Dokkyo Medical University Repository / 獨協医科大学リポジトリ
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The Improvement of QOL of Caregivers of Patients with Prader-Willi Syndrome after Growth Hormone Therapy
Get PDFPrader-Willi syndrome is a rare neurodevelopmental disorder that is characterized by neonatal hypotonia, hypogonadism, hyperphagia, and cognitive impairment. We compared the quality of life of caregivers of patients with Prader-Willi syndrome before and after the patients received growth hormone therapy.
Caregivers' quality of life was assessed using the Japanese version of the World Health Organization Quality of Life 26 (WHO-QOL26). We examined the impacts of two genotypes of Prader-Willi syndrome (deletion and maternal uniparental disomy) and growth hormone therapy on caregivers' quality of life. Using paired t-tests, we compared the caregivers' quality of life scores before and after the patients with Prader-Willi syndrome received growth hormone therapy.
The study included 141 individuals with Prader-Willi syndrome (68 males and 73 females) definitively identified with the deletion genotype and 35 (13 males and 22 females) who exhibited maternal uniparental disomy on chromosome 15. Our findings revealed that the caregivers' quality of life scores of the individuals with Prader-Willi syndrome-deletion before and after growth hormone therapy differed significantly. On the contrary, a statistically significant difference was not noted in all domains of quality of life scores of the caregivers of patients with Prader-Willi syndrome-maternal uniparental disomy on chromosome 15 genotype before and after growth hormone therapy.
The results of this study highlight that the caregivers of individuals with Prader Willi syndrome, particularly those with the Prader-Willi syndrome-deletion genotype receiving growth hormone therapy, had improved quality of life across multiple domains, including physical health, psychological well-being, social connections, and environmental experience.journal articl
Effect of remifentanil on the Tpeak-Tend interval during electroconvulsive therapy
Get PDF獨協医科大学博士（医学）令和5年度doctoral thesi
Inhibition of IL-33 signaling ameliorate hepatic fibrosis with decreasing MCP-1 in a mouse model of diabetes and non-alcoholic steatohepatitis; comparison for luseogliflozin, an SGLT2 inhibitor
Get PDF獨協医科大学博士（医学）令和5年度doctoral thesi
Association of CYP2R1 Gene Polymorphisms with Asthma and COPD in Japanese Patients
Get PDFCYP2R1 is an enzyme involved in vitamin D metabolism, and SNPs in the CYP2R1 gene are associated with asthma. We compared the SNPs rs10741657 and rs12794714 in CYP2R1 among 69 patients with chronic obstructive pulmonary disease (COPD), 77 patients with bronchial asthma (BA), and 50 healthy donors (HDs). The SNPs were identified in oral mucosal cells using specific thermal-elution chromatography. For both SNPs, the A allele frequency was higher in COPD than in BA patients and HDs. For both SNPs, the AA/AG genotype with COPD was associated with significantly lower peripheral eosinophil counts and higher peripheral neutrophil counts than the AA/AG genotypes with BA. In addition, the AA/AG genotype with COPD was associated with significantly lower FEV1 than the AA/AG genotype with BA. Moreover, for rs12794714, the GG genotype with COPD was associated with significantly lower FEV1 than the AA/AG and GG genotypes with BA p < 0.01 and 0.05, respectively. The AA/AG genotype of both SNPs with COPD appears associated with neutrophilic, rather than eosinophilic inflammation, and the GG genotype of rs12794714 with COPD seems associated with bronchial obstruction versus BA. CYP2R1 SNPs might relate to neutrophilic inflammation and bronchial obstruction in COPD in Japanese people.journal articl
Preemptive Medicine for Diabetes from the Viewpoint of the DOHaD Theory
Get PDFThe Developmental Origins of Health and Disease (DOHaD) theory posits that prenatal and infancy environmental factors influence future health and disease susceptibility.
Epidemiological and animal studies reveal that factors like nutritional status, maternal illness, chemical exposure, and drug use during pregnancy influence offspring's diabetes risk. Low birthweight correlates with later cardiovascular diseases (Barker's theory), later expanded into DOHaD theory. Dutch Famine links fetal malnutrition to adult diabetes. Animal studies replicating prenatal undernutrition show insulin resistance and altered gene expression.
Maternal hypernutrition studies using high-lipid or high-fructose diets demonstrate offspring's increased diabetes risk. Gestational Diabetes Mellitus (GDM) research shows maternal hyperglycemia affects offspring's glucose tolerance. Other maternal factors like deficiency in zinc, vitamin D, sleep disturbances, endocrine disruptor exposure, and substance intake contribute to diabetes risk.
Paternal factors, including protein restriction, high-lipid diets, and hyperglycemia, also affect offspring's diabetes risk, possibly through DNA methylation. Pathogenesis involves oxidative stress, gut microbiota, and nutrient-sensing signal disruption. Reprogramming efforts involve interventions during pregnancy or infancy, including antioxidants, green tea, flavonoids, melatonin, resveratrol, and folic acid.
The concept of "preemptive medicine" is introduced for diabetes prevention. The "First 1000 days" from fetal life to age 2 and adolescence to young adulthood are critical periods. Understanding epigenomic memory's role and promoting life-course medicine is crucial for preemptive diabetes treatment. Epigenetics, especially DNA methylation, emerges as a key molecular mechanism. Reprogramming epigenomic memory becomes a potential therapy. Overall, this review underscores the importance of comprehensive approaches for diabetes prevention in the context of DOHaD theory.journal articl