56,079 research outputs found

    Mapping the significance of green venture capital for sustainable development: A systematic review and future research agenda

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    Sustainable Development has become a key concern throughout the world after the United Nations set 2030 as the SDGs deadline. A lot of concerted efforts have already been taken and currently undergoing to combat the global menace of climate change, carbon dioxide removal, adoption of renewable energy, and many more. All of these cannot be achieved with the sole support of public funds or traditional sources of finance. This is where venture capital (VC) steps in and fulfill the gap. Over the past few years, VCs have also been channelizing their investment flows as per the ‘triple bottom line’ towards startups and businesses which comes under the aspect of cleantech, sustainable entrepreneurship, technological innovations, green innovation, and sustainability. These VCs which focus on environmental protection are the Green Venture Capital (GVC). This research study provides a holistic overview of the available literature to highlight the significance of GVCs for attaining sustainable development. The present study has summarized 179 research articles from the time period 2002 to 2022 through a systematic literature review. The research articles gave four major thematic clusters, namely- Transition towards GVC, GVC and Cleantech, GVC and Sustainability, and Policy-Push for GVC. The present study provides a brief summary of these themes and the future research directions which can be explored

    Search for CPCP violation in D(s)+K+KS0h+hD^{+}_{(s)}\rightarrow K^{+}K^{0}_{S}h^{+}h^{-} (h=K,π)(h=K,\pi) decays and observation of the Cabibbo-suppressed decay Ds+K+KKS0π+D^{+}_{s}\rightarrow K^{+}K^{-}K^{0}_{S}\pi^{+}

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    We search for CPCP violation by measuring a TT-odd asymmetry in the Cabibbo-suppressed D+K+KS0π+πD^{+}\rightarrow K^{+}K^{0}_{S}\pi^{+}\pi^{-} decay, and in the Cabibbo-favored Ds+K+KS0π+πD^{+}_{s}\rightarrow K^{+}K^{0}_{S}\pi^{+}\pi^{-} and D+K+KKS0π+D^{+}\rightarrow K^{+}K^{-}K^{0}_{S}\pi^{+} decays. We use 980 fb1{\rm fb}^{-1} of data collected by the Belle detector running at the KEKB asymmetric-energy e+ee^{+}e^{-} collider. The C ⁣PC\!P-violating TT-odd parameter aCPT-odd{a}^{T\text{-}\rm{odd}}_{CP} is measured to be aCPT-odd(D+K+KS0π+π)=(0.34±0.87±0.32)%,{a}^{T\text{-}\rm{odd}}_{CP}(D^{+}\rightarrow K^{+}K^{0}_{S}\pi^{+}\pi^{-})=(0.34\pm0.87\pm0.32)\%, aCPT-odd(Ds+K+KS0π+π)=(0.46±0.63±0.38)%,{a}^{T\text{-}\rm{odd}}_{CP}(D^{+}_{s}\rightarrow K^{+}K^{0}_{S}\pi^{+}\pi^{-})=(-0.46\pm0.63\pm0.38)\%, and aCPT-odd(D+K+KKS0π+)=(3.34±2.66±0.35)%,{a}^{T\text{-}\rm{odd}}_{CP}(D^{+}\rightarrow K^{+}K^{-}K^{0}_{S}\pi^{+})=(-3.34\pm2.66\pm0.35)\%, where the first uncertainty is statistical and the second is systematic. We also report the first observation of the Cabibbo-suppressed decay Ds+K+KKS0π+D^{+}_{s}\rightarrow K^{+}K^{-}K^{0}_{S}\pi^{+}. The branching fraction is measured relative to that of the analogous Cabibbo-favored decay : B(Ds+K+KKS0π+)/B(Ds+K+KS0π+π)=(1.36±0.15±0.04)%B(D^{+}_{s}\rightarrow K^{+}K^{-}K^{0}_{S}\pi^{+}) / B(D^{+}_{s}\rightarrow K^{+}K^{0}_{S}\pi^{+}\pi^{-}) = (1.36\pm 0.15\pm 0.04)\%

    Search for CP violation in D s + → K S 0 K − π + π + D(s)+KS0Kπ+π+ {D}_{(s)}^{+}\to {K}_S^0{K}^{-}{\pi}^{+}{\pi}^{+} decays using triple and quadruple products

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    Abstract We perform the first search for CP violation in D s + → K S 0 K − π + π + D(s)+KS0Kπ+π+ {D}_{(s)}^{+}\to {K}_S^0{K}^{-}{\pi}^{+}{\pi}^{+} decays. We use a combined data set from the Belle and Belle II experiments, which study e + e − collisions at center-of-mass energies at or near the Υ(4S) resonance. We use 980 fb −1 of data from Belle and 428 fb −1 of data from Belle II. We measure six CP-violating asymmetries that are based on triple products and quadruple products of the momenta of final-state particles, and also the particles’ helicity angles. We obtain a precision at the level of 0.5% for D + → K S 0 K − π + π + D+KS0Kπ+π+ {D}^{+}\to {K}_S^0{K}^{-}{\pi}^{+}{\pi}^{+} decays, and better than 0.3% for D s + → K S 0 K − π + π + Ds+KS0Kπ+π+ {D}_s^{+}\to {K}_S^0{K}^{-}{\pi}^{+}{\pi}^{+} decays. No evidence of CP violation is found. Our results for the triple-product asymmetries are the most precise to date for singly-Cabibbo-suppressed D + decays. Our results for the other asymmetries are the first such measurements performed for charm decays

    Measurement of the branching fractions for Cabibbo-suppressed decays D+→K+K−π+π0 and D(s)+→K+π−π+π0 at Belle

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    We present measurements of the branching fractions for the singly Cabibbo-suppressed decays D+→K+K−π+π0 and D+s→K+π−π+π0, and the doubly Cabibbo-suppressed decay D+→K+π−π+π0, based on 980 fb−1 of data recorded by the Belle experiment at the KEKB e+e− collider. We measure these modes relative to the Cabibbo-favored modes D+→K−π+π+π0 and D+s→K+K−π+π0. Our results for the ratios of branching fractions are B(D+→K+K−π+π0)/B(D+→K−π+π+π0)=(11.32±0.13±0.26)%, B(D+→K+π−π+π0)/B(D+→K−π+π+π0)=(1.68±0.11±0.03)%, and B(D+s→K+π−π+π0)/B(D+s→K+K−π+π0)=(17.13±0.62±0.51)%, where the uncertainties are statistical and systematic, respectively. The second value corresponds to (5.83±0.42)×tan4θC, where θC is the Cabibbo angle; this value is larger than other measured ratios of branching fractions for a doubly Cabibbo-suppressed charm decay to a Cabibbo-favored decay. Multiplying these results by world average values for B(D+→K−π+π+π0) and B(D+s→K+K−π+π0) yields B(D+→K+K−π+π0)=(7.08±0.08±0.16±0.20)×10^−3, B(D+→K+π−π+π0)=(1.05±0.07±0.02±0.03)×10^−3, and B(D+s→K+π−π+π0)=(9.44±0.34±0.28±0.32)×10^−3, where the third uncertainty is due to the branching fraction of the normalization mode. The first two results are consistent with, but more precise than, the current world averages. The last result is the first measurement of this branching fraction

    Branching fraction and CP asymmetry of the decays B+→K0Sπ+ and B+→K0SK+

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    An analysis of B+ → K0 Sπ+ and B+ → K0 S K+ decays is performed with the LHCb experiment. The pp collision data used correspond to integrated luminosities of 1 fb−1 and 2 fb−1 collected at centre-ofmass energies of √ s = 7 TeV and √ s = 8 TeV, respectively. The ratio of branching fractions and the direct CP asymmetries are measured to be B(B+ → K0 S K+ )/B(B+ → K0 Sπ+ ) = 0.064 ± 0.009 (stat.) ± 0.004 (syst.), ACP(B+ → K0 Sπ+ ) = −0.022 ± 0.025 (stat.) ± 0.010 (syst.) and ACP(B+ → K0 S K+ ) = −0.21 ± 0.14 (stat.) ± 0.01 (syst.). The data sample taken at √ s = 7 TeV is used to search for B+ c → K0 S K+ decays and results in the upper limit ( fc · B(B+ c → K0 S K+ ))/( fu · B(B+ → K0 Sπ+ )) < 5.8 × 10−2 at 90% confidence level, where fc and fu denote the hadronisation fractions of a ¯b quark into a B+ c or a B+ meson, respectively

    Structural pathology and functional analysis of vitamin K-dependent protein S

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    Protein S deficiency is an autosomal dominant trait affecting around 10% of families thrombophilic families. The high affinity interaction of approximately 60% of protein S with C4b -binding protein (C4BP) has raised a complicated situation for the diagnosis of deficiency states. Because only free protein S functions as cofactor in the protein C anticoagulant, it is important to measure free protein S level precisely. In this study a free protein S assay was developed using its natural ligand C4BP to capture free protein S from plasma for routine clinical purpose. Although interference by C4BP is so far considered as the major hindrance for developing ELISA, the new approach has utilized this phenomenon of high affinity interaction between protein S and C4BP, thereby reversing the adverse effect of C4BP to one of good use. (1) Mutations in a variety of human genes are now known to predispose to venous thrombosis. Characterization of the wide spectrum of gene mutations causing thrombosis may allow us to relate specific gene lesions to the probability of thromboembolism as well as to the severity of thrombotic episodes, beside providing the molecular mechanism of deficiency states. To establish the relationship between genetic abnormalities of protein S and their phenotypic expressions, four naturally occurring missense mutations were chosen to analyze thier in vitro secretion profiles and functional characteristics, which illustrated the importance of in vitro experimental characterization in each and individual cases of naturally occurring missense mutations before marking them as the underlying genetic defect. (2) Since early nineties, the suggestion about the synergistic effect between two thrombotic risk factors when associated in one patient has been lacking a biochemical basis. The now observed deficient APC-cofactor activity of protein S Heerlen in the degradation of FVa Leiden suggests a possible synergistic pathogenic mechanism between these two genetic traits resulting in increased risk of thrombosis. (3) In addition, using two monoclonal antibodies as probes the structure-function relationship studies on protein S and APC interaction were carried out. R49, Q52 in TSR was found to be part of the epitope of monoclonal HPS 67 and K97, T103 in EGF1 for monoclonal HPS 54. These data implicated indirectly as the key amino acids for APC interaction, based on the fact that these two antibodies could completely block the APC-cofactor activity of protein S. The observation that HPS 67 did not inhibit phospholipid binding of protein S has implications for the possible orientation of protein S on the membrane surface, suggesting that TSR is free to interact with membrane-bound APC. (4) Also, evaluation of the importance of amino acid residues 447-460 in protein S for binding to C4BP was performed. One amino acid Y456 was found to be important residue for C4BP interaction in this region. However, blocking this region by monoclonal antibody HPS 34 was not sufficient enough to inhibit protein S-C4BP interaction completely, suggesting that the interaction site constitute a fairly large binding surface

    Depolarization and decreased surface expression of K+ channels contribute to NSAID-inhibition of intestinal restitution

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    Non-steroidal anti-inflammatory drugs (NSAIDs) contribute to gastrointestinal ulcer formation by inhibiting epithelial cell migration and mucosal restitution; however, the drug-affected signaling pathways are poorly defined. We investigated whether NSAID inhibition of intestinal epithelial migration is associated with depletion of intracellular polyamines, depolarization of membrane potential (Em) and altered surface expression of K+ channels. Epithelial cell migration in response to the wounding of confluent IEC-6 and IEC-Cdx2 monolayers was reduced by indomethacin (100μM), phenylbutazone (100μM) and NS-398 (100μM) but not by SC-560 (1μM). NSAID-inhibition of intestinal cell migration was not associated with depletion of intracellular polyamines. Treatment of IEC-6 and IEC-Cdx2 cells with indomethacin, phenylbutazone and NS-398 induced significant depolarization of Em, whereas treatment with SC-560 had no effect on Em. The Em of IEC-Cdx2 cells was: −38.5±1.8mV under control conditions; −35.9±1.6mV after treatment with SC-560; −18.8±1.2mV after treatment with indomethacin; and −23.7±1.4mV after treatment with NS-398. Whereas SC-560 had no significant effects on the total cellular expression of Kv1.4 channel protein, indomethacin and NS-398 decreased not only the total cellular expression of Kv1.4, but also the cell surface expression of both Kv1.4 and Kv1.6 channel subunits in IEC-Cdx2. Both Kv1.4 and Kv1.6 channel proteins were immunoprecipitated by Kv1.4 antibody from IEC-Cdx2 lysates, indicating that these subunits co-assemble to form heteromeric Kv channels. These results suggest that NSAID inhibition of epithelial cell migration is independent of polyamine-depletion, and is associated with depolarization of Em and decreased surface expression of heteromeric Kv1 channels.ID: S0006295207001931; M3: Article; Accession Number: S0006295207001931; Author: L.C. Freeman (b); Author: D.F. Narvaez (a); Author: A. McCoy (a); Author: F.B. von Stein (c); Author: S. Young (b); Author: K. Silver (a); Author: S. Ganta (b); Author: D. Koch (b); Author: R. Hunter (b); Author: R.F. Gilmour (c); Author: J.D. Lillich (a, ⁎); Affiliation: Department of Clinical Sciences, Kansas State University, Manhattan, KS 66506, United States; Affiliation: Department of Anatomy and Physiology, Kansas State University, Manhattan, KS 66506, United States; Affiliation: Department of Biomedical Sciences, Cornell University, Ithaca, NY 14853, United States; Keyword: Non-steroidal anti-inflammatory drugs; Keyword: Intestinal epithelial cells; Keyword: Membrane potential; Keyword: Potassium channels; Number of Pages: 12; Language: English;Source type: Electronic(1)http://search.ebscohost.com/login.aspx?direct=true&db=edselp&AN=S0006295207001931&site=eds-live&scope=sit

    Structural pathology and functional analysis of vitamin K-dependent protein S

    No full text
    Protein S deficiency is an autosomal dominant trait affecting around 10% of families thrombophilic families. The high affinity interaction of approximately 60% of protein S with C4b -binding protein (C4BP) has raised a complicated situation for the diagnosis of deficiency states. Because only free protein S functions as cofactor in the protein C anticoagulant, it is important to measure free protein S level precisely. In this study a free protein S assay was developed using its natural ligand C4BP to capture free protein S from plasma for routine clinical purpose. Although interference by C4BP is so far considered as the major hindrance for developing ELISA, the new approach has utilized this phenomenon of high affinity interaction between protein S and C4BP, thereby reversing the adverse effect of C4BP to one of good use. (1) Mutations in a variety of human genes are now known to predispose to venous thrombosis. Characterization of the wide spectrum of gene mutations causing thrombosis may allow us to relatespecific gene lesions to the probability of thromboembolism as well as to the severity of thrombotic episodes, beside providing the molecular mechanism of deficiency states. To establish the relationship between genetic abnormalities of protein S and their phenotypic expressions, four naturally occurring missense mutations were chosen to analyze thier in vitro secretion profiles and functional characteristics, which illustrated the importance of in vitro experimental characterization in each and individual cases of naturally occurring missense mutations before marking them as the underlying genetic defect. (2) Since early nineties, the suggestion about the synergistic effect between two thrombotic risk factors when associated in one patient has been lacking a biochemical basis. The now observed deficient APC-cofactor activity of protein S Heerlen in the degradation of FVa Leiden suggests a possible synergistic pathogenic mechanism between these two genetic traits resulting in increased risk of thrombosis. (3) In addition, using two monoclonal antibodies as probes the structure-function relationship studies on protein S and APC interaction were carried out. R49, Q52 in TSR was found to be part of the epitope of monoclonal HPS 67 and K97, T103 in EGF1 for monoclonal HPS 54. These data implicated indirectly as the key amino acids for APC interaction, based on the fact that these two antibodies could completely block the APC-cofactor activity of protein S. The observation that HPS 67 did not inhibit phospholipid binding of protein S has implications for the possible orientation of protein S on the membrane surface, suggesting that TSR is free to interact with membrane-bound APC. (4) Also, evaluation of the importance of amino acid residues 447-460 in protein S for binding to C4BP was performed. One amino acid Y456 was found to be important residue for C4BP interaction in this region. However, blocking this region by monoclonal antibody HPS 34 was not sufficient enough to inhibit protein S-C4BP interaction completely, suggesting that the interaction site constitute a fairly large binding surface

    Duygusal zekan n kad n giri imcili i üzerine etkisi: Samsun ili örne i

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    Gerçekle tirilen bu çal ma duygusal zekân n kad n giri imcilik üzerine etkisini incelemesi aç s ndan önem arz etmektedir. Bu ba lamda duygusal zekây desteklemeye yönelik çal malar kad n giri imcilikte ba ar n n artmas na sebep olarak görülerek, duygusal zekân n kad n giri imcilik üzerinde pozitif etki olu turaca varsay m ile çal ma gerçekle tirilmi tir. Duygusal zekân n kad n giri imcili i üzerinde etkisi tüm zekâ, duygu kavramlar ve alt boyutlar çal ma kapsam nda yer alm bu ili ki bütün yönleri ile inceleme alan bulmu tur. Ara t rman n örneklemini, evren içerisinde kolayda örneklem yöntemi ile seçilen, Samsun Ticaret ve Sanayi Odas na kay tl 82 kad n giri imci olu turmaktad r. Yap lan analizlerde; kat l mc lar n demografik özelliklerine göre gruplara ait frekans (n) ve yüzde (%) de erlerine birlikte yer verilmi tir. Daha sonra ara t rma kapsam nda kullan lan ölçekler, güvenilirlik analizleri, ortalama kar la t rma testleri, ilgile im analizleri ve basit do rusal regresyon analizi teknikleri yer almaktad r. Yine bu çal mada; ara t rmaya kat lanlar n medeni durum, çocuk say s , ayl k gelir, e itim durumu, e in e itim durumu, anne ve baban n e itim durumu, anne ve baban n çal ma durumu, ailedeki giri imci durumu ve yak nl k derecesine yer verilmi tir. ya am na ili kin bilgiler ise; faaliyet gösterilen sektör, y l, konum, toplam çal an say s , daha önceden giri imcilik faaliyetinde bulunuldu mu, kaç y l olmak üzere kat l mc lar n demografik de i kenler aç s nda incelenmi ve elde edilen analiz sonuçlar yorumlanm t r. Sonuç olarak yap lan bu çal mada duygusal zekâ ile kad n giri imcilik aras ndaki ili ki irdelenmi tir
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