Uusing the KDJ as a trading strategy on biotech companies

Mean Reversion is the most commonly used model in quantitative trading. This model is associated with several factors, like ma5 and ma10 line. These factors are the most significant in stock markets. However, the disadvantages of this model are lag and inaccuracy. In this research, we get the historical and current stock data by web crawler, analyze the quantitative data and build a new model involved with the KDJ. Taking biotech companies marketed in the United States and B-share marketed in China as the research subjects, the result shows increased profits compared with the Mean Reversion model. It also shows that as long as we clearly understand the relationship between the turnover and fluctuation of share price, we can find the trading signals more accurately and generate more profit

Fracture Closure Empirical Model and Theoretical Damage Model of Rock under Compression

The rock or rock mass in engineering often contains joints, fractures, voids, and other defects, which are the root cause of local or overall failure. In response to most of the current constitutive models that fail to simulate the nonlinear fracture compaction deformation in the whole process of rock failure, especially brittle rocks, a piecewise constitutive model was proposed to represent the global constitutive relation of rocks in this study, which was composed of the fracture compaction empirical model and the damage statistical constitutive model. The fracture empirical compaction model was determined by fitting the expressions of fracture closure curves of various rocks, while the rock damage evolution equation was derived underpinned by the fracture growth. According to the effective stress concept and strain equivalence hypothesis, the rock damage constitutive model was deduced. The model parameters of the fracture compaction empirical model and damage statistical constitutive model were all calculated by the geometrical characteristics of the global axial stress–strain curve to guarantee that the models are continuous and smooth at the curve intersection, which is also simple and ready to program. Finally, the uniaxial compression test data and the triaxial compression test data of different rocks in previous studies were employed to validate the models, and the determination coefficient was used to measure the accuracy. The results showed great consistency between the model curves and test data, especially in the pre-peak stage

Targeting mitochondrial biogenesis to overcome drug resistance to MAPK inhibitors

Targeting multiple components of the MAPK pathway can prolong the survival of patients with BRAF(V600E) melanoma. This approach is not curative, as some BRAF-mutated melanoma cells are intrinsically resistant to MAPK inhibitors (MAPKi). At the systemic level, our knowledge of how signaling pathways underlie drug resistance needs to be further expanded. Here, we have shown that intrinsically resistant BRAF-mutated melanoma cells with a low basal level of mitochondrial biogenesis depend on this process to survive MAPKi. Intrinsically resistant cells exploited an integrated stress response, exhibited an increase in mitochondrial DNA content, and required oxidative phosphorylation to meet their bioenergetic needs. We determined that intrinsically resistant cells rely on the genes encoding TFAM, which controls mitochondrial genome replication and transcription, and TRAP1, which regulates mitochondrial protein folding. Therefore, we targeted mitochondrial biogenesis with a mitochondrium-targeted, small-molecule HSP90 inhibitor (Gamitrinib), which eradicated intrinsically resistant cells and augmented the efficacy of MAPKi by inducing mitochondrial dysfunction and inhibiting tumor bioenergetics. A subset of tumor biopsies from patients with disease progression despite MAPKi treatment showed increased mitochondrial biogenesis and tumor bioenergetics. A subset of acquired drug-resistant melanoma cell lines was sensitive to Gamitrinib. Our study establishes mitochondrial biogenesis, coupled with aberrant tumor bioenergetics, as a potential therapy escape mechanism and paves the way for a rationale-based combinatorial strategy to improve the efficacy of MAPKi.ope