Search

Background: Plyometric training is an effective training method to improve explosive strength. However, the ability to perform plyometric training in the adolescent population is still controversial, with insufficient meta-analyses about plyometric training on lower limb explosive strength in adolescent athletes. Objective: To investigate the influence of plyometric training on the explosive strength of lower limbs in adolescent athletes. Methods: We performed a search of six databases (Web of Science, PubMed, Scopus, ProQuest databases, China National Knowledge Infrastructure (CNKI), and Wan-fang database) from the starting year of inclusion in each database to April 4, 2022. The quality of the included literature was assessed using the Cochrane risk assessment tool, and data were analyzed using the Review Manager 5.4 software. Result: Plyometric training had significant effects on the performance of adolescent athletes in countermovement jump (MD = 2.74, 95% CI: 1.62, 3.85, p < 0.01), squat jump (MD = 4.37, 95% CI: 2.85, 5.90, p < 0.01), standing long jump (MD = 6.50, 95% CI: 4.62, 8.38, p < 0.01), 10-m sprint (MD = −0.04, 95% CI: −0.08, −0.00, p = 0.03), and 20-m sprint (MD = −0.12, 95% CI: −0.20, −0.04, p = 0.03); all had positive and statistically significant effects (p < 0.05). Conclusion: Plyometric training can significantly enhance the explosive strength of lower limbs in adolescent athletes.

Under the background of digital finance, this paper uses Stata to empirically study the impact of digital transformation on the profitability of commercial banks. This study examines how digital transformation affects the profitability of commercial banks by developing a fixed effect regression model using data from 16 Chinese listed commercial banks from 2012 to 2021 as research samples. Furthermore, the heterogeneity analysis is conducted to investigate the difference of the impact of digital transformation of different types of commercial banks on profitability. The research results show that digital transformation significantly increases the profitability of commercial banks. The digital transformation of large state-owned commercial banks cannot significantly improve their profitability, while the digital transformation of joint-stock commercial banks and urban commercial banks can significantly improve their profitability. Finally, based on the research results, suggestions are made for commercial banks and financial regulators.

The selective transport of ions in nanopores attracts broad interest due to their potential applications in chemical separation, ion filtration, seawater desalination, and energy conversion. The ion selectivity based on the ion dehydration and steric hindrance is still limited by the very similar diameter between different hydrated ions. The selectivity can only separate specific ion species, lacking a general separation effect. Herein, we report the highly ionic selective transport in charged nanopore through the combination of hydraulic pressure and electric field. Based on the coupled Poisson–Nernst–Planck (PNP) and Navier–Stokes (NS) equations, the calculation results suggest that the coupling of hydraulic pressure and electric field can significantly enhance the ion selectivity compared to the results under the single driven force of hydraulic pressure or electric field. Different from the material-property-based ion selective transport, this method endows the general separation effect between different kinds of ions. Through the appropriate combination of hydraulic pressure and electric field, an extremely high selectivity ratio can be achieved. Further in-depth analysis reveals the influence of nanopore diameter, surface charge density and ionic strength on the selectivity ratio. These findings provide a potential route for high-performance ionic selective transport and separation in nanofluidic systems.

Introduction: Oral diseases including periodontitis, periapical periodontitis, and peri-implantitis are characterized by inflammation and loss of alveolar bone. Signal transducer and activator of transcription 3 (Stat3) involved in bone formation and maintenance. This study aimed to investigate the effect of Stat3 on the osteoblast-mediated bone remodeling in the inflammatory lesion.Methods: The conditional knockout of Stat3 in osteoblasts (Stat3 CKO) was generated via the Cre-loxP recombination system using Osterix-Cre (Osx-Cre) transgenic mice. The lipopolysaccharide (LPS)-induced calvarial bone inflammatory lesions were harvested at day 3, 7 and 14 for micro-CT scanning, histological staining, quantitative real-time PCR (qRT-PCR) and western blot to assess the bone remodeling. Osteoblasts were harvested from Stat3 CKO and wildtype mice and were cultured in vitro. In response to LPS-stimulation, the cells were subjected to alizarin red staining, qRT-PCR and western blot to examine the formation of calcium deposit, the expression of osteogenic markers (i.e. Runx2, OPN, COL1A1) and osteoclast-related markers (i.e. RANKL, OPG). The EdU and transwell assays were performed to assess the proliferation and migration of the cells.Results: Compared with the wildtype control, a decrease of bone mass and an increase of osteolysis were found in the inflammatory lesions on Stat3 CKO mice. More osteoclastic-like cells, as well as an increased expression of RANKL, were observed in the lesions on Stat3 CKO mice. Both mRNA and protein expressions of Stat3 and osteogenic markers in the lesions was significantly decreased on Stat3 CKO mice. After co-cultured with osteogenic medium, the Stat3-deficient osteoblasts were found with a significant decrease of calcium deposits and the expression of osteogenic markers, and with a significant increased expression of RANKL, when compared with the control osteoblasts. The impaired ossification of Stat3-deficient osteoblasts was even more pronounced with the presence of LPS in vitro. According to the EdU and transwell assays, the most decrease of cell proliferation and migration was found in Stat3-deficient osteoblasts in response to LPS. Conclusions: Loss of Stat3 in osteoblasts impaired bone regeneration in inflammatory microenvironment, which might be resulted from the effect of Stat3 on the ossification, activation of osteoclast activationic signals, proliferation and migration of osteoblasts.

This case report describes an uncommon artifact of ultrawide-field imaging derived from a large pterygium, which mimicked an intraocular tumor.

Activation of microglia and inflammation-mediated vascular damages are suggested to play a decisive role in the pathogenesis of various retinopathies. The inducible nitric oxide synthase (iNOS) was required for activated microglia-mediated injuries. However, the induction mechanism of microglia activation during retinal vascular diseases is still elusive. Here we showed that IL-17 induced microglia activation with high expression of iNOS and promoted the development of retinal vascular diseases. IL-17-dependent activation of the STAT3-iNOS pathway was essentially required for microglia activation, which promoted endothelial cell growth and accelerated vascular leakage and leukostasis via IL-6 in vitro and in vivo. Taken together, our data provide novel mechanistic insights on microglia activation-mediated retinopathy, unveil the specific role of IL-17 on microglia, and define novel therapeutic targets for treating retinal vascular diseases.

Purpose To compare slit-lamp microscopy teaching outcomes with digital camera real-time display and conventional teaching tube in undergraduate education of clinical ophthalmology. Methods Thirty-seven Year 4 medical students were assigned to two groups for slit lamp microscopy teaching with digital camera real-time display (n = 18) and teaching tube (n = 19). The outcome measures included a 5-item questionnaire on their experience and the quality of slit lamp photos taken by the students. Results The overall satisfaction score was significantly higher in the group of digital camera real-time display compared with the group of teaching tube (4.5 ± 0.5 vs. 4.2 ± 0.7, P = .013). The former group also achieved higher quality score of the slit-lamp photography (4.1 ± 0.3 vs. 3.6 ± 0.5, P = .002). Conclusions The digital camera real-time display attachment is more effective in undergraduate ophthalmic education over conventional slit-lamp teaching tube. It is also more favored by students and is thus highly recommended for clinical ophthalmology education.

Recent deep convolution-based stereo matching methods have shown significant progress. However, most state-of-the-art models achieve high accuracy by using 3D convolutions during cost aggregation, which come with more floating-point computations and makes it difficult for deployment in real-time applications. In this paper, we propose an effective and efficient multi-scale aggregation module (without 3D convolution) to build our fast Multi-Scale Residual Fusion Network (MSRFNet). Three lightweight components are involved in our aggregation module: combination block, attention block, and residual fusion block. The combination block combines features with different receptive fields and the attention block emphasizes salient regions in various cost volumes. The residual fusion module focuses on extracting the differences between adjacent cost volumes, using progressively residual aggregation instead of simply stacking or adding. Extensive experiments on Scene Flow and KITTI benchmarks demonstrate that our method achieves competitive accuracy com-pared with state-of-the-art methods while running at 56ms.

Purpose To investigate the incidence and impact factors of intraoperative loss of light perception (LP) under sub-Tenon’s anesthesia in patients with macular diseases. Methods Eighty-five consecutive patients received standard phacoemulsification combined pars plana vitrectomy (PPV) under sub-Tenon’s anesthesia. At several checkpoints during the surgery (the end of phacoemulsification, the end of vitrectomy, and the end of surgery), participants were interviewed about whether they had LP or not after removing the influence of contralateral eye and the photo-bleaching effect. In patients treated with retinal photocoagulation, visual experience on laser flashes was evaluated. Results Under routine draping, no patients reported loss of LP at all the checkpoints. When the contralateral eye was tightly covered, the rates of LP loss were 84.7%, 97.6%, and 87.1% at the end of phacoemulsification, the end of vitrectomy, and the end of surgery, respectively. When the photo-bleaching effect was also removed, the rates of LP loss were 61.2%, 82.4%, and 56.5% at each checkpoint, respectively, and there were 87.1% (74/85) of patients reporting visual loss in at least one checkpoint. In addition, 76.9% (50/65) of patients could not feel laser flashes during retinal photocoagulation. Conclusion Intraoperative loss of LP under sub-Tenon’s anesthesia was a relatively common and reversible event. The conduction block of optic nerve by anesthetic mainly contributed to the visual loss during surgery. Photo-bleaching effect also has some effect on the LP evaluation. Surgeons need to inform and counsel the patients about the intraoperative loss of LP, to prevent any sudden panic attacks in them.

Nowadays, CNN-based stereo matching methods achieved remarkable performance, and how to efficiently exploit contextual information in cost aggregation stage is the key to improve performance. In this paper, we propose a simple yet efficient network named Hierarchical Context Guided Aggregation Network (HCGANet). Specifically, a novel cost aggregation module is developed to replace widely used 3D convolutions. Firstly, we construct pyramid cost volumes which carry multi-level distinctive and discriminative representation. Additionally, an intra-level aggregation module is presented for single-level regularization and contextual information learning. Moreover, we develop an inter-level aggregation module to hierarchically regularize cost volumes via the guidance from coarser scales. The proposed aggregation module is lightweight and complementary, further improving the robustness and performance of disparity estimation. Extensive experiments demonstrate that the proposed method achieves superior results for both efficiency and accuracy on Scene-Flow and KITTI benchmarks.

Significance Retinopathy is the leading cause of blindness, and development of effective therapy is urgently needed. Here, we defined an unprecedented subgroup of microglia that is responsible for causing retinopathy under hypoxia. Mechanistic studies demonstrated the signaling pathway of hypoxia-induced necroptosis of retinal microglia, i.e., the hypoxia–RIP1–RIP3–MLKL signaling axis, triggered an explosive release of FGF2, which in its turn to induce retinal neovascularization. Simultaneous targeting of necroptosis–FGF2 pathway and VEGF produces synergistic effects for treating retinopathy. On the basis of our findings, we propose a concept of necroptotic microglia-induced retinal angiogenesis and highlight a combination therapy for effective treatment of retinopathy., Retinal neovascularization is a leading cause of severe visual loss in humans, and molecular mechanisms of microglial activation-driven angiogenesis remain unknown. Using single-cell RNA sequencing, we identified a subpopulation of microglia named sMG2, which highly expressed necroptosis-related genes Rip3 and Mlkl. Genetic and pharmacological loss of function demonstrated that hypoxia-induced microglial activation committed to necroptosis through the RIP1/RIP3-mediated pathway. Specific deletion of Rip3 gene in microglia markedly decreased retinal neovascularization. Furthermore, hypoxia induced explosive release of abundant FGF2 in microglia through RIP3-mediated necroptosis. Importantly, blocking signaling components of the microglia necropotosis–FGF2 axis largely ablated retinal angiogenesis and combination therapy with simultaneously blocking VEGF produced synergistic antiangiogenic effects. Together, our data demonstrate that targeting the microglia necroptosis axis is an antiangiogenesis therapy for retinal neovascular diseases.

The frequency and intensity of heat waves (HWs) has increased in subtropical regions in recent years. The mechanism underlying the HW response of subtropical trees remains unclear. In this study, we conducted an experiment with broad-leaved Schima superba (S. superba) and coniferous Cunninghamia lanceolata (C. lanceolata) seedlings to examine HW (5-day long) effects on stem water transport, leaf water use efficiency (WUE), morphology and growth, and to elucidate differences in the responses of both species. Our results indicated that HWs can significantly reduce hydraulic conductivity in both species. C. lanceolata experienced significant xylem embolism, with the percentage loss of conductivity (PLC) increasing by 40%, while S. superba showed a non-significant increase in PLC (+25%). Furthermore, HW also caused a reduction in photosynthesis rates (An), but transpiration rates (Tr) increased on the 5th day of the HW, together leading to a significant decrease in leaf WUE. From diurnal dynamics, we observed that the HW caused significant decrease of S. superba An only in the morning, but nearly the all day for C. lanceolata. During the morning, with a high vapor pressure deficit (VPD) environment, the HW increased Tr, which contributed a lot to latently cooling the foliage. In comparing the two tree species, we found that HW effects on S. superba were mostly short-term, with leaf senescence but limited or no xylem embolism. The surviving S. superba recovered rapidly, forming new branches and leaves, aided by their extensive root systems. For C. lanceolata, continued seedling growth initially but with subsequent xylem embolism and withering of shoots, led to stunted recovery and regrowth. In conclusion, apart from the direct thermal impacts caused by HW, drought stress was the main cause of significant negative effects on plant water transport and the photosynthetic system. Furthermore, S. superba and C. lanceolata showed clearly different responses to HW, which implies that the response mechanisms of broad-leaved and coniferous tree species to climate change can differ.

Background Receptor tyrosine kinase-like orphan receptor 2 (Ror2) plays a key role in bone formation, but its signaling pathway is not completely understood. Signal transducer and activator of transcription 3 (Stat3) takes part in maintaining bone homeostasis. The aim of this study is to reveal the role and mechanism of Ror2 in the osteogenic differentiation from mouse bone marrow mesenchymal stem cells (mBMSCs) and to explore the effect of Stat3 on Ror2-mediated osteogenesis. Methods Ror2 CKO mice were generated via the Cre-loxp recombination system using Prrx1-Cre transgenic mice. Quantitative real-time PCR and western blot were performed to assess the expression of Stat3 and osteogenic markers in Ror2-knockdown mBMSCs (mBMSC-sh-Ror2). After being incubated in osteogenic induction medium for 3 weeks, Alizarin Red staining and western blot were used to examine the calcium deposit and osteogenic markers in Stat3 overexpression in mBMSC-sh-Ror2. Results Loss of Ror2 in mesenchymal or osteoblast progenitor cells led to a dwarfism phenotype in vivo. The mRNA expression of osteogenic markers (osteocalcin, osteopontin (OPN), and collagen I) in the ulna proximal epiphysis of Ror2 CKO mice was significantly decreased (P P Conclusions Ror2 was essential for skeleton development by regulating mBMSCs’ osteogenesis and osteoblast differentiation. Loss of Ror2 may impair the osteogenesis of mBMSCs by inhibiting Stat3.

Introduction Proliferative vitreoretinopathy (PVR), which is regulated by growth factors and cytokines, is the leading cause of failure in vitreoretinal surgery. In this study, we aimed to investigate the role of the human serum and vitreous inflammation-related factors in the development of proliferative vitreoretinopathy (PVR). Methods Blood and vitreous samples were obtained from patients undergoing pars plana vitrectomy. Inflammation-related factors were detected using an immunology multiplex assay on a Luminex® xMAP® platform. Patients with PVR and rhegmatogenous retinal detachment (RRD) were compared with macular hole (MH) or epiretinal membrane (ERM) patients without any other ocular or systemic disease. Results Thirty-six serum samples and 34 vitreous samples were obtained. Thirty-one different growth factors and cytokines were detected in serum samples. However, none of the circulating growth factors and cytokines were found to be different from the controls. Ten different growth factors and cytokines were measured in the vitreous samples. The concentration levels of PDGF-AA, TGF-α, VEGF, IL-6, IL-8, and TNFβ were found to have significantly increased in the vitreous of PVR patients. Conclusion Our study found that none of the circulating inflammation-related factors were changed in PVR or RRD patients, indicating the absence of a system inflammatory biomarkers to predict the development of proliferative vitreoretinopathy. As a supplement to previous research, the concentrations of PDGF-AA, TGF-α, VEGF, IL-6, IL-8, and TNFβ were significantly upregulated in the vitreous of PVR patients. These factors should be considered for preventing PVR.

Additional file 1: Figure S1. The PCR results of genotyping Ror2 CKO mice. The protocol of genotyping was performed according to the Jackson Lab instructions. Lane 1: blank control (no DNA), Lane 2: negative control (DNA from wild-type mouse), Lane 3: Prrx1-cre; Ror2 c/+, Lane 4: Prrx1-Cre; Ror2 c/c(e.g. Ror2 CKO), Lane 5: Ror2 c/+, Lane 6: Ror2 c/c. Figure S2. The mBMSCs characterizations by flow cytometry.

The prediction of hydrogen generated from fuel cladding by steam oxidation is significant in severe accident analysis. However, the existing methods and models are difficult to make an accurate prediction of hydrogen generation rate for integrated experiments and reactor core under severe accident conditions. In this work, the current models for steam oxidation of zirconium alloy cladding were reviewed by simulating five past CORA severe fuel damage experiments. A modified model based on the best-estimated temperatures of CORA tests was proposed to improve the prediction of hydrogen generation. Then, hydrogen generation rates predicted by different correlations were compared and analyzed. Among the traditional oxidation correlations for temperatures above 1873 K, the original Urbanic-Heidrick correlation is recommended for steam oxidation of zirconium alloy cladding by this work. The modified model also presents a good performance. This paper ends up with discussions about five significant factors on forecasting precision of hydrogen generated by steam oxidation of zirconium alloy cladding. These factors include: 1) temperature prediction, 2) nodalization schema, 3) inherent conservatism, 4) undue conservatism, and 5) time-delay between hydrogen generated and hydrogen gas released. They indicate several deficiencies in current prediction method for hydrogen generated from fuel cladding by steam oxidation.

The irradiation behaviors of crystalline/amorphous ZrC films, prepared by magnetron sputtering, were investigated by the method of 30 keV He+ irradiation combined with an in-situ TEM observation at 573 K. The results indicate that the amorphous-nanocrystalline transformation occurred in amorphous layer, which is mainly attributed to He+ irradiation compared with the phenomenon of in-situ annealing at 593 K. Meanwhile, the nanocrystals in amorphous layer, nucleating and growing near the amorphous/crystalline interface firstly, are independent from pristine crystals in the inner layer. The thermal spike model is suggested to explain the evolution of crystallization. During He+ irradiation, the diffusion of Zr and C interstitials is enhanced by the deposited energy from the electronic energy loss, which contributes to the crystallization of ZrC as the C to Zr elements ratio decreases in the amorphous layer.

The FeCoNiCrTi0.2 high-entropy alloys fabricated by vacuum arc melting method, and the annealed pristine material, are face centered cubic structures with coherent γ’ precipitation. Samples were irradiated with 50 keV He+ ions to a fluence of 2 × 1016 ions/cm2 at 723 K, and an in situ annealing experiment was carried out to monitor the evolution of helium bubbles during heating to 823 and 923 K. The pristine structure of FeCoNiCrTi0.2 samples and the evolution of helium bubbles during in situ annealing were both characterized by transmission electron microscopy. The annealing temperature and annealing time affect the process of helium bubbles evolution and formation. Meanwhile, the grain boundaries act as sinks to accumulate helium bubbles. However, the precipitation phase seems have few effects on the helium bubble evolution, which may be due to the coherent interface and same structure of γ’ precipitation and matrix.

Inflammation has emerged to be a critical mechanism responsible for neural damage and neurodegenerative diseases. Microglia, the resident innate immune cells in retina, are implicated as principal components of the immunological insult to retinal neural cells. The involvement of microglia in retinal inflammation is complex and here we propose for the first time that necroptosis in microglia triggers neuroinflammation and exacerbates retinal neural damage and degeneration. We found microglia experienced receptor-interacting protein kinase 1 (RIP1)- and RIP3-dependent necroptosis not only in the retinal degenerative rd1 mice, but also in the acute retinal neural injury mice. The necroptotic microglia released various pro-inflammatory cytokines and chemokines, such as tumor necrosis factor-α and chemokine (C-C motif) ligand 2, which orchestrated the retinal inflammation. Importantly, necroptosis blockade using necrostatin-1 could suppress microglia-mediated inflammation, rescue retinal degeneration or prevent neural injury in vivo. Meanwhile, cultured microglia underwent RIP1/3-mediated necroptosis and the necroptotic microglia produced large amounts of pro-inflammatory cytokines in response to lipopolysaccharide or oxidative stress in vitro. Mechanically, TLR4 deficiency ameliorated microglia necroptosis with decreased expression levels of machinery molecules RIP1 and RIP3, and suppressed retinal inflammation, suggesting that TLR4 signaling was required in microglia necroptosis-mediated inflammation. Thus, we proposed that microglia experienced necroptosis through TLR4 activation, promoting an inflammatory response that serves to exacerbate considerable neural damage and degeneration. Necroptosis blockade therefore emerged as a novel therapeutic strategy for tempering microglia-mediated neuroinflammation and ameliorating neural injury and neurodegenerative diseases.

Objective To evaluate the apical surgery-related anatomy of two-rooted and three-rooted mandibular first molars (MFMs) in a Mongoloid population. Methods A total of 502 cone-beam computed tomographic images were used to evaluate the root configuration, the distance from the buccal bone to each root, root dimensions, and the complete root resection distance at the resection level for roots of MFMs. Results The prevalence of two-rooted and three-rooted MFMs was 85.1% and 14.9%, respectively. At the resection level, the distance from the buccal bone to the mesial and distal roots of two-rooted MFMs was 2.24 and 3.15 mm, respectively, while the distance was 2.44, 2.01, and 8.55 mm for the mesial, distobuccal, and distolingual roots of three-rooted MFMs, respectively. The distance from the buccal bone to each root was longer in men than in women. The largest distance for complete root resection was detected for the distal root in two-rooted MFMs and for the distolingual root in three-rooted MFMs. Conclusions The prevalence of three-rooted MFMs is common in the Mongoloid population. The distance from the buccal bone to root apex differs according to root configurations and sex. Surgical access to the distolingual root is difficult because of the long access distance.

To verify the correlation between sub-Tenon’s anesthesia and intraoperative visual loss in ophthalmic surgery. Sixty-four patients underwent phacoemulsification combined pars plana vitrectomy under sub-Tenon’s anesthesia. Participants were investigated about their light perception at several time points: before anesthesia, immediately after anesthesia, 10 min after anesthesia without any surgical intervention or microscope illumination, and after the whole surgery. Intraoperative amaurosis was determined as that a patient could not see any light from their operative eye. The incidence rate of amaurosis at different time points and among different anesthetists was analyzed. The rate of intraoperative amaurosis was 0%, 1.56%, 48.44%, and 95.31% at several time points, respectively: before anesthesia, immediately after anesthesia, 10 min after anesthesia without any surgical intervention or microscope light exposure during the interval, and immediately after the whole surgery, presenting a significantly time-dependent increase (P

Purpose Nattokinase (NK), an active ingredient extracted from traditional food Natto, has been studied for prevention and treatment of cardiovascular diseases due to various vasoprotective effects, including fibrinolytic, antihypertensive, anti-atherosclerotic, antiplatelet, and anti-inflammatory activities. Here, we reported an antineovascular effect of NK against experimental retinal neovascularization. Methods The inhibitory effect of NK against retinal neovascularization was evaluated using an oxygen-induced retinopathy murine model. Expressions of Nrf2/HO-1 signaling and glial activation in the NK-treated retinae were measured. We also investigated cell proliferation and migration of human umbilical vein endothelial cells (HUVECs) after NK administration. Results NK treatment significantly attenuated retinal neovascularization in the OIR retinae. Consistently, NK suppressed VEGF-induced cell proliferation and migration in a concentration-dependent manner in cultured vascular endothelial cells. NK ameliorated ischemic retinopathy partially via activating Nrf2/HO-1. In addition, NK orchestrated reactive gliosis and promoted microglial activation toward a reparative phenotype in ischemic retina. Treatment of NK exhibited no cell toxicity or anti-angiogenic effects in the normal retina. Conclusions Our results revealed the anti-angiogenic effect of NK against retinal neovascularization via modulating Nrf2/HO-1, glial activation and neuroinflammation, suggesting a promising alternative treatment strategy for retinal neovascularization.

Background Due to the variety of clinical presentation, some tumors may be concealed and easily misdiagnosed, leading to delays in management. We report a series of patients who initially presented to an Ophthalmic Clinic with ocular symptoms and were subsequently diagnosed with extraocular tumors. Methods Patients who presented to the ophthalmic outpatient clinic at the Joint Shantou International Eye Center with ocular symptoms between April 2013 and December 2019 and were subsequently diagnosed with intracranial or systemic tumors were reviewed retrospectively. Clinical data, including ocular symptoms and signs, ophthalmic and systemic imaging examinations, and the results of tumor biopsies were collected and analyzed. Results Twenty-three patients were included in this study, of which 16 were female (69.6%) and 7 were male (30.4%). Chief complaints at the first visit included visual loss (n=20), proptosis (n=2), and diplopia (n=1). Ocular examination revealed disc pallor (n=8) and swelling (n=3), choroidal mass with or without chorioretinal detachment (n=5), and proptosis (n=2). Visual field (VF) examination was performed in 11 patients of which hemianopia (n=4) and non-specific field loss (n=7) were noted. Brain CT or MRI, together with histopathological findings from surgical biopsies confirmed the diagnosis of the intracranial tumors in 18 cases, including pituitary adenoma (n=7), meningioma (n=2), oligodendroglioma (n=1), sellar tumor (n=1), suprachiasmatic arteriovenous aneurysm (n=1), orbital glioma (n=1), multiple intracranial tumors (n=1), and sphenoid ossifying fibroma (n=1). Nasopharyngeal carcinoma (NPC) (n=3) was diagnosed with brain MRI and nasal endoscopy. Five patients were confirmed as choroidal metastasis secondary to lung cancer (n=3), hepatoma (n=1), and breast cancer (n=1). Conclusions Patients with extraocular tumors may present initially to an ophthalmologist with ocular symptoms. It is important to identify and appropriately manage these patients to avoid unnecessary delays in future treatment.

Purpose To investigate the prevalence of isthmi and middle mesial (MM) canals in the mesial roots of mandibular first molars (MFM) in a Mongoloid subpopulation and to evaluate their association with demographic and anatomic characteristics. Methods Cone-beam computed tomography (CBCT) images of 496 patients with 823 MFMs were selected and analyzed. The following data were collected: patient age and gender, side, presence and distribution of MM canal and isthmus, distance between mesiobuccal (MB) and mesiolingual (ML) orifices, and MB–ML root canal system (RCS) morphology. Logistic regression was used to determine the association between demographic and anatomic characteristics and the presence of isthmi in the apical third. Results The overall prevalence of isthmus and an MM canal in MFM was 64.6% and 10.8%, respectively. The highest prevalence of isthmi and MM canals was found in patients of ≤ 20 and of 41–60 years, respectively (p

Neurodegenerative diseases are a set of disorders characterized by progressive neuronal death and are associated with microglia-mediated neuroinflammation. Recently, neuroinflammation is proposed as a promising therapeutic target for many neurodegenerative diseases. Alpha-1 antitrypsin (AAT) is recognized as a novel immunomodulatory agent in autoimmune diseases and transplantation, however, its impact on neuroinflammation and neurodegeneration remains unknown. This study aims to explore the effects of AAT on microglia-mediated neuroinflammation and retinal degeneration in rd1 mouse model. We found reduced expression of AAT in rd1 retina, and AAT supplement exhibited certain protective effect on retinal degeneration, presenting with increased amount of photoreceptor nuclei, and amplified wave amplitudes in electroretinogram analysis. Of note, AAT shifted microglia phenotype from pro-inflammatory M1 (CD16/CD32+, iNOS+) to anti-inflammatory M2 (CD206+, Arg1+) both in vivo and in vitro, underscoring the concept of immunomodulation on microglia polarization by AAT during neurodegeneration. Furthermore, AAT suppressed the activation of STAT1, promoted the expression of IRF4 while inhibited IRF8 expression, indicating the involvement of these signaling pathways in AAT immunomodulation. Collectively, our data provided evidence for a novel protective role of AAT through immunomodulation on microglia polarization. Attenuating neuroinflammation by AAT may be beneficial to retard neurodegeneration in rd1 mice.

Background/Aims: Platelet-derived growth factors (PDGFs) have emerged as pivotal in pathological angiogenesis, which is a hallmark of various tumors and retinal diseases. Here we evaluated the anti-angiogenic effect of imatinib, an inhibitor of PDGF receptors α and β (PDGFR-α and -β), in retinal neovascularization using an oxygen-induced retinopathy (OIR) model. Methods: The OIR model was established and given imatinib or vehicle treatments daily from P12 to P16. At the peak of angiogenesis at P17, the neovascularization area was quantified on retinal whole-mounts with isolectin B4 staining. Immunofluorescence staining and western blots were used to determine the effect of imatinib on different vascular cells and the pathway molecules involved. Results: Imatinib effectively suppressed pathological angiogenesis in OIR mice and reduced the number of all three types of vascular cells, including endothelial cells, pericytes, and smooth muscle cells. Moreover, the expression and activation of PDGFR-α and -β were inhibited by imatinib. The imatinib-treated OIR mice presented with reduced expression of other potent pro-angiogenic factors such as VEGF and FGF2. No obvious retinal or systemic side effects were observed in the imatinib treatment group. Conclusions: Imatinib appears to be safe and effective in suppressing retinal neovascularization. Targeting PDGFs/PDGFRs may also be important for anti-angiogenic treatment and offer a viable alternative treatment for retinal angiogenic diseases.

Tungsten was irradiated with 400 keV Kr + ions using the IVEM-Tandem Facility at Argonne National Laboratory. The evolution of microstructure and gas bubbles during the irradiation was observed by in situ transmission electron microscopy. Under irradiation, dislocation loops were created and grew into an increased density of network dislocations with increasing Kr + ion fluence. The irradiation induced final microstructure consists of dislocation cells ∼50 nm in diameter separated by dislocation walls. The irradiation also induced formation of Kr gas bubbles with an average diameter of 1.4 nm after 3.0 × 10 16 ions/cm 2 at 525 K. The gas bubbles were observed to grow to 2.6 nm diameter after additional Kr-irradiation of 5.0 × 10 16 ions/cm 2 at 815 K. The relationship between bubble size and irradiation time was obtained from experimental data obtained at 815 K and an empirical formula for calculating Kr bubble size was developed by fitting bubble growth equations with experiment data. The growth mechanisms of Kr gas bubbles in tungsten are discussed.

Blood vessel degeneration is critically involved in nearly all types of degenerative diseases. Therefore strategies to enhance blood vessel protection and survival are highly needed. In this study, using different animal models and cultured cells, we show that PDGF-CC is a potent vascular protective and survival factor. PDGF-CC deficiency by genetic deletion exacerbated blood vessel regression/degeneration in various animal models. Importantly, treatment with PDGF-CC protein not only increased the survival of retinal blood vessels in a model of oxygen-induced blood vessel regression but also markedly rescued retinal and blood vessel degeneration in a disease model of retinitis pigmentosa. Mechanistically, we revealed that heme oxygenase-1 (HMOX1) activity is critically required for the vascular protective/survival effect of PDGF-CC, because blockade of HMOX1 completely abolished the protective effect of PDGF-CC in vitro and in vivo. We further found that both PDGF receptors, PDGFR-β and PDGFR-α, are required for the vasoprotective effect of PDGF-CC. Thus our data show that PDGF-CC plays a pivotal role in maintaining blood vessel survival and may be of therapeutic value in treating various types of degenerative diseases.

Oxide dispersion strengthened (ODS) alloys are considered advanced structural materials for nuclear application due to their radiation tolerance and creep resistance. Ion beam irradiation is used to study the property changes due to displacement damage. In this work 1 dpa displacement damage in an ODS was produced followed by a nanoindentation creep study at temperatures up to 600 °C to evaluate the changes in mechanical properties due to irradiation. Converted yield strength (YS) and creep related parameters are reported.

Vascular degeneration is a critical pathological process in many human degenerative diseases, which need efficient ways to revascularization. However, little is known about cellular and molecular mechanisms that are used during vascular degeneration and revascularization. Here, we show that Toll-like receptor 2 and 4 (TLR2/4) double deficiency suppressed hyperoxia induced retinal vessel regression in an oxygen-induced retinopathy (OIR) model. Notably, the TLR2/4−/− mice experienced more revascularization after reduced vessel regression compared with wild-type mice, accompanied with less activation of glial cells. Mechanistically, TLR2/4 activation can tip the balance between Th17 cells and regulatory T cells towards Th17 cells, a critical source of the IL-17A. Less migration and infiltration of IL-17A-expressing proinflammatory cells but elevated regulatory T cells were observed in OIR-retinae from TLR2/4−/− mice. Coincidentally, TLR2/4 deficiency suppressed IL-17A production and increased expressions of anti-inflammatory genes. Furthermore, IL-17A promoted activation of glial cells. IL-17A blockade using a neutralizing antibody alleviated retinal cell apoptosis and glial activation in C57/B6-OIR mice, demonstrating the important role of IL-17A pathway in glial function during revascularization. Thus TLR2/4-mediated IL-17A inflammatory signaling is involved in vessel degeneration and revascularization, indicating that modulation of the TLR2/4-IL-17A pathway may be a novel therapeutic strategy for degenerative diseases.