53 research outputs found
カラードップラー超音波検査を用いた経皮経管的血管形成術スクリーニングの評価
広島大学(Hiroshima University)博士(保健学)Doctor of Philosophy in Health Sciencedoctora
Basal Cell Carcinoma of the Head and Neck
Basal cell carcinoma (BCC) is a malignant neoplasm derived from nonkeratinizing cells that originate from the basal layer of the epidermis and is the most frequent type of skin cancer in humans, with cumulative exposure to ultraviolet radiation as an important risk factor. BCC occurs most frequently at sun-exposed sites, with the head and neck being common areas. Tumors can be classified as nodular, superficial, morpheaform, infiltrating, metatypic, and fibroepithelioma of Pinkus. Several treatment options such as surgical excision and nonsurgical procedures are available. The choice of treatment should be determined based on the histological subtype of a lesion, cost, its size and location, patient age, medical condition of the patient, treatment availability, and the patient's wishes. The aim of any therapy selected for BCC treatment involving the head and neck is to ensure complete removal, the preservation of function, and a good cosmetic outcome
Early Detection of Nasopharyngeal Carcinoma
Nasopharyngeal carcinoma (NPC) is a unique disease with a clinical presentation, epidemiology, and histopathology differing from other squamous cell carcinomas of the head and neck. NPC is an Epstein-Barr virus-associated malignancy with a marked racial and geographic distribution. Specifically, it is highly prevalent in southern China, Southeast Asia, and the Middle East. To date, most NPC patients have been diagnosed in the advanced stage, but the treatment results for advanced NPC are not satisfactory. This paper provides a brief overview regarding NPC, with the focus on the early detection of initial and recurrent NPC lesions
Study for mechanisms and treatments of cochlear injury induced by ototoxic agents
課題番号:2059196
Inhibitory effect of guinea pig serum on JTC-11 cell growth in vitro
The growth of JTC-11 cell line which was established from Ehrlich ascites carcinoma in vitro was inhibited by the addition of 2 per cent guinea pig serum to the control medium composed of 10 per cent bovine serum, 0.4 per cent
lactalbumin hydrolysate and saline D. The concentration of guinea pig serum could be reduced to 0.02 per cent (lOγ of guinea pig serum protein/ml) with
positive result, but 0.002 per cent guinea pig serum did not inhibit the growth at all. The inhibitory effect was not abolished by heating at 56°C, 66°C, and 70°C for 30 min but it was completely lost by heating at 100°C for 30 min. The inhibitory factor was undialyzable, and was inactivated with the treatment of 1mM HgCl2- Morphologically, the cells exposed to guinea pig serum
showed pycnotic changes of the nuclei, accompanied by the formation of fine vacuole-like particles in the cytoplasm. Electron microscopic study revealed poor development of endoplasmic reticulum. There were more multivesicular bodies and large vacuoles with amorphous content in the cytoplasm of the damaged cells. The DNA synthesis in these cells was remarkably disturbed by 2 per cent guinea pig serum.</p
Ischemia-Reperfusion Injury of the Cochlea: Pharmacological Strategies for Cochlear Protection and Implications of Glutamate and Reactive Oxygen Species
A large amount of energy produced by active aerobic metabolism is necessary for the cochlea to maintain its function. This makes the cochlea vulnerable to blockade of cochlear blood flow and interruption of the oxygen supply. Although certain forms of human idiopathic sudden sensorineural hearing loss reportedly arise from ischemic injury, the pathological mechanism of cochlear ischemia-reperfusion injury has not been fully elucidated. Recent animal studies have shed light on the mechanisms of cochlear ischemia-reperfusion injury. It will help in the understanding of the pathology of cochlear ischemia-reperfusion injury to classify this injury into ischemic injury and reperfusion injury. Excitotoxicity, mainly observed during the ischemic period, aggravates the injury of primary auditory neurons. On the other hand, oxidative damage induced by hydroxyl radicals and nitric oxide enhances cochlear reperfusion injury. This article briefly summarizes the generation mechanisms of cochlear ischemia-reperfusion injury and potential therapeutic targets that could be developed for the effective management of this injury type
Ceramide-1-phosphate protection of cochlear hair cells against cisplatin ototoxicity
BackgroundCeramide-1-phosphate (C1P) is a phosphorylated form of ceramide. While ceramide is known to be an inducer of apoptosis of cochlear hair cells in cisplatin ototoxicity, little is known about the function of C1P in cochlear diseases.PurposeThe present study was designed to examine whether C1P could protect cochlear hair cells against cisplatin ototoxicity.Materials and methodsExplants of cochlear basal turns collected from C57BL/6J mice at postnatal days 3–5 were used in all experiments. Cochlear explants were exposed to 5 or 10 μM cisplatin for 48 h to assess the effects of C1P, NVP-231 (a ceramide kinase inhibitor), or ceramide. Western blotting of pAkt/Akt and pMAPK/MAPK was examined to check whether this pathway was modulated by C1P.ResultsC1P activated the Akt and MAPK pathway and significantly reduced cochlear cell death induced by cisplatin. Coadministration of cisplatin and ceramide significantly increased cochlear hair cell death. In addition, when treating cochlear hair cells with NVP-231 in the presence of cisplatin or ceramide, a remarkable increase in apoptosis of hair cells was observed.ConclusionThe present findings confirmed the protective effects of C1P in the cisplatin ototoxicity. The balance between ceramide and C1P may play a critical role in the determination of hair cell fate in cisplatin ototoxicity
Synchronous unilateral parotid gland neoplasms of three different histological types
A 67-year-old male with three synchronous tumors in the unilateral parotid gland is reported. Postoperative histological examinations confirmed the presence of three synchronous primary tumors, specifically pleomorphic adenoma, Warthin\u27s tumor and salivary duct carcinoma, in the right parotid gland. To our knowledge, this is the first case report describing three different histological types in the unilateral parotid gland
Ceramide/sphingomyelin cycle involvement in gentamicin-induced cochlear hair cell death
Ceramide, a sphingolipid metabolite, regulates diverse cellular processes including apoptosis, cell senescence, the cell cycle, and cellular differentiation. Exogenously administered ceramide reportedly increased cochlear hair cell death due to gentamicin-induced ototoxicity. Ceramide is mainly generated via a ceramide/sphingomyelin cycle by sphingomyelinase and sphingomyelin synthase or via de novo synthesis by serine palmitoyltransferase and ceramide synthase. This study was designed to investigate the possible involvement of neutral sphingomyelinase, sphingomyelin synthase, or serine palmitoyltransferase in hair cell death due to gentamicin. The basal turns of the organ of Corti of Sprague–Dawley rats were dissected on postnatal days 3–5. Cochlear cultures were exposed to media containing 35 μM gentamicin for 48 h to assess the effects of GW4869 (a neutral sphingomyelinase inhibitor), 2-hydroxyoleic acid (a sphingomyelin synthase activator), and myriocin (a serine palmitoyltransferase inhibitor). Hair cell loss was significantly decreased in the presence of GW4869 or 2-hydroxyoleic acid. Myriocin had no significant effects against gentamicin-induced hair cell loss. In addition, neutral sphingomyelinase was activated by gentamicin exposure. The present findings strongly suggest that the ceramide/sphingomyelin cycle plays an important role in the protection of hair cells against gentamicin-induced ototoxicity
Protective effects of exogenous GM-1 ganglioside on acoustic injury of the mouse cochlea
GM-1 ganglioside (GM-1), a glycosphingolipid, is embedded in the lipid layer of neuronal membranes and is one of the neuroprotective agents. To the best of our knowledge, the role of GM-1 has never been examined in hair cell injury. The purpose of this study was therefore to evaluate the effects of GM-1 on acoustic injury of the cochlea. Mice were exposed to 4-kHz pure tone of 128 dB SPL (sound pressure level) for 4 h. GM-1 was intraperitoneally administered immediately before the onset of acoustic overexposure. The threshold shift of the auditory brainstem response (ABR) and hair cell loss were then evaluated 2 weeks after acoustic overexposure. Immunostaining for 4-hydroxynonenal (4-HNE), indicative of lipid peroxidation, was also examined in animals subjected to acoustic overexposure. GM-1 treatment significantly decreased the ABR threshold shifts and hair cell loss after acoustic overexposure. And immunostaining for 4-HNE was reduced by GM-1 treatment. These findings suggest that GM-1 is involved in the protection of the cochlea against acoustic injury through inhibiting lipid peroxidation
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