The Capability Approach: Comparing Amartya Sen and Martha Nussbaum

Capability approach pioneered by Amartya Sen has been a new milestone for analyzing poverty through gender perspective. Since the introduction of the approach, numerous scholars from various fields have applied this approach in their studies. One of the prominent scholars who has contributed and expanded the approach is Martha Nussbaum. Though there have been some agreements but the arguments between the two scholars have shed new insights about the poor and their situation. Therefore, this paper attempts to compare Sen‘s and Nussbaum‘s capability approach by focusing on their core concepts, main arguments and rationality of the criticism of the approach. The methodology of this paper is based on document research

Gender socialization and capability deprivation on child urban poverty: experiences of Malaysian Indian women

Child poverty is a crucial component of the urban poverty issue, especially in developing countries, such as Malaysia. The negative effects of deprivation due to gender socialization and capability expansion during childhood are likely to have more difficulty escaping poverty as adults. This study shows the influence of gender socialization experiences of Indian women living in poverty and the state of development of their capabilities due to the constraints faced in their household during their childhood. Hence, Amartya Sen’s capability approach was applied throughout the study to be able to analyze the gender complexities in poor households in two selected urban areas: Seberang Perai Tengah and Timur Laut in Penang, Malaysia. Data were collected from in-depth interviews with ten urban poor Indian women participants who retrospectively described their experiences growing up in poverty during their childhood era. The finding of this study reveals traditional feminine norms, unequal distribution of resources and differential treatment of boys and girls as three important themes. The themes reaffirm that girls face differentiation based on their gender and unequal access to resources in the household. The implications of these findings of the study ensure us to revisit the child poverty from gender lens with more in-depth and multidimensional perspective

A36-dependent Actin Filament Nucleation Promotes Release of Vaccinia Virus

Cell-to-cell transmission of vaccinia virus can be mediated by enveloped virions that remain attached to the outer surface of the cell or those released into the medium. During egress, the outer membrane of the double-enveloped virus fuses with the plasma membrane leaving extracellular virus attached to the cell surface via viral envelope proteins. Here we report that F-actin nucleation by the viral protein A36 promotes the disengagement of virus attachment and release of enveloped virus. Cells infected with the A36(YdF) virus, which has mutations at two critical tyrosine residues abrogating localised actin nucleation, displayed a 10-fold reduction in virus release. We examined A36(YdF) infected cells by transmission electron microscopy and observed that during release, virus appeared trapped in small invaginations at the plasma membrane. To further characterise the mechanism by which actin nucleation drives the dissociation of enveloped virus from the cell surface, we examined recombinant viruses by super-resolution microscopy. Fluorescently-tagged A36 was visualised at sub-viral resolution to image cell-virus attachment in mutant and parental backgrounds. We confirmed that A36(YdF) extracellular virus remained closely associated to the plasma membrane in small membrane pits. Virus-induced actin nucleation reduced the extent of association, thereby promoting the untethering of virus from the cell surface. Virus release can be enhanced via a point mutation in the luminal region of B5 (P189S), another virus envelope protein. We found that the B5(P189S) mutation led to reduced contact between extracellular virus and the host membrane during release, even in the absence of virus-induced actin nucleation. Our results posit that during release virus is tightly tethered to the host cell through interactions mediated by viral envelope proteins. Untethering of virus into the surrounding extracellular space requires these interactions be relieved, either through the force of actin nucleation or by mutations in luminal proteins that weaken these interactions.This work was outlined and supported by Project Grant #632785 of the National Health and Medical Research Council of Australia and The Australian Research Council Federation Discovery Project #1096623. CBW was supported by a National Health and Medical Research Council of Australia Senior Research Fellowship #571905. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript

Acute effects of parainfluenza virus on epithelial electrolyte transport

Parainfluenza viruses are important causes of respiratory disease in both children and adults. In particular, they are the major cause of the serious childhood illness croup (laryngotracheobronchitis). The infections produced by parainfluenza viruses are associated with the accumulation of ions and fluid in the respiratory tract. It is not known, however, whether this accumulation is because of a direct effect of the viruses on ion and fluid transport by the respiratory epithelium. Here we show that a model parainfluenza virus (the Sendai virus), in concentrations observed during respiratory infections, activates Cl- secretion and inhibits Na+ absorption across the tracheal epithelium. It does so by binding to a neuraminidase-insensitive glycolipid, possibly asialo-GM1, triggering the release of ATP, which then acts in an autocrine fashion on apical P2Y receptors to produce the observed changes in ion transport. These findings indicate that fluid accumulation in the respiratory tract associated with parainfluenza virus infection is attributable, at least in part, to direct effects of the virus on ion transport by the respiratory epithelium

The nexus of time poverty and well-being of women from poor households: a Malaysian Indian case scenario

Time autonomy is a core component in measuring the well-being of humans. The interrelation of time and well-being explains the autonomy one holds towards their time and improves their well-being. Scholars have noted that gendered aspects of well-being are always reflected through time poverty. Time autonomy is not always equal for men and women due to the interference of gender complexities in a household. In traditional societies, men’s time is often dedicated to their role as breadwinners while women’s time is often allocated for multiple roles (i.e. caregiver, mother and wife) in the household. Studies have shown that women’s time allocation is always dedicated to their unpaid roles, which add value for the household members but often reduces their own personal well-being. Poor women have been identified as a group greatly affected by time poverty, which pushes them away from attaining well-being. This study intends to show the spectrum of time poverty experiences of Malaysian Indian women which constraints them from attaining physical and mental well-being. Data was gathered through in-depth interviews with twelve Indian women from B40 households in Sungai Petani and Kulim, Kedah, Malaysia. The findings of this study revealed that excessive weight of household chores, performing multiple roles simultaneously and minimal investment towards personal development as the three important themes. Using the themes and narration of poor Indian women, time poverty and its effects on well-being were explored in this study

Cutting edge: Conventional CD8α+ dendritic cells are generally involved in priming CTL immunity to viruses

Dendritic cells (DCs) play a central role in initiating immune responses. Despite this, there is little understanding how different DC subsets contribute to immunity to different pathogens. CD8α DC have been shown to prime immunity to HSV. Whether this very limited capacity of a single DC subset priming CTL immunity is restricted to HSV infection or is a more general property of anti-viral immunity was examined. Here, we show that the CD8α DCs are the principal DC subset that initiates CTL immunity to s.c. infection by influenza virus, HSV, and vaccinia virus. This same subset also dominated immunity after i.v. infection with all three viruses, suggesting a similar involvement in other routes of infection. These data highlight the general role played by CD8α DCs in CTL priming to viral infection and raises the possibility that this DC subset is specialized for viral immunity

Breakdown in repression of IFN-y mRNA leads to accumulation of self-reactive effector CD8+ T Cells

Free to read Tight regulation of virus-induced cytotoxic effector CD8+ T cells is essential to prevent immunopathology. Naturally occurring effector CD8+ T cells, with a KLRG1hi CD62Llo phenotype typical of short-lived effector CD8+ T cells (SLECs), can be found in increased numbers in autoimmune-prone mice, most notably in mice homozygous for the san allele of Roquin. These SLEC-like cells were able to trigger autoimmune diabetes in a susceptible background. When Roquin is mutated (Roquinsan), effector CD8+ T cells accumulate in a cell-autonomous manner, most prominently as SLEC-like effectors. Excessive IFN-γ promotes the accumulation of SLEC-like cells, increases their T-bet expression, and enhances their granzyme B production in vivo. We show that overexpression of IFN-γ was caused by failed posttranscriptional repression of Ifng mRNA. This study identifies a novel mechanism that prevents accumulation of self-reactive cytotoxic effectors, highlighting the importance of regulating Ifng mRNA stability to maintain CD8+ T cell homeostasis and prevent CD8-mediated autoimmunity.</p

Breakdown in repression of IFN-y mRNA leads to accumulation of self-reactive effector CD8+ T cells

Tight regulation of virus-induced cytotoxic effector CD8+ T cells is essential to prevent immunopathology. Naturally occurring effector CD8+ T cells, with a KLRG1hi CD62Llo phenotype typical of short-lived effector CD8+ T cells (SLECs), can be found in increased numbers in autoimmune-prone mice, most notably in mice homozygous for the san allele of Roquin. These SLEC-like cells were able to trigger autoimmune diabetes in a susceptible background. When Roquin is mutated (Roquinsan), effector CD8+ T cells accumulate in a cell-autonomous manner, most prominently as SLEC-like effectors. Excessive IFN-y promotes the accumulation of SLEC-like cells, increases their T-bet expression, and enhances their granzyme B production in vivo. We show that overexpression of IFN-y was caused by failed posttranscriptional repression of Ifng mRNA. This study identifies a novel mechanism that prevents accumulation of self-reactive cytotoxic effectors, highlighting the importance of regulating Ifng mRNA stability to maintain CD8+ T cell homeostasis and prevent CD8-mediated autoimmunity.This work was supported by a Viertel Senior Medical Research Fellowship (to C.G.V.), National Health and Medical Research Council program grants (to C.G.V., J.S., and W.R.H.), and National Institutes of Health Contract BAA-NIAID-DAIT-07-35 (to E.M.B. and G.K.)

A36^YdF is invaginated at the cell membrane during egress.

<p>Representative transmission electron micrographs of BSC-1 cells infected with (<b>A</b>) WR and (<b>B</b>) A36^YdF at an MOI of 5 and fixed at 9 hpi. In contrast to WR, distinct membrane pits containing virus are apparent during A36^YdF virus egress. Scale bar = 0.2 µm. (<b>C</b>) Average percentage of viral membrane circumference in contact with cell membrane calculated from 14 (WR) or 16 (YdF) viruses randomly selected from the transmission electron micrographs. *** = P value of <0.001.</p