Introduction: Asthma is a complex and multifactorial disorder, with severe public health implications. Over the last several years, our knowledge in the field of human gut microbiota has expanded and allowed us to understand its crucial role in the development of many diseases. Aim: To analyse the nature of human gut microbiota patterns among patients with asthma compared to healthy controls. Material and methods: Composition of the complex gut microbiota was analysed in faecal samples from 13 asthma patients and 7 healthy volunteers using Next-Generation Sequencing technology (NGS). The Kruskal-Wallis Analysis of Variance (ANOVA) and Mann-Whitney tests were used to compare the above two groups of subjects. Results: The composition of the gut microbiota of asthma patients differed from that of healthy volunteers at each of the analysed levels (p < 0.05). Compared to healthy individuals, bacterial diversity was significantly lowered among the asthma group, which is the evidence of gut microbiota depletion in asthma patients. The analysis of beta diversity showed that the gut community compositions of asthma are widely dispersed in contrast to the tight clustering observed in the control group. Finally, the similarity index was found to be lower in the inter-group comparison than in the intra-group comparison, which confirmed changes in the gut microbial composition in the asthmatic group. Conclusions: The study revealed significant differences in the human gut microbiome composition between asthma patients and the healthy control group.
Background: The biological role of EGFRvIII (epidermal growth factor receptor variant three) remains unclear. Methods: Three glioblastoma DK-MG sublines were tested with EGF (epidermal growth factor) and TGFβ (transforming growth factor β). Sublines were characterized by an increased percentage of EGFRvIII-positive cells and doubling time (DK-MGlow to DK-MGextra-high), number of amplicons, and EGFRvIII mRNA expression. The influence of the growth factors on primary EGFRvIII positive glioblastomas was assessed. Results: The overexpression of exoEGFRvIII in DK-MGhigh did not convert them into DK-MGextra-high, and this overexpression did not change DK-MGlow to DK-MGhigh; however, the overexpression of RASG12V increased the proliferation of DK-MGlow. Moreover, the highest EGFRvIII phosphorylation in DK-MGextra-high did not cause relevant AKT (known as protein kinase B) and ERK (extracellular signal-regulated kinase) activation. Further analyses indicate that TGFβ is able to induce apoptosis of DK-MGhigh cells. This subline was able to convert to DK-MGextra-high, which appeared resistant to this proapoptotic effect. EGF acted as a pro-survival factor and stimulated proliferation; however, simultaneous senescence induction in DK-MGextra-high cells was ambiguous. Primary EGFRvIII positive (and SOX2 (SRY-Box Transcription Factor 2) positive or SOX2 negative) glioblastoma cells differentially responded to EGF and TGFβ. Conclusions: The roles of TGFβ and EGF in the EGFRvIII context remain unclear. EGFRvIII appears as a weak oncogene and not a marker of GSC (glioma stem cells). Hence, it may not be a proper target for CAR-T (chimeric antigen receptor T cells).
Background: Autoimmune metabolic diseases generate numerous healthy and social problems. The possible association of SNPs in the ubiquitin-proteasome system (UPS) with human pathology is under intensive study. Objective: In the present study, the genetic variations in PSMB5 (rs11543947), PSMA6 (rs2277460, rs1048990), PSMC6 (rs2295826, rs2295827) and PSMA3 (rs2348071) UPS gene cluster was investigated in type 1 diabetes and healthy donors in the Polish population. Methods: The study comprised 105 patients with type 1 diabetes mellitus (T1DM) and 214 controls. All were genotyped by PCR and restriction digestion analysis or Sanger sequencing. Results: Rs1048990 and rs2348071 were found to be neutral to T1DM (p-value: 0.499 and 0.656, respectively). According to the multiple loci genotype (MLG) analysis, the major homozygote of the tested polymorphisms had a protective effect. The most common MLG in the T1DM group was characterised by simultaneous risk factors at rs11543947, rs2277460, rs2295826 and rs2295827 (p-value: <0.0001 vs. MGL1). Multiple locus haplotype analysis revealed a similar dependence, with common alleles at all tested loci demonstrating a protective effect, and the rare alleles increasing T1DM risk (p-value: <0.0001 vs. MLH1). Conclusion: Our study suggests that the proteasome gene polymorphisms rs11543947, rs2277460, rs2295826, and rs2295827 could be potential markers for T1DM susceptibility in the Polish population.
Abstrakt Ostatnie cztery dekady przyniosły znaczący rozwój archeologii molekularnej i badania nad kopalnym DNA (aDNA). Nowatorskie metody uwzględniają szeroki zakres badań, począwszy od sekwencjonowania niewielkich fragmentów mitochondrialnego DNA po wielkoskalowe badania całych populacji, łączące sekwencjonowanie genomów mitochondrialnych, genów podlegających doborowi naturalnemu, jak i całych genomów jądrowych. Postęp, zwłaszcza w dziedzinie technologii sekwencjonowania DNA, umożliwił pozyskanie informacji ze szczątków paleontologicznych i materiału archeologicznego, umożliwiając zbadanie związków filogenetycznych między wymarłymi i współczesnymi gatunkami. Dzięki zastosowaniu technologii sekwencjonowania nowej generacji możliwe stało się poznanie sekwencji DNA nie tylko bezpośrednio ze szczątków ludzkich lub zwierzęcych, ale także z osadów sedymentacyjnych z głębin jezior oraz jaskiń. W artykule przedstawiono możliwości i ograniczenia występujące w badaniach nad kopalnym DNA ludzi, zwierząt czy bakterii z podkreśleniem wkładu polskich badaczy w rozwój tej dziedziny nauki.
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