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Ching-Min Kuo,Wei-Jen Liao,Chun-Che Huang,Tsuo-Hung Lan,Ching-Heng Lin,Shun-Ping Wang,Cheng-Hung Lee,Ping-Wing Lui 대한정신약물학회 2020 CLINICAL PSYCHOPHARMACOLOGY AND NEUROSCIENCE Vol.18 No.4
Objective: The relationship of antipsychotics and the risk of refracture in treated patients is unclear. The aim of this study is to evaluate the association between prolonged antipsychotic and the incidences of bone fractures and refractures in schizophrenia. Methods: This is a retrospective nested case-control study using Taiwan National Health Insurance Research Database recorded from 2000 to 2005, with cases followed up to end of 2011. Total of 7,842 schizophrenic patients, 3,955 had developed bone fractures were compared with 3,887 control subjects matched in age, sex, and index date. Antipsychotic drug exposure was classified based on the drug type and medication duration. Conditional logistic regression analyses were performed. Odds ratio (OR) and confidence interval (CI) were calculated. Results: We found (after adjustments) higher risks of developing fractures under continued use of typical (OR = 1.70; 95% CI, 1.51−1.91) or atypical antipsychotics (OR = 1.43; 95% CI, 1.28−1.60) were found. Additionally, continued use typical (OR = 1.84; 95% CI, 1.35−2.50) or atypical antipsychotics (OR = 1.44; 95% CI, 1.06−1.95) was positively associated with refracture risks. Moreover, refractures were associated with continuous use of chlorpromazine (one typical antipsychotics, OR = 2.45; 95% CI, 1.14−5.25), and risperidone (OR = 1.48; 95% CI, 1.01−2.16) or zotepine (OR = 2.15; 95% CI, 1.06−4.36) (two atypical antipsychotics). Conclusion: Higher risks of bone fracture and refracture were found in schizophrenia under prolonged medication with typical or atypical antipsychotics. We therefore recommend that clinicians should pay more attention on bone density monitoring for patients using long-term antipsychotics.
Reusing indigenous plant materials to restore vegetation: A practical case in Shei-Pa National Park
Ching-An Chiu,Sheng-Shan Lu,Mei-Fen Lee,Chen-Chang Pan,Kuo-Min Fu 국립중앙과학관 2020 Journal of Asia-Pacific Biodiversity Vol.13 No.2
Using only local gene pools to restore native vegetation is challenging. This practice enabled native forestin a post-fired pine and silvergrass woodland to be rehabilitated by reusing indigenous materials in asimple and effective manner. We designed vegetation restoration processes, including uprooting silvergrassand removing pine leaf from woodland ground, collecting tree saplings on sliding slopes andtransplanting them, and collecting humus and seeds from roadsides and redistributing them at restorationsites. Volunteers, tourists, and employees of Shei-Pa National Park participated in the restorationpractices. Through 5-year practices, the native vegetation and forest floor environment exhibited aremarkable recovery, inducing the reappearance of the Guanwu salamander. This restoration practicecost little money but required much time and labor. The approach may be suitable for small restorationsites. We believe that this practice could enhance knowledge, technology, and enthusiasm for localecological restoration.
Kuo-Feng Hua,A-Ching Chao,Ting-Yu Lin,Wan-Tze Chen,Yu-Chieh Lee,Wan-Han Hsu,Sheau-Long Lee,Hsin-Min Wang,Ding-I. Yang,Tz-Chuen Ju 고려인삼학회 2022 Journal of Ginseng Research Vol.46 No.4
Background: Huntington's disease (HD) is a neurodegenerative disorder caused by the expansion oftrinucleotide CAG repeat in the Huntingtin (Htt) gene. The major pathogenic pathways underlying HDinvolve the impairment of cellular energy homeostasis and DNA damage in the brain. The protein kinaseataxia-telangiectasia mutated (ATM) is an important regulator of the DNA damage response. ATM isinvolved in the phosphorylation of AMP-activated protein kinase (AMPK), suggesting that AMPK plays acritical role in response to DNA damage. Herein, we demonstrated that expression of polyQ-expandedmutant Htt (mHtt) enhanced the phosphorylation of ATM. Ginsenoside is the main and most effectivecomponent of Panax ginseng. However, the protective effect of a ginsenoside (compound K, CK) in HDremains unclear and warrants further investigation. Methods: This study used the R6/2 transgenic mouse model of HD and performed behavioral tests,survival rate, histological analyses, and immunoblot assays. Results: The systematic administration of CK into R6/2 mice suppressed the activation of ATM/AMPK andreduced neuronal toxicity and mHTT aggregation. Most importantly, CK increased neuronal density andlifespan and improved motor dysfunction in R6/2 mice. Conversely, CK enhanced the expression of Bcl2protected striatal cells from the toxicity induced by the overactivation of mHtt and AMPK. Conclusions: Thus, the oral administration of CK reduced the disease progression and markedlyenhanced lifespan in the transgenic mouse model (R6/2) of HD.