Endophthalmitis in silicone oil-filled eye: A case report

BACKGROUND Endophthalmitis occurring in silicone oil-filled eyes is a very rare occurrence,with reported incidence rates ranging between 0.07%and 0.039%.Traditional methods of management of infectious endophthalmitis include the removal of silicone oil,washout of the vitreous cavity,administration of intravitreal antibiotics,and reinjection of silicone oil.CASE SUMMARY Herein,we report the case of a 39-year-old man with unilateral endophthalmitis after pars plana vitrectomy and silicone oil tamponade.Intravitreal injections of full-dose antibiotics and anterior chamber washout were used to treat the patient.No signs of retinal toxicity were observed during the follow-up period.CONCLUSION Intravitreal full-dose antibiotic injections and anterior chamber washout are promising alternatives to traditional therapies for endophthalmitis in silicone oilfilled eyes.

Recurrence after spontaneous separation of epiretinal membrane in a young woman:a case report

Dear Editor,We report a case of recurrence after spontaneous separation of epiretinal membrane (ERM) in a young woman with suspected retinal vasculitis.ERM is defined as the fibrocellular membrane that proliferates on the inner surface of neurosensory retina at the macular area.Idiopathic ERM(iERM) usually occurs without a clearly identifiable cause in patients of more than 50 years of age and a great discrepancy in its prevalence from 1.02%to 28.9%among different ethnic groups were noted in previous epidemiologic studies^([1-3]).

Inhibition of corneal neovascularization by topical application of nintedanib in rabbit models

AIM:To evaluate the potential efficacy and mechanisms of nintedanib in corneal neovascularization(NV)in rabbit models.METHODS:Corneal NV was induced using 1 mol/L Na OH.Rabbits(n=21)were randomized to 3 groups:Group 1 were treated with 0.9%NaCl,Group 2 with Avastin(5 mg/mL),and Group 3 with nintedanib(1 mg/mL).All treatments star ted 1 d af ter alkaline burns and were topically performed 3 times a day for 2 wk.Photographs were taken on a slit lamp microscope on day 7 and 14.The NV area,the length of the vascularization and angiogenesis index(AI)were used to evaluate the corneal NV.On day 14,the immunohistochemical(IHC)studies of the cornea were examined.Western blot was performed to test the expression levels of vascular endothelial growth factor(VEGF),Akt,p-Akt,P38,p-P38,MMP-2 and MMP-9.RESULTS:The corneal NV area,vessel length and AI in Group 3 were significantly lower than Group 2,with both being lower than Group 1.IHC staining showed that VEGF was significantly overexpressed in the epithelium and stroma of cornea following alkaline burns.In contrast,the level of VEGF was significantly suppressed in both Group 2 and Group 3.Western blot results further confirmed that,compared with Group 1,Group 3 had significantly reduced expressions of VEGF,Akt,p-Akt,p-P38,MMP-2,and MMP-9 in corneal tissues.Trends of lower levels of MMP-2,AKT,and p-AKT in Group 3 than Group 2 were identified.CONCLUSION:Nintedanib and Avastin can effectively inhibit corneal NV,with P38 MAPK and AKT signaling pathways being possibly involved.Nintedanib seems more effective than Avastin and has the potential to be a novel therapy for preventing corneal NV.

Inhibitory effects of safranal on laser-induced choroidal neovascularization and human choroidal microvascular endothelial cells and related pathways analyzed with transcriptome sequencing

AIM:To determine the effects of safranal on choroidal neovascularization(CNV)and oxidative stress damage of human choroidal microvascular endothelial cells(HCVECs)and its possible mechanisms.METHODS:Forty-five rats were used as a laser-induced CNV model for testing the efficacy and safety of safranal(0.5 mg/kg·d,intraperitoneally)on CNV.CNV leakage on fluorescein angiography(FA)and CNV thickness on histology was compared.HCVECs were used for a H_(2)O_(2)-induced oxidative stress model to test the effect of safranal in vitro.MTT essay was carried to test the inhibition rate of safranal on cell viability at different concentrations.Tube formation was used to test protective effect of safranal on angiogenesis at different concentrations.mRNA transcriptome sequencing was performed to find the possible signal pathway.The expressions of different molecules and their phosphorylation level were validated by Western blotting.RESULTS:On FA,the average CNV leakage area was 0.73±0.49 and 0.31±0.11 mm^(2)(P=0.012)in the control and safranal-treated group respectively.The average CNV thickness was 127.4±18.75 and 100.6±17.34μm(P=0.001)in control and safranal-treated group.Under the condition of oxidative stress,cell proliferation was inhibited by safranal and inhibition rates were 7.4%-35.4%at the different concentrations.For tube formation study,the number of new branches was 364 in control group and 35,42,and 17 in 20,40,and 80μg/mL safranal groups respectively(P<0.01).From the KEGG pathway bubble graph,the PI3K-AKT signaling pathway showed a high gene ratio.The protein expression was elevated of insulin receptor substrate(IRS)and the phosphorylation level of PI3K,phosphoinositide-dependent protein kinase 1/2(PDK1/2),AKT and Bcl-2 associated death promoter(BAD)was also elevated under oxidative stress condition but inhibited by safranal.CONCLUSION:Safranal can inhibit CNV both in vivo and in vitro,and the IRS-PI3K-PDK1/2-AKT-BAD signaling pathway is involved in the pathogenesis of CNV.

Habitual rapid food intake and ineffective esophageal motility

AIM:To study non-cardiac chest pain(NCCP) in relation to ineffective esophageal motility(IEM) and rapid food intake.METHODS:NCCP patients with a self-reported habit of fast eating underwent esophageal manometry for the diagnosis of IEM.Telephone interviews identified eating habits of additional IEM patients.Comparison of manometric features was done among IEM patients with and without the habit of rapid food intake and healthy controls.A case study investigated the effect of 6-mo gum chewing on restoration of esophageal motility in an IEM patient.The Valsalva maneuver was performed in IEM patients and healthy controls to assess the compliance of the esophagus in response to abdominal pressureincrease.RESULTS:Although most patients diagnosed with NCCP do not exhibit IEM,remarkably,all 12 NCCP patients who were self-reporting fast eaters with a main complaint of chest pain(75.0%) had contraction amplitudes in the mid and distal esophagus that were significantly lower compared with healthy controls [(23.45 mmHg(95%CI:14.06-32.85)vs 58.80 mmHg(95%CI:42.56-75.04),P < 0.01 and 28.29 mmHg(95%CI:21.77-34.81) vs 50.75 mmHg(95%CI:38.44-63.05),P < 0.01,respectively)].In 7 normal-eating IEM patients with a main complaint of sensation of obstruction(42.9%),the mid amplitude was smaller than in the controls [30.09 mmHg(95%CI:19.48-40.70) vs 58.80 mmHg(95%CI:42.56-75.04),P < 0.05].There was no statistically significant difference in manometric features between the fast-eating and normal-eating groups.One NCCP patient who self-reported fast eating and was subsequently diagnosed with IEM did not improve with proton-pump inhibition but restored swallow-induced contractions upon 6-mo gum-chewing.The Valsalva maneuver caused a markedly reduced pressure rise in the mid and proximal esophagus in the IEM patients.CONCLUSION:Habitual rapid food intake may lead to IEM.A prospective study is needed to validate this hypothesis.Gum-chewing might strengthen weakened esophageal muscles.

Placental growth factor expression is reversed by anti-vascular endothelial growth factor therapy under hypoxic conditions

Background:Clinical trials have revealed that the antivascular endothelial growth factor(VEGF)therapies are effective in retinopathy of prematurity(ROP).But the low level of VEGF was necessary as a survival signal in healthy conditions,and endogenous placental growth factor(PIGF)is redundant for development.The purpose of this study was to elucidate the PIGF expression under hypoxia as well as the infl uence of anti-VEGF therapy on PIGF.Methods:CoCl2-induced hypoxic human umbilical vein endothelial cells(HUVECs)were used for an in vitro study,and oxygen-induced retinopathy(OIR)mice models were used for an in vivo study.The expression patterns of PIGF under hypoxic conditions and the infl uence of anti-VEGF therapy on PIGF were evaluated by quantitative reverse transcription-polymerase chain reaction(RTPCR).The retinal avascular areas and neovascularization(NV)areas of anti-VEGF,anti-PIGF and combination treatments were calculated.Retina PIGF concentration was evaluated by ELISA after treatment.The vasoactive effects of exogenous PIGF on HUVECs were investigated by proliferation and migration studies.Results:PIGF mRNA expression was reduced by hypoxia in OIR mice,in HUVECs under hypoxia and anti-VEGF treatment.However,PIGF expression was reversed by anti-VEGF therapy in the OIR model and in HUVECs under hypoxia.Exogenous PIGF significantly inhibited HUVECs proliferation and migration under normal conditions,but it stimulated cell proliferation and migration under hypoxia.Anti-PIGF treatment was effective for neovascular tufts in OIR mice(P<0.05).Conclusion:The finding that PIGF expression is iatrogenically up-regulated by anti-VEGF therapy provides a consideration to combine it with anti-PIGF therapy.