Geraniin, a polyphenol derived from the fruit peel of Nephelium lappaceum L., has been shown to possess anti-inflammatory and antioxidant properties in the cardiovascular system. The present study explored whether geraniin could protect against an isoproterenol (ISO)-induced cardiac hypertrophy model. Mice in the ISO group received an intraperitoneal injection of ISO (5 mg/kg) once daily for 9 days, and the administration group were injected with ISO after 5 days of treatment with geraniin or spironolactone. Potential therapeutic effects and related mechanisms analysed by anatomical coefficients, histopathology, blood biochemical indices, reverse transcription-PCR and immunoblotting. Geraniin decreased the cardiac pathologic remodeling and myocardial fibrosis induced by ISO, as evidenced by the modifications to anatomical coefficients, as well as the reduction in collagen I/III á1mRNA and protein expression and cross-sectional area in hypertrophic cardiac tissue. In addition, geraniin treatment reduced ISO-induced increase in the mRNA and protein expression levels of interleukin (IL)-6, IL-1β and tumor necrosis factor-α, whereas ISO-induced IL-10 showed the opposite behaviour in hypertrophic cardiac tissue.Further analysis showed that geraniin partially reversed the ISO-induced increase in malondialdehyde and nitric oxide, and the ISO-induced decrease in glutathione, superoxide dismutase and glutathione. Furthermore, it suppressed the ISO-induced cellular apoptosis of hypertrophic cardiac tissue, as evidenced by the decrease in Bcell lymphoma-2 (Bcl-2)-associated X/caspase-3/caspase-9 expression, increase in Bcl-2 expression, and decrease in TdT-mediated dUTP nick-end labeling-positive cells.These findings suggest that geraniin can attenuate ISO-induced cardiac hypertrophy by inhibiting inflammation, oxidative stress and cellular apoptosis.

Geraniin, a polyphenol derived from the fruit peel of Nephelium lappaceum L., has been shown to possess anti-inflammatory and antioxidant properties in the cardiovascular system. The present study explored whether geraniin could protect against an isoproterenol (ISO)-induced cardiac hypertrophy model. Mice in the ISO group received an intraperitoneal injection of ISO (5 mg/kg) once daily for 9 days, and the administration group were injected with ISO after 5 days of treatment with geraniin or spironolactone. Potential therapeutic effects and related mechanisms analysed by anatomical coefficients, histopathology, blood biochemical indices, reverse transcription-PCR and immunoblotting. Geraniin decreased the cardiac pathologic remodeling and myocardial fibrosis induced by ISO, as evidenced by the modifications to anatomical coefficients, as well as the reduction in collagen I/III á1mRNA and protein expression and cross-sectional area in hypertrophic cardiac tissue. In addition, geraniin treatment reduced ISO-induced increase in the mRNA and protein expression levels of interleukin (IL)-6, IL-1β and tumor necrosis factor-α, whereas ISO-induced IL-10 showed the opposite behaviour in hypertrophic cardiac tissue.Further analysis showed that geraniin partially reversed the ISO-induced increase in malondialdehyde and nitric oxide, and the ISO-induced decrease in glutathione, superoxide dismutase and glutathione. Furthermore, it suppressed the ISO-induced cellular apoptosis of hypertrophic cardiac tissue, as evidenced by the decrease in Bcell lymphoma-2 (Bcl-2)-associated X/caspase-3/caspase-9 expression, increase in Bcl-2 expression, and decrease in TdT-mediated dUTP nick-end labeling-positive cells.These findings suggest that geraniin can attenuate ISO-induced cardiac hypertrophy by inhibiting inflammation, oxidative stress and cellular apoptosis.

Geraniin, a polyphenol derived from the fruit peel of Nephelium lappaceum L., has been shown to possess anti-inflammatory and antioxidant properties in the cardiovascular system. The present study explored whether geraniin could protect against an isoproterenol (ISO)-induced cardiac hypertrophy model. Mice in the ISO group received an intraperitoneal injection of ISO (5 mg/kg) once daily for 9 days, and the administration group were injected with ISO after 5 days of treatment with geraniin or spironolactone. Potential therapeutic effects and related mechanisms analysed by anatomical coefficients, histopathology, blood biochemical indices, reverse transcription-PCR and immunoblotting. Geraniin decreased the cardiac pathologic remodeling and myocardial fibrosis induced by ISO, as evidenced by the modifications to anatomical coefficients, as well as the reduction in collagen I/III á1mRNA and protein expression and cross-sectional area in hypertrophic cardiac tissue. In addition, geraniin treatment reduced ISO-induced increase in the mRNA and protein expression levels of interleukin (IL)-6, IL-1β and tumor necrosis factor-α, whereas ISO-induced IL-10 showed the opposite behaviour in hypertrophic cardiac tissue.Further analysis showed that geraniin partially reversed the ISO-induced increase in malondialdehyde and nitric oxide, and the ISO-induced decrease in glutathione, superoxide dismutase and glutathione. Furthermore, it suppressed the ISO-induced cellular apoptosis of hypertrophic cardiac tissue, as evidenced by the decrease in Bcell lymphoma-2 (Bcl-2)-associated X/caspase-3/caspase-9 expression, increase in Bcl-2 expression, and decrease in TdT-mediated dUTP nick-end labeling-positive cells.These findings suggest that geraniin can attenuate ISO-induced cardiac hypertrophy by inhibiting inflammation, oxidative stress and cellular apoptosis.

Geraniin, a polyphenol derived from the fruit peel of Nephelium lappaceum L., has been shown to possess anti-inflammatory and antioxidant properties in the cardiovascular system. The present study explored whether geraniin could protect against an isoproterenol (ISO)-induced cardiac hypertrophy model. Mice in the ISO group received an intraperitoneal injection of ISO (5 mg/kg) once daily for 9 days, and the administration group were injected with ISO after 5 days of treatment with geraniin or spironolactone. Potential therapeutic effects and related mechanisms analysed by anatomical coefficients, histopathology, blood biochemical indices, reverse transcription-PCR and immunoblotting. Geraniin decreased the cardiac pathologic remodeling and myocardial fibrosis induced by ISO, as evidenced by the modifications to anatomical coefficients, as well as the reduction in collagen I/III á1mRNA and protein expression and cross-sectional area in hypertrophic cardiac tissue. In addition, geraniin treatment reduced ISO-induced increase in the mRNA and protein expression levels of interleukin (IL)-6, IL-1β and tumor necrosis factor-α, whereas ISO-induced IL-10 showed the opposite behaviour in hypertrophic cardiac tissue.Further analysis showed that geraniin partially reversed the ISO-induced increase in malondialdehyde and nitric oxide, and the ISO-induced decrease in glutathione, superoxide dismutase and glutathione. Furthermore, it suppressed the ISO-induced cellular apoptosis of hypertrophic cardiac tissue, as evidenced by the decrease in Bcell lymphoma-2 (Bcl-2)-associated X/caspase-3/caspase-9 expression, increase in Bcl-2 expression, and decrease in TdT-mediated dUTP nick-end labeling-positive cells.These findings suggest that geraniin can attenuate ISO-induced cardiac hypertrophy by inhibiting inflammation, oxidative stress and cellular apoptosis.

Geraniin, a polyphenol derived from the fruit peel of Nephelium lappaceum L., has been shown to possess anti-inflammatory and antioxidant properties in the cardiovascular system. The present study explored whether geraniin could protect against an isoproterenol (ISO)-induced cardiac hypertrophy model. Mice in the ISO group received an intraperitoneal injection of ISO (5 mg/kg) once daily for 9 days, and the administration group were injected with ISO after 5 days of treatment with geraniin or spironolactone. Potential therapeutic effects and related mechanisms analysed by anatomical coefficients, histopathology, blood biochemical indices, reverse transcription-PCR and immunoblotting. Geraniin decreased the cardiac pathologic remodeling and myocardial fibrosis induced by ISO, as evidenced by the modifications to anatomical coefficients, as well as the reduction in collagen I/III á1mRNA and protein expression and cross-sectional area in hypertrophic cardiac tissue. In addition, geraniin treatment reduced ISO-induced increase in the mRNA and protein expression levels of interleukin (IL)-6, IL-1β and tumor necrosis factor-α, whereas ISO-induced IL-10 showed the opposite behaviour in hypertrophic cardiac tissue.Further analysis showed that geraniin partially reversed the ISO-induced increase in malondialdehyde and nitric oxide, and the ISO-induced decrease in glutathione, superoxide dismutase and glutathione. Furthermore, it suppressed the ISO-induced cellular apoptosis of hypertrophic cardiac tissue, as evidenced by the decrease in Bcell lymphoma-2 (Bcl-2)-associated X/caspase-3/caspase-9 expression, increase in Bcl-2 expression, and decrease in TdT-mediated dUTP nick-end labeling-positive cells.These findings suggest that geraniin can attenuate ISO-induced cardiac hypertrophy by inhibiting inflammation, oxidative stress and cellular apoptosis.

We will review a case of adrenal aldosterone-cortisol co-producing adenoma (A/CPA) admitted to our hospital on May 7, 2021. By reviewing the clinical courses of this case and its relevant literatures, we hope to improve the understanding and treatment level of this disease.

Objective To evaluate the degree of brain atrophy in spinocerebellar ataxia type 3(SCA3)patients based on artificial intelligence(AI)technology,and to explore the correlation between the degree of brain atrophy and the severity of the disease.Methods The clinical and imaging data of 23 SCA3 patients(SCA3 group)and 24 healthy controls(HC)(HC group)were collected.The International Cooperative Ataxia Rating Scale(ICARS)was used to evaluate the severity of ataxia in patients with SCA3.AI technology was used to process the 3D-T1 WI MR image data of the SCA3 and HC groups to segment and measure the volume and volume percentage of brain,followed by correlation analyses between brain structural alterations and the severity of ataxia in SCA3 patients.Results There were no significant differences in gender and age between the two groups(P＞0.05).The SCA3 group had a significant reduction in the volume and volume percentage of various brain regions,such as the frontal,temporal,parietal,occipital,limbic,right cerebral white mat-ter,subcortical gray matter,cerebellum and brainstem,compared to the HC group(multiple hypothesis testing adjusted P＜0.01).In the SCA3 group,the ICARS showed positive correlation with patient age(r=0.571,P=0.004)and negative correlation with the vol-ume of the left cerebellar white matter,vermis,medulla oblongata,and the volume percentages of bilateral cerebellar white matter,vermis,pons,medulla oblongata(P＜0.05).Conclusion The significant atrophy of the supratentorial and subtentorial regions of the brain in SCA3 patients.The globus pallidus exhibits the most substantial atrophy,suggesting its potential as an imaging diagnostic marker of SC A3.

Objective:To observe the effect of rhGLP-1 (7-36) on Akt/GSK3 signaling pathway in hepatocytes.Methods:Human HL7702 cell line was cultured to the logarithmic growth stage and divided into experimental group and blank control group. The cultures were incubated with 100nM medium containing rhglp-1 (7-36) and without rhglp-1 (7-36) for 90min. The levels of Akt, Glycogen synthase Kinase 3 (GSK3) and Glycogen synthase (GS) in the two groups were detected by Western Blot.Results:Compared with blank control group, the protein expression of p-Akt (Thr308) in experimental group (1.81±0.28) was significantly increased ( P=0.01), but the protein expression of Akt and p-Akt (Ser473) was not significantly changed. The protein expression levels of p-GSK3α (Ser21) (1.27±0.09) and p-GSK3β (Ser9) (1.24±0.09) in the experimental group were significantly increased ( P=0.003, 0.002), while the protein expression levels of GSK3α and GSK3β were not significantly changed. The protein expression level of p-GS (Ser641) (0.70±0.16) was decreased in the experimental group ( P=0.03), but the protein expression level of GS did not change significantly. Conclusion:Glp-1 can inhibit GSK3/GS signaling pathway, activate GS activity and promote glycogen synthesis.

Objective:To assess the safety and efficiency of left atrial appendage closure (LAAC) combined delayed anticoagulant therapy in atrial fibrillation (AF) patients combined with cardiogenic stroke during anticoagulant therapy.Methods:Using prospective research methods, 35 AF patients combined with cardiogenic stroke during anticoagulant therapy from September 2020 to June 2022 in Xuanwu Hospital, Capital Medical University were selected. All patients were treated with LAAC and delayed anticoagulant therapy. The endpoints were the safety and efficacy of LAAC combined with delayed anticoagulant therapy. The primary endpoint of efficacy was the composite endpoint of postoperative death, myocardial infarction, hemorrhagic stroke and systemic embolism. The safety endpoint was major bleeding as defined by the International Society for Thrombosis and Hemostasis and clinically relevant non-major bleeding.Results:Among 35 patients, 21 were males and 14 were females; the age was (68.5 ± 9.3) years old; the CHA 2DS 2-VASc score was 5 (4, 6) scores; the time to the last stroke was 95 (42, 98) d; the National Institutes of Health stroke scale score at the time of stroke was 3 (1, 6) scores. All patients successfully completed LAAC without perioperative instrument-surface thrombosis, death, new stroke or bleeding events. Thirty-two patients continued oral anticoagulant therapy 45 d after LAAC. The patients were followed up for (12.6 ± 4.3) months, 1 patient experienced recurrent ischemic stroke, 2 patients endured mucosal bleeding, there were no adverse events such as all-cause death, cardiovascular death, systemic embolism and hemorrhagic stroke. Conclusions:The LAAC combined delayed anticoagulant therapy is efficient and safe in patients with AF. For AF patients combined with cardiogenic stroke during anticoagulant therapy, LAAC combined with delayed anticoagulation therapy may be considered to further prevent ischemic stroke events.

Objective:To compare surgery-related indicators, patient recovery status, perioperative complications and risk factors affecting the occurrence of postoperative grade Ⅲ or higher complications in patients undergoing laparoscopic gastric mesenchymal tumor surgery with different visceral fat areas.Methods:Clinical data of 116 patients with gastric interstitial tumor in Shaanxi Provincial People′s Hospital from April 2014 to June 2020 were retrospectively analyzed, including 44 male patients and 72 female patients, with patient aged from 25 to 88 years old and the mean age was (61.8±10.7) years, including 54 patients in the high VFA group and 62 patients in the low VFA group. SPSS 23.0 was used for statistical analysis, and t-test and χ2 test were applied to compare and analyze the patients′ surgery-related indexes, postoperative recovery status, complications within 30 d after surgery and differences in Clavien-Dindo classification of complications, while univariate and multifactorial analyses were used to study the factors affecting the occurrence of postoperative grade Ⅲ or higher complications. Results:Patients in the high VFA group had a higher body mass index than in the low VFA group, and the difference was statistically significant ( t=4.48, P<0.001); patients in the high VFA group had longer operative time ( t=2.88, P=0.005), more intraoperative bleeding ( t=2.17, P=0.032), longer period of fasting ( t=2.73, P=0.008), longer time for defecation ( t=4.46, P<0.001) and bowel movement ( t=4.62, P<0.001), and longer postoperative hospital stay ( t=3.43) compared with those in the low VFA group ( t=2.73, P=0.001), prolonged defecation ( t=4.46), prolonged bowel movement ( t=4.62), and prolonged postoperative hospitalization ( t=3.43), with statistically significant differences ( P<0.05); the incidence of postoperative complications was significantly higher in the high VFA group (31.4%) compared with the low VFA group (14.5%) ( χ2=4.78, P=0.029); among them, the incidence of postoperative pulmonary infection was significantly higher in patients in the high VFA group (12.9%) compared with those in the low VFA group (1.6%), and the difference between them was statistically significant ( χ2=4.16, P<0.05); while the differences in postoperative incision-related complications, anastomotic fistula, lower limb venous thrombosis, and intestinal obstruction were not statistically significant ( P>0.05). The incidence of postoperative complications above grade Ⅲ of the Clavien-Dindo complication classification was significantly higher in patients in the high VFA group (16.7%) compared with those in the low VFA group (4.8%), and the difference between the two was statistically significant ( χ2=4.35, P<0.05); univariate analysis revealed that operative time ≥300 min and increased VFA were the risk factors for postoperative grade Ⅲ or higher complications, while VFA was not an independent risk factor. Conclusion:Larger visceral fat area increases the difficulty of laparoscopic gastric mesenchymal tumor surgery operation, and also affects patients′ postoperative recovery, leading to increased postoperative complications, but VFA is not an independent risk factor affecting the occurrence of postoperative grade Ⅲ or higher complications in patients with gastric mesenchymal tumor.