Data-Driven Dynamic Inversion Method for Complex Fractures in Unconventional Reservoirs

Hydraulic fracturing is a crucial technology for enhancing the recovery of oil and gas from unconventional reservoirs. Accurately describing fracture morphology is essential for accurately predicting production dynamics. This article proposes a new fracture inversion model based on dynamic data-driven methods, which is different from the conventional linear elastic fracture mechanics model. This method eliminates the need to consider complex mechanical mechanisms, resulting in faster simulation speeds. In the model, the fracture morphology is constrained by combining microseismic data and fracturing construction data, and the fracture tip propagation domain is introduced to characterize the multi-directionality of fracture propagation. The simulated fracture exhibits a multi-branch fracture network morphology, aligning more closely with geological understanding. In addition, the influence of microseismic signal intensity on the direction of fracture propagation is considered in this study. The general stochastic approximation (GSA) algorithm is employed to optimize the direction of fracture propagation. The proposed method is applied to both the single-stage fracturing model and the whole well fracturing model. The research findings indicate that in the single-stage fracturing model, the inverted fracture morphology aligns closely with the microseismic data, with a fitting rate of the fracturing construction curve exceeding 95%, and a microseismic data fitting rate exceeding 93%. In the whole well fracturing model, a total of 18 sections were inverted. The fitting rate between the overall fracture morphology and the microseismic data reached 90%. The simulation only took 5 minutes, demonstrating high computational efficiency and meeting the needs of large-scale engineering fracture simulation. This method can effectively support geological modeling and production dynamic prediction

TAp73α enhances the cellular sensitivity to cisplatin in ovarian cancer cells via the JNK signaling pathway

Ovarian cancer is the most lethal gynecological malignancy. Most of ovarian cancer patients relapse and subsequently die due to the development of resistance to chemotherapy. P73 belongs to the tumor suppressor p53 family. Like p53, the transcriptionally active TAp73 can bind specifically to p53 responsive elements and transactivates some of the p53 target genes, and finally leads to cell cycle arrest and apoptosis. TAp73 can be induced by DNA damage to enhance cellular sensitivity to anticancer agents in human cancer cells. However, the functions of TAp73 in ovarian cancer cells and the role in the regulation of cellular response to commonly used chemotherapeutic agents cisplatin are still poorly understood. The aims of this study were to examine the functions of TAp73 in ovarian cancer cells and its role in cellular response to cisplatin, as well as the relationship between TAp73 and p53 in ovarian cancer cells. Functional studies showed that over-expression of TAp73alpha (TAp73α) inhibited cell proliferation, colony formation ability and anchorage-independent growth of ovarian cancer cells, and this was irrespective of p53 expression status. In addition, TAp73α inhibited cell growth by arresting cell cycle at G2/M phase and up-regulating the expressions of G2/M regulators of p21, 14-3-3sigma and GADD45α. TAp73α enhanced the cellular sensitivity to cisplatin through the activation of JNK signaling pathway, at least partially, in ovarian cancer cells. TAp73α activated the JNK pathway through the up-regulation of its target gene GADD45α and subsequent activation of MKK4, the JNK up-stream kinase. Inhibition of JNK activity by a specific inhibitor (SP600125) or small interfering RNAs (siRNAs) significantly abrogated TAp73-mediated apoptosis induced by cisplatin. Moreover, the activations of MKK4, JNK and c-Jun were abolished when GADD45α was knocked down by siRNAs, and the JNK-dependent apoptosis was not observed. Collectively, these results supported that TAp73α was able to mediate apoptotic response to cisplatin through the GADD45α/MKK4/JNK signaling pathway, which was respective of p53 expression status. Further investigation on the relationship between TAp73α and p53 demonstrated that TAp73α increased p53 protein, but not mRNA expression by attenuating p53 protein degradation in wild-type p53 ovarian cancer cells. TAp73α could directly interact with p53 protein, which might interfere with the binding ability of MDM2 to p53, and consequently block the p53 protein degradation. In addition, TAp73α inactivated the Akt and ERK pathways and activated the p38 pathway in response to cisplatin in wild-type p53 OVCA433, but not in null-p53 SKOV3 cells, suggesting that the effect of TAp73α on these pathways might be p53-dependent. These results indicated that a functional cooperation of TAp73α and p53, to some extent, existed in ovarian cancer cells. In conclusion, this study demonstrated that TAp73α acted as a tumor suppressor in ovarian carcinogenesis. It promoted the cellular sensitivity to cisplatin via, at least partially, the activation of JNK signaling pathway. These TAp73α functions were irrespective of p53 expression. In addition, TAp73α was able to bind to p53 and increase p53 expression.published_or_final_versionObstetrics and GynaecologyDoctoralDoctor of Philosoph

A novel surface active polymer oil displacement agent

Based on the relationship between the molecule structure of monomers and their performance, two types of polymerizable monomers with low oil/water interfacial tension have been synthesized, which coplymerizes acrylamide to synthesize a novel polymer oil displacement agent under compound initiator and low polymeric temperature. Its structure and distribution status in brine solution were characterized by infrared spectroscopy and freeze etching electron microscope. The results show that the polymer has good water solubility, viscosifying properties, salt-resistance and temperature-tolerance, shearing-resistance in brines. Due to the graft polymerization of acrylamide and the polymerizable surface-active monomers, the polymer overcomes chromatographic separation effect, and has low oil/water interfacial tension. Interfacial tension of 0.15% polymer solution (prepared in Daqing simulation brine) is around 10−1 mN/m in Daqing No.1 oil plant crude oil. Core flooding experiments show that the oil recovery of the novel surface active polymer is 5.2% higher than that of ordinary hydrolyzed polyacrylamide because of its better viscosifying performance and lower oil/water interfacial tension. Key words: oil displacement agent, polymer, interfacial tension, recovery facto

Progress of Research into Preformed Particle Gels for Profile Control and Water Shutoff Techniques

Gel treatment is an economical and efficient method of controlling excessive water production. The gelation of in situ gels is prone to being affected by the dilution of formation water, chromatographic during the transportation process, and thus controlling the gelation time and penetration depth is a challenging task. Therefore, a novel gel system termed preformed particle gels (PPGs) has been developed to overcome the drawbacks of in situ gels. PPGs are superabsorbent polymer gels which can swell but not dissolve in brines. Typically, PPGs are a granular gels formed based on the crosslinking of polyacrylamide, characterized by controllable particle size and strength. This work summarizes the application scenarios of PPGs and elucidates their plugging mechanisms. Additionally, several newly developed PPG systems such as high-temperature-resistant PPGs, re-crosslinkable PPGs, and delayed-swelling PPGs are also covered. This research indicates that PPGs can selectively block the formation of fractures or high-permeability channels. The performance of the novel modified PPGs was superior to in situ gels in harsh environments. Lastly, we outlined recommended improvements for the novel PPGs and suggested future research directions

The State Journal

Weekly newspaper from Mulhall, Oklahoma that includes local, territorial, and national news along with advertising. The newspaper was established on December 19, 1902

A bull-heading water control technique of thermo-sensitive temporary plugging agent

Abstract: Aimed at the disadvantages of secondary damage to oil layers caused by the conventional bull-heading water control technique, a thermo-sensitive temporary plugging agent for water control was synthesized by water solution polymerization and applied in the field with a new secondary temporary plugging technique. The optimization and performance evaluation of thermo-sensitive temporary plugging agent were carried out through laboratory experiments. The optimized formula is as follows: (6% − 8%) acrylamide + (0.08% − 0.12%) ammonium persulfate + (1.5% − 2.0%) sepiolite + (0.5% − 0.8%) polyethylene glycol diacrylate. The thermo-sensitive temporary plugging agent is suitable for formation temperatures of 70−90 °C, it has high temporary plugging strength (5−40 kPa), controllable degradation time (1−15 d), the apparent viscosity after degradation of less than 100 mPa(S and the permeability recovery value of simulated cores of more than 95%. Based on the research results, secondary temporary plugging technique was used in a horizontal well in the Jidong Oilfield. After treament, the well saw a drop of water cut to 27%, and now it has a water cut of 67%, its daily increased oil production was 4.8 t, and the cumulative oil increment was 750 t, demonstrating that the technique worked well in controlling water production and increasing oil production. Key words: bull-heading water control technique, thermo-sensitive temporary plugging agent, secondary temporary plugging technique, thermal degradation property, reservoir protectio

Activation of JNK was involved in TAp73α-mediated apoptosis induced by cisplatin.

<p>(A) TAp73α-overexpressed cells (SKOV3 C8 and OVCA433 C1) were treated with 20 μM SP600125 for different periods of time (indicated). The phosphorylation levels of JNK and c-Jun were measured. (B and C) TAp73α-overexpressed cells (SKOV3 C8 and OVCA433 C1) and the empty vector controls (V) were treated with 20 μM SP600125 or DMSO and then with cisplatin. The cell apoptosis were assessed by TUNEL assay (error bars indicated mean ± SD from three independent experiments; *: p<0.05) and the cleavage of PARP analysis. Inhibition of JNK attenuated TAp73α-mediated apoptosis in response to cisplatin. (D) TAp73α-overexpressed cells (SKOV3 C8 and OVCA433 C1) were treated with JNK siRNAs (Si-JNK) or the scrambled control siRNA (Control). The activations of JNK and c-Jun were absent upon cisplatin treatment, and associated with markedly reduced cell apoptosis (E and F).</p

Caffeine Sensitizes U87-MG Human Glioblastoma Cells to Temozolomide through Mitotic Catastrophe by Impeding G2 Arrest

Temozolomide (TMZ) is the first-line chemotherapeutic agent in the treatment of glioblastoma multiforme (GBM). Despite its cytotoxic effect, TMZ also induces cell cycle arrest that may lead to the development of chemoresistance and eventual tumor recurrence. Caffeine, a widely consumed neurostimulant, shows anticancer activities and is reported to work synergistically with cisplatin and camptothecin. The present study aimed to investigate the effects and the mechanisms of action of caffeine used in combination with TMZ in U87-MG GBM cells. As anticipated, TMZ caused DNA damage mediated by the ATM/p53/p21 signaling pathway and induced significant G2 delay. Concurrent treatment with caffeine repressed proliferation and lowered clonogenic capacity on MTT and colony formation assays, respectively. Mechanistic study showed that coadministration of caffeine and TMZ suppressed the phosphorylation of ATM and p53 and downregulated p21 expression, thus releasing DNA-damaged cells from G2 arrest into premature mitosis. Cell cycle analysis demonstrated that the proportion of cells arrested in G2 phase decreased when caffeine was administered together with TMZ; at the same time, the amount of cells with micronucleation and multipolar spindle poles increased, indicative of enhanced mitotic cell death. Pretreatment of cells with caffeine further enhanced mitotic catastrophe development in combined treatment and sensitized cells to apoptosis when followed by TMZ alone. In conclusion, our study demonstrated that caffeine enhanced the efficacy of TMZ through mitotic cell death by impeding ATM/p53/p21-mediated G2 arrest

Overexpression of TAp73α enhanced cellular sensitivity to cisplatin.

<p>(A) The GFP-TAp73α overexpressing stable clones in SKOV3 (C8, C24 and C28) and OVCA433 (C1, C7 and C12) cells were verified by western blot analysis. (B and C) Both XTT viability assay and clonogenic assay showed significantly reduced cell proliferation in TAp73α-overexpressed cells of SKOV3 and OVCA433 compared to the empty vector controls (V) in response to cisplatin treatment. The percentage of cells/colonies surviving in cisplatin relative to cells/colonies in drug-free medium control was measured. Data was shown as mean ± SD from three independent experiments (*: p<0.05; **: p<0.01).</p