Conversion of a conventional superconductor into a topological superconductor by topological proximity effect.

Realization of topological superconductors (TSCs) hosting Majorana fermions is a central challenge in condensed-matter physics. One approach is to use the superconducting proximity effect (SPE) in heterostructures, where a topological insulator contacted with a superconductor hosts an effective p-wave pairing by the penetration of Cooper pairs across the interface. However, this approach suffers a difficulty in accessing the topological interface buried deep beneath the surface. Here, we propose an alternative approach to realize topological superconductivity without SPE. In a Pb(111) thin film grown on TlBiSe2, we discover that the Dirac-cone state of substrate TlBiSe2 migrates to the top surface of Pb film and obtains an energy gap below the superconducting transition temperature of Pb. This suggests that a Bardeen-Cooper-Schrieffer superconductor is converted into a TSC by the topological proximity effect. Our discovery opens a route to manipulate topological superconducting properties of materials.

Macrophage invasion into injured cochlear nerve and its modification by methylprednisolone.

Post-traumatic invasion of macrophages into the cochlear nerve of the rat and measurement of how their invasion was modified by the administration of methylprednisolone were investigated for the first time by using a reproducible and quantifiable experimental model of cochlear nerve injury. Two weeks after precise cochlear nerve compression, a massive invasion of ED1 immunostained macrophages was observed at the compressed portion of the cochlear nerve, and this invasion of macrophages was markedly reduced in the rats to which methylprednisolone had been administered during the pre- and post-compression period. Concomitantly, the residual number of spiral ganglion cells was found to be greater in the compression+methylprednisolone group than in the control compression group. The tissue loss observed in the lesion epicenter was also significantly less in the compression+methylprednisolone group than in the control compression group. The results of our present study demonstrated the effectiveness of methylprednisolone treatment to ameliorate trauma induced cochlear nerve degeneration in the acute phase. However, these results may reflect the sum effects of methylprednisolone on macrophages, including both its beneficial effect by inhibiting the negative aspects of macrophages through attenuating macrophage recruitment to the lesion site, and at the same time an undesirable effect by sacrificing the positive aspects of macrophage function. Moreover, one reservation should be added that the protective effects of steroid to injured cochlear nerve may have operated via a pathway not related to macrophage function. Besides macrophages, various cells and factors participate in the process of CNS injury, and their effects may potentially work either positively or negatively with respect to CNS protection and regeneration at each particular time during the on-going process of CNS injury. Therefore, future investigation in CNS injury should be directed toward understanding such complex mechanisms involved in this process.

Intraoperative electrophysiological monitoring of oculomotor nuclei and their intramedullary tracts during midbrain tumor surgery.

OBJECTIVE: During surgery for intrinsic midbrain lesions, we intraoperatively recorded evoked compound muscle action potentials (ECMAPs) from the extraocular muscles and evaluated how this type of intraoperative electrophysiological monitoring could minimize postoperative oculomotor nerve palsy (ptosis and/or diplopia). METHODS: The ECMAPs were recorded through a spring electrode applied to the extraocular muscle (Method 1, seven cases) or a needle electrode inserted into the superior intraorbital space (Method 2, five cases). The surgeon repeated electrical stimulations whenever tissue of unknown origin was encountered intraoperatively, and this information was used to safely guide surgical resection of the tumors. RESULTS: Using these monitoring techniques, the response-free areas were resected and the areas from which ECMAP responses were recorded were avoided. For all 12 patients, ECMAPs were successfully recorded from the extraocular muscles. Ten patients did not exhibit any postoperative deterioration of oculomotor nerve function. Two patients exhibited deterioration of oculomotor nerve function immediately after surgery, which resolved within 1 month. Equally robust ECMAPs could be recorded with Method 2, compared with Method 1. CONCLUSION: Intraoperative ECMAP recordings from the extraocular muscles precisely indicated the locations of the oculomotor nuclei and/or intramedullary oculomotor tracts. Although Method 2 is a more indirect method for recording ECMAPs than is Method 1, Method 2 was equally useful in recording ECMAPs, which seemed to be the summed potentials from the superior rectus muscle and the levator palpebrae superioris muscle. These monitoring techniques are valuable in guiding surgeons to avoid causing inadvertent harm to the oculomotor nuclei and tracts during midbrain surgery, particularly when the neuroanatomic features are distorted by the presence of tumor.

Effectiveness of preoperative administration of an N-methyl-D-aspartate antagonist to enhance cochlear neuron resistance to intraoperative traumatic stress: an experimental study.

OBJECT: Cochlear neurons are inevitably exposed to traumatic stress during surgical removal of an acoustic neuroma; that event is an important cause of postoperative cochlear neuronal degeneration, with subsequent loss of spiral ganglion cells (SGCs). The object of this study was to investigate whether preoperative pharmacological treatment can enhance the resistance of cochlear neurons to the traumatic stress of surgery. METHODS: Cochlear neuronal degeneration was induced in 17 rats by controlled compression of the cerebellopontine angle portion of the cochlear nerve. Dizocilpine maleate (MK-801; 10 mg/kg), an N-methyl-D-aspartate (NMDA) antagonist, was administered intraperitoneally to six of the 17 rats 30 minutes before compression occurred. Two weeks after compression, each rat was killed, and the numbers of SGCs in histological preparations of temporal bones were counted. CONCLUSIONS: Spiral ganglion cells were more numerous in rats administered dizocilpine maleate (p < 0.03) than in rats that did not receive treatment, indicating that receptor-mediated glutamate neurotoxicity may participate in the pathogenesis of trauma-induced cochlear neuron death and that administration of an NMDA antagonist before surgery may protect the nerve from injury leading to hearing loss.

Methylprednisolone ameliorates cochlear nerve degeneration following mechanical injury.

We investigated whether methylprednisolone sodium succinate can ameliorate cochlear nerve degeneration following compression injury on the cerebellopontine angle portion of the cochlear nerve, using a quantitative animal experimental model that we have developed recently. In this model, cochlear nerve degeneration after compression could be quantitatively evaluated, while cochlear ischemia induced by the compression carefully maintained below the critical limit that causes irreversible damage to the cochlea. Eleven rats were treated with methylprednisolone during the pre- and post-compression period. Two weeks after compression, the numbers of SGC were compared between the rats that received the compression without and with methylprednisolone treatment. Methylprednisolone treatment improved the survival of SGC following cochlear nerve injury statistically highly significantly in the basal turn where the traumatic stress had been less than in the other cochlear turns in our experimental setting. Although it was not statistically significant, greater survival was also observed in the other cochlear turns. The results of this experimental study indicated that at least a portion of injured cochlear nerve had been potentially treatable, and that methylprednisolone might prevent such cochlear neurons from entering into the vicious process of irreversible damaging process.

A comprehensive classification system of vestibular schwannomas.

Because traditional classifications of vestibular schwannomas (according to relative size) cannot comprehensively describe lesions that grow in different patterns after arising in regions as diverse as the cerebellopontine (CP) angle, the internal auditory canal, and the region lateral to the fundus of the internal auditory canal (labyrinth), we developed a new system to classify vestibular schwannomas, a system that describes the anatomical structures involved by the tumour, rather than size alone. The vestibular schwannoma is classified first by location and then by extent. Our system provides surgeons information helpful in choosing the surgical approach, in estimating the difficulty of tumour excision, and in determining whether hearing might be preserved. Our system also avoids confusion and misunderstanding in discussions of treatment results because it reflects the diverse biological characteristics of vestibular schwannomas.

Cerebellopontine angle cisternal infusion of NGF, BDNF and NT-3: effects on cochlear neurons disconnected from central target, cochlear nucleus. An in vivo quantitative study.

Cochlear neurons need their synaptic contacts with both their peripheral (organ of Corti) and central (cochlear nucleus) targets for survival. We examined the in vivo effectiveness of the neurotrophins (NGF, BDNF and NT-3) on cochlear neuronal survival using our in vivo model, in which the central connection alone was selectively and quantitatively interrupted. The particular neurotrophins evaluated in the present study did not appear to have cochlear nerve rescue potential. However, the experimental model reported here can serve as a useful tool to investigate cochlear neuronal degeneration from the central side, which may lead to identification of effective mediators in the future.

Bone formation under the influence of bone morphogenetic protein/self-setting apatite cement composite as a delivery system.

Self-setting apatite cement (apatite cement) with a phase of hydroxyapatite (HAP) was employed as a delivery system for bone morphogenetic protein (BMP). A composite of BMP and apatite cement (BMP/HAP composite) was implanted both in thigh muscle and surgically created defect of a critical size of 5 mm, which is a size that does not heal spontaneously in the femur of mice, to evaluate its osteogenetic potential as an augmentation and reconstructive material for clinical usage. The histological and immunohistochemical assessment of proteoglycans reiterated osteogenesis in the muscle tissue. On day 14 postimplantation of BMP/HAP composite, chondroid tissue was formed in the muscle, and HAP particles were seen in newly formed chondroid tissue. On the 21st day, endo-chondral ossification had occurred, however, small HAP particles remained in the newly formed bone, i.e., HAP particles and newly formed osseous tissues coexisted in a central area. BMP/HAP composite was incorporated by newly formed osseous tissue in the experimented animals. HAP particle found in BMP/HAP composite implanted into the bone defect was resorbed and replaced by osseous tissue. The apatite cement was proved to have advantages for its shaping as well as collapsing properties, and thus, apatite cement containing BMP is suggested as a favorable augmentation material in clinical usage for delivery system of BMP.

[Establishment of the criteria to evaluate intraoperative changes of brainstem auditory evoked potentials during microvascular decompression and acoustic neurinoma excision].

Although monitoring of brainstem auditory evoked potentials (BAEP) is helpful to preserve hearing during operations in the cerebellopontine angle such as microvascular decompression and excision of an acoustic neurinoma, criteria for what and when changes in BAEP should be communicated to the surgeon have not been well established. An exhaustive review was, therefore, conducted of the English and Japanese literature on this topic. Analysis of the results of this literature review led to the conclusion that during a microvascular decompression procedure, the surgeon should be warned as soon as progressive prolongation of the latency of wave V of the BAEP exceeds 1.5 msec. It is reasonable to apply stricter criteria in acoustic neurinoma excision; prolongation of wave V latency even less than 0.5 msec should be regarded as the warning sign to the surgeon who is trying to preserve hearing. Whenever BAEP monitoring is performed, it is crucial that changes in the BAEP are evaluated in light of the particular surgical procedure in progress and that the person who evaluates these changes is well versed in the conduct of the surgical procedure.

[A simplified method to monitor oculomotor nerve function in midbrain surgery: recordings of compound muscle action potentials by percutaneous superior orbital electrode].

We report a simple and easily-applicable method to intraoperatively monitor the oculomotor nerve and oculomotor nucleus in the brainstem. A needle electrode is inserted into the space just beneath the superior root of the orbit. With this superior orbital electrode, evoked compound muscle action potentials from the superior rectus and the levator palpebrae superioris muscles were recorded. The nuclei for these two muscles are located caudally in the midline of the midbrain. The responses from the superior orbital electrode, therefore, give the surgeons useful intraoperative guidance during surgery for pineal region tumors and midbrain gliomas.

[Intraoperative electrophysiological monitoring for functional preservation of the cauda equina during lumbosacral surgery].

Adequate electrophysiological techniques to monitor function of the cauda equina have been proposed for surgery in patients with lumbosacral lipoma or myeloschisis. Motor fibers were identified by electrical stimulation in the operating field with bipolar rectangular impulses of 200 mu sec duration at 2 Hz under 5 mA and compound muscle action potentials (CMAPs) recorded from the leg and anal muscles. By recording CMAPs from the tibialis anterior, the biceps femoris, the gastrocnemius, and the external anal sphincter muscles, all of the roots from the fourth lumbar to the fourth sacral segment were continuously monitored. To spare recording channels, recordings were obtained from the right versus the left side. In our institute, 5 patients have undergone lumbosacral surgery while using this monitoring system, and the results indicated that there was no postoperative neurological exacerbation in any of the cases. According to a combination of the CMAPs produced by stimulation, the segment of the stimulated motor root could be identified electrophysiologically. Monitoring of somatosensory evoked potentials was not performed because this would have required too much time and would have prolonged surgery. However, some sensory fibers, which appeared to be posterior roots of the cauda equina on intraoperative inspection, could be identified indirectly with CMAPs recording because of current spreading from the stimulation to motor fibers.

[A case of giant cell-rich gliosarcoma].

We report a case of gliosarcoma with numerous giant cells resembling ganglion cells and having clear nucleoli. A 75-year woman was admitted to our hospital suffering from progressive left hemiparesis and ambulatory disturbance of one week's duration. CT and MRI studies showed ring enhancement on a clear margin mass in the right parieto-occipital lobe. The mass was totally removed macroscopically. Her left hemiparesis had improved and self walk came to be possible. But the tumor was regrowthed during next two months and she died for three months and a week. The gross and microscopic appearances of the tumors showed the double structure. The surface of the tumor was well enhanced and consisted of soft, gray, and easily bleeding tissue. The central core, however, was poorly enhanced and consisted of hard, yellow, non-bleeding tissue. Macroscopically, the central area included numerous giant ganglion-like cells which were negative for GFAP but positive for EMA in the cytoplasm. These giant cells had abundant collagen fibers and were surrounded by such fibers. Microscopic findings of the surrounding area included numerous spindle shaped cells which were positive for GFAP and vimentin. The origins of giant cells or tumor tissues have long been discussed, but no consensus has yet been obtained. Therefore, we speculated as to the origin in our patient based on immunohistochemical study and the findings of electronmicroscopy. We concluded, in sharp contrast to the old theory of one origin, epithelial tissue of a hamartomatous nature existed initially, followed by the growth of malignant tissue of a reactive astrocytic tumor with a sarcomatous component.

[A case report of mirror writing with low perfusion of bilateral anterior cerebral arteries].

A 20-year-old female experienced temporary unintentional mirror writing associated with low perfusion of the bilateral anterior cerebral arteries. When she was 17 years old, she had developed multiple idiopathic intracerebral hemorrhages and right hemiparesis. At the age of 20, she had a generalized convulsion for which she was transferred to our department. Computed tomography (CT) and magnetic resonance images of the brain were obtained, but no fresh abnormal lesion could be detected. The following day, after she had recovered from postictal symptoms, she wrote mirror image words, and her mirror writing then gradually improved within one week. Single photon emission CT showed low perfusion of both anterior cerebral arteries. We concluded that bilateral vascular insufficiency to the supplementary motor areas and corpus callosum caused mirror writing in this case.

An in vivo quantifiable model of cochlear neuronal degeneration induced by central process injury.

In the available in vivo experimental models for cochlear neuronal degeneration, the peripheral (hair cell side) process of the cochlear nerve has been injured in order to induce neuronal degeneration. However, there has been no dependable experimental model in which cochlear neuronal degeneration begins from the central (brain stem side) process. This lack of a central process injury model has probably been due to the experimental difficulties that had to be overcome in order to reproducibly and selectively injure the central process of the cochlear neurons while maintaining the patency of the internal auditory artery in small experimental animals such as rats. Using rats, we first developed a central process injury model in which the reduction of the spiral ganglion cells due to retrograde degeneration of cochlear neurons can be quantitatively evaluated. In our experimental model, the cochlear nerve was compressed and injured by a compression-recording (CR) electrode placed at the internal auditory meatus. First, the cochlear nerve was compressed until the compound action potentials of the cochlear nerve became flat, and then the CR electrode was advanced by various compression speeds (5, 10, or 200 micrometer/s) to reach the same depth (400 micrometer). In our model, therefore, the reduction of the spiral ganglion cells was caused compression speed dependently. This method made it possible to produce compression injury to the cochlear nerve without evidence of damage to the blood supply to the cochlea via the internal auditory artery. This model gives us the means to obtain knowledge that was previously impossible to derive from the peripheral process injury models.