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1.
J Infect Chemother ; 30(5): 459-462, 2024 May.
Article in English | MEDLINE | ID: mdl-37940037

ABSTRACT

BACKGROUND: The cumulative antibiogram is essential to guide empirical therapy for infectious diseases and monitor the trend of antimicrobial resistance. However, the status of antibiogram generation at medical institutions in Japan is uncertain. METHODS: A web-based questionnaire survey was conducted in February 2023 on the status of antibiogram preparation among facilities participating in the Japan Surveillance for Infection Prevention and Healthcare Epidemiology (J-SIPHE), an infection control surveillance system in Japan. RESULTS: The questionnaire collection rate was 19.6% (379/1931). Of all facilities, 47% (178/379) performed microbiological tests mainly in-house, while 53% (201/379) performed microbiological tests mainly outsourced. Of all facilities, 78% (296/379) prepared antibiograms. Of those without antibiograms, 33% (27/83) were considering the development in the future. Some facilities cited staff shortage as a barrier to preparing antibiograms. Of the 214 facilities with antibiograms that could use the J-SIPHE system to prepare antibiograms, 19% (41/214) were using the J-SIPHE system to prepare their antibiograms. CONCLUSIONS: One-quarter of the facilities that responded to the survey had not prepared antibiograms. Technical support for surveillance and awareness activity for using cumulative antibiograms might promote antibiogram preparation in Japan, which may improve antimicrobial stewardship and antimicrobial resistance measures.


Subject(s)
Anti-Bacterial Agents , Hospitals , Humans , Anti-Bacterial Agents/therapeutic use , Japan/epidemiology , Microbial Sensitivity Tests , Delivery of Health Care
2.
Biol Pharm Bull ; 36(10): 1650-2, 2013.
Article in English | MEDLINE | ID: mdl-24088258

ABSTRACT

We assessed the effects of oseltamivir on the conduction velocity and effective refractory period in the guinea-pig atrium in comparison with those of a class Ic antiarrhythmic drug pilsicainide. The recording and stimulating electrodes were attached on the epicardium close to the sinus nodal region and on the left atrial appendage. Oseltamivir (10-100 µM) as well as pilsicainide (1-10 µM) decreased the atrial conduction velocity in a frequency-dependent manner. Both drugs also increased the effective refractory period in both atria; but the frequency-dependent property of oseltamivir was lacking in the left atrium, and it was less obvious in the right atrium compared with that of pilsicainide. These results suggest that oseltamivir can directly modify the electrophysiological functions in the guinea-pig atrium possibly via combination of Na(+) and K(+) channel-blocking actions.


Subject(s)
Antiviral Agents/pharmacology , Atrial Function/drug effects , Electrophysiological Phenomena/drug effects , Heart Atria/drug effects , Lidocaine/analogs & derivatives , Oseltamivir/pharmacology , Animals , Anti-Arrhythmia Agents/pharmacology , Antiviral Agents/therapeutic use , Atrial Fibrillation , Atrial Function, Left/drug effects , Atrial Function, Right/drug effects , Guinea Pigs , Humans , Influenza, Human/drug therapy , Lidocaine/pharmacology , Oseltamivir/therapeutic use , Potassium Channel Blockers/pharmacology , Refractory Period, Electrophysiological/drug effects , Sodium Channel Blockers/pharmacology
3.
FASEB J ; 16(6): 601-3, 2002 Apr.
Article in English | MEDLINE | ID: mdl-11919167

ABSTRACT

Alzheimer's disease (AD) is characterized by the accumulation of fibrillar amyloid-beta (Abeta) peptides to form amyloid plaques. Understanding the balance of production and clearance of Abeta peptides is the key to elucidating amyloid plaque homeostasis. Microglia in the brain, associated with senile plaques, are likely to play a major role in maintaining this balance. Here, we show that heat-shock proteins (HSPs), such as HSP90, HSP70, and HSP32, induce the production of interleukin 6 and tumor necrosis factor alpha and increase the phagocytosis and clearance of Abeta peptides. This suggests that microglial interaction with Abeta peptides is highly regulated by HSPs. The mechanism of microglial activation by exogenous HSPs involves the nuclear factor kB and p38 mitogen-activated protein kinase pathways mediated by Toll-like receptor 4 activation. In AD brains, levels of HSP90 were increased in both the cytosolic and membranous fractions, and HSP90 was colocalized with amyloid plaques. These observations suggest that HSP-induced microglial activation may serve a neuroprotective role by facilitating Abeta clearance and cytokine production


Subject(s)
Alzheimer Disease/metabolism , Amyloid beta-Peptides/metabolism , Drosophila Proteins , Heat-Shock Proteins/pharmacology , Microglia/physiology , Peptide Fragments/metabolism , Alzheimer Disease/pathology , Animals , Cells, Cultured , Cytokines/biosynthesis , HSP70 Heat-Shock Proteins/pharmacology , HSP90 Heat-Shock Proteins/metabolism , HSP90 Heat-Shock Proteins/pharmacology , Heme Oxygenase (Decyclizing)/pharmacology , Heme Oxygenase-1 , Humans , Kinetics , Membrane Glycoproteins/metabolism , Membrane Proteins , Mice , Microglia/drug effects , Models, Biological , Neuroprotective Agents/pharmacology , Phagocytosis , Rats , Receptors, Cell Surface/metabolism , Toll-Like Receptor 4 , Toll-Like Receptors
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