predominantly in a modified 29-kilodalton form, and there was increased activity of an IGFBP-3 protease. Therefore, although IGF concentrations are much lower in interstitial fluid than in the circulation, a greater proportion of this IGF is in forms more readily available for interaction with tissue receptors. The blister fluid appears to represent physiological interstitial fluid and may provide a model for studying the physiology and pathophysiology of growth factors in the interstitial environment.
Blister↗
Multistage selection for maximum economic return with an application to beef cattle breeding.
Methodology for selection index updating was developed to allow multistage selection. The program determines truncation points for each stage of selection that will maximize either profit or the ratio of aggregate economic gain to cost (R = delta H/C). Either maximum profit or R may be attained by reducing the cost of performance testing in later stages of a multistage program. In order to eliminate the need for multiple integration and assure convergence, a piecewise algorithm was developed. Examples of beef bull selection compared single-stage selection at 1 yr of age, two-stage selection at birth and 1 yr, two-stage selection at 205 d and 1 yr, and three-stage selection at birth, 205 d, and 1 yr. Selection based on three traits (birth weight, gain birth to 205 d, and gain 205 to 365 d) was compared with selection based on four traits (the above three plus ultrasound fat depth) and selection based on five traits (the above four plus feed:gain ratio). Five scenarios were used that allowed variation in proportion of candidates selected for breeding, number of progeny per selected bull, and proportion of profit returned to the nucleus herd. General conclusions based on the examples were 1) multistage selection reduced aggregate economic gain relative to that attained by single-stage selection, 2) inclusion of feed conversion in the index of traits resulted in reduced profit and aggregate economic gain, 3) measurement of feed conversion could be justified when selected bulls produced a large number of progeny, and 4) three-trait selection produced greater profit in all five scenarios than did four- or five-trait selection. Use of the selection updating program described here provides a new source of information that can be used in developing economically sound performance testing and selection programs.
Aging↗