Optical Imaging of the Motor Cortex Following Antidromic Activation of the Corticospinal Tract after Spinal Cord Injury.

Spinal cord injury (SCI) disrupts neuronal networks of ascending and descending tracts at the site of injury, leading to a loss of motor function. Restoration and new circuit formation are important components of the recovery process, which involves collateral sprouting of injured and uninjured fibers. The present study was conducted to determine cortical responses to antidromic stimulation of the corticospinal tracts, to compare changes in the reorganization of neural pathways within normal and spinal cord-injured rats, and to elucidate differences in spatiotemporal activity patterns of the natural progression and reorganization of neural pathways in normal and SCI animals using optical imaging. Optical signals were recorded from the motor cortex in response to electrical stimulation of the ventral horn of the L1 spinal cord. Motor evoked potentials (MEPs) were evaluated to demonstrate endogenous recovery of physiological functions after SCI. A significantly shorter N1 peak latency and broader activation in the MEP optical recordings were observed at 4 weeks after SCI, compared to 1 week after SCI. Spatiotemporal patterns in the cerebral cortex differed depending on functional recovery. In the present study, optical imaging was found to be useful in revealing functional changes and may reflect conditions of reorganization and/or changes in surviving neurons after SCI.

Combined analysis of AFP and HCCR-1 as an useful serological marker for small hepatocellular carcinoma: a prospective cohort study.

Hepatocellular carcinoma (HCC) is one of the most frequent malignant tumors in the world. The only serological marker widely used for the diagnosis of HCC is alpha-fetoprotein (AFP). Despite that AFP is widely used for the diagnosis of HCC, it has a limit as a serological marker due to its low sensitivity and specificity. The human cervical cancer proto-oncogene 1 (HCCR-1) was previously reported as a new biomarker for HCC. To further evaluate the HCCR-1 as a biomarker for HCC, we conducted the prospective cohort study. We evaluated the significance of simultaneous measurement of 2 tumor markers in the diagnosis of HCC in China, Japan and Korea. Two markers for HCC, AFP and HCCR-1, were measured in the sera obtained from 1,338 patients at the time of initial diagnosis of HCC. Of the 1338 HCC patients, 616 (46%) and 686 (51.3%) were sero-positive for AFP and HCCR-1, respectively. The positive rate for HCC was increased up to 74.1% in combined use of AFP and HCCR-1. Many cases (54%) for AFP-negative HCC were positive for HCCR-1 and vice versa. More importantly, the diagnostic rate for small HCC (< 2 cm) was significantly improved in the combined analysis of AFP and HCCR-1 to 56.9% although it was only 40.1% and 23.4% in the single analysis of HCCR-1 and AFP, respectively. Our result suggests that the HCCR-1 could be an useful biomarker for HCC while the diagnostic rate could be significantly improved in the combined use of HCCR-1 and AFP.

Transdifferentiation-inducing HCCR-1 oncogene.

BACKGROUND: Cell transdifferentiation is characterized by loss of some phenotypes along with acquisition of new phenotypes in differentiated cells. The differentiated state of a given cell is not irreversible. It depends on the up- and downregulation exerted by specific molecules. RESULTS: We report here that HCCR-1, previously shown to play an oncogenic role in human cancers, induces epithelial-to-mesenchymal transition (EMT) and mesenchymal-to-epithelial transition (MET) in human and mouse, respectively. The stem cell factor receptor CD117/c-Kit was induced in this transdifferentiated (EMT) sarcoma tissues. This MET occurring in HCCR-1 transfected cells is reminiscent of the transdifferentiation process during nephrogenesis. Indeed, expression of HCCR-1 was observed during the embryonic development of the kidney. This suggests that HCCR-1 might be involved in the transdifferentiation process of cancer stem cell. CONCLUSIONS: Therefore, we propose that HCCR-1 may be a regulatory factor that stimulates morphogenesis of epithelia or mesenchyme during neoplastic transformation.

Reoperation for persistent or recurrent hemifacial spasm after microvascular decompression.

OBJECTIVE: The objective of this study was to investigate the outcome of reoperation for persistent or recurrent hemifacial spasm (HFS) after microvascular decompression (MVD). METHODS: Repeat MVD was performed on 13 patients with an HFS between June 1994 and May 2004. Patients who had compressing offending vessels identified on postoperative (prerevision) three-dimensional short-range magnetic resonance angiography were selected for repeat MVD. RESULTS: Six patients were found to have no improvement in HFS with the first MVD. All of these patients exhibited excellent improvement after the second MVD. In one patient who had mild improvement with the first MVD, but with more than 50% of remaining spasm, complete abolition of spasm occurred immediately after the second MVD. Six patients showed initial relief and subsequent aggravation of HFS after the first MVD. Of these patients, four had excellent results with the second MVD, one had a good result, and one had a fair outcome. Adverse effects after the second MVD were found in two patients (one patient with permanent mild facial weakness and one patient with hearing impairment). There was no serious morbidity associated with the second MVD. CONCLUSION: Our data suggest that repeat MVD of the facial nerve may be sufficient to resolve symptoms in selected patients with persistent or recurrent HFS. Additionally, three-dimensional short-range magnetic resonance angiography may help to identify the offending vessels and to select the patients with persistent or recurrent HFS.