In developing mammalian telencephalon, the loss of adherens junctions and cell cycle exit represent crucial steps in the differentiation of neuroepithelial cells into neurons, but the relationship between these cellular events remains obscure. Atypical protein kinase C (aPKC) is known to contribute to junction formation in epithelial cells and to cell fate determination for Drosophila neuroblasts. To elucidate the functions of aPKCλ, one out of two aPKC members, in mouse neocortical neurogenesis, a Nestin-Cre mediated conditional gene targeting system was employed. In conditional aPKCλ knockout mice, neuroepithelial cells of the neocortical region lost aPKCλ protein at embryonic day 15 and demonstrated a loss of adherens junctions, retraction of apical processes and impaired interkinetic nuclear migration that resulted in disordered neuroepithelial tissue architecture. These results are evidence that aPKCλ is indispensable for the maintenance of adherens junctions and may function in the regulation of adherens junction integrity upon differentiation of neuroepithelial cells into neurons. In spite of the loss of adherens junctions in the neuroepithelium of conditional aPKCλ knockout mice, neurons were produced at a normal rate. Therefore, we concluded that, at least in the later stages of neurogenesis, regulation of cell cycle exit is independent of adherens junctions.

The signals that prompt the axons to send out processes in peripheral nerves after axotomy are not well understood. Here, we report that galectin-1 can play an important role in this initial stage. We developed an in vitro nerve regeneration model that allows us to monitor the initial axon and support cell outgrowth from the proximal nerve stump, which is comparable to the initial stages of nerve repair. We isolated a factor secreted from COS1 cells that enhanced axonal regeneration, and we identified the factor as galectin-1. Recombinant human galectin-1 (rhGAL-1) showed the same activity at low concentrations (50 pg/ml) that are two orders of magnitude lower than those of lectin activity. A similarly low concentration was also effective in in vivo experiments of axonal regeneration with migrating reactive Schwann cells to a grafted silicone tube after transection of adult rat peripheral nerve. Moreover, the application of functional anti-rhGAL-1 antibody strongly inhibited the regeneration in vivo as well as in vitro. The same effect of rhGAL-1 was confirmed in crush/freeze experiments of the adult mouse sciatic nerve. Because galectin-1 is expressed in the regenerating sciatic nerves as well as in both sensory neurons and motor neurons, we suggest that galectin-1 may regulate initial repair after axotomy. This high activity of the factor applied under nonreducing conditions suggests that galectin-1 may work as a cytokine, not as a lectin.

BackgroundThe high recurrence rate after surgery for colorectal cancer liver metastasis (CLM) remains a crucial problem. The aim of this trial was to evaluate the efficacy of adjuvant therapy with uracil-tegafur and leucovorin (UFT/LV).MethodsIn the multicenter, open-label, phase III trial, patients undergoing curative resection of CLM were randomly assigned in a 1:1 ratio to either the UFT/LV group or surgery alone group. The UFT/LV group orally received 5 cycles of adjuvant UFT/LV (UFT 300mg/m2 and LV 75mg/day for 28 days followed by a 7-day rest per cycle). The primary endpoint was recurrence-free survival (RFS). Secondary endpoints included overall survival (OS).ResultsBetween February 2004 and December 2010, 180 patients (90 in each group) were enrolled into the study. Of these, 3 patients (2 in the UFT/LV group and 1 in the surgery alone group) were excluded from the efficacy analysis. Median follow-up was 4.76 (range, 0.15–9.84) years. The RFS rate at 3 years was higher in the UFT/LV group (38.6%, n = 88) than in the surgery alone group (32.3%, n = 89). The median RFS in the UFT/LV and surgery alone groups were 1.45 years and 0.70 years, respectively. UFT/LV significantly prolonged the RFS compared with surgery alone with the hazard ratio of 0.56 (95% confidence interval, 0.38–0.83; P = 0.003). The hazard ratio for death of the UFT/LV group against the surgery alone group was not significant (0.80; 95% confidence interval, 0.48–1.35; P = 0.409).ConclusionAdjuvant therapy with UFT/LV effectively prolongs RFS after hepatic resection for CLM and can be recommended as an alternative choice.Trial RegistrationUMIN Clinical Trials Registry C000000013

Anterograde and retrograde transport of horseradish peroxidase was used to examine the afferent and efferent projections of the VIIIth cranial nerve in the lamprey Lampetra japonica. Ganglion cells of the VIIIth nerve are classified into three types on the basis of their morphology. The central processes of these ganglion cells enter the medulla in two groups: the anterior group (mostly thick fibers) and the posterior group (mostly thin fibers). Afferent fibers mainly terminate within the ipsilateral ventral and octavomotor nuclei of the octavolateralis area and within the granular and molecular layer of the cerebellum. Some fibers terminate in the contralateral cerebellum, the medial and dorsal nuclei of the octavolateralis area, the descending nucleus of the trigeminal nerve, some cranial motor nuclei, and the lateral octavus nucleus, which has not been described previously. This small nucleus is located beneath the descending nucleus of the trigeminal nerve near the obex. Within the ventral nucleus, thin fibers occupy the dorsal part and thick fibers occupy the ventral part. The basic projection pattern of the primary afferents of the VIIIth nerve in the lampreys was similar to that of gnathostome fishes that have been studied to date. Cell bodies of the efferent vestibular neurons are located between the ipsilateral trigeminal motor nucleus and the facial motor nucleus. The lateral location of these cell bodies differs from that of all other fish species that have been studied.

We have fabricated highly packed and ordered In0.4Ga0.6As quantum dots (QDs) array on GaAs(311)B substrate without coalescence of QDs. Reflection high-energy electron diffraction and Auger spectra suggest the inhomogeneous distribution of In and Ga in QD. In concentration near the surface of QD is larger than that of the inside, and the inhomogeneous distribution of In and Ga in QDs prevents QDs from merging.