Scleral-fixated intraocular lens implants-evolution of surgical techniques and future developments.

Varied options are available for the implantation of secondary intraocular lens implants in the absence of zonular or capsular support. Loss of the capsule can occur in the context of complicated cataract surgery, trauma or inherited conditions such as Marfan syndrome or pseudoexfoliation. Approaches to overcome this include optical measures such as the use of spectacles or contact lenses, and surgical therapy incorporating the use of anterior chamber, iris-fixated or scleral-fixated lenses. Surgical techniques to implant scleral-fixated lenses have undergone various modifications, since the first publication of sutured intrascleral fixation described in the 1980s. However, despite the advances in surgical techniques, studies are limited either by their retrospective nature, small sample size and most importantly small duration of follow-up. This comprehensive review aims to amalgamate the evolution of various surgical techniques with regards to intrascleral lens fixation and suggests areas for future development.

The association of GSTM1 and GSTT1 polymorphisms with squamous cell carcinoma of cervix in Pakistan.

Gene deletions in GSTM1 and GSTT1 may result in tempering the activation and detoxification of several carcinogens and thereby may increase the risk of cancer pre-disposition. This study aims to investigate the clinical impact of glutathione-S-transferase GSTM1 and GSTT1 polymorphisms on squamous cell carcinoma of cervix (SCCA).The GSTM1 and GSTT1 polymorphisms were analyzed in cervical cancer patients and healthy controls. Touch down multiplex polymerase chain reaction (PCR) strategy was adopted for genotyping of GSTM1 and GSTT1 polymorphisms. The null genotype of GSTM1 exhibited a significantly higher percentage in patients with SCCA (74 %) than in the control group (34.0 %). However, no significant difference was observed in the null genotype of GSTT1 among SCC patients and healthy subjects, respectively. GSTM1 exhibited a significant association with increased risk of squamous cell carcinoma (p < 0.001). The odds ratio for the GSTM1 null genotype was also calculated (odds ratio 3.7484; 95 % confidence interval 1.6562-84834). This suggests that GSTM1 null genotype in cervical cell samples may be associated with more severe precancerous lesions of the cervix.

Molecular Docking of Known Carcinogen 4- (Methyl-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK) with Cyclin Dependent Kinases towards Its Potential Role in Cell Cycle Perturbation.

Cell cycle is maintained almost all the times and is controlled by various regulatory proteins and their complexes (Cdk+Cyclin) in different phases of interphase (G1, S and G2) and mitosis of cell cycle. A number of mechanisms have been proposed for the initiation and progression of carcinogenesis by abruption in cell cycle process. One of the important features of cancer/carcinogenesis is functional loss of these cell cycle regulatory proteins particularly in CDKs and cyclins. We hypothesize that there is a direct involvement of these cell cycle regulatory proteins not only at the genetic level but also proteins level, during the initiation of carcinogenesis. Therefore, it becomes significant to determine inconsistency in the functioning of regulatory proteins due to interaction with carcinogen 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). Hence, we investigated the interaction efficiency of NNK, against cell cycle regulatory proteins. We found a different value of ΔG (free energy of binding) among the studied proteins ranging between -3.29 to -7.25 kcal/mol was observed. To validate the results, we considered Human Oxy-Hemoglobin at 1.25 Å Resolution, [PDB_ID:1HHO] as a +ve control, (binding energy -6.06 kcal/mol). Finally, the CDK8 (PDB_ID:3RGF) and CDK2 (PDB_ID:3DDP) regulatory proteins showing significantly strong molecular interaction with NNK -7.25 kcal/mol, -6.19 kcal/mol respectively were analyzed in details. In this study we predicted that CDK8 protein fails to form functional complex with its complementary partner cyclin C in presence of NNK. Consequently, inconsistency of functioning in regulatory proteins might lead to the abruption in cell cycle progression; contribute to the loss of cell cycle control and subsequently increasing the possibility of carcinogenesis.