Alzheimer’s disease (AD) is characterized by the accumulation of β-amyloid peptide (Aβ) and loss of neurons. Recently, a growing body of evidences have indicated that as a herbal compound naturally derived from grapes, resveratrol modulates the pathophysiology of AD, however, with a largely unclear mechanism. Therefore, we aimed to investigate the protection of resveratrol against the neurotoxicity of β-amyloid peptide 25–35 (Aβ25–35) and further explore its underlying mechanism in the present study. PC12 cells were injuried by Aβ25–35, and resveratrol at different concentrations was added into the culture medium. We observed that resveratrol increased cell viability through the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and lactate dehydrogenase (LDH) colorimetric assays. Flow cytometry indicated the reduction of cell apoptosis by resveratrol. Moreover, resveratrol also stabilized the intercellular Ca2+ homeostasis and attenuated Aβ25–35 neurotoxicity. Additionally, Aβ25–35-suppressed silent information regulator 1 (SIRT1) activity was significantly reversed by resveratrol, resulting in the downregulation of Rho-associated kinase 1 (ROCK1). Our results clearly revealed that resveratrol significantly protected PC12 cells and inhibited the β-amyloid-induced cell apoptosis through the upregulation of SIRT1. Moreover, as a downstream signal molecule, ROCK1 was negatively regulated by SIRT1. Taken together, our study demonstrated that SIRT1-ROCK1 pathway played a critical role in the pathomechanism of AD.

Gold nanoparticles (Au NPs) have a wide range of applications because of their localized surface plasmon resonance properties. Femtosecond laser is considered to be an effective method for preparing Au NPs because of its characteristics of ultrashort irradiation periods and ultrahigh intensities. In this study, a novel method is proposed to produce an Au NP-attached substrate using the spatially and temporally shaped femtosecond laser. Laser-induced periodic surface structures (LIPSS) are designed to obtain the localized optical field enhancement, which leads to the femtosecond laser spatially reshaping, enabling the deposition of Au NPs by photoreduction on silicon substrates. The Au NPs prepared by this method exhibit morphological controllability and chemical stability, especially excellent spatial selectivity and uniformity, resulting in the tunable and stable surface-enhanced Raman scattering (SERS) applications. Also, the temporally shaped femtosecond pulses are introduced to further increase the enhancement factors of the SERS. This method successfully achieves the controllable morphology synthesis and selective deposition of Au NPs on the substrate simultaneously, which provides a promising candidate for SERS substrates fabrication, and holds potential applications in optoelectronics, such as molecular detection and biosensors.

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Spina bifida, which results from failure of fusion in the spinal region of neural tube, is among the most common birth defects associated with diabetic pregnancy. However, the mechanism underlying maternal diabetes-induced congenital malformations including spina bifida is not fully understood. It was hypothesized that hyperglycemic conditions affect the proliferation and apoptosis of neural progenitor cells in the developing spinal neural tube, leading to abnormal neurodevelopment. In the present study, biological processes such as proliferation and apoptosis were investigated in the neuroepithelial cells of the developing spinal neural tube of embryos from diabetic mice, and in embryonic spinal neural tube derived neural progenitor cell cultures exposed to high glucose in vitro. Maternal diabetes caused decreased proliferation and increased apoptosis of the neuroepithelial cells in the developing spinal cord of embryos from diabetic mouse. Decreased proliferation and increased apoptosis were also found in neural progenitor cells exposed to high glucose. In addition, high glucose-induced apoptosis in neural progenitor cells was associated with activation of caspase-3. Thus, high glucose disturbs both proliferation and cell death of neural progenitors in the developing spinal neural tube. This could provide a cellular mechanism by which maternal hyperglycemia induces spina bifida in embryos from diabetic pregnancy.

We investigate the current and temperature dependence of GaN-based high power blue light-emitting diodes and identify a set of temperature sensitive optical parameters (TSOPs) that can provide a real-time solution for determining the junction temperature (T-j). The relationships among T-j, forward current and TSOPs, "center of mass" wavelength, and, in particular, full width at half maximum (FWHM) have been studied, and the relevant mathematic models have been developed. The analysis indicates that using FWHM may yield higher accuracy than using other parameters as TSOPs. (C) 2012 American Institute of Physics. [http://dx.doi.org/10.1063/1.4718612]Major Science and Technology Project between University-Industry Cooperation in Fujian Province [2011H6025]; "863 Solid-State Lighting Project" of China [2006AA03A175]; NSF [11104230]; NSF of Fujian Province [2008J0030]; CR

Islet cell transplantation is one of the most promising therapies for diabetes mellitus (DM). However, the limited availability of purified islets for transplantation and the risk of immunological rejection severely limit its use. In vitro transdifferentiation of autologous bone marrow-derived mesenchymal stem cells (BMSCs) into insulin-producing cells (IPCs) could provide an abundant source of cells for this procedure and avoid immunological rejection. Here, we isolated and characterized BMSCs and induced their in vitro differentiation into IPCs. Reverse-transcription polymerase chain reaction analysis revealed that these IPCs could express Ins1, Ins2, glucagon, glucose transporter 2, and pancreatic duodenal homeobox-1. Insulin production by the IPCs was confirmed by immunocytochemistry and Western blot analysis. On this basis, donor rats supplying BMSCs were made diabetic by a single intraperitoneal injection of streptozotocin. The IPCs were then autologously transplanted into the duodenal submucosa of diabetic rats. Grafted cells could be visualized in sections after 2, 4, and 8 weeks by immunohistochemical staining for insulin. Furthermore, in the IPC-implanted group, hyperglycemia was normalized, compared with a persistent increase in glucose levels in the diabetic group and intraperitoneal glucose tolerance test-induced responses were observed in the IPC-implanted group. These results on autologous transplantation of IPCs derived from BMSCs into the duodenal wall could offer a novel potential therapeutical protocol for DM. Anat Rec, 292:728-735, 2009. V V C 2009 Wiley-Liss, Inc.

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