Erratum: Trehalose inhibits H2O2-induced autophagic death in dopaminergic SH-SY5Y cells via mitigation of ROS-dependent endoplasmic reticulum stress and AMPK activation: Erratum.

[This corrects the article DOI: 10.7150/ijms.25656.].

Retraction Notice to: lncRNA ILF3-AS1 promotes proliferation and metastasis of colorectal cancer cells by recruiting histone methylase EZH2.

[This retracts the article DOI: 10.1016/j.omtn.2021.04.007.].

Alterations of Ocular Surface Parameters in Type 2 Diabetic Patients.

OBJECTIVE: The purpose of the study was to evaluate the changes in the ocular surface parameters of type 2 diabetic patients. METHODS: This study is a cross-sectional observational study. It included 76 eyes of 38 patients with type 2 diabetes and 183 eyes of 92 non-diabetic controls. The diabetic subjects were divided into two groups based on diabetic duration. Ocular surface parameters were assessed for all participants. RESULTS: The diabetic group had a significantly thinner lipid layer thickness (LLT) (p = 0.008) than non-diabetic controls. LLT in the subgroup with diabetic duration ≥10 years was significantly thinner than that in the subgroup with diabetic duration <10 years (p = 0.006). Multivariate linear regression analysis showed that LLT was associated with the duration of diabetes (ß = -1.497, p = 0.009) and Schirmer I test (SIT) score (ß = 0.852, p = 0.04) in diabetic. Diabetic duration was significantly negatively associated with LLT (ß = -0.062, p = 0.004) and significantly positively associated with ocular surface disease index (OSDI) (ß = 0.087, p = 0.039). CONCLUSION: Diabetic patients exhibit significantly reduced LLT and this trend becomes more pronounced with increased duration of diabetes.

lncRNA ILF3-AS1 promotes proliferation and metastasis of colorectal cancer cells by recruiting histone methylase EZH2.

The role of long non-coding RNA (lncRNA) has been displayed in colorectal cancer (CRC). Here, we aimed to discuss the role of lncRNA interleukin enhancer-binding factor 3-antisense RNA 1 (ILF3-AS1)/enhancer of zeste homolog 2 (EZH2)/cyclin-dependent kinase inhibitor 2 (CDKN2A)/histone 3 (H3) lysine 27 trimethylation (H3K27me3) in cell proliferation and metastasis of CRC. ILF3-AS1, EZH2, and CDKN2A levels in CRC tissues and cells were detected. The relationship between ILF3-AS1/EZH2 expression and the clinicopathological features of CRC was analyzed. High/low expression of ILF3-AS1/EZH2 plasmids were composed to explore the function of ILF3-AS1/EZH2 in invasion, migration, proliferation, colony formation, and apoptosis of CRC cells. The growth status of nude mice was observed to verify the in vitro results from in vivo experiment. ILF3-AS1 and EZH2 increased, whereas CDKN2A reduced in CRC tissues and cells. ILF3-AS1 and EZH2 expression was linked to Dukes stage, distant metastasis, vascular invasion, and lymph node metastasis of CRC patients. Depleted ILF3-AS1 or reduced EZH2 suppressed proliferation, migration, colony-formation, and invasion ability, as well as facilitated apoptosis of CRC cells and attenuated the tumor growth in CRC mice. ILF3-AS1 accelerates the proliferation and metastasis of CRC cells by recruiting histone methylase EZH2 to induce trimethylation of H3K27 and downregulate CDKN2A.

Sporadic multiple renal angiomyolipoma with lymph node involvement: a case report and literature review.

Angiomyolipoma (AML) is a benign tumor that mainly occurs in the kidneys. Simultaneous involvement of the kidney and local regional lymph nodes is very rare and might be misdiagnosed as a metastasizing malignant cancer. In the present study, a 50-year-old woman was referred to our hospital after a routine health screening ultrasound. Sporadic multiple renal AML with lymph node involvement was suspected based on the clinical manifestations and radiologic features. Partial nephrectomy was performed and a para-inferior vena cava lymph node was removed. The pathologic results confirmed multiple AML with lymph node invasion. We also reviewed the English-language literature regarding renal AML with lymph node involvement. We found that middle-aged women were likely to develop this disease and that loin pain was the main presenting feature. Most patients had no history of tuberous sclerosis complex. Radical nephrectomy was the predominant treatment. No local recurrence or distant metastasis occurred in any patients after radical nephrectomy or partial nephrectomy. In conclusion, renal AML with lymph node involvement is rare but can occur in both patients with tuberous sclerosis complex and those with multiple sporadic AML. Partial nephrectomy should be the first-line treatment, after which further treatment is not necessary.

Correlation Between Immune Lymphoid Cells and Plasmacytoid Dendritic Cells in Human Colon Cancer.

Background: Innate lymphoid cells (ILCs), so far studied mostly in mouse models, are important tissue-resident innate immune cells that play important roles in the colorectal cancer microenvironment and maintain mucosal tissue homeostasis. Plasmacytoid dendritic cells (pDCs) present complexity in various tumor types and are correlated with poor prognosis. pDCs can promote HIV-1-induced group 3 ILC (ILC3) depletion through the CD95 pathway. However, the role of ILC3s in human colon cancer and their correlation with other immune cells, especially pDCs, remain unclear. Methods: We characterized ILCs and pDCs in the tumor microenvironment of 58 colon cancer patients by flow cytometry and selected three patients for RNA sequencing. Results: ILC3s were negatively correlated, and pDCs were positively correlated, with cancer pathological stage. There was a negative correlation between the numbers of ILC3s and pDCs in tumor tissues. RNA sequencing confirmed the correlations between ILC3s and pDCs and highlighted the potential function of many ILC- and pDC-associated differentially expressed genes in the regulation of tumor immunity. pDCs can induce apoptosis of ILC3s through the CD95 pathway in the tumor-like microenvironment. Conclusions: One of the interactions between ILC3s and pDCs is via the CD95 pathway, which may help explain the role of ILC3s in colon cancer.

A rare case report of immunoglobulin G4-related sclerosing mesenteritis and review of the literature.

INTRODUCTION: Immunoglobulin G4 (IgG4)-related disease (IgG4-RD) is a rare autoimmune disorder involving 1 or multiple organs, most commonly the pancreas, lacrimal glands, and salivary glands. However, IgG4-related sclerosing mesenteritis (SM) involving the small-bowel mesentery is rare. Given that IgG4-related SM usually mimics the imaging characteristics of mesenteric malignancies, its preoperative diagnosis remains challenging. In addition, no specific consensus has been reached regarding the treatment of IgG4-related SM. Therefore, a better understanding of the characteristics, treatment, and prognosis of IgG-related SM is urgently needed. Herein, we report a rare case of IgG-related SM. PATIENT CONCERNS: A 67-year-old man was admitted to our hospital after incidental detection of an abdominal mass on ultrasound imaging, although he reported being generally well. The findings on triple-phase abdominal computed tomography were highly consistent with a malignant mesenteric tumor. DIAGNOSES: The hallmark histopathological features along with elevated levels of IgG4 (145 mg/dL) and imaging findings were indicative of IgG-related SM. INTERVENTIONS: The patient was treated surgically. Postoperative histopathological examinations exhibited tissue infiltration with lymphocytes and IgG4-positive plasma cells, as well as fibrosis. OUTCOMES: Ten days after surgery, the patient was discharged from the hospital, and did not show any clinical sign of IgG-related SM within 1-year follow-up. CONCLUSION: This case highlights the mesentery as an uncommon site of involvement as well as how early IgG-related SM can be completely asymptomatic. Thus, this study has advanced our knowledge of IgG-related SM and may improve treatments for similar conditions.

Radiation therapy enhanced therapeutic efficacy of anti-PD1 against gastric cancer.

Radiation therapy is an important method in tumor treatment with distinct responses. This study aimed to investigate the immune effects of radiation therapy on the syngeneic gastric tumor model. Mouse forestomach carcinoma (MFC) cells were irradiated with different X-ray doses. Cell proliferation was determined by clonogenic assay. Gene and protein expression were determined by real-time quantitative PCR and western blot, respectively. The tumor model was established by subcutaneously injecting tumor cells in 615-(H-2 K) mice. Levels of immune-related factors in tumor tissues were determined by immunohistochemistry and flow cytometry. 5 Gy × 3 (three subfractions with 4 h interval) treatment significantly inhibited cell proliferation. Protein expression of stimulator of interferon genes (Sting) and gene expression of IFNB1, TNFα as well as CXCL-9 significantly increased in MFC cells after irradiation. In the MFC mouse model, no obvious tumor regression was observed after irradiation treatment. Further studies showed Sting protein expression, infiltration of dendritic cells and T cells, and significantly increased PD-1/PD-L1 expression in tumor tissues. Moreover, the irradiation treatment activated T cells and enhanced the therapeutic effects of anti-PD1 antibody against MFC tumor. Our data demonstrated that although the MFC tumor was not sensitive to radiation therapy, the tumor microenvironment could be primed after irradiation. Radiation therapy combined with immunotherapy can greatly improve anti-tumor activities in radiation therapy-insensitive tumor models.

Type II enteropathy-associated T cell lymphoma in the duodenum: A rare case report.

INTRODUCTION: Enteropathy-associated T-cell lymphoma (EATL) is a very rare form of lymphoma in the gastrointestinal tract. The proximal jejunum and ileum are the most common sites of EATL, whereas EATL rarely arises in the duodenum, and EATL involving metastasis of the bilateral ovaries is even rarer. PATIENT CONCERNS: A 43-year-old female suffered from upper abdominal pain and weight loss for 3 months. DIAGNOSIS: Type II EATL. INTERVENTIONS: The patient was initially treated with chemotherapies, including 4 cycles of the CHOP-E and 2 cycles of the DHAP+ chidamide chemotherapy regimens. However, the patient did not respond well to chemotherapy. Surgical treatment of the duodenal obstruction, with perforation of small intestine and the duodenum, was performed successively. OUTCOMES: The patient died of septic shock only 1 day after the surgery for the second perforation. Her overall survival was 11 months from the time of initial diagnosis. CONCLUSION: This case suggests that EALT is highly invasive and its clinical course is very aggressive. Intestinal perforation, intestinal obstruction, or involvement of extraintestinal organs may occur in EALT patients. Additionally, EALT patients respond poorly to chemotherapy and have an extremely unfavorable prognosis.

Refractory solitary cervical lymph node metastasis after esophageal squamous cell carcinoma surgery and its successful treatment with immune checkpoint inhibitor: A case report and literature review.

RATIONALE: Although the early detection and treatment of non-metastatic esophageal cancer has improved, these patients' prognoses are still poor. Most patients with radical treatment for esophageal cancer will relapse in 3 years, and the best treatment strategy after recurrence has not been uniformly accepted. Multiform treatments may be beneficial to recurrent patients. PATIENT CONCERNS: A 60-year-old male patient, due to routinely health examination, ulcerated lesions 30 cm away from the incisors were found by gastroscopy, pathology showed esophageal squamous cell carcinoma (ESCC). DIAGNOSIS: Due to the patient's pathology, he was diagnosed with ESCC. INTERVENTIONS: The patient underwent radical surgery for ESCC on June 28, 2015. The left cervical lymph node metastasis occurred after 20 months, and lymph node metastasis carcinoma resection was performed. After that, concurrent chemoradiotherapy was implemented, 40 days after the end of the 4 courses of chemotherapy, the left cervical metastatic lymph nodes relapsed, radioactive particle implantation was carried out, and progressed again after 1 month. The patient took apatinib for 1 week but could not tolerate due to hand-foot syndrome. Immune checkpoint inhibitor (ICI) was administered since October 27, 2017. OUTCOMES: The therapeutic effect of immune checkpoint inhibitor was evaluated as partial response (PR) after 6 courses of treatment and complete response (CR) after 15 courses of treatment. To our knowledge, this is the first case report of successful immunotherapy for refractory esophageal squamous cell carcinoma. LESSONS: The emergence of ICIs promotes the treatment of esophageal cancer to a new era. Our observations suggest that patients for whom schedule to receive anti-programmed cell death protein-1 (anti-PD-1)/programmed cell death-ligand 1 (PD-L1) immunotherapy may require genomic testing to predict whether tumors respond to ICIs. In this case, we also present the predictors for the efficacy of targeted immunotherapy. At present, no matter which predictor of PD-L1 expression, tumor mutational burden (TMB), microsatellite instability (MSI), and tumor-infiltrating lymphocyte (TIL), a single predictor may be unconvincing and cannot accurately estimate the efficacy of immunotherapy. Multiplex detecting methods and combined biomarkers may provide new strategies. Consensus need to be reached in order to be widely applied in future studies.

The Long Non-coding RNA HOTTIP Is Highly Expressed in Colorectal Cancer and Enhances Cell Proliferation and Invasion.

Long non-coding RNAs (lncRNAs) are associated with a spectrum of biological processes such as gene regulation on transcriptional and post-transcriptional levels. The HOXA transcript at the distal tip (HOTTIP) lncRNA plays an important role in carcinogenesis; however, the underlying role of HOTTIP in colorectal carcinoma (CRC) remains unknown. The aim of the present study was to evaluate the expression and function of HOTTIP in CRC. In the present study, we analyzed HOTTIP expression levels of CRC patients in tumor and adjacent normal tissue by real-time quantitative PCR. Knockdown of HOTTIP by RNA interference was performed to explore its roles in cell proliferation, migration, and invasion. Our results found that HOTTIP was upregulated in human primary CRC tissues. Knockdown of HOTTIP inhibited CRC cell proliferation, migration, and invasion. Above all, knockdown of HOTTIP could represent a rational therapeutic strategy for CRC.

miR-663b promotes colorectal cancer progression by activating Ras/Raf signaling through downregulation of TNK1.

MiR-663b has been demonstrated to be abnormally expressed in several cancer types and was involved in the progression of cancer. Although overexpression of miR-663b in colorectal cancer was observed, the role of miR-663b in colorectal cancer cells has not been identified yet. In this study, we analyzed expression of miR-663b in colorectal tumors and explored the molecular mechanism of miR-663b in colorectal cancer cells. MiR-663b was significantly overexpressed in colorectal tumors and cell lines. Downregulation of miR-663b inhibited cell proliferation and sphere forming ability in colorectal cancer cells. In addition, miR-663b downregulation inactivated Ras/Raf signaling activity and subsequently decreased YAP1 and CD44 expression in colorectal cancer cells. Using TargetScan software, TNK1, a negative regulator of Ras/Raf signaling, was predicted to be a target gene of miR-663b. Western blotting and RT-qPCR showed that TNK1 expression was negatively regulated by miR-663b. In addition, the direct binding of miR-663b to TNK1 mRNA was proved by dual luciferase reporter assay. Furthermore, downregulation of miR-663b inhibited colorectal cancer cell proliferation and stemness, which was reversed after siRNA-mediated silencing of TNK1. In conclusion, the current study revealed a pivotal role of miR-663b in the progression of colorectal cancer.

In Situ Seed-Mediated Growth of Polymer-Grafted Gold Nanoparticles.

We report a facile yet general in situ seed-mediated method for the synthesis of polymer-grafted gold nanoparticles with narrow size distributions (<10%), accurately tunable sizes, and excellent colloidal stability. This method can be extended to a broad range of types and molecular weights of polymer ligands. Nanoparticles with different shapes can also be prepared by using preformed shaped nanoparticles directly as the seeds.

Exosomes: Versatile Nano Mediators of Immune Regulation.

One of many types of extracellular vesicles (EVs), exosomes are nanovesicle structures that are released by almost all living cells that can perform a wide range of critical biological functions. Exosomes play important roles in both normal and pathological conditions by regulating cell-cell communication in cancer, angiogenesis, cellular differentiation, osteogenesis, and inflammation. Exosomes are stable in vivo and they can regulate biological processes by transferring lipids, proteins, nucleic acids, and even entire signaling pathways through the circulation to cells at distal sites. Recent advances in the identification, production, and purification of exosomes have created opportunities to exploit these structures as novel drug delivery systems, modulators of cell signaling, mediators of antigen presentation, as well as biological targeting agents and diagnostic tools in cancer therapy. This review will examine the functions of immunocyte-derived exosomes and their roles in the immune response under physiological and pathological conditions. The use of immunocyte exosomes in immunotherapy and vaccine development is discussed.

MicroRNAs: Key Players in Bladder Cancer.

Bladder cancer (BC) is the second highest morbid malignancy of the urinary tract and the fifth most common cancer worldwide. BC is highly malignant with significant morbidity and mortality, especially muscle-invasive BC (MIBC), which has a poor prognosis and frequently recurs after the first resection. Therefore, more sensitive diagnostic tools and effective therapeutic methods are urgently needed. MicroRNAs (miRNAs) are small noncoding RNAs that regulate the expression of protein-coding genes by repressing their translation or cleaving RNA transcripts in a sequence-specific manner. miRNAs play very important roles in regulating genes related to tumorigenesis, tumor development, progression, metastasis and angiogenesis. With the rapid development of high-throughput sequencing technology, an increasing number of miRNAs with aberrant expression between either BC patients and healthy volunteers or between BC tumor tissues and matched peripheral control tissues have been recently examined. The tumor etiopathogenesis must be determined to promote the development of new markers as diagnostic and prognostic tools and targets for bladder tumor therapy, it is therefore vital to elucidate the function of miRNAs with aberrant expression in BC. In the present study, we examined the published data of BC-related miRNAs by reviewing their expression levels, possible functions, potential target genes, related molecular regulatory networks, candidate markers for prognosis and diagnosis, and prospective therapeutic cases, and we summarized the status of research on BC-related miRNAs in recent years.

Up-regulation of microRNA-497-5p inhibits colorectal cancer cell proliferation and invasion via targeting PTPN3.

To investigate the role of microRNA-497-5p (miR-497-5p) in the tumorigenesis of colorectal cancer (CRC), the present study applied qRT-PCR to detect the expression level of miR-497-5p in both clinical samples and CRC cell lines. Furthermore, to specifically evaluate the carcinogenic role of miR-497-5p in CRC, the expression of miR-497-5p was monitored by transfecting with the mimics or inhibitors of miR-497-5p. Transwell assay as well as CCK-8 assay were used to determine the functions of miR-497-5p on cell invasion, migration and proliferation, respectively. miR-497-5p expression was remarkably down-regulated in clinical samples with cancer development as well as in CRC cell lines. Additionally, low miR-497-5p expression was remarkably correlated with higher TNM stage and lymph node metastasis of CRC patients. Up-regulation of miR-497-5p significantly inhibited proliferation, migration, and invasion of LOVO CRC cell line. Conversely, antagonizing miR-497-5p significantly promoted cell proliferation, migration and invasion. Mechanistic analysis revealed that miR-497-5p directly bound to its downstream target, protein tyrosine phosphatase non-receptor type 3 (PTPN3), whose aberrant expression partially reversed inhibition of cell proliferation and migration. Taken together, the present study elucidated the inhibitory role of miR-497-5p in CRC via targeting PTPN3, which potentiated miR-497-5p as a potential therapeutic target for combating CRC.

Expression of miR-124 in gastric adenocarcinoma and the effect on proliferation and invasion of gastric adenocarcinoma SCG-7901 cells.

Expression of miR-124 in gastric adenocarcinoma cell line SGC-7901 and its effect on biological functions was investigated. Expression of miR-124 in cancer tissues and paracancerous tissues of gastric adenocarcinoma patients was detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). RT-qPCR was used to detect the expression of miR-124 in human normal gastric epithelial cells GES-1 and gastric adenocarcinoma SGC-7901 cells. Cells in miR-124 group were transfected with miR-124 agomir, cells in NC group were transfected with agomir-negative control sequence and cells in the control group were not transfected. MTT assay was used to detect cell proliferation, and Transwell invasion assay to detect cell invasion ability, and the effect of transfected miR-124 agonist on the proliferation and invasive ability of gastric adenocarcinoma cells was evaluated. RT-qPCR results showed that miR-124 expression was significantly downregulated in gastric adenocarcinoma tumor tissues compared with paracancerous tissues. Compared with cells of normal human gastric epithelial cell line GES-1, the expression of miR-124 human gastric adenocarcinoma SGC-7901 cells was significantly downregulated. At 12 h, there was no significant difference in OD at 490 nm in the three groups (P>0.05). OD (490) in the three groups showed a gradual upward trend. After transfection, proliferation curves of the three groups showed an upward trend, proliferation rate of miR-124 group was significantly lower than that of NC and control groups (P<0.05). The number of invading cells in miR-124 group was significantly lower than that in NC group and control group, but there was no significant difference in the number of cell invasion between the NC and control groups. miR-124 can inhibit the proliferation and invasion of gastric adenocarcinoma cells. Downregulation of miR-124 expression in gastric adenocarcinoma may be closely related to the development of gastric adenocarcinoma.

Morphine regulates adult neurogenesis and contextual memory extinction via the PKCε/Prox1 pathway.

We have previously reported that the miR-181a/Prox1/Notch1 pathway mediates the effect of morphine on modulating lineage-specific differentiation of adult neural stem/progenitor cells (NSPCs) via a PKCε-dependent pathway, whereas fentanyl shows no such effect. However, the role of the PKCε/Prox1 pathway in mediating drug-associated contextual memory remains unknown. The current study investigated the effect of PKCε/Prox1 on morphine-induced inhibition of adult neurogenesis and drug-associated contextual memory in mice, while the effect of fentanyl was tested simultaneously. By using BrdU labeling, we were able to examine the lineages of differentiated NSPCs in adult DG. PKCε knockout blocked morphine's effects on inducing in vivo astrocyte-preferential differentiation of NSPCs, but did not alter NSPC lineages upon fentanyl treatment. Inhibited adult neurogenesis further resulted in prolonged extinction and enhanced reinstatement of morphine-induced CPP, as well as prolonged extinction of space reference memory indicated by the Morris water maze paradigm. However, after fentanyl administration, no significant changes were found between wild-type and PKCε knockout mice, during either CPP or water maze tasks. When the lentivirus encoding Nestin-promoter-controlled Prox1 cDNA was injected into hippocampi of wildtype and PKCε knockout adult mice to modulate PKCε/Prox1 activity, similar effects were discovered in adult mice injected with lentivirus encoding Prox1, and more dramatic effects were found in PKCε knockout mice with concurrent Prox1 overexpression. In conclusion, morphine mediates lineage-specific NSPC differentiation, inhibits adult neurogenesis and regulates contextual memory retention via the PKCε/Prox1 pathway, which are implicated in the eventual context-associated relapse.

Trehalose inhibits H2O2-induced autophagic death in dopaminergic SH-SY5Y cells via mitigation of ROS-dependent endoplasmic reticulum stress and AMPK activation.

Autophagy is a catabolic process to maintain intracellular homeostasis via removal of cytoplasmic macromolecules and damaged cellular organelles through lysosome-mediated degradation. Trehalose is often regarded as an autophagy inducer, but we reported previously that it could prevent ischemic insults-induced autophagic death in neurons. Thus, we further investigated in this study whether trehalose could protect human dopaminergic SH-SY5Y cells against H2O2-induced lethal autophagy. We found pretreatment with trehalose not only prevented H2O2-induced death in SH-SY5Y cells, but also reversed H2O2-induced upregulation of LC3II, Beclin1 and ATG5 and downregulation of p62. Then, we proved that either autophagy inhibitor 3MA or genetic knockdown of ATG5 prevented H2O2-triggered death in SH-SY5Y cells. These indicated that trehalose could inhibit H2O2-induced autophagic death in SH-SY5Y cells. Further, we found that trehalose inhibited H2O2-induced AMPK activation and endoplasmic reticulum (ER) stress. Moreover, inhibition of AMPK activation with compound C or alleviation of ER stress with chemical chaperone 4-PBA obviously attenuated H2O2-induced changes in autophagy-related proteins. Notably, we found that trehalose inhibited H2O2-induced increase of intracellular ROS and reduction in the activities of CAT and SOD. Consistently, our data revealed as well that mitigation of intracellular ROS levels with antioxidant NAC markedly attenuated H2O2-induced AMPK activation and ER stress. Therefore, we demonstrated in this study that trehalose prevented H2O2-induced autophagic death in SH-SY5Y cells via mitigation of ROS-dependent endoplasmic reticulum stress and AMPK activation.

Comparison of 2 modified methods for the active removal of silicone oil with a 23-gauge transconjunctival vitrectomy system.

To report and compare 2 modified approaches for the active removal of silicone oil (ROSO) with a 23-gauge transconjunctival vitrectomy system.This prospective single blinded study was conducted from January 2015 to December 2016. Eighty-nine eyes of 86 patients who underwent silicone oil removal were enrolled. Patients were randomly divided into either group A or B. In group A, the fluid-air exchange tube was connected to a 1 mL syringe with the plunger removed and the tip was dilated with a hemostat so that it fit into the cap of the 23-gauge cannula to form a seal for oil drainage. In group B, the tip of the syringe was closely attached to the cap of the 23-gauge cannula by a tube adaptor, which was salvaged from a used silicone oil inject and aspirate pack and sterilized. Main outcome measures were time required for silicone oil removal, silicone oil residual, intraoperative and postoperative complications including hypotony, bleeding, and retinal redetachment.The mean time required was 6.08 ±â€Š0.31 minutes and 6.11 ±â€Š0.31 minutes for groups A and B, respectively. No silicone oil residual, severe hypotony, recurrence of retinal detachment, or impairment of visual acuity were observed in either group. Conjunctival injection and hyperemia were slightly more severe in group A, but spontaneously resolved in 2 to 3 days.Both methods described in this paper were demonstrated to be safe, effective, and cost-effective for the ROSO. The syringe dilation method caused more severe conjuntival irritation, thus we suggest using the tube adaptor method for hospitals equipped with cold sterilization equipment.