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PubMed1990

T cell reactivity to the purified mycobacterial antigens p65 and p70 in leprosy patients and their household contacts.

T cell reactivity to the 70 and 65 kD (p70 and p65) protein antigens derived from Mycobacterium bovis BCG strain was studied by measuring the proliferative responses of peripheral blood mononuclear cells from members of an isolated Aboriginal community resident in the Torres Straits islands. In the nine index leprosy cases the pattern of responsiveness to the purified antigens paralleled that to whole sonicates from M. leprae and BCG. In the 40 contacts of the index cases, a high correlation was observed between the responses to p70 and p65 as well as to the crude sonicates. Significant T cell responses to the purified antigens, as well as the crude sonicates, were obtained with cells from the majority of contacts. Limiting dilution analysis of precursor frequencies in the contacts confirmed the immunogenicity of the purified antigens and excluded both a mitogenic component and the presence of suppressor cells in those moderate or low responders whose blood contained sufficient precursors to be tested. p70 appeared to be more potent in stimulating a proliferative response than p65 at equivalent protein concentrations. No correlation between responder status to either antigen and disease type was detected in families. These findings provide confirmation of the importance of p70 and p65 as major T cell immunogens in man and indicate that they are both potential candidates for inclusion in a bivalent vaccine for leprosy and tuberculosis.

Antigens, Bacterial↗
PubMed1988

Monoclonal antibodies against leucoagglutinin-reactive human T-lymphocyte surface components. II. Studies on the mechanism of K46M-induced activation and determination of the frequency of responding cells.

A monoclonal antibody, K46M (IgM kappa), obtained after immunization with leucoagglutinin (La)-reactive T-cell surface components, stimulated human lymphocytes to proliferate. It induced maximal proliferation at greater than 20 micrograms IgM/ml after 3-4 days of culture. Cells stimulated by K46M produced interleukin 2 (IL-2) and gamma interferon (IFN-gamma) and expressed receptors for IL-2 and transferrin. The majority of the activated cells were phenotypically T cells as defined by monoclonal antibodies against CD3 and CD2, and an increase in the K46M-positive cells was also observed during the activation period. K46M-activated cells display major histocompatibility complex (MHC)-unrestricted cytotoxicity against several cultured target cells. The frequencies of the cytotoxic and of the proliferative precursor cells were determined using a limiting dilution assay. K46M seems to activate a larger fraction of cytotoxic precursor cells against Molt 4 than against K562, but the statistical significance of these observations requires further exploration. Both K46M or La activated 40% of PBL to proliferate, whereas 70% of PBL were induced by OKT3. However, the frequency of K46M-activated cells was 40% only when the lymphocytes were plated at low cell densities, i.e. less than 0.5 cells per well. At higher densities an inhibition of proliferation was seen that resulted in a biphasic response curve, indicating that the activation of PBL by K46M was not a single hit event. This was not found with either La or OKT3. Whether K46M, in contrast to OKT3 and La, activates a subpopulation with suppressor activity remains to be established.

Animals↗
PubMed1972

Effect of the folic acid analogue, trimethoprim, on growth, macromolecular synthesis, and incorporation of exogenous thymine in Escherichia coli.

The effect of trimethoprim [2,4-diamino-5(2',4',5'trimethoxybenzyl)-pyrimidine] in the presence of thymine on Escherichia coli B temperature-sensitive and non-temperature-sensitive Thy(') strains and a phosphodeoxyribomutase-negative mutant was studied. The inhibitory effect of 5 mug of trimethoprim per ml on the growth of E. coli B was not overcome by thymine, thymidine, or thymidylate even in the presence of one-carbon metabolites and related metabolites. Deoxyribonucleic acid (DNA) and protein synthesis were more severely inhibited than ribonucleic acid (RNA) synthesis. The inhibition of DNA synthesis was partially reversed by addition of deoxyadenosine to increase the incorporation of exogenous thymine. By contrast, the inhibition of protein was not reversed even with one-carbon metabolites present, in keeping with the requirement for formylmethionyl-transfer RNA(F) for initiation. However, the inhibition of both DNA and protein synthesis in a phosphodeoxyribomutase-negative strain by 1 mug of trimethoprim per ml with thymine present was partially reversed by deoxyadenosine and one-carbon metabolites, and nearly normal growth occurred. 5-Fluorodeoxyuridine added at the time of addition of trimethoprim prevented the inhibition. Sulfadiazine in the presence of thymine inhibited both Thy(+) and Thy(-) strains whereas trimethoprim (with thymine) did not inhibit Thy(-) organisms. The effect of trimethoprim on the incorporation of labeled thymine into DNA was also studied. These experiments support the concept that trimethoprim in conjunction with the action of thymidylate synthetase inhibits the growth of Thy(+) cells because of a depletion of tetrahydrofolate. DNA synthesis is inhibited initially by a limitation of thymine nucleotide precursor, resulting from the indirect inhibition of thymidylate synthetase and the poor incorporation of exogenous thymine.

Anti-Bacterial Agents↗
PubMed1995

Characterization of a ubiquitinated protein which is externally located in African swine fever virions.

An antiserum was raised against the African swine fever virus (ASFV)-encoded ubiquitin-conjugating enzyme (UBCv1) and used to demonstrate by Western blotting (immunoblotting) and immunofluorescence that the enzyme is present in purified extracellular virions, is expressed both early and late after infection of cells with ASFV, and is cytoplasmically located. Antiubiquitin serum was used to identify novel ubiquitin conjugates present during ASFV infections. This antiserum stained virus factories late after infection, suggesting that virion proteins may be ubiquitinated. This possibility was confirmed by Western blotting, which identified three major antiubiquitin-immunoreactive proteins with molecular masses of 5, 18, and 58 kDa in purified extracellular virions. The 18-kDa protein was solubilized from virions at relatively low concentrations of the detergent n-octyl-beta-D-glucopyranoside, indicating that it is externally located and is possibly in the virus capsid. The 18-kDa protein was purified, and N-terminal amino acid sequencing confirmed that the protein was ubiquitinated and was ASFV encoded. The ASFV gene encoding this protein (PIG1) was sequenced, and the encoded protein expressed in an Escherichia coli expression vector. Recombinant PIG1 was ubiquitinated in the presence of E. coli expressed UBCv1 in vitro. These results suggest that PIG1 may be a substrate for UBCv1. The predicted molecular masses of the PIG1 protein and recombinant ubiquitinated protein were larger than the 18-kDa molecular mass of the ubiquitinated protein present in virions. Therefore, during viral replication, a precursor protein may undergo limited proteolysis to generate the ubiquitinated 18-kDa protein.

African Swine Fever Virus↗
PubMed1983

Glucose production measured by tracer and balance data in conscious miniature pig.

The rate of glucose production was estimated in the conscious, unrestrained miniature pig during metabolic adaptation to starvation (up to 120 h) by the simultaneous use of three different techniques: 1) the isotopedilution technique, 2) the arteriohepatovenous catheter technique, and 3) the urinary nitrogen balance. During the experimental period 1) whole-body glucose turnover decreased, whereas the amount of glucose recycling increased; 2) splanchnic glucose output decreased, whereas the rate of splanchnic precursor extraction increased up to 48 h, followed by a decrease; 3) gut glucose consumption amounted to about 30% of splanchnic glucose output; and 4) urinary nitrogen excretion declined continuously. The comparison of the different methods revealed that during starvation 1) tracer-determined glucose production rate was within the range (+/- 10%) of the splanchnic glucose output; 2) mean hepatic glucose output overestimated the tracer data by about 30-40%; 3) splanchnic glucose output underestimated hepatic glucose production by the amount of gut glucose consumption; 4) tracer-determined glucose recycling corrected for isotope dilution and amino acid contribution was within the range of splanchnic gluconeogenic precursor extractions. Considering the limitations (e.g., gut glucose consumption, gut lactate and alanine release, blood flow measurement) and methodological problems of the different approaches applied, it is evident that each method reflects different events. It is suggested that the versatile tracer technique combined with nitrogen balance should be preferred for measurement of endogenous glucose production.

Alanine Transaminase↗
PubMed1993

Inhibition by a stable factor derived from neutrophils of endothelium-dependent relaxation in rat aorta.

Polymorphonuclear leukocytes (PMNs) may play an important role in many pathophysiological states. The effect of a factor derived from PMNs on endothelium-dependent relaxation was studied using rat aortic rings in organ chambers. PMNs were obtained from cardiac surgical patients and healthy volunteers. After incubation in Krebs solution for 3 h, supernatants of PMN suspensions were isolated and used to pretreat the aortic rings for 30 min. The results showed that the supernatants derived from 1 x 10(4) to 5 x 10(6) cells/ml PMNs produced a concentration-dependent inhibition of endothelium-dependent relaxation to acetylcholine but not endothelium-independent relaxation to sodium nitroprusside. The effect could not be prevented by oxygen free radical scavenger superoxide dismutase (150 U/ml), catalase (1,200 U/ml), or mannitol (20 mM) used alone or in combination. Heating the supernatants at 95 degrees C for 30 min did not reduce the inhibitory effect. L-Arginine at 3 x 10(-5) to 3 x 10(-3) M did not significantly reverse the inhibitory effect of the PMN-derived factor. In conclusion, this study reveals that a heat-stable factor derived from human PMNs potently inhibits acetylcholine-induced endothelium-dependent relaxation but not sodium nitroprusside-induced endothelium-independent relaxation in rat aorta. This inhibitory effect is not caused by oxygen free radicals, a limitation of nitric oxide precursor or other unstable factors.

Animals↗
PubMed2005

Steroidogenesis in aldosterone-producing adenoma revisited by transcriptome analysis.

CONTEXT: Primary aldosteronism (PAL) is the most frequent cause of secondary arterial hypertension. In PAL, aldosterone production is chronic, excessive, and autonomous. OBJECTIVE: The objective of this study was to identify the angiotensin-II independent alterations of steroidogenesis responsible for PAL. DESIGN: Genomewide gene expression was compared in two tissues differentiated for aldosterone production, both nonstimulated by circulating angiotensin II and differing in their autonomy to produce aldosterone: aldosterone-producing adenoma (APA) and its adjacent dissected zona glomerulosa (ZG). SETTING: The setting of this study was the Comete Network. PATIENTS: Patients with APA were studied. INTERVENTION: Transcriptome comparison was made of one APA and its adjacent ZG by serial analysis of gene expression; validation by in situ hybridization was performed for 19 genes in 11 samples. OUTCOME: The study outcome was genes differentially expressed in APA and adjacent ZG. RESULTS: Activation of steroidogenesis in PAL is restricted to the overexpression of the enzymes producing aldosterone-specific steroids, aldosterone synthase and also 21-hydroxylase, suggesting that upstream precursor production is not limiting. Increased expression of high-density lipoprotein receptor, adrenodoxin and P450 oxidoreductase suggests that these systems provide cholesterol and electrons to the mitochondrial steroidogenic enzymes. As for acute stimulation of aldosterone production, an activation of calcium signaling is suggested by concordant overexpression of calcium-binding proteins or effectors. Calcium activation may result from an abnormal activity of G(q) protein-coupled receptors. This calcium activation may be the starting point of the other gene expression changes observed in APA. Finally, other differentially expressed genes include three genes encoding unidentified proteins. CONCLUSION: This work provides an original and integrated view of the mechanisms of aldosterone production in PAL.

Adenoma↗
PubMed2001

Nuclear p26, a small heat shock/alpha-crystallin protein, and its relationship to stress resistance in Artemia franciscana embryos.

The role of the small heat shock/alpha-crystallin protein, p26, in transcription in Artemia franciscana embryos was examined using isolated nuclei, containing either control or elevated levels of p26, in transcription run-on assays. Heat shock or anoxia in vivo and acid pH in vitro were used to transfer p26 into nuclei. The results suggest that parameters other than, or in addition to, p26 are responsible for the reduced transcription rates observed and that decreases in pHi are involved. In vivo experiments indicate that RNA synthesis and, to a lesser extent, protein synthesis are downregulated in intact embryos recovering from heat shock and that the precursor pool is not limiting. Confocal microscopy confirmed that p26 moves into nuclei in response to heat shock and anoxia in vivo, and to low pH in vitro, and indicated that the nuclear distribution of p26 is similar under all three conditions. We present evidence that unstressed (control) embryos containing p26 in all their nuclei will not hatch, even under permissive conditions, and propose that they are unable to terminate diapause. Potential nuclear targets of p26 chaperone activity are discussed.

Animals↗
PubMed1997

High glucose inhibits nitric oxide production in cultured rat mesangial cells.

Hyperglycemia directly contributes to the development of diabetic nephropathy. A high-serum glucose concentration alters intraglomerular hemodynamics and promotes deposition of extracellular matrix in the kidney. Nitric oxide (NO) is a short-lived messenger molecule that participates in the regulation of renal blood flow, GFR, and mesangial matrix accumulation. Therefore, in this study it was tested whether high glucose directly modulates NO synthesis by rat mesangial cells in vitro by measuring the accumulation of nitrite, the stable metabolite of NO, in the incubation media. Raising the external glucose concentration to 33.3 mM for 24 to 72 h reduced nitrite levels in cell supernatants in a time-dependent manner to a nadir of 14 +/- 3% of the amount in normal glucose media (5.6 mM) (P < 0.01). The decline in NO synthesis in high glucose media was paralleled by decreased cyclic guanosine monophosphate generation; however, there was no alteration in rat mesangial cell expression of inducible NO synthase protein. The suppressive effect of high glucose on NO production by mesangial cells was not modified by inhibition of protein kinase C (H-7), the addition of antioxidants (vitamin E or superoxide dismutase), or a pan-specific anti-transforming growth factor-beta antibody. An elevated ambient glucose caused a time-dependent reduction in mesangial cell L-arginine content. Addition of L-arginine (10 to 20 mM) to external media partially reversed the inhibitory effect of high glucose on mesangial cell NO production in a dose-dependent manner. The highest dose of L-arginine (20 mM) increased mesangial cell L-arginine content to comparable levels in normal and high glucose media. These results indicate that high glucose causes depletion of L-arginine in mesangial cells and compromises NO synthesis. Limitation in the metabolic precursor and other, as yet unidentified, factors act to reduce NO production by mesangial cells in the presence of an elevated ambient glucose level, a change that may play a role in the development of diabetic glomerulosclerosis.

Amino Acids↗
PubMed1994

What beta-cell defect could lead to hyperproinsulinemia in NIDDM? Some clues from recent advances made in understanding the proinsulin-processing mechanism.

Pancreatic beta-cell dysfunction is a characteristic of non-insulin-dependent diabetes mellitus (NIDDM). An aspect of this dysfunction is that an increased proportion of proinsulin is secreted, but an actual beta-cell defect that leads to hyperproinsulinemia is unknown. Nevertheless, an impairment in beta-cell proinsulin conversion mechanism has been suggested as the most likely cause. Insulin is produced from its precursor molecule, proinsulin, by limited proteolytic cleavage at two dibasic sequences (Arg31, Arg32 and Lys64, Arg65). Two endopeptidase activities catalyze this cleavage: PC2 and PC3. PC2 endopeptidase cleaves predominately at Lys64, Arg65, and PC3 endopeptidase cleaves at Arg31, Arg32. The recent identification and characterization of these endopeptidases has enabled a better understanding of the human proinsulin-processing mechanism. In particular, experimental evidence suggests that the majority of human proinsulin processing is sequential. PC3 cleaves proinsulin first to generate a proinsulin conversion intermediate that is the preferred substrate of PC2. Both PC2 and PC3 activities are influenced by Ca2+ and pH, but the more stringent Ca2+ and pH requirements of PC3 suggest it as the most likely enzyme to regulate proinsulin conversion, as well as initiate it. When an increased demand is placed on the proinsulin-processing mechanism by a glucose-stimulated increase in proinsulin biosynthesis, there is a coordinate increase in PC3 biosynthesis (but not in PC2). This supports PC3 as the key endopeptidase that regulates proinsulin processing. In this perspective, the current concepts of the enzymology and regulation of proinsulin conversion at a molecular level are reviewed.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed1982

Incorporation of [U-14C] palmitate into lipids by the stable fly, Stomoxys calcitrans (L.).

The incorporation in vivo of [U-14C] palmitate into fat body lipids was studied in the blood feeding stable fly, Stomoxys calcitrans. Palmitate was rapidly esterified into triacylglycerol and after one-half h, nearly one third of the total recovered label was in the triacylglycerol fraction with a concomitant loss of radioactivity in the free fatty acids. The fat body, from one day sugar-water-fed flies incorporated more label into triacylglycerol than those from flies fed on blood. The present study indicates that fat body from sugar-water-fed stable flies retains a high lipogenic ability and that availability of proper precursors may be a limiting factor in lipogenesis. The incorporation of [14C] palmitate into triacylglycerol decreased during subsequent blood meals, except for an increased incorporation into triacylglycerol by the fat body of males after the fourth blood meal. Flies fed five blood meals showed the least incorporation of label into fat body lipids after [14C] palmitate injection. The capacity for incorporation of [14C] palmitate into fat body lipids was reduced in starved stable flies. In addition, the lipids isolated from starved flies showed reduced specific activities.

Adipose Tissue↗
PubMedDate not supplied

Mathematical modeling of human embryonic and fetal growth rates.

A mathematical model for human embryonic/fetal growth data from implantation to birth is developed. In previous work, it was shown that an unbiased estimate for human fetal growth data from about day 50 post-conception until term could be calculated from the Gompertz equation. This period represents a range of embryonic/fetal weights from one to 3500 g. When the Gompertz equation is extended, with no change of parameters, to the prenatal period before 50 days, the predicted weights have a consistent bias which might have a biological basis. Early embryonic growth immediately following fertilization is exponential; i.e., one cell goes to 2, then 4, then 8... etc., with essentially no decrease in relative growth rate. Except for possible small changes in cell size and cell mitosis cycle time, such exponential growth can be considered as a special case of the Gompertz equation with a, the relative rate of decrease of the relative growth rate, equal to zero. The relative growth rate begins to decrease about 20 days post-conception, at the time of cell differentiation into organ precursors. Although the "Hayflick Limit" of the maximum of 50 to 60 cell divisions for human cells would tend to cause a decrease in growth rate, it can be shown that the effect is insignificant during embryonic/fetal growth. The observed decrease in the growth rate might be a result of a decreasing fraction of cells in the pool of dividing cells. For the Gompertz equation model, a at this time changes from zero to a positive number. Analysis of fetal growth data shows that a rapidly becomes large and then decreases over a period of several days to become a constant positive value for the remainder of the prenatal term. Good fits of empirical embryonic/fetal growth data were obtained by nonlinear regression with calculation of the embryonic/fetal weights through numerical integration of the differential Gompertz equations and the functionality of alpha.

Body Weight↗
PubMed1992

CD11b (Mac-1): a marker for CD8+ cytotoxic T cell activation and memory in virus infection.

We have found that CD11b, a cell surface integrin of macrophages, granulocytes, and NK cells, is expressed by a subset of CD8+ T cells that include both the active virus-specific CTL and the virus-specific memory CTL populations. CD8+CD11b+ cells comprise less than 3% of naive mouse splenocytes, but after lymphocytic choriomeningitis virus (LCMV) infection increase by 9- to 12-fold by the peak (day 8) of the virus-specific CTL response. Depletion of day-8 splenocytes with anti-Mac-1 and C' or enrichment by sorting for CD11b+ or CD8+CD11b+ spleen cells demonstrated that LCMV-specific CTL are CD11b+. The CD11b+ subpopulation also contained the bulk of the IL-2-responsive CD8+ cells. MEL-14, a homing marker down-regulated on activated T cells, was down-regulated on the majority of CD8+ cells that became CD11b+. Less than 1% of LCMV-immune splenic lymphocytes expressed CD11b. Antibody and C' depletion of this population severely impaired the ability of immune splenocytes to respond to in vitro secondary stimulation with LCMV-infected peritoneal macrophages, but did not affect the generation of a primary allospecific CTL response in MLC. Mixing of CD8-depleted and CD11b-depleted LCMV-immune splenocytes failed to restore the ability of these cells to mount a virus-specific memory CTL response, indicating that a cell coexpressing CD8 and CD11b is essential for this response. As determined by limiting dilution analysis, the precursors for the LCMV-specific memory CTL response were enriched in the CD11b+ population of LCMV-immune splenocytes. CD11b stained far fewer CD8+ splenocytes from naive mice than did CD44 (Pgp-1), and among immune splenocytes it identified a small subpopulation of CD44hi cells, indicating that CD11b may be the best single marker available for discriminating between naive and memory CD8+ T cells.

Animals↗
PubMed1977

Studies on a cyclic nucleotide-independent protein kinase and its proenzyme in mammalian tissues. I. Purification and characterization of an active enzyme from bovine cerebellum.

A protein kinase which phosphorylated histone and protamine was partially purified from bovine cerebellum. Casein and phosvitin were inert as substrates. The enzyme did not require any cyclic nucleotide. A sulfhydryl compound such as 2-mercaptoethanol, glutathione, or cysteine was necessary for the reaction. The optimum pH was 8.5 to 9.0 Km values for ATP and whole histone were 3.3 X 10(-6) M and 150 microgram/ml, respectively. The optimum concentration of Mg2+ varied with histone fractions employed; with H2B histone as substrate the enzyme was most active at 50 to 100 nM Mg2", whereas with H1 and H2A histones the maximum activity was observed at 5 to 10 mM Mg2+ and with H3 and H4 histones the enzyme was active over a range of 5 to 75 mM Mg2+. The enzyme phosphorylated Ser-32 and Ser-36 in H2B histone and Ser-38 in H1 histone, although the reaction with Ser-36 in H2B histone was very slow. The molecular weight was 6.4 X 10(4). The sedimentation coefficient and Stokes radium were about 4.5 and 29 A, respectively. The enzyme showed heterogeneity upon isoelectrofocusing electrophoresis with isoelectric points of 5.6, 6.0, and 6.6. The enzyme was not inhibited by protein inhibitor nor by the regulatory subunit of cyclic AMP-dependent protein kinase. Preliminary analysis suggested that the enzyme was produced from its precursor protein by a limited proteolytic reaction.

Animals↗
PubMedDate not supplied

The pancreatic duct cell: proliferative capabilities, specific characteristics, metaplasia, isolation, and culture.

The pancreatic duct cell, although a minor cell type of the pancreas, plays an important role in fluid/electrolyte and mucin secretion, and has been implicated in the development of pancreatic cancer, alcoholic pancreatitis, and cystic fibrosis. In the normal pancreas, the duct cell has the same low proliferative rate as acinar and endocrine cells. Under certain pathological circumstances, duct cells, as well as acinar and islet cells, may be stimulated to proliferate more rapidly. Pancreatic duct cells exhibit certain features not shared by acinar and/or endocrine cells, including a variety of antigens, mucins, enzymes, and morphological features. Adult duct cells resemble fetal pancreatic duct-like cells morphologically, but they have differentiated to at least a limited extent from their precursor cell type. Although there is no evidence that duct cells differentiate into acinar cells after pancreatic morphogenesis is complete, some islet cells develop from duct epithelium in the early postnatal period. Some pathological conditions may lead to the postnatal formation of islet cells from duct cells and may cause acinar cells to become duct-like in morphology or to die and be replaced by duct cells. A better understanding of duct cells is now possible because of the development of techniques for their isolation and culture free from other cell types. Several such techniques are reviewed.

Animals↗
PubMedDate not supplied

[Amino acid composition and properties of fibrin self-assembly inhibitors].

Three peptides, inhibitors of fibrin self-assembly, were shown to be responsible for stable antipolymerization activity of blood plasma. Similarity of amino acid composition of these inhibitors might be considered as an indication of their origin from a common precursor by means of limited proteolysis. Inhibition of the self-assembly occurred due to interaction of the peptides with monomeric fibrin in the region of domain D, which was accompanied by loosening of electrostatic interactions between molecules of fibrin.

Amino Acids↗
PubMed1987

Tissue tropism and temporal expression of Rous sarcoma virus in embryonic avian limb in ovo.

Embryonic avian tissue is resistant to the transforming potential of Rous sarcoma virus (RSV) in ovo. Analysis of the pattern of host-viral interactions in the first semester of chick development has demonstrated that RSV is first expressed in a limited population of muscle precursor cells and proceeds to spread throughout the developing dorsal and ventral limb musculature. The number of non-muscle cells participating in the infection is initially low but gradually increases as development continues. The data show that RSV infection in ovo is both compatible with the process of differentiation and the maintenance of the differentiated state of the limb. The kinetics of viral spreading and competence for transformation are developmentally regulated in the embryo. The contrasting properties of embryonic cells in ovo as compared with those of the adult provide an opportunity for evaluating host related regulatory factors that are of significance to the expression of viral transforming function.

Animals↗