The application of artificial intelligence(AI)in the medical field, particularly for predicting, diagnosing and treating retinal detachment(RD), has made remarkable achievements. This paper reviews the advancements in AI applications for RD across multiple dimensions, including predicting RD incidence, assessing surgical success rates, forecasting postoperative visual outcomes, and evaluating recurrence rates. In diagnostic support, AI technology has demonstrated significant value, especially in ophthalmic imaging, with applications in the intelligent analysis of ultra-wide-angle fundus photography, optical coherence tomography(OCT), ophthalmologic ultrasound images, and AI chatbots models. Furthermore, AI has proven uniquely beneficial in surgical decision-making, robotic-assisted surgical systems, and the assessment of surgical complications. This paper provides a comprehensive overview of the current state of AI applications in RD, underscoring its potential to address numerous challenges in clinical practice. It also explores existing limitations and offers insights into future directions for development in this field.

The application of artificial intelligence(AI)in the medical field, particularly for predicting, diagnosing and treating retinal detachment(RD), has made remarkable achievements. This paper reviews the advancements in AI applications for RD across multiple dimensions, including predicting RD incidence, assessing surgical success rates, forecasting postoperative visual outcomes, and evaluating recurrence rates. In diagnostic support, AI technology has demonstrated significant value, especially in ophthalmic imaging, with applications in the intelligent analysis of ultra-wide-angle fundus photography, optical coherence tomography(OCT), ophthalmologic ultrasound images, and AI chatbots models. Furthermore, AI has proven uniquely beneficial in surgical decision-making, robotic-assisted surgical systems, and the assessment of surgical complications. This paper provides a comprehensive overview of the current state of AI applications in RD, underscoring its potential to address numerous challenges in clinical practice. It also explores existing limitations and offers insights into future directions for development in this field.

Objective To evaluate whether Vibrio vulnificus secreted exotoxin-hemolysin (VVH) can activate platelet, an important blood immune cell, and to explore the possible molecular mechanism of platelet activation by VVH. Methods Transcriptomics and immunohistochemistry were used to analyze whether Vibrio vulnificus infection caused platelet activation in mice. Then, flow cytometry was used to identify whether VVH was the main stimulator of platelet activation. Naturally expressed VVH toxin was purified and prepared. The effects of extracellular and intracellular Ca²⁺ signal inhibitors on VVH activated platelets were evaluated by flow cytometry and Western blotting. The immune activation effect of VVH in the early stage of Vibrio vulnificus infection was analyzed in vivo. Results VVH was the main stimulator of platelet activation in Vibrio vulnificus culture supernatant. Natural VVH can induce the increase of P-selectin (CD62P) on platelet surface, the formation of platelet-neutrophil complex (PNC), and the release of platelet microvesicles. The activation mechanism may be related to the VVH pore-dependent Ca²⁺-calmodulin (CaM) -myosin light chain kinase (MLCK) signaling pathway, which led to the release of platelet alpha particles and cascade activation of platelets. In a mouse model of ALD infected by Vibrio vulnificus gavage, VVH was strongly associated with platelet activation. Conclusion This study shows that VVH is an important platelet activating molecule in the early stage of Vibrio vulnificus infection, and its induction of platelet activation may be related to the pathogenic process.
Animals ; Platelet Activation/drug effects* ; Hemolysin Proteins/pharmacology* ; Vibrio vulnificus/metabolism* ; Mice ; Blood Platelets/drug effects* ; Vibrio Infections/immunology* ; P-Selectin/metabolism* ; Bacterial Proteins ; Female

Stresses induced by the deficiency or excess of trace mineral elements, such as manganese (Mn), represent a common limiting factor for the production of crops like Brassica napus. To identify key genes involved in Mn allocation in B. napus and elucidate the underlying mechanisms, a member of the metal tolerance protein (MTP) family obtained in the previous screening of cDNA library of B. napus under Mn stress was selected as the research subject. Based on the sequence information and phylogenetic analysis, it was named as BnMTP10. It belongs to the Mn-cation diffusion facilitator (CDF) subfamily. Expression of BnMTP10 in yeast significantly improved the tolerance of transformants to excessive Mn and iron (Fe) and reduced the accumulation of Mn and Fe. However, the yeast transformants exhibited no significant changes in tolerance to excess cadmium, boron, aluminum, zinc, or copper. The qRT-PCR results demonstrated that the flowers of B. napus had the highest expression of BnMTP10, followed by roots and leaves. Subcellular localization studies revealed that BnMTP10 was localized in the endoplasmic reticulum (ER). Compared with wild-type plants, transgenic Arabidopsis overexpressing BnMTP10 exhibited enhanced tolerance to excessive Mn stress but showed no significant difference under Fe stress. Correspondingly, under excessive Mn stress, the Mn content in the roots of transgenic Arabidopsis increased significantly. However, under excessive Fe stress, the Fe content in transgenic Arabidopsis did not alter significantly. According to the results, we hypothesize that BnMTP10 may alleviate excessive Mn stress in plants by mediating Mn transport to the ER. This study facilitated our understanding of efficient mineral nutrients, and provided theoretical foundations and gene resources for breeding B. napus.
Brassica napus/genetics* ; Manganese/metabolism* ; Plants, Genetically Modified/genetics* ; Plant Proteins/physiology* ; Arabidopsis/metabolism* ; Gene Expression Regulation, Plant ; Phylogeny ; Cation Transport Proteins/metabolism* ; Stress, Physiological

Objective To explore the clinical significance of miR-423-5p in ischemic stroke and its effects on SH-SY5Y cell apoptosis along with the underlying mechanisms.Methods Plasma samples were collected from three stroke-prone patients who subsequently developed acute ischemic stroke(AIS)within 24 hours.High-throughput sequencing was used to identify miR-423-5p as a key target.Venous blood samples were collected from 46 AIS pa-tients within 24 hours of onset and from 46 matched control cases.RT-qPCR was performed to measure the plasma expression of miR-423-5p in both groups.The diagnostic value of miR-423-5p for AIS was evaluated using receiver operating characteristic(ROC)curve.After overexpression and knockdown of miR-423-5p in SH-SY5Y cells,flow cytometry was performed to detect apoptosis in each group to analyze the potential relationship between miR-423-5p and SH-SY5Y cell apoptosis.Western blot was used to measure changes in the expression level of the ap-optotic protein cleaved caspase-3 and the anti-apoptotic proteins Bcl-2 and Bcl-xL.Results The expression of miR-423-5p in 3 AIS patients showed significant difference before and after onset.Plasma miR-423-5p expression was significantly elevated in AIS patients versus controls(P＜0.001).ROC analysis indicated its strong diagnostic potential for AIS.Overexpression of miR-423-5p increased the apoptosis rate and cleaved caspase-3 ex-pression of SH-SY5Y cells after OGD/R,and decreased the expression of Bcl-2 and Bcl-xL,while knocking down miR-423-5p had the opposite effect.Conclusions The expression of miR-423-5p is upregulated in the plasma of patients with ischemic stroke compared to healthy controls.Furthermore,miR-423-5p promotes OGD/R-induced apoptosis in SH-SY5Y cells by increasing the level of cleaved caspase-3 and suppressing the expression of Bcl-2 and Bcl-xL.

Objective To investigate the effect of glycine N-methyl transferase (GNMT)on intrauterine adhesion (IUA)fibrosis and its related mechanism.Methods In vivo experiment:A total of 36 healthy female SD rats (SPF grade,6～8 weeks old and weighing from 180～220 g)were subjected in this study.IUA model of SD rats and IUA model of GNMT overexpressed rats were established.RT-qPCR and immunofluorescence assay were applied to detect GNMT expression level in normal uterus and model group.RT-qPCR and Western blotting were used to detect the mRNA and protein levels of fibrosis-related molecules and the activation of TGF-β1/Smad3 signaling pathway in each group.The number of endometrial glands in each group was observed by HE staining.Masson staining was used to analyze the severity of endometrial fibrosis in each group.In vitro experiment:transformed human endometrial stromal cells (THESCs)fibrotic phenotype model was constructed using TGF-β1,and THESCs stably transfected with GNMT overexpression lentvirus were treated with TGF-β1.RT-qPCR and Western blotting were used to detect the mRNA and protein expression of fibrosis-related molecules.The expression of TGF-β1/Smad3 signaling pathway was detected by Western blotting.TGF-β1/Smad3 signaling pathway was activated by TGF-β1/Smad signaling pathway activator (SRI-011381),and the expression of TGF-β1/Smad3 signaling pathway and key molecular proteins of fibrosis phenotype was measured with Western blotting.Results In vivo experiment,the mRNA and protein expression levels of GNMT were significantly decreased in the IUA rats than the control rats (P<0.05).Overexpression of GNMT decreased the mRNA and protein levels of fibrosis related molecules,Collagen Ⅰ,Collagen Ⅲ and FN in the IUA rats (P<0.05),and decreased the phosphorylation levels of TGF-β1 and its downstream Smad3 protein (P<0.05).HE and Masson staining showed that overexpression of GNMT could increase the number of endometrial glands and reduce the severity of fibrosis in the IUA rats (P<0.05).In vitro experiments:overexpression of GNMT decreased the mRNA and protein levels of Collagen Ⅰ,Collagen Ⅲ and FN associated with fibrotic phenotype of THESCs (P<0.05),and reduced the phosphorylation level of Smad3 protein,downstream of TGF-β1 (P<0.05).After activation of TGF-β1/Smad3 signaling pathway,the protein levels of TGF-β1/Smad3 signaling pathway and downstream fibrosis phenotype molecules,Collagen Ⅲ and FN,were significantly decreased in the LV-GNMT+SRI-011381 group.Conclusion Overexpression of GNMT can inhibit endometrial fibrosis by regulating TGF-β1/Smad3 signaling pathway,thus achieving therapeutic effect on IUA.

Objective:To investigate the interaction of platelet factor 4(PF4)with tumor necrosis factor-α(TNF-α)in the pathoge-nesis of chronic periodontitis(Ⅲ-C).Methods:22 patients with chronic periodontitis(Ⅲ-C)and 22 subjects with periodontal health were recruited.Before and after periodontal treatment,the concentration of PF4 and TNF-α in gingival crevicular fluid(GCF)and ser-um,the amount of PF4 released by platelets after lipopolysaccharide(LPS)stimulated peripheral blood platelets were measured by ELISA.Flow cytometry was used to calculate the number of platelets in GCF before and after treatment.Results:The concentrations of PF4 and TNF-α in the GCF and serum of the patients were higher than those in the periodontal healthy group(P＜0.05).After treat-ment,the concentrations of PF4 and TNF-α in the GCF were significantly lower than those before treatment(P＜0.05),and the con-centrations of PF4 and TNF-α in the serum were unchanged(P＞0.05).After LPS stimulation of the platelets in blood before and after treatment,the concentration of PF4 released by the platelets was much higher in the patients than that in the healthy controls(P＜0.01),and the concentration was significantly lower after periodontal treatment than before treatment(P＜0.01).The number of CD41/CD61 double positive platelets and CD45 negative cells in GCF before periodontal treatment were 85 times and 87 times higher than those in periodontal healthy subjects,respectively(P＜0.01).Conclusion:PF4 and TNF-α have synergistic effect in the patho-genesis of chronic periodontitis.

Objective:To compare the efficacy between Kirschner wire and clavicular hook plate in the fixation of distal clavicle fractures in older children.Methods:A retrospective analysis was conducted of the 28 pediatric patients with distal clavicle fracture who had undergone surgical treatment at Department of Pediatric Orthopedics, The Second General Hospital of Fuzhou from December 2014 to December 2023. There were 20 boys and 8 girls. Age: 10.0 (9.0, 12.8) years old; 22 left sides and 6 right sides; by the Craig modified Neer classification: 22 cases of type Ⅱ, 5 cases of type Ⅳ, and 1 case of type Ⅴ. The patients were divided into 2 groups based on their internal fixation methods. The Kirschner wire group of 12 cases were treated with open reduction and Kirschner wire fixation; the hook plate group of 16 cases were treated with open reduction and clavicular hook plate fixation. Operation time, hospital stay, fracture healing time, incidence of complications, and scores at the final follow-up (the Constant-Murley shoulder function score, quick disabilities of the arm, shoulder, and hand (quickDASH) score, and visual analog scale (VAS) for aesthetic satisfaction) were recorded and compared between the 2 groups.Results:There were no statistically significant differences in the baseline data between the 2 groups, indicating comparability ( P>0.05). The postoperative follow-up period for the 28 patients was (14.8±6.5) months. The operation time in the Kirschner wire group [(34.3±12.1) min] was significantly shorter than that in the hook plate group [(49.4±16.8) min] ( P<0.05), and the VAS score for aesthetic satisfaction at the final follow-up in the Kirschner wire group [(8.2±1.1) points] was significantly higher than that in the hook plate group [(6.2±2.6) points] ( P<0.05). There were no statistically significant differences between the 2 groups in terms of fracture healing time, hospital stay, incidence of complications, or Constant-Murley score and quickDASH score at the final follow-up ( P>0.05). Conclusions:For pediatric patients with distal clavicle fracture, both Kirschner wire fixation and clavicular hook plate fixation can achieve good functional outcomes. However, Kirschner wire fixation has advantages of shorter operation time, higher postoperative aesthetic satisfaction, and no need of a secondary surgery for implant removal.

Objective:To explore the high-risk factors for parenteral nutrition associated cholestasis（PNAC）in extremely/ultra-low birth weight infants，and establish a risk Alignment Diagram prediction model.Methods:We retrospectivly analyzed the clinical data of hospitalized extremely/ultra-low birth weight infants admitted to Neonatology Department at Quanzhou Children's Hospital from January 2019 to December 2020，using multivariate Logistic regression analysis to screen for independent risk factors for the occurrence of PNAC.An Alignment Diagram model prediction model for PNAC was constructed by using R software，and the performance of the model was evaluated through receiver operating characteristic curves.Results:A total of 203 extremely/ultra-low birth weight infants were included，with a median gestational age of 29.14（28.00，30.86）weeks and a median birth weight of 1　170（1　000,1　300）g.Among them，26（12.81%）cases developed PNAC.Multivariate Logistic regression analysis showed that the duration of parenteral nutrition（ OR=1.015 ，95% CI 1.003-1.034），the cumulative amount of glucose（ OR=1.014 ，95% CI 1.001-1.028），small for gestational age（ OR=3.455 ，95% CI 1.127-10.589），and neonatal sepsis（ OR=3.142 ，95% CI 1.039-9.503）were independent risk factors for PNAC（ P＜0.05）；The four independent risk factors mentioned above were introduced into R software to construct an Alignment Diagram model，the area under the receiver operating characteristic curve was 0.835（95% CI 0.842-0.731），and the results of the Hosmer Limeshow goodness of fit test show that：χ 2=5.34，degree of freedom=8， P=0.72.A calibration curve indicated good consistency between the predicted probability of the model and the actual occurrence rate，with good accuracy. Conclusion:The Alignment Diagram model constructed based on four independent risk factors of the duration of parenteral nutrition，glucose accumulation，small for gestational age infants，and neonatal sepsis exhibits high predictive ability，and is expected to provide an intuitive and convenient visualization tool for preventing or reducing the occurrence of PNAC in extremely/ultra-low birth weight infants

Objective:To study clinical outcomes, genetic etiology, efficacy and safety of continuous renal replacement therapy (CRRT) for neonatal hyperammonemia.Methods:From September 2016 to June 2023, neonates with hyperammonemia receiving CRRT in NICU of our hospital were retrospectively analyzed. Their perinatal conditions, clinical manifestations, laboratory results, genetic tests, treatments and outcomes were collected. The patients were assigned into survival group and death group according to their conditions at discharge. SPSS 22.0 statistical software was used to analyze the differences between the two groups.Results:A total of 10 patients were enrolled, including 8 males and 2 females. The gestational age was 39.3(38.2,39.8)weeks and birth weight 3 300(3 050, 3 583) g. The age of onset was 2.0(2.0, 4.3) d. The main clinical manifestations included seizures, coma and high blood ammonia level (up to 586-1 250 μmol/L). The patients received CRRT at 3.0(2.0, 8.3) d of age and CRRT lasted for 20.5(16.5, 42.8) h. Before CRRT, average time of coma was 10.0(3.5, 12.8) h and the total duration of coma was 20.5(12.5, 29.0) h. After CRRT, blood ammonia decreased (52.6±22.2) μmol/L every hour for 6 h. The genetic tests showed ornithine transcarbamylase deficiency in 5 cases, methylmalonic acidemia in 2 cases, propionic acidemia in 1 case, carnitine acylcarnitine translocase deficiency in 1 case and transient hyperammonemia in 1 case. 6 patients survived. 4 patients died at discharge, including 2 withdrawal treatment. The duration of coma before CRRT and the total duration of coma in the death group were significantly longer than the survival group ( P<0.05). Conclusions:Inborn metabolic error are common causes of neonatal hyperammonemia. Timely CRRT can safely and effectively reduce blood ammonia levels and may improve clinical outcomes.