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We have identified and isolated a novel human gene, HMBOX1 (homeobox containing 1) from a pancreatic cDNA library. Human HMBOX1 is widely expressed in 18 tissues, and it is highly expressed in pancreas. According to the genome database, HMBOX1 is located at the boundary of 8p12.3 and 8p21.1. HMBOX1 proteins are highly conserved in human, mouse, rat, chicken and Xenopus laevis. A phylogenetic tree shows that HMBOX1 may represent a distinct group in HNF (Hepatocyte Nuclear Factor) transcriptional factors. Functional HMBOX1::EGFP (enhanced green fluorescent protein) fusion protein revealed that HMBOX1 accumulated more in cytoplasm than in nucleus. Co-transfection of HEK-293T cells with pM-HMBOX1 plasmid and reporter plasmid pGAL4₅tkLUC indicates that HMBOX1 is a transcription repressor. In situ hybridization on paraffin sections of mouse tissues demonstrated that Hmbox1 is widely expressed in pancreas and the expression of this gene can also be detected in pallium, hippocampus and hypothalamus.

Spinal cord injury (SCI) leads to a loss of sensitive and motor functions. Currently, there is no therapeutic intervention offering a complete recovery. Here, we report that repetitive trans-spinal magnetic stimulation (rTSMS) can be a noninvasive SCI treatment that enhances tissue repair and functional recovery. Several techniques including immunohistochemical, behavioral, cells cultures, and proteomics have been performed. Moreover, different lesion paradigms, such as acute and chronic phase following SCI in wild-type and transgenic animals at different ages (juvenile, adult, and aged), have been used. We demonstrate that rTSMS modulates the lesion scar by decreasing fibrosis and inflammation and increases proliferation of spinal cord stem cells. Our results demonstrate also that rTSMS decreases demyelination, which contributes to axonal regrowth, neuronal survival, and locomotor recovery after SCI. This research provides evidence that rTSMS induces therapeutic effects in a preclinical rodent model and suggests possible translation to clinical application in humans. Keywords Rehabilitation. spinal cord injury. glial scar. magnetic stimulation and neuroregeneration Abbreviations BDA biotinylated dextran amine DAPI 4′,6-diamidino-2-phénylindole GFAP glial fibrillary acidic protein Iba1 ionized calcium-binding adapter molecule 1 MBP myelin basic protein * C. Chalfouh

Traumatic brain injury (TBI) is a devastating condition, often leading to life-long consequences for patients. Even though modern neurointensive care has improved functional and cognitive outcomes, efficient pharmacological therapies are still lacking. Targeting peripherally derived, or resident inflammatory, cells that are rapid responders to brain injury is promising, but complex, given that the contribution of inflammation to exacerbation versus improved recovery varies with time post-injury. The injury-induced inflammatory response is triggered by release of alarmins, and in the present study we asked whether interleukin-33 (IL-33), an injury-associated nuclear alarmin, is involved in TBI. Here, we used samples from human TBI microdialysate, tissue sections from human TBI, and mouse models of central nervous system injury and found that expression of IL-33 in the brain was elevated from nondetectable levels, reaching a maximum after 72 h in both human samples and mouse models. Astrocytes and oligodendrocytes were the main producers of IL-33. Post-TBI, brains of mice deficient in the IL-33 receptor, ST2, contained fewer microglia/macrophages in the injured region than wild-type mice and had an altered cytokine/chemokine profile in response to injury. These observations indicate that IL-33 plays a role in neuroinflammation with microglia/macrophages being cellular targets for this interleukin post-TBI.