Estimation of genetic parameter for feed efficiency and resilience traits in three pig breeds.

Recently, automatic feeders have become popular for collecting daily feed intake data in the pig industry, making it possible to evaluate genetic effects on feed efficiency and resilience traits, expressed as day-to-day fluctuations in feeding records. This study aimed to understand the influence of genetic factors on feed efficiency traits, including residual intake and BW gain (RIG), and resilience traits, as well as to compare the differences in genetic parameter estimates among three purebred pig breeds. A total of 6 103 pigs from three breeds (Large White: 1 193 pigs, Landrace: 3 010 pigs, and Duroc: 1 900 pigs) were raised in a specific pathogen-free environment. The growth and feed intake records during the testing period were obtained using automatic feeders, and the average daily gain (ADG) and average feed intake (AFI) were calculated. Feed conversion ratio (FCR), residual feed intake (RFI), residual gain, and RIG were calculated as feed efficiency traits, and the log-transformed variance of deviation for the daily feed intake (LnVar_FI), daily occupation time (LnVar_OC), and the daily number of visits to the feeder (LnVar_VT) was calculated as resilience traits. After estimating the genetic parameters for each breed, a meta-analysis was performed to obtain the weighted mean of heritability estimates (hm2) and genetic correlation estimates (GCm) for the three breeds. The hm2 were moderate and ranged from 0.31 to 0.39 for feed efficiency traits and 0.31 to 0.40 for resilience traits, and there were no significant differences in heritability estimates among the three breeds except for AFI, RFI, and RIG. For feed efficiency traits, the FCR and RIG showed favourably moderate GCm with AFI (0.29 and -0.33, respectively) and ADG (-0.39 and 0.31, respectively). For resilience traits, the LnVar_FI and LnVar_VT showed favourably low to moderate GCm with FCR (0.33 and 0.28, respectively) and RIG (-0.37 and 0.28, respectively), and there were no genetic relationships of LnVar_OC with FCR and RIG (the absolute value of GCm was 0.01). There was no significant difference in the genetic correlation estimates among the three breeds for feed efficiency and resilience traits. Our results suggest that feed efficiency and resilience traits were heritable, and resilience traits showed favourable or no genetic correlation with feed efficiency traits. In addition, the influence of genetic factors on feed efficiency and resilience traits could be the same among breeds.

Fusion of visual and infrared thermography images for advanced assessment in non-destructive testing.

For better evaluation of infrared measurements in non-destructive testing, especially for objects with complex geometry or small dimensions, it is beneficial to combine with the same viewing angle an image of a camera in the visible range with the image of an infrared camera. In the hybrid camera developed by us, a beam splitter is used which combines the visible and the infrared wavelength regions under the same viewing angle to form a hybrid image. The applications of this new technique range from the localization and the verification of false indications in non-destructive testing applications to the retrieval of 3D surface information with a hybrid picture as texture with defect indications and the filtering of laser markings displayed in the IR image to area and process monitoring.

Comparison between in vitro qualities of platelets washed with commercially available additive solutions and those washed with M-sol.

BACKGROUND AND OBJECTIVES: We previously developed a novel additive solution (M-sol) with a high ability to preserve the in vitro qualities of platelets (PLTs) in washed PLTs Here, we compared the ability of M-sol with that of commercially available additive solutions (ASs) to preserve the in vitro qualities (pH, mean PLT volume, %disc, P-selectin, %hypotonic shock response and aggregation) of PLTs at a low plasma concentration. MATERIALS AND METHODS: The platelet concentrate was divided into two equal aliquots (control group and test group). After centrifugation of both groups and removal of as much supernatant as possible, the pellet of the control group was resuspended in M-sol and those of the test group were resuspended in other ASs, and subsequently stored in polyolefin bags with agitating at 20-24 degrees C. RESULTS: Compared with those stored in M-sol, the qualities of PLTs stored in PAS-B (alternative name; PAS-II or T-sol), PAS- C (alternative name; PAS-III or Intersol) or Plasma Lyte were degraded as early as 24 h after washing. The qualities of PLTs stored in PAS-D (alternative name; Composol PS) or PAS-E (alternative name; PAS-IIIM or SSP+) were comparable to that of those stored in M-sol 24 h after washing; however, the qualities had deteriorated 72 h after washing. CONCLUSIONS: At a low plasma concentration (5% or less), the M-sol showed a higher ability to preserve PLTs than the five ASs studied here. Although PAS-D and PAS-E are available as an AS for short-term storage of washed PLTs, M-sol is thought to be preferable for longer storage.

Clinical significance of chromosome abnormalities in childhood acute lymphoblastic leukemia in Japan.

Of 240 Japanese children with acute lymphoblastic leukemia (ALL) treated between 1983 and 1990, 75 (31%) had normal diploidy, 47 (20%) hyperdiploidy with more than 50 chromosomes, 18 (8%) hyperdiploidy with 47-50 chromosomes, 77 (32%) pseudodiploidy, 22 (9%) hypodiploidy and one hypotetraploidy in the leukemic cells. Event-free survival (EFS) +/- standard error (SE) at 4 years was 74 +/- 7% in patients with hyperdiploidy > 50, 68 +/- 6% in those with normal diploidy, 55 +/- 13% in those with hyperdiploidy 47-50, 54 +/- 11% in those with hypodiploidy, and 22 +/- 5% in those with pseudodiploidy (log-rank, p < 0.0001). Seventy-four patients with translocation and 166 patients without translocation had EFS +/- SE of 26 +/- 6% and 64 +/- 4%, respectively, at 4 years (p < 0.0001). The overall prognosis of our patients was comparable to that of the patients mainly treated in the late 1970s and reported by the Sixth International Workshop on Chromosomes in Leukemia, but was much poorer than that of the patients more recently treated and reported from some American institutions. These findings may possibly reflect less appropriate chemotherapy having been applied to Japanese children with ALL.

There may be two tumor suppressor genes on chromosome arm 1p closely associated with biologically distinct subtypes of neuroblastoma.

We studied loss of heterozygosity (LOH) on chromosome arm 1p in 108 neuroblastomas using 14 polymorphic DNA markers. One-hundred and four tumors with one or more informative loci; 21 (20%) of the 104 tumors showed LOH on 1p, and were classified into three groups on the basis of interstitial or terminal allelic loss, and presence or absence of LOH on 1p. Seven of the 21 tumors showed an interstitial deletion which encompassed a small region in 1p36 (group A), and the other 14 showed a terminal deletion which encompassed the region from 1pter to 1p32 (group B). Eighty-three tumors without LOH on 1p were classified as group C. The group A patients were mostly less than 12 months of age (6/7), were frequently found by a mass screening program for infants (5/7), had a tumor of non-adrenal origin, and rarely progressed to stage IV (1/7). Most group B patients were 12 months or older (11/14), were found clinically (11/14), had tumors of adrenal origin, and progressed to stage IV (10/14). Analysis of biologic characteristics in group C tumors suggested that they may comprise group A and B tumors. While all group A tumors were in the triploid range (3n) (4/4), most group B tumors were diploid (2n) or tetraploid (4n) (7/10). MYCN amplification was found in 8 group B tumors, but in none of group A tumors. Event-free survivals of groups A, B, and C patients at 3 years were 86, 49, and 74%, respectively (P = 0.0287). These findings suggest that there may be two tumor suppressor genes on 1p which are closely associated with two biologically distinct subtypes of neuroblastoma.

Deletion of WT1 and WIT1 genes and loss of heterozygosity on chromosome 11p in Wilms tumors in Japan.

Six of 39 sporadic Wilms tumors had gross homozygous or hemizygous WT1 and WIT1 deletions. Two Wilms tumor-aniridia-genitourinary abnormalities-mental retardation syndrome patients had total hemizygous WT1 and WIT1 deletions in both constitutional and nonsporadic type tumor cells. Four of the 8 tumors with WT1 and WIT1 deletions showed loss of constitutional heterozygosity (LOH) for markers limited to the 11p13 region. Seven of 19 Wilms tumors with neither WT1 nor WIT1 deletions also had LOH on 11p; 4 in the 11p15-11p13 region, one in the 11p15 and possibly also 11p13 regions, and two solely in the 11p15 region. Thus, 15 of the 41 Wilms tumors (37%) had WT1 and WIT1 deletions or LOH on 11p, and only 2 of the 27 tumors whose nonneoplastic normal tissues were available for study showed LOH limited to the 11p15 region. None of the 7 non-Wilms childhood renal tumors showed WT1 or WIT1 deletions, or LOH on 11p. These data suggest that Japanese Wilms tumors may be characterized by a higher incidence of the gross WT1 deletion and a lower incidence of LOH limited to the 11p15 region than the Caucasian counterparts. These molecular-genetic features may be contributing to the lower incidence of Wilms tumors in Japanese children than in Caucasian ones.

The 8;21 chromosome translocation in acute myeloid leukemia is always detectable by molecular analysis using AML1.

The AML1 gene was rearranged in leukemic cells with t(8;21)(q22;q22) or its variant, complex t(8;V;21) translocations from 33 acute myeloid leukemia (AML) patients. The AML1 rearrangement was also detected in three AML patients without t(8;21); two had a normal diploid karyotype, and one had a karyotype of 45,X, - X. The AML1 rearrangement in the t(8;21) breakpoint cluster region was not detected in leukemic cells with cytogenetic abnormalities other than t(8;21), or with normal diploidy obtained from 23 AML patients. Because leukemic cells of the five patients with complex t(8;V;21) translocations had a der(8)t(8;21) chromosome with a break in band 8q22 in common, the juxtaposition of the 5' side of AML1 to a predicted counterpart gene located in the breakpoint region of 8q22 may be an essential step in the leukemogenesis of AML with t(8;21). Our findings show that the 8;21 translocation, its variants, and the masked t(8;21) may all be detectable by the Southern hybridization method using the AML1 probes.

Correlation of chromosome abnormalities with histological and clinical features in Wilms' and other childhood renal tumors.

Chromosomes and histology were successfully studied in 33 childhood renal tumors. Thirty-one tumors were classified as one of four subtypes of Wilms' tumor. Of 24 typical Wilms' tumors, 12 had hyperdiploidy with nonrandom trisomies, mostly including +6 and/or +12. Three typical Wilms' tumors with an 11p13 deletion or a pericentric inversion with a break in 11p13 were not associated with aniridia. Two other typical Wilms' tumors with the 11p13 deletion and one fetal rhabdomyomatous nephroblastoma with an 11p13 translocation were associated with aniridia. Two cystic partially differentiated nephroblastomas showed hyperdiploidy with +12. Of four clear cell sarcomas of the kidney, three had normal diploidy and the other had a 2;22 translocation. Two congenital mesoblastic nephromas had hyperdiploid karyotype with trisomy 11, which was never seen in the 31 Wilms' tumors. Our findings and a review of data on 102 reported Wilms' tumors revealed 11p13 abnormalities in 24 tumors, 11p15 abnormalities in five tumors, and partial deletions of 1p, 7p, 11q, 12q, 16q, or 17p or monosomy of No. 21 or No. 22 each in four or more tumors. These findings suggest that increased copy number of genes on the nonrandom trisomic chromosomes might contribute to the genesis of many Wilm's tumors and that deletion of various tumor suppressor genes other than a Wilms' tumor gene, WT1 in 11p13, might also play a critical role in the development of some tumors.

Establishment and characterization of a small round cell sarcoma cell line, SCCH-196, with t(11;22)(q24;q12).

A cell line designated SCCH-196 was established from an extraskeletal small round cell sarcoma developed in a 16-year-old Japanese girl. The cells grew as a monolayer, and have been continuously propagated by serial subcultures during the past 26 months. Cells from the primary tumor and those from the SCCH-196 cell line at passage 10 both showed the same karyotype, 51,XX, +8, +20, +21, t(11;22)(q24;q12), +i(1q), +i(1q). Histologically the primary tumor was difficult to classify as either Ewing's sarcoma (ES) or peripheral neuroepithelioma (NE). Neuron-specific enolase-positive cells in the primary tumor and the occurrence in the upper extremity were in favor of NE, while positive reaction of SCCH-196 cells to an ES-specific monoclonal antibody 5C11 suggested a diagnosis of ES. The SCCH-196 cell line may be useful for basic studies on differentiation of neuroectodermal tumors, and for future cloning of still unidentified genes which may be located at the breakpoints of the 11;22 translocation.

Effects of nisoldipine on sympathetic activity, the renin-angiotensin-aldosterone system, and water-sodium-calcium metabolism in patients with essential hypertension.

The effects of nisoldipine (Bay k 5552), a long-acting Ca2+ antagonist, on sympathetic activity, the renin-angiotensin-aldosterone (RAA) system, the renal metabolism of water and electrolytes, and parathyroid hormone (PTH) were investigated following single dose and 4 weeks administration. The administration of nisoldipine led to the following results: 1. Mean arterial pressure (MAP) fell and heart rate slightly increased after the first dose, but did not show any appreciable change over 4 weeks treatment. 2. The urinary excretion of sodium, fractional excretion of sodium, plasma renin activity (PRA) and plasma noradrenaline concentration (pNA) were elevated initially, but the trend was to return to pretreatment levels after 4 weeks treatment. 3. A decrease in plasma aldosterone concentration was observed from the commencement of treatment. 4. Urinary excretion of calcium, fractional excretion of calcium and 24-h urine volume (UV) increased from the beginning, and maintained elevated levels after 4 weeks treatment. A decrease in body weight was also observed. 5. Plasma Ca2+ concentration did not change significantly throughout the treatment period, but PTH was decreased significantly both after 1 week and 4 weeks. 6. The percent changes in MAP (% delta MAP) after 4 weeks showed a significant negative correlation with pretreatment levels of MAP and the increment of UV (delta UV), as well as a positive correlation with pretreatment PRA or pNA levels. These findings suggest that in addition to its direct vasodilative effect, suppression of sympathetic activity and the renin-angiotensin-aldosterone system, reduction in body fluid and sodium, and a decrease in PTH and the related calciuresis may contribute to the hypotensive mechanism of nisoldipine.

Chromosome translocations involving band 7q35 or 7p15 in childhood T-cell leukemia/lymphoma.

In a chromosome study in childhood T-cell leukemia/lymphoma, we found t(7;11)(q35;p13) in 2 patients, t(7;14) (q35;q11) in one patient, and t(7;14)(p15;q32) in 1 patient. Southern blotting and in situ chromosomal hybridization studies in one patient with the t(7;11) demonstrated that both alleles of the T-cell antigen receptor beta-subunit gene (TCRB) were rearranged, and that one TCRB allele had relocated from 7q35 to the fusion point in band p13 of the involved chromosome 11 (11p-). These findings suggest that juxtaposition of TCRB with the putative oncogene tcl-2 located in band 11p13 may be a critical step toward development of this T-cell leukemia/lymphoma. In the other two translocations, all breakpoints were sites for lymphocyte function genes, ie, 7q35 for TCRB, 14q11 for T-cell antigen receptor alpha-subunit gene (TCRA), 7p15 for T-cell antigen receptor alpha-subunit gene (TCRG), and 14q32 for immunoglobulin heavy-chain gene (IGH). Thus, the findings in these cases allow us to expand the above hypothesis and propose that the juxtaposition of TCRB or TCRG with tcl-2, TCRA, or IGH through chromosomal translocation may activate a mechanism for the genesis of T-cell leukemia/lymphoma with these chromosome translocations.

Human c-erbB-2 remains on chromosome 17 in band q21 in the 15;17 translocation associated with acute promyelocytic leukemia.

Using the human c-erbB-2 cDNA as a probe, we applied in situ hybridization techniques to acute promyelocytic leukemia cells with a 15;17 chromosome translocation, t(15;17)(q;22;q21), and were able to localize the c-erbB-2 gene on chromosome 17 to band q12 or q21 and on the proximal side of the breakpoint in the translocation. From this finding and previous observations by others, we presume that the gene and the breakpoint are both in band q21.1 of chromosome 17. We suggest possible involvement of the c-erbB-2 gene in the development of the t(15;17)-associated acute promyelocytic leukemia.