Risk of Severe Acute Respiratory Syndrome Coronavirus 2 Transmission in Seoul, Korea.

BACKGROUND: The risk of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) transmission during the endemic phase may vary from that during the previous pandemic phase. We evaluated the risk of infection in a general population with laboratory-confirmed coronavirus disease 2019 (COVID-19) in a community setting in Korea. MATERIALS AND METHODS: This study included 1,286 individuals who had been in contact with an index COVID-19 case between January 24, 2020, and June 30, 2022. Variables such as age, sex, nationality, place of contact, level of contact, the status of exposed cases, period, and level of mask-wearing were assessed. RESULTS: Among 1,286 participants, 132 (10.30%) were confirmed to have COVID-19. With increasing age, the risk of the exposed persons contracting COVID-19 from index cases tended to increase (P <0.001), especially for people in their 70s (odds ratio, 1.24; 95% confidence interval, 1.11-1.40; P <0.001). We found an increasing trend in the risk of a COVID-19 exposed case becoming a secondary infection case (P <0.001) in long-term care facilities where the attack rate was high. CONCLUSION: The risk of COVID-19 transmission is high in long-term care facilities where many older adults reside. Intensive management of facilities at risk of infection and strict mask-wearing of confirmed COVID-19 cases are necessary to prevent the risk of COVID-19 infection.

Outbreak of carbapenem-resistant Enterobacterales at a long-term care facility in Seoul, Korea: surveillance and intervention mitigation strategies.

OBJECTIVES: Because effective decolonization options are not available, and treatment options are limited, carbapenem-resistant Enterobacterales (CRE) constitute increasingly threatening nosocomial pathogens. To prevent CRE-associated transmission and ensure patient safety, healthcare personnel and everyone in contact with CRE-infected patients must implement stringent infection control practices. This report describes a CRE outbreak, possibly related to a caregiver at a long-term care facility (LTCF), and presents a new surveillance model to improve the infection control of CRE in Seoul, Korea. METHODS: The Seoul Metropolitan Government surveillance system identified an outbreak of CRE in an LTCF in 2022. We obtained data on the demographic characteristics and contact histories of the inpatients, medical staff, and caregivers. To isolate the inpatients and employees exposed to CRE, we used rectal swab samples and environmental sampling during the study period (May-December 2022). RESULTS: We identified 18 cluster cases (1 caregiver and 17 inpatients) and 12 sporadic cases with CRE, and conducted a complete 197-day follow-up of all cases in the LTCF's isolation wards. CONCLUSIONS: This investigation demonstrated that our surveillance model and targeted intervention, based on the cooperation of the municipal government, public health center, and infection control advisory committee, effectively contained the epidemic at the LTCF. Measures to improve the compliance of all employees in LTCFs with infection control guidelines should also be adopted.

Transferrin-mediated increase of labile iron Pool following simulated ischemia causes lipid peroxidation during the early phase of reperfusion.

Heart ischemia/reperfusion (I/R) injury is related to iron content. However, the occurrence and mechanism of changes in labile iron pool (LIP) during I/R is debatable. Moreover, the identity of the iron form dominant in LIP during I/R is unclear. Herein, we measured changes of LIP during simulated ischemia (SI) and reperfusion (SR), in which ischemia was simulated in vitro with lactic acidosis and hypoxia. Total LIP did not change in lactic acidosis, whereas LIP, especially Fe3+, increased in hypoxia. Under SI, accompanied by hypoxia with acidosis, both Fe2+ and Fe3+ were significantly increased. Increased total LIP was maintained at 1 h post-SR. However, the Fe2+ and Fe3+ portion was changed. The increased Fe2+ was decreased, and conversely the Fe3+ was increased. BODIPY oxidized signal increased and through the time-course these changes correlated with blebbing of cell membrane and SR-induced LDH release. These data suggested lipid peroxidation occurred via Fenton's reaction. The experiments using bafilomycin A1 and zinc protoporphyrin suggested no role of ferritinophagy or heme oxidation in the increase of LIP during SI. The extracellular source, transferrin assessed using serum transferrin bound iron (TBI) saturation showed that the depletion of TBI reduced SR-induced cell damages and additive saturation of TBI accelerated SR-induced lipid peroxidation. Furthermore, Apo-Tf dramatically blocked the increase of LIP and SR-induced damages. In conclusion, Tf-mediated iron induces the increase of LIP during SI, and it causes Fenton reaction-mediated lipid peroxidation during the early phase of SR.

The optimal model of reperfusion injury in vitro using H9c2 transformed cardiac myoblasts.

An in vitro model for ischemia/reperfusion injury has not been well-established. We hypothesized that this failure may be caused by serum deprivation, the use of glutamine-containing media, and absence of acidosis. Cell viability of H9c2 cells was significantly decreased by serum deprivation. In this condition, reperfusion damage was not observed even after simulating severe ischemia. However, when cells were cultured under 10% dialyzed FBS, cell viability was less affected compared to cells cultured under serum deprivation and reperfusion damage was observed after hypoxia for 24 h. Reperfusion damage after glucose or glutamine deprivation under hypoxia was not significantly different from that after hypoxia only. However, with both glucose and glutamine deprivation, reperfusion damage was significantly increased. After hypoxia with lactic acidosis, reperfusion damage was comparable with that after hypoxia with glucose and glutamine deprivation. Although high-passage H9c2 cells were more resistant to reperfusion damage than low-passage cells, reperfusion damage was observed especially after hypoxia and acidosis with glucose and glutamine deprivation. Cell death induced by reperfusion after hypoxia with acidosis was not prevented by apoptosis, autophagy, or necroptosis inhibitors, but significantly decreased by ferrostatin-1, a ferroptosis inhibitor, and deferoxamine, an iron chelator. These data suggested that in our SIR model, cell death due to reperfusion injury is likely to occur via ferroptosis, which is related with ischemia/reperfusion-induced cell death in vivo. In conclusion, we established an optimal reperfusion injury model, in which ferroptotic cell death occurred by hypoxia and acidosis with or without glucose/glutamine deprivation under 10% dialyzed FBS.

Bis-phosphoryl-bridged stilbenes synthesized by an intramolecular cascade cyclization.

Bis-phosphoryl-bridged stilbenes have been synthesized using an intramolecular cascade cyclization. They show intense blue fluorescences at longer wavelengths with higher quantum yields compared to those of the known element-bridged stilbenes. In addition, they have much lower reduction potentials due to the inductive effect of phosphoryl groups. The incorporation of the phosphoryl moiety is an effective way for the construction of highly electron-accepting pi-conjugated systems.

Boron trifluoride induced palladium-catalyzed cross-coupling reaction of 1-aryltriazenes with areneboronic acids.

[reaction: see text] Aryltriazenes are directly coupled with areneboronic acids in the presence of a catalytic amount of Pd(2)(dba)(3) and P(tBu)(3) together with 1 equiv of BF(3).OEt(2) in DME to afford the corresponding biaryl products in up to 98% yield. A carbonylative cross-coupling reaction under a carbon monoxide atmosphere is also found to give the corresponding diaryl ketone with a similar catalyst system.