Global Capitalism, Immigrant Labor, and the Struggle for Justice

Around the world borders are militarized, states are stepping up repressive anti-immigrant controls, and native publics are turning immigrants into scapegoats for the spiraling crisis of global capitalism. The massive displacement and primitive accumulation unleashed by free trade agreements and neo-liberal policies, as well as state and “private” violence has resulted in a virtually inexhaustible immigrant labor reserve for the global economy. State controls over immigration and immigrant labor have several functions for the system: 1) state repression and criminalization of undocumented immigration make immigrants vulnerable and deportable and therefore subject to conditions of super-exploitation, super-control and hyper-surveillance; 2) anti-immigrant repressive apparatuses are themselves ever more important sources of accumulation, ranging from private for-profit immigrant detention centers, to the militarization of borders, and the purchase by states of military hardware and systems of surveillance. Immigrant labor is extremely profitable for the transnational corporate economy; 3) the anti-immigrant policies associated with repressive state apparatuses help turn attention away from the crisis of global capitalism among more privileged sectors of the working class and convert immigrant workers into scapegoats for the crisis, thus deflecting attention from the root causes of the crisis and undermining working class unity. This article focuses on structural and historical underpinnings of the phenomenon of immigrant labor in the new global capitalist system and on how the rise of a globally integrated production and financial system, a transnational capitalist class, and transnational state apparatuses, have led to a reorganization of the world market in labor, including deeper reliance on a rapidly expanding reserve army of immigrant labor and a vicious new anti-immigrant politics. It looks at the United States as an illustration of the larger worldwide situation with regard to immigration and immigrant justice. Finally, it explores the rise of an immigrant justice movement around the world, observes the leading role that immigrant workers often play in worker’s struggles and that a mass immigrant rights movement is at the cutting edge of the struggle against transnational corporate exploitation. We call for replacing the whole concept of national citizenship with that of global citizenship as the only rallying cry that can assure justice and equality for all

Association of biomarkers for human papillomavirus with survival among adults with Barrett high-grade dysplasia and esophageal adenocarcinoma

Importance: The presence of high-risk human papillomavirus (HPV) has been associated with a favorable outcome in Barrett high-grade dysplasia (HGD) and esophageal adenocarcinoma (EAC). Nevertheless, the prognostic significance of other HPV-related biomarkers (ie, retinoblastoma protein [pRb], cyclin D1 [CD1], minichromosome maintenance protein [MCM2] and Ki-67) is unknown. Objective: To examine the association between HPV-related biomarkers and survival in adult patients with Barrett HGD and EAC. Design, Setting, and Participants: This retrospective case-control study examined the hypothesis that the HPV-related cell cycle markers (pRb, CD1, and Ki-67) and the viral surrogate marker (MCM2) may be associated with a favorable prognosis in Barrett HGD and EAC. Pretreatment biopsies were used for HPV DNA determination via polymerase chain reaction and immunohistochemistry for the HPV-related biomarkers. Recruitment of patients occurred in secondary and tertiary referral centers, with 151 patients assessed for eligibility. The study period was from December 1, 2002, to November 28, 2017, and the dates of analysis were from September 9, 2011, to November 28, 2017. Main Outcomes and Measures: Disease-free survival and overall survival. Results: Of 151 patients assessed for eligibility, 9 were excluded. Among the 142 patients with Barrett HGD or EAC (126 [88.7%] men; mean [SD] age, 66.0 [12.1] years; 142 [100%] white), 37 were HPV positive and 105 were HPV negative. No association with disease-free survival was noted for pRb, CD1, Ki-67, and MCM2. In regard to overall survival, only low expression of CD1 had a favorable prognosis (hazard ratio [HR], 0.53; 95% CI, 0.30-0.95; adjusted P = .03). All the biomarkers stratified by HPV status showed significant associations with survival. Patients with HPV-positive, low-expression pRb esophageal tumors were associated with a significantly improved disease-free survival compared with the HPV-negative, high-expression Rb tumors (HR, 0.33; 95% CI, 0.12-0.93; adjusted P = .04). Similarly, HPV-positive, low-expression CD1 was associated with a significantly favorable disease-free survival (HR, 0.26; 95% CI, 0.09-0.76; adjusted P = .01), as was HPV-positive, high-expression MCM2 (HR, 0.27; 95% CI, 0.09-0.78; adjusted P = .02). In regard to overall survival, HPV was significantly associated only with low CD1 (HR, 0.38; 95% CI, 0.15-0.94; adjusted P = .04). Conclusions and Relevance: This study's findings suggest that low expression of CD1 appears to be an independent prognostic marker in Barrett HGD and EAC. Human papillomavirus positivity in combination with pRb, CD1, MCM2, and Ki-67 was associated with a survival benefit in esophageal tumors. These findings suggest the possibility of personalization of therapy for Barrett HGD and EAC based on viral status

Selective chromo-fluorogenic detection of trivalent cations in aqueous environments using a dehydration reaction

[EN] Trivalent cations (Al3+, Fe3+, Cr3+, As3+, In3+ and Ga3+) induced a dehydration reaction of a chemodosimeter in water that is coupled with colour and emission changes.Financial support from the Spanish Government and FEDER funds (Project MAT2015-64139-C4-1) and the Generalitat Valencia (Project PROMETEO II/2014/047) is gratefully acknowledged. M. L. P. is grateful to the Generalitat Valenciana for her Santiago Grisolia grant.Lo-Presti, M.; El Sayed Shehata Nasr, S.; Martínez-Máñez, R.; Costero, AM.; Gil, S.; Parra, M.; Sancenón Galarza, F. (2016). Selective chromo-fluorogenic detection of trivalent cations in aqueous environments using a dehydration reaction. New Journal of Chemistry. 40(11):9042-9045. https://doi.org/10.1039/c6nj01957aS90429045401

Marine biodiversity research in the Ryukyu Islands, Japan: current status and trends

Marine biodiversity and derived ecosystem services are critical to the healthy functioning of marine ecosystems, and to human economic and societal well-being. Thus, an understanding of marine biodiversity in different ecosystems is necessary for their conservation and management. Coral reefs in particular are noted for their high levels of biodiversity, and among the world’s coral reefs, the subtropical Ryukyu Islands (RYS; also known as the Nansei Islands) in Japan have been shown to harbor very high levels of marine biodiversity. This study provides an overview of the state of marine biodiversity research in the RYS. First, we examined the amount of English language scientific literature in the Web of Science (WoS; 1995–2017) on six selected representative taxa spanning protists to vertebrates across six geographic sub-regions in the RYS. Our results show clear taxonomic and sub-region bias, with research on Pisces, Cnidaria, and Crustacea to be much more common than on Dinoflagellata, Echinodermata, and Mollusca. Such research was more commonly conducted in sub-regions with larger human populations (Okinawa, Yaeyama). Additional analyses with the Ocean Biogeographic Information System (OBIS) records show that within sub-regions, records are concentrated in areas directly around marine research stations and institutes (if present), further showing geographical bias within sub-regions. While not surprising, the results indicate a need to address ‘understudied’ taxa in ‘understudied sub-regions’ (Tokara, Miyako, Yakutane, Amami Oshima), particularly sub-regions away from marine research stations. Second, we compared the numbers of English language scientific papers on eight ecological topics for the RYS with numbers from selected major coral reef regions of the world; the Caribbean (CAR), Great Barrier Reef (GBR), and the Red Sea (RES). As expected, the numbers for all topics in the RYS were well below numbers from all other regions, yet within this disparity, research in the RYS on ‘marine protected areas’ and ‘herbivory’ was an order of magnitude lower than numbers in other regions. Additionally, while manuscript numbers on the RYS have increased from 1995 to 2016, the rate of increase (4.0 times) was seen to be lower than those in the CAR, RES, and GBR (4.6–8.4 times). Coral reefs in the RYS feature high levels of both endemism and anthropogenic threats, and subsequently they contain a concentration of some of the world’s most critically endangered marine species. To protect these threatened species and coral reef ecosystems, more data are needed to fill the research gaps identified in this study

Azide and sulfonylazide functionalized fluorophores for the selective and sensitive detection of hydrogen sulfide

[EN] Three fluorescent probes (1–3) for the selective and sensitive detection of hydrogen sulfide have been synthesized and characterized. Probe 1 is a coumarin derivative functionalized with an azide moiety whereas 2 contain the azide reactive group into a naphthalene fluorophore backbone. Probe 3 is composed also by a naphthalene fluorophore but, in this case, functionalized with a sulfonylazide reactive moiety. Probes 1 and 3 are non-fluorescent whereas 2 is weakly emissive in HEPES (10 mM, pH 7.4)–DMSO 99:1 (v/v). The emission behavior of the three probes was tested against selected anions, bio-thiols and oxidant molecules. Of all the chemical species tested, only HS− is able to induce an enhancement in the emission intensity (50, 11 and 20-fold for 1, 2 and 3, respectively). The observed emission in the presence of hydrogen sulfide is ascribed, in the case of probes 1 and 2, to an azide–amine reduction induced by HS− anion, whereas for probe 3 the sensing mechanism is related with a sulfonylazide–sulfonamide conversion. The three probes are very sensitive to HS− anion with limits of detection of 0.17, 0.20 and 0.40 mM for 1, 2 and 3 respectively. Cell viability studies demonstrated that 1–3 probes are essentially non-toxic at concentrations 10–50 μM and are well suited for in vivo studies. Finally, probe 1 was used for the detection on intracellular HS− anion in HeLa cells by means of confocal microscopy.Financial support from the Spanish Government (Project MAT2012-38429-004-01) and the Generalitat Valenciana (Project PROMETEO/2009/016) is gratefully acknowledged. S.E. is grateful to the Generalitat Valenciana for his Santiago Grisolia fellow. C.T. also thanks the Ministerio de Ciencia e Innovacion for her FPU grant. L.E.S.F. thanks the Carolina Foundation and UPNFM-Honduras for his doctoral grant.El Sayed Shehata Nasr, S.; De La Torre Paredes, C.; Santos Figueroa, LE.; Marín Hernández, C.; Martínez Mañez, R.; Sancenón Galarza, F.; Costero Nieto, AM.... (2015). Azide and sulfonylazide functionalized fluorophores for the selective and sensitive detection of hydrogen sulfide. Sensors and Actuators B: Chemical. 207(B):987-994. https://doi.org/10.1016/j.snb.2014.04.047S987994207

Effects of cigarette smoke on endothelial function of pulmonary arteries in the guinea pig

<p>Abstract</p> <p>Background</p> <p>Cigarette smoking may contribute to pulmonary hypertension in chronic obstructive pulmonary disease by altering the structure and function of pulmonary vessels at early disease stages. The objectives of this study were to evaluate the effects of long-term exposure to cigarette smoke on endothelial function and smooth muscle-cell proliferation in pulmonary arteries of guinea pigs.</p> <p>Methods</p> <p>19 male Hartley guinea pigs were exposed to the smoke of 7 cigarettes/day, 5 days/week, for 3 and 6 months. 17 control guinea pigs were sham-exposed for the same periods. Endothelial function was evaluated in rings of pulmonary artery and aorta as the relaxation induced by ADP. The proliferation of smooth muscle cells and their phenotype in small pulmonary vessels were evaluated by immunohistochemical expression of α-actin and desmin. Vessel wall thickness, arteriolar muscularization and emphysema were assessed morphometrically. The expression of endothelial nitric oxide synthase (eNOS) was evaluated by Real Time-PCR.</p> <p>Results</p> <p>Exposure to cigarette smoke reduced endothelium-dependent vasodilatation in pulmonary arteries (ANOVA p < 0.05) but not in the aorta. Endothelial dysfunction was apparent at 3 months of exposure and did not increase further after 6 months of exposure. Smoke-exposed animals showed proliferation of poorly differentiated smooth muscle cells in small vessels (p < 0.05) after 3 months of exposure. Prolonged exposure resulted in full muscularization of small pulmonary vessels (p < 0.05), wall thickening (p < 0.01) and increased contractility of the main pulmonary artery (p < 0.05), and enlargement of the alveolar spaces. Lung expression of eNOS was decreased in animals exposed to cigarette smoke.</p> <p>Conclusion</p> <p>In the guinea pig, exposure to cigarette smoke induces selective endothelial dysfunction in pulmonary arteries, smooth muscle cell proliferation in small pulmonary vessels and reduced lung expression of eNOS. These changes appear after 3 months of exposure and precede the development of pulmonary emphysema.</p

Global, regional, and national burden of chronic kidney disease, 1990–2017 : a systematic analysis for the Global Burden of Disease Study 2017

Background Health system planning requires careful assessment of chronic kidney disease (CKD) epidemiology, but data for morbidity and mortality of this disease are scarce or non-existent in many countries. We estimated the global, regional, and national burden of CKD, as well as the burden of cardiovascular disease and gout attributable to impaired kidney function, for the Global Burden of Diseases, Injuries, and Risk Factors Study 2017. We use the term CKD to refer to the morbidity and mortality that can be directly attributed to all stages of CKD, and we use the term impaired kidney function to refer to the additional risk of CKD from cardiovascular disease and gout. Methods The main data sources we used were published literature, vital registration systems, end-stage kidney disease registries, and household surveys. Estimates of CKD burden were produced using a Cause of Death Ensemble model and a Bayesian meta-regression analytical tool, and included incidence, prevalence, years lived with disability, mortality, years of life lost, and disability-adjusted life-years (DALYs). A comparative risk assessment approach was used to estimate the proportion of cardiovascular diseases and gout burden attributable to impaired kidney function. Findings Globally, in 2017, 1·2 million (95% uncertainty interval [UI] 1·2 to 1·3) people died from CKD. The global all-age mortality rate from CKD increased 41·5% (95% UI 35·2 to 46·5) between 1990 and 2017, although there was no significant change in the age-standardised mortality rate (2·8%, −1·5 to 6·3). In 2017, 697·5 million (95% UI 649·2 to 752·0) cases of all-stage CKD were recorded, for a global prevalence of 9·1% (8·5 to 9·8). The global all-age prevalence of CKD increased 29·3% (95% UI 26·4 to 32·6) since 1990, whereas the age-standardised prevalence remained stable (1·2%, −1·1 to 3·5). CKD resulted in 35·8 million (95% UI 33·7 to 38·0) DALYs in 2017, with diabetic nephropathy accounting for almost a third of DALYs. Most of the burden of CKD was concentrated in the three lowest quintiles of Socio-demographic Index (SDI). In several regions, particularly Oceania, sub-Saharan Africa, and Latin America, the burden of CKD was much higher than expected for the level of development, whereas the disease burden in western, eastern, and central sub-Saharan Africa, east Asia, south Asia, central and eastern Europe, Australasia, and western Europe was lower than expected. 1·4 million (95% UI 1·2 to 1·6) cardiovascular disease-related deaths and 25·3 million (22·2 to 28·9) cardiovascular disease DALYs were attributable to impaired kidney function. Interpretation Kidney disease has a major effect on global health, both as a direct cause of global morbidity and mortality and as an important risk factor for cardiovascular disease. CKD is largely preventable and treatable and deserves greater attention in global health policy decision making, particularly in locations with low and middle SDI

An Integrated TCGA Pan-Cancer Clinical Data Resource to Drive High-Quality Survival Outcome Analytics

For a decade, The Cancer Genome Atlas (TCGA) program collected clinicopathologic annotation data along with multi-platform molecular profiles of more than 11,000 human tumors across 33 different cancer types. TCGA clinical data contain key features representing the democratized nature of the data collection process. To ensure proper use of this large clinical dataset associated with genomic features, we developed a standardized dataset named the TCGA Pan-Cancer Clinical Data Resource (TCGA-CDR), which includes four major clinical outcome endpoints. In addition to detailing major challenges and statistical limitations encountered during the effort of integrating the acquired clinical data, we present a summary that includes endpoint usage recommendations for each cancer type. These TCGA-CDR findings appear to be consistent with cancer genomics studies independent of the TCGA effort and provide opportunities for investigating cancer biology using clinical correlates at an unprecedented scale. Analysis of clinicopathologic annotations for over 11,000 cancer patients in the TCGA program leads to the generation of TCGA Clinical Data Resource, which provides recommendations of clinical outcome endpoint usage for 33 cancer types

Pan-Cancer Analysis of lncRNA Regulation Supports Their Targeting of Cancer Genes in Each Tumor Context

Long noncoding RNAs (lncRNAs) are commonly dys-regulated in tumors, but only a handful are known toplay pathophysiological roles in cancer. We inferredlncRNAs that dysregulate cancer pathways, onco-genes, and tumor suppressors (cancer genes) bymodeling their effects on the activity of transcriptionfactors, RNA-binding proteins, and microRNAs in5,185 TCGA tumors and 1,019 ENCODE assays.Our predictions included hundreds of candidateonco- and tumor-suppressor lncRNAs (cancerlncRNAs) whose somatic alterations account for thedysregulation of dozens of cancer genes and path-ways in each of 14 tumor contexts. To demonstrateproof of concept, we showed that perturbations tar-geting OIP5-AS1 (an inferred tumor suppressor) andTUG1 and WT1-AS (inferred onco-lncRNAs) dysre-gulated cancer genes and altered proliferation ofbreast and gynecologic cancer cells. Our analysis in-dicates that, although most lncRNAs are dysregu-lated in a tumor-specific manner, some, includingOIP5-AS1, TUG1, NEAT1, MEG3, and TSIX, synergis-tically dysregulate cancer pathways in multiple tumorcontexts

Pan-cancer Alterations of the MYC Oncogene and Its Proximal Network across the Cancer Genome Atlas

Although theMYConcogene has been implicated incancer, a systematic assessment of alterations ofMYC, related transcription factors, and co-regulatoryproteins, forming the proximal MYC network (PMN),across human cancers is lacking. Using computa-tional approaches, we define genomic and proteo-mic features associated with MYC and the PMNacross the 33 cancers of The Cancer Genome Atlas.Pan-cancer, 28% of all samples had at least one ofthe MYC paralogs amplified. In contrast, the MYCantagonists MGA and MNT were the most frequentlymutated or deleted members, proposing a roleas tumor suppressors.MYCalterations were mutu-ally exclusive withPIK3CA,PTEN,APC,orBRAFalterations, suggesting that MYC is a distinct onco-genic driver. Expression analysis revealed MYC-associated pathways in tumor subtypes, such asimmune response and growth factor signaling; chro-matin, translation, and DNA replication/repair wereconserved pan-cancer. This analysis reveals insightsinto MYC biology and is a reference for biomarkersand therapeutics for cancers with alterations ofMYC or the PMN