10 results on '"Sudan, K."'
Search Results
2. Impact of Microfinance Institutions on Economic Growth of Nepal
- Author
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Sudan K. Oli
- Subjects
Inflation ,Microfinance ,media_common.quotation_subject ,Money supply ,Broad money ,General Medicine ,Per capita income ,Gross domestic product ,Agricultural economics ,law.invention ,law ,Negative relationship ,Loan ,Business ,health care economics and organizations ,media_common - Abstract
This study examines the impact of microfinance institutions on economic growth of Nepal. Gross domestic product and per capita income are the dependent variables. The independent variables are total number of staffs, total number of members, microenterprises credit, total assets, total loan, total deposit, inflation and broad money supply. The study is based on secondary sources of data. The data have been collected for the period of 2012/13 to 2016/17 from 24 microfinance institutions leading to a total of 120 observations. The data are collected from Bank Supervision Report, Quarterly Economic Bulletin published by Nepal Rastra Bank and Economic Survey 2016/17 published by Ministry of Finance. The multiple regression models are estimated to test the significance and impact of microfinance institutions on economic growth of Nepal. The study shows that the total number of staffs, total number of members, ratio of microenterprises loan, total assets, total loan, total deposit and broad money supply growth are positively related to economic growth. It indicates that larger the number of staffs and members of micro-finance institutions, higher would be the economic growth. The results also show that increase in total assets and total loan leads to increase in economic growth. Likewise, the study reveals that higher the amount of total deposits, higher would be the economic growth. Similarly, the study shows that higher the money supply, higher would be the economic growth. However, result shows that there is a negative relationship between inflation and economic growth in Nepal. This indicates that higher the inflation, lower would be the economic growth.
- Published
- 2018
3. Optimizing non-invasive wellness care for maximum impact: Multisensory meditation environments promote wellbeing
- Author
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Moller, H J, Saynor, L, Bal, H, Sudan, K, Moller, H J, Saynor, L, Bal, H, and Sudan, K
- Published
- 2016
4. Optimizing Non-invasive Wellness Care for Maximum Impact: Multisensory Meditation Environments Promote Wellbeing
- Author
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Moller, H J, primary, Saynor, L, additional, Bal, H, additional, and Sudan, K, additional
- Published
- 2016
- Full Text
- View/download PDF
5. Managing Data Placement in Memory Systems with Multiple Memory Controllers
- Author
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Awasthi, M., primary, Nellans, D., additional, Sudan, K., additional, Balasubramonian, R., additional, and Davis, A., additional
- Published
- 2011
- Full Text
- View/download PDF
6. CCL22-Polarized TAMs to M2a Macrophages in Cervical Cancer In Vitro Model.
- Author
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Wang Q, Sudan K, Schmoeckel E, Kost BP, Kuhn C, Vattai A, Vilsmaier T, Mahner S, Jeschke U, and Heidegger HH
- Subjects
- Animals, Biomarkers metabolism, Cell Differentiation, Lipopolysaccharides metabolism, Macrophage Activation, Macrophages metabolism, Mice, Neoplasms metabolism, Tumor-Associated Macrophages
- Abstract
Macrophages are dynamic cells susceptible to the local microenvironment which includes tumor-associated macrophages (TAMs) in cancers. TAMs are a collection of heterogeneous macrophages, including M1 and M2 subtypes, shaped by various activation modes and labeled with various markers in different tumors. CCL22+-infiltrating cells are thought to be significantly associated with the prognosis of cervical cancer patients. Moreover, CCL22 is an established marker of M2a macrophages. Although the phenotypic identification of M1 and M2 macrophages is well established in mice and human macrophages cultured in a medium with fetal calf serum (FCS), fewer studies have focused on M2 subtypes. In addition, the question of whether CCL22 affects polarization of M2a macrophages remains unanswered. This study constructed a co-culture system to shape TAMs in vitro. We found that CCL22 was mainly secreted by TAMs but not cervical cancer cell lines. Human peripheral blood monocytes were differentiated into uncommitted macrophages (M0) and then polarized to M1, M2a, M2b, and M2c macrophages using LPS plus IFNr, IL-4, LPS plus IL1β, and IL-10, respectively. Using flowcytometry, we found CD80++ was the marker of M1 and M2b, CD206++ was the marker of M2a, and CD163++ was the marker of M2c, compared with M0 macrophages. By regulating CCL22, we found that the mean fluorescence intensity (MFI) of CD206 in TAMs was significantly affected compared to the control group. Therefore, CCL22 could polarize TAMs of cervical cancer toward M2a macrophages. In conclusion, our study revealed that CCL22 could be a therapeutic target for cervical cancer, which might be because of its role in regulating macrophage polarization.
- Published
- 2022
- Full Text
- View/download PDF
7. Isolation of Decidual Macrophages and Hofbauer Cells from Term Placenta-Comparison of the Expression of CD163 and CD80.
- Author
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Lasch M, Sudan K, Paul C, Schulz C, Kolben T, Dorp JV, Eren S, Beyer S, Siniscalchi L, Mahner S, Jeschke U, and Meister S
- Subjects
- Antigens, CD, Antigens, Differentiation, Myelomonocytic metabolism, B7-1 Antigen metabolism, Cell Adhesion Molecules metabolism, Female, Humans, Macrophages metabolism, Pregnancy, Placenta metabolism, Receptors, Cell Surface metabolism
- Abstract
(1) Background: Placental immune cells are playing a very important role in a successful placentation and the prevention of pregnancy complications. Macrophages dominate in number and relevance in the maternal and the fetal part of the placenta. The evidence on the polarization state of fetal and maternal macrophages involved in both, healthy and pregnancy-associated diseases, is limited. There is no representative isolation method for the direct comparison of maternal and fetal macrophages so far. (2) Material and Methods: For the isolation of decidual macrophages and Hofbauer cells from term placenta, fresh tissue was mechanically dissected and digested with trypsin and collagenase A. Afterwards cell enrichment was increased by a Percoll gradient. CD68 is represented as pan-macrophage marker, the surface markers CD80 and CD163 were further investigated. (3) Results: The established method revealed a high cell yield and purity of the isolated macrophages and enabled the comparison between decidual macrophages and Hofbauer cells. No significant difference was observed in the percentage of single CD163
+ cells in the distinct macrophage populations, by using FACS and immunofluorescence staining. A slight increase of CD80+ cells could be found in the decidual macrophages. Considering the percentage of CD80+ CD163- and CD80- CD163+ cells we could not find differences. Interestingly we found an increased number of double positive cells (CD80+ CD163+ ) in the decidual macrophage population in comparison to Hofbauer cells. (4) Conclusion: In this study we demonstrate that our established isolation method enables the investigation of decidual macrophages and Hofbauer cells in the placenta. It represents a promising method for direct cell comparison, enzyme independently, and unaffected by magnetic beads, to understand the functional subsets of placental macrophages and to identify therapeutic targets of pregnancy associated diseases.- Published
- 2022
- Full Text
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8. Regulation of Epigenetic Modifications in the Placenta during Preeclampsia: PPARγ Influences H3K4me3 and H3K9ac in Extravillous Trophoblast Cells.
- Author
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Meister S, Hahn L, Beyer S, Paul C, Mitter S, Kuhn C, von Schönfeldt V, Corradini S, Sudan K, Schulz C, Kolben TM, Mahner S, Jeschke U, and Kolben T
- Subjects
- Adult, Benzamides pharmacology, Case-Control Studies, Female, Histones metabolism, Humans, Methylation drug effects, PPAR gamma agonists, PPAR gamma antagonists & inhibitors, PPAR gamma metabolism, Pre-Eclampsia metabolism, Pre-Eclampsia pathology, Pregnancy, Protein Isoforms genetics, Protein Isoforms metabolism, Pyridines pharmacology, Retinoid X Receptor alpha metabolism, Signal Transduction, Thiazolidinediones pharmacology, Trophoblasts drug effects, Trophoblasts pathology, Epigenesis, Genetic, Histones genetics, PPAR gamma genetics, Pre-Eclampsia genetics, Retinoid X Receptor alpha genetics, Trophoblasts metabolism
- Abstract
The aim of this study was to analyze the expression of peroxisome proliferator-activated receptor γ (PPARγ) and retinoid X receptor α (RxRα), a binding heterodimer playing a pivotal role in the successful trophoblast invasion, in the placental tissue of preeclamptic patients. Furthermore, we aimed to characterize a possible interaction between PPARγ and H3K4me3 (trimethylated lysine 4 of the histone H3), respectively H3K9ac (acetylated lysine 9 of the histone H3), to illuminate the role of histone modifications in a defective trophoblast invasion in preeclampsia (PE). Therefore, the expression of PPARγ and RxRα was analyzed in 26 PE and 25 control placentas by immunohistochemical peroxidase staining, as well as the co-expression with H3K4me3 and H3K9ac by double immunofluorescence staining. Further, the effect of a specific PPARγ-agonist (Ciglitazone) and PPARγ-antagonist (T0070907) on the histone modifications H3K9ac and H3K4me3 was analyzed in vitro. In PE placentas, we found a reduced expression of PPARγ and RxRα and a reduced co-expression with H3K4me3 and H3K9ac in the extravillous trophoblast (EVT). Furthermore, with the PPARγ-antagonist treated human villous trophoblast (HVT) cells and primary isolated EVT cells showed higher levels of the histone modification proteins whereas treatment with the PPARγ-agonist reduced respective histone modifications. Our results show that the stimulation of PPARγ-activity leads to a reduction of H3K4me3 and H3K9ac in trophoblast cells, but paradoxically decreases the nuclear PPARγ expression. As the importance of PPARγ, being involved in a successful trophoblast invasion has already been investigated, our results reveal a pathophysiologic connection between PPARγ and the epigenetic modulation via H3K4me3 and H3K9ac in PE.
- Published
- 2021
- Full Text
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9. Normal Development and Function of T Cells in Proline Rich 7 (Prr7) Deficient Mice.
- Author
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Hrdinka M, Sudan K, Just S, Drobek A, Stepanek O, Schlüter D, Reinhold D, Jordan BA, Gintschel P, Schraven B, and Kreutz MR
- Abstract
Transmembrane adaptor proteins (TRAPs) are important organisers for the transduction of immunoreceptor-mediated signals. Prr7 is a TRAP that regulates T cell receptor (TCR) signalling and potently induces cell death when overexpressed in human Jurkat T cells. Whether endogenous Prr7 has a similar functional role is currently unknown. To address this issue, we analysed the development and function of the immune system in Prr7 knockout mice. We found that loss of Prr7 partially impairs development of single positive CD4+ T cells in the thymus but has no effect on the development of other T cell subpopulations, B cells, NK cells, or NKT cells. Moreover, Prr7 does not affect the TCR signalling pathway as T cells derived from Prr7 knockout and wild-type animals and stimulated in vitro express the same levels of the activation marker CD69, and retain their ability to proliferate and activate induced cell death programs. Importantly, Prr7 knockout mice retained the capacity to mount a protective immune response when challenged with Listeria monocytogenes infection in vivo. In addition, T cell effector functions (activation, migration, and reactivation) were normal following induction of experimental autoimmune encephalomyelitis (EAE) in Prr7 knockout mice. Collectively, our work shows that loss of Prr7 does not result in a major immune system phenotype and suggests that Prr7 has a dispensable function for TCR signalling., Competing Interests: The authors have declared that no competing interests exist.
- Published
- 2016
- Full Text
- View/download PDF
10. Functional differences exist between TNFα promoters encoding the common -237G SNP and the rarer HLA-B*5701-linked A variant.
- Author
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Simpson PD, Moysi E, Wicks K, Sudan K, Rowland-Jones SL, McMichael AJ, Knight J, and Gillespie GM
- Subjects
- Animals, B-Lymphocytes drug effects, B-Lymphocytes metabolism, Base Sequence, Cell Line, DNA Methylation drug effects, DNA Methylation genetics, Epigenesis, Genetic drug effects, Genes, Reporter, HIV Infections genetics, Haplotypes genetics, Homozygote, Humans, Lipopolysaccharides pharmacology, Luciferases metabolism, Lymphocyte Activation drug effects, Mice, Molecular Sequence Data, Monocytes cytology, Monocytes drug effects, Protein Binding drug effects, RNA, Messenger genetics, RNA, Messenger metabolism, Software, Solubility, Tetradecanoylphorbol Acetate pharmacology, Transcription Factors metabolism, Tumor Necrosis Factor-alpha biosynthesis, HLA-B Antigens genetics, Polymorphism, Single Nucleotide genetics, Promoter Regions, Genetic genetics, Tumor Necrosis Factor-alpha genetics
- Abstract
A large body of functional and epidemiological evidence have previously illustrated the impact of specific MHC class I subtypes on clinical outcome during HIV-1 infection, and these observations have recently been re-iterated in genome wide association studies (GWAS). Yet because of the complexities surrounding GWAS-based approaches and the lack of knowledge relating to the identity of rarer single nucleotide polymorphism (SNP) variants, it has proved difficult to discover independent causal variants associated with favourable immune control. This is especially true of the candidate variants within the HLA region where many of the recently proposed disease influencing SNPs appear to reflect linkage with 'protective' MHC class I alleles. Yet causal MHC-linked SNPs may exist but remain overlooked owing to the complexities associated with their identification. Here we focus on the ancestral TNFα promoter -237A variant (rs361525), shown historically to be in complete linkage disequilibrium with the 'protective' HLA-B*5701 allele. Many of the ancestral SNPs within the extended TNFα promoter have been associated with both autoimmune conditions and disease outcomes, however, the direct role of these variants on TNFα expression remains controversial. Yet, because of the important role played by TNFα in HIV-1 infection, and given the proximity of the -237 SNP to the core promoter, its location within a putative repressor region previously characterized in mice, and its disruption of a methylation-susceptible CpG dinucleotide motif, we chose to carefully evaluate its impact on TNFα production. Using a variety of approaches we now demonstrate that carriage of the A SNP is associated with lower TNFα production, via a mechanism not readily explained by promoter methylation nor the binding of transcription factors or repressors. We propose that the -237A variant could represent a minor causal SNP that additionally contributes to the HLA-B*5701-mediated 'protective' effect during HIV-1 infection.
- Published
- 2012
- Full Text
- View/download PDF
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