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  <title>DSpace コレクション: 2007-08</title>
  <link rel="alternate" href="http://hdl.handle.net/10564/1562" />
  <subtitle>2007-08</subtitle>
  <id>http://hdl.handle.net/10564/1562</id>
  <updated>2026-04-10T15:42:23Z</updated>
  <dc:date>2026-04-10T15:42:23Z</dc:date>
  <entry>
    <title>A CASE OF GYNECOMASTIA ASSOCIATED WITH EFAVIRENZ</title>
    <link rel="alternate" href="http://hdl.handle.net/10564/318" />
    <author>
      <name>Kenji Uno</name>
    </author>
    <author>
      <name>Mitsuru Konishi</name>
    </author>
    <author>
      <name>Eiichiro Yoshimoto</name>
    </author>
    <author>
      <name>Kei Kasahara</name>
    </author>
    <author>
      <name>Kei Mori</name>
    </author>
    <author>
      <name>Koichi Maeda</name>
    </author>
    <author>
      <name>Keiicm Mikasa</name>
    </author>
    <id>http://hdl.handle.net/10564/318</id>
    <updated>2017-06-11T23:20:26Z</updated>
    <published>2007-08-30T15:00:00Z</published>
    <summary type="text">タイトル: A CASE OF GYNECOMASTIA ASSOCIATED WITH EFAVIRENZ
著者: Kenji Uno; Mitsuru Konishi; Eiichiro Yoshimoto; Kei Kasahara; Kei Mori; Koichi Maeda; Keiicm Mikasa
抄録: We herein report on an HIV-infected patient with gynecomastia caused by &#xD;
efavirenz (EFV). A 57-year-old man was diagnosed with HIV-1 infection in 1994. He &#xD;
started therapy with zidovudine / lamivudine, didanosine, and EFV in December 2002. He &#xD;
felt painfu1 breast hypertrophy after 5 months. There were firm, tender, unattached &#xD;
masses under the bilateral nipples, and ultrasonography showed benign enlargement of &#xD;
the breast without adipomastia. The blood levels of thyroid hormones, testosterone, &#xD;
estradiol, prolactin, and cortisol were normal. Therefore, we diagnosed him as having &#xD;
EFV-induced gynecomastia because of medication history and examinations. Although &#xD;
EFV was not stopped, his gynecomastia gradually improved.</summary>
    <dc:date>2007-08-30T15:00:00Z</dc:date>
  </entry>
  <entry>
    <title>A CASE OF BOW HUNTER'S STROKE PRESENTING SYNCOPE AS AN INITIAL SYMPTOM WHILE DRJVING</title>
    <link rel="alternate" href="http://hdl.handle.net/10564/317" />
    <author>
      <name>Takeshima, Yasuhiro</name>
    </author>
    <author>
      <name>Kawata, Kazumro</name>
    </author>
    <author>
      <name>Imanishi, Kazumi</name>
    </author>
    <author>
      <name>Kawaguchi, Shoichiro</name>
    </author>
    <author>
      <name>Tamaki, Ryo</name>
    </author>
    <author>
      <name>Nakase, Hiroyuki</name>
    </author>
    <author>
      <name>Sakaki, Toshisuke</name>
    </author>
    <author>
      <name>Hoshida, Tohru</name>
    </author>
    <id>http://hdl.handle.net/10564/317</id>
    <updated>2017-06-11T23:20:26Z</updated>
    <published>2007-08-30T15:00:00Z</published>
    <summary type="text">タイトル: A CASE OF BOW HUNTER'S STROKE PRESENTING SYNCOPE AS AN INITIAL SYMPTOM WHILE DRJVING
著者: Takeshima, Yasuhiro; Kawata, Kazumro; Imanishi, Kazumi; Kawaguchi, Shoichiro; Tamaki, Ryo; Nakase, Hiroyuki; Sakaki, Toshisuke; Hoshida, Tohru
抄録: Bow Hunter's Stroke is a consequence of vertebrobasilar insufficiency as a &#xD;
result of mechanical occlusion or stenosis of the vertebral artery at the C1-C2 level by &#xD;
head rotation. It is rarely symptomatic in daily activities. We describe a case of Bow &#xD;
Hunter's Stroke(BHS) presenting syncope as an initial symptom while driving a car. &#xD;
A 59-year-old male patient suddenly lost consciousness while driving and his car &#xD;
dropped into a ravine 20 meters deep. On admission he was conscious, but suffering &#xD;
Central Cord Syndrome (CCS). &#xD;
We examined the cause of syncope. At the time of the accident, he turned his head to &#xD;
the rear in order to back his car and lost consciousness. Magnetic resonance angiography &#xD;
demonstrated the dominant vertebral artery (VA) in the left and the hypoplastic VA in &#xD;
the right. Cerebral angiography on turning the head 90 degrees to the right revealed the &#xD;
left VA occluded at the C1-C2 level. Therefore we diagnosed the patient with BHS. The &#xD;
vertigo symptom was intractable with conservative treatment, and we therefore &#xD;
performed C1-C2 posterior fusion. The post-operative course was uneventfu1 and he does &#xD;
not have the symptoms anymore. &#xD;
Syncope sometimes induces traffic accidents, but it is rare that BHS is detected on &#xD;
examination of common trauma. Therefore when vertigo, dizziness, or syncope is found &#xD;
in common trauma, BHS must be considered as a potential cause.</summary>
    <dc:date>2007-08-30T15:00:00Z</dc:date>
  </entry>
  <entry>
    <title>転写調節因子による嗅覚神経回路の形成機構</title>
    <link rel="alternate" href="http://hdl.handle.net/10564/316" />
    <author>
      <name>吉原, 誠一</name>
    </author>
    <author>
      <name>坪井, 昭夫</name>
    </author>
    <id>http://hdl.handle.net/10564/316</id>
    <updated>2017-05-29T06:06:56Z</updated>
    <published>2007-08-30T15:00:00Z</published>
    <summary type="text">タイトル: 転写調節因子による嗅覚神経回路の形成機構
著者: 吉原, 誠一; 坪井, 昭夫
抄録: 一次嗅覚神経系は匂い分子を受容する嗅細胞とその情報の伝達先である嗅球内&#xD;
のニューロンが非常に精密な神経回路網を形成することで成立しており,脳内の複雑な神経回&#xD;
路形成のメカニズムを解明するための極めて有効なモデルとなる。また,嗅細胞及び嗅球介在&#xD;
ニューロンは胎生期のみならず成体期においても常に産生され続けることから,再生医療の観&#xD;
点からも嗅覚系は注目されてきている。近年おもにノックアウトマウスの解析から,一次嗅覚&#xD;
神経回路形成過程において様々な転写調節因子が遺伝子カスケードを作りながら,嗅細胞及び&#xD;
嗅球ニュ一ロンの増殖・分化を調節していることがわかってきた。また,Arx及びFezという&#xD;
二つの転写調節因子のノックアウトマウスの解析により,嗅細胞の軸索投射と嗅球の形態形成&#xD;
が互いに密接に影響を及ぼしながら,相互依存的に発達することが明らかになった。</summary>
    <dc:date>2007-08-30T15:00:00Z</dc:date>
  </entry>
  <entry>
    <title>神経細胞型ニコチン性アセチルコリン受容体を介した細胞保護作用と細胞増殖促進作用</title>
    <link rel="alternate" href="http://hdl.handle.net/10564/315" />
    <author>
      <name>中山, 均</name>
    </author>
    <id>http://hdl.handle.net/10564/315</id>
    <updated>2017-06-30T05:42:12Z</updated>
    <published>2007-08-30T15:00:00Z</published>
    <summary type="text">タイトル: 神経細胞型ニコチン性アセチルコリン受容体を介した細胞保護作用と細胞増殖促進作用
著者: 中山, 均
抄録: 神経細胞型ニコチン性アセチルコリン受容体はおもに神経細胞に発現し、神経伝&#xD;
達および神経伝達の調節に関与している。一方、非神経系組織でも同受容体の発現が近年確認&#xD;
され、神経系とは異なる働きが示唆されている。本稿では神経細胞型ニコチン性アセチルコリ&#xD;
ン受容体を活性化した時にみられる神経細胞の保護および非神経細胞の増殖、アポトーシス抑&#xD;
制への関与についての最近の知見を紹介し、考察する。</summary>
    <dc:date>2007-08-30T15:00:00Z</dc:date>
  </entry>
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