Branding Dissent: Nitirat, Thailand’s Enlightened Jurists

This article examines the political role of a group of academic lawyers based at Thammasat University who have been seeking to reform various aspects of the Thai legal and judicial system. The seven-member group started out by criticising the illegality of the 2006 coup. After the 2010 crackdown against redshirt protestors, the group named itself Nitirat and started to hold seminars, draft legal proposals, and campaign to amend various laws. Nitirat has repeatedly challenged the legal and constitutional underpinnings of three key elements of the Thai state: the judiciary, the military, and the monarchy. In doing so, the group has gained a mass following, drawn mainly from those sympathetic to the “redshirt” movement which broadly supports former Prime Minister Thaksin Shinawatra. Informally led by scholar Worajet Pakeerat, Nitirat has created a popular branding which is reflected in huge audiences for public events, and the sales of souvenirs. The article aims to answer the following questions: How does Nitirat combine the roles of legal academic and political activist? How does it differ from the traditional mode of Thai public intellectuals? How significant is the Nitirat phenomenon

Phenotypic variation in the Pseudomonas fluorescens clinical strain MFN1032

International audiencePseudomonas fluorescens is a highly heterogeneous species and includes both avirulent strains and clinical strains involved in nosocomial infections. We previously demonstrated that clinical strain MFN1032 has hemolytic activity involving phospholipase C (PlcC) and biosurfactants (BSs), similar to that of the opportunistic pathogen Pseudomonas aeruginosa. When incubated under specific conditions, MFN1032 forms translucent phenotypic variant colonies defective in hemolysis, but not necessarily in PlcC. We analyzed eight variants of the original strain MFN1032 and found that they clustered into two groups. Mutations of genes encoding the two-component regulatory system GacS/GacA are responsible for phenotypic variation in the first group of variants. These group 1 variants did not produce secondary metabolites and had impaired biofilm formation. The second group was composed of hyperflagellated cells with enhanced biofilm capacity: they did not produce BSs and were thus unable to swarm. Artificial reduction of the intracellular level of c-di-GMP restored the ability to form biofilm to levels shown by the wild type, but production of BSs was still repressed. Phenotypic variation might increase the virulence potential of this strain

What is the impact of blood pressure on neurological symptoms and the risk of ESKD in primary and secondary thrombotic microangiopathies based on clinical presentation: a retrospective study.

The impact of blood pressure on neurological symptoms and risk of end-stage kidney disease (ESKD) is unknown in primary and secondary thrombotic microangiopathies (TMAs). We measured baseline systolic (SBP) and diastolic (DBP) BP in consecutive 563 patients with adjudicated primary and secondary TMAs, and assessed its association with the risk of ESKD. Normal BP, grade 1, 2 and 3 hypertension were present in 243 (43.1%), 132 (23.4%), 101 (17.9%) and 88 (15.6%), respectively. Significant BP differences were noted in relation to the cause of TMA: highest BP values were found in patients with atypical hemolytic-uremic syndrome (aHUS), pregnancy, transplantation and auto-immune-related TMAs. Normal BP or grade 1 hypertension was found in 17/18 (94.4%) patients with thrombotic thrombocytopenic patients (only 1/18 (5.6%) had a SBP value>150 mmHg). In contrast, BP values could not differentiate isolated "essential" malignant hypertension (MH) from MH associated with aHUS (isolated MH (n=15): BP (median (IQR)): 220 (182-249)/132 (101-150) mmHg; MH with aHUS (n=5): BP: 223 (196-245)/131 (111-144) mmHg). The risk of vigilance disturbances (6.9%, 15.0%, 25.0%, respectively), epileptic seizures (1.5%, 4.0%, 12.5%, respectively) and posterior reversible encephalopathy syndrome (0.76%, 2.97%, 6.82%, respectively) increased with increasing baseline BP values from grade 1 to grade 3 hypertension. ESKD occurred in 35/563 (6.2%) patients (1.23%, 2.27%, 11.9% and 19.3% of patients with normal BP, grade 1, 2 and 3 hypertension, respectively). As compared to patients with normal BP (<120/139 mmHg), grade 1, grade 2 and grade 3 hypertension were associated with a greater risk of ESKD in univariate (OR: 1.91 [0.83-4.40], 13.2 [3.56-48.9] and 34.8 [9.31-130], respectively) and multivariate (OR: 0.89 [0.30-2.69], 7.00 [1.57-31.3] and 19.7 [4.53-85.2], respectively) analyses. The association between BP and the risk of ESRD was unchanged after adjustment on eculizumab use (OR: 3.46 [1.41-8.49], 17.7 [4.44-70.0] and 70.6 [8.61-579], respectively). Patients with MH, regardless of its cause, had a greater risk of ESKD (OR: 26.4 [10.0-69.8] vs other patients). Baseline BP differs in primary and secondary TMAs. High BP reduces the neurological tolerance of TMAs and is a powerful independent risk factor of ESKD, even after adjustment on TMA's cause

Fibrinogen-Like Protein 2/Fibroleukin Induces Long-Term Allograft Survival in a Rat Model through Regulatory B Cells

International audienceWe previously described that in a rat model of heart transplantation tolerance was dependent on CD8 + CD45RC low Tregs that over-expressed fibrinogen-like protein 2 (FGL2)/fibro-leukin. Little is known on the immunoregulatory properties of FGL2. Here we analyzed the transplantation tolerance mechanisms that are present in Lewis 1A rats treated with FGL2. Over-expression of FGL2 in vivo through adenovirus associated virus-mediated gene transfer without any further treatment resulted in inhibition of cardiac allograft rejection. Adoptive cell transfer of splenocytes from FGL2-treated rats with long-term graft survival (> 80 days) in animals that were transplanted with cardiac allografts inhibited acute and chronic organ rejection in a donor-specific and transferable tolerance manner, since iterative adoptive transfer up to a sixth consecutive recipient resulted in transplantation tolerance. Adoptive cell transfer also efficiently inhibited anti-donor antibody production. Analysis of all possible cell populations among splenocytes revealed that B lymphocytes were sufficient for this adoptive cell tolerance. These B cells were also capable of inhibiting the proliferation of CD4 + T cells in response to allogeneic stimuli. Moreover, gene transfer of FGL2 in B cell deficient rats did not prolong graft survival. Thus, this is the first description of FGL2 resulting in long-term allograft survival. Furthermore, allograft tolerance was transfer-able and B cells were the main cells responsible for this effect