54 research outputs found
Survivin expression in ovarian cancer
Aim: To examine the expression of survivin in benign ovarian tumors, ovarian carcinomas of different stages. Methods: We screened the expression of survivin mRNA by reverse transcription polymerase chain reaction in 114 ovarian tissue samples. Quantitative real-time PCR was used to estimate survivin mRNA levels in the samples with positive survivin expression. Results: No survivin mRNA was expressed in all normal ovarian specimens, while it appeared in 73% of ovarian carcinomas, 47% of borderline ovarian carcinomas and 19% of benign ovarian tumors. The survivin mRNA expression rate was positively associated with clinical stage (P = 0.026) and differentiation grade (P = 0.049). There was notably statistically significant difference in the survivin mRNA expression rate dependent on different histological types (serous, mucinous, endometrioid, P = 0.008), but not β dependent on lymph node metastasis (P = 0.921) and ascites (P = 0.87). In tissues with positive expression of survivin, we also found that mean survivin mRNA expression levels were higher in ovarian carcinomas than that in benign ovarian tumors and borderline ovarian carcinoma tissues (P < 0.001). Among ovarian carcinomas, the high survivin mRNA expression levels correlated with the clinical stages, differentiation grade, lymph node metastasis, but not β with ascites and histological type. Conclusion: Our study suggest that survivin is associated with progression of ovarian carcinoma.Π¦Π΅Π»Ρ: ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°ΡΡ ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΡ ΡΡΡΠ²ΠΈΠ²ΠΈΠ½Π° Π² Π΄ΠΎΠ±ΡΠΎΠΊΠ°ΡΠ΅ΡΡΠ²Π΅Π½Π½ΡΡ
ΠΈ Π·Π»ΠΎΠΊΠ°ΡΠ΅ΡΡΠ²Π΅Π½Π½ΡΡ
Π½ΠΎΠ²ΠΎΠΎΠ±ΡΠ°Π·ΠΎΠ²Π°Π½ΠΈΡΡ
ΡΠΈΡΠ½ΠΈΠΊΠ°. ΠΠ΅ΡΠΎΠ΄Ρ: ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΡ
ΠΌΠ ΠΠ ΡΡΡΠ²ΠΈΠ²ΠΈΠ½Π° ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½Π° ΠΌΠ΅ΡΠΎΠ΄ΠΎΠΌ RT-PCR Π² 114 ΠΎΠ±ΡΠ°Π·Π°Ρ
ΡΠΊΠ°Π½ΠΈ ΡΠΈΡΠ½ΠΈΠΊΠ° ΡΠ΅Π»ΠΎΠ²Π΅ΠΊΠ°. ΠΠ»Ρ ΡΡΡΠ°Π½ΠΎΠ²Π»Π΅Π½ΠΈΡ ΡΡΠΎΠ²Π½Ρ ΡΠΊΡΠΏΡΠ΅ΡΠΈΠΈ
ΠΌΠ ΠΠ ΡΡΡΠ²ΠΈΠ²ΠΈΠ½Π° ΠΏΡΠΈΠΌΠ΅Π½ΡΠ»ΠΈ ΠΊΠΎΠ»ΠΈΡΠ΅ΡΡΠ²Π΅Π½Π½ΡΠΉ PCR Π² ΡΠ΅ΠΆΠΈΠΌΠ΅ ΡΠ΅Π°Π»ΡΠ½ΠΎΠ³ΠΎ Π²ΡΠ΅ΠΌΠ΅Π½ΠΈ. Π Π΅Π·ΡΠ»ΡΡΠ°ΡΡ: ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΡ ΠΌΠ ΠΠ ΡΡΡΠ²ΠΈΠ²ΠΈΠ½Π°
Π½Π΅ Π²ΡΡΠ²Π»Π΅Π½Π° Π² ΠΎΠ±ΡΠ°Π·ΡΠ°Ρ
Π½ΠΎΡΠΌΠ°Π»ΡΠ½ΠΎΠΉ ΡΠΊΠ°Π½ΠΈ ΡΠΈΡΠ½ΠΈΠΊΠ°, Π½ΠΎ Π·Π°ΡΠ΅Π³ΠΈΡΡΡΠΈΡΠΎΠ²Π°Π½Π° Π² 73% ΡΠ»ΡΡΠ°Π΅Π² ΡΠ°ΠΊΠ° ΡΠΈΡΠ½ΠΈΠΊΠ°, 47% ΡΠ»ΡΡΠ°Π΅Π² ΡΠ΅ΡΠΎΠ·Π½ΡΡ
ΠΎΠΏΡΡ
ΠΎΠ»Π΅ΠΉ ΡΠΈΡΠ½ΠΈΠΊΠ° ΡΠ΅ΡΠΎΠ·Π½ΠΎΠ³ΠΎ ΡΠΈΠΏΠ° ΠΈ 19% ΠΎΠ±ΡΠ°Π·ΡΠΎΠ² Π΄ΠΎΠ±ΡΠΎΠΊΠ°ΡΠ΅ΡΡΠ²Π΅Π½Π½ΡΡ
ΠΎΠΏΡΡ
ΠΎΠ»Π΅ΠΉ. Π£ΡΡΠ°Π½ΠΎΠ²Π»Π΅Π½Π° ΠΏΠΎΠ»ΠΎΠΆΠΈΡΠ΅Π»ΡΠ½Π°Ρ Π·Π°Π²ΠΈΡΠΈΠΌΠΎΡΡΡ ΠΌΠ΅ΠΆΠ΄Ρ
ΡΡΠΎΠ²Π½Π΅ΠΌ ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΠΈ ΠΌΠ ΠΠ ΡΡΡΠ²ΠΈΠ²ΠΈΠ½Π° ΠΈ ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΎΠΉ ΡΡΠ°Π΄ΠΈΠ΅ΠΉ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡ (P = 0,026), ΠΈ ΡΡΠ΅ΠΏΠ΅Π½ΡΡ Π΄ΠΈΡΡΠ΅ΡΠ΅Π½ΡΠΈΡΠΎΠ²ΠΊΠΈ ΠΎΠΏΡΡ
ΠΎΠ»ΠΈ
(P = 0,049). ΠΡΡΠ²Π»Π΅Π½Π° ΡΡΠ°ΡΠΈΡΡΠΈΡΠ΅ΡΠΊΠΈ Π·Π½Π°ΡΠΈΠΌΠ°Ρ Π·Π°Π²ΠΈΡΠΈΠΌΠΎΡΡΡ ΡΡΠΎΠ²Π½Ρ ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΠΈ ΠΌΠ ΠΠ ΡΡΡΠ²ΠΈΠ²ΠΈΠ½Π° ΠΎΡ Π³ΠΈΡΡΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ ΡΠΈΠΏΠ°
ΠΎΠΏΡΡ
ΠΎΠ»ΠΈ (ΡΠ΅ΡΠΎΠ·Π½ΠΎΠ³ΠΎ, ΠΌΡΠΊΠΎΠ·Π½ΠΎΠ³ΠΎ, ΡΠ½Π΄ΠΎΠΌΠ΅ΡΡΠΈΠΎΠΈΠ΄Π½ΠΎΠ³ΠΎ, P = 0,008) ΠΈ ΠΎΡΡΡΡΡΡΠ²ΠΈΠ΅ ΡΠ°ΠΊΠΎΠ²ΠΎΠΉ ΠΎΡ Π½Π°Π»ΠΈΡΠΈΡ ΠΌΠ΅ΡΠ°ΡΡΠ°Π·ΠΎΠ² Π² Π»ΠΈΠΌΡΠ°ΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΡΠ·Π»Π°Ρ
(P = 0.921) ΠΈΠ»ΠΈ Π°ΡΡΠΈΡΠ° (P = 0.87). Π’Π°ΠΊΠΆΠ΅ ΡΡΡΠ°Π½ΠΎΠ²Π»Π΅Π½ΠΎ, ΡΡΠΎ ΡΡΠ΅Π΄Π½ΠΈΠ΅ ΡΡΠΎΠ²Π½ΠΈ ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΠΈ ΠΌΠ ΠΠ ΡΡΡΠ²ΠΈΠ²ΠΈΠ½Π° Π²ΡΡΠ΅ ΠΏΡΠΈ ΡΠ°ΠΊΠ΅
ΡΠΈΡΠ½ΠΈΠΊΠ°, ΡΠ΅ΠΌ Π² ΡΠΊΠ°Π½ΠΈ Π΄ΠΎΠ±ΡΠΎΠΊΠ°ΡΠ΅ΡΡΠ²Π΅Π½Π½ΡΡ
Π½ΠΎΠ²ΠΎΠ±ΡΠ°Π·ΠΎΠ²Π°Π½ΠΈΠΉ ΠΈΠ»ΠΈ ΡΠ΅ΡΠΎΠ·Π½ΡΡ
ΠΎΠΏΡΡ
ΠΎΠ»Π΅ΠΉ ΡΠΈΡΠ½ΠΈΠΊΠ° ΠΏΠΎΠ³ΡΠ°Π½ΠΈΡΠ½ΠΎΠ³ΠΎ ΡΠΈΠΏΠ° (P < 0,001).
ΠΡΠΈ ΡΠ°ΠΊΠ΅ ΡΠΈΡΠ½ΠΈΠΊΠ° Π²ΡΡΠΎΠΊΠΈΠΉ ΡΡΠΎΠ²Π΅Π½Ρ ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΠΈ ΠΌΠ ΠΠ ΡΡΡΠ²ΠΈΠ²ΠΈΠ½Π° ΠΊΠΎΡΡΠ΅Π»ΠΈΡΠΎΠ²Π°Π» Ρ ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΎΠΉ ΡΡΠ°Π΄ΠΈΠ΅ΠΉ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡ, ΡΡΠ΅ΠΏΠ΅Π½ΡΡ
Π΄ΠΈΡΡΠ΅ΡΠ΅Π½ΡΠΈΡΠΎΠ²ΠΊΠΈ ΠΎΠΏΡΡ
ΠΎΠ»Π΅Π²ΡΡ
ΠΊΠ»Π΅ΡΠΎΠΊ, Π½ΠΎ Π½Π΅ ΠΊΠΎΡΡΠ΅Π»ΠΈΡΠΎΠ²Π°Π» Ρ Π³ΠΈΡΡΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΠΌ ΡΠΈΠΏΠΎΠΌ Π½ΠΎΠ²ΠΎΠΎΠ±ΡΠ°Π·ΠΎΠ²Π°Π½ΠΈΡ. ΠΡΠ²ΠΎΠ΄Ρ: ΡΠ΅Π·ΡΠ»ΡΡΠ°ΡΡ
ΡΠ²ΠΈΠ΄Π΅ΡΠ΅Π»ΡΡΡΠ²ΡΡΡ ΠΎ ΡΠΎΠΌ, ΡΡΠΎ ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΡ ΡΡΡΠ²ΠΈΠ²ΠΈΠ½Π° Π°ΡΡΠΎΡΠΈΠΈΡΠΎΠ²Π°Π½Π° Ρ ΠΏΡΠΎΠ³ΡΠ΅ΡΡΠΈΠ΅ΠΉ ΡΠ°ΠΊΠ° ΡΠΈΡΠ½ΠΈΠΊΠ°.
ΠΠ»ΡΡΠ΅Π²ΡΠ΅ ΡΠ»ΠΎΠ²Π°: ΡΡΡΠ²ΠΈΠ²ΠΈΠ½, ΡΠ°ΠΊ ΡΠΈΡΠ½ΠΈΠΊΠ°, ΠΎΠΏΡΡ
ΠΎΠ»Π΅Π²Π°Ρ ΠΏΡΠΎΠ³ΡΠ΅ΡΡΠΈΡ
Equilibrium conditions for semi-clathrate hydrates formed with CO2, N2 or CH4 in the presence of tri-n-butylphosphine oxide
We measured the thermodynamic stability conditions for the N, CO, or CH semiclathrate hydrate formed from the aqueous solution of tri-n-butylphosphine oxide (TBPO) at 26 wt %, corresponding to the stoichiometric composition for TBPOΒ·34.5HO. The measurements were performed in the temperature range 283.71-300.34 K and pressure range 0.35-19.43 MPa with the use of an isochoric equilibrium step-heating pressure-search method. The results showed that the presence of TBPO made these semiclathrate hydrates much more stable than the corresponding pure N , CO, and CH hydrates. At a given temperature, the semiclathrate hydrate of 26 wt % TBPO solution + CH was more stable than that of 26 wt % TBPO solution + CO, which in turn was more stable than that of 26 wt % TBPO solution + N. We analyzed the phase equilibrium data using the Clausius-Clapeyron equation and found that, in the pressure range 0-20 MPa, the mean dissociation enthalpies for the semiclathrate hydrate systems of 26 wt % TBPO solution + N, 26 wt % TBPO solution + CO, and 26 wt % TBPO solution + CH were 177.75, 206.23, and 159.00 kJΒ·mol, respectively
Overexpression of extracellular superoxide dismutase reduces acute radiation induced lung toxicity
BACKGROUND: Acute RT-induced damage to the lung is characterized by inflammatory changes, which proceed to the development of fibrotic lesions in the late phase of injury. Ultimately, complete structural ablation will ensue, if the source of inflammatory / fibrogenic mediators and oxidative stress is not removed or attenuated. Therefore, the purpose of this study is to determine whether overexpression of extracellular superoxide dismutase (EC-SOD) in mice ameliorates acute radiation induced injury by inhibiting activation of TGFΞ²1 and downregulating the Smad 3 arm of its signal transduction pathway. METHODS: Whole thorax radiation (single dose, 15 Gy) was delivered to EC-SOD overexpressing transgenic (XRT-TG) and wild-type (XRT-WT) animals. Mice were sacrificed at 1 day, 1 week, 3, 6, 10 and 14 weeks. Breathing rates, right lung weights, total/differential leukocyte count, activated TGFΞ²1 and components of its signal transduction pathway (Smad 3 and p-Smad 2/3) were assessed to determine lung injury. RESULTS: Irradiated wild-type (XRT-WT) animals exhibited time dependent increase in breathing rates and right lung weights, whereas these parameters were significantly less increased (p < 0.05) at 3, 6, 10 and 14 weeks in irradiated transgenic (XRT-TG) mice. An inflammatory response characterized predominantly by macrophage infiltration was pronounced in XRT-WT mice. This acute inflammation was significantly attenuated (p < 0.05) in XRT-TG animals at 1, 3, 6 and 14 weeks. Expression of activated TGFΞ²1 and components of its signal transduction pathway were significantly reduced (p < 0.05) at later time-points in XRT-TG vs. XRT-WT. CONCLUSION: This study shows that overexpression of EC-SOD confers protection against RT-induced acute lung injury. EC-SOD appears to work, in part, via an attenuation of the macrophage response and also decreases TGFΞ²1 activation with a subsequent downregulation of the profibrotic TGFΞ² pathway
NOA1 Functions in a Temperature-Dependent Manner to Regulate Chlorophyll Biosynthesis and Rubisco Formation in Rice
NITRIC OXIDE-ASSOCIATED1 (NOA1) encodes a circularly permuted GTPase (cGTPase) known to be essential for ribosome assembly in plants. While the reduced chlorophyll and Rubisco phenotypes were formerly noticed in both NOA1-supressed rice and Arabidopsis, a detailed insight is still necessary. In this study, by using RNAi transgenic rice, we further demonstrate that NOA1 functions in a temperature-dependent manner to regulate chlorophyll and Rubisco levels. When plants were grown at 30Β°C, the chlorophyll and Rubisco levels in OsNOA1-silenced plants were only slightly lower than those in WT. However, at 22Β°C, the silenced plants accumulated far less chlorophyll and Rubisco than WT. It was further revealed that the regulation of chlorophyll and Rubisco occurs at the anabolic level. Etiolated WT seedlings restored chlorophyll and Rubisco accumulations readily once returned to light, at either 30Β°C or 15Β°C. Etiolated OsNOA1-silenced plants accumulated chlorophyll and Rubisco to normal levels only at 30Β°C, and lost this ability at low temperature. On the other hand, de-etiolated OsNOA1-silenced seedlings maintained similar levels of chlorophyll and Rubisco as WT, even after being shifted to 15Β°C for various times. Further expression analyses identified several candidate genes, including OsPorA (NADPH: protochlorophyllide oxidoreductase A), OsrbcL (Rubisco large subunit), OsRALyase (Ribosomal RNA apurinic site specific lyase) and OsPuf4 (RNA-binding protein of the Puf family), which may be involved in OsNOA1-regulated chlorophyll biosynthesis and Rubisco formation. Overall, our results suggest OsNOA1 functions in a temperature-dependent manner to regulate chlorophyll biosynthesis, Rubisco formation and plastid development in rice
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Cirmtuzumab inhibits ibrutinib-resistant, Wnt5a-induced Rac1 activation and proliferation in mantle cell lymphoma.
Cirmtuzumab may enhance the therapeutic activity of ibrutinib by inhibiting ROR1-dependent signaling pathway in patients with chronic lymphocytic leukemia (CLL). Mantle cell lymphoma (MCL) is B-cell malignancy that also expresses ROR1. In this study, we found that the plasma of patients with MCL had high levels of Wnt5a, a ROR1 ligand, that were comparable to those found in patients with CLL; in contrast Wnt5a was virtually undetectable in the plasma of age-matched healthy adults. We also found that Wnt5a induced Rac1 activation in the primary MCL cells. Cirmtuzumab, but not ibrutinib, could inhibit the capacity of Wnt5a to induce primary MCL cells to activate Rac1. Addition of exogenous Wnt5a in vitro significantly enhanced the numbers of MCL cell divisions and the proportion of dividing MCL cells entering S/G2 in MCL cells over time in the presence of CD154 and IL-4/10. Treatment of the MCL cells with cirmtuzumab, but not ibrutinib, blocked Wnt5a-enhanced proliferation of MCL cells. This study indicates that cirmtuzumab and ibrutinib may have complementary activity in the treatment of patients with MCL
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