Pelatihan Strategi Peningkatan Pemasaran, Penjualan dan Pelaporan Akuntansi melalui Pembuatan Website di Yayasan Duta Bangsa Indonesia di Cikarang

Duta Bangsa College of Technology was established on March 3, 2007 in accordance with the Decree of the Minister of Education and Culture Number.34/D/0/2007 concerning the establishment of STT.Duta Bangsa. STT.Duta Bangsa is located in Kp. Pulokapuk RT 01 RW 05 Mekar Mukti Village Kec. North Cikarang Kab. Bekasi. Tel/Fax number: (021) 29082747. Permit of Higher Education: Minister of Education Decree No.2740/D/T/K-IV/2010. Minister of Education Decree No.2741/D/T/K-IV/2010. Decree of Minister of National Education No.2742/D/T/K-IV/2010. The problem faced by the Indonesian ambasadors foundation is the marketing problem, where they have to compete in fighting over a limited market niche with more and more competitors. Moreover, the market share to fight over the students who are nota bene is the X generation who are literate in the world of Information Technology, which certainly requires marketing to hit their hearts. Starting from this, we from the Faculty of Economics at Bhayangkara University offered to provide training for Marketing Persons at the Duta Bangsa Foundation so that they could win a large market share of students in Bekasi, especially in the Cikarang area, in creating a web site

Functional modulation of the transient outward current Ito by KCNE beta-subunits and regional distribution in human non-failing and failing hearts

Objectives: The function of Kv4.3 (KCND3) channels, which underlie the transient outward current I,, in human heart, can be modulated by several accessory subunits such as KChIP2 and KCNE1-KCNE5. Here we aimed to determine the regional expression of Kv4.3, KChIP2, and KCNE mRNAs in non-failing and failing human hearts and to investigate the functional consequences of subunit coexpression in heterologous expression systems. Methods: We quantified mRNA levels for two Kv4.3 isoforms, Kv4.3-S and Kv4.3-L, and for KChIP2 as well as KCNE1-KCNE5 with real-time RT-PCR. We also studied the effects of KCNEs on Kv4.3 + KChIP2 current characteristics in CHO cells with the whole-cell voltage-clamp method. Results: In non-failing hearts, low expression was found for KCNE1, KCNE3, and KCNE5, three times higher expression for KCNE2, and 60 times higher for KCNE4. Transmural gradients were detected only for KChIP2 in left and right ventricles. Compared to non-failing tissue, failing hearts showed higher expression of Kv4.3-L and KCNE1 and lower of Kv4.3-S, KChIP2, KCNE4, and KCNE5. In CHO cells, Kv4.3 + KChIP2 currents were differentially modified by co-expressed KCNEs: time constants of inactivation were shorter with KCNE1 and KCNE3-5 while time-to-peak was decreased, and V-0.5 of steady-state inactivation was shifted to more negative potentials by all KCNE subunits. Importantly, KCNE2 induced a unique and prominent 'overshoot' of peak current during recovery from inactivation similar to that described for human I-to while other KCNE subunits induced little (KCNE4,5) or no overshoot. Conclusions: All KCNEs are expressed in the human heart at the transcript level. Compared to It. in native human myocytes, none of the combination of KChIP2 and KCNE produced an ideal congruency in current characteristics, suggesting that additional factors contribute to the regulation of the native I-to channel

Metabolic reprogramming of murine cardiomyocytes during autophagy requires the extracellular nutrient sensor decorin.

The extracellular matrix is a master regulator of tissue homeostasis in health and disease. Here we examined how the small, leucine-rich, extracellular matrix proteoglycan decorin regulates cardiomyocyte metabolism during fasting in vivo. First, we validated in Dcn-/- mice that decorin plays an essential role in autophagy induced by fasting. High-Throughput metabolomics analyses of cardiac tissue in Dcn-/- mice subjected to fasting revealed striking differences in the hexosamine biosynthetic pathway resulting in aberrant cardiac O-β-N-Acetylglycosylation as compared with WT mice. Functionally, Dcn-/- mice maintained cardiac function at a level comparable with nonfasted animals whereas fasted WT mice showed reduced ejection fraction. Collectively, our results suggest that reduced sensing of nutrient deprivation in the absence of decorin preempts functional adjustments of cardiac output associated with metabolic reprogramming. © 2018 Gubbiotti et al

Making up for the deficit in a marathon run

To predict the final result of an athlete in a marathon run thoroughly is the eternal desire of each trainer. Usually, the achieved result is weaker than the predicted one due to the objective (e.g., environmental conditions) as well as subjective factors (e.g., athlete's malaise). Therefore, making up for the deficit between predicted and achieved results is the main ingredient of the analysis performed by trainers after the competition. In the analysis, they search for parts of a marathon course where the athlete lost time. This paper proposes an automatic making up for the deficit by using a Differential Evolution algorithm. In this case study, the results that were obtained by a wearable sports-watch by an athlete in a real marathon are analyzed. The first experiments with Differential Evolution show the possibility of using this method in the future.Comment: ISMSI 201

Virtual Skiing as an Art Installation

The Virtual Skiing game allows the user to immerse himself into the skiing sensation without using any obvious hardware interfaces. To achieve the movement down the virtual skiing slope the skier who stands on a pair of skis attached to the floor performs the same movements as on real skis, in particular this is the case on carving skis: tilting the body to the left initiates a left turn, tilting the body to the right initiates a right turn, by lowering the body, the speed is increased. The skier observes his progress down the virtual slope projected on the wall in front of him. The skier’s movements are recorded using a video camera placed in front of him and processed on a PC in real time to drive the projected animation of the virtual slope

Mitochondrial Ca(2+) uptake by the voltage-dependent anion channel 2 regulates cardiac rhythmicity.

Tightly regulated Ca(2+) homeostasis is a prerequisite for proper cardiac function. To dissect the regulatory network of cardiac Ca(2+) handling, we performed a chemical suppressor screen on zebrafish tremblor embryos, which suffer from Ca(2+) extrusion defects. Efsevin was identified based on its potent activity to restore coordinated contractions in tremblor. We show that efsevin binds to VDAC2, potentiates mitochondrial Ca(2+) uptake and accelerates the transfer of Ca(2+) from intracellular stores into mitochondria. In cardiomyocytes, efsevin restricts the temporal and spatial boundaries of Ca(2+) sparks and thereby inhibits Ca(2+) overload-induced erratic Ca(2+) waves and irregular contractions. We further show that overexpression of VDAC2 recapitulates the suppressive effect of efsevin on tremblor embryos whereas VDAC2 deficiency attenuates efsevin\u27s rescue effect and that VDAC2 functions synergistically with MCU to suppress cardiac fibrillation in tremblor. Together, these findings demonstrate a critical modulatory role for VDAC2-dependent mitochondrial Ca(2+) uptake in the regulation of cardiac rhythmicity

Outlook Magazine, Autumn 2012

https://digitalcommons.wustl.edu/outlook/1187/thumbnail.jp