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OBJECTIVE: The aim: To evaluate the quality of cleaning and disinfection of surfaces scheduled for daily cleaning and degree of bacterial contamination of hospital rooms and the patients' inanimate environment in Kyiv acute care hospitals, Ukraine. PATIENTS AND METHODS: Materials and methods: We performed a multicenter prospectively study of the quality of cleaning and disinfection of surfaces scheduled for daily cleaning in 9 acute care hospitals by use of an ultraviolet fluorescence targeting method and microbial methods. RESULTS: Results: A total 9,104 environmental samples from were collected and tested. The cleaning and disinfection of surfaces were not being performed properly in most cases. Complete removal of the mark was 49.1%, partial removal was 37,5%, and mark was still visible, i.e. this area had not been processed was 13,4% when the ultraviolet fluorescence targeting method procedures were used, respectively. The predominant bacterial agents in hospital environment surfaces were: Escherichia coli, Enterobacter spp., Pseudomonas aeruginosa, Klebsiella pneumoniae, Proteus spp., Citrobacter spp., Acinetobacter spp., and Enterococcus spp. The overall proportion of extended spectrum beta-lactamase (ESBL) production among Enterobacteriaceae was 31.5% and of methicillin-resistance in Staphylococcus aureus (MRSA) 14.9%. Vancomycin resistance was observed in 5.2% of isolated enterococci (VRE). Resistance to third-generation cephalosporins was observed in 12.7% E.coli isolates and was in 11.2% K. pneumoniae isolates. Carbapenem resistance was identified in 24.7% of P.aeruginosa isolates and 59.3% of Acinetibacter spp. isolates. CONCLUSION: Conclusions: In a hospital rooms, patient environmental surfaces can be a vehicle for the transmission of multidrug-resistant (MDR) bacterial agents that cause healthcare-associated infections.
Assuntos
Antibacterianos , Infecção Hospitalar , Antibacterianos/farmacologia , Antibacterianos/uso terapêutico , Bactérias , Infecção Hospitalar/microbiologia , Infecção Hospitalar/prevenção & controle , Hospitais , Humanos , UcrâniaRESUMO
OBJECTIVE: The aim: To evaluate the potential of transmission of methicillin-resistance Staphylococcus aureus (MRSA) in Ukrainian acute care hospitals. PATIENTS AND METHODS: Materials and methods: We performed a multicenter cross-sectional study. Definitions of HAI were used from the CDC/ NHSN. The susceptibility to antibiotics was determined by disk diffusion method according to the EUCAST. The cefoxitin-resistant isolates S.aureus were analyzed for the presence of the mecA gene and femA endogenous control gene using PCR. The virulence factor encoding genes (lukS-PV and lukF-PV) were detected by PCR. RESULTS: Results: Of 2,421 patients with HAIs caused S.aureus included in the study, 28.7% patients had MRSA. Prevalence of nasal carriage rate of MRSA among healthcare workers (HCWs) was 33.3%. MRSA contamination of hands and uniforms/gowns of HCW were 32.2% and 29.7%, respectively. MRSA contamination in the inanimate environment surfaces in near- and extended patients areas were 26.9%. The predominant MRSA contamination in hospital environment surfaces were: room inner door knob (32.8%), bed rails (28.9%), room light switch (28.9%), chair (27.9%), bedside table handle (20.6%), bedside table (20.5%), and tray table (13.7%). The PVL gene was present in 38.7% of MRSA strains, isolated from patients with HAIs and in 55.7% of MRSA, isolated from environment surfaces in patient area. In addition, the PVL genes were detected in over 56.3% of MRSA isolated from HCWs carrier. CONCLUSION: Conclusions: The majority of MRSA is acquired during hospitalization. Environmental surfaces may serve as potential reservoirs for nosocomial MRSA and facilitate transmissions via contact.
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Infecção Hospitalar , Staphylococcus aureus Resistente à Meticilina , Infecções Estafilocócicas , Infecção Hospitalar/epidemiologia , Estudos Transversais , Hospitais , Humanos , Staphylococcus aureus Resistente à Meticilina/genética , Testes de Sensibilidade Microbiana , Epidemiologia Molecular , Infecções Estafilocócicas/epidemiologia , Ucrânia/epidemiologiaRESUMO
Ligand-free methods for the synthesis of halide perovskite nanocrystals are of great interest because of their excellent performance in optoelectronics and photonics. In addition, template-assisted synthesis methods have become a powerful tool for the fabrication of environmentally stable and bright nanocrystals. Here we develop a novel approach for the facile ligand-free template-assisted fabrication of perovskite nanocrystals with a near-unity absolute quantum yield, which involves CaCO3 vaterite micro- and submicrospheres as templates. We show that the optical properties of the obtained nanocrystals are affected not mainly by the template morphology, but strongly depend on the concentration of precursor solutions, anion and cation ratio, as well as on adding defect-passivating rare-earth dopants. The optimized samples are further tested as infrared radiation visualizers exhibiting promising characteristics comparable to those that are commercially available.
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Polymorphic Human arylamine N-acetyltransferase (NAT2) inactivates the anti-tubercular drug isoniazid by acetyltransfer from acetylCoA. There are active NAT proteins encoded by homologous genes in mycobacteria including M. tuberculosis, M. bovis BCG, M. smegmatis and M. marinum. Crystallographic structures of NATs from M. smegmatis and M. marinum, as native enzymes and with isoniazid bound share a similar fold with the first NAT structure, Salmonella typhimurium NAT. There are three approximately equal domains and an active site essential catalytic triad of cysteine, histidine and aspartate in the first two domains. An acetyl group from acetylCoA is transferred to cysteine and then to the acetyl acceptor e.g. isoniazid. M. marinum NAT binds CoA in a more open mode compared with CoA binding to human NAT2. The structure of mycobacterial NAT may promote its role in synthesis of cell wall lipids, identified through gene deletion studies. NAT protein is essential for survival of M. bovis BCG in macrophage as are the proteins encoded by other genes in the same gene cluster (hsaA-D). HsaA-D degrade cholesterol, essential for mycobacterial survival inside macrophage. Nat expression remains to be fully understood but is co-ordinated with hsaA-D and other stress response genes in mycobacteria. Amide synthase genes in the streptomyces are also nat homologues. The amide synthases are predicted to catalyse intramolecular amide bond formation and creation of cyclic molecules, e.g. geldanamycin. Lack of conservation of the CoA binding cleft residues of M. marinum NAT suggests the amide synthase reaction mechanism does not involve a soluble CoA intermediate during amide formation and ring closure.
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Arilamina N-Acetiltransferase/metabolismo , Mycobacterium/enzimologia , Sequência de Aminoácidos , Arilamina N-Acetiltransferase/genética , Conformação Molecular , Dados de Sequência Molecular , Mycobacterium/genética , Polimorfismo GenéticoRESUMO
The angiostatic nature of pharmacological doses of glucocorticoid steroids is well known. However, the consequences of pathophysiological elevation of endogenous glucocorticoids are not well established. In the current study, we hypothesized that the angiostatic effect of corticosterone, an endogenous glucocorticoid in rodents, occurs through multi-faceted alterations in skeletal muscle microvascular endothelial cell proliferation, migration, and proteolysis. Chronic corticosterone treatment significantly reduced the capillary to fiber ratio in the tibialis anterior muscle compared to that of placebo-treated rats. Corticosterone inhibited endothelial cell sprouting from capillary segments ex vivo. Similarly, 3-dimensional endothelial cell spheroids treated with corticosterone for 48 hours showed evidence of sprout regression and reduced sprout length. Endothelial cell proliferation was reduced in corticosterone treated cells, coinciding with elevated FoxO1 and reduced VEGF production. Corticosterone treated endothelial cells exhibited reduced migration, which correlated with a reduction in RhoA activity. Furthermore, corticosterone treated endothelial cells in both 3-dimensional and monolayer cultures had decreased MMP-2 production and activation resulting in decreased proteolysis by endothelial cells, limiting their angiogenic potential. Promoter assays revealed that corticosterone treatment transcriptionally repressed MMP-2, which may map to a predicted GRE between -1510 and -1386 bp of the MMP-2 promoter. Additionally, Sp1, a known transcriptional activator of MMP-2 was decreased following corticosterone treatment. This study provides new insights into the mechanisms by which pathophysiological levels of endogenous glucocorticoids may exert angiostatic effects.