Active Compensation of Unbalanced Load Currents in Grid Connected Voltage Source Converters

Raghbendra Tiwari,Roy Nilsen 전력전자학회 2019 ICPE(ISPE)논문집 Vol.2019 No.5

For a 2-level 3-phase voltage source converter connected to the grid, it should be capable of supporting the grid with maximum possible active and reactive power during balanced and unbalanced load condition. This paper discusses about the unbalanced current injection algorithm from a VSC to keep the grid currents balanced and sinusoidal in case of asymmetrical loading conditions. Positive and negative sequence synchronous reference frame control have been used to filter the unbalanced component in the grid currents and to compensate it from the converter. A case study with unbalanced reactive load has been simulated to verify the algorithm and the effect of compensation. The compensation reduces the asymmetry in PCC voltage and grid currents, and makes it close to sinusoidal shape to keep it within a standard limit of unbalance in grid power quality.

Vulnerability as Expected Poverty in Rural India

Raghbendra Jha,Woojin Kang,Hari K. Nagarajan,Kailash C. Pradhan 한국외국어대학교 인도연구소 2018 남아시아연구 Vol.24 No.1

Using a unique panel data for rural India for the periods 1999 and 2006 this paper models vulnerability to poverty. We quantify household vulnerability in rural India in 1999 and 2006, investigate the determinants of ex post poverty as well as ex ante vulnerability, assess the role of ex ante vulnerability on poverty shift during the sample periods (i.e. movement into/out of poverty) and finally, examine how the effects of the determinants of vulnerability vary at different points across the vulnerability distribution. We conclude that over time economic growth has reduced the incidence of poverty. Although chronic poverty is relatively small the high incidence of transient poverty underscores the importance of covariate and idiosyncratic shocks. Household vulnerability across the distribution of such vulnerability is also investigated. A number of factors affect such vulnerability across this distribution. Thus the paper isolates a number of characteristics of households and policy variables which can be targeted to reduce the incidence of vulnerability in rural India.

Vulnerability and Responses to Risk in Rural India

Jha, Raghbendra,Kang, Woojin(강우진),Nagarajan, Hari K.,Pradhan, Kailash C. 한국외국어대학교 인도연구소 2020 남아시아연구 Vol.26 No.3

인도의 비 도시 지역 패널 가계조사를 활용하여 비 도시 지역 가계들의 취약성을 추정한 결과 빈곤과 가계 단위의 개별적인 소득충격이 가계 취약성에 크게 영향을 미치는 것으로 나타났다. 이들 가계들은 저축, 현금 이전, 자산처분 등과 같은 가계단위에서의 비공식적 수단을 동원하여 위험에 대처하고 있다. 그러나 소비수준이 소득변화에 크게 연동되어 움직인다는 사실은 그와 같은 비공식적인 자구책이 소득감소에 대한 완충역할을 충분히 하지 못하고 있음을 의미한다. 한편, 공적 위기대처 방안의 경우 가계취약성을 줄이는 것으로 나타났으나 이들 프로그램에 대한 접근은 매우 제한적이다. 이에 따라 인도 정부는 접근성과 정책조준성이 뛰어난 공적 사회안전망을 수립 할 필요가 있으며 정부지원 프로그램의 확대는 소득 충격의 상황에서 가계소비 평준화에 큰 역할을 할 것으로 기대된다. Drawing upon a representative panel household survey for rural India, this paper demonstrates that household vulnerability in rural India is largely explained by poverty and idiosyncratic components. So far as risk coping strategies go, households rely heavily on informal instruments such as their own saving, transfers or capital depletion. Household consumption, however, is highly covariate with income and this implies that existing informal insurance instruments are not sufficient to protect household consumption against income shocks. Hence, an important policy implication of our analysis is that the government should provide readily accessible and well-targeted public safety nets given that the existing informal strategy is not very effective as a consumption insurance mechanism. Although the public risk coping programme is found to reduce vulnerability, access to such programmes is constrained. Expansion of government sponsored coping programmes is likely to protect households effectively from negative shocks.

Debt Sustainabilityin East Asia after the Financial Crisis

허현승,구정모,Raghbendra Jha 한국경제연구학회 2005 Korea and the World Economy Vol.6 No.2

Debt sustainability in East Asia after the Financial Crisis

GEN,Jha,Raghbendra,구정모 한국경제연구학회 2005 The Journal of the Korean Economy Vol.6 No.2

Catalase inhibition induces pexophagy through ROS accumulation

Lee, Joon No,Dutta, Raghbendra Kumar,Maharjan, Yunash,Liu, Zhi-qiang,Lim, Jae-Young,Kim, Se-Jin,Cho, Dong-Hyung,So, Hong-Seob,Choe, Seong-Kyu,Park, Raekil Elsevier 2018 Biochemical and biophysical research communication Vol.501 No.3

<P><B>Abstract</B></P> <P>Peroxisomes are dynamic and multifunctional organelles involved in various cellular metabolic processes, and their numbers are tightly regulated by pexophagy, a selective degradation of peroxisomes through autophagy to maintain peroxisome homeostasis in cells. Catalase, a major peroxisome protein, plays a critical role in removing peroxisome-generated reactive oxygen species (ROS) produced by peroxisome enzymes, but the contribution of catalase to pexophagy has not been reported. Here, we investigated the role of catalase in peroxisome degradation during nutrient deprivation. Both short interfering RNA-mediated silencing of catalase and pharmacological inhibition by 3-aminotriazole (3AT) decreased the number of peroxisomes and resulted in the downregulation of peroxisomal proteins, such as PMP70 and PEX14 under serum starvation. In addition, treatment with 3AT induced NBR1-dependent autophagy and PEX5 ubiquitination in the absence of serum, which was accompanied by accumulation of ROS. Co-treatment with antioxidant agent N-acetyl-<SMALL>L</SMALL>-cysteine (NAC) prevented ROS accumulation and pexophagy by modulating peroxisome protein levels and the association of NBR1, a pexophagy receptor with peroxisomes. Taken together, these findings demonstrate that catalase plays an important role in pexophagy during nutrient deprivation.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Catalase deficiency or its inhibition by 3 A T during serum starvation results in pexophagy. </LI> <LI> Pexophagy mediated by catalase inhibition is accompanied by PEX5 ubiquitination. </LI> <LI> ROS accumulation in peroxisome is the key factor to induce pexophagy. </LI> <LI> N-acetyl-<SMALL>L</SMALL>-cysteine prevents ROS-mediated pexophagy. </LI> </UL> </P>

Autophagy alteration prevents primary cilium disassembly in RPE1 cells

Maharjan, Yunash,Lee, Joon No,Kwak, SeongAe,Lim, Hyewon,Dutta, Raghbendra Kumar,Liu, Zhi-qiang,So, Hong-Seob,Park, Raekil Elsevier 2018 Biochemical and biophysical research communication Vol.500 No.2

<P><B>Abstract</B></P> <P>Primary cilium is a microtubule structure that emanates from the surface of most human cells. Primary cilia assemble during the resting stage (G<SUB>0</SUB> phase) and disassemble with cell cycle progression. Defects associated with the control of the assembly or disassembly of the primary cilium have been implicated in various human diseases, including ciliopathy and cancer. Although studies have suggested the interplay between activation of autophagy and ciliogenesis, any direct mechanism between autophagy abatement and disassembly of primary cilium remains elusive. In this study, we found that the gradual abatement in autophagy during serum-restimulation was a dynamic process and significantly correlated with the disassembly of primary cilium in human retinal pigmented epithelial (RPE1) cells. Although autophagy activity was gradually decreased during serum-restimulation, the alteration in autophagy under the same condition prevented the disassembly of the primary cilium. Autophagy inhibitors such as chloroquine, U18666A and 3-methyladenine (3-MA) retained both the number of ciliated cells and cilium length. In contrast, rapamycin treatment during serum-restimulation maintained the number of ciliated cells with shortened cilia. Taken together, alteration in autophagy during serum-restimulation prevent the disassembly of the primary cilium, and autophagy modulators may serve as useful compounds for studying mechanistic details related to the disassembly of the primary cilium and ciliopathy.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Autophagy abatement and cilia disassembly is correlated during serum-restimulation. </LI> <LI> Both activation and inhibition of autophagy flux during serum-restimulation prevents disassembly of primary cilium. </LI> <LI> Inhibition of autophagy maintains cilium length during serum-restimulation. </LI> <LI> Rapamycin-induced autophagy results in shortened cilium length during serum-restimulation. </LI> </UL> </P>

Ciliogenesis is reciprocally regulated by PPARA and NR1H4/FXR through controlling autophagy in vitro and in vivo

Liu, Zhi-qiang,Lee, Joon No,Son, Myeongjoo,Lim, Jae-Young,Dutta, Raghbendra Kumar,Maharjan, Yunash,Kwak, SeongAe,Oh, Goo Taeg,Byun, Kyunghee,Choe, Seong-Kyu,Park, Raekil Landes Bioscience 2018 AUTOPHAGY Vol.14 No.6

<P>The primary cilia are evolutionarily conserved microtubule-based cellular organelles that perceive metabolic status and thus link the sensory system to cellular signaling pathways. Therefore, ciliogenesis is thought to be tightly linked to autophagy, which is also regulated by nutrient-sensing transcription factors, such as PPARA (peroxisome proliferator activated receptor alpha) and NR1H4/FXR (nuclear receptor subfamily 1, group H, member 4). However, the relationship between these factors and ciliogenesis has not been clearly demonstrated. Here, we present direct evidence for the involvement of macroautophagic/autophagic regulators in controlling ciliogenesis. We showed that activation of PPARA facilitated ciliogenesis independently of cellular nutritional states. Importantly, PPARA-induced ciliogenesis was mediated by controlling autophagy, since either pharmacological or genetic inactivation of autophagy significantly repressed ciliogenesis. Moreover, we showed that pharmacological activator of autophagy, rapamycin, recovered repressed ciliogenesis in ppara(-/-) cells. Conversely, activation of NR1H4 repressed cilia formation, while knockdown of NR1H4 enhanced ciliogenesis by inducing autophagy. The reciprocal activities of PPARA and NR1H4 in regulating ciliogenesis were highlighted in a condition where de-repressed ciliogenesis by NR1H4 knockdown was further enhanced by PPARA activation. The in vivo roles of PPARA and NR1H4 in regulating ciliogenesis were examined in greater detail in ppara(-/-) mice. In response to starvation, ciliogenesis was facilitated in wild-type mice via enhanced autophagy in kidney, while ppara(-/-) mice displayed impaired autophagy and kidney damage resembling ciliopathy. Furthermore, an NR1H4 agonist exacerbated kidney damage associated with starvation in ppara(-/-) mice. These findings indicate a previously unknown role for PPARA and NR1H4 in regulating the autophagy-ciliogenesis axis in vivo.</P>