The Large sky Area Multi-Object Fiber Spectroscopic Telescope (LAMOST) general survey is a spectroscopic survey that will eventually cover approximately half of the celestial sphere and collect 10 million spectra of stars, galaxies and QSOs. Objects in both the pilot survey and the first year regular survey are included in the LAMOST DR1. The pilot survey started in October 2011 and ended in June 2012, and the data have been released to the public as the LAMOST Pilot Data Release in August 2012. The regular survey started in September 2012, and completed its first year of operation in June 2013. The LAMOST DR1 includes a total of 1202 plates containing 2 955 336 spectra, of which 1 790 879 spectra have observed signalto-noise ratio (SNR) ≥ 10. All data with SNR ≥ 2 are formally released as LAMOST DR1 under the LAMOST data policy. This data release contains a total of 2 204 696 spectra, of which 1 944 329 are stellar spectra, 12 082 are galaxy spectra and 5017 are quasars. The DR1 not only includes spectra, but also three stellar catalogs with measured parameters: late A,FGK-type stars with high quality spectra (1 061 918 entries), A-type stars (100 073 entries), and M-type stars (121 522 entries). This paper introduces the survey design, the observational and instrumental limitations, data reduction and analysis, and some caveats. A description of the FITS structure of spectral files and parameter catalogs is also provided.

Inflammatory cytokines, especially tumor necrosis factor a (TNF-a), have been shown to inhibit osteogenic differentiation of mesenchymal stem cells (MSCs) and bone formation in estrogen deficiency-induced osteoporosis, but the mechanism responsible remains poorly understood. MicroRNAs (miRNAs) have been shown to regulate MSC differentiation. Here, we identified a novel mechanism whereby TNF-a, suppressing the functional axis of a key miRNA (miR-21) contributes to estrogen deficiency-induced osteoporosis. In this study, we screened differentially expressed miRNAs in MSCs derived from estrogen deficiency-induced osteoporosis and found miR-21 was significantly downregulated. miR-21 was suppressed by TNF-a during the osteogenesis of MSCs. Furthermore, miR-21 was confirmed to promote the osteoblast differentiation of MSCs by repressing Spry1, which can negatively regulate the osteogenic differentiation of MSCs. Upregulating miR-21 partially rescued TNF-a-impaired osteogenesis of MSCs. Blocking TNF-a ameliorated the inflammatory environment and significantly enhanced bone formation with increased miR-21 expression and suppressed Spry1 expression in ovariectomized (OVX) mice. Our results revealed a novel function for miR-21 and suggested that suppressed miR-21 may contribute to impaired bone formation by elevated TNF-a in estrogen deficiency-induced osteoporosis. This study may indicate a molecular basis for novel therapeutic strategies against osteoporosis and other inflammatory bone diseases. ß

Obesity and alcohol consumption often coexist and work synergistically to promote steatohepatitis; however, the underlying mechanisms remain obscure. Here, we demonstrated that feeding mice a high-fat diet (HFD) for as little as 3 days markedly exacerbated acute ethanol binge-induced liver neutrophil infiltration and injury. Feeding mice with a HFD for 3 months plus a single binge of ethanol induced much more severe steatohepatitis. Moreover, 3-day or 3-month HFD-plus-ethanol binge (3d-HFD+ethanol or 3m-HFD+ethanol) treatment markedly upregulated the hepatic expression of several chemokines, including chemokine (C-X-C motif) ligand 1 (Cxcl1), which showed the highest fold (approximately 20-fold and 35-fold, respectively) induction. Serum CXCL1 protein levels were markedly elevated after the HFD+ethanol treatment. Blockade of CXCL1 with a CXCL1 neutralizing antibody or genetic deletion of the Cxcl1 gene reduced the HFD+ethanol-induced hepatic neutrophil infiltration and injury; whereas overexpression of the Cxcl1 exacerbated steatohepatitis in HFD-fed mice. Furthermore, the expression of Cxcl1 mRNA was upregulated in hepatocytes, hepatic stellate cells and endothelial cells isolated from HFD+ethanol-fed mice compared to mice that were only given a HFD, with the highest fold induction observed in hepatocytes. In vitro stimulation of hepatocytes with palmitic acid upregulated the expression of Cxcl1 mRNA, and this upregulation was attenuated after treatment with ERK1/2, JNK, or NF-κB inhibitors. In addition, hepatic or serum levels of free fatty acids (FFAs) were higher in HFD+ethanol-fed mice than in the control groups. In conclusion, a HFD combined with acute ethanol consumption synergistically induces acute liver inflammation and injury via the elevation of hepatic or serum FFAs and subsequent upregulation of hepatic CXCL1 expression and promotion of hepatic neutrophil infiltration.