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PubMed1999

Comparison of horse chromosome 3 with donkey and human chromosomes by cross-species painting and heterologous FISH mapping.

The melanocortin 1 receptor (MC1R), mast/stem cell growth factor receptor (KIT), and platelet-derived growth factor receptor alpha (PDGFRA) are loci that all belong to equine linkage group 2 (LG2). Of these, KIT was fluorescent in situ hybridization (FISH) mapped to ECA3q21 with equine cDNA and heterologous porcine BAC probes, while MC1R was localized to ECA3p12 and PDGFRA to ECA3q21 with heterologous porcine BAC probes. A three-step comparison between ECA3 and donkey chromosomes was carried out. First, microdissected ECA3 painting probe was used on donkey chromosomes, which showed disruption of the equine synteny. Next, human (HSA) Chromosomes (Chrs) 16q and 4 specific paints, known to be homologous to ECA3p and 3q, respectively, were applied to detect homologous chromosomal segment(s) in donkey. Finally, four genes (MC1R, ALB, PDGFRA, KIT) and two equine microsatellite markers (SGCV18 and SGCV33) located on ECA3 were FISH mapped to donkey chromosomes. The findings refined the cross species painting homology results and added six new markers to the nascent donkey gene map. The hypothesis that Tobiano coat color in horses may be associated with a chromosomal inversion involving genes within LG2 was tested by G-banding-based cytogenetic analysis and ordering of four loci-KIT, PDGFRA, albumin (ALB), and MC1R-in Tobiano and non-tobiano (homozygous as well as heterozygous) horses. However, no difference either in banding patterns or location/relative order of the genes was observed in the three classes. The study highlights successful FISH mapping of BAC probes across evolutionarily diverged species, viz., pig and horse/donkey, and represents the first use of large-sized individual clones across distantly related farm animals.

Animals↗
PubMed2005

Generation of hybrid hepatocytes by cell fusion from monkey embryoid body cells in the injured mouse liver.

Monkey embryonic stem (ES) cells have characteristics that are similar to human ES cells, and might be useful as a substitute model for preclinical research. When embryoid bodies (EBs) formed from monkey ES cells were cultured, expression of many hepatocyte-related genes including cytochrome P450 (Cyp) 3a and Cyp7a1 was observed. Hepatocytes were immunocytochemically observed using antibodies against albumin (ALB), cytokeratin-8/18, and alpha1-antitrypsin in the developing EBs. The in vitro differentiation potential of monkey ES cells into the hepatic lineage prompted us to examine the transplantability of monkey EB cells. As an initial approach to assess the repopulation potential, we transplanted EB cells into immunodeficient urokinase-type plasminogen activator transgenic mice that undergo liver failure. After transplantation, the hepatocyte colonies expressing monkey ALB were observed in the mouse liver. Fluorescence in-situ hybridization revealed that the repopulating hepatocytes arise from cell fusion between transplanted monkey EB cells and recipient mouse hepatocytes. In contrast, neither cell fusion nor repopulation of hepatocytes was observed in the recipient liver after undifferentiated ES cell transplantation. These results indicate that the differentiated cells in developing monkey EBs, but not contaminating ES cells, generate functional hepatocytes by cell fusion with recipient mouse hepatocytes, and repopulate injured mouse liver.

Animals↗
PubMed1997

Occupational exposure to antineoplastic agents and parameters for renal dysfunction.

To study the nephrotoxic effects of occupational exposure to antineoplastic agents, the early renal effect parameters retinol-binding protein (RBP) and albumin (ALB) were determined in the urine of 11 hospital workers involved in the preparation and administration of antineoplastic agents and in 23 hospital workers not involved in drug handling, who served as nonexposed controls. No significant difference was found between the exposed group and the nonexposed control group with respect to the early renal effect parameters RBP and ALB. Although it was demonstrated that the hospital workers were exposed to cyclophosphamide (CP) and probably other antineoplastic agents, the results of the present study show that these exposure levels did not cause nephrotoxic effects.

Adult↗
PubMed1997

Surfactant proteins and stable microbubbles in tracheal aspirates of infants with respiratory distress syndrome: relation to the degree of respiratory failure and response to exogenous surfactant.

UNLABELLED: Surfactant proteins (SP-A and SP-BC), albumin (ALB), and stable microbubble (SM) count were measured in tracheal aspirates from infants with respiratory distress syndrome (RDS) receiving single-dose Surfactant-TA (surfactant group, n = 32) or no surfactant (control group, n = 12), and those without RDS (non-RDS group, n = 8) to determine biochemical and biophysical status of surfactant in the course of RDS after surfactant replacement. Surfactant therapy resulted in immediate and sustained elevations of SP-BC/ALB and SM count with a rapid fall in ventilatory index to levels measured in the non-RDS group, whereas these indices improved slowly in the control group. The SP-A/ ALB was initially low in both RDS groups and increased to levels measured in the non-RDS group by age 48 h. Multiple regression analysis showed that SP-BC/ALB, postnatal age, SM count, SM count/SP-A plus SP-BC, and surfactant therapy were independently associated with the severity of RDS as assessed by ventilatory index (r = 0.75, P < 0.0001; number of samples = 256). Infants with a relapse response to surfactant (n = 9) had levels of SP-A/ALB and SP-BC/ALB similar to those measured in the sustained group (n = 23), but had significantly lower SM count and SM count/SP-A plus SP-BC between 24 and 96 h of age. CONCLUSION: Surfactant therapy normalizes the surfactant and respiratory status of infants with RDS. Surfactant dysfunction rather than depletion may explain the relapse response seen in some surfactant recipients.

Albumins↗
PubMed2004

Trace elements and some extracellular antioxidant proteins levels in serum of patients with systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a chronic progressive autoimmune disorder with a wide spectrum of clinical and immunological abnormalities. In this study, we aimed to investigate the levels of serum zinc (Zn), copper (Cu), magnesium (Mg), manganese (Mn), iron (Fe), ceruloplasmin (Cp), transferrin (Trf), and albumin (Alb) in SLE and whether it is related to the severity of the clinical condition of this chronic disease. Cp and Cu levels were higher, while Trf, Alb, Zn, Mg, Mn, and Fe levels were lower in serum of patients with SLE (n = 27) compared with healthy controls (n = 20). The mechanisms by which these alterations occur in certain inflammatory conditions need to be elucidated. It is also obscure whether these alterations are a cause or a consequence of the inflammation. As a conclusion, alterations in the levels of the parameters in SLE may not be a reason for, but in fact a consequence of the disease itself.

Adolescent↗
PubMed1992

Serum protein concentrations in Plasmodium falciparum malaria.

In patients with uncomplicated Plasmodium falciparum infection cytokine-mediated serum protein levels of C-reactive protein (CRP), coeruloplasmin (COE), beta 2-microglobulin (B2M), alpha 1-acid glycoprotein (AAG), alpha 1-antitrypsin (AAT), haptoglobin (HPT), prealbumin (PRE), retinol binding protein (RBP), albumin (ALB) and transferrin (TRF) were measured in an endemic area of the Amazonian rain forest. Semi-immune (SI) and nonimmune (NI) patients were investigated. In both patient groups the serum concentrations of CRP, COE and B2M were elevated on admission. In addition AAG and AAT concentrations were increased in NI patients compared to control subjects. Significantly lower serum concentrations of HPT, PRE, RBP, ALB and TRF were seen in both patient groups during the acute phase of the disease, and were more pronounced in NI patients. After a 28-day follow-up, AAT and B2M were normal in SI patients but HPT, AAT and B2M were still significantly altered in NI patients.

Acute-Phase Proteins↗
PubMed1985

Concentration of bronchoalveolar lavage fluid by ultrafiltration: evidence of differential protein loss and functional inactivation of proteinase inhibitors.

Bronchoalveolar lavage samples were concentrated using positive-pressure ultrafiltration. The starting material, concentrates, and eluates were assayed for immunoglobulin A (IgA), albumin (Alb), alpha 1-proteinase inhibitor (alpha 1-PI), antileukoprotease (ALP), and total leukocyte elastase inhibitory capacity (LEIC). No enzyme inhibitory capacity or protein was detected in membrane eluates, confirming the selectivity of the membrane used (Mr cutoff 2000 or 500). However, the concentrated lavages showed a generated loss of protein. The proportion of each protein recovered using the 500 Mr cutoff membrane was: IgA, 50.6% (+/- 15%); albumin, 43% (+/- 8.4); alpha 1-PI, 53.6 (+/- 17.3); ALP, 43% (+/- 2.1); and LEIC, 18.4% (+/- 2.6). Similar results were obtained with the 200 Mr cutoff membrane. The alpha 1-PI/Alb and the IgA/alb ratios were higher (2P less than 0.05) in the concentrates than in the starting material, suggesting differential protein loss. Protein losses were due to binding to the membrane since the wash with saline solution improved recoveries: IgA, 80%; Alb, 56%; alpha 1-PI, 64%; ALP, 66%; LEIC, 29%. Concentration of bronchoalveolar lavage fluids therefore resulted in substantial differential losses in elastase inhibitory capacity and protein concentrations, suggesting analysis of these fluids should be performed on unconcentrated samples.

Body Fluids↗
PubMed1987

Protein transfer at the blood cerebrospinal fluid barrier and the quantitation of the humoral immune response within the central nervous system.

The cerebrospinal fluid (CSF)/serum concentration quotients of albumin and the immunoglobulins G, A and M have been determined for 396 patients with a normal blood CSF barrier function or a pure barrier impairment without a humoral immune response within the central nervous system. The ratios between the concentration quotients of the three immunoglobulins and that of albumin increase in a nonlinear fashion with progressive impairments of the blood CSF barrier, i.e. the molecular size dependent discrimination of the protein transfer ('selectivity') decreases. The upper reference values of the concentration quotients for the whole range of passive transfer comply with the hyperbolic function: Q(IgX) = a/b square root Q(Alb)2 + b2 - c with different constants a/b, b2, c for IgG (0.8, 15 X 10(-6), 1.8 X 10(-3), IgA (0.72, 80 X 10(-6), 5.1 X 10(-3) and IgM (0.65, 150 X 10(-6), 7.5 X 10(-3). With these discriminatory functions the locally synthesized fractions IgX(loc) of IgG, IgA and IgM in CSF can be calculated by the general formula: IgX(loc) = [Q(IgX) - a/b square root Q(Alb)2 + b2 + c] X IgX(Ser).

Albumins↗
PubMed1991

Complete hepatic regeneration after somatic deletion of an albumin-plasminogen activator transgene.

We previously demonstrated that expression of an albumin-urokinase-type plasminogen activator (Alb-uPA) fusion construct in transgenic mice resulted in elevated plasma uPA concentration, hypofibrinogenemia, and neonatal hemorrhaging. Two lines of Alb-uPA mice were established in which only one half of the transgenic pups died at birth; surprisingly, plasma uPA concentrations in survivors gradually returned to normal by 2 months of age. The basis for this phenomenon is DNA rearrangement within hepatocytes that affects the transgene tandem array and abolishes transgene expression. Transgene-deficient cells selectively proliferate relative to surrounding liver, and this process culminates in replacement of the entire liver by clonal hepatic nodules derived from transgene-deficient progenitor cells. In some cases as few as two nodules can reconstitute over 90% of liver mass, highlighting the remarkable regenerative capacity of individual liver cells.

Animals↗
PubMed1990

The influence of blood chemistry on T4 and FT4I in major depression.

The pathophysiology underlying thyroid dysfunction in some depressed patients has not yet been determined. In order to clarify possible biochemical influences on thyroid regulation in these patients, we retrospectively examined several thyroid indices in charts from 81 depressed inpatients and 82 psychiatric controls. The depressed group had significantly higher T4 levels and free T4 index (FT4I), as well as lower chloride (CL) levels than controls. Albumin (ALB) also tended to be higher in the depressives. After adjustment for previously reported effects of ALB and CL on thyroid hormone binding in plasma, the initial differences in thyroid indices became non-significant. We suggest from these findings that plasma biochemical factors contribute significantly to the transient changes in thyroid function observed in some acutely depressed patients. Potential explanations for these biochemical alterations are discussed.

Chlorides↗
PubMed1991

Anthropometric and biochemical assessment of the nutritional state in depression: evidence for lower visceral protein plasma levels in depression.

Severe depression is characterized by anorexia and weight loss, symptoms that could endanger the patient's nutritional state. In order to investigate the nutritional state of depressed patients we determined the following in 113 healthy controls and depressed inpatients: (1) anthropometric variables such as body weight, ideal body weight (IBW), percentage of IBW, mean arm circumference, triceps skinfold thickness and arm muscle circumference, and (2) biochemical parameters such as albumin (Alb), prealbumin (Prealb), and transferrin (Tf). We were unable to detect any differences in the anthropometric parameters between healthy controls, minor and major depressed patients. Depressed patients exhibited significantly lower Alb and Tf levels than healthy controls. The drop in both plasma proteins was highly sensitive (72%) and specific (92%) for melancholia. These results may point towards the existence of a disorder in protein homeostasis or protein malnutrition without a marasmic component.

Adult↗
PubMed1992

Higher alpha 1-antitrypsin, haptoglobin, ceruloplasmin and lower retinol binding protein plasma levels during depression: further evidence for the existence of an inflammatory response during that illness.

Recently, a few reports have shown that severe depression may be associated with higher levels of positive acute phase proteins (APPs), such as haptoglobin (Hp), alpha 1-acid glycoprotein (alpha 1S) and lower levels of negative APPs (visceral proteins), such as albumin (Alb) and transferrin (Tf). In order to reassess whether depression is related to alterations in the expression of plasma APP concentrations, we measured in 84 normal controls and depressed inpatients positive APPs such as Hp, alpha 1-antitrypsin (alpha 1AT), hemopexin (Hpx), ceruloplasmin (Cp), complement component C3C and one visceral protein, i.e., retinol binding protein (RBP). We found increased plasma concentrations of Hp, alpha 1AT, and Cp in major depressed subjects as compared with healthy controls, with minor depressives exhibiting an intermediate position. RBP was significantly lower in minor and major depressives than in normal controls. The disorders in these proteins were rather sensitive (62%) for major depression, with a specificity equalling 96%. Our findings are compatible with the hypothesis that major depression may be accompanied by inflammatory changes with higher levels of positive APPs (i.e., alpha 1AT, Hp, Cp, alpha 1S) and lower levels of visceral proteins (i.e., RBP, Tf, Alb).

Acute-Phase Reaction↗
PubMed1994

Micronuclei, chromosomal aberrations and aflatoxin-albumin adducts in experimental animals after exposure to aflatoxin B1.

Rats and mice differ markedly in sensitivity to aflatoxin B1 (AFB1) hepatocarcinogenicity, the former being sensitive and the latter resistant. Animals were treated with single doses of different concentrations of AFB1, between 0.01 and 1.0 microgram AFB1/g body weight. The frequency of chromosomal aberrations and micronuclei in the bone marrow was measured and compared to the level of AFB1 bound covalently to albumin in the peripheral blood. Both chromosomal aberrations and micronuclei were significantly increased in treated rats compared to the control group at doses above 0.1 microgram/g. In contrast, in mice, a slight increase in chromosome aberrations was seen in the highest dose group (1.0 microgram/g) but no increase in micronuclei was observed at any of the doses. The level of chromosomal aberrations was about 10 times higher in rats than in mice at the highest dose of AFB1. AFB1-albumin (AF-alb) adducts did not show a strong dose-response increase after treatment in mice, whereas in rats the levels increased linearly with dose of AFB1 and there were strong correlations at the individual rat level with both chromosomal aberrations (r = 0.92; p < 0.0001) and micronucleus frequency (r = 0.86; p < 0.0001). These data suggest that the AF-alb may reflect the level of genetic alteration resulting from the initial binding of this carcinogen to cellular DNA. Therefore, this adduct used as a biomarker in studies of human exposure to aflatoxin may provide information not only on exposure but also on the risk of genetic alterations consequent to that exposure.

Aflatoxin B1↗
PubMed1988

IgM/IgG solid-phase antibody-capture assay with biotin/125I-streptavidin amplification: application to normal human sural nerve biopsies.

A highly sensitive and specific solid-phase antibody-capture assay was developed to measure IgM and IgG in endoneurial preparations of human sural nerve biopsies. Assay amplification was obtained by utilizing biotin-labeled anti-IgM or anti-IgG antibody and 125I-streptavidin, resulting in multiple streptavidin molecules binding per biotinylated antibody molecule. A minimal detectable dose of 0.16 +/- 0.08 ng (mean +/- SD; n = 7) for IgM and 0.03 +/- 0.02 ng (mean +/- SD; n = 5) for IgG was obtained in a 100 microliters sample. When this assay was applied to normal fascicular biopsies from human sural nerve, the percent of IgM and IgG, respectively, of the total endoneurial protein was 0.026 +/- 0.015% (n = 9) and 0.27 +/- 0.15% (n = 10; mean +/- SD). When these endoneurial concentrations of IgM and IgG were related to the plasma concentrations (mg IgM or IgG/mg total plasma protein), an IgM-blood-nerve barrier (BNB) index of 4.09 +/- 1.95 and an IgG-BNB index of 2.07 +/- 1.10 were obtained (X10(2); mean +/- SD). These values were also related to the albumin (Alb) concentration in the biopsies as a percent of total endoneurial protein (2.48 +/- 1.07%; mean +/- SD) and with the Alb-BNB index (5.40 +/- 2.53; X10(2); mean +/- SD; n = 10). Although these normal values will be expected to change with age, sex, nerve, and proximal-distal distance from nerve root, they should provide a basis for the comparison of BNB indices from patients with peripheral neuropathy.

Adult↗
PubMed1996

Comparison of saturable transport and extracellular pathways in the passage of interleukin-1 alpha across the blood-brain barrier.

Blood-borne cytokines enter the brain by transport across the blood-brain barrier (BBB) or by leakage through extracellular pathways at sites, such as circumventricular organs (CVOs), without a BBB. We used radioactively labeled albumin (T-Alb) to differentiate the relative contribution of transport and extracellular pathways to the passage of interleukin-1 alpha ([125I]IL-1 alpha) across the BBB. The major mechanism of entry for [125I]IL-1 alpha after intravenous (i.v.) injection was a saturable transport system with extracellular pathways accounting for only a small fraction of entry into brain. CVOs concentrated blood-borne [125I]IL-1 alpha in a saturable manner to a much greater extent than did the cerebral cortex and cerebellum, but accounted for less that 5% of total brain uptake. After intracerebroventricular (i.c.v.) injection, [125I]IL-1 alpha and T-Alb were concentrated in the CVOs, especially the median eminence, although CVOs contained less that 1% of the substances injected. Distribution after i.c.v. injection was largely due to diffusion and leakage through extracellular pathways. We conclude that after i.c.v. injection, leakage across extracellular pathways accounts for the small but concentrated amount of [125I]IL-1 alpha found in CVOs. After i.v. injection, transport across the BBB accounts for the majority of [125I]IL-1 alpha in brain.

Albumins↗
PubMed1992

Physiologic concentrations of inorganic phosphate accelerate fructosamine synthesis.

The effect of physiologic concentrations of inorganic phosphate (Pi) on fructosamine (FRA) synthesis was studied. After 75 g oral glucose administration (OGTT), 'delta FRA/24 h', defined as delta FRA after incubating serum or other specimens at 37 degrees C for 24 h after adding 1000 mg/dl glucose, was significantly decreased in parallel to the decrease of plasma Pi concentrations. 'The FRA index', defined as the FRA value divided by the corresponding glucose concentration, both at fasting, correlated significantly with plasma Pi concentrations. In vitro incubation of serum total protein (TP), albumin (ALB), gamma-globulin (GLB), free lysine (Lys), and free valine (Val) with glucose at different concentrations of Pi showed a Pi-dependent increase of FRA synthesis throughout 48 h of incubation. The accelerating effect of 5 mg/dl Pi on FRA synthesis from TP, ALB, GLB, Lys, and Val at pH 7.4 was, respectively, as great as 48, 20, 24, 13 or 25% of those without Pi. Increase of pH from 6 to 10 logarithmically increased delta FRA/24 h in contrast to a logarithmic decrease of the accelerating effect of Pi on delta FRA/24 h. These data show that physiologic concentrations of Pi accelerate protein glycation by accelerating dehydrogenation during the Amadori rearrangement through the negative charge of Pi. Because this accelerating effect of physiologic Pi presumably exists in vivo, Pi concentration must be taken into account as an accelerating factor for FRA synthesis in evaluating diabetic control, and further studies must be carried out to elucidate whether hyperphosphatemia accelerates glycation-induced diabetic complications.

Adult↗
PubMed1980

Molecular mechanisms of control of albumin and alphafetoprotein production: a system to study the early effects of chemical hepatocarcinogens.

The cellular mechanism of control of alphafetoprotein (AFP) and albumin (ALB) production during normal and pathologic permissive states is being examined using complementary DNA probes. AFP is the major serum protein for most of fetal life, but normally is produced in very small amounts in the adult. AFP production recurs in the adult during restitutive proliferation of the liver following partial hepatectomy or chemical injury, early after the exposure to chemical carcinogens and in animals with hepatocellular or yolk sac carcinomas. AFP production is roughly proportional in each case examined so far to the amount of mRNA available. On the other hand, there appears to be no difference in the gene number or gene organization in permissive or non-permissive states and there is no evidence of selective degradation of AFP or AFP (and ALB) production is probably at the level of gene transcription. Understanding of how carcinogens act to permit expression of the AFP gene may lead to important insights into carcinogenic mechanisms.

Albumins↗
PubMed1984

Molecular cloning of a cDNA for Chinese hamster ovary asparagine synthetase.

In previous reports we have described the isolation and characterization of a number of Chinese hamster ovary (CHO) cell mutants resistant to the amino acid analogue albizziin (Alb). Multistep mutants were derived which showed a high degree of drug resistance and expressed increased levels of asparagine synthetase (AS) levels up to 300-fold over that of the parental cell line. Karyotypic analysis of these mutants revealed homogeneously staining regions (HSRs) usually indicative of gene amplification. In the present work, we provide further proof for gene amplification by showing that the mutants greatly overproduce functional AS mRNA, as evidenced by in vitro translation of purified mRNA and immunoprecipitation of AS. By using these overproducing mutants as sources of mRNA coupled with velocity centrifugation, we have been able to greatly enrich for AS sequences in our mRNA preparations to the point where they represent 1-5% of the total message. This facilitated cloning and selection of the cDNA sequences complementary to the gene. Utilizing these cloned cDNAs, we have demonstrated a correlation between gene copy number and enzyme expression in the parent and Alb-resistant mutants, thus providing direct evidence that drug resistance is due to gene amplification.

Animals↗