Detachment of cell-cell adhesion is indispensable for the first step of invasion and metastasis of cancer. This mechanism is frequently associated with the impairment of either E-cadherin expression or function. However, mechanisms of such abnormalities have not been fully elucidated. In this study, we demonstrated that the function of E-cadherin was completely abolished in the human gastric cancer cell line HSC-39, despite the high expression of E-cadherin, because of mutations in one of the E-cadherin-associated cytoplasmic proteins, ␤-catenin. Although immunofluorescence staining of HSC-39 cells by using an anti-E-cadherin antibody (HECD-1) revealed the strong and uniform expression of E-cadherin on the cell surface, cell compaction and cell aggregation were not observed in this cell. Western blotting (immunoblotting) using HECD-1 exhibited a 120-kDa band which is equivalent to normal E-cadherin. Northern (RNA) blotting demonstrated a 4.7-kb band, the same as mature E-cadherin mRNA. Immunoprecipitation of metabolically labeled proteins with HECD-1 revealed three bands corresponding to E-cadherin, ␣-catenin, and ␥-catenin and a 79-kDa band which was apparently smaller than that of normal ␤-catenin, indicating truncated ␤-catenin. The 79-kDa band was immunologically identified as ␤-catenin by using immunoblotting with anti-␤-catenin antibodies. Examination of ␤-catenin mRNA by the reverse transcriptase-PCR method revealed a transcript which was shorter than that of normal ␤-catenin. The sequencing of PCR product for ␤-catenin confirmed deletion in 321 bases from nucleotides ؉82 to ؉402. Southern blotting of ␤-catenin DNA disclosed mutation at the genomic level. Expression vectors of ␤-catenin were introduced into HSC-39 cells by transfection. In the obtained transfectants, E-cadherin-dependent cell-cell adhesiveness was recovered, as revealed by cell compaction, cell aggregation, and immunofluorescence staining. From these results, it was concluded that in HSC-39 cells, impaired cell-cell adhesion is due to mutations in ␤-catenin which results in the dysfunction of E-cadherin.

Using high‐quality data for dissolved inorganic carbon and related properties obtained about 10 years apart (1992/1993–2003), we examined decadal increases of anthropogenic CO2 (ΔnCTCAL) along 30°S (WHP A10 section) in the subtropical South Atlantic. Significant ΔnCTCAL was detectable down to an isopycnal surface of σθ = 27.3 (∼1000 m water depth). Averaged ΔnCTCAL in Sub‐Antarctic Mode Water (SAMW; 26.6–27.0 σθ, 350–700 m) was 6.8 ± 1.6 μmol kg−1 and that in Antarctic Intermediate Water (AAIW; 27.1–27.4 σθ, 700–1200 m) was 3.6 ± 1.4 μmol kg−1. In SAMW, ΔnCTCAL was higher by ∼7 μmol kg−1 west of 15°W than east of it, while ΔnCTCAL in AAIW did not show such a distinct east‐west difference. For deep waters, significant ΔnCTCAL was detected in Antarctic Bottom Water at depths greater than 4500 m in the Cape Basin (longitude 2°E–10°E). No significant ΔnCTCAL could be detected for North Atlantic Deep Water (NADW). We attributed ΔnCTCAL being higher west of 15°W in SAMW to differences of water mass distributions and flows. From a water column inventory, we estimated the uptake rate of anthropogenic CO2 over the decade from 1992/1993 to 2003 to be 0.6 ± 0.1 mol m−2 a−1, which is half the rate in the South Pacific (1.0 ± 0.4 mol m−2 a−1).

A case of cervical radiculomyelopathy caused by multiple calcified nodules in the ligamenta flava is presented. Roentgenological examination of the cervical spine showed radiopaque nodular lesions, 7 x 7 x 5 mm in size, located in the paramedian portion of the posterior spinal canal. The nodules were removed surgically and they were confirmed to be calcifications of ligamenta flava. Microscopic examination of the nodules with the polarized light revealed extensive deposition of crystals. By x-ray diffraction study, the crystal was determined as calcium pyrophosphate dihydrate (CPPD: Ca2P2O7 . 2H2O). Although CPPD deposition in the cartilage has been known as pseudo-gout syndrome, deposition in the ligament has been reported only in a few cases. This is the first case with radiopaque calcified nodules in the ligamenta flava causing spinal cord compression, the composition of which proved to be CPPD.

Abstract. Rising atmospheric CO 2 contents have led to greater CO 2 uptake by the oceans, lowering both pH due to increasing hydrogen ions and CaCO 3 saturation states due to declining carbonate ion (CO 2− 3 ). Here we used previously compiled data sets and new data collected in 2010 and 2011 to investigate ocean acidification of the North Pacific western subarctic gyre. In winter, the western subarctic gyre is a source of CO 2 to the atmosphere because of convective mixing of deep waters rich in dissolved inorganic carbon (DIC). We calculated pH in winter mixed layer from DIC and total alkalinity (TA), and found that it decreased at the rate of −0.0011 ± 0.0004 yr −1 from 1997 to 2011. This decrease rate is slower than that expected under the condition of seawater/atmosphere equilibration, and it is also slower than the rate in the subtropical regions (−0.002 yr −1 ). The slow rate is caused by a reduction of CO 2 emission in winter due to an increase in TA. Below the mixed layer, the calcite saturation horizon (∼ 185 m depth) shoaled at the rate of 2.9 ± 0.9 m yr −1 as the result of the declining CO 2− 3 concentration (−0.03 ± 0.01 µmol kg −1 yr −1 ). Between 200 m and 300 m depth, pH decline during the study period (−0.0051 ± 0.0010 yr −1 ) was larger than ever reported in the open North Pacific. This enhanced acidification rate below the calcite saturation horizon reflected not only the uptake of anthropogenic CO 2 but also the increase in the decomposition of organic matter evaluated from the increase in AOU, which suggests that the dissolution of CaCO 3 particles increased.

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