Purpose: This study aimed to determine whether genetic factors affect the location of dilated perivascular spaces (dPVS) by comparing healthy young twins and non-twin (NT) siblings. Materials and Methods: A total of 700 healthy young adult twins and NT siblings [138 monozygotic (MZ) twin pairs, 79 dizygotic (DZ) twin pairs, and 133 NT sibling pairs] were collected from the Human Connectome Project dataset. dPVS was automatically segmented and normalized to standard space. Then, spatial similarity indices [mean squared error (MSE), structural similarity (SSIM), and dice similarity (DS)] were calculated for dPVS in the basal ganglia (BGdPVS) and white matter (WMdPVS) between paired subjects before and after propensity score matching of dPVS volumes between groups. Within-pair correlations for the regional volumes of dVPS were also assessed using the intraclass correlation coefficient. Results: The spatial similarity of dPVS was significantly higher in MZ twins [higher DS (median, 0.382 and 0.310) and SSIM (0.963 and 0.887) and lower MSE (0.005 and 0.005) for BGdPVS and WMdPVS, respectively] than in DZ twins [DS (0.121 and 0.119), SSIM (0.941 and 0.868), and MSE (0.010 and 0.011)] and NT siblings [DS (0.106 and 0.097), SSIM (0.924 and 0.848), and MSE (0.016 and 0.017)]. No significant difference was found between DZ twins and NT siblings. Similar results were found even after the subjects were matched according to dPVS volume. Regional dPVS volumes were also more correlated within pairs in MZ twins than in DZ twins and NT siblings. Conclusion Our results suggest that genetic factors affect the location of dPVS.

Aplastic anemia, mental retardation, and dwarfism (AMeD) syndrome, also known as aldehyde degradation deficiency (ADD) syndrome, is an autosomal recessive disorder caused by mutations in the ALDH2 and ADH5 genes, leading to decreased activity of the aldehyde dehydrogenase 2 (ALDH2) and alcohol dehydrogenase 5 (ADH5) enzymes, subsequently triggering enhanced cellular levels of formaldehyde and diverse multisystem manifestations. Herein, we present the case of a 7-year-old girl with AMeD syndrome, characterized by pancytopenia, developmental delay, microcephaly, epilepsy, and myelodysplastic syndrome. Whole-exome sequencing revealed compound heterozygous variants (c.832G＞C and c.678delA) in the ADH5 gene and a heterozygous pathogenic variant (c.1510G＞A) in the ALDH2 gene. This case underscores the complexity of AMeD syndrome, emphasizing the importance of genetic testing to ensure diagnosis and aid in the development of potential targeted therapeutic approaches.

Purpose: The purpose of this study was to explore and assess the experiences of cancer patients and their caregivers who had been admitted to comprehensive nursing care service wards. Methods: Data were collected from 10 patients and 10 caregivers by in-depth interviews. The data were analyzed using content analysis of Downe-Wamboldt. Results: Three categories and seven subcategories were extracted. 1) Realizing institutional limitations of comprehensive nursing care service: ‘Wishing for precise operating systems based on patient severity,’ ‘Anticipating active caregiver participation in treatment process,’ ‘Requiring a countermeasure for safety accidents,’ 2) Professional nursing service which provides relief: ‘Patient-centered professional nursing service,’ ‘Inpatient service that provides relief for patients and caregivers,’ 3) Anticipating continuous use of the service: ‘Inpatient service which users are willing to reuse,’ ‘Wishing for expansion and reinforcement of the service.’ Conclusion Cancer patients and their caregivers experienced institutional limitations while satisfied with professional nursing service and willing to reuse the service. To improve this situation, institutional support such as separate wards for severe patients, measures for active caregiver participation and prevention of safety accidents, and adequate staffing would be helpful for relatively severe level cancer patients and their caregivers.

Purpose: This study aimed to determine whether genetic factors affect the location of dilated perivascular spaces (dPVS) by comparing healthy young twins and non-twin (NT) siblings. Materials and Methods: A total of 700 healthy young adult twins and NT siblings [138 monozygotic (MZ) twin pairs, 79 dizygotic (DZ) twin pairs, and 133 NT sibling pairs] were collected from the Human Connectome Project dataset. dPVS was automatically segmented and normalized to standard space. Then, spatial similarity indices [mean squared error (MSE), structural similarity (SSIM), and dice similarity (DS)] were calculated for dPVS in the basal ganglia (BGdPVS) and white matter (WMdPVS) between paired subjects before and after propensity score matching of dPVS volumes between groups. Within-pair correlations for the regional volumes of dVPS were also assessed using the intraclass correlation coefficient. Results: The spatial similarity of dPVS was significantly higher in MZ twins [higher DS (median, 0.382 and 0.310) and SSIM (0.963 and 0.887) and lower MSE (0.005 and 0.005) for BGdPVS and WMdPVS, respectively] than in DZ twins [DS (0.121 and 0.119), SSIM (0.941 and 0.868), and MSE (0.010 and 0.011)] and NT siblings [DS (0.106 and 0.097), SSIM (0.924 and 0.848), and MSE (0.016 and 0.017)]. No significant difference was found between DZ twins and NT siblings. Similar results were found even after the subjects were matched according to dPVS volume. Regional dPVS volumes were also more correlated within pairs in MZ twins than in DZ twins and NT siblings. Conclusion Our results suggest that genetic factors affect the location of dPVS.

Purpose: This study aimed to determine whether genetic factors affect the location of dilated perivascular spaces (dPVS) by comparing healthy young twins and non-twin (NT) siblings. Materials and Methods: A total of 700 healthy young adult twins and NT siblings [138 monozygotic (MZ) twin pairs, 79 dizygotic (DZ) twin pairs, and 133 NT sibling pairs] were collected from the Human Connectome Project dataset. dPVS was automatically segmented and normalized to standard space. Then, spatial similarity indices [mean squared error (MSE), structural similarity (SSIM), and dice similarity (DS)] were calculated for dPVS in the basal ganglia (BGdPVS) and white matter (WMdPVS) between paired subjects before and after propensity score matching of dPVS volumes between groups. Within-pair correlations for the regional volumes of dVPS were also assessed using the intraclass correlation coefficient. Results: The spatial similarity of dPVS was significantly higher in MZ twins [higher DS (median, 0.382 and 0.310) and SSIM (0.963 and 0.887) and lower MSE (0.005 and 0.005) for BGdPVS and WMdPVS, respectively] than in DZ twins [DS (0.121 and 0.119), SSIM (0.941 and 0.868), and MSE (0.010 and 0.011)] and NT siblings [DS (0.106 and 0.097), SSIM (0.924 and 0.848), and MSE (0.016 and 0.017)]. No significant difference was found between DZ twins and NT siblings. Similar results were found even after the subjects were matched according to dPVS volume. Regional dPVS volumes were also more correlated within pairs in MZ twins than in DZ twins and NT siblings. Conclusion Our results suggest that genetic factors affect the location of dPVS.

Aplastic anemia, mental retardation, and dwarfism (AMeD) syndrome, also known as aldehyde degradation deficiency (ADD) syndrome, is an autosomal recessive disorder caused by mutations in the ALDH2 and ADH5 genes, leading to decreased activity of the aldehyde dehydrogenase 2 (ALDH2) and alcohol dehydrogenase 5 (ADH5) enzymes, subsequently triggering enhanced cellular levels of formaldehyde and diverse multisystem manifestations. Herein, we present the case of a 7-year-old girl with AMeD syndrome, characterized by pancytopenia, developmental delay, microcephaly, epilepsy, and myelodysplastic syndrome. Whole-exome sequencing revealed compound heterozygous variants (c.832G＞C and c.678delA) in the ADH5 gene and a heterozygous pathogenic variant (c.1510G＞A) in the ALDH2 gene. This case underscores the complexity of AMeD syndrome, emphasizing the importance of genetic testing to ensure diagnosis and aid in the development of potential targeted therapeutic approaches.

Purpose: The purpose of this study was to explore and assess the experiences of cancer patients and their caregivers who had been admitted to comprehensive nursing care service wards. Methods: Data were collected from 10 patients and 10 caregivers by in-depth interviews. The data were analyzed using content analysis of Downe-Wamboldt. Results: Three categories and seven subcategories were extracted. 1) Realizing institutional limitations of comprehensive nursing care service: ‘Wishing for precise operating systems based on patient severity,’ ‘Anticipating active caregiver participation in treatment process,’ ‘Requiring a countermeasure for safety accidents,’ 2) Professional nursing service which provides relief: ‘Patient-centered professional nursing service,’ ‘Inpatient service that provides relief for patients and caregivers,’ 3) Anticipating continuous use of the service: ‘Inpatient service which users are willing to reuse,’ ‘Wishing for expansion and reinforcement of the service.’ Conclusion Cancer patients and their caregivers experienced institutional limitations while satisfied with professional nursing service and willing to reuse the service. To improve this situation, institutional support such as separate wards for severe patients, measures for active caregiver participation and prevention of safety accidents, and adequate staffing would be helpful for relatively severe level cancer patients and their caregivers.

Aplastic anemia, mental retardation, and dwarfism (AMeD) syndrome, also known as aldehyde degradation deficiency (ADD) syndrome, is an autosomal recessive disorder caused by mutations in the ALDH2 and ADH5 genes, leading to decreased activity of the aldehyde dehydrogenase 2 (ALDH2) and alcohol dehydrogenase 5 (ADH5) enzymes, subsequently triggering enhanced cellular levels of formaldehyde and diverse multisystem manifestations. Herein, we present the case of a 7-year-old girl with AMeD syndrome, characterized by pancytopenia, developmental delay, microcephaly, epilepsy, and myelodysplastic syndrome. Whole-exome sequencing revealed compound heterozygous variants (c.832G＞C and c.678delA) in the ADH5 gene and a heterozygous pathogenic variant (c.1510G＞A) in the ALDH2 gene. This case underscores the complexity of AMeD syndrome, emphasizing the importance of genetic testing to ensure diagnosis and aid in the development of potential targeted therapeutic approaches.

Purpose: This study aimed to determine whether genetic factors affect the location of dilated perivascular spaces (dPVS) by comparing healthy young twins and non-twin (NT) siblings. Materials and Methods: A total of 700 healthy young adult twins and NT siblings [138 monozygotic (MZ) twin pairs, 79 dizygotic (DZ) twin pairs, and 133 NT sibling pairs] were collected from the Human Connectome Project dataset. dPVS was automatically segmented and normalized to standard space. Then, spatial similarity indices [mean squared error (MSE), structural similarity (SSIM), and dice similarity (DS)] were calculated for dPVS in the basal ganglia (BGdPVS) and white matter (WMdPVS) between paired subjects before and after propensity score matching of dPVS volumes between groups. Within-pair correlations for the regional volumes of dVPS were also assessed using the intraclass correlation coefficient. Results: The spatial similarity of dPVS was significantly higher in MZ twins [higher DS (median, 0.382 and 0.310) and SSIM (0.963 and 0.887) and lower MSE (0.005 and 0.005) for BGdPVS and WMdPVS, respectively] than in DZ twins [DS (0.121 and 0.119), SSIM (0.941 and 0.868), and MSE (0.010 and 0.011)] and NT siblings [DS (0.106 and 0.097), SSIM (0.924 and 0.848), and MSE (0.016 and 0.017)]. No significant difference was found between DZ twins and NT siblings. Similar results were found even after the subjects were matched according to dPVS volume. Regional dPVS volumes were also more correlated within pairs in MZ twins than in DZ twins and NT siblings. Conclusion Our results suggest that genetic factors affect the location of dPVS.

Purpose: The purpose of this study was to explore and assess the experiences of cancer patients and their caregivers who had been admitted to comprehensive nursing care service wards. Methods: Data were collected from 10 patients and 10 caregivers by in-depth interviews. The data were analyzed using content analysis of Downe-Wamboldt. Results: Three categories and seven subcategories were extracted. 1) Realizing institutional limitations of comprehensive nursing care service: ‘Wishing for precise operating systems based on patient severity,’ ‘Anticipating active caregiver participation in treatment process,’ ‘Requiring a countermeasure for safety accidents,’ 2) Professional nursing service which provides relief: ‘Patient-centered professional nursing service,’ ‘Inpatient service that provides relief for patients and caregivers,’ 3) Anticipating continuous use of the service: ‘Inpatient service which users are willing to reuse,’ ‘Wishing for expansion and reinforcement of the service.’ Conclusion Cancer patients and their caregivers experienced institutional limitations while satisfied with professional nursing service and willing to reuse the service. To improve this situation, institutional support such as separate wards for severe patients, measures for active caregiver participation and prevention of safety accidents, and adequate staffing would be helpful for relatively severe level cancer patients and their caregivers.