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: This study aimed to develop an animal model suitable for coronectomy research. Materials and Methods: Eighteen Sprague-Dawley rats were divided into six groups: incisor control (InC), incisor flap (InF), incisor non-flap (InNF), molar control (MC), molar flap (MF), and molar non-flap (MNF). Coronectomy was not performed in the control groups (InC and MC). In the incisor (In) groups, coronectomy was performed on the mandibular incisors, with flap elevation in the InF group and without flap elevation in the InNF group. In the molar (M) groups, coronectomy was performed on the maxillary first molar, with flap elevation in the MF group and without flap elevation in the MNF group. The incisor groups were sacrificed on day 7, and the molar groups on days 7 and 14. Clinical healing, tooth movement, and histological and immunohistochemical analyses were performed. Results: InF and InNF groups showed tooth eruption similar to or the same as that before coronectomy, whereas the MF and MNF groups’ roots moved slowly. In InF and InNF groups, the pulp at the maturation zone was mineralized, but apical pulp vitality was maintained. MF and MNF groups showed bacterial infection and inflammation on day 7, with mineralization on day 14; however, apical pulp vitality was maintained. The MF group showed varied healing patterns, whereas the MNF group had consistent results across individuals. Conclusion Both incisors and molars are meaningful models for coronectomy. However, for consistent experimental results, coronectomy without flap elevation on the maxillary first molar is recommended.

Purpose: This study aimed to develop an animal model suitable for coronectomy research. Materials and Methods: Eighteen Sprague-Dawley rats were divided into six groups: incisor control (InC), incisor flap (InF), incisor non-flap (InNF), molar control (MC), molar flap (MF), and molar non-flap (MNF). Coronectomy was not performed in the control groups (InC and MC). In the incisor (In) groups, coronectomy was performed on the mandibular incisors, with flap elevation in the InF group and without flap elevation in the InNF group. In the molar (M) groups, coronectomy was performed on the maxillary first molar, with flap elevation in the MF group and without flap elevation in the MNF group. The incisor groups were sacrificed on day 7, and the molar groups on days 7 and 14. Clinical healing, tooth movement, and histological and immunohistochemical analyses were performed. Results: InF and InNF groups showed tooth eruption similar to or the same as that before coronectomy, whereas the MF and MNF groups’ roots moved slowly. In InF and InNF groups, the pulp at the maturation zone was mineralized, but apical pulp vitality was maintained. MF and MNF groups showed bacterial infection and inflammation on day 7, with mineralization on day 14; however, apical pulp vitality was maintained. The MF group showed varied healing patterns, whereas the MNF group had consistent results across individuals. Conclusion Both incisors and molars are meaningful models for coronectomy. However, for consistent experimental results, coronectomy without flap elevation on the maxillary first molar is recommended.

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: This study aimed to develop an animal model suitable for coronectomy research. Materials and Methods: Eighteen Sprague-Dawley rats were divided into six groups: incisor control (InC), incisor flap (InF), incisor non-flap (InNF), molar control (MC), molar flap (MF), and molar non-flap (MNF). Coronectomy was not performed in the control groups (InC and MC). In the incisor (In) groups, coronectomy was performed on the mandibular incisors, with flap elevation in the InF group and without flap elevation in the InNF group. In the molar (M) groups, coronectomy was performed on the maxillary first molar, with flap elevation in the MF group and without flap elevation in the MNF group. The incisor groups were sacrificed on day 7, and the molar groups on days 7 and 14. Clinical healing, tooth movement, and histological and immunohistochemical analyses were performed. Results: InF and InNF groups showed tooth eruption similar to or the same as that before coronectomy, whereas the MF and MNF groups’ roots moved slowly. In InF and InNF groups, the pulp at the maturation zone was mineralized, but apical pulp vitality was maintained. MF and MNF groups showed bacterial infection and inflammation on day 7, with mineralization on day 14; however, apical pulp vitality was maintained. The MF group showed varied healing patterns, whereas the MNF group had consistent results across individuals. Conclusion Both incisors and molars are meaningful models for coronectomy. However, for consistent experimental results, coronectomy without flap elevation on the maxillary first molar is recommended.

Purpose: This study aimed to develop an animal model suitable for coronectomy research. Materials and Methods: Eighteen Sprague-Dawley rats were divided into six groups: incisor control (InC), incisor flap (InF), incisor non-flap (InNF), molar control (MC), molar flap (MF), and molar non-flap (MNF). Coronectomy was not performed in the control groups (InC and MC). In the incisor (In) groups, coronectomy was performed on the mandibular incisors, with flap elevation in the InF group and without flap elevation in the InNF group. In the molar (M) groups, coronectomy was performed on the maxillary first molar, with flap elevation in the MF group and without flap elevation in the MNF group. The incisor groups were sacrificed on day 7, and the molar groups on days 7 and 14. Clinical healing, tooth movement, and histological and immunohistochemical analyses were performed. Results: InF and InNF groups showed tooth eruption similar to or the same as that before coronectomy, whereas the MF and MNF groups’ roots moved slowly. In InF and InNF groups, the pulp at the maturation zone was mineralized, but apical pulp vitality was maintained. MF and MNF groups showed bacterial infection and inflammation on day 7, with mineralization on day 14; however, apical pulp vitality was maintained. The MF group showed varied healing patterns, whereas the MNF group had consistent results across individuals. Conclusion Both incisors and molars are meaningful models for coronectomy. However, for consistent experimental results, coronectomy without flap elevation on the maxillary first molar is recommended.

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.

This paper describes a community effort to improve earlier versions of the full-text corpus of Genomics & Informatics by semi-automatically detecting and correcting PDF-to-text conversion errors and optical character recognition errors during the first hackathon of Genomics & Informatics Annotation Hackathon (GIAH) event. Extracting text from multi-column biomedical documents such as Genomics & Informatics is known to be notoriously difficult. The hackathon was piloted as part of a coding competition of the ELTEC College of Engineering at Ewha Womans University in order to enable researchers and students to create or annotate their own versions of the Genomics & Informatics corpus, to gain and create knowledge about corpus linguistics, and simultaneously to acquire tangible and transferable skills. The proposed projects during the hackathon harness an internal database containing different versions of the corpus and annotations.