Abstract: Objective　Through analyzing the epidemiological characteristics of imported Plasmodium falciparum (P. falciparum) cases in China from 2017 to 2022, to understand the trend of imported P. falciparum epidemic before and after malaria elimination, and to provide data support for further prevention and control of imported P. falciparum. Methods　Epidemiological questionnaires of P. falciparum cases in 31 provinces (autonomous regions and municipalities directly under the Central Government, excluding Taiwan, Hong Kong, and Macao) and Xinjiang Production and Construction Corps were collected from the parasitic disease control information management system from 2017 to 2022, and the epidemic situation, overseas foci, and distribution of three were statistically analyzed. Results　From 2017 to 2022, a total of 7 026 cases of P. falciparum were reported nationwide, accounting for 64.2% (7 026/10 943) of the total number of cases, all of which were imported cases. The infected cases were distributed across 60 countries in 4 continents, mainly in African countries. P. falciparum was reported every month from 2017 to 2022, with uneven distribution throughout the year and a peak occurring at the beginning. The top five provinces with the highest number of P. falciparum malaria cases were Guangdong Province (13.1%, 922/7 026), Jiangsu Province (9.1%, 636/7 026), Shandong Province (8.1%, 569/7 026), Guangxi Zhuang Autonomous Region (7.6%, 537/7 026), and Zhejiang Province (7.6%, 534/7 026). The majority of cases were Chinese nationals (94.9%, 6 668/7 026), with a male-to-female ratio of 17.2∶1. Among the reported cases of P. falciparum, 239 were critically ill and 48 died. Conclusions　In the stage of preventing imported malaria retransmission, although all the reported malaria cases in China were imported cases, P. falciparum accounted for the high proportion. Considering the complexity and rapid progression of P. falciparum, which can lead to critical illness or even death, timely detection, accurate diagnosis and standardized treatment of malaria cases should be done to reduce critical illness or death.

OBJECTIVE:To investigate the effects of hydrophilic polymers on the stability of self-microemulsifying drug deliv-ery systems (SMEDDS). METHODS:Taking felodipine (FDP) as model drug,the content of FDP was determined by HPLC method. The effects of pure water,0.5% Kollidon VA64,HPMC E5,HPMC K100LV,HPMC K4M,PVP K30 solution,while 0.1%,0.5% and 1.0% HPMC E5 and Kollidon VA64 on residual content of dissolved FDP were determined in SMEDDS. RE-SULTS:The residual contents of dissolved FDP in SMEDDS placed in Kollidon VA64,HPMC E5,HPMC K100LV,PVP K30, HPMC K4M and pure water for 1 h were 92.7%,63.6%,50.2%,46.2%,36.0%and 24.0%,respectively. The order of maintain-ing the supersaturation state was Kollidon VA64>HPMC E5>HPMC K100LV>PVP K30>HPMC K4M>pure water. The residu-al contents of dissolved FDP in SMEDDS placed in 0.1%,0.5%,1% Kollidon VA64 and HPMC E5 and pure water for 1 h were 93.2%,95.1%,96.0% and 48.4%,62.1%,75.1%. CONCLUSIONS:Kollidon VA64 and HPMC E5 can significantly inhibit drug release in SMEDDS and be used as stabilizer of SMEDDS,wherein Kollidon VA64 was better.

This study was aimed to establish the pharmacokinetics-pharmacodynamics (PK-PD) model of ginsenoside Rb1 following the intravenous administration of Shengmai injection in subjects with stable angina pectoris.A total of stable angina pectoris were selected and received Shengmai injection for 14 days.Plasma samples were collected at different time points.Plasma concentrations of ginsenoside Rb1 were determined by liquid chromatography-mass spectrometry (LC/MS).The concentration-time curves (AUC) were drawn,and then the PK parameters were calculated.The systolic pressure and diastolic pressure were monitored,and the combined PK-PD model was established based on the theory of effect compartment.The results showed that PK of ginsenoside Rb1 conformed to a mono-compartment model.The effect of Shengmai injection lagged behind the concentrations of ginsenoside Rb1 in plasma.The effect exhibited good correlation with ginsenoside Rb1 in effect compartment.The relationship between effect and plasma concentrations fits the Inhibitory Effect Imax model.It was concluded that the study successfully established the combined PK-PD model of ginsenoside Rb1 in subjects with angina pectoris.The model can efficiently evaluate the effective substance of Shengmai injection.

Objective:To investigate the relationship between body mass index (BMI) and gestational hypertension using two-sample Mendelian randomization analysis.Methods:The summary level data for BMI and gestational hypertension were obtained from the genome-wide association study (the deadline for data inclusion was October 31, 2023). All data were analyzed by inverse variance weighting, MR-Egger regression, weighted median, simple model and weighted model methods. Cochrane Q test was used to evaluate heterogeneity, MR-Egger regression intercept test and funnel plot were used to assess horizontal pleiotropy. Results:Inverse variance weighting result under fixed effects and random effects models showed that the risk of gestational hypertension increased with the increase of BMI ( OR = 1.62 and 1.62, 95% CI 1.39 to 1.88 and 1.39 to 1.88, P<0.01). Sensitivity analysis results including MR-Egger regression, weighted median and weighted model methods showed that BMI increased the risk of gestational hypertension ( OR = 1.51, 1.56 and 1.71; 95% CI 1.01 to 2.26, 1.23 to 1.99 and 1.09 to 2.69; P<0.05 or <0.01). Although Cochrane Q test result showed evidence of heterogeneity ( P = 0.04), inverse variance weighting under a random model suggested that BMI increased the risk of gestational hypertension. Horizontal pleiotropy was not observed in the above analysis ( P = 0.73). Conclusions:Obesity may increase the risk of gestational hypertension. Pregnant women should pay attention to weight control to decrease the risk of gestational hypertension.

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.

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.