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101.
OBJECTIVE: The purpose of this study was to compare the left atrial appendage (LAA) tissue Doppler imaging (TDI) with the classical LAA function parameters in patients with mitral valve disease. METHODS: Twenty patients who had pure mitral regurgitation (group 1), 20 patients who had pure rheumatic mitral stenosis (group 2), and 20 healthy patients (group 3) were included in this study. All the cases were sinus rhythm. In order to determine the LAA functions, LAA late filling (LAALF), and late emptying (LAALE) flow velocities and LAA fractional area change (LAAFAC) were measured. LAA tissue Doppler evaluations were obtained from the PW Doppler, which was placed on the LAA lateral wall in a transverse basal short-axis approach. LAA late systolic (LAALSW) and late diastolic (LAALDW) wave velocities were obtained from TDI records transesophageal echocardiography (TEE). RESULTS: There were no significant differences among groups 1, 2, and 3 in terms of age, left ventricular (LV) ejection fraction, gender, and heart rate. No differences were observed between group 1 and the control group with respect to LAALE, LAALF, and LAAFAC. LAALE velocity and LAAFAC were significantly decreased in group 2 than group 1. LV diastolic diameter was significantly greater, whereas LAALSW and LAALDW velocities were significantly decreased in group 1 compared with group 3. There were no differences between groups 1 and 2 regarding to LAALSW and LAALDW velocities. LAALE, LAALF, LAALSW, LAALDW velocities, and LAAFAC were significantly decreased in group 2 than group 3. CONCLUSION: The TDI method may detect the LAA systolic dysfunctions, which cannot be detected using classical methods, on tissue level in patients with mitral regurgitation. In addition, the deterioration of the LAA functions at tissue level in patients with rheumatic mitral stenosis was also detected.  相似文献   
102.
Acute coronary ischemia augments inhomogeneity in ventricular repolarization, which significantly correlates with ventricular fibrillation. The effects of glycoprotein IIb/IIIa receptor inhibition on QT interval dispersion (QTd), and the effects of QTd changes on in-hospital, 30 day, and long-term cardiac events in patients with unstable angina (UA) and non-Q-wave myocardial infarction (MI) have not been investigated previously. Eighty-three patients presenting with Braunwald class IIIB UA or non-Q-wave MI were randomized to standard therapy (aspirin and unfractionated heparin, 42 patients) or tirofiban therapy: addition to standard therapy (41 patients). QT interval dispersion (QTd) and corrected QTd (QTcd) were measured prior to therapy, and 6, 24, 48, 72, and 96 hours after the initiation of the treatment. In both groups QTd and QTcd were higher than normal limits during the admission, prior to therapy. The first QTd and QTcd were not different between two groups; the remaining values were significantly lower in tirofiban group except the first and last QTd (p values for QTd at 6, 24, 48, 72, and 96 hours are 0.057, 0.045, 0.0006, 0.04, and NS, respectively, and for QTcd, they are 0.017, 0.046, 0.0004, 0.012, and 0.01, respectively). When the first QTd and QTcd compared to the following measurements in each group, the first significant decrease occurred at 6th hour (p = 0.004 for QTd, and 0.004 for QTcd) in tirofiban group, whereas in standard therapy group it was occurred at 48th hour (p = 0.02) for QTd, and 72nd hour (p = 0.019) for QTcd. While the incidence of in-hospital acute MI, recurrent refractory angina, and total major cardiac events were significantly lower in the tirofiban group (p = 0.03, 0.04, and 0.01, respectively) that early QTd recovery observed, the 30 day and long-term incidence of major cardiac events were not different between the two groups. GP IIb/IIIa receptor inhibition in addition to heparin treatment causes a faster recovery of increased QT dispersion, and the early recovery of QTd is associated with a reduction in in-hospital major cardiac events.  相似文献   
103.
Coronary artery ectasia (CAE) is characterised by irregular, diffuse, saccular, or fusiform dilatation of the coronary arteries. Although the underlying mechanisms are not fully understood, CAE is considered to be an original form of vascular remodelling in response to atherosclerosis. However, it is not clear why some patients develop CAE while most do not. Experimental data suggest that activation of the renin angiotensin system may lead to an increased inflammatory response in the vessel wall or to an activation of matrix metalloproteinases. In addition, an insertion/deletion (ID) polymorphism of angiotensin converting enzyme (ACE) has been associated with coronary vascular tone and the development of aneurysms. Accordingly, we hypothesised that the gene polymorphism of ACE may be a potential factor influencing the genesis of CAE. We retrospectively evaluated 112 patients who underwent coronary angiography. ACE ID genotype was determined in two groups of patients. Group 1 consisted of 56 patients who were found to have CAE. Group 2 consisted of 56 patients with significant coronary artery disease (CAD) (> 50% stenosis in any of the major epicardial coronary arteries or their branches) but without any evidence of coronary ectasia. Polymerase Chain Reaction (PCR) was used to detect ACE genotype. The ratio of DD genotype was found to be greater in group 1 than group in 2 (39% versus 18%, respectively, P < 0.05). When assessed according to the presence of the I allele, it was greater was greater in group 2 than in group 1 (82.1% versus 60.7%, respectively, P < 0.05). The results indicate that an ACE DD genotype may be a risk factor for CAE.  相似文献   
104.
The purpose of the current study was to compare the characteristics of lung cancer patients who had exposure to asbestos and asbestos-related radiological findings (ARRF) to the characteristics of patients who had no exposure. Of the 766 lung cancer patients evaluated, 607 had no exposure to asbestos and no ARRF, 88 had ARRF and a history of exposure, remaining 71 patients had no exposure to asbestos occupationally and no ARRF, but we could not obtain environmental exposure history from them. So we excluded these 71 patients' data. The study patients were compared with respect to age, gender, smoking history, duration and nature of symptoms, findings on physical examination, tumor histological types, chest X-ray (CXR) findings, tumor site and stage, and survival. Lung cancer patients with ARRF were more often males, former smokers, and older than patients with no history of exposure to asbestos. There were no differences between the groups of patients in terms of the duration of symptoms, the distribution of symptoms, the findings on physical examination, tumor histological type, and the CXR findings. There was no difference between the two groups of patients in the distribution among tumor stages and median survival. The anatomic site of origin of the tumor in the group with ARRF was peripheral and in the lower zone of the lung. We suggest that specific attention should be given to the peripheral and lower zones of the lungs on CRX during the evaluation of the patients with ARRF for lung cancer.  相似文献   
105.

Background

To our knowledge, no study so far investigated the importance of post‐procedural frontal QRS‐T angle f(QRS‐T) in ST segment elevation myocardial infarction (STEMI). The aim of our study was to investigate the role of baseline and post‐procedural f(QRS‐T) angles for determining high risk STEMI patients, and the success of reperfusion.

Methods

A total of 248 patients with first acute STEMI that underwent primary percutaneous coronary intervention (pPCI) or thrombolytic therapy (TT) between 2013 and 2014 were included in this study. Baseline f(QRS‐T) angle was defined as the angle which measured from the first ECG at the time of hospital admission. Post‐procedural (QRS‐T) angle was defined according to the treatment strategy as follows: the angle which measured from the post‐PCI ECG in patients treated with pPCI; the angle which measured from the ECG taken 90 min after onset of therapy in patients treated with TT.

Results

The baseline (101.9° ± 48.0 vs. 72.1° ± 49.1, p = 0.014) and post‐procedural f(QRS‐T) angles (95.7° ± 48.1 vs. 58.1° ± 47.1, p = 0.002) were significantly higher in patients who developed in‐hospital mortality than the patients who did not develop in‐hospital mortality. Also, f(QRS‐T) angle measured at 90 min was significantly lower in patients with successful thrombolysis group compared to failed thrombolysis group (53.2° ± 42.8 vs. 77.3° ± 52.9, p = 0.033), whereas baseline f(QRS‐T) angle was similar between two groups (78.6° ± 53.4 vs. 78.9° ± 54.0, p = 0.976). Multivariate analysis showed that post‐procedural f(QRS‐T) angle ≥89.6° (odds ratio: 3.541, 95% confidence interval: 1.235–10.154, p = 0.019), but not baseline f(QRS‐T) angle, was independent predictor of in‐hospital mortality.

Conclusion

f(QRS‐T) angle may be used as a beneficial tool for determining high risk patients in acute STEMI. Unlike previous studies, we showed for the first time that that post‐procedural f(QRS‐T) can predict in‐hospital mortality and TT failure.
  相似文献   
106.
107.
For both the B2O3-Bi2O3-CaO and B2O3-Bi2O3-SrO glass systems, γ-ray and neutron attenuation qualities were evaluated. Utilizing the Phy-X/PSD program, within the 0.015–15 MeV energy range, linear attenuation coefficients (µ) and mass attenuation coefficients (μ/ρ) were calculated, and the attained μ/ρ quantities match well with respective simulation results computed by MCNPX, Geant4, and Penelope codes. Instead of B2O3/CaO or B2O3/SrO, the Bi2O3 addition causes improved γ-ray shielding competence, i.e., rise in effective atomic number (Zeff) and a fall in half-value layer (HVL), tenth-value layer (TVL), and mean free path (MFP). Exposure buildup factors (EBFs) and energy absorption buildup factors (EABFs) were derived using a geometric progression (G–P) fitting approach at 1–40 mfp penetration depths (PDs), within the 0.015–15 MeV range. Computed radiation protection efficiency (RPE) values confirm their excellent capacity for lower energy photons shielding. Comparably greater density (7.59 g/cm3), larger μ, μ/ρ, Zeff, equivalent atomic number (Zeq), and RPE, with the lowest HVL, TVL, MFP, EBFs, and EABFs derived for 30B2O3-60Bi2O3-10SrO (mol%) glass suggest it as an excellent γ-ray attenuator. Additionally, 30B2O3-60Bi2O3-10SrO (mol%) glass holds a commensurably bigger macroscopic removal cross-section for fast neutrons (ΣR) (=0.1199 cm−1), obtained by applying Phy-X/PSD for fast neutrons shielding, owing to the presence of larger wt% of ‘Bi’ (80.6813 wt%) and moderate ‘B’ (2.0869 wt%) elements in it. 70B2O3-5Bi2O3-25CaO (mol%) sample (B: 17.5887 wt%, Bi: 24.2855 wt%, Ca: 11.6436 wt%, and O: 46.4821 wt%) shows high potentiality for thermal or slow neutrons and intermediate energy neutrons capture or absorption due to comprised high wt% of ‘B’ element in it.  相似文献   
108.
Eighteen carbapenem-resistant, OXA-48-positive enterobacterial isolates recovered from Turkey, Lebanon, Egypt, France, and Belgium were analyzed. In most isolates, similar 70-kb plasmids carrying the carbapenemase gene blaOXA-48 were identified. That gene was located within either transposon Tn1999 or transposon Tn1999.2, which was always inserted within the same gene. This work highlights the current plasmid-mediated dissemination of the OXA-48 carbapenemase worldwide.Carbapenem-hydrolyzing β-lactamases belonging to Ambler classes A, B, and D have been reported worldwide among Enterobacteriaceae (22). The extensive spread of Ambler class A carbapenemases of the KPC type highlights that carbapenemases may rapidly become threatening (17). Acquired class D ß-lactamases possessing carbapenemase properties have been reported previously, being identified mainly in Acinetobacter sp. (18, 21) and occasionally in Enterobacteriaceae. The chromosome-encoded oxacillinase OXA-23 was previously described for Proteus mirabilis (4), and the oxacillinase OXA-48 was first identified in a Klebsiella pneumoniae isolate from Turkey (20). Since then, several other OXA-48-producing isolates of various enterobacterial species (Citrobacter freundii and Escherichia coli) have been reported, mainly from Turkey (1, 6, 11, 16) but also from Belgium (8), from Lebanon (15), and more recently from the United Kingdom (14, 23a), India (3a), and Argentina (6a). So far, the blaOXA-48 gene has been found to be plasmid borne and located between two identical insertion sequences, IS1999, forming the composite transposon Tn1999 (3). We have analyzed here the genetic backgrounds associated with the blaOXA-48 gene among Enterobacteriaceae isolates collected from different countries.The study included 18 OXA-48-positive clinical isolates of K. pneumoniae (13 isolates), Enterobacter cloacae (2 isolates), Providencia rettgeri (1 isolate), C. freundii (1 isolate), and E. coli (1 isolate). Isolates were mainly from the Turkish cities Istanbul, Ankara, and Izmir (n = 14) (Table (Table1).1). Among the 13 K. pneumoniae isolates, at least Kp11978 (20) and KpB had been sources of nosocomial outbreaks (6). A single K. pneumoniae isolate (KpBEL) was recovered from Brussels, Belgium (8); another K. pneumoniae isolate (KpL) from Beirut, Lebanon (15); another K. pneumoniae isolate from the Bicêtre Hospital (KpBIC), Paris, France (this study); and another K. pneumoniae isolate from Gizah, Egypt (KpE) (8a). Samples were isolated from blood (KpI1, KpI2, KpB, and Enc1), urine (PR, KpBEL, KpL, Kp11978, and KpBIC), cerebrospinal fluid (Enc2), and catheter (KpE). Isolates from Belgium, France, Egypt, and Lebanon were from patients who did not report recent travel history.

TABLE 1.

MICs of β-lactams for the 18 isolates of Enterobacteriaceae and their transconjugants and/or transformants (pOXA-48) E. coli J53 and E. coli TOP10
β-Lactam(s)aMIC (μg/ml) of β-lactam forb:
MIC (μg/ml) of β-lactam forb:
Kp11978 (Istanbul; OXA-48, SHV-2a, TEM-1)E. coli J53(pA-1)KpB (Istanbul; OXA-48, CTX-M-15)E. coli J53(pBb)Kp3A (Ankara; OXA-48)E. coli J53(p3A)Kp4A (Ankara; OXA-48, CTX- M-15), Kp5A (Ankara; OXA-48, SHV-5), Kp6A (Ankara; OXA-48, TEM-150)E. coli J53(p4A, p5A, p6A)Kp7A (Ankara; OXA-48)E. coli J53(p7A)KpI-1 and KpI-2 (Izmir; OXA- 48, CTX-M-15)E. coli J53(pI-1, pI-2)KpBIC (Paris; OXA-48)E. coli TOP10(pBIC)KpE (Gizah; OXA-48, CTX-M-15)E. coli J53(pE)KpBEL (Brussels; OXA-48)E. coli J53(pBEL)KpL (Beirut; OXA-48)E. coli J53(pL)PR (Izmir; OXA-48, TEM-101)E. coli TOP10(pPR)Enc1 (Istanbul; OXA-48, SHV-5)E. coli J53(pEnc1)Enc2 (Istanbul; OXA-48, SHV-2a)E. coli J53(pEnc2)CF (Istanbul; OXA-48, VEB-1)E. coli J53(pCF)EcA (Ankara; OXA-48, TEM-150)E. coli J53(pEcA)E. coli J53E. coli TOP10
Imipenem642160.5>320.75>320.38>320.75240.50.50.5220.750.75>164>321.50.50.50.750.75>320.75240.750.060.06
Ertapenem640.19>320.25>320.25>320.12>320.19240.2520.53342>164>320.750.50.1250.750.19>320.25>320.250.060.06
Meropenem640.25320.12>320.12>320.094>320.12160.0940.50.5220.50.5>160,19>320.250.50.0940.750.12>320.12240.190.060.06
Amoxicillin>512>512>512>512>512>512>512>512>512>512>512>512>512>512>512>512>256>256>256>256>256>256>512>512>512>512>512>512>256>25644
Amoxicillin + clav. acid>512128>512>512>512>512>512>512>512>512>512>512>512>512>512>512>256>256>256>256>256>256>512>512>512>512>512>512>256>25644
Ticarcillin>512>512>512>512>512>512>512>512>512>512>512>512>512>512>512>512>256>256>256>256>256>256>512>512>512>512>512>512>256>25624
Ticarcillin + clav. acid>512128>512>512>512>512>512>512>512>512>512>512>512>512>512>512>256>256>256>256>256>256>512>512>512>512>512>512>256>25624
Piperacillin>5128>512>512>512512>512>512>512>512>512512>512>512>512512>2561289664>256128>512>512>512>512>512>512>25612812
Piperacillin + tazobactam5124>512>512>512512>512>512>512>512>512512>512>512>512512>2561289664>256128>512>512>512>512>512>512>25612812
Cephalotin>5120.5>51216>51216>51216>51216>51216>51216>512161616328>51216>51216>51216>512>512>5121644
Cefotaxime640.06>5120.510.5640.120.50.5640.120.50.5640.120.120.121.50.256432>5120.255120.25640.12640.120.060.06
Ceftazidime5120.12>51210.250.255120.120.120.125120.120.120.125120.1210.750.750.75512512>5120.75320.755120.755120.750.060.06
Cefepime320.06>512<0.50.50.12320.120.50.5320.120.50.5320.120.120.120.120.06320.540.12320.12320.12320.120.030.06
Aztreonam5120.06>512<0.120.060.065120.060.060.065120.060.060.065120.060.060.060.060.065120.06>5120.065120.065120.065120.060.030.06
Cefoxitin12821284221282128212821282128222821284>512251221282128224
Open in a separate windowaclav. acid, clavulanic acid.bKp, K. pneumoniae; Enc, E. cloacae; CF, C. freundii; PR, P. rettgeri; Ec, E. coli.Antibiotic susceptibility of the isolates was determined by the disk diffusion method (7). MICs of β-lactams were determined using Etest strips (AB bioMérieux, Solna, Sweden). All isolates were resistant to penicillins. Fourteen of the 18 isolates were resistant to carbapenems according to the CLSI guidelines (Table (Table1)1) (7). The four remaining isolates (KpBIC, KpE, Enc1, and Enc2) exhibited MICs of carbapenems remaining in the intermediate or in the susceptible range. Resistance to broad-spectrum cephalosporins was observed for most of the isolates. However, isolates Kp3A, Kp7A, KpBEL, KpL, and KpBIC remained susceptible to broad-spectrum cephalosporins (Table (Table1).1). All isolates were resistant to fluoroquinolones, except isolates Kp6A, Enc1, and Enc2. All isolates were resistant to aminoglycosides and sulfamethoxazole, except isolate CF, which remained susceptible to the latter antibiotic.Carbapenemase- and extended-spectrum-β-lactamase (ESBL)-encoding genes were identified by PCR experiments using previously designed primers (6, 8), followed by sequencing. Additional ESBL production was detected by synergy tests as described previously (12). Positive results for ESBL production were observed for isolates EcA, Enc1, Enc2, Kp4A, Kp5A, Kp6A, KpI-1, KpI-2, and KpE. Several ESBL determinants were identified, including CTX-M-15, SHV-5, SHV-2a, TEM-101, TEM-150, and VEB-1 (Table (Table11).Isolates belonging to the same species (13 K. pneumoniae isolates or two E. cloacae isolates) were compared by pulsed-field gel electrophoresis (PFGE) as described previously (6). Ten pulsotypes were identified among the 13 K. pneumoniae isolates. The two K. pneumoniae isolates from Izmir were clonally related, and the three K. pneumoniae isolates from Ankara (Kp4A, Kp5A, and Kp6A) shared very similar PFGE patterns. The two E. cloacae isolates recovered from Istanbul were not clonally related (Fig. (Fig.11).Open in a separate windowFIG. 1.Pulsed-field gel electrophoresis patterns of the 13 OXA-48-producing K. pneumoniae isolates and the two OXA-48-producing E. cloacae isolates. (A) Lane 1, Kp3A; lane 2, Kp4A; lane 3, Kp5A; lane 4, Kp6A; lane 5, Kp7A; lane 6, KpI-1; lane 7, KpI-2; lane 8, unrelated K. pneumoniae isolate (included as a comparative strain); lane 9, Enc1; lane 10, Enc2; lane 11, unrelated E. cloacae isolate (included as a comparative strain); lane M, molecular size marker. (B) Lane 1, Kp3A; lane 2, Kp11978; lane 3, Kp4A; lane 4, Kp7A; lane 5, KpI-1; lane 6, KpL; lane 7, KpB; lane 8, KpBEL; lane 9, KpE; lane 10, KpBIC; lane M, molecular size marker.Transferability of the blaOXA-48 gene was studied by conjugation experiments as described previously (6). When conjugation experiments failed, plasmid DNA extract was used for transformation as described previously (20). Transformants were selected on LB agar containing ticarcillin (50 μg/ml). Transconjugants and transformants with decreased susceptibility to carbapenems were obtained for all isolates (Table (Table1),1), and MICs for the transconjugants/transformants remained in the susceptible range. The E. coli transformant obtained from the P. rettgeri isolate exhibited reduced susceptibility to carbapenems associated with resistance to cefotaxime and ceftazidime.Plasmids were analyzed by using the Kieser technique (13). A 70-kb plasmid was identified in all transconjugants/transformants (data not shown). However, a 150-kb plasmid was identified in the blaOXA-48-positive transformant obtained with the PR isolate. The blaOXA-48 and blaTEM-101 genes were codetected on the same 150-kb plasmid, as confirmed by Southern blot hybridization as described previously (20) (data not shown), explaining the resistance to all β-lactams of the PR isolate and its transformant (Table (Table1).1). Plasmid restriction profiles were compared as described previously (10) (data not shown), and very similar restriction patterns (suggesting highly related structures) were obtained for all of the 70-kb plasmids but not for the 150-kb plasmid pPR.PCR mapping was used to assess the presence of insertion sequence IS1999 upstream of the blaOXA-48 gene, to confirm the presence of transposon Tn1999, and to identify the transposon insertion site for all of the OXA-48-positive isolates (3, 20). In all isolates, the blaOXA-48 gene was flanked by two copies of IS1999, as described previously (3). The prototype IS1999 located at the left extremity of transposon Tn1999 was identified in isolates Kp3A, Kp4A, Kp5A, Kp6A, Kp7A, CF, PR, Enc1, and Enc2. Insertion of IS1R into IS1999 as described for KpB (6) and giving rise to Tn1999.2 was identified for isolates EcA, KpBIC, KpI, KpL, KpBEL, and KpE (Fig. (Fig.2).2). In isolate Kp11978, transposon Tn1999 had been identified to be inserted into the tir gene, being functionally homologous to the F3 gene encoding the factor F involved in the plasmid replicative machinery (23). By use of a primer located upstream of Tn1999 inserted into the tir gene, insertion of Tn1999 at the same target site was evidenced in all of the blaOXA-48-positive plasmids except for the pPR plasmid (Fig. (Fig.2).2). Inverse PCR performed as described previously (3) was used for identifying the blaOXA-48-surrounding structures in isolate PR. Sequencing of the obtained amplicons indicated that Tn1999 had targeted a gene encoding a phosphoadenosine phosphosulfate reductase (ΔPPR).Open in a separate windowFIG. 2.Genetic environments of the blaOXA-48-carrying plasmids identified among the 18 OXA-48-positive Enterobacteriaceae isolates. (A) Structure described for pA-1, p3A, p4A, p5A, p6A, p7A, pCF, pEnc1, and pEnc2. (B) Structure of the 150-kb pPR plasmid. (C) Structure described for pBb, pI, pL, pBEL, pEcA, pBIC, and pE.Attempts to identify the incompatibility group of the 70-kb OXA-48-positive plasmids failed using a PCR-based replicon typing method as described previously (5). Since rep genes are often located close to the hot spots for resistance gene integration, cloning experiments were performed to study these plasmids further. A gene encoding phage replication protein P (RepP) was identified upstream of the blaOXA-48 gene. Primers specific for the repP gene were designed (RepPA, 5′-AATGGTTAACTTTGACTGTG-3′; RepPB, 5′-GCACGATTTAGAGGTCTAC-3′), and positive results were obtained for all 70-kb plasmids. Association of the repP gene with the blaOXA-48 gene on the 70-kb plasmid was confirmed by hybridization with a specific RepP probe (data not shown). However, the repP gene could not be detected on the 150-kb plasmid identified from isolate PR. Our study showed the spread of a blaOXA-48-carrying plasmid among different enterobacterial species, being identified first in Turkey and later in other European countries and in the Middle East. The present work indicates that dissemination of the blaOXA-48 gene is not driven by the dissemination of a single K. pneumoniae clone. Since the blaOXA-48-carrying plasmid confers by itself a low level of resistance to carbapenems, clinical laboratory detection of OXA-48-producing strains may be difficult. Since the reservoir of blaOXA-48 has been identified in the waterborne Gram-negative organism Shewanella oneidensis (19), it is likely that the process leading to the dissemination of this gene may be the consequence of a wide interspecies exchange. In addition, since plasmids belonging to the RepP group have been described among Pseudomonas sp., phytopathogenic Xanthomonas sp., and samples from soils and sludges (2, 9, 24), it may be hypothesized that the blaOXA-48 gene could also be identified in those species. This work underlines that besides class B (VIM and IMP) and class A (KPC) carbapenemases, the class D carbapenemase OXA-48 type might contribute significantly to carbapenem resistance in Enterobacteriaceae.  相似文献   
109.
Thirty-one female Sprague-Dawley rats were used to determine the effects of subacromial corticosteroid injections on the rotator cuff. The injection technique was tested in 6 animals, which were excluded from the study. The remaining 25 rats were randomly divided into three groups of 8 animals each; a single rat received no injections. Every other week for 8 weeks, one shoulder in each rat was injected with methylprednisolone, betamethasone, or saline in a dosage equivalent to that used in humans. The supraspinatus and infraspinatus tendons were removed 10 days after the last injection and evaluated. There were no pathologic changes in the tendons injected with saline. In 43% of the methylprednisolone-treated rats and 29% of the betamethasone-treated rats, the tendons were abnormally soft and light-colored. In 43% of the methylprednisolone group and 71% of the betamethasone group, fragmentation of collagen bundles and inflammatory cell infiltration were evident. Subacromial injections of methylprednisolone or betamethasone repeated frequently can cause deleterious changes in the normal structure of the rat rotator cuff. In light of these findings, therapy for subacromial impingement syndrome of the shoulder with frequent, repeated steroid injections is potentially harmful.  相似文献   
110.
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