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PubMed1992

[Leukocyte number, protein-inhibitor, and complement in smokers].

In the present study, the number of leukocytes was increased in smokers, dependent on the amount of exposure to smoke (duration and cigarette number/day). The differential leukocyte count did not differ between smokers and non-smokers. Leucocyte-associated serum components such as alpha 1-antitrypsin, alpha 2 globulin, and complements did not differ in smokers. There was no relationship between neutrophils in peripheral blood and BAL fluid. These findings suggest that an increased number of leukocytes in smokers is not attributable to activation of complement, and that anti-proteinase serum levels including alpha 1-antitrypsin and alpha 2 globulin are unchanged in both smokers and ex-smokers.

Adult↗
PubMed2004

[Procalcitonin as an indicator of infection in patients with liver cirrhosis].

Incidence of bacterial infections in hospitalised patients with liver disease is high. Due to a liver dysfunction immune reactivity is significantly impaired and bacterial infections are more frequent. Also incidence of nosocomial infections is higher in patients with liver disease compared to patients hospitalised for other conditions. To make a differential diagnosis of infectious and non-infectious aetiology of an inflammation is very difficult. Characteristic laboratory tests for bacterial infection include test of a number of leucocytes in peripheral blood, differential count of leucocytes, erythrocyte sedimentation, procalcitonin, C-reactive protein, tumor necrosis factor alpha, interleukin-1, interleukin-6, interleukin-8, and complement fragment C3a. Clinically the most significant are C-reactive protein test and procalcitonin test. Procalcitonin is a protein, a calcitonin precursor, which is in healthy individuals produced by cells of thyroid gland. A half-life of procalcitonin in serum is 20-24 hours which makes it suitable for daily monitoring and enables to control a course of treatment and to distinguish bacterial infection from other types of inflammations. Procalcitonin levels rise in bacterial, parasite, and yeast infections. Elevated procalcitonin levels appear only in inflammations of an infectious etiology with systemic signs. In patients with liver cirrhosis bacterial infections are more frequent. They usually include spontaneous bacterial peritonitis, infection of the respiratory system, urinary infections, and bacteremia. A timely proof of a bacterial infection and an appropriate and effective antibiotic therapy lead to an improvement of the general state of a patient and to his/her better prognosis. Procalcitonin determination is appropriate for diagnosing infections and control of treatment.

Bacterial Infections↗
PubMed2004

Inflammatory response after coronary revascularization: off-pump versus on-pump (heparin-coated circuits and poly2methoxyethylacrylate-coated circuits).

OBJECTIVE: Off-pump coronary artery bypass grafting (OPCAB) may reduce the inflammatory response associated with cardiopulmonary bypass (CPB) and contribute to minimizing postoperative complications. Heparin-coated circuits and poly2methoxyethylacrylate (PMEA)-coated circuits were developed to reduce such complications. We compared the postoperative inflammatory response with or without CPB. METHODS: Eighteen consecutive patients undergoing isolated coronary artery bypass grafting (CABG) were divided into three groups: OPCAB group (n=6), heparin-coated circuits group (n=6), PMEA-coated circuits group (n=6). The plasma concentrations of the following inflammatory markers were measured: cytokines [interleukin (IL-10)], polymorphonuclear elastase (PMNE), coagulofibrinolytic factor [thrombin-antithrombin III complex (TAT)], complement factor (C3a). RESULTS: At the end of CPB, IL-10 and TAT concentrations were significantly different among the three groups (OPCAB group < PMEA-coated group < heparin-coated group). The PMNE concentration was significantly lower in the OPCAB group and the heparin-coated group as compared to the PMEA-coated group both at the end of CPB and 4 hours after CPB. C3a concentration was significantly lower in the OPCAB group than in the CPB groups at the end of CPB. Clinical variables did not differ significantly among the three groups. CONCLUSION: Off-pump CABG is associated with a reduction in the inflammatory response when compared with on-pump CABG, using either PMEA-coated or heparin-coated circuits.

Acrylates↗
PubMed1992

The relation between triglyceride synthesis in peripheral tissues and postprandial plasma triglyceride levels: preliminary evidence of a role for acylation stimulating protein.

The present study examines the hypothesis that the rate at which peripheral tissues synthesize triglycerides is a key determinant of the rate at which they are removed from plasma. The cells of greatest interest in this regard would, of course, be the adipocytes. However, serial sampling of this tissue is not possible in man. We have approached the question indirectly, by studying triglyceride synthesis in human mononuclear cells before and after an oral fat load. In addition, plasma levels of Acylation Stimulating Protein (ASP) were measured after an overnight fast and 4 h after ingestion of the oral fat load. Similar measurements were made in the same subjects after fasting overnight and with the fast extended for 4 additional hours. With the extended fast, no parameter measured changed significantly. However, after the oral fat load, the following changes were found to be significant: plasma triglycerides increased (63.6 +/- 31.1 vs 101.5 +/- 43 mg/dl, p less than 0.005) as did d less than 1.006 g/ml triglycerides (42.3 +/- 22.8 vs 78.0 +/- 39.7 mg/dl, p less than 0.005) and plasma ASP (10.4 +/- 2.2 vs 14.7 +/- 2.3 mg/dl, p less than 0.005). In addition, the rate of triglyceride synthesis in the mononuclear cells increased significantly (1.22 +/- 0.3 vs 1.52 +/- 0.3 nmol oleate/mg cell protein per h, p less than 0.005). There was also a significant inverse relation between the increase in the d less than 1.006 triglycerides between 0 and 4 h and the increase in triglyceride synthesis in the mononuclear cells (r = 0.91, p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Acylation↗
PubMed2006

[Acylation stimulating protein--its role in control of metabolism in the adipose tissue].

Multiple hormones and enzymes participate in the lipid storage. One of them is acylation stimulating protein. Acylation stimulating protein is produced predominantly by adipocytes. After the binding on specific receptor at the surface of adipocytes, acylation stimulating protein leads to enhancement of triglyceride synthesis. This process is mediated by protein-kinase C. Concurrently, glucose transporters move from the cytoplasm to the adipocyte surface. Higher glucose disposal leads to a sufficient substrate availability for triglyceride synthesis. Acylation stimulating protein also stimulates pancreatic insulin secretion. Total acylation stimulating protein level in plasma is related to the adipose tissue mass and it positively correlates with many anthropometric parameters and with serum insulin level. In acylation stimulating protein deficient mice, resistance to the obesity development after a high fat diet was observed. Adipose tissue mass is lower in the acylation stimulating protein deficient mice and higher insulin sensitivity was shown in acylation stimulating protein deficient mice compared to a wild type mice. Acylation stimulating protein pathway may have an important role in the obesity development.

Adipose Tissue↗
PubMed2006

[Arrested coronary artery bypass grafting with modified percutaneous cardiopulmonary support circuit (mini-pump system)].

Therapeutic strategy for ischemic heart disease has been changing in this decade. We attempted to improve the conventional extracorporeal circulation with the aim of less invasive coronary artery revascularization. Our extracorporeal circulation has been used since 2002, and called the 'mini-pump system' or 'MECC (minimized extracorporeal circulation) system'. The mini-pump system has a centrifugal pump, a membrane oxygenator, a soft reservoir and the characteristics of low prime volume completely closed circuit and low volume cardioplegia. We investigated the degree of invasiveness of the mini-pump system by examining the clinical outcomes (minimum hematocrit, the amount of transfusion and so on), thrombin-antithrombin III complex (TAT), complement factor (C3a) and interleukin (IL)-10 levels. The mini-pump system demonstrated better value than the conventional extracorporeal circulation (TAT; 19.5 : 66.1 ng/ml, C3a; 1,349 : 1,895 mg/dl, IL-10; 105 : 486 pg/ml, respectively) and proved to be less invasive. The incidence of postoperative atrial fibrillation using the mini-pump system was less than that of the conventional extracorporeal circulation. In this issue we presented the vista of the mini-pump system by showing how it decreased invasiveness.

Aged↗
PubMed1990

[Inflammation and rejection].

The inflammation represents an important cause of allograft tissue lesions during ongoing rejection episodes. Such inflammation is mediated, at least in part, via the release of different soluble mediators. Some of these endogenous inflammation mediators are well known and include prostaglandins, leukotriens, histamine or histaminergic compounds and factors induced by the activation of the complement cascade (C3a, C5a). More recently, different molecules have been characterized, namely cytokines that are potent mediators of both immune and inflammatory reactions. Cytokines are produced by a wide variety of cells types (i.e., inducing immune and non immune cells) and expressing pleiotropic effects. The synergism between these various inflammation mediators finally provoke the anatomopathological lesions characteristic of a rejection process that are vascular lesions, edema formation and white blood cell chemotaxis leading to massive cellular infiltration. The aim of this brief review is to analyze the more recent data of the literature concerning cytokines that, applied to the field of organ transplantation, may provide further insights onto the relationships existing between inflammation and allograft rejection.

Cytokines↗
PubMed1991

Complement activation by dental implants.

Activation of complement leads to the generation of C3a and C5a inflammatory peptides. C5a is a potent chemotactic factor, stimulating the secretion of proteolytic enzymes by neutrophils and osteoclast activating factor/Interleukin-1 by monocytes. In vitro generation of C3a and C5a was measured by radioimmunoassay techniques. The results showed significant complement activation by all implants tested when compared to the control serum incubation. It is concluded that all of the implants studied activated the complement system and are not physiologically inert. Complement activation, therefore, may contribute either positively to healing or negatively to a poor outcome in osseoadaptation initially or over time.

Complement Activation↗
PubMed1991

Levels of acylation stimulating protein in obese women before and after moderate weight loss.

Acylation stimulating protein (ASP) is a small (MW 14,000) basic (pI 9.0) protein which has only recently been purified from human plasma. Since ASP is the most potent known stimulant of triglyceride synthesis in human adipose tissue, the present study was designed to determine if plasma ASP was elevated in patients with moderate obesity, and if so, whether this level changed with weight loss. Fasting plasma ASP levels were determined by competitive ELISA immunoassay in 10 obese women before weight loss, immediately after weight loss, and 3 months after maintaining weight reduction. Their plasma ASP results were compared to 17 age and sex-matched lean controls. With weight loss, plasma ASP decreased significantly: 19.6 +/- 10.7 mg/dl before weight loss vs 15.0 +/- 9.5 mg/dl after weight loss vs 13.8 +/- 7.7 mg/dl 3 months after being weight stable, P less than 0.05 initial vs final value. Nevertheless, plasma ASP was significantly higher than the control value at all three times. Thus, before weight loss, the average ASP in the obese group was four times that in the control group (19.6 +/- 10.7 vs 5.1 +/- 3.6 mg/dl, P less than 0.0005) while even 3 months after weight loss, it remained almost three times above the control group (13.8 +/- 7.7 vs 5.1 +/- 3.6 mg/dl, P less than 0.0005). The data suggest, therefore, that an elevated plasma level of ASP is common in obesity, that the level of plasma ASP may reflect the fat cell mass present in an individual, and raises the possibilities that ASP may play a role in initiation or maintenance of the obese state.

Adult↗
PubMed1990

Regulation of apoB secretion from HepG2 cells: evidence for a critical role for cholesteryl ester synthesis in the response to a fatty acid challenge.

Secretion of hepatic apoB lipoproteins removes excess triglyceride from the liver. However, the mechanism by which synthesis of apoB, which occurs on the rough endoplasmic reticulum, is coordinated with synthesis of triglyceride, which takes place in the smooth endoplasmic reticulum, is not known. To examine this question, we have manipulated intracellular synthesis of triglyceride and cholesteryl ester in HepG2 cells and determined the impact of these maneuvers on apoB secretion. Since cholesteryl ester is the only major lipid class synthesized in the rough endoplasmic reticulum, our hypothesis was that, in response to a fatty acid challenge, synthesis of cholesteryl ester rather than synthesis of triglyceride would be the immediate trigger to apoB secretion. Oleate complexed to bovine serum albumin caused intracellular triglyceride synthesis to increase 6-fold and cholesteryl ester synthesis to increase almost 3-fold, while apoB secretion into the medium increased by 2.5-fold (P less than 0.0125) at all time points between 4 and 24 h. Addition of acylation stimulating protein to the medium further stimulated both triglyceride and cholesteryl ester synthesis (58% and 108%, respectively) above oleate alone and this resulted in a 50% increase in apoB secretion (P less than 0.0025). By contrast, both progesterone and 2-bromooctanoate inhibited triglyceride and cholesteryl ester synthesis and these effects were associated with reduced apoB secretion. Lovastatin inhibited cholesteryl ester synthesis (45%, P less than 0.0025); however, at the doses used, triglyceride formation was unaffected. Under these circumstances, apoB secretion was reduced by 25% (P less than 0.05). Similarly, 58-035 (an inhibitor of acyl CoA:cholesterol acyltransferase) on the one hand reduced cholesteryl ester synthesis markedly (59%, P less than 0.005), but on the other increased triglyceride synthesis though not statistically significantly (65%, P NS), and again this resulted in decreased apoB secretion (25%, P less than 0.005). Control experiments established that changes in low density lipoprotein catabolism did not contribute importantly to the quantity of apoB in the medium. Taken together, the data indicate that, at least in HepG2 cells, there are parallel changes in cholesteryl ester synthesis and apoB secretion and suggest that it is cholesteryl ester synthesis, not triglyceride synthesis, that is the immediate regulator of apoB secretion when these cells are exposed to an increased influx of fatty acids. However, alternative or additional regulatory mechanisms, such as, for example, a role for acylation of apoB, are not excluded by these studies.

Apolipoproteins B↗
PubMed1990

Receptor expression and functional status of cultured human eosinophils derived from umbilical cord blood mononuclear cells.

Selective use of recombinant human cytokines has enabled the culture of large numbers of eosinophils from human cord blood mononuclear cells, raising the possibility of their use as a model of eosinophil function. Cultured eosinophils (CE) were compared with normal-density peripheral blood eosinophils (PBE) in terms of their membrane receptor expression and function. Fc gamma R and CR1 expression of CE and PBE was similar. In contrast, the specific mean fluorescence for LFA-1 alpha, p150,95 alpha, ICAM-1, and HLA-DR was significantly elevated for CE compared with PBE. CE responded in PAF-induced chemotaxis in a similar fashion to PBE. CE gave higher numbers of both resting and platelet activating factor (PAF)-stimulated immunoglobulin G (IgG)- and C3b-dependent rosettes than PBE. CE and PBE had comparable capacity to kill IgG- and C-opsonized schistosomula in terms of both baseline values and PAF-induced enhancement of cytotoxicity. Baseline adherence by CE and PBE to plasma-coated glass was essentially the same, but stimulated adhesion (PAF) of CE was lower. Compared with PBE, CE generated less than half the amounts of extracellular and cell-associated PAF induced by calcium ionophore A23187 stimulation. Unlike PBE, CE did not generate PAF after exposure to IgG-coated Sepharose particles. CE stimulated with IgG-coated beads generated small quantities of LTC4, while A23187 stimulation resulted in approximately half the LTC4 levels observed with PBE. The total cell content of eosinophil peroxidase (EPO) was similar for CE and PBE. These data suggest that although CE and PBE have many phenotypic and functional properties in common there are quantitative differences that may be a consequence of their immaturity and/or the influence of the cytokines used in their culture.

Animals↗
PubMed1991

Further insights into the pathophysiology of hyperapobetalipoproteinemia: role of basic proteins I, II, III.

Hyperapobetalipoproteinemia (hyperapoB), a familial lipoprotein disorder characterized by an increase in small, dense, low-density lipoprotein (LDL) particles, is strongly associated with coronary artery disease. There are two metabolic defects in hyperapoB: an increased synthesis of a very-low-density lipoprotein in liver, resulting in an overproduction of LDL, and a delayed clearance of post-prandial triglyceride and free fatty acids. To date, defects in the apolipoprotein B gene do not appear to explain the hyperapoB phenotype. Defect(s) in the uptake or intracellular metabolism of free fatty acids have been found in cells from hyperapoB patients. Three basic proteins (BPs)--BP I (Mr 14,000, pI 9.10), BP II (Mr 27,500, pI 8.48), and BP III (Mr 55,000, pI 8.73)--were isolated from normal human serum. Compared with normal fibroblasts, cultured hyperapoB fibroblasts incubated with BP I, which appears to be the same protein as acylation-stimulating protein (ASP), showed 50% less stimulation of triglyceride acylation and cholesterol esterification, whereas BP II markedly stimulated cholesteryl ester formation, and BP III caused no difference in response vs normal fibroblasts. However, in cultured normal human monocyte macrophages, BP III, but not BP I or BP II, stimulated cholesteryl esterification two- to threefold. BP I, BP II, and BP III may provide new insights into normal metabolism of lipids, lipoproteins, and free fatty acids and the pathophysiology of hyperapoB.

Animals↗