Anterior chamber depth (ACD) is becoming a hot topic and plays an important role in correcting the refractive errors (REs) after cataract surgery. The aim of this study was to assess the ACD changes and their relationship with the REs after phacoemulsification and intraocular lens (IOL) implantation in patients with age-related cataracts. One hundred forty-five eyes of 125 age-related cataract patients from the Department of Ophthalmology, Tangdu Hospital, China, were recruited. IOL Master was used for axial length (AL) and the IOL power calculation measurements, and the Pentacam HR device was used for the ACD and lens thickness (LT) measurements. Every patient underwent uncomplicated phacoemulsification by a single surgeon using a single technique. Postoperative refraction results were obtained at 1 month. The appropriate formula used for the IOL power calculation was chosen depending on the AL, specifically the Hoffer Q (AL < 22.0 mm), SRK/T (22.0 mm ≤ AL ≤ 30.0 mm), and Haigis (AL > 30.0 mm) formulas. The postoperative ACD was deepened and tended to stabilize gradually after 2 weeks. A concurrent hyperopic shift (0.57 ± 0.47 D) was observed when the change in the ACD was less than 1.65 mm, whereas a myopic shift (− 0.18 ± 0.62 D) occurred contrarily, and the difference between the two groups was statistically significant (P < 0.0001). The change in ACD was significantly larger in the shallow anterior chamber (1.92 ± 0.40 mm) than in the deep chamber (1.33 ± 0.42 mm) (P < 0.0001). Similarly, the change in ACD was larger in the short AL (2.12 ± 0.37 mm) than in the long AL (1.32 ± 0.49 mm). The postoperative ACD and refractive changes were correlated with the preoperative ACD and AL (P < 0.0001), respectively. Two regression formulas were proposed: postoperative ACD = 3.524 + 0.294 × preoperative ACD and postoperative ACD = 3.361 + 0.228× (preoperative ACD + 1/2 LT). The results of this study showed that the ACD deepened and was associated with a concurrent RE after cataract surgery. Postoperative changes in the ACD were related to the preoperative ACD and AL, which determined the refraction status and visual quality. The regression formula of the postoperative ACD could provide a theoretical basis for predicting refractive errors in the clinic.

Cataract is a blinding disease worldwide. It is an age-related disease that mainly occurs in people over 65 years old. Cataract is also prevalent in patients with diabetes mellites (DM). The pathological mechanisms underlying diabetic cataract (DC) are more complex than that of age-related cataract. Studies have identified that polyol pathway, advanced glycation end products (AGEs) and oxidative stress are the primary pathogenesis of DC. In recent years, molecular-level regulations and pathological processes of lens epithelial cells (LECs) have been confirmed to play roles in the initiation and progression of DC. A comprehensive understanding and elucidation of how chronic hyperglycemia drives molecular-level regulations and cytopathological processes in the lens will shed lights on the prevention, delay and treatment of DC. Excessive glucose in the lens enhances polyol pathway and AGEs formation. Polyol pathway causes imbalance in the ratio of NADPH/NADP⁺ and NADH/NAD⁺. Decrease in NADPH/NADP⁺ ratio compromises antioxidant enzymes, while increase in NADH/NAD⁺ ratio promotes reactive oxygen species (ROS) overproduction in mitochondria, resulting in oxidative stress. Oxidative stress in the lens causes oxidation of DNA, proteins and lipids, leading to abnormalities in their structure and functions. Glycation of proteins by AGEs decreases solubility of proteins. High glucose triggered epigenetic regulations directly or indirectly affect expressions of genes and proteins in LECs. Changes in autophagic activity, increases in fibrosis and apoptosis of LECs destroy the morphological structure and physiological functions of the lens epithelium, disrupting lens homeostasis. In both diabetic animal models and diabetics, oxidative stress plays crucial roles in the formation of cataract. Epigenetic regulations, include lncRNA, circRNA, microRNA, methylation of RNA and DNA, histone acetylation and pathological processes, include autophagy, fibrosis and apoptosis of LECs also involved in DC.

Context Type 2 diabetes mellitus (T2DM) and cancer share a variety of risk factors and pathophysiological features. It is becoming increasingly accepted that the 2 diseases are related, and that T2DM increases the risk of certain malignancies. Objective This review summarizes recent advancements in the elucidation of functions of insulin-like growth factor 2 (IGF-2) messenger RNA (mRNA)-binding protein 2 (IGF2BP2) in T2DM and cancer. Methods A PubMed review of the literature was conducted, and search terms included IGF2BP2, IMP2, or p62 in combination with cancer or T2DM. Additional sources were identified through manual searches of reference lists. The increased risk of multiple malignancies and cancer-associated mortality in patients with T2DM is believed to be driven by insulin resistance, hyperinsulinemia, hyperglycemia, chronic inflammation, and dysregulation of adipokines and sex hormones. Furthermore, IGF-2 is oncogenic, and its loss-of-function splice variant is protective against T2DM, which highlights the pivotal role of this growth factor in the pathogenesis of these 2 diseases. IGF-2 mRNA-binding proteins, particularly IGF2BP2, are also involved in T2DM and cancer, and single-nucleotide variations (formerly single-nucleotide polymorphisms) of IGF2BP2 are associated with both diseases. Deletion of the IGF2BP2 gene in mice improves their glucose tolerance and insulin sensitivity, and mice with transgenic p62, a splice variant of IGF2BP2, are prone to diet-induced fatty liver disease and hepatocellular carcinoma, suggesting the biological significance of IGF2BP2 in T2DM and cancer. Conclusion Accumulating evidence has revealed that IGF2BP2 mediates the pathogenesis of T2DM and cancer by regulating glucose metabolism, insulin sensitivity, and tumorigenesis. This review provides insight into the potential involvement of this RNA binding protein in the link between T2DM and cancer.

Diabetic retinopathy (DR) is one of the most common diseases causing blindness in the world, and most patients are already in advanced stage. Recent years, many studies reported mean platelet volume (MPV) may be associated with development of DR, but there was no consistent conclusion reached. Literature was retrieved by formally searching PubMed, Embase, Cochrane library and Scopus and by hand searching of reference lists of related articles. Finally, a total of 14 literatures included, and Review manager 5.3 and STATA 14.0 statistical software were utilized for processing. Meta-analysis showed that MPV values in DR were significantly higher than health controls [SMD (95% CI) = 0.92 (0.60–1.24)] and type 2 diabetes mellitus without diabetic retinopathy (T2DM without DR) [SMD (95% CI) = 0.36 (0.19–0.53)]. Subgroup analysis indicated that MPV level in proliferative diabetic retinopathy (PDR) patients was higher than T2DM without DR patients [SMD (95% CI) = 0.48 (0.28, 0.68)], but this difference didn’t appear in non-proliferative diabetic retinopathy (NPDR). The study demonstrated that increased MPV level was significant associated with the development of DR, and it might reflect the severity of DR, which could be provided to monitor development and progression of DR clinically.