Midazolam is a short acting sedative with small number of adverse effects. Administered orally, it is currently the most common form of conscious sedation in children. The objective of this paper is to describe effect of midazolam administered to children during dental treatment on their vital signs, and to monitor changes in children’s behavior. We described values of vital signs and behavior in 418 sedations conducted in 272 children between 1-12 years of age. To achieve the following results, we used data from 272 all first-time sedations. After administration of midazolam arterial blood pressure and blood oxygen saturation decreased by values which were not clinically significant. The heart rate increased, with values staying within the limits of physiological range. The speed of onset of midazolam’s clinical effects depends on age and dose. The lower age and dose correlated with the higher behavior score. The effectiveness of midazolam treatment is 97.8 %. Unwillingness of child to receive midazolam is predictor for disruptive behavior during sedation. 1.8 % of all sedation cases showed paradoxical reactions. The administration of midazolam in dose of 0.5 mg per 1 kg of child’s body weight is safe and could be recommended for dental treatment in pediatric dentistry., Jana Vasakova, Jana Duskova, Jitka Lunackova, Klara Drapalova, Lucie Zuzankova, Luboslav Starka, Michaela Duskova, Zdenek Broukal., and Obsahuje bibliografii
Gastropathy is one of the most common diseases of the human gastrointestinal tract. Apart from its consequences in the stomach, it is also manifested in other parts of the digestive tract, particularly in the duodenum. The aim of this pilot study was to verify on animal model the empirically observed alleviation of gastropathy symptoms in patients who underwent a drinking treatment of Vincentka natural mineral water during their spa treatment. Sixteen male Wistar rats were included in the study. The animals were randomly divided into two groups: experimental group (E; n=8) and control group (C; n=8). The experimental protocol consisted of three phases: (1) handling phase (7 days); (2) mineral water (E)/tap water (C) administration (7 days); (3) acute gastritis induction (1 day). Twenty-four hours after the induction of acute gastritis, the animals were sacrificed. The collected tissues (stomach and duodenum) and blood were examined by standard histological microscopy, and by immunohistochemical and biochemical methods. Histopathological analysis revealed significantly reduced damage to the gastric mucosa in the experimental group. Significantly different values of blood plasma antioxidant capacity, oxidative stress parameters and blood plasma biochemical parameters were also found. Based on these results, we conclude that the mineral water Vincentka has a positive impact on development and symptoms of acute gastric ulcers.
The study aimed to recognize whether the activity of a semi-aquatic invasive carnivore – the American mink Neovison vison – is related to the distribution of waterbird colonies. For this reason, we monitored mink occurrence in lake reedbeds and the fate of artificial nests imitating those of the great crested grebe Podiceps cristatus. The location of artificial nests in the grebe colony increased the probability of their survival compared to those placed outside the grebe colony. During the study, mink activity increased over time. In general, it was lower in colonies than outside of them, suggesting that the presence of natural nests does not increase the probability of mink occurrence in lake reedbeds. However, mink activity was negatively correlated with the distance from the lake shoreline and differed spatially according to the presence or absence of natural grebe nests. In grebe colonies, the probability of mink occurrence at greater distances from the lake shoreline was higher than outside, which can be explained by optimizing swimming effort while searching for prey. In conclusion, mink activity in colonies was lower than in areas with no waterbird nests, and nest location in a colony decreased predation risk by mink.
The main goal of our prospective randomized study was
comparing compare the effectiveness of ventilation control
method „Automatic proportional minute ventilation (APMV)
“versus manually set pressure control ventilation modes in
relationship to lung mechanics and gas exchange. 80 patients
undergoing coronary artery bypass grafting (CABG) were
randomized into 2 groups. 40 patients in the first group No. 1
(APMV group) were ventilated with pressure control (PCV) or
pressure support ventilation (PSV) mode with APMV control. The
other 40 patients (control group No.2) were ventilated with
synchronized intermittent mandatory ventilation (SIMV-p) or
pressure control modes (PCV) without APMV. Ventilation control
with APMV was able to maintain minute ventilation more
precisely in comparison with manual control (p<0.01), similarly
deviations of ETCO2 were significantly lower (p<0.01). The
number of manual corrections of ventilation settings was
significantly lower when APMV was used (p<0.01). The
differences in lung mechanics and hemodynamics were not
statistically significant. Ventilation using APMV is more precise in
maintaining minute ventilation and gas exchange compared with
manual settings. It required less staff intervention, while
respiratory system mechanics and hemodynamics are
comparable. APMV showed as effective and safe method
applicable on top of all pressure control ventilation modes.
The increased proliferation and migration of airway smooth muscle cells (ASMCs) is a key process in the formation of airway remodeling in asthma. In this study, we focused on the expression of mircoRNA-18a (miR-18a) in airway remodeling in bronchial asthma and its related mechanisms. ASMCs are induced by platelet-derived growth factor BB (PDGF-BB) for in vitro airway remodeling. The expression of miR-18a in sputum of asthmatic patients and healthy volunteers was detected by qRT-PCR. The expression of miR-18a was over-expressed or interfered with in PDGF-BB-treated ASMCs. Cell proliferation, apoptosis and migration were detected by MTT, flow cytometry and Transwell, respectively, the expression of contractile phenotype marker proteins (SM-22α, α-SM-actin, calponin) and key molecules of the phosphatidylinositol 3-kinase (PI3K)/AKT pathway (PI3K, p-PI3K, AKT and p-AKT) in ASMCs were detected by Western blot. The expression of miR-18a was down-regulated in the sputum and PDGF-BB-treated ASMCs of asthma patients. PDGF-BB could promote the proliferation and migration of ASMCs and inhibit their apoptosis, it could also promote the phenotypic transformation of ASMCs and activate the PI3K/AKT pathway. MiR-18a could inhibit the proliferation, migration ability and phenotypic transformation of ASMCs induced by PDGF-BB to a certain extent and alleviate the effect of PDGF-BB in supressing apoptosis, while miR-18a could inhibit the activation of the PI3K/AKT pathway. MiR-18a inhibits PDGF-BB-induced proliferation, migration and phenotypic conversion of ASMCs by inhibiting the PI3K/AKT pathway, thus attenuating airway remodeling in asthma.
Circulating miRNAs have been proposed as the effective diagnostic biomarkers for muscular fibrosis-associated diseases. However, circulating biomarkers for early diagnosis of contracture muscles are limited in gluteal muscle contracture (GMC) patients. Here we sought to explore the abnormally expressed miRNAs in plasma and contraction bands of GMC patients. The results showed miR-29a-3p expression in plasma and contraction bands tissue was significantly reduced in GMC patients compared with normal control. Cell viability and levels of proliferation-associated protein cyclin D1 and cyclindependent-kinase 2 (CDK2) were powerfully inhibited by miR-29a mimics and enhanced by miR-29a inhibitor compared with negative control. Furthermore, miR-29a mimics effectively impeded, while miR-29a inhibitor enhanced the expression of collagen I and collagen III, followed by the secretion of transforming growth factor β1 (TGF-β1), TGF-β3 and connective tissue growth factor (CTGF) in primary human contraction bands (CB) fibroblasts. The miR-29a-3p negatively regulated the expression of TGF-β1 through binding to the 3′ UTR region of SERPINH1 (encoding heat shock protein HSP47), but had no effect on Smad2 activity. The miR-29a-3p was inversely correlated with HSP47 in contraction bands tissue from GMC patients. Collectively, miR-29a was notably depressed and regulated cell viability and fibrosis by directly targeting HSP47 in GMC, which suggest that circulating miR-29a might be a potential biomarker for early diagnosis and provides a novel therapeutic target for GMC.
Acute myocardial infarction (AMI) represents the acute manifestation of coronary artery disease. In recent years, microRNAs (miRNAs) have been extensively studied in AMI. This study focused on the role of miR-431-5p in AMI and its effect on cardiomyocyte apoptosis after AMI. The expression of miR-431-5p was analyzed by quantitative real-time PCR (qRT-PCR). By interfering with miR-431-5p in hypoxiareoxygenation (H/R)-induced HL-1 cardiomyocytes, the effect of miR-431-5p on cardiomyocyte apoptosis after AMI was examined. The interaction between miR-431-5p and selenoprotein T (SELT) mRNA was verified by dual-luciferase reporter assay. Cell apoptosis was determined by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay and flow cytometry. Cell viability was examined by 3-(4,5)- dimethylthiahiazo(-z-y1)-3,5-di-phenytetrazoliumromide (MTT) assay. The results of qRT-PCR showed that the expression of miR-431-5p in AMI myocardial tissues and H/R-induced HL-1 cardiomyocytes was significantly increased. After interfering with miR-431-5p, the expression of SELT in HL-1 cells was up-regulated, cell apoptosis was decreased, cell viability was increased, and lactate dehydrogenase (LDH) activity was decreased. The dual-luciferase reporter assay confirmed the targeting relationship between miR-431-5p and SELT1 3’ untranslated region (UTR). In H/R-induced HL-1 cells, the simultaneous silencing of SELT and miR-431-5p resulted in a decrease of Bcl-2 expression, an increase of Bax expression, and an increase of cleaved-caspase 3 expression compared with silencing miR-431-5p alone. Also, cell viability was decreased, while LDH activity was increased by the simultaneous silencing of SELT and miR-431-5p. Interfering miR-431-5p protected cardiomyocytes from AMI injury via restoring the expression of SELT, providing new ideas for the treatment of AMI.
Gluteal muscle contracture (GMC) is a chronic fibrotic disease of gluteal muscles due to multiple etiologies. Emilin 1 plays a determinant role in fibers formation, but its role in the progression of GMC remains unclear. The present study was aimed to search for the predictive role and regulatory mechanism of Emilin 1 on GMC. Here, Protein and mRNA expression of Emilin 1 were decreased in GMC tissues compared to normal muscle tissues. Using the analysis of target prediction, Emilin 1 was observed to be a potential downstream sponge of miR-491-5p. In comparison to Emilin 1, miR-491-5p showed an aberrant elevation in GMC tissues, which was further proven to have a negative correlation with Emilin 1. The direct binding of miR-491-5p to Emilin 1 mRNA was confirmed by luciferase reporter gene assay, and miR-491-5p mimics inhibited, while miR-491-5p inhibitor promoted the protein expression and secretion of Emilin 1 in contraction bands (CB) fibroblasts. Additionally, miR-491-5p mimics promoted the expression of cyclin-dependent kinase 2 and cyclin D1 and the proliferation of CB fibroblasts, which could be reversed by Emilin 1 overexpression. Mechanistically, miR-491-5p mimics possibly activated transforming growth factor β1 (TGF-β1)/Smad3 signal cascade via binding to 3’-untranslated region of Emilin 1 mRNA, thereby promoting the progression of fibrosis of CB fibroblasts. Collectively, miR-491-5p inhibited Emilin 1 expression, and subsequently promoted CB fibroblasts proliferation and fibrosis via activating TGF-β1/Smad3 signal axis. MiR-491-5p might be a potentially effective biomarker for predicting GMC, providing a novel therapeutic strategy for GMC.
Chloroplast PSII photochemical efficiency is upregulated more rapidly than CO2 assimilation during photosynthesis induction, suggesting the existence of other electron sinks than that of CO2 assimilation. We hypothesized that the mitochondrial alternative oxidase (AOX) pathway could be such a sink. Inhibition of the AOX restricted light activation of the malate-oxaloacetate shuttle and caused an excessive reduction of PSI acceptor side and substantial accumulation of QA-, hindering the photosynthetic linear electron transport rate (ETR) and leading to an imbalance between light energy absorption and exploitation during photosynthetic induction. ETR limitation also restricted the formation of thylakoid pH gradient, evidenced by a decreased de-epoxidation of the xanthophyll cycle, thus preventing nonphotochemical quenching. Delayed CO2 assimilation due to thylakoid pH gradient restriction was partially reversed by exogenous ATP application. The AOX pathway acts as a photosynthetic electron sink, protecting the photosynthetic apparatus against photoinhibition and accelerating the induction of CO2 assimilation during photosynthetic induction in Rumex K-1 leaves.