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The ability to use induced pluripotent stem cells（i PSC）to model brain diseases is a powerful tool for unraveling mechanistic alterations in these disorders.Rodent models of brain diseases have spurred understanding of pathology but the concern arises that they may not recapitulate the full spectrum of neuron disruptions associated with human neuropathology.iPSC derived neurons,or other neural cell types,provide the ability to access pathology in cells derived directly from a patient＇s blood sample or skin biopsy where availability of brain tissue is limiting.Thus,utilization of iPSC to study brain diseases provides an unlimited resource for disease modelling but may also be used for drug screening for effective therapies and may potentially be used to regenerate aged or damaged cells in the future.Many brain diseases across the spectrum of neurodevelopment,neurodegenerative and neuropsychiatric are being approached by iPSC models.The goal of an iPSC based disease model is to identify a cellular phenotype that discriminates the disease-bearing cells from the control cells.In this mini-review,the importance of iPSC cell models validated for pluripotency,germline competency and function assessments is discussed.Selected examples for the variety of brain diseases that are being approached by iPSC technology to discover or establish the molecular basis of the neuropathology are discussed.

Receptor for activated C kinase 1（RACK1）is an evolutionarily conserved scaffolding protein within the tryptophan-aspartate（WD）repeat family of proteins.RACK1 can bind multiple signaling molecules concurrently,as well as stabilize and anchor proteins.RACK1 also plays an important role at focal adhesions,where it acts to regulate cell migration.In addition,RACK1 is a ribosomal binding protein and thus,regulates translation.Despite these numerous functions,little is known about how RACK1 regulates nervous system development.Here,we review three studies that examine the role of RACK1 in neural development.In brief,these papers demonstrate that（1）RACK-1,the C.elegans homolog of mammalian RACK1,is required for axon guidance;（2）RACK1 is required for neurite extension of neuronally differentiated rat PC12cells;and（3）RACK1 is required for axon outgrowth of primary mouse cortical neurons.Thus,it is evident that RACK1 is critical for appropriate neural development in a wide range of species,and future discoveries could reveal whether RACK1 and its signaling partners are potential targets for treatment of neurodevelopmental disorders or a therapeutic approach for axonal regeneration.

Semaphorins were originally identified as axon guidance factors involved in the development of the neuronal system. However, accumulating evidence indicates that several members of semaphorins, so-called ＇immune semaphorins＇, are crucially involved in various phases of immune responses. These semaphorins regulate both immune cell interactions and immune cell trafficking during physiological and pathological immune responses. Here, we review the following two functional aspects of semaphorins and their receptors in immune responses： their functions in cell-cell interactions and their involvement in immune cell trafficking.

Fibroblast growth factors （FGFs） can be classified as secretory （FGFI-10 and FGF15-23） or intracellular non-secretory forms （FGF 11-14）. Secretory forms of FGF and their receptors are best known for their regulatory roles in cell growth, differentiation and morphogenesis in the early stages of neural development. However, the functions of intracellular FGFs remain to be ex- plored. FGF12 and FGF14 are found to interact with voltage-gated sodium channels, and regulate the channel activity in neu- rons. FGF13 is expressed in primary sensory neurons, and is colocalized with sodium channels at the nodes of Ranvier along the myelinated afferent fibers. FGF13 is also expressed in cerebral cortical neurons during the late developmental stage. A re- cent study showed that FGFI3 is a microtubule-stabilizing protein required for regulating the neuronal development in the cerebral cortex. Thus, non-secretory forms of FGF appear to have important roles in the brain, and it would be interesting to further investigate the functions of intracellular FGFs in the nervous system and in neural diseases.

Aim： Our previous studies have showed that ursodeoxycholic acid （UA） and jasminoidin （JA） effectively reduce cerebral infarct volume in mice. In this study we explored the pure synergistic mechanism of these compounds in treatment of mouse cerebral ischemia, which was defined as synergistic actions specific for phenotype variations after excluding interference from ineffective compounds. Methods： Mice with focal cerebral ischemia were treated with UA, JA or a combination JA and UA （JU）. Concha margaritifera （CM） was taken as ineffective compound. Cerebral infarct volume of the mice was determined, and the hippocampi were taken for microarray analysis. Particular signaling pathways and biological functions were enriched based on differentially expressed genes, and corresponding networks were constructed through Ingenuity Pathway Analysis. Results： In phenotype analysis, UA, JA, and JU significantly reduced the ischemic infarct volume with JU being superior to UA or JA alone, while CM was ineffective. As a result, 4 pathways enriched in CM were excluded. Core pathways in the phenotype-positive groups （UA or JA） were involved in neuronal homeostasis and neuropathology. JU-contributing pathways included all UA-contributing and the majority （71.7%） of JA-contributing pathways, and 10 new core pathways whose effects included inflammatory immunity, apoptosis and nervous system development. The functions of JU group included all functions of JA group, the majority （93.1%） of UA-contributing functions, and 3 new core functions, which focused on physiological system development and function. Conclusion： The pure synergism between UA and JA underlies 10 new core pathways and 3 new core functions, which are involved in inflammation, immune responses, apoptosis and nervous system development.

Axonal and dendritic outgrowth are fundamental processes in the development of the nervous system.During this period neurons change their morphology from a simple bipolar shape into a mature complex shape.Neurons develop dendrites and extend long or short axons that travel through a complex path until reaching target cells and form functional and accurate neuronal circuits.

Neural cell differentiation and maturation is a critical step during central nervous system devel-opment. The oligodendrocyte transcription family （Olig family） is known to be an important factor in regulating neural cell differentiation. Because of this, the Olig family also affects acute and chronic central nervous system diseases, including brain injury, multiple sclerosis, and even gliomas. Improved understanding about the functions of the Olig family in central nervous system development and disease will greatly aid novel breakthroughs in central nervous system diseases. This review investigates the role of the Olig family in central nervous system develop- ment and related diseases.

Adolescence is a critical period for neurodevelopment. Evidence from animal studies suggests that isolated rearing can exert negative effects on behavioral and brain development. The present study aimed to investigate the effects of adolescent social isolation on latent inhibition and brain-derived neurotrophic factor levels in the forebrain of adult rats. Male Wistar rats were randomly divided into adolescent isolation （isolated housing, 38-51 days of age） and social groups. Latent inhibition was tested at adulthood. Brain-derived neurotrophic factor levels were measured in the medial prefrontal cortex and nucleus accumbens by an enzyme-linked immunosorbent assay. Adolescent social isolation impaired latent inhibition and increased brain-derived neurotrophic factor levels in the medial prefrontal cortex of young adult rats. These data suggest that adolescent social isolation has a profound effect on cognitive function and neurotrophin levels in adult rats and may be used as an animal model of neurodevelopmental disorders.

The primary role of the gonadal steroid hormones in mammals is to regulate reproduction and related behaviors; however, both androgens and estrogens are also integrally involved in mediating higher brain function and processes including cognition, neural development, and neural plasticity. In particular, a number of studies show that estradiol modulates dendritic spine growth and synapse density （synaptic plasticity） in the hippocampus of females, and that increased estradiol levels are generally associated with improvements on a variety of learning and memory tasks. While the majority of research has focused on the beneficial effects of estradiol in females, much less attention has been given to testosterone and its effects on learning and memory in males. Similar to estradiol titers in females, testosterone titers in males decline with age, albeit more gradually, and this decline has been correlated with impairment of certain cognitive tasks. Moreover, studies involving both humans and animals indicate that testosterone and its metabolites can augment responding on certain behavioral tasks, depending on the subject＇s current hormonal state, the response required, and the stimuli involved （e.g., those involving spatial or nonspatial stimuli）. While the exact mechanisms by which testosterone exerts its effects on learning and memory are not fully understood, recent findings suggest that testosterone modulates learning and memory in males through an interaction with the cholinergic system. The overall objective of this review is to discuss studies investigating the role of the gonadal hormones in mediating learning and memory processes in male mammals [Current Zoology 57 （4）： 543-558, 2011].

Sir, the recent report on ＂ultrasound measurement of the corpus callo- sum and neural development＂ is very interesting[1]. Liu et al. reported that ＂corpus callosum growth in premature infants is associated with neurobehavioral development during the early extrauterine stage[1].＂ In fact, the use of 3D ultrasound seems to be useful to determine corpus callosum abnormality[2]. However, the genetic counseling based on its result remains controversial[2]. Santo et al. found that normal outcome could be observed in about 65-75% of cases with detected abnormali- ties of corpus callosum[3]. The diagnostic sensitivity of the ultrasound is also the topic to be considered[4]. Inaccuracy of ultrasound can be commonly seen and this leads to the requirement of additional MRI investigation[5].