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[Blood group and human diseases (review of literature).]

AB0 blood group antigens were discovered over a century ago; however, it is still important to study their role in development of various pathological conditions. Today it is known that antigenic determinants of this blood group are present not only on erythrocyte membrane but also on other cells and tissues: platelets, gastrointestinal epithelium and salivary glands, respiratory system cells. In the last decade, a large number of studies have appeared to reveal the relationship between a specific disease and blood group type, meta-analyses have been published. Previously, the authors have studied the metabolic status, cell composition and coagulation profile of clinically healthy individuals for more than on 180,000 donations, that allowed to identify groupspecific features for each blood group. This review presents generalized data on the association of such pathological conditions as coronary heart disease, thromboembolic complications, tumors of various localizations, inflammatory and destructive oral diseases, psychiatric and some infectious diseases with the presence or absence of antigenic determinants A and B. Carriers of blood group 0 (I) are generally more resistant to diseases, with the exception of H.pylori-associated gastrointestinal diseases. Carriers of «antigenic» blood groups A (II), B (III), AB (IV) are more susceptible to development of infectious, cardiovascular and cancer diseases. The presented data demonstrate clinical significance of the definition of group typing not only for selection of blood and its components during transfusion and transplantation, but also for diagnostics, determination of risk group and tactics for treatment patients with different nosologies.

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Triflumuron induces cytotoxic effects on hepatic and renal human cell lines.

Insect growth regulator insecticides are a new class of pesticides, commonly used around the world to control insect damages. Among those compounds, we focused our interest on triflumuron (TFM), which is less toxic than other conventional insecticides. However, not much is known about its toxic effects on mammalian systems. Therefore, our study aimed toward evaluating the cytotoxic and genotoxic effects of TFM using two different cell lines, the human renal embryonic cells (HEK 293) and hepatocytes (Hep G2). We showed, according to the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, that TFM reduced significantly the cell viability and increased the reactive oxygen species generation, malondialdehyde levels, and mitochondrial membrane potential in both cell lines. The antioxidant system was disturbed as assessed by the increased activities in both catalase and superoxide dismutase. We demonstrated also, that TFM is an inductor of DNA damages quantified by the comet assay. Moreover, we showed an overexpression of proapoptotic Bax and a decrease in antiapoptotic Bcl-2 expression. As a conclusion, we demonstrate that the liver presents the major target organ to TFM, in which the cytotoxicity and the genotoxic effects were significantly higher in hepatic cells than in renal cells and by consequence its uses must be controlled.

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Extracorporeal and advanced therapies for progressive refractory near-fatal acute severe asthma in children.

Asthma is the most common chronic illness and is one of the most common medical emergencies in children. Progressive refractory near-fatal asthma requiring intubation and mechanical ventilation can lead to death. Extracorporeal membrane oxygenation (ECMO) can provide adequate gas exchange during acute respiratory failure although data on outcomes in children requiring ECMO support for status asthmaticus is sparse with one study reporting survival rates of nearly 85% with asthma being one of the best outcome subsets for patients with refractory respiratory failure requiring ECMO support. We describe the current literature on the use of ECMO and other advanced extracorporeal therapies available for children with acute severe asthma. We also review other advanced invasive and noninvasive therapies in acute severe asthma both before and while on ECMO support.

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Tomentosin induces apoptotic pathway by blocking inflammatory mediators via modulation of cell proteins in AGS gastric cancer cell line.

In this study, we investigated the in vitro effect of tomentosin on cell proliferation by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, reactive oxygen species by 2',7'-dichlorofluorescein diacetate staining assay, apoptosis (AO/EtBr, propidium iodide, and 4',6-diamidino-2-phenylindole staining, mitochondrial membrane potential), cell adherent, cell migration, inflammation, apoptosis, and oxidative stress from gastric cancer cells (GCCs) AGS. Upon their relative cell proliferative, inflammatory, and apoptotic molecular markers were analyzed by using the enzyme-linked immunosorbent assay and Western blot analysis method. Treatment with tomentosin (IC  = 20 µM) significantly inhibited cell proliferation and oxidative stress-induced anti-cell proliferative (proliferating cell nuclear antigen and cyclin-D1) also regulated expression, drastically diminished tumor necrosis factor-α, nuclear factor-κB, interleukin-6, and interleukin-1β expression levels, significantly upregulated Bcl-2 and Bax expression. Thus, this tomentosin can significantly reduce GCC proliferation via cytotoxicity which is stimulated apoptosis markers via morphology staining changes and inhibitory inflammatory markers. The tomentosin-induced oxidative stress may be involved to stimulate apoptotic mechanisms via mitochondria-mediated signaling by the inhibition of inflammation. Taken together, our findings suggest a possible future use of chemotherapeutic agents for pharmacological benefits and as an anti-cancer treatment option.

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