Objective To investigate the effects of Tongfengding capsule combined with diclofenac sodium on blood uric acid level, joint swelling and pain in gout patients. Methods 120 cases of gout patients enrolled in our hospital from January 2014 to June 2016 were selected for the study and divided into the control group and the observation group according to the random number table, with 60 cases in each group. The two groups were given anti-infection, low purine diet and other basic treatment, and both treated with sodium bicarbonate tablets and diclofenac sodium. The observation group was given Tongfengding capsule on this basis and the two groups were treated for four weeks. After treatment, gout related factors erythrocyte sedimentation rate (ESR) was observed in the two groups, and TCM symptoms of redness and swelling, pain scores were evaluated and the onset of gout was observed again at six months after treatment. Results The level of UA (463.47±50.28) CB/(μmol?L) in the control group was significantly higher than that in the control group (434.52±51.63) CB/(μmol?L) (P<0.05). The pain and swelling score of the control group were significantly higher than those in the observation group (P<0.05). The recurrence rate in the observation group (5%) was significantly lower than that in the control group (18.33%) (P<0.05). Conclusion Tongfengding capsule combined with diclofenac sodium can effectively relieve joint swelling, pain symptoms of gout patients and reduce blood uric acid levels with significant clinical efficacy.

Objective To investigate the molecule phenotype, epidemiology, and resistance genes of the New Delhi metallo- β-lactamase-1 ( NDM-1 ) producing Klebsiella pneumoniae ( K. pneumoniae ) . Methods Retrospective study was made on one hundred and ten non-repetitive carbepenem-resistant K. pneumoniae clinical isolated strains, which were collected from January 2011 to December 2012 in our hospital. The minimal inhibitory concentrations ( MICs ) of antibiotics were tested by the GN13 cards of BioMerieux Company. Modified Hodge test were used for the detection of carbapenemases. The blaNDM-1 encoding gene and linkage of ISAba125-NDM were detected by PCR method. The purified PCR products were cloned and sequenced. The homology of the K. pneumoniae were analyzed by the multilocus sequence typing ( MLST ) . Plasmid conjugation experiment and curing method were used to study the transfer of bacterial resistance. The Fisher′s exact probability test was used to compare the data. Results 13% NDM-1-producing K. pneumoniae were detected and confirmed as blaNDM-1 by sequencing (14/110). The resistance rates of the 14 NDM-1-producing K. pneumoniae strains to imipenem, meropenem, ertapenem, ciprofloxacin, levofloxacin, amikacin, and aztreonam were 14/14, 14/14, 13/14, 10/14, 9/14, 5/14, and 11/14. Meanwhile, the positive rate of ISAba125-NDM linkage of those 14 NDM-1-producing K. pneumoniae strains was 14/14. The E. coli J53 transconjugants, whose MICs of imipenem, meropenem, and ertapenem were increased by 4 to 64 times, were blaNDM-1 gene and ISAba125-NDM linkage positive. In addition, it was showed that the blaNDM-1 gene and ISAba125-NDM linkage were located on a plasmid with a size of approximately 65 000 bp. Conclusions The NDM-1 producing K. pneumoniae strains in this study were resistant to many commonly used antibiotics, however, the resistance rate to aminoglycoside and aztreonam were relatively low. The carbapenemase-resistant genotype spread by blaNDM-1 carried plasmid. Attention should be paid to its easily transmissible feature among the strains in clinic. The insertion sequence ISAba125 may be involved in the blaNDM-1 gene mediated carbapenemase-resistant genotype.

Objective: To investigate the occurrence of masked hypertension (MH) and the degree of damage to target organs in people with family history of hypertension. Methods: 987 cases of family history of hypertension who had been examined in our hospital from January 2017 to November 2017 were selected as observation group with the approval of hospital ethics committee. At the same time, 987 subjects without family history of hypertension who had been examined in our hospital during the same period were selected as control group. The incidence of masked hypertension, left ventricular mass index (LVMI) and carotid intima-media thickness (IMT) were observed. Results: The incidence of hypertension and masked hypertension in the observation group was significantly higher than that in the control group (P<0.05). LVMI and IMT in patients with masked hypertension were significantly higher than those in normal blood pressure group. LVMI and IMT in patients with hypertension were higher than those in patients with masked hypertension and normal blood pressure group. The LVMI and IMT of patients with family history of masked hypertension were higher than those without family history of masked hypertension. Conclusions Family history of hypertension can increase the incidence of masked hypertension and organ damage of patients. The monitoring of masked hypertension should be strengthened for those with family history of hypertension.

OBJECTIVETo study the resistance mechanism and homology of carbapenems-resistant Pseudomonas aeruginosa (PA).

METHODSA total of 812 strains of PA (identified) were isolated from sputum, urine, blood, pus, and drainage of patients with burn, severe pneumonia, diabetes, chronic obstructive pneumonia, myocarditis, liver transplantation, or brainstem hemorrhage hospitalized from January to September 2012. Drug resistance of the 812 strains of PA to 15 antibiotics commonly used in clinic, including piperacillin, imipenem, etc., was tested using the automatic microorganism identifying and drug sensitivity analyzer. Among the carbapenems-resistant PA isolates, synergism test with imipenem-ethylene diamine tetraacetic acid (EDTA) and enhancement test with imipenem-EDTA and ceftazidime-EDTA were used to screen metallo-β-lactamase (MBL)-producing strains; modified Hodge test was used to screen strains producing Klebsiella pneumoniae carbapenemases (KPC); the carbapenemase gene, plasmid mediated quinolone resistant (PMQR) gene, and mobile genetic elements (MGE) were detected by polymerase chain reaction (PCR). In addition, a comparative analysis of the PMQR gene carrying level between the carbapenemase gene positive strains and carbapenemase gene negative strains was carried out. The repetitive consensus sequence of Enterobacteriaceae genome PCR (ERIC-PCR) was carried out for gene typing. Moreover, the source and resistance genes of strains with the same genotype were analyzed. Data were processed with Fisher's exact probability test.

RESULTSThe sensitive rates of the 812 strains of PA to ceftriaxone and trimethoprim-sulfamethoxazole were high, respectively 83.07% and 88.19%, and those of the other antibiotics ranged from 17.30% to 55.18%. Twenty-four carbapenems-resistant PA strains were screened, including 11 MBL-producing strains and 2 KPC-producing strains. Eleven carbapenems-resistant PA strains were found to harbor the blaVIM-2 gene, accounting for 45.83%; 2 carbapenems-resistant PA strains carried the blaKPC-2 gene, accounting for 8.33%. Fourteen carbapenems-resistant PA strains only harbored the PMQR gene acc (6')-Ib-cr, accounting for 58.33%; 3 carbapenems-resistant PA strains (12.50%) harbored the PMQR genes acc (6')-Ib-cr and qnr, including 1 strain with qnr A1 and 2 strains with qnr B4. Ten carbapenems-resistant PA strains carried the MGE gene ISCR1, accounting for 41.67%; 6 carbapenems-resistant PA strains carried the MGE gene ISEcp1, accounting for 25.00%. In addition, 3 carbapenems-resistant PA strains co-harbored the MGE genes ISCR1 and ISEcp1 (accounting for 12.50%), while only 1 carbapenems-resistant PA strain co-harbored the MGE genes class 1 integron and ISEcp1, accounting for 4.17%. Twelve out of the 13 carbapenemase gene positive strains carried one or two PMQR gene (s), which was significantly higher than that of the carbapenemase gene negative strains (with only five strains harboring one PMQR gene, P = 0.023). The 24 carbapenems-resistant PA strains were classified into 6 genotypes by the ERIC-PCR. Thirteen strains (accounting for 54.17%), mainly isolated from pus and blood samples, which were collected from burn department, were in genotype A. Eight out of the 13 strains harbored genes blaVIM-2, acc (6')-Ib-cr, and ISCR1. Five strains (accounting for 20.83%), mainly isolated from sputum samples which were collected from ICU, were in genotype B. Only 2 out of the 5 strains co-harbored the carbapenemase gene, PMQR gene, and MGE gene. There were respectively 2 strains in genotypes C and D, both accounting for 8.33%; the strains in different pattern were isolated from different wards, and they harbored diverse resistance genes. There were respectively 1 strain in genotypes E and F, both accounting for 4.17%.

CONCLUSIONSThe resistance mechanism of PA to carbapenems is mainly mediated by the VIM-2 type MBL in our hospital during 2012, followed by KPC-2 type carbapenemase, and the prevalent genotype is type A. The carbapenemase genes and PMQR genes co-carrying phenomenon exists among these strains of PA, which disseminated by clones.

Anti-Bacterial Agents ; pharmacology ; Bacterial Proteins ; genetics ; Carbapenems ; pharmacology ; DNA, Bacterial ; Drug Resistance, Bacterial ; Humans ; Microbial Sensitivity Tests ; Pseudomonas aeruginosa ; drug effects ; genetics ; isolation & purification ; beta-Lactamases ; genetics