The Lhasa terrane is one of the major segments of the Tibetan Plateau, with widespread Mesozoic to Cenozoic magmatic and metallogenic records. Here, we investigate timing and characteristics of magmatism associated with the Lunggar Fe skarn deposit in Central Lhasa. We also present Sr–Nd–Pb and Hf (zircon) isotopic data on three associated intrusions to gain insights on the tectonic and metallogenic evolution of the region. Our data reveal at least two magmatic pulses in Lunggar represented by Early Cretaceous I‐type granodiorite (112.9 ± 1.5 Ma) and granite porphyry (112.6 ± 1.3 Ma) with magma generation related to slab break‐off associated with the Bangong–Nujiang Ocean during closure of the Meso‐Tethyan ocean at ~113 Ma. Iron skarn mineralization at Lunggar was contemporaneous with local Early Cretaceous intrusive activity. Following this, Late Cretaceous adakitic diorite (90.5 ± 1.5 Ma) formed from delaminated thickened crust at ~91 Ma related to the northern subduction of the Yarlung‐Zangbo oceanic plate. We also provide a comprehensive review of the Cretaceous tectonic evolution of Central Lhasa, which trace the tectonic evolution as follows: (a) 145–120 Ma: southward subduction of the Bangong–Nujiang oceanic plate under the Lhasa terrane; (b) 120–115 Ma: Lhasa‐Qiangtang continental collision; (c) 115–110 Ma: slab break‐off of the Bangong–Nujiang Ocean; (d) 110–95 Ma: crustal thickening of the Central Lhasa lower crust; (e) 95–80 Ma: delamination of lithospheric mantle; and (f) 80–65 Ma: northward subduction of the Yarlung‐Zangbo oceanic plate and subsequent slab rollback. The related metallogenic events in Central Lhasa include (a) ~115–110 Ma skarn Fe mineralization associated with slab break‐off; (b) ~90–80 Ma porphyry Cu–Au mineralization formed in delaminated thickened crust of Central Lhasa; and (c) ~65 Ma skarn Pb–Zn mineralization produced from slab rollback of the Yarlung‐Zangbo Ocean.

Spinal cord injury (SCI) results in a series of severe dysfunction of sensory and motor functions, while the molecular mechanisms that cause these dysfunctions remain elusive. Using proteomics technology, Western blot (WB), and immunohistochemistry (IHC), we found endoplasmic reticulum protein 29 (ERp29) was substantially downregulated in the motor cortex 3 days postoperation (dpo) after spinal cord transection (SCT, T10) followed by a gradual recovery 28 dpo. IHC showed that ERp29 is expressed in cortical neurons. In order to investigate the role of ERp29 in axotomized cortical neurons, we developed an in vitro axotomy injury model. ERp29 overexpression in cortical neurons after axotomy protected them from apoptosis; prevented the reduction of the number of neurons, and prevented reduction of neurite length. Moreover, we found that ERp29 overexpression increased neuronal regeneration assessed by neurite number and length. Furthermore, overexpression of ERp29 in cortical neurons after axotomy increased expression of Erk-1 and PI3K while decreasing the expression of caspase-3 expression. The present data therefore provides evidence to address the role of ERp29 in axotomized cortical neurons and identifies new therapeutic targets for the treatment of SCI.