Transmission And Distribution Bakshi Pdf 21
Vinnie Breidenthal
The book covers all the aspects of Transmission and Distribution for undergraduate course. The various aspects of transmission and distribution systems, FACTS, sag calculations, parameters and performance of transmission lines, insulators, cables, substations and grounding systems are explained in the book with the help of comprehensive approach.
Background: Rational development of drugs to prevent human immunodeficiency virus (HIV) transmission benefits from an understanding HIV distribution in the female genital tract after intercourse. This study describes HIV distribution using surrogates of cell-free and cell-associated HIV and semen.
Methods: Apheresis-derived, autologous, lymphocyte-rich cells radiolabeled with 3.7-MBq (100-μCi) indium 111 ((111)In)-oxine (cell-associated HIV surrogate) and 18.5-MBq (500-μCi) technetium 99m ((99m)Tc)-sulfur colloid (HIV-sized 100-nm particle, cell-free HIV surrogate) were resuspended in 3 mL of hydroxyethylcellulose gel (semen simulant) with gadoteridol and dosed via artificial phallus after simulated intercourse. Postdosing dual-isotope single photon emission computed tomography with computed tomography (SPECT/CT) and magnetic resonance (MR) images were acquired to determine the surrogates' distribution. Seven hours after dosing, vaginal biopsy and luminal samples were collected at discrete locations in 8 subjects.
Results: SPECT/CT and MR analysis showed HIV and semen surrogate distribution with highest signal intensity in the vaginal pericervical area, without detectable signal in the uterus. One-third of the administered dose was retained in the female genital tract after 4 hours. Cell-free and cell-associated surrogate distribution coincided.
Conclusions: We demonstrate the feasibility of dual-isotope SPECT/CT and MR imaging to determine the distribution of HIV and semen surrogates after simulated intercourse without disrupting vaginal contents. Surrogate distribution suggests topical microbicides do not need to reach the uterus for efficacy.
Traditional asset pricing models have mainly focused oncharacterizing the reward for equity risk. However, such modelstypically fail to capture the reward for bearing variance risk. Thevariance risk premium is formally defined as the difference betweenthe risk neutral and the physical expectation of the total returnvariation. It can be estimated using model-free measures as thedifference between the option implied variance and the expectedrealized variance. The observed variance premium in the US is largeand varies significantly over time. In order to generate atime-varying variance premium, standard asset pricing models havebeen adjusted in different ways. One strand of the literature, andthe one that will be followed in this paper, links the variancerisk premium to macroeconomic uncertainty. This strand follows theintuition behind the long-run risk model in Bansal and Yaron (2004)(BY hereafter), and the idea that agents have a preference for anearly resolution of uncertainty in Bansal et. al. (2005). ExtendingBY's model, Bollerslev, Tauchen and Zhou (2009) (BTZ hereafter)show that the variance premium predicts equity returns; animplication for which they find empirical evidence for the US. Analternative strand of the literature relates the variance premiumto agents' attitudes towards non-normalities in the distribution ofreturns. In Bakshi and Madam (2006), for example, the variance riskpremium is explained by the desire of risk averse agents to buyprotection against extreme events. In a similar vein, Bekaert andEngstrom (2010), Todorov (2010), and Gabaix (2009), using differentmethodologies, focus on the interplay between returns, riskaversion and extreme events to explain many asset pricingregularities, including the variance risk premium.
The strictly domestic nature of the existing models motivatesthe theoretical contribution of this paper. In the second part, Ipropose a model to investigate the role of the variance premium inexplaining the interactions across international equity and optionmarkets. The model is a two-country extension of that in BTZ andextends the intuition that agents have a preference for an earlyresolution of uncertainty to an international setting. Themacroeconomic uncertainty is characterized in my model by thedynamics of the consumption growth volatility of each country andis allowed to be transmitted across countries given a uniquerepresentative agent endowed with recursive preferences. In such asetting, the shocks to macroeconomic uncertainty in any countrycharacterize the variance premium in all countries. In particular,the variance premiums of the two countries reveal the volatility ofvolatility of consumption generated in both countries. Given thatchanges in the volatility of volatility also explain a portion ofthe total risk premiums of any country, the model not only impliesthat variance risk is priced but also provides the intuition forthe potential role of the variance premium of any country inpredicting local and foreign equity returns. In other words, agentsdemand a reward for the existing local and foreign sources of risk(i.e., the volatility and the volatility of volatility ofconsumption). Although this uncertainty transmission mechanism isbidirectional, the model explicitly features a leader economy. Theconsumption process of this leader economy is entirely driven bylocal shocks. However, the shocks of the leader country consumptionprocess can be partially transmitted to a second country, thefollower.
In this section, I present some numerical simulations of mymodel in order to investigate the mechanism of transmission of VoVshocks across countries. The purpose of these simulations is toanalyze the qualitative implications of my model for the variancepremiums and for the interaction between the variance premiums andthe equity returns. Understanding these qualitative implicationsprovides a natural step between the model and the empiricalevidence presented in the next section.
The possibility of VoV loading negatively on the equity premiumscan actually be explained by the mechanism of transmission ofshocks to VoV implied by the model. According to this mechanism, apositive shock to VoV in the follower country has a negative impacton the leader country's equity premium. This effect can beinterpreted as a macroeconomic uncertainty induced flight-to-safetyfrom the follower to the leader economy. The possibility of anuncertainty flight-to-safety in this direction is actuallygenerated by the fact that the leader country consumption processis, by construction, not sensitive to the shocks generated in thefollower country (Eq. (1)). Investingin equities in the leader country is then expected to become a moreattractive investment alternative with respect to this foreignsource of risk. In contrast, an uncertainty flight-to-safety in theother direction (leader to follower) is not always possible. Thisis due to the fact that the follower country consumption process isaffected by the shocks in the leader economy (Eq. (2)).Therefore, a flight-to-safety in this direction is only possible ifthe economies are assumed to be quite independent from each other.For example, in the case of totally independent economies in PanelJ, any equity market is free from the uncertainty risk generated inthe foreign economy. Thus, in this extreme case, the VoV of onecountry will always load negatively on the other country's equitypremium.
Natural gas is one of the cheapest forms of energy and is the source of more than 30% of the energy produced in the USA [1]. 280,000 miles of gas transmission lines, 90,000 miles of gathering lines and 835,000 miles of distribution lines form a vast network across the country. It is imperative to assure the integrity of this vast network, for safe and economical transport of gas.
Background: CAB LA dosed at 2-month intervals demonstrated viro-logic efficacy in maintaining HIV-1 suppression as part of a dual regimen with rilpivirine LA and is undergoing Phase 3 evaluation as a single agent for HIV-1 pre-exposure prophylaxis (PrEP). CAB pharma-cokinetics (PK) in plasma and mucosal tissues associated with sexual HIV-1 transmission were evaluated following single CAB LA IM injection.
Conclusions: Plasma CAB PK was consistent with prior studies, and CAB concentrations in tissue and fluid were proportional to plasma over time. Correlations with plasma concentrations were stronger for tissue (RT, CT, VT) than for luminal fluid (CF and RF). Tissue concentrations were 1/6th (CT, VT) to 1/10th (RT) of plasma concentrations. With sufficient distribution into mucosal tissues associated with sexual HIV-1 transmission, CAB tissue:plasma ratios may serve as important measurements in evaluating CAB LA as an effective PrEP agent.
Recent results have suggested a role for prolactin (PRL) as a regeneration factor in the liver. In order to investigate the involvement of prolactin in the pathogenesis of liver cirrhosis, we studied the expression of the prolactin receptor (PRLR) and PRL during the development of cirrhosis in an animal model. 30 male rats were exposed to CCl4 by inhalation. Phenobarbitone was added to the drinking water to accelerate the formation of toxic metabolites by enzyme induction. Two control groups of 30 animals each were treated with phenobarbitone only or received no treatment. 10 animals of each group were sacrificed 35, 55, and 70 days after initiation of treatment. Liver tissue was subjected to histological examination, which demonstrated fibrosis of different grades and cirrhosis in the CCl4-treated rats. Expression of PRLR mRNA was investigated by mRNA extraction, RT-PCR and computer-supported densitometric evaluation. Compared to control liver, PRLR mRNA was expressed at a higher level in fibrotic and cirrhotic liver specimens. In normal tissue, immunohistochemical staining showed a high concentration of PRLR around the central vein and in the epithelium of the bile ducts. This pattern of distribution was lost in fibrosis and cirrhosis. An accumulation of PRLR was demonstrated within the damaged cells. Neither PRL nor PRL mRNA was detectable in normal, fibrotic, or cirrhotic liver. We conclude that PRLR is distributed in normal rat liver in a typical pattern which is lost with increasing fibrosis. PRL is not produced by rat liver, indicating that PRL does not act through autocrine or paracrine mechanisms.
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