含歯性嚢胞より生じた原発性骨内歯原性癌腫

Malignant tumors arising from dentigerous cysts are classified as primary squamous cell carcinoma derived from an odontogenic cyst or as odontogenic carcinoma according to the 2005 WHO classification and are extremely rare. We report a malignant tumor arising from a dentigerous cyst in the right maxillary anterior teeth , together with a literature review. The patient was a 75-year-old man who visited a hospital with complaining of discomfort in the lingual part of the right maxillary anterior teeth. On panoramic radiography and plain computed tomography (CT), dentigerous cyst, keratocystic odontogenic tumor or ameloblastoma was suspected. The extirpated material was histopathologically diagnosed as an odontogenic carcinoma (in situ) arising from the dentigerous cyst. Postoperative ultrasonography (US) and contrast enhanced CT revealed no metastasis to the cervical lymph nodes. The patient is currently being followed up without resection or anticancer drug administration. Neither local recurrence nor metastases were observed 18 month after surgery.症例は75歳男性で、右上顎前歯の舌部不快感を主訴として受診した。パノラマX線撮影とCT検査により含歯性嚢胞、角化細胞歯原性腫瘍またはエナメル上皮腫が疑われた。切除切片の病理組織学的検査の結果、含歯性嚢胞より生じた歯原性癌腫と診断した。術後超音波検査と造影増強CT画像では頸部リンパ節への転移は見られなかった。抗癌剤投与はせずに経過観察中で、術後18ヵ月時点で再発や転移は見られていない。含歯性嚢胞より生じる悪性腫瘍は2005年のWHO分類によれば歯原性嚢胞由来の原発性扁平上皮癌または歯原性癌腫に分類され、極めて稀である。本症例は右上顎前歯の含歯性嚢胞より生じた悪性腫瘍であった。他の症例についても文献レビューした

Conceptual design of DEMO blanket materials test modules for A-FNS

A conceptual design of Advanced Fusion Neutron Source, A-FNS, has been conducted to achieve early realization of fusion-like neutron irradiation test for fusion reactor materials in Japan. A-FNS provides eight test modules to obtain irradiation data for fusion reactor materials. Conceptual design activities on Blanket Functional Materials Test Module (BFMTM), Tritium Release Test Module (TRTM) and Activated Corrosion Products Module (ACPM) were described among the A-FNS test modules. Also, basic concepts of the sub-system cells for the TRTM and the ACPM were also discussed

Active Hippocampal Networks Undergo Spontaneous Synaptic Modification

The brain is self-writable; as the brain voluntarily adapts itself to a changing environment, the neural circuitry rearranges its functional connectivity by referring to its own activity. How the internal activity modifies synaptic weights is largely unknown, however. Here we report that spontaneous activity causes complex reorganization of synaptic connectivity without any external (or artificial) stimuli. Under physiologically relevant ionic conditions, CA3 pyramidal cells in hippocampal slices displayed spontaneous spikes with bistable slow oscillations of membrane potential, alternating between the so-called UP and DOWN states. The generation of slow oscillations did not require fast synaptic transmission, but their patterns were coordinated by local circuit activity. In the course of generating spontaneous activity, individual neurons acquired bidirectional long-lasting synaptic modification. The spontaneous synaptic plasticity depended on a rise in intracellular calcium concentrations of postsynaptic cells, but not on NMDA receptor activity. The direction and amount of the plasticity varied depending on slow oscillation patterns and synapse locations, and thus, they were diverse in a network. Once this global synaptic refinement occurred, the same neurons now displayed different patterns of spontaneous activity, which in turn exhibited different levels of synaptic plasticity. Thus, active networks continuously update their internal states through ongoing synaptic plasticity. With computational simulations, we suggest that with this slow oscillation-induced plasticity, a recurrent network converges on a more specific state, compared to that with spike timing-dependent plasticity alone

Podoplanin promotes progression of MPM

Malignant pleural mesothelioma (MPM) is characterized by dissemination and aggressive growth in the thoracic cavity. Podoplanin (PDPN) is an established diagnostic marker for MPM, but the function of PDPN in MPM is not fully understood. The purpose of this study was to determine the pathogenetic function of PDPN in MPM. Forty-seven of 52 tumors (90%) from Japanese patients with MPM and 3/6 (50%) MPM cell lines tested positive for PDPN. Knocking down PDPN in PDPN-high expressing MPM cells resulted in decreased cell motility. In contrast, overexpression of PDPN in PDPN-low expressing MPM cells enhanced cell motility. PDPN stimulated motility was mediated by activation of the RhoA/ROCK pathway. Moreover, knocking down PDPN with short hairpin (sh) RNA in PDPN-high expressing MPM cells resulted in decreased development of a thoracic tumor in mice with severe combined immune deficiency (SCID). In sharp contrast, transfection of PDPN in PDPN-low expressing MPM cells resulted in an increase in the number of Ki-67-positive proliferating tumor cells and it promoted progression of a thoracic tumor in SCID mice. Interestingly, PDPN promoted focus formation in vitro, and a low level of E-cadherin expression and YAP1 activation was observed in PDPN-high MPM tumors. These findings indicate that PDPN is a diagnostic marker as well as a pathogenetic regulator that promotes MPM progression by increasing cell motility and inducing focus formation. Therefore, PDPN might be a pathogenetic determinant of MPM dissemination and aggressive growth and may thus be an ideal therapeutic target

Prolapse of Intussusception through the Anus as a Result of Sigmoid Colon Cancer

Adult intussusception is rare and most often associated with cancer. We report a case of intussuscepted sigmoid colon into the rectum protruding from the anus of a 47-year-old woman. The cause of the intussusception was sigmoid colon cancer. We removed the intussuscepted part of the sigmoid colon as well as the rectum and regional lymph nodes. The patient recovered uneventfully and there has been no evidence of recurrence of the cancer