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Li W.-P.,National Cheng Kung University | Liao P.-Y.,National Cheng Kung University | Su C.-H.,Center for Translational Research in Biomedical science | Yeh C.-S.,National Cheng Kung University
Journal of the American Chemical Society | Year: 2014

A new multifunctional nanoparticle to perform a near-infrared (NIR)-responsive remote control drug release behavior was designed for applications in the biomedical field. Different from the previous studies in formation of Fe3O4-Au core-shell nanoparticles resulting in a spherical morphology, the heterostructure with polyhedral core and shell was presented with the truncated octahedral Fe3O4 nanoparticle as the core over a layer of trisoctahedral Au shell. The strategy of Fe3O4@polymer@Au was adopted using poly-l-lysine as the mediate layer, followed by the subsequent seeded growth of Au nanoparticles to form a Au trisoctahedral shell. Fe3O4@Au trisoctahedra possess high-index facets of {441}. To combine photothermal and chemotherapy in a remote-control manner, the trisoctahedral core-shell Fe3O 4@Au nanoparticles were further covered with a mesoporous silica shell, yielding Fe3O4@Au@mSiO2. The bondable oligonucleotides (referred as dsDNA) were used as pore blockers of the mesoporous silica shell that allowed the controlled release, resulting in a NIR-responsive DNA-gated Fe3O4@Au@mSiO2 nanocarrier. Taking advantage of the magnetism, remotely triggered drug release was facilitated by magnetic attraction accompanied by the introduction of NIR radiation. DNA-gated Fe3O4@Au@mSiO2 serves as a drug control and release carrier that features functions of magnetic target, MRI diagnosis, and combination therapy through the manipulation of a magnet and a NIR laser. The results verified the significant therapeutic effects on tumors with the assistance of combination therapy consisting of magnetic guidance and remote NIR control. © 2014 American Chemical Society. Source

Lin P.-Y.,Chang Gung University | Lin P.-Y.,Center for Translational Research in Biomedical science | Tseng P.-T.,Tsyr Huey Mental Hospital
Journal of Psychiatric Research | Year: 2015

Glial cell-line derived neurotrophic factor (GDNF) has been shown to promote development, differentiation, and protection of CNS neurons and was thought to play an important role in various neuropsychiatric disorders. Several studies have examined the GDNF levels in patients with depression but shown inconsistent results. In this study, we compared blood GDNF levels between depressive patients and control subjects through meta-analytic method. The effect sizes (ESs) from all eligible studies were synthesized by using a random effect model. In this meta-analysis, we included 526 patients and 502 control subjects from 12 original articles. Compared to control subjects, blood GDNF levels are significantly decreased in patients with depression (ES=-0.62, p=0.0011). However, significant heterogeneity was found among included studies. Through subgroup analysis, we found that GDNF was still decreased in studies with major depressive disorder (ES=-0.73, p=0.0001); in studies with non-old-age depression (ES=-1.25, p=0.0001), but not with old-age depression; and in studies using serum samples (ES=-0.86, p<0.0001), but not in studies using plasma sample. Meta-regression did not show moderating effects of mean age of subjects, gender distribution, and age of onset of depression. Our findings support blood GDNF levels as a biomarker of depression as a whole, but the results were modulated by psychiatric diagnosis, age of included subjects, and sampling sources. With these results, future studies are required to examine whether effective antidepressant treatment is associated with an increase in serum GDNF levels. © 2015 Elsevier Ltd. Source

Tsai M.-F.,Center for Micro Nano Science and Technology | Chang S.-H.G.,National Cheng Kung University | Cheng F.-Y.,National Cheng Kung University | Shanmugam V.,Center for Micro Nano Science and Technology | And 3 more authors.
ACS Nano | Year: 2013

Photothermal cancer therapy using near-infrared (NIR) laser radiation is an emerging treatment. In the NIR region, two biological transparency windows are located in 650-950 nm (first NIR window) and 1000-1350 nm (second NIR window) with optimal tissue transmission obtained from low scattering and energy absorption, thus providing maximum radiation penetration through tissue and minimizing autofluorescence. To date, intensive effort has resulted in the generation of various methods that can be used to shift the absorbance of nanomaterials to the 650-950 nm NIR regions for studying photoinduced therapy. However, NIR light absorbers smaller than 100 nm in the second NIR region have been scant. We report that a Au nanorod (NR) can be designed with a rod-in-shell (rattle-like) structure smaller than 100 nm that is tailored to be responsive to the first and second NIR windows, in which we can perform hyperthermia-based therapy. In vitro performance clearly displays high efficacy in the NIR photothermal destruction of cancer cells, showing large cell-damaged area beyond the laser-irradiated area. This marked phenomenon has made the rod-in-shell structure a promising hyperthermia agent for the in vivo photothermal ablation of solid tumors when activated using a continuous-wave 808 m (first NIR window) or a 1064 nm (second NIR window) diode laser. We tailored the UV-vis-NIR spectrum of the rod-in-shell structure by changing the gap distance between the Au NR core and the AuAg nanoshell, to evaluate the therapeutic effect of using a 1064 nm diode laser. Regarding the first NIR window with the use of an 808 nm diode laser, rod-in-shell particles exhibit a more effective anticancer efficacy in the laser ablation of solid tumors compared to Au NRs. © 2013 American Chemical Society. Source

Chang A.Y.,Center for Translational Research in Biomedical science
Journal of Biomedical Science | Year: 2012

Background: Based on an experimental brain stem death model, we demonstrated previously that activation of the mitogen-activated protein kinase kinase 1/2 (MEK1/2)/extracellular signal-regulated kinase 1/2 (ERK1/2)/ mitogen-activated protein kinase signal-interacting kinase 1/2 (MNK1/2) cascade plays a pro-life role in the rostral ventrolateral medulla (RVLM), the origin of a life-and-death signal detected from systemic arterial pressure, which sequentially increases (pro-life) and decreases (pro-death) to reflect progressive dysfunction of central cardiovascular regulation during the advancement towards brain stem death in critically ill patients. The present study assessed the hypothesis that, in addition to ERK1/2, c-Jun NH2-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38MAPK), the other two mammalian members of MAPKs that are originally identified as stress-activated protein kinases, are activated specifically by MAPK kinase 4 (MAP2K4) or MAP2K6 and play a pro-life role in RVLM during experimental brain stem death. We further delineated the participation of phosphorylating activating transcriptional factor-2 (ATF-2) and c-Jun, the classical transcription factor activated by JNK or p38MAPK, in this process. Results: An experimental model of brain stem death that employed microinjection of the organophosphate insecticide mevinphos (Mev; 10 nmol) bilaterally into RVLM of Sprague-Dawley rats was used, alongside cardiovascular, pharmacological and biochemical evaluations. Results from ELISA showed that whereas the total JNK, p38MAPK, MAP2K4 and MAP2K6 were not affected, augmented phosphorylation of JNK at Thr183 and Tyr185 and p38MAPK at Thr180 and Tyr182, accompanied by phosphorylation of their upstream activators MAP2K4 at Ser257 and Thr261 and MAP2K6 at Ser207 and Thr211 in RVLM occurred preferentially during the pro-life phase of experimental brain stem death. Moreover, the activity of transcription factors ATF-2 at Thr71 and c-Jun at Ser73, rather than Elk-1 at Ser383 in RVLM were also augmented during the pro-life phase. Furthermore, pretreatment by microinjection into the bilateral RVLM of specific JNK inhibitors, JNK inhibitor I (100 pmol) or SP600125 (5 pmol), or specific p38MAPK inhibitors, p38MAPK inhibitor III (500 pmol) or SB203580 (2 nmol), exacerbated the depressor effect and blunted the augmented life-and-death signal exhibited during the pro-life phase. On the other hand, pretreatment with the negative control for JNK or p38MAPK inhibitor, JNK inhibitor I negative control (100 pmol) or SB202474 (2 nmol), was ineffective in the vehicle-controls and Mev-treatment groups. Conclusions: Our results demonstrated that activation of JNK or p38MAPK in RVLM by their upstream activators MAP2K4 or MAP2K6 plays a preferential pro-life role by sustaining the central cardiovascular regulatory machinery during experimental brain stem death via phosphorylation and activation of nuclear transcription factor ATF-2 or c-Jun. © 2012 Chang; licensee BioMed Central Ltd. Source

Cheng F.-Y.,National Cheng Kung University | Su C.-H.,Center for Translational Research in Biomedical science | Wu P.-C.,National Cheng Kung University | Yeh C.-S.,National Cheng Kung University
Chemical Communications | Year: 2010

Multifunctional Taxol-loaded PLGA nanoparticles show chemotherapeutic and photothermal destruction of cancer cells in vitro and in vivo. © The Royal Society of Chemistry 2010. Source

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