Modulating the gut microbiome and its influence on human health is the subject of intense research. The gut microbiota could be associated not only with gastroenterological diseases but also with psychiatric disorders. The importance of factors such as stress, mode of delivery, the role of probiotics, circadian clock system, diet, and occupational and environmental exposure in the relationship between the gut microbiota and brain function through bidirectional communication, described as “the microbiome–gut–brain axis”, is especially underlined. In this review, we discuss the link between the intestinal microbiome and the brain and host response involving different pathways between the intestinal microbiota and the nervous system (e.g., neurotransmitters, endocrine system, immunological mechanisms, or bacterial metabolites). We review the microbiota alterations and their results in the development of psychiatric disorders, including major depressive disorder (MDD), schizophrenia (SCZ), bipolar disorder (BD), autism spectrum disorder (ASD), and attention-deficit hyperactivity disorder (ADHD).

the ABCB1 gene belongs to Atp binding cassette (ABc) transporter genes that has been previously implicated in cancer progression and drug response. this study aimed to evaluate the association between the SNP 3435 and the expression of the ABCB1 gene in lung cancer patients in the polish population in comparison to clinicopathological parameters and treatment. 150 RNA and 47 DNA samples were isolated from 49 lung cancer cases including both tissue samples and blood taken from the same patients at three time points: diagnosis, 100 days and one year after the surgical intervention. Qualitative and real-time pcR analysis of expression were done, also genotyping by PCR-RFLP. Mutant homozygous TT and allele T are present statistically significantly more frequently in the group of patients with lung cancer. There is no difference with expression level in lung cancer tissue and blood sample taken from the same patients before surgical treatment. on the basis of blood samples analysis it was observed that the expression level of ABCB1 mRnA was growing in time. Higher levels were marked after 100 days and one year after the surgical intervention. The complementary pharmacological treatment induced higher expression levels of ABCB1. the presented data suggest an important role of ABCB1 in lung cancer, the increasing level of ABCB1 mRnA which can be connected with induction of multidrug resistance mechanism is also significant, that observation must be confirmed in further analysis.

Abstract. The aim of the present study was to evaluate the mRNA expression level of the runt-related transcription factor 1 (RUNX1) and runt-related transcription factor 3 (RUNX3) genes in patients with acute myeloid leukemia (AML). The etiology of AML is not yet fully known, but certain genetic factors may contribute to its manifestation. The RUNX1 and RUNX3 genes have been demonstrated to serve a role in the transcription process. The group investigated in the present study included 43 patients diagnosed with AML, and the relative RUNX1 and RUNX3 expression levels were determined using reverse transcription-quantitative polymerase chain reaction. The results indicated that RUNX1 and RUNX3 expression was associated with clinicopathological features, including sex and mortality risk. Expression levels of the RUNX1 gene were higher and more variable among females (P=0.044), and mortality was more frequent among patients with a higher RUNX3 expression level (P=0.036). The data obtained from the present study suggested that RUNX3 expression may have potential value as a prognostic factor; furthermore, sex is potentially a factor that may affect the difference in RUNX1 gene expression level among females and males. Further analyses in this field will aid in the identification and elucidation of the molecular basis of leukemia.

Gastric cancer is one of the most common worldwide types of cancer. It is a multifactorial disease and both environmental and genetic factors play an important role in its etiology. Evaluation of the relative expression level of NFKB2 gene in two groups of patients: peptic ulcer and gastric cancer and its role in the pathomechanism of these diseases was the aim of this study. RNA was isolated from: 79 samples of peptic ulcer, 22 gastric cancer and 11 control tissue. The real-time PCR technique was used to study the expression of NFKB2 gene. The relative expression level of NFKB2 gene was a variable in all three studied groups. The relative NFKB2 gene expression depends on the type of a disease. Peptic ulcer cases showed the increased relative NFKB2 gene expression to control group (p = 0.0000). Cancer cases presented decreased relative NFKB2 gene expression to normal stomach tissue (p = 0.0183). There are statistically important differences in the investigated gene expression between peptic ulcer, where the expression level is higher comparing to gastric cancer and control tissue which confirmed that such an activation is connected with an inflammatory process. The relative expression level of NFKB2 is decreased in cancer cases as opposed to control tissue and peptic ulcer cases which could suggest that during carcinogenesis of gastric cancer inhibition of NF-kB pathway takes place which could be a promising factor for patients.

The global scope and scale of the SARS-CoV-2 pandemic led to huge amounts of important data from clinical observations and experimental analyses being collected, in particular, regarding the long-term impact of COVID-19 on lung tissue. Visible changes in lung tissue mainly relate to the destruction of the alveolar architecture, dense cellularity, and pulmonary fibrosis with myofibroblast proliferation and collagen deposition. These changes are the result of infection, mainly with virus variants from the first pandemic waves (Alpha to Delta). In addition, proper regulation of immune responses to pathogenic viral stimuli is critical for the control of and recovery from tissue/organ damage, including in the lungs. We can distinguish three main processes in the lungs during SARS-CoV-2 infection: damage or deficiency of the pulmonary surfactant, coagulation processes, and fibrosis. Understanding the molecular basis of these processes is extremely important in the context of elucidating all pathologies occurring after virus entry. In the present review, data on the abovementioned three biochemical processes that lead to pathological changes are gathered together and discussed. Systematization of the knowledge is necessary to explore the three key pathways in lung tissue after SARS-CoV-2 virus infection as a result of a prolonged and intense inflammatory process in the context of pulmonary fibrosis, hemostatic disorders, and disturbances in the structure and/or metabolism of the surfactant. Despite the fact that the new Omicron variant does not affect the lungs as much as the previous variants, we cannot ignore the fact that other new mutations and emerging variants will not cause serious damage to the lung tissue. In the future, this review will be helpful to stratify the risk of serious complications in patients, to improve COVID-19 treatment outcomes, and to select those who may develop complications before clinical manifestation.

Currently, acute lymphoblastic leukemia (ALL) has an overall survival of nearly 80% when it occurs in children, however cure rates among adults are far reduced. Leukemogenesis can be driven up by a slight change in the expression or function of certain transcription factors. CCAAT Enhancer Binding Protein Alpha (CEBPA) is a transcription factor with role in cell cycle regulation, granulocytic differentiation and more. Some studies suggest its oncogenic function. The potential role of CEBPA as an oncogene in ALL development has not been completely elucidated so far. Therefore, the aim of the present study was to evaluate mRNA level of CEBPA gene in 60 adult patients diagnosed with ALL. Quantitative analysis was performed by qPCR reaction. Analysis revealed that men tended to have higher and more variable CEBPA expression levels (P = 0.032). No associations for other parameters (ALL subtype, age, leukocytosis, blast percentage, Philadelphia chromosome presence, CD10 marker presence) were found. When comparing the results of CEBPA expression with patients suffering from acute myeloid leukemia, ALL cases showed statistically significant lower levels of CEBPA (P < 0.0000). It may seem that CEBPA expression level itself has potentially no effect on arising and progression of acute lymphoblastic leukemia, although it is a matter that needs further investigation. Acute lymphoblastic leukemia (ALL) is a malignant disease of lymphoid progenitor cells affecting both children and adults 1. At present, ALL is successfully curable in almost 80% of cases if it comes to children, however, it shows poor prognosis when arising in adults 2,3. Despite the high cure rates, the complexity, expenditure and toxic side-effects of contemporary multidrug treatments must be mentioned 2. Thus, it is advisable to continue analyzing genetic abnormalities of leukemic cells and to transform them further into enhanced diagnostic methods, targeted novel therapeutics and treatment strategies 1,4. Furthermore, specific predisposing factors leading to acute lymphoblastic leukemia development are not fully known yet, however, leukemogenesis can be driven up by a slight change in the expression or function of certain transcription factors 4. CCAAT Enhancer Binding Protein Alpha (CEBPA) is an intronless gene located on chromosome 19q13.1 5,6. It encodes protein belonging to transcription factors family containing a basic leucine zipper (bZIP) motif 6,7. CEBPA function includes the following modulation of the genes expression involved in the cell cycle regulation and body weight homeostasis 8-10 , it is also crucial in granulocytic differentiation 10,11 and probably acts as a tumor suppressor in hematologic and non-hematologic malignancies 10. On the other hand, some results indicate that CEBPA may act as an oncogene in lymphoid malignancies, in contrast to its role as a tumor suppressor in myeloid leukemia 12. The potential role of CEBPA as an oncogene in ALL development has not been completely elucidated so far. Therefore, the aim of the present study ...

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CEBPA and c-MYC genes belong to TF and play an essential role in hematologic malignancies development. Furthermore, these genes also co-regulate with RUNX1 and lead to bone marrow differentiation and may contribute to the leukemic transformation. Understanding the function and full characteristics of selected genes in the group of patients with AML can be helpful in assessing prognosis, and their usefulness as prognostic factors can be revealed. The aim of the study was to evaluate CEBPA and c-MYC mRNA expression level and to seek their association with demographical and clinical features of AML patients such as: age, gender, FAB classification, mortality or leukemia cell karyotype. Obtained results were also correlated with the expression level of the RUNX gene family. To assess of relative gene expression level the qPCR method was used. The expression levels of CEBPA and c-MYC gene varied among patients. Neither CEBPA nor c-MYC expression levels differed significantly between women and men (p=0.8325 and p=0.1698, respectively). No statistically significant correlation between age at the time of diagnosis and expression of CEBPA (p=0.4314) or c-MYC (p=0.9524) was stated. There were no significant associations between relative CEBPA (p=0.4247) or c-MYC (p=0.4655) expression level and FAB subtype and mortality among the enrolled patients (p=0.5858 and p=0.8437, respectively). However, it was observed that c-MYC and RUNX1 expression levels were significantly positively correlated (rS=0.328, p=0.0411). Overall, AML pathogenesis involves a complex interaction among CEBPA, c-MYC and RUNX family genes.