A gastric tube has been widely used for reconstruction of the esophagus after esophagectomy for esophageal cancer. Reflux esophagitis after esophagectomy is frequently observed. Therefore we retrospectively investigated the risk factors for reflux esophagitis after gastric pull-up esophagectomy in 74 outpatients with thoracic esophageal cancer. Reflux esophagitis was diagnosed endoscopically. Esophagitis was classified according to the Los Angeles classification. Reflux symptoms, medications, and the surgical procedure were reviewed. The relation between reflux symptoms and reflux esophagitis and the influence of the anastomotic site were evaluated. Reflux esophagitis was observed in 53 patients. Severe esophagitis (grade C or D) was found in 75.6% of these patients. Although all patients with esophagitis took antacid agents, histamine receptor-2 blocker was effective in only 35% of them. The correlation between reflux symptoms and reflux esophagitis was not significant. Reflux esophagitis was present in 56.4% of patients with neck anastomosis and in 88.6% of patients with intrathoracic anastomosis ( p = 0.0039). We concluded that routine endoscopic examination is necessary after gastric pull-up esophagectomy because reflux esophagitis is not diagnosed based on reflux symptoms. When a gastric tube is used for reconstruction after esophagectomy, neck anastomosis is recommended to lower the risk of reflux esophagitis.
IntroductionIn 2011, Fukushima was struck by a triple disaster: an earthquake, tsunamis, and a nuclear accident. In the aftermath, there was much fear among hospital staff members about radiation exposure and many staff members failed to report to work.ObjectivesOne objective is to measure this shortage in hospital staff and another is to compare the difference in recovery by hospital types and by categories of hospital staff.DesignThe monthly records of the number of staff members from May 2011 to September 2012 were extracted anonymously from the records of 7 local hospitals in the Soso district in Fukushima. Change in the number of staff was analyzed.ResultsStaff shortages at hospitals reached a maximum within one month after the disaster (47% reported to work). The shortage of clerks was the most severe (38% reported to work), followed by nurses (48% reported to work). The shortages remained even 18 months after the disaster.ConclusionAfter a disaster in which the damage to hospital functions surpasses the structural damage, massive support of human resources in the acute phase and a smaller volume of support in the mid-term phase appear to be required, particularly for non-medical staff.
Increased sialylation in cell surface glycoproteins is one characteristic feature of cancer cells, particularly related to their metastatic potential and invasiveness. Expression of lysosomal-type sialidase, which plays a major role in hydrolysis of such sialo-glycoproteins, is therefore considered to have a great influence on malignant properties of cancer cells. To investigate whether the sialidase expression level is linked to the malignant phenotype, we transfected B16-BL6 murine melanoma cells, a highly invasive and metastatic line, with an expression vector harboring a rat lysosomal sialidase cDNA; then clones were isolated and examined for changes in biological character. Sialidase-overexpressing cells showed suppression of experimental pulmonary metastasis and tumor progression. The transfectants exhibited diminished cell growth, anchorage-independent growth and increased sensitivity to apoptosis induced by suspension culture or serum depletion in vitro, but no significant alterations in invasiveness, cell motility and cell attachment to fibronectin, collagen IV and laminin. Flow cytometric analysis with either peanut agglutinin (PNA) or Ricinus communis agglutinin (RCA) lectin revealed that desialylated forms of glycoproteins on the cell surfaces were increased. In particular, a desialylated form of a cell surface glycoprotein of 83 kDa was prominent in the transfectants, as determined by galactose oxidase labeling. These observations indicate that sialidase expression is inversely associated with metastatic potential and tumor growth in cancer cells, probably through a regulation mechanism that suppresses cell growth and anchorage-independent growth and promotes apoptosis with deprivation of cell anchorage. © 2001 Wiley-Liss, Inc. Key words: sialidase; metastasis; anchorage-independent growth; sialic acidsSialidase (EC 3.2.1.18) is a key enzyme in catabolism of glycoproteins and glycolipids. Desialylation of these glycoconjugates is a crucial event leading to modulation of cellular functions in numerous physiological and pathological processes. 1,2 Alterations in sialylation during malignant transformation have been observed to be closely associated with the malignant phenotype in terms of metastatic potential and invasiveness. [3][4][5][6][7] To understand how sialidases are involved in this aberrant sialylation, our study has focused on mammalian forms in cancer cells.Mammalian sialidases are classified into 3 to 4 forms based on their subcellular localization and substrate preference. Cytosolic, lysosomal and membrane forms of the sialidases have been cloned; their primary sequences revealed that they are proteins encoded by distinct genes with different major subcellular locations and enzymatic properties. 8 We previously demonstrated that metastatic potential is inversely correlated with lysosomal-type sialidase activity in transformed rat 3Y1 cells 9 and in murine B16 melanoma cells, 10 whereas it did not have a significant relation to sialic acid levels. We also investigated the role of sialidas...
Sialidase expression levels are inversely correlated with the metastatic potential of mouse colon adenocarcinoma 26 sublines, as assessed by activity assays and RT-PCR, irrespective of total and cell surface sialic acid contents. Compared with low metastatic NL4 and NL44 cell lines, the highly metastatic NL17 and NL22 cells exhibit low expression of sialidases, accompanied with higher levels of sialylLe x and GM3. To investigate whether these properties of NL17 cells can be altered by sialidase overexpression, we transfected a cytosolic sialidase gene into NL17 cells. The result was markedly inhibited lung metastasis, invasion and cell motility with a concomitant decrease in sialylLe x and GM3 levels, in line with the case of spontaneously low metastatic sublines having relatively high endogenous sialidase levels, implying that sialidase level is a determining factor affecting metastatic ability. Treatment of the cells with antibodies against sialylLe x and GM3 affected cell adhesion and/or cell motility, providing evidence that desialylation of these molecules, as targets of sialidase, is involved in the suppression of metastasis. Aberrant sialylation in cancer cells is generally accepted as one characteristic feature associated with metastatic potential. 1-5 Cellular sialic acid contents are controlled mainly by expression levels of sialyltransferases and sialidases. To elucidate the molecular mechanisms and significance of aberrant sialylation, our studies have been focused on sialidase. In the 1970s, exogenous sialidases of microbial origin were often used for studies on treatment with cancer cells to enhance tumor growth regression or cellular immunity. However, observations on endogenous sialidase of malignant cells can facilitate further understanding of the pathologic desialylation. Mammalian sialidases have so far been classified into 3 or 4 types differing in subcellular localization and enzymatic properties. Three types, located mainly in cytosol, lysosomes and plasma membranes, have been cloned. 6 Although many functional aspects of each sialidase have yet to be clarified, they are likely to be involved not only in catabolism of glycoconjugates but also in functional modulation through desialylation of molecules, depending on their particular subcellular location and substrate specificity. The lysosomal form may have a major role in glycoprotein catabolism by collaborating with lysosomal proteases or endoglycosidase, as fragmentation into glycopeptides or oligosaccharide chains is required before cleavage by this sialidase. 7 Cytosolic sialidase may participate in regulatory desialylation because of its ability to act on native glycoproteins and gangliosides at neutral pH. 8 Plasma membrane sialidase hydrolyzes gangliosides specifically 9,10 and has been suggested to participate in cell surface events.To understand the role of sialidases in metastasis, we previously measured activity levels in transformed rat 3Y1 cell lines and found an inverse correlation with metastatic potential. 11 No significant...
Stat3, a member of signal transducers and activators of transcription (STAT), is activated by a variety of cytokines. Recently, mice lacking Stat3 specifically in T cells have been generated and shown to be defective in IL-6-induced proliferation due to the impairment in IL-6-mediated prevention of apoptosis. In the present study, we show that Stat3-deficient T cells are partially defective in IL-2-induced proliferation. Stat3-deficient T cells show impaired IL-2-mediated IL-2 receptor (IL-2R) alpha chain expression. When Stat3-deficient T cells are stimulated with high-dose IL-2, these T cells express IL-2Ralpha and proliferate to similar extents as wild-type T cells. These demonstrate that Stat3 activation is required for efficient T cell proliferation by IL-2 through IL-2Ralpha induction. Taken together, these findings demonstrate that Stat3 activation in T cells is responsible for IL-2- and IL-6-induced proliferation through distinct mechanisms.
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