Scanning Electron Microscopy of Nerve Fibers in the Dog Cochlea

The nerve fiber arrangement inside the organ of Corti in the dog was studied. Thick sections were cut serially from celloidin-embedded cochleas and observed with a scanning electron microscope (SEM). The nerve fibers in the organ of Corti were clearly exposed in sections cut in the horizontal plane. The arrangement of nerve fibers in the dog showed considerable difference from that of other species. The tunnel basilar fibers in the dog curved basalward, and took a long longitudinal course to form a broad bundle in the center of the tunnel floor. This bundle has not been found in adult animals of other species. Two distinct types of tunnel radial fibers, upper tunnel radial fibers and underpassing radial fibers, were recognized. The latter type of radial fibers ran beneath the bundle of basilar fibers, and seemed to be characteristic of the dog cochlea. From the morphological characteristics, these underpassing radial fibers were thought to be efferent in nature

Scanning Electron Microscopy of the Celloidin-Embedded Inner Ear Sections

The nerve fibers running inside the organ of Corti were studied in cats by scanning electron microscopy (SEM). The fixed temporal bones were decalcified and embedded in celloidin according to the conventional method. Thick serial sections (100-150 μm) were cut parallel to the basilar membrane. After removing the celloidin, the sections were freeze-dried in t-butyl alcohol. Though some outer hair cells had been deformed, the nerve fibers were well preserved for analysis. Some new findings were observed in the present SEM study. The tunnel spiral bundle in a kitten took an atypical course on the floor of Corti\u27s tunnel apart from the previously reported site. In the barely-patent tunnels of Corti in kittens, nerve fibers were stuck together into thick bundles and took different courses compared to those in the mature cochleas. Filiform projections of nerve fibers were climbing around the first row of the outer hair cells in the immature cochlea. These were thought to be growing ends of efferent nerves which would later grow into nerve endings

Scanning Electron Microscopic Study of the Postnatal Development of the Rabbit Cochlea, with an Emphasis on Innervation

The development of nerve fiber arrangements of the organ of Corti was studied in rabbits 1, 3, 5, 7 and 12-days-old using thick sections from celloidin-embedded cochleas which were examined under a scanning electron microscope. The arrangements of nerve fibers varied with developmental age. The tunnel spiral bundle was thick and loosely collected in the immature cochlea. The outer spiral fibers were recognized even in the narrow space of Nuel in the one-day-old cochlea. As Nuel\u27s space is extending, the fibers course along the medial side of Deiters\u27 cells. The arrangement of the outer spiral fibers was irregular and sparse in the five-day-old cochlea, in contrast to the regular parallel pattern of the adult cochlea. Adult-like parallel arrangement of the outer spiral fibers was seen in the twelve-day-old cochlea. In the three-day-old cochlea, irregularly running nerve fibers were seen along the outer spiral fibers. They may be efferent axons which develop afterwards. Club-like immature nerve endings were recognized at the base of the outer hair cells in the seven-day-old cochlea. Some fibers climbed high up along the medial wall of the outer hair cells. A nearly mature pattern was seen in the twelve-day-old cochlea. This study confirms previous reports on the development of cochlear innervation

Scanning Electron Microscopy of Age-Related Changes in the C57BL/6J Mouse Cochlea

Hair cells and nerve fibers inside the organ of Corti of the C57BL/6J mouse, which is known as the precocious presbycusis model, were studied using the scanning electron microscope. For this study, we used thick serial sections cut from celloidin blocks. In the 5-week-old mice, hair cell loss was not seen. The upper tunnel radial fibers crossed the upper part of the tunnel of Corti and entered the Nuel\u27s space between the outer pillar cells. The fibers varied in diameter and showed many varicosities. The basilar fibers emerged into the tunnel of Corti beneath the upper tunnel radial fibers and crossed the floor of tunnel slightly curving basalward. The outer spiral fibers ran along the lateral wall of the Nuel\u27s spaces, sometimes buried in the cytoplasm of Deiters\u27 cells. The nerve endings were clearly seen on the modiolar sides of the outer hair cell bases in the basal turn. In the 30-, 42- and 60-week-old mice, hair cell degeneration was seen both at the basal and apical portions, more pronounced in the former. The outer hair cells were affected more than the inner hair cells. In the basal turn where most of outer hair cells had degenerated, the upper tunnel radial fibers disappeared while the basilar fibers remained. These results suggest that degeneration of the efferent fibers occur earlier than those of the afferent to the outer hair cells

Draft Genome Sequence of a Clinical Isolate of Streptococcus mutans Strain HM

We report the draft genome sequence of Streptococcus mutans strain HM isolated from a 4-year-old girl with infective endocarditis. The genomics information will provide information on the genetic diversity and virulence potential of S. mutans strain HM

Activation of Cdc42 by trans interactions of the cell adhesion molecules nectins through c-Src and Cdc42-GEF FRG

Nectins, Ca2+-independent immunoglobulin-like cell–cell adhesion molecules, initiate cell–cell adhesion by their trans interactions and recruit cadherins to cooperatively form adherens junctions (AJs). In addition, the trans interactions of nectins induce the activation of Cdc42 and Rac small G proteins, which increases the velocity of the formation of AJs. We examined here how nectins induce the activation of Cdc42 in MDCK epithelial cells and L fibroblasts. Nectins recruited and activated c-Src at the nectin-based cell–cell adhesion sites. FRG, a GDP/GTP exchange factor specific for Cdc42, was then recruited there, tyrosine phosphorylated by c-Src, and activated, causing an increase in the GTP-bound active form of Cdc42. Inhibition of the nectin-induced activation of c-Src suppressed the nectin-induced activation of FRG and Cdc42. Inhibition of the nectin-induced activation of FRG or depletion of FRG by RNA interference suppressed the nectin-induced activation of Cdc42. These results indicate that nectins induce the activation of Cdc42 through c-Src and FRG locally at the nectin-based cell–cell adhesion sites

Transcriptional repression induces a slowly progressive atypical neuronal death associated with changes of YAP isoforms and p73

Transcriptional disturbance is implicated in the pathology of polyglutamine diseases, including Huntington's disease (HD). However, it is unknown whether transcriptional repression leads to neuronal death or what forms that death might take. We found transcriptional repression-induced atypical death (TRIAD) of neurons to be distinct from apoptosis, necrosis, or autophagy. The progression of TRIAD was extremely slow in comparison with other types of cell death. Gene expression profiling revealed the reduction of full-length yes-associated protein (YAP), a p73 cofactor to promote apoptosis, as specific to TRIAD. Furthermore, novel neuron-specific YAP isoforms (YAPΔCs) were sustained during TRIAD to suppress neuronal death in a dominant-negative fashion. YAPΔCs and activated p73 were colocalized in the striatal neurons of HD patients and mutant huntingtin (htt) transgenic mice. YAPΔCs also markedly attenuated Htt-induced neuronal death in primary neuron and Drosophila melanogaster models. Collectively, transcriptional repression induces a novel prototype of neuronal death associated with the changes of YAP isoforms and p73, which might be relevant to the HD pathology

Nonfunctioning endocrine tumor of the pancreas：A case report

We report a rare case of a very large nonfunctioning endocrine tumor of the pancreas without malignant histological features. A 63-year-old woman referred for appetite loss and general fatigue was found to have a tumor in the pancreas head. Computed tomography demonstrated a well-defined pancreatic tumor 45mm in diameter with hypervascular staining in the pancreas head. Angiography showed a hypervascular tumor of the pancreas head and a dilatation of the anterior superior and posterior superior pancreaticoduodenal arteries. The preoperative diagnosis was an endocrine tumor of the pancreas, with undeniable malignancy. Pylorus-preserving pancreaticoduodenectomy was performed. The histopathological diagnosis was a benign nonfunctioning endocrine tumor of the pancreas based on immunohistochemical staining for Chromogranin A, Synaptophysin, and NSE, but not for hormones. The tumor revealed a low labeling index (<2.0%) of Ki-67 indicating its benign character. No tumor recurrence has been identified in the 18 months since surgery

Forebrain Ptf1a Is Required for Sexual Differentiation of the Brain

The mammalian brain undergoes sexual differentiation by gonadal hormones during the perinatal critical period. However, the machinery at earlier stages has not been well studied. We found that Ptf1a is expressed in certain neuroepithelial cells and immature neurons around the third ventricle that give rise to various neurons in several hypothalamic nuclei. We show that conditional Ptf1a-deficient mice (Ptf1a cKO) exhibit abnormalities in sex-biased behaviors and reproductive organs in both sexes. Gonadal hormone administration to gonadectomized animals revealed that the abnormal behavior is caused by disorganized sexual development of the knockout brain. Accordingly, expression of sex-biased genes was severely altered in the cKO hypothalamus. In particular, Kiss1, important for sexual differentiation of the brain, was drastically reduced in the cKO hypothalamus, which may contribute to the observed phenotypes in the Ptf1a cKO. These findings suggest that forebrain Ptf1a is one of the earliest regulators for sexual differentiation of the brain