Constrained populism in Indonesia: Joko Widodo, electoral institutions and party power

Populism -- a political strategy in which a personalist leader aims to mobilise voters through charismatic appeals, and with a minimum of institutional intermediation -- is squarely implicated in the global crisis of liberal democracy. The literature has settled upon two broad areas of consensus. First, populism fares better in contexts where ties between voters and traditional parties have degraded, leaving voters available for recruitment by populist candidates. By the same token, the prevalence of strong, stable patronage or identity-based linkages between parties and voters serves to limit the constituency for populism. Second, that the relationship between the structural conditions borne of the decline of parties and other institutionalised forms of political representation on the one hand, and the actual viability of populist politics on the other, is intermediated by several key institutional variables. These start with the overall form of government, with presidential democracies offering an easier path to executive power for populists than parliamentary systems. Within presidential systems, more specific electoral system features can also facilitate the success of populist presidential candidacies. In Indonesia, key structural and institutional correlates of populism exist in tension with some distinctive features of the country's electoral system. Hollowed-out parties, fragmented patronage systems, and direct presidential elections combine to create strategic opportunity for political entrepreneurs to 'reach past' sclerotic party and patronage machines to amass national popularity through populist tactics. Yet as this thesis demonstrates via an in-depth study of the career of President Joko Widodo (or Jokowi), Indonesia's electoral rules force populist candidates to channel their political ambitions through incumbent non-populist parties, on account of onerous party registration rules, and the legal requirement that presidential candidates gain the nomination of incumbent parties/coalitions. The result, as Widodo's presidency has illustrated, is a populism shorn of the anti-establishment, anti-party character of populist presidencies often seen in national contexts where the structural correlates of populism coexist with electoral rules that allow outsiders to ascend to the presidency without entering into political alliances with incumbent elites. This thesis uses the Indonesian case to highlight the role that electoral 'barriers to entry' play in shaping the form populism takes if and when it does emerge. Jokowi's accommodative approach to oligarchic interests, in spite of his initial desire to assert his autonomy from them, was conditioned by the alliances he was forced to form with party leaders as part of gaining the nomination in 2014. Indonesia's institutions did not prevent the rise of a populist outsider to the presidency, but they have been greatly important in shaping the character of his populism in a party-friendly direction. The Indonesian example does not invalidate the core assumptions about the relationship between populism and party strength. Rather, it invites scholars to consider the issue of 'party strength' as it relates to populism with more nuance. Indonesian parties are 'weak' in the sense usually implied by the literature: organisationally hollowed-out, elitist, and growing more disembedded from society. Yet they are 'strong' where it counts: their grassroots weakness is mitigated by the electoral-system barriers to entry that force outsiders into accommodation with incumbents. My thesis suggests that models of the relationship between party weakness and populism must take more account of the critical role that electoral rules can play in affording parties an artificial strength at the apex of the political system that mitigates against their weakness at the grassroots

Age-specific risk factor profiles of adenocarcinomas of the esophagus: A pooled analysis from the international BEACON consortium: Age-specific risk factors of esophageal adenocarcinomas

Esophageal (EA) and esophagogastric junction (EGJA) adenocarcinoma have been steadily increasing in frequency in younger people, however the etiology of these cancers is poorly understood. We therefore investigated associations of body- mass index (BMI), cigarette smoking, alcohol consumption, gastroesophageal reflux, and use of non-steroidal anti-inflammatory drugs (NSAIDs) in relation to age-specific risks of EA and EGJA. We pooled individual participant data from eight population-based, case-control studies within the international Barrett’s and Esophageal Adenocarcinoma Consortium (BEACON). The analysis included 1,363 EA patients, 1,472 EGJA patients, and 5,728 control participants. Multivariable logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for age-specific (<50, 50–59, 60–69, ≥70 years) cancer outcomes, as well as interactions by age. BMI, smoking status and pack-years, recurrent gastroesophageal reflux, and frequency of gastroesophageal reflux were positively associated with EA and EGJA in each age group. Early-onset EA (<50 years) had stronger associations with recurrent gastroesophageal reflux (OR=8.06, 95%CI: 4.52, 14.37; Peffect modification=0.01) and BMI (ORBMI ≥30 vs. <25=4.19, 95%CI: 2.23, 7.87; Peffect modification=0.04), relative to older age groups. In contrast, inverse associations of NSAID use were strongest in the oldest age group (≥70 years), although this apparent difference was not statistically significant. Age-specific associations with EGJA showed similar, but slightly weaker patterns and no statistically significant differences by age were observed. Our study provides evidence that associations between obesity and gastroesophageal reflux are stronger among earlier onset EA cancers

Gastroesophageal reflux GWAS identifies risk loci that also associate with subsequent severe esophageal diseases

Funder: The Swedish Esophageal Cancer Study was funded by grants (R01 CA57947-03) from the National Cancer Institute he California Tobacco Related Research Program (3RT-0122; and; 10RT-0251) Marit Peterson Fund for Melanoma Research. CIDR is supported by contract HHSN268200782096CAbstract: Gastroesophageal reflux disease (GERD) is caused by gastric acid entering the esophagus. GERD has high prevalence and is the major risk factor for Barrett’s esophagus (BE) and esophageal adenocarcinoma (EA). We conduct a large GERD GWAS meta-analysis (80,265 cases, 305,011 controls), identifying 25 independent genome-wide significant loci for GERD. Several of the implicated genes are existing or putative drug targets. Loci discovery is greatest with a broad GERD definition (including cases defined by self-report or medication data). Further, 91% of the GERD risk-increasing alleles also increase BE and/or EA risk, greatly expanding gene discovery for these traits. Our results map genes for GERD and related traits and uncover potential new drug targets for these conditions

A genome-wide association study identifies new susceptibility loci for esophageal adenocarcinoma and Barrett's esophagus.

Esophageal adenocarcinoma is a cancer with rising incidence and poor survival. Most such cancers arise in a specialized intestinal metaplastic epithelium, which is diagnostic of Barrett's esophagus. In a genome-wide association study, we compared esophageal adenocarcinoma cases (n = 2,390) and individuals with precancerous Barrett's esophagus (n = 3,175) with 10,120 controls in 2 phases. For the combined case group, we identified three new associations. The first is at 19p13 (rs10419226: P = 3.6 × 10(-10)) in CRTC1 (encoding CREB-regulated transcription coactivator), whose aberrant activation has been associated with oncogenic activity. A second is at 9q22 (rs11789015: P = 1.0 × 10(-9)) in BARX1, which encodes a transcription factor important in esophageal specification. A third is at 3p14 (rs2687201: P = 5.5 × 10(-9)) near the transcription factor FOXP1, which regulates esophageal development. We also refine a previously reported association with Barrett's esophagus near the putative tumor suppressor gene FOXF1 at 16q24 and extend our findings to now include esophageal adenocarcinoma

Finishing the euchromatic sequence of the human genome

The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead

Meet Joko Widodo

What does Joko Widodo’s presidential candidacy mean for the future of Indonesian democracy? . The announcement that Joko Widodo had been given his party’s presidential candidacy was cathartic and oddly anticlimactic. More than a year of speculation about whether PDI-P party matriarch, former President Megawati Soekarnoputri, would give the wildly popular Governor of Jakarta a shot at the presidency came to an end with a hastily convened media conference in a poor neighbourhood of the capital. There, Jokowi (as he is universally known) made what must be the most succinct declaration of a presidential candidacy in the history of democracy.&nbsp;He said, “I have gotten the mandate from PDI-Perjuangan Chairwoman Mrs Megawati Soekarnoputri to be the candidate for the President of the Republic for Indonesia from PDI-Perjuangan. In the name of God, most gracious and most merciful, I am ready to do it”, before kissing the Indonesian flag placed conveniently behind him. Not exactly stirring. Then again, this skinny, self-effacing populist has never been known for his oratory. He lets his actions—impromptu visits to lower-class neighbourhoods and tours of public works projects, wearing cheap clothes and doing more listening than talking—speak for themselves. They say: I understand you, I understand your problems, and I’m going to find a way to help you. Getting to the essence of why the punters like the 52-year old governor so much is easy—as Dave McRae pithily put it, for the first time ‘Indonesians look at a politician and they see themselves in him’. Read the full article&gt; &nbsp; Image: Flickr / US Embassy Jakarta, Indonesi

Age-specific risk factor profiles of adenocarcinomas of the esophagus: a pooled analysis from the international BEACON consortium

Esophageal (EA) and esophagogastric junction (EGJA) adenocarcinoma have been steadily increasing in frequency in younger people; however, the etiology of these cancers is poorly understood. We therefore investigated associations of body mass index (BMI), cigarette smoking, alcohol consumption, gastroesophageal reflux and use of nonsteroidal anti-inflammatory drugs (NSAIDs) in relation to age-specific risks of EA and EGJA. We pooled individual participant data from eight population-based, case-control studies within the international Barrett's and Esophageal Adenocarcinoma Consortium (BEACON). The analysis included 1,363 EA patients, 1,472 EGJA patients and 5,728 control participants. Multivariable logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for age-specific

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