The bovine genetic resources in China are diverse, but their value and potential are yet to be discovered. To determine the genetic diversity and population structure of Chinese cattle, we analysed the whole genomes of 46 cattle from six phenotypically and geographically representative Chinese cattle breeds, together with 18 Red Angus cattle (RAN) genomes, 11 Japanese black cattle (JBC) genomes and taurine and indicine genomes available from previous studies. Our results showed that Chinese cattle originated from hybridization between Bos taurus and Bos indicus. Moreover, we found that the level of genetic variation in Chinese cattle depends upon the degree of indicine content. We also discovered many potential selective sweep regions associated with domestication related to breed-specific characteristics, with selective sweep regions including genes associated with coat colour (ERCC2, MC1R, ZBTB17 and MAP2K1), dairy traits (NCAPG, MAPK7, FST, ITFG1, SETMAR, PAG1, CSN3 and RPL37A), and meat production/quality traits (such as BBS2, R3HDM1, IGFBP2, IGFBP5, MYH9, MYH4 and MC5R). These findings substantially expand the catalogue of genetic variants in cattle and reveal new insights into the evolutionary history and domestication traits of Chinese cattle.

Resveratrol could be beneficial to health and provides protection against a wide array of pathologies and age-associated problems, as evident from preclinical studies. However, a comparison of animal and human studies reveals that this dietary polyphenol cannot protect against metabolic diseases and their associated complications. The clinical outcomes are affected by many factors such as sample size. This article not only presents a comprehensive review of the current advances concerning the dose, the extent of absorption, interaction and toxicity of resveratrol in human studies, but also describes its therapeutic effects against several chronic diseases such as diabetes mellitus, obesity, cardiovascular diseases, cancer and aging and the related diseases.

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Excitotoxicity induced by NMDA receptor-mediated intracellular Ca 2+ ([Ca 2+ ] i ) overload is a major cause of delayed neuronal death in cerebral ischemia. Transient receptor potential canonical (TRPC) 6 protects neurons from ischemic brain damage. However, the mechanisms by which TRPC6 protects neurons are largely unknown. Here, we reported that TRPC6 suppressed the [Ca 2+ ] i elevation induced by NMDA and protected neurons from excitotoxicity. Over-expressing or down-regulating TRPC6 suppressed or aggravated Ca 2+ overload under excitotoxicity, respectively. TRPC6 protected cultured neurons from damage caused by NMDA toxicity or oxygen glucose deprivation (OGD). Moreover, the infarct volume in TRPC6 transgenic (Tg) mice was smaller than that in wild-type (WT) littermates. The TRPC6 Tg mice had better behavior performance and lower mortality than their WT littermates. Thus, TRPC6 inhibited NMDA receptor-triggered neurotoxicity and protected neurons from ischemic brain damage. Increase in TRPC6 activity could be a potential strategy for stroke prevention and therapy. Keywords: excitotoxicity, focal ischemia, neuroprotection, transgenic mice, TRPC6. Excitotoxicity elicited by excitatory amino acid releasing during ischemia-reperfusion process is a major factor inducing ischemic insults in cerebral stroke (Dirnagl et al. 1999;Lo et al. 2003). Overactivation of NMDA receptors is a key event in excitotoxicity that acutely elevates the [Ca 2+ ] i concentration of neurons in a short time (Sattler et al. 1998;Arundine and Tymianski 2004). This sudden Ca 2+ overload in neurons activates several endonucleases, kinases, and proteases that induce severe damage to cell functions and constructions, and finally leads to cell apoptosis or necrosis (Szydlowska and Tymianski 2010). Furthermore, a wealth of evidence indicates that suppressing the Ca 2+ overload by blocking NMDA receptors can be neuroprotective in various experiment models. However, directly inhibiting NMDA receptors by antagonists for the treatment of stroke could induce severe adverse effects in the central nervous system (CNS) (Smith 2003). Finding endogenous pathways that block NMDA toxicity might provide new approaches for stroke therapy.TRPC proteins belong to the TRP superfamily. They form Ca 2+ -permeable non-selective cation channels in various cell types in mammals. TRPC family has seven members falling into four subgroups based on sequence similarity: TRPC1, TRPC2, TRPC3/6/7, and TRPC4/5. Homo-or hetero-tetramers of these subunits form functional channels (Clapham 2003;Vazquez et al. 2004). TRPC channels have high expression levels in all the regions of the CNS (Riccio et al. 2002) and have various roles, including growth cone guidance (Li et al. 2005), fear memory (Riccio et al. 2009), and neuronal development (Jia et al. 2007;Tai et al. 2008;Zhou et al. 2008). In TRPC family, TRPC6 is notable for its important roles in Received June 27, 2012; revised manuscript received September 26, 2012; accepted September 27, 2012. Address c...

Sonic hedgehog (Shh), both as a mitogen and as a morphogen, plays an important role in cell proliferation and differentiation during early development. Here, we show that Shh inhibits glutamate transporter activities in neurons, rapidly enhances extracellular glutamate levels, and affects the development of epilepsy. Shh is quickly released in response to epileptic, but not physiological, stimuli. Inhibition of neuronal glutamate transporters by Shh depends on heterotrimeric G protein subunit Ga i and enhances extracellular glutamate levels. Inhibiting Shh signaling greatly reduces epileptiform activities in both cell cultures and hippocampal slices. Moreover, pharmacological or genetic inhibition of Shh signaling markedly suppresses epileptic phenotypes in kindling or pilocarpine models. Our results suggest that Shh contributes to the development of epilepsy and suppression of its signaling prevents the development of the disease. Thus, Shh can act as a modulator of neuronal activity, rapidly regulating glutamate levels and promoting epilepsy.