Phosphoinositide-dependent regulation of VAN3 ARF-GAP localization and activity essential for vascular tissue continuity in plants

ACAP-type ARF GTPase activating proteins (ARF-GAPs) regulate multiple cellular processes, including endocytosis, secretion, phagocytosis, cell adhesion and cell migration. However, the regulation of ACAP functions by other cellular proteins is poorly understood. We have reported previously that a plant ACAP, VAN3, plays a pivotal role in plant venation continuity. Here, we report on newly identified VAN3 regulators: the CVP2 (cotyledon vascular pattern 2) 5 PTase, which is considered to degrade IP3 and also to produce PtdIns(4) P from PtdIns(4,5) P-2; and a PH domain-containing protein, VAB (VAN3 binding protein). Combinational mutations of both CVP2 and its closest homologue CVL1 (CVP2 like 1) phenocopied the strong allele of van3 mutants, showing severe vascular continuity. The phenotype of double mutants between van3, cvp2 and vab suggested that VAN3, CVP2 and VAB function in vascular pattern formation in the same pathway. Localization analysis revealed that both CVP2 and VAB colocalize with VAN3 in the trans-Golgi network (TGN), supporting their functions in the same pathway. The subcellular localization of VAN3 was dependent on its PH domain, and mislocalization of VAN3 was induced in cvp2 or vab mutants. These results suggest that CVP2 and VAB cooperatively regulate the subcellular localization of VAN3 through the interaction between its PH domain and phosphoinositides and/or inositol phosphates. In addition, PtdIns(4) P, to which VAN3 binds preferentially, enhanced the ARF-GAP activity of VAN3, whereas IP3 inhibited it. These results suggest the existence of PtdIns(4) P and/or IP3-dependent subcellular targeting and regulation of VAN3 ACAP activity that governs plant vascular tissue continuity

New Large Bowel Segmentation on Plain Abdominal Radiography in Comparison with the Conventional Method

Plain abdominal radiography is a very basic examination and plays an important role in primary care. The objectives of this study were to clarify colon distributions on plain abdominal radiographs. Forty-three healthy volunteers underwent gastric fluoroscopy, and 2 hours later, plain abdominal radiography in the supine position. A region of interest (ROI) was defined uniformly on each X-ray image to divide the image into 600 zones. The area corresponding to the large bowel within the ROI was divided into 4 segments (ascending colon, transverse colon, descending colon, and sigmoid colon＋rectum). The percentage of barium in each segment relative to the total volume of barium used was calculated to evaluate the percent ROI occupancy. The large bowel covered 76.7% of the entire ROI, with the percent duplication being 55%. The duplicated area corresponded to the transverse colon region. When the method proposed by Arhan et al. was used, the percentage of the colon actually present in each segment relative to that determined theoretically was 99.6% for the right colon segment, 92.2% for the left colon segment, and 92.2% for the sigmoid/rectal segment. However, in cases in which the transverse colon descended partially from the fifth lumbar vertebra, the percentage occupied by the sigmoid colon＋rectum decreased to 57.2%. We applied a new large bowel segmentation method especially for patients with ptosis, by devising a line joining the lateral side of the right lesser pelvis and the lower ends of both sacroiliac joints

Huge right ventricle–right coronary artery fistula compromising right ventricular function in a patient with pulmonary atresia and intact ventricular septum: A case report

AbstractJ Thorac Cardiovasc Surg 2001;122:1030-

Effect of Taurine on Acinar Cell Apoptosis and Pancreatic Fibrosis in Dibutyltin Dichloride-induced Chronic Pancreatitis

The relationship between pancreatic fibrosis and apoptosis of pancreatic acinar cells has not been fully elucidated. We reported that taurine had an anti-fibrotic effect in a dibutyltin dichloride (DBTC)-chronic pancreatitis model. However, the effect of taurine on apoptosis of pancreatic acinar cells is still unclear. Therefore, we examined apoptosis in DBTC-chronic pancreatitis and in the AR42J pancreatic acinar cell line with/without taurine. Pancreatic fibrosis was induced by a single administration of DBTC. Rats were fed a taurine-containing diet or a normal diet and were sacrificed at day 5. The AR42J pancreatic acinar cell line was incubated with/without DBTC with taurine chloramines. Apoptosis was determined by using terminal deoxynucleotidyl transferase-mediated dUTP-digoxigenin nick end labeling (TUNEL) assay. The expression of Bad and Bcl-2 proteins in the AR42J cells lysates was detected by Western blot analysis. The apoptotic index of pancreatic acinar cells in DBTC-administered rats was significantly increased. Taurine treatment inhibited pancreatic fibrosis and apoptosis of acinar cells induced by DBTC. The number of TUNEL-positive cells in the AR42J pancreatic acinar cell lines was significantly increased by the addition of DBTC. Incubation with taurine chloramines ameliorated these changes. In conclusion, taurine inhibits apoptosis of pancreatic acinar cells and pancreatitis in experimental chronic pancreatitis

食道痛細胞におけるWntのベータカテ二ンTCF経路の活性化の検討

Although, accumulation of nuclear and cytoplasmic beta-catenin has been observed in ESCCs, mutation of APC and beta-catenin are not found in ESCCs. Therefore, another mechanism for cytoplasmic beta- catenin accumulation might exist in ESCCs. Materials and Methods: Human ESCCs cell lines and the 293 stable transfectants expressing Wnt-1, Wnt-5A, and Wnt-7A were cultured under standard conditions. The TOPFlash or FOPFlash reporter plasmids were transfected. Results: Transfected mutant beta-catenin as well as an axin fragment harbing the GSK3 beta interaction domain, the latter a potent GSK3 beta inhibitor. both robustly activated pTOPFlash in ESCCs cells. When pTOPFlash/pFOPFlash reporters were transfected in ESCCs cell lines followed by cocultivation with 293 cells that stably express Wnt -1, all cell lines except one demonstrated TCF mediated transcriptional. But, cells were co- cultured, Wnt - 7A or Wnt - 5A did not activate TCF mediated transcription in a cell number dependent fashion. Discussion; We report the activation of TCF promoter gene by extemal Wnt stimuli in ESCCs cells.背景:食道癌細胞にベータカテニンの蓄積があることは報告されているが,大腸癌とことなり,ベータカテニン,Axin,APC変異の報告がなく,そのメカニズムは不明である｡ 方法:8種類の食道癌細胞株において,3種類のWntの刺激によるベータカテニンTCF系の活性化への影響をTCFプロモーターを持つルシュフフェラーゼプラスミドを癌細胞にトランスフェクションして検討した｡ 結果:代表的な食道癌細胞は変異ベータカテニン,変異APC,変異Axinのいずれも,TCFの活性化をおこした｡8種類中7種類の癌細胞はWnt1により量依存性のTCFの活性化が認められたが,Wnt5A,Wnt7Aでは活性化が認められなかった｡ 結語:食道癌の進展にWnt1の関与が示唆された