REPAIR MATERIAL COMPOSITE DAMAGE DEBONDING FORWARD OF FRAME X6630 PADA EUROCOPTER 155

Suatu fenomena yang sangat mengagumkan ketika peradaban manusia di dunia mampu menerbangkan benda yang lebih berat dari udara. Fenomena tersebut dikenal dengan dirgantara (aerospace) telah menjadi salah satu rumpun perkembangan ilmu pengetahuan yang berkembang sangat pesat di tengah banyaknya perkembangan ilmu-ilmu pengetahuan lain juga. Perpaduan berbagai disiplin ilmu seperti halnya aerodinamika, struktur, kinematika dan dinamika benda, propulsi, desain dan sebagainya telah berpartisipasi menciptakan wahana-wahana terbang yang dapat memberikan akses transportasi dari dan ke berbagai tempat yang tergolong relatif jauh hanya dalam waktu yang jauh lebih singkat daripada menggunakan sarana transportasi lainnya. Penelitian ini merupakan penelitian deskriptif yaitu penelitian terhadap masalah-masalah berupa fakta-fakta saat ini dari suatu populasi yang meliputi kegiatan penelitian sikap atau pendapat terhadap individu, organisasi, keadaan, ataupun prosedur. Repair Material adalah proses perbaikan bagian yang telah mengalami kerusakan/cacat agar kekuatan bagian memenuhi standar yang telah ditetapkan oleh perancang. Di mana kerusakan material dapat diidentifikasi dengan cara pengujian NDT/non destructive test dan DT/Destructive test serta limitasi kerusakan mengacu pada dokumen RADS PT. Indonesia Air Transport. Proses removing dan installing dilakukan dengan 4 tahap dan monitoring pasca repair material dilakukan oleh Eurocopter Airbus Indonesia

Blocking airway mucous cell metaplasia by inhibiting EGFR antiapoptosis and IL-13 transdifferentiation signals

Epithelial hyperplasia and metaplasia are common features of inflammatory and neoplastic disease, but the basis for the altered epithelial phenotype is often uncertain. Here we show that long-term ciliated cell hyperplasia coincides with mucous (goblet) cell metaplasia after respiratory viral clearance in mouse airways. This chronic switch in epithelial behavior exhibits genetic susceptibility and depends on persistent activation of EGFR signaling to PI3K that prevents apoptosis of ciliated cells and on IL-13 signaling that promotes transdifferentiation of ciliated to goblet cells. Thus, EGFR blockade (using an irreversible EGFR kinase inhibitor designated EKB-569) prevents virus-induced increases in ciliated and goblet cells whereas IL-13 blockade (using s-IL-13Rα2-Fc) exacerbates ciliated cell hyperplasia but still inhibits goblet cell metaplasia. The distinct effects of EGFR and IL-13 inhibitors after viral reprogramming suggest that these combined therapeutic strategies may also correct epithelial architecture in the setting of airway inflammatory disorders characterized by a similar pattern of chronic EGFR activation, IL-13 expression, and ciliated-to-goblet cell metaplasia

IL-13-induced airway mucus production is attenuated by MAPK13 inhibition

Increased mucus production is a common cause of morbidity and mortality in inflammatory airway diseases, including asthma, chronic obstructive pulmonary disease (COPD), and cystic fibrosis. However, the precise molecular mechanisms for pathogenic mucus production are largely undetermined. Accordingly, there are no specific and effective anti-mucus therapeutics. Here, we define a signaling pathway from chloride channel calcium-activated 1 (CLCA1) to MAPK13 that is responsible for IL-13–driven mucus production in human airway epithelial cells. The same pathway was also highly activated in the lungs of humans with excess mucus production due to COPD. We further validated the pathway by using structure-based drug design to develop a series of novel MAPK13 inhibitors with nanomolar potency that effectively reduced mucus production in human airway epithelial cells. These results uncover and validate a new pathway for regulating mucus production as well as a corresponding therapeutic approach to mucus overproduction in inflammatory airway diseases

TME quality in rectal cancer surgery

<p>Abstract</p> <p>Background</p> <p>The concept of total mesorectal excision has revolutionised rectal cancer surgery. TME reduces the rate of local recurrence and tumour associated mortality. However, in clinical trials only 50% of the removed rectal tumours have an optimal TME quality. Patients: During a period of 36 months we performed 103 rectal resections. The majority of patients (76%; 78/103) received an anterior resection. The remaining patients underwent either abdominoperineal resection (16%; 17/103), Hartmann's procedure (6%; 6/103) or colectomy (2%; 2/103).</p> <p>Results</p> <p>In 90% (93/103) TME quality control could be performed. 99% (92/93) of resected tumours had optimal TME quality. In 1% (1/93) the mesorectum was nearly complete. None of the removed tumours had an incomplete mesorectum. In 98% (91/93) the circumferential resection margin was negative. Major surgical complications occurred in 17% (18/103). 5% (4/78) of patients with anterior resection had anastomotic leakage. 17% (17/103) developed wound infections. Mortality after elective surgery was 4% (4/95).</p> <p>Conclusion</p> <p>Optimal TME quality results can be achieved in all stages of rectal cancer with a rate of morbidity and mortality comparable to the results from the literature. Future studies should evaluate outcome and local recurrence in accordance to the degree of TME quality.</p