Degenerative retinoschisis(RS)is a common peripheral retinal degeneration that typically remains asymptomatic and follows a benign clinical course. However, its morphological resemblance to rhegmatogenous retinal detachment(RRD)presents a diagnostic challenge, as the two conditions demand fundamentally different management and carry distinct prognoses. Precise differentiation is therefore clinically imperative. Recent advances in multimodal imaging have substantially refined the diagnostic accuracy and differential assessment of degenerative RS, establishing spectral-domain optical coherence tomography(SD-OCT)as the definitive reference standard. When the disease progresses to progressive symptomatic schisis-related retinal detachment(PSSRD), prompt surgical intervention, including scleral buckling, pars plana vitrectomy, or a combined approach, is mandated to preserve visual function. Clinical decision-making must be individualized, with the surgical strategy carefully tailored to the specific characteristics of eachcase. This review provides a systematic synthesis of current evidence on the natural history, imaging hallmarks, and surgical management of degenerative RS and its complications, aiming to inform and optimize clinical practice.

Objective:To investigate the impacts of nuclear receptor-interacting protein 1(NRIP1)on sepsis-evoked intesti-nal epithelial injury via transcriptional regulation of high mobility group box 1(HMGB1).Methods:The expression levels of NRIP1 and HMGB1 were detected by RT-qPCR and Western blot.The pathological changes of intestinal tissue were detected by HE staining.CCK-8 assay determined the optimal treatment time of LPS.Caco-2 cells were transfected with NRIP1 small interfering RNA(siRNA-NRIP1-1/2),and cell viability and apoptosis were detected by CCK-8 assay and flow cytometry,respectively.RT-qPCR and Western blot examined the expressions of inflammation-associated factors.Transepithelial resistance(TEER)was used to detect intestinal epi-thelial permeability.Western blot was used to detect the expressions of apoptosis and tight-junction related proteins.The binding rela-tionship between NRIP1 and HMGB1 was verified by luciferase reporting assay and chromatin immunoprecipitation assay(ChIP).After knocking down NRIP1 and overexpressing HMGB1 in LPS-treated Caco-2 cells,the functional experiment was performed again.Results:NRIP1 expression was fortified in the intestinal tissues of sepsis rats and LPS-treated Caco-2 cells.Interference with NRIP1 attenuated LPS-elicited Caco-2 cell viability injury,apoptosis,inflammatory response and barrier damage.Additionally,NRIP1 might activate HMGB1 expression at transcriptional level and HMGB1 elevation might reverse the impacts of NRIP1 absence on Caco-2 cell viability,apoptosis,inflammatory response as well as barrier function.Conclusion:NRIP1 may promote sepsis-elicited intestinal epi-thelial injury,which may be related to transcriptional activation of HMGB1.

Objective To observe the anti apoptotic effect of salidroside on heart function in arsenic poisoned rats.Methods Forty male rats were randomly divided into low-dose salidroside group(Sal-L group),high-dose salidroside group(Sal-H group),sodium arsenite(SA)poisoning group(SA group),non-SA group and control group(each n=8).Rats in Sal-L,Sal-H and SA groups were given SA solution(10 mg/[kg·d]),while in non-SA and control groups were given sterile distilled water for 30 days.Then,rats in Sal-L,Sal-H and non-SA groups underwent gavage with salidroside solution at doses of 15,30 and 30 mg/(kg·d),while those in SA and control groups underwent gavage with physiological saline for consecutive 21 days.Echocardiogram was performed,then myocardial tissue was obtained for HE staining and TUNEL apoptosis analysis,and the content of apoptosis related proteins were measured.The improvement effect of salidroside on heart function in arsenic poisoned rats was evaluated.Results Significant differences of left ventricular fraction shortening,left ventricular ejection fraction and peak strain were found among 5 groups(all P＜0.05),basically presented as SA group＜Sal-L group＜Sal-H group＜non-SA group=control group(all P＜0.05).After arsenic poisoning,myocardial cells were damaged,apoptotic cells increased,B-cell lymphoma 2 associated X protein increased but B-cell lymphoma 2 protein decreased.After intervention with salidroside,improvement of the above situation was observed,especially in Sal-H group.Conclusion Salidroside could protect heart function in arsenic poisoned rats through anti apoptotic effect,with certain dose dependence.

Objective To observe the anti apoptotic effect of salidroside on heart function in arsenic poisoned rats.Methods Forty male rats were randomly divided into low-dose salidroside group(Sal-L group),high-dose salidroside group(Sal-H group),sodium arsenite(SA)poisoning group(SA group),non-SA group and control group(each n=8).Rats in Sal-L,Sal-H and SA groups were given SA solution(10 mg/[kg·d]),while in non-SA and control groups were given sterile distilled water for 30 days.Then,rats in Sal-L,Sal-H and non-SA groups underwent gavage with salidroside solution at doses of 15,30 and 30 mg/(kg·d),while those in SA and control groups underwent gavage with physiological saline for consecutive 21 days.Echocardiogram was performed,then myocardial tissue was obtained for HE staining and TUNEL apoptosis analysis,and the content of apoptosis related proteins were measured.The improvement effect of salidroside on heart function in arsenic poisoned rats was evaluated.Results Significant differences of left ventricular fraction shortening,left ventricular ejection fraction and peak strain were found among 5 groups(all P＜0.05),basically presented as SA group＜Sal-L group＜Sal-H group＜non-SA group=control group(all P＜0.05).After arsenic poisoning,myocardial cells were damaged,apoptotic cells increased,B-cell lymphoma 2 associated X protein increased but B-cell lymphoma 2 protein decreased.After intervention with salidroside,improvement of the above situation was observed,especially in Sal-H group.Conclusion Salidroside could protect heart function in arsenic poisoned rats through anti apoptotic effect,with certain dose dependence.

Objective:To discuss the anti-tumor effect of low dose of methotrexate(MTX)combined with sorafenib(SFN)on the human osteosarcoma(OS),and to clarify the possible mechanism.Methods:Four types of human OS cells(143B cells,HOS cells,U2OS cells,and MG63 cells)were cultured in vitro.Western blotting method was used to detect the expression levels of vascular endothelial growth factor(VEGF)and vascular endothelial growth factor receptor 2(VEGFR2)proteins in the above four kinds of cells.The human OS xenograft model was established in the nude mice,and 20 successfully modeled BALB/C nude mice were randomly divided into control group(given 2％dimethyl sulfoxide+98％corn oil),low dose of MTX group(given 2 mng·kg-1 MTX),SFN group(given 15 mng·kg-1 SFN),and combined drug group(given 2 mng·kg-1 MTX+15 mng·kg-1 SFN);there were 5 mice in each group.The tumor volumes of the mice in various groups were detected and tumor growth curves were plotted;HE staining was used to observe the morphology of tumor tissue of the mice in various groups;immunohistochemistry was used to detect the positive expression rates of VEGFR2,proliferation marker Ki-67,and hypoxia-inducible factor-1(HIF-1)proteins in tumor tissue of the mice in various groups.The human OS 143B cells were divided into 0,0.125,0.250,0.500,1.000,2.000,and 4.000 μmol·L-1 MTX groups(given 0,0.125,0.250,0.500,1.000,2.000,and 4.000 μmol·L-1 MTX,respectively).CCK-8 method was used to detect the proliferation rates of the 143B cells in various groups,and half inhibityory concentration(IC50)was calculated;the concentration of MTX that had no effect on 143B cell survival was selected as low dose of MTX.The human OS 143B cells were divided into control and low dose of MTX groups(given 0 and 0.250 μmol·L-1 MTX).ELISA method was used to detect the levels of VEGF in the 143B cells in various groups.Results:Compared with 143B cells,the expression levels of VEGF and VEGFR2 proteins in the HOS cells,U2OS cells,and MG63 cells were significantly increased(P＜0.001).In the xenograft model,compared with control group,the tumor volumes of the mice in SFN group,and combined drug group were decreased(P＜0.001);compared with low dose of MTX group and SFN group,the tumor volume of the mice in combined drug group was decreased(P＜0.01).The immunohistochemical results showed that compared with control group,the positive expression rates of Ki-67,VEGFR2,and HIF-1 proteins in tumor tissue of the mice in combined drug group were significantly decreased(P＜0.05).The CCK-8 results showed that there was no change in the proliferation of the 143B cells treated with 0.25 μmol·L-1 MTX.The ELISA results showed that compared with control group,the level of VEGF in the 143B cells in MTX group was signyicantly decreased(P＜0.05).Conclusion:Low dose of MTX enhances the anti-tumor effect of SFN on the human OS,which may be due to the inhibition of VEGF secretion by the OS cells,thereby enhancing the anti-tumor effect of SFN on the human OS.

Objective:To investigate the impacts of nuclear receptor-interacting protein 1(NRIP1)on sepsis-evoked intesti-nal epithelial injury via transcriptional regulation of high mobility group box 1(HMGB1).Methods:The expression levels of NRIP1 and HMGB1 were detected by RT-qPCR and Western blot.The pathological changes of intestinal tissue were detected by HE staining.CCK-8 assay determined the optimal treatment time of LPS.Caco-2 cells were transfected with NRIP1 small interfering RNA(siRNA-NRIP1-1/2),and cell viability and apoptosis were detected by CCK-8 assay and flow cytometry,respectively.RT-qPCR and Western blot examined the expressions of inflammation-associated factors.Transepithelial resistance(TEER)was used to detect intestinal epi-thelial permeability.Western blot was used to detect the expressions of apoptosis and tight-junction related proteins.The binding rela-tionship between NRIP1 and HMGB1 was verified by luciferase reporting assay and chromatin immunoprecipitation assay(ChIP).After knocking down NRIP1 and overexpressing HMGB1 in LPS-treated Caco-2 cells,the functional experiment was performed again.Results:NRIP1 expression was fortified in the intestinal tissues of sepsis rats and LPS-treated Caco-2 cells.Interference with NRIP1 attenuated LPS-elicited Caco-2 cell viability injury,apoptosis,inflammatory response and barrier damage.Additionally,NRIP1 might activate HMGB1 expression at transcriptional level and HMGB1 elevation might reverse the impacts of NRIP1 absence on Caco-2 cell viability,apoptosis,inflammatory response as well as barrier function.Conclusion:NRIP1 may promote sepsis-elicited intestinal epi-thelial injury,which may be related to transcriptional activation of HMGB1.

Objective To observe the value of myocardial contrast echocardiography(MCE)combined with speckle tracking imaging(STI)for evaluating the protective effect of 2-aminoethoxydiphenyl borate(2-APB)on heart of arsenic poisoned rats.Methods Forty rats were randomly divided into low-and high-dose 2-APB intervention after arsenic trioxide(ATO)poisoned group(2-APBL group and 2-APBH group),simple ATO poisoned group(ATO group),simple 2-APB intervention group(2-APB group)and control group(each n=8).5 mg/kg ATO were intraperitoneally injected in 2-APBL group,2-APBH group and ATO group,while equal dose physiological saline were injected in 2-APB group and control group,respectively.Then 2,4 and 4 mg/kg 2-APB were intraperitoneally injected in 2-APBL group,2-APBH group and 2-APB group,while equal doses physiological saline were injected in ATO group and control group,respectively.MCE and STI were performed,serum myocardial injury markers were tested,sarcoplasmic reticulum Ca2+-ATPase(SERCA)was examinated,and finally myocardial pathological examination was performed.The above indexes were compared among groups and between each 2 groups,and correlation analysis was performed.Results Significant differences of left ventricular fractional shortening(LVFS),left ventricular ejection fraction(LVEF),wash in slope(WIS),peak intensity(PI),WIS×PI,area under the curve(AUC),global circumferential strain(GCS)in each layer of myocardium,as well as glutamic-oxaloacetic transaminase(GOT),creatine kinase(CK),lactate dehydrogenase(LDH)and SERCA were found among 5 groups(all P＜0.05).The above indexes substantially increased or decreased sequentially ATO group,2-APBL group,2-APBH group and 2-APB group/control group(all P＜0.05).WIS,PI,WIS × PI and GCS of rat endo-myocardium,GSC of mid-myocardium and GCS of epi-myocardium all positively correlated with SERCA(r=0.874,0.893,0.920,0.916,0.848,0.783,all P＜0.05).Conclusion MCE combined with STI,especially WISXPI and GCS of endo-myocardium could be used to evaluate the protective effect of 2-APB on heart of arsenic poisoned rats.

AIM: To observe the changes of corneal densitometry(CD)in patients with keratoconus after corneal cross-linking(CXL).METHODS: Retrospective study. A total of 32 patients(43 eyes)with keratoconus in Ningxia Eye Hospital from April 2020 to April 2022 were selected. Pentacam analysis system divided the cornea into three layers: anterior 120 μm, middle layer and posterior 60 μm, and divides it into five regions with diameters of 0-2, 2-6, 6-10, 10-12 mm and full diameter according to the diameter, and measures the CD in different ranges. The changes of CD were compared before operation and at 1, 3 and 6 mo after operation.RESULTS: There were differences in uncorrected visual acuity, best corrected visual acuity and intraocular pressure before and 6 mo after operation(all P<0.05), and there was no difference in corneal endothelial cells(P=0.477). CD reached its peak at 1 mo after operation, and decreased at 3 mo and 6 mo after operation, but it was still higher than that before operation. There is a significant positive correlation between CD and Kmax in the anterior layer and the whole layer(r=0.164, P=0.016; r=0.152, P=0.023).CONCLUSION: The values of CD peaked at 1 mo after CXL, then it gradually decreased, tending to become stable at 6 mo postoperatively.

Objective:To understand the impact of diet on glycemic control in community-managed patients with type 2 diabetes mellitus (T2DM) and provide evidence for implementing prevention strategies and measures for diabetes patients.Methods:Eight communities were randomly selected from Changshu and Wuhan in 2015, and T2DM patients managed in the community were selected to conduct questionnaire surveys, physical measurements, and blood glucose testing. Factor analysis was used to obtain dietary patterns. A binary logistic regression model was used to analyze the factors affecting glycemic control.Results:Finally, 1 818 T2DM patients were included, and the control rate of FPG was 57.59% (95% CI: 55.30%-59.86%), and the control rate of 2 h postprandial blood glucose (2 h PBG) was 24.90% (95% CI: 22.93%- 26.91%). Five dietary patterns were obtained by factor analysis: animal food pattern, fruit-aquatic products-potato patterns, vegetable-grain pattern, egg-milk-bean pattern, and oil-salt patterns. No-conditional multivariate logistic regression analysis showed that after adjusting for confounding factors, the reduced probability of FPG control was related to animal food pattern ( OR=0.71, 95% CI: 0.52-0.98) and fruit-aquatic products-potato patterns ( OR=0.71, 95% CI: 0.51-0.97). The decrease in the 2 h PBG control probability was related to fruit-aquatic products-potato patterns ( OR=0.60, 95% CI: 0.40-0.90). The increased probability of FPG and 2 h postprandial glucose control were both related to vegetable-grain pattern ( OR=1.41, 95% CI: 1.03-1.94; OR=1.68, 95% CI: 1.13-2.51) and egg-milk-bean pattern ( OR=1.75, 95% CI: 1.25-2.46; OR=1.56, 95% CI: 1.00-2.42). Compared with the Q4 group of egg-milk-bean pattern, the FPG control rate of the combination of "fruit-aquatic products-potato pattern ( Q4 group), vegetable-grain pattern ( Q2 group), egg-milk-bean pattern ( Q3 group)" was higher ( OR=6.79, 95% CI: 1.15-40.23, P=0.035). Compared with the Q4 group of vegetable-grain pattern, the combination of "fruit-aquatic products-potato pattern ( Q4 group), vegetable-grain pattern ( Q3 group), egg-milk-bean pattern ( Q2 group), oil-salt pattern ( Q2 group)" had higher control rate of 2 h PBG ( OR=12.78, 95% CI: 1.26-130.05, P=0.031). Conclusions:A proper combination of dietary patterns and dietary patterns are more conducive to the control of FPG and 2 h PBG in T2DM patients managed in the communities of Wuhan and Changshu. Patient nutrition education should be strengthened, and the food-matching ability of patients should be improved.