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The high mortality rate of COVID-19 patients is mainly caused by the progression from mild to critical illness. To identify the key laboratory indicators and stratify high-risk COVID-19 patients with progression to severe/critical illness, we compared 474 moderate patients and 74 severe/critical patients. The laboratory indicators, including lactate dehydrogenase (LDH), monocytes percentage, etc. were significantly higher in the severe/critical patients (P <0.001) and showed a noticeable change at about a week before the diagnosis. Based on these indicators, we constructed a risk-stratification model, which can accurately grade the severity of patients with COVID-19 (accuracy = 0.96, 95% CI: 0.94 - 0.989, sensitivity = 0.98, specificity = 0.84). Also, compared with non-COVID-19 viral pneumonia, we found that COVID-19 had weaker dysfunction to the heart, liver, and kidney. The prognostic model based on laboratory indicators could help to diagnose, monitor, and predict severity at an early stage to those patients with COVID-19.
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Objective@#Analysis of the effect of triggering receptor-1 expressed on myeloid cells (TREM-1) in nonalcoholic fatty liver disease (NAFLD) and the mechanism.@*Methods@#The oleic acid-treated HepG2 cells were divided into model group, overexpression group, interference group A, interference group B and negative control group. The mouse model of NAFLD was generated and randomly divided into (nuclear factor-κB) NF-κB inhibition group, protein kinase B (AKT) inhibition group, knockout group A, knockout group B and control group. The expression of inflammatory factors and TREM-1 in liver tissue was detected by PCR, and fat accumulation was detected by oil red O staining. Western blotting was used to detect the expression of TREM-1 and signaling pathway proteins, and HE staining was used to detect liver tissue changes.@*Results@#TREM-1 was up-regulated in liver tissue of NAFLD mice [(0.936±0.127) vs. (0.432±0.105)] and in oleic acid-treated HepG2 cells. In oleic acid-treated HepG2 cells, overexpression of TREM-1 increased inflammatory factor expression and increased lipid droplets; inhibition of TREM-1 expression decreased inflammatory factor expression, and lipid droplets decreased. Knockout of TREM-1 and inhibition of NF-κB in NAFLD mice reduced hepatocyte inflammatory factor expression and reduced liver damage; knockout of TREM-1 and inhibition of AKT reduced liver tissue lipids and drops accumulate.@*Conclusions@#The overexpression of TREM-1 in NAFLD mice liver tissue can regulate inflammatory factor expression and lipid droplets through NF-κB and AKT signal pathway. TREM-1 might be a potential therapeutic target of NAFLD.
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0bjective Analysis of the effect of triggering receptor-1 expressed on myeloid cells(TREM-1)in nonalcoholic fatty liver disease(NAFLD)and the mechanism.Methods The oleic acid-treated HepG2 ceils were divided into model group,overexpression group,interference group A,interference group B and negative control group.The mouse model of NAFLD was generated and randomly divided into(nuclear factor-κB)NF-κB inhibition group,protein kinase B(AKT)inhibition group,knockout group A,knockout group B and control group.The expression of inflammatory factors and TREM.1 in liver tissue was detected by PCR,and fat accumulation was detected by oil red O staining.Western blotting was used to detect the expression of TREM-1 and signaling pathway proteins,and HE staining was used to detect liver tissue changes.Results TREM-1 was up.regulated in liver tissue of NAFLD mice J(0.936±0.127)vs.(0.432±0.105)] and in oleic acid-treated HepG2 cells.In oleic acid.treated HepG2 cells.overexpression of TREM-1 increased inflammatory factor expression and increased 1ipid droplets:inhibition of TREM-1 expression decreased inflammatory factor expression.and lipid droplets decreased.Knockout of TREM-1 and inhibition of NF-κB in NAFLD mice reduced hepatocyte inflammatory factor expression and reduced liver damage;knockout of TREM-1 and inhibition of AKT reduced liver tissue lipids and drops accumulate,Conclusions The overexpression of TREM-1 in NAFLD mice liver tissue can regulate inflammatory factor expression and lipid droplets through NF-κB and AKT signal pathway.TREM-1 might be a potential thera-peutic target of NAFLD.
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Objective To observe the effect of atmospheric pollution on workers'α1-antitrypsin concentrationb in petrochemical enterprises.Methods During health examination,the workers were indivded into 3 groups according tO the length of job experience.Ⅰ group(<10 years)included 291 cases,aged 22-35 years old,Ⅱ group(10-20 years)included 634 cases,aged 33-45 years old,and Ⅲgroup(>20 years)included 427 cases,aged 44-55 years old.The normal control were individed int different group according to the status of petrochemical workers.,all the serum samples were detected on automatic biochemical analyzer,α1-antitrypsin levels were analyzed between the different groups.Results In group Ⅰ,the α1-AT concentration was 2.58±0.38 g/L(P>0.05)without significant difference compared with control.In group Ⅱ and Ⅲ,the concentration α1-AT were 2.02±0.43 g/L and 1.72±0.41 g/L respectively with significant differences compared with control.And the significant difference existed among the three groups of petrochemical workers..But the sigficant difference did not exist between different group of control people.Conclusion During the process of oil refining,the plants exhausted the polluted gas of nitrogen dioxide,olefins,alkanes,alcohols,carbonyl and other harmful substances,it influenced theα-AT levels of body.It is a good suggestion to decreas the petrochemical pollution,and to monitor the serum concentration of α-AT content among petrochemical workers,it might to reduce the incidence of lung disease of great significance.