Caspase-3, p53 and Bcl-2 expression in basal cell carcinoma of the eyelid.

INTRODUCTION: Eyelid tumours mostly originated from skin and its appendeges. External carcinogens like UV radiation causes cell damages in the eyelid skin and contributes to carcinogenesis. Apoptosis is a very important mechanism to prevent these damage and probable neoplatic change. AIM: To compare caspase-3, p53 and Bcl-2 levels between patients with basal cell carcinoma (BCC) of the eyelid and healthy individuals. MATERIAL AND METHODS: Pathology archives from October 2012 to April 2015 were scanned for BCC biopsies of the eyelid and tissue removed during blepharoplasty and entropion procedures. A total of 36 specimens were found. The specimens were divided into two groups: BCC group and controls (consisting of eyelid tissue removed during routine blepharoplasty). The pathology specimens were then stained using p53, Bcl-2 and caspase-3 stains and the intensity of staining was graded on a 0-3 scale. RESULTS: Samples from a total of 36 patients were included in the study. Eighteen (50.0%) patients were female. There were 13 patients in the BCC group and 23 patients in the control group. The mean age was 66.0 ±10.8 years in the BCC group, and 65.61 ±11.22 years in the control group. The caspase-3 staining was lower in the BCC group than in the control group. No significant differences were found between the BCC group and the control group in terms of p53 levels or Bcl-2 levels (both of them, p = 1.000). CONCLUSIONS: The caspase-3 level was lower in the BCC group. This result suggests that these enzymes can play a significant role in carcinogenesis of eyelid BCC.

Cilioretinal artery: Vasculogenesis might be promoted by plasminogen activator inhibitor-1 5G allele.

BACKGROUND: Cilioretinal arteries (CAs) represent enlargements of microscopic and early established collaterals formed via vasculogenesis between choroidal and retinal circulations. We aimed to investigate whether genetic tendency to thrombosis due to well-known gene polymorphisms may induce CA vasculogenesis in embryonic life. METHODS: We assessed plasminogen activator inhibitor-1 (PAI-1) 4G/5G, methylenetetrahydrofolatereductase (MTHFR), FACTOR V LEIDEN and PROTHROMBIN gene polymorphisms on 130 patients [82/48 females/males; Median age: 57 (18-84) with visible CAs and 100 (64/36: female/male; Median age: 55 (19-90)] without visible CAs. RESULTS: Using multiple logistic regression models, we found PAI-1 4G/5G; MTHFR (C677T and A1298C) polymorphisms to have significant effects on the probability of visible CAs, that having at least one 5G allele would increase the odds of having visible cilioretinal artery by 98.4% [Odds ratio: 1984 (95% CI: 1.320-3.000, p = 0.001)], and having at least one MTHFR C677T or A1298C allele would decrease the odds of having visible CAs by approximately 38% (OR = 0.618, 95% CI: 0.394-0.961, p = 0.035) or 44% (OR = 0.558, 95% CI: 0.354-0.871, p = 0.011), respectively. CONCLUSIONS: This is the first study to test the existence of significant association between presence of enlarged and visible CAs and genetic factors predisposing to thrombosis, according to the literature. Here we suggest that not only the lack of genetic predisposition to thrombosis by MTHFR gene polymorphisms, but also the PAI-1 5G allele might promote vasculogenesis of CAs.

Measurements of central corneal thickness and endothelial parameters with three different non-contact specular microscopy devices.

We aimed to compare the measurements of central corneal thickness (CCT) and endothelial parameters with three different non-contact specular microscopy (SM) devices. Fifteen eyes of 15 healthy individuals (6 males; 9 females) were enrolled in the study. Mean age was 37.93 ± 15.13 years. Endothelial parameters and CCT were measured with Nidek CEM-530, Topcon SP-3000P, and Tomey EM-3000 SM devices by the same physician. Endothelial parameters included endothelial cell count (ECC), maximum, minimum, and average endothelial cell size. and hexagonality ratio. There were no statistically significant differences in ECC, CTT, and average endothelial size (AES) between the devices (p > 0.05). The measurement of maximum endothelial size (MES) was different between Nidek SM and Topcon SM devices (p = 0.001), but there was no difference in MES between Nidek SM and Tomey SM (p = 0.058), and between Topcon SM and Tomey SM (p = 0.081). There was no difference in minimum endothelial size (MinES) between Nidek SM and Topcon SM (p = 0.794); however, there was a significant difference in MinES between Tomey SM and Nidek SM (p < 0.001), and between Tomey SM and Topcon SM (p < 0.001). Comparison of hexagonality ratio showed statistically significant difference between the devices (p < 0.001). No significant differences in the measurements of ECC, CCT, and AES were detected between different SM devices, whereas a statistically significant difference in hexagonality ratio was detected between the devices. These devices should not be used alternatively in the endothelial morphology assessment in patient's follow-up.