Medication Rules and Pharmaceutical Care of 875 Cases of COVID-19Treated by Traditional Chinese Medicine / 中国实验方剂学杂志

Objective:This paper analyzed the prescriptions of traditional Chinese medicine（TCM） for all patients diagnosed with novel coronavirus pneumonia（corona virus disease-2019，COVID-19）in Wuhan third hospital，analyzed the medication rules of the prescription，summarized the characteristics and thoughts of medication，and discussed the contents of TCM pharmaceutical care. Method:Use the data analysis software Excel 2007 and SQL server 2017 to perform statistical analysis for all inpatients in Wuhan Third Hospital from January 25，2020 to March 18，2020 who were treated by the prescriptions of TCM. The usage quantity，frequency，average dosage and dosage range of TCM were counted and compared with the dosage stipulated in the 2015 edition of Chinese Pharmacopoeia. Result:In this study，a total of 875 patients were included in the treatment prescription，involving 233 TCMs，and 20 high-frequency herbs were obtained，which were mainly used to dissolve phlegm，relieve cough and asthma，and tonify body. In the analysis of the characteristics of TCM，it is mainly composed of plain drugs，followed by cold drugs and warm drugs. The main taste of medicine is bitter，followed by spicy and sweet. The main meridians were the lung meridians，followed by the spleen and stomach meridians. By using association rule analysis and complex network analysis，it was found that the correlation degree of Artemisiae Scopariae Herba，Amomi Fructus Rotundus，Akebiae Caulis，Talcum and Fritillariae Cirrhosae Bulbus was very high，which could treat symptoms such as fever，cough，sputum，thirst，chest tightness and abdominal distension after COVID-19 infection. Conclusion:In this study，it was found that the core prescription for the treatment of COVID-19 in Wuhan Third Hospital was the addition and reduction of clearing damp agent，modified Ganlu Xiaodudan，and the reduction of expectorant modified Qingjin Jianghuotang，all the drugs were excess used than pharmacopoeia prescribed dosage. As a clinical Chinese pharmacist，we should distinguish the syndrome types according to the symptoms of the patients，and medication monitoring should be conducted from the aspects of usage and dosage of specific medication，processing product selection，compatibility，patient education，etc.

Prognostic Impact of Fasting Plasma Glucose on Mortality and Re-Hospitalization in Patients with Acute Heart Failure / 中华医学杂志(英文版)

Background@#The impact of fasting plasma glucose (FPG) on survival outcomes in patients with acute heart failure (HF) is unclear, and the relationship between intensity of glycemic control of FPG in diabetes mellitus (DM) patients and HF prognosis remains uncertain. This retrospective study aimed to evaluate the prognostic impact of FPG in patients with acute HF.@*Methods@#A total of 624 patients hospitalized with acute HF from October 2000 to April 2014 were enrolled in this study. All patients were stratified by three groups according to their admission FPG levels (i.e., DM, impaired fasting glucose [IFG], and non-DM). All-cause and cardiovascular mortality was the primary end point, and HF re-hospitalization was the secondary end point during follow-up period.@*Results@#A total of 587 patients were included in final analysis. The all-cause mortality rates of patients with DM, IFG, and non-DM were 55.5%, 40.3%, and 39.2%, with significant difference (P = 0.001). Moreover, compared with those with IFG (34.3%) and non-DM (32.6%), patients with DM had significantly higher rate of cardiovascular mortality (45.1%). Multiple Cox regression analysis showed that DM as well as IFG was related to all-cause mortality (DM: hazard ratio [HR] = 1.936, P < 0.001; IFG: HR = 1.672, P = 0.019) and cardiovascular mortality (DM: HR = 1.739, P < 0.001; IFG: HR = 1.817, P = 0.013). However, they were both unrelated to HF re-hospitalization. DM patients with strictly controlled blood glucose (FPG <3.9 mmol/L) had higher all-cause mortality than patients with non-DM, IFG, and DM patients with moderately controlled glucose (3.9 mmol/L≤ FPG <7.0 mmol/L). Likewise, both the primary end point and secondary end point were found to be worse in DM patients with poorly controlled blood glucose (FPG ≥7.0 mmol/L).@*Conclusions@#IFG and DM were associated with higher all-cause mortality and cardiovascular mortality in patients with acute HF. The association between mortality and admission FPG in DM patients with acute HF appeared U-shaped.

Role of Circulating Fibrocytes in Cardiac Fibrosis / 中华医学杂志(英文版)

<p><b>OBJECTIVE</b>It is revealed that circulating fibrocytes are elevated in patients/animals with cardiac fibrosis, and this review aims to provide an introduction to circulating fibrocytes and their role in cardiac fibrosis.</p><p><b>DATA SOURCES</b>This review is based on the data from 1994 to present obtained from PubMed. The search terms were "circulating fibrocytes " and "cardiac fibrosis ".</p><p><b>STUDY SELECTION</b>Articles and critical reviews, which are related to circulating fibrocytes and cardiac fibrosis, were selected.</p><p><b>RESULTS</b>Circulating fibrocytes, which are derived from hematopoietic stem cells, represent a subset of peripheral blood mononuclear cells exhibiting mixed morphological and molecular characteristics of hematopoietic and mesenchymal cells (CD34+/CD45+/collagen I+). They can produce extracellular matrix and many cytokines. It is shown that circulating fibrocytes participate in many fibrotic diseases, including cardiac fibrosis. Evidence accumulated in recent years shows that aging individuals and patients with hypertension, heart failure, coronary heart disease, and atrial fibrillation have more circulating fibrocytes in peripheral blood and/or heart tissue, and this elevation of circulating fibrocytes is correlated with the degree of fibrosis in the hearts.</p><p><b>CONCLUSIONS</b>Circulating fibrocytes are effector cells in cardiac fibrosis.</p>

Effect of Metabolic Syndrome on Risk Stratification for Left Atrial or Left Atrial Appendage Thrombus Formation in Patients with Nonvalvular Atrial Fibrillation / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Metabolic syndrome (MS) is a risk factor for stroke and thromboembolism event. Left atrial or LA appendage (LA/LAA) thrombus is a surrogate of potential stroke. The relationship between MS and atrial thrombus remains unclear. In this study, we sought to investigate the effect of MS on risk stratification of LA/LAA thrombus formation in patients with nonvalvular atrial fibrillation (NVAF).</p><p><b>METHODS</b>This cross-sectional study enrolled 294 consecutive NVAF patients without prior anticoagulant and lipid-lowering therapies. LA/LAA thrombus was determined by transesophageal echocardiography. Risk assessment of LA/LAA thrombus was performed using the CHADS2 , CHA2DS2 -VASc, MS, CHADS2 -MS, and CHA2DS2 -VASc-MS scores. Logistic regression analyses were performed to determine which factors were significantly related to LA/LAA thrombus. Odds ratio (OR) including 95% confidence interval was also calculated. The predictive powers of different scores for the risk of LA/LAA thrombus were represented by C-statistics and compared by receiver operating characteristic (ROC) analysis.</p><p><b>RESULTS</b>LA/LAA thrombi were identified in 56 patients (19.0%). Logistic analysis showed that MS was the strongest risk factor for LA/LAA thrombus in NVAF patients (OR = 14.698, P < 0.001). ROC curve analyses revealed that the C-statistics of CHADS2 -MS and CHA2DS2 -VASc-MS was significantly higher than those of CHADS2 and CHA2DS2 -VASc scores (CHADS2 -MS vs. CHADS2 , 0.807 vs. 0.726, P = 0.0019). Furthermore, MS was helpful for identifying individuals with a high risk of LA/LAA thrombus in the population with a low risk of stroke (CHADS2 or CHA2DS2 -VASc score = 0).</p><p><b>CONCLUSIONS</b>MS is associated with LA/LAA thrombus risk in patients with NVAF. In addition to the CHADS2 and CHA2DS2 -VASc scores, the CHADS2 -MS and CHA2DS2 -VASc-MS scores provide additional information on stroke risk assessment.</p>

Effect of RNAi-mediated silencing of SREBP2 gene on inflammatory cytokine-induced cholesterol accumulation in HepG2 cells / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To investigate the effect of RNA interference (RNAi)-mediated silencing of the SREBP2 on inflammatory cytokine-induced cholesterol accumulation in HepG2 cells.</p><p><b>METHODS</b>Short-hairpin (sh)RNA targeting SREBP2 or negative control (NC) shRNA were transfected into HepG2 cells by a liposomal method. G418-selective culturing was used to obtain the SREBP2 shRNA HepG2 and NC shRNA HepG2 cell lines. The two cell lines were cultured in serum-free medium and left untreated (control) or treated with TNF-a (20 ng/ml), low-density lipoprotein (LDL) loading (100 mug/ml), or a combination LDL plus TNF-a treatment. Lipid accumulation was evaluated by oil red O (ORO) staining. Intracellular cholesterol level was measured by enzymatic assay. The mRNA and protein levels of SREBP2 and its downstream target genes, LDL receptor (LDLr), and HMGCoA reductase, were measured by real-time PCR and Western blotting, respectively.</p><p><b>RESULTS</b>SREBP2 shRNA HepG2 and NC shRNA HepG2 stable cell lines were successfully established. ORO staining and cholesterol quantitative analysis showed that LDL loading significantly increased intracellular cholesterol and that expression of SREBP2 further exacerbated the inflammatory cytokine-induced lipid accumulation, as seen in NC shRNA HepG2 cells. LDL loading of NC shRNA HepG2 decreased the gene and protein expressions of SREBP2, LDLr, and HMGCoA reductase, but the suppressive effect was overridden by inflammatory cytokine. SREBP2 shRNA HepG2 cells showed lower levels of cholesterol accumulation under LDL loading and inflammatory stress conditions. Moreover, the mRNA and protein levels of SREBP2, LDLr, and HMGCoA reductase were much lower than in NC shRNA HepG2 cells under the same conditions.</p><p><b>CONCLUSION</b>Inflammatory cytokine exacerbated cholesterol accumulation in HepG2 via disrupting SREBP2. RNAi-mediated inhibition of SREBP2 expression significantly ameliorated the cholesterol accumulation induced by inflammatory cytokine.</p>