A primary aorto-duodenal fistula associated with an inflammatory abdominal aortic aneurysm: a case report.

Primary aorto-enteric fistula (PAEF)is a serious complication of abdominal aortic aneurysm(AAA). We report a patient with PAEF associated with inflammatory AAA who underwent emergent surgery. A 52-year-old male presented with recurrent hematemesis. A computer tomography scan showed a sealed rupture of the AAA adjacent to the duodenum. At surgery, a coin-sized PAEF was noted. The aorta was replaced with a Dacron graft in situ . Histological examination revealed the characteristics of an inflammatory AAA. The postoperative course was uneventful, and there has been no evidence of infection during a follow-up period of 3 years. We discuss the etiologic and surgical considerations regarding this unusual entity.</p

ｶｲｺ体液中に存在する細胞増殖抑制ならびに脂肪蓄積促進活性因子に関する研究

ｶｲｺ(Bombyx mori)の幼虫体液中にはｶｲｺ由来培養細胞の増殖を抑制する活性があることを見出した｡また､ｶｲｺ体液によって増殖を阻害された細胞中には脂肪滴の形成が認められた｡本研究ではこれらの細胞増殖抑制および脂肪蓄積促進活性の実体となるｶｲｺ体液因子の解明を行った｡ｶｲｺ体液を出発材料として､細胞増殖抑制活性を指標にﾀﾝﾊﾟｸ質の精製を行った｡6段階の精製過程の後､SDS-ﾎﾟﾘｱｸﾘﾙｱﾐﾄﾞｹﾞﾙ電気泳動において単一ﾊﾞﾝﾄﾞを示す画分を得た｡ｱﾐﾉ酸配列解析の結果､このﾀﾝﾊﾟｸ質はｶｲｺ Niemann-Pick disease type C2(BmNPC2)ﾀﾝﾊﾟｸ質であると同定された｡ﾘｺﾝﾋﾞﾅﾝﾄ BmNPC2 ﾀﾝﾊﾟｸ質は細胞増殖抑制活性を示したことから BmNPC2 ﾀﾝﾊﾟｸ質がｶｲｺ体液中の細胞増殖抑制活性の実体であることが示唆された｡さらに､ﾘｺﾝﾋﾞﾅﾝﾄ BmNPC2 ﾀﾝﾊﾟｸ質をｶｲｺ培養細胞に添加することによって､細胞内ﾄﾘｸﾞﾘｾﾘﾄﾞ量の増大が認められた｡以上の結果は､BmNPC2 ﾀﾝﾊﾟｸ質がｶｲｺにおいて細胞増殖と脂質代謝を制御する体液性因子であることを示唆している｡Silkworm hemolymph induced both the cessation of growth and an increase in neutral lipids storage in the silkworm-derived cell line, BmN4. In this study, we identified a responsible blood factor showing growth-inhibitory and lipid-accumulating activity. We subjected the silkworm hemolymph to successive column chromatographies and measured the growth-inhibitory activity of each fraction. The final purified fraction showed the highest specific activity and a single band of 15kDa protein on SDS-PAGE. The amino acid sequence revealed that the 15kDa protein was Bombyx mori Niemann-Pick disease type C2 (BmNPC2) protein. A recombinant BmNPC2 protein exhibited growth-inhibitory activity comparable with the final purified fraction, indicating that this protein is responsible for the activitiy of silkworm hemolymph. Moreover, the recombinant BmNPC2 protein induced an increase in triglyceride storage in BmN4 cells. These results indicate that BmNPC2 protein regulates both cell growth and lipid metabolism in silkworm

Wortmannin, a specific inhibitor of phosphatidylinositol-3 kinase, blocks osteoclastic bone resorption

AbstractThe biological role of phosphatidylinositol (PI)-3 kinase was examined in osteoclast-like multinucleated cells (OCLs) formed in co-cultures of mouse osteoblastic cells and bone marrow cells. The expression of PI-3 kinase in OCLs was confirmed by Western blot analysis. Wortmannin (WT), a specific inhibitor of PI-3 kinase, inhibited PI-3 kinase activity in OCLs both in vitro and in vivo. WT also inhibited pit-forming activity on dentine slices and disrupted a ringed structure of F-actin-containing dots (an actin ring) in OCLs in a dose-dependent manner. The inhibitory profiles of WT for pit and actin ring formation were similar to that for PI-3 kinase activity in OCLs. Electron microscopic analysis revealed that OCLs treated with WT did not form ruffled borders. Instead, numerous electron lucent vacuoles of differing sizes were found throughout the cytoplasm. These results suggest that PI-3 kinase is important in osteoclastic bone resorption

Probable IgG4-related thyroiditis with cervical lymphadenopathy

　We present a case of probably IgG4-related thyroiditis with lymphadenopathy. The patient was a 70-year-old Japanese female who was undergoing hemodialysis and had undergone a right hemi-thyroidectomy in 1989 due to carcinoma. In December 2010, an ultrasonography study revealed a hypoechoic small lesion in thyroid gland. When the patient was admitted to our hospital in November 2013, the lesion and regional lymph nodes had enlarged and we suspected that they were metastatic thyroid cancer. We performed a residual total thyroidectomy and regional lymph node dissection in August 2014. At that time, lymphoplasmacytic infiltration and fibrosis were observed histopathologically in thyroid tissue. Immunohistochemical studies revealed infiltrated lymphocytes and plasma cells were markedly IgG-positive, and the ratio of IgG4-positive to IgG-positive cells was over 40%. We therefore diagnosed the patient with IgG4-related thyroiditis. The cervical lymph nodes were metastases of papillary carcinoma from 25 years earlier. The patient remains well without any recurrences 33 months after the surgery

Id4, a New Candidate Gene for Senile Osteoporosis, Acts as a Molecular Switch Promoting Osteoblast Differentiation

Excessive accumulation of bone marrow adipocytes observed in senile osteoporosis or age-related osteopenia is caused by the unbalanced differentiation of MSCs into bone marrow adipocytes or osteoblasts. Several transcription factors are known to regulate the balance between adipocyte and osteoblast differentiation. However, the molecular mechanisms that regulate the balance between adipocyte and osteoblast differentiation in the bone marrow have yet to be elucidated. To identify candidate genes associated with senile osteoporosis, we performed genome-wide expression analyses of differentiating osteoblasts and adipocytes. Among transcription factors that were enriched in the early phase of differentiation, Id4 was identified as a key molecule affecting the differentiation of both cell types. Experiments using bone marrow-derived stromal cell line ST2 and Id4-deficient mice showed that lack of Id4 drastically reduces osteoblast differentiation and drives differentiation toward adipocytes. On the other hand knockdown of Id4 in adipogenic-induced ST2 cells increased the expression of Pparγ2, a master regulator of adipocyte differentiation. Similar results were observed in bone marrow cells of femur and tibia of Id4-deficient mice. However the effect of Id4 on Pparγ2 and adipocyte differentiation is unlikely to be of direct nature. The mechanism of Id4 promoting osteoblast differentiation is associated with the Id4-mediated release of Hes1 from Hes1-Hey2 complexes. Hes1 increases the stability and transcriptional activity of Runx2, a key molecule of osteoblast differentiation, which results in an enhanced osteoblast-specific gene expression. The new role of Id4 in promoting osteoblast differentiation renders it a target for preventing the onset of senile osteoporosis