Monitorowanie zapalenia płuc związanego z wentylacją mechaniczną według projektu INICC — doświadczenia jednego ośrodka

Background: Pneumonia is a common complication of hospitalisation in severely ill patients who need mechanical ventilation. The aim of this study was to assess the usefulness of the International Nosocomial Infection Control Consortium programme for the surveillance of ventilator-associated pneumonia (VAP). Methods: A prospective study (1 Jan 2012-30 June 2014) was conducted in the 20-bed ICU. The device utilisation ratios for lung ventilation and the frequency (density and incidence) and aetiology of VAP were estimated in ICU patients. Results: From a total of 1097 patients, VAP infections were diagnosed in 93. Thirty percent of patients with VAP died. The incidence index was 8.47 per 100 admissions to the ICU. VAP infections accounted for 46% of the overall count of device-associated healthcare-associated infections. Mechanical ventilation was used in 71 +/- 8 patients during the 11 862 patient days and 8425 ventilation days. The rate of VAP per 1000 ventilator days was 11.15/9.34/10.23 in years 2012/2013/2014 (half a year), respectively. The main VAP pathogens were Acinetobacter baumannii (45%) and Pseudomonas aeruginosa (17%). Conclusion: During the reported time span, the incidence of VAP was lower than in the INICC report (2007-2012), but it was tenfold higher than in the NHSN/CDC report (dated 2012). Because of the unchanged VAP level during the 2.5-year observation period, the root cause needs to be determined and action should be taken to resolve this issue

Rep protein accommodates together dsDNA and ssDNA which enables a loop-back mechanism to plasmid DNA replication initiation

17 p.-8 fig.-1 graph. abst.For DNA replication initiation in Bacteria, replication initiation proteins bind to double-stranded DNA (dsDNA) and interact with single-stranded DNA (ssDNA) at the replication origin. The structural–functional relationship of the nucleoprotein complex involving initiator proteins is still elusive and different models are proposed. In this work, based on crosslinking combined with mass spectrometry (MS), the analysis of mutant proteins and crystal structures, we defined amino acid residues essential for the interaction between plasmid Rep proteins, TrfA and RepE, and ssDNA. This interaction and Rep binding to dsDNA could not be provided in trans, and both are important for dsDNA melting at DNA unwinding element (DUE). We solved two crystal structures of RepE: one in a complex with ssDNA DUE, and another with both ssDNA DUE and dsDNA containing RepE-specific binding sites (iterons). The amino acid residues involved in interaction with ssDNA are located in the WH1 domain in stand β1, helices α1 and α2 and in the WH2 domain in loops preceding strands β1’ and β2’ and in these strands. It is on the opposite side compared to RepE dsDNA-recognition interface. Our data provide evidence for a loop-back mechanism through which the plasmid replication initiator molecule accommodates together dsDNA and ssDNA.Polish National Science Centre grant [2017/26/D/NZ1/00239]; E.Z. was supported by the MPD/2010/5 project operated within the Foundation for Polish Science International PhD Projects (MPD) Programme co-financed by the EU European Regional Development Fund; I.K. was supported by Foundation for Polish Science [TEAM, POIR.04.04.00-00-5C75/17-00]; R.G. is the recipient of a grant by Spanish MICIN/AEI [PID2021-124866OB-I00]. Funding for open access charge: University of Gdansk.Peer reviewe

Rosiglitazone Ameliorates Cardiac and Skeletal Muscle Dysfunction by Correction of Energetics in Huntington’s Disease

Huntington’s disease (HD) is a rare neurodegenerative disease that is accompanied by skeletal muscle atrophy and cardiomyopathy. Tissues affected by HD (central nervous system [CNS], skeletal muscle, and heart) are known to suffer from deteriorated cellular energy metabolism that manifests already at presymptomatic stages. This work aimed to test the effects of peroxisome proliferator-activated receptor (PPAR)-γ agonist—rosiglitazone on grip strength and heart function in an experimental HD model—on R6/1 mice and to address the mechanisms. We noted that rosiglitazone treatment lead to improvement of R6/1 mice grip strength and cardiac mechanical function. It was accompanied by an enhancement of the total adenine nucleotides pool, increased glucose oxidation, changes in mitochondrial number (indicated as increased citric synthase activity), and reduction in mitochondrial complex I activity. These metabolic changes were supported by increased total antioxidant status in HD mice injected with rosiglitazone. Correction of energy deficits with rosiglitazone was further indicated by decreased accumulation of nucleotide catabolites in HD mice serum. Thus, rosiglitazone treatment may not only delay neurodegeneration but also may ameliorate cardio- and myopathy linked to HD by improvement of cellular energetics

Monocyte chemoattractant protein-induced protein 1 impairs adipogenesis in 3T3-L1 cells

Monocyte chemoattractant protein-induced protein 1 (MCPIP1) encoded by the ZC3H12a gene (also known as Regnase-1) is involved in the regulation of degradation of mRNA of inflammatory modulators and for processing of pre-miRNA. These functions depend on the presence of the PIN domain. Moreover, MCPIP1 was described as a negative regulator of NF-?B and AP-1 signaling pathways although mechanisms underlying such activity remain unknown. We aimed at determining the role of MCPIP1 in adipogenesis. Here, we present evidence that Mcpip1 transcription is transiently activated during 3T3-L1 transition from pre- to adipocytes. However Mcpip1 protein expression is also strongly decreased at day one after induction of adipogenesis. Knockdown of Mcpip1 results in an upregulation of C/EBP? and PPAR? mRNAs, whereas overexpression of MCPIP1 reduces the level of both transcription factors and impairs adipogenesis. MCPIP1-dependend modulation of C/EBP? and PPAR? levels results in a modulation of the expression of downstream controlled genes. In addition, decreased C/EBP?, but not PPAR?, depends on the activity of the MCPIP1 PIN domain, which is responsible for RNase properties of this protein. Together, these data confirm that MCPIP1 is a key regulator of adipogenesi

Mimitin - a novel cytokine-regulated mitochondrial protein

Background: The product of a novel cytokine-responsive gene discovered by differential display analysis in our earlier studies on HepG2 cells was identified as mimitin - a small mitochondrial protein. Since proinflammatory cytokines are known to affect components of the respiratory chain in mitochondria, and mimitin was reported as a possible chaperone for assembly of mitochondrial complex I, we looked for the effects of modulation of mimitin expression and for mimitin-binding partners. Results: By blocking mimitin expression in HepG2 cells by siRNA we found that mimitin has no direct influence on caspase 3/7 activities implicated in apoptosis. However, when apoptosis was induced by TNF and cycloheximide, and mimitin expression blocked, the activities of these caspases were significantly increased. This was accompanied by a slight decrease in proliferation of HepG2 cells. Our observations suggest that mimitin may be involved in the control of apoptosis indirectly, through another protein, or proteins. Using the yeast two-hybrid system and coimmunoprecipitation we found MAP1S among proteins interacting with mimitin. MAP1S is a recently identified member of the microtubule-associated protein family and has been shown to interact with NADH dehydrogenase I and cytochrome oxidase I. Moreover, it was implicated in the process of mitochondrial aggregation and nuclear genome destruction. The expression of mimitin is stimulated more than 1.6-fold by IL-1 and by IL-6, with the maximum level of mimitin observed after 18 - 24 h exposure to these cytokines. We also found that the cytokine-induced signal leading to stimulation of mimitin synthesis utilizes the MAP kinase pathway. Conclusion: Mimitin is a mitochondrial protein upregulated by proinflammatory cytokines at the transcriptional and protein levels, with MAP kinases involved in IL-1-dependent induction. Mimitin interacts with a microtubular protein (MAP1S), and some changes of mimitin gene expression modulate activity of apoptotic caspases 3/7, suggesting that this protein may indirectly participate in apoptosi

New national and regional bryophyte records, 49

International audienceBryological Note

New national and regional bryophyte records, 48

International audience[No abstract available