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BACKGROUND: Echocardiography is a tool used in neonatal period to screen for congenital heart defects and to assess the function of the cardiovascular system. It enables obtaining a three-vessel view (3VV) to show how the superior vena cava, the aorta and the pulmonary trunk relate to each other. A 3VV also provides a view of the thymus gland. METHODS: It is a preliminary study. Using the thymus measurements obtained in echocardiography of neonates delivered in one healthcare centre, a total of 1,331 thymus records were collected and statistically analysed. The study was conducted on group of 321 preterm neonates and 1,010 full-term neonates. The superior mediastinal view (three-vessel view, 3VV) was chosen for thymus measurements, with the parallel vascular system, including the superior vena cava, the aorta and the pulmonary trunk, with visible branching to the right and left pulmonary artery. Thymus width, depth and thymic 3VV index were measured. Thymic 3VV index (TI 3VV) is defined as a product of multipling the width and the depth of the thymus in three-vessel view projection. RESULTS: Based on a statistical analysis, a correlation was found of 3VV thymus dimensions and thymic 3VV index with body weight, gestational age and body surface area (BSA). These measurements led to the important finding that the TI 3VV value depends on thymus width and depth, more prominently the latter. The 3VV measurement of thymus depth alone can serve as a screening tool to assess the size of the gland. CONCLUSIONS: Inclusion of thymic measurements in neonatal echocardiography protocol can be used as a screening tool to assess the size of thymus gland.
Assuntos
Ecocardiografia , Timo , Humanos , Timo/diagnóstico por imagem , Timo/anatomia & histologia , Recém-Nascido , Feminino , Masculino , Ecocardiografia/métodos , Recém-Nascido Prematuro , Idade Gestacional , Estudos de CoortesRESUMO
Background: Currently, no evidence exists on the expression of apoptosis (CASP3), autophagy (BECN1), and mitophagy (BNIP3) genes in the CA3 area after ischemia with long-term survival. Objective: The goal of the paper was to study changes in above genes expression in CA3 area after ischemia in the period of 6-24 months. Methods: In this study, using quantitative RT-PCR, we present the expression of genes associated with neuronal death in a rat ischemic model of Alzheimer's disease. Results: First time, we demonstrated overexpression of the CASP3 gene in CA3 area after ischemia with survival ranging from 0.5 to 2 years. Overexpression of the CASP3 gene was accompanied by a decrease in the activity level of the BECN1 and BNIP3 genes over a period of 0.5 year. Then, during 1-2 years, BNIP3 gene expression increased significantly and coincided with an increase in CASP3 gene expression. However, BECN1 gene expression was variable, increased significantly at 1 and 2 years and was below control values 1.5 years post-ischemia. Conclusions: Our observations suggest that ischemia with long-term survival induces neuronal death in CA3 through activation of caspase 3 in cooperation with the pro-apoptotic gene BNIP3. This study also suggests that the BNIP3 gene regulates caspase-independent pyramidal neuronal death post-ischemia. Thus, caspase-dependent and -independent death of neuronal cells occur post-ischemia in the CA3 area. Our data suggest new role of the BNIP3 gene in the regulation of post-ischemic neuronal death in CA3. This suggests the involvement of the BNIP3 together with the CASP3 in the CA3 in neuronal death post-ischemia.
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Doença de Alzheimer , Apoptose , Autofagia , Proteína Beclina-1 , Caspase 3 , Modelos Animais de Doenças , Proteínas de Membrana , Mitofagia , Animais , Proteína Beclina-1/genética , Proteína Beclina-1/metabolismo , Doença de Alzheimer/genética , Doença de Alzheimer/patologia , Proteínas de Membrana/genética , Proteínas de Membrana/metabolismo , Mitofagia/genética , Mitofagia/fisiologia , Autofagia/genética , Autofagia/fisiologia , Apoptose/genética , Masculino , Caspase 3/metabolismo , Caspase 3/genética , Ratos , Região CA3 Hipocampal/patologia , Região CA3 Hipocampal/metabolismo , Isquemia Encefálica/genética , Isquemia Encefálica/patologia , Proteínas Reguladoras de Apoptose/genética , Proteínas Reguladoras de Apoptose/metabolismo , Proteínas Mitocondriais/genética , Proteínas Mitocondriais/metabolismo , Ratos WistarRESUMO
Background: Understanding the phenomena underlying the non-selective susceptibility to ischemia of pyramidal neurons in the CA3 is important from the point of view of elucidating the mechanisms of memory loss and the development of dementia. Objective: The aim of the study was to investigate changes in genes expression of amyloid precursor protein, its cleaving enzymes and tau protein in CA3 post-ischemia with survival of 12-24 months. Methods: We used an ischemic model of Alzheimer's disease to study the above genes using an RT-PCR protocol. Results: The expression of the amyloid precursor protein gene was above the control values at all times post-ischemia. The expression of the α-secretase gene also exceeded the control values post-ischemia. The expression of the ß-secretase gene increased 12 and 24 months post-ischemia, and 18 months was below control values. Presenilin 1 and 2 genes expression was significantly elevated at all times post-ischemia. Also, tau protein gene expression was significantly elevated throughout the observation period, and peak gene expression was present 12 months post-ischemia. Conclusions: The study suggests that the genes studied are involved in the non-amyloidogenic processing of amyloid precursor protein. Additionally data indicate that brain ischemia with long-term survival causes damage and death of pyramidal neurons in the CA3 area of the hippocampus in a modified tau protein-dependent manner. Thus defining a new and important mechanism of pyramidal neuronal death in the CA3 area post-ischemia. In addition expression of tau protein gene modification after brain ischemia is useful in identifying ischemic mechanisms occurring in Alzheimer's disease.
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Doença de Alzheimer , Isquemia Encefálica , Humanos , Doença de Alzheimer/genética , Doença de Alzheimer/metabolismo , Precursor de Proteína beta-Amiloide/genética , Precursor de Proteína beta-Amiloide/metabolismo , Secretases da Proteína Precursora do Amiloide/genética , Secretases da Proteína Precursora do Amiloide/metabolismo , Proteínas tau/genética , Proteínas tau/metabolismo , Hipocampo/metabolismo , Isquemia Encefálica/genética , Isquemia Encefálica/metabolismo , Isquemia/metabolismo , Peptídeos beta-Amiloides/metabolismoRESUMO
INTRODUCTION: In recent years, a very close relationship between miRNA and cardiovascular diseases has been found. RAH and T2DM are accompanied by a change in the microRNA expression spectrum. OBJECTIVES: This study aimed to evaluate the clinical characteristics and expression of selected microRNAs in patients with idiopathic RAH and T2DM. PATIENTS AND METHODS: A total of 115 patients with RAH were included in this study. Among them were 53 patients (46.09%) with T2DM. miRNA levels were determined using quantitative real-time polymerase chain reaction. The expression of the examined genes was calculated from the formula RQ = 2-ΔΔCT. RESULTS: Analysis using the Mann-Whitney U test showed a statistically significant (p < 0.05) difference in the expression of MIR1-1 (p = 0.031) and MIR195 (p = 0.042) associated with the occurrence of T2DM in the subjects. The value of MIR1-1 gene expression was statistically significantly higher in patients with T2DM (median: 0.352; mean: 0.386; standard deviation: 0.923) compared to patients without T2DM (median: 0.147; mean: -0.02; standard deviation: 0.824). The value of MIR195 gene expression was statistically significantly higher in patients with T2DM (median: 0.389, mean: 0.442; standard deviation: 0.819) compared to patients without T2DM (median: -0.027; mean: 0.08; standard deviation: 0.942). CONCLUSIONS: The values of MIR1-1 and MIR195 gene expression were statistically significantly higher in patients with RAH and T2DM compared to patients with RAH and without T2DM. Further studies are necessary to precisely clarify the roles of miRNAs in patients with RAH and T2DM. They should demonstrate the utility of these genetic markers in clinical practice.
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INTRODUCTION AND OBJECTIVE: Lung cancer is the most common malignant tumour. More than 80% of all diagnosed cases are non-small cell carcinoma which can be effectively treated by radical resection. Despite significant progress in the field of diagnostic and therapeutic methods, the results of lung cancer treatment are still unsatisfactory. Lung cancer is detected relatively late, which leads to an unfavourable prognosis. Kynurenine aminotransferases are an important element of the kynurenine pathway of tryptophan metabolism, which has recently aroused great interest from the aspect of possible use as a target point of personalized therapies in malignant tumours.The aim of the study was to analyze the expression of the selected gene of kynurenine aminotransferases GOT 2 at the mRNA level in peripheral blood leukocytes of patients with lung cancer. MATERIAL AND METHODS: The mRNA expression of the GOT 2 gene was tested on blood samples from 50 patients treated surgically for non-small cell lung cancer.The control group consisted of 15 healthy individuals.The determination of mRNA expression of the GOT 2 gene was performed using the real-time PCR method.The GAPDH gene was used as the endogenous reference level. RESULTS: The mRNA expression of the GOT2 gene on the 6th day after surgery was statistically significantly lower than before surgery (p = 0,05). In the study group, the average LogRQ mRNA expression of the GOT2 gene before the procedure was 0.192082±0.292174 in woman. This was statistically significantly higher than in men whose average LogRQ mRNA expression of the GOT2 gene before the procedure was 0.004210±0.235065 (p=0.0183). CONCLUSIONS: Surgical resection of lung cancer results in inhibition of GOT2 mRNA expression in leukocytes. Further studies are expected to show whether it may be used as a target point for personalized therapies in lung cancer.