Objective To explore the clinical factors influencing complete response in patients with locally advanced rectal cancer (LARC) after neoadjuvant chemoradiotherapy (nCRT). Methods Clinical data of LARC patients treated in the Department of Radiation Oncology at Beijing Shijitan Hospital between January 2013 and December 2024 were retrospectively collected. All patients received nCRT, after which surgery or a watch-and-wait approach was adopted based on treatment response. Univariable and multivariable logistic regression analyses were performed to identify prognostic factors influencing complete response. A clinical prediction model was constructed based on the multivariable analysis results, and its predictive performance was evaluated using the receiver operating characteristic curve. Results A total of 113 eligible patients were included. After nCRT, 19 patients (16.8%) achieved complete response, including 3 with clinical complete response and 16 with pathological complete response. Univariable analysis indicated that pretreatment clinical N stage, extramural venous invasion, carcinoembryonic antigen level, and neoadjuvant treatment regimen were associated with complete response after nCRT (P<0.05). Multivariable logistic regression analysis identified pretreatment extramural venous invasion, carcinoembryonic antigen level, and neoadjuvant treatment regimen as independent influencing factors for complete response (P<0.05). A prediction model incorporating these independent factors yielded an area under the receiver operating characteristic curve of 0.813 (95% confidence interval: 0.713-0.913), with a sensitivity of 89.5% and a specificity of 60.6%, demonstrating good predictive performance. Conclusion Pretreatment extramural venous invasion, carcinoembryonic antigen level, and neoadjuvant treatment regimen are independent factors influencing complete response after nCRT in LARC patients. The prediction model combining these factors may assist in evaluating treatment efficacy following nCRT in LARC patients.

Intravitreal anti-vascular endothelial growth factor(anti-VEGF)therapy has been widely used, but the variability in its therapeutic efficacy limits individualized treatment. In recent years, the application of artificial intelligence(AI)has opened up new avenues for personalized treatment response prediction, and its core branches include machine learning(ML)and deep learning(DL). This review systematically retrieved and analyzed 41 relevant studies published up to April 2025. Comprehensive analysis reveals that AI predictive models are evolving from forecasting single endpoints(such as visual acuity or central retinal thickness)to integrating multi-dimensional endpoints(encompassing anatomical, functional, and treatment demand parameters)and generating predictive imaging outputs. In terms of technical approaches, DL models(28 studies, accounting for 68.3%)dominate this field due to their robust image interpretation capabilities, while ML models(10 studies, 24.4%)retain significant value in the analysis of structured clinical data. Cross-disease comparisons indicate that research efforts are most concentrated on age-related macular degeneration(ARMD)and diabetic macular edema(DME), with shared conceptual frameworks for model construction, yet distinct anatomical and functional indicators are prioritized for each disease. Currently, the field confronts several key challenges, including insufficient prospective clinical validation, limited model interpretability(the “black box problem”), and a scarcity of high-quality multi-center datasets. Moving forward, it is imperative to advance real-world validation and develop explainable AI techniques to expedite the clinical translation of these predictive models.

ObjectiveTo investigate the effect of bone morphogenetic protein 3 （BMP3） on the expression of inflammatory factors and joint damage in adjuvant arthritis （AA） induced by Freund′s complete adjuvant （FCA） in rats. MethodsThe AIA model was established in SD rats by intradermal injection of FCA into the toes of the left hind limb， and BMP3 overexpressing adenovirus （Ad-BMP3） or control adenovirus （Ad-NC） was injected in situ into the knee joint cavity on day 8 after modeling. Subsequently， HE staining was used to observe the histopathological changes in the synovium， immunohistochemistry was used to detect the expression of BMP3 in the synovium， and ELISA was used to analyze the expression levels of IL-6， IL-1β and TNF-α in the serum. Primary fibroblast-like synoviocytes （FLS） were isolated from AIA rats， the expression of BMP3 in FLS was knocked down or overexpressed， and Western blot and qRT-PCR were used to detect the expression levels of BMP3 and inflammatory factors in FLS. ResultsHE staining confirmed the successful establishment of the AIA model. Compared with normal rats， AIA rats showed decreased BMP3 expression in synovial tissue. Knockdown of BMP3 promoted the protein expression of inflammatory factors （IL-6， IL-1β， IL-17A， TNF-α） and the mRNA expression of chemokines ［C-C motif chemokine ligand 2 （CCL2）， C-C motif chemokine ligand 3 （CCL3）， Vascular Cell Adhesion Molecule-1 （VCAM-1）］ in FLS. In contrast， overexpression of BMP3 suppressed the expression of these inflammatory factors and chemokines. Intra-articular injection of BMP3-overexpressing adenovirus in AIA rats upregulated BMP3 expression in synovial tissue and inhibited synovial inflammation and bone erosion. ConclusionBMP3 suppresses the production of inflammatory factors and chemokines in FLS， thereby alleviating synovial hyperplasia and bone erosion in arthritis.

Exosomes are ubiquitous in all types of body fluids, exhibiting a high degree of abundance and diversity. Given their distinctive structure and function, exosomes are involved in a range of life activities, including intercellular communication, material transport, and immune regulation. An increasing number of studies have identified exosomes as a source of diagnostic markers for diabetic retinopathy. Furthermore, exosomes represent a novel avenue for therapeutic intervention, with promising clinical applications. This paper examines the diagnostic and therapeutic mechanisms of exosomes in diabetic retinopathy, reviews the advancements in exosomes-based diagnostics and therapeutics for diabetic retinopathy, and aims to enhance the precision and efficiency of clinical diagnosis and treatment of diabetic retinopathy.

Objective To investigate the mechanism of long non-coding RNA(LncRNA)FUT8-AS1 on diabetic ischemia-reperfusion injury by regulating growth differentiation factor 15(GDF15).Methods Male SD rats were randomly divided into Sham group,cerebral ischemia-reperfusion injury(MCAO/R)group,diabetic cerebral ischemia-reperfusion injury(DM-MCAO/R)group,DM-MCAO/R+sh NC group,and DM-MCAO/R+sh FUT8-AS1 group.TTC staining was used to assess the size of cerebral infarction.Tunel staining was selected to evaluate the apoptosis of neurons in brain tissue.Nissl staining was used to assess the number of neurons in brain tissue.The expression of LncRNA FUT8-AS1,GDF15 mRNA in Willis arterial loop and internal carotid artery tissues were detected by qRT-PCR.The expression of α-SMA,eNOS,p-eNOS,GDF15 protein in Willis arterial loop and internal carotid artery was detected by Western blot.The rat brain microvascular endothelial cells were divided into control(Con)group,OGD/R group,HG-OGD/R group,HG-OGD/R+sh NC group,HG-OGD/R+sh FUT8-AS1 group,HG-OGD/R+sh FUT8-AS1+oe NC group,and HG-OGD/R+sh FUT8-AS1+oe GDF15 group.MTT assay was used to detect cell viability.Lactate dehydrogenase(LDH)assay was used to detect cell damage.The expression ofα-smooth muscle actin(α-SMA),endothelial nitric oxide synthase(eNOS),p-eNOS protein was detected by Western blot.Results Compared with the Sham group,the percentage of cerebral infarction,the number of Tunel-positive cells,the FUT8-AS1 and mRNA expression of GDF15 and the expression of GDF-15 protein increased(P<0.05),and the expression of α-SMA,eNOS,p-eNOS proteins decreased in the MCAO/R group(P<0.05),and the number of neurons in the hippocampus decreased,the morphology was shrunk,and the color was dark in the MCAO/R group.Compared with the MCAO/R group,the percentage of cerebral infarction,the number of Tunel-positive cells,the FUT8-AS1 and mRNA expression of GDF15 and the expression of GDF-15 protein increased(P<0.05),and the expression of α-SMA,eNOS,p-eNOS proteins decreased in the DM-MCAO/R group(P<0.05),and the number of neurons in the hippocampus decreased in the DM-MCAO/R group.Compared with the DM-MCAO/R+sh NC group,the percentage of cerebral infarction,the number of Tunel-positive cells,the FUT8-AS1 and mRNA expression of GDF15 and the expression of GDF-15 protein decreased(P<0.05),and the expression of α-SMA,eNOS,p-eNOS proteins increased in the DM-MCAO/R+sh FUT8-AS1 group(P<0.05),and the number of neurons in the hippocampus increased in the DM-MCAO/R+sh FUT8-AS1 group.Compared with the Con group,the LDH release,FUT8-AS1 expression,GDF15 mRNA and protein expression increased(P<0.05),and the cell activity,α-SMA,eNOS,and p-eNOS protein expressions decreased in the OGD/R group(P<0.05).Compared with the OGD/R group,the LDH release,FUT8-AS1 expression,GDF15 mRNA and protein expression increased(P<0.05),and the cell activity,α-SMA,eNOS,and p-eNOS protein expressions decreased in the HG-OGD/R group(P<0.05).Compared with the HG-OGD/R+sh NC group,the LDH release,FUT8-AS1 expression,GDF15 mRNA and protein expression decreased(P<0.05),and the cell activity,α-SMA,eNOS,and p-eNOS protein expressions increased in the HG-OGD/R+sh FUT8-AS1 group(P<0.05).Compared with the HG-OGD/R+sh NC group,the LDH release,GDF15 mRNA and protein expression increased(P<0.05),and the cell activity decreased in the HG-OGD/R+oe GDF15 group(P<0.05).Compared with the HG-OGD/R+sh FUT8-AS1+oe NC group,the expression of α-SMA,eNOS,p-eNOS proteins decreased in the HG-OGD/R+sh FUT8-AS1+oe GDF15 group(P<0.05).Conclusions LncRNA FUT8-AS1 may exacerbate diabetic cerebral ischemia-reperfusion injury by regulating GDF15.

Objective:To establish a detection method for fatty acid composition and methoxylaniline value in pharmaceutical excipient castor oil.Methods:The detection of fatty acid composition involves pre-test of the sam-ple using the methanol sodium methylation method,followed by direct injection analysis using gas chromatography,and finally calculating the content of each fatty acid composition using the area normalization method with correction factors.The detection of methoxylaniline value is achieved by dissolving and diluting the sample with isooctane:isopropanol(8∶2,volume ratio),reacting with 4-methoxylaniline,measuring the absorbance at a wavelength of 350 nm,and calculating the methoxylaniline value.Results:Under the composition of fatty acids,the 8 kinds of fatty acids have good separation degree.The methyl ricinoleate and methyl stearate have good linear relationship in the range of 0.1-5.0 mg·mL-1.The repeatabilityand intermediate precision(RSD)ofthe determination results of each fatty acid in the sample are all less than 5%.It is also found that only α-type of linolenic acid is present in castor oil,without γ-type.In the determination of methoxyaniline value,the blank solvent does not interfere with the determination of the sample,and the repeatability RSD is 3.6%.Conclusion:The detection method for fatty acid composition and meth-oxylaniline value established in this article is accurate and reliable,and can be used for the detection of fatty acid composition and methoxylaniline value in pharmaceutical excipient castor oil.

Objective To investigate the mechanism of long non-coding RNA(LncRNA)FUT8-AS1 on diabetic ischemia-reperfusion injury by regulating growth differentiation factor 15(GDF15).Methods Male SD rats were randomly divided into Sham group,cerebral ischemia-reperfusion injury(MCAO/R)group,diabetic cerebral ischemia-reperfusion injury(DM-MCAO/R)group,DM-MCAO/R+sh NC group,and DM-MCAO/R+sh FUT8-AS1 group.TTC staining was used to assess the size of cerebral infarction.Tunel staining was selected to evaluate the apoptosis of neurons in brain tissue.Nissl staining was used to assess the number of neurons in brain tissue.The expression of LncRNA FUT8-AS1,GDF15 mRNA in Willis arterial loop and internal carotid artery tissues were detected by qRT-PCR.The expression of α-SMA,eNOS,p-eNOS,GDF15 protein in Willis arterial loop and internal carotid artery was detected by Western blot.The rat brain microvascular endothelial cells were divided into control(Con)group,OGD/R group,HG-OGD/R group,HG-OGD/R+sh NC group,HG-OGD/R+sh FUT8-AS1 group,HG-OGD/R+sh FUT8-AS1+oe NC group,and HG-OGD/R+sh FUT8-AS1+oe GDF15 group.MTT assay was used to detect cell viability.Lactate dehydrogenase(LDH)assay was used to detect cell damage.The expression ofα-smooth muscle actin(α-SMA),endothelial nitric oxide synthase(eNOS),p-eNOS protein was detected by Western blot.Results Compared with the Sham group,the percentage of cerebral infarction,the number of Tunel-positive cells,the FUT8-AS1 and mRNA expression of GDF15 and the expression of GDF-15 protein increased(P<0.05),and the expression of α-SMA,eNOS,p-eNOS proteins decreased in the MCAO/R group(P<0.05),and the number of neurons in the hippocampus decreased,the morphology was shrunk,and the color was dark in the MCAO/R group.Compared with the MCAO/R group,the percentage of cerebral infarction,the number of Tunel-positive cells,the FUT8-AS1 and mRNA expression of GDF15 and the expression of GDF-15 protein increased(P<0.05),and the expression of α-SMA,eNOS,p-eNOS proteins decreased in the DM-MCAO/R group(P<0.05),and the number of neurons in the hippocampus decreased in the DM-MCAO/R group.Compared with the DM-MCAO/R+sh NC group,the percentage of cerebral infarction,the number of Tunel-positive cells,the FUT8-AS1 and mRNA expression of GDF15 and the expression of GDF-15 protein decreased(P<0.05),and the expression of α-SMA,eNOS,p-eNOS proteins increased in the DM-MCAO/R+sh FUT8-AS1 group(P<0.05),and the number of neurons in the hippocampus increased in the DM-MCAO/R+sh FUT8-AS1 group.Compared with the Con group,the LDH release,FUT8-AS1 expression,GDF15 mRNA and protein expression increased(P<0.05),and the cell activity,α-SMA,eNOS,and p-eNOS protein expressions decreased in the OGD/R group(P<0.05).Compared with the OGD/R group,the LDH release,FUT8-AS1 expression,GDF15 mRNA and protein expression increased(P<0.05),and the cell activity,α-SMA,eNOS,and p-eNOS protein expressions decreased in the HG-OGD/R group(P<0.05).Compared with the HG-OGD/R+sh NC group,the LDH release,FUT8-AS1 expression,GDF15 mRNA and protein expression decreased(P<0.05),and the cell activity,α-SMA,eNOS,and p-eNOS protein expressions increased in the HG-OGD/R+sh FUT8-AS1 group(P<0.05).Compared with the HG-OGD/R+sh NC group,the LDH release,GDF15 mRNA and protein expression increased(P<0.05),and the cell activity decreased in the HG-OGD/R+oe GDF15 group(P<0.05).Compared with the HG-OGD/R+sh FUT8-AS1+oe NC group,the expression of α-SMA,eNOS,p-eNOS proteins decreased in the HG-OGD/R+sh FUT8-AS1+oe GDF15 group(P<0.05).Conclusions LncRNA FUT8-AS1 may exacerbate diabetic cerebral ischemia-reperfusion injury by regulating GDF15.

Objective:To establish a detection method for fatty acid composition and methoxylaniline value in pharmaceutical excipient castor oil.Methods:The detection of fatty acid composition involves pre-test of the sam-ple using the methanol sodium methylation method,followed by direct injection analysis using gas chromatography,and finally calculating the content of each fatty acid composition using the area normalization method with correction factors.The detection of methoxylaniline value is achieved by dissolving and diluting the sample with isooctane:isopropanol(8∶2,volume ratio),reacting with 4-methoxylaniline,measuring the absorbance at a wavelength of 350 nm,and calculating the methoxylaniline value.Results:Under the composition of fatty acids,the 8 kinds of fatty acids have good separation degree.The methyl ricinoleate and methyl stearate have good linear relationship in the range of 0.1-5.0 mg·mL-1.The repeatabilityand intermediate precision(RSD)ofthe determination results of each fatty acid in the sample are all less than 5%.It is also found that only α-type of linolenic acid is present in castor oil,without γ-type.In the determination of methoxyaniline value,the blank solvent does not interfere with the determination of the sample,and the repeatability RSD is 3.6%.Conclusion:The detection method for fatty acid composition and meth-oxylaniline value established in this article is accurate and reliable,and can be used for the detection of fatty acid composition and methoxylaniline value in pharmaceutical excipient castor oil.

ObjectiveTo explore the effect of timosaponin BⅡ （TBⅡ） combined with icariin （ICA） on osteoclast （OC）-osteoblast （OB） coupling and decipher the mechanism from the cellular level. MethodsThe cell counting kit-8 （CCK-8） was used to assess the effects of different concentrations of TBⅡ and different concentrations of TBⅡ+ICA on the growth of RAW264.7 cells. Soluble receptor activator of nuclear factor-κB ligand （sRANKL） was used to induce the differentiation of RAW264.7 pre-osteoclasts into osteoclasts. The cells were allocated into sRANKL， TBⅡ （1， 5， 10 μmol·L^-1）， and TBⅡ+ICA groups. Tartrate-resistant acid phosphatase staining was performed to assess the effects of TBⅡ and TBⅡ+ICA on osteoclast differentiation. Real-time quantitative polymerase chain reaction （Real-time PCR） was conducted to examine the effects of TBⅡ+ICA on the expression of key genes involved in osteoclast differentiation and osteoclast-derived coupling factors. The osteogenic differentiation conditioned medium mixed with osteoclast supernatant was used to induce osteogenic differentiation of MC3T3-E1 cells. Alkaline phosphatase staining and alizarin red S staining were employed to determine the effect of TBⅡ+ICA on osteogenic differentiation. Real-time PCR was employed to evaluate the effects of conditioned medium on key genes involved in osteogenic differentiation. ResultsTBⅡ at 1， 5， 10 μmol·L^-1 had no significant effect on the cell survival rate. Compared with the sRANKL group， TBⅡ inhibited osteoclast differentiation in a dose-dependent manner and achieved the best effect at 10 μmol·L^-1 （P<0.01）. Compared with the sRANKL group， different concentrations of TBⅡ down-regulated the mRNA levels of osteoclast differentiation-related genes c-Fos， RANK， and RANKL （P<0.05）. None of 10 μmol·L^-1 TBⅡ， 10 μmol·L^-1 TBⅡ+10^-4 μmol·L^-1 ICA， or 10 μmol·L^-1 TBⅡ+10^-3 μmol·L^-1 ICA affected the viability of RAW264.7 cells. TBⅡ and/or ICA inhibited osteoclast differentiation （P<0.01）， and TBⅡ + ICA had the best effect （P<0.01）. Compared with the sRANKL group， TBⅡ and/or ICA down-regulated the mRNA levels of c-Fos， RANK， and RANKL （P<0.05）. The single application of TBⅡ and ICA had no significant effect on the mRNA levels of Wnt10b， Cthrc1， and C3a， while TBⅡ+ICA exerted up-regulating effects （P<0.05）. Compared with those in the blank group， the bone differentiation and mineralization abilities of the normal osteogenic induction group and each osteogenic induction + osteoclast supernatant group were improved （P<0.01）. Compared with the blank group， the normal osteogenic induction group and the osteogenic induction + osteoclast supernatant group showed up-regulated mRNA levels of Runx2 and OCN （P<0.01）. ConclusionTBⅡ+ICA can inhibit osteoclast differentiation， maintain the normal osteoclast-osteoblast coupling， and promote osteogenic differentiation.

OBJECTIVES: To explore the association between GPSM2 expression level and gastric cancer progression and analyze the functional pathways and action mechanism of GPSM2. METHODS: We analyzed GPSM2 expression levels in gastric cancer tumors based on data from the GEPIA database and the clinical data of 109 patients. Public databases enrichment analysis were used to assess the impact of GPSM2 expression level on survival outcomes and the functional pathways and action mechanism of GPSM2. We further observed the effects of GPSM2 knockdown and overexpression on proliferation, migration and apoptosis of MGC803 cells using CCK-8 assay, colony formation assay, flow cytometry and immunoblotting and on the growth of MGC803 cell xenografts in nude mice. RESULTS: Bioinformatic analysis and immunohistochemical staining of the clinical specimens both revealed high GPSM2 expressions in gastric cancer (P<0.01). A high GPSM2 expression was significantly correlated with T3-4 stages, N2-3 stages, a carcinoembryonic antigen (CEA) level ≥5 μg/L, and a carbohydrate antigen (CA) 19-9 level ≥37 kU/L (P<0.05). Cox regression analysis identified high GPSM2 expression as an independent risk factor affecting 5-year survival of the patients (P<0.05). Gene ontology (GO) analysis suggested that GPSM2 was involved in cell cycle regulation. In MGC803 cells, GPSM2 overexpression significantly promoted cell proliferation and G1/S transition and xenograft growth in nude mice. KEGG pathway enrichment analysis indicated that GPSM2 executed its biological functions by regulating the p53 signaling pathway, which was confirmed by the results of immunoblotting experiments showing suppression of p53 signaling pathway activity in GPSM2-over expressing MGC803 cells. CONCLUSIONS GPSM2 is highly expressed in gastric cancer to affect patient prognosis by promoting tumor cell proliferation and G1/S transition possibly via inhibiting the p53 pathway.
Stomach Neoplasms/metabolism* ; Humans ; Cell Proliferation ; Prognosis ; Animals ; Mice, Nude ; Cell Line, Tumor ; Mice ; Apoptosis ; Tumor Suppressor Protein p53/metabolism* ; Cell Movement