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The mechanical response of liver tissue is commonly characterized by compression tests of specimens. The preloading force between the compression platform and the specimen is often ignored in compression tests. In the present study, unconfined and no-slip compression tests of liver tissue with preloading forces were performed. Based on collected mechanical responses of unconfined compression tests with five preloading forces, the influences of the preloading force on the constitutive model parameters and elastic moduli were analyzed. An indirect optimization method was proposed to eliminate the influence of the preloading force. Pre-strain caused by the preloading force is considered in the constitutive model in this method. The collected mechanical responses are applied to obtain the constitutive model and preloading model PUCT parameters with proposed indirect optimization method. Based on the optimization constitutive model parameters, FE models with different sample sizes were established. Preloading model PNSCT was established by numerical tests with different sample sizes. Based on the preloading model PNSCT, the collected mechanical response of no-slip compression test with a preloading force (0.05 N) was corrected. The results show that the indirect optimization method can eliminate the effect of the preloading force on liver tissue properties, and the corrected mechanical response is closer to the actual mechanical response.

Background: We investigated the application of a predictive nursing education process on the degree of comfort and quality of life for cancer patients. Methods: A total of 168-cancer patient in Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong, China between June 2014 and June 2016 were enrolled and admitted for surgery or radiotherapy/chemotherapy treatment. Patients were randomly divided into control and observation groups, each containing 84 cases. Patients in the control group received routine cancer care, whereas the observation group received care incorporating a predictive nursing education process. Patients were assessed after admission and prior to discharge via the Kolcaba's comfort status scale (through a General Comfort Questionnaire (GCQ)), quality of life scale (QOL), and Barthel Index (BI) for activities of daily living (ADL). Patient mental state was also evaluated using the Hamilton Anxiety Rating Scale (HAMA) and Hamilton Depression Rating Scale (HAMD). Results: GCQ, QOL, and BI scores of the observation group were all significantly higher than those of the control group (P

Background: The long non-coding RNA (lncRNA) HOX transcript antisense RNA (HOTAIR) serves as a powerful predictor of tumor progression and overall survival in patients. Our previous studies showed that HOTAIR modulated HOXA1 DNA methylation by reducing DNMT1 and DNMT3b expression in drug-resistant small cell lung cancer (SCLC). Moreover, H3 lysine 27 trimethylation (H3K27me3) is catalyzed by enhancer of zeste homolog 2 (EZH2) and plays a critical role in SCLC chemoresistance. However, it is not completely clear whether H3K27me3 affects HOXA1 DNA methylation or whether this effect is mediated by HOTAIR. Methods: The levels of EZH2 and H3K27me3 were identified in SCLC tissues by immunohistochemical (IHC) staining and in SCLC multidrug-resistant cells by Western blotting. Cell counting kit-8 (CCK-8) and flow cytometry were used to detect and analyze the biological function of H3K27me3. Then, we assessed the role of HOTAIR in the regulation of EZH2 and H3K27me3 by using lentivirus and small interfering RNA. Further, bisulfite sequencing PCR was conducted to detect the methylation levels of HOXA1 DNA. Finally, Western blotting was performed to examine the regulatory role of H3K27me3 in controlling HOTAIR expression in SCLC. Results: In this study, we found that EZH2 and H3K27me3 levels were markedly higher in SCLC tissues and multidrug-resistant SCLC cells. The results indicated that H3K27me3 was related to multidrug resistance. HOTAIR overexpression and knockdown showed that EZH2 and H3K27me3 were regulated by HOTAIR. Moreover, H3K27me3 affected HOXA1 DNA methylation levels. Strikingly, we found that H3K27me3 acted as a negative feedback regulator of HOTAIR. Conclusions: Our study showed that H3K27me3 affects HOXA1 DNA methylation via HOTAIR regulation, indicating that H3K27me3 may be a potential therapy target for SCLC chemoresistance.