Despite advances in the treatment of ST-segment elevation myocardial infarction (STEMI), little is known about how this evolving knowledge is applied in current clinical practice in China.
Objective
To evaluate hospital performance and temporal trends in the management of STEMI.
Design, Setting, and Participants
This study used data from the Improving Care for Cardiovascular Disease in China–Acute Coronary Syndrome Project, a nationwide quality improvement registry, in collaboration with the American Heart Association and the Chinese Society of Cardiology. Participants included patients with STEMI admitted to 143 tertiary hospitals across China from November 2014 to July 2019, and data were analyzed from November 2020 to December 2021.
Main Outcomes and Measures
Levels, hospital-level variations, and trends for utilization rates of the 9 management strategies with Class I recommendations in Chinese and US guidelines.
Results
A total of 57 560 hospitalizations with STEMI were included. Overall, 20.0% of patients received all the care according to the 9 guideline-recommended strategies. The performance rate of quality measures was low for reperfusion therapy (61.0%, 35 115/57 560 patients), β-blocker at discharge (68.3%, 37 750/55 285 patients), angiotensin-converting enzyme inhibitor or angiotensin receptor blocker at discharge (55.1%, 2524/4578 patients), and smoking cessation counseling (36.5%, 9586/26 265 patients) among those who were eligible. Of 25 563 patients who underwent primary percutaneous coronary intervention (PCI), 66.8% underwent this procedure within 90 minutes of hospital arrival. Of 1128 patients who underwent fibrinolysis therapy, 253 (22.4%) underwent this treatment within 30 minutes of hospital arrival. Measures with high performance rates included receipt of dual antiplatelet therapy within 24 hours (95.5%, 54 263/56 848 patients) and at discharge (91.8%, 51 452/56 019 patients) and receipt of statin at discharge (93.0%, 52 214/56 141 patients) for those eligible. There was significant variation between hospitals in all-or-none score (ranging from 0 to 61.9%) and performance of individual measures. The quality of care improved during the study period, especially for reperfusion therapy, primary PCI within the first 90 minutes of hospital arrival, and smoking cessation counseling.
Conclusions and Relevance
The quality of care for patients hospitalized with STEMI does not meet guideline-recommended strategies in China, with only 1 in 5 patients receiving all the care according to the 9 guideline-recommended strategies. Large disparities in the quality of care exist across hospitals.
To study the expressions of phosphorylated STAT5 (P-STAT5) in CD34(+)CD59(-) and CD34(+)CD59(+) bone marrow cells of the patients with paroxysmal nocturnal hemoglobinuria (PNH) before and after in vitro G-CSF or SCF stimulation, then evaluate the functions of G-CSF and SCF receptors in PNH clone cells.Bone marrow mononuclear cells (BMMNC) of 26 PNH patients and 14 normal controls were stimulated in vitro with G-CSF (100 ng/ml) or SCF (100 ng/ml) for 10 min. Before and after these stimulations, the mean fluorescence intensity (MFI) of P-STAT5 in CD34(+)CD59(+) BMMNC and CD34(+)CD59(-) BMMNC were measured by flow cytometry.(1) The P-STAT5 MFI was (24 ± 18) in unstimulated CD34(+)CD59(-) cells. And it was significantly lower than that in unstimulated CD34(+)CD59(+) cells of PNH patients (64 ± 49) and normal controls (61 ± 33) (both P < 0.01). No statistic difference existed between the latter two. (2) The P-STAT5 MFI was (36 ± 35) in G-CSF stimulated CD34(+)CD59(-) cells of PNH patients. And it was significantly lower than that in G-CSF stimulated CD34(+)CD59(+) cells of PNH patients (124 ± 84) and normal controls (116 ± 59) (both P < 0.01). There was no statistic difference between the latter two. (3) The P-STAT5 MFI was (34 ± 27) in SCF stimulated CD34(+)CD59(-) cells of PNH patients. And it was significantly lower than that in SCF stimulated CD34(+)CD59(+) cells of PNH patients (124 ± 97) and normal controls (128 ± 62) (both P < 0.01). And no statistic difference existed between the latter two. (4) The increased P-STAT5 MFI in G-CSF stimulated CD34(+)CD59(-) cells of PNH patients was significantly lower than that in G-CSF stimulated CD34(+)CD59(+) cells of PNH patients and normal controls (both P < 0.01). No statistic difference existed between the latter two. The increase of P-STAT5 MFI in SCF stimulated CD34(+)CD59(-) cells of PNH patients was significantly lower than that in SCF stimulated CD34(+)CD59(+) cells of PNH patients and normal controls (both P < 0.01). No statistic difference existed between the latter two.There is a lower expression of P-STAT5 expressed in G-CSF or SCF stimulated PNH clone cells compared to that in normal clone cells.
AIM:To investigate the protective effect of ketamine on the endotoxin-induced proinflammatory cytokines and NFkappa B activation in the intestine. METHODS:Adult male Wistar rats were randomly divided into 6 groups: (a) normal saline control, (b) challenged with endotoxin (5 mg/kg) and treated by saline, (c) challenged with endotoxin (5 mg/kg) and treated by ketamine (0.5 mg/kg), (d) challenged with endotoxin (5 mg/kg) and treated by ketamine (5 mg/kg ), (e) challenged with endotoxin (5 mg/kg) and treated by ketamine (50 mg/kg), and (f) saline injected and treated by ketamine (50 mg/kg).After 1, 4 or 6 h, TNF-α and IL-6 mRNA were investigated in the tissues of the intestine (jejunum) by RT-PCR.TNF-α and IL-6 were measured by ELISA.We used electrophoretic mobility shift assay (EMSA) to investigate NF-kappa B activity in the intestine.RESULTS: NF-kappa B activity, the expression of TNF-α and IL-6 were enhanced in the intestine by endotoxin.Ketamine at a dose of 0.5 mg/kg could suppress endotoxininduced TNF-α mRNA and protein elevation and inhibit NFkappa B activation in the intestine.However the least dosage of ketamine to inhibit IL-6 was 5 mg/kg in our experiment.CONCLUSION: Ketamine can suppress endotoxin-induced production of proinflammatory cytokines such as TNF-α and IL-6 production in the intestine.This suppressive effect may act through inhibiting NF-kappa B.
The aim of our study is to investigate the effects of IL-15 on the apoptosis of CD4+CD25+ regulatory T cells(Tregs) and the mechanism.We isolated Tregs from the human peripheral blood mononuclear cells in two steps by magnetic cell sorting system,and measured the purity rate of the sorted cells was by flowcytometry(FC).Then the prepared Tregs were co-cultured with Dynabeads CD3/CD28 T cell expander and divided into 3 groups(control group,IL-2 group,and IL-15 group) without or with IL-2(100 U/ml) and IL-15(50 ng/ml).FC was used to detect the Tregs apoptosis;the incorporation of [3H] thymidine was used to evaluate the suppressive function of the Tregs on the Teff in the presence of IL-2 or IL-15;Western blotting was used to observe the expression of Bcl-2,Bcl-xl,and p-Bad(ser112).FC showed that the purity of sorted CD4+ CD25+ T cells was 95.2 %;the intracellular staining indicated that the expression rate of Foxp3 was 94.2% in Tregs.Compared with Tregs cultured without cytokines,IL-15 and IL-2 were able to promote survival of activated Tregs.IL-2 profoundly reversed the Tregs-mediated suppression of Teff proliferation,however IL-15 had almost no effects on Tregs-mediated suppression.We also found that addition of IL-15 and IL-2 did not affect Bcl-2 expression.In contrast,Bcl-xl and p-Bad(ser112) was selectively up-regulated by IL-15 and IL-2 in Tregs.All the results indicated that IL-15 can reduce the Tregs apoptosis,which maybe associated with up-regulating the Bcl-xl and p-Bad(ser112) expression.Furthermore,IL-15 could maintain Tregs suppression function.
Cell adhesion-mediated drug resistance is an important factor that influences the effects of chemotherapy in multiple myeloma. DTX3L, a ubiquitin ligase, plays a key role in cell-cycle-related process. Here, we found that the expression of DTX3L gradually increased during the proliferation of myeloma cells, which resulted in arrest of the cell cycle in the G1 phase and promoted the adherence of myeloma cells to fibronectin or bone marrow stromal cells. In addition, silencing of DTX3L improved sensitivity to chemotherapy drugs in multiple myeloma cell lines adherent to bone marrow stromal cells and increased the expression of caspase-3 and poly-adenosine diphosphate-ribose polymerase, two markers of apoptosis. Finally, we also found that DTX3L expression was regulated by focal adhesion kinase. Taken together, the results of this study show that DTX3L plays an important role in the proliferation and cell adhesion-mediated drug resistance of multiple myeloma cells and as such may play a key role in the development of multiple myeloma.
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