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991.
重复采动覆岩裂隙率空间分布相似模拟研究——以陕北矿区为例 总被引:1,自引:0,他引:1
由于水资源短缺,陕北矿区利用采空区储存矿井水进行再利用,采空区储水量与采动裂隙空间分布密切相关,为准确预测采空区储水量,基于工作面上覆岩层断裂分带划分结果,确定煤矿地下水库的主要储水空间为垮落带与断裂带的裂隙空间,建立了采动覆岩裂隙率空间分布的计算方法,采用相似模拟试验得出了柠条塔矿1-2煤和2-2煤重复采动后上覆岩层的下沉曲线,计算出重复采动覆岩裂隙率在垂直和水平方向的空间分布情况。结果表明:沿垂直方向,随着高度增加,覆岩裂隙率逐渐减小,1-2煤开采后岩层裂隙率由1.87%逐渐下降为1.18%,2-2煤开采后,裂隙率由12.85%下降为4.11%;沿水平方向,垮落带、断裂带和弯曲下沉带的裂隙率在采空区边缘附近都会产生2个峰值,并且峰值位置逐渐向采空区中央移动,1-2煤开采后,中间压实区的最大裂隙率为1.21%,两边离层区的最大裂隙率为2.19%,2-2煤开采后,压实区和离层区最大裂隙率分别为16.1%和6.54%;重复开采后,上覆岩层的裂隙率显著增加,有... 相似文献
994.
根据剪切解络-超滤过程中金属离子的动态浓度关系和质量守恒定律,采用CodeBlocks17.12软件编写程序,建立了剪切解络-超滤工艺关键指标预测模型,实现了金属离子浓度、回收率、体积稀释倍数等指标的预测,并用实验加以验证。依次在转速800 r/min、1 400 r/min、3 000 r/min下回收模拟废水中43 μg/L的Co2+、995 μg/L的Ni2+和88 μg/L的La3+,3种金属的回收率均达99.8%以上时,超滤过程体积稀释倍数的预测值分别为7.0、7.5、5.75,实验值分别为7.5、7.25、6.25,可见预测值与实验值基本一致。本模型对研究方案制定和调整有实际指导意义。 相似文献
995.
996.
QIANSHAN TAO QING ZHANG HUIPING WANG HAO XIAO MEI ZHOU LINLIN LIU HUI QIN JIYU WANG FURUN AN ZHIMIN ZHAI YI DONG 《Biocell》2022,46(1):159-169
Acute myeloid leukemia (AML) is regarded as a stem cell disease. However, no one unique marker is expressed
on leukemia stem cells (LSC) but not on leukemic blasts nor normal hematopoietic stem cells (HSC). CD34+
CD38- with
or without CD123 or CD44 subpopulations are immunophenotypically defined as putative LSC fractions in AML.
Nevertheless, markers that can be effectively and simply held responsible for the intrinsical heterogeneity of LSC is
still unclear. In the present study, we examined the frequency of three different LSC subtypes (CD34+
CD38-,
CD34+
CD38-
CD123+
, CD34+
CD38-
CD44+
) in AML at diagnosis. We then validated their prognostic significance on
the relevance of spectral features for diagnostic stratification, immune status, induction therapy response, treatment
effect maintenance, and long-term survival. In our findings, high proportions of the above three different LSC
subtypes were all significantly characterized with low complete remission (CR) rate, high relapse/refractory rate, poor
overall survival (OS), frequent FLT3-ITD mutation, the high level of regulatory T cells (Treg) and monocytic
myeloid-derived suppressor cells (M-MDSC). However, there was no significant statistical difference in all kinds of
other clinical performance among the three different LSC groups. It was demonstrated that CD34+
CD38-
subpopulation without CD123 and CD44 might be held responsible for LSC and correlated with an imbalance of
immune cell subsets in AML. 相似文献
997.
BING WANG KAORU TANAKA KOUICHI MARUYAMA YASUHARA NINOMIYA TAKANORI KATSUBE MITSURU NENOI 《Biocell》2022,46(10):2315-2325
Investigation on possible induction of adaptive response (AR) by high-liner energy transfer (LET) particle
radiation for protection against low-LET photon radiation-induced detrimental effects has not yet been performed in
utero. This study verified if an AR could be induced by high-LET particle radiation from accelerated heavy ions
against low-LET X-ray radiation-induced detrimental effects on fetal mice. Total body irradiation of pregnant
C57BL/6J mice were performed by delivering a priming dose ranging from 10 mGy to 320 mGy of particle radiation
on gestation day 11 followed one day later by a challenge dose at 3500 mGy from X-ray radiation. The monoenergetic
beams of carbon, silicon and iron with the LET values of about 15, 55, and 200 KeV/μm, respectively, were examined.
Significant suppression by the priming radiation of the detrimental effects (fetal death, malformation, or low body
weight) was used as the endpoints for judgment of a successful AR induction on gestation day 18. Existence of AR
was not observed. On the other hand, the priming dose of high-LET particle radiation, in some cases, even increased
the detrimental effects induced by the challenge dose from low-LET X-ray radiation. Although existence of AR
induced by high-LET radiation in cultured mammalian cells in vitro
and in certain tissues of laboratory mice in vivo
was demonstrated, the present study did not suggest that low dose of high-LET particle radiation could induce an AR
in fetal mice in
utero under the setup of our experimental system. 相似文献
998.
Esophageal cancer (EC) was an aggressive malignant neoplasm characterized by high morbidity and poor prognosis. Identifying the changes in DNA damage repair genes helps to better understand the mechanisms of carcinoma progression. In this study, by comparing EC samples and normal samples, we found a total of 132 DDR expression with a significant difference. Moreover, we revealed higher expression of POLN, PALB2, ATM, PER1, TOP3B and lower expression of HMGB1, UBE2B were correlated to longer OS in EC. In addition, a prognostic risk score based on 7 DDR gene expression (POLN, HMGB1, TOP3B, PER1, UBE2B, ATM, PALB2) was constructed for the prognosis of EC. Meanwhile, EC cancer samples were divided into 3 subtypes based on 132 DDR genes expressions. Clinical profile analysis showed cluster C1 and C2 showed a similar frequency of T2, which was remarked higher than that in cluster 3. Moreover, we found the immune cell inflation levels were significantly changed in different subtypes of EC. The infiltration levels of T cell CD8+, B cell and NK cells were greatly higher in cluster 2 than that in cluster 1 and cluster 3. The results showed T cell CD4+ infiltration levels were dramatically higher in cluster 1 than that in cluster 2 and cluster 3. Finally, we perform bioinformatics analysis of DEGs among 3 subtypes of EC and found DDR genes may be related to multiple signaling, such as Base excision repair, Cell cycle, Hedgehog signaling pathway, and Glycolysis/Gluconeogenesis. These results showed DDR genes may serve as new target for the prognosis of EC and prediction of the potential response of immune therapy in EC. 相似文献
999.
LI PAN WENTING YI DONGMIN LIANG YULONG ZHAO RANRAN WANG PINGYU WANG YOUJIE LI JIAXUAN XIN YUNFEI YAN SHUYANG XIE 《Biocell》2022,46(2):417-431
Tumor progression is usually characterized by proliferation, migration, and angiogenesis, which is essential for
supplying both nutrients and oxygen to the tumor cells. Therefore, targeting angiogenesis has been considered a
promising therapeutic strategy for cancer prevention and treatment. In the present study, we demonstrated that in
addition to suppressing lung cancer cell proliferation and migration in vitro, 10-hydroxycamptothecin (10-HCPT) is
also capable of inhibiting angiogenesis in vivo with a miR-181a-dependent manner. Mechanistically, by upregulating
miR-181a, which in turn downregulating FOXP1, 10-HCPT can inhibit the PI3K/Akt/ERK signaling pathwaymediated angiogenesis. Furthermore, reduced levels of miR-181a have been found in both lung cancer cell lines and
xenograft with concurrently elevated levels of FOXP1, VEGF, bFGF, and HDGF. Consistent with the findings from
the in vitro experiments, miR-181a impairs neovascularization in our xenograft model. In summary, our findings have
not only established the anti-oncogenic role of miR-181a in lung cancer angiogenesis but also suggest that 10-HCPT
could be a potential therapeutic reagent for lung cancer treatment. 相似文献
1000.
The pathogenesis of high altitude-related gastric mucosal injury remains poorly understood, this study aimed to
investigate the role of autophagy in hypoxia-induced apoptosis of rat gastric mucosal cells. Rats were randomized into
four groups which were maintained at an altitude of 400 m (P) or received no treatment (H), autophagy inducer
rapamycin (H+AI) or autophagy inhibitor 3-MA (H+AB) at an altitude of 4,300 m for 1, 7, 14 and 21 days,
respectively, and the morphology, ultrastructure, autophagy, and apoptosis of gastric mucosal tissues were examined.
Gastric mucosal epithelial cells CC-R039 were cultured under conditions of normoxia, 2% O2 (hypoxia), or 2%
O2+anti-mTORC1 for 0, 24, 48, and 72 h, respectively, and the autophagy and apoptosis were analyzed. CC-R039
cells were transfected with siHIF-1α, siTERT, or siRNA and the autophagy was examined. The results showed that the
exposure to hypoxia increased the autophagy and apoptosis of gastric mucosal cells in rats, and apoptosis was
aggravated by rapamycin treatment but alleviated by 3-MA treatment. Increased duration of hypoxia from 0 to 72 h
could increase the autophagy and apoptosis but decrease the proliferation of gastric mucosal cells. Inhibition of
mTORC1 with rapamycin led to further increase in apoptosis and even substantial cell death, and inhibition of HIF-
1α and TERT increased mTORC1 expression and reduced autophagy. Moreover, the inhibition of HIF-1α reduced
TERT expression. In conclusion, hypoxia could induce apoptosis of rat gastric mucosal cells by activating autophagy
through HIF-1α/TERT/mTORC1 pathway 相似文献