Objective:Severe fever with thrombocytopenia syndrome (SFTS), caused by the novel bunyavirus, is an emerging infectious disease with a high fatality rate. Co-infections with bacteria or fungi can exacerbate the disease. This study aimed to investigate the characteristics of co-infections in SFTS patients.Methods:A retrospective analysis was conducted on 143 SFTS patients admitted to Qilu Hospital of Shandong University and Juxian People’s Hospital from April 2021 to October 2024.Results:The result showed that 35.7% (51/143) of patients had co-infections, with 85.5% diagnosed within 48 hours of hospitalization. The co-infection group exhibited higher incidences of neurological and respiratory symptoms, lower median platelet counts, and significantly elevated levels of C-reactive protein (CRP), procalcitonin (PCT), blood urea nitrogen (BUN), creatinine (Cr), and ferritin ( P<0.01). Pathogen analysis revealed a predominance of lower respiratory tract Aspergillus infections. Co-infected patients had higher rates of ICU admission (31.4% vs 5.4%), mechanical ventilation (43.1% vs 6.5%), longer hospital stays, higher costs, and lower survival rates (74.5% vs 90.2%). The score within 6 days of disease onset (including age, neutrophil percentage, aspartate transaminase (AST), lactate dehydrogenase (LDH), and BUN) was a significant risk factor for co-infection. A predictive model combining CRP, BUN, and the composite score demonstrated superior performance (AUC=0.851). Conclusions:This study provides critical evidence for early diagnosis and identification of high-risk populations for co-infections in SFTS patients.

Objective:Severe fever with thrombocytopenia syndrome (SFTS), caused by the novel bunyavirus, is an emerging infectious disease with a high fatality rate. Co-infections with bacteria or fungi can exacerbate the disease. This study aimed to investigate the characteristics of co-infections in SFTS patients.Methods:A retrospective analysis was conducted on 143 SFTS patients admitted to Qilu Hospital of Shandong University and Juxian People’s Hospital from April 2021 to October 2024.Results:The result showed that 35.7% (51/143) of patients had co-infections, with 85.5% diagnosed within 48 hours of hospitalization. The co-infection group exhibited higher incidences of neurological and respiratory symptoms, lower median platelet counts, and significantly elevated levels of C-reactive protein (CRP), procalcitonin (PCT), blood urea nitrogen (BUN), creatinine (Cr), and ferritin ( P<0.01). Pathogen analysis revealed a predominance of lower respiratory tract Aspergillus infections. Co-infected patients had higher rates of ICU admission (31.4% vs 5.4%), mechanical ventilation (43.1% vs 6.5%), longer hospital stays, higher costs, and lower survival rates (74.5% vs 90.2%). The score within 6 days of disease onset (including age, neutrophil percentage, aspartate transaminase (AST), lactate dehydrogenase (LDH), and BUN) was a significant risk factor for co-infection. A predictive model combining CRP, BUN, and the composite score demonstrated superior performance (AUC=0.851). Conclusions:This study provides critical evidence for early diagnosis and identification of high-risk populations for co-infections in SFTS patients.

[This corrects the article DOI: 10.1016/j.apsb.2021.04.013.].

[This corrects the article DOI: 10.1016/j.apsb.2021.04.013.].

Vascular smooth muscle cell (VSMC) migration plays a critical role in the pathogenesis of many cardiovascular diseases. We recently showed that TMEM16A is involved in hypertension-induced cerebrovascular remodeling. However, it is unclear whether this effect is related to the regulation of VSMC migration. Here, we investigated whether and how TMEM16A contributes to migration in basilar artery smooth muscle cells (BASMCs). We observed that AngII increased the migration of cultured BASMCs, which was markedly inhibited by overexpression of TMEM16A. TMEM16A overexpression inhibited AngII-induced RhoA/ROCK2 activation, and myosin light chain phosphatase (MLCP) and myosin light chain (MLC20) phosphorylation. But AngII-induced myosin light chain kinase (MLCK) activation was not affected by TMEM16A. Furthermore, a suppressed activation of integrin

Volume regulated chloride channel (VRCC) enhances cell proliferation through PI3K/Akt signal pathway ,and inhibits cell apoptosis through mitochondrial pathway in vascular smooth muscle cells ,and accelerates the process of atherosclerosis through JNK/p38 MAPK signal pathway,resulting in increasing SR-A expression and ox-LDL uptake. Cerebrovascular remodeling is mediated by VRCC. This effect of VRCC on remodeling is related to accelerating cell proliferation ,migration and accumulation of. extracellular matrix. As to the molecular identification of VRCC ,it is very complex. VRCC is diversity in various cells or tissues , rather than a single ubiquitous channel,VRCC may be contain variedcell type-or tissue-specific subunitcompositions. ClC-3 volume regulated Cl-channel is regulated by both integrin-Src and Rho/RhA-Rock signal pathways.

Aim To investigate change in Cl- channels of hypertensive rats aortic smooth muscle cells. Methods 2 kidney-2 clip renovascular hypertensive rats(RVHR) model was established. In thoracic aorta smooth muscles from the hypertensive rats 1～12 weeks after operation,the changes of tension of aortic rings were recorded in vitro. Effects of Cl- channel blookers,DIDS(4,4-diisothiocyanato-stilbene-2,2'disulphonate)and NPPB[5-nitro-2-(3-phenylpropy-lamino) benzonic acid], in different concentration on contractile response of hypertensive rats aorta smooth muscle induced by 10 ?mol?L -1 phenylephrine were observed.Results The difference of inhibitory effects of 300 ?mol?L -1 DIDS and 100 ?mol?L -1 NPPB on Phe-induced contractile response between RVHR and sham-operated rats was not evident.Inhibitory effects of 300 ?mol?L -1 DIDS and 100 ?mol?L -1 NPPB on contractile response of hypertensive rats aorta smooth muscle induced by 10 ?mol?L -1 phenylephrine were lower than those of sham-operated rats in 8 weeks and 12 weeks after operation. With extension of time after operation and gradual increase of blood pressure in RVHR,inhibitory effects of DIDS and NPPB on Phe-induced contractile response gradually reduced.Conclusion Action of DIDS-sensitive and NPPB-sensitive Cl- channels in hypertensive rats aortic vascular smooth muscle cells changes. DIDS-sensitive and NPPB-sensitive Cl- channels play an important role in development and maintenance of hypertension.

Pleiotropic effects of a drug are actions other than that for which the agents were developed.These effects may be desired or undesired,and may be unrelated to their primary mechanism.Statins were designed as a drug for reducing cholesterol,but now pleiotropic effect are found including improvement of endothelial dysfunction,inhancement of eNOS bioavailability antioxide effect,antiinflammatory properties and reduction of hypertension.Understanding those effects is important for treatment and prevention of cardiovascular disease.

Acid-sensing ion channels( ASICs )are ubiquitously expressed both in periphery nervous system, where they are involved in nociception,mechanosensation,inflammation ,cardiac angina, and in central nervous system,where they are essential to a variety of physiologic and pathophysiologic processes,such as synaptic plasticity ,learning ,memory and ischemic brain injury. Here in the article, we present a collection of key points about ASICs, ranging from molecular identity and expression, regulatory mechanisms responsible for channel gating to their multiple functions. Finally, a future prospect for the investigation of ASICs is outlined.

Myocardial hypertrophy is the complication of many cardiovascular diseases that induce cardiac remodeling.The molecular mechanism of cardiac remodeling involves abnormal changes in various transmembrane ionic currents in the heart.Recent studies suggest the potential involvement of volume-regulated Cl-current(ICl.Vol)in cardiac hypertrophy.Although the molecular basis of ICl.Vol remains to be elucidated,recent progress is reviewed in the potential role of ICl.Vol in cardiac remodeling.