A novel HLA-B allele, HLA-B*39:01:16, identified by super high-resolution single-molecule sequence-based typing in a Japanese individual.

HLA-B*39:01:16 differs from B*39:01:03 by one nucleotide 348 (codon 116) T to C.

Induction of urokinase-type plasminogen activator by the anthracycline antibiotic in human RC-K8 lymphoma and H69 lung-carcinoma cells.

Current evidence has suggested the possible involvement of ROS as signaling messengers in IL-1beta- or LPS-induced gene expression. We previously reported that both IL-1beta and LPS induce uPA in RC-K8 human lymphoma cells. Here, we provide evidence that ROS-generating anthracycline antibiotics, including doxorubicin and aclarubicin, upregulate uPA expression in 2 human malignant cell lines, RC-K8 and H69 small-cell lung-carcinoma cells. Both doxorubicin and aclarubicin markedly increased uPA accumulation in RC-K8- and H69-conditioned medium in a dose-dependent manner. In each case, maximal induction was observed at a sublethal concentration, i.e., at a concentration where cell growth was slightly inhibited. Both doxorubicin and aclarubicin increased uPA mRNA levels, and induction in each case reached the maximal level 9 hr after stimulation. Doxorubicin barely changed the half-life of uPA mRNA and activated uPA gene transcription. Antioxidants such as NAC and PDTC inhibited doxorubicin-induced uPA mRNA accumulation. Microarray analysis, using Human Cancer CHIP version 2 (Takara Shuzo, Kyoto, Japan), in which 425 human cancer-related genes were spotted on glass plates, revealed that uPA is 1 of 3 genes that were clearly upregulated in H69 cells by doxorubicin stimulation. These findings suggest that the anthracycline induces uPA in human malignant cells by activating gene transcription in which ROS may be involved. Therefore, by upregulating uPA expression, the anthracycline may influence many biologic cell functions mediated by the uPA/plasmin system.

Paraaortic lymphadenectomy in patients with advanced carcinoma of the upper-third of the stomach.

BACKGROUND/AIMS: According to current TNM classification, paraaortic nodes involvement in gastric cancer is now distant metastasis. Anatomically, however, proximal gastric cancer may drain preferentially to the left-paraaortic area which represents a regional lymph-node basin. METHODOLOGY: Seventy-five patients who underwent an extended gastrectomy with paraaortic lymphadenectomy for advanced carcinoma of the upper-third of the stomach were retrospectively studied. RESULTS: Of the 75 patients, 55 (73.3%) were positive for nodal metastasis and 21 (28.0%) had paraaortic nodes involvement. Paraaortic nodes involvement tended to be left-sided (the left side of the aorta around the left renal vein) and its incidence did not increase as the overall number of infiltrated nodes increased. Five (23.8%) of the 21 patients with paraaortic nodes involvement did not have nodal metastases in the paraceliac area. Overall survival was not different whether or not paraaortic nodes involvement was present, but was dependent on the overall number of infiltrated nodes (viz. 10 vs. > 10). Eight (22.2%) of 36 patients with 1-10 infiltrated nodes had PNI, with a 5-year survival rate of 46.9%. CONCLUSIONS: Removal of lymph nodes around the left renal vein should be included during extended gastrectomy in patients with advanced carcinoma of the upper-third of the stomach. Left-paraaortic lymphadenectomy may benefit such patients if the overall number of infiltrated nodes is low (viz. 10).

[A case of pharyngeal-cervical-brachial variant of Guillain-Barré syndrome with positive anti-galactocerebroside (Gal-C) IgM antibody].

A 49-year-old man presented with hoarseness, dysphagia, muscle atrophy and weakness of deltoid, trapezius, sternocleidomastoid, rhomboid, anterior serratus, infraspinatus and supraspinatus. Anti-Gal-C IgM antibody was positive in the serum. The other antiganglioside antibodies (GM1, GM2, GM3, GD1a, GD1b, GD3, GT1a, GT1b, GQ1b, GA1, GalNAc-GD1a, GM1b) were negative. Patient contracted pneumonia but whether it was due to mycoplasma was not evident. Plasmapheresis improved his clinical state including a decrease of the antibody. This case was diagnosed pharyngeal-cervical-brachial variant of Guillain-Barré syndrome, and anti-Gal-C antibody seemed to be correlated with the pathogenesis of this syndrome. Gal-C is a major glycolipid of myelin and the cell membrane of the myelin-forming cell (oligodendrocytes and Schwann cells) and is free of specific localization and distribution. The mechanism how the anti-Gal-C IgM antibody induced bulbar paralysis and the symptoms localizing neck and upper limbs remains to be known.

Eosinophilic pneumonia with eosinophilic gastroenteritis.

A 48-year-old man was admitted to our hospital with cough, fever and dysphagia. He had a past history of bronchial asthma and surgery for nasal polyp. Chest radiograph and computed tomography showed atelectasis in the right lower field and infiltrative shadow in the left lower field and overall thickening of the esophageal wall. Transbronchial lung biopsy (TBLB) specimens revealed infiltration of eosinophils and lymphocytes under the bronchial mucosa. Gastrointestinal tract biopsy specimens showed submucosal infiltration of eosinophils. These findings led to a definite diagnosis of eosinophilic pneumonia associated with eosinophilic gastroenteritis, a disease which has been rarely reported.

Case report: intrahepatic portal-hepatic venous shunts associated with a huge pelvic leiomyoma.

We present a case of portal-systemic encephalopathy due to intrahepatic multiple portal-hepatic venous shunts. A 71-year-old woman was admitted to our hospital because of recurrent episodes of disturbed consciousness. She showed no clinical signs of portal hypertension. Liver function was normal, except for an indocyanine green retention rate of 34% at 15 min and blood ammonia level of 282 microg/dL. Portal venography revealed dilatation of the portal vein and multiple portal-hepatic venous shunts, and a liver biopsy specimen revealed almost normal liver. Further clinical examination revealed a huge pelvic tumour. At laparotomy, two dilated veins were seen to arise from the pelvic tumour with blood flow into the mesentery. The tumour was resected successfully and a histological diagnosis of leiomyoma was made. The blood ammonia concentration decreased to the normal range postoperatively. A follow-up portal venogram demonstrated decreased portal vein dilatation and minor portal-hepatic venous shunts, considered to be congenital in origin. It is concluded that hepatic encephalopathy was produced in this patient due to an excess portal blood flow from the huge pelvic leiomyoma via the mesentery, with portosystemic shunting through pre-existent (probably congenital) intrahepatic anastomoses.