102 research outputs found
Implementasi Program Wirausaha Baru Oleh Dinas Tenaga Kerja Dan Transmigrasi Dalam Mendukung Gerdu Kempling Kota Semarang Tahun 2014
The Government of Semarang through Local Regulation Number 4 of 2008 about poverty reduction in Semarang City which is an acceleration in poverty reduction efforts. The strategy called Gerdu Kempling (Integrated Health, Economy, Education, Infrastructure, and Environment ) and one of the program that is New Entrepreneur Program by Dinas Tenaga Kerja dan Transmigrasi Kota Semarang. This research was meant to find out how the implementation of New Entrepreneur Program by Dinas Tenaga Kerja Dan Transmigrasi that supports Gerdu Kempling Kota Semarang in 2014 and knowing the influence factors of this implementation. New Entrepreneur Program has been part of Gerdu Kempling starting in 2011. There are three locations in this research: Village of Bulusan, Ngadirgo and Padangsari. This research using qualitative descriptive research methods. The subject in this study consisted of eight (8) informants. The results showed that the implementation of New Entrepreneur Program are still less effective that is seen from the precision implementation aspects. The factors that influence the implementation such as the goals and basic of policy, resource policy, communication and implementation activities, the implementing agency characteristics, external conditions as well as the disposition of the implementor are still less optimal too. Based on these conclusions, the researcher recommend to the implementation agency and target of this program need high commitment and take maximal advantages for sustainable in order to achieve the purpose of this program
1 Pengaruh Mengkonsumsi Rebusan Daun Sirsak Terhadap Penurunan Nyeri Pada Penderita Gout Artritis Di Wilayah Kerja Puskesmas Pineleng
Gout artritis merupakan penyakit yang ditandai dengan nyeri yang terjadi berulang-ulang yang disebabkan adanya endapan kristal monosodium urat yang tertumpuk di dalam sendi sebagai akibat tingginya kadar asam urat di dalam darah. Mengkonsumsi rebusan daun sirsak (Anonna muricata) adalah salah satu jenis terapi nonfamakologi yang bertujuan untuk menurunkan tingkat nyeri pada penderita gout artritis karena senyawa yang terkandung dalam daun sirsak berfungsi sebagai analgetik yang mempu mengurangi nyeri gout.Tujuan penelitan ini adalah untuk menganalisis pengaruh mengkonsumsi rebusan daun sirsak terhadap penurunan nyeri pada penderita gout artritis di wilayah kerja Puskesmas Pineleng.Sampel diambil dengan menggunakan total sampling yaitu 34 orang yang memenuhi kriteria inklusi.Desain penelitian yang digunakan adalah Time Series Design dan data yang dikumpulkan dari responden menggunakan lembar observasi.Hasil penelitian uji Wilcoxon sign rank test pada hasil akhir didapatkan nilai p = 0,004 < Ξ± = 0,005 sehingga dapat diambil Kesimpulan bahwa hipotesis penelitian diterima, hal ini menunjukan bahwa ada pengaruh mengkonsumsi rebusan daun sirsak terhadap penurunan nyeri pada penderita gout artritis di wilayah kerja Puskesmas Pineleng.Saran untuk penelitian selanjutnya dapat menggunakan populasi yang lebih besar untuk hasil yang lebih akurat serta dapat mengembangkan penelitian tentang pengaruh mengkonsumsi rebusan daun sirsak terhadap variabel yang lain seperti penurunan tekanan darah pada penderita hipertensi
Effects of Cdc5 kinase and of Cdc14 and PP2A phosphatase activities on Cdc14 re-sequestration.
<p>A stabilized version of Cdc5 (3Γ<i>CDC5ΞN70</i>) causes a delay in Cdc14 re-sequestration both in wild-type cells (panel A) and <i>bub2Ξ</i> background (panel B). (<b>A</b>) Cdc20 block-and-release was pre-simulated for 180 min with no degradation of Cdc5 (<i>k</i><sub>d,poloβ²</sub>β=β0, <i>k</i><sub>s,polo</sub>β=β0.011). (<b>B</b>) Simulation was done as in A with the rates of inactivation of Tem1 set to zero (<i>k</i><sub>i,temβ²</sub>β=β<i>k</i><sub>i,temβ³</sub>β=β0). (<b>C</b>) Cdc14 stays released from the nucleolus in <i>cdc14-1</i> cells arrested in telophase. Cdc20 block-and-release was presimulated with no Cdc14 activity (<i>effc14</i>β=β0). (<b>D</b>, <b>E</b> and <b>F</b>) Cdc20 block-and-release in wild-type cells; after 24 min (when cells start to enter G1 phase), either PP2A activity (panel D, <i>effpa</i>β=β0) or Cdc14 activity (panel E, <i>effc14</i>β=β0) was inhibited. In either case, Cdc14 is re-sequestered into the nucleoulus. In panel F, when both PP2A and Cdc14 phosphatase activities are inhibited after 24 min (<i>effpa</i>β=β<i>effc14</i>β=β0), Cdc14 does not return to the nucleolus.</p
Flux diagrams in wild-type cells.
<p>Initially cells are in the metaphase steady state by Cdc20 deprivation. Cdc20 activation at time zero (<i>k</i><sub>s,20</sub>β=β0.015) induces mitotic progression through anaphase, telophase and G1. Flux definitions are given in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0030810#pone.0030810.s001" target="_blank">Table S1</a>.</p
Simulations of mitotic progression of cells containing <i>cdc15-2</i>, <i>NET1-6cdk</i>, <i>tem1-3, cdc28-as1</i>, and <i>GAL-CLB2dbΞ cdc5-as1</i> mutations.
<p>(<b>A</b>) In MEN mutants such as <i>cdc15-2</i>, Cdc14 is transiently released and resequestered. Cdc20 block-and-release was presimulated with inactive Cdc15 (<i>effc15</i>β=β0). (<b>B</b>) In <i>tem1-3</i> temperature sensitive mutant (MEN inactive), Cdc14 is transiently released and cells are arrested in telophase. Simulation was started at metaphase by Cdc20 deprivation (<i>k</i><sub>s,20</sub>β=β0) for 15 min with total concentration of Tem1, initial conditions of Tem1 and MEN were set to zero. Cdc20 was activated at time zero (<i>k</i><sub>s,20</sub>β=β0.015) (<b>C</b>) In <i>NET1-6cdk</i> cells ME occurs with a delay, as typical of FEAR mutants. Cdc20 block-and-release was presimulated with no Net1 phosphorylation by Cdk/Clb2 (<i>k</i><sub>k,12</sub>β=β<i>k</i><sub>k,34</sub>β=β0). (<b>D</b>) Double MEN and FEAR mutations, such as <i>NET1-6cdk cdc15-2</i>, do not show transient release of Cdc14 and arrest in telophase. Cdc20 block-and-release was presimulated with inactive Cdc15 (<i>effc15</i>β=β0) and no Net1 phosphorylation by Cdk/Clb2 (<i>k</i><sub>k,12</sub>β=β<i>k</i><sub>k,34</sub>β=β0). (<b>E</b>) When Cdk kinase activity is inhibited, there is no Cdc14 release. Both Cdk/Clb2 and Cdc5 phosphorylation on Net1 are diminished in <i>cdc28-as1</i> mutant. Simulation was done similar to wild-type cells except that INH was set to 5 to inhibit Cdk kinase activity. (<b>F</b>) Our model predicts that when Cdc5 is inhibited, overexpressed Clb2 cannot induce Cdc14 release with or without active Cdc20. Simulation was started at metaphase by Cdc20 deprivation, overexpression of Clb2 and inactive Cdc5 for 15 min (<i>k</i><sub>s,20</sub>β=β0, <i>k</i><sub>s,b2</sub>β=β0.6, <i>k</i><sub>d,b2</sub>β=β<i>k</i><sub>d,b2β²</sub>β=βeffpolβ=β0). Cdc20 was added back at time zero (<i>k</i><sub>s,20</sub>β=β0.015).</p
Simulation of mitotic progression of cells containing overexpressed <i>CDC5</i> and inactive <i>cdc5</i> mutations.
<p>(<b>A</b>) Cdc5 is necessary for ME. Cdc20 block-and-release was simulated as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0030810#pone-0030810-g002" target="_blank">Figure 2</a> with inactive Cdc5 (<i>cdc5-as1</i>; <i>effpol</i>β=β0). Cdc14 is not released, nor is Cdh1 activated. (<b>B</b>) The MEN requirement for ME can be bypassed by overexpressed Cdc5. Cdc20 block-and-release was simulated as usual, with inactive Cdc15 (<i>cdc15-2</i>; <i>effc15</i>β=β0) and with Cdc5 overexpressed 30-fold (<i>GAL-CDC5</i>; <i>k</i><sub>s,polo</sub>β=β0.3). (<b>C</b>) Overexpressed Cdc5 is sufficient for Cdc14 release when FEAR and MEN are inactive. Simulation was started in an arrested steady state with initial conditions of Clb2 and Polo were set less than metaphase values to represent an earlier stage of the arrest by hydroxyurea (Clb2β=β0.8, Poloβ=β0.6, Poloiβ=β0.2, <i>k</i><sub>s,b2</sub>β=β0.024, <i>k</i><sub>s,polo</sub>β=β0.006) and with inactive Cdc15 (<i>effc15</i>β=β0) for 15 min. Then Cdc5 and Pds1 overexpressions were induced at time zero (<i>k</i><sub>s,polo</sub>β=β0.3, <i>k</i><sub>s,pds</sub>β=β0.45, <i>k</i><sub>d,pdsβ²</sub>β=β0). (<b>D</b>) The Cdc5 requirement for Cdc14 release and ME can be bypassed by overexpression of a truncated version of Cdc15. Cdc20 block-and-release was pre-simulated for 60 min with no synthesis of either Cdc20 or Cdc5 (<i>k</i><sub>s,polo</sub>β=β<i>k</i><sub>s,20</sub>β=β0; setting also the initial conditions for Cdc5 active and inactive forms to zero) while the total concentration of Cdc15 was increased 20-fold and inhibition of Cdc15 by Cdk was reduced 1000-fold (<i>k</i><sub>i,c15</sub>β²β=β0.00009, <i>CDC15T</i>β=β20). At <i>t</i>β=β0, Cdc20 synthesis is induced as usual (<i>k</i><sub>s,20</sub>β=β0.015). (<b>E</b>) Cdc14 is not released in <i>cdc5-1</i> and <i>cdc5-1 cdc14-1</i> cells in E and F. Therefore, Cdc14 release in the <i>cdc14-1</i> mutant may be attributable solely to Net1 phosphorylation by Cdc5. Simulation in E was done similar to <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0030810#pone-0030810-g004" target="_blank">Figure 4A</a> except that <i>effpol</i> was set to 0.1 for the small residual activity of Cdc5. (<b>F</b>) Simulation in F was done similar to A except that activity of Cdc14 was set to zero (<i>effc14</i>β=β0).</p
Temporal changes of RENT, Net1 forms and fluxes in <i>cdc15-2</i> cells blocked at telophase in mitosis.
<p>Simulation was done similar to <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0030810#pone-0030810-g005" target="_blank">Figure 5A</a>.</p
<i>clb2Ξ</i> and <i>bub2Ξ cdh1Ξ</i> mutants.
<p>(<b>A</b>) When Clb2 is inhibited Cdc14 is released with a delay. Simulation was started at metaphase Cdc20 block for 80 min with rate of synthesis of Clb2 in the model decreased to 1/3 of baseline due to residual Clb1 activity (<i>k</i><sub>s,b2</sub>β=β0.1) and Cdc20 was added back at time zero. (<b>B</b>) In <i>bub2Ξ cdh1Ξ</i> cells, Cdc14 stays released after ME. Simulation was done as wild-type cells except that rates of inactivation of Tem1 and total concentration of Cdh1 were set to zero (<i>k</i><sub>i,temβ²</sub>β=β<i>k</i><sub>i,temβ³</sub>β=β<i>CDH1T</i>β=β0).</p
Model predicts that Cdc14 is responsible for its own re-sequestration after ME.
<p>(<b>AβC</b>) All simulations were done similar to <i>cdc15-2</i> mutant simulations in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0030810#pone-0030810-g005" target="_blank">Figure 5A</a> except that after 20 min either Cdc14 (in A, <i>effc14</i>β=β0) or PP2A (in B, <i>effppa</i>β=β0) or both (in C, <i>effc14</i>β=β<i>effppa</i>β=β0)) were inactivated by setting their corresponding activity factors to zero.</p
Flux diagrams and temporal changes of RENT, Net1 forms in <i>NET1-6cdk</i> mutants.
<p>Simulation was done similar to <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0030810#pone-0030810-g005" target="_blank">Figure 5C</a>.</p
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