Background: To improve local radicality of surgical treatment for left-sided pancreatic cancer, radical antegrade modular pancreatosplenectomy (RAMPS) was developed. However, no evidences are available regarding the superiority of RAMPS to conventional distal pancreatectomy (cDP) in terms of long-term outcomes. Objective: To assess the oncological benefit of RAMPS by comparing outcomes between patients who underwent cDP and RAMPS. Methods: Clinical data of patients undergoing cDP and RAMPS between 2009 and 2016 at two high-volume centers were analyzed. Patients having tumors of less than 5cm in size and those whose CA19-9 was less than 500ng/ml were included. Exclusion criteria were as follows; R2 resection, concomitant portal vein or celiac axis resection. Surgical outcomes were compared between patients who underwent cDP (cDP group) and RAMPS (RAMPS group). Results: The cDP and RAMPS groups were composed of 49 and 56 patients, respectively. No differences were found in tumor characteristics (tumor size, CA19-9 level, and lymph node positive rate) between the two groups. Compared to the cDP group, operation time was longer (cDP/RAMPS: 275min/309min, p=0.03) and the amount of blood loss was larger (125ml/435ml, p< 0.01) in the RAMPS group. However, the incidence of major complications was similar between the two groups (4%/14%, p=0.08). No differences were found in the R0 resection rate (cDP/RAMPS: 92%/95%, p=0.57), 3-year overall survival rate (65.6%/60.1%, p=0.86), and 3-year recurrence-free survival rate (53.3%/52.0%, p=0.68). However, 3-year local recurrence rate was lower in the RAMPS group (26.7%/8.6%, p=0.04). Conclusion: RAMPS is superior to conventional procedure in terms of long-term control of local recurrence.

1. Invited lecture: Problems and progress in ERCP Dr. Peter B. Cotton, M.D., M.R.C.P. (Middlesex Hospital, London) 2. Speclal lectures: (1) Aging and the digestive tract Dr. Kenji Tsuneoka (Nippon Medical University) (2) Cholelithiasis Dr. Toshio Sato (Tohoku University) 3. Symposia: (1) Progressive course from viral hepatitis to liver carcinoma Co-Moderators: Dr. Fumihiro Ichida (Niigata University) Dr. Kunio Okuda (Chiba University) (2) Recent advances in the diagnosis and treatment of pancreatocholangio carcinoma Co-Moderators: Dr. Kaneo Ishii (Asahikawa Medical College) Dr. Ryoichi Tsuchiya (Nagasaki University) (3) Cancer found in the observation of gastric ulcer Co-Moderators: Dr. Tadashige Murakami (Tokyo Medical and Dental University) Dr. Takao Sakita (Tsukuba University) (4) Diagnosis of the ileocecal disorders Co-Moderators: Dr. Hikoo Shirakabe (Juntendo University) Dr. Tadayoshi Takemoto (Tokyo Women's Medical College) 4. Closing dates for the submission of papers: Symposia: May 5, 1976 Free papers: May 31, 1976 Further information may be obtained from Prof. I-Iiroshi Takasaki, M.D., Department of Medicine, Mie University Hospital, Edobashi 2-174, Tsu City, Mie Prefecture, 514 Japan.

2) S y m p o s i a : (1) Polyposis of the digestive tract Co-Moderators: Prof. Tadashige Murakami, M.D. Prof. Takao Sakita, M.D. (2) Alcohol and digestive diseases Co-Moderators: Prof. Fumihiro Ichida, M.D. Prof. Toshio Sato, M.D. (3) Pathology and clinic of bile stagnation Co-Moderators: Prof. Hachinen Akita, M.D. Prof. Haruo Kameta, M.D. (4) Problems on fulminant hepatitis Co-Moderators: Prof. Kiyowo Kosaka, M.D. Prof. Yoshiyata Takahashi, M.D. (5) Malabsorption syndrome Co-Moderators: Prof. Masasuke Masuda, M.D. Prof. Toshio Honda, M.D.

The 69th Annual Meeting of the Japanese Society of Gastroenterology will be held under the chairmanship of Dr. Sukeo Yamamoto, M.D., Professor of Medicine, Osaka City University Medical School, from April 11 to 13, 1983, at Osaka Royal Hotel and Royal NCB Annex, Osaka, Japan. The outline of the scientific program is as follows: 1. Special lectures 2. Chairman's lecture 3. Symposia: (1) Immune Hepatic Disorders. (2) Problems on Defence Mechanism of the Gastric Mucosa. 4. Workshops: (1) Intestinal Diseases and Bacteria. (2) Biliary Stenosis. 5. Poster Symposium: The session will be conducted in the form of symposium. 6. Poster Session: This session is scheduled to be organized with papers selected from the General Session. For further information, please contact: Sukeo YAMAMOTO, M.D., Chairman, 69th Annual Meeting of the Japanese Society of Gastroenterology, 3rd Department of Internal Medicine, Osaka City University School of Medicine 5-7 Asahi-machi 1-chome, Abeno-ku, Osaka, 545 JAPAN.

Abnormal biosynthesis of thromboxane and prostacyclin has been implicated in patients with primary pulmonary hypertension and secondary pulmonary hypertension associated with congenital heart disease, and could be involved in the pathogenesis of pulmonary vascular disease. The chronic effects of an oral prostacyclin analogue, beraprost sodium, on thromboxane and prostacyclin biosynthesis and on pulmonary circulation were investigated in 15 children with pulmonary hypertension. The plasma concentrations of thromboxane B2 and 6-keto-prostaglandin F1 alpha were measured, as was the urinary excretion of 11-dehydro-thromboxane B2 and 2,3-dinor-6-keto-prostaglandin F1 alpha, which are stable metabolites of thromboxane A2 and prostacyclin, respectively. In patients with pulmonary hypertension, the plasma concentration of thromboxane B2 and the ratio of thromboxane B2 to 6-keto-prostaglandin F1 alpha were greater than in healthy controls: 210 +/- 49 versus 28 +/- 4 pg/mL (P < 0.05) and 32.6 +/- 8.9 versus 5.7 +/- 1.8 (P < 0.01), respectively. After 3 months of administration of beraprost, the plasma concentration of thromboxane B2 and the ratio of thromboxane B2 to 6-keto-prostaglandin F1 alpha were reduced significantly: 210 +/- 49 to 98 +/- 26 pg/mL (P < 0.01) and 32.6 +/- 8.9 to 18.0 +/- 6.7 (P < 0.05), respectively. In contrast, the plasma concentrations of 6-keto-prostaglandin F1 alpha in patients were slightly but not significantly higher than in controls, and did not change significantly after administration of beraprost. The concentrations of 11-dehydro-thromboxane B2 and 2,3-dinor-6-keto-prostaglandin F1 alpha in urine correlated significantly with thromboxane B2 and 6-keto-prostaglandin F1 alpha, respectively, in plasma. Beraprost improved the imbalance of thromboxane and prostacyclin biosynthesis and has a potential efficacy for preventing the progressive development of pathological changes in pulmonary vasculature.

2) S y m p o s i a : (1) Polyposis of the digestive tract Co-Moderators: Prof. Tadashige Murakami, M.D. Prof. Takao Sakita, M.D. (2) Alcohol and digestive diseases Co-Moderators: Prof. Fumihiro Ichida, M.D. Prof. Toshio Sato, M.D. (3) Pathology and clinic of bile stagnation Co-Moderators: Prof. Hachinen Akita, M.D. Prof. Haruo Kameta, M.D. (4) Problems on fulminant hepatitis Co-Moderators: Prof. Kiyowo Kosaka, M.D. Prof. Yoshiyata Takahashi, M.D. (5) Malabsorption syndrome Co-Moderators: Prof. Masasuke Masuda, M.D. Prof. Toshio Honda, M.D.

The 63rd Annual Meeting will be held under the presidency of Prof. Kaizo Ariga, M.D., Nihen University School of Medicine, Tokyo, as follows: 1. Meet ing date: April 1 to 4th, 1977. 2. Meeting site: Kosei Nenkin Kaikan (The Welfare Annuity Hall) and Tokyo Kinzoku Kenpo Kaikan, Shinjuku-ku, Tokyo. 3. Scientific p r o g r a m : 1) Special l ec tures : (1) Biochemical study on digestive absorption Prof. Mosaburo Kobayashi, M.D., Dept. of Biochemistry, Nihon University School of Medicine, Tokyo, Japan. (2) Contribution of ammonia to the pathogenesis of hepatic coma Prof. Charles S. Davidson, M.D., Dept. of Medicine, Harvard Medical School, U.S.A.

Although both osteoblasts and adipocytes have a common origin, i.e., mesenchymal cells, the molecular mechanisms that define the direction of two different lineages are presently unknown. In this study, we investigated the role of a transcription factor, CCAAT/enhancer binding protein beta (C/EBPbeta), and its isoform in the regulation of balance between osteoblast and adipocyte differentiation. We found that C/EBPbeta, which is induced along with osteoblast differentiation, promotes the differentiation of mesenchymall cells into an osteoblast lineage in cooperation with Runx2, an essential transcription factor for osteogenesis. Surprisingly, an isoform of C/EBPbeta, liver-enriched inhibitory protein (LIP), which lacks the transcriptional activation domain, stimulates transcriptional activity and the osteogenic action of Runx2, although LIP inhibits adipogenesis in a dominant-negative fashion. Furthermore, LIP physically associates with Runx2 and binds to the C/EBP binding element present in the osteocalcin gene promoter. These data indicate that LIP functions as a coactivator for Runx2 and preferentially promotes the osteoblast differentiation of mesenchymall cells. Thus, identification of a novel role of the C/EBPbeta isoform, provides insight into the molecular basis of the regulation of osteoblast and adipocyte commitment.

Isolated left ventricular noncompaction (LVNC) is a form of cardiomyopathy that most commonly presents in infancy with a hypertrophic and dilated left ventricle characterized by deep trabeculations and intertrabecular recesses. Our goal was to determine the frequency of mutations in G4.5, α-dystrobrevin, and FK Binding protein-12 in isolated LVNC patients. No mutations were identified in 47 of the 48 patients studied, while a splice site acceptor site mutation of intron 10 of G4.5 was identified in one patient, resulting in the deletion of exon 10 from the mRNA.

Mice deficient in the Msx2 gene manifest defects in skull ossification and a marked reduction in bone formation associated with decreases in osteoblast numbers, thus suggesting that Msx2 is involved in bone formation. However, the precise role of Msx2 during osteoblast differentiation is not fully understood. In the present study, we investigated the role of Msx2 in the regulation of osteoblast differentiation in the multipotent mesenchymal cell lines C3H10T1/2 and C2C12 and in murine primary osteoblasts. Introduction of Msx2 induced alkaline phosphatase activity in C3H10T1/2 and C2C12 cells and promoted the calcification of murine primary osteoblasts. This effect of Msx2 was also observed in mesenchymal cells isolated from Runx2-deficient mice. Interestingly the expression of Msx2 was induced by bone morphogenetic protein 2 treatment in Runx2-deficient mesenchymal cells. In contrast, Msx2 diminished peroxisome proliferator-activated receptor gamma (PPARgamma) expression and adipogenesis of the preadipocytic cell line 3T3-F442A. Moreover Msx2 inhibited the transcriptional activity of PPARgamma, CCAAT/enhancer-binding protein beta (C/EBPbeta), and C/EBPdelta and blocked adipocyte differentiation of mesenchymal cells induced by overexpression of PPARgamma, C/EBPalpha, C/EBPbeta, or C/EBPdelta. These data indicate that Msx2 promotes osteoblast differentiation independently of Runx2 and negatively regulates adipocyte differentiation through inhibition of PPARgamma and the C/EBP family.

We report a 10-month-old boy who underwent a bi-directional Glenn procedure and repair of coronary sinus orifice atresia. The left superior vena cava was the only vessel communicating with the coronary sinus in this case. The coronary sinus was allowed to communicate freely with the left atrium by creating a partially unroofed coronary sinus using a left superior vena cava flap.

The calcium-binding protein S100A12 causes inflammation through interaction with the multiligand receptor for advanced glycation end products (RAGE). Blocking of S100A12 showed promising therapeutic effects in mice. We investigated 31 individuals with Kawasaki disease, and recorded an association between expression of S100A12 and activity of Kawasaki disease. Serum concentrations of S100A12 decreased quickly in 28 patients who responded to treatment with gammaglobulin (from 463 microg/L [SD 316] to 184 microg/L [147] within 24 h, p<0.0001). Since the interaction of S100A12 with multiligand receptors has a key role in inflammatory responses, this protein could serve as a novel target for future therapeutic interventions in inflammatory disorders.

Bone morphogenetic proteins, BMPs, are members of the transforming growth factor-beta (TGF-beta) superfamily, which are implicated in embryogenesis, organogenesis, skeletogenesis, osteogenesis, cellular differentiation and apoptosis by regulating the expression of specific target genes. Recent progresses in studying the BMP signaling reveal that a cytoplasmic protein family, Smad, plays a central role in mediating the biological effects of BMPs. Smad transduces the signal from the cytoplasm to the nucleus where Smad regulates the transcription of the target genes through the direct association with the specific biding elements or with assistance of other transcription factors or co-activators such as p300/CBP. In addition, the signals mediated by Smad are also positively or negatively controlled by cross-talks with other hormone, growth factor or cytokine signalings, thereby modulating the biological actions of BMPs. Moreover, Smad signaling has negative feedback regulations at the cytoplasmic or nuclear level, which are important to restrict or terminate the biological effect of BMPs. Here we provide an overview of recent knowledge about the roles of Smad family in the regulation of BMP signaling.