Linear stability of an alternating-magnetic-field-driven flow in a spinning cylindrical container.

We present a numerical analysis of free-surface liquid metal flow and its three-dimensional linear stability. The flow is driven by an alternating magnetic field in a spinning cylindrical container. The electromagnetic and hydrodynamic fields are fully coupled via the shape of the liquid free surface.

[Lymphocytic sensitization to antigens of viruses of the family Paramyxoviridae in diabetes mellitus].

The purpose of this investigation was to study cellular immunity to parotiditis and measles viruses in patients with diabetes mellitus (DM). Lymphocytic sensitization to parotiditis and measles viral antigens and insulin was determined by peripheral blood lymphocytic blast-transformation reaction (a morphological method for reaction assessment) In 10 patients with measles, 18 patients with epidemic parotiditis, 52 patients with DM (23 and 29 patients types 1 and 2 DM, respectively), and 46 apparently healthy individuals. The studies revealed lymphocytic sensitization to parotiditis and measles viral antigens and insulin in most patients in the acute phase of infection with a subsequent reduction in the intensity of proliferation until the point of complete cessation during 12 months.

Induced expression of manganese superoxide dismutase by non-toxic concentrations of oxidized low-density lipoprotein (oxLDL) protects against oxLDL-mediated cytotoxicity.

Oxidized low-density lipoprotein (oxLDL) affects macrophages and plays a critical role in the development of atherosclerosis. In the present paper, we demonstrate that high concentrations of oxLDL provoked apoptosis of human Mono-Mac-6 cells, which was blocked by diphenylene-iodonium (DPI), an inhibitor of flavin-containing enzymes, such as NADPH oxidase, suggesting the involvement of reactive oxygen species (ROS). Importantly, pre-treatment of cells with low concentrations of oxLDL prevented apoptosis in response to high concentrations of oxLDL by up-regulating manganese superoxide dismutase (MnSOD).

Oxidized low-density lipoprotein (oxLDL) triggers hypoxia-inducible factor-1alpha (HIF-1alpha) accumulation via redox-dependent mechanisms.

Oxidized low-density lipoprotein (oxLDL) and macrophages play a central role in atherosclerosis. Here, we obtained evidence that oxLDL induced hypoxia-inducible factor-1alpha (HIF-1alpha) protein accumulation in human macrophages (Mono-Mac-6) under normoxia. HIF-1alpha accumulation was attenuated by pretreatment with the antioxidant N-acetyl-L-cysteine (NAC), the nitric oxide (NO) donor S-nitrosoglutathione (GSNO), and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitors such as diphenyleniodonium (DPI) or 4-(2-aminoethyl)-benzenesulfonyl fluoride (AEBSF), thus implicating the contribution of oxLDL-generated reactive oxygen species (ROS).

Adenovirus-mediated wild-type-p53-gene expression sensitizes TNF-resistant tumor cells to TNF-induced cytotoxicity by altering the cellular redox state.

We have shown that the loss of p53 function contributed to resistance of tumor cells to TNF-induced cytotoxicity. In the present study, we evaluated the effect of wild-type p53 (wt-p53) expression on TNF sensitivity, by introducing wt-p53 into MCF7/Adr cells in which p53 was deleted, via a recombinant adenovirus encoding p53 (Ad-p53). Our results indicate that infection with Ad-p53 (50-100 viral particles per cell) resulted in pronounced cytotoxicity, whereas infection with 10 viral particles per cell, which was weakly toxic for the MCF7/Adr cells, sensitized these cells to TNF-induced cell death.

Adenovirus-mediated transfer of wild-type p53 gene sensitizes TNF resistant MCF7 derivatives to the cytotoxic effect of this cytokine: relationship with c-myc and Rb.

Tumor suppressor p53 is a nuclear transcription factor that blocks cell cycle progression and induces apoptosis. We have previously shown that the MCF7 resistance to the cytotoxic action of TNF correlates with p53 mutations. In the present study, we used a recombinant adenovirus carrying a wild-type p53 gene (Adwtp53) in order to investigate the effect of wt p53 transfer on modulation of cell resistance to the cytotoxic action of TNF.

Methyltransferase inhibitor S-adenosyl-L-homocysteine sensitizes human breast carcinoma MCF7 cells and related TNF-resistant derivatives to TNF-mediated cytotoxicity via the ceramide-independent pathway.

In this study we investigated the signalling requirements for TNF-induced cytotoxicity modulated by the methyltransferase inhibitor S-adenosyl-L-homocysteine (AdoHcy) using the TNF-sensitive human breast carcinoma MCF7 cells and its established TNF-resistant clones (R-A1 and clone 1001). Our data indicate that inhibition of methylation reactions by adenosine plus homocysteine, which are known to condense within cells to AdoHcy, markedly potentiated TNF-induced cytotoxicity in MCF7 cells and rendered related TNF-resistant variants, TNF-sensitive by a mechanism independent from the ceramide pathway. We demonstrated that the dominant-negative derivative of FADD (FADD-DN) blocked methylation inhibition/TNF-induced cell death.

Modulation of tumor necrosis factor-alpha-mediated cytotoxicity by changes of the cellular methylation state: mechanism and in vivo relevance.

A combination of adenosine (Ado) and homocysteine (Homo) enhances tumor necrosis factor (TNF)-alpha cytotoxicity in vitro and in vivo in several tumor cells. Ado and Homo at concentrations that enhanced TNF-alpha-mediated cytotoxicity accumulated S-adenosylhomocysteine (AdoHcy) and as consequence decreased the cellular methylation state, i.e.

Analysis of human breast adenocarcinoma MCF7 resistance to tumor necrosis factor-induced cell death. Lack of correlation between JNK activation and ceramide pathway.

Considerable progress has been made in the understanding of tumor necrosis factor (TNF) signaling; however, the molecular and biochemical basis of tumor resistance to the cytotoxic action of TNF are still not definitively identified yet. Although a role of c-Jun N-terminal kinase (JNK) pathway has been suggested as an effector in TNF signaling, its exact relative contribution and its interaction with ceramide pathway and tumor resistance to TNF remain unknown. The relationship between JNK activation and human breast adenocarcinoma MCF7 resistance acquisition to the cytotoxic action of TNF was therefore investigated.

[The status of the immunity system in diphtheria].

The complex study of cell-mediated and humoral immunity characteristics, as well as nonspecific protective factors, in 30 diphtheria patients, 9 clinically healthy carriers and 54 healthy subjects was carried out. In healthy immunized subjects normal characteristics of all elements of immunity were observed in combination with high titers of antitoxins and sensitization of lymphocytes to diphtheria toxoid. In healthy carriers the presence of cell-mediated and humoral immunity to diphtheria was associated with disturbances of the metabolic activity of phagocytes and a decrease in the proliferation of lymphocytes in response to the mitogen.

[Immune system in residents of territories contaminated with radionuclides after Chernobyl accident].

Aim: Study of the immunity and nonspecific defense factors in subjects living at a territory contaminated with radionuclides at a density of 1-5 Ci/km2 after the Chernobyl accident.

Materials And Methods: A total of 144 subjects aged 18 to 82 years living in the Sasovo region of the Ryazan district were examined. Three groups were distinguished with different density of contamination: 1) n = 54, 1-5 Ci/km2; 2) n = 36, conditionally pure territory; and 3) n = 54, living at the interface of the two territories.

Sphingosine-1-phosphate mobilizes intracellular calcium and activates transcription factor NF-kappa B in U937 cells.

Sphingosine-1-phosphate (SPP), a metabolite of sphingolipids, has been implicated as a second messenger in cell growth regulation and signal transduction via calcium mobilization from internal stores. This study shows that SPP mobilizes intracellular calcium in U937 cells and demonstrates for the first time the ability of SPP to activate the transcription factor NF-kappa B in these cells. Furthermore, calcium release from the internal stores by thapsigargin (TG), an inhibitor of the endoplasmic reticulum Ca2+ pump, was associated with activation of NF-kappa B.

Iron chelation decreases human immunodeficiency virus-1 Tat potentiated tumor necrosis factor-induced NF-kappa B activation in Jurkat cells.

TNF-alpha stimulates HIV-1 replication via activation of the transcription factor NF-kappa B. TNF-mediated activation of NF-kappa B is known to involve the intracellular formation of reactive oxygen intermediates (ROIs). We recently demonstrated that HIV-1 Tat protein potentiates TNF-induced NF-kappa B activation by downregulation of manganese-dependent superoxide dismutase (MnSOD), shifting the cellular redox state towards pro-oxidative conditions.

HIV type 1 glycoprotein 120 amplifies tumor necrosis factor-induced NF-kappa B activation in Jurkat cells.

This article demonstrates that human immunodeficiency virus type 1 (HIV-1) gp120 amplifies the activity of tumor necrosis factor alpha (TNF-alpha), a cytokine that stimulates HIV-1 replication through activation of NF-kappa B. In CD4-positive Jurkat cells, gp120 potentiates TNF-induced NF-kappa B activation. TNF-mediated activation of NF-kappa B is known to involve the intracellular formation of reactive oxygen intermediates (ROIs).

Induction of NO synthesis in macrophages by Newcastle disease virus is associated with activation of nuclear factor-kappa B.

Newcastle disease virus (NDV) has received much attention recently because of its non-specific immune stimulating potential and its various anti-tumor activities. Here we describe that NDV induces synthesis of NO and causes an activation of nuclear factor-kappa B (NF-kappa B) in murine macrophages. These reactions were part of an activation process which included also stimulation of adenosine deaminase and inhibition of 5'-nucleotidase.

HIV-1 Tat potentiates TNF-induced NF-kappa B activation and cytotoxicity by altering the cellular redox state.

This study demonstrates that human immunodeficiency virus type 1 (HIV-1) Tat protein amplifies the activity of tumor necrosis factor (TNF), a cytokine that stimulates HIV-1 replication through activation of NF-kappa B. In HeLa cells stably transfected with the HIV-1 tat gene (HeLa-tat cells), expression of the Tat protein enhanced both TNF-induced activation of NF-kappa B and TNF-mediated cytotoxicity. A similar potentiation of TNF effects was observed in Jurkat T cells and HeLa cells treated with soluble Tat protein.

Adenosine and homocysteine together enhance TNF-mediated cytotoxicity but do not alter activation of nuclear factor-kappa B in L929 cells.

This paper shows that a combination of adenosine and homocysteine potentiates TNF-alpha-mediated cytotoxicity, but does not modulate activation of NF-kappa B transcription factor controlling the expression of various TNF-alpha-inducible genes. Adenosine and homocysteine at concentrations (1 mM each) that enhance TNF-alpha-induced cytotoxicity accumulate S-adenosyl-L-homocysteine (AdoHcy), a potent inhibitor of S-adenosyl-L-methionine-dependent methylation reactions. In addition, preloading L929 cells with AdoHcy resulted in enhanced responses to TNF-alpha, suggesting that AdoHcy potentiates TNF-alpha-induced cytotoxicity.

[The functional activity of the urethral neutrophilic granulocytes in patients with chronic urethroprostatitis and its correction].

The functional state of urethral neutrophil granulocytes in patients with chronic urethro-prostatitis, and possibility of miramistin use in complex treatment of the disease were investigated. The data revealed functional suppression of these granulocytes in the patients. Complex treatment with miramistin normalized indices of urethral phagocytic activity, on the contrary, after treatment of the patients without the agent there was no tendency to normalize urethral phagocytic function.

[The effect of miramistin on the phagocytic activity of the urethral neutrophilic granulocytes in patients with chronic urethroprostatitis].

It was found that addition of mirastimin to the traditional anti-inflammatory treatment results in stimulation of the absorptive capacity of the urethral phagocytes and improves the results of treatment of patients with chronic urethroprostatitis. The immunomodulator mirastimin should be given with consideration of the initial functional state of urethral neutrophilic granulocytes.

[An immunological analysis of the hemagglutinin from the influenza A virus (H1N1) isolated by using various detergents].

Immunogenic properties of influenza virus hemagglutinin, isolated by new detergents O-14 (desintegron-O) and B-14 (desintegron-B) have been studied. Hemagglutinin isolated by desintegron-O has been found to be more immunogenic than virions. It has been shown that hemagglutinin isolated by desintegron-B induces a lower humoral immune response than the influenza virus.

[Effect of antimicrobial surface-active agents on the immune response to thymus-dependent antigen in mice].

The study showed that miramystin, a cationi surfactant, was an immunostimulant inducing an increase in humoral and cellular immunity in response to sheep red blood cells. The observed dose-dependent stimulating effect of miramystin on antibody production and development of DTH recommends its use as an immunologic adjuvant in the laboratory practice. It also indicated to the prospects in investigation of immunologic adjuvant properties of other preparations belonging to surface-active substances.

[Effects of embryonal bone tissue on hemopoiesis].

The influence of human fetal bone (FB) on the hemopoietic and stromal cells were studied in the morphometric assay of the bone marrow trephine biopsy samples after a preliminary cultivation using the Marbrook system for 1-5 weeks. The rat FB effect on the hemopoiesis and survival were also studied in experiment with FB transplantation to rats with prior administration of lethal and sublethal doses of cyclophosphamide. In long-term cultivation of the bone marrow trephine biopsy samples, enhanced proliferation of the fibrous tissue and elimination of hemopoietic elements were seen.

[Immunostimulating effect of synthetic surface-active agents in experimental tuberculosis].

The influence of synthetic surfactants of different classes (BX-14, O-14, B-14) on an immunologic reactivity of mice with evolving experimental tuberculosis was studied. The use of the substances leads to an increase of the E-rosette forming cells (E-RFC) in the mice thymus gland and spleen, and stimulates the inhibited function of spleen natural killers, without modifying (except the agent O-14) the cytotoxicity level of thymus gland natural killers. The above substances can enhance the absorbing capacity of the spleen macrophages as well as their ability to reduce nitro blue tetrazolium.

[The effect of miramistin on the phagocytic activity of urethral neutrophil granulocytes].

Secondary immunodeficiency, one of whose manifestations is depressed phagocytic activity of urethral neutrophilic granulocytes, develops in patients with chronic urethroprostatitis. Miramistin exerts a dose-dependent stimulating effect on the urethral neutrophilic granulocytes; the maximum stimulating effect is observed when phagocytes are treated with 0.001% solution of the drug.