Purpose: This study aimed to describe adult living donor liver transplantation (LDLT) for acute liver failure and evaluate its clinical significance by comparing its surgical and survival outcomes with those of deceased donor liver transplantation (DDLT). Methods: We retrospectively reviewed the medical records of 267 consecutive patients (161 LDLT recipients and 106 DDLT recipients) aged 18 years or older who underwent liver transplantation between January 2006 and December 2020. Results: The mean periods from hepatic encephalopathy to liver transplantation were 5.85 days and 8.35 days for LDLT and DDLT, respectively (P = 0.091). Among these patients, 121 (45.3%) had grade III or IV hepatic encephalopathy (living, 34.8% vs. deceased, 61.3%; P < 0.001), and 38 (14.2%) had brain edema (living, 16.1% vs. deceased, 11.3%; P = 0.269) before liver transplantation. There were no significant differences in in-hospital mortality (living, 11.8% vs. deceased, 15.1%; P = 0.435), 10-year overall survival (living, 90.8% vs. deceased, 84.0%; P = 0.096), and graft survival (living, 83.5% vs. deceased, 71.3%;P = 0.051). However, postoperatively, the mean intensive care unit stay was shorter in the LDLT group (5.0 days vs. 9.5 days, P < 0.001). In-hospital mortality was associated with vasopressor use (odds ratio [OR], 3.40; 95% confidence interval [CI], 1.45–7.96; P = 0.005) and brain edema (OR, 2.75; 95% CI, 1.16–6.52; P = 0.022) of recipient at the time of transplantation. However, LDLT (OR, 1.26; 95% CI, 0.59–2.66; P = 0.553) was not independently associated with in-hospital mortality. Conclusion LDLT is feasible for acute liver failure when organs from deceased donors are not available.

Purpose: This study is to explore the antecedent factors of daycare teacher behaviors concerning the eye health of preschool children by applying an extended parallel process model. Methods: Focus group interviews were conducted with ten daycare center teachers on September 4 and 14, 2023. A data analysis was performed according to the content analysis method by clustering the data into the four categories: the two threat factors of severity and susceptibility and the two efficacy factors of self-efficacy and response-efficacy. Results: Daycare center teachers’ perception of the severity of eye health problems in preschool children was high in relation to eye trauma, but it was recognized that viewing the electronic devices were of a less severe because symptoms were not noticed in a short period of time. They also showed low susceptibility because they were not sufficiently interested in the eye health hazard behaviors of preschool children. The self-efficacy of daycare center teachers was low because this was a lack of knowledge about symptoms of eye problems. However, they recognized that eye health activities performed in the preschool age could prevent negative eye health outcomes, thus showing a high response efficacy. Conclusion In the future, it is necessary to increase the sensitivity and engagement of daycare center teachers concerning with the eye health of preschool children and to increase their self-efficacy. It will also be necessary to develop various interventions to improve eye health for preschool children that can be implemented by daycare center teachers.

Background: Uncoupling protein 1 (UCP1) is a proton uncoupler located across the mitochondrial membrane gener‑ ally involved in thermogenesis of brown adipose tissues. Although UCP1 is known to be strongly expressed in brown adipocytes, recent evidence suggest that white adipocytes can also express UCP1 under certain circumstances such as cold- or β-adrenergic receptor-stimulation, allowing them to acquire brown adipocyte-like features thereby becoming ’beige’ adipocytes. Results: In this study, we report that UCP1 can be expressed in adipose-tissue macrophages (ATM) lacking func‑ tional hypoxia-inducible factor-1 (HIF-1) and this does not require cold- nor β-adrenergic receptor activation. By using myeloid-specific Hif-1α knockout (KO) mice, we observed that these mice were protected from diet-induced obesity and exhibited an improved thermogenic tolerance upon cold challenge. ATM isolated from white adipose tissues (WAT) of these mice fed with high fat diet exhibited significantly higher M2-polarization, decreased gly‑ colysis, increased mitochondrial functions and acetyl-CoA levels, along with increased expression of Ucp1, peroxisome proliferator activated receptor-gamma co-activator-1a, and others involved in histone acetylation. Consistent with the increased Ucp1 gene expression, these ATM produced a significant amount of heat mediating lipolysis of cocultured adipocytes liberating free fatty acid. Treating ATM with acetate, a substrate for acetyl-CoA synthesis was able to boost the heat production in wild-type or Hif-1α-deficient but not UCP1-deficient macrophages, indicating that UCP1 was necessary for the heat production in macrophages. Lastly, we observed a significant inverse correlation between the number of UCP1-expressing ATM in WAT and the body mass index of human individuals. Conclusions UCP1-expressing ATM produce the heat to mediate lipolysis of adipocytes, indicating that this can be a novel strategy to treat and prevent diet-induced obesity.

Background: Uncoupling protein 1 (UCP1) is a proton uncoupler located across the mitochondrial membrane gener‑ ally involved in thermogenesis of brown adipose tissues. Although UCP1 is known to be strongly expressed in brown adipocytes, recent evidence suggest that white adipocytes can also express UCP1 under certain circumstances such as cold- or β-adrenergic receptor-stimulation, allowing them to acquire brown adipocyte-like features thereby becoming ’beige’ adipocytes. Results: In this study, we report that UCP1 can be expressed in adipose-tissue macrophages (ATM) lacking func‑ tional hypoxia-inducible factor-1 (HIF-1) and this does not require cold- nor β-adrenergic receptor activation. By using myeloid-specific Hif-1α knockout (KO) mice, we observed that these mice were protected from diet-induced obesity and exhibited an improved thermogenic tolerance upon cold challenge. ATM isolated from white adipose tissues (WAT) of these mice fed with high fat diet exhibited significantly higher M2-polarization, decreased gly‑ colysis, increased mitochondrial functions and acetyl-CoA levels, along with increased expression of Ucp1, peroxisome proliferator activated receptor-gamma co-activator-1a, and others involved in histone acetylation. Consistent with the increased Ucp1 gene expression, these ATM produced a significant amount of heat mediating lipolysis of cocultured adipocytes liberating free fatty acid. Treating ATM with acetate, a substrate for acetyl-CoA synthesis was able to boost the heat production in wild-type or Hif-1α-deficient but not UCP1-deficient macrophages, indicating that UCP1 was necessary for the heat production in macrophages. Lastly, we observed a significant inverse correlation between the number of UCP1-expressing ATM in WAT and the body mass index of human individuals. Conclusions UCP1-expressing ATM produce the heat to mediate lipolysis of adipocytes, indicating that this can be a novel strategy to treat and prevent diet-induced obesity.

Background: Uncoupling protein 1 (UCP1) is a proton uncoupler located across the mitochondrial membrane gener‑ ally involved in thermogenesis of brown adipose tissues. Although UCP1 is known to be strongly expressed in brown adipocytes, recent evidence suggest that white adipocytes can also express UCP1 under certain circumstances such as cold- or β-adrenergic receptor-stimulation, allowing them to acquire brown adipocyte-like features thereby becoming ’beige’ adipocytes. Results: In this study, we report that UCP1 can be expressed in adipose-tissue macrophages (ATM) lacking func‑ tional hypoxia-inducible factor-1 (HIF-1) and this does not require cold- nor β-adrenergic receptor activation. By using myeloid-specific Hif-1α knockout (KO) mice, we observed that these mice were protected from diet-induced obesity and exhibited an improved thermogenic tolerance upon cold challenge. ATM isolated from white adipose tissues (WAT) of these mice fed with high fat diet exhibited significantly higher M2-polarization, decreased gly‑ colysis, increased mitochondrial functions and acetyl-CoA levels, along with increased expression of Ucp1, peroxisome proliferator activated receptor-gamma co-activator-1a, and others involved in histone acetylation. Consistent with the increased Ucp1 gene expression, these ATM produced a significant amount of heat mediating lipolysis of cocultured adipocytes liberating free fatty acid. Treating ATM with acetate, a substrate for acetyl-CoA synthesis was able to boost the heat production in wild-type or Hif-1α-deficient but not UCP1-deficient macrophages, indicating that UCP1 was necessary for the heat production in macrophages. Lastly, we observed a significant inverse correlation between the number of UCP1-expressing ATM in WAT and the body mass index of human individuals. Conclusions UCP1-expressing ATM produce the heat to mediate lipolysis of adipocytes, indicating that this can be a novel strategy to treat and prevent diet-induced obesity.

Purpose: In chronic inflammatory diseases, neutrophils release NETs (neutrophil extracellular traps), web-like structures composedof DNA and citrullinated histones, to eliminate bacteria and regulate the inflammatory response. In periodontitis, NETosis acts asa crucial defense mechanism, characterized by the expression of citrullinated histones. This study aims to evaluate the impact ofage and smoking on the expression of citrullinated histones in patients with periodontitis and the feasibility of using saliva for their detection. Materials and Methods: A total of 19 patients participated in the experiment. Among them, 15 were grouped accord-ing to smoking status and age, with 5 patients assigned to each group. After clinical and radiographic examinations, blood sampleswere collected from the subjects, and serum was separated. For 4 subjects, both blood and saliva samples were collected. Thelevels of citrullinated histones in the samples were quantified using an ELISA kit, and the results were compared and statisticallyanalyzed. Results: The concentration of citrullinated histones was significantly higher in younger individuals (P < 0.05). Although the expression of citrullinated histones was higher in the smoking group compared to the non-smoking group, the difference was not statistically significant. In patients with periodontitis, the levels of citrullinated histones detected in saliva were comparable to those found in serum. Conclusion Age may be potential risk factors influencing the expression of citrullinated histones in patients with periodontitis. Additionally, saliva, which is easier to collect, could be used as a viable sample for detecting citrullinated histones in periodontitis patients.

Purpose: In chronic inflammatory diseases, neutrophils release NETs (neutrophil extracellular traps), web-like structures composedof DNA and citrullinated histones, to eliminate bacteria and regulate the inflammatory response. In periodontitis, NETosis acts asa crucial defense mechanism, characterized by the expression of citrullinated histones. This study aims to evaluate the impact ofage and smoking on the expression of citrullinated histones in patients with periodontitis and the feasibility of using saliva for their detection. Materials and Methods: A total of 19 patients participated in the experiment. Among them, 15 were grouped accord-ing to smoking status and age, with 5 patients assigned to each group. After clinical and radiographic examinations, blood sampleswere collected from the subjects, and serum was separated. For 4 subjects, both blood and saliva samples were collected. Thelevels of citrullinated histones in the samples were quantified using an ELISA kit, and the results were compared and statisticallyanalyzed. Results: The concentration of citrullinated histones was significantly higher in younger individuals (P < 0.05). Although the expression of citrullinated histones was higher in the smoking group compared to the non-smoking group, the difference was not statistically significant. In patients with periodontitis, the levels of citrullinated histones detected in saliva were comparable to those found in serum. Conclusion Age may be potential risk factors influencing the expression of citrullinated histones in patients with periodontitis. Additionally, saliva, which is easier to collect, could be used as a viable sample for detecting citrullinated histones in periodontitis patients.

Background: Uncoupling protein 1 (UCP1) is a proton uncoupler located across the mitochondrial membrane gener‑ ally involved in thermogenesis of brown adipose tissues. Although UCP1 is known to be strongly expressed in brown adipocytes, recent evidence suggest that white adipocytes can also express UCP1 under certain circumstances such as cold- or β-adrenergic receptor-stimulation, allowing them to acquire brown adipocyte-like features thereby becoming ’beige’ adipocytes. Results: In this study, we report that UCP1 can be expressed in adipose-tissue macrophages (ATM) lacking func‑ tional hypoxia-inducible factor-1 (HIF-1) and this does not require cold- nor β-adrenergic receptor activation. By using myeloid-specific Hif-1α knockout (KO) mice, we observed that these mice were protected from diet-induced obesity and exhibited an improved thermogenic tolerance upon cold challenge. ATM isolated from white adipose tissues (WAT) of these mice fed with high fat diet exhibited significantly higher M2-polarization, decreased gly‑ colysis, increased mitochondrial functions and acetyl-CoA levels, along with increased expression of Ucp1, peroxisome proliferator activated receptor-gamma co-activator-1a, and others involved in histone acetylation. Consistent with the increased Ucp1 gene expression, these ATM produced a significant amount of heat mediating lipolysis of cocultured adipocytes liberating free fatty acid. Treating ATM with acetate, a substrate for acetyl-CoA synthesis was able to boost the heat production in wild-type or Hif-1α-deficient but not UCP1-deficient macrophages, indicating that UCP1 was necessary for the heat production in macrophages. Lastly, we observed a significant inverse correlation between the number of UCP1-expressing ATM in WAT and the body mass index of human individuals. Conclusions UCP1-expressing ATM produce the heat to mediate lipolysis of adipocytes, indicating that this can be a novel strategy to treat and prevent diet-induced obesity.

Purpose: In chronic inflammatory diseases, neutrophils release NETs (neutrophil extracellular traps), web-like structures composedof DNA and citrullinated histones, to eliminate bacteria and regulate the inflammatory response. In periodontitis, NETosis acts asa crucial defense mechanism, characterized by the expression of citrullinated histones. This study aims to evaluate the impact ofage and smoking on the expression of citrullinated histones in patients with periodontitis and the feasibility of using saliva for their detection. Materials and Methods: A total of 19 patients participated in the experiment. Among them, 15 were grouped accord-ing to smoking status and age, with 5 patients assigned to each group. After clinical and radiographic examinations, blood sampleswere collected from the subjects, and serum was separated. For 4 subjects, both blood and saliva samples were collected. Thelevels of citrullinated histones in the samples were quantified using an ELISA kit, and the results were compared and statisticallyanalyzed. Results: The concentration of citrullinated histones was significantly higher in younger individuals (P < 0.05). Although the expression of citrullinated histones was higher in the smoking group compared to the non-smoking group, the difference was not statistically significant. In patients with periodontitis, the levels of citrullinated histones detected in saliva were comparable to those found in serum. Conclusion Age may be potential risk factors influencing the expression of citrullinated histones in patients with periodontitis. Additionally, saliva, which is easier to collect, could be used as a viable sample for detecting citrullinated histones in periodontitis patients.

Background: Uncoupling protein 1 (UCP1) is a proton uncoupler located across the mitochondrial membrane gener‑ ally involved in thermogenesis of brown adipose tissues. Although UCP1 is known to be strongly expressed in brown adipocytes, recent evidence suggest that white adipocytes can also express UCP1 under certain circumstances such as cold- or β-adrenergic receptor-stimulation, allowing them to acquire brown adipocyte-like features thereby becoming ’beige’ adipocytes. Results: In this study, we report that UCP1 can be expressed in adipose-tissue macrophages (ATM) lacking func‑ tional hypoxia-inducible factor-1 (HIF-1) and this does not require cold- nor β-adrenergic receptor activation. By using myeloid-specific Hif-1α knockout (KO) mice, we observed that these mice were protected from diet-induced obesity and exhibited an improved thermogenic tolerance upon cold challenge. ATM isolated from white adipose tissues (WAT) of these mice fed with high fat diet exhibited significantly higher M2-polarization, decreased gly‑ colysis, increased mitochondrial functions and acetyl-CoA levels, along with increased expression of Ucp1, peroxisome proliferator activated receptor-gamma co-activator-1a, and others involved in histone acetylation. Consistent with the increased Ucp1 gene expression, these ATM produced a significant amount of heat mediating lipolysis of cocultured adipocytes liberating free fatty acid. Treating ATM with acetate, a substrate for acetyl-CoA synthesis was able to boost the heat production in wild-type or Hif-1α-deficient but not UCP1-deficient macrophages, indicating that UCP1 was necessary for the heat production in macrophages. Lastly, we observed a significant inverse correlation between the number of UCP1-expressing ATM in WAT and the body mass index of human individuals. Conclusions UCP1-expressing ATM produce the heat to mediate lipolysis of adipocytes, indicating that this can be a novel strategy to treat and prevent diet-induced obesity.