The impact of platelet transfusion on prognosis in adult burn patients with thrombocytopenia: A propensity score matching analysis.

BACKGROUND AND OBJECTIVES: Thrombocytopenia is common among burn patients. Platelet transfusion is frequently administered to increase platelet counts. However, it is not clear whether platelets affect the outcome after transfusion among adult burn patients with thrombocytopenia. Our aim is to explore whether platelet transfusion affects the prognosis of adult burn patients with thrombocytopenia. METHODS: We undertook a retrospective analysis of 368 adult burn victims with thrombocytopenia from the Department of Burn at the First Affiliated Hospital of Nanchang University, China, from January 2014 to July 2021. Propensity score matching (PSM) was utilized to reduce selection bias and confounding factors. After PSM, the platelet transfusion group and the no-platelet transfusion group each had 46 patients. Our primary outcome was 30-day all-cause mortality. RESULTS: Logistic multivariate regression analysis showed that third-degree burn area [ß = -0.040, odds ratio (OR) = 1.052, 95 % confidence interval (CI) = 1.015-1.091] and platelet transfusion (OR =2.227, 95 % CI = 0.473-10.483) were independent risk factors (P < 0.05). KaplanMeier analysis showed that the 30-day mortality of patients in the platelet transfusion group and no-platelet transfusion group were 47.8 % and 19.6 %, respectively (P < 0.05) CONCLUSION: Platelet transfusion was an independent risk factor for 30-day mortality in adult burn patients with thrombocytopenia.

Regulation of renal ischemia-reperfusion injury and tubular epithelial cell ferroptosis by pparγ m6a methylation: mechanisms and therapeutic implications.

This study aimed to elucidate the role and underlying mechanisms of Peroxisome proliferator-activated receptor gamma (PPARγ) and its m6A methylation in renal ischemia-reperfusion (I/R) injury and ferroptosis of tubular epithelial cells (TECs). High-throughput transcriptome sequencing was performed on renal tissue samples from I/R injury models and sham-operated mice, complemented by in vivo and in vitro experiments focusing on the PPARγ activator Rosiglitazone and the manipulation of METTL14 and IGF2BP2 expression. Key evaluations included renal injury assessment, ferroptosis indicator measurement, and m6A methylation analysis of PPARγ. Our findings highlight the critical role of the PPARγ pathway and ferroptosis in renal I/R injury, with Rosiglitazone ameliorating renal damage and TEC ferroptosis. METTL14-mediated m6A methylation of PPARγ, dependent on IGF2BP2, emerged as a pivotal regulator of PPARγ expression, renal injury, and ferroptosis. This study reveals that PPARγ m6A methylation, orchestrated by METTL14 through an IGF2BP2-dependent mechanism, plays a crucial role in mitigating renal I/R injury and TEC ferroptosis. These insights offer promising avenues for therapeutic strategies targeting acute kidney injury.

S-adenosyl-L-methionine supplementation alleviates aortic dissection by decreasing inflammatory infiltration.

Methionine, an indispensable amino acid crucial for dietary balance, intricately governs metabolic pathways. Disruption in its equilibrium has the potential to heighten homocysteine levels in both plasma and tissues, posing a conceivable risk of inducing inflammation and detriment to the integrity of vascular endothelial cells. The intricate interplay between methionine metabolism, with a specific focus on S-adenosyl-L-methionine (SAM), and the onset of thoracic aortic dissection (TAD) remains enigmatic despite acknowledging the pivotal role of inflammation in this vascular condition. In an established murine model induced by ß-aminopropionitrile monofumarate (BAPN), we delved into the repercussions of supplementing with S-adenosyl-L-methionine (SAM) on the progression of TAD. Our observations uncovered a noteworthy improvement in aortic dissection and rupture rates, accompanied by a marked reduction in mortality upon SAM supplementation. Notably, SAM supplementation exhibited a considerable protective effect against BAPN-induced degradation of elastin and the extracellular matrix. Furthermore, SAM supplementation demonstrated a robust inhibitory influence on the infiltration of immune cells, particularly neutrophils and macrophages. It also manifested a notable reduction in the inflammatory polarization of macrophages, evident through diminished accumulation of MHC-IIhigh macrophages and reduced expression of inflammatory cytokines such as IL1ß and TNFα in macrophages. Simultaneously, SAM supplementation exerted a suppressive effect on the activation of CD4 + and CD8 + T cells within the aorta. This was evidenced by an elevated proportion of CD44- CD62L + naïve T cells and a concurrent decrease in CD44 + CD62L- effector T cells. In summary, our findings strongly suggest that the supplementation of SAM exhibits remarkable efficacy in alleviating BAPN-induced aortic inflammation, consequently impeding the progression of thoracic aortic dissection.

COMMD10 inhibited DNA damage to promote the progression of gastric cancer.

PURPOSE: The copper metabolism MURR1 domain 10 (COMMD10) plays a role in a variety of tumors. Here, we investigated its role in gastric cancer (GC). METHODS: Online prediction tools, quantitative real-time PCR, western blotting and immunohistochemistry were used to evaluate the expression of COMMD10 in GC. The effect of COMMD10 knockdown was investigated in the GC cell lines and in in vivo xenograft tumor experiments. Western blotting and immunofluorescence were used to explore the relationships between COMMD10 and DNA damage. RESULTS: The expression of COMMD10 was upregulated in GC compared to that in para-cancerous tissue and correlated with a higher clinical TNM stage (P = 0.044) and tumor size (P = 0.0366). High COMMD10 expression predicted poor prognosis in GC. Knockdown of COMMD10 resulted in the suppression of cell proliferation, migration, and invasion, accompanied by cell cycle arrest and an elevation in apoptosis rate. Moreover, the protein expression of COMMD10 was decreased in cisplatin-induced DNA-damaged GC cells. Suppression of COMMD10 impeded DNA damage repair, intensified DNA damage, and activated ATM-p53 signaling pathway in GC. Conversely, restoration of COMMD10 levels suppressed DNA damage and activation of the ATM-p53 signaling cascade. Additionally, knockdown of COMMD10 significantly restrained the growth of GC xenograft tumors while inhibiting DNA repair, augmenting DNA damage, and activating the ATM-p53 signaling pathway in xenograft tumor tissue. CONCLUSION: COMMD10 is involved in DNA damage repair and maintains genomic stability in GC; knockdown of COMMD10 impedes the development of GC by exacerbating DNA damage, suggesting that COMMD10 may be new target for GC therapy.

[Analysis of Plasma Metabolic Profile in Children with Transfusion-Dependent Thalassemia].

OBJECTIVE: To explore the plasma metabolomic characteristics of children with transfusion-dependent thalassemia (TDT), and reveal the changes of metabolic pattern in children with TDT. METHODS: 23 children with TDT who received regular blood transfusion in Ganzhou Women and Children's Health Care Hospital in 2021 were selected, and 11 healthy children who underwent physical examination during the same period were selected as the control group. The routine indexes between children with TDT and the control group were compared, and then the metabolic composition of plasma samples from children with TDT and the control group was detected by liquid chromatography-mass spectrometry. An OPLS-DA model was established to perform differential analysis on the detected metabolites, and the differential metabolic pathways between the two groups were analyzed based on the differential metabolites. RESULTS: The results of routine testing showed that the indexes of ferritin, bilirubin, total bile acid, glucose and triglycerides in children with TDT were significantly higher than those in healthy controls, while hemoglobin and total cholesterol were significantly lower (all P <0.05). However there was no significant difference in lactate dehydrogenase between the two groups (P >0.05). Compared with the control group, 190 differential metabolites (VIP>1) were identified in TDT children. Among them, 168 compounds such as arginine, proline and glycocholic acid were significantly increased, while the other 22 compounds such as myristic acid, eleostearic acid, palmitic acid and linoleic acid were significantly decreased. The metabolic pathway analysis showed that the metabolic impact of TDT on children mainly focused on the upregulation of amino acid metabolism and downregulation of lipid metabolism. CONCLUSION: The amino acid and lipid metabolism in children with TDT were significantly changed compared with the healthy control group. This finding is helpful to optimize the treatment choice for children with TDT, and provides a new idea for clinical treatment.

Redistribution and Activation of CD16brightCD56dim NK Cell Subset to Fight against Omicron Subvariant BA.2 after COVID-19 Vaccination.

With the alarming surge in COVID-19 cases globally, vaccination must be prioritised to achieve herd immunity. Immune dysfunction is detected in the majority of patients with COVID-19; however, it remains unclear whether the immune responses elicited by COVID-19 vaccination function against the Omicron subvariant BA.2. Of the 508 enrolled patients infected with Omicron BA.2, 102 were unvaccinated controls, and 406 were vaccinated. Despite the presence of clinical symptoms in both groups, vaccination led to a significant decline in nausea or vomiting, abdominal pain, headache, pulmonary infection, and overall clinical symptoms and a moderate rise in body temperature. The individuals infected with Omicron BA.2 were also characterised by a mild increase in both serum pro- and anti-inflammatory cytokine levels after vaccination. There were no significant differences or trend changes between T- and B-lymphocyte subsets; however, a significant expansion of NK lymphocytes in COVID-19-vaccinated patients was observed. Moreover, the most effective CD16brightCD56dim subsets of NK cells showed increased functional capacities, as evidenced by a significantly greater IFN-γ secretion and a stronger cytotoxic potential in the patients infected with Omicron BA.2 after vaccination. Collectively, these results suggest that COVID-19 vaccination interventions promote the redistribution and activation of CD16brightCD56dim NK cell subsets against viral infections and that they could facilitate the clinical management of patients infected with Omicron BA.2.

Tanshinone IIA relieves arthritis by inhibiting autophagy of fibroblast-like synoviocytes via matrix metalloproteinase9/receptor for advanced glycation end product/toll-like receptor 9 signal axis in mice with collagen-induced arthritis.

In this study, we probed into the related mechanism underlying the role of Tanshinone IIA (TIIA) in RA fibroblast-like synoviocytes (RA-FLSs). We constructed a mouse model of RA using the collagen-induced arthritis (CIA) method. Gain- or loss-of-function approaches were used to manipulate matrix metalloproteinase9 (MMP9), receptor for advanced glycation end product (RAGE), and toll-like receptor 9 (TLR9) in both CIA mice and RA-FLSs following treatment with TIIA to study the in vivo and in vitro effect of TIIA through analysis of cell viability, and measurement of autophagy and inflammatory proteins as well as severity of RA. In vitro and in vivo animal experiments results showed that TIIA could inhibit the proliferation of RA-FLSs and affect autophagy, thereby improving the symptoms of RA in mice. Mechanically, TIIA could inhibit the expression of MMP9 in RA-FLSs, thereby inhibiting the shedding of RAGE and thus inhibiting the activation of TLR9. Finally, animal experiments confirmed that TIIA affected autophagy by regulating the MMP9/RAGE/TLR9 axis, and finally improve the symptoms of RA in mice. Conclusively, TIIA may inhibit expression of MMP9 to suppress the combination of RAGE and TLR9, thereby inhibiting RA-FLS proliferation and affecting autophagy, eventually improve the RA.

Prevalence and clinical characteristics of T2DM patients with OTUD3 gene rs78466831 SNP at a single academic center in China.

Background: A novel, rare OTUD3 c.863G>A (rs78466831) in humans has been reported associated with diabetes, but the prevalence and clinical characteristics of T2DM patients with rs78466831 have not been reported before. Objective: To investigate the prevalence and clinical characteristics of T2DM patients with rs78466831 and provide a basis for clinical diagnosis and treatment. Methods: OTUD3 gene rs78466831 SNP was detected by Sanger sequencing in all the collected specimens of laboratory-confirmed T2DM patients and healthy people. Clinical characteristics indexes inconsisting of fasting blood glucose (FBG), glycosylated hemoglobin (HbA1c), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), total cholesterol (TC), triglyceride (TG) and a body mass index (BMI), T2DM-associated chronic complications (myocardial infarction, cerebrovascular disease, retinopathy, arterial plaque, peripheral neuropathy and nephropathy) were obtained from the clinical laboratory information systems and electronic medical record system. Clinical characteristic indicators were compared between the wild-type and variant (rs78466831) patients with T2DM. Results: The prevalence of rs78466831 in the T2DM patients group was significantly higher than the healthy control in our academic center. The general characteristic indicators were not significantly different between the wild-type and rs78466831 patients with T2DM, except the family history of diabetes. Clinical laboratory indicators including HbA1c, FBG, OGTT, TC, HDL-C, LDL-C and CP had no significant difference between the two groups. The therapeutic drug and target achievement rates were not significantly different between the two groups. The incidence of diabetic retinopathy in the variant group was significantly higher than the wild-type group. Conclusions: The OTUD3 gene rs78466831 was associated with T2DM and may be a biological risk factor of diabetes retinopathy.

Polymorphonuclear neutrophil activation by Src phosphorylation contributes to HLA-A2 antibody-induced transfusion-related acute lung injury.

Human leukocyte antigen (HLA)-A2 antibody contributes to the pathogenesis of transfusion-related acute lung injury (TRALI) via polymorphonuclear neutrophil (PMN) activation, but the signaling pathways involved this process remain largely undefined. In this study, we sought to study the signaling pathways involved in the pathogenesis of HLA-A2-induced TRALI. Lipopolysaccharide (LPS), and the plasma from the HLA-A2 antibody-positive donors were utilized to establish a rat model of TRALI. Human pulmonary endothelial cells (HPMECs) were in vitro co-cultured with HLA-A2 antibody-treated PMNs and then treated with LPS to induce a cytotoxicity model. The effects of HLA-A2 antibody on HPMEC injury were evaluated in this model. Besides, dasatinib was used to block the Src phosphorylation to explore whether Src involved in the TRALI or HPMEC injury induced by HLA-A2 antibody. The HLA-A2 antibody plus LPS induced TRALI and stimulated PMN activation in rats. HLA-A2 antibody-induced TRALI could be attenuated via depletion of PMN. HLA-A2 antibody activated NF-κB and NLRP3 inflammasome. In addition, HLA-A2 antibody aggravated the HPMEC injuries and the release of PMN surfaces makers, but dasatinib treatment reversed this effect, indicating that HLA-A2 antibody activated PMNs and exacerbated TRALI by stimulating phosphorylation of Src followed by activation of NF-κB and NLRP3 inflammasome, which was validated in vivo. In summary, HLA-A2 induced PMNs by activating NF-κB/NLRP3 inflammasome via phosphorylated-Src elevation, thereby exacerbating TRALI. This study highlights promising target for the treatment of antibody-mediated TRALI.

Extracellular Vesicle-Derived circITGB1 Regulates Dendritic Cell Maturation and Cardiac Inflammation via miR-342-3p/NFAM1.

Acute myocardial infarction (AMI) is a complication of atherosclerosis-related cardiovascular illness that is caused by prolonged ischemia. Circular RNAs (circRNAs) are concentrated in extracellular vesicles (EVs) and have been linked to cardiovascular disease. However, additional research is needed into the expression and function of circRNAs in AMI. In this study, circITGB1 (has_circRNA_0018146), derived from exon 1 of the ITGB1 gene localized on chromosome 10, was shown to be considerably increased in plasma from patients with AMI compared to healthy controls, as demonstrated by the comparison of EV-circRNA expression patterns. Using a luciferase screening assay and a biotin-labeled circITGB1 probe to identify microRNA(s) complementary to circITGB1 sequences, we discovered that circITGB1 competitively binds to miR-342-3p and inhibits its expression, which in turn increase the expression of NFAT activating molecule 1 (NFAM1). Based on western blotting and immunological studies, circITGB1 controls dendritic cell maturation by targeting miR-342-3p and NFAM1. circITGB1 also exacerbated cardiac damage and regulated miR-342-3p and NFAM1 expression in a mouse AMI model. This implies that EV-circITGB1 is involved in dendritic cell maturation and cardiac damage via miR-342-3p/NFAM1, and that is linked to AMI-associated pathogenic processes.

Curcumin activates NLRC4, AIM2, and IFI16 inflammasomes and induces pyroptosis by up-regulated ISG3 transcript factor in acute myeloid leukemia cell lines.

Curcumin, the primary bioactive component isolated from turmeric, has been found to possess a variety of biological functions, including anti-leukemia activity. However, the effect of curcumin in different leukemia cells vary. In this study, we demonstrated that curcumin induced the expression of AIM2, IFI16, and NLRC4 inflammasomes in leukemia cells U937 by increasing the expression levels of ISG3 transcription factor complex, which activated caspase 1, promoted cleavage of GSDMD, and induced pyroptosis. We also found that pyroptosis executor GSDMD was not expressed in two curcumin-insensitive cells HL60 and K562 cells. In addition, exogenous overexpression of GSDMD by lentiviral transduction in K562 cells increased the anti-cancer activity of curcumin, and inhibiting the expression of GSDMD by shRNA enhanced U937 cells to resist curcumin. The results showed that inducing pyroptosis is a novel mechanism underlying the anti-leukemia effects of curcumin.

CREM Is Correlated With Immune-Suppressive Microenvironment and Predicts Poor Prognosis in Gastric Adenocarcinoma.

The transcriptional repressor cAMP response element modulator (CREM) has an important role in T-cell development. In this study, we used the integrated Bioinformatics Methods to explore the role of CREM in gastric adenocarcinoma (GAC). Our results showed that high CREM expression was closely related with poorer overall survival in GAC. By GSEA cluster analysis, we found that the high expression of CREM was associated with the cancer-associated pathway in GAC. Moreover, single-cell sequencing data showed that CREM is mainly localized in exhausted CD8+ T cells. Its prognostic value and the potential function lead to T-cell exhaustion in the tumor microenvironment (TME). Similar results were also obtained in glioma and lung cancer. High expression of CREM, correlated with clinical relevance of GAC, was associated with T-cell exhaustion and M2 polarization in GAC. These findings suggest that CREM can be used as a prognostic biomarker in GAC, which might provide a novel direction to explore the pathogenesis of GAC.

Neuraminidase 1 Exacerbating Aortic Dissection by Governing a Pro-Inflammatory Program in Macrophages.

Inflammation plays an important role in aortic dissection (AD). Macrophages are critically involved in the inflammation after aortic injury. Neuraminidases (NEUs) are a family of enzymes that catalyze the cleavage of terminal sialic acids from glycoproteins or glycolipids, which is emerging as a regulator of macrophage-associated immune responses. However, the role of neuraminidase 1 (NEU1) in pathological vascular remodeling of AD remains largely unknown. This study sought to characterize the role and identify the potential mechanism of NEU1 in pathological aortic degeneration. After ß-aminopropionitrile monofumarate (BAPN) administration, NEU1 elevated significantly in the lesion zone of the aorta. Global or macrophage-specific NEU1 knockout (NEU1 CKO) mice had no baseline aortic defects but manifested improved aorta function, and decreased mortality due to aortic rupture. Improved outcomes in NEU1 CKO mice subjected to BAPN treatment were associated with the ameliorated vascular inflammation, lowered apoptosis, decreased reactive oxygen species production, mitigated extracellular matrix degradation, and improved M2 macrophage polarization. Furthermore, macrophages sorted from the aorta of NEU1 CKO mice displayed a significant increase of M2 macrophage markers and a marked decrease of M1 macrophage markers compared with the controls. To summarize, the present study demonstrated that macrophage-derived NEU1 is critical for vascular homeostasis. NEU1 exacerbates BAPN-induced pathological vascular remodeling. NEU1 may therefore represent a potential therapeutic target for the treatment of AD.

Early correction of coagulopathy reduces the 28-day mortality in adult patients with large-area burns. / æ—©æœŸçº æ­£å‡è¡€åŠŸèƒ½éšœç¢é™ä½Žå¤§é¢ç§¯çƒ§ä¼¤æˆå¹´æ‚£è€ 28 dç— æ­»çŽ‡.

OBJECTIVES: Coagulation dysfunction caused by large-area burns is an independent risk factor for the 28-day mortality of adult patients. However, whether early (48 hours after admission) correction of coagulopathy can reduce the 28-day mortality of adult patients with large-area burns has not been clarified. The purpose of this study was to investigate the effect of early correction of coagulopathy on the 28-day mortality in the adult patients with large-area burns. METHODS: Medical records of burn patients with blood transfusion who were hospitalized in the Department of Burn, First Affiliated Hospital of Nanchang University from April 2014 to July 2019 were retrieved. Among them, 573 adult patients with large-area burns were selected as the research subjects. The patients were divided into an experimental group (patients had early rectification of coagulation dysfunction, n=290) and a control group (patients without early rectification of coagulation dysfunction, n=283). The basic clinical data and prognostic indicators of the 2 groups were compared. Logistic univariate regression analysis was used to screen the influential factors of 28-day mortality in adult patients with large-area burns, and further logistic multivariate regression analysis was carried out to obtain independent risk factors and protective factors. Kaplan-Meier method was used to draw the survival curve for the 2 groups of patients, and log-rank test was used. RESULTS: The differences of the burn area/the total body surface area (TBSA), III° burn area, 24-hour urine volume and rehydration volume, 48-hour fresh frozen plasma transfusion volume, and 48-hour activated partial thromboplastin time (APTT) between the 2 groups were statistically significant (all P<0.05). The duration of mechanical ventilation in the experimental group was shorter than that in the control group, and the 28-day mortality in the experimental group was significantly lower than that in the control group (10% vs 24%, both P<0.05). The results of logistic univariate regression analysis showed that burn area/TBSA, III° burn area, inhalation injury, length of hospital stay, mechanical ventilation time, 48-hour frozen plasma infusion, and 48-hour coagulation dysfunction correction were the influential factors of 28-day mortality of adult patients with large-area burns and coagulation dysfunction at admission (all P<0.05). Logistic multivariate regression analysis showed that the burn area/TBSA (OR=1.058, 95% CI 0.921 to 1.214, P=0.022) and III° burn area (OR=1.085, 95% CI 1.009 to 1.168, P=0.027) were independent risk factors for 28-day mortality of adult patients with large-area burns, while 48-hour frozen plasma transfusion volume (OR=0.098, 95% CI 0.012 to 0.789, P=0.029) and 48-hour coagulation dysfunction correction (OR=0.103, 95% CI 0.015 to 0.679, P=0.018) were independent protective factors. Kaplan-Meier survival curve analysis showed that 28-day survival rates of the experimental group and the control group were 90% and 76%, respectively. The difference between them was statistically significant (χ2=14.270, P<0.001). CONCLUSIONS: The burn area/TBSA and III° burn area are independent risk factors for 28-day mortality in adult patients with large-area burns. The 48-hour frozen plasma transfusion volume and 48-hour correction of coagulopathy are independent protective factors. Early correction of coagulation dysfunction is beneficial to reducing the 28-day mortality for the adult patients with large-area burns.

MiR-144-induced KLF2 inhibition and NF-kappaB/CXCR1 activation promote neutrophil extracellular trap-induced transfusion-related acute lung injury.

Transfusion-related acute lung injury (TRALI) is a clinical syndrome which is associated with the formation of neutrophil extracellular trap (NET). Recent studies have demonstrated the roles of microRNAs (miRNAs) in the pathophysiological process of TRALI. Here, the study focused on the role of miR-144 and the molecular mechanisms in NET-induced TRALI. Up-regulated miR-144 and under-expressed KLF2 were determined in patients with TRALI. In the mouse model of a two-event TRALI induced by intraperitoneal injections with lipopolysaccharide and anti-H-2Kd mAb, we determined expression patterns of miR-144, Krüppel-like factor 2 (KLF2), chemokine (C-X-C motif) receptor 1 (CXCR1) and nuclear factor kappa-B (NF-kappaB) p65. The results confirmed that miR-144 was highly expressed, while KLF2 was poorly expressed in mice with TRALI. Dual-luciferase reporter gene assay identified that miR-144 could target KLF2. Using gain- and loss-of-function approaches, we analysed the effects of miR-144 and its interaction with KLF2 on TRALI. Enforced expression of miR-144 was found to aggravate NET-induced TRALI by down-regulating KLF2 and activating the NF-kappaB/CXCR1 signalling pathway in TRALI mice. Collectively, miR-144-targeted inhibition of KLF2 and activation of NF-kappaB/CXCR1 are possible mechanisms responsible for NET-caused TRALI. These findings aid in the development of therapeutic modalities for the treatment of TRALI.

Effect of the infusion ration between frozen plasma and plasma substitutes on the prognosis of adult patients with major burn in shock stage. / ä¼‘å ‹æœŸå†°å†»è¡€æµ†ä¸Žè¡€æµ†ä»£ç”¨å“è¾“æ³¨æ¯”ä¾‹å¯¹å¤§é¢ç§¯çƒ§ä¼¤æˆå¹´æ‚£è€ é¢„åŽçš„å½±å“.

OBJECTIVES: In recent years, it has been reported that the anti-shock effect of plasma substitutes in adult patients with major burn in shock stage is not good. However, due to the shortage of clinical frozen plasma supply, it is impossible to guarantee that frozen plasma is used as colloidal solution for anti-shock treatment. The purpose of this study is to explore the effect of the infusion ration between frozen plasma and plasma substitutes on the prognosis of adult patients with major burn in shock stage. METHODS: This study enrolled 586 adult patients with major burn by selecting the hospitalization burn patients, who had been hospitalized at the Jiangxi province burn center from September 2014 to April 2019. The patients with the infusion ratio of frozen plasma to plasma substitutes ≥2꞉1 at 48 hours after admission were included in the experimental group, otherwise they were included in the control group. The basic clinical data and clinical prognosis indicator in the 2 groups were compared. Logistic univariate regression analysis was used to screen the influential factors of 30-day mortality in adult patients with major burn, and logistic multivariate regression analysis was used to obtain independent risk and protective factors; Kaplan-Meier method was used to draw the survival curve of the 2 groups, and log-rank test was used to compare the 30-day survival rate of the 2 groups. RESULTS: There were significant differences in the infusion volume of frozen plasma and plasma substitutes between the 2 groups at 48 hours after admission (both P<0.05). The duration of mechanical ventilation in the experimental group was shorter than that in the control group, the percentage of continuous renal replacement therapy (CRRT) in the experimental group was lower than that in the control group, and the in-hospital mortality and 30-day mortality in the experimental group were lower than those in the control group, the differences were statistically significant (all P<0.05). The percentage of burn area and total body surface area (TBSA) was an independent risk factor for 30-day mortality of adult patients with major burn (OR=1.228, 95% CI 1.010 to 1.439, P=0.039), while the infusion ration between of frozen plasma and plasma substitutes 48 hours after admission was an independent protective factor (OR=0.016, 95% CI 0.001 to 0.960, P=0.023). The 30-day survival rate of the experimental group was significantly higher than that in the control group (P<0.001). CONCLUSIONS: Infusion ration between frozen plasma to plasma substitutes at 48 hours after admission is an independent protective factor for 30-day mortality of adult patients with major burn. In the early stage of adult patients with major burn, frozen plasma should be used as the anti-shock therapy as far as possible (frozen plasma꞉plasma substitute ≥2꞉1) to improve the prognosis and reduce the of 30-day mortality.

Elevated frequencies of CD14+HLA-DRlo/neg MDSCs in COVID-19 patients.

BACKGROUND: The immune responses, hyper-inflammation or immunosuppression, may be closely related to COVID-19 progression. We aimed to evaluate the changes of frequency of CD14+HLA-DRlo/neg MDSCs, a population of cells with potent immunosuppressive capacity, in COVID-19 patients. METHODS: The levels of CD14+HLA-DRlo/neg MDSCs were determined by flow cytometry in 27 COVID-19 patients, and their association with clinical characteristics and laboratory data were analyzed. RESULTS: The frequency of CD14+HLA-DRlo/neg MDSCs was elevated in COVID-19 patients, particularly severe patients. A follow-up comparison revealed a decline of CD14+HLA-DRlo/neg MDSCs percentages in most patients 1 day after testing negative for SARS-CoV-2 nucleic acid, but the levels of CD14+HLA-DRlo/neg MDSCs were still greater than 50.0% in 3 ICU patients 4-10 days after negative SARS-CoV-2 results. Elevated frequency of CD14+HLA-DRlo/neg MDSCs was positively correlated with oropharyngeal viral loads and length of hospital stay, while negatively correlated with lymphocyte counts and serum albumin. Moreover, strong correlations were observed between the frequency of CD14+HLA-DRlo/neg MDSCs and T cell subsets, NK cell counts, and B cell percentages. The frequency of CD14+HLA-DRlo/neg MDSCs could be used as a predictor of COVID-19 severity. CONCLUSIONS: A high frequency of CD14+HLA-DRlo/neg MDSCs, especially in severe patients, may indicate an immunoparalysis status and could be a predictor of disease severity and prognosis.

Clinical significance of long noncoding RNA maternally expressed gene 3 in acute promyelocytic leukemia.

INTRODUCTION: Long noncoding RNA maternally expressed gene 3 (MEG3) expression was significantly decreased in acute myeloid leukemia (AML). However, its expression and clinical significance in acute promyelocytic leukemia (APL) remain unclear. Thus, the present study aimed to investigate the expression of MEG3 in APL and explore its clinical value. METHODS: A total of 287 AML patients derived from The Cancer Genome Atlas (TCGA) and Vizome database were enrolled. A development and validation cohort, including APL, AML with AML1/ETO, and other types of AML patients and disease controls, from the First Affiliated Hospital of Nanchang University, were also enrolled in this study. The correlation between MEG3 expression and the clinicopathological features in APL was investigated. The diagnostic values of MEG3 expression in APL were analyzed by receiver operating characteristic (ROC) curves. RESULT: In the development set, MEG3 expression was significantly increased in APL than AML with AML1/ETO, other types of AML, and disease controls, which was consistent with the results from the database analysis. MEG3 expression in APL was associated with age (P = .0053) but did not correlate with other clinicopathological features (P > .05). ROC curve analysis in the development set and diagnostic test analysis in the validation set suggested that MEG3 expression has a significant value in the diagnosis of APL. Furthermore, the expression of MEG3 decreased during the follow-up of patients with negative PML/RARα fusion gene. CONCLUSION: MEG3 serves as a novel marker for the diagnosis of APL, evaluates the curative effect, and provides a novel direction for further research.

Influential factor and trend of specific IgG antibody titer in coronavirus disease 2019 convalescents. / 2019å† çŠ¶ç— æ¯’ç— åº·å¤è€ ç‰¹å¼‚æ€§IgGæŠ—ä½“æ•ˆä»·çš„å½±å“å› ç´ åŠå˜åŒ–è¶‹åŠ¿.

OBJECTIVES: To explore the influential factors and titer trend of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) specific IgG antibody in convalescent patients with coronavirus disease 2019 (COVID-19), and to provide theoretical basis for the feasibility of clinical treatment of convalescent plasma. METHODS: Colloidal gold immunochromatography assay was used to detect the SARS-CoV-2 specific IgG antibody and its titer in 113 convalescent patients with COVID-19 who were followed up from February 19, 2020 to April 6, 2020. The basic characteristics and treatment factors of patients in the high titer group (antibody titer≥1꞉160, n=22) and the low titer group (antibody titer <1꞉160, n=91) were analyzed. The IgG antibody titer in the high titer group was continuously monitored and the trend of titer was analyzed. RESULTS: The difference in the clinical type of COVID-19, onset time, first admission C-reactive protein, absolute value of lymphocyte, absolute value of CD19+CD3- lymphocytes, and the treatment of glucocorticoid were not statistically significant between the patients in the high titer group and the low titer group (all P>0.05). The male patients in the high titer group were more than those in the low titer group (P<0.05). The titer of SARS-CoV-2 specific IgG antibody in the high titer group decreased to less than 1꞉160 28 d after discharge. CONCLUSIONS: Male COVID-19 patients might be more likely to produce high titer SARS-CoV-2 specific IgG antibodies than female. The peak level of SARS-CoV-2 specific IgG antibody in convalescent patients is maintained for a short period. Using plasma from convalescent COVID-19 patients for treatment should be within 28 d after discharge.