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It's common to use multi-stage hydraulic fracturing in horizontal wells for the development of tight gas reservoirs. Therefore, accurate productivity prediction is crucial. Concerning the theory of equivalent wellbore radius and the principle of pressure drop superposition, the effects of secondary fractures and water-blocking damage were treated as distinct skin effects innovatively. Consequently, the productivity model for tight gas reservoirs in hydraulic fracturing horizontal wells was established, taking into account the effects of slippage effect, stress sensitivity, threshold pressure gradient and high-velocity non-Darcy flow. Then the accuracy of the model was verified in two ways. The calculated results are basically consistent with different models from the literature without considering the influence of various factors. In addition, the open flow capability of the proposed model by using the data of a gas field block is 1617.85Mscfd, while that of one fractured well through field well testing is 1696.79Mscfd, resulting in a relative error of 4.65%. Furthermore, the factors affecting productivity were subjected to a sensitivity analysis using this model. The results indicate that water-blocking damage can significantly impact productivity, while threshold pressure gradient, fracture number, and high-velocity non-Darcy flow have a relatively small influence on productivity. [ABSTRACT FROM AUTHOR]

Long-chain acyl-CoA synthetase (ACSL) family members include five different ACSL isoforms, each encoded by a separate gene and have multiple spliced variants. ACSLs on endoplasmic reticulum and mitochondrial outer membrance catalyze fatty acids with chain lengths from 12 to 20 carbon atoms to form acyl-CoAs, which are lipid metabolic intermediates and involved in fatty acid metabolism, membrane modifications and various physiological processes. Gain- or loss-of-function studies have shown that the expression of individual ACSL isoforms can alter the distribution and amount of intracellular fatty acids. Changes in the types and amounts of fatty acids, in turn, can alter the expression of intracellular ACSLs. ACSL family members affect not only the proliferation of normal cells, but the proliferation of malignant tumor cells. They also regulate cell apoptosis through different signaling pathways and molecular mechanisms. ACSL members have individual functions in fatty acid metabolism in different types of cells depending on substrate preferences, subcellular location and tissue specificity, thus contributing to liver diseases and metabolic diseases, such as fatty liver disease, obesity, atherosclerosis and diabetes. They are also linked to neurological disorders and other diseases. However, the mechanisms are unclear. This review addresses new findings in the classification and properties of ACSLs and the fatty acid metabolism-associated effects of ACSLs in diseases.