Artificial intelligence-aided diagnosis and treatment in the field of optometry.

With the rapid development of computer technology, the application of artificial intelligence (AI) to ophthalmology has gained prominence in modern medicine. As modern optometry is closely related to ophthalmology, AI research on optometry has also increased. This review summarizes current AI research and technologies used for diagnosis in optometry, related to myopia, strabismus, amblyopia, optical glasses, contact lenses, and other aspects. The aim is to identify mature AI models that are suitable for research on optometry and potential algorithms that may be used in future clinical practice.

Silencing of the TPM1 gene induces radioresistance of glioma U251 cells.

The present study was designed to investigate the relationship between tropomyosin 1 (TPM1) and radioresistance in human U251 cells. Radioresistant U251 (RR-U251) cells were established by repeated small irradiating injury. TPM1 levels in the U251 and RR-U251 cells were inhibited by transfection with TPM1-short hairpin RNA (shRNA) while overexpression was induced by treatment with pcDNA3.1­TPM1. The radiosensitivity of the U251 and RR-U251 cells and the plasmid-transfected cells was evaluated by cell viability, migration and invasion assays. Cell apoptosis was also examined in vitro. The radiosensitivity of U251 xenografts was observed by tumor growth curve after radiotherapy in an in vivo experiment. Western blotting and immunohistochemistry were used to detect the level of TPM1 in vivo. The expression of TPM1 was significantly decreased in the RR-U251 cells, which may be correlated with the radioresistance of the glioma U251 cells. In the TPM1-silenced RR-U251 and TPM1-silenced U251 cells, cell viability, migration and invasion ability were significantly increased, and the rate of cell apoptosis was decreased. Consistent with these results, in the TPM1-overexpressing U251 and RR-U251 cells, cell viability, migration and invasion abilities were markedly decreased, and increased apoptosis was noted when compared to the control group. Tumor growth of the U251 xenografts was significantly inhibited following treatment with pcDNA3.1­TPM1 combined with radiotherapy. Taken together, these results indicate that TPM1 may be one mechanism underlying radiation resistance, and TPM1 may be a potential target for overcoming the radiation resistance in glioma.

Increasing radiosensitivity with the downregulation of cofilin-1 in U251 human glioma cells.

The aim of the present study was to examine the association between cofilin­1 (CFL1) and radioresistance in human glioma U251 cells. CFL1 expression was downregulated and upregulated in U251 cells through the transfection of CFL1­small interfering (si)RNA and pcDNA3.1­CFL1, respectively. The radiosensitivity of U251 cells and established radioresistant U251 cells (RR­U251) was evaluated using cell viability, migration and invasion ability assays. Cell cycle distribution was also examined. The results showed that CFL1 expression was significantly increased in RR­U251 cells; in addition, the cell viability, migration and invasion ability of RR­U251 cells were significantly enhanced compared to those of the normal U251 cells, whereas the number of cells arrested in G2 phase was markedly decreased. In CFL1­silenced RR­U251 and CFL1­silenced U251 cells, the cell viability, migration and invasion abilities were significantly downregulated and the number of cells arrested in G2 phase was increased compared to that of the untransfected cells. In U251 cells overexpressing CFL1, cell viability, migration and invasion abilities were markedly upregulated and the number of cells arrested in G2 phase was decreased. In conclusion, the results of the present study suggested that downregulation of CFL1 may increase radiosensitivity in U251 cells.

Downregulation of phosphoglycerate kinase 1 by shRNA sensitizes U251 xenografts to radiotherapy.

Phosphoglycerate kinase 1 (PGK1) has been demonstrated to be involved in radioresistance. The present study was designed to investigate the effect of PGK1 on the radioresistance in vivo. U251 glioma cells were transfected with the short hairpin RNA (shRNA)-PGK1 and pcDNA3.1-PGK1 using Lipofectamine 2000. The radiosensitivity of U251 xenografts was observed by tumor growth curve following radiotherapy. Quantitative PCR, western blot analysis and immunohistochemistry were performed to evaluate PGK1 expression in the xenografts from the different tumor models. The expression of PGK1 was maximally inhibited in response to shRNA4 at 24 h after the transfection in vitro. Tumor growth of the U251 xenografts was significantly inhibited following treatment with shRNA-PGK1 and radiotherapy. The expression of PGK1 in vivo at the mRNA and protein levels was downregulated by the treatment of shRNA1 when compared to levels following treatment with shNC and PBS after radiotherapy. The results showed that suppression of PGK1 enhanced the radiosensitivity of U251 xenografts and suggest that PGK1 may serve as a useful target in the treatment of radioresistant glioma.

A cross-sectional study on cerebrospinal fluid biomarker levels in cognitively normal elderly subjects with or without a family history of Alzheimer's disease.

BACKGROUND: Cerebrospinal fluid (CSF) biomarkers reflect changes in the brain, and contribute to early screening. Maternal inheritance is putatively stronger than paternal inheritance for late-onset Alzheimer's disease (LOAD). METHODS: Clinical data of 162 cognitively normal subjects were reviewed. A standard questionnaire was used to identify LOAD family history. Mini-mental state examination (MMSE) was used to evaluate cognition. CSF Aß1-40, Aß1-42, total and phosphorylated tau were measured using ELISA. AIMS: To compare biomarkers in cognitively normal elderly subjects with versus without LOAD family history. RESULTS: Among the 162 subjects, 38 and 60 had LOAD family history on paternal and maternal sides, respectively. The remaining 60 subjects had no family history. No difference was noted in age, gender, education level, MMSE score, and memory impairment complaint in the three groups. Aß42 and the Aß42/40 ratio were lower than in subjects with a maternal history than in subjects with a paternal history or without family history (P < 0.05 in both). Phosphorylated and total tau did not differ among the three groups. CONCLUSION: Offspring with a family history of LOAD on the maternal side have lower Aß42 and Aß42/40 ratio in the CSF, and maybe at higher risk for developing AD.