Search

Background: Collapsin response mediator protein-2 (CRMP2) has been shown to be involved in ischemia/hypoxia (IH) injury. We determined whether CRMP2 modulates ischemic injury in the retinal of Ocular ischemic syndrome (OIS). This study was to explore the molecular mechanisms underlying OIS in a novel mice model. Methods: Experiments were performed on adult male C57/BL6 mice that received bilateral internal carotid arteries ligation for 1, 2, or 4 weeks. The mice received injection of calpeptin group before occlusion for 4 weeks or not. The expression of CRMP2 in the retinal was examined by western blotting (WB) analysis and immunohistochemical analysis (IHC). The effects of ischemic injury on retinal were evaluated by fundus examination, fundus fluorescein angiography, electroretinogram, cell counting of retinal ganglion cell (RGC), and measurement of the thickness of the retina. Results: The veins dilated after chronic ischemia. In the electroretinography, the amplitudes of a- and b-waves kept diminishing in an ischemia time-dependent manner. Moreover, the tail vein-retinal circulation time prolonged in the 1- and 2-week group. In comparison, thickness of the retina decreased gradually with the ischemia time elapsed. WB analysis showed the CRMP2 and p-CRMP2 levels decreased in the 2- and 4-week groups. The results of IHC analysis were compatible with our results of WB. The loss of RGCs, decrease of the total reaction time and reduction of CRMP2 was alleviated by intravitreal injection of calpeptin. Conclusions: These results revealed that bilateral ligation of the internal carotid artery causes retinal ischemia in mice. Moreover, CRMP2 might play a pivotal role during the ischemic injury in the retina and inhibit the cleavage of CRMP2 can ameliorate the IH injury. Key words: Calpeptin; Collapsin Response Mediator Protein 2; Ischemia Injury; Ocular Ischemic Syndrome; Phosphorylation

Corneal curvatures measured by conventional instruments after refractive surgeries were greater than the real values. This study on the instruments and methods for measuring corneal curvature was carried out with the aim of determining an accurate, simple and effective method to evaluate corneal refractive power after radial keratotomy (RK).A retrospective study was carried out on 52 eyes of 42 patients with a history of RK. The postoperative measurements after RK were performed with a manual keratometer (Rodenstock, Munchen-Hamburg, Germany), a corneal topographer (Tomey TMS-1) and an automated IOLMaster keratometer (Carl Zeiss GmbH, USA). The results obtained from analyzing clinical histories (clinical history method, CHM) were compared to the postoperative measurements with a two-way analysis of variance. Adjusted keratometry was used to correct the corneal central refractive power (K) values of the three keratometers. The CHM results were also compared to the corrected K values obtained with the three keratometers using the same statistical method.The smallest mean value was found for the CHM ((36.61 ± 2.23) diopters). The K values obtained with the CHM were very different from the results obtained with the three different instruments. The corrected K values obtained with the IOLMaster were the closest to the K values from the CHM.It was shown that K values from measurements with the three instruments were higher. When the power of the intraocular lens of the patients after RK was calculated, the errors of the K values measured with the instruments should be taken into consideration.

Large drusen is a known risk factor for the development of late complications of age-related macular degeneration (AMD) and drusen reduction has been found by our previous study. To prospectively evaluate the efficacy and safety of prophylactic laser treatment in Chinese patients with bilateral soft drusen, we examined the structure and function of the macula 8 years after treatment.Ten patients with more than 10 soft drusen (125 mm) and best corrected visual acuity ≥ 20/25 in each eye participated in the study. One eye, with relatively more drusen, was exposed to an argon laser (514 nm) to achieve a barely visible retinal lesion. The contralateral eye was used as a control. Fluorescein angiography, Amsler tests, Fourier-domain optical coherence tomography and visual evoked potential tests were carried out 8 years later.No choroidal neovascularization was seen in the laser-treated eyes or control eyes. There were no significant differences in visual acuity or P100 latency and amplitude between the laser treated eyes and contralateral eyes (t = 1.685, 1.184; P0.05). The thickness of the retinal pigment epithelium of the treated eyes was less than that of the contralateral eyes (t = -4.540; P0.05). The full retinal thickness in treated eyes was slightly, but insignificantly, reduced relative to contralateral eyes (t = -1.746; P0.05).The treatment was associated with a reduction in retinal pigment epithelium thickness elevation compared with the contralateral eyes. Macular function was not impaired.

Small cell lung cancer (SCLC) is the most aggressive form of lung cancer. This study aimed to investigate the mechanism of human small cell lung cancer cell line resistance to etoposide (VP-16), H446/VP.The cell viability was measured by MTT assay. Immunocytochemistry, reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting methods were used to detect the multidrug resistance gene (MDR1), bcl-2, bax and the topoisomerase II (Topo II) expressions in H446 and H446/VP cells after treated with or without VP-16.The 50% inhibition concentration (IC50) of VP-16 on H446 cells was 49 mg/L, and 836 mg/L was for H446/VP cells. The expressions of MDR1 and bcl-2 were up-regulated, while the amounts of bax and Topo II were reduced in H446/VP cells. After treated with 49 mg/L of VP-16, it showed that the drug could significantly inhibit bcl-2 and Topo II expressions, and increase bax expression in H446 cells compared with that of H446/VP cells.The H446/VP cell was stably resistant to VP-16. The decreased expression of Topo II was correlated with the H446/VP multidrug resistance. The elevated expressions of MDR1, and the altered apoptotic pathways also played an important role in VP-16 induced multidrug resistance of SCLC.

Ophthalmic gel has been developed to increase the drug concentration in aqueous humor and to retard the loss of drug from the conjunctival sac. The research was to compare the drug concentration in aqueous humor of cataract patients administered 0.3% gatifloxacin ophthalmic gel with that in patients administered 0.3% gatifloxacin ophthalmic solution.Ninety-six patients with cataract (96 eyes) were randomly assigned to 8 groups. The patients in groups 1-4 received topical gatifloxacin 0.3% ophthalmic gel and those in groups 5-8 received gatifloxacin 0.3% ophthalmic solution. The dose regimen was 1 drop, 4 times a day for 3 consecutive days prior to cataract surgery. On the day of surgery, 1 drop was applied at 15, 30, 60 or 120 minutes before commencement of cataract surgery in groups 1 and 5, groups 2 and 6, groups 3 and 7, and groups 4 and 8, respectively. Aqueous humor was extracted during the cataract surgery for the analysis of gatifloxacin concentration..The concentrations of gatifloxacin in aqueous humor were (0.24 +/- 0.25) microg/ml, (1.11 +/- 0.74) microg/ml, (2.32 +/- 2.01) microg/ml and (1.85 +/- 1.14) microg/ml in groups 1 to 4, and (0.16 +/- 0.25) microg/ml, (0.31 +/- 0.24) microg/ml, (0.75 +/- 0.28) microg/ml and (0.33 +/- 0.22) microg/ml in groups 5 to 8, respectively. Patients receiving gatifloxacin ophthalmic gel showed greater mean values of gatifloxacin concentration in aqueous humor than those receiving gatifloxacin solution, and such differences were significant with P0.05 for all comparisons except that between groups 1 and 5.Topical gatifloxacin ophthalmic gel can attain significantly greater drug concentrations in human aqueous humor than gatifloxacin ophthalmic solution.