A risk model based on the tumor microenvironment to predict survival and immunotherapy efficacy for ovarian cancer.

OBJECTIVE: Based on the interactions between immune components in the tumor microenvironment and ovarian cancer (OC) cells, immunotherapies have been demonstrated to be effective in dramatically increasing survival rates. This study aimed to identify landmark genes, develop a prognostic risk model, and explore its relevance to the efficacy of immunotherapy. MATERIALS AND METHODS: A risk model was built based on the immune- and stromal-related genes, which were extracted from the OC gene expression data of "The Cancer Genome Atlas" (TCGA) database. Survival analysis and receiver operating characteristic (ROC) analysis were then conducted through the model's risk score pattern, which was established depending on the TCGA training cohort and verified based on the internal TCGA cohort and external "Gene Expression Omnibus" (GEO) datasets. Furthermore, the immune-related characteristics and prognostic values of the risk model were evaluated. RESULTS: The prognostic risk model for ovarian cancer demonstrated excellent performance in predicting survival rates, as validated in both the TCGA and GEO databases. The model showed significant associations with 17 functional immune cells, 17 immune checkpoints, PD-1, and several immune pathways, suggesting its potential to enhance the efficacy of immunotherapy in OC. CONCLUSIONS: The risk model developed in this study has the potential to serve as a prognostic marker for OC, enabling the development of personalized immunotherapy protocols and providing a theoretical basis for novel combinations of immunotherapeutic approaches.

Effects of lncRNA MALAT1 and lncRNA NKILA on proliferation, invasion and apoptosis of retinoblastoma.

OBJECTIVE: To assess the expression of LncRNA NKILA and MALAT1 in retinoblastoma and its related mechanisms. PATIENTS AND METHODS: Tixty-eight cases of retinoblastoma patients admitted to our hospital from February 2017 to February 2019 were collected as a research group, while 70 healthy people who came to our hospital for checkup at the same time were chosen as a control group. Both retinoblastoma and human colorectal mucosa cells were purchased, expression and clinical value of NKILA and MALAT1 in serum of Rb patients were tested, and sh-NKILA, si-NKILA, NC, sh-MALAT1 and si-MALAT1 were transfected into Weri-Rb1 and Y79 cells. qRT-PCR was adopted to detect the NKILA and MALAT1 levels in samples, and WB was adopted to detect the cle-caspase-3, cle-caspase-9, Bax, Cyclin B1, CDC2 and p-CDC2 protein levels in cells. Cell proliferation was conducted via MTT assay, invasion was carried out through transwell assay, and apoptosis was confirmed by flow cytometry assay. RESULTS: NKILA and MALAT1 were low expressed in retinoblastoma, and AUC of LncRNA NKILA and MALAT1 was over 0.8. LncRNA NKILA and MALAT1 were associated with tumor size, classification and clinical grading in children with retinoblastoma. Over-expression of NKILA and MALAT1 could promote apoptosis, inhibit cell growth and Bcl-2 protein, and promote upregulation of the expression levels of clecaspase-3, clecaspase-9 and Bax. CONCLUSIONS: By regulating MALAT1 and NKILA, we controlled the growth and apoptosis of Rb cells, which was expected to be a potential clinical therapeutic target for Rb.

Debye-waller factors of compounds with the caesium chloride structure

The lattice dynamics of five compounds with the caesium chloride structure have been investigated using shell models. Debye-Waller factors for these compounds are calculated over the temperature range from 1 to 1000 K and the results are presented analytically in a polynomial form. When experimental results are available, the calculated results are compared to the experimentally measured Debye-Waller factors and typically the discrepancies between these factors are less than 10%.

Parameterization of the temperature dependence of the Debye-Waller factors.

Parameterization has been made for the temperature dependence of the Debye-Waller factors of 68 elemental crystals and 17 compounds with the zinc-blende structure. The Debye-Waller factors of 46 elemental crystals were calculated based on the available phonon density of states, and those of the remaining 22 elemental crystals were estimated using the Debye approximation for the phonon density of states. The Debye-Waller factors of the zinc-blende compounds were obtained from the 14-parameter shell-model calculations of Reid [Acta Cryst. (1983), A39, 1-13].

Lattice dynamics and Debye-Waller factors of some compounds with the sodium chloride structure.

The lattice dynamics of 19 compounds with the sodium chloride structure have been investigated using shell models. The models are compared with existing experimentally measured phonon-dispersion curves and refined using a multidimensional downhill simplex method. Debye-Waller factors for these compounds are calculated over the temperature range from 1 to 1000 K where appropriate and the results are fitted analytically using polynomial regression. The results are compared with experimentally measured room-temperature Debye-Waller factors and for most of the compounds the agreement is found to be better than 10%. At lower temperatures, it is expected that these results would be more accurate, since the harmonic approximation, which is crucial to the calculation of the Debye-Waller factors, works better. In choosing the models for particular applications, it is recommended that the model with the smallest standard error sigma is used for fitting the experimentally measured phonon-dispersion curves, or the model that shows best agreement with reliable experimental measurements of more relevant physical quantities, such as Debye-Waller factors in crystallography.