Objective To investigate the prevalence and resistance mechanisms of Proteus mirabilis in the ward of neurology de‐partment of our hospital .Methods For a total of 20 clinic isolates of Proteus mirabilis ,PCR were used for the detection of AmpC , ESBLs ,KPC and MBLs and then DNA sequencing was performed .The integrons were also detected by using PCR and then sequen‐cing was carried out .The genetic relationship between isolates were detected and analysed by pulsed‐field gel electrophoresis(PF‐GE) .The results of drug sensitivity tests were analysed .Results TEM‐1 and CTX‐M‐14 gene were found in all the 20 isolates ,the 10 isolates of Proteus mirabilis were also found carrying CMY‐2 gene .Class Ⅰ integrons were amplified from 19 strains carrying gene cassettes aacA4+cmlA1,dfrA12+orfF+aadA2and dfrA32+ereA+aadA2 respectively .PFGE analysis revealed that the 20 isolates were grouped into 11 PFGE types P1-P11 ,the 12 isolates of P1-P3 were same clones .The sensitive rates of the i‐solates to Meropenem ,Amikacin ,Aztreonam ,Ceftazidime and Tazocin were high .Conclusion Nosocomial transmission of the same clone of Proteus mirabilis was appeared in the ward of neurology department of our hospital .The predominance drug‐resistance genes were CTX‐M‐14 andCMY‐2 .The incidence of carrying class Ⅰ integrons was high ,and the major gene cassettes wereaacA4+cmlA1and dfrA12+orfF+aadA2.The 20 isolates were all sensitive to Meropenem ,Amikacin and Aztreonam .Other Clinical departments should also pay attention to the nosocomial infection caused by Proteus mirabilis and strengthen the infection control measures .

OBJECTIVETo study the gene polymorphism of the Auberger antigens in Lutheran blood group system in Chinese population and establish a stable, accurate molecular method detecting Auberger antigens.

METHODSPeripheral blood samples from 162 randomly collected and unrelated volunteer blood donors were directly sequenced for the exon 12 at the gene locus of Auberger antigens. PCR products with novel nucleotide were further investigated by restriction fragment length polymorphism (RFLP) analysis.

RESULTSAuberger genotypes in the 162 Chinese individuals were obtained: Au(a+ b- )(nt1615A) was found in 119 individuals, Au(a+ b+ ) (nt1615A/G) in 40 individuals and Au(a- b+ ) (nt1615G) in 3 individuals. The allele frequencies of the Au(a) and Au(b) were 0.8580 and 0.1420, respectively. An individual with homozygous Au(a) genotype had a nucleotide mutation (1595 G to T). The mutation was confirmed by digesting the DNA with Hha I.

CONCLUSIONThe distribution of gene polymorphism of Auberger antigens in a Chinese population was investigated and obtained. And a molecular method determining the Auberger antigen was established. A novel Lutheran allele was deposited in GenBank (accession number EU260043).

Amino Acid Sequence ; Asian Continental Ancestry Group ; genetics ; Base Sequence ; DNA Mutational Analysis ; Female ; Gene Frequency ; Haplotypes ; Humans ; Lutheran Blood-Group System ; chemistry ; genetics ; Male ; Molecular Sequence Data ; Polymorphism, Genetic

Objective:To investigate the in-stent thrombosis after carotid artery stenting revealed by optical coherence tomography (OCT) and its possible risk factors.Methods:Consecutive patients with carotid artery stenosis underwent carotid artery stenting and intraoperative OCT between January 2015 and December 2019 were selected through the Stroke Registration Center of the Second Affiliated Hospital of Guangzhou Medical University and Nanjing Stroke Registry Program. The clinical characteristics of the patients were recorded, OCT images were analyzed, and postoperative in-stent thrombosis was observed. At the same time, OCT image features such as plaque calcification, thin fiber cap, stent apposition, plaque prolapse and microdissection were collected. The risk factors for in-stent thrombosis were analyzed.Results:A total of 63 patients were included. OCT showed that 17 of them (23.3%) had in-stent thrombosis. Perioperative vascular events occurred in 4 patients due to in-stent thrombosis. One of them was more serious. There were no perioperative vascular events in the in-stent non-thrombosis group. Multivariate logistic regression analysis showed that microdissection was an independent risk factor for in-stent thrombosis after carotid artery stenting (odds ratio 5.439, 95% confidence interval 1.102-26.837; P=0.038). Conclusions:OCT can reveal in-stent thrombosis after carotid artery stenting, which was associated with perioperative vascular events, and microdissection was one of the possible causes of in-stent thrombosis.

Objective:To explore the value of cardiodynamicsgram (CDG) obtained from electrocardiogram (ECG) data by radial basis functionradial basis function (RBF) neural network in early diagnosis of patients with acute coronary syndrome (ACS).Methods:Retrospective analysis method was used. Patients with chest pain as the main initial symptom in the emergency department of Baoan District People's Hospital of Shenzhen from October 2021 to September 2022 were enrolled. Baseline data were collected, including gender, age, smoking history, family history of coronary heart disease and history of hypertension, diabetes, hyperlipidemia, and atherosclerosis. The first 12-lead ECG was recorded after admission to the emergency department, and electrocardiodynamics analysis was performed to generate CDG. Receiver operator characteristic curve (ROC curve) was plotted to analyze the value of CDG and ECG in the early diagnosis of ACS and non-ST segment elevation ACS (NSTE-ACS). Sensitivity, specificity, area under the ROC curve (AUC), and 95% confidence interval (95% CI) were calculated. CDG and coronary angiography results of 3 patients with ACS with normal ECG were observed and analyzed. Non-ACS patients with normal ECG but positive CDG were followed for 30 days for adverse cardiovascular events. Results:A total of 384 patients with chest pain were included, including 169 patients with ACS and 215 patients without ACS. The proportion of male (87.0% vs. 53.0%), smoking history (37.9% vs. 12.1%), hypertension (46.2% vs. 22.3%), diabetes (24.3% vs. 7.9%), hyperlipidemia (55.0% vs. 14.0%) and history of atherosclerosis (22.5% vs. 2.3%) in ACS group were significantly higher than those in non-ACS group (all P < 0.05). The ROC curve showed that the AUC of CDG diagnosis of ACS was higher than that of ECG [AUC (95% CI): 0.88 (0.66-0.76) vs. 0.71 (0.84-0.92)], the sensitivity was 92.8%, 78.6%, and the specificity was 83.3%, 64.2%, respectively. The AUC of CDG diagnosis of NSTE-ACS was higher than that of ECG [AUC (95% CI): 0.85 (0.80-0.90) vs. 0.63 (0.56-0.69)], the sensitivity was 87.1%, 61.3%, and the specificity was 83.3%, 64.2%, respectively. CDG of 3 patients with ACS with normal ECG showed disordered state, and coronary angiography showed ≥70% stenosis of major coronary branches. Of 215 non-ACS patients, 20 had a normal ECG but positive CDG, and 3 developed ST segment elevation myocardial infarction (STEMI) within 30 days, and 2 developed unstable angina (UA) within 30 days. Conclusion:CDG has high value in early diagnosis of ACS patients and is expected to become an important means of early diagnosis of ACS in emergency.

Schistosomiasis-associated pulmonary arterial hypertension (Sch-PAH) is categorized as WHO Group I PAH because its clinical manifestations, laboratory and hemodynamic features share with PAH of other etiologies, such as idiopathic, heritable, HIV and autoimmune disorders. Sch-PAH is usually a life-threatening complication of hepatosplenic schistosomiasis characterized by changes in the vascular wall, remodeling and vasoconstriction with lesions primarily located in the precapillary segments of the pulmonary vasculature, which may result in a marked and sustained increase in pulmonary vascular resistance, right ventricular failure and ultimately death. Although egg deposition into lung and subsequent inflammatory cascades are key factors in the pathogenesis of Sch-PAH, the exact pathogenesis, course of disease and treatment of Sch-PAH remain largely uncertain. This review mainly discusses the pathophysiological and immunological mechanisms of Sch-PAH, so as to provide insights into the clinical diagnosis and treatment of Sch-PAH.