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A channel layer substitution of a wider bandgap AlGaN for a conventional GaN in high electron mobility transistors (HEMTs) is an effective method of enhancing the breakdown voltage. Wider bandgap AlGaN, however, should also increase the ohmic contact resistance. Si ion implantation doping technique was utilized to achieve sufficiently low resistive source/drain contacts. The fabricated AlGaN channel HEMTs with the field plate structure demonstrated good pinch-off operation with sufficiently high drain current density of 0.5 A/mm without noticeable current collapse. The obtained maximum breakdown voltages was 1700 V in the AlGaN channel HEMT with the gate-drain distance of 10 μm. These remarkable results indicate that AlGaN channel HEMTs could become future strong candidates for not only high-frequency devices such as low noise amplifiers but also high-power devices such as switching applications.
Adenosquamous carcinoma is a very rare tumour which is characterised pathologically by the simultaneous presence of distinct areas of adenocarcinoma and squamous cell carcinoma. Generally, adenosquamous carcinoma has an aggressive clinical course and is associated with a poor prognosis. Most cases have been treated by surgery alone or combined with radiotherapy. Chemotherapy is rarely used in treating adenosquamous carcinoma, and it has been difficult to establish treatment guidelines due to the paucity of cases.
We report a case of adenosquamous carcinoma which arose in the maxillary sinus of a 77-year-old man. Despite surgical treatment and chemoradiotherapy to the primary site, he developed bilateral neck metastases after the surgery. The patient was treated with S-1, a novel oral fluoropyrimidine anticancer agent, with a complete (albeit finite) response.
This report presents the aggressive character of adenosquamous carcinoma and the possible role of S-1 in the treatment of this uncommon neoplasm.
Decreased function of the melanocortin-4 receptor (MC4R) was reported to cause late-onset
obesity and insulin resistance in rodents. Thus mutations in the MC4R gene drew strong attention
as a possible cause of obesity and diabetes. We screened for mutations in the MC4R gene in extremely
obese [body mass index (BMI) [ges ] 35 kg/m2] Japanese with diabetes by direct sequencing. A
heterozygous mutation (V103I) was detected in one case (2.0 %), however the frequency was not
significantly different from that in non-obese (BMI [les ] 24 kg/m2) and non-diabetic subjects (2.7 %).
No other mutations were detected. These results suggest that mutations including V103I in the
MC4R gene are not a major cause of obesity or diabetes in Japanese.
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