Inflammatory predictors (eosinophil, C-RP and IL-6) and effectiveness of oral Azvudine tablets treatment in COVID-19 hospitalized patients: A retrospective, self-controlled study.

Background: Although vaccinations and antiviral drugs are widely used in the clinical treatment worldwide, there is little investigation on the clinical outcomes and effectiveness of oral Azvudine tablets (FNC) treatment in COVID-19 hospitalized patients. The previous data showed Azvudine treatment was closely related to reduced virus shedding time, but the potential role of Azvudine on inflammatory response is scarce. Thus, this study is to investigate inflammatory predictors and effectiveness of oral Azvudine tablets treatment in COVID-19 hospitalized patients. Methods: A total of 600 out of hospitalized patients were retrospectively collected over a 2-month period, of whom 60 out of hospitalized patients infected SARS-CoV-2. 32 of hospitalized patients who received Azvudine tablets were collected and the rest did not. Oral Azvudine tablets treatment: 5 mg/day for 7-14 days. We analyzed the routine blood tests, blood coagulation test, NT-proBNP, Troponin (cTNl), Creatine kinase MB (CK-MB) after oral Azvudine tablets treatment compared with that in before oral Azvudine tablets treatment. Also, we compared the CT chest and length of Stay after Azvudine treatment. Results: We found that the number and percentage of eosinophil increased significantly, but the levels of C-reactive protein (C-RP) and IL-6 reduced remarkably after Azvudine treatment. In blood coagulation tests, the results showed that activated partial thromboplastin time (APTT) (mean ± SEM: 2.950 ± 2.268s) and fibrinogen (mean ± SEM: 0.8910 ± 0.5134g/L) downregulated slightly, while there was similar in the level of D-Dimer (mean ± SEM: 0.1660 ± 0.3108 µg/mL) before and after Azvudine treatment. The expression of NT-proBNP reduced in Azvudine treatment (mean ± SEM: 897.1 ± 557.1pg/mL). Chest computed tomography (CT) scan reports also demonstrated that Azvudine treatment improved lung symptoms in COVID-19 hospitalized patients. Moreover, there is no difference in the average of length of stay in Azvudine treatment (the average of LOS days: 9.0) and no treatment (the average of LOS days: 9.0). Conclusion: Oral Azvudine tablets treatment was associated with decreased inflammatory response and improved blood coagulation function, which should be substantial clinical benefits in COVID-19 hospitalized patients.

Kaempferol improves acute kidney injury via inhibition of macrophage infiltration in septic mice.

Sepsis contributes to life-threatening circulatory and organ dysfunction by dysregulating the host response to infection in critically ill patients. Treatment in an Intensive Care Unit (ICU) can improve the survival of patients who suffer from severe sepsis, but sepsis-associated acute kidney injury (SAKI) is still one of the main causes of death. The existing treatment is mainly focused on controlling microorganism induced infections by using drugs, such as ulinastatin and glucocorticoid. Also, it is well documented that kaempferol, a flavonoid derived from plant sources, improves septic mouse survival via anti-inflammatory response. However, the mechanism of anti-inflammatory response mediated by this flavonoid compound was little known. This study aims to demonstrate the mechanisms of inflammatory response regulated by kaempferol treatment during sepsis. We perform cecal ligation and puncture (CLP) injury as a sepsis mouse model and evaluate organ injury in sepsis. The molecular (qRT-PCR and Western Blot) and cellular profiling (IHC staining and Flow Cytometry) of the immune responses illustrates that kaempferol decreases the expression of adhesion molecular genes (ICAM-1 and VCAM-1) and monocyte chemoattractant protein-1 (MCP-1), thereby inhibiting F4/80+ macrophages infiltration in CLP-induced acute kidney injury. Our data suggested that kaempferol alleviates acute kidney injury via regulating F4/80+ macrophages infiltration in CLP-induced acute kidney injury.

High-Fructose Diet Induces Cardiac Dysfunction via Macrophage Recruitment in Adult Mice.

Cardiovascular diseases are the leading cause of death globally, including cardiac fibrosis, myocardial infarction, cardiac hypertrophy, and heart failure. High fat/ fructose induces metabolic syndrome, hypertension and obesity, which contributes to cardiac hypertrophy and fibrosis. Excessive fructose intake accelerates inflammation in different organs and tissues, and molecular and cellular mechanisms of organ and tissue injury have been demonstrated. However, the mechanisms of cardiac inflammation have not been fully documented in high-fructose diet. This study shows that there are significantly increased in cardiomyocytes size and relative wall thickness of LV in high-fructose fed adult mice. With echocardiographic analysis of cardiac function, the ejection fraction (EF%) and fractional shortening (FS%) are significantly reduced at 12 weeks after 60% high-fructose diet. The mRNA and protein levels of MCP-1 are notably increased in high-fructose treated HL-1 and primary cardiomyocyte respectively. Also, the increased protein level of MCP-1 has been detected in vivo mouse model after 12 weeks feeding, resulting in the production of pro-inflammatory makers, pro-fibrotic genes expression, and macrophage infiltration. These data demonstrate that high-fructose intake induces cardiac inflammation via macrophage recruitment in cardiomyocyte, which contributes to impair cardiac function.

Severe pneumonia caused by Parvimonas micra: a case report.

BACKGROUND: Parvimonas micra (P. micra) is a gram-positive anaerobic coccus that is detected widely on the skin, in the oral mucosa and in the gastrointestinal tract. In certain circumstances, P. micra can cause abdominal abscesses, bacteraemia and other infections. To the best of our knowledge, there have been no case reports describing the biological characteristics of P. micra-related pneumonia. These bacteria do not always multiply in an aerobic organ, such as the lung, and they could be easily overlooked because of the clinical mindset. CASE PRESENTATION: A 35-year-old pregnant woman was admitted to the emergency department 4 weeks prior to her due date who was exhibiting 5 points on the Glasgow coma scale. A computed tomography (CT) scan showed a massive haemorrhage in her left basal ganglia. She underwent a caesarean section and brain surgery before being admitted to the ICU. She soon developed severe pneumonia and hypoxemia. Given that multiple sputum cultures were negative, the patient's bronchoalveolar lavage fluid was submitted for next-generation sequencing (NGS) to determine the pathogen responsible for the pneumonia; as a result, P. micra was determined to be the causative pathogen. Accordingly the antibiotic therapy was altered and the pneumonia improved. CONCLUSION: In this case, we demonstrated severe pneumonia caused by the anaerobic organism P. micra, and the patient benefited from receiving the correct antibiotic. NGS was used as a method of quick diagnosis when sputum culture failed to distinguish the pathogen.