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ObjectiveThe effect of early intravenous (IV) beta-blockers (BBs) administration in patients undergoing primary percutaneous coronary intervention (pPCI) on ST-segment deviation is unknown. We undertook a prespecified secondary analysis of the Early Beta-blocker Administration before primary PCI in patients with ST-elevation Myocardial Infarction (EARLY-BAMI) trial to investigate the effect of early IV BB on ST-segment deviation.MethodsThe EARLY-BAMI trial randomised patients with ST-elevation myocardial infarction (STEMI) to IV metoprolol (2×5 mg bolus) or matched placebo before pPCI. The prespecified outcome, evaluated by an independent core laboratory blinded to study treatment, was the residual ST-segment deviation 1 hour after pPCI (ie, the percentage of patients with >3 mm cumulative ST deviation at 1 hour after pPCI).ResultsAn ECG for the evaluation of residual ST-segment deviation 1 hour after pPCI was available in 442 out of 683 randomised patients. The BB group had a lower heart rate after pPCI compared with placebo (71.2±13.2 vs 74.3±13.6, p=0.016); however, no differences were noted in the percentages of patients with >3 mm cumulative ST deviation at 1 hour after pPCI (58.6% vs 54.1%, p=0.38, in BB vs placebo, respectively) neither a significant difference was found for the percentages of patients in each of the four prespecified groups (normalised ST-segment; 1–3 mm; 4–6 mm;>6 mm residual ST-deviation).ConclusionsIn patients with STEMI, who were being transported for primary PCI, early IV BB administration did not significantly affect ST-segment deviation after pPCI compared with placebo. The neutral result of early IV BB administration on an early marker of pharmacological effect is consistent with the absence of subsequent improvement of clinical outcomes.

Contains fulltext : 182904.pdf (Publisher’s version ) (Open Access) BACKGROUND: To eliminate some of the potential late limitations of permanent metallic stents, the bioresorbable coronary stents or 'bioresorbable vascular scaffolds' (BVS) have been developed. METHODS: We reviewed all currently available clinical data on BVS implantation. RESULTS: Since the 2015 position statement on the appropriateness of BVS in percutaneous coronary interventions, several large randomised trials have been presented. These have demonstrated that achieving adequate 1 and 2 year outcomes with these first-generation BVS is not straightforward. These first adequately powered studies in non-complex lesions showed worse results if standard implantation techniques were used for these relatively thick scaffolds. Post-hoc analyses hypothesise that outcomes similar to current drug-eluting stents are still possible if aggressive lesion preparation, adequate sizing and high-pressure postdilatation are implemented rigorously. As long as this has not been confirmed in prospective studies the usage should be restricted to experienced centres with continuous outcome monitoring. For more complex lesions, results are even more disappointing and usage should be discouraged. When developed, newer generation scaffolds with thinner struts or faster resorption rates are expected to improve outcomes. In the meantime prolonged dual antiplatelet therapy (DAPT, beyond one year) is recommended in an individualised approach for patients treated with current generation BVS. CONCLUSION: The new 2017 recommendations downgrade and limit the use of the current BVS to experienced centres within dedicated registries using the updated implantation protocol and advise the prolonged usage of DAPT. In line with these recommendations the manufacturer does not supply devices to the hospitals without such registries in place.

Background The impact of intravenous (IV) beta-blockers before primary percutaneous coronary intervention (PPCI) on infarct size and clinical outcomes is not well established. Objectives This study sought to conduct the first double-blind, placebo-controlled international multicenter study testing the effect of early IV beta-blockers before PPCI in a general ST-segment elevation myocardial infarction (STEMI) population. Methods STEMI patients presenting

Salmonella Enteritidis has developed the potential to contaminate eggs by surviving in the antimicrobial environment of the hen's egg white. This has led to a worldwide pandemic of foodborne salmonellosis infections in humans due to the consumption of contaminated eggs and egg-derived products. The molecular mechanisms of Salmonella Enteritidis egg white survival are not fully clear. Using in vivo expression technology and promoter-reporter fusions we showed that the promoter of the tolC gene, encoding the TolC outer membrane channel that is used by multidrug efflux pumps to export harmful molecules and to secrete bacterial products, is activated by egg white at the chicken body temperature. Using a Salmonella Enteritidis tolC deletion mutant we showed that TolC has an important role in egg white survival. Chromatographic separation techniques and subsequent testing of antimicrobial activities of separated egg white fractions led to the identification of ovotransferrin as the egg white antimicrobial factor which is capable of inhibiting growth of a tolC deletion strain but not the wild type strain. We provide evidence that TolC protects Salmonella Enteritidis against ovotransferrin-mediated growth inhibition in egg white.

Aims: Interleukin-6 receptor (IL-6R) signalling has been suggested to play a causal role in the development and outcome of coronary heart disease (CHD). The aim of this study was to investigate the association of sIL-6R levels with myocardial reperfusion after percutaneous coronary intervention (PCI) for acute ST-elevated myocardial infarction (STEMI).Methods: Blood was sampled from 70 patients presenting with STEMI at 6 different time-points (baseline, post-PCI, t = 1 h, t = 6 h, t = 24 h, t = 2w). Coronary angiograms post-PCI were analysed for myocardial blush grade (MBG) as indicator of myocardial reperfusion. Serum IL-6 and sIL-6R were measured using IL-6 and sIL-6R enzyme-linked immunosorbent assays (ELISA).Results: sIL-6R levels fluctuated biphasic during the two weeks after STEMI. Reduced MBG was associated with a larger change in sIL-6R levels between baseline and post-PCI compared to optimal MBG (-13.40; SEM 2.78 ng/ml vs -1.99; SEM 2.35 ng/ml, respectively; p Conclusions: sIL-6R levels fluctuate biphasic during the two weeks after MI with larger changes and increased IL-6/sIL-6R ratio in patients with reduced MBG. Further research is needed to increase our understanding of the possible causality of these associations. (C) 2015 Elsevier Ltd. All rights reserved.

Importance Metformin treatment is associated with improved outcome after myocardial infarction in patients with diabetes. In animal experimental studies metformin preserves left ventricular function. Objective To evaluate the effect of metformin treatment on preservation of left ventricular function in patients without diabetes presenting with ST-segment elevation myocardial infarction (STEMI). Design, Setting, and Participants Double-blind, placebo-controlled study conducted among 380 patients who underwent primary percutaneous coronary intervention (PCI) for STEMI at the University Medical Center Groningen, the Netherlands, between January 1, 2011, and May 26, 2013. Interventions Metformin hydrochloride (500 mg) (n = 191) or placebo (n = 189) twice daily for 4 months. Main Outcomes and Measures The primary efficacy measure was left ventricular ejection fraction (LVEF) after 4 months, assessed by magnetic resonance imaging. A secondary efficacy measure was the N-terminal pro-brain natriuretic peptide (NT-proBNP) concentration after 4 months. The incidence of major adverse cardiac events (MACE; the combined end point of death, reinfarction, or target-lesion revascularization) was recorded until 4 months as a secondary efficacy measure. Results At 4 months, all patients were alive and none were lost to follow-up. LVEF was 53.1% (95% CI, 51.6%-54.6%) in the metformin group (n = 135), compared with 54.8% (95% CI, 53.5%-56.1%) ( P = .10) in the placebo group (n = 136). NT-proBNP concentration was 167 ng/L in the metformin group (interquartile range [IQR], 65-393 ng/L) and 167 ng/L in the placebo group (IQR, 74-383 ng/L) ( P = .66). MACE were observed in 6 patients (3.1%) in the metformin group and in 2 patients (1.1%) in the placebo group ( P = .16). Creatinine concentration (79 µmol/L [IQR, 70-87 µmol/L] vs 79 µmol/L [IQR, 72-89 µmol/L], P = .61) and glycated hemoglobin (5.9% [IQR, 5.6%-6.1%] vs 5.9% [IQR, 5.7%-6.1%], P = .15) were not significantly different between both groups. No cases of lactic acidosis were observed. Conclusions and Relevance Among patients without diabetes presenting with STEMI and undergoing primary PCI, the use of metformin compared with placebo did not result in improved LVEF after 4 months. The present findings do not support the use of metformin in this setting. Trial Registration clinicaltrials.gov Identifier:NCT01217307.

Background Aromatase inhibitors (AIs) frequently lead to the AI-induced musculoskeletal syndrome (AIMSS). Looking into its pathophysiology, 6 months of AI therapy thickens the tendon sheath with intra-articular fluid (IAF) retention and loss of grip strength. We here report 24-month follow-up data. Patients and methods A prospective cohort study of 33 postmenopausal breast cancer patients received adjuvant endocrine therapy; 27 received an AI and 6 received tamoxifen. At baseline, 6 and 24 months patients had a rheumatologic examination, including a grip strength test, and magnetic resonance imaging of both hands and wrists. The primary end point was tenosynovial changes; secondary end points were changes in morning stiffness, grip strength and IAF. Results Twenty-three AI and 5 tamoxifen patients completed all investigations. Between month 6 and 24, IAF further increased in AI users (P = 0.04) but not in tamoxifen users, and grip strength further decreased in both groups. The worsened tenosynovial changes were strongly correlated with a decrease in grip strength. At 24 months, morning stiffness continued to be present in over a third of AI users. Conclusion AIMSS represents a substantial problem in breast cancer patients. It is associated with tenosynovial changes, IAF retention, joint stiffness and loss of grip strength that do not improve with prolonged use.

Cigarette smokers with ST-segment elevation myocardial infarction (STEMI) may present different response to potent antithrombotic therapy compared to nonsmokers. We assessed the impact of smoking status and intracoronary abciximab in patients with STEMI undergoing primary percutaneous coronary intervention (PCI). We pooled data from 5 randomized trials comparing intracoronary versus intravenous abciximab bolus in patients undergoing primary PCI. The primary end point was the composite of death or reinfarction at a mean follow-up of 292 ± 138 days. Of 3,158 participants, 1,369 (43.3%) were smokers, and they had a lower risk of the primary end point in crude, but not in adjusted analyses (hazard ratio [HR] 0.87, 95% confidence interval [CI] 0.63 to 1.21, p = 0.405). Intracoronary versus intravenous abciximab was associated with a significant reduction in the risk of primary end point among smokers (3.6% vs 8.0%; HR 0.43, 95% CI 0.26 to 0.72, p = 0.001), but not in nonsmokers (10.2% vs 9.9%; HR 0.99, 95% CI 0.72 to 1.36, p = 0.96), with a significant interaction (p = 0.009). Furthermore, intracoronary abciximab decreased the risk of reinfarction in smokers (HR 0.30, 95% CI 0.15 to 0.62, p = 0.001), with no difference in nonsmokers (HR 1.20, 95% CI 0.71 to 2.01, p = 0.50). Stent thrombosis was lowered by intracoronary abciximab in smokers (HR 0.28, 95% CI 0.06 to 0.66, p = 0.009), but was ineffective in nonsmokers (HR 1.04, 95% CI 0.54 to 2.00, p = 0.903). Interaction testing showed heterogeneity in treatment effect for reinfarction (p = 0.002) and stent thrombosis (p = 0.018) according to smoking status. In conclusion, among patients with STEMI undergoing primary PCI, smoking status did not affect the adjusted risk of clinical events. Intracoronary abciximab bolus improved clinical outcomes by reducing the risk of death or reinfarction. Sin financiación 3.398 JCR (2016) Q2, 47/126 Cardiac & Cardiovascular Systems UEC

Background Left ventricular dysfunction and the development of heart failure is a frequent and serious complication of myocardial infarction. Recent animal experimental studies suggested that metformin treatment reduces myocardial injury and preserves cardiac function in non-diabetic rats after experimental myocardial infarction. We will study the efficacy of metformin with the aim to preserve left ventricular ejection fraction in non-diabetic patients presenting with ST elevation myocardial infarction (STEMI). Methods The Glycometabolic Intervention as adjunct to Primary percutaneous intervention in ST elevation myocardial infarction (GIPS)-III trial is a prospective, single center, double blind, randomized, placebo-controlled trial. Three-hundred-and-fifty patients, without diabetes, requiring primary percutaneous coronary intervention (PCI) for STEMI will be randomized to metformin 500 mg twice daily or placebo treatment and will undergo magnetic resonance imaging (MRI) after 4 months. Major exclusion criteria were prior myocardial infarction and severe renal dysfunction. The primary efficacy parameter is left ventricular ejection fraction 4 months after randomization. Secondary and tertiary efficacy parameters include major adverse cardiac events, new onset diabetes and glycometabolic parameters, and echocardiographic diastolic function. Safety parameters include renal function deterioration and lactic acidosis. Conclusions The GIPS-III trial will evaluate the efficacy of metformin treatment to preserve left ventricular ejection fraction in STEMI patients without diabetes.

Multislice computed tomography (MSCT) has emerged as a noninvasive imaging modality allowing anatomical imaging of the heart. The presence of coronary artery stenosis can be reliably ruled out, without development of cardiovascular events on follow-up, which currently makes MSCT particularly useful for the evaluation of patients with chest pain and low-to-intermediate pretest likelihood of coronary artery disease. In addition, MSCT may be useful for guiding interventions such as those for cardiac valves or treating cardiac rhythm disorders. Since the technology behind MSCT continues to evolve at a rapid pace and the radiation doses decrease, further expansion of the applications of MSCT across the clinical practices is expected.

Background Our preliminary results showed that tenosynovial changes and decrease in grip strength are associated with the aromatase inhibitor-induced musculoskeletal syndrome (AIMSS). Here, we report the final results and assess the relationship between grip strength and body mass index (BMI). Patients and methods We conducted a prospective study including postmenopausal early breast cancer patients receiving either an aromatase inhibitor (AI) or tamoxifen. Primary end point was change from baseline in tenosynovial abnormalities. Secondary end points were changes from baseline in morning stiffness, intra-articular fluid and grip strength and its association with BMI. Results After 6 months of therapy, 74% [95% confidence interval (CI) 51% to 89%] of AI-treated patients had worsened tenosynovial abnormalities, 56% (95% CI 34% to 75%) had increased intra-articular fluid, and 22% (95% CI 9% to 45%) had increased morning stiffness. Grip strength decreased 8% for the left hand (95% CI 2% to 21%) and 11% for the right (95% CI 4% to 17%). Regression analysis suggested that grip strength decreased more for subjects with high or with low BMI. Conclusions AIMSS is characterized by tenosynovial changes, intra-articular fluid and morning stiffness. We hypothesize that the quadratic association between BMI and loss of grip strength reflects AI-induced changes on the endocrine control of the growth hormone insulin-like growth factor-I pathway.

Aims To evaluate non-invasive angiography using dual-source computed tomography (CT) for the determination of the most appropriate therapeutic strategy in patients with suspected coronary artery disease (CAD). Methods and results CT angiography (Dual Source CT, Somatom Definition, Siemens Medical Systems, Forchheim, Germany) was performed in 60 consecutive patients [51 men, median age 64 (57–70) years] scheduled for elective coronary angiography. Both techniques were used to evaluate the presence of CAD, significant stenosis, and the need for revascularization therapy. Sensitivity and specificity for the presence of significant stenosis were: per segment ( n = 766) 62% (95% CI 50–72) (64/104) and 79% (95% CI 74–84) (526/662), respectively; per patient ( n = 60) 100% (95% CI 91–100) (38/38) and 45% (95% CI 24–68) (10/22), respectively. In therapeutic decision-making based on CT angiography, sensitivity, specificity, positive and negative predictive values for intervention were 97% (95% CI 84–100) (36/37), 48% (95% CI 27–69) (11/23), 75% (95% CI 60–86) (36/48), and 92% (95% CI 60–100) (11/12), respectively. If a revascularization procedure was needed, the CT angiographic data indicated the appropriate modality (percutaneous coronary intervention or coronary artery bypass grafting) in 70% (26/36) of patients. Conclusion Although imaging qualities have improved considerably, CT angiography cannot be used for definitive therapeutic decision-making with regard to revascularization procedures in patients with suspected CAD.

Purpose: To explore the hypothesis that stent placement decreases dilator function of various arteries outside the stented segment and that angiotensin(1-7) improves this function, and to assess the contribution of dilator signal compounds. A further objective was to test the hypothesis that on-stent delivery of Ang-(1-7) reduces neointima formation and improves endothelial function. Methods. Abdominal aortic stenting or sham operation was performed in the rat four weeks after stenting and treatment with intravenous saline or Ang-(1-7) infusion (24 ug/kg/h); vasomotor function in isolated thoracic aorta and brachial and iliac artery was measured in organ baths. Furthermore, Ang-(1-7)-eluting stents were designed and placed in rat abdominal aorta. Neointima formation and aortic function were tested after four weeks. Results: Relaxation of the thoracic aorta to metacholine was decreased after stenting compared with shams due to a decrease in nitric oxide-mediated response (67% reduction in maximal NO-dependent response). Ang-(1-7)restored the response mainly through increased prostaglandin- and possibly also endothelial-derived hyperpolarising factor-mediated relaxation. Relaxation in the brachial artery decreased after stenting (maximal response dropped by 50%), whilst contractions to phenylephrine increased. Ang-(1-7) normalised vasomotor function. Iliac artery function remained unaltered after stenting but Ang-(1-7) increased maximal relaxations by 65%. Delivery of Ang-(1-7) by means of a drug-eluting stent improved endothelial function. Conclusion: Stenting differentially affects dilator and contractile function in various arterial beds. Ang-(1-7) both improves dilator function and normalises contractile function. Delivery of protective peptides such as Ang-(1-7) from the stent is a new therapy option that merits further development and exploration.

Objectives The objective of this study was to compare 2 manual thrombus aspiration catheters in unselected patients with ST-segment elevation myocardial infarction.Background Distal embolization is common during percutaneous coronary intervention in ST-segment elevation myocardial infarction and can induce impaired myocardial perfusion. Several aspiration thrombectomy devices have been introduced to prevent distal embolization, however, with conflicting clinical results. Currently, it is unclear to what extent this variance in outcome can be explained by device-related factors, such as internal lumen size.Methods We performed a prospective cohort study in which patients undergoing primary percutaneous coronary intervention were treated with a large-internal-lumen catheter (Diver, Invatec, Roncadelle, Italy). Outcomes were compared with a matched population of the Thrombus Aspiration during Percutaneous coronary intervention in Acute myocardial infarction Study (TAPAS) trial, in which patients were treated with a medium-sized catheter (Export, Medtronic, Minneapolis, Minnesota). A histopathological analysis was performed of retrieved material.Results A total of 160 patients, treated with the Diver (n = 80) or Export (n = 80) aspiration catheter, were enrolled. Effective thrombus aspiration was seen in 70.3% of the patients treated with the Diver catheter versus 81.8% with the Export catheter (p = 0.10) No significant difference was found in myocardial blush grade or electrocardiographic outcome between the 2 devices. Size distribution of retrieved thrombotic particles was similar per device. Erythrocyte-rich thrombi were found in 34.8% of the cases and were predominately seen in patients with low initial Thrombolysis In Myocardial Infarction flow grade (p = 0.008).Conclusions A larger internal lumen diameter does not result in retrieval of larger thrombotic particles, nor in improved angiographic or electrocardiographic outcomes. (J Am Coll Cardiol Intv 2008; 1:258-64) (C) 2008 by the American College of Cardiology Foundation

Background Controversy exists regarding the factors influencing the duration of work incapacity after surgically treated carpal tunnel syndrome (CTS). Aim To determine relevant factors related to return to work. Methods Surgical technique, clinical factors, demographic factors, other medical problems, psychosocial factors, work-related and economical factors were reviewed in patients operated on for CTS. Statistical multivariate analyses were performed to identify the baseline factors influencing the work incapacity period. Results A total of 107 cases were reviewed. Professional exposure to repetitive movements and heavy manual handling activity were associated with a longer return-to-work interval. The duration of work incapacity period was not significantly related to the socioprofessional category of the patient (self-employed or employee) or to the type of the procedure (open versus endoscopic surgery). Conclusion Work-related features have a more important influence on return to work than personal, pathological or surgical features.

Background —Inhibition of matrix metalloproteinase (MMP) activity after balloon angioplasty by intraperitoneal injection of batimastat reduces late lumen loss by inhibition of constrictive remodeling. In the present study, we investigated whether the oral MMP inhibitor marimastat inhibits constrictive remodeling in favor of neutral or expansive remodeling. Methods and Results —In 26 pigs, balloon dilation was performed in 101 peripheral arteries. Pigs were treated with marimastat or served as controls and were euthanized 42 days after intervention. Intravascular ultrasound was performed at all time points. Vessel area (VA) loss was assessed by calculating the change in VA at termination relative to after intervention. Arteries were divided in 3 categories: expansive remodeling (VA loss < −5%), neutral (−5% ≤ VA loss ≤ +5%), and constrictive remodeling (VA loss > +5%). In the marimastat group, a significant reduction (53%) of late lumen loss was observed that was fully explained by impaired constrictive remodeling. In the marimastat group, the prevalence of constrictive remodeling was reduced (38% versus 75% in the control group) in favor of not only neutral but also expansive remodeling (21% and 42% versus 4% and 21% in the control group, respectively, P Conclusions —Irrespective of the acute luminal gain by balloon dilation, the oral MMP inhibitor marimastat inhibited constrictive arterial remodeling in favor of both neutral and expansive remodeling.

Background —Arterial remodeling after balloon angioplasty has been recognized as a major determinant of restenosis. Perturbation of collagen metabolism might be important. After balloon injury, matrix metalloproteinase (MMP) expression is upregulated. We investigated the effect of Batimastat, a nonspecific MMP inhibitor, on late lumen loss, arterial remodeling, and neointima formation after balloon dilation. Methods and Results —In atherosclerotic iliac arteries of 12 Yucatan micropigs, balloon dilation was performed, with intravascular ultrasound and quantitative angiography used before and after balloon dilation and at 42-day follow-up. The animals were randomly divided into 2 groups, the Batimastat group (n=6) and the vehicle group (n=6). All animals were intraperitoneally injected with either Batimastat or a vehicle immediately after balloon dilation and at 2 weeks and 4 weeks after balloon dilation. Angiographic and echographic late lumen loss in the Batimastat group versus the vehicle group was 0.3±0.1 versus 0.8±0.1 mm ( P =0.01) and 2.2±0.5 versus 4.9±0.7 mm 2 ( P =0.004), respectively. Late media-bounded area loss was used as a measure of remodeling after balloon dilation and was 0.9±0.6 mm 2 in the Batimastat group compared with 3.8±0.8 mm 2 in the vehicle group ( P =0.003, mixed model analysis P =0.01). Neointima formation was 1.3±0.3 mm 2 in the Batimastat group and 1.0±0.2 mm 2 in the vehicle group ( P =0.542). Conclusions —Metalloproteinase inhibition by Batimastat significantly reduced late lumen loss after balloon angioplasty by inhibition of constrictive arterial remodeling, whereas neointima formation was not inhibited by MMP inhibition.

Trehalose is present as a free disaccharide in the cytoplasm of mycobacteria and as a component of cell-wall glycolipids implicated in tissue damage associated with mycobacterial infection. To obtain an overview of trehalose metabolism, we analysed data from the Mycobacterium tuberculosis genome project and identified ORFs with homology to genes encoding enzymes from three trehalose biosynthesis pathways previously characterized in other bacteria. Functional assays using mycobacterial extracts and recombinant enzymes derived from these ORFs demonstrated that mycobacteria can produce trehalose from glucose 6-phosphate and UDP-glucose (the OtsA-OtsB pathway) from glycogen-like alpha(1--4)-linked glucose polymers (the TreY-TreZ pathway) and from maltose (the TreS pathway). Each of the pathways was found to be active in both rapid-growing Mycobacterium smegmatis and slow-growing Mycobacterium bovis BCG. The presence of a disrupted treZ gene in Mycobacterium leprae suggests that this pathway is not functional in this organism. The presence of multiple biosynthetic pathways indicates that trehalose plays an important role in mycobacterial physiology.

Mycobacterium tuberculosis has innate resistance to a range of broad-spectrum antimicrobial agents. This may in part reflect the relative impermeability of the mycobacterial cell wall, but additional specific mechanisms may also be important. In the case of fosfomycin, it has been suggested that a key difference in the active site of the M. tuberculosis MurA enzyme might confer resistance. In Escherichia coli, fosfomycin covalently binds to a cysteine normally involved in the enzymic activity, while protein alignments predict an aspartate at this position in the M. tuberculosis MurA. In the present study, it is demonstrated that the wild-type M. tuberculosis MurA is indeed resistant to fosfomycin, and that it becomes sensitive following replacement of the aspartate residue in position 117 by a cysteine. In addition, the study illustrates the use of an inducible expression system in mycobacteria to allow functional characterization of an M. tuberculosis enzyme that is unstable during constitutive expression.

A recombinant plasmid isolated from a Mycobacterium fortuitum genomic library by selection for gentamicin and 2- N ′-ethylnetilmicin resistance conferred low-level aminoglycoside and tetracycline resistance when introduced into M. smegmatis . Further characterization of this plasmid allowed the identification of the M. fortuitum tap gene. A homologous gene in the M. tuberculosis H37Rv genome has been identified. The M. tuberculosis tap gene (Rv1258 in the annotated sequence of the M. tuberculosis genome) was cloned and conferred low-level resistance to tetracycline when introduced into M. smegmatis . The sequences of the putative Tap proteins showed 20 to 30% amino acid identity to membrane efflux pumps of the major facilitator superfamily (MFS), mainly tetracycline and macrolide efflux pumps, and to other proteins of unknown function but with similar antibiotic resistance patterns. Approximately 12 transmembrane regions and different sequence motifs characteristic of the MFS proteins also were detected. In the presence of the protonophore carbonyl cyanide m -chlorophenylhydrazone (CCCP), the levels of resistance to antibiotics conferred by plasmids containing the tap genes were decreased. When tetracycline accumulation experiments were carried out with the M. fortuitum tap gene, the level of tetracycline accumulation was lower than that in control cells but was independent of the presence of CCCP. We conclude that the Tap proteins of the opportunistic organism M. fortuitum and the important pathogen M. tuberculosis are probably proton-dependent efflux pumps, although we cannot exclude the possibility that they act as regulatory proteins.

To the Editor: Early risk stratification has the potential to play an important role in ST-elevation myocardial infarction (STEMI)1 patients who are to be treated with primary percutaneous coronary intervention (PCI). Several risk scores have been developed for STEMI patients; however, most risk scores require many variables, making them more difficult to use in clinical practice. The long-term prognostic value of biomarker measurements for glucose, N-terminal pro–brain type natriuretic peptide (NT-proBNP), and estimated glomerular filtration rate (eGFR) taken early after admission has recently been demonstrated for STEMI patients (1). Damman and coworkers have shown that a multimarker model including these biomarkers improved the prediction of mortality over that provided by established risk factors derived from the Thrombolysis In Myocardial Infarction (TIMI) score, which include age, body mass index, diabetes, hypertension, systolic blood pressure, heart rate, anterior myocardial infarction, and time to treatment (1, 2). Moreover, a simplified risk score developed with the 3 biomarkers identified low-, intermediate- and high-risk subgroups with respect to mortality. The best way to evaluate such a model is to perform an external validation study of the predictors in a new and independent …

The causative agents of leprosy and tuberculosis, Mycobacterium leprae and Mycobacterium tuberculosis, have a lipid-rich cell envelope which contributes to virulence and antibiotic resistance. Acyl coenzyme A carboxylase, which catalyzes the first committed step of lipid biosynthesis, consists in mycobacteria of two subunits, one of which is biotinylated. Genes from M. leprae and M. tuberculosis encoding a biotinylated protein have been cloned and sequenced. Analysis of the derived protein sequences demonstrated the presence of biotin-binding sites and putative ATP-bicarbonate interactions sites, consistent with the proteins having a biotin carboxylase function as well as their being biotin carrier proteins.

Objective— Shorter leukocyte telomeres are associated with atherosclerosis and predict future heart disease. The goal of the present study was to determine whether leukocyte telomere length is related to atherosclerotic plaque telomere length and whether it is associated with plaque characteristics or recurrence of disease. Methods and Results— Telomere length was measured by real-time quantitative polymerase chain reaction in atherosclerotic plaques and leukocytes in patients with carotid atherosclerosis undergoing carotid endarterectomy (n=684) and of leukocytes in age- and gender-balanced subjects without clinical atherosclerosis (n=780). Leukocyte telomere length was shorter in patients versus controls (0.99 [interquartile range (IQR): 0.79 to 1.26] versus 1.06 [0.80 to 1.39]; P =0.0007). Plaque telomeres were longer than leukocyte telomeres (1.42 [IQR: 1.21 to 1.77] versus 1.01 [IQR: 0.75 to 1.34]; P −6 ) and independent of age. Leukocyte and plaque telomere length were only weakly correlated (correlation coefficient r 2 =0.04, P =0.03). Patients, whose plaques showed marked macrophage infiltration and large lipid core, had longer plaque telomeres (1.61 [IQR: 1.32 to 2.04] versus 1.40 [IQR: 1.15 to 1.57]; P =0.006) and shorter leukocyte telomeres (0.88 [IQR: 0.75 to 1.20] versus 1.03 [IQR: 0.83 to 1.34]; P =0.02). Plaque telomere length was associated with restenosis 1 year after endarterectomy (OR 1.58±0.206; P =0.026 per SD decrease of plaque telomere length). Conclusion— Leukocyte telomere length is associated with the presence of atherosclerotic carotid plaques but is not a proxy for local plaque telomere length. Plaque telomere length is related to plaque characteristics and development of restenosis following endarterectomy.

We have constructed a cosmid vector, Tropist3, based on the λ, origin double-cos-site vector Lawrist4, which is designed for efficient cloning and mapping of genomic DNA. Tropist3 contains two cloning sites in addition to the Hind III and Bam HI sites present in Lawrist4; a SalI site allows cloning of Sau 3 AI partial digests following partial filling in of the ends, and a Pml I site is suitable for blunt-end cloning. Both these strategies reduce the chance of co-cloning two inserts. Tropist3 also contains Not I, PacI , Sac II and Kpn I sites flanking the cloning region; these allow most inserts to be excised cleanly and mapped by partial digestion followed by hybridization with short vector sequences which lie adjacent to the cloning sites. This will also be useful for recloning inserts into different vectors, or for cosmid sequencing projects.

The purposes of this study were to investigate whether, in patients with ST-segment elevation myocardial infarction (STEMI) and multivessel disease (MVD), percutaneous coronary intervention (PCI) should be confined to the culprit or also nonculprit vessels and, when performing PCI for nonculprit vessels, whether it should take place during primary PCI or staged procedures.A significant percentage of STEMI patients have MVD. However, the best PCI strategy for nonculprit vessel lesions is unknown.Pairwise and network meta-analyses were performed on 3 PCI strategies for MVD in STEMI patients: 1) culprit vessel only PCI strategy (culprit PCI), defined as PCI confined to culprit vessel lesions only; 2) multivessel PCI strategy (MV-PCI), defined as PCI of culprit vessel as well as ≥1 nonculprit vessel lesions; and 3) staged PCI strategy (staged PCI), defined as PCI confined to culprit vessel, after which ≥1 nonculprit vessel lesions are treated during staged procedures. Prospective and retrospective studies were included when research subjects were patients with STEMI and MVD undergoing PCI. The primary endpoint was short-term mortality.Four prospective and 14 retrospective studies involving 40,280 patients were included. Pairwise meta-analyses demonstrated that staged PCI was associated with lower short- and long-term mortality as compared with culprit PCI and MV-PCI and that MV-PCI was associated with highest mortality rates at both short- and long-term follow-up. In network analyses, staged PCI was also consistently associated with lower mortality.This meta-analysis supports current guidelines discouraging performance of multivessel primary PCI for STEMI. When significant nonculprit vessel lesions are suitable for PCI, they should only be treated during staged procedures.

The 236 U(n,f) cross section has been measured in the neutron energy region from 0.5eV to 25keV at the GELINA neutron facility of the IRMM in Geel, Belgium. A highly enriched 236 U sample was mounted back-to-back with a 10 B sample in the centre of a Frisch-gridded ionisation chamber; a control measurement was performed with a 235 U sample in the same configuration. Besides a dominant resonance at 5.45eV, for which a resonance analysis was performed, the next resonance (cluster) only occurs at about 1.3keV. It is demonstrated that the fission resonance integral and the thermal fission cross section adopted in all commonly used evaluated data libraries are too large by two orders of magnitude.

A case of soft tissue chondroma or extraskeletal chondroma is described. The tumour caused compression of the posterior interosseous nerve. Excision and biopsy were performed with complete resolution of the symptoms.

Oculo-dento-digital dysplasia (ODDD) is an autosomal dominant disorder characterized by developmental anomalies of the face, the eyes, the limbs and the teeth. Patients with ODDD usually present with complete syndactyly of the fourth and fifth fingers (type III syndactyly), ocular changes, abnormalities of primary and permanent dentition and specific craniofacial malformations. Mutations in GJA1, a gene that encodes the gap junction protein connexin 43, are responsible for ODDD. Gap junctions are assemblies of intercellular channels that allow exchange of various ions and signaling molecules between cells. In this way, gap junctions play an important regulatory role in a variety of physiologic and developmental processes. We identified three novel and one previously described GJA1 mutation in two large ODDD families and two sporadic ODDD cases.

Shewanella oneidensis couples anaerobic oxidation of lactate, formate, and pyruvate to the reduction of vanadium pentoxide (V V ). The bacterium reduces V V (vanadate ion) to V IV (vanadyl ion) in an anaerobic atmosphere. The resulting vanadyl ion precipitates as a V IV -containing solid.

Hox genes encode a highly conserved family of transcription factors with fundamental roles in body patterning during embryogenesis.1 Studies in mouse and chick have shown that the 5‘ HoxD and HoxA genes are critical for vertebrate limb and urogenital tract development.2 In humans, mutations in HOXD13 and HOXA13 cause the rare dominantly inherited limb malformation syndromes synpolydactyly (SPD, MIM 186000) and hand-foot-genital syndrome (HFGS, MIM 140000), respectively. SPD is characterised by syndactyly between the third and fourth fingers and between the fourth and fifth toes, with variable digit duplication in the syndactylous web. Most cases result from expansions of a polyalanine tract in the N-terminal region of HOXD13 3–6 but frameshifting deletions have been identified in three families with an atypical foot phenotype.7,8 HFGS is characterised by short thumbs and halluces, hypospadias in males, Mullerian duct fusion defects in females, and urinary tract malformations in both sexes. Most cases result from nonsense mutations in HOXA13 , but two polyalanine tract expansions and one missense mutation have also been described.9–11 Here we report two Belgian families, one with the first missense mutation to be identified in HOXD13 and the other with only the third polyalanine tract expansion to be identified in HOXA13. Remarkably, intermarriage between the two families has resulted in a girl heterozygous for both mutations, the first human HOXD13 / HOXA13 double heterozygote to be reported. Her digital abnormalities are strikingly more severe than those in carriers of each individual mutation, suggesting that the two mutations act synergistically. ### The proband The proband (fig 1) was born with severe bilateral hand abnormalities (fig 2A-F). She had complete cutaneous syndactyly between the third and fourth fingers, duplication of the distal and proximal phalanges of the fourth fingers, and a rudimentary extra central metacarpal. In addition, both …

A glomus tumour of the finger is a benign tumour that develops from the neuromyoarterial elements of the glomus body, which is a specialised arteriovenous anastomosis involved in thermoregulation. In this structure the arterioles that connect with venules have a thick layer of concentrically arranged epitheloid smooth muscle cells. Contraction of the layer of smooth muscle cells results in closure of the arteriovenous anastomosis and this will force blood to flow through the capillary network. Control of the function of the arteriovenous anastomoses is mainly neural. Most glomus tumours are localised in the distal phalanx. It is a small tumour with a subungual or pulpar localisation and with typical symptoms consisting of the triad pain, cold intolerance, and very localised tenderness.1 Most cases of phalangeal glomus tumours are solitary. A related condition called multiple glomuvenous malformations of the skin shows autosomal dominant inheritance2 and is linked to the chromosome 1p21-22 region.3 The abnormalities in the skin consist of cutaneous venous malformations with smooth muscle-like glomus cells. Recently the gene involved in this familial condition has been cloned and named glomulin.4 Glomuvenous malformations of the skin are clinically and aetiologically different from the sporadic glomus tumours of the distal phalanx. The jugular glomus tumours seen …

Item does not contain fulltext Molecular analysis of the reciprocal chromosomal translocation t(12;22)(p11.2;q13.3) cosegregating with a complex type of synpolydactyly showed involvement of an alternatively spliced exon of the fibulin-1 gene (FBLN1 located in 22q13.3) and the C12orf2 (HoJ-1) gene on the short arm of chromosome 12. Investigation of the possible functional involvement of the fibulin-1 protein (FBLN1) in the observed phenotype showed that FBLN1 is expressed in the extracellular matrix (ECM) in association with the digits in the developing limb. Furthermore, fibroblasts derived from patients with the complex type of synpolydactyly displayed alterations in the level of FBLN1-D splice variant incorporated into the ECM and secreted into the conditioned culture medium. By contrast, the expression of the FBLN1-C splice variant was not perturbed in the patient fibroblasts. Based on these findings, we propose that the t(12;22) results in haploinsufficiency of the FBLN1-D variant, which could lead to the observed limb malformations.

Background —Constrictive vascular remodeling (VR) is the most significant component of restenosis after balloon angioplasty (PTA). Whereas in physiological conditions VR is associated with normalization of shear stress (SS) and wall stress (WS), after PTA the role of SS and WS in VR is unknown. Furthermore, whereas matrix metalloproteinase inhibition (MMPI) has been shown to modulate VR after PTA, its effect on the SS and WS control mechanisms after PTA is unknown. Methods and Results —PTA was performed in external iliac arteries of 12 atherosclerotic Yucatan pigs, of which 6 pigs (7 vessels) received the MMPI batimastat and 6 pigs (10 vessels) served as controls. Before and after the intervention and at 6-week follow-up, intravascular ultrasound pullback was performed, allowing 3D reconstruction of the treated segment and computational fluid dynamics to calculate the media-bounded area and SS. WS was derived from the Laplace formula. Immediately after PTA, media-bounded area, WS, and SS changed by 20%, 16%, and −49%, respectively, in both groups. VR was predicted by SS and WS. In the control group, SS and WS had been normalized at follow-up with respect to the reference segment. In contrast, for the batimastat group, the SS had been normalized, but not the WS. The latter is attributed to an increase in wall area at follow-up. Conclusions —Vascular remodeling after PTA is controlled by both SS and WS. MMPI inhibited the WS control system.

The prognosis of patients with acute myocardial infarction (AMI) has been considerably improved following the introduction of reperfusion therapies. The primary aim in the acute phase of an AMI is rapid and sustained restoration of blood flow through the infarct-related artery. When logistically feasible, primary percutaneous coronary intervention (PCI) has emerged as the preferred reperfusion modality. Compared with balloon angioplasty, implantation of a bare metal stent (BMS) results in a lower rate of reocclusion and restenosis. Nevertheless, rates of target vessel revascularization after BMS implantation in patients with AMI range from 7 to 15%.1,2 The clinical presentation of the restenotic process is most often recurrence of angina, and is usually not associated with death or myocardial infarction. BMS eliminate elastic recoil and negative remodelling. However, they may induce marked neointima proliferation, resulting in in-stent restenosis. In elective PCI, drug-eluting stents (DES) have been shown to reduce neointima proliferation and thereby the risk of in-stent restenosis. These initial positive outcomes have resulted in widespread use of DES in high-risk patients, such as patients with AMI. Kastrati et al. have reported their findings on the use of DES for primary PCI.3 The authors have performed a careful meta-analysis of eight randomized controlled trials (RCTs), comparing DES with BMS in 2786 patients. Individual patient data were available from seven of the eight studies (2476 … *Corresponding author. Tel: +31 50 3611413; fax: +31 50 3614391. E-mail address : p.j.j.vlaar{at}thorax.umcg.nl

In the last year, following several publications in peer reviewed journals and presentations during the 2006 European Society of Cardiology congress,1 concerns have been raised about a possible increase in the incidence of death and myocardial infarction in patients treated with drug eluting stents (DESs) due to the occurrence of stent thrombosis. The incidence of stent thrombosis in the bare metal stent (BMS) era has become low after the introduction of dual antiplatelet therapy.2 Stent thrombosis in this setting is associated with persistent dissection, stent length, and final diameter.3 With paclitaxel and sirolimus-eluting stents, premature discontinuation of thienopyridine therapy has become the most important risk factor for stent thrombosis.4 In event-free patients 6 months after stent implantation, there was still an increase in death and/or myocardial infarction at 24 months follow-up in patients treated with DES without long-term thienopyridine therapy compared with DES with thienopyridine therapy.5 This impact on outcome of clopidogrel was not … *Corresponding author. Tel: +31 50 3611347; fax: +31 50 3611347. E-mail address : b.j.g.l.de.smet{at}thorax.umcg.nl

Brachyspira pilosicoli (formerly Serpulina pilosicoli) causes swine spirochaetosis and can also be isolated fro human faeces, although its role in human disease remains unclear. The genetic and biochemical variations amongst 19 isolates of human spirochaetes from five different countries were evaluated and compared to those found amongst swine isolates of B. pilosicoli. All isolates were negative for beta-glucosidase and all but one were positive for hippurate hydrolysis, which are characteristics typical of B. pilosicoli. The isolates showed variation in indole production and alpha-galactosidase and alpha-glucosidase activity, other characteristics which can be used to identify B. pilosicoli. The DNA sequences of part of the 16S rRNA gene differed from each other and from that of B. pilosicoli by 0-3 bp out of 283 bp. It is concluded that there is considerable variation amongst human intestinal spirochaetes. Since few of the isolates reported here match the current criteria for B. pilosicoli, it is concluded that this species is more heterogeneous than previously appreciated. However, it cannot be excluded that some isolates may belong to uncharacterized related Brachyspira/Serpulina species.

Objective: Remodeling in de novo atherosclerosis and in restenosis after balloon angioplasty constitutes a change in total arterial circumference which, together with plaque growth or neointimal formation, determines the lumen of the artery. To better understand the fundamental biology of neointimal formation, remodeling and their interaction, animal studies are needed. In this study, we described in detail the methodology used and the natural history of neointimal formation and remodeling after balloon angioplasty in atherosclerotic Yucatan micropigs. Methods and results: Atherosclerosis was induced in 60 peripheral arteries of sixteen Yucatan micropigs by a combination of denudation and atherogenic diet. Balloon angioplasty was performed in 38 arteries, with serial intravascular ultrasound (IVUS) and quantitative angiography before and after intervention and at 2, 4, 7, 14 or 42 days follow-up. Remodeling, expressed as late media-bounded area (MBA) loss, increased progressively over time. At 42 days, late MBA loss after balloon angioplasty was significantly different compared to late MBA loss in control arteries, 2.2±1.0 versus −0.3±1.1 mm2 and p =0.02. Late lumen loss increased over time and was highest at 42 days after balloon angioplasty (2.8±0.7 mm2). The contribution of neointimal formation to late lumen loss decreased over time and the contribution of late MBA loss to late lumen increased over time and was highest at 42 days (78%). Medial necrosis was 48% at two days after balloon angioplasty and the repopulation of the media was almost completed at seven days. Conclusion: Remodeling following balloon angioplasty has an early onset and progresses with neointimal formation to cause restenosis over the standard 42-day time course for Yucatan micropigs. This correlates to six months renarrowing in humans. In this model, atherosclerosis and the natural history of restenosis, both with respect to neointimal formation and remodeling, resemble the human disease quite closely.

The nucleotide sequence and mechanism of action of a tetracycline resistance gene from Mycobacterium smegmatis were determined. Analysis of a 2.2-kb sequence fragment showed the presence of one open reading frame, designated tet (V), encoding a 419-amino-acid protein (molecular weight, 44,610) with at least 10 transmembrane domains. A database search showed that the gene is homologous to membrane-associated antibiotic efflux pump proteins but not to any known tetracycline efflux pumps. The steady-state accumulation level of tetracycline by M. smegmatis harboring a plasmid carrying the tet (V) gene was about fourfold lower than that of the parental strain. Furthermore, the energy uncoupler carbonyl cyanide m -chlorophenylhydrazone blocked tetracycline efflux in deenergized cells. These results suggest that the tet (V) gene codes for a drug antiporter which uses the proton motive force for the active efflux of tetracycline. By primer-specific amplification the gene appears to be restricted to M. smegmatis and M. fortuitum .

Abstract —Geometric remodeling in de novo atherosclerosis and in restenosis after balloon angioplasty constitutes a change in total arterial circumference that, together with plaque growth or neointima formation, determines the lumen of the artery. The heterogeneous nature of arterial obstructions raises the question of whether early and late outcomes (restenosis) of angioplasty are affected by the degree and direction of de novo atherosclerotic remodeling. This study was designed to assess the relationship between atherosclerotic remodeling and the degree and mechanism of restenosis after balloon angioplasty. Atherosclerosis was induced in 27 peripheral arteries of 18 Yucatan micropigs by a combination of denudation and atherogenic diet. Balloon angioplasty was performed, with serial intravascular ultrasound and quantitative angiography before and after intervention and at 42 days’ follow-up. We used the relative media-bounded area (MBA), defined as the MBA of the treated site divided by the MBA of the reference, before angioplasty as a measure of remodeling in de novo atherosclerosis and late MBA loss as a measure of remodeling after balloon angioplasty. Relative MBA before angioplasty was not correlated with angiographic and echographic acute gain after balloon angioplasty ( r= .22, P =.28 and r= .14, P =.48) or with late lumen loss ( r= −.05, P =.81 and r= .19, P =.33). No correlation was found between relative MBA and late MBA loss ( r= .14 and P =.48). In the atherosclerotic Yucatan micropig, remodeling during de novo atherosclerosis has no relevance for acute gain and late lumen loss after balloon angioplasty. Both the direction and the extent of remodeling after balloon angioplasty are not related to the direction and extent of remodeling during de novo atherosclerosis.

Background Recent studies have indicated that coronary restenosis after balloon angioplasty is the sum of geometric remodeling and neointimal formation. A proportional relationship between acute gain and late lumen loss has been observed in clinical trials. The aims of this study were to evaluate (1) the contribution of geometric remodeling and neointimal formation to the proportional gain-loss relationship after PTA or stenting and (2) the relationship between geometric remodeling and neointimal formation. Methods and Results In atherosclerotic iliac arteries of 29 Yucatan micropigs, PTA or stenting was performed, with serial intravascular ultrasound (IVUS) and quantitative angiography before and after intervention and at 2 or 42 days of follow-up, followed by histomorphometrical analysis. For PTA at 42 days, late lumen loss by IVUS correlated strongly with geometric remodeling, expressed as late media-bounded area (MBA) loss ( R 2 =.843, P R 2 =.214, P =.02). For stented arteries, however, late lumen loss correlated moderately with intimal hyperplasia ( R 2 =.367, P =.01, n=18) and only weakly with geometric remodeling ( R 2 =.195, P =.04). Late lumen loss and late MBA loss of reference segments were observed at 42 days, especially in PTA arteries. Intimal hyperplasia and geometric remodeling were not correlated. Conclusions In this experimental model, the proportional relationship between acute gain and late lumen loss is mainly due to the proportional relationship between acute gain and geometric remodeling for PTA and between acute gain and intimal hyperplasia for stents. Finally, neointimal formation and remodeling seem to be unrelated processes.

Summary: Sequencing 280 bp of the internal transcribed spacer (ITS) between the 16S and 23S rRNA genes in a collection of 46 clinical isolates of the Mycobacterium avium-intracellulare complex (MAI complex) identified nine different sequences, grouping these isolates in nine ‘ITS sequevars’. This analysis extends the subdivision within the MAI complex to 18 ITS sequevars and also improves discrimination from other mycobacterial species. Evaluation of the sequevar grouping among different clinical sources revealed strong association of the M. avium sequevar Mav-B with AIDS and with lymphadenitis in children (18 out of 20 and 3 out of 3 respectively). Isolates from elderly patients with pulmonary disease and not suspected of being HIV infected belonged predominantly to M. intracellulare ITS sequevars and sequevars not assigned to either M. avium or M. intracellulare. On the other hand, animal isolates were of both the Mav-A and Mav-B sequevars. We conclude that ITS sequevar typing is an accurate way of identifying distinct MAI complex strains. The observed differences between clinical sources suggest that ITS sequevars reflect possibly important, biologically and clinically relevant polymorphisms between MAI complex organisms.

Objectives The aim of this study was to perform an individual patient-level pooled analysis of randomised trials, comparing intracoronary versus intravenous abciximab bolus use in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI). Background Abciximab represents a cornerstone in the treatment of STEMI patients undergoing primary PCI. Intracoronary abciximab bolus administration has been proposed as an alternative strategy to the standard intravenous route. However, whether intracoronary abciximab effectively improves clinical outcomes compared with standard route remains unknown. Methods Individual data of 1198 patients enrolled in five trials were entered into the pooled analysis. The primary endpoint of the study was the occurrence of all-cause death and reinfarction at 30-day follow-up. Secondary endpoints were all-cause death, reinfarction and target-vessel revascularisation (TVR). Results No significant heterogeneity was found across trials. Compared with the intravenous route, intracoronary abciximab administration significantly reduced the risk of the composite of death and reinfarction (HR 0.52, 95% CI 0.29 to 0.94; p=0.03), death (HR 0.44, 95% CI 0.20 to 0.95; p=0.04) and TVR (HR 0.53, 95% CI 0.29 to 0.99; p=0.045), without a significant impact on the risk of reinfarction (HR 0.54, 95% CI 0.24 to 1.21; p=0.13). However, after correction for baseline differences, only the composite of death/reinfarction and death remained significant. Conclusions In STEMI patients undergoing primary PCI, intracoronary abciximab administration, when compared with the intravenous standard route, can improve short-term clinical outcomes mainly by reducing the risk of death.

Chromosome investigation in six localized forms of tenosynovial giant cell tumors, also known as modular tenosynovitis, revealed an identical translocation between chromosomes 1 and 2, t(1;2)(p11;q35-36) in three tumors, a variant translocation t(1;5)(p11;q22) in a fourth case, and a t(2;16)(q33;q24) in a fifth case. One case showed a normal karyotype. Although morphologically rather uniform, these benign tumors appear to be cytogenetically heterogeneous, but the chromosome changes seem to cluster in 2 regions, 1p11 and 16q24.