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PubMed1995

Fetal-adult phenotype transition, in terms of the serum dependency and growth factor requirements, of human skin fibroblast migration.

Since the migration of human fetal skin fibroblasts into a denuded area of a cell monolayer has been demonstrated to be serum-independent (fetal phenotype), whereas that of adult-donor skin fibroblasts is serum-dependent (adult phenotype), a study was carried out to determine at which life stage the fetal-adult phenotype transition, in terms of serum dependency of human skin fibroblast migration, occurs. The results demonstrated that this phenotype transition occurred before birth, and, therefore, the fetal skin fibroblast phenotype differed from those of infant-, child-, adult-, and elderly-donor skin fibroblasts. But, the fetal-, child-, and adult-donor skin fibroblast phenotypes did not change during in vitro aging. On the other hand, the growth factor requirement for human skin fibroblast migration changed similarly to the serum dependency for fibroblast migration: the signal for fibroblast migration changed from basic fibroblast growth factor for the fetal phenotype to platelet-derived growth factor for the adult phenotype.

Adult↗
PubMed1988

Genetics of the quantitative Lp(a) lipoprotein trait. I. Relation of LP(a) glycoprotein phenotypes to Lp(a) lipoprotein concentrations in plasma.

The Lp(a) lipoprotein is a complex particle composed of a low density lipoprotein (LDL)-like lipoprotein and the disulfide bonded Lp(a) glycoprotein. The complex represents a quantitative genetic trait. SDS gel electrophoresis under reducing conditions of sera followed by immunoblotting with affinity-purified polyclonal anti-Lp(a) demonstrated inter- and intra-individual size heterogeneity of the glycoprotein with apparent Mr in the range 400-700kDa. According to their relative mobilities compared to apo B-100 the Lp(a) patterns were categorized into phenotypes F, B, S1, S2, S3 und S4 and into the respective double-band phenotypes. This size heterogeneity seems to be controlled by multiple alleles designated LpF, LpB, LpS1, LpS2, LpS3, LpS4 and a null allele (LpO) at a single locus. Phenotype frequencies observed in 441 unrelated subjects were in good agreement with those expected from the genetic hypothesis. Comparison of Lp(a) lipoprotein concentrations in the different phenotypes revealed a highly significant association of phenotypes B, S1 and S2 with high, and phenotypes S3 und S4 with intermediate Lp(a) concentrations. A third mode is represented by the null phenotype were no Lp(a) band is detected upon immunoblotting and Lp(a) lipoprotein is low or absent. We conclude that the same gene locus is involved in determining Lp(a) glycoprotein phenotype and Lp(a) lipoprotein concentrations in plasma. This major gene seems to be the Lp(a) glycoprotein structural gene locus.

Alleles↗
PubMed1988

Variation in adhesion and cell surface hydrophobicity in Candida albicans white and opaque phenotypes.

A previous study had established that a select group of pathogenic isolates of Candida albicans was capable of switching heritably, reversibly and at a high frequency (10(-2) to 10(-3)) between two phenotypes ('white' or 'opaque') readily distinguishable by the size, shape, and color of colonies formed on agar at 25 degrees C. This paper describes experiments designed to determine the ability of these two phenotypes to attach to buccal epithelial cells (BECs) and plastic, and to compare the cell surface hydrophobicities of white and opaque phenotypes from three clinical isolates. 'White cells' were found to be significantly more adhesive to BECs, and a strong correlation was also found between phenotype adhesiveness and the percentage of BECs to which C. albicans had attached. The percentage of BECs with one or more attached C. albicans was approximately 90% for the white phenotype and approximately 50% for the opaque phenotype. 'Opaque cells', in contrast, were twice as hydrophobic as white cells, and the percentage of opaque cells bound to BECs by coadhesion was also double that of white cells. The differences in adhesion to plastic between the two phenotypes were not statistically significant and there was no distinct trend to suggest which phenotype might be more adhesive to plastic. These results indicate that several factors are involved in the adhesion of C. albicans to plastic, and confirm the hypothesis that cell surface hydrophobicity is of minor importance in direct adhesion to epithelial cells but that it may contribute to indirect attachment to epithelial cells by promoting yeast coadhesion.(ABSTRACT TRUNCATED AT 250 WORDS)

Candida albicans↗
PubMed1994

Immunochemical and immunohistological expression of Lewis histo-blood group antigens in small intestine including individuals of the Le(a+b+) and Le(a-b-) nonsecretor phenotypes.

Histological samples and total non-acid glycosphingolipids were prepared from small intestine of human cadavers with the Le(a+b+) and Le(a-b-) nonsecretor phenotypes and contrasted with the more common Lewis phenotypes. Glycolipid fractions were analysed by thin-layer chromatography and tested for Lewis activity with monoclonal antibodies reactive to Lewis epitopes. Paraffin-embedded small intestine sections were also fluorescently immunostained with anti-Lewis antibodies. Unlike the common Lewis positive phenotypes, we were immunochemically able to demonstrate the copresence of large amounts of Lea and Leb glycolipids in the Le(a+b+) sample. In addition we demonstrated increased formation of extended Lewis structures in this phenotype. By immunohistochemistry Lea, Leb and type 1 precursor chain epitopes could be demonstrated in the brush border. These results show that the expression of the Le(a+b+) phenotype at the erythrocyte phenotyping level parallels the small intestinal expression of this phenotype, and the patterns of Lewis antigen expressions are unique to this phenotype. By immunohistochemistry and immunochemistry we also demonstrated the presence of trace amounts of Lewis active glycoconjugates in the small intestine of the Le(a-b-) nonsecretor and Le(a+b-) samples. In the Le(a-b-) nonsecretor Lea and Leb activity was absent and type 1 precursor was present in brush border, while Leb activity was immunohistologically demonstrated in the Golgi apparatus of the deep glands. Trace amounts of both Lea and Leb glycolipids were identified in this sample. In parallel trace Leb activity could also be detected in the glycolipids of the Le(a+b-) sample and could be immunohistologically demonstrated to be fully expressed in occasional cells in the deep glands of the small intestine, a pattern quite dissimilar to that of the Le(a-b-) nonsecretor.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1995

Characterization of aberrant phenotypes in acute myeloblastic leukemia.

The existence of leukemic-associated phenotypes has been suggested to be a valuable tool for the detection of minimal residual disease (MRD) in AML patients, as they would allow to distinguish leukemic blast cells from normal hematopoietic progenitors. The present study was designed to analyze in which proportion of AML patients the immunological detection of MRD is feasible, based on the presence of aberrant phenotypes that allow the distinction of leukemic from normal cells. For this purpose we have prospectively investigated the blast cells from 40 AML patients at diagnosis with a large panel of MoAb in double and triple staining combinations analyzed at flow cytometry, in order to detect aberrant phenotypes on blast cells (lineage infidelity, antigenic overexpression, and asynchronous antigenic expression, as well as aberrant light-scatter pattern). In the analysis of the 40 AML cases more than one blast cell subset, distinguished by its different antigenic expression, was detected in 85% of the patients: five different phenotypic blast cell subsets were observed in six cases, four in 13 patients, three subsets in three cases, and two in 12 patients; only six cases showed a homogeneous phenotypical blast cell population. Twenty-nine of the 40 AML cases analyzed (73%) showed the existence of at least one aberrant phenotype: in 15 cases the myeloid blast cells co-expressed lymphoid-associated antigens (CD2, CD5, CD7, and/or CD19)--lineage infidelity--; asynchronous antigen expression was detected in 25 patients (CD34+CD56+, CD34+CD11b+, CD34+CD14+, CD117+CD15+, CD33-CD13+, CD13-CD15+, HLADR + CD15 , HLADR-CD14+CD11b+ CD4+); seven cases displayed antigen overexpression (CD13, CD33, CD15, or CD14); and in 13 patients leukemic cells had an abnormal FSC/SSC distribution according to their phenotype. These results suggest that immunological methods for the detection of MRD based on the existence of aberrant phenotypes could be used in the majority of AML patients.

Antibodies, Monoclonal↗
PubMed1985

Phenotypic variations among enterotoxinogenic Escherichia coli from Swedish piglets with diarrhoea.

Escherichia coli strains causing diarrhoea in Swedish piglets were isolated; this investigation was made over a 20-year period, from 1964 to 1984. Many of the isolates belonged to O-groups 8, 141 and 149. These strains were separated into different phenotypes with the aid of a new method, "biochemical fingerprinting". This method has been especially designed to sort E. coli-isolates into various phenotypes based on a pattern of quantitatively measured biochemical reactions. It was found that most pathogenic isolates carrying O-antigen 8 belonged to the same phenotype. This phenotype was common in the 1960's, but later it disappeared from the population and was replaced by a wide variety of different phenotypes, most of them non-enterotoxinogenic, but still belonging to O-group 8. In O-group 141 one phenotype dominated in the 1960's, but in the 1970's a new phenotype appeared, which further increased in number in the 1980's. By contrast, in the O-group 149 practically all strains isolated during the 20-year period were found to carry the relevant virulence factors and belong to the same phenotype.

Animals↗
PubMed2005

Comparison of phenotypic and molecular distances to predict heterosis and F1 performance in Ethiopian mustard (Brassica carinata A. Braun).

Predicting heterosis and F1 performance from the parental generation could largely enhance the efficiency of breeding hybrid or synthetic cultivars. This study was undertaken to determine the relationship between parental distances estimated from phenotypic traits or molecular markers with heterosis, F1 performance and general combining ability (GCA) in Ethiopian mustard (Brassica carinata). Nine inbred lines representing seven different geographic regions of Ethiopia were crossed in half-diallel. The nine parents along with their 36 F1s were evaluated in a replicated field trail at three locations in Ethiopia. Distances among the parents were calculated from 14 phenotypic traits (Euclidean distance, ED) and 182 random amplified polymorphic DNA (RAPD) markers (Jaccard's distances, JD), and correlated with heterosis, F1 performance and GCA sum of parents (GCAsum). The correlation between phenotypic and molecular distances was low (r=0.34, P< or =0.05). Parents with low molecular distance also had low phenotypic distance, but parents with high molecular distance had either high, intermediate or low phenotypic distance. Phenotypic distance was highly significantly correlated with mid-parent heterosis (r=0.53), F1 performance (r=0.61) and GCA (r=0.79) for seed yield. Phenotypic distance was also positively correlated with (1) heterosis, F1 performance and GCA for plant height and seeds plant(-1), (2) heterosis for number of pods plant(-1), and (3) F1 performance for 1,000 seed weight. Molecular distance was correlated with GCAsum (r=0.36, P< or =0.05) but not significantly with heterosis and F1 performance for seed yield. For each parent a mean distance was calculated by averaging the distances to the eight other parents. Likewise, mean heterosis was estimated by averaging the heterosis obtained when each parent is crossed with the other eight. For seed yield, both mean ED and JD were significantly correlated with GCA (r=0.90, P< or =0.01 for ED and r=0.68, P< or =0.05 for JD) and mean heterosis (r=0.79, P< or =0.05 for ED and r=0.77, P< or =0.05 for JD). In conclusion, parental distances estimated from phenotypic traits better predicted heterosis, F1 performance and GCA than distances estimated from RAPD markers.

Brassica↗
PubMed2005

Genetic and environmental correlations between bone phenotypes and anthropometric indices in Chinese.

Height, weight, bone mineral density (BMD), and bone size are all influenced by genetic and environmental factors as well as interactions between them. Height and weight are often used in population studies to adjust the bone phenotypes. However, it is still unknown what proportion of genetic and environmental variability is shared between these anthropometric characteristics and the bone phenotypes. The genetic and environmental correlations between the bone phenotypes and anthropometric indices in Chinese subjects were studied by bivariate quantitative genetic analysis on a sample of 931 healthy subjects from 292 Chinese nuclear families aged from 19 to 79 years. BMD and bone size at the lumbar spine (L1-L4) and the hip of all subjects were measured by dual-energy X-ray absorptiometry. We found significant genetic correlations between weight and spine BMD, hip BMD, spine bone size and hip bone size, which were 0.50 (P<0.01), 0.45 (P<0.01), 0.36 (P=0.02), and 0.38 (P<0.01), respectively. Likewise, significant genetic correlations between height and spine BMD, spine bone size, and hip bone size were 0.30 (P=0.02), 0.54 (P<0.01), and 0.58 (P<0.01), respectively. The environmental correlations were found to be significant only between height and spine bone size (P<0.001) and weight and hip BMD (P=0.02). These results suggest the probability that the same genetic and environmental factors contribute to these different phenotypes. Moreover, when a candidate gene or genomic region is responsible for the variation of both bone phenotypes and anthropometric indices, its true genetic effect on the bone phenotypes may be lost after one has adjusted the phenotypic values with weight and height as random environmental factors. It may have implications for population studies of candidate genes that underlie the complex bone phenotypes and for the development of strategies for therapeutic application.

Absorptiometry, Photon↗
PubMed2000

Bone sialoprotein (BSP) is a crucial factor for the expression of osteoblastic phenotypes of bone marrow cells cultured on type I collagen matrix.

In this study, we demonstrated that type I collagen matrix induced the expression of osteoblastic phenotypes of bone marrow cells, and that antibone sialoprotein (BSP) monoclonal antibody suppressed the expression of these phenotypes. On the other hand, BSP accelerated the expression of osteoblastic phenotypes of bone marrow cells. The adherent bone marrow cells were harvested from rat femur and cultured on type I collagen matrix gels in medium containing 15% fetal calf serum, neither beta-glycerophosphate nor glucocorticoid. Cells showed osteoblastic phenotypes (high alkaline phosphatase activity, osteocalcin synthesis, and responsiveness against parathyroid hormone) on collagen matrix gels at week 3 after the inoculation, and simultaneously, BSP was detected in the conditioned medium by Western blotting using an anti-BSP monoclonal antibody. However, cells in the conventional culture dishes did not show osteoblastic phenotypes during the experimental period. To investigate the physiological function of BSP in osteoblastic differentiation, bone marrow cells were cultured on collagen matrix with an anti-BSP monoclonal antibody for 3 weeks. This treatment suppressed the expression of the osteoblastic phenotypes, and the effect of the antibody was abolished by the addition of bovine bone BSP. Furthermore, bovine bone BSP stimulated the expression of osteoblastic phenotypes of bone marrow cells. Our results indicate that BSP plays a crucial role in the expression of osteoblastic phenotypes of bone marrow cells.

Animals↗
PubMed1998

Low glutathione pools in the original pso3 mutant of Saccharomyces cerevisiae are responsible for its pleiotropic sensitivity phenotype.

The original pso3-1 mutant isolate of the yeast Saccharomyces cerevisiae exhibits a pleiotropic mutagen-sensitivity phenotype that includes sensitivity to UVA-activated 3-carbethoxypsoralen, to UVC-light, to mono- and bi-functional nitrogen mustard, to paraquat, and to cadmium; on the other hand, it shows hyper-resistance (HYR) to nitrosoguanidine when compared to established wild-type strains. Also, the original pso3-1 mutant exhibits a low UVC-induced mutability and mitotic gene conversion and a high rate of spontaneous and UVC-induced petite mutations. Since the HYR to the nitrosoguanidine (MNNG) phenotype resembles that of low glutathione-containing yeast cells, the original pso3-1 mutant was crossed to a gsh1 knock-out mutant that lacks the enzyme for the first step in glutathione biosynthesis and the resulting diploid was tested for complementation. While there was none for HYR to nitrosoguanidine, and other low glutathione-related phenotypes, some other phenotypic characteristics of pso3-1, e.g. UVC sensitivity and UVC-induced mutability were restored to a wild-type level. Tetrad analysis of a diploid derived from a cross of the original haploid pso3-1 isolate with a repair-proficient, normal glutathione-containing, PSO3 GSH1 wild-type led to the separation of a leaky gsh1 mutation phenotype from that of the repair-deficient pso3-1 phenotype. Linkage studies by tetrad and random spore analyses indicated no linkage of the two genes. This shows that the low glutathione content in the original pso3-1 isolate is due to a second, additional, mutation in the GSH1 locus and is unrelated to the pso3-1 mutation. Thus, the original pso3-1 isolate is a pso3-1 gsh1 double mutant with most of the particular characteristics of the pleiotropic sensitivity phenotype contributed by either the pso3-1 or the gsh1-leaky mutant allele. The expression of a few phenotypic characteristics of pso3, however, were most pronounced in pso3-1 mutants with a low glutathione pool.

Fungal Proteins↗
PubMed1996

Identification of NF2 germ-line mutations and comparison with neurofibromatosis 2 phenotypes.

Neurofibromatosis 2 (NF2) is an autosomal inherited disorder that predisposes carriers to nervous system tumors. To examine genotype-phenotype correlations in NF2, we performed mutation analyses and gadolinium-enhanced magnetic resonance imaging of the head and full spine in 59 unrelated NF2 patients. In patients with vestibular schwannomas (VSs) or identified NF2 mutations, the mild phenotype was defined as < 2 other intracranial tumors and < or = 4 spinal tumors, and the severe phenotype as either > or = 2 other intracranial tumors of > 4 spinal tumors. Nineteen mutations were found in 20 (34%) of the patients and were distributed in 12 of the 17 exons of the NF2 gene, including intron-exon boundaries. Seven mutations were frameshift, six were nonsense, four were splice site, two were missense, and one was a 3-bp in frame deletion. The nonsense mutations included one codon 57 and two codon 262 C-->T transition in CpG dinucleotides. The frameshift and nonsense NF2 mutations occurred primarily in patients with severe phenotypes. The two missense mutations occurred in patients with mild phenotypes, and three of the four splice site mutations occurred in families with both mild and severe phenotypes. Truncating NF2 mutations are usually associated with severe phenotypes, but the association of some mutations with mild and severe phenotypes indicates that NF2 expression is influenced by stochastic, epigenetic, or environmental factors.

DNA Mutational Analysis↗
PubMed1998

The relationship between apolipoprotein E and serum oxidation-related variables is apolipoprotein E phenotype dependent.

To examine the relationship between apolipoprotein E and serum oxidation status, we assayed apolipoprotein E level, apolipoprotein E phenotype, and levels of lipid peroxides and transition metal ions and their binding proteins in sera from apparently healthy individuals. The study group included 129 women aged 22-63 years and 53 men aged 22-56 years. Among subjects with apolipoprotein E 4/3 phenotype, lipid peroxide levels were higher compared with E 3/2 phenotype (786 +/- 182 nmol/l vs. 659 +/- 174 nmol/l, P = 0.015), and ceruloplasmin levels were slightly higher compared with apolipoprotein E 3/3 phenotype (0.28 +/- 0.08 mg/l vs. 0.26 +/- 0.06 mg/l, P = 0.035). In the study group as a whole, there were significant associations between serum apolipoprotein E level, and serum levels of ceruloplasmin (r = 0.266, P < 0.001) and ferritin (r = 0.2, P < 0.007). Among subjects with apolipoprotein E 4/3 phenotype, there was a significant association between serum apolipoprotein E and lipid peroxide levels (r = 0.470, P < 0.01), which was not apparent among subjects with E 3/3 or E 3/2 phenotypes. In multivariate analysis, apolipoprotein E phenotype was a small but significant independent contributor to variation in serum lipid peroxide levels. These data suggest that there may be heterogeneity among apolipoprotein E phenotypes in their relationships with serum lipid oxidation status.

Adult↗
PubMed2005

Microsatellite instability is linked to loss of hMLH1 expression in advanced gastric cancers: lack of a relationship with the histological type and phenotype.

BACKGROUND: It has been suggested that the prevalence of microsatellite instability (MSI) is high in intramucosal differentiated gastric cancers with gastric foveolar phenotypic expression, and that these tumors are prone to lose their glandular structures and progress to undifferentiated-type lesions. To test this hypothesis, we examined the relationships among human MutL homologue 1 (hMLH1) expression (which is linked to MSI), the phenotype, and the histological type in patients with advanced and intramucosal gastric cancer. METHODS: We analyzed hMLH1 expression by immunohistochemistry in 70 advanced and 30 intramucosal gastric cancers with histological evaluation and assessment of the phenotype, and Cdx2 expression determined by immunohistochemistry. The MSI status was also examined in 20 cases. RESULTS: Thirteen (18.6%) advanced and 5 (16.7%) intramucosal gastric cancers were judged to be hMLH1-negative. In the advanced cases, no association was observed between the histological type and the phenotype and loss of hMLH1. In the intramucosal cases, MUC5AC expression was observed in all 5 hMLH1-negative differentiated-type cancers. However, no hMLH1-negative lesions were detected in the intramucosal undifferentiated cancers (0/14; P < 0.05 vs differentiated types). In the advanced cases, MSI-positivity (MSI +) and loss of hMLH1 expression did correlate (P < 0.0001), while no association was observed between MSI +, histological type, and phenotype. CONCLUSION: Our data support the hypothesis that, phenotypically, some MSI-positive differentiated gastric cancers of gastric foveolar phenotypic expression may easily change, from gastric to intestinal phenotypic expression, also changing, histologically, from differentiated to undifferentiated type with progression.

Adaptor Proteins, Signal Transducing↗
PubMed2006

Caveolin-1 expression is associated with a basal-like phenotype in sporadic and hereditary breast cancer.

The role of caveolin 1 (CAV1), a structural component of caveolae in breast cancer is controversial, although most studies suggest that it functions as a tumor-suppressor gene. In addition, some studies have identified CAV1 as a marker of myoepithelial cells. Since myoepithelial markers are frequently expressed in breast carcinomas with a basal-like phenotype, which are frequently occurring tumors in women with BRCA1 germline mutations, we evaluated whether CAV1 was associated with a basal-like phenotype in 509 sporadic and 47 hereditary BRCA1-/BRCA2-associated carcinomas. Immunohistochemistry was performed on tissue microarrays and cases were classified as having a basal-like-phenotype if they were estrogen-receptor- and HER2-negative but cytokeratin 5/6- and/or epidermal growth factor receptor-positive. In sporadic carcinomas, CAV1 expression was found in 21 out of 496 valuable cases (4.2%). A basal-like-phenotype was found in 53 out of 498 (10.6%) cases. A strong association was found between CAV1 expression and a basal-like-phenotype, since 52% of tumors that expressed CAV1 had this phenotype, compared with only 9% of CAV1-negative carcinomas (p<0.001). CAV1 was expressed in six (12.8%) familial cases, five of which had a basal-like-phenotype (p = 0.009). Moreover, these six CAV1-positive cases were BRCA1 tumors. The difference in the frequency of CAV1 expression between BRCA1- and BRCA2-associated tumors was statistically significant (p = 0.024). In conclusion, this study reports for the first time CAV1 expression in BRCA1 and BRCA2 hereditary breast cancer and identifies CAV1 as a marker associated with a basal-like-phenotype in both hereditary and sporadic breast cancer.

Breast Neoplasms↗
PubMed1988

Study on the possible factors influencing the expression of H-2 restriction specificity and Ir phenotype of antigen-specific proliferative T cells with various types of radiation chimeras.

To better understand the factors described previously as influencing the manifestation of H-2 restriction specificity and Ir phenotype of T cells from radiation bone marrow chimeras, we also examined H-2 restriction specificity (Ir phenotype) of antigen (DNP-OVA, (T, G)-A-L, (H, G)-A-L)-specific proliferative T cells generated in various types of H-2 incompatible radiation chimeras prepared under our specific-pathogen-free (SPF) condition. The results indicated the following: (a) T cells generated in F1----parent bone marrow chimeras preferentially manifested host-type H-2 restriction specificity and Ir phenotype, regardless of the radiation dose (8.70 vs 11.59 Gy); (b) T cells recovered from twice-reconstituted F1----(PA----PB) chimeras manifested primary host (PB)-type Ir phenotype; (c) T cells which were recovered from (B10.Thy-1.1 X B10.BR.Thy-1.1)F1----parent (Thy-1.2) bone marrow chimeras and treated with anti-Thy-1.2 plus complement to deplete host-derived T cells still manifested preferentially the restriction specificity for host-type H-2; (d) PA-derived T cells which had differentiated in a fully allogeneic host (PB) environment of (PA + PB)----PB chimeras manifested fully allogeneic host-type Ir phenotype; (e) T cells from F1----parent chimeras that were prepared with 13-day fetal liver cells also manifested host H-2-restricted Ir phenotype; and (f) host preference for Ir phenotype of antigen-specific proliferative T cells was observed even in the case of F1----parent bone marrow chimeras reconstituted with "intact" bone marrow cells. The data suggest that thymic APCs, surviving host T cells or the source of stem cells (adult bone marrow vs 13-day fetal liver), do not necessarily play a significant role in the manifestation of H-2 restriction specificity and Ir phenotype of T cells generated in H-2 incompatible radiation chimeras.

Animals↗
PubMed1991

Determination of apolipoprotein E phenotypes from stored or postmortem serum samples.

In order to assess the validity of Apo E phenotyping from stored specimens, phenotypes determined from fresh serum samples were compared with those from stored (8 years at -20 degrees C) samples from the same individuals (n = 42). The effect of early postmortem period on Apo E phenotype determinability was studied by taking four duplicate blood samples from eight cadavers 2, 6, 12, and 24 h after death. Apo E phenotyping was performed directly from serum by isoelectric focusing and immunoblotting. From the cadavers, the same Apo E phenotypes were obtained 2, 6, 12, and 24 h after death. After eight years' storage five out of ten Apo E4/4 phenotypes were falsely recorded as Apo E4/3 and one out of six Apo E4/3, one out of 12 Apo E4/2 were falsely interpreted as Apo E3/3. Phenotypes Apo E2/2 (n = 2), Apo E3/2 (n = 10), and Apo E3/3 (n = 2) were correctly assessed after 8 years of storage. In the total material, 17% (7/42) of Apo E phenotypes were incorrectly assessed after the storage.

Apolipoproteins E↗
PubMed1988

Influence of apolipoprotein E polymorphism on plasma lipid and apolipoprotein levels, and clinical characteristics of type III hyperlipoproteinemia due to apolipoprotein E phenotype E2/2 in Japan.

Apolipoprotein (apo) E phenotype was examined in 188 healthy subjects and in 447 patients seen between 1984 and 1986. The frequency of the apo E2, 3, and 4 genes in the clinically healthy subjects was 0.035 +/- 0.0288, 0.872 +/- 0.0310, and 0.093 +/- 0.0152, respectively. The frequency of the apo E3 gene was higher and that of the apo E genes 2 and 4 lower than that reported in western countries. Clinical features and apo E phenotype are presented from the 5 patients with type III hyperlipoproteinemia (HLP) due to apo E phenotype E2/2 (E2-III); all patients in E2-III were post-menopausal women. In contrast to the clinical characteristics so far reported, no notable findings of atherosclerosis, such as coronary angiographic findings or xanthoma, were evident in any of these 5 patients. Glucose intolerance was seen in 4 of them. Four patients were normolipidemic with apo E phenotype E2/2 (E2-N). In addition, plasma lipid and apolipoprotein concentrations were determined in patients with different apo E phenotypes. Plasma total cholesterol (TC) and apo B levels were elevated in the order of E2-N, E2/3, E2/4, E3/3, E3/4 and E4/4 except for E2-III. The plasma apo E level was highest in E2-III but was not significantly different from other phenotypes. The apo B/apo E and apo C-III/apo E ratios were significantly lower in E2/2 than in other phenotypes. The TC/apo B ratio was significantly higher in E2/2 than in other phenotypes.

Adult↗
PubMed1992

Phenotypic diversity and prognosis of adult T-cell leukemia.

We examined phenotypically 107 patients with adult T-cell leukemia (ATL), using a panel of monoclonal antibodies, in order to clarify the occurrence of aberrant phenotypes, and to determine the correlation between phenotypic diversity and prognosis. The incidence of the typical (CD4+.CD8-) phenotype, the double-negative (CD4-.CD8-), the double-positive (CD4+.CD8+), and the CD8-positive (CD4-.CD8+) phenotypes was 81%, 7%, 7%, and 4%, respectively. The median survival time (MST) for all patients was 10.0 months with 17% survival at 2 years. The patients with typical phenotypes had a 10.2 month MST with 20% survival at 2 years, significantly better than the patients with the unusual phenotypes whose MST were 4.9, 7.8, and 2.6 months, respectively, for the double-negative, double-positive, and CD8-positive phenotypes. Lack of antigens reactive with CD2, CD3, CD5, and WT31 monoclonal antibody panels was one factor in bad prognosis, but the presence of CD4 and CD8 antigen abnormalities was much more significant.

Antigens, CD↗