Chondroitin 4-sulfotransferase (C4ST) catalyzes the transfer of sulfate from 3'-phosphoadenosine 5'-phosphosulfate to position 4 of the N-acetylgalactosamine residues of chondroitin. We previously reported the cloning of C4ST cDNA from mouse brain. We here report the cloning and expression of human C4ST cDNA. The cDNA was isolated from a human fetal brain cDNA library by hybridization with a DNA probe prepared from rat poly(A)(+) RNA used for the cloning of mouse C4ST cDNA. The cDNA comprises a single open reading frame that predicts a Type II transmembrane protein composed of 352 amino acids. The protein has an amino acid sequence homology of 96% with mouse C4ST. When the cDNA was introduced into a eukaryotic expression vector and transfected in COS-7 cells, the sulfotransferase activity that transfers sulfate to both chondroitin and desulfated dermatan sulfate was overexpressed. Northern blot analysis indicated that human C4ST mRNAs (6.0 and 1.9 kb) are expressed ubiquitously in various adult human tissues. Dot blot analysis has shown that human C4ST is strongly expressed in colorectal adenocarcinoma and peripheral blood leukocytes, whereas strong expression of human chondroitin 6-sulfotransferase (C6ST) is observed in aorta and testis. These observations suggest that the expression of C4ST and C6ST may be controlled differently in human tissues. The C4ST gene was localized to chromosome 12q23.2-q23.3 by fluorescence in situ hybridization.

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Currently, no three-dimensional reference data exist for the normal coccyx in the standing position on computed tomography (CT); however, this information could have utility for evaluating patients with coccydynia and pelvic floor dysfunction. Thus, we aimed to compare coccygeal parameters in the standing versus supine positions using upright and supine CT and evaluate the effects of sex, age, and body mass index (BMI) on coccygeal movement. Thirty-two healthy volunteers underwent both upright (standing position) and conventional (supine position) CT examinations. In the standing position, the coccyx became significantly longer and straighter, with the tip of the coccyx moving backward and downward (all p < 0.001). Additionally, the coccygeal straight length (standing/supine, 37.8 ± 7.1/35.7 ± 7.0 mm) and sacrococcygeal straight length (standing/supine, 131.7 ± 11.2/125.0 ± 10.7 mm) were significantly longer in the standing position. The sacrococcygeal angle (standing/supine, 115.0 ± 10.6/105.0 ± 12.5°) was significantly larger, while the lumbosacral angle (standing/supine, 21.1 ± 5.9/25.0 ± 4.9°) was significantly smaller. The migration length of the tip of the coccyx (mean, 7.9 mm) exhibited a moderate correlation with BMI (r = 0.42, p = 0.0163). Our results may provide important clues regarding the pathogenesis of coccydynia and pelvic floor dysfunction.

Serous cystic neoplasms are relatively uncommon and rarely possess malignant potential. We report a rare case of pancreatic serous cystadenoma with splenic invasion in a female in her 60s. Dynamic contrast-enhanced CT revealed a 3 cm mass in the tail of the pancreas. The lesion showed marked enhancement in the arterial phase on dynamic CT, which extended into the spleen. No cystic components were detected in the pancreatic mass on either magnetic resonance cholangiopancreatography or T2 weighted imaging. No metastasis or lymph node swelling was detected. Based on the hypervascularity of the tumour, the pre-operative diagnosis was pancreatic neuroendocrine tumour with splenic invasion. The patient underwent laparoscopic distal pancreatectomy with splenectomy. The pathological diagnosis was microcystic serous cystadenoma with locally aggressive features (infiltration into spleen, lymph nodes, and splenic vein). A few cases of pancreatic serous cystadenomas with splenic invasion have been reported; all were symptomatic, with diameters greater than approximately 9 cm. This is the first known case of incidentally detected serous cystadenoma with splenic invasion, reported with detailed imaging findings of dynamic CT and MRI.