ObjectiveTo construct a risk prediction model for carotid artery plaques in high-risk populations of stroke based on five machine learning methods. MethodsThe clinical information of the high-risk population of stroke was collected. Factor analysis and statistical analysis of syndrome elements were conducted on their traditional Chinese medicine （TCM） symptoms and tongue and pulse manifestations. On the basis of the results of factor analysis and variable screening， five machine learning methods-classification and regression tree （CART） decision tree， support vector machine （SVM）， back propagation（BP） neural network， logistic regression， and random forest-were used to construct the risk prediction model for carotid artery plaques. ResultsThe most common TCM syndrome elements in the high-risk population of stroke was Qi deficiency. The scores of Qi deficiency， Yin deficiency， and Yang deficiency in the population with carotid artery plaques were higher than those without carotid artery plaques （P<0.05）. The CART decision tree， SVM， logistic regression， BP neural network， and random forest models showed the areas under the receiver operating characteristic （ROC） curves of 0.71， 0.75， 0.76， 0.76， and 0.75， the accuracy rates of 68.94%， 69.27%， 69.44%， 70.10%， and 69.60%， the precision rates of 68.56%， 68.53%， 68.75%， 69.74%， and 69.42%， the recall rates of 68.91%， 67.93%， 67.92%， 68.10%， and 67.31%， and the F₁ values of 0.69， 0.68， 0.68， 0.68， and 0.68， respectively. ConclusionAmong the high-risk population of stroke， the most frequently distributed TCM syndrome element is Qi deficiency， with the rest mainly being fire heat， Yin deficiency， Yang deficiency， phlegm dampness， blood stasis， and Qi stagnation. Deficiency syndrome may be a major factor leading to carotid artery plaques in the high-risk population of stroke. The BP neural network model demonstrates better performance in predicting the risk of carotid artery plaques in the high-risk population of stroke. People with carotid artery plaques are more likely to present with symptoms such as a heavy head， dizziness， headache， and thready pulse. The primary community benefits more widely when the BP neural network model is adopted to predict the risk of carotid artery plaques in the high-risk population of stroke over 40 years old.

ObjectiveTo construct a risk prediction model for carotid artery plaques in high-risk populations of stroke based on five machine learning methods. MethodsThe clinical information of the high-risk population of stroke was collected. Factor analysis and statistical analysis of syndrome elements were conducted on their traditional Chinese medicine （TCM） symptoms and tongue and pulse manifestations. On the basis of the results of factor analysis and variable screening， five machine learning methods-classification and regression tree （CART） decision tree， support vector machine （SVM）， back propagation（BP） neural network， logistic regression， and random forest-were used to construct the risk prediction model for carotid artery plaques. ResultsThe most common TCM syndrome elements in the high-risk population of stroke was Qi deficiency. The scores of Qi deficiency， Yin deficiency， and Yang deficiency in the population with carotid artery plaques were higher than those without carotid artery plaques （P<0.05）. The CART decision tree， SVM， logistic regression， BP neural network， and random forest models showed the areas under the receiver operating characteristic （ROC） curves of 0.71， 0.75， 0.76， 0.76， and 0.75， the accuracy rates of 68.94%， 69.27%， 69.44%， 70.10%， and 69.60%， the precision rates of 68.56%， 68.53%， 68.75%， 69.74%， and 69.42%， the recall rates of 68.91%， 67.93%， 67.92%， 68.10%， and 67.31%， and the F₁ values of 0.69， 0.68， 0.68， 0.68， and 0.68， respectively. ConclusionAmong the high-risk population of stroke， the most frequently distributed TCM syndrome element is Qi deficiency， with the rest mainly being fire heat， Yin deficiency， Yang deficiency， phlegm dampness， blood stasis， and Qi stagnation. Deficiency syndrome may be a major factor leading to carotid artery plaques in the high-risk population of stroke. The BP neural network model demonstrates better performance in predicting the risk of carotid artery plaques in the high-risk population of stroke. People with carotid artery plaques are more likely to present with symptoms such as a heavy head， dizziness， headache， and thready pulse. The primary community benefits more widely when the BP neural network model is adopted to predict the risk of carotid artery plaques in the high-risk population of stroke over 40 years old.

Objective To investigate the protective effect of LncRNA MEG3 on the retina in early-stage diabetic rats through regulation of the COX-2/PGE2/VEGF signaling pathway.Methods 50 male SD rats of SPF grade were selected for the study.Among them,10 rats were assigned to the control group,while 40 rats were used to establish diabetic retinopathy models.A total of 32 rats successfully underwent modeling and were subsequently divided into four groups(n=8 per group):model group,negative control group,MEG3 overexpression group,and MEG3 overexpression+COX-2 inhibitor group.Histopathological changes,vascular permeability,glucose and lipid metabolism,inflammatory factors,oxidative stress indices,PGE2 levels,as well as the relative mRNA and protein expression levels of COX-2 and VEGF were evaluated in each group.Results Compared with the control group,HDL-C,CAT,GSH-PX,and SOD levels were significantly decreased,whereas the mRNA and protein expression levels of vascular permeability,TG,TC,LDL-C,IL-6,IL-1β,TNF-α,MDA,PGE2,COX-2,and VEGF were significantly increased in the model group(P<0.05).Compared with the negative control group,HDL-C,CAT,GSH-PX,and SOD levels were significantly increased in the MEG3 overexpression group,while the mRNA and protein expression levels of vascular permeability,TG,TC,LDL-C,IL-6,IL-1β,TNF-α,MDA,PGE2,COX-2,and VEGF were significantly decreased(P<0.05).Compared with the MEG3 overexpression group,HDL-C,CAT,GSH-PX,and SOD levels were further increased in the MEG3 overexpression+COX-2 inhibitor group,and the mRNA and protein expression levels of vascular permeability,TG,TC,LDL-C,IL-6,IL-1β,TNF-α,MDA,PGE2,COX-2,and VEGF were further decreased(P<0.05).Conclusion LncRNA MEG3 is capable of regulating the COX-2/PGE2/VEGF pathway,enhancing glucose and lipid metabolism in rats,suppressing the expression of inflammatory factors,attenuating stress responses,and alleviating diabetic retinopathy.

Objective To investigate the protective effect of LncRNA MEG3 on the retina in early-stage diabetic rats through regulation of the COX-2/PGE2/VEGF signaling pathway.Methods 50 male SD rats of SPF grade were selected for the study.Among them,10 rats were assigned to the control group,while 40 rats were used to establish diabetic retinopathy models.A total of 32 rats successfully underwent modeling and were subsequently divided into four groups(n=8 per group):model group,negative control group,MEG3 overexpression group,and MEG3 overexpression+COX-2 inhibitor group.Histopathological changes,vascular permeability,glucose and lipid metabolism,inflammatory factors,oxidative stress indices,PGE2 levels,as well as the relative mRNA and protein expression levels of COX-2 and VEGF were evaluated in each group.Results Compared with the control group,HDL-C,CAT,GSH-PX,and SOD levels were significantly decreased,whereas the mRNA and protein expression levels of vascular permeability,TG,TC,LDL-C,IL-6,IL-1β,TNF-α,MDA,PGE2,COX-2,and VEGF were significantly increased in the model group(P<0.05).Compared with the negative control group,HDL-C,CAT,GSH-PX,and SOD levels were significantly increased in the MEG3 overexpression group,while the mRNA and protein expression levels of vascular permeability,TG,TC,LDL-C,IL-6,IL-1β,TNF-α,MDA,PGE2,COX-2,and VEGF were significantly decreased(P<0.05).Compared with the MEG3 overexpression group,HDL-C,CAT,GSH-PX,and SOD levels were further increased in the MEG3 overexpression+COX-2 inhibitor group,and the mRNA and protein expression levels of vascular permeability,TG,TC,LDL-C,IL-6,IL-1β,TNF-α,MDA,PGE2,COX-2,and VEGF were further decreased(P<0.05).Conclusion LncRNA MEG3 is capable of regulating the COX-2/PGE2/VEGF pathway,enhancing glucose and lipid metabolism in rats,suppressing the expression of inflammatory factors,attenuating stress responses,and alleviating diabetic retinopathy.

Objective To analyze the differences of brain activity between first-episode untreated depressive patients with and without suicidal ideation(SI),and its correlations with clinical characteristics.Methods A total of 40 major depressive disorder(MDD)patients with SI(MDD+SI group),40 patients without SI MDD(MDD+NSI group),and 40 healthy controls(HC)(HC group)were enrolled.The 17-item Hamilton depression scale(HAMD-17)and Beck scale for suicide ideation(BSI)were used to assess the severity of depression and SI,respectively.MRI data were collected.The values of fractional amplitude of low-frequency fluctuation(fALFF)were calculated.Results(1)Compared with the HC group,the MDD+NSI group showed decreases in the fALFF val-ues of the default network and attention network.The fALFF values of the attention network in the MDD+SI group showed decreases.Compared with the MDD+NSI group,the MDD+SI group showed decreases in the fALFF values of the attention network.(2)The fALFF values in the left middle frontal gyrus were negatively correlated with the total score of HAMD-17(r=-0.55;P<0.001)in the MDD+NSI group,while the fALFF values in the left middle frontal gyrus were negatively correlated with the total score of HAMD-17(r=-0.53;P<0.001)and the total score of BSI(r=-0.51;P<0.001)in the MDD+SI group.(3)The optimal critical value of fALFF value in left middle frontal gyrus for predicting SI occurrence in MDD patients was-0.039,area under the curve(AUC)was 0.76,sensitivity was 0.63,and specificity was 0.80.Conclusion The decreased local activity intensity in the left middle frontal gyrus of the brain might be the central mechanism for the occurrence of SI in MDD patients.In addition,the left middle frontal gyrus might have certain value in identifying SI and predicting the severity of SI.

Objective To investigate the protective effect and mechanism of calcium dobesilate on oxidative damage induced by high-glucose in Müller cells.Methods The oxidative damage model of Müller cells induced by high-glucose was established and the cells were divided into 4groups.The control group was cultured normally,and the high glucose group was cultured in the medium of 35mmol/L glucose.The control+calcium dobesilate group was treated with 0.5μmol/L calcium dobesilate intervention cells on the basis of routine culture,and the high sugar+calcium dobesilate group was treated with 0.5μmol/L calcium dobesilate intervention cells on the basis of high glucose.Cell proliferation was assessed by CCK-8,apoptosis was detected by flow cytometry,and oxidative stress markers were detected by the kit.Intracellular correction potassium channel subtype 4.1(Kir4.1)and aquaporin 4(AQP4)protein levels were detected by western blot.Results Compared with the control group,the proliferative activity of Müller cells of the high glucose group was decreased,apoptosis rate was increased,oxidative stress occurred,AQP4 protein expression level was increased and Kir4.1 protein level was decreased(P＜0.05).Compared with the high glucose group,the cell activity and apoptosis rate of the high glucose+calcium do-besilate group were increased,the oxidative stress damage was alleviated,the AQP4 protein expression level was decreased and the Kir4.1 protein level was increased(P＜0.05).Conclusion Calcium dobesilate may inhibit the oxidative damage of Müller cells induced by high-glucose by regulating the AQP4/Kir4.1 axis.

Background Existing studies have confirmed that fine particulate matter (PM_2.5)is one of the important factors inducing pulmonary fibrosis. Pulmonary fibrosis is the terminal stage of a major category of lung diseases characterized by the destruction of tissue structure, and eventually leading lung ventilation and ventilation dysfunction. No effective pulmonary fibrosis treatment is available yet. Objective To investigate the protective effect of salidroside on pulmonary fibrosis induced by the exposure of PM_2.5 and its molecular mechanism. Methods Seventy 7-week-old male C57BL/6 mice were randomly divided into four groups: control group (intratracheal instillation of normal saline + saline by gavage, n=25), Sal group (intratracheal instillation of normal saline + Sal 60 mg·kg⁻¹ by gavage, n=10), PM_2.5 group (intratracheal instillation of PM_2.5 5 mg·kg⁻¹ + saline by gavage, n=10), and Sal + PM_2.5 group (intratracheal instillation of PM_2.5 5 mg·kg⁻¹ +Sal 60 mg·kg⁻¹ by gavage, n=10). The mice were administered by gavage once daily, intratracheal instillation once every 3 d, and every 3 d constituted an experimental cycle. At the end of the 26-30th cycles, 3 mice in the control group and 3 mice in the PM_2.5 group were randomly sacrificed, and the lung tissues were collected for Masson staining to verify whether the pulmonary fibrosis model was successfully established. After 30 cycles, the model was successfully constructed. After 1 week of continuous observation, the mice were sacrificed, and the blood and lung tissues of the mice were collected to make lung tissue sections. Assay kits were correspondingly employed to detect oxidative stress indicators such as serum malondialdehyde (MDA) and superoxide dismutase (SOD). Western blotting was used to detect the expression of fibrosis-related proteins (Collagen-III, α-SMA), mitochondrial dynamics-related proteins (MFN1, Drp1), and mitophagy-related proteins (PINK1, Parkin, and LC3). Results Compared with the control group, the weight gain rate of the PM_2.5 group was slowed down (P<0.05), which was alleviated by the Sal intervention (P<0.05). The lung coefficient increased after the PM_2.5 exposure (P<0.05), which was alleviated by Sal intervention. Compared with the control group, the PM_2.5 group showed severe alveolar structure damage, inflammatory cell infiltration, and blue collagen deposition, and significantly increased the lung injury score, collagen volume fraction (CVF), Szapiel score, and Ashcroft score (P<0.05), as well as serum oxidative stress levels (P<0.05). The protein expression levels of Collagen-III, α-SMA, Drp1, PINK1, Parkin, and LC3 II/I were increased (P<0.05), and the expression of MFN1 was decreased (P<0.05). Compared with the PM_2.5 group, the Sal intervention alleviated lung injury, reduced inflammatory cell infiltration and collagen deposition, showing decreased lung injury score, CVF, Szapiel score, and Ashcroft score (P<0.05), and decreased serum oxidative stress levels (P<0.05); the protein expression levels of Collagen-III, α-SMA, PINK1, Parkin, and LC3 II/I were decreased (P<0.05), the expression level of Drp1 was decreased, and the expression level of MFN1 was increased. Conclusion In the process of pulmonary fibrosis induced by PM_2.5 exposure in mice, Sal may affect mitochondrial autophagy through PINK1/Parkin pathway and play a protective role. The specific mechanism needs to be further verified.

Objective To analyze the differences of brain activity between first-episode untreated depressive patients with and without suicidal ideation(SI),and its correlations with clinical characteristics.Methods A total of 40 major depressive disorder(MDD)patients with SI(MDD+SI group),40 patients without SI MDD(MDD+NSI group),and 40 healthy controls(HC)(HC group)were enrolled.The 17-item Hamilton depression scale(HAMD-17)and Beck scale for suicide ideation(BSI)were used to assess the severity of depression and SI,respectively.MRI data were collected.The values of fractional amplitude of low-frequency fluctuation(fALFF)were calculated.Results(1)Compared with the HC group,the MDD+NSI group showed decreases in the fALFF val-ues of the default network and attention network.The fALFF values of the attention network in the MDD+SI group showed decreases.Compared with the MDD+NSI group,the MDD+SI group showed decreases in the fALFF values of the attention network.(2)The fALFF values in the left middle frontal gyrus were negatively correlated with the total score of HAMD-17(r=-0.55;P<0.001)in the MDD+NSI group,while the fALFF values in the left middle frontal gyrus were negatively correlated with the total score of HAMD-17(r=-0.53;P<0.001)and the total score of BSI(r=-0.51;P<0.001)in the MDD+SI group.(3)The optimal critical value of fALFF value in left middle frontal gyrus for predicting SI occurrence in MDD patients was-0.039,area under the curve(AUC)was 0.76,sensitivity was 0.63,and specificity was 0.80.Conclusion The decreased local activity intensity in the left middle frontal gyrus of the brain might be the central mechanism for the occurrence of SI in MDD patients.In addition,the left middle frontal gyrus might have certain value in identifying SI and predicting the severity of SI.

Objective To investigate the protective effect and mechanism of calcium dobesilate on oxidative damage induced by high-glucose in Müller cells.Methods The oxidative damage model of Müller cells induced by high-glucose was established and the cells were divided into 4groups.The control group was cultured normally,and the high glucose group was cultured in the medium of 35mmol/L glucose.The control+calcium dobesilate group was treated with 0.5μmol/L calcium dobesilate intervention cells on the basis of routine culture,and the high sugar+calcium dobesilate group was treated with 0.5μmol/L calcium dobesilate intervention cells on the basis of high glucose.Cell proliferation was assessed by CCK-8,apoptosis was detected by flow cytometry,and oxidative stress markers were detected by the kit.Intracellular correction potassium channel subtype 4.1(Kir4.1)and aquaporin 4(AQP4)protein levels were detected by western blot.Results Compared with the control group,the proliferative activity of Müller cells of the high glucose group was decreased,apoptosis rate was increased,oxidative stress occurred,AQP4 protein expression level was increased and Kir4.1 protein level was decreased(P＜0.05).Compared with the high glucose group,the cell activity and apoptosis rate of the high glucose+calcium do-besilate group were increased,the oxidative stress damage was alleviated,the AQP4 protein expression level was decreased and the Kir4.1 protein level was increased(P＜0.05).Conclusion Calcium dobesilate may inhibit the oxidative damage of Müller cells induced by high-glucose by regulating the AQP4/Kir4.1 axis.

Objective:To observe the effect of point injection at Zusanli(ST36)plus abdominal point application on gastrointestinal dysfunction after laparoscopic surgery.Methods:A total of 204 patients with gastrointestinal dysfunction after laparoscopic surgery were recruited and divided into four groups using the random number table method,with 51 cases in each group.The control group received conventional postoperative intervention.In addition to the treatment in the control group,the point injection group was given point injection at Zusanli(ST36),the application group was offered abdominal point application,and the integrated group received point injection at Zusanli(ST36)and abdominal point application.The treatment lasted 3 consecutive days in all four groups.The recovery time of gastrointestinal function indicators and the incidence rate of postoperative nausea and vomiting(PONV)were observed and recorded.Before and after treatment,the visual analog scale(VAS)was used to assess abdominal pain intensity,the venous blood type 1 helper T cells/type 2 helper T cells(Th1/Th2)was determined,the serum levels of interleukin(IL)-6 and interferon(IFN)-γ were detected using the enzyme-linked immunosorbent assay,and the plasma levels of motilin and gastrin were measured using radioimmunoassay.Results:Compared to the control group,the first exhaust time,the first defecation time,and the time of restoring fluid diet came earlier in the other three groups(P<0.05)and were earlier in the integrated group than in the point injection and application groups(P<0.05).The point injection,application,and integrated groups had a lower PONV incidence rate than the control group,and the integrated group was lower than the point injection and application groups(P<0.05).The intra-group comparisons showed that the VAS score and the levels of IL-6 and INF-γ decreased after treatment in all four groups(P<0.05);the point injection,application,and integrated groups were lower than the control group(P<0.05),and the integrated group was lower than the point injection and application groups(P<0.05).The intra-group comparisons also demonstrated that the levels of Th1/Th2,motilin,and gastrin increased after the intervention in the four groups(P<0.05);the point injection,application,and integrated groups were higher than the control group(P<0.05),and the integrated group was higher than the point injection and application groups(P<0.05).Conclusion:Point injection at Zusanli(ST36)plus abdominal point application can encourage postoperative exhaust,defecation,and the recovery of diet fluid,alleviate postoperative abdominal pain,reduce PONV,balance Th1/Th2,and regulate the secretion of motilin and gastrin in patients with gastrointestinal dysfunction after laparoscopic surgery.