Model Kebijakan Penanggulangan Korupsi di Universitas Negeri YOGYAKARTA

Penelitian ini bertujuan untuk mengetahui kebijakan Universitas Negeri Yogyakarta dalam menanggulangi korupsi dan menemukan model kebijakan yang diinginkan Universitas Negeri Yogyakarta dalam menanggulangi korupsi. Penelitian ini adalah penelitian survei dengan pendekatan kuantitatif dan kualitatif. Sampel penelitian ditentukan secara multy stage sampling dengan teknik pengumpulan data dengan angket, dokumen dan diperkuat dengan pengumpulan data melalui Focus Group Discussion (FGD), dan validasi instrumen melalui validitas isi (content validity). Data dianalisis secara deskriptif. Hasil penelitian menunjukkan bahwa kebijakan penanggulangan korupsi di UNY tidak ada secara khusus dikeluarkan. Kebijakan yang ada mengikuti dan mempertahankan kebijakan yang lebih tinggi, yaitu dari Pemerintah. Model kebijakan penangggulangan korupsi di UNY yang digunakan adalah Model Rasional, yaitu kebijakan penanggulangan korupsi yang dikeluarkan merupakan aspirasi semua staf yang ada di unit kerja dan harus menekankan pada aspek efisiensi atas beban kerja pada unit kerja yang bersangkutan. Adapun kebijakan yang sudah ada yang berasal dari Pemerintah pusat dijadikan pedoman

Control of the replication initiator DnaA by an anti-cooperativity factor

Proper coordination of DNA replication with cell growth and division is critical for production of viable progeny. In bacteria, coordination of DNA replication with cell growth is generally achieved by controlling activity of the replication initiator DnaA and its access to the chromosomal origin of replication, oriC. Here we describe a previously unknown mechanism for regulation of DnaA. YabA, a negative regulator of replication initiation in Bacillus subtilis, interacts with DnaA and DnaN, the sliding (processivity) clamp of DNA polymerase. We found that in vivo, YabA associated with the oriC region in a DnaA-dependent manner and limited the amount of DnaA at oriC. In vitro, purified YabA altered binding of DnaA to DNA by inhibiting cooperativity. Although previously undescribed, proteins that directly inhibit cooperativity may be a common mechanism for regulating replication initiation. Conditions that cause release of DnaN from the replisome, or overproduction of DnaN, caused decreased association of YabA and increased association of DnaA with oriC. This effect of DnaN, either directly or indirectly, is likely responsible, in part, for enabling initiation of a new round of replication following completion of a previous round.United States. Public Health Service (grant GM41934)National Institutes of Health (U.S.) (NIH Kirschstein NRSA postdoctoral fellowship F32GM093408

Cell Surface Sialylation and Fucosylation Are Regulated by L1 via Phospholipase Cγ and Cooperate to Modulate Neurite Outgrowth, Cell Survival and Migration

BACKGROUND: Cell surface glycosylation patterns are markers of cell type and status. However, the mechanisms regulating surface glycosylation patterns remain unknown. METHODOLOGY/PRINCIPAL FINDINGS: Using a panel of carbohydrate surface markers, we have shown that cell surface sialylation and fucosylation were downregulated in L1(-/y) neurons versus L1(+/y) neurons. Consistently, mRNA levels of sialyltransferase ST6Gal1, and fucosyltransferase FUT9 were significantly reduced in L1(-/y) neurons. Moreover, treatment of L1(+/y) neurons with L1 antibodies, triggering signal transduction downstream of L1, led to an increase in cell surface sialylation and fucosylation compared to rat IgG-treated cells. ShRNAs for both ST6Gal1 and FUT9 blocked L1 antibody-mediated enhancement of neurite outgrowth, cell survival and migration. A phospholipase Cgamma (PLCgamma) inhibitor and shRNA, as well as an Erk inhibitor, reduced ST6Gal1 and FUT9 mRNA levels and inhibited effects of L1 on neurite outgrowth and cell survival. CONCLUSIONS: Neuronal surface sialylation and fucosylation are regulated via PLCgamma by L1, modulating neurite outgrowth, cell survival and migration

Does rapid HIV disease progression prior to combination antiretroviral therapy hinder optimal CD4 + T-cell recovery once HIV-1 suppression is achieved?

Objective: This article compares trends in CD4+ T-cell recovery and proportions achieving optimal restoration (>=500 cells/µl) after viral suppression following combination antiretroviral therapy (cART) initiation between rapid and nonrapid progressors. Methods: We included HIV-1 seroconverters achieving viral suppression within 6 months of cART. Rapid progressors were individuals experiencing at least one CD4+ less than 200 cells/µl within 12 months of seroconverters before cART. We used piecewise linear mixed models and logistic regression for optimal restoration. Results: Of 4024 individuals, 294 (7.3%) were classified as rapid progressors. At the same CD4+ T-cell count at cART start (baseline), rapid progressors experienced faster CD4+ T-cell increases than nonrapid progressors in first month [difference (95% confidence interval) in mean increase/month (square root scale): 1.82 (1.61; 2.04)], which reversed to slightly slower increases in months 1–18 [-0.05 (-0.06; -0.03)] and no significant differences in 18–60 months [-0.003 (-0.01; 0.01)]. Percentage achieving optimal restoration was significantly lower for rapid progressors than nonrapid progressors at months 12 (29.2 vs. 62.5%) and 36 (47.1 vs. 72.4%) but not at month 60 (70.4 vs. 71.8%). These differences disappeared after adjusting for baseline CD4+ T-cell count: odds ratio (95% confidence interval) 0.86 (0.61; 1.20), 0.90 (0.38; 2.17) and 1.56 (0.55; 4.46) at months 12, 36 and 60, respectively. Conclusion: Among people on suppressive antiretroviral therapy, rapid progressors experience faster initial increases of CD4+ T-cell counts than nonrapid progressors, but are less likely to achieve optimal restoration during the first 36 months after cART, mainly because of lower CD4+ T-cell counts at cART initiation

FORENSIC SCIENCES Case Work Guidelines and Interpretation of Short Tandem Repeat Complex Mixture Analysis

Interpretation guidelines for short tandem repeat casework analysis are difficult to construct. As soon as a set of guidelines are developed, a new case evolves that does not fit the painstakingly written document. The casework analysts gather and amend the guidelines again, and again. This article seeks to demonstrate that general guidelines can be set and written such that it can be used for any detection format. Guidelines published by the Scientific Working Group for DNA Analysis Methods, a working group of DNA forensic experts in the United States, are used to set the format for the written protocol on interpretations. The rule "the interpretation of results in casework is a matter of professional judgment and expertise. Not every situation can or should be covered by a preset rule" is stressed. Development of minimum and maximum threshold values, heterozygote ratios, stochastic limits, and determination of major and minor components based on validation studies is discussed. The paper travels through setting criteria to evaluate internal lane standards and amplification controls. It continues with establishing ranges for interpretation and defining true alleles versus anomalies. Examples of a variety of profiles are given and the potential interpretation, using signal intensities and genetics. In addition, report writing strategies and wording routinely used by the Pennsylvania State Police DNA Laboratory System are given

Virologic and Immunologic Response to cART by HIV-1 Subtype in the CASCADE Collaboration

Background: We aimed to compare rates of virologic response and CD4 changes after combination antiretroviral (cART) initiation in individuals infected with B and specific non-B HIV subtypes. Methods: Using CASCADE data we analyzed HIV-RNA and CD4 counts for persons infected >= 1996, >= 15 years of age. We used survival and longitudinal modeling to estimate probabilities of virologic response (confirmed HIV-RNA <500 c/ml), and failure (HIV-RNA>500 c/ml at 6 months or >= 1000 c/ml following response) and CD4 increase after cART initiation. Results: 2003 (1706 B, 142 CRF02_AG, 55 A, 53 C, 47 CRF01_AE) seroconverters were included in analysis. There was no evidence of subtype effect overall for response or failure (p = 0.075 and 0.317, respectively) although there was a suggestion that those infected with subtypes CRF01_AE and A responded sooner than those with subtype B infection [HR (95% CI): 1.37 (1.01-1.86) and 1.29 (0.96-1.72), respectively]. Rates of CD4 increase were similar in all subtypes except subtype A, which tended to have lower initial, but faster long-term, increases. Conclusions: Virologic and immunologic response to cART was similar across all studied subtypes but statistical power was limited by the rarity of some non-B subtypes. Current antiretroviral agents seem to have similar efficacy in subtype B and most widely encountered non-B infections in high-income countries