François Hollande is by no means certain to win the French Presidential election. He may yet fall foul of France’s well-known ‘Frontrunner Syndrome’, as Sarkozy’s fightback begins.

In the run up to France’s presidential election on 22 April opinion polls place President Nicolas Sarkozy on the back foot against the Socialist candidate François Hollande. Yet Rainbow Murray argues that the contest is far from over yet. Sarkozy can draw on his recent experience on the European and world stages, and Hollande must overcome historical trends where election frontrunners in France see their support fall dramatically in the immediate run up to Presidential elections

More than a year after the presidential elections, France is still in search of a leader

A little over a year since being elected, French President François Hollande’s popularity in the polls has plummeted as the French economy continues to struggle. Rainbow Murray writes that while Hollande’s first year has been beset by scandals and disappointments, France’s main opposition party, the UMP, have their own share of problems following a divisive leadership contest between François Fillon and Jean-François Copé. She notes that the in-fighting within the UMP may yet pave the way for a political comeback from ex-president Nicolas Sarkozy

French regional elections: failure for the Front National, but little to celebrate for the mainstream

France held the second round of its regional elections on 13 December. As Rainbow Murray writes, the key story to emerge from the election was the failure of the Front National to win in any of the French regions, following a strong showing in the first round of voting. She notes that while the second round will ultimately be regarded as a failure for the Front National, there remains little to celebrate for either the governing Socialist Party or Nicolas Sarkozy’s Republicans

Quotas, Citizens, and Norms of Representation

The author gratefully acknowledges the financial support of the Leverhulme Trust, who funded this research via a Research Fellowship grant

Merit vs Equality? The argument that gender quotas violate meritocracy is based on fallacies

The case against gender quotas often involves the argument of merit. The logic is that we should recruit on the basis of merit, not gender; quotas recruit on the basis of gender and so are by definition unmeritocratic. This is a myth used to justify the privilege-based status quo, argues Rainbow Murray. By focusing on political recruitment, she explains why merit and quotas are not mutually exclusive but that in fact, quotas are essential to a meritocratic system for they open up politics to everyone

The impact of online misogyny on women’s participation: democracy experts respond

Many women, including a number of high-profile British politicians, have been the targets of misogynistic abuse via social media. Democratic Audit recently featured an article by Laura Bates, arguing that this trend has negative effect on rates of female participation in public life. In this post we ask leading democracy and gender experts to respond, sharing their experiences and views on how misogyny undermines democracy

Quotas for Men: Reframing Gender Quotas as a Means of Improving Representation for All

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Genetic regulation of pituitary gland development in human and mouse

Normal hypothalamopituitary development is closely related to that of the forebrain and is dependent upon a complex genetic cascade of transcription factors and signaling molecules that may be either intrinsic or extrinsic to the developing Rathke’s pouch. These factors dictate organ commitment, cell differentiation, and cell proliferation within the anterior pituitary. Abnormalities in these processes are associated with congenital hypopituitarism, a spectrum of disorders that includes syndromic disorders such as septo-optic dysplasia, combined pituitary hormone deficiencies, and isolated hormone deficiencies, of which the commonest is GH deficiency. The highly variable clinical phenotypes can now in part be explained due to research performed over the last 20 yr, based mainly on naturally occurring and transgenic animal models. Mutations in genes encoding both signaling molecules and transcription factors have been implicated in the etiology of hypopituitarism, with or without other syndromic features, in mice and humans. To date, mutations in known genes account for a small proportion of cases of hypopituitarism in humans. However, these mutations have led to a greater understanding of the genetic interactions that lead to normal pituitary development. This review attempts to describe the complexity of pituitary development in the rodent, with particular emphasis on those factors that, when mutated, are associated with hypopituitarism in humans

The impact of viral mutations on recognition by SARS-CoV-2 specific T cells.

We identify amino acid variants within dominant SARS-CoV-2 T cell epitopes by interrogating global sequence data. Several variants within nucleocapsid and ORF3a epitopes have arisen independently in multiple lineages and result in loss of recognition by epitope-specific T cells assessed by IFN-γ and cytotoxic killing assays. Complete loss of T cell responsiveness was seen due to Q213K in the A∗01:01-restricted CD8+ ORF3a epitope FTSDYYQLY207-215; due to P13L, P13S, and P13T in the B∗27:05-restricted CD8+ nucleocapsid epitope QRNAPRITF9-17; and due to T362I and P365S in the A∗03:01/A∗11:01-restricted CD8+ nucleocapsid epitope KTFPPTEPK361-369. CD8+ T cell lines unable to recognize variant epitopes have diverse T cell receptor repertoires. These data demonstrate the potential for T cell evasion and highlight the need for ongoing surveillance for variants capable of escaping T cell as well as humoral immunity.This work is supported by the UK Medical Research Council (MRC); Chinese Academy of Medical Sciences(CAMS) Innovation Fund for Medical Sciences (CIFMS), China; National Institute for Health Research (NIHR)Oxford Biomedical Research Centre, and UK Researchand Innovation (UKRI)/NIHR through the UK Coro-navirus Immunology Consortium (UK-CIC). Sequencing of SARS-CoV-2 samples and collation of data wasundertaken by the COG-UK CONSORTIUM. COG-UK is supported by funding from the Medical ResearchCouncil (MRC) part of UK Research & Innovation (UKRI),the National Institute of Health Research (NIHR),and Genome Research Limited, operating as the Wellcome Sanger Institute. T.I.d.S. is supported by a Well-come Trust Intermediate Clinical Fellowship (110058/Z/15/Z). L.T. is supported by the Wellcome Trust(grant number 205228/Z/16/Z) and by theUniversity of Liverpool Centre for Excellence in Infectious DiseaseResearch (CEIDR). S.D. is funded by an NIHR GlobalResearch Professorship (NIHR300791). L.T. and S.C.M.are also supported by the U.S. Food and Drug Administration Medical Countermeasures Initiative contract75F40120C00085 and the National Institute for Health Research Health Protection Research Unit (HPRU) inEmerging and Zoonotic Infections (NIHR200907) at University of Liverpool inpartnership with Public HealthEngland (PHE), in collaboration with Liverpool School of Tropical Medicine and the University of Oxford.L.T. is based at the University of Liverpool. M.D.P. is funded by the NIHR Sheffield Biomedical ResearchCentre (BRC – IS-BRC-1215-20017). ISARIC4C is supported by the MRC (grant no MC_PC_19059). J.C.K.is a Wellcome Investigator (WT204969/Z/16/Z) and supported by NIHR Oxford Biomedical Research Centreand CIFMS. The views expressed are those of the authors and not necessarily those of the NIHR or MRC