Catecholamines may undergo iron-promoted oxidation resulting in formation of reactive intermediates (aminochromes) capable of redox cycling and reactive oxygen species (ROS) formation. Both of them induce oxidative stress resulting in cellular damage and death. Iron chelation has been recently shown as a suitable tool of cardioprotection with considerable potential to protect cardiac cells against catecholamine-induced cardiotoxicity. However, prolonged exposure of cells to classical chelators may interfere with physiological iron homeostasis. Prochelators represent a more advanced approach to decrease oxidative injury by forming a chelating agent only under the disease-specific conditions associated with oxidative stress. Novel prochelator (lacking any iron chelating properties) BHAPI [(E)-Ń-(1-(2-((4-(4,4,5,5-tetramethyl-1,2,3-dioxoborolan-2-yl)benzyl)oxy)phenyl)ethylidene) isonicotinohydrazide] is converted by ROS to active chelator HAPI with strong iron binding capacity that efficiently inhibits iron-catalyzed hydroxyl radical generation. Our results confirmed redox activity of oxidation products of catecholamines isoprenaline and epinephrine, that were able to activate BHAPI to HAPI that chelates iron ions inside H9c2 cardiomyoblasts. Both HAPI and BHAPI were able to efficiently protect the cells against intracellular ROS formation, depletion of reduced glutathione and toxicity induced by catecholamines and their oxidation products. Hence, both HAPI and BHAPI have shown considerable potential to protect cardiac cells by both inhibition of deleterious catecholamine oxidation to reactive intermediates and prevention of ROS-mediated cardiotoxicity.

• MeSH
• Epinephrine antagonists & inhibitors   toxicity   MeSH
• Biocatalysis MeSH
• Cell Line MeSH
• Iron Chelating Agents pharmacology   MeSH
• Glutathione metabolism   MeSH
• Hydroxyl Radical metabolism   MeSH
• Isoproterenol antagonists & inhibitors   toxicity   MeSH
• Cardiotonic Agents pharmacology   MeSH
• Catecholamines antagonists & inhibitors   toxicity   MeSH
• Rats MeSH
• Boronic Acids pharmacology   MeSH
• Humans MeSH
• Membrane Potential, Mitochondrial drug effects   MeSH
• Oxidative Stress drug effects   MeSH
• Prodrugs pharmacology   MeSH
• Reactive Oxygen Species metabolism   MeSH
• Semicarbazones pharmacology   MeSH
• Boron Compounds pharmacology   MeSH
• Iron chemistry   MeSH
• Animals MeSH
• Check Tag
• Rats MeSH
• Humans MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH

• MeSH
• Angina Pectoris pathology   MeSH
• Adult MeSH
• Drug Therapy methods   MeSH
• Heparin administration & dosage   therapeutic use   MeSH
• Coronary Disease complications   therapy   MeSH
• Hemorrhage therapy   MeSH
• Humans MeSH
• Check Tag
• Adult MeSH
• Humans MeSH
• Male MeSH
• Female MeSH
• Publication type
• Multicenter Study MeSH
• Randomized Controlled Trial MeSH

Autor osvětluje využití bioenergie jako rezervy lidského organismu.

• Keywords
• bioenergie,
• MeSH
• Biophysics MeSH
• Respiration MeSH
• Holistic Health MeSH
• Massage MeSH
• Energy Transfer MeSH
• Exercise Movement Techniques MeSH
• Publication type
• Essay MeSH

• Conspectus
• Fyzioterapie. Psychoterapie. Alternativní lékařství
• NML Fields
• fyzika, biofyzika
• alternativní lékařství

Oxidative stress is a common denominator of numerous cardiovascular disorders. Free cellular iron catalyzes the formation of highly toxic hydroxyl radicals, and iron chelation may thus be an effective therapeutic approach. However, using classical iron chelators in diseases without iron overload poses risks that necessitate more advanced approaches, such as prochelators that are activated to chelate iron only under disease-specific oxidative stress conditions. In this study, three cell-membrane-permeable iron chelators (clinically used deferasirox and experimental SIH and HAPI) and five boronate-masked prochelator analogs were evaluated for their ability to protect cardiac cells against oxidative injury induced by hydrogen peroxide. Whereas the deferasirox-derived agents TIP and TRA-IMM displayed negligible protection and even considerable toxicity, the aroylhydrazone prochelators BHAPI and BSIH-PD provided significant cytoprotection and displayed lower toxicity after prolonged cellular exposure compared to their parent chelators HAPI and SIH, respectively. Overall, the most favorable properties in terms of protective efficiency and low inherent cytotoxicity were observed with the aroylhydrazone prochelator BSIH. BSIH efficiently protected both H9c2 rat cardiomyoblast-derived cells and isolated primary rat cardiomyocytes against hydrogen peroxide-induced mitochondrial and lysosomal dysregulation and cell death. At the same time, BSIH was nontoxic at concentrations up to its solubility limit (600 μM) and in 72-h incubation. Hence, BSIH merits further investigation for prevention and/or treatment of cardiovascular disorders associated with a known (or presumed) component of oxidative stress.

• MeSH
• Aldehydes chemistry   pharmacology   MeSH
• Apoptosis drug effects   MeSH
• Benzoates chemistry   pharmacology   MeSH
• Cell Line MeSH
• Iron Chelating Agents chemistry   pharmacology   MeSH
• Cytoprotection * MeSH
• Hydrazones chemistry   pharmacology   MeSH
• Myocytes, Cardiac drug effects   physiology   MeSH
• Rats MeSH
• Boronic Acids chemistry   pharmacology   MeSH
• Isonicotinic Acids chemistry   pharmacology   MeSH
• Membrane Potential, Mitochondrial drug effects   MeSH
• Oxidative Stress drug effects   MeSH
• Cell Membrane Permeability drug effects   MeSH
• Hydrogen Peroxide metabolism   MeSH
• Rats, Wistar MeSH
• Semicarbazones chemistry   pharmacology   MeSH
• Boron Compounds chemistry   pharmacology   MeSH
• Mitochondria, Heart drug effects   physiology   MeSH
• Triazoles chemistry   pharmacology   MeSH
• Iron chemistry   metabolism   MeSH
• Animals MeSH
• Check Tag
• Rats MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Research Support, N.I.H., Extramural MeSH
• Comparative Study MeSH

In 2018 Polish health IT community faces critical challenges related to the national eHealth agenda. The mission of HL7 Poland is to establish a community around interoperability standards and integration profiles with health IT vendors, medical providers and public authorities. One of the activities that would support this goal is providing tooling for specification publication and implementation validation. HL7 Poland has started a project to create a central hub for specifications and tools. The Tukan is an online platform dedicated to Polish healthcare IT community, where national specifications for interoperability are published together with a set of testing tools supporting their implementation. The platform is based on software components originating from various sources: open source release of IHE Gazelle components, development tooling of Polish National Implementation Guide of HL7 CDA, ART-DECOR platform software components, HAPI FHIR reference implementation for FHIR STU3 standard and Central Authentication Server (CAS) software components. Tukan platform is ready to be used as an environment supporting peer-to-peer testing in connectathon-like events. The pilot phase of Tukan platform has shown that there is a significant interest in testing services, especially when there are official specifications of interoperability standards published. In 2018 the first Polish connectathon will be held by HL7 Poland on Tukan platform in cooperation with national and regional projects.

• Keywords
• HL7,
• MeSH
• Health Information Interoperability standards   MeSH
• Software standards   MeSH
• Geographicals
• Poland MeSH

Oxidative stress is known to contribute to a number of cardiovascular pathologies. Free intracellular iron ions participate in the Fenton reaction and therefore substantially contribute to the formation of highly toxic hydroxyl radicals and cellular injury. Earlier work on the intracellular iron chelator salicylaldehyde isonicotinoyl hydrazone (SIH) has demonstrated its considerable promise as an agent to protect the heart against oxidative injury both in vitro and in vivo. However, the major limitation of SIH is represented by its labile hydrazone bond that makes it prone to plasma hydrolysis. Hence, in order to improve the hydrazone bond stability, nine compounds were prepared by a substitution of salicylaldehyde by the respective methyl- and ethylketone with various electron donors or acceptors in the phenyl ring. All the synthesized aroylhydrazones displayed significant iron-chelating activities and eight chelators showed significantly higher stability in rabbit plasma than SIH. Furthermore, some of these chelators were observed to possess higher cytoprotective activities against oxidative injury and/or lower toxicity as compared to SIH. The results of the present study therefore indicate the possible applicability of several of these novel agents in the prevention and/or treatment of cardiovascular disorders with a known (or presumed) role of oxidative stress. In particular, the methylketone HAPI and nitro group-containing NHAPI merit further in vivo investigations.

• MeSH
• Aldehydes blood   chemistry   pharmacology   MeSH
• Antioxidants chemistry   metabolism   pharmacology   MeSH
• Cell Line MeSH
• Iron Chelating Agents chemical synthesis   metabolism   pharmacology   MeSH
• Hydrazones blood   chemistry   pharmacology   MeSH
• Hydrolysis MeSH
• Hydroxyl Radical toxicity   MeSH
• Rabbits MeSH
• Rats MeSH
• Oxidative Stress MeSH
• Drug Stability MeSH
• Animals MeSH
• Check Tag
• Rabbits MeSH
• Rats MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH

Nozokomiální pneumonie – Hospital-acquired pneumonia (HAP) je jednou z nejzávažnějších komplikací zdravotního stavu pacientů v průběhu hospitalizace a je významným prvkem ovlivňujícím ekonomiku péče o nemocné a často souvisí s problematikou bakteriální rezistence. Zastoupení jednotlivých etiologických patogenů HAP a jejich odolnost k antimikrobním přípravkům má rozhodující vliv na antimikrobiální léčbu. Nemožnost časné identifikace původců komplikuje kauzální antibiotickou terapii v úvodu HAP. Jejich určení trvá řadu hodin až dní a v tomto časovém intervalu je nutné zahájit antibiotickou léčbu empiricky. V etiologii HAP se většinou uplatňují bakteriální kmeny endogenního původu, přičemž u časné formy se předpokládá jejich původ z primární mikroflóry, zatímco u pozdních ze sekundárně kolonizujících bakterií s vyšší mírou rezistence. Nástup HAP se často projevuje klinickými známkami sepse a významně zhoršuje prognózu pacienta. Proto bylo naším cílem získání aktuálních epidemiologických dat o původcích HAP a určení citlivosti těchto etiologických agens k antibiotikům. Porovnáním výsledků s údaji protokolu referenční iniciální empirické antibiotické léčby HAP jsme formulovali optimální nastavení iniciální antimikrobiální terapie HAP.

Hospital-acquired pneumonia (HAP) is one of the most severe complications occurring in patients during their hospital stayand an important factor affecting the economy of health care; it is often associated with bacterial resistance. The presence ofindividual etiological pathogens causing HAP and their resistance to antimicrobial agents play a key role in the selection of adequateantibiotic therapy. However, not knowing these pathogens usually complicates causative antibiotic therapy at the onsetof pneumonia. It takes hours to days to identify them and, in the meantime, empirical antibiotic therapy must be initiated. Theusual pathogens causing HAP are endogenous bacterial strains originating from the primary microflora in early-onset HAP andsecondary colonizing bacteria with a higher level of resistance in late-onset HAP. The onset of HAP is often manifested by clinicalsigns of sepsis and considerably worsens the prognosis of patients. Therefore, the aims were to obtain current epidemiologicaldata on pathogens causing HAP and to determine their susceptibility to antibiotics. The results were compared with data froma protocol for reference initial empirical antibiotic therapy of HAP so that optimal initial antibiotic therapy of HAP could be set.

• Keywords
• empirická terapie,
• MeSH
• Anti-Bacterial Agents * therapeutic use   MeSH
• Drug Resistance, Microbial MeSH
• Bacteria isolation & purification   drug effects   MeSH
• Pneumonia, Bacterial * diagnosis   ethnology   drug therapy   microbiology   MeSH
• Adult MeSH
• Cross Infection * etiology   drug therapy   MeSH
• Clinical Protocols MeSH
• Drug Therapy, Combination MeSH
• Middle Aged MeSH
• Humans MeSH
• Microbial Sensitivity Tests MeSH
• Healthcare-Associated Pneumonia MeSH
• Prospective Studies MeSH
• Aged, 80 and over MeSH
• Aged MeSH
• Treatment Outcome MeSH
• Check Tag
• Adult MeSH
• Middle Aged MeSH
• Humans MeSH
• Male MeSH
• Aged, 80 and over MeSH
• Aged MeSH
• Female MeSH
• Publication type
• Multicenter Study MeSH
• Observational Study MeSH
• Research Support, Non-U.S. Gov't MeSH

• MeSH
• Speech MeSH

• Conspectus
• Lingvistika. Jazyky
• NML Fields
• lingvistika, lékařská terminologie

Nozokomiální pneumonie (hospital-acquired pneumonia – HAP) je pneumonie, jejíž příznaky vznikly za dobu delší než 2 dny ( > 48 hod) od přijetí do nemocnice nebo až 14 dnů od propuštění z nemocnice. Nozokomiální pneumonie představují 13–18 % všech nozokomiálních infekcí. Výskyt HAP je nejčastější u uměle ventilovaných nemocných. Druh a zastoupení původců HAP závisí především na délce pobytu pacienta v nemocnici a na jeho stavu a charakteru léčby. Diagnostika pneumonie je opřena o anamnézu, fyzikální a RTG nález, o výsledky mikrobiologického vyšetření vzorků z respiračního traktu, hemokultury, vyšetření pleurálního výpotku, sérologického vyšetření, hematologického a biochemického vyšetření. Antibiotická léčba je klíčová v komplexní léčbě HAP. Léčba HAP vyžaduje vždy použití dávkování antibiotik na horní hranici možného rozmezí. Předpokladem úspěšného předcházení nozokomiální pneumonii je vytvoření preventivního programu, kterého se aktivně účastní zdravotnický personál.

Nosocomial pneumonia (hospital-acquired pneumonia – HAP) is the form of pneumonia the symptoms of which present after more than 2 days ( > 48 hours) of admission to hospital or as late as 14 days of discharge from hospital. The HAP pneumonias represent 13–18 % of all nosocomial infections. Incidence of HAP is the most frequent in mechanically ventilated patients. The type and representation of HAP agents primarily depends on the length of a patient’s stay in hospital and on their condition and character of treatment. Diagnosing of pneumonia is based on anamnesis, physical and X-ray findings, results of examination of microbiological samples from the respiratory tract, hemoculture, the pleural effusion test, serological, hematological and biochemical tests. Antibiotic treatment is key to the comprehensive treatment of HAP. The HAP treatment always requires the dosing of antibiotics near the upper limit of the possible range. A precondition for successful avoidance of HAP pneumonias is the creation of a preventive programme with active engagement of medical staff.

• MeSH
• Anti-Bacterial Agents therapeutic use   MeSH
• Diagnostic Imaging MeSH
• Hospitalization MeSH
• Cross Infection * diagnosis   etiology   drug therapy   physiopathology   MeSH
• Humans MeSH
• Microbiological Techniques MeSH
• Pneumonia * diagnosis   etiology   drug therapy   physiopathology   MeSH
• Risk Factors MeSH
• Sputum microbiology   MeSH
• Pneumonia, Ventilator-Associated * diagnosis   etiology   drug therapy   physiopathology   MeSH
• Check Tag
• Humans MeSH
• Publication type
• Review MeSH