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PubMed1978

Improved continuous-flow (SMAC) determination of serum albumin.

The albumin values determined by the bromcresol green methods do not compare well with values by more specific methods for albumin determination. The discrepancies have been related to, among other things, acute-phase reactants and are especially pronounced in the lower albumin range. These disadvantages are also inherent in a routine continuous-flow method for albumin (SMAC). The bromcresol green method has been improved considerably by shortening the reaction time before the absorbance is measured, as is described here. The modified method yields values that better agree with those by more specific methods and an influence of acute-phase reactants is no longer observed.

Autoanalysis↗

PubMed1992

Lipoprotein(a) and acute-phase proteins in acute myocardial infarction.

Lipoprotein(a) (Lp(a)) and the acute-phase proteins, orosomucoid, haptoglobin and alpha 1-antitrypsin, were studied in 32 patients with acute myocardial infarction. Samples were taken at admission and, after fasting overnight, on the following 6 days. In a subgroup of 21 patients total serum cholesterol, high-density lipoprotein (HDL) cholesterol and triglycerides were also estimated. In a linear regression model a significant relation between the relative values of Lp(a) and the time in days was obtained (p = 0.001). Compared with the acute-phase proteins, however, Lp(a) showed a weak increase and the individual responses were very variable. There were no correlations between the individual changes in Lp(a) and the changes in the acute-phase proteins, but Lp(a) changes correlated significantly with the changes in total cholesterol and low-density lipoprotein (LDL) cholesterol. It is suggested that the Lp(a) reaction in myocardial infarction is linked to the reaction of the lipoproteins. There may also be several clinical conditions, including different medications, which influence the Lp(a) level.

Acute-Phase Proteins↗

PubMed1992

Heparin cofactor II deficiency in the elderly: comparison with antithrombin III.

We investigated heparin cofactor II (HC II) levels and their relationship to other haemostatic factors in the elderly in comparison with antithrombin III (AT III). We measured plasma HC II activity levels in 166 subjects aged from 61 to 99 years using a chromogenic method. HC II levels (94.4 +/- 18.5%) in the healthy elderly subjects were significantly (p less than 0.001) lower than in 40 healthy adult controls under 60 years of age (mean age: 51.5 years; 111.6 +/- 21.2%). HC II levels in the elderly subjects decreased further with age (r = 0.308, p less than 0.001) and the extent of the decrease was more marked than that for AT III (r = 0.179, p less than 0.05). There was no significant sex difference in HC II levels in the elderly. HC II levels correlated significantly with AT III levels and with acute phase reactants including sialic acid, fibrinogen, and PAI-1. HC II levels also correlated with factor VII, plasminogen, alpha 2-plasmin inhibitor, serum lipid, pseudocholinesterase, and albumin levels. These correlations were also found for AT III except active PAI-1 and tPA-PAI-1 complexes, but the correlations with acute phase reactants were stronger for HC II than AT III. We divided 154 elderly subjects into 4 groups by their pseudocholinesterase and albumin levels to estimate the effect of nutritional status on antithrombin activity in the elderly. HC II levels were normal in the elderly subjects with a good nutritional state (103 +/- 18%), but were significantly decreased in those with malnutrition (85 +/- 15%, p less than 0.001). AT III levels also showed the same tendency. These results indicate a decrease in the reserve capacity to inhibit thrombin generation at sites of atherosclerosis in response to trigger events. The deficiency of two major antithrombin factors in the elderly may indicate a tendency to thrombosis, especially in individuals with malnutrition. When considering the clinical significance of HC II, several other parameters, including age, nutritional status, hepatic synthetic ability, and the presence or absence of acute phase reaction should also be assessed.

Acute-Phase Proteins↗

PubMed1978

Isolation of the etiologic agent of Korean Hemorrhagic fever.

Lung tissues from 73 rodents (Apodemus agrarius coreae) gave specific immunofluorescent reactions when they reacted with sera from patients convalescing from Korean hemorrhagic fever. Similar staaining was observed in the lungs of A. agrarius inoculated with acute-phase sera obtained from two patients with this disease. The unidentified agent was successfully propagated in adult A. agrarius through eight passages representing a cumulative dilution of greater than 10(-17). Experimentally inoculated rodents developed specific fluorescent antigen in the lung, kidney, liver, parotid glands, and bladder. Organs, especially lungs, were positive beginning 10 days and continuing through 69 days after inoculation. The agent could not be cultivated in several types of cell cultures nor in laboratory animals. No fluorescence was observed when infected A. agrarius lung tissues were reacted with antisera to Marburg virus, Ebola virus, and serval arenaviruses. Diagnostic increases in immunofluorescent antibodies occurred in 113 of 116 severe and 11 of 34 milder cases of clinically suspected Korean hemorrhagic fever. Antibodies were present during the first week of symptoms, reached a peak at the end of the second week, and persisted for up to 14 years. Convalescent-phase sera from four persons suffering a similar disease in the Soviet Union were also positive for antibodies.

Animals↗

PubMed1992

Role of CAAT-enhancer binding protein isoforms in the cytokine regulation of acute-phase plasma protein genes.

Rat hepatic cells respond to interleukin (IL) -1, IL-6, and dexamethasone treatment by increasing the transcription rate of acute-phase plasma protein genes. The same conditions lead to changes in the expression of CAAT-enhancer binding protein (C/EBP) isoforms which are specific to the hepatic cell line. To identify the relationship between C/EBP isoforms and acute-phase protein gene activation, the hormone-specific expression of C/EBP alpha, beta, and delta was determined in H-35 and HTC cells and was compared to acute-phase liver. C/EBP beta was found to be the principal isoform in hepatoma cells and to be strongly stimulated by cytokines and dexamethasone in H-35 cells. Transactivating functions were observed for all three C/EBP isoforms by cotransfection of CAT gene reporter constructs containing cytokine and glucocorticoid response elements of acute-phase protein genes and expression plasmids for mouse C/EBP alpha, beta, and delta into rat and human hepatoma cells. The degree of C/EBP-mediated transactivation was, however, extremely variable among the different regulatory elements. Transcription run-on reactions with nuclei from transiently transfected H-35 cells indicated that cotransfected C/EBP beta increases basal expression of reporter gene constructs as well as the dexamethasone-mediated stimulation of constructs containing the glucocorticoid response elements of the rat alpha 1-acid glycoprotein gene, but did not accelerate or enhance hormone-dependent transcription activation of reporter gene plasmids containing the IL-6 regulatory element of the beta-fibrinogen gene. Activation of the reporter gene constructs appeared to be temporally and quantitatively correlated with the amount of nuclear C/EBP as determined by two-dimensional Western and Southwestern blot analyses.

Acute-Phase Proteins↗

PubMed1992

Cytomegalovirus DNA detection in sera from patients with active cytomegalovirus infections.

Using a specific and sensitive polymerase chain reaction method, we detected reliably the presence of human cytomegalovirus (HCMV) DNA directly in serum samples collected at an early stage of HCMV infection, even before immunoglobulin M (IgM) antibodies were measurable. HCMV DNA was detected in serum from all patients with active HCMV infection; in 91% of these patients, HCMV DNA was found in the acute-phase serum. In 13 of 44 patients, HCMV DNA was found in serum before HCMV-specific IgM. For four kidney transplant recipients, the occurrence of HCMV DNA in serum, virus isolation from urine and leukocytes, and HCMV IgG and IgM serology were determined. We found a correlation between HCMV DNA in serum and positive virus isolation from leukocytes. In three of five congenitally infected infants, HCMV DNA and HCMV IgM were detected in the same sample. Two other infants were HCMV DNA positive, although no HCMV IgM antibodies were measurable. HCMV was found in urine from these infants either by virus isolation or with the polymerase chain reaction. Serum from one of the 22 healthy HCMV-seropositive blood donors was HCMV polymerase chain reaction positive.

Antibodies, Viral↗

PubMed1992

Influence of 4 different membrane oxygenators on inflammation-like processes during extracorporeal circulation with pulsatile and non-pulsatile flow.

The influence of four different membrane oxygenators (HF 4000, BOS-CM 50, CML 2, Maxima) on leucocyte count, concentrations of PMN-elastase, clotting factor XII, AT-III, C1-INH, alpha 2-antiplasmin and C3a was registered before, during and after CPB with pulsatile and nonpulsatile flow in 80 male patients aged between 36 and 67 years. With all systems tested, there was a drop in the concentrations of clotting factor XII, AT-III, C1-INH and alpha 2-antiplasmin in the early extracorporeal circulation (ECC) phase, exceeding the average hematocrit reduction accounted for by dilution. This drop was the least distinct with CML 2 systems, both with pulsatile and nonpulsatile perfusion, indicating system-inherent influences. Leucocyte cound and PMN-elastase concentration rose significantly during ECC irrespective of oxygenator tested of flow type applied. The rise in leucocyte count even continued for about 4 h after ECC. During the first 40 min of ECC, these changes were paralleled by a significant rise in C3a concentration, suggesting complement activation as a main cause for PMN activation. However, there is reason to suppose involvement of further mechanisms operating in PMN activation, since the elevated C3a-concentrations began to fall off while leucocyte count and PMN-elastase concentrations were still increasing.

Acute-Phase Proteins↗

PubMed1978

[Acute-phase proteins in women with a copper IUD (author's transl)].

Acute-phase (AP) proteins haptoglobin, alpha1-antitrypsin and C-reactive protein were measured in 50 women before and 10 to 30 weeks after insertion of a copper T-200. No statistically significant increase in AP proteins was found. Since these proteins are synthesized in the liver, the results indicate the lack of a systemic humoral reaction of the organism in women with a copper-containing IUD.

C-Reactive Protein↗

PubMed1992

Cotrimoxazole therapy of Toxoplasma gondii encephalitis in AIDS patients.

Twenty-four consecutive HIV-positive patients affected by Toxoplasma gondii encephalitis received trimethoprim-sulfamethoxazole (cotrimoxazole) as acute-phase treatment. Two dosage regimens of cotrimoxazole were used: 40 mg/kg/day (12 patients) or 120 mg/kg/day (12 patients) of total compound (trimethoprim plus sulfamethoxazole). Clinical and radiological responses to treatment were evaluated, and the product-limit method for survival data analysis was used. Eighteen of 24 patients showed both a clinical and radiological response (75% response rate). There were no differences in response rates between patients receiving the two dosage regimens of cotrimoxazole. Adverse reaction consisted of leukopenia (two cases) and skin rash (three cases) which led to the discontinuation of the drug in one case. These results suggest that a randomized, controlled clinical trial should be carried out comparing cotrimoxazole versus sulfadiazine-pyrimethamine in AIDS patients with Toxoplasma gondii encephalitis.

Acquired Immunodeficiency Syndrome↗

PubMedDate not supplied

Agarose gel filtration of concentrated fecal extracts containing virus-like particles associated with hepatitis A.

Virus-like particles shown to be associated with hepatitis A infection were recently visualized by immune electron microscopy in human and chimpanzee acute-phase fecal extracts. Agarose gel filtration of concentrated chimpanzee fecal extracts containing those 27-nm diameter particles separated more than 99% of the high molecular weight fecal impurities into two major peaks as determined by absorbance at 280 and 260 nm. The hepatitis A-associated particles were found between these two peaks by both immune electron microscopy and a new immunoradiometric assay.

Animals↗

PubMed2024

Systematic Proteome Profiling of Maternal Plasma for Development of Preeclampsia Biomarkers.

Preeclampsia (PE) is a hypertensive disorder of pregnancy with various clinical symptoms. However, traditional markers for the disease including high blood pressure and proteinuria are poor indicators of the related adverse outcomes. Here, we performed systematic proteome profiling of plasma samples obtained from pregnant women with PE to identify clinically effective diagnostic biomarkers. Proteome profiling was performed using TMT-based liquid chromatography-mass spectrometry (LC-MS/MS) followed by subsequent verification by multiple reaction monitoring (MRM) analysis on normal and PE maternal plasma samples. Functional annotations of differentially expressed proteins (DEPs) in PE were predicted using bioinformatic tools. The diagnostic accuracies of the biomarkers for PE were estimated according to the area under the receiver-operating characteristics curve (AUC). A total of 1307 proteins were identified, and 870 proteins of them were quantified from plasma samples. Significant differences were evident in 138 DEPs, including 71 upregulated DEPs and 67 downregulated DEPs in the PE group, compared with those in the control group. Upregulated proteins were significantly associated with biological processes including platelet degranulation, proteolysis, lipoprotein metabolism, and cholesterol efflux. Biological processes including blood coagulation and acute-phase response were enriched for down-regulated proteins. Of these, 40 proteins were subsequently validated in an independent cohort of 26 PE patients and 29 healthy controls. APOM, LCN2, and QSOX1 showed high diagnostic accuracies for PE detection (AUC >0.9 and p < 0.001, for all) as validated by MRM and ELISA. Our data demonstrate that three plasma biomarkers, identified by systematic proteomic profiling, present a possibility for the assessment of PE, independent of the clinical characteristics of pregnant women.

Humans↗

PubMed1992

[The pathogenesis of psoriasis--new results].

A great deal of new immunological, biochemical, and cell biological information has been published on the pathogenesis of psoriasis. Many of these findings must be considered to be epi-phenomena of the inflammatory reaction (clinical correlate--erythema) and hyperproliferation of keratinocytes (scaling). The mechanisms of the psoriatic inflammatory reaction and of the specific neutrophil infiltration can now be more readily understood following the discovery of adhesion molecules, and the identification of new mediators--in particular NAP-1/IL-8. Proliferation-promoting factors for keratinocytes in vitro, that is, possible mediators of psoriatic scaling, are listed, and currently known changes in expression and concentration in psoriatic lesions are discussed.

Acute-Phase Proteins↗

PubMed1978

The in vitro interactions of rat pancreatic elastase and normal and inflammatory ray serum.

The partition of labelled rat pancreatic elastase (EC 3.4.21.11) between the different protease inhibitors of rat plasma was studied at different levels of saturation of the inhibitors of rat plasma was studied at different levels of saturation of the inhibitor capacity of plasma with the enzyme. The reaction mixtures were analysed by immunoelectrophoretic methods utilizing specific antisera against the different inhibitors and by gel filtration on Sephadex G-200. Rat serum was shown to contain four elastase binding proteins. alpha 1-antitrypsin, alpha 1-macroglobulin and alpha 2-acute phase protein and alpha 1-inhibitor 3 which exhibits immunologic cross-reaction with human inter-alpha-trypsin inhibitor and is of similar molecular weight. With minute amounts of labelled elastase the partition among the binding protein was alpha 1-macroglobulin 60%, alpha 1-antitrypsin 24% and alpha 1-I3 16%. The 60% value of alpha 1-M bound radioactivity in normal serum corresponds to the sum of alpha 1-M and alpha 2-AP labelling in inflammatory serum.

Acute-Phase Proteins↗

PubMed1979

Effect of human cord and postoperative serum on experimental inflammation in the rat.

Human cord and postoperative serum depressed the oedema provoked by mediators of the inflammatory reaction such as bradykinin, histamine, serotonin and prostaglandin E2 and also the experimental inflammation caused by carrageenin. Normal human and pregnancy serum did not have such an effect. In two cases of open neural tube defect, one of anencephaly and another of spina bifida, human amniotic fluid also had a strongly depressing effect on the experimental oedema provoked by serotonin. Human amniotic fluid from normal pregnancies did not inhibit this experimental inflammation. A protein-fraction of mol. wt 30,000--100,000 has been isolated from the inhibiting sera and shows the anti-inflammatory activity to be dose-related towards all the oedema-provoking substances used. Immunological studies showed that the inhibiting factor could be a protein in the pre-albuminic region, while alpha-foetoprotein did not appear to be responsible for the anti-inflammatory activity. Our conclusion is that human serum contains a protein of foetal origin with an acute-phase character and strong anti-inflammatory activities analogous to rat alpha 2-macrofoetoprotein.

Amniotic Fluid↗

PubMed1992

Evidence for lipopolysaccharide binding in human granulosa-luteal cells.

We investigated whether human granulosa-luteal (GL) cells exhibited lipopolysaccharide (LPS)-binding protein, and the response of follicular aspirate cells to LPS in vitro. Follicular aspirates taken from a human in-vitro fertilization and gamete intra-fallopian-tube transfer programme were subjected to Percoll gradients in order to isolate an enriched population of GL cells. GL cells exhibited specific LPS-binding protein, detected by autoradiography of the cellular lysate on SDS-PAGE after the cells were specifically labelled with a radioiodinated, photoactivable and reducible LPS derivative. LPS binding to the cells was also detected by the appearance of immunofluorescence associated with the cellular membrane when incubated with a fluorescent conjugated LPS receptor antibody. Ninety-four per cent of the cells exhibiting immunofluorescent LPS-binding protein were also positive for the steroidogenic enzyme 3 beta-hydroxysteroid dehydrogenase, as detected by cytochemistry. In order to detect a response to LPS, the enriched population of GL cells were cultured in vitro in the presence or absence of LPS; after 16 h of culture, tumour necrosis factor-alpha (TNF) mRNA was detected by reverse transcription-polymerase chain reaction and Southern blot analysis of the amplified cDNA. The expression of TNF mRNA was enhanced when the cells were cultured in the presence of LPS, which also significantly enhanced TNF secretion into the media during the 16-h period. These results reveal that GL cells exhibit LPS-binding protein and thus increased TNF secretion occurs in response to LPS in follicular aspirate cells. The source of ovarian TNF may be leukocytes, macrophages and/or GL cells.

3-Hydroxysteroid Dehydrogenases↗

PubMed1976

Conformational flexibility of the serum amyloid precursor SAA.

SAA is a normal acute-phase serum protein and is thought to be the precursor of amyloid protein AA which is deposited as insoluble beta-pleated sheet fibrils in secondary amyloidosis. Native SAA has a molecular weight of 160,000 and has not been isolated; it has been most frequently purified as a species (designated SAAL) of 12,500 mol. wt. by gel filtration in dissociating solutions. The conformational properties of SAA proteins in patients with and without amyloidosis have been compared in an effort to determine the factors involved in the induction of the beta-pleated sheet conformation in the amyloid SAA protein prior to fibril deposition. Amyloid and nonamyloid SAA proteins are similar in that they readily undergo conformational changes which result in the formation of heterogenous mol. wt. SAA species and in an increased exposure of antigenic determinants which cross-react with AA fibril proteins. Amyloid and nonamyloid SAA are different, however, in that amyloid SAA is more resistant to dissociation to SAAL. Amyloid SAAL, while similar to nonamyloid SAAL in immunoreactivity, shows a greater tendency toward aggregation. The relative resistance of both amyloid SAA and SAAL to complete dissociation may play an important role in amyloid fibril formation from these precursors.

Amyloid↗

PubMed1977

Acute-phase proteins from the liver and enzymes from myocardial infarction; a quantitative relationship.

In 14 patients with acute myocardial infarction (M.I.) not having any other disease, the possible quantitative relationship between enzymes from M.I. and changes in concentration of acute phase reactants coming from the liver were studied. The patients were followed up until 1 1/2 years after M.I. and comparison of baseline-protein values took place using a control group of 18 healthy individuals. Quantitation of protein changes was done by planimetric determination of the area under the concentration curve and by taking peak values. The myocardial infarction was quantitatively estimated by mathematical analysis of the time course of alpha-hydroxybutyrate dehydrogenase (alpha-HBDH) plasma concentrations and by taking peak values. A quantitative relationship with enzymatic infarct size was found for haptoglobin, alpha1-acid glycoprotein, alpha1-antitrypsin, C-reactive protein, fibrinogen and E.S.R. Albumin and transferrin did not show a negative quantitative relationship with enzymatic infarct size. Humoral factors originating from the site of tissue injury and evoking in proportion a positive acute phase reaction by the liver are probably the basis for this observed quantitative relationship.

Acute Disease↗

PubMed1992

Interleukin-6 and its receptor in autoimmunity.

Interleukin-6 (IL-6) is a multifunctional cytokine which acts on a wide variety of cells, regulating immune response, acute phase reaction and hematopoiesis. In accordance with its pleiotropic functions, IL-6 is indicated to be involved in the pathogenesis of several diseases including autoimmunities, lymphoid malignancies and inflammations. An elevated level of IL-6 is demonstrated in patients with rheumatoid arthritis and cardiac myxoma, which can explain symptoms of these diseases, such as autoantibody production and increase in acute phase proteins. Therefore, inhibitors of IL-6 production or IL-6 receptor-mediated signal transduction may be used for treatment of IL-6-related diseases. The IL-6 receptor system consists of two membrane proteins, a ligand-binding chain (IL-6R) and a non-ligand-binding signal transducer, gp130, both of which belong to the cytokine receptor family. Binding of IL-6 to IL-6R triggers the association of IL-6R and gp130, and gp130 in turn transduces the signal. A nuclear factor for controlling IL-6 gene expression (NF-IL6) is also involved in the transcriptional regulation of various acute-phase protein genes. IL-6-stimulation of hepatocytes, through modification of pre-existing NF-IL6 protein, leads to binding of NF-IL6 to IL-6-responsive elements and activation of acute-phase protein genes. NF-IL6 is shown to recognize the enhancer core sequence of several viruses, suggesting a possible relationship of virus infection and IL-6 expression.

Acute-Phase Proteins↗