HLA-G14 bp polymorphism Hainan Li nationality and severe preeclampsia susceptibility related research

Objective:To explore the correlation between the distribution of 14bp polymorphism in exon 8 of human leukocyte antigen-G(HLA-G)gene in Hainan Li nationality and susceptibility to severe preeclampsia.Methods:100 cases of severe preeclampsia inpatients(experimental group)admitted to our hospital from June 2018 to September 2019 were selected.Among them,50 were Li and 50 were Han,and 100 were admitted to our hospital during the same period Normal pregnant women were the control group,including 50 cases of Li nationality and 50 cases of Han nationality.Venous blood was collected to detect the 14bp polymorphism in HLA-G gene exon 8,and the correlation between the 14bp polymorphism in HLA-G gene exon 8 and susceptibility to severe preeclampsia was analyzed.Results:There was a statistically significant difference in the 14-bp genotyping and allele frequency in HLA-G exon 8 of the Li ethnic group in the control group and the experimental group(P<0.05).The SBP and DBP of the Li 14-14/14bp typing,+14bp/-14bp typing,and allele-14bp typing were lower in the experimental group than in the Han group in the experimental group(P<0.05),and the SBP of+14bp/-14bp typing DBP was higher than that of Han patients in the experimental group(P<0.05).Binary Logistic Regression Analysis+14bp/-14bp was associated with the incidence of severe preeclampsia in Li women in Hainan region(P<0.05).The-14bp/-14bp classification was a protective factor for severe preeclampsia in Li women in Hainan region(P<0.05).Conclusion:The HLA-G gene exon 8 carrying a 14bp deletion polymorphism in the Hainan Li nationality is associated with preeclampsia susceptibility and progression.

METTL14 upregulates m6A modification of pri‑miR‑141 inhibiting ZEB1 to promote proliferation and inflammation of lung fibroblasts

Objective: To explore whether METTL14 is involved in regulating the fibroblast proliferation and inflammatory cytokine secretion by regulating the m6A modification of pri‑miR‑141. Methods: MRC‑5 cells were transfected via METTL14 overexpression lentivirus to increase METTL14 expression. Levels of METTL14 and ZEB1 were measured by qPCR and western blot. The effect of METTL14 on MRC‑5 proliferation and apoptosis was determined by CCK‑8 and flow cytometry, respectively. The ELISA kits of IL‑2, IL6 and TNF‑α were used to detect the effect of METTL14 on MRC‑5 inflammatory secretion. m6A modification site on pri‑miR‑141 was detected by meRIP. The binding site between pri‑miR‑141 and METTL14 was determined by RIP. Results: We successfully upregulated METTL14 expression in MRC‑5 cells. Elevated METTL14 promoted MRC‑5 cell proliferation, suppressed its apoptosis and promoted inflammatory factors secretion in MRC‑5 cells. pri‑miR‑141 had m6A modification sites. pri‑miR‑141 can directly bind to METTL14. METTL14 upregulation increased miR‑141 while suppressed ZEB1 expression. Conclusion: METTL14 can promote the expression of miR‑141 by increasing the m6A modification site of pri‑miR‑141, and inhibit ZEB1, thereby promoting the proliferation of fibroblasts and the secretion of inflammatory factors.

Prevalence of allergic rhinitis and associated risk factors in middle school students from Haikou,China

Objective:To identify the prevalence and influencing factors of allergic rhinitis among middle school students in Haikou,and to provide reference for the prevention and treatment of allergic rhinitis among middle school students in Haikou.Methods:The stratified cluster sampling method was adopted to randomly select the middle school students(aged 12-18)from 8 ordinary or vocational middle schools in Xiuying District,Longhua District,Meilan District and Qiongshan District of Haikou as the survey subjects.The self-made questionnaire was used to conduct the survey from April to May in 2022.Results:A total of 2169 valid questionnaires were collected,the effective rate was 86.6%(2169/2479),814(37.5%)male students and 1355(62.5%)female students.The prevalence rate of allergic rhinitis reported by middle school students in Haikou was 39.8%(863/2169),including 599 cases of intermittent allergic rhinitis(69.4%)and 264 cases of persistent allergic rhinitis(30.6%).The January,February,November and December were the periods of high incidence of symptoms each year.The results of multivariate logistic regression analysis showed that:using antibiotics 5 times a year[OR=2.07,95%CI(1.24-3.45),P=0.005],using antibiotics 3-4 times a year[OR=1.77,95%CI(1.23-2.55),P=0.002],family history of allergic rhinitis[OR=3.84,95%CI(2.67-5.54),P<0.001],history of sinusitis[OR=7.77,95%CI(3.22-18.76),P<0.001],damp living environment[OR=2.87,95%CI(2.00-4.13),P<0.001],history of asthma[OR=8.69,95%CI(1.93-39.12),P=0.005],urban residents[OR=1.68,95%CI(1.35-2.09),P<0.001],frequent exposure to dust[OR=1.59,95%CI(1.20-2.12),P=0.001],male[OR=1.35,95%CI(1.10-1.66),P=0.005],furry pet[OR=1.39,95%CI(1.10-1.75),P=0.006],daily sleep time<8 hours[OR=1.30,95%CI(1.07-1.58),P=0.009]were risk factors for allergic rhinitis.Conclusion:The prevalence of allergic rhinitis among middle school students in Haikou was higher than reported in most areas of China.Male,urban residents,antibiotic use,sleeping less than 8 hours a day,feeding furry pets,living in humid environment,frequent exposure to dust,family history of allergic rhinitis,history of sinusitis and history of asthma were risk factors for allergic rhinitis.Family history of allergic rhinitis,sinusitis and asthma were the most significant factors.

MiR-873 regulates cell autophagy by targeting Beclin1 to promot inflammation and apoptosis of bronchial epithelial cells

Objective:Investigating the effects of miR-873 on apoptosis and autophagy in bronchial epithelial cells,as well as its regulatory role on Beclin1.Methods:Following transfection of miR-873 mimic into 16HBE cells for 48 hours,the mRNA level of miR-873 was quantified by qRT-PCR,and cell viability was evaluated by CCK-8 assay.The levels of IL-2,IL-6,IL-10,and TNF-αin the cell supernatant were determined using ELISA assay,while cell apoptosis was detected by TUNEL staining.LC-3 protein expression was examined by immunofluorescence,and mRNA and protein expression levels of Beclin1 were analyzed by qRT-PCR and Western blot,respectively.Moreover,dual-luciferase reporter gene technology was employed to investigate the binding site between miR-873 and Beclin1.Results:Transfection of miR-873 mimic into 16HBE cells significantly upregulated the mRNA level of miR-873,which led to the inhibition of cell proliferation and the promotion of secretion of pro-inflammatory cytokines IL-2,IL-6,and TNF-α,while suppressing the secretion of anti-inflammatory cytokine IL-10.Moreover,miR-873 induced cell apoptosis and inhibited the expression of LC-3.Dual-luciferase reporter gene assay further confirmed the presence of binding sites between miR-873 and Beclin1 gene.Besides,miR-873 could target and suppress the mRNA and protein expression levels of Beclin1.Conclusion:miR-873 might modulate cell autophagy by targeting the Beclin1 gene,which can potentially promote inflammation and apoptosis in bronchial epithelial cells.

Mechanical thrombectomy and postoperative complications after acute ischemic stroke with large vessel occlusion

Acute ischemic stroke is one of the common discases in Chinese,among which acute ischemic stroke with large vessel occlusion(AIS-LVO)has thc most serious complications and has the risk of death.Studies have shown that reperfusion is a first-line treatment for the effective rescue of ischemic brain tissue,usually mainly by mechanical|hrombectomy(MT),supplemented by intravenous thrombolysis.However,there are still complications after large blood vessel occlusion and MT.such as blecding and infection at the puncture point,vasospasm,vascular dissection,subarachnoid hemorrhage,hcmonhagic transfomation,reembolization,and massive cerebral infarction,ctc.The high risk factors and corresponding measures of complications after MT by revicwing the rescarch analysis.

Recent research progress from biological perspective on the mechanism of formation of osteoarthritis after anterior cruciate ligament injury

The anterior cruciate ligament(ACL)mainly plays a role in stabilizing the knee joint by limiting the forward translation of tibial force and rotational force at the tibial joint,and if this ligament is damaged,it will cause joint pain,limited mobility,knee instability,etc.According to related studies,the incidence of traumatic osteoarthritis(PTOA)after ACL injury is as high as 87%,although many studies have shown that patients with ACL injury are susceptible to PTOA,but the exact mechanism is currently unknown.This may be related to biological,structural,and mechanical factors caused by the ligament injury.Previous studies have shown that elevated inflammatory mediators in the joint cavity following ACL injury can lead to chondrocytes necrosis and degradation of the cartilage matrix.These potential biochemical mediators contribute to PTOA formation,and early intervention can reduce future episodes of PTOA.In recent years,many scholars have devoted themselves to studying the potential important factors and signaling pathways involved in the formation of osteoarthritis after ACL injury,and exploring its molecular mechanism,which has led to great progress in this field.This paper mainly studies and discusses the mechanism of osteoarthritis formation after ACL injury from the biological perspective.

Effects of Sirt1 on proliferation,migration,and apoptosis of endothelial progenitor cells in peripheral blood of SD rats with chronic obstructive pulmonary disease

Objective:To explore the effect of Sirt1 on the function of endothelial progenitor cells(EPCs)in rats with chronic obstructive pulmonary disease(COPD).Methods:A rat COPD model was established via smoking and endotoxin administration for three months.The peripheral circulating EPCs were isolated by gradient centrifugation,and their functions,cell cycle distribution,apoptosis,and Sirt1 expression were examined.The function changes of EPCs in the presence or absence of Sirt1 agonist and inhibitor were estimated;meanwhile,the expressions of Sirt1,FOXO3a,NF-κB,and p53 were also evaluated.Results:The proliferation,adhesion,and migration of EPCs decreased while the apoptosis rate was increased in the COPD rats.The expression of Sirt1 protein in EPCs of the COPD group was significantly lower than that in the control group(P<0.01).The overexpression of the Sirt1 gene using a gene transfection technique or Sirt1 agonists(SRT1720)improved the proliferation,migration,and adhesion,and decreased the apoptosis of EPC.However,Sirt1 inhibitor(EX527)decreased EPC functions in the COPD group.The effect of Sirt1 expression on EPC function may be related to reduction of FOXO3a and increase of NF-κB and p53 activity.Conclusions:Increased expression of Sirt1 can improve the proliferation and migration of EPCs and reduce their apoptosis in COPD rats.This change may be related to FOXO3a,NF-κB,and p53 signaling pathways.

Transcriptome sequencing analysis of lncRNA expression in peripheral blood mononuclear cells from patients with COPD

Objective:To screen abnormally expressed lncRNAs in peripheral blood mononuclear cells from patients with COPD.Methods:The peripheral blood of 3 COPD patients and 3 normal controls were collected from our hospital,mononuclear cells were isolated,RNA was extracted and then transcriptome sequencing was performed.The expression difference between the two groups of samples was calculated based on p<0.05 and|log2FC|>1.Plot the difference lncRNA heat map and volcano map.The Lncpro database may predict mRNAs regulated by differential lncRNA,and perform the GO function and KEGG signaling clustering.Results:There were 67 lncRNAs between the COPD group and the control group that met the difference of p<0.05 and|log2FC|>1,of which 33 were up-regulated and 34 were down-regulated.Between the two groups.The target genes are mainly enriched in GO functions:regulatory functions of multicellular biological processes,regulatory functions of development processes,structured morphogenesis functions,system development functions,and development process functions.Target genes are mainly enriched in KEGG signaling pathways:multi-species apoptotic pathway,TGF-βsignaling pathway,complement and coagulation cascade pathway,colorectal cancer pathway and apoptosis pathway.Conclusion:Our results provide general information and possible regulatory functions and pathways of lncRNA expression changes in peripheral blood mononuclear cells of COPD,which may help clarify the underlying mechanism of COPD.

Incidence of adverse reactions to COVID-19 vaccination:A meta-analysis of randomized controlled trials

Objective:To systematically evaluate the incidence of adverse reactions to coronavirus disease 2019(COVID-19)vaccination.Methods:We systematically searched PubMed,Embase,The Cochrane Library,Web of Science,CNKI,WanFang Data,and VIP Database from the inception of each database to August 31,2021.Randomized controlled clinical trials(RCTs)on the safety of different types of COVID-19 vaccines were retrieved and analyzed.A random or fixed-effects model was used with an odds ratio as the effect size.The quality of each reference was evaluated.The incidence of the adverse reactions of the placebo group and the vaccination group was compared.Heterogeneity and publication bias were taken care of by meta-regression and sub-group analyses.Results:A total of 13 articles were included,with 81287 subjects.Compared with the placebo group,the vaccination group showed a higher combined risk ratio(RR)of total adverse reactions(RR=1.67,95%CI:1.46-1.91,P<0.01),local adverse reactions(RR=2.86,95%CI:2.11-3.87,P<0.01),systemic adverse reactions(RR=1.25,95%CI:0.92-1.72,P=0.16),pain(RR=2.55,95%CI:1.75-3.70,P<0.01),swelling(RR=4.16,95%CI:1.71-10.17,P=0.002),fever(RR=2.34,95%CI:1.84-2.97,P<0.01),fatigue(RR=1.36,95%CI:1.32-1.41,P<0.01)and headache(RR=1.22,95%CI:1.18-1.26,P<0.01).The subgroup analysis showed the incidence of adverse reactions of the vaccination group after injection of the three COVID-19 vaccines(inactivated viral vaccines,mRNA vaccines and adenovirus vector vaccines)was higher than that of the placebo group,and the difference between the placebo group and the vaccination group in the mRNA vaccine subgroup and the adenovirus vector vaccine subgroup was statistically significant(P<0.01).The incidence of adverse reactions after injection of COVID-19 vaccine in subgroups of different ages was significantly higher than that in the placebo group(P<0.01).Conclusions:COVID-19 vaccines have a good safety,among which adenovirus vector vaccine has the highest incidence of adverse reactions.Both adolescents and adults vaccinated with novel coronavirus vaccine have a certain proportion of adverse reactions,but the symptoms are mild and can be relieved by themselves.Our meta-analysis can help boost global awareness of vaccine safety,promote mass vaccination,help build regional and global immune barriers and effectively curb the recurrency of COVID-19.

Anatomical study of Rubens'flap in breast reconstruction

Objective:To investigate the anatomical basis of Rubens'flap based on the deep circumflex iliac artery,and to apply more donor site tissue amount for big chest wall defect.Methods:Gross anatomical study was carried on 8 sides of fresh specimens of 4 cases and data was measured by mean of the Vernier caliper.Besides,the surgical simulation was carried on 1 specimen(2 sides).Results:At the inguinal segment,the via artery gave off(9.16±6.22)branches;the diameter of the origin was(3.97±0.86)mm;the distance from starting point to the first branch was(15.87±9.24)mm;amount of osteomusculocutaneous branch was 3.12±1.34;the biggest diameter of perforator was(1.48±1.02)mm;pedicle length was(132.51±48.24)mm.In the surgical simulation,the layers of Ruben's flap from up to down ranged in skin,subcutaneous tissue,obliquus externus abdominis,oblique internal abdominis and transversus abdominis.Conclusion:Rubens'flap,with large tissue amount,based on the deep circumflex iliac artery,near to traditional abdominal flap,has a good clinical application prospect in breast reconstruction and repair of big chest wall defect,for its thin waist effect and slight donor site defect.

Exosome-derived miR-146a-5p from decidual macrophages in preeclampsia inhibits the viability and invasive ability of trophoblast cells by targeting HIF1α

Objective:To investigate the effect of exosomes secreted by decidual macrophages on trophoblast cells and their molecular mechanism.Methods:The decidual tissues of patients with preeclampsia(PE)and normal-term pregnant women were collected.Macrophages were obtained by the density gradient method and then flow cell sorting,then the exosomes were extracted.The structure of the exosomes was observed by transmission electron microscope.The expression of CD63,a marker protein of the exocrine body,was detected by western blot,and the exosomes were identified.CCK-8 was used to detect the effect of exosomes on trophoblast cell viability.Transwell migration experiment was used to detect the influence on migration ability.The expression of miR-146a-5p in exosomes was detected by qPCR.The effect of exosomes on the expression of HIF1αprotein in trophoblasts was detected by western blot and detection of the binding site between miR-146a-5p and HIF1αby double luciferase reporter gene was conducted.Results:The exosomes of macrophages present a"cake"structure with a middle depression about 30-130 nm in diameter,and CD63 is highly expressed,which conforms to the characteristics of exosomes.Compared with the normal group,the exosomes of decidual macrophages in the PE group inhibited the activity and migration of trophoblast cells(P<0.001).The expression of miR-146a-5p in the exosomes of decidual macrophages in the PE decreased significantly,and after exosomes of PE decidual macrophages treating trophoblast cells,the protein expression of HIF1αin trophoblast cells was significantly increased.There are targeted binding sites between miR-146a-5p and HIF1α.Conclusion:PE decidual macrophage exosomes can inhibit the viability and migration of trophoblast cells,which may be related to the decreased expression of miR-146a-5p in exosomes,thus promoting HIF1αprotein expression of trophoblast cells.

The effect of Huayu Lifei formula on the expression of miR-27a and α-SMA in lung tissue of bleomycin-induced rat lung fibrosis model

Objective:Investigating the inhibitory effect of Huayu Lifyei Formula on bleomycininduced rat pulmonary fibrosis and its impact on the expression of miR-27a andα-SMA.Methods:Wistar rats were arbitrarily classified into a normal group,a model group,and a group treated with Huayu Lifyei Formula,each consisting of ten rats.Pulmonary fibrosis rat model was established by injecting bleomycin.Subsequent to the modeling,the Huayu Lifyei Formula treatment group was administered Huayu Lifyei Formula via gavage for a period of 7 days.Rats were sacrificed on the 14th day after modeling.The right lung was taken for HE staining,Masson staining,and immunohistochemical observation of alpha-smooth muscle actin(α-SMA)expression.The expression of miR-27a was measured by qRT-PCR,with the miR-27a binding site on ACTA2(the gene encodingα-SMA protein)confirmed using dualluciferase reporter gene technology.Results:When compared to the model group,the Huayu Lifyei Formula treatment group showed considerable alleviation of pathological morphological changes in lung tissue,with significant reductions in alveolitis,fibrosis,collagen deposition in lung tissue,and the expression ofα-SMA protein.Meanwhile,the expression of miR-27a in the Huayu Lifyei Formula treatment group significantly increased,and the dual-luciferase reporter gene confirmed the binding site of miR-27a with the ACTA2 gene.Conclusion:Huayu Lifyei Formula can inhibit bleomycin-induced pulmonary fibrosis in rats,and its mechanism may be related to the promotion of miR-27a expression.

Abnormal expression of TGFβ1 in acute myeloid leukemia and its regulation effect on leukemia cells

Objective:To explore the level of acute myeloid leukemia(COX-2),transforming growth factorβ1(TGFβ1),basic fibroblast growth factor(bFGF),and vascular endothelial growth factor(VEGF)in acute myeloid leukemia(AML)patients and to investigate the role of TGFβ1 on the proliferation,apoptosis and cycle of AML cells,providing new targets and research bases for the treatment and prognostic evaluation of AML.Methods:Peripheral blood was collected from 80 AML patients and 60 normal people.The levels of COX-2,TGFβ1,bFGF and VEGF in peripheral blood mononuclear cells and serum were determined by using quantitative polymerase chain reaction and enzyme linked immunosorbent assay,respectively.The proliferation,apoptosis and cycle of AML cells affected by overexpression and silencing of TGFβ1 was detected using cell counting kit-8 and flow cytometry.Results:The expression of COX-2,TGFβ1,bFGF and VEGF increased significantly in peripheral blood mononuclear cells and serum in AML patients.TGFβ1 promoted AML cell proliferation,inhibited its apoptosis,and increased stage G2 cell proportion.Conclusion:COX-2,TGFβ1,bFGF and VEGF play important roles in the progression of AML.TGFβ1 is a new potential biomarker for the diagnosis and treatment of AML.

Expression and clinical significance of miR-186 in serum exosomes of patients with chronic obstructive pulmonary disease

Objective:To study the expression of miR-186 in serum exosomes of patients with chronic obstructive pulmonary disease,and to explore its clinical significance with chronic obstructive pulmonary disease.Methods:The peripheral blood sera of 53 COPD patients and 53 normal persons in our hospital were collected.Extraction of exosomes and electron microscopy to identify the characteristics of exosomes.RT-PCR method was used to detect the miR-186 expression level in serum exosomes.And statistical analysis of the expression difference between the COPD group and the normal group,alysis of the correlation between miR-186 and FEV1%predicted value,and ROC curve analysis of the diagnostic value of serum exosome miR-186 in COPD.Results:The relative expression of miR-186 in serum exosomes of COPD group was 3.24±0.14,which was significantly higher than that of normal control group 1.03±0.04(t=15.47,P<0.001).The expression level of miR-186 was negatively correlated with the predicted FEV1%of COPD patients(r=-0.5024,p<0.0001).The area under the ROC curve between miR-186 and COPD patients was 0.8409(95%confidence interval:0.6875-0.9943).Conclusion:The high expression of miR-186 in serum exosomes may be a risk factor and may be used as a diagnostic indicator of COPD.

Research progress on the correlation between lncRNA and the pathogenesis of COPFD

Chronic obstructive pulmonary disease is a common chronic disease with high morbidity and mortality.Early prevention,diagnosis and treatment of chronic obstructive pulmonary disease can effectively reduce its morbidity,improve prognosis,and reduce the economic burden of patients'families.With the deepening of molecular biology research,lncRNAs have become a research hotspot in recent years.They are involved in the occurrence,development and prognosis of diseases,providing new directions for disease research.This article reviews the research progress on the biological characteristics of lncRNAs and their association with the causes,pathological changes and therapeutic drugs of chronic obstructive pulmonary disease.

Mechanism of PD‑1/PD‑L1 signaling pathway regulating Treg/Th17 in the occurrence and development of preeclampsia

Objective:To detect the expression levels of programmed cell death 1(PD‑1)and its ligand PD‑L1,regulatory cell(Treg)and T helper cell 17(Th17)specific nuclear transcription factors forkhead box protein 3(Foxp3)and the retinoic acid‑related orphan nuclear receptorgammat(RORγc)in the placenta of normal pregnant women and in preeclamptic(PE)women,and to study the relationship between their differential expression and the development of PE.Methods:Between March 2021 and March 2022,40 patients with pre‑eclampsia who were treated at the Obstetrical Department in Hainan Hospital were selected,including 20 cases of mild(PE)and 20 cases of severe(sPE),and 20 normal pregnant women with singleton cesarean section in the same period were selected to collect placental tissue.PD‑1,PD‑L1,Foxp3 and RORγc in placenta were detected by qRT‑PCR and Western blot.Results:(1)The results of qRT‑PCR assay showed that the mRNA expression of PD‑1,PD‑L1,Foxp3 protein decreased significantly compared with the control group.The changes in PD‑1,PD‑L1 and Foxp3 became more obvious as the disease progressed(P<0.05);The mRNA expression of RORγc increased significantly compared with the control group.The changes of RORγc mRNA became more obviousas as the disease progressed(P<0.05);(2)The results of Western blot assay show,compared with the normal group,the protein expression of PD‑1,PD‑L1,Foxp3 mRNA decreased significantly.With the aggravation of the disease,the changes of PD‑1 and PD‑L1 became more obvious,with significant difference(P<0.05);Compared with the normal group,the protein expression of RORγc increased significantly.With the aggravation of the disease,the changes of RORγc protein became more obvious with significant difference(P<0.05).Conclusion:PD‑1/PD‑Ll participates in the occurrence and development of preeclampsia by regulating Treg/Th17 immune balance.

Expression and clinical significance of lncRNA SNHG3 in peripheral blood mononuclear cells of patients with chronic obstructive pulmonary disease

Objective: To investigate the expression of lncRNA SNHG3 in peripheral blood mononuclear cells of patients with chronic obstructive pulmonary disease (COPD), and to explore its clinical significance with chronic obstructive pulmonary disease. Methods: Mononuclear cells were collected from 120 patients with COPD and 110 normal controls. The expression of lncRNA SNHG3 in peripheral blood mononuclear cells was detected by RT-PCR and the difference between COPD group and normal group, and the difference between mild, moderate, severe, extremely severe COPD and health volunteers was analyzed. Results: The relative expression of SNHG3 in peripheral blood mononuclear cells of COPD patients was 1.52 ± 0.52, which was lower than that of the normal control group (2.51 ± 0.59) (P < 0.001). The relative expression of SNHG3 in peripheral blood mononuclear cells of mild COPD was 2.16 ± 0.23, which was higher than that of moderate group (1.55 ± 0.10) (P < 0.001), severe group 1.19 ± 0.11 (P< 0.001), and extremely severe group 0.89 ± 0.06(P < 0.001). In addition, lncRNA SNHG3 can bind to miR-186 and regulate its expression. Conclusions: The expression of lncRNA SNHG3 in peripheral blood mononuclear cells of COPD patients may be a risk factor for COPD and an indicator of the severity of COPD patients. The lncRNA SNHG3/miR-186 regulatory network may play an important role in the development of COPD.

Basic research and clinical progress of sepsis-associated encephalopathy

Sepsis-associated encephalopathy(SAE),a major cerebral complication of sepsis,occurs in 70%of patients admitted to the intensive care unit(ICU).This condition can cause serious impairment of consciousness and is associated with a high mortality rate.Thus far,several experimental screenings and radiological techniques(e.g.,electroencephalography)have been used for the non-invasive assessment of the structure and function of the brain in patients with SAE.Nevertheless,the pathogenesis of SAE is complicated and remains unclear.In the present article,we reviewed the currently available literature on the epidemiology,clinical manifestations,pathology,diagnosis,and management of SAE.However,currently,there is no ideal pharmacological treatment for SAE.Treatment targeting mitochondrial dysfunction may be useful in the management of SAE.