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.

Objective:To compare the diagnostic efficacy of 68Ga-prostate-specific membrane antigen (PSMA)-617 PET/CT and multiparametric magnetic resonance imaging (mpMRI) in detecting extraprostatic extension (EPE) and seminal vesicle invasion (SVI) in prostate cancer. Methods:A retrospective analysis was conducted on the clinical data of 113 patients with localized prostate cancer who underwent both 68Ga-PSMA-617 PET/CT and mpMRI at Xiangya Hospital, Central South University, from May 2018 to May 2024 prior to radical prostatectomy (RP). The median age of the patients was 66.0 (61.3, 71.0) years old, with a median body mass index of 28.86 (19.01, 24.77) kg/m 2, and a median prostate-specific antigen (PSA) level of 13.50(9.26, 21.99) ng/ml. The pathological results after RP were used as the gold standard to compare the sensitivity, specificity, positive predictive value, and negative predictive value of the two imaging modalities in diagnosing EPE and SVI. Additionally, the diagnostic value of combining both imaging modalities was explored, employing a parallel strategy where a positive result from either modality was deemed positive, and only when both tests were negative was the result considered negative. Results:Pathological results after RP indicated EPE in 46 cases (40.71%) and SVI in 11 cases (9.70%). In diagnosing EPE, the sensitivity, specificity, positive predictive value, and negative predictive value of 68Ga-PSMA-617 PET/CT were 17.39% (8/46), 97.01% (65/67), 80.00% (8/10), and 63.11% (65/103), respectively, while for mpMRI they were 34.78% (16/46), 83.58% (56/67), 59.26% (16/27), and 65.12% (56/86), respectively. The sensitivity of mpMRI was significantly higher than that of 68Ga-PSMA-617 PET/CT ( P=0.048), while the specificity was the opposite ( P=0.008). When combining both imaging modalities, the sensitivity, specificity, positive predictive value, and negative predictive value were 45.65% (21/46), 80.60% (54/67), 61.76% (21/34), and 68.35% (54/79), respectively. In diagnosing SVI, the sensitivity, specificity, positive predictive value, and negative predictive value of 68Ga-PSMA-617 PET/CT were 27.27% (3/11), 96.08% (98/102), 42.86% (3/7), and 92.45% (98/106), respectively, while for mpMRI they were 36.36% (4/11), 88.24% (90/102), 25.00% (4/16), and 92.78% (90/97), respectively. The specificity of 68Ga-PSMA-617 PET/CT was significantly higher than that of mpMRI ( P=0.033). When combining both imaging modalities, the sensitivity, specificity, positive predictive value, and negative predictive value were 45.45% (5/11), 85.29% (87/102), 25.00% (5/20), and 93.55% (87/93), respectively. Conclusions:mpMRI has higher sensitivity in diagnosing EPE and SVI in prostate cancer, while 68Ga-PSMA-617 PET/CT shows higher specificity. The combined use of both imaging modalities can increase diagnostic sensitivity but may reduce specificity. PSMA PET/MRI may be a more accurate diagnostic tool for discerning EPE and SVI.

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.

The ribosomal protein S11(RPS11)from Enterococcus faecalis is was heterologously ex-pressed using the Pichia pastoris system.The RPS11 gene sequence was optimized to match the yeast codon preference,and the recombinant expression vector pPIC9K-RPS11 was constructed.Electroporation was used to transform the vector into the Pichia pastoris GS115 strain,and high-copy recombinant strains were selected through G418 resistance screening.Protein expression was induced with methanol,and the expression was verified by SDS-PAGE.The recombinant protein was applied in a mouse melanoma treatment model to evaluate its therapeutic effects.The results showed that the recombinant expression vector pPIC9K-RPS11 successfully expressed the target protein with an approximate molecular weight of 14 kDa in Pichia pastoris.The optimal fermenta-tion conditions were determined to be an induction temperature of 30 ℃,induction time of 72 h,and methanol concentration of 1％.Analysis using a mouse peritoneal macrophage trained immuni-ty model revealed that recombinant RPS11 possessed biological activity capable of inducing trained immunity.Additionally,therapeutic experiments in a mouse melanoma model demonstrated that recombinant RPS11 significantly inhibited tumor growth.These findings suggest that the recombi-nant RPS11 secreted by Pichia pastoris not only possesses biological activity in inducing trained immunity but also inhibits tumor cell growth in a mouse melanoma model,providing theoretical support for the heterologous expression and potential applications of recombinant RPS11.

Objective: To investigate the effects of paeoniflorin (Pae) on acute kidney injury ( AKI) and mouse renal tubular epithelial cell ( mRTEC) damage induced by lansoprazole (LPZ) and cisplatin (CIS) through in vivo and in vitro experiments . Methods : The C57BL/6J mice or mRTECs were divided into four groups : normal control (NC) group , NC + LPZ group , CIS group , and CIS + LPZ group . Serum creatinine (CRE) and blood urea nitro- gen (BUN) levels in mice were measured , and kidney pathology was observed with HE staining. Western blot , im- munohistochemistry , and immunofluorescence were used to detect the expression levels of kidney injury molecule-1 (KIM-1) and receptor-interacting protein kinase (RIPK) 1 , RIPK3 , and mixed lineage kinase domain-like protein (MLKL) . Subsequently , C57BL/6J mice or mRTECs were divided into six groups : NC group , NC + Pae group , CIS + LPZ (M) group , and CIS + LPZ + Pae ( M + Pae) group . Serum CRE and BUN levels in each group were measured , kidney pathology was observed with HE staining , and ultrastructural changes in the kidney were observed with transmission electron microscopy. The KIM-1 and necroptosis-related protein expression levels were detected by Western blot , immunohistochemistry , and immunofluorescence . Results: Compared with the NC group , CRE and BUN levels were elevated in the CIS group , and these levels were further increased after LPZ in- tervention (all P < 0. 001) . Compared with the CIS group , renal tubular dilation and brush border loss were evi- dent in the CIS + LPZ group based on HE staining of kidney tissue (P < 0. 001) . Compared with the NC group , the expression levels of KIM-1 , RIPK1 , RIPK3 , and MLKL in the renal tissues of mice in the CIS group increased ( all P < 0. 001) , and compared with the CIS group , The expression levels of KIM-1 , RIPK1 , RIPK3 and MLKL in the renal tissues of mice in the CIS + LPZ group increased (all P < 0. 001) . After Pae treatment , compared with group M , the expression levels of CRE , BUN , KIM-1 , RIPK1 , RIPK3 and MLKL in each group of mice decreased significantly and in a dose-dependent manner (all P < 0. 001) . Conclusion LPZ promotes CIS-induced AKI by enhancing necroptosis in renal tubular epithelial cells , and Pae can improve CIS and LPZ-induced AKI by inhibi- ting necroptosis .

Objective To investigate the interference of varying degrees of lipemia on serum lithium(Li)measurement using the phosphatase method and explore effective mitigation strategies.Methods A pooled sample of severe lipemic serum without lithium was collected and concentrated to obtain lipemic serum concentrate.A pooled serum sample from patients with normal lipid levels taking lithium carbonate was used for triglyceride(TG)interference experiments.Additionally,28 serum samples from patients not taking lithium carbonate were collected.Based on the results of TG interference experiments,the maximum TG concentration that did not interfere with serum lithium measurement was determined as the target concentration for dilution,and the corresponding dilution factor was calculated.Lithium solution was added to each sample to determine the theoretical lithium concentration.Samples were divided into three groups and analyzed using direct detection,physiological saline dilution,and high-speed centrifugation(13 000 r/min,10 min).The results obtained from different methods were compared.Results Lipemic serum with TG concentrations>4.77mmol/L interfered with lithium measurement by the phosphatase method.The physiological saline dilution method showed the largest deviation(t=10.87,P<0.000 1)and significant differences from theoretical values,making it unsuitable for accurate measurement.In contrast,the high-speed centrifugation method provided results closest to the theoretical values(t=2.97,P=0.036 9)with higher accuracy.Although the direct detection method was highly correlated with the high-speed centrifugation method(r=0.976 5,P<0.000 1),with a significant mean difference remained(t=5.37,P<0.000 1).Conclusion For lipemic serum samples with TG concentrations>4.77mmol/L,the physiological saline dilution method should be avoided due to its inaccuracy.High-speed centrifugation effectively removes lipemic interference,yielding results closer to theoretical values,and is recommended as the optimized method for serum lithium measurement in lipemic samples.

Objective:To explore the distant metastatic characteristics of metastatic hormone-sensitive prostate cancer (mHSPC) and metastatic castration-resistant prostate cancer (mCRPC) based on prostate-specific membrane antigen (PSMA) PET-CT.Methods:This is a retrospective cohort study. Ultimately, data from 227 patients with metastatic prostate cancer who underwent PSMA PET-CT examinations at Xiangya Hospital, Central South University between March 2016 and May 2025 were retrospectively reviewed, including 117 mHSPC patients with an age of (68.8±7.6) years (range:53 to 89 years) and 110 mCRPC patients with an age of (69.4±7.5) years (range: 49 to 88 years). Clinical and pathological data, along with metastatic characteristics identified via PSMA PET-CT, were collected and compared. Intergroup comparisons were performed using χ 2 tests. Results:The incidence rates of lymph node metastasis, bone metastasis, and visceral metastasis in the mHSPC group were 71.8% (84/117), 89.7% (105/117), and 11.1% (13/117), respectively, while those in the mCRPC group were 52.7% (58/110), 91.8% (101/110), and 15.5% (17/110), respectively. The incidence of lymph node metastasis in the mHSPC group was significantly higher than that in the mCRPC group ( χ2=8.800, P=0.003). Among patients with bone metastasis, the rates of osteoblastic metastasis, osteolytic metastasis, and mixed metastasis in the mHSPC group were 76.2% (80/105), 8.6% (9/105), and 15.2% (16/105), respectively, while the corresponding rates in the mCRPC group were 74.3% (75/101), 7.3% (8/101), and 16.4% (18/101), respectively, all indicating a relatively high probability of osteolytic and mixed bone metastases ( χ2=0.260, P=0.878). Among patients with mHSPC and mCRPC who tested positive for visceral metastasis, lung metastasis (9/13 and 8/17) and liver metastasis (4/13 and 9/17) were the most common sites of metastasis, but there was no significant difference in the composition of visceral metastasis between the two groups ( χ2=0.933, P=0.564). In this study, among 20 patients who progressed from mHSPC to mCRPC, 35.0% (7/20) had persistent or progressive activity at the original metastatic site, 35.0% (7/20) developed new metastatic lesions, and 30.0% (6/20) showed inhibitory changes in the original metastatic lesions. Among patients with imaging progression, 1/14 of patients with osteoblastic metastatic lesions at the mHSPC stage exhibited osteolytic changes upon progression to mCRPC. Conclusion:Compared with the mCRPC group, the mHSPC group has a higher lymph node metastasis rate,and both groups have common rates of osteolytic and mixed bone metastases and visceral metastasis.