Left Ventricle Longitudinal Strain Parameters Are Effective for Differentiating Cardiac Amyloidosis from Primary Hypertensive Left Ventricular Hypertrophy / 中山大学学报(医学科学版)

ObjectiveTo clarify the value of the left ventricular longitudinal strain（LVLS）parameters in patients with cardiac amyloidosis （CA） and primary hypertension with left ventricular hypertrophy （HLVH）. MethodsForty-one patients confirmed with CA were selected and assigned to CA with hypertension group （n =14） and pure CA group （n=27） based on the initial diagnosis with or without hypertension. Twenty patients with primary hypertension-induced left ventricular hypertrophy （HLVH group） and twenty healthy controls were also selected， matching for gender， age， and body surface area. Clinical data， conventional echocardiography parameters were collected and LVLS parameters were measured. Within-group variations were compared among the four groups， and pairwise comparisons were conducted between groups. The sensitivity and specificity of each parameter in predicting CA were judged by the receiver operator characteristic （ROC） curvy in CA and HLVH patients with left ventricular ejection fraction （LVEF） preserved. ResultsAmong the conventional echocardiography parameters， LVEF and left ventricular end-diastolic diameter （LVEDD） were lower in the CA with hypertension group and pure CA group compared with the higher values in the HLVH group and control group. Whereas， left ventricular posterior wall thickness （LVPWT）， relative wall thickness （RWT）， and average E/e' were higher in the two CA groups compared with the HLVH group （all P＜0.05）.Among the LVLS parameters， Global longitudinal strain （GLS） was the worst in the CA with hypertension group so as pure CA group， modest in the HLVH group， and highest in the control group. On the contrary， relative longitudinal strain and ejection fraction strain ratio （EFSR） were the highest in the CA with hypertension group so as to pure CA group， modest in the HLVH group， and lowest in the control group （all P＜0.05）. ROC analysis showed that when LVEF was preserved， the absolute value of GLS less than 14.35% and EFSR higher than 4.28 could effectively distinguish CA from HLVH （all AUCs＞0.9，all P＜0.05）； meanwhile GLS showed high sensitivity（100%） and EFSR showed great specificity（95%）. There were not statistically significance in any parameter between CA with hypertension group and pure CA group（all P＞0.05）. ConclusionWhether CA was complicated with hypertension or not， there were statistically significance among routine echocardiography and LVLS parameters compared with HLVH. In particular， GLS and EFSR are accurate in predicting CA in patients with myocardial hypertrophy and preserved LVEF.

Effects of Ginkgo biloba extract on periodontal pathogens and its clinical efficacy as adjuvant treatment / 中国结合医学杂志

<p><b>OBJECTIVE</b>To determine the effects of Ginkgo biloba extract (EGB) on major periodontal pathogens in subgingival plaque.</p><p><b>METHODS</b>Sixty patients with moderate to severe periodontitis were selected and randomly assigned to 3 groups: EGB group, a positive (periocline) and a negative control groups. Subgingival plaque samples were collected before treatment and 1 week, 2 months and 4 months after treatment. The detection rates of 4 major periodontal pathogens-Treponema denticola (Td), Tannerella forsythus (Tf), Prevotella intermedia (Pi), and Porphyromonas gingivalis (Pg)-were detected by polymerase chain reaction (PCR). Clinical indicators were examined before treatment, 3 and 6 months after treatment.</p><p><b>RESULTS</b>EGB significantly decreased the detection rate of all the 4 pathogens 1 week after treatment, and then gradually increased at 2 and 4 months. EGB's inhibition effect was better than or comparable to periocline, except for Pg in short-term. The difference of plaque index (PLI) and bleeding index (BI) was not statistically significant among the groups, while for probing depth (PD) and attachment loss (AL), the difference was statistically significant between the EGB group and negative control group at 3 and 6 months after treatment.</p><p><b>CONCLUSION</b>EGB significantly inhibited major periodontal pathogens and can be used as an adjuvant for periodontitis treatment.</p>

Investigation of the prevalence of patients co-colonized or infected with methicillin-resistant Staphylococcus aureus and vancomycin-resistant enterococci in China: a hospital-based study / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Nosocomial infection caused by methicillin-resistant Staphylococcus aureus (MRSA) and vancomycin-resistant enterococci (VRE) could lead to increased morbidity and mortality. In 2006, VRE nosocomial spread became a reality in our hospital since the first VRE nosocomial infection in 2003. Little is known about the prevalence of coexistence with VRE and MRSA in the patients. The primary objective of the study was to identify the molecular characteristics of epidemic MRSA clones in our hospital and the prevalence of the coexistence with MRSA and VRE in same patients during the 2-year period, 2006 - 2007.</p><p><b>METHODS</b>The clinical features, laboratory test results, and therapeutic outcomes of 129 cases who isolated MRSA collected from January 2006 to December 2007 were retrospectively analyzed. Polymerase chain reaction (PCR) was used to determine mecA-femB type and staphylococcal cassette chromosome mec (SCCmec) type. All the participants were screened for clinical and microbiological data to identify the coexistence of VRE strains with MRSA.</p><p><b>RESULTS</b>One hundred and twenty-nine MRSA isolates were included in the study: 71 (55%) from the intensive care unit, 35 (27.2%) from the surgical wards and 23 (17.8%) from the medical wards. The most frequent source of isolation of MRSA was sputum (76.7%). From seven patients we isolated MRSA and VRE (E. faecium) simultaneously during their inpatient stay. One hundred and twenty-seven (127/129, 98.4%) MRSA isolates harboured SCCmec type III, only 2 MRSA strains contained SCCmec type II. All of the 129 MRSA isolates remained sensitive to vancomycin, teicoplanin and linezolid. Higher sensitivity rates were noted for chloramphenicol 99.2% (128/129). Only 20.2% (26/129) of the MRSA isolates were sensitive to rifampin. All isolates presented resistance to multiple antimicrobial agents with high minimum inhibitory concentrations (MICs), including: beta-lactams (penicillin, oxacillin, cefoxitin, and cefazolin), tetracycline, erythromycin, gentamicin, and quinolones (ciprofloxacin, levofloxacin, and moxifloxacin).</p><p><b>CONCLUSIONS</b>The predominant MRSA clone at Beijing Chaoyang Hospital from 2006 to 2007 had the type III SCCmec element. All of the MRSA isolates were multiresistant to antimicrobial agents. Emergence of coexistence of MRSA and VRE in the same patient was not rare. Physicians should pay more attention to infections resulting from MRSA and VRE. Aggressive infection control measures should be taken to prevent the transmission of the multidrug resistance organism.</p>

R25G mutation in exon 1 of LMNA gene is associated with dilated cardiomyopathy and limb-girdle muscular dystrophy 1B / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Mutations of the LMNA gene encoding lamin A and C are associated with dilated cardiomyopathy (DCM), conduction system defects and skeletal muscle dystrophy. Here we report a family with a mutation of the LMNA gene to identify the relationship between genotype and phenotype.</p><p><b>METHODS</b>All 30 members of the family underwent clinical and genetic evaluation. A mutation analysis of the LMNA gene was performed. All of the 12 exons of LMNA gene were extended with polymerase chain reaction (PCR) and the PCR products were screened for gene mutation by direct sequencing.</p><p><b>RESULTS</b>Ten members of the family had limb-girdle muscular dystrophy (LGMD) and 6 are still alive. Two patients suffered from DCM. Cardiac arrhythmias included atrioventricular block and atrial fibrillation; sudden death occurred in 2 patients. The pattern of inheritance was autosomal dominant. Mutation c.73C > G (R25G) in exon 1 encoding the globular domains was confirmed in all of the affected members, resulting in the conversion of arginine (Arg) to glycine (Gly).</p><p><b>CONCLUSIONS</b>The mutation R25G in exon 1 of LMNA gene we reported here in a Chinese family had a phenotype of malignant arrhythmia and mild LGMD, suggesting that patients with familial DCM, conduction system defects and skeletal muscle dystrophy should be screened by genetic testing for the LMNA gene.</p>

Mechanism of carbapenems resistance in Acinetobacter baumannii / 中国医学科学院学报

<p><b>OBJECTIVE</b>To investigate the mechanism of carbapenems resistance in Acinetobacter baumannii.</p><p><b>METHODS</b>WHONET-5 software was used to analyze the trend of carbapenem resistance in Acinetobacter baumannii collected from 1999 to 2001 at Peking Union Medical College Hospital. Analytical isoelectric focusing was used to measure the pI of the beta-lactamase. Conjugation experiment was used to study the transfer of carbapenem resistance and plasmid DNA was extracted and purified with Qiagen Plasmid Mini Kit. The homology of the isolates was determined by pulsed field gel electrophoresis (PFGE). Integrase genes and blaIMP-, blaVIM-, blaOXA- genes for resistant isolates were amplified and sequenced.</p><p><b>RESULTS</b>Imipenem resistance in A. baumannii was ranged from 1.8%-8.5%, but only 9 resistant isolates were viable. They were co-resistant to other carbapenems, ceftazidime, aztreonam, and gentamicin, and four isolates were resistant to ciprofloxacin. Impipenem resistance could not be transferred to susceptible strains. No plasmid was extracted. Each isolate produced TEM-1, AmpC, and two enzymes (pI 6.7, 6.0), which can not be inhibited by cloxacillin and clavulanic acid. Each isolate had class I intergase gene. Nine isolates were all negative for PCR of blaIMP- and blaVIM- genes, but positive for blaOXA-23 specific PCR. Sequencing found 100% homology with blaOXA-23. PFGE found 3 clones (A type: 5 isolates; B type: 3 isolates; C type: 1 isolate). Control isolates (imipenem-susceptible, but ceftazidime, ciprofloxacin, and gentamicin resistant) were also A clone.</p><p><b>CONCLUSIONS</b>Production of OXA-23 carbapenemase in A. baumannii was one of the main mechanisms of carbapenems resistance at our hospital. It brings concern that imipenem-resistant clone has evoluted from nosocomial multiple-resistant strains.</p>