Objective:To explore the predictive value of human cartilage glycoprotein 39 (YKL-40) and growth differentiation factor 15 (GDF-15) for clinical outcomes of patients with Parkinson disease (PD).Methods:A total of 109 patients with PD admitted to Xinxiang Central Hospital from February 2021 to February 2023 were selected and treated with regular anti-PD medications for 4 weeks, with dosage appropriately adjusted according to clinical status and individual response.Clinical outcomes were evaluated after 2 months of treatment, and the predictive value of serum YKL-40 and GDF-15 at admission for clinical outcomes was analyzed.Data were analyzed by independent sample t-test, χ2 test and Logistic regression using SPSS 26.0. Results:PD patients with poor outcomes exhibited higher serum levels of YKL-40((3.18±0.67)mg/L, (2.34±0.41)mg/L) and GDF-15((457.82±142.83)pg/mL, (282.95±105.96)pg/mL) than those with good outcomes, and the differences were statistically significant ( t=8.082, 7.349, both P<0.05).Logistic regression analysis showed that elevated serum levels of YKL-40( B=0.664, OR=1.943, 95% CI=1.237-3.052) and GDF-15( B=0.185, OR=1.787, 95% CI=1.145-2.789) both influenced the clinical outcomes of PD patients(both P<0.05).Serum YKL-40 combined with GDF-15 demonstrated a predictive sensitivity of 87.23%, specificity of 90.32%, and AUC of 0.927(95% CI=0.861-0.968) for clinical outcomes in PD patients.The AUC was significantly higher than that achieved by either indicator alone (YKL-40: AUC (95% CI)=0.722 (0.628-0.804); GDF-15: AUC (95% CI)=0.797 (0.709-0.868)). Conclusion:The elevated levels of YKL-40 and GDF-15 in PD patients are associated with clinical outcomes, which may be the potential markers for predicting clinical outcomes of patients with PD.

Objective:To explore the predictive value of human cartilage glycoprotein 39 (YKL-40) and growth differentiation factor 15 (GDF-15) for clinical outcomes of patients with Parkinson disease (PD).Methods:A total of 109 patients with PD admitted to Xinxiang Central Hospital from February 2021 to February 2023 were selected and treated with regular anti-PD medications for 4 weeks, with dosage appropriately adjusted according to clinical status and individual response.Clinical outcomes were evaluated after 2 months of treatment, and the predictive value of serum YKL-40 and GDF-15 at admission for clinical outcomes was analyzed.Data were analyzed by independent sample t-test, χ2 test and Logistic regression using SPSS 26.0. Results:PD patients with poor outcomes exhibited higher serum levels of YKL-40((3.18±0.67)mg/L, (2.34±0.41)mg/L) and GDF-15((457.82±142.83)pg/mL, (282.95±105.96)pg/mL) than those with good outcomes, and the differences were statistically significant ( t=8.082, 7.349, both P<0.05).Logistic regression analysis showed that elevated serum levels of YKL-40( B=0.664, OR=1.943, 95% CI=1.237-3.052) and GDF-15( B=0.185, OR=1.787, 95% CI=1.145-2.789) both influenced the clinical outcomes of PD patients(both P<0.05).Serum YKL-40 combined with GDF-15 demonstrated a predictive sensitivity of 87.23%, specificity of 90.32%, and AUC of 0.927(95% CI=0.861-0.968) for clinical outcomes in PD patients.The AUC was significantly higher than that achieved by either indicator alone (YKL-40: AUC (95% CI)=0.722 (0.628-0.804); GDF-15: AUC (95% CI)=0.797 (0.709-0.868)). Conclusion:The elevated levels of YKL-40 and GDF-15 in PD patients are associated with clinical outcomes, which may be the potential markers for predicting clinical outcomes of patients with PD.

The specific mechanisms of interferon regulatory factor 8(IRF8)in porcine intestinal in-nate immunity and resistance to enteric virus infection remain to be elucidated.To investigate the immunoregulatory role of IRF8,establishing an IRF8 gene knockout porcine intestinal epithelial cell(IPEC-J2)monoclonal cell line is of significant importance.This study initially aimed to obtain recombinant adeno-associated virus rAAV-sgIRF8-eGFP capable of knocking out the IRF8 gene through co-transfection of HEK-293T cells with three plasmids.Subsequently,IPEC-J2 cells were infected with the virus,and those expressing eGFP were selected by flow cytometry and cultured to form monoclonal cell lines.These cell lines were then identified by Sanger sequencing and West-ern blot techniques.Lastly,qPCR analysis was used to measure the expression levels of interferon factors IFN-α,IFN-β,IFN-γ and IFN-λ,providing preliminary insights into the impact of IRF8 gene knockout on IPEC-J2 cell immunity.The results demonstrated successful generation of rAAV-sgIRF8-eGFP,which successfully infected IPEC-J2 cells leading to eGFP fluorescence.Flow cytometry followed by cell culture led to the establishment of two monoclonal cell lines,IRF8-KO1 and IRF8-KO3.Sanger sequencing revealed a five-base deletion in IRF8-KO1 and a seven-base dele-tion in IRF8-KO3.Western blot confirmed the absence of IRF8 protein expression in IRF8-KO1,making it an ideal candidate monoclonal cell line.qPCR analysis of interferon factors indicated sig-nificant decrease in IFN-γ(P＜0.05)and IFN-λ(P＜0.01)transcription level in IRF8-knockout cells,while the transcription levels of IFN-α and IFN-β remained relatively unchanged.This study successfully established an IRF8 gene knockout IPEC-J2 monoclonal cell line,providing a founda-tion for further research on IRF8-related porcine intestinal immune regulation and mechanisms of intestinal virus infection.

Monotropein is a compound classified into iridoid which is found in herbaceous plants Morindae officinalis. It possesses anti-inflammatory, antioxidant, and anti-osteoarthritic activities. Previous study indicates that monotropein may have the potential to combat cardiovascular disease, although the related mechanism remains unclear. In this study, we constructed the model of atherosclerosis by oxidized low density lipoprotein-induced vascular smooth muscle cells and LDLR –/–mice given high-fat diet to investigate the effects of monotropein on atherosclerosis.Our results showed that monotropein treatment significantly reduced the area of atherosclerotic plaques and necrotic cores in mice, inhibited the proliferation and migration of vascular smooth muscle cells, and reduced inflammatory responses and oxidative stress, which in turn alleviated atherosclerosis. In addition, we found that monotropein reduced the expression levels of P-NF-κB and P-AP-1. In conclusion, our data suggest that monotropein inhibited the proliferation and migration of vascular smooth muscle cells by mediating the activity of NF-κB, AP-1, reducing the level of inflammation and oxidative stress, and thus resisting the development of atherosclerosis. These findings demonstrate the efficacious therapeutic impact of monotropein on atherosclerosis and elucidate its specific target.

Monotropein is a compound classified into iridoid which is found in herbaceous plants Morindae officinalis. It possesses anti-inflammatory, antioxidant, and anti-osteoarthritic activities. Previous study indicates that monotropein may have the potential to combat cardiovascular disease, although the related mechanism remains unclear. In this study, we constructed the model of atherosclerosis by oxidized low density lipoprotein-induced vascular smooth muscle cells and LDLR –/–mice given high-fat diet to investigate the effects of monotropein on atherosclerosis.Our results showed that monotropein treatment significantly reduced the area of atherosclerotic plaques and necrotic cores in mice, inhibited the proliferation and migration of vascular smooth muscle cells, and reduced inflammatory responses and oxidative stress, which in turn alleviated atherosclerosis. In addition, we found that monotropein reduced the expression levels of P-NF-κB and P-AP-1. In conclusion, our data suggest that monotropein inhibited the proliferation and migration of vascular smooth muscle cells by mediating the activity of NF-κB, AP-1, reducing the level of inflammation and oxidative stress, and thus resisting the development of atherosclerosis. These findings demonstrate the efficacious therapeutic impact of monotropein on atherosclerosis and elucidate its specific target.

Monotropein is a compound classified into iridoid which is found in herbaceous plants Morindae officinalis. It possesses anti-inflammatory, antioxidant, and anti-osteoarthritic activities. Previous study indicates that monotropein may have the potential to combat cardiovascular disease, although the related mechanism remains unclear. In this study, we constructed the model of atherosclerosis by oxidized low density lipoprotein-induced vascular smooth muscle cells and LDLR –/–mice given high-fat diet to investigate the effects of monotropein on atherosclerosis.Our results showed that monotropein treatment significantly reduced the area of atherosclerotic plaques and necrotic cores in mice, inhibited the proliferation and migration of vascular smooth muscle cells, and reduced inflammatory responses and oxidative stress, which in turn alleviated atherosclerosis. In addition, we found that monotropein reduced the expression levels of P-NF-κB and P-AP-1. In conclusion, our data suggest that monotropein inhibited the proliferation and migration of vascular smooth muscle cells by mediating the activity of NF-κB, AP-1, reducing the level of inflammation and oxidative stress, and thus resisting the development of atherosclerosis. These findings demonstrate the efficacious therapeutic impact of monotropein on atherosclerosis and elucidate its specific target.

Monotropein is a compound classified into iridoid which is found in herbaceous plants Morindae officinalis. It possesses anti-inflammatory, antioxidant, and anti-osteoarthritic activities. Previous study indicates that monotropein may have the potential to combat cardiovascular disease, although the related mechanism remains unclear. In this study, we constructed the model of atherosclerosis by oxidized low density lipoprotein-induced vascular smooth muscle cells and LDLR –/–mice given high-fat diet to investigate the effects of monotropein on atherosclerosis.Our results showed that monotropein treatment significantly reduced the area of atherosclerotic plaques and necrotic cores in mice, inhibited the proliferation and migration of vascular smooth muscle cells, and reduced inflammatory responses and oxidative stress, which in turn alleviated atherosclerosis. In addition, we found that monotropein reduced the expression levels of P-NF-κB and P-AP-1. In conclusion, our data suggest that monotropein inhibited the proliferation and migration of vascular smooth muscle cells by mediating the activity of NF-κB, AP-1, reducing the level of inflammation and oxidative stress, and thus resisting the development of atherosclerosis. These findings demonstrate the efficacious therapeutic impact of monotropein on atherosclerosis and elucidate its specific target.

Monotropein is a compound classified into iridoid which is found in herbaceous plants Morindae officinalis. It possesses anti-inflammatory, antioxidant, and anti-osteoarthritic activities. Previous study indicates that monotropein may have the potential to combat cardiovascular disease, although the related mechanism remains unclear. In this study, we constructed the model of atherosclerosis by oxidized low density lipoprotein-induced vascular smooth muscle cells and LDLR –/–mice given high-fat diet to investigate the effects of monotropein on atherosclerosis.Our results showed that monotropein treatment significantly reduced the area of atherosclerotic plaques and necrotic cores in mice, inhibited the proliferation and migration of vascular smooth muscle cells, and reduced inflammatory responses and oxidative stress, which in turn alleviated atherosclerosis. In addition, we found that monotropein reduced the expression levels of P-NF-κB and P-AP-1. In conclusion, our data suggest that monotropein inhibited the proliferation and migration of vascular smooth muscle cells by mediating the activity of NF-κB, AP-1, reducing the level of inflammation and oxidative stress, and thus resisting the development of atherosclerosis. These findings demonstrate the efficacious therapeutic impact of monotropein on atherosclerosis and elucidate its specific target.

The specific mechanisms of interferon regulatory factor 8(IRF8)in porcine intestinal in-nate immunity and resistance to enteric virus infection remain to be elucidated.To investigate the immunoregulatory role of IRF8,establishing an IRF8 gene knockout porcine intestinal epithelial cell(IPEC-J2)monoclonal cell line is of significant importance.This study initially aimed to obtain recombinant adeno-associated virus rAAV-sgIRF8-eGFP capable of knocking out the IRF8 gene through co-transfection of HEK-293T cells with three plasmids.Subsequently,IPEC-J2 cells were infected with the virus,and those expressing eGFP were selected by flow cytometry and cultured to form monoclonal cell lines.These cell lines were then identified by Sanger sequencing and West-ern blot techniques.Lastly,qPCR analysis was used to measure the expression levels of interferon factors IFN-α,IFN-β,IFN-γ and IFN-λ,providing preliminary insights into the impact of IRF8 gene knockout on IPEC-J2 cell immunity.The results demonstrated successful generation of rAAV-sgIRF8-eGFP,which successfully infected IPEC-J2 cells leading to eGFP fluorescence.Flow cytometry followed by cell culture led to the establishment of two monoclonal cell lines,IRF8-KO1 and IRF8-KO3.Sanger sequencing revealed a five-base deletion in IRF8-KO1 and a seven-base dele-tion in IRF8-KO3.Western blot confirmed the absence of IRF8 protein expression in IRF8-KO1,making it an ideal candidate monoclonal cell line.qPCR analysis of interferon factors indicated sig-nificant decrease in IFN-γ(P＜0.05)and IFN-λ(P＜0.01)transcription level in IRF8-knockout cells,while the transcription levels of IFN-α and IFN-β remained relatively unchanged.This study successfully established an IRF8 gene knockout IPEC-J2 monoclonal cell line,providing a founda-tion for further research on IRF8-related porcine intestinal immune regulation and mechanisms of intestinal virus infection.

Objective:To observe the long-term efficacy and safety of macular buckling (MB) in the treatment of high myopia traction maculopathy.Methods:A retrospective clinical study. From January 2014 to December 2017, 57 eyes of 57 patients with high myopia traction maculopathy who underwent MB treatment at Zhongshan Ophthalmic Center of Sun Yat-sen University were included in the study. Among them, there were 15 males with 15 eyes, average age was 51.80±10.72 years; there were 42 females with 42 eyes, average age was 59.14±11.51 years. There were 21 eyes of 21 cases with highly myopic macular hole with macular detachment (MHMD), and 36 eyes in 36 cases with highly myopic foveoschisis with macular detachment (FSMD), and they were grouped accordingly. All patients underwent best corrected visual acuity (BCVA), optical coherence tomography (OCT), and axial length (AL) measurements. The standard logarithmic visual acuity chart was used for BCVA examination, which was converted into logarithm of the minimum angle of resolution (logMAR) visual acuity during statistics. All patients underwent MB, either on its own or combined with vitrectomy. Patients with significant vitreous macular traction on OCT were treated with combined surgery. One, 3, 6 months and 1, 2, 3, and 4 years after the operation, the same equipment and methods before the operation were used to conduct related examinations, and the long-term efficacy and safety of the two groups of eyes were observed.Results:Before surgery, the logMAR BCVA of eyes in MHMD group and FSMD group were 1.35±0.47 and 1.17±0.59, respectively; 4 years after surgery, they were 1.02±0.49 and 0.73±0.55, respectively. The BCVA improved significantly at postoperative 4 years than preoperative in both groups ( P=0.039, 0.001). In the eyes with MHMD, the BCVA was found to be significant improved 3 years after surgery ( P=0.042). Whereas, in the eyes with FSMD, the BCVA was found to be significantly improved 3 months after surgery ( P=0.013). Macular reattachment was achieved in 100% of cases, while macular hole closure rate was achieved in 66.7% in the MHMD group. In the FSMD group, either macular reattachment rate or the foveoschisis resolution rate was 97.2%. After surgery, choroidal neovascularization was observed in 2 eyes, and 3 eyes with intraretinal cyst. Conclusion:MB may represent a safe and effective surgical option for the treatment of high myopia maculopathy.