19 research outputs found

    Overexpression of DNA Polymerase ζAffects Cisplatin Resistance in Ovarian Cancer: An Immunohistochemical Study

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    DNA polymerase ζ (Pol ζ) participates in translesional bypass replication. Pol ζ has been shown to be an important contributor to cis-diamminedichloroplatinum (II)(DDP; cisplatin) -induced genomic instability and the subsequent emergence of resistance in vitro. We immunohistochemically examined the expression of Pol ζ in ovarian cancer tissues to determine whether its expression affects the DDP resistance of human ovarian cancers and also to determine whether Pol ζ expression is a prognostic factor for ovarian cancers. We assessed 76 archival, formalin-fixed, paraffin-embedded tissue samples obtained from patients with epithelial ovarian cancers who underwent their first operation between 2003 and 2011. An ovarian cancer tissue array was also used in this study. Immunohistochemical staining of Pol ζ was performed using an anti-human Pol ζ monoclonal rabbit antibody. The strength of expression of Pol ζ was compared with the DDP resistance and clinical features of the study population. The Pol ζ over-expression in ovarian cancer tissue which compared with epithelial cells in normal ovaries was not affected by the histological types, FIGO stage, or patient age, but Pol ζ was significantly more overexpressed in the DDP-resistant group than in the DDP-sensitive group (P = 0.043). Pol ζ over-expression did not significantly affect the survival rate of the ovarian cancer patients; however, the Pol ζ positive group tended to have a poorer long-term prognosis. In conclusion, ovarian carcinoma patients with Pol ζ over-expression are likely to be resistant to DDP, especially in cases of recurrent disease. These results confirm the previous findings in vitro, wherein Pol ζ modulated the cytotoxicity and mutagenicity of DDP

    血清アデノシンデアミナーゼ活性の測定法の改良とその臨床的応用

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    An improved method was devised for the estimation of serum adenosine deaminase activity. The principle of the method consists in measurement of a liberated ammonia by the action of the deaminase with a direct colorimetric determination of ammonia concentration [Okuda et al.]. The technique is relatively easy to estimate the serum enzyme activity and can be applied for routine clinical use. The serum adenosine deaminase activity assayed by this method was elevated in patients with hepatic disease and the others, such as auto-immune diseases, rheumatoid arthritis, malignant lymphoma, leukemia and multiple myeloma. The presented experiments were designed to clarify the origin of the elevated adenosine deaminase in serum. The heat stability and pH optimum were found to be essentially identical in sera from hepatic disease and the others. However, Michael is constant (Km) for adenosine and V max were higher in the sera from patients with hepatic diseases than those of the others. The isoelectrofocusing pattern of the serum enzyme was shown quite different between hepatic disease and the others. The results in the present investigation indicated that the enhanced serum adenosine deaminase activity and its isoenzyme pattern were very useful for clinical diagnosis

    Role of tube size and intranasal compression of the nasotracheal tube in respiratory pressure loss during nasotracheal intubation: a laboratory study

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    Abstract Background Small nasotracheal tubes (NTTs) and intranasal compression of the NTT in the nasal cavity may contribute to increasing airway resistance. Since the effects of size, shape, and partial compression of the NTT on airway resistance have not been investigated, values of airway resistance with partial compression of preformed NTTs of various sizes were determined. Methods To determine the factors affecting the respiratory pressure loss during the nasotracheal intubation, physical and fluid dynamics simulations were used. The internal minor axes of NTTs in the nasal cavity of intubated patients were measured using dial calipers. In physical and fluid dynamics simulations, pressure losses through the tubular parts, compressed parts, and slip joints of NTTs with internal diameters (IDs) of 6.0, 6.5, 7.0, 7.5, and 8.0 mm were estimated under partial compression. Results The median internal minor axes of the 7.0- and 7.5-mm ID NTTs in the nasal cavity were 5.2 (4.3–5.6) mm and 6.0 (4.2–7.0) mm, respectively. With a volumetric air flow rate of 30 L/min, pressure losses through uncompressed NTTs with IDs of 6.0-, 6.5-, 7.0-, 7.5- and 8.0-mm were 651.6 ± 5.7 (6.64 ± 0.06), 453.4 ± 3.9 (4.62 ± 0.04), 336.5 ± 2.2 (3.43 ± 0.02), 225.2 ± 0.2 (2.30 ± 0.00), and 179.0 ± 1.1 Pa (1.82 ± 0.01 cmH2O), respectively; the pressure losses through the slip joints were 220.3 (2.25), 131.1 (1.33), 86.8 (0.88), 57.1 (0.58), and 36.1 Pa (0.37 cmH2O), respectively; and the pressure losses through the curvature of the NTT were 71.6 (0.73), 69.0 (0.70), 64.8 (0.66), 32.5 (0.33), and 41.6 Pa (0.42 cmH2O), respectively. A maximum compression force of 34.1 N increased the pressure losses by 82.0 (0.84), 38.0 (0.39), 23.5 (0.24), 16.6 (0.17), and 9.3 Pa (0.09 cmH2O), respectively. Conclusion Pressure losses through NTTs are in inverse proportion to the tubes’ IDs; greater pressure losses due to slip joints, acute bending, and partial compression of the NTT were obvious in small NTTs. Pressure losses through NTTs, especially in small NTTs, could increase the work of breathing to a greater extent than that through standard tubes; intranasal compression further increases the pressure loss

    Changes in Magnesium Ion Concentration in Patients with Esophagectomy

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    HGP44 Induces Protection against Porphyromonas gingivalis-Induced Alveolar Bone Loss in Mice▿

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    The protective effect of DNA vaccines expressing the Arg-gingipain A domain against bone loss induced by Porphyromonas gingivalis infection was investigated in a murine model. phgp44, which expresses the 44-kDa adhesion/hemagglutinin domain of Arg-gingipain A, prevented P. gingivalis-induced alveolar bone loss. The results indicate that phgp44 could be a candidate antigen for a vaccine against P. gingivalis infection
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