The proper orthogonal decomposition reduced-order models (POD-ROMs) have been widely used as a computationally efficient surrogate models in large-scale numerical simulations of complex systems. However, when it is applied to a Hamiltonian system, a naive application of the POD method can destroy its Hamiltonian structure in the reduced-order model. In this paper, we develop a new reduce-order modeling approach for the Hamiltonian system, which uses the traditional framework of Galerkin projection-based model reduction but modifies the ROM so that the appropriate Hamiltonian structure is preserved. Since the POD truncation can degrade the approximation of the Hamiltonian function, we propose to use the POD basis from shifted snapshots to improve the Hamiltonian function approximation. We further derive a rigorous a priori error estimate of the structure-preserving ROM and demonstrate its effectiveness in several numerical examples. This approach can be readily extended to dissipative Hamiltonian systems, port-Hamiltonian systems etc.

A large proportion (40–60%) of patients with human epidermal growth factor receptor 2 (HER2)-overexpressing breast cancer do not benefit from trastuzumab treatment, potentially due to the lack of complement-dependent cytotoxicity (CDC) activation. In the present study, the effect of complement decay-accelerating factor (CD55) and CD59 glycoprotein precursor (CD59) expression on trastuzumab-induced CDC in HER2-positive breast cancer cell lines was investigated. The CD55 and CD59-overexpressing and HER2-positive cell lines SK-BR-3 and BT474 were selected for subsequent experiments. Blocking CD55 and CD59 function using targeting monoclonal antibodies significantly enhanced the cell lysis of SK-BR-3 and BT474 cells following treatment with trastuzumab. In addition, following treatment with 0.1 U/ml phosphatidylinositol-specific phospholipase C (PI-PLC) for 1 h, CD55 and CD59 surface expression was significantly decreased, and the cell lysis rate was further enhanced. Treatment of SK-BR-3 cells with short hairpin RNA (shRNA) targeting CD55 and CD59 downregulated CD55 and CD59 expression at the mRNA and protein levels, and resulted in significantly enhanced trastuzumab-induced CDC-dependent lysis. The data from the present study suggested that CD55 and CD59 serve roles in blocking trastuzumab-induced CDC, therefore strategies targeting CD55 and CD59 may overcome breast cancer cell resistance to trastuzumab. The results from the present study may provide a basis for developing suitable, personalized treatment strategies to improve the clinical efficacy of trastuzumab for patients with HER2-positive breast cancer.

In consideration of budget and efficiency, we suggest OCT as the best storing method that not only preserves RNA quality during the freezing-thawing process well, but also ensures more secure and stable DNA and protein.

Period2 (Per2) is a key circadian clock gene, and its deregulation contributes to tumour development, including breast cancer. However, the biological function and clinicopathological significance of Per2 in non‑small cell lung cancer (NSCLC) remain unclear. The present study aimed to explore the role of Per2 and its relative clinical significance in NSCLC. To analyse Per2 expression in NSCLC specimens, reverse transcription‑quantitative polymerase chain reaction was performed, and the results indicated that Per2 expression was markedly downregulated in 83.87% (26/31) of NSCLC samples compared with their adjacent matched tissues. Increased Per2 expression was associated with increased differentiation (P<0.01) and reduced lymph node metastasis (P<0.0001). Functional studies identified that enhancing Per2 expression in A549 cells by lentivirus transduction not only significantly suppressed cell growth, migration and invasion (P<0.05) but also inhibited NSCLC growth and metastasis in vivo. Animal studies and histopathological analysis identified that Per2 expression in A549 cells not only markedly increased expression of tumour anti‑oncogenes Bax, P53 and P21 but also inhibited expression of pro‑oncogenes vascular endothelial growth factor, CD44 and c‑Myc. These results indicate that the loss of Per2 is one of the factors underlying tumourigenesis in NSCLC, and it may function as a novel molecular target for NSCLC.

Adjuvant chemotherapy may cause alterations in serum lipids in postoperative breast cancer (BC) patients, but the specific alterations caused by different chemotherapy regimens remain unclear. The aim of this study was to investigate the status of serum lipids pre- and post-chemotherapy and to compare the side effects of different chemotherapy regimens on serum lipid. We retrospectively analysed the lipid profiles of 1934 consecutive postoperative BC patients who received one of the following chemotherapy regimens: doxorubicin and cyclophosphamide followed by paclitaxel (AC-T); epirubicin and cyclophosphamide followed by paclitaxel (EC-T); cyclophosphamide and paclitaxel (TC); and fluorouracil, cyclophosphamide, and epirubicin (FEC). The levels of triglycerides (TG), total cholesterols (TC), and low-density lipoprotein (LDL-C) were significantly elevated in patients who received chemotherapy regimens above ( P < .001). With respect to different chemotherapy regimens, FEC had less side effects on lipid profiles (TG ( P = .006), high-density lipoprotein (HDL-C) ( P < .001), and LDL-C ( P < .001)) than TC regimen and AC-T and EC-T regimen. Also, the incidence of newly diagnosed dyslipidemia after chemotherapy was lower in FEC group than TC group and AC-T and EC-T group ( P < .001). Additionally, the magnitude of the alterations in lipid profiles (TG, TC, HDL-C, and LDL-C) was greater in premenopausal patients than that of the postmenopausal patients ( P = .004; P < .001; P = .002; P = .003, respectively). Moreover, after adjusting for multiple baseline covariates, anthracycline-plus-taxane-based regimens (AC-T and EC-T) were still statistically associated with a high level of TG ( P = .004) and a low level of HDL-C ( P = .033) after chemotherapy compared with FEC regimen. Also, body mass index (BMI) > 24 was associated with abnormal lipid profiles (TG, TC, HDL-C, LDL-C) post-chemotherapy compared with BMI ≤ 24 ( P < .001; P = .036; P = .012; P = .048, respectively). BC patients receiving chemotherapy may have elevated lipid profiles, and anthracycline-based regimen had less side effects on lipid profiles compared with regimens containing taxane. Therefore, it is necessary to take lipid metabolism into consideration when making chemotherapy decisions and dyslipidemia prevention and corresponding interventions are indispensable during the whole chemotherapy period.