Objective. To investigate refractive development and prevalence of myopia in children aged 3-6 years in Hebei Province, China, and to explore the developmental law of refraction, so as to clinically guide the prediction and intervention of myopia. Methods. In May 2019, a total of 6120 people were inspected in 68 kindergartens in 11 cities in Hebei Province. Child refractive refraction was checked under noncycloplegia using a handheld binocular vision screener (SW-800, SUOER, Tianjin, China). Axial length (AL) and corneal radius of curvature (CR) were measured using an ocular biometry (IOLMaster 500, Carl Zeiss, Germany). Myopia was defined as spherical equivalent SE ≤ − 0.75 D . Results. A total of 5506 children aged 3-6 years met the criteria and were included in the statistical analysis. The prevalence of myopia was 3.49% (1.93% at age 3, 2.90% at age 4, 3.78% at age 5, and 3.88% at age 6). Overall, the mean SE was + 0.67 ± 1.05 D ( + 0.81 ± 1.00 D at age 3, + 0.79 ± 1.05 D at age 4, + 0.67 ± 1.08 D at age 5, and + 0.13 ± 1.01 D at age 6); the mean CR was 7.76 ± 0.26 mm ( 7.78 ± 0.26 mm at age3, 7.75 ± 0.25 mm at age 4, 7.77 ± 0.26 mm at age 5, and 7.76 ± 0.25 mm at age 6); the mean AL was 22.31 ± 0.73 mm ( 21.98 ± 0.63 mm at age 3, 22.12 ± 0.69 mm at age 4, 22.34 ± 0.73 mm at age 5, and 22.49 ± 0.73 mm at age 6). Conclusions. Prevalence of myopia increases with age in children aged 3-6 years in Hebei, China. With the increase of age, CR is basically stable, and AL increases gradually. AL/CR, which is closely related to SE, can be used as an indicator to predict myopia and guide clinical work.
Tamoxifen (TAM) is the most commonly used adjuvant endocrine drug for hormone receptor-positive (HR+) breast cancer patients. However, how to accurately evaluate the risk of breast cancer recurrence and metastasis after adjuvant TAM therapy is still a major concern. In recent years, many studies have shown that the clinical outcomes of TAM-treated breast cancer patients are influenced by the activity of some cytochrome P450 (CYP) enzymes that catalyze the formation of active TAM metabolites like endoxifen and 4-hydroxytamoxifen. In this study, we aimed to first develop and validate an algorithm combining polymorphisms in CYP genes and clinicopathological signatures to identify a subpopulation of breast cancer patients who might benefit most from TAM adjuvant therapy and meanwhile evaluate major risk factors related to TAM resistance. Specifically, a total of 256 patients with invasive breast cancer who received adjuvant endocrine therapy were selected. The genotypes at 10 loci from three TAM metabolism-related CYP genes were detected by time-of-flight mass spectrometry and multiplex long PCR. Combining the 10 loci with nine clinicopathological characteristics, we obtained 19 important features whose association with cancer recurrence was assessed by importance score via random forests. After that, a logistic regression model was trained to calculate TAM risk-of-recurrence score (TAM RORs), which is adopted to assess a patient’s risk of recurrence after TAM treatment. The sensitivity and specificity of the model in an independent test cohort were 86.67% and 64.56%, respectively. This study showed that breast cancer patients with high TAM RORs were less sensitive to TAM treatment and manifested more invasive characteristics, whereas those with low TAM RORs were highly sensitive to TAM treatment, and their conditions were stable during the follow-up period. There were some risk factors that had a significant effect on the efficacy of TAM. They were tissue classification (tumor Grade < 2 vs. Grade ≥ 2, p = 2.2e−16), the number of lymph node metastases (Node-Negative vs. Node < 4, p = 5.3e−07; Node < 4 vs. Node ≥ 4, p = 0.003; Node-Negative vs. Node ≥ 4, p = 7.2e−15), and the expression levels of estrogen receptor (ER) and progesterone receptor (PR) (ER < 50% vs. ER ≥ 50%, p = 1.3e−12; PR < 50% vs. PR ≥ 50%, p = 2.6e−08). The really remarkable thing is that different genotypes of CYP2D6*10(C188T) show significant differences in prediction function (CYP2D6*10 CC vs. TT, p < 0.019; CYP2D6*10 CT vs. TT, p < 0.037). There are more than 50% Chinese who have CYP2D6*10 mutation. So the genotype of CYP2D6*10(C188T) should be tested before TAM therapy.
Efficacy of clinical chemotherapeutic agents depends not only on direct cytostatic and cytotoxic effects but also involves in eliciting (re)activation of tumour immune effects. One way to provoke long‐lasting antitumour immunity is coined as immunogenic cell death (ICD), exploiting the host immune system against tumour cells as a “second hit”. Although metal‐based antitumour complexes hold promise as potential chemotherapeutic agents, ruthenium (Ru)‐based ICD inducers remain sparse. Herein, we report a half‐sandwich complex Ru(II) bearing aryl‐bis(imino) acenaphthene chelating ligand with ICD inducing properties for melanoma in vitro and in vivo. Complex Ru(II) displays strong anti‐proliferative potency and potential cell migration inhibition against melanoma cell lines. Importantly, complex Ru(II) drives the multiple biochemical hallmarks of ICD in melanoma cells, i. e., the elevated expression of calreticulin (CRT), high mobility group box 1 (HMGB1), Hsp70 and secretion of ATP, followed by the decreased expression of phosphorylation of Stat3. In vivo the inhibition of tumour growth in prophylactic tumour vaccination model further confirms that mice with complex Ru(II)‐treated dying cells lead to activate adaptive immune responses and anti‐tumour immunity by the activation of ICD in melanoma cells. Mechanisms of action studies show that complex Ru(II)‐induced ICD could be associated with mitochondrial damage, ER stress and impairment of metabolic status in melanoma cells. We believe that the half‐sandwich complex Ru(II) as an ICD inducer in this work will help to design new half‐sandwich Ru‐based organometallic complexes with immunomodulatory response in melanoma treatments.
Ultrasonic treatment is an effective method to disintegrate sludge and extract organic matter and nutrients, including nitrogen and phosphorus, from the sludge. This study investigated the transformation of phosphorus species during the ultrasonic treatment of sludge, to reveal the mechanism of phosphorus migration in the activated sludge structure. The experimental results indicated that power density and ultrasonic time were critical parameters affecting the energy input for sludge integration. The optimal phosphorus release performance was achieved at 2.5 W/mL 10 min. The release of phosphorus showed as a layer-by-layer pattern from the inner sludge core to the outer sphere of the multiple-layer structure of the sludge. The complex sludge structure played an important role in buffering the ultrasonication process and transfer of phosphorus. Mg-P, Ca-P, and organic phosphorus are the main phosphorus species that can be extracted from the sludge core into the supernatant. The three-stage process of phosphorus migration through the sludge layers, including dissolution, reprecipitation, and equilibrium, has been revealed.
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