scholarly journals Immunological indices in flu patients

2012 ◽  
Vol 17 (5) ◽  
pp. 16-21
Author(s):  
N. V. Svistunova ◽  
I. P. Baranova

The results of the analysis of immunological features of influenza during the epidemic rise in incidence are presented. In 39 patients aged from 8 to 34 years with moderate disease course changes in the serum concentration of the proinflammatory cytokine tumor necrosis factor alpha (TNF-alpha) and levels of production of interferons alpha and gamma (IFN = alpha and IFN=gamma) at beginning of the disease and in early recovery period were studied. The features and differences of the cytokine response during influenza in dependence on the etiology of the disease, presence of complications, gender, age of the patient, in women during pregnancy, as well as the various types of causal treatment have been revealed. Based on the characteristics of the dynamic fluctuations in the concentration of IFN-alpha, IFN gamma =, TNF-alpha in flu patients predictors of adverse clinical course are identified.

2019 ◽  
Vol 17 (7) ◽  
pp. 95-99
Author(s):  
O. V. Kurushina ◽  
◽  
E. A. Kurakova ◽  

2020 ◽  
Vol 98 (11) ◽  
pp. 51-56
Author(s):  
G. V. Neklyudova ◽  
А. V. Chernyak ◽  
N. А. Tsareva ◽  
S. N. Аvdeev

The article describes a clinical case demonstrating the results of the lungs ultrasound examination in the COVID-19 patient during the acute period of the disease and early recovery period.


2021 ◽  
Vol 63 (1) ◽  
pp. 22-25
Author(s):  
Denys N. Khramtsov ◽  
Olexandr N. Stoyanov ◽  
Tetiana N. Muratova ◽  
Olexandr R. Pulyk

Aim: The aim of the study was to evaluate the clinical outcome in the use of neuroprotective agents in the acute period of ischemic stroke. Material and Methods: The study was performed on the basis of the stroke of the Center for Reconstructive and Rehabilitation Medicine (University Clinic) of the Odessa National Medical University. A retrospective analysis of clinical outcomes of 115 patients with acute stroke was conducted. Results: An average NIHSS score at discharge was 4.1±0.1 points when treated with no refinery, then it reached 3.6±0.1 points when using peptidergic drugs, and 3.4±0.1 when using D-fdf. 3.1±0.1 points. When using D-FDF, the MMSE score was 3.5±0.1 points, whereas when using cholinergic agents, this index did not exceed 26.9±1.5 points, and when using peptidergic agents - 26.8±1.4 points. Conclusion: The use of neuroprotective agents positively affects the effectiveness of neuro-rehabilitation in patients with acute stroke. The best results in three months after the hospitalization were obtained for peptidergic agents and D-fructose-1,6-diphosphate.


Blood ◽  
1994 ◽  
Vol 84 (8) ◽  
pp. 2622-2631 ◽  
Author(s):  
N Oyaizu ◽  
TW McCloskey ◽  
S Than ◽  
R Hu ◽  
VS Kalyanaraman ◽  
...  

Abstract We have recently shown that, in unfractioned peripheral blood mononuclear cells (PBMCs), the cross-linking of CD4 molecules (CD4XL) is sufficient to induce T-cell apoptosis. However, the underlying mechanism for the CD4XL-mediated T-cell apoptosis is largely unknown. Several recent studies have shown that Fas antigen (Ag), a cell-surface molecule, mediates apoptosis-triggering signals. We show here that cross-linking of CD4 molecules, induced either by anti-CD4 monoclonal antibody (MoAb) Leu3a or by human immunodeficiency virus-1 (HIV-1) envelope protein gp160, upregulates Fas Ag expression as well as Fas mRNA in normal lymphocytes. Addition of the tyrosine protein kinase inhibitor genistein or of the immunosuppressive agent cyclosporin A abrogated these effects. The upregulation of Fas Ag closely correlated with apoptotic cell death, as determined by flow cytometry. In addition, CD4XL resulted in the induction of interferon-gamma (IFN- gamma) and tumor necrosis factor-alpha (TNF-alpha) in the absence of interleukin-2 (IL-2) and IL-4 secretion in PBMCs. Both INF-gamma and TNF-alpha were found to contribute to Fas Ag upregulation and both anti- IFN-gamma and anti-TNF-alpha antibodies blocked CD4XL-induced Fas Ag upregulation and lymphocyte apoptosis. These findings strongly suggest that aberrant cytokine secretion induced by CD4XL and consequent upregulation of Fas Ag expression might play a critical role in triggering peripheral T-cell apoptosis and thereby contribute to HIV disease pathogenesis.


1990 ◽  
Vol 259 (5) ◽  
pp. E672-E676
Author(s):  
P. E. Walton ◽  
M. J. Cronin

Prolactin binds to lymphocytes and monocytes and can modulate immune cell function. It was postulated that proteins released from activated macrophages and lymphocytes could directly influence prolactin release and thus form an endocrine control loop during infection, tumor invasion, or inflammation. This hypothesis was tested by exposing cultured rat anterior pituitary cells to murine tumor necrosis factor-alpha (TNF-alpha) and/or interferon-gamma (IFN-gamma) for 24 h before a 4-h test of cell function. Overall prolactin accumulation during this first 24 h was inhibited by TNF-alpha and markedly reduced by TNF-alpha plus IFN-gamma. In contrast, thyroid-stimulating hormone levels were unchanged in these same media. During the subsequent 4-h challenge, both cytokines reduced thyrotropin-releasing hormone-stimulated prolactin release but had no effect on inhibited prolactin release mediated by dopamine and somatostatin receptors. Cellular viability (assessed by trypan blue and chromium release assays) and prolactin cell content were unchanged after TNF-alpha or IFN-gamma treatment. We conclude that both TNF-alpha and IFN-gamma have the potential to act directly on anterior pituitary cells to slow the rate of prolactin release.


1993 ◽  
Vol 178 (4) ◽  
pp. 1435-1440 ◽  
Author(s):  
R Kamijo ◽  
J Le ◽  
D Shapiro ◽  
E A Havell ◽  
S Huang ◽  
...  

Mice with a targeted disruption of the interferon gamma receptor gene (IFN-gamma R0/0 mice) and control wild-type mice were inoculated with the Bacillus Calmette-Guérin (BCG) strain of Mycobacterium bovis. BCG infection was not lethal for wild-type mice whereas all IFN-gamma R0/0 mice died approximately 7-9 wk after inoculation. Histological examination at 2 and 6 wk after BCG inoculation showed that livers of IFN-gamma R0/0 mice had higher numbers of acid-fast bacteria than wild-type mice, especially at 6 wk. In parallel, the livers of IFN-gamma R0/0 mice showed a reduction in the formation of characteristic granulomas at 2 wk after inoculation. Injection of lipopolysaccharide (LPS) 2 wk after BCG inoculation was significantly less lethal for IFN-gamma R0/0 mice than for wild-type mice. Reduced lethality of LPS correlated with a drastically reduced production of tumor necrosis factor alpha (TNF-alpha) in the IFN-gamma R0/0 mice. Interleukin 1 alpha (IL-1 alpha) and IL-6 levels in the serum were also significantly reduced in the IFN-gamma R0/0 mice after BCG infection and LPS challenge. The greatly reduced capacity of BCG-infected IFN-gamma R0/0 mice to produce TNF-alpha may be an important factor in their inability to resist BCG infection. These results show that the presence of a functional IFN-gamma receptor is essential for the recovery of mice from BCG infection, and that IFN-gamma is a key element in the complex process whereby BCG infection leads to the sensitization to endotoxin.


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