An Optimization Method for Lightweight Rock Classification Models: Transferred Rich Fine-Grained Knowledge.

Rock image classification represents a challenging fine-grained image classification task characterized by subtle differences among closely related rock categories. Current contrastive learning methods prevalently utilized in fine-grained image classification restrict the model's capacity to discern critical features contrastively from image pairs, and are typically too large for deployment on mobile devices used for in situ rock identification. In this work, we introduce an innovative and compact model generation framework anchored by the design of a Feature Positioning Comparison Network (FPCN). The FPCN facilitates interaction between feature vectors from localized regions within image pairs, capturing both shared and distinctive features. Further, it accommodates the variable scales of objects depicted in images, which correspond to differing quantities of inherent object information, directing the network's attention to additional contextual details based on object size variability. Leveraging knowledge distillation, the architecture is streamlined, with a focus on nuanced information at activation boundaries to master the precise fine-grained decision boundaries, thereby enhancing the small model's accuracy. Empirical evidence demonstrates that our proposed method based on FPCN improves the classification accuracy mobile lightweight models by nearly 2% while maintaining the same time and space consumption.

PARP-1 modulates the expression of miR-223 through histone acetylation to involve in the hydroquinone-induced carcinogenesis of TK6 cells.

The upstream regulators of microRNAs were rarely reported. Hydroquinone (HQ) is the main metabolite of benzene, one of the important environmental factors contributing to leukemia and lymphoma. In HQ-induced malignant transformed TK6 (TK6-HT) cells, the expression of PARP-1 and miR-223 were upregulated. When in PARP-1 silencing TK6-HT cells, miR-223 was downregulated and the apoptotic cell number correspondingly increased. In TK6 cells treated with HQ for different terms, the expression of miR-223 and PARP-1 were dynamically observed and found to be decreased and increased, respectively. Trichostatin A could increase the expression of miR-223, then the expression of HDAC1-2 and nuclear factor kappa B were found to be increased, but that of mH2A was decreased. PARP-1 silencing inhibited the protein expression of H3Ac, mH2A, and H3K27ac. By co-immunoprecipitation experiment, PARP-1 and HDAC2 were found to form a regulatory complex. In conclusion, we demonstrated that the upregulation of PARP-1 mediated activation of acetylation to promote the transcription of miR-223 possibly via coregulating with HDAC2, an epigenetic regulation mechanism involved in cell malignant transformation resulting from long-term exposure to HQ, in which course, H3K27ac might be a specific marker for the activation of histone H3, which also gives hints for benzene exposure research.

Inhibition of PARP1 by small interfering RNA enhances docetaxel activity against human prostate cancer PC3 cells.

Though poly(ADP-ribose) polymerase 1 (PARP1) inhibitors have benefits in combination with radiotherapy in prostate cancers, few is known about the exactly role and underlying mechanism of PARP1 in combination with chemotherapy agents. Here our data revealed that inhibition of PARP1 by small interfering RNA (siRNA) could enhance docetaxel's activity against PC3 cells, which is associated with an accelerate repression of EGF/Akt/FOXO1 signaling pathway. Our results provide a novel role of PARP1 in transcription regulation of EGFR/Akt/FOXO1 signaling pathway and indicate that PARP1 siRNA combined with docetaxel can be an innovative treatment strategy to potentially improve outcomes in CRPC patients.

NXPH4 Used as a New Prognostic and Immunotherapeutic Marker for Muscle-Invasive Bladder Cancer.

Background: One of the most common malignant tumors of the urinary system is muscle-invasive bladder cancer (MIBC). With the increased use of immunotherapy, its importance in the field of cancer is becoming abundantly evident. This study classifies MIBC according to GSVA score from the perspective of the GSEA immune gene set. Methods: This study integrated the sequencing and clinical data of MIBC patients in TCGA and GEO databases, then scored the data using the GSVA algorithm, the CNMF algorithm was implemented to divide the subtypes of GEO and TCGA datasets, respectively, and finally screened and determined the key pathways in combination with clinical data. Simultaneously, LASSO Cox regression model was constructed based on key pathway genes to assess the model's predictive ability (ROC) and describe the immune landscape differences between high- and low-risk groups; key genes were further analyzed and verified in patient tissues. Results: 404 TCGA and 297 GEO datasets were divided into C1-3 groups (TCGA-C1:120/C2:152/C3:132; GEO- C1:112/C2:101/C3:84), of which TCGA-C2 (n = 152) subtype and GEO-C1 (n = 112) subtype had the worst prognosis. LASSO Cox regression model with ROC (train set = 0.718, test set = 0.667) could be constructed. When combined with the Cancer Immunome Atlas database, it was found that patients with high-risk scores were more sensitive to PD-1 inhibitor and PD-1 inhibitor combined with CTLA-4. NXPH4, as a key gene, plays a role in MIBC with tissue validation results show that nxph4 is highly expressed in tumor. Conclusion: The immune gene score of MIBC data in TCGA and GEO databases was successfully evaluated using GSVA in this research. The lasso Cox expression model was successfully constructed by screening immune genes, the high-risk group had a worse prognosis and higher sensitivity to immunotherapy, PD-1 inhibitors or PD-1 combined with CTLA-4 inhibitors can be preferentially used in high-risk patients who are sensitive to immunotherapy, and NXPH4 may be a molecular target to adjust the effect of immunotherapy.

Regulatory loop between lncRNA FAS-AS1 and DNMT3b controls FAS expression in hydroquinone-treated TK6 cells and benzene-exposed workers.

Hydroquinone (HQ), one of the main metabolites of benzene, is a well-known human leukemogen. However, the specific mechanism of how benzene or HQ contributes to the development of leukemia is unknown. In a previous study, we demonstrated the upregulation of DNA methyltransferase (DNMT) expression in HQ-induced malignant transformed TK6 (HQ-TK6) cells. Here, we investigated whether a regulatory loop between the long noncoding RNA FAS-AS1 and DNMT3b exists in HQ-TK6 cells and benzene-exposed workers. We found that the expression of FAS-AS1 was downregulated in HQ-TK6 cells and workers exposed to benzene longer than 1.5 years via histone acetylation, and FAS-AS1 expression was negatively correlated with the time of benzene exposure. Restoration of FAS-AS1 in HQ-TK6 cells promoted apoptosis and inhibited tumorigenicity in female nude mice. Interestingly, treatment with a DNMT inhibitor (5-aza-2-deoxycytidine), histone deacetylase inhibitor (trichostatin A), or DNMT3b knockout led to increased FAS-AS1 through increased H3K27ac protein expression in HQ-TK6 cells, and DNMT3b knockout decreased H3K27ac and DNMT3b enrichment to the FAS-AS1 promoter region, which suggested that DNMT3b and/or histone acetylation involve FAS-AS1 expression. Importantly, restoration of FAS-AS1 resulted in reduced expression of DNMT3b and SIRT1 and increased expression of FAS in both HQ-TK6 cells and xenograft tissues. Moreover, the average DNMT3b expression in 17 paired workers exposed to benzene within 1.5 years was decreased, but that of the remaining 103 paired workers with longer exposure times was increased. Conversely, DNMT3b was negatively correlated with FAS-AS1 expression. Both FAS-AS1 and DNMT3b influenced the enrichment of H3K27ac in the FAS promoter region by regulating the expression of SIRT1, consequently upregulating FAS expression. Taken together, these observations demonstrate crosstalk between FAS-AS1 and DNMT3b via a mutual inhibition loop and indicate a new mechanism by which FAS-AS1 regulates the expression of FAS in benzene-related carcinogenesis.

[Treatment of urinary tract calculi in preschool children with endoscopy].

OBJECTIVES: To investigate the safety and feasibility of endoscopy in treating urinary tract calculi in preschool children. METHODS: From August 2004 to August 2008, 28 preschool children with urinary tract calculi were treated by endoscopy, 11 cases received ureterolithotripsy (URL) and 17 cases received minimally invasive percutaneous nephrolithotomy (MPCNL). RESULTS: Of 11 cases with ureteric calculi, 5 cases were rendered stone free in the first session, the other 6 cases received passive dilation by indwelling of ureteric stents for 1 to 3 weeks and underwent successful ureteroscopy with a 8/9.8 Fr rigid ureteroscope. Seventeen cases with renal calculi received MPCNL and were rendered stone free. CONCLUSION: Our study shows that endoscopy in treating urinary tract calculi is safe and feasible in preschool children.

Poly(ADP-ribose) polymerase-1 promotes expression of miR-155 by the up-regulation of methyl-CpG binding domain protein 2 in TK6 cells exposed to hydroquinone.

Hydroquinone (HQ), one of the major metabolites of benzene, can induce aberrant gene expression. MiR-155, a tumor activator, participates in various biological processes, including DNA damage response. However, the molecular mechanism of aberrant miR-155 expression is still not completely elucidated. Here, we investigated the mechanism of abnormal expression of miR-155 induced by poly(ADP-ribose)polymerase-1 (PARP-1) expression in HQ-treated TK6 lymphoblastoid cells. We examined the expression of genes related to abnormal expression of miR-155 to explore the reason for this phenomenon. The results of the present study showed that miR-155 was significantly increased and reactive oxygen species (ROS) were decreased in cells treated with HQ for 72 h compared with PBS-treated cells. Meanwhile, E4F1, PARP-1 and PARP-1 related co-regulators (NF-κB, HDAC1, and HDAC2), acetylated histone H3 (H3Ac) were increased in a concentration-dependent manner. Experiments for treatment with 5-AzaC (DNMTs inhibitor), TSA (HDACs inhibitor), DOX (to activate PARP-1) or MG132 (proteasome inhibitor) revealed that the MBDs and PARP-1 was positively associated with miR-155 expression. Moreover, in cells treated with HQ in conjunction with PARP-1 knockdown, expression of miR-155, H3Ac and MBD2 protein were decreased, compared with negative control. In conclusion, PARP-1 activates expression of miR-155 via acetylation by regulating MBD2 in TK6 cells exposed to HQ.