Objective:Over the previous decade, fibroblast growth factor 23 (FGF23) has been identified as a key biomarker in the context of cardiovascular diseases(CVD). The primary goal of this investigation was to determine the association between FGF23 and the susceptibility to CVD among children and adolescents. Methods:We performed an electronic search of the Cochrane Library, PubMed, Web of Science, and Embase databases, covering the period from their inception until August 4, 2022. The random effects model was applied. Additionally, we conducted stratified analyses and performed a sensitivity analysis as part of our further investigation. Results:A total of 11 studies involving 1,428 participants, including 366 individuals with cardiovascular disease and 1,062 control subjects, were included in the analysis. Children and adolescents with cardiovascular disease exhibited significantly higher serum FGF-23 levels compared to the control group [standardized mean difference [SMD] = 1.28, 95% confidence interval [CI] 0.53-2.03; I 2 = 93.0%], as determined using a random-effects model. In categorical analyses across six studies, the pooled odds ratio did not demonstrate a statistically significant association with disease risk [odds ratio (OR) = 1.64, 95% CI 0.86-3.12; I 2 = 100.0%]. Meta-regression analysis, accounting for variables such as type of cardiovascular disease, assay type, chronic kidney disease (CKD) status, and CKD stage, yielded a restricted maximum likelihood (REML) estimate of (τ 2 = 0.2321) for the SMD outcome, indicating residual heterogeneity (I 2_res ≈ 70.3%) and an adjusted R2 of 83.6%. The joint test for covariates was not statistically significant (Knapp-Hartung corrected Prob > F = 0.3165). For the categorical outcome, the meta-regression analysis produced a boundary estimate (τ 2 = 0) with I 2_res = 0% and a non-significant joint test (Prob > F = 0.3479); however, these findings are likely influenced by the limited number of studies and restricted degrees of freedom. Conclusion:Serum FGF-23 levels are elevated in pediatric populations with cardiovascular disease, but study-specific thresholds have not shown a clear independent association with risk. The variability in findings, reliance on observational study designs, and differences in assay methods contribute to the uncertainty about its prognostic value. Therefore, standardized prospective studies reporting on renal function and mineral metabolism markers are needed. Systematic Review Registration:https://www.crd.york.ac.uk/PROSPERO/view/CRD42023480899, PROSPERO CRD42023480899.

Osteoarthritis (OA) is characterized by inflammatory and catabolic disruption of cartilage extracellular matrix (ECM) homeostasis. An increased relative abundance of activin receptor-like kinase 1 (ALK1) relative to ALK5, together with altered Smad signaling, has been associated with chondrocyte dysfunction during OA progression. This study examined whether eugenol attenuates IL-1β-induced ECM dysregulation in primary human chondrocytes and whether ALK1/ALK5-associated Smad signaling contributes to this response. Primary human chondrocytes were treated to IL-1β in the presence or absence of eugenol and analyzed using RT-qPCR, Western blotting, immunofluorescence, exploratory RNA sequencing, and siRNA-mediated loss-of-function experiments. Receptor-expression profiles were also assessed in juvenile and aged mouse cartilage and in cartilage from a previously established ACLT cohort. Eugenol attenuated IL-1β-induced decreases in ACAN, COL2A1, and SOX9 expression and reduced IL-1β-induced increases in MMP13, ADAMTS5, COL10A1, RUNX2, and IL-6 immunoreactivity. At the protein level, eugenol increased COL2A1 abundance and reduced MMP13 and ADAMTS5 level. Exploratory pairwise RNA-seq analysis identified IL-1β-responsive genes that were directionally counter-regulated by both eugenol concentrations; these genes were enriched in inflammatory, cell-behavior, and TGF-β/BMP-related pathways. Prolonged IL-1β exposure increased the ALK1/ALK5 protein ratio, primarily because ALK5 declined more markedly than ALK1. Eugenol treatment was associated with a lower ALK1/ALK5 ratio, reduced Smad1/5/9 phosphorylation, and increased Smad2/3 phosphorylation. ALK1 knockdown phenocopied selected eugenol-associated ECM responses, whereas ALK5 knockdown weakened several matrix-restorative and anti-catabolic responses. Computational docking, short molecular-dynamics simulations, and Y279A/H280A mutagenesis provided exploratory observations but did not demonstrate direct eugenol–ALK1 binding. In mouse cartilage, receptor-expression profiles differed between juvenile and aged animals, and eugenol partially normalized ACLT-associated changes in ALK1 and ALK5 immunostaining. These findings indicate that eugenol attenuates IL-1β-induced ECM dysregulation in chondrocytes. Modulation of ALK1/ALK5-associated Smad signaling may contribute to this response; however, direct target engagement and ligand-specific signaling mechanisms remain to be established.

AIM: To explore how vacuolar protein sorting 35 (VPS35) regulates astrocytic inflammation, impairs retinal endothelial function and drives early diabetic retinopathy (DR) neurovascular lesions in diabetic mouse model. METHODS: A streptozotocin (STZ)-induced C57BL/6J diabetic mouse model was established. Retinal tissues were collected from 0 to 12wk after successful induction of diabetes. Protein expression levels of VPS35, glial fibrillary acidic protein (GFAP), excitatory amino acid transporter 2 (EAAT2), leucine-rich repeat kinase 2 (LRRK2), and vascular endothelium-associated proteins were assessed by Western blotting (WB). The interaction between VPS35 and LRRK2 was verified by co-immunoprecipitation. Vascular leakage and astrocyte activation were evaluated by fundus fluorescein angiography and retinal flat-mount immunofluorescence staining. Primary astrocytes were cultured in vitro and subjected to high-glucose stimulation or VPS35 knockdown. Cell activation, expression of glutamate transport-associated proteins, and inflammatory cytokine expression were examined. Supernatant fluid from the primary astrocytes was applied to human umbilical vein endothelial cells (HUVECs) to assess cell migration, proliferation, and tube formation capacity. The expression of proteins related to the nuclear factor kappa-B (NF-κB) pathway was also evaluated. RESULTS: In diabetic mice, retinal VPS35 protein expression exhibited a progressive decline beginning at 4wk post-diabetes onset, whereas GFAP protein expression increased significantly. By 8wk, marked astrocyte activation was observed, accompanied by retinal microvascular leakage and a reduction in vascular area. In vivo and in vitro experiments further confirmed that under high-glucose conditions, retinal VPS35 and EAAT2 protein levels were markedly decreased, while GFAP and LRRK2 protein levels were significantly elevated. Co-immunoprecipitation verified the physical interaction between VPS35 and LRRK2 in astrocytes. Finally, in vitro experiments demonstrated that both high-glucose stimulation and VPS35 knockdown led to astrocyte activation, upregulation of inflammatory cytokine expression, downregulation of EAAT2 and AMPA receptor subunit GLUA2, and upregulation of LRRK2. Treatment of HUVECs with supernatant fluid from these astrocytes enhanced cell migration but significantly inhibited cell proliferation and tube formation. WB analysis revealed markedly increased levels of NF-κB and phosphorylated NF-κB in the treated HUVECs. CONCLUSION: During early DR in mice model, decreased retinal VPS35 protein expression induces astrocyte-mediated inflammatory responses and glutamate transport dysfunction. Through the interaction between VPS35 and LRRK2, paracrine inflammatory cytokines subsequently activate the NF-κB signaling pathway in vascular endothelial cells, leading to endothelial dysfunction and further driving DR-associated neurovascular injury. This study provides novel insights into the pathogenesis of DR and highlights the potential of VPS35 as a target for early intervention in DR.

BackgroundThe management of bone metastases requires careful balancing of therapeutic efficacy against distinct safety profiles. Current understanding of differential adverse event patterns between zoledronic acid and denosumab warrants more sophisticated analytical approaches to identify clinically relevant risk biomarkers and underlying molecular mechanisms.MethodsWe conducted an advanced pharmacovigilance study utilizing the FDA Adverse Event Reporting System (FAERS) database (2004-2024). Our multidimensional analytical framework integrated five established signal detection algorithms (ROR, PRR, BCPNN, MGPS, and MHRA) with comprehensive temporal and demographic stratification to identify clinically relevant safety patterns. Additionally, a network pharmacology approach was employed to explore the molecular mechanisms of zoledronic acid-associated osteonecrosis, involving target prediction, protein-protein interaction (PPI) network construction, and functional enrichment analysis.ResultsAnalysis of 8849 reports revealed distinct toxicity profiles: Denosumab demonstrated significant associations with metabolic complications including hypocalcemia (ROR: 4.32; 95% CI: 3.87-4.82) and osteonecrosis of the jaw, whereas zoledronic acid showed stronger signals for nonjaw osteonecrosis and renal impairment. Temporal analysis revealed significantly earlier onset of adverse events with denosumab (median: 178 days) compared to zoledronic acid (median: 378 days). Network pharmacology identified 271 common targets shared by bone metastasis, zoledronic acid, and osteonecrosis. Subsequent PPI network and module analysis prioritized 76 key genes, with hub genes (e.g., TP53, TNF, IL-6, AKT1, and STAT3) enriched in inflammatory signaling, apoptosis regulation, and pathways such as PI3K-Akt and TNF signaling.ConclusionThis comprehensive safety analysis demonstrates distinct risk architectures for these bone-targeting therapies. The integration of real-world pharmacovigilance with network pharmacology provides data-driven insights for personalized treatment selection and reveals potential molecular mechanisms underlying zoledronic acid-associated osteonecrosis. The identification of key risk-modifying factors, temporal patterns, and candidate molecular pathways enables the development of biomarker-informed monitoring strategies, representing a significant advancement in pharmacovigilance methodology for optimizing safety in cancer patients with bone metastases.

Diabetic retinopathy (DR) is one of the major complications of diabetes and can cause severe visual impairment. Blood-retina barrier (BRB) destruction resulted from chronic hyperglycemia underlines its major pathological process. However, current treatments have limited efficacy and may even cause serious complications. Remote ischemic conditioning (RIC), through repeated transient mechanical occlusion of limb blood vessels, has been confirmed to promote blood-brain barrier integrity after stroke, but its role in BRB disruption has not been elucidated. This study aimed to investigate the protective effects of RIC on the BRB in diabetic rats and its potential mechanisms. 48 Sprague-Dawley rats were randomly assigned to the Sham group, Sham + RIC group, diabetes mellitus (DM) group and DM+RIC group. The diabetic model was successfully induced by intraperitoneal injection of streptozotocin. RIC treatment was administered daily and lasted for 9 weeks. In functional analysis, RIC improved the retinal function based on electroretinogram data and reduced the leakage of BRB in diabetic rats. In proteomic analysis, tight junction pathway was enriched after RIC treatment, in which Patj gene was significantly increased. We also found that RIC increased mRNA levels of Patj, claudin-1 and zonula occludens (ZO)-1, protein expression of claudin-1 when compared with diabetic models. In conclusion, RIC slowed BRB damage in diabetic rats, which may be related to the preservation of tight junction proteins. RIC may be a promising protective strategy for the treatment of DR.

Objective:This study aimed to develop a predictive model for sudden cardiac death (SCD) in children with hypertrophic cardiomyopathy (HCM). Methods:The retrospective study included children diagnosed with HCM who visited Beijing Children's Hospital, Capital Medical University between January 2006 and August 2022. Cox regression analysis was used to identify risk factors for SCD. A nomogram was constructed based on risk factors identified through multivariate analysis. Results:A total of 184 children (115 boys and 69 girls) were included in the study. The median (IQR) age at the initial diagnosis was 4.54 (0.50-10.25) years. Of these, 141 children were diagnosed with primary HCM, while 43 had secondary HCM. The multivariate analysis showed that age <1 year [hazard ratio (HR), 95% confidence interval (CI): 6.232 (2.858-13.591)], female sex [HR: 2.547 (1.460-4.444)], a family history of HCM [HR: 2.622 (1.468-4.683)], pathological Q-waves [HR: 2.290 (1.285-4.082)], fragmented QRS waves [HR: 3.526 (1.786-6.963)], combined arrhythmias (HR: 2.218 [1.136-4.333]), increased interventricular septal thickness [HR: 1.055 (1.008-1.105)], and increased left ventricular posterior wall thickness [HR: 1.060 (1.026-1.096)] were significantly associated with SCD. The nomogram-based SCD prediction model demonstrated strong discriminatory ability, with areas under the curve (AUC) of 0.887 (95% CI: 0.829-0.945) at 1 year, 0.839 (95% CI: 0.777-0.902) at 2 years, 0.847 (95% CI: 0.782-0.912) at 3 years, 0.855 (95% CI: 0.791-0.919) at 4 years, 0.850 (95% CI: 0.789-0.911) at 5 years, and 0.845 (95% CI: 0.763-0.926) at 10 years. Predicted probabilities closely aligned with observed probabilities, indicating good calibration of the model. Conclusion:A predictive model for SCD in children with HCM was developed, demonstrating strong internal consistency and reliability. External validation is recommended before clinical implementation.

AIM: To compare the effects of different types of negative pressure suction on the macular and optic disc retinal vessel density (VD) in myopic patients with different axial lengths (ALs) undergoing femtosecond laser-assisted excimer laser in situ keratomileusis (FS-LASIK) by optical coherence tomography angiography (OCTA). METHODS: A prospective, nonrandomized, controlled study. Participants underwent FS-LASIK surgery were divided into the short AL group (SAL, 22≤AL<26 mm) and the long AL group (LAL, 26≤AL<28 mm) according to the different ALs. Further, the two groups were divided into subgroups according to the corneal flap using VisuMax or WaveLight FS200 femtosecond laser (FS) platform. All patients underwent OCTA before the surgery and 1-day/1-week/1-month after the surgery. ANOVA statistically analyzed data with two-factor repeated measurement in SPSS. RESULTS: Totally 108 participants (108 eyes, 18–35y) were divided into SAL group [22 patients (4 males and 18 females) were treated with VisuMax, and 24 (3 males and 21 females) were treated with WaveLight FS200] and LAL group [34 patients (4 males and 30 females) were treated with VisuMax, and 28 patients (6 males and 22 females) were treated with WaveLight FS200]. In the LAL group, there was no significant difference in macular superficial capillary plexuses vessel density (SCP-VD) in the fovea and perifovea region, but compared with the VisuMax subgroup, SCP-VD in the parafoveal region (t=2.647, P=0.010) and the whole area (t=2.030, P=0.047) in WaveLight FS200 subgroup decreased at one day after the operation and increased to a preoperative level at 1-week and 1-month after operation. There was no significant difference between SCP-VD in the two SAL subgroups, neither of deep capillary plexuses vessel density (DCP-VD) and optic nerve head vessel density (ONH-VD) in the SAL and LAL groups. CONCLUSION: With the increase of AL and suction intensity, a transient decrease of SCP-VD in the macular region is observed at 1d postoperatively during FS-LASIK, and it increases to preoperative level at 1-week and 1-month postoperatively. However, the AL and suction intensity do not affect the macular DCP-VD and ONH-VD.

Cone cell death is a characteristic shared by various retinal degenerative disorders, such as cone-rod dystrophy, Stargardt disease, achromatopsia, and retinitis pigmentosa. This leads to conditions like color blindness and permanently impaired visual acuity. Stem cell therapy focused on photoreceptor replacement holds promise for addressing these conditions. However, identifying surface markers that aid in enriching retinal progenitor cells (RPCs) capable of differentiating into cones remains a complex task. In this study, we employed single-cell RNA sequencing to scrutinize the transcriptome of developing retinas in C57BL/6J mice. This revealed the distinctive expression of somatostatin receptor 2 (Sstr2), a surface protein, in late-stage RPCs exhibiting the potential for photoreceptor differentiation. In vivo lineage tracing experiments verified that Sstr2+ cells within the late embryonic retina gave rise to cones, amacrine and horizontal cells during the developmental process. Furthermore, Sstr2+ cells that were isolated from the late embryonic mouse retina displayed RPC markers and exhibited the capability to differentiate into cones in vitro. Upon subretinal transplantation into both wild-type and retinal degeneration 10 (rd10) mice, Sstr2+ cells survived and expressed cone-specific markers. This study underscores the ability of Sstr2 to enrich late-stage RPCs primed for cone differentiation to a large extent. It proposes the utility of Sstr2 as a biomarker for RPCs capable of generating cones for transplantation purposes.

Retinal ischemia is a significant factor in various vision-threatening diseases, but effective treatments are currently lacking. This study explores the potential of stem cell factor (SCF) in regulating the neurovascular unit as a therapeutic intervention for retinal ischemic diseases. A chronic retinal ischemia model was established in Brown Norway rats using bilateral common carotid artery occlusion (BCCAO). Subsequent SCF treatment resulted in a remarkable recovery of retinal function, as indicated by electroretinogram, light/dark transition test, and optokinetic head tracking test results. Histological examination demonstrated a significant increase in the number of retinal neurons and an overall thickening of the retina. Immunofluorescence confirmed these findings and further demonstrated that SCF treatment regulated retinal remodeling. Notably, SCF treatment ameliorated the disrupted expression of synaptic markers in the control group's BCCAO rats and suppressed the activation of Müller cells and microglia. Retinal whole-mount analysis revealed a significant improvement in the abnormalities in retinal vasculature following SCF treatment. Transcriptome sequencing analysis revealed that SCF-induced transcriptome changes were closely linked to the Wnt7 pathway. Key members of the Wnt7 pathway, exhibited significant upregulation following SCF treatment. These results underscore the protective role of SCF in the neurovascular unit of retinal ischemia rats by modulating the Wnt7 pathway. SCF administration emerges as a promising therapeutic strategy for retinal ischemia-related diseases, offering potential avenues for future clinical interventions.

Purpose: To quantitatively characterize the posterior morphology of high myopia eyes with posterior staphyloma. Methods: Surface points of the eyeball were automatically extracted from magnetic resonance imaging scans using deep learning. Subsequently, the topography of posterior staphylomas was constructed to facilitate accurate visualization and quantification of their location and severity. In the three-dimensional Cartesian coordinate system established with surface points, measurements of distances (D) from each point to the hypothetical pre-elongation eye center within the eyeball and local curvatures (C) at each point on the posterior sclera were computed. Using this data, specific parameters were formulated. The concordance of these parameters with traditional staphyloma classification methods and their association with myopic traction maculopathy (MTM) grades based on the ATN classifications were investigated. Results: The study included 102 eyes from 52 participants. The measured parameters, particularly the variance of distance (Dvar) and the maximum value of the curvature and distance product (C Dmax), demonstrated efficacy in differentiating various types of posterior staphyloma and exhibited strong correlations with the grades of MTM. Conclusions: The automated generation of the posterior scleral topography facilitated visualization and quantification of staphyloma location and severity. Simple geometric parameters can quantify staphyloma shape and correlate well with retinal complications. Future works on expanding these measures to more imaging modalities could improve their clinical use and deepen insights into the link between posterior staphyloma and related retinal diseases.

Purpose: To investigate gender differences in orbital morphology using large MRI datasets. Methods: Using a deep learning-based approach, the orbit and eyeball were automatically segmented from high resolution 3D MRI images of the IXI and OASIS3 datasets. Orbital and eyeball morphological parameters, including orbital volume, eyeball volume, effective orbital volume (EOV, defined as the orbital cavity volume excluding the eyeball), and coronal orbital dimensions and shape, were quantitatively assessed. The volume index was defined as the ratio of orbital volume to eyeball volume. Results: This study included 1926 subjects with a mean age of 63.9 +/- 15.3 years. The mean volumes of the eyeball and orbit were 7.1 +/- 1.0 ml and 25.9 +/- 3.5 ml, respectively. Significant gender differences (all P < 0.001) were observed in the following parameters (males versus females): orbital volume (28.3 +/- 3.0 ml versus 24.0 +/- 2.7 ml), EOV (25.1 +/- 3.0 ml versus 21.1 +/- 2.6 ml), eyeball volume (7.3 +/- 1.0 ml versus 6.9 +/- 1.0 ml), volume index (3.9 +/- 0.6 versus 3.5 +/- 0.5), orbital depth (40.0 +/- 3.1 mm versus 37.4 +/- 2.9 mm), coronal orbital height (40.8 +/- 3.0 mm versus 38.4 +/- 2.4 mm), coronal orbital width (38.0 +/- 1.9 mm versus 36.6 +/- 1.7 mm) and coronal orbital area (1292.5 +/- 97.1 mm(2) versus 1177.9 +/- 89.7 mm(2)). Conclusions: This study employed deep learning to analyze a large dataset of 3D head MRI scans, achieving accurate and objective measurements of orbital morphology. We identified significant gender differences in orbital parameters, with males generally having larger structures. Additionally, we established a normative database for orbital dimensions, providing a valuable resource for future research on orbital disorders and potentially improving clinical diagnosis and treatment.

BackgroundOcular ischemic syndrome (OIS), attributable to chronic hypoperfusion caused by marked carotid stenosis, is one of the important factors that cause ocular neurodegenerative diseases such as optic atrophy. The current study aimed to detect blood flow perfusion in a visual pathway by arterial spin labeling (ASL) and magnetic resonance imaging (MRI) for the differential diagnosis of OIS.MethodsThis diagnostic, cross-sectional study at a single institution was performed to detect blood flow perfusion in a visual pathway based on 3D pseudocontinuous ASL (3D-pCASL) using 3.0T MRI. A total of 91 participants (91 eyes) consisting of 30 eyes with OIS and 61 eyes with noncarotid artery stenosis-related retinal vascular diseases (39 eyes with diabetic retinopathy and 22 eyes with high myopic retinopathy) were consecutively included. Blood flow perfusion values in visual pathways derived from regions of interest in ASL images, including the retinal-choroidal complex, the intraorbital segments of the optic nerve, the tractus optics, and the visual center, were obtained and compared with arm-retinal circulation time and retinal circulation time derived from fundus fluorescein angiography (FFA). Receiver operating characteristic (ROC) curve analyses and the intraclass correlation coefficient (ICC) were performed to evaluate the accuracy and consistency.ResultsPatients with OIS had the lowest blood flow perfusion values in the visual pathway (all p < 0.05). The relative intraorbital segments of optic nerve blood flow values at post-labeling delays (PLDs) of 1.5 s (area under the curve, AUC = 0.832) and the relative retinal–choroidal complex blood flow values at PLDs of 2.5 s (AUC = 0.805) were effective for the differential diagnosis of OIS. The ICC of the blood flow values derived from the retinal–choroidal complex and the intraorbital segments of the optic nerve between the two observers showed satisfactory concordance (all ICC > 0.932, p < 0.001). The adverse reaction rates of ASL and FFA were 2.20 and 3.30%, respectively.Conclusion3D-pCASL showed that the participants with OIS had lower blood flow perfusion values in the visual pathway, which presented satisfactory accuracy, reproducibility, and safety. It is a noninvasive and comprehensive differential diagnostic tool to assess blood flow perfusion in a visual pathway for the differential diagnosis of OIS.

Objective To explore the effect of the application of the ‘Internet+’ nursing teaching mode on the comprehensive teaching ‘Fundamentals of Nursing’. Trial design Parallel design and convenient sampling were used to select vocational nursing students from the Nursing College of Capital Medical University. Methods Selected students were randomly divided into two groups. The control group consisted of 30 students in Grade 2020 higher vocational nursing education (traditional teaching mode). The observation group consisted of 30 students in Grade 2021 higher vocational nursing education (Internet+ mixed teaching mode). Training assessment results, automatic learning ability, professional identity, and satisfaction were compared between the two groups. Results Compared with the control group, the students in the observation group scored higher in the following operation practices: venous blood sampling, intradermal injection, cardiopulmonary resuscitation (CPR), sputum aspiration, and putting on and taking off robes (84.01 ± 0.87 vs. 92.14 ± 1.23; 91.41 ± 0.82 vs. 96.86 ± 0.27; 87.56 ± 0.31 vs. 93.91 ± 2.79; 88.11 ± 0.51 vs. 93.75 ± 0.29; and 82.29 ± 0.29 vs. 90.96 ± 0.34, respectively, with p < 0.05 for all scores). The total scores for autonomous learning ability and subjective satisfaction were also higher in the observation group compared with the control group (82.98 ± 4.72 vs. 93.17 ± 5.01 and 96.67% vs. 90.00%, respectively, with p < 0.05 for all scores). Conclusion In the post-epidemic era, the ‘Internet+ hybrid teaching mode’ was applied to comprehensive nursing teaching. This changed the traditional education mode, which focuses only on professional knowledge. The ‘Internet+’ teaching mode results showed that the professional, ideological, and political courses exhibited the same value guidance, which improved students’ independent learning ability, practical operation ability, professional identity, and satisfaction.

OPINION article Front. Med., 25 April 2023Sec. Healthcare Professions Education Volume 10 - 2023 | https://doi.org/10.3389/fmed.2023.1174677

目的 探讨不同类型高度近视视网膜劈裂患者脉络膜特征及临床意义.方法 采用横断面研究.2019 年 1 月至 2022年 3 月于首都医科大学附属北京友谊医院眼科就诊的患者中,选取根据黄斑病变萎缩-牵拉-新生血管(atrophic,tractional,neovascular components,ATN)分型符合T0～T3 级高度近视患者 74 例 74 只眼纳入研究.其中,男性 20 例 20 只眼、女性 54例 54 只眼;平均年龄(64.3±11.2)岁;眼轴长度(axial length,AL)(29.2±2.78)mm.患者均行加强深度成像模式光学相干断层扫描.依据ATN分型将患者按照病变程度分为T0～T3 级,分别为 20、23、18、13 只眼.获取黄斑中心凹多个部位脉络膜厚度数据,采用MATLAB软件计算该区域的脉络膜容积(macular choroidal volume,MCV).参数间行相关性分析.组间差异比较采用单因素分析和多因素分析.结果 T0～T3组患者MCV分别为(4.6±2.3)mm3、(3.1±1.2)mm3、(2.9±1.3)mm3、(2.1±1.1)mm3,差异有统计学意义(P=0.006).与T0 组患者相比,T1～T3 组患者最佳矫正视力明显下降,AL和等效球镜绝对值明显增加,黄斑中心凹下脉络膜厚度(subfoveal choroidal thickness,SFCT)明显下降,差异均有统计学意义(P＜0.05).T1 与T3组间及T2 与T3 组间等效球镜的差异,以及T1 与T2 组间及T1 与T3 组间SFCT和MCV的差异依赖AL和年龄,T2 和T3 组间SFCT和MCV的差异不依赖AL和年龄.结论 高度近视患者随着视网膜劈裂程度加重,MCV逐步下降,MCV的变化受到AL、年龄等多种因素影响.

ObjectiveTo construct risk factors assessment table of intensive care unit⁃acquired weakness，in order to provide basis for the establishment of risk assessment tools for acquired weakness.MethodsLiterature review and group discussion were used to screen the risk factors of intensive care unit⁃acquired weakness，and the risk factors assessment table was formed by Delphi method.ResultsThere were two rounds of expert consultation.The expert positivity coefficient of 2 rounds of expert letter questionnaires were 100.00% and 95.65%.The expert authority coefficients were 0.91 and 0.93.And Kendall coordination coefficients were 0.43 and 0.49，respectively（P<0.001）.The final constructed risk factors assessment table of intensive care unit⁃acquired weakness included 7 dimensions with a total of 45 items.The S⁃CVI was 0.86.The average score of the dimensions ranged from 4.28 to 4.90，and the coefficient of variation ranged from 0.06 to 0.18.The average score of item importance ranged from 3.80 to 5.00，and the coefficient of variation ranged from 0.00 to 0.29.ConclusionsThe risk factors assessment table of intensive care unit⁃acquired weakness was scientific and practical，which can provide tool for the risk identification of acquired frailty in critically ill patients.

C-kit/CD117, expressed in a series of tissue-specific progenitor cells, plays an important role in tissue regeneration and tissue homeostasis. We previously demonstrated that organoid-derived c-kit+ retinal progenitor cells can facilitate the restoration of degenerated retina. Meanwhile, we have identified a population of endogenous c-kit+ cells in retinas of adult mouse. However, the exact role of these cells in retinal degeneration remains unclear. Here, we demonstrated that stimulation of endogenous c-kit+ cells by stem cell factor (SCF) conferred protection against retinal degeneration. Retinal degeneration was induced by intravitreal injection of N-methyl-D-aspartate (NMDA). NMDA challenge increased the total number of c-kit+ cells in the retinal ganglion cell layer (GCL), while deregulated the protein level of SCF, which was mainly expressed in Müller cells. Both flash electroretinogram (fERG) and light/dark transition tests showed that intravitreal injection of SCF effectively improved the visual function of NMDA-treated mice. Mechanistically, SCF administration not only prevented the loss of retinal ganglion cells (RGCs), but also maintained the function of RGCs as quantified by fERG. Further, we performed transcriptome sequencing analysis of the retinal cells isolated from SCF-treated mice and the parallel control. Gene Ontology analysis showed that SCF-induced transcriptome changes were closely correlated with eye development-related pathways. Crystallins and several protective factors such as Pitx3 were significantly upregulated by SCF treatment. Our results revealed the role of SCF stimulated c-kit+ cells in the protection of RGCs in NMDA-treated mice, via inhibiting the loss of RGCs. Administration of SCF can act as a potent strategy for treating retinal degeneration-related diseases.

Introduction To compare the efficacy and safety of non-steroidal anti-inflammatory drugs (NSAID), corticosteroid (CS), and a combination of both drugs to prevent cystoid macular edema (CME) after cataract surgery. Methods We searched Pubmed, Cochrane Library, and Embase electronic databases to assess the relevant randomized controlled trials (RCTs) up to 28 April 2021. Network meta-analysis was registered on PROSPERO (CRD42020182520). Results Twenty-four RCTs were included in this review. The NSAID and combination of both drugs were significantly reduced the risk of developing CME than CS alone in non-diabetics and mix populations. In the ranking profiles, the combination therapy showed a significant advantage over the single drugs and was less likely to develop CME. Diclofenac was the most likely to reduce the odds of developing CME compared with bromfenac and nepafenac. Dexamethasone was the most likely to reduce the odds of developing CME compared with betamethasone and fluorometholone. Conclusion NSAID combination with CS has significantly reduced the risk of developing CME postoperatively than the single drug. Diclofenac was superior to bromfenac and nepafenac in preventing CME. Dexamethasone was superior to betamethasone and fluorometholone in preventing CME.