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Notes: The Rfm1 gene restores the fertility of the msm1 and msm2 male-sterile cytoplasms in barley. Rfm1 is located on the short arm of chromosome 6H. To develop molecular markers tightly linked to Rfm1 for use in sophisticated marker-assisted selection and map-based cloning, an amplified fragment-length polymorphism (AFLP) marker system with isogenic lines and a segregating BC1F1 population was used. Nine hundred primer combinations were screened and a linkage map was constructed around the Rfm1 locus by using 25 recombinant plants selected from 214 BC1F1 plants. Three AFLP markers were identified, e34m2, e46m19 and e48m17, linked to the locus. The most closely linked markers were e34m2, at 1.0 cM distally and e46m19, at 1.1 cM proximally. The two AFLP markers were converted to dominant STS markers. These markers should accelerate programmes for breeding restorer lines and will be useful for map-based cloning.

Notes: General knowledge of the closed flowering trait, or cleistogamy, of barley is still limited. The relationship between cleistogamy and spike morphology characters was studied and linkage of cleistogamy genes with a highly significant quantitative trait locus (QTL) for rachis internode length on the long arm of chromosome 2H was detected. The mapping populations consisted of 129 doubled haploid lines of ‘Mikamo Golden’ × ‘Harrington’ and 150 F2 plants of ‘Misato Golden’ × ‘Satsuki Nijo’. The phenotypic variance explained by this QTL accounted for 77.5% and 82.6% of the variance in rachis internode lengt, respectively, in these two populations. The peaks of the QTL coincided with the positions of the cleistogamy gene loci.

Notes: Two types of male-sterile cytoplasm, designated msm1 and msm2, in barley were investigated to determine whether these cytoplasms confer resistance to barley yellow mosaic virus (Ba YMV) and Fusarium head blight (FHB). Alloplasmic lines and isogenic lines of two cultivars showed the same reaction to each Ba YMV as that of their euplasmic lines. This demonstrates that the barley male-sterile cytoplasms msm1 and msm2 have no effect on resistance to BaYMV. No significant difference in reactions to FHB was recognized among fertile alloplasmic lines of ‘Adorra’, but the difference in reactions to FHB between fertile and sterile isogenic lines of ‘Adorra’ was significant. The damage caused by FHB in the male-sterile lines that produced sterile pollen was significantly greater than the damage in a sterile line that did not produce pollen. These results suggest that pollen or anthers are important factors in infection with or spread of FHB. For production of hybrid seeds, male-sterile lines with no pollen production, such as those with msm1 male-sterile cytoplasm, would reduce FHB infestation.

Notes: Abstract. Background: Compared with esophageal varices, gastrointestinal varices are relatively rare, but they are clinically important because they tend to bleed massively. Color Doppler sonography is now widely used to diagnose the collaterals, but few color Doppler findings of gastric or intestinal varices have been reported. The aim of this study was to investigate the sonographic and color Doppler findings of gastrointestinal varices and to determine the role of color Doppler sonography in the diagnosis of these varices. Methods: We studied 30 patients who were diagnosed by endoscopy as having gastrointestinal varices (24 gastric, four duodenal, two intestinal) with color Doppler sonography and compared the results with the clinical data. The causes of gastric varices included liver cirrhosis (16/24, 66.7%), idiopathic portal hypertension (3/24, 12.5%), chronic pancreatitis with splenic vein thrombosis (2/24, 8.3%), congenital biliary atresia (1/24, 4.2%), congenital hepatic fibrosis (1/24, 4.2%), and unknown (1/24, 4.2%). The causes of duodenal varices included idiopathic portal hypertension with portal thrombosis (3/4, 75%) and liver cirrhosis (1/4, 25%). Results: The gastric wall at the fundus was thickened in 17 of 24 cases (70.8%) with gastric varices, and the duodenal wall was thickened in four of four cases (100%) with duodenal varices. Sonography revealed thrombosis in the splenic vein in two of two cases with gastric varices secondary to chronic pancreatitis and in the confluence of the superior mesenteric vein and the splenic vein in three of four cases with duodenal varices. Color Doppler sonography demonstrated multiple, slow constant blood flows in the thickened wall in 15 of 24 cases (62.5%) with gastric varices and in four of four cases (100%) with duodenal varices. It demonstrated accumulated slow constant blood flows in the cecum in the case with cecal varices. Color Doppler showed also the communication between the varices and the neighboring vascular system (superior mesenteric vein and inferior vena cava) in the case with cecal varices, but it did not directly reveal such a communication in the other 29 cases (96.7%). Color Doppler showed a hepatofugal flow in the left gastric vein in all the hemorrhagic gastric varicose patients with esophageal varices, but it showed a hepatopetal flow in the left gastric vein in the isolated nonhemorrhagic gastric varicose patients. Conclusion: Color Doppler sonography was very useful for the diagnosis of gastric and duodenal varices and for visualizing fine venous flows in the thickened gastric or duodenal wall. When it shows portal thrombosis in the confluence of the splenic vein and the superior mesenteric vein, duodenal varices should be suspected. The flow direction of the left gastric vein helps to differentiate hemorrhagic gastric varices from nonhemorrhagic ones.

Notes: Abstract. Background: The aim of this study was to reevaluate the causes and sites of intrahepatic venous collaterals and to determine the role of color Doppler sonography in the diagnosis of this relatively rare vascular abnormality. Methods: Real-time color Doppler sonography was used to study 21 patients with intrahepatic venous collaterals. The cause, distribution, and clinical manifestations of collaterals were determined, and Doppler waveforms obtained from the collaterals were also analyzed. Results: First, the causes of intrahepatic venous collaterals were divided roughly into two groups according to the presence or absence of veno-occlusions. The former group included liver tumors (six cases), primary Budd-Chiari syndrome (five cases), and metastatic adrenal tumors invading the inferior vena cava (two cases). The latter group consisted of diaphragmatic hernia (three cases), Osler-Weber-Rendu disease (two cases), and congestive liver (one case). The cause was not determined in two cases. Second, venous collaterals were distributed throughout the entire liver in primary Budd-Chiari syndrome but localized in the other cases. Third, Doppler waveforms of the collaterals were divided into two patterns: flat flow and multiphasic flow. Flat flow pattern was seen in patients with veno-occlusive diseases, and multiphasic flow pattern was seen in patients without veno-occlusive disease. Conclusion: The relationship between intrahepatic venous collaterals and veno-occlusive diseases has been emphasized in the literature, but the results of our series showed that they occurred under a wide variety of conditions, even without veno-occlusive diseases, including diaphragmatic hernia and Osler-Weber-Rendu disease. The analysis of the Doppler waveforms of the collaterals was useful in differentiating those due to veno-occlusive diseases and those not.

Notes: Abstract. Color Doppler sonograms and angiographic findings in 23 hepatic hemangioma patients were compared to clarify how arterioportal shunts influence color Doppler findings of hepatic hemangiomas. The results of our study showed that the presence of arterioportal shunts (six cases) gave rise to large feeding arteries (five cases), multiple intratumoral flows (six cases), and reversal of portal flow within (five cases) or around (four cases) the tumor. These color Doppler findings mimicked hypervascular malignant tumors. Knowledge of such unusual color Doppler findings in hepatic hemangiomas may help in avoiding misinterpretations of color Doppler sonograms. RID=""ID=""〈e5〉Correspondence to:〈/e5〉 H. Naganuma

Notes: Abstract We present two patients with hepatocellular carcinoma (HCC) on liver cirrhosis in whom color Doppler sonography documented an incidental peripheral arterioportal fistula due to a previous liver biopsy under laparoscopy. Detection of the fistula helped in preventing the occurrence of a portal thrombus. Color Doppler sonography should be performed prior to transarterial embolization in patients with HCC on liver cirrhosis with a past history of liver biopsy under laparoscopy.

Notes: Abstract Background: Mesenteric cyst (MC) is a relatively rare disease, and its sonographic characteristics have not been sufficiently analyzed. Methods: We studied the sonographic findings of eight patients with MC, with attention paid to its size, shape, internal echoes, and especially the presence or absence of lateral shadowing and the mode of back echoes. In four cases, the sound velocity and acoustic impedance of cystic fluid were also measured. The mode of blood flow was evaluated by color Doppler sonography. Results: Six cases showed an oval or comma-shaped mass. Internal echoes were present in six cases, and two of them showed a pseudosolid pattern. In these cases, M-mode sonography confirmed the movement of these internal echoes. Only one case showed a posterior echo enhancement, and no case showed lateral shadowing. Sound velocity measured in four cases was 1515–1537 m/s, with an acoustic impedance of 1.550–1.576 kg/m2/s. No blood flow signals were obtained from the lesion. Conclusion: MC exhibits so many patterns on ultrasound that we should consider the possibility of MC when encountering an avascular oval mesenteric mass.

Notes: Abstract Background and methods: Sonographic (US) findings of Chilaiditi syndrome have been rarely reported in the literature. We reviewed 18 cases of Chilaiditi syndrome to pinpoint its US pattern. Results: (1) US showed gas echoes of different sizes superimposed over the entire liver in two cases and over the right hepatic lobe in six cases, leading to a high suspicion of Chilaiditi syndrome. (2) US showed a small gas echo in the hepatodiaphragmatic space, mimicking pneumoperitoneum in eight cases. In this instance, altering the patient's position allowed for confirmation of the lack of a change in the location of the gas echo, unlike cases of pneumoperitoneum. (3) The hepatic surface appeared as a hyperechoic mass in two cases. Conclusion: Knowledge of US patterns of Chilaiditi syndrome helps avoid confusion with pneumoperitoneum or hepatic masses.

Notes: Abstract Background: Neurofibromatosis 1 (NF1) has been studied from many viewpoints, but its abdominal involvement has rarely been reported. Sonography (US) is now the initial diagnostic tool for abdominal exploration, which prompted us to determine the clinical manifestations and US findings of abdominal involvement in NF1. Methods: We analyzed the US findings and clinical data of eight NF1 cases with abdominal involvement. Results: Abdominal involvement included neurofibromatous tumor growth in the liver, mesentery, and retroperitoneum, in addition to mesenteric leiomyomatosis and gastric carcinoma. Color Doppler US was useful not only in detecting blood flows in the lesions but also in preventing hazardous vascular injury during tumor biopsy. Conclusion: A better understanding of the clinical manifestations and US findings of abdominal involvement in NF1 translates into improved NF1 patient care.