Background and objectiveOur objective was to investigate the efficacy and safety of dexa methasone (DEX) implant for the treatment of pseudophakic cystoid macular edema (PCME) in diabetic patients.Study designThis was a prospective, non-randomized, interventional case series of 43 participants. Eighteen patients were enrolled in the DEX implant group and 25 were enrolled in an intravitreal triamcinolone acetonide (IVTA) group.Main outcome measuresThe primary efficacy measurement was the percentage of patients who gained improvements of more than ten letters in best corrected visual acuity (BCVA) during 6 months of follow-up. Other efficacy measurements included change in BCVA, change in central macular thickness (CMT), and number of retreatments. The primary safety evaluation was the percentage of patients with intraocular hypertension and variation in intraocular pressure (IOP) during 6 months of follow-up. Other adverse events, such as conjunctival hemorrhage, eye pain, secondary infection, endophthalmitis, noninfectious inflammation, retinal detachment, and implant migration, were also recorded during follow-up.ResultsAt month 1, we observed that the percentage of patients gaining improvement of more than ten letters was similar in both groups (P=0.625). As patients in the IVTA group were retreated several times, this effect persisted throughout the study (P=0.941 at month 2, P=0.553 at month 3, P=0.856 at month 6). Variations in CMT were noticed at week 1 and reached their maximum at month 1. No significant difference was found between the two groups (P=0.831 at week 1, P=0.783 at month 1). At month 1, the variation in IOP reached its maximum in the DEX implant group and then decreased slightly. However, in the IVTA group, it increased continuously throughout the study. Conjunctival hemorrhage and eye pain were found in both groups, but both were rated as mild in severity, and no significant difference was found (P=0.184, P=0.766, respectively).ConclusionBoth IVTA and DEX implants could effectively restore visual function and recover morphological change in diabetic patients with PCME for at least 6 months, but repeated intravitreal injection was required in the IVTA group. DEX implant is well tolerated. We suggest that intravitreal injection of DEX implant is a promising new therapeutic option for diabetic patients with PCME.

PurposeTo evaluate the effect of Helicobacter pylori (H. pylori) eradication on the remission of acute idiopathic central serous chorioretinopathy (ICSCR).Study designA prospective, randomized, placebo-controlled study of 53 participants.Main outcome measureTwenty-seven acute ICSCR patients tested positive for H. pylori were given an eradication H. pylori therapy, and another 26 patients with the same diagnosis received matching placebo medication. All participants were tested for the following items: (1) disappearance rate of subretinal fluid (SRF); (2) best-corrected visual acuity (BCVA); and (3) central retinal sensitivity at baseline, 2 weeks, 4 weeks, 8 weeks, and 12 weeks after treatment. The difference between the two groups was analyzed by PASW statistics version 18.0.ResultsAt each follow-up, the disappearance rate of SRF in the active treatment group seemed slightly better than in the control group, but no statistically significant differences were observed (P > 0.05 at each follow-up). The BCVA between the two groups also did not demonstrate statistically significant differences (P > 0.05 at each follow-up). Unlike the BCVA and the disappearance rate of SRF, we compared the change in central retinal sensitivity at 12 weeks after treatment; a statistical difference was observed (P = 0.042).ConclusionOur findings suggested that H. pylori eradication does not improve BCVA and the disappearance rate of SRF, but it could improve the central retinal sensitivity in acute ICSCR patients. We recommend that chronic ICSCR patients and more sensitive methods for H. pylori diagnosis should be involved in evaluating the effect of H. pylori eradication.

ObjectiveTo investigate the effects of papaverine (PAP) on lipopolysaccharide (LPS)-induced microglial activation and its possible mechanisms.Materials and methodsBV2 microglial cells were first pretreated with PAP (0, 0.4, 2, 10, and 50 μg/mL) and then received LPS stimulation. Transcription and production of proinflammatory factors (IL1β, TNFα, iNOS, and COX-2) were used to evaluate microglial activation. The transcriptional changes undergone by M1/M2a/M2b markers were used to evaluate phenotype transformation of BV2 cells. Immunofluorescent staining and Western blot were used to detect the location and expression of P65 and p-IKK in the presence or absence of PAP pretreatment.ResultsPretreatment with PAP significantly inhibited the expression of IL1β and TNFα, and suppressed the transcription of M1/M2b markers Il1rn, Socs3, Nos2 and Ptgs2, but upregulated the transcription of M2a markers (Arg1 and Mrc1) in a dose-dependent manner. In addition, PAP pretreatment significantly decreased the expression of p-IKK and inhibited the nuclear translocation of P65 after LPS stimulation.ConclusionPAP not only suppressed the LPS-induced microglial activity by inhibiting transcription/production of proinflammatory factors, but also promoted the transformation of activated BV2 cells from cytotoxic phenotypes (M1/M2b) to a neuroprotective phenotype (M2a). These effects were probably mediated by NF-κB signaling pathway. Thus, it would be a promising candidate for the treatment of neurodegenerative diseases.

Alveolar echinococcosis (AE) is a parasitic disease caused by E. multilocularis metacestodes and it is highly prevalent in the northern hemisphere. We have previously found that vaccination with E. multilocularis Leucine aminopeptidase (EM-LAP) induced specific immune response and had an inhibiting effect on the parasites. In this study, the therapeutic effect of recombinant EM-LAP (rEM-LAP) on AE was evaluated and verified using Ubenimex, a broad-spectrum inhibitor of LAP. The results reveal that rEM-LAP could inhibit cyst growth and invasion and induce specific immunity response in BALB/c mice infected with E. multilocularis protoscoleces. The ultrasonic, MRI, and morphological results show that treatment with rEM-LAP inhibits E. multilocularis infection and reduces cyst weight, number, fibrosis and invasion. The same effect is observed for the treatment with Ubenimex by inhibiting LAP activity. The indirect ELISA shows that rEM-LAP could induce specific immunity response and produce high levels of IgG, IgG1, IgG2a, IgM, and IgA, and the serum levels of IFN-γ and IL-4 are significantly increased compared to the control groups, indicating that treatment with rEM-LAP leads to a Th1 and Th2 mixed-type immune response. This study suggests that EM-LAP could be a potential therapeutic target of E. multilocularis infection.

Low-level laser irradiation (LLLI) modulates a set of biological effects in many cell types such as fibroblasts, keratinocytes, and stem cells. However, no study to date has reported the effects of LLLI on retinal pigment epithelia (RPE) cells. The aim of this study was to investigate whether LLLI could enhance the proliferation of RPE cells and increase the expression of RPE functional genes/proteins. Human ARPE-19 cells were seeded overnight and treated with 8 J/cm(2) of LLLI. Cell proliferation was measured by CCK8 assay and cell cycle distribution was evaluated by FACS. The transcription of cell cycle-specific genes and RPE functional genes was quantified by RT-PCR. Moreover, the expression of ZO-1 and CRALBP were evaluated by immunostaining. A dose of 8 J/cm(2) of LLLI significantly increased proliferation and promoted cell cycle progression while upregulating the transcription of CDK4 and CCND1 and decreasing the transcription of CDKN2A, CDKN2C, and CDKN1B in human ARPE-19 cells. Additionally, LLLI enhanced the expression of ZO-1 and CRALBP in human ARPE-19 cells. In conclusion, LLLI could enhance the proliferative ability of human ARPE-19 cells by modulating cyclin D1, CDK4, and a group of cyclin-dependent kinase inhibitors. It also could increase the expression of RPE-specific proteins. Thus, LLLI may be a potential approach for the treatment of RPE degenerative diseases.