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Chia-Lun Kuo,Pei-Chen Lee,Li-Jung Elizabeth Ku,Yu Sun,Tsung-Hsueh Lu,Muhammad Atoillah Isfandiari,Chung-Yi Li 한국역학회 2023 Epidemiology and Health Vol.45 No.-
OBJECTIVES: Information regarding the underlying causes of death (UCODs) and standardized mortality ratio (SMR) of dementia is instrumental in formulating medical strategies to prolong life in persons with dementia (PWD). We examined the leading UCODs among PWD and estimated the overall and cause-specific SMRs in relation to dementia in Taiwan. METHODS: Data were retrieved from 2 national datasets: the Taiwan Death Registry and the medical claim datasets of the National Health Insurance program. The observed person-years for each study participant were counted from the date of cohort enrollment to either the date of death or the final day of 2016. Sex-specific and age-specific SMRs were then calculated. RESULTS: The leading UCOD was circulatory disease, accounting for 26.0% of total deaths (n=3,505), followed by respiratory disease at 21.3% (n=2,875). PWD were at significantly increased risk of all-cause mortality (SMR, 2.01), with SMR decreasing with advancing age. A cause-specific analysis revealed that the highest SMRs were associated with nervous system diseases (SMR, 7.58) and mental, behavioral, and neurodevelopmental disorders (SMR, 4.80). Age appeared to modify SMR, suggesting that younger age at cohort enrollment was linked to higher SMRs for nearly all causes of mortality. CONCLUSIONS: Circulatory and respiratory diseases were the leading UCODs among PWD. The particularly elevated mortality due to nervous system diseases and mental disorders suggests that allocating more resources to neurological and psychiatric services is warranted. The elevated SMRs of various UCODs among younger PWD underscore the need for clinicians to pay particular attention to the medical care provided to these patients.
Manikandan, Arumugam,Ilango, P. Robert,Chen, Chia-Wei,Wang, Yi-Chung,Shih, Yu-Chuan,Lee, Ling,Wang, Zhiming M.,Ko, Hyunhyub,Chueh, Yu-Lun The Royal Society of Chemistry 2018 Journal of Materials Chemistry A Vol.6 No.31
<P>Here, we demonstrate the successful synthesis of (1T/2H) MoS2/α-MoO3 heterostructured nanoflowers at a low temperature of 200 °C by a one-step hydrothermal method. By tuning the reaction time under the influence of thiourea and hydrazine hydrate, we established a complete phase-engineered MoS2 with 1T and 2H phases on the surface of α-MoO3. Active sites associated with the phase-engineered (1T/2H) MoS2/α-MoO3 hybrid nanoflowers enable them to exhibit dual roles as a superior dye adsorbent and an electrocatalyst towards the hydrogen evolution reaction. The 2H-rich (1T/2H) MoS2/α-MoO3 hybrid heterostructured nanoflowers prepared at 16 h achieved a high surface area of 37.97 m<SUP>2</SUP> g<SUP>−1</SUP>, and 97% of the RhB dye with an initial concentration of 47.9 mg L<SUP>−1</SUP> was removed within 10 min through the adsorption process, which is the highest known removal efficiency reported in the literature. As a hydrogen evolution reaction (HER) electrocatalyst in acidic solution, the 1T-rich (1T/2H) MoS2/α-MoO3 hybrid heterostructured nanoflowers prepared at 12 h exhibited a highly efficient catalytic activity by achieving a low overpotential of 232 mV at a current density of 10 mA cm<SUP>−2</SUP>, which is comparable to those of previously reported HER catalysts based on MoS2. Moreover, this sample reached a low Tafel slope of 81 mV dec<SUP>−1</SUP> and was stable when operated for more than 1000 cycles.</P>
Chun-Yu Liu,Tzu-Ting Huang,Pei-Yi Chu,Chun-Teng Huang,Chia-Han Lee,Wan-Lun Wang,Ka-Yi Lau,Wen-Chun Tsai,Tzu-I Chao,Jung-Chen Su,Ming-Huang Chen,Chung-Wai Shiau,Ling-Ming Tseng,Kuen-Feng Chen 생화학분자생물학회 2017 Experimental and molecular medicine Vol.49 No.-
Triple-negative breast cancer (TNBC) remains difficult to treat and urgently needs new therapeutic options. Nintedanib, a multikinase inhibitor, has exhibited efficacy in early clinical trials for HER2-negative breast cancer. In this study, we examined a new molecular mechanism of nintedanib in TNBC. The results demonstrated that nintedanib enhanced TNBC cell apoptosis, which was accompanied by a reduction of p-STAT3 and its downstream proteins. STAT3 overexpression suppressed nintedanib-mediated apoptosis and further increased the activity of purified SHP-1 protein. Moreover, treatment with either a specific inhibitor of SHP-1 or SHP-1-targeted siRNA reduced the apoptotic effects of nintedanib, which validates the role of SHP-1 in nintedanib-mediated apoptosis. Furthermore, nintedanib-induced apoptosis was attenuated in TNBC cells expressing SHP-1 mutants with constantly open conformations, suggesting that the autoinhibitory mechanism of SHP-1 attenuated the effects of nintedanib. Importantly, nintedanib significantly inhibited tumor growth via the SHP-1/p-STAT3 pathway. Clinically, SHP-1 levels were downregulated, whereas p-STAT3 was upregulated in tumor tissues, and SHP-1 transcripts were associated with improved disease-free survival in TNBC patients. Our findings revealed that nintedanib induces TNBC apoptosis by acting as a SHP-1 agonist, suggesting that targeting STAT3 by enhancing SHP-1 expression could be a viable therapeutic strategy against TNBC.