Academic literature on the topic 'MI 24030'

The aim of the article is to analyze and evaluate the effect of dual-fuel feed on diesel and natural gas on Indicated Engine Ignition Indicators Perkins 1104D-E44TA. The actual indicator diagrams prepared during engine operation according to the external speed characteristic in the engine crankshaft speed range from 1000 to 2400 rpm were analyzed. On the basis of the average pressure courses in the cylinder, open indicator diagrams were made, which were then analyzed. The operating parameters of the tested motor were determined as: average indicated pressure pi, average effective pressure pe, indicated power Ni, indicated torque Mi, indicated efficiency ηi, mechanical efficiency ηm, and unit-specific fuel consumption gi.

Advances in the field of Brain-Computer Interfaces (BCIs) aim, among other applications, to improve the movement capacities of people suffering from the loss of motor skills. The main challenge in this area is to achieve real-time and accurate bio-signal processing for pattern recognition, especially in Motor Imagery (MI). The significant interaction between brain signals and controllable machines requires instantaneous brain data decoding. In this study, an embedded BCI system based on fist MI signals is developed. It uses an Emotiv EPOC+ Brainwear®, an Altera SoCKit® development board, and a hexapod robot for testing locomotion imagery commands. The system is tested to detect the imagined movements of closing and opening the left and right hand to control the robot locomotion. Electroencephalogram (EEG) signals associated with the motion tasks are sensed on the human sensorimotor cortex. Next, the SoCKit processes the data to identify the commands allowing the controlled robot locomotion. The classification of MI-EEG signals from the F3, F4, FC5, and FC6 sensors is performed using a hybrid architecture of Convolutional Neural Networks (CNNs) and Long Short-Term Memory (LSTM) networks. This method takes advantage of the deep learning recognition model to develop a real-time embedded BCI system, where signal processing must be seamless and precise. The proposed method is evaluated using k-fold cross-validation on both created and public Scientific-Data datasets. Our dataset is comprised of 2400 trials obtained from four test subjects, lasting three seconds of closing and opening fist movement imagination. The recognition tasks reach 84.69% and 79.2% accuracy using our data and a state-of-the-art dataset, respectively. Numerical results support that the motor imagery EEG signals can be successfully applied in BCI systems to control mobile robots and related applications such as intelligent vehicles.

Background:Cardiovascular (CVS) diseases are the leading cause of death worldwide and patients with rheumatic diseases have an increased CVS risk including stroke and myocardial infarction (MI) (1-3). CVS risk factors and CVS events are common in SpA (4). Delineating the CVS risk and the association with medications in patients with SpA would be useful.Objectives:The objective of this study was to delineate the CVS risk and the association with medications in patients with SpA.Methods:Patients with SpA and patients with non-specific back pain (NSBP) were identified in rheumatology and orthopedics clinics respectively. Clinical information and CVS events were retrieved. Incidence rates were calculated. Association analysis was performed to determine the CVS risk of SpA and other modifiable risk factors.Results:A total of 5046 patients (SpA 2616 and NSBP 2430) were included from eight centers. Over 56 484 person-years of follow-up, 160 strokes, 84 MI and 262 major adverse cardiovascular events (MACE) were identified. Hypercholesterolemia was more prevalent in SpA (SpA 34.2%, NSBP 28.7%, P<0.01). Crude incidence rates of stroke and MI were higher in SpA patients. SpA was associated with a higher risk of MACE (HR 1.66, 95%CI 1.22-2.27, P<0.01) and cerebrovascular events (HR 1.42, 95%CI 1.01-2.00, p=0.04). The use of anti-tumor necrosis factor (TNF) drugs was associated with a reduced risk of MACE (HR 0.37, 95%CI 0.17-0.80, P=0.01) and cerebrovascular events (HR 0.21, 95%CI 0.06-0.78, P=0.02).Conclusion:SpA is an independent CVS risk factor. Anti-TNF drugs were associated with a reduced CVS risk in these patients.References:[1]Crowson CS, Liao KP, Davis JM, 3rd, Solomon DH, Matteson EL, Knutson KL, et al. Rheumatoid arthritis and cardiovascular disease. Am Heart J. 2013;166(4):622-8 e1.[2]Verhoeven F, Prati C, Demougeot C, Wendling D. Cardiovascular risk in psoriatic arthritis, a narrative review. Joint Bone Spine. 2020;87(5):413-8.[3]Liew JW, Ramiro S, Gensler LS. Cardiovascular morbidity and mortality in ankylosing spondylitis and psoriatic arthritis. Best Pract Res Clin Rheumatol. 2018;32(3):369-89.[4]Molto A, Etcheto A, van der Heijde D, Landewe R, van den Bosch F, Bautista Molano W, et al. Prevalence of comorbidities and evaluation of their screening in spondyloarthritis: results of the international cross-sectional ASAS-COMOSPA study. Ann Rheum Dis. 2016;75(6):1016-23.Disclosure of Interests:None declared.

Background: Cardiovascular (CVS) diseases are the leading cause of death worldwide and patients with rheumatic diseases have an increased CVS. CVS risk factors and CVS events are common in spondyloarthritis (SpA). Delineating the CVS risk in patients with SpA and identifying modifiable risk factors would be useful. Methods: Patients with SpA and patients with non-specific back pain (NSBP) were identified in rheumatology and orthopedics clinics, respectively. Clinical information and CVS events were retrieved. Baseline characteristics and incidence rates of CVS events were compared between two groups of patients using an age- and sex-matched cohort. Propensity score adjustment and Cox regression analysis were performed to determine the CVS risk associated with SpA. Results: A total of 5046 patients (SpA 2616 and NSBP 2430) were included from eight centers. Over 56,484 person-years of follow up, 160 strokes, 84 myocardial infarction (MI) and 262 major adverse cardiovascular events (MACE) were identified. Hypercholesterolemia was more prevalent in SpA (SpA 34.2%, NSBP 28.7%, p < 0.01). Crude incidence rates of MACE and stroke were higher in SpA patients. SpA was associated with a higher risk of MACE [hazard ratio (HR) 1.70; 95% confidence interval (CI) 1.29–2.26; p < 0.01] and cerebrovascular events (HR 1.50; 95% CI 1.08–2.07; p = 0.02). SpA patients with anti-TNF use had a reduced risk of MACE (HR 0.37, 95%CI 0.17–0.80, p = 0.01) and cerebrovascular events (HR 0.21, 95%CI 0.06–0.78, p = 0.02) compared with SpA patients without anti-TNF use. Conclusion: SpA is an independent CVS risk factor. Anti-tumor necrosis factor (TNF) drugs were associated with a reduced CVS risk in these patients.

3557 Background: Cetuximab, an IgG1 monoclonal antibody targeting the EGFR, is currently approved for second line treatment of metastatic colorectal cancer (CRC). This phase II trial was designed to evaluate the safety and efficacy of cetuximab combined with FOLFOX6 as first line therapy in this patient population. Promising results have been reported at ESMO in a similar small pilot study. Methods: Eligibility: Age ≥ 18, locally advanced or metastatic CRC, no prior therapy for advanced disease, EGFR expression positive or undetectable. Regimen: Cetuximab 400 mg/M2 (2 hour infusion) day 1; 250 mg/M2 day 8 (and 250 mg/M2 for all subsequent doses); and modified FOLFOX 6 (2 hour infusion); and 5FU bolus 400 mg/M2 day 1 followed by 5FU-CI 2400 mg/M2 over 46 hours (days 1 and 2). Cycles were repeated every 14 days. Results: 82 patients were enrolled in the study. The median number of treatment cycles administered was 8. (range 1–28) At the time of this report, 23 patients are still on study. Reasons for discontinuation of therapy included: Toxicity (14 patients), disease progression (20), investigator /patient decision (11), planned therapy completed (3). Five patients (6%) died on study. Causes of death included: PD (2 patients), acute MI (1), respiratory failure secondary to pneumonia (1), sudden death of unknown cause (1). The most frequently observed toxicity was neutropenia. Grade 3/4 toxicities are listed in the table below. At this early analysis time point, 32 of 60 patients evaluable for response have documented CR/PR (3 CR, 29 PR, overall response rate of 53%). A pre-meeting update is planned for presentation purposes. Conclusion: These findings suggest that the combination of cetuximab with FOLFOX6 is safe and active in first line treatment of patients with metastatic CRC. Updated efficacy and safety data will be presented. [Table: see text] No significant financial relationships to disclose.

3506 Background: This multicenter, randomized study assessed efficacy & safety for 3 irinotecan/fluoropyrimidines combinations in previously untreated mCRC. In a 3 × 2 factorial design, we also assessed whether celecoxib added to chemotherapy (CT) improved CT efficacy and/or reduced toxicity. Methods: Pts were randomized to: FOLFIRI - irinotecan (I) 180 mg/m2, leucovorin (LV) 400 mg/m2, 5-FU bolus 400 mg/m2, & infusional 5-FU 2400 mg/m2 over 46 hours q 2 wks; modified IFL (m-IFL) - I 125 mg/m2, LV 20 mg/m2, & bolus 5-FU 500 mg/m2 wkly × 2, q 3 wks; or CapeIri - I 250 mg/m2 day 1 & capecitabine 1000 mg/m2 po BID × 14 days, q 3 wks. Pts were also randomized to concurrent celecoxib (400 mg po BID) or placebo in a double-blind fashion. Time to progression (TTP) was the primary endpoint. Results: 430 pts were enrolled from 2/03 to 4/04, prior to an amendment that added bevacizumab to CT arms. Baseline characteristics were balanced. TTP for FOLFIRI (median = 8.2 mos) was significantly better than for either m-IFL (6.0 mos; p = 0.01) or CapeIri (5.7 mos; p = 0.01). Overall survival (OS) also favored FOLFIRI (median = 23.1 mos) compared to either m-IFL (17.6 mos; p=0.10) or CapeIri (18.8 mos; p = 0.19). Common grade ≥ 3 toxicities are listed below. CapeIri had the highest rates of nausea, vomiting, diarrhea, dehydration & hand-foot syndrome, whereas FOLFIRI had lower rates. Among all 430 pts, median TTP did not differ for pts randomized to celecoxib compared to placebo (6.9 vs 6.9 mos; p=0.71). Median OS was also similar for celecoxib vs placebo (19.5 vs 18.8 mos; p=0.63). CT toxicities did not differ for celecoxib vs placebo. Rates for MI/stroke were 1.5% for celecoxib and 1.9% for placebo. Conclusions: First-line FOLFIRI offers a superior TTP when compared to m-IFL or CapeIri; OS & toxicity analyses also favored FOLFIRI. Celecoxib neither improved CT efficacy nor reduced CT toxicity. Updated survival data & data on pts enrolled after the addition of bevacuzimab will be presented. [Table: see text] [Table: see text]

533^ Background: Vascular endothelial growth factor (VEGF) and the VEGF receptor-2 (VEGFR-2) are overexpressed in CRC and mediate angiogenesis. Ramucirumab (RAM; IMC-1121B) is a fully human IgG1 MAb that inhibits binding of VEGF ligands to VEGFR-2 and inhibits VEGFR-2 activation and signaling. In preclinical CRC models VEGFR-2 inhibition confers antitumor activity. RAM was administered with mFOLFOX-6 as 1st-line therapy (rx) in mCRC. Methods: Eligible pts had mCRC with no prior chemo Rx (prior adjuvant rx was allowed), at least 1 measurable target lesion by RECIST v1.0, ECOG PS 0-1, and adequate organ function. Pts received RAM (8 mg/kg IV on D1), oxaliplatin (85 mg/m² IV on D1), folinic acid (400 mg/m² IV on D1), fluorouracil (5-FU, 400 mg/m² bolus followed by 2400 mg/m² continuous infusion over 46 hours on D1). Rx cycles were q2w and tumor assessments were q8w. Endpoints included progression-free survival (PFS), objective response rate (ORR), overall survival (OS), safety, and pharmacokinetics/immunogenicity. Sample size was based on an improved median (medn) PFS from 8 to 11 months (m). Results: 48 pts received therapy. All were white; 25 M/23 F; median age 60.5 y. ECOG PS was 0/1 in 30/18 pts. 42 pts (88%) had metastatic disease, with liver (79%) and lung (35%) as most frequent sites. 13 (27%) pts had liver-only mCRC. The most frequently observed RAM-related adverse events (AEs) included hypertension 46% (15% Grade [G] ≥3); diarrhea 31% (2% G≥3); and nausea and infusion-related reactions, each 19% (0% G≥3). 2 pts died on study due to acute MI or cardiopulmonary arrest. Medn PFS was 11.5 m (9-13 m 95% CI) with 1-yr PFS of 48% (32-62% 95% CI). ORR: 67% (52-80% 95% CI); disease control rate (DCR: CR+PR+SD): 94% (83-99% 95% CI; 5 pts had CR, 27 had PR and 13 had SD). Medn duration of response was 11.0 m (7-12 m 95% CI). One-year OS was 85% (72-93% 95% CI). As of 4/15/2011, 2 pts continued to receive rx, 20 had died and 28 (58.3%) remained alive. Conclusions: RAM combined with mFOLFOX-6 was reasonably tolerated in pts with mCRC. Median PFS exceeds 11 m. PFS, ORR, and DCR are encouraging and favor investigation of this regimen and of RAM in mCRC.

Background:Knowledge of changes over time in baseline characteristics and tumor necrosis factor inhibitor (TNFi) response in bio-naïve axial spondyloarthritis (axSpA) patients treated in routine care is limited.Objectives:To investigate secular trends in baseline characteristics and retention, remission and response rates in axSpA patients initiating a first TNFi.Methods:Prospectively collected data on bio-naïve axSpA patients starting TNFi in routine care from 15 European countries were pooled. According to year of TNFi initiation, three groups were defined a priori based on bDMARD availability: Group A (1999–2008), Group B (2009–2014) and Group C (2015–2018). Retention rates (Kaplan-Meier), crude and LUNDEX adjusted1 remission (Ankylosing Spondylitis Disease Activity Score (ASDAS) <1.3, Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) <20) and response (ASDAS Major and Clinically Important Improvement (MI/CII), BASDAI 50) rates were assessed at 6, 12 and 24 months. No statistical comparisons were made.Results:In total, 27189 axSpA patients were included (5945, 11255 and 9989 in groups A, B and C).At baseline, patients in group A were older, had longer disease duration and a larger proportion of male and HLA-B27 positive patients compared to B and C, whereas disease activity was similar across groups.Retention rates at 6, 12 and 24 months were highest in group A (88%/81%/71%) but differed little between B (84%/74%/64%) and C (85%/76%/67%).In all groups, median ASDAS and BASDAI had decreased markedly at 6 months (Table 1). The ASDAS values at 12 and 24 months and BASDAI at 24 months were higher in group A compared with groups B and C. Similarly, crude remission and response rates were lowest in group A. After adjustments for drug retention (LUNDEX), remission and response rates showed less pronounced between-group differences regarding ASDAS measures and no relevant differences regarding BASDAI measures.Conclusion:Nowadays, axSpA patients initiating TNFi are younger with shorter disease duration and more frequently female and HLA-B27 negative than previously, while baseline disease activity is unchanged. Drug retention rates have decreased, whereas crude remission and response rates have increased. This may indicate expanded indication but also a stable disease activity threshold for TNFi initiation over time, an increased focus on targeting disease remission and more available treatment options.References:[1]Arthritis Rheum 2006; 54: 600-6.Table 1.Secular trends in baseline characteristics, treatment retention, remission and response rates in European axSpA patients initiating a 1st TNFiBaseline characteristicsGroup A(1999–2008)Group B(2009–2014)Group C(2015–2018)Age, years, median (IQR)57 (49–66)51 (42–60)46 (37–56)Male, %666057HLA-B27, %877772Years since diagnosis, median (IQR)5 (1–12)2 (0–8)2 (0–7)Smokers, %232425ASDAS, median (IQR)3.5 (2.8–4.1)3.4 (2.8–4.1)3.5 (2.8–4.1)BASDAI, median, (IQR)57 (42–71)59 (43–72)57 (41–71)TNFi drug, % (Adalimumab /Etanercept / Infliximab /Certolizumab / Golimumab)22 / 35 / 43 / 0 / 037 / 21 / 20 / 4 / 1827 / 28 / 24 / 8 / 13Follow up6 months12 months24 monthsGr AGr BGr CGr AGr BGr CGr AGr BGr CRetention rates, %, (95% CI)88 (88–89)84 (83–85)85 (84–86)81 (80–82)74 (74–75)76 (75–76)71 (70–72)64 (63–65)67 (66–68)ASDAS, median, (IQR)1.8 (1.2–2.8)1.9 (1.2–2.8)1.8 (1.2–2.6)1.9 (1.3–2.6)1.7 (1.2–2.5)1.6 (1.1–2.4)1.9 (1.4–2.6)1.7 (1.1–2.4)1.5 (1.1–2.2)ASDAS inactive disease, %, c/L28 / 2528 / 2430 / 2624 / 1932 / 2434 / 2623 / 1634 / 2039 / 23ASDAS CII, %, c/L57 / 5159 / 5063 / 5461 / 5063 / 4767 / 5159 / 4168 / 4074 / 45ASDAS MI, %, c/L31 / 2732 / 2737 / 3232 / 2637 / 2741 / 3130 / 2042 / 2546 / 28BASDAI, median, (IQR)23 (10–40)26 (11–48)24 (10–44)21 (10–38)23 (10–42)20 (8–39)22 (9–40)20 (8–39)16 (6–35)BASDAI remission, %, c/L44 / 4040 / 3443 / 3645 / 3645 / 3450 / 3844 / 3048 / 2956 / 34BASDAI 50 response, %, c/L53 / 4750 / 4253 / 4557 / 4656 / 4258 / 4457 / 3960 / 3563 / 38Gr, Group; c/L, crude/LUNDEX adjusted.Acknowledgements:Novartis Pharma AG and IQVIA for supporting the EuroSpA Research Collaboration Network.Disclosure of Interests:Lykke Midtbøll Ørnbjerg Grant/research support from: Novartis, Sara Nysom Christiansen Speakers bureau: BMS and GE, Grant/research support from: Novartis, Simon Horskjær Rasmussen: None declared, Anne Gitte Loft Speakers bureau: AbbVie, Janssen, Lilly, MSD, Novartis, Pfizer, UCB, Consultant of: AbbVie, Janssen, Lilly, MSD, Novartis, Pfizer, UCB, Grant/research support from: Novartis, Ulf Lindström: None declared, Jakub Zavada: None declared, Florenzo Iannone: None declared, Fatos Onen: None declared, Michael J. Nissen Speakers bureau: Novartis, Eli Lilly, Celgene, and Pfizer, Consultant of: Novartis, Eli Lilly, Celgene, and Pfizer, Brigitte Michelsen Consultant of: Novartis, Grant/research support from: Novartis, Maria Jose Santos Speakers bureau: AbbVie, Novartis, Pfizer, Gary Macfarlane Grant/research support from: GlaxoSmithKline, Dan Nordström Consultant of: Abbvie, BMS, MSD, Novartis, Pfizer, Roche, UCB, Manuel Pombo-Suarez: None declared, Catalin Codreanu Speakers bureau: AbbVie, Amgen, Egis, Novartis, Pfizer, UCB, Grant/research support from: AbbVie, Amgen, Egis, Novartis, Pfizer, UCB, Matija Tomsic Speakers bureau: Abbvie, Amgen, Biogen, Medis, MSD, Novartis, Pfizer, Consultant of: Abbvie, Amgen, Biogen, Medis, MSD, Novartis, Pfizer, Irene van der Horst-Bruinsma Speakers bureau: Abbvie, BMS, MSD, Novartis, Pfizer, Lilly, UCB, Björn Gudbjornsson Speakers bureau: Amgen and Novartis, Johan Askling: None declared, Bente Glintborg Grant/research support from: Pfizer, Biogen, AbbVie, Karel Pavelka Speakers bureau: AbbVie, Roche, MSD, UCB, Pfizer, Novartis, Egis, Gilead, Eli Lilly, Consultant of: AbbVie, Roche, MSD, UCB, Pfizer, Novartis, Egis, Gilead, Eli Lilly, Elisa Gremese: None declared, Nurullah Akkoc: None declared, Adrian Ciurea Speakers bureau: Abbvie, Eli-Lilly, MSD, Novartis, Pfizer, Eirik kristianslund: None declared, Anabela Barcelos: None declared, Gareth T. Jones Grant/research support from: Pfizer, AbbVie, UCB, Celgene, Amgen, GSK, Anna-Mari Hokkanen Grant/research support from: MSD, Carlos Sánchez-Piedra: None declared, Ruxandra Ionescu Speakers bureau: Abbvie, Amgen, Boehringer-Ingelheim Eli-Lilly,Novartis, Pfizer, Sandoz, UCB, Ziga Rotar Speakers bureau: Abbvie, Amgen, Biogen, Medis, MSD, Novartis, Pfizer, Consultant of: Abbvie, Amgen, Biogen, Medis, MSD, Novartis, Pfizer, Marleen G.H. van de Sande: None declared, Arni Jon Geirsson: None declared, Mikkel Østergaard Speakers bureau: AbbVie, BMS, Boehringer-Ingelheim, Celgene, Eli-Lilly, Centocor, GSK, Hospira, Janssen, Merck, Mundipharma, Novartis, Novo, Orion, Pfizer, Regeneron, Schering-Plough, Roche, Takeda, UCB and Wyeth, Consultant of: AbbVie, BMS, Boehringer-Ingelheim, Celgene, Eli-Lilly, Centocor, GSK, Hospira, Janssen, Merck, Mundipharma, Novartis, Novo, Orion, Pfizer, Regeneron, Schering-Plough, Roche, Takeda, UCB and Wyeth, Merete L. Hetland Speakers bureau: Abbvie, Biogen, BMS, Celltrion, Eli Lilly, Janssen Biologics B.V, Lundbeck Fonden, MSD, Pfizer, Roche, Samsung Biopies, Sandoz, Novartis.

BACKGROUND : We significantly reduced door-to-balloon-time (DBT) after instituting prehospital cath lab activation for STEMI, without EKG transmittal or MD involvement. OBJECTIVE: To study the effect of the protocol on DBT in normal workday hours (cath lab team is in-house) vs. after-hours (cath lab team is not in-house). METHODS : For all STEMI patients (pts), data are collected prospectively. Since 2001 all pts transported by our institution’s EMS, with symptoms suggesting MI, have had prehospital EKG. In April 2005, we started the following additional protocol (with no other changes in our acute MI program): if the chief complaint is Chest Pain and the Zoll® M Series Interpretive EKG (Marquette 12SL algorithm) reads ``**Acute MI**,” Paramedics call the ED unit coordinator from the scene to activate the cath lab without MD involvement. For all EMS transported pts from Jan 2004 to Jan 2007, we analyzed demographics, symptoms, Zoll interpretation, door-to-EKG-time, and DBT. We compared the time saved before and after protocol change for normal workday hours vs. after hours. Statistics were by Kruskal Wallis and the two-tailed Fisher Exact test. RESULTS: There were 104 patients with STEMI transported in the time period. 36 were excluded: 26 with no chest pain (14 cardiac arrest), 8 with a non-diagnostic Zoll EKG and 2 others. Of 68 eligible patients (65% of all STEMI), 36 had prehospital activation (20 workday, 16 after hours) and 32 did not get prehospital activation (12 Workday and 20 after hours). See table for results. Overall mean DBT was reduced from 86.0 ± 9.6 (CI) min. in the before group to 56.1 ± 7.7 min. in the prehospital activation group. CONCLUSION : Prehospital activation significantly reduces DBT in STEMI patients presenting during both normal workday hours and after hours. Significant time savings and exceptionally short DBTs (< 60 min) were achieved by prehospital activation for STEMI patients presenting during normal workday hours.

Abstract Background There are limited comparative data concerning long-term major clinical outcomes between male and female in dyslipidemic AMI patients after PCI with new-generation DES. Purpose We thought to investigate the impact of gender difference on the 2-year clinical outcomes. Methods Finally, a total of 2403 eligible dyslipidemic AMI patients who underwent PCI with new-generation DES were enrolled and they were separated into two groups; the male group (n=1800) and the female group (n=603). The primary endpoint was major adverse cardiac events (MACE) defined as all-cause death, recurrent myocardial infarction (re-MI), target lesion revascularization (TLR), and target vessel revascularization (TVR). The secondary endpoints were the incidence of the individual components of MACE and target vessel failure (TVF), a composite of death related to the target vessel, re-MI, or clinically driven TVR Results Two propensity score-matched (PSM) groups (422 pairs, n=844, C-statistic = 0.850) were generated. In the total study population, the cumulative incidences of MACE, all-cause death, re-MI, and TVF were significantly higher in the female group compared with the male group. However, after propensity score-matched (PSM) analysis, the cumulative incidences of MACE (HR, 0.971; 95% CI, 0.628–1.501; p=0.895), all-cause death (HR, 1.061; 95% CI, 0.536–2.100; p=0.865), re-MI (HR, 1.212; 95% CI, 0.433–2.907; p=0.813), and TVF (HR, 0.764; 95% CI, 0.474–1.229; p=0.267) were similar between the two groups. In addition, the cumulative incidences of cardiac death, TLR, TVR were not significantly different between the two groups (Table 1). Outcomes Cumulative Events at 2-year (%) Hazard Ratio (95% CI) p value Male Female Log-rank Propensity score matched patients MACE 41 (10.4) 40 (10.3) 0.895 0.971 (0.628–1.501) 0.895 All-cause death 16 (4.0) 17 (4.2) 0.865 1.061 (0.536–2.100) 0.865 Cardiac death 13 (3.3) 9 (2.2) 0.391 0.691 (0.295–1.616) 0.393 Re-MI 8 (2.0) 9 (2.4) 0.813 1.212 (0.433–2.907) 0.813 TLR 7 (1.8) 6 (1.6) 0.781 0.857 (0.298–2.550) 0.781 TVR 16 (4.3) 10 (2.7) 0.236 0.623 (0.283–1.373) 0.241 TVF 39 (10.2) 30 (7.8) 0.265 0.764 (0.474–1.229) 0.267 Conclusion The gender difference was not apparent in these dyslipidemic South Korean AMI patients who underwent PCI with new-generation DES during 2-year follow-up period.

Bildung ist ein Instrument, das zur Bekämpfung von Armut, Ungleichheit und sozialer Ausgrenzung in jeder Gesellschaft eingesetzt werden kann. Für eine nachhaltige und ganzheitliche nationale Entwicklung ist daher eine gerechte Verteilung der Bildungsressourcen unter den Menschen erforderlich. Dies ist jedoch nicht immer ohne Weiteres zu erreichen, insbesondere in Afrika, wo der Kolonialismus in vielen Ländern teilweise zu einer ungleichen Entwicklung unter den Menschen geführt hat. Schon bald nach der Eingliederung der Northern Territories of the Gold Coast (heute Ghana) in die Kolonialherrschaft vernachlässigte die Bildungspolitik der Kolonialisten den nördlichen Teil des Landes. Obwohl es einige Studien zum Kolonialismus in Afrika im Allgemeinen gibt, wurde nur wenig darüber berichtet, welche Rolle er bei der Schaffung eines ungleichen Bildungswesens spielte. Auch die Auswirkungen von aktiven Förderungsmaßnahmen, die zur Überbrückung der Kluft zwischen dem Nord-Süd-Gefälle in Ghana eingeführt wurden. Die wichtigsten Fragen, die diese Studie daher zu beantworten versucht, sind die Folgenden: Was waren die kolonialen Begegnungen mit dem Norden Ghanas, die die Unterentwicklung des Bildungswesens in der Region bewirkten? Wie überbrücken die aktiven Förderungsmaßnahmen bzw. die positive Diskriminierung die Kluft zwischen dem Norden und dem Süden des Landes? Zur Beantwortung der Forschungsfragen wurde in der Studie ein methodengemischter Ansatz verwendet, bei dem Tiefeninterviews, Q-Methoden, Dokumentenanalyse und Beobachtung als Datenerhebungsmethoden Einsatz fanden. Es stellte sich heraus, dass die Kolonialisten eine bewusste Strategie verfolgten, den Norden zu einer Reserve ungelernter Arbeitskräfte zu machen, was erklärt, warum sie dort anfangs nur wenige Schulen bauten. Die Ergebnisse der Studie zeigen darüber hinaus, dass die positive Diskriminierung die Nord-Süd-Lücke nicht wie erwartet schließt. So kommt man zu dem Schluss, dass die Ausbeutung weitesgehend für die Unterentwicklung des Bildungswesens in Nordghana verantwortlich ist.
Education is a tool that can be used to fight poverty, inequality, and social exclusion in every given society. Thus, for a sustainable and holistic national development, there is the need for an equitable distribution of educational resources among the people. This is however hardly achievable, especially in Africa where colonialism has partly brought about unequal development among the people in many countries. Soon after the Northern Territories of the Gold Coast (now Ghana) was incorporated under colonial rule, the educational policy of the colonialists did not favour the northern part of the country. Even though, there have been some studies on the colonialism of Africa in general, little has been done regarding the role it played in (re)producing unequal development of education in Africa. Likewise, the impact of an affirmative action instituted to bridge the gap between the north-south divide in Ghana has not been evaluated. The main questions this study thus seek to answer are: What were the colonial encounters with the north that brought about the underdevelopment of education in the area? How is the affirmative action bridging the gap between the north and the south? To answer the research questions, the study used a mixed-methods approach where in-depth interviews, Q methods, document analysis and observation were adapted as data collection methods. It was revealed that the colonialists adopted a deliberate strategy of making the north an unskilled labour reserve, thus accounting for why they did not build many schools there in the beginning. The findings of the study also show that the effect of the affirmative action has not been able to appreciably contribute to closing the north-south gap as expected. It is concluded that exploitation largely accounted for the underdevelopment of education in northern Ghana.