Xi Huang

Objectives: To evaluate whether the corneal densitometry graph can visualise the demarcation line (DL) and measure its depth early after corneal collagen cross-linking (CXL). Methods: A total of 53 eyes of 53 patients with progressive keratoconus underwent accelerated CXL. Visual acuity and corneal topography were measured preoperatively and at 1 month. The apex of the cross-linking reaction (CLR) peak on corneal densitometry graph was compared with the DL depth on anterior segment optical coherence tomography (AS-OCT); the reaction-initiating and reaction-ending depths were compared with those on in vivo confocal microscopy (IVCM). Pearson correlation coefficient was used to assess the linear association between the densitometry-derived depths and the reference measurements. Agreement was evaluated with Bland–Altman analysis together with an absolute-agreement intraclass correlation coefficient (ICC) and changes were analysed with linear mixed-effects models. Results: At 1 month postoperatively, uncorrected distance visual acuity (UDVA) did not change significantly (p = 0.851), whereas CDVA improved slightly (p = 0.022). Corneal densitometry increased in the central region (0–2, 2–6, 6–10 mm) (p < 0.001). Corneal densitometry increased significantly in the central region (0–2, 2–6 and 6–10 mm annuli; total layer, all p ≤ 0.001) but not in the 10–12 mm annulus (p = 0.827). Correlation analysis showed a strong association with AS-OCT and IVCM (r = 0.82–0.88, p < 0.001). Agreement with AS-OCT and IVCM was good at the group level (ICC(2,1), 0.82–0.87), although all 95% limits of agreement exceeded the ±5% limit. A CLR peak was identified in all 53/53 eyes versus 50/53 eyes on AS-OCT, but the detection rates did not differ significantly (McNemar exact test, p = 0.25). Conclusions: The corneal densitometry graph provides an initial, non-contact evaluation of the depth and extent of the early cross-linking reaction, with good group-level agreement with AS-OCT and IVCM.

Diabetes is a major global health problem that affects the entire body and is a significant cause of cardiovascular disease, amputations, blindness, renal failure and heart failure; by 2040, it is ...

Purpose Research on the correlation between ocular dominance and macular structure and function is inconsistent. This clinical observational study explored the effect of ocular dominance on retinal structure and the correlation between binocular structural asymmetry and ocular dominance. Methods Forty healthy young adults (aged 20–29 years) were enrolled. Ocular dominance, refractive error, pattern visual evoked potential (PVEP), multifocal electroretinography (mfERG), swept-source optical coherence tomography (SS-OCT), and optical coherence tomography angiography (OCTA)tests were performed. Results Among the 40 subjects, 24 (60%) were right-eye dominant. The dominant eye had a larger amplitude density of Ring 1 in the mfERG (198.52 ± 51.43 vs. 175.92 ± 50.17, p = 0.003), larger density of the superficial capillary plexus of the macula within the 4–12 mm diameter range (dominant eyes vs. nondominant eyes: 4–6 mm: 80.89 (78.24,83.58) vs. 78.93 (74.85,81.77), p < 0.001; 7–9 mm: 73.01 (69.22,75.90) vs. 71.75 (69.43,74.37), p = 0.009; 10–12 mm: 55.79 ± 5.40 vs. 54.46 ± 7.03, p = 0.033), and a thicker choroidal layer (dominant eyes vs. nondominant eyes: 7–9 mm: 289.70 ± 58.85 vs. 279.86 ± 59.16, p = 0.045; 10–12 m: 270.05 ± 44.87 vs. 259.64 ± 43.50, p = 0.014). The right eye had a higher choroidal vascular density (right eyes vs. left eyes: 0–1 mm: 95.45 (84.56,98.67) vs. 91.04 (79.79,97.04), p = 0.018) and lower superficial retinal vascular density (right eyes vs. left eyes: 10–12 mm: 54.29 ± 5.98 vs. 55.82 ± 6.34, p = 0.027) and choroidal vascular density (right eyes vs. left eyes: 7–9 mm: 90.98 ± 2.89 vs. 92.18 ± 2.61, p = 0.041). Conclusion Ocular dominance influenced macular foveal function, parafoveal vessel density and choroidal thickness. The functional and morphological differences in ocular dominance and laterality are inconsistent.

Retinal ischemia/reperfusion injury (RI/R) is a common pathological process in ophthalmic diseases, which can cause severe visual impairment. The mechanisms underlying RI/R damage and repair are still unclear. Scholars are actively exploring effective intervention strategies to restore impaired visual function. With the development of nucleic acid nanomaterials, tetrahedral framework nucleic acids (tFNAs) have shown promising therapeutic potential in various fields such as stem cells, biosensors, and tumour treatment due to their excellent biological properties. Besides, miRNA‐22‐3p (miR‐22), as an important regulatory factor in neural tissue, has been proven to have positive effects in various neurodegenerative diseases. By stably constructing a complex of tetrahedral framework nucleic acids miR22 (tFNAs‐miR22), we observed that tFNAs‐miR22 had a positive effect on the repair of RI/R injury in retinal neural tissue. Previous studies have shown that tFNAs can effectively deliver miR‐22 into damaged retinal neurons, subsequently exerting neuroprotective effects. Interestingly, we found that there was a certain synergistic effect between tFNAs and miR‐22. tFNAs‐miR22 can selectively activated the ERK1/2 signalling pathway to reduce neuronal apoptosis, accelerate cell proliferation, and restore synaptic functional activity. In this study, we established a simple yet effective small molecule drug for RI/R treatment which may become a promising neuroprotectant for treating this type of vision impairment disease in the future.

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Purpose To determine whether the GNAQ/11 mutation correlated with the outcome of patients with uveal melanoma (UM) when genetic heterogeneity was considered. Methods We performed a retrospective study of sixty-seven patients with UM. The heterogeneity of GNAQ/11 was examined by using droplet digital PCR. The correlation between metastasis and heterogeneity of the GNAQ/11 mutation was analysed. Disease free survival curves were constructed using the Kaplan-Meier method, and the Wilcoxon log-rank test was used to compare the curves. Results The GNAQ/11 mutation ratio was varied between each case. Among these patients, 28.35% of them harboured homogeneous mutation of GNAQ/11, 62.69% present heterogeneous mutation and 8.96% didn’t present either GNAQ or GNA11 mutation. The tumour with heterogeneous mutation of GNAQ/11 has a higher metastatic rate than that with homogeneous mutation (13/29 vs 1/18, p=0.027). In Kaplan-Meier analysis, metastasis-free survival was not significantly associated with either homogeneous or heterogeneous mutation of GNAQ/11. Conclusion The mutation ratio of GNAQ/11 in UM was quite variable. The tumour with heterogeneous mutation of GNAQ/11 is more likely to develop a poor prognosis than that with homogeneous mutation of GNAQ/11.

It has previously been reported that cardamonin is able to regulate glycometabolism and vasodilation whilst also exhibiting anti‑inflammatory and antitumor properties. The antitumor effect of cardamonin is multifaceted, and so it is necessary to investigate the antitumor mechanisms of cardamonin at the molecular level. Cardamonin alters chemotherapy‑resistant colon cancer cell growth; however, the underlying mechanism is unknown. The present study was conducted to investigate the effect of cardamonin on chemotherapy‑resistant colon cancer cells and the possible mechanisms of action. Cardamonin significantly suppressed the growth of chemotherapy‑resistant colon cancer cells, induced apoptosis and promoted caspase‑3/9 activity and Bax protein expression in 5‑fluorouracil (5‑FU)‑resistant HCT‑116 cells. Cardamonin significantly suppressed c‑MYC, octamer‑binding transcription factor 4, cyclin E, testes‑specific protease 50 and nuclear factor‑κB protein expression in 5‑FU‑resistant HCT‑116 cells. The findings of the present study demonstrate that cardamonin suppresses chemotherapy‑colon cancer cell via the NF‑κB pathway in vitro.

Interleukin-32 promotes the proliferation of multiple myeloma cells by inducing production of IL-6 in bone marrow stromal cells Interleukin-32α promotes the proliferation of multiple myeloma cells by inducing production of IL-6 in bone marrow stromal cells