Objective:To study the inhibitory effect of endothelial progenitor cells (EPCs) on aortic injury in mice with systemic lupus erythematosus (SLE) arteriosclerosis.Methods:APOE -/- mice were injected with norphytane and high fat diet to establish lupus vascular injury model. Then the mice were divided into normal control group (ND group), high fat diet group (HFD group), high fat diet+ SLE vascular injury group (HFD+ SLE group), high fat diet+ SLE vascular injury+ hydroxychloroquine treatment group (HFD+ SLE+ Hydro group), high fat diet+ SLE vascular injury+ EPCs treatment group (HFD+ SLE+ EPCs group). At the end of the experiment, urine, blood and aortic tissues of mice in each group were collected, and the content of urinary protein and the depth of serum type I interferon (IFN-Ⅰ) were detected by enzyme linked immunosorbent assay (ELISA). The activation of cyclic guanosine monophosphate synthase/interferon gene stimulating factor/type I interferon (cGAS/STING/IFN-Ⅰ) pathway, the levels of inflammatory factors, adhesion fractions and chemokines in the aorta of mice in each group were detected by immunohistochemistry and Western blotting (WB). The lipid deposition in the aorta was detected by oil red staining. Results:The results of ELISA showed that the levels of urinary protein and serum IFN-Ⅰ in HFD+ SLE group were higher than those in normal control group. EPCs treatment could reduce the levels of urinary protein and serum IFN-Ⅰ in SLE atherosclerotic mice. WB results showed that the expression of CD19, CD68, CD34, chemokine, cGAS, p-STING, phosphorylated TANK binding kinase 1 (p-TBK1), phosphorylated interferon regulatory factor 3 (p-IRF3) and IFN-Ⅰ increased in HFD+ SLE group, and hydroxychloroquine and EPCs decreased the levels of these factors. CGAS/STING/IFN-Ⅰ signal pathway is involved in the occurrence and development of atherosclerosis in SLE patients; both EPCs and hydroxychloroquine can inhibit the activation of cGAS/STING/IFN-Ⅰ signal, thus reducing atherosclerosis in SLE mice.Conclusions:cGAS/STING/IFN-Ⅰ pathway is involved in the development of SLE atherosclerosis. EPCs can inhibit the activation of cGAS/STING signal, reduce the expression and secretion of IFN-Ⅰ, and then reduce vascular inflammation and inhibit the development of SLE-related atherosclerosis.

Objective:To study the inhibitory effect of endothelial progenitor cells (EPCs) on aortic injury in mice with systemic lupus erythematosus (SLE) arteriosclerosis.Methods:APOE -/- mice were injected with norphytane and high fat diet to establish lupus vascular injury model. Then the mice were divided into normal control group (ND group), high fat diet group (HFD group), high fat diet+ SLE vascular injury group (HFD+ SLE group), high fat diet+ SLE vascular injury+ hydroxychloroquine treatment group (HFD+ SLE+ Hydro group), high fat diet+ SLE vascular injury+ EPCs treatment group (HFD+ SLE+ EPCs group). At the end of the experiment, urine, blood and aortic tissues of mice in each group were collected, and the content of urinary protein and the depth of serum type I interferon (IFN-Ⅰ) were detected by enzyme linked immunosorbent assay (ELISA). The activation of cyclic guanosine monophosphate synthase/interferon gene stimulating factor/type I interferon (cGAS/STING/IFN-Ⅰ) pathway, the levels of inflammatory factors, adhesion fractions and chemokines in the aorta of mice in each group were detected by immunohistochemistry and Western blotting (WB). The lipid deposition in the aorta was detected by oil red staining. Results:The results of ELISA showed that the levels of urinary protein and serum IFN-Ⅰ in HFD+ SLE group were higher than those in normal control group. EPCs treatment could reduce the levels of urinary protein and serum IFN-Ⅰ in SLE atherosclerotic mice. WB results showed that the expression of CD19, CD68, CD34, chemokine, cGAS, p-STING, phosphorylated TANK binding kinase 1 (p-TBK1), phosphorylated interferon regulatory factor 3 (p-IRF3) and IFN-Ⅰ increased in HFD+ SLE group, and hydroxychloroquine and EPCs decreased the levels of these factors. CGAS/STING/IFN-Ⅰ signal pathway is involved in the occurrence and development of atherosclerosis in SLE patients; both EPCs and hydroxychloroquine can inhibit the activation of cGAS/STING/IFN-Ⅰ signal, thus reducing atherosclerosis in SLE mice.Conclusions:cGAS/STING/IFN-Ⅰ pathway is involved in the development of SLE atherosclerosis. EPCs can inhibit the activation of cGAS/STING signal, reduce the expression and secretion of IFN-Ⅰ, and then reduce vascular inflammation and inhibit the development of SLE-related atherosclerosis.

The clinical data of a child with chemical pneumonia caused by kerosene in Hainan Maternal and Children′s Medical Center in June 2019 were retrospectively analyzed.The patient was a 2 years and 1 month old boy with a history of kerosene inhalation and fever.The clinical features included low breath sounds in the left lung and dry and wet rales in both lungs.The white blood cells (WBC) level, C-reactive protein (CRP) level, and erythrocyte se-dimentation rate (ESR) were significantly increased.Chest CT showed inhalation pneumonia.Chest ultrasound suggested medium pleural effusion on the left side.The patient was given antibiotics, nebulization and other treatment.On the 12 th day of the course of the disease, his temperature returned to normal, and breath sounds on the left side were stronger than before.The WBC level, CRP level and ESR were improved according to the re-check results, but pulmonary ventilation was still obstructed mildly to moderately.Fourteen days after hospital discharge, the patient coughed less.Reexamination of chest CT prompted the lesions were further absorbed, but the mild to moderate obstructive lesions were still observed.With the reduction of kerosene use in daily life, kerosene-induced chemical pneumonia is rare, but due to its diverse and complex clinical manifestations and slow absorption of pulmonary inflammation, attention should be paid to its progression into chronic cough.

Objective: To detect the single nucleotide polymorphism (SNP) at locus 1 165 of β1-adrenoceptor (β1-AR) and to investigate the association between the SNP and the infection by enterovirus A71(EV-A71). Methods: Polymerase chain reaction (PCR) amplification technique was used to detect the SNP at locus 1 165 of β1-AR between hand, foot and mouth disease (HFMD) and healthy controls by sanger sequencing method . Results: There was a G1165C SNP and three kinds of genotypes (GG, GC, CC) in β1-AR gene in the 77 cases of EV-A71 HFMD patients and 66 cases of healthy controls. For HFMD patients, frequencies of GG, GC and CC genotypes of the G1165C locus were 10%, 47% and 43%, respectively, and alleles frequency of G and C were 34% and 66%, respectively. But in healthy children, GG, GC, CC genotype frequencies were 7%, 41% and 52%, respectively, and G and C allele frequencies were 28% and 72% respectively. Chi-square analysis showed that there were no significant differences in distribution of genotypes (χ²=1.154, df=2, P=0.562) and alleles frequency (χ²=1.091, df=2, P=0.296) between the EV-A71-infected group and the healthy control group. Between mild and severe EV-A71-infected group, there were no significant differences in distribution of genotypes (χ²=3.945, df=2, P=0.139) and alleles frequency (χ²=3.763, df=2, P=0.052). Conclusions The 1 165 SNP in the coding region of β1-AR was not associated with EV-A71 infection and its severity.

Enterovirus 71 (EV71) has a high degree of nerve absorption and which is an important neurotoxic pathogen causing severe hand,foot and mouth disease and central nervous system(CNS) diseases.EV71 infection is at a high incidence in Asia Pacific region.The CNS damage caused by EV71 mainly includes aseptic meningitis,encephalitis,brain stem encephalitis,acute flaccid paralysis,etc,which has a high mortality and poor prognosis,while its injury mechanism is not clear.Now,EV71 related etiology,epidemiology,pathogenesis of CNS damage caused by EV71 infection and EV71 vaccine research progress were summarized,in order to provide theoretical basis for EV71 related studies.

Objective To investigate the influence of tethered cord syndrome (TCS) on the up-per urinary tract and its etiology. Methods Forty patients with TCS diagnosed by spinal MRI were enrolled in this study. There were 21 males and 19 females with mean age of 23 years old. The course of disease ranged from 1 to 40 years. Urinalysis, mid-stream urine culture, serum creatinine(SCr), urinary system ultrasound, IVU, eystography and urodynamic study were carried out on all patients. Results Urinary tract infection was found in 17 patients and increased level of SCr was found in 6 pa-tients (251.64±98.5μmol/L). Of the 29 patients who underwent urinary system ultrasound examina-tion, 12 cases had hydronephroais and dilated upper ureter. Of the 30 patients who underwent IVU, 10(33.3%) had ureterectasia and hydronephrosis, 22 cases had bladder turriform or Christmas tree like deformity with diverticulum and trabeculum. Of the 22 patients accepted cystography, 17 cases had vesieoureteral reflux on 27 sides. Post-void residual (PVR) was evaluated in 35 patients and found increased in 31 cases. Cystometry had been done in 33 patients. The mean value of maximal detrusor pressure (Pdetmax) during filling phase was 41.2±20.9 cm H2O. The detrusor compliance was 22.35±18.8 ml/cm H2O. During voiding phase, detrusor-sphincter dyssynergia(DSD)was observed in 16 patients, detrusor areflexia was observed in 16 patients and detrusor underactivity was observed in 13 patients. Resting urethral pressure profilemetry was measured in 16 patients. Maximal urethral closure pressure (MUCP) was 76.1±33.1 cm H2O. The upper urinary tract deterioration was de-fined as increased SCr, hydronephrosis or vesicoureteral reflux. There were 20 patients diagnosed as upper urinary tract deterioration. The compliance of the upper urinary tract deteriorating group and the no-deteriorating group was 9.4±7.8 vs 19.3±15.8 ml/cm H2O, Pdetmax was 43.1±21.2 vs 24.0±11.9 cm H2O, PVR 189.0±138.0 vs 47.8±36.8 ml, MUCP 86.2±32.4 vs 46.8 5±20.8 cm H2O, incidence of damaged detrusor 100.0% vs 69.2% and DSD 65.0% vs 23.1%, respectively. There were significant differences between the 2 groups(P<0.05). And when comparing the VUR group with no VUR group, the incidence of urinary tract infection was 94.1%(16/17) vs 20.0%(1/ 5) (P=0.003). And when comparing urinary tract infection group with no infection group, the inci-dence of upper urinary tract deterioration was 88.2% (15/17) vs 21.7%(5/23)(P=0.000). Condn-sion Low compliance bladder, high Pdetmax during filling phase, increased PVR, high MUCP, damage of detrusor contractive function and DSD are the risk factors for upper urinary tract deteriora-tion in the TCS patients.

4.00 ng/ml) were divided into BPH group (without inflammation), acute inflammation group and chronic inflammation group. The diagnosis was confirmed by transrectal-ultrasound guided needle biopsies. Prostate volumes were measured in all patients by the transrectal-ultrasound. A total of 126 patients were included in this study. The biopsy results showed 47 patients in BPH group, 45 patients in acute inflammation group and 34 patients in chronic inflammation group. Results The serum PSA value in the BPH group, acute inflammation group and chronic inflammation group were (5.76?3.21),( 8.67 ?2.92 ) and (5.54?3.01) ng/ml respectively. The serum PSA value in acute inflammation group was much higher than that of BPH group and chronic inflammation group(P

OBJECTIVE:To compare the cost and efficacy between three different haemostatics in treating postoperative bleeding following suprapubic prostatectomy.METHODS:Using cost-effectiveness analysis,reptilase,aprotinin and minirin were evaluated.RESULTS & CONCLUSION:From pharmacoeconomic view,use of reptilase in treating postoperative bleeding is the best therapeutic regimen.