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Mei Cheng Lim(Mei Cheng Lim),Sarbhan Singh(Sarbhan Singh ),Chee Herng Lai(Chee Herng Lai ),Balvinder Singh Gill(Balvinder Singh Gill ),Mohd Kamarulariffin Kamarudin(Mohd Kamarulariffin Kamarudin ),Ahm 한국역학회 2023 Epidemiology and Health Vol.45 No.-
OBJECTIVES: This study aimed to develop susceptible-exposed-infectious-recovered-vaccinated (SEIRV) models to examine the effects of vaccination on coronavirus disease 2019 (COVID-19) case trends in Malaysia during Phase 3 of the National COVID-19 Immunization Program amidst the Delta outbreak. METHODS: SEIRV models were developed and validated using COVID-19 case and vaccination data from the Ministry of Health, Malaysia, from June 21, 2021 to July 21, 2021 to generate forecasts of COVID-19 cases from July 22, 2021 to December 31, 2021. Three scenarios were examined to measure the effects of vaccination on COVID-19 case trends. Scenarios 1 and 2 represented the trends taking into account the earliest and latest possible times of achieving full vaccination for 80% of the adult population by October 31, 2021 and December 31, 2021, respectively. Scenario 3 described a scenario without vaccination for comparison. RESULTS: In scenario 1, forecasted cases peaked on August 28, 2021, which was close to the peak of observed cases on August 26, 2021. The observed peak was 20.27% higher than in scenario 1 and 10.37% lower than in scenario 2. The cumulative observed cases from July 22, 2021 to December 31, 2021 were 13.29% higher than in scenario 1 and 55.19% lower than in scenario 2. The daily COVID-19 case trends closely mirrored the forecast of COVID-19 cases in scenario 1 (best-case scenario). CONCLUSIONS: Our study demonstrated that COVID-19 vaccination reduced COVID-19 case trends during the Delta outbreak. The compartmental models developed assisted in the management and control of the COVID-19 pandemic in Malaysia.
Phloroglucinol inhibits ultraviolet B radiation-induced oxidative stress in the mouse skin
Piao, Mei Jing,Ahn, Mee Jung,Kang, Kyoung Ah,Kim, Ki Cheon,Zheng, Jian,Yao, Cheng Wen,Cha, Ji Won,Hyun, Chang Lim,Kang, Hee Kyoung,Lee, Nam Ho,Hyun, Jin Won Informa Healthcare 2014 International journal of radiation biology Vol.90 No.10
<P><I>Purpose</I>: Previously we demonstrated that phloroglucinol (1,3,5-trihydroxybenzene) protected human HaCaT keratinocytes against ultraviolet B (UVB, 280-320 nm)-induced oxidative stress <I>in vitro</I> by scavenging intracellular reactive oxygen species (ROS). The current study investigated whether phloroglucinol could similarly protect the mouse skin against UVB-induced oxidative tissue damage <I>in vivo</I>.</P><P><I>Materials and methods</I>: Male 7-week-old Balb/c mice were divided into the following untreated normal control, phloroglucinol only-treated, vehicle plus UVB (30 or 60 mJ/cm<SUP>2</SUP>)-exposed, and phloroglucinol (10 or 50 mg/ml) plus UVB (30 or 60 mJ/cm<SUP>2</SUP>)-treated groups. Following UVB exposure, phloroglucinol or phosphate buffered saline vehicle was applied to the dorsal skin of each mouse daily for 3 days. Studies were conducted at 24 h after the last of the UVB exposures. Histopathological analyses of dorsal skin lesions were performed on all mice. In addition, the levels of UVB-provoked injury to cellular components, including DNA, proteins, and lipids were detected by levels of 8-oxoguanine (8-oxoG), protein carbonyls, and 8-isoprostane. Apoptosis were assessed by using western blot for B-cell lymphoma-2-associated X protein (Bax) and activated caspase-3 expression, by using immunohistochemistry.</P><P><I>Results</I>: UVB radiation increased the thickness of the epidermis and the dermis, and also stimulated the accumulation of mast cells in the irradiated skin. However, treatment with phloroglucinol significantly decreased all of these parameters. Furthermore, phloroglucinol decreased UVB-provoked injury to cellular components, including DNA, proteins, and lipids; down-regulated the expression of phospho-histone H2A.X in the injured skin; and reduced the UVB-generated levels of 8-oxoG, protein carbonyls, and 8-isoprostane, which are all markers of oxidative stress. In addition, phloroglucinol attenuated the UVB-induced expression of the pro-apoptotic proteins, Bax protein, and activated caspase-3.</P><P><I>Conclusion</I>: These results suggest that phloroglucinol safeguards the mouse skin against UVB-induced oxidative stress and apoptosis.</P>
Ryu, Min Ju,Kang, Kyoung Ah,Piao, Mei Jing,Kim, Ki Cheon,Zheng, Jian,Yao, Cheng Wen,Cha, Ji Won,Hyun, Chang Lim,Chung, Ha Sook,Park, Jong Cook,Cho, Suk Ju,Hyun, Jin Won Springer 2014 In vitro cellular & developmental biology Animal Vol.50 No.6
<P>The cytoprotective mechanism of 7, 8-dihydroxyflavone (DHF) against oxidative stress-induced cell damage with respect to its stimulatory effect on the expression of heme oxygenase-1 (HO-1), a potent antioxidant enzyme, was investigated in the present study. Up-regulation of HO-1 expression by DHF was both dose and time dependent in lung fibroblast V79-4 cells. DHF also increased the protein expression level of the transcription factor nuclear factor erythroid-2-related factor 2 (Nrf2), and induced the translocation of Nrf2 from the cytosol into the nucleus, leading to elevated HO-1 expression. The siNrf2 RNA-transfection attenuated HO-1 expression induced by DHF treatment. In addition, DHF induced the activation of extracellular signal-regulated kinase (ERK), while U0126 (a specific pharmacological inhibitor of ERK kinase) abrogated DHF-activated Nrf2 and HO-1 expression. This suggests that DHF increased the levels of Nrf2 and HO-1 via ERK-dependent pathways. Furthermore, DHF significantly prevented the reduction of cell viability in response to oxidative stress; however, U0126 attenuated the protective effect of DHF. Taken together, these results demonstrate that DHF protected cells from oxidative stress via the activation of an ERK/Nrf2/HO-1 signaling pathway.</P>
( Jin Won Hyun ),( Ji Won Cha ),( Mei Jing Piao ),( Ki Cheon Kim ),( Cheng Wen Yao ),( Jian Zheng ),( Seong Min Kim ),( Chang Lim Hyun ),( Yong Seok Ahn ) 한국응용약물학회 2014 Biomolecules & Therapeutics(구 응용약물학회지) Vol.22 No.2
We investigated the protective effects of chlorogenic acid (CGA), a polyphenol compound, on oxidative damage induced by UVBexposure on human HaCaT cells. In a cell-free system, CGA scavenged 1,1-diphenyl-2-picrylhydrazyl radicals, superoxide anions,hydroxyl radicals, and intracellular reactive oxygen species (ROS) generated by hydrogen peroxide and ultraviolet B (UVB). Furthermore, CGA absorbed electromagnetic radiation in the UVB range (280-320 nm). UVB exposure resulted in damage to cellularDNA, as demonstrated in a comet assay; pre-treatment of cells with CGA prior to UVB irradiation prevented DNA damage andincreased cell viability. Furthermore, CGA pre-treatment prevented or ameliorated apoptosis-related changes in UVB-exposedcells, including the formation of apoptotic bodies, disruption of mitochondrial membrane potential, and alterations in the levelsof the apoptosis-related proteins Bcl-2, Bax, and caspase-3. Our findings suggest that CGA protects cells from oxidative stressinduced by UVB radiation.
Dictyopteris undulata Extract Induces Apoptosis in Human Colon Cancer Cells
Kim, Areum Daseul,Kang, Kyoung Ah,Piao, Jing Mei,Kim, Ki Cheon,Zheng, Jian,Yao, Cheng Wen,Cha, Ji Won,Hyun, Chang Lim,Boo, Sun Jin,Lee, Nam Ho,Na, Soo Young,Hyun, Jin Won 한국생물공학회 2014 Biotechnology and Bioprocess Engineering Vol.19 No.3
The present study investigated the cytotoxic and apoptotic effects of an ethanol extract derived from the marine brown alga Dictyopteris undulata against human colon adenocarcinoma cells. The Dictyopteris undulata extract (DUE) showed cytotoxic activity against SW480 cells in a dose-dependent manner, with 50% inhibition of cell viability at a concentration of $40{\mu}g/mL$. DUE also induced programmed cell death in SW480 cells, as evidenced by apoptotic body formation, DNA fragmentation, an increase in the population of apoptotic sub-$G_1$ phase cells, and mitochondrial membrane depolarization. Moreover, DUE significantly modulated the expression of apoptosis-associated proteins, resulting in a decrease in B cell lymphoma-2 expression and an increase in Bcl-2-associated X protein expression, as well as the activation of caspase-9 and caspase-3. Furthermore, DUE showed apoptotic cell death in two other colon cancer cell lines, SNU407 and HT29. These observations suggest that DUE may prove useful as a therapeutic agent for the attenuation of colon cancer.