Direct neural decompression is not always necessary, and the majority of patients can be treated with a less-invasive procedure such as short-segment posterior spinal fusion with indirect decompression combined with vertebroplasty. The high-priority issue is careful evaluation of patients' general health and osteoporosis severity, so that the surgeon can choose the procedure best suited for each patient.

Background:LacCer is known to regulate PLA 2 activity in cells, but the precise mechanisms have not been elucidated. Results: LacCer binds to cPLA 2 ␣ and increases its enzymatic activity. Conclusion: LacCer is identified as a novel and direct activator of cPLA 2 ␣. Significance: This research provides new insights into the regulatory mechanisms of cPLA 2 ␣ and the physiological functions of LacCer as a signaling molecule.

This study elucidated symptoms specific to anatomical pathology or compressed segments in thoracic myelopathy. These relationships can be helpful in the initial investigation of thoracic diseases, although additional measures such as MRI or CT are necessary for definitive diagnosis.

The cFos immunostaining allowed the identification of multiple populations of neurons involved in the generation of paradoxical sleep. We adopted the transgenic (targeted recombination in active populations) mouse model, which following injection of tamoxifen, allows expression of Cre-dependent reporter constructs (i.e., mCherry) in neurons expressing cFos during waking or paradoxical sleep hypersomnia following automatic paradoxical sleep deprivation. Three groups of mice were subjected to two periods of waking, one period of waking and one of paradoxical sleep hypersomnia, or two periods of paradoxical sleep hypersomnia. A high percentage of doublelabelled neurons was observed in the lateral hypothalamic area and zona incerta of two periods of waking and two periods of paradoxical sleep hypersomnia in mice, but not in those of one period of waking and one of paradoxical sleep hypersomnia in animals. Melanin-concentrating hormone neurons in the lateral hypothalamic area and Lhx6+ cells in the zona incerta constituted 5.7 ± 1.5% and 8.8 ± 2.3% of all mCherry+ cells and 20.6 ± 4.8% and 24.6 ± 5.9% of all cFos+ neurons in two periods of paradoxical sleep hypersomnia in animals. In addition, melanin-concentrating hormone cells as well as Lhx6+ neurons rarely expressed mCherry (or cFos) in the waking condition, in contrast to orexin neurons, which constituted approximately 30% of mCherry+ and cFos+ neurons. Our results validate the TRAP methodology and open the way to use it for identifying the neurons activated during waking and paradoxical sleep hypersomnia. Furthermore, they indicate for the first time that Lhx6+ neurons in the zona incerta, like melanin-concentrating hormone cells in the lateral hypothalamic area, are activated during paradoxical sleep hypersomnia but not during waking. These results indicate that Lhx6+ neurons might play a role in the control of paradoxical sleep, like the melanin-concentrating hormone cells. K E Y W O R D S hypothalamic neuropeptides, sleep-wake cycle 2 of 11 | LEE Et aL. 1 | INTRODUC TI ON The cFos immunostaining has long been utilized to identify the neurons activated during waking (W), slow-wave sleep (SWS) and paradoxical (i.e., rapid eye movement [REM]) sleep (PS). By this means,