Timely vitrectomy without intraocular lens removal for acute endophthalmitis after cataract surgery.

AIM: To investigate the clinical features, causative organisms and effects of timely vitrectomy and silicone oil tamponade without intraocular lens (IOL) removal in the treatment of acute-onset endophthalmitis after cataract surgery (APCE). METHODS: We retrospectively analyzed the clinical features and microbiological factors in 10 eyes of 10 patients with APCE at Tianjin Medical University General Hospital from January 2010 to December 2018. Data on the clinical features, causative organisms, visual acuity, intraocular pressure (IOP) and complications were collected. The mean follow-up period was 25.5mo. RESULTS: The mean age of the patients was 71.4y. The mean time between cataract surgery and the onset of endophthalmitis was 2.0d. Preoperative visual acuity ranged from no light perception to hand motion. After vitrectomy, the visual acuity increased in nine eyes (90%), and was unchanged in one eye (10%). A significant difference was observed between the mean preoperative (36.3±7.1 mm Hg) and postoperative IOP (14.9±4.3 mm Hg, P<0.05). Staphylococcus epidermidis was isolated in 5 eyes, S. aureus in 2 eyes, and Enterococcus in 1 eye. Postoperative complications mainly included fibrin exudates in the anterior chamber at the early stages in all eyes and temporary IOP elevation in one eye. No retinal detachment or ocular atrophy was observed during the follow-up period. CONCLUSION: Under systemic antibiotic treatment and timely diagnosis, vitrectomy and silicone oil tamponade without IOL removal is a safe and effective method for APCE.

The anti-infection drug furazolidone inhibits NF-κB signaling and induces cell apoptosis in small cell lung cancer.

Targeting nuclear factor kappa B (NF-κB) signaling pathway has become a promising strategy for the development of new antitumor drugs. In this paper, we found that anti-infection drug furazolidone (FZD) could significantly inhibit NF-κB-driven luciferase activity, and FZD could markedly inhibit both of the constitutive and tumor necrosis factor-α (TNFα)-triggered phosphorylation of NF-κB p65 in small cell lung cancer (SCLC). Further studies revealed that FZD inhibited the expression of inhibitor of kappa B kinase ß (IKKß) in SCLC cells. In addition, we found that FZD had significant antitumor activities in SCLC cells. FZD could markedly suppress the cell viability of SCLC cells dose-dependently, and FZD could significantly induce the cleavages of poly ADP-ribose polymerase (PARP) and Caspase3, the biomarkers of cell apoptosis, in SCLC cells. The flow cytometry also revealed that FZD induced cell apoptosis in SCLC cells. Finally, we also found that overexpression of constitutively activated IKKß could significantly abolish FZD-induced cell growth inhibition in SCLC cells, which further confirmed that FZD displayed its anti-SCLC activity through regulating NF-κB signaling pathway.

Nitroxoline induces cell apoptosis by inducing MDM2 degradation in small-cell lung cancer.

The proto-oncogene MDM2 is a nuclear-localized E3 ubiquitin ligase, which promotes tumor formation by targeting tumor suppressor proteins, such as p53, for proteasomal degradation. In this study, the anti-infective drug nitroxoline (NXQ) was screened out to effectively inhibit cell survival of small-cell lung cancer (SCLC) cells, and induce SCLC cell apoptosis by suppressing antiapoptotic proteins (such as Bcl-2 and MCL1) and upregulating proapoptotic protein Bim. In the mechanistic study, NXQ was found to downregulate MDM2 expression by inducing its proteasomal degradation, and thus upregulated p53 expression, which was a substrate protein of MDM2. Moreover, overexpression of MDM2 decreased the cytotoxicity of NXQ on SCLC cells. These results demonstrated that NXQ displayed anti-SCLC activity by suppressing MDM2 expression, which suggested that anti-infective NXQ had potential for SCLC treatment by targeting the MDM2/p53 axis.

MicroRNA-26b suppresses tumorigenicity and promotes apoptosis in small cell lung cancer cells by targeting myeloid cell leukemia 1 protein.

The aim of this study was to investigate the role of microRNA-26b (miR-26b) in regulating the proliferation, migration, and apoptosis of small cell lung cancer (SCLC) cells. First, we examined the expression level of miR-26b in human normal fetal lung fibroblasts (NFLFs) and three SCLC cell lines NCI-H466, NCI-H1688, and NCI-H196. In the following experiments, the three SCLC cell lines were transfected with miR-26b mimic and inhibitor. Cell growth and survival, as well as migration and invasion capacities were determined by MTT, colony formation, Transwell migration and invasion, and wound healing assays. Cell apoptosis, production of reactive oxygen species, and mitochondrial membrane potential were also measured in the three cell lines following various treatments. As a result, we found that the level of miR-26b was significantly lower in SCLC cells than in NFLFs. Additionally, transfection with miR-26b mimic could inhibit proliferation, colony formation, and migration, as well as induce apoptosis in these SCLC cell lines; while miR-26b inhibitor showed the opposite effects. Further mechanistic experiment revealed that miR-26b could suppress the expression of myeloid cell leukemia 1 protein (Mcl-1) and the 3'-untranslated region (3'-UTR) of Mcl-1 may be the direct binding site of miR-26b, suggesting that the effect of miR-26b may be mediated by targeting Mcl-1. Collectively, our findings offer a new insight into the role of miR-26b in the pathogenesis of SCLC, and provide primary evidence supporting the potential of miR-26b-based therapy for the treatment of SCLC.

[Manipulative reduction and plaster external fixation for the treatment of the scaphoid fracture and perilunate dislocation].

OBJECTIVE: To investigate the efficacy and complications of manual reduction and external fixation for the treatment of scaphoid fractures and perilunate dislocations. METHODS: From January 2009 to January 2013, 43 patients suffered from scaphoid fractures and perilunate dislocations were retrospective analyzed. Among them, 17 cases were treated with manipulative reduction and plaster external fixation as conservation group including 10 males and 7 females, the other 26 cases were treated with application of surgical as operation group including 15 males and 11 females. The clinical effects were assessed by Cooney function score, radiological analysis and observation of complications. RESULTS: All patients were followed up for(45.00±8.72) months ranging from 36 to 60 months. At the final follow-up, the Cooney score of wrist function was 88.53±4.24 in conservation group and 89.58±4.59in operation group(t=0.455, P>0.05). During the follow-up, 4 patients were found scaphoid avascular necrosis in the imaging performance in the conservation group(χ²=4.32, P<0.05). The difference of other complications between two groups was not statistically significant(P>0.05). CONCLUSIONS: For patients suffered from the scaphoid fractures and perilunate dislocation, the early manipulative reduction and plaster external fixation after injury as soon as possible is necessary. Maintaining a satisfactory reduction and reliable fixation at the same time can lead to good treatment effect and there's no weakness compared to surgical treatment. But there was an increase in danger of complications. The key of conservative treatment lies in early diagnosis and maintenance of reduction, reliable fixation, and timely and appropriate functional exercise.

Changes in TL1A levels and associated cytokines during pathogenesis of diabetic retinopathy.

Tumor necrosis factor (TNF) ligand related molecule 1A (TL1A), also termed TNF superfamily member 15 and vascular endothelial growth inhibitor is important for tumorigenicity and autoimmunity. However, the function of TL1A in diabetic retinopathy (DR) remains to be elucidated. The present study established a diabetes mellitus (DM) rat model to investigate TL1A, vascular endothelial growth factor (VEGF), tumor necrosis factor­α (TNF­α) and interleukin­1ß (IL­1ß) expression levels in the retina, vitreous and serum of rats with DM at different stages (1 month group, 3 month group and 6 month group). The present study determined that TL1A expression levels in the retina and vitreous from the DM 1 month group were significantly lower compared with the control group. However, TL1A levels in the retina and vitreous were significantly increased in advanced stages of DM compared with the control group. Furthermore, the levels of VEGF in the retina and vitreous were significantly higher in the DM groups compared with the control group. The expression levels of TNF­α and IL­1ß in the retina and vitreous were significantly higher in DM 3 month and 6 month groups compared with the control group. It is of note that the expression levels of TL1A were significantly lower in the DM 1 and 3 month groups compared with the control group; however, they were significantly increased in the DM 6 month group compared with the DM 3 month group. The expression levels of VEGF, TNF­α and IL­1ß in blood serum have been observed to exhibit similar expression change dynamics as those of the retina and vitreous. Therefore, these findings suggest that TL1A may be a protective factor of DR, and may provide a rationale for the development of novel therapeutic strategies to treat DR.

[Experimental study on treatment of rabbits optic nerve injury with Caspase-3 inhibitor z-DEVD-fmk].

OBJECTIVE: To observe the effects of caspase-3 inhibitor z-DEVD-fmk on optic nerve injury of rabbits. METHODS: It was an experimental study. Two to three month-old rabbits were used in this study. The rabbit model of optic nerve injury was created by fluid percussion brain injury device (FPI). DMSO (5 µl 2% solution) was injected intravitreally to the left eyes (control group). Caspase-3 inhibitor z-DEVD-fmk (5 µl) was injected intravitreally to the right eyes (experimental group). Flash-visual evoked potential (F-VEP) and histopathological examination of the retina were used to check the variations in optic nerve injury at 1, 4, 7, 10, 14, and 21 days after the treatment. Immunohistochemistry was used to detect the expression of caspase-3 in the retina. T-test, variance analysis, q-test and linear correlation analysis were used to analyze these data. RESULTS: At the 7th day after treatment, the latency of F-VEP P1 in experimental group was shorter than that in the control group [(90.50±7.61) ms vs (113.59±12.92) ms, t=4.060, P<0.05] and the number of retinal ganglion cells (RGC) in the experimental group was greater than that in the control group (237.62±8.50 vs 207.03±11.04, t=-5.843, P<0.05). Both of these trends continued to the 21st day after treatment [(67.97±7.93) ms vs. (134.22±8.50) ms, t=13.950, P<0.05; 156.32±8.45 vs. 207.13±12.21, t=-10.307, P<0.05]. The absorbency (A) of caspase-3 in the experimental group (0.396±0.023) was lower than that in the control group (0.458±0.024) and this difference was statistically significant (t=6.200, P<0.05) at the 7th day after treatment. The latency of F-VEP P1 and the absorbency of caspase-3 in the retina were positively correlated with each other (r=0.95, P<0.05). CONCLUSION: z-DEVD-fmk is effective in treating rabbit optic nerve injury by inhibiting the expression of caspase-3 in the retina. It can promote the recovery of optic nerve function.

[Treatment of postoperative endophthalmitis following cataract surgery without intraocular lens removal].

OBJECTIVE: To explore the effects of vitrectomy combined with silicone oil injection on the treatment of postoperative endophthalmitis following cataract surgery without intraocular lens removal, and to analyze the relative factors. METHODS: This was a retrospective case series study. Clinical data of 7 eyes of 7 patients with postoperative endophthalmitis following cataract surgery underwent the treatment of vitrectomy combined with silicone oil injection without intraocular lens removal from 2003 to 2008 were collected. The outcomes of vision, slit lamp examination, direct and indirect ophthalmoscopy, IOP, and B-scan were observed, and the surgical effects were analyzed. RESULTS: Five patients were male, and 2 patients were female. The age ranged from 67.0 to 84.0 years with a mean of 70.0 + or - 4.5. The onset of endophthalmitis ranged from 1 to 3 days with a mean of 2 days. Silicone oil was removed in 5 eyes 3 to 6 months postoperatively. Preoperative visual acuity ranged from non light perception to hand moving. The mean preoperative intraocular pressure (IOP) was (35.0 + or - 0.5) mmHg with a range from 35.0 to 56.0 mmHg. Follow-up periods ranged from 6 to 43 months with a mean of (10 + or - 6) months. Postoperative visual acuity ranged from non light perception to 0.8. Postoperative vision increased in 6 eyes (86%), and was stable in 1 eye (14%). The mean postoperative IOP was (18.0 + or - 1.5) mmHg with a range from 10.0 to 20.0 mmHg, this was significantly lower than that preoperatively (t = 1.94, P < 0.05). Postoperative complications mainly included fibrous exudates in the anterior chamber at early stage after the surgery (7 eyes) and temporary intraocular pressure elevation (1 eye). There was no retinal detachment and atrophia bulbi. CONCLUSION: Vitrectomy combined with silicone oil injection may be a safe and effective method in treating postoperative endophthalmitis following cataract surgery without intraocular lens removal.

[The expression of vascular endothelial growth factor of vitreous in patients with proliferative diabetic retinopathy].

OBJECTIVE: To explore the expression of vascular endothelial growth factor of vitreous in patients with proliferative diabetic retinopathy, and to analyze the relative factors. METHODS: It was a case-control study. Data of 50 eyes of 50 PDR patients who underwent vitrectomy were retrospectively analyzed. The vitreous fluid samples were obtained during surgery. The VEGF level in vitreous fluid was determined by enzyme linked immunosorbent assay, and the expression of vascular endothelial growth factor of vitreous in patients with proliferative diabetic retinopathy was analyzed. The mean follow-up was 9 months with a range from 6 to 26 months. The VEGF levels in vitreous fluid were compared between PDR patients and normal control, and silicone oil tamponade group and without silicone oil tamponade group by t-test. The changes of VEGF levels in vitreous fluid in eyes with regression, stabilization, and progression were analyzed by analysis of variance. The effects of VEGF levels in vitreous fluid on PDR were analyzed by analysis of variance. RESULTS: The mean VEGF level of vitreous was (592.4801 +/- 587.4267) ng/L in PDR patients, and it was (131.3022 +/- 26.9192) ng/L in normal control. VEGF level was significantly higher in PDR patients than that in normal control (t = 3.2315, P < 0.05). There were 10 eyes (20%) with progression of PDR, 10 eyes (20%) with stabilization, and 30 eyes (60%) with regression. Vitreous level of VEGF was significantly higher in eyes with progression of PDR than that in eyes with stabilization or regression of PDR (q = -3.3187, -4.0843; P < 0.05). Vitreous level of VEGF was significantly higher in eyes without retinal photocoagulation than that in eyes underwent panretinal photocoagulation or local photocoagulation (q = -4.2187, -3.9672; P < 0.05). CONCLUSION: There is a correlation between the expression of VEGF of vitreous and the severity of PDR. The expression of VEGF of vitreous presents a relatively lower level in patients with stabilization and regression of PDR.