“The land belonged to Nepal but the people belonged to Tibet”: Overlapping sovereignties and mobility in the Limi Valley borderland

Recent scholarship on the lived experiences of borderlands has foregrounded and theorized the pervasiveness of anxiety, violence, and lawlessness. While useful, these do not capture all of the ways in which borderland residents relate to diverse constellations of power. This paper examines the China (Tibet Autonomous Region) &ndash; Nepal borderland through the case of the Limi Valley, in the northwest corner of Nepal&rsquo;s Humla district. Before 1959, the valley was considered part of Nepalese territory, yet its residents belonged administratively to the Tibetan government, an arrangement at odds with contemporary understandings of state territorial sovereignty. The non-postcolonial state formations of Nepal and China have created their own specific forms of border citizenship and overlapping sovereignties. The article shows how multiple sovereignties can stretch beyond state borders in unexpected ways by tracing how Limi Valley residents negotiate overlapping sovereignties of the Nepali and Chinese states, as well as the non-state sovereignty of the Tibetan government-in-exile. Furthermore, it demonstrates that these in turn overlap with a form of social sovereignty grounded in the community&rsquo;s body of laws, codes, and practices, which are at once a historically sedimented trace of Limi&rsquo;s governance before the nation-state, and a product of navigating political transformations. However, challenges to this social sovereignty, expressed through the idiom of statist law, have recently emerged. Whereas states typically exert sovereign power in borderlands by restricting mobility, some Limi villagers now selectively invoke state sovereignty through law to enable greater mobility.</p

Pests, keystone species, and hungry ghosts: the Gesar epic and human-pika relations on the Tibetan Plateau

For over half a century, the Chinese government has carried out large-scale poisoning campaigns on the Tibetan Plateau in an effort to exterminate the plateau pika, which is viewed as a pest that competes with livestock and causes grassland degradation. Since the 1990s, an ecological counternarrative has emerged in which pikas are keystone species rather than pests, and indicators rather than prime causes of grassland degradation. Virtually ignored in this debate are the ways in which Tibetan pastoralists understand and relate to pikas. We investigate Tibetan analytics of what pikas are, and what draws them to specific sites, based on interviews and observations in two pastoral communities, as well as readings of the Epic of King Gesar. Performed by bards since the twelfth century, the epic is grounded in the cultural milieu of Tibetan nomadic society and continues to be an important part of everyday life. As such, it shapes Tibetan analytics, a term we use to refer to forms of reason that cannot be reduced to &lsquo;cultural belief.&rsquo; Because large numbers of pikas, as hungry ghosts, are drawn to places where the essence or fertility of the earth has been depleted, causing irritation to territorial deities, Tibetan practices include rituals to feed hungry ghosts, appease territorial deities, and return treasures to restore the fertility of the earth. Bringing Tibetan analytics together with proposals for political ontology, the article examines the ways in which these different ontologies, or practices of worlding, cooperate and conflict in a context of asymmetric power relations and non-liberal recognition of difference. This approach takes seriously both the agency of the nonhuman as well as human difference, while rejecting notions of rigidly bounded ontologies.</p

Development and divergent post-disaster trajectories in a mountain village: Temporal dynamics of differentiation after the 2008 Wenchuan Earthquake

Following the massive and devastating 2008 Wenchuan Earthquake, the Chinese state called for major reconstruction to be completed within three years. Reconstruction was subsequently folded into longer-term development goals, an approach often considered &lsquo;building back better.&rsquo; However, few studies have examined long-term trajectories of household recovery following the earthquake and reconstruction-as-development. We conducted a case study of long-term trajectories in a mountain village in Pengzhou City, Chengdu Municipality, which was severely impacted by the earthquake. Based on in-depth qualitative methods, including semi-structured interviews conducted with 59 villagers and local leaders between September 2018 and May 2019, we analyze a variety of distinct post-earthquake trajectories, including different patterns of recovery and experiences of development for villagers in a concentrated settlement and those who chose owner-driven reconstruction on their pre-earthquake house lots. We find that concentrated settlement created significant barriers to income generation and problems of inadequate housing to accommodate demographic growth and family reproduction. For those who chose in-situ reconstruction, differentiation happened over a span of a decade, as a result of changing development visions and construction regulations, as well as secondary earthquake hazards. These processes have both exacerbated existing inequalities in a small, relatively homogenous village, and created new ones. Some households experience the post-earthquake period as an acceleration of development, whereas others experience a sense of moving backwards in time to a less-developed status. Our study demonstrates that earthquake recovery cannot be considered a single, discrete event, but must instead be understood through long-term trajectories that intersect with both political processes and place-based events. Moreover, we show how qualitative, in-depth studies can shed light on processes otherwise obscured when earthquake recovery and development are conceptualized as apolitical, technical problems.</p

Molecular testing for the clinical diagnosis of fibrolamellar carcinoma.

Fibrolamellar carcinoma has a distinctive morphology and immunophenotype, including cytokeratin 7 and CD68 co-expression. Despite the distinct findings, accurate diagnosis of fibrolamellar carcinoma continues to be a challenge. Recently, fibrolamellar carcinomas were found to harbor a characteristic somatic gene fusion, DNAJB1-PRKACA. A break-apart fluorescence in situ hybridization (FISH) assay was designed to detect this fusion event and to examine its diagnostic performance in a large, multicenter, multinational study. Cases initially classified as fibrolamellar carcinoma based on histological features were reviewed from 124 patients. Upon central review, 104 of the 124 cases were classified histologically as typical of fibrolamellar carcinoma, 12 cases as 'possible fibrolamellar carcinoma' and 8 cases as 'unlikely to be fibrolamellar carcinoma'. PRKACA FISH was positive for rearrangement in 102 of 103 (99%) typical fibrolamellar carcinomas, 9 of 12 'possible fibrolamellar carcinomas' and 0 of 8 cases 'unlikely to be fibrolamellar carcinomas'. Within the morphologically typical group of fibrolamellar carcinomas, two tumors with unusual FISH patterns were also identified. Both cases had the fusion gene DNAJB1-PRKACA, but one also had amplification of the fusion gene and one had heterozygous deletion of the normal PRKACA locus. In addition, 88 conventional hepatocellular carcinomas were evaluated with PRKACA FISH and all were negative. These findings demonstrate that FISH for the PRKACA rearrangement is a clinically useful tool to confirm the diagnosis of fibrolamellar carcinoma, with high sensitivity and specificity. A diagnosis of fibrolamellar carcinoma is more accurate when based on morphology plus confirmatory testing than when based on morphology alone

Assistants, Guides, Collaborators, Friends: The Concealed Figures of Conflict Research

Recent scholarship has demonstrated an increasing awareness of the need for more grounded, empirical research into the micro-level dynamics of violent contexts. Research in these difficult, dangerous, and potentially violent conflict or post-conflict settings necessitates the formation of new relationships of dependency, and assistants, friends, collaborators, and guides become central figures in the field. However, all too often, these figures are written out of academic accounts and silenced in our analyses. This not only does them a significant disservice, but it also obscures potential biases, complexities, and ethical dilemmas that emerge in the way in which such research is carried out. Drawing upon fieldwork exploring the 2007–2008 Kenyan postelection violence, this paper argues that reliance upon insider-assistants is essential in conflict settings and explores the challenges inherent in these relationships. As researchers become increasingly engaged in micro-level studies of violent contexts, we must interrogate the realities of how our knowledge has been produced and engage in more open and honest discussions of the methodological and ethical challenges of conflict research

Oxidative stress in the developing brain: effects of postnatal glucocorticoid therapy and antioxidants in the rat.

In premature infants, glucocorticoids ameliorate chronic lung disease, but have adverse effects on long-term neurological function. Glucocorticoid excess promotes free radical overproduction. We hypothesised that the adverse effects of postnatal glucocorticoid therapy on the developing brain are secondary to oxidative stress and that antioxidant treatment would diminish unwanted effects. Male rat pups received a clinically-relevant tapering course of dexamethasone (DEX; 0.5, 0.3, and 0.1 mg x kg(-1) x day(-1)), with or without antioxidant vitamins C and E (DEXCE; 200 mg x kg(-1) x day(-1) and 100 mg x kg(-1) x day(-1), respectively), on postnatal days 1-6 (P1-6). Controls received saline or saline with vitamins. At weaning, relative to controls, DEX decreased total brain volume (704.4±34.7 mm(3) vs. 564.0±20.0 mm(3)), the soma volume of neurons in the CA1 (1172.6±30.4 µm(3) vs. 1002.4±11.8 µm(3)) and in the dentate gyrus (525.9±27.2 µm(3) vs. 421.5±24.6 µm(3)) of the hippocampus, and induced oxidative stress in the cortex (protein expression: heat shock protein 70 [Hsp70]: +68%; 4-hydroxynonenal [4-HNE]: +118% and nitrotyrosine [NT]: +20%). Dexamethasone in combination with vitamins resulted in improvements in total brain volume (637.5±43.1 mm(3)), and soma volume of neurons in the CA1 (1157.5±42.4 µm(3)) and the dentate gyrus (536.1±27.2 µm(3)). Hsp70 protein expression was unaltered in the cortex (+9%), however, 4-HNE (+95%) and NT (+24%) protein expression remained upregulated. Treatment of neonates with vitamins alone induced oxidative stress in the cortex (Hsp70: +67%; 4-HNE: +73%; NT: +22%) and in the hippocampus (NT: +35%). Combined glucocorticoid and antioxidant therapy in premature infants may be safer for the developing brain than glucocorticoids alone in the treatment of chronic lung disease. However, antioxidant therapy in healthy offspring is not recommended

Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018.

Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. The mission of the NCCD is to provide a widely accepted nomenclature on cell death in support of the continued development of the field

Cardiovascular disease, chronic kidney disease, and diabetes mortality burden of cardiometabolic risk factors from 1980 to 2010: A comparative risk assessment

Background: High blood pressure, blood glucose, serum cholesterol, and BMI are risk factors for cardiovascular diseases and some of these factors also increase the risk of chronic kidney disease and diabetes. We estimated mortality from cardiovascular diseases, chronic kidney disease, and diabetes that was attributable to these four cardiometabolic risk factors for all countries and regions from 1980 to 2010. Methods: We used data for exposure to risk factors by country, age group, and sex from pooled analyses of population-based health surveys. We obtained relative risks for the effects of risk factors on cause-specific mortality from meta-analyses of large prospective studies. We calculated the population attributable fractions for each risk factor alone, and for the combination of all risk factors, accounting for multicausality and for mediation of the effects of BMI by the other three risks. We calculated attributable deaths by multiplying the cause-specific population attributable fractions by the number of disease-specific deaths. We obtained cause-specific mortality from the Global Burden of Diseases, Injuries, and Risk Factors 2010 Study. We propagated the uncertainties of all the inputs to the final estimates. Findings: In 2010, high blood pressure was the leading risk factor for deaths due to cardiovascular diseases, chronic kidney disease, and diabetes in every region, causing more than 40% of worldwide deaths from these diseases; high BMI and glucose were each responsible for about 15% of deaths, and high cholesterol for more than 10%. After accounting for multicausality, 63% (10·8 million deaths, 95% CI 10·1-11·5) of deaths from these diseases in 2010 were attributable to the combined effect of these four metabolic risk factors, compared with 67% (7·1 million deaths, 6·6-7·6) in 1980. The mortality burden of high BMI and glucose nearly doubled from 1980 to 2010. At the country level, age-standardised death rates from these diseases attributable to the combined effects of these four risk factors surpassed 925 deaths per 100 000 for men in Belarus, Kazakhstan, and Mongolia, but were less than 130 deaths per 100 000 for women and less than 200 for men in some high-income countries including Australia, Canada, France, Japan, the Netherlands, Singapore, South Korea, and Spain. Interpretation: The salient features of the cardiometabolic disease and risk factor epidemic at the beginning of the 21st century are high blood pressure and an increasing effect of obesity and diabetes. The mortality burden of cardiometabolic risk factors has shifted from high-income to low-income and middle-income countries. Lowering cardiometabolic risks through dietary, behavioural, and pharmacological interventions should be a part of the global response to non-communicable diseases. Funding: UK Medical Research Council, US National Institutes of Health. © 2014 Elsevier Ltd

Dissecting the Shared Genetic Architecture of Suicide Attempt, Psychiatric Disorders, and Known Risk Factors

Background Suicide is a leading cause of death worldwide, and nonfatal suicide attempts, which occur far more frequently, are a major source of disability and social and economic burden. Both have substantial genetic etiology, which is partially shared and partially distinct from that of related psychiatric disorders. Methods We conducted a genome-wide association study (GWAS) of 29,782 suicide attempt (SA) cases and 519,961 controls in the International Suicide Genetics Consortium (ISGC). The GWAS of SA was conditioned on psychiatric disorders using GWAS summary statistics via multitrait-based conditional and joint analysis, to remove genetic effects on SA mediated by psychiatric disorders. We investigated the shared and divergent genetic architectures of SA, psychiatric disorders, and other known risk factors. Results Two loci reached genome-wide significance for SA: the major histocompatibility complex and an intergenic locus on chromosome 7, the latter of which remained associated with SA after conditioning on psychiatric disorders and replicated in an independent cohort from the Million Veteran Program. This locus has been implicated in risk-taking behavior, smoking, and insomnia. SA showed strong genetic correlation with psychiatric disorders, particularly major depression, and also with smoking, pain, risk-taking behavior, sleep disturbances, lower educational attainment, reproductive traits, lower socioeconomic status, and poorer general health. After conditioning on psychiatric disorders, the genetic correlations between SA and psychiatric disorders decreased, whereas those with nonpsychiatric traits remained largely unchanged. Conclusions Our results identify a risk locus that contributes more strongly to SA than other phenotypes and suggest a shared underlying biology between SA and known risk factors that is not mediated by psychiatric disorders.Peer reviewe