Trapped in white space : the allegations and denials of organ trafficking

Allegations of body parts trafficking implicating the West have been surfacing persistently in the media of many non Western countries for almost 20 years. Western media has responded to the allegations with denials and denunciations. This thesis considers the competing accounts and places them in a framework for analysis.

MSP119 miniproteins can serve as targets for invasion inhibitory antibodies in plasmodium falciparum provided they contain the correct domains for cell surface trafficking.

Antibodies from malaria-exposed individuals can agglutinate merozoites released from Plasmodium schizonts, thereby preventing them from invading new erythrocytes. Merozoite coat proteins attached to the plasma membrane are major targets for host antibodies and are therefore considered important malaria vaccine candidates. Prominent among these is the abundant glycosylphosphatidylinositol (GPI)-anchored merozoite surface protein 1 (MSP1) and particularly its C-terminal fragment (MSP1(19)) comprised of two epidermal growth factor (EGF)-like modules. In this paper, we revisit the role of agglutination and immunity using transgenic fluorescent marker proteins. We describe expression of heterologous MSP1(19)'miniproteins' on the surface of Plasmodium falciparum merozoites. To correctly express these proteins, we determined that GPI-anchoring and the presence of a signal sequence do not allow default export of proteins from the endoplasmic reticulum to merozoite surface and that extra sequence elements are required. The EGFs are insufficient for correct trafficking unless they are fused to additional residues that normally reside upstream of this fragment. Antibodies specifically targeting the surface-expressed miniprotein can inhibit erythrocyte invasion in vitro despite the presence of endogenous MSP1. Using a line expressing a green fluorescent protein-MSP1 fusion protein, we demonstrate that one mode of inhibition by antibodies targeting the MSP1(19) domain is the rapid agglutinating of merozoites prior to erythrocyte attachment.

Enlistment and non-enlistment in wartime Australia : responses to the 1916 call to arms appeal

This article examines men’s responses to the 1916 ‘Call to Arms’ appeal, in which Australia’s federal government questioned military-aged male citizens on their willingness to enlist voluntarily in the armed forces for service at the front. It argues that the appeal illuminated men’s difficult negotiation of choice, in which they weighed their personal sense of obligation to the state at war, to their families, and to themselves. It shows how men not only confronted their decision, but measured their responsibilities against others’, producing a subjective order of sacrifice that paralysed recruiting. In the absence of conscription, that private decision-making was critical to the nature of Australia’s commitment to the war, as men assessed and re-assessed the limits of obligation for themselves.

Innate immunity and intracellular trafficking : insights for novel anti-HIV-1 therapeutics

It is now evident that host cells have evolved a remarkable variety of antiretroviral activities to defend themselves against viral invaders and in return viruses have developed ingenious ways to circumvent these defences and, in some cases, actually hijack cellular proteins in order to facilitate their replication. Study of this cat and mouse interplay between viruses and their host cells throughout evolution has lead to the identification of some of the most sophisticated antiviral strategies that mammals have developed to prevent viral infection. Recently, a wave of publications has significantly enhanced our understanding of the relationship between human immunodeficiency virus type 1 (HIV-1) and its host, including: 1) the HIV-1 protein Vif and its interaction with host cell nucleic acid editing enzymes; 2) the host cell restrictive factors that provide protection against retroviral infection, such as TRIM5; and 3) the late domains of retroviruses and their relationship with the host cell vacuolar protein sorting pathway. The focus of this review is to provide an up-to-date account of these important areas of HIV-1 research and highlight how some of these new discoveries can potentially be exploited for the development of novel anti-retroviral therapeutics.

Illegal immigration, technology adoption and welfare

A debate in the illegal immigration and technology adoption literature suggests that hiring illegal immigrants may be hindering the adoption of new technology, which in turn harms a country’s productivity growth. This paper analyses an individual firm’s behaviour regarding new technology adoption in the presence of illegal immigrants. We assume a Ricardian economy and analyse immigration of illegal unskilled workers in a model of Cournot duopoly where firms are producing homogenous and non-traded goods, and hiring illegal immigrants. A two-stage simultaneous move game is set up: in Stage 1, given the opportunity of hiring illegal immigrants, an individual firm decides whether to adopt the new technology or not, where technology adoption is costly. In Stage 2, each firm will choose the Cournot output level. Solving this two-stage game, we conclude that (i) given the opportunity of hiring illegal immigrants, an individual firm may adopt the new technology and (ii) in the case of zero tolerance of illegal immigration, technology adoption may increase but such technology adoption is immiserizing as it reduces the total surplus.

Host cell remodelling and protein trafficking

Inside their respective vertebrate hosts, Plasmodium spp spend most of their life residing within hepatocytes and erythrocytes, with large-scale infection of the latter responsible for the clinical symptoms associated with malaria. These parasites extensively remodel these host cells for a variety of purposes relating to both pathogenesis and maintaining growth. Remodelling of the erythrocytic stage has been most intensively studied in P. falciparum and is the subject of this chapter. To help remodel their hosts these parasites export hundreds of proteins into the erythrocytic compartment. This principally alters the architecture of the erythrocyte, rendering the host membrane more permeable to solutes and nutrients, and also increasing the rigidity and adhesiveness of the infected erythrocyte. Moreover, because erythrocytes lack a secretory apparatus, the parasite must also export many additional proteins to help traffic other proteins to their correct destination within the host cell. The functions of some of these exported proteins will be discussed as will recent progress that has been made in unravelling how exported proteins gain access to the host compartment.