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Based on experience during our life, neuronal connectivity continuously changes through structural remodeling of synapses. Recent studies have shown that the complex interaction between astrocytes and synapses regulates structural synapse remodeling by inducing the formation and elimination of synapses, as well as their functional maturation. Defects in this astrocyte-mediated synapse remodeling cause problems in not only neuronal network activities but also animal behaviors. Moreover, in various neurological disorders, astrocytes have been shown to play central roles in the initiation and progression of synaptic pathophysiology through impaired interactions with synapses. In this review, we will discuss recent studies identifying the novel roles of astrocytes in neuronal circuit remodeling, focusing on synapse formation and elimination. We will also discuss the potential implication of defective astrocytic function in evoking various brain disorders.

Acamprosate, also known as N-acetyl homotaurine, is an N-methyl-d-aspartate receptor antagonist that is used for treating alcohol dependence. Although the exact mechanism of acamprosate has not been clearly established, it appears to work by promoting a balance between the excitatory and inhibitory neurotransmitters, glutamate, and gamma-aminobutyric acid, respectively. Several studies have demonstrated that acamprosate provides neuroprotection against ischemia-induced brain injury. However, no studies have been performed evaluating the effect of acamprosate on traumatic brain injury (TBI). In the present study, we sought to evaluate the therapeutic potential of acamprosate to protect against neuronal death following TBI. Rats were given oral acamprosate (200 mg/kg/d for 2weeks) and then subjected to a controlled cortical impact injury localized over the parietal cortex. Histologic analysis was performed at 3hours, 24hours, and 7days after TBI. We found that acamprosate treatment reduced the concentration of vesicular glutamate and zinc in the hippocampus. Consequently, this reduced vesicular glutamate and zinc level resulted in a reduction of reactive oxygen species production after TBI. When evaluated 24hours after TBI, acamprosate administration reduced the number of degenerating neurons, zinc accumulation, blood-brain barrier disruption, neutrophil infiltration, and dendritic loss. Acamprosate also reduced glial activation and neuronal loss at 7days after TBI. In addition, acamprosate rescued TBI-induced neurologic and cognitive dysfunction. The present study demonstrates that acamprosate attenuates TBI-induced brain damage by depletion of vesicular glutamate and zinc levels. Therefore, this study suggests that acamprosate may have high therapeutic potential for prevention of TBI-induced neuronal death.

Introduction Lumbar herniated intervertebral disc (HIVD) is a common chronic disease, and in Korea many patients use Korean medicine (KM) for treatment. However, KM clinical practice guideline (CPG) for HIVD remain poor. Therefore, this aim is to describe the KM approach for managing HIVD in Korea from an evidence-based medicine (EBM) perspective. Methods A systematic review was undertaken of literature focusing on key areas of KM practice aimed at managing HIVD. The evidence obtained was based on the study design and the risk of bias. Recommendations were formulated, taking the quality, quantity, and level of the evidence into consideration, as well as the likely clinical impact and the applicability of the evidence to KM practice in Korea. Preliminary CPGs were then recommended for the application of KM for the management of HIVD. After several rounds of expert consensus meetings, the final guideline was endorsed by relevant professional committees. Results The final recommendation was made based on a draft of the recommendations of the working group during the consensus process. A total of 15 recommendation statements were made regarding KM treatments for HIVD, which included acupuncture (n = 3), pharmacopuncture (n = 3), herbal medicine (n = 3), chuna (n = 2), moxibustion (n = 2), and cupping therapy (n = 2). Conclusions Following on from the above development, we sought to carry out a high-quality follow-up KM clinical study with the objective of improving HIVD patients understanding of medical treatments for the condition. Also, future research in this area will formally examine the success of the guideline’s implementation.

We synthesized oleic acid capped tetrapod nanocrystals of CdSe, CdTe and type II heterostructured CdTe/CdSe to investigate the effects of nanocrystal compositions and type II heterojunction on the photovoltaic properties of hybrid solar cells. The hybrid solar cell based on the blend of CdSe tetrapod nanocrystals and P3HT with a weight ratio of 6:1 showed the maximum power conversion efficiency of 1.03% under AM 1.5 G condition, and the maximum incident photon to current conversion efficiency of the solar cell was 43% at 415 nm. Although CdTe and CdTe/CdSe tetrapod nanocrystals showed relatively poor performance, the power conversion efficiency and the short circuit current density of the hybrid solar cell based on type II heterostructured CdTe/CdSe tetrapod nanocrystals was 4.4 and 3.9 times higher than that of the solar cell based on CdTe tetrapod nanocrystals, respectively. These results can be explained by the effects of nanocrystal compositions and type II heterojunction on the photovoltaic properties of hybrid solar cells.

A simple wiper coating method was introduced to coat large area of PEDOT:PSS film for the polymer solar cell module. A thin and smooth film of PEDOT:PSS was prepared by the method. The efficiency of 4.46% was obtained from the single cell having wiper-coated PEDOT:PSS layer. The efficiency is comparable to the polymer single cell prepared by spin coating method. The atomic force microscopy result confirms that the surface of the film prepared by the coating method is smooth uniform. The large area module was prepared by the method and the V OC of 5.30 V, I SC of 19.88 mA and FF of 53.29% was obtained from the polymer solar cell module. The resulted power conversion efficiency was 1.21% with on aperture size 46.2 cm 2 .

A solution processed polymer tandem cell has been fabricated by utilizing organic layer coated TiO 2 nanoparticle (OL-TiO 2 ) as an interlayer. The crystalline phase of the OL-TiO 2 was anatase. The dispersed solution of the OL-TiO 2 showed high optical transparency and excellent film forming property. The top and bottom cell were clearly separated by the OL-TiO 2 interlayer without interlayer mixing, which was not observed for the tandem cell utilizing commercially available TiO 2 nanoparticle (N-TiO 2 ) as an interlayer. The conversion efficiency of a polymer tandem cell was enhanced from 1.43% to 3.44% by replacing the interlayer from N-TiO 2 to OL-TiO 2 . The tandem cell performance was further enhanced by adjusting the thicknesses of the active layers in the subcells and adjusting the conductivity of the PEDOT:PSS layer in the bottom cell. The highest conversion efficiency of 3.66% was obtained from the tandem cell having the structure of ITO/Baytron P VP AI 4083/P3HT:PCBM (100 nm)/OL-TiO 2 /Baytron PH 500/P3HT:PCBM (100 nm)/Al. In addition that, it was found that the OL-TiO 2 interlayer enhanced the stability of the tandem cell comparing to that of the single junction cell by the reduction of the oxygen diffusion to the bottom layer by the interlayer. It is expected that the performance of the tandem cell can be further enhanced by adopting efficient low band gap materials.

In zebrafish, the endoderm originates at the blastula stage from the most marginal blastomeres. Through a series of complex morphogenetic movements and differentiation events, the endodermal germ layer gives rise to the epithelial lining of the digestive tract as well as its associated organs such as the liver, pancreas, and swim bladder. How endodermal cells differentiate into distinct cell types such as hepatocytes or endocrine and exocrine pancreatic cells remains a major question. In a forward genetic screen for genes regulating endodermal organ development, we identified mutations at the shiri locus that cause defects in the development of a number of endodermal organs including the liver and pancreas. Detailed phenotypic analyses indicate that these defects are partially due to a reduction in endodermal expression of the hairy/enhancer of split-related gene, her5, at mid to late gastrulation stages. Using the Tg(0.7her5:EGFP)ne2067 line, we show that her5 is expressed in the endodermal precursors that populate the pharyngeal region as well as the organ-forming region. We also find that knocking down her5 recapitulates some of the endodermal phenotypes of shiri mutants, further revealing the role of her5 in endoderm development. Positional cloning reveals that shiri encodes Med12, a regulatory subunit of the transcriptional Mediator complex recently associated with two human syndromes. Additional studies indicate that Med12 modulates the ability of Casanova/Sox32 to induce sox17 expression. Thus, detailed phenotypic analyses of embryos defective in a component of the Mediator complex have revealed new insights into discrete aspects of vertebrate endoderm development, and provide possible explanations for the craniofacial and digestive system defects observed in humans with mutations in MED12.

The cellular origin of signals that regulate pancreatic beta cell induction is not clearly defined. Here, we investigate the seeming paradox that Hedgehog/Smoothened signaling functions during gastrulation to promote pancreatic beta cell development in zebrafish, yet has an inhibitory role during later stages of pancreas development in amniotes. Our cell transplantation experiments reveal that in zebrafish, Smoothened function is not required in beta cell precursors. At early somitogenesis stages, when the zebrafish endoderm first forms a sheet, pancreatic beta cell precursors lie closest to the midline; however, the requirement for Smoothened lies in their lateral neighbors, which ultimately give rise to the exocrine pancreas and intestine. Thus, pancreatic beta cell induction requires Smoothened function cell-nonautonomously during gastrulation, to allow subsequent intra-endodermal interactions. These results clarify the function of Hedgehog signaling in pancreas development, identify an unexpected cellular source of factors that regulate beta cell specification, and uncover complex patterning and signaling interactions within the endoderm.

It has been reported from our laboratories that expression of CYP2E1 significantly increased and decreased in rats with acute renal failure induced by uranyl nitrate (U-ARF) treated with recombinant human growth hormone (rGH) for one day (U-ARF1) compared with those in control rats and rats with U-ARF, respectively. Chlorzoxazone (CZX) primarily undergoes hydroxylation to form 6-hydroxychlorzoxazone (OH-CZX) catalyzed mainly by CYP2E1 in rats. Hence, the effects of rGH on the pharmacokinetics of intravenous CZX (20 mg/kg) were investigated in rats with U-ARF. Based on CYP2E1 expression, it could be expected that in rats with U-ARF1, the formation of OH-CZX significantly increased and decreased compared with those in control rats and rats with U-ARF, respectively. This was proven in the following results. First, the total area under the plasma concentration-time curve from time zero to 8 hr (AUC(0--8 hr)) of OH-CZX in rats with U-ARF1 (36,100 microg min/ml) was significantly greater and smaller than those in control rats (1040 microg min/ml) and rats with U-ARF (50,300 microg min/ml), respectively. Second, the AUC(0--8 hr, OH-CZX)/AUC(CZX) ratio in rats with U-ARF1 (28.9) was significantly greater and smaller than those in control rats (0.468) and rats with U-ARF (72.6), respectively.