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Root Causes of Rohingya Crisis Must Not be Ignored Expert comment sysadmin 28 September 2017

The focus on Aung San Suu Kyi masks the complete lack of an adequate response to the crisis in Myanmar, whether at the global or regional level.

Aung San Suu Kyi’s recent speech on the Rohingya crisis was - at best - light on details on how the current situation could be remedied and - at worst - full of easily disproven assertions.

While she does not directly control the military, it is her government that is blocking humanitarian access to the areas affected by the violence. And the Rohingya have faced systemic persecution and discrimination for decades.

Some may argue this is simply realpolitik and that any public support for the Rohingya could mean facing a backlash from the military and a large part of her support base. But arguably, she does have moral authority (which helped her in the past to stand up to the military generals) that is now being eroded by her ambivalence in speaking out.

However, the focus on Aung San Suu Kyi masks the complete lack of an adequate response to the crisis – whether at the global or regional level.

Undertaking dangerous and perilous journeys

Since the attacks on border and military posts by the armed group Arakan Rohingya Salvation Army (ARSA) in August 2017, there has been a strong military crackdown against the Rohingya in Rakhine state: a substantial number of Rohingya villages destroyed; close to half a million people Rohingya fleeing into Bangladesh and tens of thousands internally displaced within Myanmar.

Prince bin Ra’ad , UN High Commissioner for Human Rights, has called the crisis a “textbook example of ethnic cleansing” and tens of thousands of Rohingya are still undertaking dangerous and perilous journeys seeking sanctuary. In response, the UN and EU have focused on addressing the immediate humanitarian crisis in Bangladesh, which is already home to many formerly displaced Rohingya communities.

Within the region, Sheikh Hasina’s secular Awami League government in Bangladesh initially proposed joint military operations with Myanmar against the ARSA - in part because of concerns about the long standing relationship between Rohingya political or armed groups and the Jamaat-e-Islami, an ally of the main opposition Bangladesh Nationalist Party (BNP).

However, faced with massive refugee flows, Bangladesh turned its focus to the humanitarian crisis while stressing that Myanmar must allow the return of refugees. Bangladesh’s concern is partly motivated by internal security concerns. If the current situation becomes protracted, with no clear resolution in sight, frustration could create the conditions for further radicalisation within Rohingya communities.

The Association of South East Asian Nations (ASEAN) has yet to come to grips with the situation. Despite its mandate to ensure peace and stability within the region, its policy of non-interference and consensus trumps the need to secure and maintain stability. Instead countries have responded bilaterally - for example, Indonesia sent its foreign minister to both Myanmar and Bangladesh while Malaysia has been consistently vocal about its concerns.

So this raises broader questions on the effectiveness of ASEAN. Currently celebrating its 50th anniversary, ASEAN needs to decide how to mediate and resolve issues with regional implications as its principle of non-intervention effectively blocks any constructive discussion on the Rohingyas ongoing statelessness and impact of this on the region.

However, there is also an opportunity here for ASEAN to consider how mediation and negotiation could potentially manage such crises. And there is a historical precedent: the 1989 Comprehensive Plan of Action on Indo-Chinese refugees saw cooperation between recipient countries in the region and the international community on how to resettle Vietnamese refugees (although Cold War considerations did play a part in that specific crisis).

India and China have both backed Myanmar, reflecting their economic and security interests in the country but also motivated by each wanting to contain the influence of the other within Myanmar. Rakhine is important with its natural resources and coastal location and, as China is not directly affected by the refugee crisis, it has less to lose than others in standing by Aung San Suu Kyi and her government.

India is nearing completion of the Kaladan Multi-modal Transit Transport Project, connecting the Bay of Bengal with the northeast Indian state of Mizoram, and sees Myanmar as an important market for its regional ambitions. For parts of the Indian administration, the crisis plays to a domestic narrative that some of the Rohingya already settled in Jammu and Kashmir have links to armed groups in Pakistan and are an internal security concern.

So while India is providing humanitarian aid to Bangladesh, it is also threatening to deport almost 40,000 Rohingya. The case is currently being heard at the Indian Supreme Court, but given that the Rohingya lack citizenship in Myanmar, it is not clear to where they would be deported.

Myanmar, ASEAN and other affected countries need to show political will to find a solution to the Rohingya’s long-standing issue of statelessness - discrimination was legally formalised in a 1982 Burma Citizenship Law, which recognised 135 ethnicities for citizenship but excluded the Rohingya.

The root causes of this crisis – long standing discrimination, persecution and lack of citizenship – cannot be ignored. There is a need for a comprehensive peace process, which recognises the ethnic and religious diversity within Myanmar.

And incentives, such as improving infrastructure, access to services and livelihoods, may also be needed to ensure there is a lasting solution that allows the Rohingya return and thrive as part of Myanmar society.

Without such a response, it is difficult to see an end to the current impasse.

Claudio Macci and Barbara Pacchiarotti
Theor. Probability and Math. Statist. 111 (), 21-43.
Abstract, references and article information

Chris A.J. Klaassen
Theor. Probability and Math. Statist. 111 (), 9-19.
Abstract, references and article information

Shengyu Tang
Proc. Amer. Math. Soc. 152 (), 5381-5394.
Abstract, references and article information

Carnosine (β-alanyl-l-histidine) and anserine (β-alanyl-3-methyl-l-histidine) are abundant peptides in the nervous system and skeletal muscle of many vertebrates. Many in vitro and in vivo studies demonstrated that exogenously added carnosine can improve muscle contraction, has antioxidant activity, and can quench various reactive aldehydes. Some of these functions likely contribute to the proposed anti-aging activity of carnosine. However, the physiological role of carnosine and related histidine-containing dipeptides (HCDs) is not clear. In this study, we generated a mouse line deficient in carnosine synthase (Carns1). HCDs were undetectable in the primary olfactory system and skeletal muscle of Carns1-deficient mice. Skeletal muscle contraction in these mice, however, was unaltered, and there was no evidence for reduced pH-buffering capacity in the skeletal muscle. Olfactory tests did not reveal any deterioration in 8-month-old mice lacking carnosine. In contrast, aging (18–24-month-old) Carns1-deficient mice exhibited olfactory sensitivity impairments that correlated with an age-dependent reduction in the number of olfactory receptor neurons. Whereas we found no evidence for elevated levels of lipoxidation and glycation end products in the primary olfactory system, protein carbonylation was increased in the olfactory bulb of aged Carns1-deficient mice. Taken together, these results suggest that carnosine in the olfactory system is not essential for information processing in the olfactory signaling pathway but does have a role in the long-term protection of olfactory receptor neurons, possibly through its antioxidant activity.

Proteins in the α-macroglobulin (αM) superfamily use thiol esters to form covalent conjugation products upon their proteolytic activation. αM protease inhibitors use theirs to conjugate proteases and preferentially react with primary amines (e.g. on lysine side chains), whereas those of αM complement components C3 and C4B have an increased hydroxyl reactivity that is conveyed by a conserved histidine residue and allows conjugation to cell surface glycans. Human α2-macroglobulin–like protein 1 (A2ML1) is a monomeric protease inhibitor but has the hydroxyl reactivity–conveying histidine residue. Here, we have investigated the role of hydroxyl reactivity in a protease inhibitor by comparing recombinant WT A2ML1 and the A2ML1 H1084N mutant in which this histidine is removed. Both of A2ML1s' thiol esters were reactive toward the amine substrate glycine, but only WT A2ML1 reacted with the hydroxyl substrate glycerol, demonstrating that His-1084 increases the hydroxyl reactivity of A2ML1's thiol ester. Although both A2ML1s conjugated and inhibited thermolysin, His-1084 was required for the conjugation and inhibition of acetylated thermolysin, which lacks primary amines. Using MS, we identified an ester bond formed between a thermolysin serine residue and the A2ML1 thiol ester. These results demonstrate that a histidine-enhanced hydroxyl reactivity can contribute to protease inhibition by an αM protein. His-1084 did not improve A2ML1's protease inhibition at pH 5, indicating that A2ML1's hydroxyl reactivity is not an adaption to its acidic epidermal environment.

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Adult progenitor cell populations typically exist in a quiescent state within a controlled niche environment. However, various stresses or forms of damage can disrupt this state, which often leads to dysfunction and aging. We built a glucocorticoid (GC)-induced liver damage model of mice, found that GC stress induced liver damage, leading to consequences for progenitor cells expansion. However, the mechanisms by which niche factors cause progenitor cells proliferation are largely unknown. We demonstrate that, within the liver progenitor cells niche, Galectin-3 (Gal-3) is responsible for driving a subset of progenitor cells to break quiescence. We show that GC stress causes aging of the niche, which induces the up-regulation of Gal-3. The increased Gal-3 population increasingly interacts with the progenitor cell marker CD133, which triggers focal adhesion kinase (FAK)/AMP-activated kinase (AMPK) signaling. This results in the loss of quiescence and leads to the eventual stemness exhaustion of progenitor cells. Conversely, blocking Gal-3 with the inhibitor TD139 prevents the loss of stemness and improves liver function. These experiments identify a stress-dependent change in progenitor cell niche that directly influence liver progenitor cell quiescence and function.

When you use SAS/ACCESS Interface to PostgreSQL to query a Yellowbrick database, the SAS OBS= option is not generating a limit clause on the query that is passed to the database. Click the

Genetic variants that increase the risk of fatty liver disease (FLD) and cirrhosis have recently been identified in the proximity of membrane bound O-acyltransferase domain-containing 7 (MBOAT7).  To elucidate the link between these variants and FLD we characterized Mboat7 liver-specific knock-out mice (Mboat7-LSKO).  Chow-fed Mboat7-LSKO mice developed fatty livers and associated liver injury.  Lipidomic analysis of liver using mass spectrometry revealed a pronounced reduction in 20-carbon polyunsaturated fatty acid content in phosphatidylinositols (PIs), but not in other phospholipids. The change in fatty acid composition of PIs in these mice was associated with a marked increase in de novo lipogenesis due to activation of SREBP-1c, a transcription factor that coordinates the activation of genes encoding enzymes in the fatty acid biosynthesis pathway. Hepatic removal of both SREBP cleavage activating protein (Scap) and Mboat7 normalized hepatic triglycerides relative to Scap only hepatic knock-out showing increased SREBP-1c processing is required for Mboat7 induced steatosis.  This study reveals a clear relationship between PI fatty acid composition and regulation of hepatic fat synthesis and delineates the mechanism by which mutations in MBOAT7 cause hepatic steatosis.

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