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Cataract is a disease opacifying the crystalline, leading to a blurred vision and ultimately to blindness. With an aging population, the incidence of cataract is increasing, as well as the number of treatments. The solution available is its complete removal, followed by an implant of an intraocular lens (IOL). Although the post-operative complications on cataract surgeries have been decreasing in general, the bag-IOL complex dislocation is still an issue, probably being the most serious complication under this procedure. In this work, an axisymmetric Finite Element (FE) modelling strategy of the crystalline complex during the process of accommodation under cataract surgery is proposed. The goal was to understand the influence of biomechanical alterations promoted by the IOL on bag-IOL dislocation after surgery. An increase of force and stress in the zonules was verified in the pseudophakic eye compared to the complete eye, which could explain why zonules break years after surgery, leading to the bag-IOL dislocation. The axisymmetric FE model proposed in this work is innovative in this field, which still lacks detailed research, and can be an important complement for the clinical and biomechanical work on the crystalline complex.

Cervical cancer is one of the most common cancers in women worldwide, being high-risk group the HPV infected, the leading etiological factor. The raf kinase inhibitory protein (RKIP) has been associated with tumor progression and metastasis in several human neoplasms, however its role on cervical cancer is unclear. In the present study, 259 uterine cervix tissues, including cervicitis, cervical intraepithelial lesions and carcinomas, were analyzed for RKIP expression by immunohistochemistry. We found that RKIP expression was significantly decreased during malignant progression, being highly expressed in non-neoplastic tissues (54% of the samples; 73/135), and expressed at low levels in the cervix invasive carcinomas (∼15% (19/124). Following in vitro downregulation of RKIP, we observed a viability and proliferative advantage of RKIP-inhibited cells over time, which was associated with an altered cell cycle distribution and higher colony number in a colony formation assay. An in vitro wound healing assay showed that RKIP abrogation is associated with increased migratory capability. RKIP downregulation was also associated with an increased vascularization of the tumors in vivo using a CAM assay. Furthermore, RKIP inhibition induced cervical cancer cells apoptotic resistance to cisplatin treatment. In conclusion, we described that RKIP protein is significantly depleted during the malignant progression of cervical tumors. Despite the lack of association with patient clinical outcome, we demonstrate, in vitro and in vivo, that loss of RKIP expression can be one of the factors that are behind the aggressiveness, malignant progression and chemotherapy resistance of cervical cancer.