The LAMOST-Kepler (LK-) project was initiated to use the Large Sky Area Multi-Object Fiber Spectroscopic Telescope (LAMOST) to make spectroscopic follow-up observations for the targets in the field of the Kepler mission. The Kepler field is divided into 14 subfields that are adapted to the LAMOST circular field with a diameter of 5 degrees. During the regular survey phase of LAMOST, the LK-project took data from 2012 June to 2017 June and covered all the 14 subfields at least twice. In particular, we describe in this paper the second Data Release of the LK-project, including all spectra acquired through 2015 May to 2017 June together with the first round observations of the LK-project from 2012 June to 2014 September. The LK-project now counts 227 870 spectra of 156 390 stars, among which we have derived atmospheric parameters (log g, T eff and [Fe/H]) and heliocentric radial velocity (RV) for 173 971 spectra of 126 172 stars. These parameters were obtained with the most recent version of the LAMOST Stellar Parameter Pipeline v 2.9.7. Nearly one half, namely 76 283 targets, are observed both by LAMOST and Kepler telescopes. These spectra, establishing a large spectroscopy library, will be useful for the entire astronomical community, particularly for planetary science and stellar variability on Kepler targets.

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The power conversion efficiency (PCE) of 2D/3D perovskite solar cells (PSCs) is still significantly low compared with 3D PSCs due to the poor charge transport ability of 2D perovskite thin films and a large number of defects in 3D thin films. Herein, to address these two issues, multifunctional TiO2 nanoparticles (NPs)‐modified carbon nanotubes (CNT:TiO2) additives are incorporated into 3D perovskite layer for the first time, and demonstrate three positive effects for CNT:TiO2 material application: firstly, it passivates the defect state of the 3D perovskite layer and enhances the charge mobility of the 3D layer; secondly, its interaction with the 2D film increases the conductivity of the 2D layer and produces the interface polarization electric field to promote the hole extraction. As a consequence, not only the PCE of the optimized 2D/3D PSCs with the CNT:TiO2 is greatly improved to 22.7% from 19.8% of the control PSCs, but also the stability is significantly improved.

The development of a hole transport layer (HTL) with persistent high conductivity, good moisture/oxygen barrier ability, and suitable passivation ability of perovskite defects is very important for achieving high power conversion efficiency (PCE) and long‐term stability of perovskite solar cells (PSCs). However, the state‐of‐the art HTL, lithium bis(trifluoromethanesulfonyl)‐imide (Li‐TFSI)‐doped 2,2′,7,7′‐tetrakis‐(N,N‐di‐p‐methoxyphenylamine)‐9,9′‐spirobifluorene (spiro‐OMeTAD), does not have these abilities. Herein, the incorporation of antimony sulfide (Sb2S3) nanoparticles as a multifunctional additive into spiro‐OMeTAD is demonstrated. The Sb2S3 effectively improve the compactness of composite spiro‐OMeTAD:Sb2S3 HTL by inhibiting the Li‐TFSI aggregation and effectively prevent the infiltration of moisture and oxygen into the perovskite layer, resulting in its high chemical stability. More importantly, Sb2S3 not only improves the conductivity and hole mobility of the spiro‐OMeTAD:Sb2S3 through the oxidation of spiro‐OMeTAD by Sb2S3, but also makes the high conductivity more durable and stable in the atmospheric environment. In addition, Sb2S3 also effectively passivates the perovskite defects and accelerates the charge transfer from perovskite layer to HTL. As a consequence, the optimized PSCs based on spiro‐OMeTAD:Sb2S3 HTL exhibit a much higher PCE (22.13%) than that (19.29%) of the PSCs without Sb2S3 and show a greatly improved stability.

The universal N6-threonylcarbamoyladenosine (t6A) modification occurs at position 37 of tRNAs that decipher codons starting with adenosine. Mechanistically, t6A stabilizes structural configurations of the anticodon stem loop, promotes anticodon–codon pairing and safeguards the translational fidelity. The biosynthesis of tRNA t6A is co-catalyzed by two universally conserved protein families of TsaC/Sua5 (COG0009) and TsaD/Kae1/Qri7 (COG0533). Enzymatically, TsaC/Sua5 protein utilizes the substrates of L-threonine, HCO3−/CO2 and ATP to synthesize an intermediate L-threonylcarbamoyladenylate, of which the threonylcarbamoyl-moiety is subsequently transferred onto the A37 of substrate tRNAs by the TsaD–TsaB –TsaE complex in bacteria or by the KEOPS complex in archaea and eukaryotic cytoplasm, whereas Qri7/OSGEPL1 protein functions on its own in mitochondria. Depletion of tRNA t6A interferes with protein homeostasis and gravely affects the life of unicellular organisms and the fitness of higher eukaryotes. Pathogenic mutations of YRDC, OSGEPL1 and KEOPS are implicated in a number of human mitochondrial and neurological diseases, including autosomal recessive Galloway–Mowat syndrome. The molecular mechanisms underscoring both the biosynthesis and cellular roles of tRNA t6A are presently not well elucidated. This review summarizes current mechanistic understandings of the catalysis, regulation and disease implications of tRNA t6A-biosynthetic machineries of three kingdoms of life, with a special focus on delineating the structure–function relationship from perspectives of conservation and diversity.