A Survey of Near-Miss Dispensing Errors in Hospital Pharmacies in Japan: DEPP-J Study-Multi-Center Prospective Observational Study-

The aim of this study was to determine the proportion of near-miss dispensing errors in hospital pharmacies in Japan. A prospective multi-center observational study was conducted between December 2018 and March 2019. The primary objective was to determine the proportion of near-miss dispensing errors in hospital pharmacy departments. The secondary objective was to determine the predictive factors for near-miss dispensing errors using multiple logistic regression analysis. The study was approved by the ethical committee at The Institute of Medical Sciences, University of Tokyo, Japan. A multi-center prospective observational study was conducted in 20 hospitals comprising 8862 beds. Across the 20 hospitals, we assessed data from 553 pharmacists and 53039 prescriptions. A near-miss dispensing error proportion of 0.87% (n = 461) was observed in the study. We found predictive factors for dispensing errors in day-time shifts: a higher number of drugs in a prescription, higher number of quantified drugs, such as liquid or powder formula, in a prescription, and higher number of topical agents in a prescription; but we did not observe for career experience level for clinical pharmacists. For night-time and weekend shifts, we observed a negative correlation of near-miss dispensing errors with clinical pharmacist experience level. We found an overall incidence of near-miss dispensing errors of 0.87%. Predictive factors for errors in night-time and weekend shifts was inexperienced pharmacists. We recommended that pharmacy managers should consider education or improved work flow to avoid near-miss dispensing errors by younger pharmacists, especially those working night or weekend shifts.

Predominant synaptic potentiation and activation in the right central amygdala are independent of bilateral parabrachial activation in the hemilateral trigeminal inflammatory pain model of rats.

Nociceptive signals originating in the periphery are conveyed to the brain through specific afferent and ascending pathways. The spino-(trigemino-)parabrachio-amygdaloid pathway is one of the principal pathways mediating signals from nociception-specific ascending neurons to the central amygdala, a limbic structure involved in aversive signal-associated emotional responses, including the emotional aspects of pain. Recent studies suggest that the right and left central amygdala play distinct roles in the regulation of nociceptive responses. Using a latent formalin inflammatory pain model of the rat, we analyzed the right-left differences in synaptic potentiation at the synapses formed between the fibers from the lateral parabrachial nucleus and central amygdala neurons as well as those in the c-Fos expression in the lateral parabrachial nucleus, central amygdala, and the basolateral/lateral amygdala after formalin injection to either the right or left side of the rat upper lip. Although the single-sided formalin injection caused a significant bilateral increase in c-Fos-expressing neurons in the lateral parabrachial nucleus with slight projection-side dependence, the increase in the amplitude of postsynaptic excitatory currents and the number of c-Fos-expressing neurons in the central amygdala occurred predominantly on the right side regardless of the side of the inflammation. Although there was no significant correlation in the number of c-Fos-expressing neurons between the lateral parabrachial nucleus and central amygdala in the formalin-injected animals, these numbers were significantly correlated between the basolateral amygdala and central amygdala. It is thus concluded that the lateral parabrachial nucleus-central amygdala synaptic potentiation reported in various pain models is not a simple Hebbian plasticity in which raised inputs from the lateral parabrachial nucleus cause lateral parabrachial nucleus-central amygdala potentiation but rather an integrative and adaptive response involving specific mechanisms in the right central amygdala.

Gold Coating of Silver Nanoplates for Enhanced Dispersion Stability and Efficient Antimicrobial Activity against Intracellular Bacteria.

Silver nanoparticles have antibacterial activity. However, the nanoparticles are unstable and easily form aggregates, which decreases their antibacterial activity. To improve the dispersion stability of silver nanoparticles in aqueous media and to increase their effectiveness as antibacterial agents, we coated triangular plate-like silver nanoparticles (silver nanoplates, Ag NPLs) with one or two layers of gold atoms (Ag@Au1L NPLs and Ag@Au2L NPLs, respectively). These gold coatings improved the dispersion stability in aqueous media with high salt concentrations. Ag@Au1L NPLs showed stronger antibacterial activity on pathogenic bacteria than Ag NPLs and Ag@Au2L NPLs. Furthermore, the Ag@Au1L NPLs decreased the number of bacteria in RAW 264.7 cells. The Ag@Au1L NPLs displayed no cytotoxicity towards RAW 264.7 cells and could be used as antibacterial agents for intracellular bacterial infections.

Effects of pulsed laser irradiation on gold-coated silver nanoplates and their antibacterial activity.

Gold-coated silver nanoplates, when subjected to pulsed laser irradiation, changed their shape from triangular to spherical, accompanied by a shift of their extinction spectra. The simple single crystal structure of the silver nanoplates changed to multiple small crystal domains. The ratio of silver to gold of the particles also changed from 22 : 1 to 4.5 : 1, enabling more silver to be released. As a result, the antibacterial activity of the gold-coated silver nanoplates was significantly increased after pulsed laser irradiation.

The 24-bp consensus sequence responsible for regulation of the BphS1T1 two-component system in a hybrid promoter.

Rhodococcus jostii RHA1 degrades polychlorinated biphenyls (PCBs) by cometabolism with biphenyl. The bphS1T1-coding two-component system, which is composed of a sensor kinase, BphS1, and a response regulator, BphT1, activates the transcription of biphenyl/PCB degradation genes from the five promoters of bphAa, etbAa1, etbAa2, etbAd, and etbD1 in the presence of aromatics, such as biphenyl and ethylbenzene. The transcription start sites of etbAd and etbD1 were determined and the results indicated that the 18-bp consensus sequence is shared by all five promoters at the equivalent position from their transcriptional start sites. To investigate the involvement of the 18-bp consensus sequence in the regulation of BphS1T1, a hybrid promoter was constructed by connecting the 18-bp consensus sequence of bphAa promoter to a portion of the benzoate dioxygenase gene promoter, which is not under the control of BphS1T1. The ethylbenzene-dependent induction of the hybrid promoter by BphS1T1 was not observed. Recently, a 24-bp consensus sequence that included the 18-bp consensus sequence of the bphAa promoter was identified in the regions conserved among RHA1 and other rhodococcal degraders. When the 24-bp consensus sequence was employed instead, both BphS1T1-dependent basal activation and ethylbenzene-dependent induction of the hybrid promoter were observed. Mutations in the six extra residues outside the 18-bp sequence in the 24-bp consensus sequence, affected not only ethylbenzene-dependent induction but also BphS1T1-dependent basal activation. The outstanding conservation of the 24-bp consensus sequence was confirmed by multiple sequence alignment. These results indicate that the 24-bp consensus sequence is really responsible for the regulation of BphS1T1.