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The clinical features and risk factors for survival time were analysed in haemodialysis patients complicated with infective endocarditis. A total of 101 infective endocarditis (IE) patients treated at Hangzhou First People's Hospital, from January 1, 2012, to April 1, 2022, were included in the present study. Baseline demographic data and laboratory data were collected for statistical analysis of risk factors and survival time in the IE with haemodialysis group (HD-IE group, n=15) and the IE without haemodialysis group (NHD-IE group, n=86). Haemoglobin, red blood cells, C-reactive protein, procalcitonin, serum albumin, diabetes, invasive procedures, positive blood bacteria culture, heart valve calcification ratio, and left ventricular ejection fraction level were risk factors for infective endocarditis complicated with haemodialysis (P<0.05). Compared with the NHD-IE group, the HD-IE group had an obviously increased risk of mortality (χ2=6.323, P=0.012). The univariate Cox regression analysis showed that age, haemoglobin, red blood cells, serum albumin, left ventricular ejection score, longest vegetation diameter, combined hypotension and diabetes were risk factors for death; furthermore, multivariate Cox regression showed that age (HR=1.187, P=0.015), combined hypotension (HR=0.921, P=0.025) and the longest vegetation diameter (HR=9.191, P=0.004) were independent risk factors affecting the survival of patients. Collectively, the present study revealed that the mortality rate of HD-IE patients was higher than that of NHD-IE patients. Older age, hypotension, and the longest vegetation diameter were independent risk factors affecting the survival of patients. For HD-IE patients, active and effective antibiotic treatment or surgical treatment should be strongly recommended.
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BACKGROUND AND AIMS: The genotypic method could significantly shorten the time needed to obtain antibiotic susceptibility data for Helicobacter pylori. The aim of this study was to explore the profile of H. pylori from gastric biopsies and strains with antibiotic-induced resistance. METHODS: A total of 124 gastric biopsies were used to perform gene sequencing and to perform bacterial culture and susceptibility testing. Seven susceptible strains were selected to develop resistance to clarithromycin, levofloxacin, and metronidazole. Four susceptible strains were selected to transfer candidate mutations. The genotype profiles of these groups were analyzed by sequencing analysis. The antibiotic susceptibility of these strains was detected using the E-test method. RESULTS: Phenotypic resistance to clarithromycin, levofloxacin, and metronidazole was observed in 35.5%, 40.0%, and 79.8% strains, respectively. Point mutations in 23 S rRNA, gyrA, and rdxA genes were observed in 39.5%, 38.7%, and 86.3% of gastric biopsies, respectively. The A2143G mutation in the 23S rRNA occurs in most clarithromycin-resistant samples. The A2142C point mutation showed a higher efficacy than A2142G and A2143G for inducing clarithromycin resistance. The D91N and N87K mutations in gyrA occurs in most levofloxacin-resistant samples, and double point mutations showed a higher efficacy than single mutations for inducing levofloxacin resistance. Phenotypic resistance and mutations in rdxA lacked consistency. CONCLUSION: Genotype-based gastric biopsy analysis was reliable for determining clarithromycin and levofloxacin resistance. A2143G in 23S rRNA and N87K/D91N in the gyrA gene occurred in most resistant strains. Mutations in the rdxA gene were not good indicators of metronidazole resistance.
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OBJECTIVE: To identify the genotypes of the blood sample whose blood grouping showed discrepancies and study the ABO alleles' molecular characteristics of the involved ancestry. METHODS: Blood samples were preliminary genotyped by PCR-SSP. Complete exon 6 and 7 in the ABO genes were amplified by PCR and the PCR products were directly sequenced and cloning sequenced to identify its genotype. RESULTS: Sequence analysis indicated that 3 samples of the family had an nt905A>G mutation in the B gene compared with ABO*B101. Combined with the serological results, the propositus could be typed as Bx02/O102. CONCLUSION: DNA sequencing analysis is able to identify the serological phenotype samples that forward and reverse group methods were incongruous.
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Alelos , Sistema del Grupo Sanguíneo ABO , Secuencia de Bases , Tipificación y Pruebas Cruzadas Sanguíneas , Exones , Pruebas Genéticas , Genotipo , Humanos , Mutación , Fenotipo , Reacción en Cadena de la PolimerasaRESUMEN
OBJECTIVE: To explore the effect of syndecan-1 (Sdc-1) in the pathogenesis of colitis. METHODS: Thirty BALB/c mice were forced to drink 4% dextran sodium sulphate (DSS) in distilled water as the sole source of drinking fluid for 7 days, distilled water for 10 days, and 4% DSS in distilled water for another 7 days so as to establish colitis models and then were randomly divided into 3 equal groups: model groups 1, 2, and 3 to be killed 8, 18, and 25 days after the DSS drinking respectively to take their colons. Another 10 mice were fed with distilled water as control group and were killed on Day 8. Microscopy was used to evaluate the histological score of the colon. RT-PCR was used to detect the expression of Sdc-1 mRNA and IL-1 mRNA in the colon mucosa. Immunohistochemistry was conducted to detect the Sdc-1 protein level. RESULTS: The histological scores of the 3 model groups were all significantly higher than that of the control group (F = 448.717, P < 0.01) and the score was the highest in the model group 1 and then gradually decreased. There was not significant differences in the Sdc-1 mRNA expression among different groups (F = 0.822, P > 0.05). The levels of Sdc-1 protein of the 3 model groups were all significantly lower than that of the control group (F = 865.586, P < 0.01), and the Sdc-1 protein level was the lowest level in the model group1, and then increased gradually. The expression of IL-1 mRNA of the 3 model groups were all significantly higher than that of the control group (F = 103.833, P < 0.01), and the IL-1 mRNA level was the highest in the model group1 and then decreased gradually. CONCLUSION: The severity of colitis is associated with the reduction of Sdc-1 protein level, but not with the Sdc-1 mRNA level in the colon mucosa. The reduction of Sdc-1 protein level may be associated to increase of IL-1 level.