OBJECTIVES: To compare the efficacy of toric implantable collamer lens (Toric-ICL) and femtosecond laser-assisted in situ keratomileusis (FS-LASIK) for myopia correction in patients with moderate to high myopia complicated with astigmatism. METHODS: We retrospectively collected data from 64 patients (aged 18-42 years) with moderate to high myopia complicated with astigmatism (128 eyes) undergoing either Toric-ICL (28 patients/56 eyes) or FS-LASIK (36 patients/72 eyes) at our department between January, 2019 and December, 2020. The changes of uncorrected distance visual acuity (UCVA), spherical equivalent (SE), mean astigmatism correction index (CI), corneal endothelial cell density (ECD) and intraocular pressure (IOP) following the procedures were compared between the two groups. RESULTS: In FS-LASIK group, all the eyes (72/72) achieved an UCVA≥1.0, similar to the rate in Toric-ICL group (55/56 eyes; P=0.2374). The postoperative SE was also comparable between FS-LASIK and Toric-ICL groups [0.43±0.06 D (range: -1.0 to 1.50 D) vs 0.38±0.05 D (range: -0.75 to 1.00 D); P=0.56]. The mean astigmatism CI was significantly higher in FS-LASIK group than in Toric-ICL group (0.8561 vs 0.7176; P<0.0001), and 88.89% of the eyes in FS-LASIK group and 69.64% in Toric-ICL group had postoperative astigmatism ≤0.50 D. No significant changes were observed in postoperative corneal ECD in FS-LASIK group, whereas ECD decreased significantly after the procedure in Toric-ICL group (P=0.0057). The patients undergoing Toric-ICL exhibited no significant changes of postoperative IOP, but the patients receiving FS-LASIK had significantly reduced IOP after the procedure (P<0.001). CONCLUSIONS Although the patients included in Toric-ICL group had higher myopia and astigmatism, Toric-ICL still showed better predictability and efficacy for astigmatic correction in Toric-ICL group. Toric-ICL is an effective and safe equivalent of FS-LASIK for correcting moderate myopia but can be more advantageous for correcting high myopia with astigmatism.
Humans ; Astigmatism/complications* ; Myopia/complications* ; Keratomileusis, Laser In Situ/methods* ; Retrospective Studies ; Adult ; Visual Acuity ; Adolescent ; Young Adult ; Treatment Outcome ; Male ; Lens Implantation, Intraocular/methods* ; Female ; Phakic Intraocular Lenses ; Intraocular Pressure

Objective To investigate the effects of exosome-derived miR-1246 on metastasis and autophagy of esophageal squamous cell carcinoma(ESCC).Methods The exosomes of ESCC cells were extracted by exosome extraction kit,the morphology was observed under electron microscope,the particle size was detected by nano-particle size analyzer,and the expression of exosome markers TSG101 and Calnexin was detected by Western blot.The RNA of exosomes of ESCC cells and normal esophageal epithelial cells were sequenced to analyze the differentially expressed miRNAs,which were analyzed by KEGG Pathway enrichment.The expression of miR-1246 in tumor tissues and paracancer tissues of 155 patients with ESCC was evaluated by transcriptome sequencing.The effect of miR-1246 on the migration ability of ESCC cells was detected by Transwell assay and the effect on autophagy was detected by Western blot.Results The exosomes derived from ESCC cells were intact in shape and similar to spherical vesicle-like structure with the particle size of 50～80 nm.The exosome marker TSG101 protein was positive and Calnexin protein was negative.There were 59 common differentially expressed miRNAs between exosomes of ESCC cells and normal esophageal epithelial cells.Exosome miR-1246 was highly expressed in ESCC cells,and the differentially expressed miRNAs were mainly enriched in autophagy metabolic pathway.Exosome miR-1246 was highly expressed in cancer tissues of patients with ESCC.Overexpression of miR-1246 significantly promoted the migration and autophagy of ESCC cells(t=4.119 and 48.150,P <0.05 and <0.001,respectively).Inhibition of miR-1246 expression inhibited the migration and autophagy of ESCC cells(t=9.067 and 51.270,P <0.01 and <0.001,respectively).Conclusion miR-1246 derived from exosomes can significantly affect the metastasis and autophagy of ESCC cells.

Objective To investigate the effects of rotavirus ( RV) on the expression and bioactiv-ity of Na+-H+ exchanger 3 ( NHE3 ) in Caco-2 cells and the possible regulatory mechanism. Methods Caco-2 cells expressing NHE3 were constructed and divided into four groups as follows: control ( CTL ) group, RV group, BAPTA-AM ( a Ca2+ chelator) group and BAPTA-AM+RV group. Na+-H+ exchanger ac-tivity and NHE3 expression on cell surface were determined using BCECF-AM and biotinylation assay, re-spectively. Expression of Cdc42 at protein level was measured by Western blot. Results Compared with the control group, RV infection significantly decreased the activity of NHE3 and its expression on cell surface. BATPA-AM antagonized the inhibitory effects on NHE3. Moreover, the expression of Cdc42 at protein level was increased following RV infection, which was also antagonized by BATPA-AM. Conclusions Intracellu-lar Ca2+-mediated Cdc42-dependent endocytosis pathway might be involved in regulating the expression and bioactivity of NHE3 during RV infection.

Objective To observe the effect of rotavirus (RV) infection on expression level and bioactivity of Na+-H+ exchanger 3 (NHE3) in Caco-2 cells. Methods Model of NHE3-expressing Caco-2 cells was constructed and studied in terms of intervention: control, RV, clathrin antagonist chlorpromazine (CPZ), and CPZ + RV. NHE3 activity and NHE3 protein amount on cell surface were determined by BCECF-AM and biotinylation, respectively. Expression level of clathrin was assayed by Western blot. Results Compared with control group, NHE3 activity and NHE3 surface protein level significantly decreased when the cells were treated with RV. These effects could not be completely cancelled by clathrin antagonist CPZ. Moreover, RV treatment could increase cellular protein level of clathrin, which was cancelled by CPZ. Conclusions The effect of RV infection on NHE3 expression level and biological activity may be related to clathrin-dependent endocytosis pathway, and may be also affected by other endocytosis pathways.

Objective To analyze the clinical characteristics and therapy of levofloxacin-induced prolonged Q-T interval in patients with multi-drug resistant tuberculosis ( MDR-TB) . Methods Clinical materials of 6 patients with MDR-TB who developed prolonged Q-T/QTc interval caused by levofloxacin therapy were analyzed. Those cases were collected from the Tuberculosis Prevention and Control of Wuhan City form April 2010 to August 2014. Results The proportion of patients with levofloxacin-induced prolonged Q-T interval was approximately 3.0%.The condition occurred 2-8 months after the administration. The initial value of QTc interval ranged from 397 ms to 439 ms, while the average was (410.17±14.62) ms.The value of QTc interval was extended to 470-486 ms after treatment of levofloxacin, while the average was (476.33±6.16) ms.The increase of QTc interval was 47-85 ms, while the average was ( 66 ± 11. 48 ) ms. None of them developed Tdp. Conclusion The application of high dosage and long treatment course of levofloxacin in patients with MDR-TB could result in the extension of the Q-T/QTc interval, which should arouse our serious attention. In order to detect the abnormal Q-T/QTc interval in early stage, electrolyte level examination as well as ECG examination should be considered as routine tests before initiation of treatment and during the follow-up treatment.