PubMed Health⌕ Search

Biomedical subjects

M Barna

Publications and source records attributed to M Barna.

At least 19 recordsLinked to original sources
PubMed2001

Modeling the effects of VOC/NOx emissions on ozone synthesis in the cascadia airshed of the Pacific Northwest.

A modeling system consisting of MM5, Calmet, and Calgrid was used to investigate the sensitivity of anthropogenic volatile organic compound (VOC) and oxides of nitrogen (NOx) reductions on ozone formation within the Cascadia airshed of the Pacific Northwest. An ozone episode that occurred on July 11-14, 1996, was evaluated. During this event, high ozone levels were recorded at monitors downwind of Seattle, WA, and Portland, OR, with one monitor exceeding the 1 hr/120 ppb National Ambient Air Quality Standard (at 148 ppb), and six monitors above the proposed 8 hr/80 ppb standard (at 82-130 ppb). For this particular case, significant emissions reductions, between 25 and 75%, would be required to decrease peak ozone concentrations to desired levels. Reductions in VOC emissions alone, or a combination of reduced VOC and NOx emissions, were generally found to be most effective; reducing NOx emissions alone resulted in increased ozone in the Seattle area. When only VOC emissions were curtailed, ozone reductions occurred in the immediate vicinity of densely populated areas, while NOx reductions resulted in more widespread ozone reductions.

Air Movements↗
PubMed2000

Plzf regulates limb and axial skeletal patterning.

The promyelocytic leukaemia zinc finger (Plzf) protein (encoded by the gene Zfp145) belongs to the POZ/zinc-finger family of transcription factors. Here we generate Zfp145-/- mice and show that Plzf is essential for patterning of the limb and axial skeleton. Plzf inactivation results in patterning defects affecting all skeletal structures of the limb, including homeotic transformations of anterior skeletal elements into posterior structures. We demonstrate that Plzf acts as a growth-inhibitory and pro-apoptotic factor in the limb bud. The expression of members of the abdominal b (Abdb) Hox gene complex, as well as genes encoding bone morphogenetic proteins (Bmps), is altered in the developing limb of Zfp145-/- mice. Plzf regulates the expression of these genes in the absence of aberrant polarizing activity and independently of known patterning genes. Zfp145-/- mice also exhibit anterior-directed homeotic transformation throughout the axial skeleton with associated alterations in Hox gene expression. Plzf is therefore a mediator of anterior-to-posterior (AP) patterning in both the axial and appendicular skeleton and acts as a regulator of Hox gene expression.

Animals↗
PubMed1998

Anti-gliadin and anti-endomysium antibodies in children with celiac disease consuming a gluten free diet.

A group of 26 children (13 boys and 13 girls; average age 12.2 years) with CD who had been on a gluten free diet for 5-15 years was examined in order to find out how effectively they could manage their diet. The diagnosis of CD was established on the basis of ESPGAN criteria (1969). 5-15 years ago. Antigliadin antibodies, IgG-, and IgA-AGA (by fluorescence enzyme immunoassay), Gliastick by ELISA technique, and Anti-endomysium antibodies (by indirect immunofluorescence on sections of monkey esophagus) were examined in the serum. Only 5 patients had no antigliadin or anti-endomysium antibodies. In 21 cases the IgG-AGA showed positive results; the IgA-AGA was positive in 6, the Gliastick in 19, and the anti-endomysium antibodies in 8 cases. The main cause of the mismanagement of the diet was inadequate food labeling; so it seems to be important to also establish a Food Intolerance Data Bank in Hungary. The 5 sero-negative children volunteered for a gluten challenge; 3 of them became positive in a few weeks or months. Two patients remained negative even after 1 year. Their gluten sensitivity may not prove to be permanent.

Adolescent↗
PubMed1997

Interleukin-12 promotes recovery from viral encephalitis.

Infusion of interleukin-12 (IL-12) enhances recovery from lethal experimental vesicular stomatitis virus (VSV) infection of the central nervous system (CNS). Interleukin-12 treatment resulted in: 1) increased survival frequency; 2) faster recovery from weight loss; 3) substantially decreased VSV titers in brain homogenates and diminished immunohistochemical detection of VSV antigens in tissue sections; 4) earlier and increased CNS expression of types 1, 2, and 3 nitric oxide synthase (NOS) and both major histocompatibility complex (MHC) class I and class II antigens; 5) earlier and increased blood and CNS levels of tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma). These results suggest that IL-12 enhances recovery from VSV infection of the CNS.

Animals↗
PubMed1997

Effect of calcitriol on the production of T-cell-derived cytokines in psoriasis.

Although the use of vitamin D analogues in the treatment of psoriasis has been an important new development, the mechanisms of action of these drugs are not fully understood. Psoriasis results from hyperproliferation of keratinocytes, and various studies attribute a crucial role to the locally infiltrating T lymphocytes. In an attempt to add to the understanding of the mechanisms of calcitriol therapy, we determined the effect of this drug on T cells by studying its effect on proliferation and on the production of various cytokines by T-cell clones prepared from psoriatic skin after non-specific activation with the combination of phytohaemagglutinin (PHA) and phorbol myristate acetate (PMA). The addition of increasing doses (10(-9)-10(-5) mol/l) of calcitriol to these T cells resulted in a dose-dependent inhibition in lymphocyte proliferation and in production of the type 1 cytokines IFN-gamma and IL-2, the type 2 cytokines IL-4 and IL-5. The general cytokines TNF-alpha and GM-CSF were not significantly inhibited. These data suggest that calcitriol is involved in the treatment of psoriasis via inhibition of the expansion, and cytokine production, of skin-infiltrating T lymphocytes.

Calcitriol↗
PubMed1996

Activation of type III nitric oxide synthase in astrocytes following a neurotropic viral infection.

Type III nitric oxide synthase (type III NOS), also known as endothelial cell nitric oxide synthase (eNOS or ecNOS or NOS-3), is a constitutively expressed, calcium- and calmodulin-dependent, isoform of NOS. Its expression has been localized to endothelial cells and a subset of neurons in the brain. We report here that resident astrocytes of the central nervous system (CNS) of mice express type III NOS. Following an experimental neurotropic viral infection, the expression of type III NOS on reactive astrocytes increases substantially, predominantly in virally infected regions of the brain. This upregulation of type III NOS expression is also evident following cytokine treatment in vitro. The intraperitoneal (i.p.) administration of IL-12, a potent activator of IFN-gamma and TNF-alpha production, results in a substantial increase in type III NOS immunoreactivity in astrocytes. Cytokine-mediated activation of type III NOS is observed in vitro following exposure of a C6 glioma cells, which constitutively express type III NOS, to IL-12, IFN-gamma, and TNF-alpha treatment. We conclude that astrocytes of the murine CNS express type III NOS, which may be positively regulated by a number of cytokines following viral infection. Type III NOS expression by astrocytes represents a novel source of nitric oxide in the brain. It may be important in regulating perfusion and maintaining the blood-brain barrier. Given the intimate association of astrocytes with endothelial cells and neurons, increased activity of type III NOS following viral infection may be beneficial in inhibition of viral infection in neighboring cells.

Animals↗
PubMed1996

Sex differences in susceptibility to viral infection of the central nervous system.

We have characterized striking differences in recovery of male and female BALB/c and BALB/c-H-2dm2 (dm2) mice from an experimental neurotropic viral infection of the central nervous system (CNS). Following intranasal inoculation of vesicular stomatitis virus (VSV), assays of tissue homogenates from female mice produced lower viral titers. There was also a significant reduction in the spread of virus from the rostral to caudal end of the brain in female mice. Enhanced recovery by female mice of both strains in response to this viral insult correlates with increased levels of Nitric Oxide Synthase (NOS) types I, II, and III expression, an increased prevalence of reactive astrocytes, earlier and enhanced levels of expression of Major Histocompatibility Complex (MHC) class II molecules on astrocytes, endothelial and microglial cells, and increased T cell infiltration in the female BALB/c mouse. Taken together, these findings document sexual dimorphism in CNS immunity, and may provide an understanding of some of the mechanisms underlying many sex-biased diseases.

Animals↗
PubMed1996

Host immune response to vesicular stomatitis virus infection of the central nervous system in C57BL/6 mice.

In this report, the kinetics of cellular inflammatory changes in the brain of vesicular stomatitis virus (VSV)-infected C57BL/6 (B6) mice was determined. The behavior and survival rate of infected B6 were carefully monitored each day. Infectious viral titers and VSV antigen distribution were determined at several time points during the course of infection. Strong activation of both astrocytes and microglia was observed after VSV infection. Induction of type II nitric oxide synthase (iNOS) was detected in activated microglia in the olfactory bulb (OB) starting at day 4 postinfection. Induced expression of major histocompatibility complex (MHC) molecules and rapid infiltration of both T cells and natural killer (NK) cells were detected in the VSV-infected CNS. Collectively, these data indicate that the response to CNS infection in B6 mice, which is often primarily Th1 in characteristics, is comparable to BALB/c mice, a strain that often shows a Th2-dominated immune response.

Animals↗
PubMed1995

IL-12 promotes enhanced recovery from vesicular stomatitis virus infection of the central nervous system.

To investigate the role of a cytokine in host defense against the vesicular stomatitis virus (VSV) infection of the central nervous system (CNS), IL-12 was injected i.p. into groups of 10 BALB/c mice on days -1, 0, 1, 2, and 3 postinfection. Four days postinfection, mice were examined. IL-12 strongly enhanced immunity to VSV infection in the CNS as demonstrated by 1) decreased VSV titers in brain homogenate of IL-12-injected mice compared with those of controls; 2) increased expression of inducible nitric oxide synthase in the CNS; 3) enhanced expression of both MHC class I and class II Ags in the CNS; 4) increased T cell infiltration in the CNS, especially in the olfactory bulb; and 5) diminished VSV-induced apoptosis in olfactory bulb. No detrimental effect was observed even with the 200 ng/mouse dose of IL-12. Protective effects of IL-12 were dose dependent. Collectively, these results demonstrate that exogenously added IL-12, even when injected peripherally, significantly enhances recovery from VSV infection of the CNS.

Animals↗
PubMed1995

Vesicular stomatitis virus infection of the central nervous system activates both innate and acquired immunity.

Vesicular stomatitis virus (VSV) causes acute infection of the central nervous system (CNS) when intranasally applied. We have examined cellular inflammatory changes in the CNS following VSV infection. As early as 1 day postinfection (p.i.), astrocytes were activated in the olfactory bulb (OB). This was followed by activation of microglia, first observed in the OB at day 3 p.i. Expression of inducible nitric oxide synthase was observed in activated microglia in the OB at day 3 p.i., and increased inducible nitric oxide synthase expression coincided with decreased virus titers in tissue homogenates. Expression of major histocompatibility complex (MHC) class I molecules on astrocytes and microglial, endothelial, and ependymal cells was also rapidly induced and followed by induced expression of MHC class II molecules on astrocytes and microglial and endothelial cells. Consistent with the pattern of viral dissemination, MHC molecules were expressed temporally from the rostral-to-caudal direction. Infiltration of CD8+ cells was observed as early as 1 day p.i. in the OB. CD4+ cells were detected in the OB at day 4 p.i. Increasing T-cell infiltration coincided with decreased virus titers. In contrast, B-cell infiltration of the CNS was not detected until day 14 p.i., after the virus was cleared and mice were showing behavioral signs of recovery. Breakdown of the blood-brain barrier was detected beginning at day 6 p.i., was most severe at day 8 p.i., and was followed by full recovery. Collectively, these data show that both innate immunity (production of nitric oxide) and acquired immunity (expression of MHC molecules and T-cell infiltration) are activated following VSV infection in the CNS.

Amino Acid Oxidoreductases↗
PubMed1994

Characterization of lesional psoriatic skin T lymphocyte clones.

T cells are considered to play a role in the pathomechanism of psoriasis. Therefore we investigated the cytokine production patterns of T cell clones that were randomly prepared from chronic plaque psoriasis lesions of 2 patients. 67% of the 49 T lymphocyte clones (TLC) expressed CD4 and 33% expressed CD8 (ratio 2:1), while gamma delta-TCR expression was absent. The production of IL-4, IFN-gamma, IL-2 and IL-6 was measured in supernatants of TLC following PHA plus PMA stimulation. Different groups of clones could be distinguished according to their IL-4/IFN-gamma production ratio. In addition to Th0 cells (low IL-4/low IFN-gamma), low IL-4/high IFN-gamma producers as well as high IL-4/low IFN-gamma producing clones were found, suggesting the presence of Th1- and Th2-like subsets. Upon stimulation, all TLC secreted low levels of IL-2 whereas a minority of the TLC secreted low levels of IL-6. These results may imply that T cells in psoriasis lesions do not show shifts towards either a Th1 or a Th2 cytokine production profile.

CD4-CD8 Ratio↗
PubMed1993

Repolarization pattern of body surface potential maps (BSPM) in coronary artery disease.

The aim of our study was to assess if repolarization BSPM were able to evaluate the site, size and severity of chronic ischaemic damages and if BSPM were in any way related to the regional attenuation of myocardial contractility or to the site of coronary artery occlusion. The BSPM were obtained from 69 patients suffering from coronary artery disease confirmed by coronarography, with at least 75% occlusion of at least one coronary artery. According to the site of single occlusion, or a combination of the sites of multiple occlusions, the patients were divided into 6 subgroups. According to the region of attenuated kinetics the same group of 69 patients was also divided into other 6 subgroups. As in the polarity distribution there was only a limited accordance in BSPM with coronarographic and echocardiographic findings, in the localization of extreme values there were very important specific changes in patients with normal kinetics as determined by both contrast ventriculography and two-dimensional echocardiography. The repolarization maps can distinguish patients with coronary artery disease and normal echocardiography from healthy persons with a sensitivity of 85% and a specificity of 65% in the case of the isoareal map from the ST segment (RIAM) and 90% and 85%, respectively, in the case of the isointegral map from the whole ST-T segments (RIIM).

Adult↗
PubMed1990

[Cryptosporidium as a co-pathogen in infantile diarrhea and pneumonia].

The authors describe a case of cryptosporidiosis in a 10 month old immunocompetent infant, who suffered from prolonged diarrhoea and pneumonia. Cryptosporidium oocysts, Giardia lamblia were detected by using modified Kinyoun stain, and klebsiella was identified in the stool culture. According to the clinical presentation and the laboratory data the streptococcus infection is presumed as cause of the pneumonia, but the authors could not exclude the role of cryptosporidium in predisposing and/or causing the pneumonia.

Animals↗