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Taking the SaErTU and Putaohua oil layers in the L29 well area of LHP oilfield in the northern Songliao Basin as the research object, In response to the difficulty of interference between thin interbedded sand and mudstone and strong reflection between strata, which have a significant impact on fine prediction of sand bodies, a stratigraphic model is established based on the geological characteristics of the target layer to eliminate the impact of stratigraphic reflection; Then add a thin layer of sand body to its interior, establish a thin interlayer model, and obtain a geological model that is more in line with the actual situation of the target layer. Using forward simulation, analyze the seismic response characteristics of sand bodies, extract 30 seismic attributes from 4 categories: amplitude statistics, composite seismic trace statistics, sequence and frequency spectrum statistics, and calculate the correlation between cumulative sandstone thickness and seismic attributes, and select a sensitive seismic attribute set;By combining sedimentary and drilling data, the seismic attribute with the highest sensitivity to the target layer is selected. The multi-level dimensionality reduction and gradual improvement of seismic attribute selection methods using “model forward modeling, attribute analysis, relevant optimization, and drilling implementation” can effectively improve the prediction accuracy of thin interbedded sand bodies and greatly reduce the risk of oilfield exploration and development.

Psoriasis is a recurrent and protracted disease that severely impacts the patient's physical and mental health. Thus, there is an urgent need to explore its pathogenesis to identify therapeutic targets. The expression level of protein tyrosine phosphatase nonreceptor type 2 (PTPN2) was analyzed by immunohistochemistry techniques in psoriatic tissues and imiquimod‐induced psoriatic mouse models. PTPN2 and signal transducer and activator of transcription 3 (STAT3) were overexpressed or silenced in human keratinocytes or an interleukin (IL)‐6‐induced psoriasis HaCaT cell model using overexpression plasmid transfection or small interfering RNA technology in vitro, and the effects of PTPN2 on STAT3, HaCaT cell function, and autophagy levels were investigated using reverse transcription‐quantitative polymerase chain reaction, Western blot, Cell Counting Kit 8, 5‐ethynyl‐20‐deoxyuridine, flow cytometry, and transmission electron microscopy. PTPN2 expression was found to be significantly downregulated in psoriatic tissues. Then, the in vitro antipsoriatic properties of PTPN2 were investigated in an IL‐6‐induced psoriasis‐like cell model, and the results demonstrated that inhibition of keratinocyte proliferation by PTPN2 may be associated with elevated STAT3 dephosphorylation and autophagy levels. These findings provide novel insights into the mechanisms of autophagy in psoriatic keratinocytes and may be essential for developing new therapeutic strategies to improve inflammatory homeostasis in psoriatic patients. Significance statement: Psoriasis is a recurrent and chronic systemic inflammatory skin disease, which seriously affects the physical and mental health of patients. In this manuscript, we report for the first time that protein tyrosine phosphatase nonreceptor type 2 (PTPN2) is significantly underexpressed in psoriasis. PTPN2 mediates signal transducer and activator of transcription 3 dephosphorylation, promoting autophagy levels and inhibiting keratinocyte proliferation. To the best of our knowledge, psoriasis cannot be adequately controlled even though the clinical efficacy of the present treatment for the etiology of the condition has greatly improved. The search explores the mechanism of pathogenesis of PTPN2 in psoriasis, providing new insights into the mechanism of autophagy in psoriatic keratinocytes, and may have important implications for the development of new therapeutic strategies to improve inflammatory homeostasis in patients with psoriasis. [ABSTRACT FROM AUTHOR]

Psoriasis is a chronic inflammatory skin disease. Although miRNAs are reported to be associated with the pathogenesis of psoriasis, the contribution of individual microRNAs toward psoriasis remains unclear. The miR-17-92 cluster regulates cell growth and immune functions that are associated with psoriasis. miR-17-3p is a member of miR-17-92 cluster; however, its role in dermatological diseases remains unclear. Our study aims at investigating the effects of miR-17-3p and its potential target gene on keratinocytes proliferation and secretion of pro-inflammatory cytokine and their involvement in psoriasis. Initially, we found that miR-17-3p was upregulated in psoriatic skin lesions, and bioinformatic analyses suggested that CTR9 is likely to be a target gene of miR-17-3p. Quantitative reverse-transcriptase PCR and immunohistochemical analysis revealed that CTR9 expression was downregulated in psoriatic lesions. Using dual-luciferase reporter assays, we identified CTR9 as a direct target of miR-17-3p. Further functional experiments demonstrated that miR-17-3p promoted the proliferation and pro-inflammatory cytokine secretion of keratinocytes, whereas CTR9 exerted the opposite effects. Gain-of-function studies confirmed that CTR9 suppression partially accounted for the effects of miR-17-3p in keratinocytes. Furthermore, Western blot revealed that miR-17-3p activates the downstream STAT3 signaling pathway while CTR9 inactivates the STAT3 signaling pathway. Together, these findings indicate that miR-17-3p regulates keratinocyte proliferation and pro-inflammatory cytokine secretion partially by targeting the CTR9, which inactivates the downstream STAT3 protein, implying that miR-17-3p might be a novel therapeutic target for psoriasis.