Effects of two different dexamethasone dosing regimens on ventilator-free days and long-term mortality in COVID-19 patients with moderate-to-severe ARDS: the REMED randomized clinical trial.

Background: Dexamethasone 6 mg in patients with severe COVID-19 has been shown to decrease mortality and morbidity. The effects of higher doses of corticosteroid, that would further increase anti-inflammatory effects, are uncertain. The objective of our study was to assess the effect of 20 mg dexamethasone vs.

Bacterial Community- and Hospital-Acquired Pneumonia in Patients with Critical COVID-19-A Prospective Monocentric Cohort Study.

The impact of bacterial pneumonia on patients with COVID-19 infection remains unclear. This prospective observational monocentric cohort study aims to determine the incidence of bacterial community- and hospital-acquired pneumonia (CAP and HAP) and its effect on mortality in critically ill COVID-19 patients admitted to the intensive care unit (ICU) at University Hospital Olomouc between 1 November 2020 and 31 December 2022. The secondary objectives of this study include identifying the bacterial etiology of CAP and HAP and exploring the capabilities of diagnostic tools, with a focus on inflammatory biomarkers.

[Resistance of bacterial pathogens isolated from the lower respiratory tract and their clonality in intensive care patients in a post-COVID-19 period].

Objectives: The period of the COVID-19 pandemic had a significant impact on the healthcare system, including its effect on compliance with the established procedures of a rational antibiotic policy, especially in the context of nosocomial pneumonia, where it was very difficult to distinguish a possible bacterial superinfection from a severe inflammatory reaction caused by the SARS-CoV-2 virus. The aim of the present study was to analyze the antimicrobial resistance of bacterial pathogens isolated from the lower respiratory tract and their clonality in intensive care patients in 2022 and to compare it with the previous COVID-19 period.

Material And Methods: Bacterial strains isolated from the lower respiratory tract (LRT) of patients hospitalized at the Department of Anaesthesiology, Resuscitation and Intensive Care, Olomouc University Hospital (DARIC) over a three-year period (January 1, 2020 - December 31, 2022) were included in the study.

[Impact of the COVID-19 pandemic on antimicrobial resistance].

Objectives: The COVID-19 pandemic has had a major impact on the healthcare system, which has been forced to manage large numbers of patients, including those with respiratory insufficiency and in need of oxygen therapy. Due to concerns about bacterial co-infection, antibiotic therapy was administered to many patients. The aim of the present study was to compare antimicrobial resistance in intensive care patients in the pre-pandemic and pandemic periods.

Bacterial Resistance to Antibiotics and Clonal Spread in COVID-19-Positive Patients on a Tertiary Hospital Intensive Care Unit, Czech Republic.

This observational retrospective study aimed to analyze whether/how the spectrum of bacterial pathogens and their resistance to antibiotics changed during the worst part of the COVID-19 pandemic (1 November 2020 to 30 April 2021) among intensive care patients in University Hospital Olomouc, Czech Republic, as compared with the pre-pandemic period (1 November 2018 to 30 April 2019). A total of 789 clinically important bacterial isolates from 189 patients were cultured during the pre-COVID-19 period. The most frequent etiologic agents causing nosocomial infections were strains of Klebsiella pneumoniae (17%), Pseudomonas aeruginosa (11%), Escherichia coli (10%), coagulase-negative staphylococci (9%), Burkholderia multivorans (8%), Enterococcus faecium (6%), Enterococcus faecalis (5%), Proteus mirabilis (5%) and Staphylococcus aureus (5%).

[Acute care treatment of COVID-19 pneumonia with acute respiratory failure].

Treatment of COVID-19 patients and their extreme numbers represented an unprecedented challenge for the intensive care system in healthcare facilities throughout the Czech Republic, a country particularly affected by the new coronavirus SARS-CoV-2 pandemic. A steep increase in the need for intensive care placed an excess burden on bed and staff capacity. For a severe and critical course of COVID-19, bilateral pneumonia with acute hypoxemic respiratory failure is pathognomonic.

and Vancomycin-Resistant Enterococci in COVID-19 Patients with Severe Pneumonia.

Broad-spectrum antibiotics administered to patients with severe COVID-19 pneumonia pose a risk of infection caused by . This risk is reduced mainly by strict hygiene measures and early de-escalation of antibiotic therapy. Recently, oral vancomycin prophylaxis (OVP) has also been discussed.

[Antibiotic treatment issues in patients with COVID-19].

The COVID-19 pandemic may increase the current threat of antimicrobial resistance and exacerbate another, rather silent, pandemic posed by the increasing frequency of multidrug-resistant bacterial pathogens and the associated potential for loss of effective antibiotics. Antibiotic treatment has often been used in patients hospitalized for COVID-19 due to concerns about possible bacterial co-infection, as confirmed by previous experience with viral respiratory infections such as H1N1 influenza, SARS and MERS. Concerns or unknowns related to the COVID-19 pandemic have also affected physicians behavior, including the use of antibiotics.

Nosocomial pneumonias.

The paper provides clear definitions of the basic concepts of nosocomial pneumonias. Specifically, definitions and classifications of HAP and VAP, general treatment principles and specific recommended procedures for antibiotic therapy are given as applicable in the Czech Republic.

Human myotubularin-related protein 9 regulates ER-to-Golgi trafficking and modulates WNT3A secretion.

Regulation of phosphatidylinositol phosphates plays a crucial role in signal transduction, membrane trafficking or autophagy. Members of the myotubularin family of lipid phosphatases contribute to phosphoinositide metabolism by counteracting the activity of phosphoinositide kinases. The mechanisms determining their subcellular localization and targeting to specific membrane compartments are still poorly understood.

[Hospital-acquired pneumonia in the light of current recommendations - is there a space for improving patient care?].

Hospital-acquired pneumonia (HAP) is an infection of the lung parenchyma. It is the second most frequent nosocomial infection and the leading cause of death from infection in critically ill patients. Hospital-acquired and, particularly, ventilator-associated pneumonia prolong the hospital stay and increase treatment costs.

Detection of the etiological agents of hospital-acquired pneumonia - validity and comparison of different types of biological sample collection: a prospective, observational study in intensive care patients.

Background: There is still a lack of evidence as to which method of biological sample collection is optimal for identifying bacterial pathogens causing hospital-acquired pneumonia (HAP). Much effort has been made to find an easy and valid approach to be used in clinical practice.

Methods: The primary endpoint of this prospective, observational study was to determine the predictive value of oropharyngeal swab (OS) and gastric aspiration (GA) as simple and non-invasive methods for diagnosing HAP.

Epidemiology of hospital-acquired pneumonia: Results of a Central European multicenter, prospective, observational study compared with data from the European region.

Background: Hospital-acquired pneumonia (HAP) is associated with high mortality. In Central Europe, there is a dearth of information on the prevalence and treatment of HAP. This project was aimed at collecting multicenter epidemiological data on patients with HAP in the Czech Republic and comparing them with supraregional data.

[Validity comparison of various biological samples from lower airway and their contribution for the detection of nosocomial pneumonia etiological agents].

Background: The aim of the study was to compare the validity of bronchial secretion sampling and bronchoscopy-assisted protected specimen brushing (PSB) in patients with hospital-acquired pneumonia (HAP).

Materials And Methods: In patients with HAP, bronchial secretion samples (aspiration of lower airway secretions from an orotracheal tube with a suctioning catheter) and PSB (bronchoscopy-assisted sampling from the most affected area of the lung, verified by CT scan) were taken at the same time. Both samples were processed by semiquantitative routine microbiological techniques.

Fatty acid modification of Wnt1 and Wnt3a at serine is prerequisite for lipidation at cysteine and is essential for Wnt signalling.

The Wnt family of proteins is a group of extracellular signalling molecules that regulate cell-fate decisions in developing and adult tissues. It is presumed that all 19 mammalian Wnt family members contain two types of post-translational modification: the covalent attachment of fatty acids at two distinct positions, and the N-glycosylation of multiple asparagines. We examined how these modifications contribute to the secretion, extracellular movement and signalling activity of mouse Wnt1 and Wnt3a ligands.

Incidence of postoperative nausea and vomiting in patients at a university hospital. Where are we today?

Aim: To determine the incidence of postoperative nausea and vomiting (PONV), identify risk factors, assess treatment and its effectiveness.

Design: A prospective, observational, questionnaire- and interview-based study.

Setting: Standard and intensive care units of the following university hospital departments: abdominal, thoracic and vascular surgery; gynecology; plastic and esthetic surgery; urology; and traumatology.

Functional analysis of the posttranslational modifications of the death receptor 6.

Death receptor 6 (DR6/TNFRSF21) is a death domain-containing receptor of the TNFR superfamily with an apparent regulatory function in hematopoietic and neuronal cells. In this study we document that DR6 is an extensively posttranslationally modified transmembrane protein and that N- and O-glycosylations of amino acids in its extracellular part are mainly responsible for its approximately 40 kDa mobility shift in SDS polyacrylamide gels. Site-directed mutagenesis confirmed that all six extracellular asparagines are N-glycosylated and that the Ser/Thr/Pro cluster in the "stalk" domain juxtaposed to the cysteine-rich domains (CRDs) is a major site for the likely mucine-type of O-glycosylation.

Dazap2 modulates transcription driven by the Wnt effector TCF-4.

A major outcome of the canonical Wnt/beta-catenin-signalling pathway is the transcriptional activation of a specific set of target genes. A typical feature of the transcriptional response induced by Wnt signalling is the involvement of Tcf/Lef factors that function in the nucleus as the principal mediators of signalling. Vertebrate Tcf/Lef proteins perform two well-characterized functions: in association with beta-catenin they activate gene expression, and in the absence of Wnt ligands they bind TLE/Groucho proteins to act as transcriptional repressors.

Wnt-expressing rat embryonic fibroblasts suppress Apo2L/TRAIL-induced apoptosis of human leukemia cells.

Wnt signaling enhances cell proliferation and the maintenance of hematopoietic cells. In contrast, cytotoxic ligand Apo2L/TRAIL induces the apoptosis of various transformed cells. We observed that co-culture of human pre-B leukemia cells KM3 and REH with Wnt1- or Wnt3a-producing rat embryonic fibroblasts efficiently suppressed Apo2L/TRAIL-induced apoptosis of the lymphoid cells.

Quercetin enhances TRAIL-mediated apoptosis in colon cancer cells by inducing the accumulation of death receptors in lipid rafts.

Cytokines such as tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) can induce apoptosis in colon cancer cells through engagement of death receptors. Nevertheless, evading apoptosis induced by anticancer drugs characterizes many types of cancers. This results in the need for combination therapy.

HIC1 attenuates Wnt signaling by recruitment of TCF-4 and beta-catenin to the nuclear bodies.

The hypermethylated in cancer 1 (HIC1) gene is epigenetically inactivated in cancer, and in addition, the haploinsufficiency of HIC1 is linked to the development of human Miller-Dieker syndrome. HIC1 encodes a zinc-finger transcription factor that acts as a transcriptional repressor. Additionally, the HIC1 protein oligomerizes via the N-terminal BTB/POZ domain and forms discrete nuclear structures known as HIC1 bodies.

Binding of the Galanthus nivalis agglutinin to thymocytes reveals alterations in surface glycosylation during T-cell development.

Surface binding of the Galanthus nivalis agglutinin (GNA) to thymocyte subsets has been studied in pigs and rodents by multicolour flow cytometry. In all the species examined, analogous staining profiles have been recorded. Counter-staining with anti-CD3epsilon, anti-CD4 and anti-CD8 monoclonal antibodies (MoAb) revealed that a significant increase of the GNA targets on the cell surface occurred during early thymocyte differentiation and reached its maximum at the level of the CD3loCD4+CD8+ small cortical thymocyte.