Lithographic precision is as or more important than resolution. For decades, the semiconductor industry has been able to work with Ϯ5% precision. However, for other applications such as micronanoelectromechanical systems, optical elements, and biointerface applications, higher precision is desirable. Lyding et al. ͓Appl. Phys. Lett. 64, 11 ͑1999͔͒ have demonstrated that a scanning tunneling microscope can be used to remove hydrogen ͑H͒ atoms from a silicon ͑100͒ 2 ϫ 1 H-passivated surface through an electron stimulated desorption process. This can be considered e-beam lithography with a thin, self-developing resist. Patterned hydrogen layers do not make a robust etch mask, but the depassivated areas are highly reactive since they are unsatisfied covalent bonds and have been used for selective deposition of metals, oxides, semiconductors, and dopants. The depassivation lithography has shown the ability to remove single H atoms, suggesting the possibility of precise atomic patterning. This patterning process is being developed as part of a project to develop atomically precise patterned atomic layer epitaxy of silicon. However, significant challenges in sample preparation, tip technology, subnanometer pattern placement, and patterning throughput must be overcome before an automated atomic precision lithographic technology evolves.

Microglia are the resident immune cells in the central nervous system (CNS). After traumatic spinal cord injury (SCI), microglia undergo activation, proliferation, and changes in gene and protein expression and morphology, with detrimental and beneficial effects. Activated microglia cause secondary neuronal injury via the production of proinflammatory cytokines, reactive oxygen species, and proteases. However, activated microglia also promote neuronal repair through the secretion of anti-inflammatory growth factors and cytokines. Proinflammatory cytokines increase endothelial permeability, promote A1 astrocyte activation and axonal demyelination, and reduce neural stem/progenitor cells (NSPCs), leading to the exacerbation of neuronal injury. In contrast, anti-inflammatory factors facilitate angiogenesis, reduce reactive astrocytes, and promote axonal remyelination and the propagation of NSPCs, contributing to tissue repair and locomotor recovery. Due to its limited regenerative capacity, the CNS requires beneficial microglia for continuous protection against injury. Understanding and regulating microglial activation status are beneficial to reducing detrimental effects and promoting repair behaviors and to obtain more information on efficient therapies for traumatic SCI. This review discusses microglial activation and the differences between microglia and similar immune cells, microglial interactions with other cells in the spinal cord, and the progress in the development of therapies targeting microglia in SCI.

The mechanisms underlying the potentially beneficial effect of bone marrow stem cells (BMSCs) on spinal cord injury (SCI) are unknown. Therefore, the aim of the present study was to explore the protective effect of BMSCs in rats with SCI. A total of 45 adult male Sprague-Dawley rats were randomly divided into three groups; the SCI group (n=15), the BMSC group (n=15) and the sham-operation group (n=15). In the SCI and BMSC treatment groups, a modified Allen’s weight-drop technique was used to induce SCI. The BMSC treatment group received an injection of BMSCs using a microneedle into the epicenter of the spinal cord 24 h after injury. Rats in the sham-operation group were not subjected to SCI; however, the corresponding vertebral laminae were removed. Seven days after transplantation, a rapid recovery was observed in the Basso, Beattie and Bresnahan (BBB) scores of the BMSC treatment group, whereas the BBB scores in the SCI group remained low (P<0.05). Caspase-12 expression in the SCI group was increased compared with that in the sham-operation group, whereas caspase-12 expression was attenuated 24 h after transplantation in the BMSC treatment group (P<0.05). In conclusion, the transplantation of BMSCs may improve locomotor function and attenuate caspase-12 expression following SCI. Therefore, it is likely to be an effective strategy for preventing severe injury of the spinal cord.

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