Establishing chronic models of age-related macular degeneration via long-term iron ion overload.

Age-related macular degeneration (AMD) is characterized by the degenerative senescence in the retinal pigment epithelium (RPE) and photoreceptors, which is accompanied by the accumulation of iron ions in the aging retina. However, current models of acute oxidative stress are still insufficient to simulate the gradual progression of AMD. To address this, we established chronic injury models by exposing the aRPE-19 cells, 661W cells, and mouse retina to iron ion overload over time. Investigations at the levels of cell biology and molecular biology were performed. It was demonstrated that long-term treatment of excessive iron ions induced senescence-like morphological changes, decreased cell proliferation, and impaired mitochondrial function, contributing to apoptosis. Activation of the mitogen-activated protein kinase (MAPK) pathway and the downstream molecules were confirmed both in the aRPE-19 and 661W cells. Furthermore, iron ion overload resulted in dry AMD-like lesions and decreased visual function in the mouse retina. These findings suggest that chronic exposure to overloading iron ions plays a significant role in the pathogenesis of retinopathy and provide a potential model for future studies on AMD.NEW & NOTEWORTHY To explore the possibility of constructing reliable research carriers on age-related macular degeneration (AMD), iron ion overload was applied to establish models in vitro and in vivo. Subsequent investigations into cellular physiology and molecular biology confirmed the presence of senescence in these models. Through this study, we hope to provide a better option of feasible methods for future researches into AMD.

Protective effect of ginsenoside Rg1 on 661W cells exposed to oxygen-glucose deprivation/reperfusion via keap1/nrf2 pathway.

AIM: To construct an in vitro model of oxygen-glucose deprivation/reperfusion (OGD/R) induced injury to the optic nerve and to study the oxidative damage mechanism of ischemia-reperfusion (I/R) injury in 661W cells and the protective effect of ginsenoside Rg1. METHODS: The 661W cells were treated with different concentrations of Na2S2O4 to establish OGD/R model in vitro. Apoptosis, intracellular reactive oxygen species (ROS) levels and superoxide dismutase (SOD) levels were measured at different time points during the reperfusion injury process. The injury model was pretreated with graded concentrations of ginsenoside Rg1. Real-time polymerase chain reaction (PCR) was used to measure the expression levels of cytochrome C (cyt C)/B-cell lymphoma-2 (Bcl2)/Bcl2 associated protein X (Bax), heme oxygenase-1 (HO-1), caspase9, nuclear factor erythroid 2-related factor 2 (nrf2), kelch-like ECH-associated protein 1 (keap1) and other genes. Western blot was used to detect the expression of nrf2, phosphorylated nrf2 (pnrf2) and keap1 protein levels. RESULTS: Compared to the untreated group, the cell activity of 661W cells treated with Na2S2O4 for 6 and 8h decreased (P<0.01). Additionally, the ROS content increased and SOD levels decreased significantly (P<0.01). In contrast, treatment with ginsenoside Rg1 reversed the cell viability and SOD levels in comparison to the Na2S2O4 treated group (P<0.01). Moreover, Rg1 reduced the levels of caspase3, caspase9, and cytC, while increasing the Bcl2/Bax level. These differences were all statistically significant (P<0.05). Western blot analysis showed no significant difference in the protein expression levels of keap1 and nrf2 with Rg1 treatment, however, Rg1 significantly increased the ratio of pnrf2/nrf2 protein expression compared to the Na2S2O4 treated group (P<0.001). CONCLUSION: The OGD/R process is induced in 661W cells using Na2S2O4. Rg1 inhibits OGD/R-induced oxidative damage and alleviates the extent of apoptosis in 661W cells through the keap1/nrf2 pathway. These results suggest a potential protective effect of Rg1 against retinal I/R injury.

MAP4K4 is involved in the neuronal development of retinal photoreceptors.

Mitogen-activated protein kinase kinase kinase kinase-4 (MAP4K4) is a potential regulator of photoreceptor development. To investigate the mechanisms underlying MAP4K4 during the neuronal development of retinal photoreceptors, we generated knockout models of C57BL/6j mice in vivo and 661 W cells in vitro. Our findings revealed homozygous lethality and neural tube malformation in mice subjected to Map4k4 DNA ablation, providing evidence for the involvement of MAP4K4 in early stage embryonic neural formation. Furthermore, our study demonstrated that the ablation of Map4k4 DNA led to the vulnerability of photoreceptor neurites during induced neuronal development. By monitoring transcriptional and protein variations in mitogen-activated protein kinase (MAPK) signaling pathway-related factors, we discovered an imbalance in neurogenesis-related factors in Map4k4 -/- cells. Specifically, MAP4K4 promotes jun proto-oncogene (c-JUN) phosphorylation and recruits other factors related to nerve growth, ultimately leading to the robust formation of photoreceptor neurites. These data suggest that MAP4K4 plays a decisive role in regulating the fate of retinal photoreceptors through molecular modulation and contributes to our understanding of vision formation.

Oxidative stress-induced lncRNA CYLD-AS1 promotes RPE inflammation via Nrf2/miR-134-5p/NF-κB signaling pathway.

Oxidative stress-induced damage to and dysfunction of retinal pigment epithelium (RPE) cells are important pathogenetic factors of age-related macular degeneration (AMD); however, the underlying molecular mechanism is not fully understood. Long noncoding RNAs (lncRNAs) have important roles in various biological processes. In this study, using an oxidative damage model in RPE cells, we identified a novel oxidation-related lncRNA named CYLD-AS1. We further revealed that the expression of CYLD-AS1 was increased in RPEs during oxidative stress. Depletion of CYLD-AS1 promoted cell proliferation and mitochondrial function and protected RPE cells against hydrogen peroxide (H2 O2 )-induced damage. Mechanistically, CYLD-AS1 also regulated the expression of NRF2, which is related to oxidative stress, and NF-κB signaling pathway members, which are related to inflammation. Remarkably, these two signaling pathways were mediated by the CYLD-AS1 interactor miR-134-5p. Moreover, exosomes secreted by CYLD-AS1 knockdown RPE cells had a lower proinflammatory effect than those secreted by control cells. In summary, our study revealed that CYLD-AS1 affects the oxidative stress-related and inflammatory functions of RPE cells by sponging miR-134-5p to mediate NRF2/NF-κB signaling pathway activity, suggesting that targeting CYLD-AS1 could be a promising strategy for the treatment of AMD and related diseases.

Primary Vitreoretinal Lymphoma: A Retrospective Study of 20 Eyes.

Purpose: This study aimed to describe and analyze the clinical features of 20 eyes of 15 primary vitreoretinal lymphoma (PVRL) patients. Methods: This was a retrospective case series and a review of the literature. Fifteen PVRL patients (20 affected eyes) referred between February 2011 and December 2019 were recruited, and their medical records were retrospectively reviewed. Results: Among these 15 PVRL patients, seven were men (46.67%), and five had bilateral PVRL (33.33%). The median onset age was 66 ± 9.26 years and six (40%) patients had central nervous system (CNS) involvement, and two of them died of CNS-related complications. The ocular symptoms varied from decreased vision to binocular diplopia. The ocular manifestations were diverse and involved both the anterior and posterior segments, including the vitreous cells, subretinal white-yellow lesions, cotton-wool spots, and ophthalmoplegia. The rate of misdiagnosis and failure to diagnose was 100%, and 30% of them were misdiagnosed as uveitis. We found five cases revealing rare characteristics of this malignancy. Among them, there were two cases with mild hypertensive retinopathy exhibiting cotton-wool spots, one case mimicking age-related macular degeneration (AMD), one case with systemic lupus erythematosus (SLE), and one patient had extraocular muscle involvement. To the best of our knowledge, we reported PVRL exhibiting cotton-wool spots as the main manifestation and coexisting with extraocular myopathy for the first time. Conclusions: PVRL is a rare intraocular malignancy that commonly masquerades as uveitis. As the clinical signs and symptoms are atypical, ophthalmologists must carefully examine patients to avoid misdiagnosis or a failure to diagnose. Cotton-wool spots and extraocular myopathy might be the dominant initial symptoms in PVRL patients, and AMD should be considered a differential diagnosis of PVRL. SLE patients under immunosuppressive treatment could have spontaneous PVRL.

Clinical Features of Endogenous Endophthalmitis Secondary to Minimally Invasive Upper Urinary Tract Calculus Removal.

PURPOSE: To evaluate endogenous endophthalmitis clinical features following minimally invasive removal of upper urinary tract calculi. METHODS: Medical records of twelve patients (17 eyes) with endogenous endophthalmitis secondary to minimally invasive upper urinary tract calculus removal were retrospectively reviewed. RESULTS: Diabetes mellitus was found in 7 patients (58%). 10 patients (83%) suffered from fever. The stone extraction and ocular symptom onset interval ranged from 2 to 22 days. All eyes presented as vitritis and fluffy yellow-white retinal exudates. Hypopyon was only found in 3 eyes (18%). 5 patients (42%) were misdiagnosed as uveitis which led to mismanagement. Ocular fluids were culture positive for only C. albicans in 12 eyes (71%). 10 of 12 eyes (83%) with silicon oil tamponade obtained a final BCVA≥0.05. CONCLUSIONS: C. albicans was the most common endogenous endophthalmitis pathogen after urinary calculus removal by minimally invasive surgery. Pars plana vitrectomy with silicon oil tamponade may be helpful to achieve a favorable visual outcome. Routine ophthalmologic evaluation by the uveitis or vitreoretinal specialist may be necessary within 2 weeks after the urological procedures.

2,3,5,6-Tetramethylpyrazine protects retinal photoreceptors against endoplasmic reticulum stress by modulating ATF4-mediated inhibition of PRP aggregation.

Endoplasmic reticulum (ER) stress is a common threat to photoreceptors during the pathogenesis of chronic retinopathies and often results in irreversible visual impairment. 2,3,5,6-Tetramethylpyrazine (TMP), which possesses many beneficial pharmacological activities, is a potential drug that could be used to protect photoreceptors. In the present study, we found that the cellular growth rate of 661 W cells cultured under low glucose conditions was lower than that of control cells, while the G2/M phase of the cell cycle was longer. We further found that the mitochondrial membrane potential (ΔΨm) was lower and that ER stress factor expression was increased in 661 W cells cultured under low glucose conditions. TMP reversed these trends. Visual function and cell counts in the outer nuclear layer (ONL) were low and the TUNEL-positive rate in the ONL was high in a C3H mouse model of spontaneous retinal degeneration. Similarly, visual function was decreased, and the TUNEL-positive rate in the ONL was increased in fasted C57/BL6j mice compared with control mice. On the other hand, ER stress factor expression was found to be increased in the retinas of both mouse models, as shown by reverse transcription real-time PCR (RT-qPCR) and western blotting. TMP reversed the physiological and molecular biological variations observed in both mouse models, and ATF4 expression was enhanced again. Further investigation by using western blotting illustrated that the proportion of insoluble prion protein (PRP) versus soluble PRP was reduced both in vitro and in vivo. Taken together, these results suggest that TMP increased the functions of photoreceptors by alleviating ER stress in vitro and in vivo, and the intrinsic mechanism was the ATF4-mediated inhibition of PRP aggregation. TMP may potentially be used clinically as a therapeutic agent to attenuate the functional loss of photoreceptors during the pathogenesis of chronic retinopathies. KEY MESSAGES: • Already known: TMP is a beneficial drug mainly used in clinic to enhance organ functions, and the intrinsic mechanism is still worthy of exploring. • New in the study: We discovered that TMP ameliorated retinal photoreceptors function via ER stress alleviation, which was promoted by ATF4-mediated inhibition of PRP aggregation. • Application prospect: In prospective clinical practices, TMP may potentially be used in the clinic as a therapeutic agent to attenuate the photoreceptors functional reduction in chronic retinopathies.

Risk Factors and Prognosis of Pediatric Open Globe Injuries without Initial Light Perception.

PURPOSE: The aim of this study was to investigate the possible risk factors and prognosis of initial no light perception (NLP) in pediatric open globe injuries (POGI). PROCEDURES: This retrospective, comparative, interventional case-control study included 865 eyes of POGI patients presenting to a tertiary referral ophthalmic center from January 1, 2011 to December 31, 2015. Eyes were divided into 2 groups: the NLP group included eyes with initial NLP, and the light perception (LP) group included eyes with initial LP or vision better than LP. RESULTS: The following risk factors were significantly related to initial NLP: severe intraocular hemorrhage (OR 3.287, p = 0.015), retinal detachment (RD; OR 2.527, p = 0.007), choroidal damage (OR 2.680, p = 0.016), and endophthalmitis (OR 4.221, p < 0.001). Choroidal damage is related to remaining NLP after vitreoretinal surgery (OR 12.384, p = 0.003). At the last visit, more eyes in the NLP group suffered from silicone oil-sustained status (OR 0.266, p = 0.020) or ocular atrophy (OR 0.640, p = 0.004), and fewer eyes benefitted from final LP (OR 41.061, p < 0.001) and anatomic success (OR 4.515, p < 0.001). CONCLUSION: Severe intraocular hemorrhage, RD, choroidal damage, and endophthalmitis were possible predictors of initial NLP in POGI. Choroidal damage was the major factor related to an NLP prognosis. Traumatized eyes with initial NLP could be anatomically and functionally preserved by vitreoretinal surgery.

m6A methyltransferase METTL3 promotes retinoblastoma progression via PI3K/AKT/mTOR pathway.

Retinoblastoma (RB) is a common intraocular malignancy in children. Due to the poor prognosis of RB, it is crucial to search for efficient diagnostic and therapeutic strategies. Studies have shown that methyltransferase-like 3 (METTL3), a major RNA N (6)-adenosine methyltransferase, is closely related to the initiation and development of cancers. Nevertheless, whether METTL3 is associated with RB remains unexplored. Therefore, we investigated the function and mechanisms of METTL3 in the regulation of RB progression. We manipulated METTL3 expression in RB cells. Then, cell proliferation, apoptosis, migration and invasion were analysed. We also analysed the expression of PI3K/AKT/mTOR pathway members. Finally, we incorporated subcutaneous xenograft mouse models into our studies. The results showed that METTL3 is highly expressed in RB patients and RB cells. We found that METTL3 knockdown decreases cell proliferation, migration and invasion of RB cells, while METTL3 overexpression promotes RB progression in vitro and in vivo. Moreover, two downstream members of the PI3K/AKT/mTOR pathway, P70S6K and 4EBP1, were affected by METTL3. Our study revealed that METTL3 promotes the progression of RB through PI3K/AKT/mTOR pathways in vitro and in vivo. Targeting the METTL3/PI3K/AKT/mTOR signalling axis could be a promising therapeutic strategy for the treatment of RB.

Curcumin Inhibits Proliferation and Epithelial-Mesenchymal Transition in Lens Epithelial Cells through Multiple Pathways.

BACKGROUND: Posterior capsule opacification (PCO), a complication of extracapsular lens extraction surgery that causes visual impairment, is characterized by aberrant proliferation and epithelial-mesenchymal transition (EMT) of lens epithelial cells (LECs). Curcumin, exerting inhibitive effects on cell proliferation and EMT in cancer, serves as a possible antidote towards PCO. METHODS: Cellular proliferation of LECs after treatment of curcumin was measured with MTT assay and flow cytometry. The transcriptional and expressional levels of proteins related to proliferation and EMT of LECs were quantified by western blotting and real-time PCR. RESULTS: Curcumin was found to suppress the proliferation of LECs by inducing G2/M arrest via possible inhibition of cell cycle-related proteins including CDK1, cyclin B1, and CDC25C. It had also inactivated proliferation pathways involving ERK1/2 and Akt pathways in LECs. On the other hand, curcumin downregulated the EMT of LECs through blocking the TGF-ß/Smad pathway and interfering Notch pathway which play important roles in PCO. CONCLUSIONS: This study shows that curcumin could suppress the proliferation and EMT in LECs, and it might be a potential therapeutic protection against visual loss induced by PCO.

Risk Factors Associated with Failure of Direct Cyclopexy in the Treatment of Small to Moderate Tramatic Cyclodialysis Clefts.

BACKGROUND: To evaluate the risk factors associated with failure to correct hypotony using direct cyclopexy in patients with traumatic cyclodialysis cleft. METHODS: In a series of 116 patients with traumatic cyclodialysis who underwent direct cyclopexy at Zhongshan Ophthalmic Center from January 2008 to August 2018, the clinical correlation between the risk factors and failure of the operation were retrospectively studied, after adjusting for other potential confounders. RESULTS: The curative ratio after one procedure was 82.76%, whereas 20 (17.24%) eyes experienced treatment failure after the first surgery. The degree of anterior chamber angle closure was significantly wider in patients with a failed first surgery than in patients for whom one procedure was a success (p = .046). The risk of failure to achieve closure increased as the angle-closure exceeded 5 clock hour (odds ratio, 10.39; 95% confidence interval, 1.75-61.72; p = .010). An analysis of the recurrent position indicated that an angle closure exceeding 5 clock hour may impede accurate cleft location and is thus associated with an increased risk of failure to correct hypotony. CONCLUSION: Exceeding the threshold of 5 clock hour in anterior chamber angle closure may impede accurate cleft location and, thus, present a higher risk of failure to correct hypotony using direct cyclopexy. These patients may need injection of a viscoelastic agent into the anterior chamber by paracentesis to deepen the anterior chamber and to delineate the clefts using gonioscopy pre- or intraoperatively.

Anti-tumor Drug THZ1 Suppresses TGFß2-mediated EMT in Lens Epithelial Cells via Notch and TGFß/Smad Signaling Pathway.

Selective covalent CDK7 inhibitor THZ1 is a promising potential anti-tumor drug in many kinds of cancers. Epithelial-mesenchymal Transition (EMT) is highly related to cancer initiation, development, invasion and metastasis and other pathogenesis processes. We treated cancer cell line Hela229 and three retinoblastoma cell lines so-RB50, WERI-Rb-1, Y79 with gradient concentration of THZ1, and found that THZ1 could inhibit cell viability and EMT, suggesting that THZ1 may be a promising drug for human cervical cancer and retinoblastoma treatment. Our results verified the role of THZ1 in EMT for the first time, however, the mechanism needs further study. Here we report that THZ1 suppresses the TGFß2 induced EMT in human SRA01/04 lens epithelial cells (LECs), rabbit primary lens epithelial cells, and whole rat lens culture semi-in vivo model. RNA-sequencing and KEGG analysis revealed that the THZ1 inhibits EMT by down-regulating phosphorylate Smad2 and Notch signaling pathway. On the other hand, we found that THZ1 could strongly inhibit LECs proliferation through G2/M phase arrest as well as attenuating of MAPK, PI3K/AKT signaling pathway. Our results uncovered the function and underlying mechanism of THZ1 in regulation of EMT, which provides a new perspective of the anti-tumor effect by THZ1 and may offer a novel treatment for PCO.

Covalent CDK7 Inhibitor THZ1 Inhibits Myogenic Differentiation.

Covalent CDK7 inhibitor THZ1 is a newly discovered anti-tumor drug.THZ1 affects the function of transcription factor TFIIH by inhibiting CDK7, which in turn affects RNA polymerase II, and ultimately affects transcription initiation. Study found that THZ1 could inhibit proliferation and promote apoptosis of several tumor cell lines. However, there is no report of the potential side effect of THZ1 in normal tissues. In the course of cancer, the muscle consumption of cachexia needs to be supplemented by the differentiation of muscle cells. However, the effect of THZ1 on myogenic differentiation remains unclear. Our study in this article found that THZ1 could both inhibit the differentiation of C2C12 cells and mouse primary myoblasts, also repressing the expression of differentiation-related transcription factors and muscle structural proteins, such as and myogenin, myh3 and MCK. Moreover, THZ1 could inhibit C2C12 cell proliferation and migration, increase its oxidative stress and promote its apoptosis. Our data indicates that THZ1 inhibits myogenic differentiation, suggesting that therapies based on THZ1 might have potential side effects on muscle functions.

Notch signaling pathway mediates Doxorubicin-driven apoptosis in cancers.

BACKGROUND: Doxorubicin is a widely used chemotherapy drug for the treatment of a variety of cancers, however it also has serious side effects such as anaphylaxis and heart damage. Therefore, it's very important to understand the downstream molecular pathways that are essential for Doxorubicin function in cancer treatment. METHODS: HeLa S3 cells were treated with different concentrations of Doxorubicin for 24 hours. Then, the mRNA levels of Notch pathway components in the Doxorubicin treated cells were determined by Real-Time qRT-PCR. Lentiviral transfection was used to up-regulate and down-regulate HES1 expression. Cell proliferation and apoptosis were measured with MTT assay and flow cytometry. Finally, immunofluorescence was used to detect protein subcellular location. RESULT: Doxorubicin treatment strongly increases the expression of multiple Notch pathway components in cancer cells. The Notch target HES1 is activated by Doxorubicin and is required for the Doxorubicin driven apoptosis. In addition, over-expression of HES1 can further enhances Doxorubicin's role in promoting apoptosis. Mechanistically, HES1 activates PARP1 and regulates the subcellular location of AIF to mediate the apoptosis response under Doxorubicin treatment. CONCLUSION: Our results provided novel insights into the downstream molecular pathways underlying Doxorubicin treatment and suggested that manipulation of Notch signaling pathway could have synergistic effect with Doxorubicin for cancer treatment.

The inhibition of NOTCH2 reduces UVB-induced damage in retinal pigment epithelium cells.

Age-related macular degeneration (AMD) is the leading cause of irreversible blindness in the elderly. The pathogenesis of dry AMD remains indistinct and the mechanism of retinal pigment epithelium (RPE) cells death in dry AMD is controversial. The aim of the present study was to investigate the functions of Notch signaling in ultraviolet B (UVB)-induced damage of RPE cells. It was identified that, in RPE cells, UVB increased intracellular reactive oxygen species (ROS) and induced cell apoptosis. In addition, UVB activated Notch signaling in a dose dependent manner. Surprisingly, NOTCH2, but not NOTCH1, was demonstrated to be the major Notch receptor in RPE cells. Under normal conditions, the inhibition of NOTCH2 reduced cell growth and cell migration, but had no impact on intracellular ROS and cell apoptosis. However, in the presence of UVB, the inhibition of NOTCH2, but not NOTCH1, attenuated intracellular ROS and cell apoptosis. The function of Notch signaling involved in UVB damage of RPE cells may not only be significant to understanding the pathogenesis of AMD (especially dry AMD), but also useful for designing effective therapeutic agents for dry AMD.

PTEN Reduced UVB-Mediated Apoptosis in Retinal Pigment Epithelium Cells.

Age-related macular degeneration (AMD) is a leading cause of blindness and progressive loss of central vision in the elderly population. The important factor of AMD pathogenesis is the degeneration of retinal pigment epithelial (RPE) cells by oxidative stress. Inactivation of PTEN can disrupt intercellular adhesion in the RPE cells, but the mechanism of oxidative stress is less known. Here we presented evidence that UVB-mediated oxidative stress induced apoptosis in ARPE-19 cells. Downregulation of the expression of PTEN in UVB-irradiative RPE cells triggered DNA damage and increased the level of UVB-induced apoptosis by activating p53-dependent pathway. However, overexpression of PTEN increased cell survival by suppressing p-H2A in response to DNA damage and apoptosis. When using Pifithrin-α (one of p53 inhibitors), the level of p53-dependent apoptosis was significantly lower than untreated, which suggested that p53 was possibly involved in PTEN-dependent apoptosis. Thus, it elucidated the molecular mechanisms of UVB-induced damage in RPE cells and may offer an alternative therapeutic target in dry AMD.

Modified technique for transscleral fixation of posterior chamber intraocular lenses.

BACKGROUND: Suture exposure remains to be a potential problem of transscleral fixated posterior chamber intraocular lens (PCIOL). We report a modified technique to minimize the risk of suture exposure for the transscleral fixation of PCIOL. METHODS: The modified surgical technique is as following: at first, two 3 mm × 4 mm square scleral pockets were created from groove incisions at opposite positions. A straight needle attached to a 10-0 polypropylene suture was passed through one incision groove. Then, a 27-Gauge hollow needle passed through the opposite sclera incision bed was used to retrieve the straight fine needle via its barrel. The sutures were tied to themselves after one more bite on the scleral bed. At last, the suture ends were left long (about 4 mm) and laid flat into corresponding laminar scleral pockets. This modified technique of PCIOL was performed in 48 post-traumatic aphakic vitrectomized eyes from 48 patients (47 male, one female) with mean age of 34.8 ± 14.8 years. Main outcome measures included best corrective visual acuity (BCVA), IOL decentration, IOL tilt, and postoperative complications. RESULTS: The mean follow-up was 32.3 ± 10.8 months (3-67 months). The LogMAR BCVA remained stable, from a preoperative value of 0.46 ± 0.34 to postoperative 0.44 ± 0.34 (p = 0.69). Mild IOL tilt (5-10°) was observed in five eyes, and slight IOL decentration (0.5-1.0 mm) was seen in three cases. No case of suture exposure, suture breakage, IOL dislocation, or endophthalmitis was observed during the follow up period. CONCLUSION: The modified technique allowed stable placement of PCIOLs in post-traumatic aphakic eyes with a wide range of follow-up. Our procedure might have the potential benefit to avoid suture exposure in scleral-fixated IOL implantation.

Influence of psychological intervention before emergent ocular trauma surgery on patients' negative emotions.

PURPOSE: To investigate the effect of preoperative psychological intervention on alleviating negative emotions in patients undergoing emergent ocular trauma surgery. METHODS: A total of 100 patients undergoing emergent ocular trauma surgery were selected using convenience sampling and randomly divided into control (n = 49) and experimental (n = 51) groups. Patients in the control group received conventional nursing and their counterparts in the observation group were treated with individualized psychological interventions including psychological support, relaxation training, and humanistic care based on conventional nursing care. Self-rating anxiety scale (SAS), self-rating depression scale (SDS), and fear visual analog scale (FVAS) scores were statistically compared between the two groups. RESULTS: The scores of SAS, SDS, and FAVS were significantly lower in the experimental group than in the control group (all P < 0.001). CONCLUSION: Comprehensive psychological intervention effectively eliminates negative emotions in patients undergoing emergent ocular trauma surgery and accelerates their physical and mental recovery.

Novel air-injection technique to locate the medial cut end of lacerated canaliculus.

Locating the medial cut end of the severed canaliculus is the most difficult aspect of canalicular repair, especially in patients with more medial laceration, severe oedema, persistent errhysis and a narrow canaliculus. Irrigation is a widely used technique to identify the cut end; however, we found that air injected through the intact canaliculus with a straight needle failed to reflux when the common canaliculus or lacrimal sac was not blocked. We describe a simple, safe and efficient air-injection technique to identify the medial cut edge of a lacerated canaliculus. In this method, we initially submersed the medial canthus under normal saline, then injected filtered air through the intact canaliculus using a side port stainless steel probe with a closed round tip. The tip was designed to block the common canaliculus to form a relatively closed system. The efficiency of this novel air-injection technique was equivalent to the traditional technique but does not require the cooperation of the patient to blow air. Using this technique, the medial cut end was successfully identified by locating the air-bubble exit within minutes in 19 cases of mono-canalicular laceration without any complication.

Abnormal expression of seven myogenesis-related genes in extraocular muscles of patients with concomitant strabismus.

Hyperplasia or hypoplasia of muscles gradually leads to strabismus. Myogenesis-related genes are involved in extraocular muscle development, including myogenic differentiation 1 (MYOD1), myogenin (MYOG), retinoblastoma 1 (RB1), cyclin-dependent kinase inhibitor 1A (P21), cyclin­dependent kinase inhibitor 1C (P57), insulin-like growth factor 1 (IGF1) and muscle creatine kinase (MCK). This study evaluated the expression of the above seven myogenesis-related genes by real-time quantitative RT-PCR in 18 resected extrocular muscles of patients with concomitant strabismus and 12 normal control muscle samples from one presumably healthy male 6 h after sudden mortality. We found that although there was a great divergence among the expression levels of 6 myogenesis-related regulatory factors, the relative expression patterns were similar in all the normal muscles, including the synergistic, antagonistic and yoke muscles. However, their expression levels in the 18 diseased extraocular muscles were abnormal; the expression levels of all the genes, with the exception of P57, were reduced in most of the diseased muscle tissues. These results imply that the abnormal expression of these myogenesis-related genes may contribute to concomitant strabismus.