Penggunaan IC Mikrokontroler 8951 Dalam Pembuatan Perangkat Tagihan Warnet

Teknologi internet saat ini telah merasuk hampir ke seluruh segi kehidupan. Hal tersebut telah banyak mengundang para pengusaha untuk bergerak dalam usaha jasa internet, yang disebut warung internet (warnet). Usaha jasa tersebut membutuhkan suatu sistem penagiban yang efektif. Pada dasarnya warnet-warnet yang ada sekarang ini sudah memiliki perangkat penagibannya sendiri, yaitu dengan perangkat lunak yang terdapat pada komputer pusat. Hanya saja faktor keamanannya kurang menunjang, yaitu terdapat banyak kecurangan terutama kecurangan dalam penampilan lama waktu pemakaian dari para pelanggan ataupun karyawannya sendiri. Untuk itu dirancang perangkat tagihan warnet dengan perangkat keras yang dianggap akan menghasilkan sistem penagihan yang lebih aman dari sistem penagihan yang sudah ada. Komponen utama dari alat penagihan perangkat keras tersebut adalah lC mikrokontroler AT89C51, adapun tugas dari lC mikrokontroler AT89C51 ada tiga, yang pertama adalah untuk mengatur penampilan lama waktu pemakaian internet pada tampilan (display) sebagai informasi untuk pelanggan, yang kedua adalah untuk mengatur penampilan lama waktu pemakaian internet pada PC sebagai informasi untuk karyawan, yang ketiga adalah untuk mengatur switch untuk menghubungkan kabel jaringan pada HUB agar pelanggan dapat menggunakan internet

Pyruvate kinase M2 activators promote tetramer formation and suppress tumorigenesis

Cancer cells engage in a metabolic program to enhance biosynthesis and support cell proliferation. The regulatory properties of pyruvate kinase M2 (PKM2) influence altered glucose metabolism in cancer. The interaction of PKM2 with phosphotyrosine-containing proteins inhibits enzyme activity and increases the availability of glycolytic metabolites to support cell proliferation. This suggests that high pyruvate kinase activity may suppress tumor growth. We show that expression of PKM1, the pyruvate kinase isoform with high constitutive activity, or exposure to published small-molecule PKM2 activators inhibits the growth of xenograft tumors. Structural studies reveal that small-molecule activators bind PKM2 at the subunit interaction interface, a site that is distinct from that of the endogenous activator fructose-1,6-bisphosphate (FBP). However, unlike FBP, binding of activators to PKM2 promotes a constitutively active enzyme state that is resistant to inhibition by tyrosine-phosphorylated proteins. These data support the notion that small-molecule activation of PKM2 can interfere with anabolic metabolism.National Institutes of Health (U.S.) (NIH grant R01 GM56203)National Institutes of Health (U.S.) (grant NIH 5P01CA120964)Dana-Farber/Harvard Cancer Center (NIH 5P30CA006516)National Institutes of Health (U.S.) (NIH grant R03MH085679)National Human Genome Research Institute (U.S.) (Intramural Research Program)National Institutes of Health (U.S.) (Molecular Libraries Initiative of the NIH Roadmap for Medical Research

Plasma Dynamics

Contains table of contents for Section 2 and reports on two research projects.Princeton University/National Spherical Torus Experiment Grant S04020G PPPLU.S. Department of Energy Grant DE-FGO2-91-ER-54109National Science Foundation Grant ECS 94-24282Los Alamos National Laboratory Grant No. E29060017

A novel process driving Alzheimer's disease validated in a mouse model: Therapeutic potential

Abstract Introduction The neuronal mechanism driving Alzheimer's disease (AD) is incompletely understood. Methods Immunohistochemistry, pharmacology, biochemistry, and behavioral testing are employed in two pathological contexts—AD and a transgenic mouse model—to investigate T14, a 14mer peptide, as a key signaling molecule in the neuropathology. Results T14 increases in AD brains as the disease progresses and is conspicuous in 5XFAD mice, where its immunoreactivity corresponds to that seen in AD: neurons immunoreactive for T14 in proximity to T14‐immunoreactive plaques. NBP14 is a cyclized version of T14, which dose‐dependently displaces binding of its linear counterpart to alpha‐7 nicotinic receptors in AD brains. In 5XFAD mice, intranasal NBP14 for 14 weeks decreases brain amyloid and restores novel object recognition to that in wild‐types. Discussion These findings indicate that the T14 system, for which the signaling pathway is described here, contributes to the neuropathological process and that NBP14 warrants consideration for its therapeutic potential

The global imbalances and the contradictions of US monetary hegemony

Over the last decade, the world economy has been characterised by escalating global current account imbalances between the United States (US) and East Asia in particular. This article argues that US monetary hegemony has been a necessary condition for the emergence of these imbalances. It is contended that the notion of structural power is indispensable to understanding the nature of US monetary hegemony and its relation to the imbalances. US monetary structural power has both induced East Asian states to increase their accumulation of dollar-denominated assets and allowed the US to decrease its savings. The article also shows that the mechanisms of US structural monetary power contain several contradictory dynamics that are able to undermine its own purpose, which is to avoid the burden of adjustment to balance-of-payments disequilibria. Journal of International Relations and Development (2010) 13, 105-135. doi:10.1057/jird.2009.3