BACKGROUND AND OBJECTIVES: Cochlear dead region (CDR) is a region in the cochlear where hearing loss has occurred due to damage to the inner hair cells and/or neurons. Recently, a subjective test involving a pure-tone test in the presence of threshold-equalizing noise (TEN) was introduced to identify CDR. However, for uncooperative patients, such a subjective method would be unsuitable and objective methods would be needed instead to detect CDR. The acoustic change complex (ACC) is an evoked potential elicited by changes in the ongoing sound. In this study, we developed an objective method of identifying CDR by combining ACC response with a TEN test, namely the TEN-ACC test, and investigated its feasibility in normal-hearing listeners. SUBJECTS AND METHOD: Ten normal-hearing subjects participated in this study. All subjects underwent both behavioral TEN test and electrophysiological TEN-ACC test. The stimuli for the TEN-ACC test consisted of TEN and embedded pure tones with different frequencies/signals to noise ratios (SNRs). To identify the thresholds, the range SNR of stimulation was varied from 0 to 20 dB, in stages of 4 dB. RESULTS: The ACC responses of all subjects who participated in this study were well elicited by stimuli developed for the TEN-ACC test. We confirm that the pure-tones embedded in TEN elicited the objective ACC response. CONCLUSION: The results of this study suggest that the novel TEN-ACC test can be applied to evoke ACC in normal-hearing listeners. Future research should incorporate hearing-impaired listeners to determine the feasibility of the TEN-ACC test as an objective method to identify CDR.
Acoustics* ; Evoked Potentials ; Hair Cells, Auditory, Inner ; Hearing Loss ; Humans ; Methods ; Neurons ; Noise

Purpose: Suicide ranks among the top causes of death among youth in South Korea. This study aimed to identify the characteristics of suicidal individuals treated at emergency departments between 2011 and 2020. Methods: A retrospective analysis was conducted using data from January 2011 to December 2020 in the Injury Surveillance Cohort, a prospective registry. Patients’ sex, age, mortality, methods of self-harm, and previous suicide attempts were analyzed. The methods of self-harm were categorized into falls, asphyxiation, blunt injuries, penetrating injuries, poisoning, and others. Sub-groups with and without poisoning were compared. Results: The proportion of self-harm/suicide attempts increased from 2.3% (2011) to 5.0% (2020). The mortality rate decreased from 10.8% (2011) to 6.3% (2020). Poisoning was the most common method (61.7%). Mortality rates ranged from 42.0% for asphyxiation to 0.2% for blunt injuries. Individuals in their 20s showed a marked increase in suicide/self-harm attempts, especially in the last three years. A large proportion of decedents in their 70s or older (52.6%) used poisoning as a method of suicide. The percentage of individuals with two or more previous attempts rose from 7.1% (2011) to 19.7% (2020). The death rates by poisoning decreased from 7.7% (2011) to 2.5% (2020). Conclusion Our findings underscore the urgent need for targeted interventions and suicide prevention policies. Managing and reducing suicide and self-harm in emergency settings will require a focus on poisoning, the 10–29 age group, and the elderly. This paper will be valuable for future policies aiming to reduce the societal burden of suicide and self-harm.

Objectives: This study was conducted to systematically summarize trends in research concerning patients with coronavirus disease 2019 (COVID-19) as reported in Korean medical journals. Methods: We performed a literature search of KoreaMed from January 2020 to September 2022. We included only primary studies of patients with COVID-19. Two reviewers screened titles and abstracts, then performed full-text screening, both independently and in duplicate. We first identified the 5 journals with the greatest numbers of eligible publications, then extracted data pertaining to the general characteristics, study population attributes, and research features of papers published in these journals. Results: Our analysis encompassed 142 primary studies. Of these, approximately 41.0% reported a funding source, while 3.5% disclosed a conflict of interest. In 2020, 42.9% of studies included fewer than 10 participants; however, by 2022, the proportion of studies with over 200 participants had increased to 40.6%. The most common design was the cohort study (48.6%), followed by case reports/series (35.2%). Only 3 randomized controlled trials were identified. Studies most frequently focused on prognosis (58.5%), followed by therapy/intervention (20.4%). Regarding the type of intervention/exposure, therapeutic clinical interventions comprised 26.1%, while studies of morbidity accounted for 13.4%. As for the outcomes measured, 50.7% of studies assessed symptoms/clinical status/improvement, and 14.1% evaluated mortality. Conclusions Employing a systematic approach, we examined the characteristics of research involving patients with COVID-19 that was published in Korean medical journals from 2020 onward. Subsequent research should assess not only publication trends over a longer timeframe but also the quality of evidence provided.

Background: High-alert medications (HAMs) are medications that bear a heightened risk of causing significant patient harm if used in error. To facilitate safe use of HAMs, identifying specific HAM lists for clinical setting is necessary. We aimed to develop the national level HAM list for acute care setting. Methods: We used three-step process. First, we compiled the pre-existing lists referring HAMs. Second, we analyzed medication related incidents reported from national patient safety incident report data and adverse events indicating medication errors from the Korea Adverse Event Reporting System (KAERS).We also surveyed the assistant staffs to support patient safety tasks and pharmacist in charge of medication safety in acute care hospital. From findings from analysis and survey results we created additional candidate list of HAMs. Third, we derived the final list for HAMs in acute care settings through expert panel surveys. Results: From pre-existing HAM list, preliminary list consisting of 42 medication class/ingredients was derived. Eight assistant staff to support patient safety tasks and 39 pharmacists in charge of medication safety responded to the survey. Additional 44 medication were listed from national patient safety incident report data, KAERS data and common medications involved in prescribing errors and dispensing errors from survey data. A list of mandatory and optional HAMs consisting of 10 and 6 medication classes, respectively, was developed by consensus of the expert group. Conclusion We developed national level HAM list for Korean acute care setting from pre-existing lists, analyzing medication error data, survey and expert panel consensus.

Aromadendrin is a phenolic compound with various biological effects such as anti-inflammatory properties. However, its protective effects against acute lung injury (ALI) remain unclear. Therefore, this study aimed to explore the ameliorative effects of aromadendrin in an experimental model of lipopolysaccharide (LPS)-induced ALI. In vitro analysis revealed a notable increase in the levels of cytokine/chemokine formation, nuclear factor kappa B (NF-κB) activation, and myeloid differentiation primary response 88 (MyD88)/toll-like receptor (TLR4) expression in LPS-stimulated BEAS-2B lung epithelial cell lines that was ameliorated by aromadendrin pretreatment. In LPS-induced ALI mice, the remarkable upregulation of immune cells and IL-1β/IL-6/TNF-α levels in the bronchoalveolar lavage fluid and inducible nitric oxide synthase/cyclooxygenase-2/CD68 expression in lung was decreased by the oral administration of aromadendrin. Histological analysis revealed the presence of cells in the lungs of ALI mice, which was alleviated by aromadendrin. In addition, aromadendrin ameliorated lung edema. This in vivo effect of aromadendrin was accompanied by its inhibitory effect on LPS-induced NF-κB activation, MyD88/TLR4 expression, and signal transducer and activator of transcription 3 activation. Furthermore, aromadendrin increased the expression of heme oxygenase-1/ NAD(P)H quinone dehydrogenase 1 in the lungs of ALI mice. In summary, the in vitro and in vivo studies demonstrated that aromadendrin ameliorated endotoxin-induced pulmonary inflammation by suppressing cytokine formation and NF-κB activation, suggesting that aromadendrin could be a useful adjuvant in the treatment of ALI.

Aromadendrin is a phenolic compound with various biological effects such as anti-inflammatory properties. However, its protective effects against acute lung injury (ALI) remain unclear. Therefore, this study aimed to explore the ameliorative effects of aromadendrin in an experimental model of lipopolysaccharide (LPS)-induced ALI. In vitro analysis revealed a notable increase in the levels of cytokine/chemokine formation, nuclear factor kappa B (NF-κB) activation, and myeloid differentiation primary response 88 (MyD88)/toll-like receptor (TLR4) expression in LPS-stimulated BEAS-2B lung epithelial cell lines that was ameliorated by aromadendrin pretreatment. In LPS-induced ALI mice, the remarkable upregulation of immune cells and IL-1β/IL-6/TNF-α levels in the bronchoalveolar lavage fluid and inducible nitric oxide synthase/cyclooxygenase-2/CD68 expression in lung was decreased by the oral administration of aromadendrin. Histological analysis revealed the presence of cells in the lungs of ALI mice, which was alleviated by aromadendrin. In addition, aromadendrin ameliorated lung edema. This in vivo effect of aromadendrin was accompanied by its inhibitory effect on LPS-induced NF-κB activation, MyD88/TLR4 expression, and signal transducer and activator of transcription 3 activation. Furthermore, aromadendrin increased the expression of heme oxygenase-1/ NAD(P)H quinone dehydrogenase 1 in the lungs of ALI mice. In summary, the in vitro and in vivo studies demonstrated that aromadendrin ameliorated endotoxin-induced pulmonary inflammation by suppressing cytokine formation and NF-κB activation, suggesting that aromadendrin could be a useful adjuvant in the treatment of ALI.

Aromadendrin is a phenolic compound with various biological effects such as anti-inflammatory properties. However, its protective effects against acute lung injury (ALI) remain unclear. Therefore, this study aimed to explore the ameliorative effects of aromadendrin in an experimental model of lipopolysaccharide (LPS)-induced ALI. In vitro analysis revealed a notable increase in the levels of cytokine/chemokine formation, nuclear factor kappa B (NF-κB) activation, and myeloid differentiation primary response 88 (MyD88)/toll-like receptor (TLR4) expression in LPS-stimulated BEAS-2B lung epithelial cell lines that was ameliorated by aromadendrin pretreatment. In LPS-induced ALI mice, the remarkable upregulation of immune cells and IL-1β/IL-6/TNF-α levels in the bronchoalveolar lavage fluid and inducible nitric oxide synthase/cyclooxygenase-2/CD68 expression in lung was decreased by the oral administration of aromadendrin. Histological analysis revealed the presence of cells in the lungs of ALI mice, which was alleviated by aromadendrin. In addition, aromadendrin ameliorated lung edema. This in vivo effect of aromadendrin was accompanied by its inhibitory effect on LPS-induced NF-κB activation, MyD88/TLR4 expression, and signal transducer and activator of transcription 3 activation. Furthermore, aromadendrin increased the expression of heme oxygenase-1/ NAD(P)H quinone dehydrogenase 1 in the lungs of ALI mice. In summary, the in vitro and in vivo studies demonstrated that aromadendrin ameliorated endotoxin-induced pulmonary inflammation by suppressing cytokine formation and NF-κB activation, suggesting that aromadendrin could be a useful adjuvant in the treatment of ALI.

Aromadendrin is a phenolic compound with various biological effects such as anti-inflammatory properties. However, its protective effects against acute lung injury (ALI) remain unclear. Therefore, this study aimed to explore the ameliorative effects of aromadendrin in an experimental model of lipopolysaccharide (LPS)-induced ALI. In vitro analysis revealed a notable increase in the levels of cytokine/chemokine formation, nuclear factor kappa B (NF-κB) activation, and myeloid differentiation primary response 88 (MyD88)/toll-like receptor (TLR4) expression in LPS-stimulated BEAS-2B lung epithelial cell lines that was ameliorated by aromadendrin pretreatment. In LPS-induced ALI mice, the remarkable upregulation of immune cells and IL-1β/IL-6/TNF-α levels in the bronchoalveolar lavage fluid and inducible nitric oxide synthase/cyclooxygenase-2/CD68 expression in lung was decreased by the oral administration of aromadendrin. Histological analysis revealed the presence of cells in the lungs of ALI mice, which was alleviated by aromadendrin. In addition, aromadendrin ameliorated lung edema. This in vivo effect of aromadendrin was accompanied by its inhibitory effect on LPS-induced NF-κB activation, MyD88/TLR4 expression, and signal transducer and activator of transcription 3 activation. Furthermore, aromadendrin increased the expression of heme oxygenase-1/ NAD(P)H quinone dehydrogenase 1 in the lungs of ALI mice. In summary, the in vitro and in vivo studies demonstrated that aromadendrin ameliorated endotoxin-induced pulmonary inflammation by suppressing cytokine formation and NF-κB activation, suggesting that aromadendrin could be a useful adjuvant in the treatment of ALI.