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Biomedical subjects

M Zembala

Publications and source records attributed to M Zembala.

At least 55 records · Page 3Linked to original sources
PubMed1998

The IL-6 gene expression by leukemic cells from acute lymphoblastic leukemia common and T type and modulation of IL-6 production by TNF.

The tumour necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) mRNA accumulation and the release of the cytokines TNF-alpha and IL-6 was determined in leukemic cells isolated from bone marrow biopsy from patients with acute lymphoblastic leukemia: ALL-common type (cALL), 11 patients; ALL-T type, nine patients. The non-leukemic bone marrow cells (BMMC) and peripheral blood mononuclear cells (PBMC) from healthy donors were used as a control. The mRNA was assessed by fluorescent in situ hybridization in cell suspension and analyzed with flow cytometry. The accumulation of cytokine mRNA was higher in cALL cells as compared to ALL-T and PBMC (control) and was comparable to cytokines mRNA accumulation in BMMC. The production of IL-6 by leukemic cells from both types of leukemia was significantly lower than in BMMC. The bioactive TNF was not detected in either of the leukemia groups studied. TNF-alpha protein was produced by ALL-T cells and BMMC but not by cALL type of leukemic cells. The synthesis of IL-6 was significantly enhanced by TNF-alpha in BMMC and ALL-T while the presence of TNF-alpha had no effect on IL-6 synthesis in the culture of cALL leukemic cells. It was concluded that despite IL-6 and TNF-alpha mRNA contents, leukemic cells representing early stage of B-cell development (CD10+) showed disregulation of production of these cytokines.

Adolescent↗
PubMed1998

Lymph node micrometastases in early gastric carcinoma alone inadequately reflect the new model of metastatic development.

Forty early gastric carcinomas were studied retrospectively for the presence of micrometastases in the regional lymph nodes by cytokeratin 18 immunostaining. Tumor typing, grading and staging were reestimated and ploidy of the tumors was assessed with the CAS 200. Micrometastases were found only in 3 cases, while macrometastases were present in 6 cases (micrometastases were present in 3 of those 6 patients). Micrometastases had no effect on patients' survival. It has been concluded that in early gastric carcinoma micrometastases do not influence typing, grading, staging of the tumor and have no prognostic significance. It has also been concluded that it takes more than the diagnosis of micrometastasis alone to estimate its real prognostic significance, especially in view of the new by emerging concept of cancer metastatic development.

Adult↗
PubMed1997

Melatonin affords protection against gastric lesions induced by ischemia-reperfusion possibly due to its antioxidant and mucosal microcirculatory effects.

Melatonin, a pineal hormone, is known to scavenge oxygen free radicals and to be present in the gut but little is known about its role in the protection of gastric mucosa against the damage accompanied by a marked increase in these radicals. This study was designed to determine the effects of melatonin on the formation of acute gastric lesions induced by ischemia-reperfusion and, for comparison, by a topical irritant such as 100% ethanol. It was found that pretreatment with melatonin at a dose of 5 mg/kg given intragastrically reduced significantly gastric lesions induced by ischemia-reperfusion and this was accompanied by a reduction in free radicals in the blood and by attenuation of the fall in gastric blood flow. In contrast, melatonin failed to affect acute gastric lesions induced by 100% ethanol. We conclude that melatonin is capable of protecting gastric mucosa from the damage caused by ischemia-reperfusion and that this action is mediated, at least in part, by limitation of the generation of free radicals and by attenuation of the fall in gastric blood flow.

Animals↗
PubMed1997

Influence of Polydispersity on Random Sequential Adsorption of Spherical Particles

Random sequential adsorption (RSA) of polydisperse mixtures of hard and interacting spherical particles was analyzed. Theoretical results were derived by performing numerical MC simulations both for Gaussian and for continuous distributions of particle sizes characterized by standard deviations below 20%. Adsorption kinetics of these mixtures was determined for a broad range of times showing that for tau < 5 the influence of polydispersity was rather minor for both Gauss and continuous particle size distributions. More significant deviations were predicted for the asymptotic adsorption regime close to jamming. In the case of continuous distributions this limiting kinetics could be described by the power law dependence thetainfinity - theta approximately tau-1/3 in accordance with the predictions of G. Tarjus and J. Talbot (1991, J. Phys. Math Gen. 24, L913). The jamming concentration thetainfinity for hard (noninteracting) particles was found to increase proportionally to sigma;. It was also shown that the polydispersity of particle mixtures can exert an effect on the structure of the adsorption layer (characterized in terms of the pair correlation function). The broadening of this function was confirmed experimentally by using colloid suspensions of spherical particles (polystyrene latex) characterized by sigma; = 6-10%.

Journal Article↗
PubMed1997

Apoptosis of human monocytes/macrophages in Mycobacterium tuberculosis infection.

Tuberculosis (TB) is still a major health problem, both as a single disease entity and as a cofactor in AIDS. The interaction between macrophage and Mycobacterium tuberculosis (MTB) is a critical step in the establishment of an early chronic infection. This study analyses the capacity of MTB to induce apoptosis in cells obtained by broncho-alveolar lavage (BAL) from patients with reactive pulmonary tuberculosis and from AIDS patients with disseminated pulmonary tuberculosis. Apoptosis was increased three-fold in BAL cells obtained from patients with pulmonary tuberculosis and even more markedly in alveolar macrophages of MTB-infected AIDS patients, compared with controls. Apoptosis was analysed and characterized by propidium iodide (PI) incorporation, terminal deoxy transferase (TDT)-mediated dUTP-biotin nick end labelling (TUNEL), and tissue transglutaminase (tTG) expression. The MTB-macrophage interaction was also investigated in vitro by infecting monocyte-derived macrophages (MDM) with MTB (virulent strain H37Rv). The induction of apoptosis by MTB required viable bacteria, was dose-dependent, and was restricted to H37Rv. Infection with either Mycobacterium avium complex (MAC) or HIV-1 and treatment with heat-killed MTB failed to induce apoptosis.

AIDS-Related Opportunistic Infections↗
PubMed1997

Cytokine production in transient hypogammaglobulinemia and isolated IgA deficiency.

BACKGROUND: Transient hypogammaglobulinemia of infancy and isolated IgA deficiency are characterized by normal numbers of circulating B lymphocytes. It is likely that no single abnormality, but rather different factors, may be relevant for the delayed onset of IgG synthesis in transient hypogammaglobulinemia or for the differentiation defect of B cells in IgA deficiency. These factors may include defective production of cytokines or an abnormal response of B cells to various mediators. Alternatively, some cytokines may act as inhibitory factors of B-cell function. METHODS: The ability of peripheral blood mononuclear cells from children with proved or probable transient hypogammaglobulinemia (30 patients) and IgA deficiency (15 patients) to secrete several cytokines on stimulation with phytohemagglutinin in vitro was analyzed. RESULTS: An enhanced production of tumor necrosis factor (TNF)-alpha, TNF-beta, and IL-10 was observed in transient hypogammaglobulinemia; whereas secretion of IL-1, IL-4, and IL-6 was essentially similar in the control and patient groups. Increased frequency of mononuclear cells secreting TNF-alpha was seen in the patient groups. Apart from elevated production of TNF-alpha, no other abnormalities in cytokine synthesis in selective IgA deficiency were observed. In vitro observations showed that exogenously added TNF-alpha and TNF-beta inhibited IgG and IgA secretion by pokeweed mitogen-stimulated mononuclear cells. During follow-up of 10 children, normalization of serum IgG level was associated with a decrease in previously elevated TNF-alpha and TNF-beta production, but IL-10 production remained unchanged. CONCLUSION: These results suggest that TNF may be involved in the regulation of IgG and IgA production and can be associated with an arrest of IgG and IgA switch of B cells in hypogammaglobulinemia. The balance between TNF and IL-10 may be important for the normal development of IgG-secreting B cells.

Agammaglobulinemia↗
PubMed1997

Vancomycin down-regulates lipopolysaccharide-induced tumour necrosis factor alpha (TNF alpha) production and TNF alpha-mRNA accumulation in human blood monocytes.

The cytokines play an important role in the cascade of the pathological events leading to septic shock. The TNF alpha produced by monocytes/macrophages upon stimulation with bacterial fragments may contribute to induction of this cytokine cascade. Moreover, the antibiotics used for antimicrobial therapy may cause the increase of TNF alpha production due to massive bacterial killing and exposure of monocytes/macrophages to bacterial cell constituents. To investigate the effect of Vancomycin on TNF alpha production, an in vitro model of LPS-stimulated monocytes was used. The level of TNF alpha protein or TNF biological activity were tested in the culture supernatants of monocytes with LPS. Vancomycin down-regulated, in dose-dependent manner, the TNF alpha production. Vancomycin also inhibited TNF alpha-mRNA accumulation in LPS-stimulated monocytes, as assessed by fluorescence in situ hybridization (FISH) in cell suspension. The down-regulation of TNF alpha production in LPS-stimulated monocytes may indicate that inhibition of this cytokine release is one of the important therapeutic effects of Vancomycin in sepsis.

Animals↗
PubMed1997

Phenotypic changes of monocytes induced by HIV-1 gp120 molecule and its fragments.

Several phenotypic and functional changes of monocytes (M phi) have been described in HIV-1+ subjects and AIDS patients. Some of these changes that are pertinent for immunopathogenesis of the disease may be induced by HIV-1 envelope glycoprotein 120 (gp120). In the present study the effect of recombinant full length gp120 (FLgp120) and its two fragments: rp120cd (aa 410-511) and rp120 (aa 446-511) on the expression of the surface molecules of M phi cultured in vitro was determined. The FLgp120 and rp120cd caused upregulation of CD14 and CD44. The rp120cd peptide significantly increased the expression of CD16 (Fc gamma receptor type III) and TNF receptor type II. In contrast, the rp120 downregulated HLA-DR, CD64 (Fc gamma RI), interferon gamma receptor and induced IL-10 production by M phi. This study indicates that gp120 molecule and its fragments may induce several phenotypic changes of M phi in particular the increased proportion of CD14+CD16+ cells that is observed in the blood of AIDS patients. These results provide further evidence for variable response of M phi to gp120 which may explain the variability of phenotypic changes and heterogeneity of M phi subsets seen in HIV-1 disease.

Cell Adhesion Molecules↗
PubMed1997

Infection of human monocytes with Mycobacterium tuberculosis enhances human immunodeficiency virus type 1 replication and transmission to T cells.

Mycobacterium tuberculosis and human immunodeficiency virus type 1 (HIV-1) are virulent intracellular pathogens that invade and multiply within macrophages. The effect of M. tuberculosis on HIV-1 infection and replication was analyzed in vitro using human monocyte-derived macrophages (MDM) isolated from peripheral blood mononuclear cells by countercurrent centrifugal elutriation. Preinfection of MDM with M. tuberculosis followed by HIV-1 infection resulted in an increase in p24 release, reverse transcriptase activity, and infective virus production. In contrast, no increase in HIV-1 production was observed when MDM were infected with Mycobacterium avium complex or heat-killed M. tuberculosis. Coinfected MDM were potent stimulators of T cell proliferation, while HIV-1-infected MDM failed to present exogenous tuberculin to T cells. Furthermore, coinfected MDM showed an increased capacity to transmit HIV-1 to activated T cells. These results suggest that M. tuberculosis infection can both up-regulate HIV-1 infection and replication within MDM and increase the efficiency of virus transmission from infected MDM to T cells.

Cells, Cultured↗
PubMed1997

The photodynamic effect of Victoria blue BO on peripheral blood mononuclear and leukemic cells.

The photodynamic effect of Victoria blue BO (VB-BO) and photoirradiation on peripheral blood mononuclear cells was studied. The cells were preincubated with VB-BO followed by photoirradiation and overnight culture. The highest percentage of dead cells (propidium iodide assay in flow cytometry) was seen in the monocyte population. The lymphocytes showed a lower sensitivity to VB-BO photodynamic action than the monocytes (12% vs 80% of PI-positive cells). The effect of VB-BO and phototreatment on lymphocyte function was studied using a mitogen-induced proliferation assay. A decrease of mitogen response was observed. The VB-BO and photoirradiation were also used on leukemic cells. The leukemic cells from acute myeloid leukemia and B precursors leukemia were sensitive to VB-BO photodynamic action. The high VB-BO sensitivity of monocytes and leukemic cells (myeloid and lymphoid B derived) suggests possible application of VB-BO for selective depletion of monocytes or sensitive leukemic cells.

Antineoplastic Agents↗
PubMed1997

Gastroprotective activity of melatonin and its precursor, L-tryptophan, against stress-induced and ischaemia-induced lesions is mediated by scavenge of oxygen radicals.

BACKGROUND: Melatonin, a pineal hormone that is biosynthesized from L-tryptophan, is known to scavenge oxygen free radicals and to be present in the gut, but little is known about the role of this hormone and its precursor, L-tryptophan, in protecting the gastric mucosa from damage accompanied by increase in the generation of oxygen radicals. METHODS: This study was designed to determine the effects of melatonin and L-tryptophan on the formation of acute gastric lesions induced by stress and ischaemia reperfusion and, for comparison, by topical irritants such as 100% ethanol or acidified acetylsalicylic acid. RESULTS: It was found that pretreatment with melatonin in doses ranging from 1.2 to 10 mg/kg dose-dependently reduced the stress-induced gastric lesions and was accompanied by a reduction in blood-free radicals and by attenuation of the fall in gastric blood flow. L-tryptophan applied intragastrically in doses ranging from 1 to 100 mg/kg also reduced dose-dependently the lesions induced by stress; this effect too was accompanied by a rise in gastric blood flow. Pretreatment with indomethacin, to block the biosynthesis of prostaglandins, significantly augmented the lesions produced by stress and completely abolished the protective effects of melatonin or L-tryptophan. Both melatonin and tryptophan reduced the formation of acute gastric lesions provoked by ischaemia reperfusion; this was accompanied by an increase in gastric blood flow. In contrast, melatonin and L-tryptophan failed to influence acute gastric lesions induced by topical irritants such as 100% ethanol or acidified aspirin. CONCLUSIONS: Melatonin and L-tryptophan protect the gastric mucosa from damage by stress and ischaemia reperfusion, and this action is mediated, at least in part, by the limitation in the free radicals, the stimulation of mucosal generation of PG and by the increase in gastric blood flow.

Acute Disease↗
PubMed1997

Cellular adhesion molecules changes in myocardium during first year post heart transplant.

The increased presence of intercellular adhesion molecule-1 (ICAM-1) and vascular adhesion molecule-1 (VCAM-1) in the myocardium after orthotropic heart transplantation (OHT) has been implicated in early and late organ rejection. The aim of this study was to investigate the changes in ICAM-1 and VCAM-1 during the first years post-OHT. Accordingly, we studied multiple endomyocardial biopsy specimens collected from 11 randomly selected patients (all males, mean age 46 +/- 11 years). Qualification criteria for OHT included: ischemic cardiomyopathy in 6 pts (55%) and idiopathic dilated cardiomyopathy in 5 pts (45%). All patients were receiving triple immunosuppressive regimen. The therapy consisted of cyclosporine, azathioprine, and prednisolone. Multiple endomyocardial biopsy specimens were collected at 7, 30, 90 and 360 days post OHT from all patients (pts), and examined routinely for histologic signs of organ rejection. To assess levels of adhesion molecules we used monoclonal antibodies (murine anti-human ICAM-1 and VCAM-1) on frozen sections. Immunoreactivity (IR) was detected using a commercially available kit. Intensity of IR was assessed based on a semiquantitative scoring system. In this study, IR scores > or = 2 + were considered positive for ICAM-1, and scores > or = 1 + were considered positive for VCAM-1. IR scores in specimens obtained from consecutive biopsies were compared with the initial biopsy collected at the day 7. The results were analyzed using nonparametric statistics. The routine evaluation revealed histological signs of organ rejection (> or = 2) in 2 pts at 7 days, in 5 pts at 30 days, in 3 pts at 90 days, and in 1 patient at 360 days. On the other hand, ICAM-1 and VCAM-1 expression were absent in the majority of patients at 7, 30 and 90 days, but their presence was significantly increased at 360 days (p < 0.05). Absence of the early expression of ICAM-1 and VCAM-1 may be related to the protective effect of triple immunosuppressive therapy in these patients. The expression of ICAM-1 and VCAM-1 strongly emerging at 1 year post OHT may reflect chronic rejection in myocardium. In conclusion, the immunohistological monitoring of the adhesion molecules in biopsy specimens during routine biopsy schedule may be helpful for the discovery of chronic rejection.

Adult↗
PubMed1996

Pentoxifylline reduces plasma tumour necrosis factor-alpha concentration in premature infants with sepsis.

UNLABELLED: Increased plasma tumour necrosis factor alpha (TNF) concentration correlates with mortality in sepsis. We suggested that pentoxifylline (PTXF), which is known to inhibit TNF production, may improve survival and attenuate clinical symptoms of sepsis in neonates. Plasma TNF levels were evaluated in 29 newborn infants with sepsis. Patients were randomly assigned into two groups, receiving PTXF in a dose of 5 mg/kg per hour for 6 h or placebo (saline), on 3 successive days. Both groups were subjected to the same conventional therapy. TNF was evaluated before and after PTXF or placebo administration on the 1st and 3rd days of therapy. There was a statistically significant decrease in plasma TNF level in the PTXF group when the values before the first and after the last PTXF infusion were compared [mean: 671.5 pg/ml; SD: 438; med: 729.6 vs mean: 41.0 pg/ml; SD: 64.1; med: 11.5; P < 0.000004]. In the placebo group, decrease was not significant [mean: 633.0 pg/ml SD: 488.6; med: 618.9 vs 246.9 pg/ml; SD: 243.9; med: 191.0]. A significantly higher plasma TNF level, evaluated after the last PTXF infusion, was found in the placebo group [246.9 pg/ml vs 41.0 pg/ml; P < 0.001]. Only one of four infants with signs of shock in the placebo group survived, whereas all of five newborns with symptoms of shock in the PTXF group survived [P < 0.04]. An increased incidence of metabolic acidosis [P < 0.05], necrotizing enterocolitis [P < 0.04] and renal insufficiency [P < 0.05] was observed in infants in the placebo group. CONCLUSION: PTXF inhibits production of TNF and may have therapeutic value in the treatment of premature infants with sepsis complicated by shock.

Humans↗
PubMed1996

Serum beta-2-microglobulin (beta-2-M) levels in heart transplant patients (HTP).

UNLABELLED: The present paper aim to answer following questions: 1. What is serum beta-2-M levels in HTP? 2. Does significant correlations between serum beta-2-M levels and serum creatinine levels or creatinine clearance (inulin clearance) exit? 3. Does any significant correlation between serum beta-2-M levels and blood cyclosporine A concentration exit? Three groups of subjects were studied. The first group consisted of 33 heart transplant patients (HTP), the second group consisted of 12 patients with small decline kidney function, and the third one consisted of 36 healthy subjects. In all examined subjects serum beta-2-M (RIA) creatinine, creatinine and inulin (steady state dosis method) clearance were assessed. CONCLUSION: 1. In observed HTP serum beta-2-M level is significantly higher then in controls and patients with small decline kidney function; 2. A significant correlation between kidney function and -2-M level in HTP as well as in other examined groups subjects exit; 3. Presence a significant positive correlation between serum beta-2-M level and blood cyclosporine A concentration suggest that beta-2-M level can be a good parametr to define cyclosporine A tubular toxicity.

Case-Control Studies↗