The performance of a deep learning system in assisting junior ophthalmologists in diagnosing 13 major fundus diseases: a prospective multi-center clinical trial.

Artificial intelligence (AI)-based diagnostic systems have been reported to improve fundus disease screening in previous studies. This multicenter prospective self-controlled clinical trial aims to evaluate the diagnostic performance of a deep learning system (DLS) in assisting junior ophthalmologists in detecting 13 major fundus diseases. A total of 1493 fundus images from 748 patients were prospectively collected from five tertiary hospitals in China. Nine junior ophthalmologists were trained and annotated the images with or without the suggestions proposed by the DLS. The diagnostic performance was evaluated among three groups: DLS-assisted junior ophthalmologist group (test group), junior ophthalmologist group (control group) and DLS group. The diagnostic consistency was 84.9% (95%CI, 83.0% ~ 86.9%), 72.9% (95%CI, 70.3% ~ 75.6%) and 85.5% (95%CI, 83.5% ~ 87.4%) in the test group, control group and DLS group, respectively. With the help of the proposed DLS, the diagnostic consistency of junior ophthalmologists improved by approximately 12% (95% CI, 9.1% ~ 14.9%) with statistical significance (P < 0.001). For the detection of 13 diseases, the test group achieved significant higher sensitivities (72.2% ~ 100.0%) and comparable specificities (90.8% ~ 98.7%) comparing with the control group (sensitivities, 50% ~ 100%; specificities 96.7 ~ 99.8%). The DLS group presented similar performance to the test group in the detection of any fundus abnormality (sensitivity, 95.7%; specificity, 87.2%) and each of the 13 diseases (sensitivity, 83.3% ~ 100.0%; specificity, 89.0 ~ 98.0%). The proposed DLS provided a novel approach for the automatic detection of 13 major fundus diseases with high diagnostic consistency and assisted to improve the performance of junior ophthalmologists, resulting especially in reducing the risk of missed diagnoses. ClinicalTrials.gov NCT04723160.

Protective role of thymoquinone in hyperlipidemia-induced liver injury in LDL-R-/-mice.

BACKGROUND: Hyperlipidemia, a heterogeneous group of disorders characterized by elevated plasma lipids in the blood, causes severe health problems, leading to fatty liver disease and nonalcoholic fatty liver disease. Thymoquinone, the major active chemical component of Nigella sativa, reportedly exerts a vast array of biological effects. Various studies have reported that Thymoquinone protects against liver injury. AIMS: The aim of this study was to investigate the possible protective effects of Thymoquinone against liver injury in hyperlipidemia-induced LDL-R-/- mice. METHODS: Eight-week-old male LDL-R-/- mice were randomly divided into three groups: a control group fed a normal diet and two groups fed a high-cholesterol diet or high-cholesterol diet mixed with Thymoquinone. All groups were fed different diets for 8 weeks. Blood samples were obtained from the inferior vena cava and collected in serum tubes. The samples were then stored at - 80 °C until used. Longitudinal sections of liver tissues were fixed in 10% formalin and then embedded in paraffin for histological evaluation. The remainder of the liver tissues were snap-frozen in liquid nitrogen for reverse transcription-polymerase chain reaction or western blotting. RESULTS: Our results demonstrated that Thymoquinone administration significantly reduced liver histological alterations by hyperlipidemia. Thymoquinone mitigated hyperlipidemia-induced liver injury as indicated by the suppression of metabolic characteristics, liver biochemical parameters, pyroptosis indicators, a macrophage marker, and the phosphatidylinositide 3-kinase signaling pathway. CONCLUSIONS: Thymoquinone is a potential therapeutic agent for hyperlipidemia-induced liver injury.

Solidification/stabilization of heavy metals and its efficiency in lead-zinc tailings using different chemical agents.

Lead-zinc tailings are generated during the mining process which is considered as hazardous solid waste due to its high heavy metal content and leachability in the natural state. At present, the most effective technology for disposing heavy metals in solid wastes is the solidification/stabilization (S/S) technique. In terms of S/S technology, chemical stabilization is one of the most potential and practical method. This paper aims to investigate the S/S property of four typical chemical agents (Na2S, NaH2PO4, TMT and Na2EDTA) on the heavy metals in lead-zinc tailings. The results reveal that the heavy metals lead and zinc in tailings are stabilized more effectively by using chelating agents TMT than by using inorganic chemical agents Na2S and NaH2PO4. When the dosage of TMT reaches 4%, the leaching concentration of lead and zinc is 0.18 and 14.60 mg/L according to toxicity characteristic leaching procedure (TCLP), and the stabilization efficiency of lead and zinc is 99.31% and 80.92%, respectively, while the leaching concentration of lead and zinc just drops to 0.41 and 16.00 mg/L with addition of 10% NaH2PO4. Furthermore, the leaching concentration of heavy metal lead in tailings treated by 4% Na2EDTA increases to 53.44 mg/L which far exceeds the standard of pollution control. Therefore, considering stabilization efficiency and dosage, TMT is the preferred agent for solidifying heavy metals in lead-zinc tailings.

G-quadruplex structural variations in human genome associated with single-nucleotide variations and their impact on gene activity.

G-quadruplexes (G4s) formed by guanine-rich nucleic acids play a role in essential biological processes such as transcription and replication. Besides the >1.5 million putative G-4-forming sequences (PQSs), the human genome features >640 million single-nucleotide variations (SNVs), the most common type of genetic variation among people or populations. An SNV may alter a G4 structure when it falls within a PQS motif. To date, genome-wide PQS-SNV interactions and their impact have not been investigated. Herein, we present a study on the PQS-SNV interactions and the impact they can bring to G4 structures and, subsequently, gene expressions. Based on build 154 of the Single Nucleotide Polymorphism Database (dbSNP), we identified 5 million gains/losses or structural conversions of G4s that can be caused by the SNVs. Of these G4 variations (G4Vs), 3.4 million are within genes, resulting in an average load of >120 G4Vs per gene, preferentially enriched near the transcription start site. Moreover, >80% of the G4Vs overlap with transcription factor-binding sites and >14% with enhancers, giving an average load of 3 and 7.5 for the two regulatory elements, respectively. Our experiments show that such G4Vs can significantly influence the expression of their host genes. These results reveal genome-wide G4Vs and their impact on gene activity, emphasizing an understanding of genetic variation, from a structural perspective, of their physiological function and pathological implications. The G4Vs may also provide a unique category of drug targets for individualized therapeutics, health risk assessment, and drug development.

A pilot study on vitrectomy combined with scleral shortening for eyes with myopic macular retinoschisis-2y follow-up results.

AIM: To evaluate the effect of vitrectomy combined with scleral shortening for eyes with myopic macular retinoschisis. METHODS: Thirty-seven patients with myopic macular retinoschisis who underwent pars plana vitrectomy (PPV) combined with scleral shortening were reviewed. Axial length (AL), the height of macular retinoschisis, the height of retinal detachment if existed, the diameter of macular hole if existed and best corrected visual acuity (BCVA) were obtained. The preoperative and postoperative parameters were compared. RESULTS: At postoperative 24mo, the mean AL and height of macular retinoschisis were reduced significantly by 0.79 mm and 256.51 µm (t=8.064, P<0.0001; Z=-5.086, P<0.0001) respectively. In addition, the mean height of retinal detachment and diameter of macular hole were also reduced significantly by 365.38 µm and 183.68 µm (Z=-4.457, P=0.000008; Z=-2.983, P=0.003) respectively. Meanwhile, the postoperative BCVA was improved markedly (Z=-2.126, P=0.033). CONCLUSION: Vitrectomy combined with scleral shortening is an effective surgical method for eyes with myopic macular retinoschisis, whether or not macular hole and retinal detachment are present.

Choroidal thickness changes and choriocapillary circulation analysis in macular holes using optical coherence tomography angiography.

BACKGROUND: To investigate the changes of subfoveal choroidal thickness (SFCT) and choriocapillary circulation in idiopathic macular holes (IMHs), the fellow eyes, and normal subjects using optical coherence tomography (OCT) and optical coherence tomography angiography (OCTA), and to explore the role of SFCT and choriocapillary circulation in the pathogenesis of IMH. METHODS: A case series of 30 patients with unilateral IMH and 30 subjects, with age- and sex-matched, were included. Thirty eyes of 30 patients with unilateral IMH, the unaffected fellow eyes, and 30 eyes of age- and sex-matched healthy patients were studied. SFCT was measured by spectral domain enhanced depth imaging optical coherence tomography (EDI SD-OCT), while vascular density and blood flow area of choriocapillary circulation were obtained by OCTA. RESULTS: The SECT in IMH eyes (236.09±79.25 µm) was lower than that in the unaffected fellow eyes (249.71±86.10 µm) (P=0.040) and healthy control eyes (283.29±64.16 µm) (P=0.001). Also, the SFCT of the unaffected fellow eyes was lower than that of the healthy control eyes (P=0.033). The superficial blood flow area and vascular density of choriocapillary in the macular area were smaller and lower in the IMH eyes (2.84±0.35 mm2, 20.74%±8.26%) than the unaffected fellow eyes (3.19±0.23 mm2, 35.18%±5.20%) and healthy control eyes (3.26±0.24 mm2, 35.20%±6.49%) (P<0.001); however, no difference was observed between the unaffected fellow eyes and healthy control eyes. CONCLUSIONS: The SFCT in IMH eyes was lower than that of unaffected fellow eyes and matched control eyes. In addition, the choriocapillary blood flow area and vascular density were smaller and lower than those of the unaffected fellow eyes and normal controls. Our findings suggested that atrophy of choriocapillary might play an important role in the formation of IMH.

Multimodal Imaging of Parry Romberg Syndrome-associated Panuveitis: A Case Report and Review of Literature.

Purpose: We describe a case of Parry-Romberg syndrome (PRS) presenting with panuveitis and retinal vasculitis.Methods: We conducted a retrospective review of our patient's case and related literature published through May 2019.Results: A 26-year-old woman with history of PRS was diagnosed with panuveitis and retinal vasculitis. Intraocular inflammation was controlled with local and systemic corticosteroids. The relationship between PRS and intraocular inflammation is discussed with references to the relevant on literature.Conclusions: Our findings and the accompanying literature review suggest that the patient's ocular involvement included multiple fundus lesions, retinal vascular disorder, and unilateral poliosis - all of which may be attribute to trigeminal neuro vasculitis. As the Varicella-zoster virus may contribute to the onset of the autoimmune processes associated with PRS, this requires further exploration. This report confirms the utility of multimodal imaging in the study, screening, and follow-up of intraocular inflammation in patients with PRS.

Protective Role of Coenzyme Q10 in Acute Sepsis-Induced Liver Injury in BALB/c Mice.

Sepsis increases the risk of the liver injury development. According to the research works, coenzyme Q10 exhibits hepatoprotective properties in vivo as well as in vitro. Current work aimed at investigating the protective impacts of coenzyme Q10 against liver injury in septic BALB/c mice. The male BALB/c mice were randomly segregated into 4 groups: the control group, the coenzyme Q10 treatment group, the puncture and cecal ligation group, and the coenzyme Q10+cecal ligation and puncture group. Cecal ligation and puncture was conducted after gavagaging the mice with coenzyme Q10 during two weeks. Following 48 h postcecal ligation and puncture, we estimated hepatic biochemical parameters and histopathological changes in hepatic tissue. We evaluated the expression of factors associated with autophagy, pyroptosis, and inflammation. Findings indicated that coenzyme Q10 decreased the plasma levels in alkaline phosphatase, alanine aminotransferase, and aspartate aminotransferase in the cecal ligation and puncture group. Coenzyme Q10 significantly inhibited the elevation of sequestosome-1, interleukin-1ß, oligomerization domain-like receptor 3 and nucleotide-binding, interleukin-6, and tumor necrosis factor-α expression levels; coenzyme Q10 also increased beclin 1 levels. Coenzyme Q10 might be a significant agent in the treatment of liver injury induced by sepsis.

Erratum to "Effect of Thymoquinone on Acute Kidney Injury Induced by Sepsis in BALB/c Mice".

[This corrects the article DOI: 10.1155/2020/1594726.].

One-Step High-Throughput Telomerase Activity Measurement of Cell Populations, Single Cells, and Single-Enzyme Complexes.

Telomerase, a key enzyme involved in telomere homeostasis, is a major player involved in or required for sustained cell proliferation. It is expressed in ∼90% tumor but rarely in normal somatic cells. Therefore, telomerase serves as a diagnostic marker and therapeutic target of cancers. Although many methods are available for measuring telomerase activity, a convenient, fast, sensitive, and reliable method is still lacking for routine use in both clinics and research. Here, we present a single-enzyme sensitivity telomere repeat amplification protocol for quantifying telomerase activity. With multiple optimizations, the protocol pushes the ultimate detection limit down to a single telomerase complex, enabling measurement of telomerase activity of not only multiple cancerous/normal cell samples but also single cancer cells alone or even in the presence of 8000 normal cells. Implemented in a one-step mix-and-run format, the protocol offers a most sensitive, fast, accurate, and reproducible quantification of telomerase activity with linearity ranging from 20,000 HeLa cancer cells to a single telomerase complex. It requires minimal manual operation and experimental skill and is convenient for either low or high throughput of samples. We expect that the protocol should provide practical routine analyses of telomerase in both research and clinical applications. As an example, we demonstrate how telomerase activity evolves at the single-cell level and partitions in cell division in early mouse embryo development.

Detection of genomic G-quadruplexes in living cells using a small artificial protein.

G-quadruplex (G4) structures formed by guanine-rich nucleic acids are implicated in essential physiological and pathological processes and serve as important drug targets. The genome-wide detection of G4s in living cells is important for exploring the functional role of G4s but has not yet been achieved due to the lack of a suitable G4 probe. Here we report an artificial 6.7 kDa G4 probe (G4P) protein that binds G4s with high affinity and specificity. We used it to capture G4s in living human, mouse, and chicken cells with the ChIP-Seq technique, yielding genome-wide landscape as well as details on the positions, frequencies, and sequence identities of G4 formation in these cells. Our results indicate that transcription is accompanied by a robust formation of G4s in genes. In human cells, we detected up to >123 000 G4P peaks, of which >1/3 had a fold increase of ≥5 and were present in >60% promoters and ∼70% genes. Being much smaller than a scFv antibody (27 kDa) or even a nanobody (12-15 kDa), we expect that the G4P may find diverse applications in biology, medicine, and molecular devices as a G4 affinity agent.

Establishing a mouse model of choroidal neovascularization to study the therapeutic effect of levotinib and its mechanism.

OBJECTIVE: To study the therapeutic effect and mechanism of levotinib on choroidal neovascularization (CNV) in mice. METHODS: 45 healthy C57BL/6 mice were selected and randomly divided into three groups: control group (group A), model group (group B) and levotinib group (group C). The model of CNV in mice was established. The fluorescence leakage of choroidal lesions in mice was observed by fundus fluorescein angiography. The morphological changes of retinal vessels in mice were observed by retinal slice preparation, the pathological changes of eyeball tissues in mice were observed by hematoxylin-eosin (HE) staining, the expression of vascular endothelial growth factor (VEGF) in mice retina was detected by real-time quantitative fluorescence PCR, and the protein expression of VEGF in mice retina was detected by Western blotting. RESULT: On the 7th, 14th and 21st day after modeling, compared with group B, the fluorescence leakage area of group C mice was significantly reduced, and the difference was statistically significant (P < 0.05). The morphology of retinal vessels in group A was normal. In group B, the retinal vessels showed large areas of ischemia without perfusion and abundant neovascularization clusters and capillaries. Compared with group B, the morphology of retinal vessels in group C was significantly improved. Group A mice had normal eyeball structure, group B mice had visible spindle-like damage to the inner and outer retina, while group C mice had significantly less spindle-like damage than group B. Compared with group A, group B mice had significantly higher expression of retinal VEGF and the difference was statistically significant (P < 0.05), but compared with group B mice, the expression of VEGF in the retina of mice in group C was significantly decreased, and the difference was statistically significant (P < 0.05). Compared with group A, the expression of VEGF in retina of group B mice was significantly increased, and the difference was statistically significant (P < 0.05). Compared with group B, the expression of VEGF in retina of group C mice was significantly decreased, and the difference was statistically significant (P < 0.05). CONCLUSION: Levatinib has obvious therapeutic effect on CNV, which may be achieved by inhibiting the high expression of VEGF in CNV.

Effect of Thymoquinone on Acute Kidney Injury Induced by Sepsis in BALB/c Mice.

Acute kidney injury (AKI) is a common complication of sepsis and has also been observed in some patients suffering from the new coronavirus pneumonia COVID-19, which is currently a major global concern. Thymoquinone (TQ) is one of the most active ingredients in Nigella sativa seeds. It has a variety of beneficial properties including anti-inflammatory and antioxidative activities. Here, we investigated the possible protective effects of TQ against kidney damage in septic BALB/c mice. Eight-week-old male BALB/c mice were divided into four groups: control, TQ, cecal ligation and puncture (CLP), and TQ+CLP. CLP was performed after 2 weeks of TQ gavage. After 48 h, we measured the histopathological alterations in the kidney tissue and the serum levels of creatinine (CRE) and blood urea nitrogen (BUN). We also evaluated pyroptosis (NLRP3, caspase-1), apoptosis (caspase-3, caspase-8), proinflammatory (TNF-α, IL-1ß, and IL-6)-related protein and gene expression levels. Our results demonstrated that TQ inhibited CLP-induced increased serum CRE and BUN levels. It also significantly inhibited the high levels of NLRP3, caspase-1, caspase-3, caspase-8, TNF-α, IL-1ß, and IL-6 induced by CLP. Furthermore, NF-κB protein level was significantly decreased in the TQ+CLP group than in the CLP group. Together, our results indicate that TQ may be a potential therapeutic agent for sepsis-induced AKI.

Selective Targeting of Guanine-Vacancy-Bearing G-Quadruplexes by G-Quartet Complementation and Stabilization with a Guanine-Peptide Conjugate.

Stabilization of G-quadruplexes (G4s) formed in guanine-rich (G-rich) nucleic acids by small-molecule ligands has been extensively explored as a therapeutic approach for diseases such as cancer. Finding ligands with sufficient affinity and specificity toward G4s remains a challenge, and many ligands reported seemed to compromise between the two features. To cope with this challenge, we focused on targeting a particular type of G4s, i.e., the G-vacancy-bearing G-quadruplexes (GVBQs), by taking a structure complementation strategy to enhance both affinity and selectivity. In this approach, a G-quadruplex-binding peptide RHAU23 is guided toward a GVBQ by a guanine moiety covalently linked to the peptide. The filling-in of the vacancy in a GVBQ by the guanine ensures an exclusive recognition of GVBQ. Moreover, the synergy between the RHAU23 and the guanine dramatically improves both the affinity toward and stabilization of the GVBQ. Targeting a GVBQ in DNA by this bifunctional peptide strongly suppresses in vitro replication. This study demonstrates a novel and promising alternative targeting strategy to a distinctive panel of G4s that are as abundant as the canonical ones in the human genome.

Targeting nucleic acids with a G-triplex-to-G-quadruplex transformation and stabilization using a peptide-PNA G-tract conjugate.

A dual-functional peptide-PNA (peptide nucleic acid) conjugate consisting of a PNA G3-tract and an RHAU23 peptide is devised to target nucleic acids bearing three tandem guanine tracts (G-tracts). The PNA G3-tract joins the three G-tracts to form a stable bimolecular G-quadruplex (G4) and the resulting G4 is then bound by the RHAU23 moiety to form an extra stable G4-peptide complex. Owing to this synergistic dual structural enforcement, the conjugate accomplished extremely high selectivity and nM to sub-nM affinities towards its targets that are up to 1000 times greater than the small molecule G4 ligands. As a result, the conjugate impacts the tracking activity of motor proteins on DNA with superior selectivity and potency that are rarely seen in other G4-targeting approaches.

DNA:RNA hybrid G-quadruplex formation upstream of transcription start site.

Bioinformatic analysis reveals an enrichment of putative DNA:RNA hybrid G-quadruplex-forming sequences (PHQS) on both sides of the transcription start sites (TSSs) in the genome of warm-blooded animals, suggesting a positive selection of PHQSs in evolution and functional role of DNA:RNA hybrid G-quadruplexes (HQs) in transcription. The formation of HQs downstream of TSS in transcribed DNA has been documented under in vitro conditions; however, it is still not known if such HQs can form at the upstream side of TSSs. In this study, we report that such HQs can form in transcription in DNA with two to three guanine tracts if RNA carrying the required number of G-tracts is supplied. We also show that the formation of such HQs is dependent on the negative supercoiling generated by RNA polymerases. These results suggest that HQs may also form at the upstream side of TSSs in vivo and play a role in transcription since the two requirements are satisfied in cells.

Kinetics, conformation, stability, and targeting of G-quadruplexes from a physiological perspective.

The particular enrichment of G-quadruplex-forming sequences near transcription start sites signifies the involvement of G-quadruplexes in the regulation of transcription. The characterization of G-quadruplex formation, which holds the key to understand the function it plays in physiological and pathological processes, is mostly performed under simplified in vitro experimental conditions. Formation of G-quadruplexes in cells, however, occurs in an environment far different from the ones in which the in vitro studies on G-quadruplexes are normally carried out. Therefore, the characteristics of G-quadruplex structures obtained under the in vitro conditions may not faithfully reveal how the G-quadruplexes would behave in a physiologically relevant situation. In this mini-review, we attempt to briefly summarize the differences in a few important characteristics, including kinetics, conformation, and stability of G-quadruplex formation observed under the two conditions to illustrate how the intracellular environment might affect the behavior of G-quadruplexes largely based on the previous work carried out in the authors' laboratory. We also propose that unstable G-quadruplex variants may be better drug target candidates to improve selectivity and potency.

Acute shock caused by Clonorchis sinensis infection: a case report.

BACKGROUND: Clonorchiasis, caused by Clonorchis sinensis (C. sinensis) infection, is a serious food-borne zoonotic disease that is often asymptomatic or shows only mild symptoms, which leads to delayed treatment and chronic clonorchiasis and results in various complications, such as cholelithiasis, cholangitis, cholecystitis and cholangiocarcinoma. However, acute shock caused by C. sinensis infection has not been reported. Here, for the first time, we describe a fatal case of acute shock caused by C. sinensis infection. CASE PRESENTATION: A patient with a history of eating raw or undercooked freshwater fish was hospitalized with acute shock caused by severe abdominal pain. Physical examination suggested acute abdomen with severe abdominal pain and rigidity. Computed tomography (CT) detection indicated acute cholecystitis and cholelithiasis. After cholecystectomy, several liver flukes were found in the drainage tube. Furthermore, morphological analysis and polymerase chain reaction (PCR) identified the pathogen as C. sinensis. The liver gradually restored normal function after anthelmintic therapy with praziquantel. CONCLUSIONS: In this fatal case, C. sinensis infection was the cause of acute shock, which is rarely found in the clinic environment. This report aims to increase awareness of the hazards and complications related to clonorchiasis. The PCR diagnosis method used in this report might be helpful in reducing the misdiagnosis of clonorchiasis and unnecessary cholecystectomy.

Decreased Serum miR-1296 may Serve as an Early Biomarker for the Diagnosis of Non-Alcoholic Fatty Liver Disease.

BACKGROUND: Circulating microRNA has become a candidate biomarker for many diseases. The purpose of this study was to investigate the significance of miR-1296 as a non-invasive biomarker in nonalcoholic fatty liver disease (NAFLD). METHODS: Serum samples were collected from normal people and NAFLD patients for biochemical detection. Serum microRNAs were isolated by the NucleoZOL method, and the stem-loop method was used to reverse transcribe the DNA. The relative quantification of miR-1296 was performed by SYBR Green method. Spearman's method was used to analyze the correlation between miR-1296 and serum biochemical parameters. RESULTS: By using 2-∆∆CT method, we found that, compared with the normal control group, the expression of serum miR-1296 increased in patients with normal lipid NAFLD and those with hyperlipidemia NAFLD. At the same time, the expression of microRNA-1296 in the NAFLD hyperlipidemia group increased more significantly than that in the NFALD group with normal lipid. Spearman's correlation assay demonstrated that the correlation between the expression of miR-1296 and blood lipids, including TC, TG, HDL-c, and LDL-c, was TC (r = 0.4951, p = 0.0013), TG (r = 0.054, p = 0.6425), HDL-C (r = 0.3435, p = 0.07522), and LDL-C (r = 0.3307, p = 0.0699. The data showed that miR-1296 was positively correlated with serum TC level. CONCLUSIONS: In summary, serum microRNA-1296 is a more sensitive marker of NAFLD than blood lipids, which provides a new method for noninvasive early screening of NAFLD.

APC-Cdh1 Inhibits the Proliferation and Activation of Oligodendrocyte Precursor Cells after Mechanical Stretch Injury.

The incidence of spinal cord injury (SCI) continues to increase; however, the involved mechanisms remain unclear. Anaphase promoting complex (APC) and its regulatory subunit Cdh1 play important roles in the growth, development, and repair of the central nervous system (CNS). Cdh1 is involved in the pathophysiological processes of neuronal apoptosis and astrocyte-reactive proliferation after ischemic brain injury, whereas the role played by APC-Cdh1 in the proliferation and activation of oligodendrocyte precursor cells (OPCs) after SCI remains unresolved. Using primary cultures of spinal oligodendrocyte precursor cells, we successfully established an in vitro mechanical stretch injury model to simulate SCI. Cell viability and proliferation were determined by MTT assay and flow cytometric analysis of the cell cycle. Real-time fluorescent quantitative PCR and Western blot analysis determined the mRNA and protein expression levels of Cdh1 and its downstream substrates Skp2 and Id2. Mechanical stretch injury decreased the proliferative activity of OPCs and enhanced cellular Cdh1 expression. Dampened expression of Cdh1 in primary OPCs significantly promoted proliferation and activation of OPCs after SCI. In addition, the expression of the downstream substrates of Cdh1, Skp2, and Id2 was decreased following mechanical injury, whereas adenovirus-mediated Cdh1 RNA interference increased postinjury expression of Skp2 and Id2. These findings suggest that APC-Cdh1 might be involved in regulating the proliferation and activation of OPCs after mechanical SCI. Moreover, degraded ubiquitination of the downstream substrates Skp2 and Id2 might play an important role, at least in part, in the beneficial effects of OPCs activity following SCI.