To overcome the limited mixing efficiency associated with conventional steady-state side blowing in molten pool smelting,this study proposes a gas injection strategy that combines a swirl lance configuration with sinu...To overcome the limited mixing efficiency associated with conventional steady-state side blowing in molten pool smelting,this study proposes a gas injection strategy that combines a swirl lance configuration with sinusoidal pulsed blowing.Using a volume-of-fluid(VOF)multiphase flow framework coupled with the Realizable k-ε turbulence model,the performance of constant-velocity blowing is systematically compared with sinusoidal pulsed blowing over a range of amplitudes(5,10,and 15 m/s)and frequencies(0.5,1,and 2 Hz).The results demonstrate that sinusoidal pulsed blowing markedly enhances gas-liquid mixing within the melt pool relative to constant-speed injection.Mixing efficiency increases with blowing amplitude,while its dependence on pulse frequency is nonlinear.Within the investigated parameter space,the optimal configuration,an amplitude of 15 m/s and a frequency of 1 Hz,raises the average gas volume fraction by 8%,reduces the mixing dead-zone area by 81%,and expands the active mixing region by 25%.Overall,the imposed sinusoidal pulsing promotes bubble breakup beneath the free surface,leading to more complete bubble collapse,intensified turbulent agitation,and,ultimately,improved gas–liquid mixing.展开更多
In Chin.Phys.B 34114704(2025),Eq.(7)and the associated unit notation were incorrect.The correct ones are present here.Since Eq.(7)is an in-built expression in the simulation package,the correction is purely typographi...In Chin.Phys.B 34114704(2025),Eq.(7)and the associated unit notation were incorrect.The correct ones are present here.Since Eq.(7)is an in-built expression in the simulation package,the correction is purely typographical and does not affect the simulation procedure,numerical results,or the conclusions.展开更多
Quantum key distribution(QKD)achieves information-theoretic security based on quantum mechanics principles,where single-photon detectors(SPDs)serve as critical components.This study focuses on the sinusoidal gated SPD...Quantum key distribution(QKD)achieves information-theoretic security based on quantum mechanics principles,where single-photon detectors(SPDs)serve as critical components.This study focuses on the sinusoidal gated SPDs widely used in high-speed QKD systems.We investigate the mechanisms underlying the rising-edge jitter in detection signals,identifying contributions from factors such as the temporal width of injected optical pulses,avalanche generation processes,avalanche signal extraction,and pulse discrimination.To address the issue of excessive jitter-induced bit errors,we propose a retiming scheme that utilizes coincidence signals synchronized with the sinusoidal gating signal.This approach effectively suppresses detection signal jitter and reduces the after-pulse probability of the detector.Experimental validation using a high-precision time-to-digital converter(TDC)demonstrates a significant reduction in the rising-edge jitter distribution after applying the suppression scheme.The proposed method features clear principles and straightforward engineering implementation,avoiding direct interference with the detector’s operational processes.The designed high-speed sinusoidal gated InGaAs/InP SPD operates at 1.25 GHz,achieving a remarkable reduction in after-pulse probability from 10.7%(without jitter suppression)to 0.72%,thereby enhancing the overall performance of QKD systems.展开更多
BACKGROUND The progression of non-alcoholic fatty liver disease(NAFLD)to non-alcoholic steatohepatitis(NASH)and liver fibrosis remains poorly understood,though liver sinusoidal endothelial cells(LSECs)are thought to p...BACKGROUND The progression of non-alcoholic fatty liver disease(NAFLD)to non-alcoholic steatohepatitis(NASH)and liver fibrosis remains poorly understood,though liver sinusoidal endothelial cells(LSECs)are thought to play a central role in disease pathogenesis.AIM To investigate the role of TSC22D1 in NAFLD fibrosis through its regulation of LSEC dysfunction and macrophage polarization.METHODS We analysed single-cell transcriptomic data(GSE129516)from NASH and normal INTRODUCTION Non-alcoholic fatty liver disease(NAFLD)is a global health issue associated with increasing rates of obesity and metabolic syndrome.NAFLD encompasses a spectrum of conditions,ranging from simple steatosis to more severe manifestations such as non-alcoholic steatohepatitis(NASH),fibrosis,cirrhosis,and hepatocellular carcinoma.Liver fibrosis represents a critical stage in NAFLD progression because of its strong association with impaired liver function,progression to end-stage liver disease,and increased disease-related mortality[1].The pathogenesis of NAFLD is multifactorial and involves complex interactions between genetic predispositions,insulin resistance,dietary factors,and chronic inflammation[2].Liver sinusoidal endothelial cells(LSECs),which are highly specialized endothelial cells lining the hepatic sinusoids,critically contribute to both the pathogenesis and progression of NAFLD[3,4].In NAFLD,LSECs undergo structural alterations such as reduced fenestrations,which impair hepatic microcirculation and hinder the exchange of lipids and other substances,thereby promoting lipid accumulation in hepatocytes[5].Furthermore,dysfunctional LSECs exacerbate hepatic inflammation and fibrogenesis by releasing pro-inflammatory cytokines and fibrogenic mediators,such as transforming growth factor-β(TGF-β).These factors activate hepatic stellate cells(HSCs),resulting in the pathological accumulation of extracellular matrix components[6].LSECs are also highly susceptible to oxidative stress,further aggravating hepatic injury[7,8].Importantly,LSECs influence macrophage polarization by producing chemotactic and immunomodulatory factors,thereby promoting the recruitment and activation of M1-type pro-inflammatory CONCLUSION In conclusion,this study provides a comprehensive understanding of the role of TSC22D1 in the pathogenesis of NAFLD fibrosis.We elucidated the mechanisms through which TSC22D1 drives LSEC microvascularization and EndMT,as well as its role in promoting the secretion of TWEAK,which induces macrophage polarization towards the M1 phenotype.These findings offer novel insights into the pathophysiology of NAFLD,particularly the interplay between endothelial dysfunction,inflammation,and fibrosis.Importantly,our results highlight the potential of TSC22D1 as a therapeutic target for NAFLD.Future research should focus on validating these mechanisms in human clinical cohorts and deve-loping targeted interventions,such as TSC22D1 inhibitors or modulators of the TWEAK/FN14 signalling pathway,to translate these findings into effective treatments for NAFLD progression to fibrosis.展开更多
太阳能空气集热器(Solar Air Heater,SAH)与空气供暖相结合,在冬季为室内进行通风供暖是复合供暖的重要研究点。文章对提升SAH的集热性能做出模拟研究分析,在平板双风道SAH基础上,建立双层正弦波纹板SAH数学模型,分析正弦波纹板双风道SA...太阳能空气集热器(Solar Air Heater,SAH)与空气供暖相结合,在冬季为室内进行通风供暖是复合供暖的重要研究点。文章对提升SAH的集热性能做出模拟研究分析,在平板双风道SAH基础上,建立双层正弦波纹板SAH数学模型,分析正弦波纹板双风道SAH的集热性能,对室内供暖热舒适性环境做出研究。研究结果表明,正弦波纹板双风道SAH具有更高的出口温度和集热效率,与平板SAH之间的最大温差约为13.2 K,最大集热效率差约为21.6%。正弦波纹板SAH的散热系数较平板SAH低约10%,正弦波纹板双风道SAH的上下层空气出口温度及集热效率在10:00时最低,在13:00时最高,集热效率最高约为71.04%,最大散热系数约为4.5 W/m^(2)·K。根据SAH逐时计算所得到的出口温度,而研究室内平均温度可得出:室内平均温度在10:00时最低约为287 K,13:00时最高约为290.52 K。正弦波纹板双风道SAH可为冬季室内直接热风供暖使用。展开更多
Hepatic sinusoidal obstruction syndrome (HSOS) can be caused by the intake of pyrrolizidine alkaloids (PAs). To date, PAs-induced HSOS has not been extensively studied. In view of the difference in etiology of HSOS be...Hepatic sinusoidal obstruction syndrome (HSOS) can be caused by the intake of pyrrolizidine alkaloids (PAs). To date, PAs-induced HSOS has not been extensively studied. In view of the difference in etiology of HSOS between the West and China, clinical profiles, imaging findings, treatment, and outcomes of HSOS associated with hematopoietic stem cell transplantation or oxaliplatin might be hardly extrapolated to PAs-induced HSOS. Reactive metabolites derived from PAs form pyrrole-protein adducts that result in toxic destruction of hepatic sinusoidal endothelial cells. PAs-induced HSOS typically manifests as painful hepatomegaly, ascites, and jaundice. Laboratory tests revealed abnormal liver function tests were observed in most of the patients with PAs-induced HSOS. In addition, contrast computed tomography and magnetic resonance imaging scan show that patients with PAs-induced HSOS have distinct imaging features, which reveal that radiological imaging provides an effective noninvasive method for the diagnosis of PAs-induced HSOS. Liver biopsy and histological examination showed that PAs-induced HSOS displayed distinct features in acute and chronic stages. Therapeutic strategies for PAs-induced HSOS include rigorous fluid management, anticoagulant therapy, glucocorticoids, transjugular intrahepatic portosystemic shunt, liver transplantation, etc. The aim of this review is to describe the pathogenesis, clinical profiles, diagnostic criteria, treatment, and outcomes of PAs-induced HSOS.展开更多
Sinusoidal obstruction syndrome(SOS), previously known as hepatic veno-occlusive disease, is a rare disorder in solid organ transplant patients, and is an uncommon complication after liver transplantation. Severe SOS ...Sinusoidal obstruction syndrome(SOS), previously known as hepatic veno-occlusive disease, is a rare disorder in solid organ transplant patients, and is an uncommon complication after liver transplantation. Severe SOS with hepatic failure causes considerable mortality. Tacrolimus has been reported to be an offending agent, which potentially plays a role in the pathophysiological process of SOS. SOS due to tacrolimus has been reported in lung and pancreatic transplantations, but has never been described in a liver transplant recipient. Herein, we present a case of SOS after liver transplantation, which was possibly related to tacrolimus. A 27-year-old man developed typical symptoms of SOS with painful hepatomegaly, ascites and jaundice after liver transplantation, which regressed following withdrawal of tacrolimus. By excluding other possible predisposing factors, we concluded that tacrolimus was the most likely cause of SOS.展开更多
基金Supported by Yunnan Fundamental Research Projects(202301AT070469,202301AT070275)Supported by Yunnan Provincial Integrated Special Fund for Key Laboratories(Integrated for Provincial and Municipal Levels)(No.202302AN360004).
文摘To overcome the limited mixing efficiency associated with conventional steady-state side blowing in molten pool smelting,this study proposes a gas injection strategy that combines a swirl lance configuration with sinusoidal pulsed blowing.Using a volume-of-fluid(VOF)multiphase flow framework coupled with the Realizable k-ε turbulence model,the performance of constant-velocity blowing is systematically compared with sinusoidal pulsed blowing over a range of amplitudes(5,10,and 15 m/s)and frequencies(0.5,1,and 2 Hz).The results demonstrate that sinusoidal pulsed blowing markedly enhances gas-liquid mixing within the melt pool relative to constant-speed injection.Mixing efficiency increases with blowing amplitude,while its dependence on pulse frequency is nonlinear.Within the investigated parameter space,the optimal configuration,an amplitude of 15 m/s and a frequency of 1 Hz,raises the average gas volume fraction by 8%,reduces the mixing dead-zone area by 81%,and expands the active mixing region by 25%.Overall,the imposed sinusoidal pulsing promotes bubble breakup beneath the free surface,leading to more complete bubble collapse,intensified turbulent agitation,and,ultimately,improved gas–liquid mixing.
文摘In Chin.Phys.B 34114704(2025),Eq.(7)and the associated unit notation were incorrect.The correct ones are present here.Since Eq.(7)is an in-built expression in the simulation package,the correction is purely typographical and does not affect the simulation procedure,numerical results,or the conclusions.
基金supported by the Major Scientific and Technological Special Project of Anhui Province(202103a13010004)the Major Scientific and Technological Special Project of Hefei City(2021DX007)the Manufacturing Industry Project of Attracting Talents and Wisdom of Anhui Province(JB24179).
文摘Quantum key distribution(QKD)achieves information-theoretic security based on quantum mechanics principles,where single-photon detectors(SPDs)serve as critical components.This study focuses on the sinusoidal gated SPDs widely used in high-speed QKD systems.We investigate the mechanisms underlying the rising-edge jitter in detection signals,identifying contributions from factors such as the temporal width of injected optical pulses,avalanche generation processes,avalanche signal extraction,and pulse discrimination.To address the issue of excessive jitter-induced bit errors,we propose a retiming scheme that utilizes coincidence signals synchronized with the sinusoidal gating signal.This approach effectively suppresses detection signal jitter and reduces the after-pulse probability of the detector.Experimental validation using a high-precision time-to-digital converter(TDC)demonstrates a significant reduction in the rising-edge jitter distribution after applying the suppression scheme.The proposed method features clear principles and straightforward engineering implementation,avoiding direct interference with the detector’s operational processes.The designed high-speed sinusoidal gated InGaAs/InP SPD operates at 1.25 GHz,achieving a remarkable reduction in after-pulse probability from 10.7%(without jitter suppression)to 0.72%,thereby enhancing the overall performance of QKD systems.
基金Supported by the Changzhou Science and Techology Program,No.CJ20241048Changzhou High-Level Medical Talents Training Project,No.2022CZBJ105+1 种基金Development Foundation of the Affiliated Hospital of Xuzhou Medical University,No.XYFC202304 and No.XYFM202307The Open Project of Jiangsu Provincial Key Laboratory of Laboratory Medicine,No.JSKLM-Z-2024-002.
文摘BACKGROUND The progression of non-alcoholic fatty liver disease(NAFLD)to non-alcoholic steatohepatitis(NASH)and liver fibrosis remains poorly understood,though liver sinusoidal endothelial cells(LSECs)are thought to play a central role in disease pathogenesis.AIM To investigate the role of TSC22D1 in NAFLD fibrosis through its regulation of LSEC dysfunction and macrophage polarization.METHODS We analysed single-cell transcriptomic data(GSE129516)from NASH and normal INTRODUCTION Non-alcoholic fatty liver disease(NAFLD)is a global health issue associated with increasing rates of obesity and metabolic syndrome.NAFLD encompasses a spectrum of conditions,ranging from simple steatosis to more severe manifestations such as non-alcoholic steatohepatitis(NASH),fibrosis,cirrhosis,and hepatocellular carcinoma.Liver fibrosis represents a critical stage in NAFLD progression because of its strong association with impaired liver function,progression to end-stage liver disease,and increased disease-related mortality[1].The pathogenesis of NAFLD is multifactorial and involves complex interactions between genetic predispositions,insulin resistance,dietary factors,and chronic inflammation[2].Liver sinusoidal endothelial cells(LSECs),which are highly specialized endothelial cells lining the hepatic sinusoids,critically contribute to both the pathogenesis and progression of NAFLD[3,4].In NAFLD,LSECs undergo structural alterations such as reduced fenestrations,which impair hepatic microcirculation and hinder the exchange of lipids and other substances,thereby promoting lipid accumulation in hepatocytes[5].Furthermore,dysfunctional LSECs exacerbate hepatic inflammation and fibrogenesis by releasing pro-inflammatory cytokines and fibrogenic mediators,such as transforming growth factor-β(TGF-β).These factors activate hepatic stellate cells(HSCs),resulting in the pathological accumulation of extracellular matrix components[6].LSECs are also highly susceptible to oxidative stress,further aggravating hepatic injury[7,8].Importantly,LSECs influence macrophage polarization by producing chemotactic and immunomodulatory factors,thereby promoting the recruitment and activation of M1-type pro-inflammatory CONCLUSION In conclusion,this study provides a comprehensive understanding of the role of TSC22D1 in the pathogenesis of NAFLD fibrosis.We elucidated the mechanisms through which TSC22D1 drives LSEC microvascularization and EndMT,as well as its role in promoting the secretion of TWEAK,which induces macrophage polarization towards the M1 phenotype.These findings offer novel insights into the pathophysiology of NAFLD,particularly the interplay between endothelial dysfunction,inflammation,and fibrosis.Importantly,our results highlight the potential of TSC22D1 as a therapeutic target for NAFLD.Future research should focus on validating these mechanisms in human clinical cohorts and deve-loping targeted interventions,such as TSC22D1 inhibitors or modulators of the TWEAK/FN14 signalling pathway,to translate these findings into effective treatments for NAFLD progression to fibrosis.
基金Supported by National Natural Science Foundation of China,No.81570555 and No.81770582
文摘Hepatic sinusoidal obstruction syndrome (HSOS) can be caused by the intake of pyrrolizidine alkaloids (PAs). To date, PAs-induced HSOS has not been extensively studied. In view of the difference in etiology of HSOS between the West and China, clinical profiles, imaging findings, treatment, and outcomes of HSOS associated with hematopoietic stem cell transplantation or oxaliplatin might be hardly extrapolated to PAs-induced HSOS. Reactive metabolites derived from PAs form pyrrole-protein adducts that result in toxic destruction of hepatic sinusoidal endothelial cells. PAs-induced HSOS typically manifests as painful hepatomegaly, ascites, and jaundice. Laboratory tests revealed abnormal liver function tests were observed in most of the patients with PAs-induced HSOS. In addition, contrast computed tomography and magnetic resonance imaging scan show that patients with PAs-induced HSOS have distinct imaging features, which reveal that radiological imaging provides an effective noninvasive method for the diagnosis of PAs-induced HSOS. Liver biopsy and histological examination showed that PAs-induced HSOS displayed distinct features in acute and chronic stages. Therapeutic strategies for PAs-induced HSOS include rigorous fluid management, anticoagulant therapy, glucocorticoids, transjugular intrahepatic portosystemic shunt, liver transplantation, etc. The aim of this review is to describe the pathogenesis, clinical profiles, diagnostic criteria, treatment, and outcomes of PAs-induced HSOS.
基金Supported by National Natural Science Foundation of China,No.81373160
文摘Sinusoidal obstruction syndrome(SOS), previously known as hepatic veno-occlusive disease, is a rare disorder in solid organ transplant patients, and is an uncommon complication after liver transplantation. Severe SOS with hepatic failure causes considerable mortality. Tacrolimus has been reported to be an offending agent, which potentially plays a role in the pathophysiological process of SOS. SOS due to tacrolimus has been reported in lung and pancreatic transplantations, but has never been described in a liver transplant recipient. Herein, we present a case of SOS after liver transplantation, which was possibly related to tacrolimus. A 27-year-old man developed typical symptoms of SOS with painful hepatomegaly, ascites and jaundice after liver transplantation, which regressed following withdrawal of tacrolimus. By excluding other possible predisposing factors, we concluded that tacrolimus was the most likely cause of SOS.
