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AIM: To observe the changes in Schlemm's canal (SC), trabecular meshwork (TM), and anterior chamber relevant parameters after small incision lenticule extraction (SMILE) of myopia patients. METHODS: A total of 58 eyes from 30 patients who underwent SMILE were divided into a low and moderate myopia group (group A, 32 eyes) and a high myopia group (group B, 26 eyes). The diameter and area of the SC, the width and thickness of TM obtained by CIRRUS HD-OCT5000, and the related anterior chamber parameters obtained by Pentacam anterior segment analysis system, accommodation amplitude (AMP) were observed pre- and postoperatively. The preoperative intraocular pressure (IOP) and postoperative correction of intraocular pressure (IOPcc) were measured. RESULTS: The diameter and area of the SC in the two groups were significantly increased postoperatively (all P0.05). The corneal curvature, central anterior chamber depth, and anterior chamber volume decreased after SMILE surgery (all P

AIM: To study the changes of anterior chamber morphology and related parameters in patients with myopia after small incision lenticule extraction(SMILE).METHODS: A total of 39 patients with myopia(74 eyes)who underwent SMILE surgery in our hospital during December 2018 to January 2019 were selected. They were divided into two groups: 23 patients(44 eyes)in low and medium myopia group(≤-6.00D)and 16 patients(30 eyes)in the high myopia group(>-6.00D). Changes of central anterior chamber depth(ACD), anterior chamber volume(ACV), anterior chamber angle(ACA), posterior central elevation(PCE), and accommodation amplitude(AMP)were observed in the two groups before the surgery and 1d, 1wk, and 1mo after surgery. The related data were statistically analyzed, and the changes before and after the surgery were compared. The causes of the morphological changes of the anterior chamber in the early stage after the SMILE were discussed.RESULTS: The ACD before and 1d, 1wk, 1mo after surgery were 3.18±0.21, 3.10±0.21, 3.11±0.21 and 3.12±0.2mm, respectively, the ACV were 201.1±29.3, 187.9±27.1, 187±26.4 and 187.7±24.9mm3, respectively, the AMP were 8.4±2.6, 6.5±1.6, 7±1.7 and 8.3±1.9D, respectively, the ACD in the high myopia group before and 1d, 1wk, 1mo after surgery were 3.25±0.2, 3.18±0.19, 3.16±0.19 and 3.23±0.24mm, respectively, the ACV were 204.1±31mm3, 194.5±27mm3, 194.5±28.6mm3 and 196.5±31.7mm3, respectively, the AMP were 8.9±2D, 6.8±1.9D, 7.9±1.4D and 8.9±1.5D, respectively, the PCE 2.4±2.7μm, 1.4±2.7μm, 1.1±2.8μm and 1.4±2.9μm, respectively, the ACA were 42.40°±3.1°, 42.30°±3.6°, 42.10°±4.6°and 40.70°±4.5°, respectively. Pearson correlation analysis showed that postoperative ACD was positively correlated with ACA and ACV in both groups(Pr=0.301, Pr=0.161,Pr=0.069, 0.103, P>0.05).CONCLUSION: In the early stage after SMILE, the diopter is different and the morphology of the anterior chamber is different. We believe that the change of ACD in the early stage after SMILE is related to changes of the corneal posterior elevation and postoperative accommodation.

Macroautophagy/autophagy dysregulation has been noted in diabetic nephropathy; however, the regulatory mechanisms controlling this process remain unclear. In this study, we showed that SMAD3 (SMAD family member 3), the key effector of TGFB (transforming growth factor beta)-SMAD signaling, induces lysosome depletion via the inhibition of TFEB-dependent lysosome biogenesis. The pharmacological inhibition or genetic deletion of SMAD3 restored lysosome biogenesis activity by alleviating the suppression of TFEB, thereby protecting lysosomes from depletion and improving autophagic flux in renal tubular epithelial cells in diabetic nephropathy. Mechanistically, we found that SMAD3 directly binds to the 3ʹ-UTR of TFEB and inhibits its transcription. Silencing TFEB suppressed lysosome biogenesis and resulted in a loss of the protective effects of SMAD3 inactivation on lysosome depletion under diabetic conditions. In conclusion, SMAD3 promotes lysosome depletion via the inhibition of TFEB-dependent lysosome biogenesis; this may be an important mechanism underlying autophagy dysregulation in the progression of diabetic nephropathy. Abbreviations: AGEs: advanced glycation end products; ATP6V1H: ATPase H+ transporting V1 subunit H; CTSB: cathepsin B; ChIP: chromatin immunoprecipitation; Co-BSA: control bovine serum albumin; DN: diabetic nephropathy; ELISA: enzyme-linked immunosorbent assay; FN1: fibronectin 1; HAVCR1/TIM1/KIM-1: hepatitis A virus cellular receptor 1; LAMP1: lysosomal associated membrane protein 1; LMP: lysosome membrane permeabilization; MAP1LC3B/LC3B: microtubule associated protein 1 light chain 3 beta; NC: negative control; SIS3: specific inhibitor of SMAD3; SMAD3: SMAD family member 3; siRNA: small interfering RNA; SQSTM1/p62: sequestosome 1; TECs: tubular epithelial cells; TFEB: transcription factor EB; TGFB1: transforming growth factor beta 1; TGFBR1: transforming growth factor beta receptor 1; UTR: untranslated region; VPS11: VPS11 core subunit of CORVET and HOPS complexes. [ABSTRACT FROM AUTHOR]

Sebocyte differentiation is a continuous process, but its potential molecular mechanism remains unclear. We aimed to establish a novel sebocyte differentiation model using human primary sebocytes and to identify the expression profiles of differentiation-associated proteins. Primary human sebocytes were cultured on Sebomed medium supplemented with 2% serum for 7 days. Flow cytometry showed that S phase cells were decreased time-dependently, while G1 and subG1 (apoptosis) phase cells increased under serum starvation. Transmission electron microscopy and Oil Red O staining revealed a gradual increase of intracellular lipid accumulation. Expression of proliferation marker was diminished, while expression of differentiation, apoptosis, and lipogenic markers elevated gradually during 7-day culture. iTRAQ analysis identified 3582 expressed proteins in this differentiation model. Compared with day 0, number of differentially expressed proteins was 132, 54, 321, and 96 at days 1, 3, 5, and 7, respectively. Two overexpressed proteins (S100 calcium binding protein P and ferredoxin reductase) and 2 downexpressed proteins (adenosine deaminase and keratin 10) were further confirmed by Western blot and immunohistochemistry. [ABSTRACT FROM AUTHOR]