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Health

Strategies for Fighting Ebola: A Columbia University Summit to Help End the Epidemic


Monday, December 1, 2014 
9:00am - 12:00pm


Columbia Club of New York


15 West 43rd Street
New York, NY
 
Where do we stand in the fight against Ebola -- and what should be done now?
 
Columbia is convening leading experts -- from the University and other institutions – to recommend and discuss specific strategies to:
 
·        Arrest the transmission of the virus and accelerate the delivery of needed care.
·        Marshal the financial resources – and the health care personnel – required to address the crisis.
·        Mobilize and coordinate international, national, and private-sector responses.
·        Accelerate the development, testing, and distribution of an Ebola vaccine.
 
 
A full list of distinguished panelists is included below.
 
Please note that Dr. Ranu Dhillon and Dr. Estrella Lasry will be joining the summit life via Skype from West Africa.
 
A live webcast will be available here:
http://www.livestream.com/columbiaalumniassociation
 
This event is sponsored by: Columbia Business School Alumni Club of New York, The Columbia Alumni Association, The Columbia University Club of New York,  Columbia University College of Physicians and Surgeons, Columbia University Mailman School of Public Health, Columbia University School of Nursing, Columbia’s School of International and Public Affairs.
 
Panelists include:
Kathleen Crowley PA-C, MPH, DrPH is the Associate Vice President of Environment Health and Safety for Columbia University.
Ranu Dhillon MD will join the panel discussion via Skype from Guinea. Dr. Dhillon is Senior Technical Advisor, Center on Globalization and Sustainable Development, at Columbia University’s Earth Institute. He has been a consultant to support public health systems in Liberia, Nigeria, and India, and has served with the World Health Organization and UNICEF.
Jennifer Dohrn DNP, RN, FAAN directs the Columbia University School of Nursing’s Office of Global Initiatives. She directed a project that provided technical assistance to build nursing and midwifery capacity in 10 Sub-Saharan countries. She serves on the Global Committee for the Association of Nurses in AIDS Care, and the Global Network of WHO Collaborating Centers for Nursing and Midwifery Development.
Wafaa El-Sadr MD, MPH directs the Global Health Initiative at the Mailman School of Public Health, where she is a professor of Epidemiology. She is an expert in building public health and healthy system capacity.
Les Funtleyder  directs strategic investments for Opko Health, is the health care portfolio manager for E Squared Asset Management, and a partner with Bluecloud Healthcare, a U.K.-based incubator of health care companies in Africa. Widely quoted in the business and financial media, he is the author of Healthcare Investing: Profiting from the New World of Pharma, Biotech, and Health Care Services.
Scott Hammer MD is the Chief for the Division of Infectious Diseases, Department of Medicine, Columbia University Medical Center. Hammer is a professor of Epidemiology at the Mailman School of Public Health and is an investigator with the National Institutes of Health where he performs clinical trials to improve the treatment of infectious disease.
Elaine Larson  PhD, RN, FAAN is an internationally recognized expert in promoting infection prevention and control worldwide. She is Associate Dean for Research at the Columbia University School of Nursing and holds a joint appointment at the Mailman School of Public Health, where she is a professor of Epidemiology. Dr. Larson is the editor of the American Journal of Infection Control.
Estrella Lasry, MD, MSc, DTM, Tropical Medicine Advisor, Médecins Sans Frontières, will join the panel via Skype from Guinea,  She is currently supporting the MSF intervention in the West Africa Ebola outbreak
Susan Michaels-Strasser PhD, MPH, RN, FAAN is the associate director for nursing programs and project director of the Global Nurse Capacity Building Program (GNCBP) at ICAP. In this role, she oversees a HRSA-funded, multi-country initiative to strengthen and sustain nursing’s role in the care of people living with HIV. She has served at senior management and training levels at various locations throughout Southern Africa, and has recently returned from Sierra Leone.
Stephen Morse PhD is professor of Epidemiology at the Mailman School of Public Health and is the global Co-Director of PREDICT, a USAID initiative to strengthen global capacity for surveillance and detection of new infectious diseases. He is also the founding Chair of the Program to Monitor Emerging Diseases (ProMED).
Fernando Ortiz Jr. works in the Department of Peacekeeping Operations at the United Nations and is currently on special assignment to the United Nations Mission in Liberia.
Alexander Preker is president and CEO of the Health Investment & Financing Corp, a founding member of the NY Chapter of the Keiretsu Forum, and served as chief economist of health, nutrition, and population at The World Bank.
Irwin Redlener MD is professor of Health Policy and Management and co-founder and president of the Children’s Health Fund and director of the National Center for Disaster Preparedness at The Earth Institute. Dr. Redlener is a nationally recognized expert on disaster preparedness policies, pandemic influenza, the threat of terrorism in the U.S., and the impact and consequences of major natural disasters and related issues.
Christopher Reim is the managing director of the Community Development Venture Capital Alliance and a managing general partner of Innovate NY Fund, LP.
Witney Schneidman is a senior international advisor for Africa at Covington & Burling, who provides strategic advice on political, economic, social and regulatory issues that are critical to companies’ success in Africa. Previously, he was Deputy Assistant Secretary of State for African Affairs and played a key role in ensuring the passage and implementation of the Africa Growth and Opportunity Act, and the establishment of the U.S.-SADC Forum, the U.S.-Angola Bilateral Consultative Commission and the U.S. Nigeria Joint Economic Partnership Committee.

Event Date: 
Monday, December 1, 2014 - 9:00am to 12:00pm
Event Location: 

Columbia Club of New York 
15 West 43rd Street
New York, NY
Topic: 

Associated Global A-Z item

News

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Friday, July 5, 2019

Experts from across Columbia University came together on Tuesday, January 29 with practitioners from government, business, the media, philanthropies, and grassroots and international organizations to discuss nearly 20 proposals for projects aimed at addressing some of the greatest challenges in...

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Columbia Neuroscientist Rafael Yuste Awarded Eliasson Global Leadership Prize

Date: 
Wednesday, October 17, 2018

Rafael Yuste, a professor of Biological Sciences at Columbia University, has been awarded the Eliasson Global Leadership Prize by the Tällberg Foundation for his seminal contributions in inspiring the US and International BRAIN initiatives and for his efforts toward building ethical guidelines...

Image: 
Rafael Yuste

Long-term Exposure to Ambient Air Pollution and Trajectories of Cognitive Decline in Northern Manhattan

Age-related cognitive decline is a growing public health issue as increases in life expectancy are expected to substantially raise the prevalence of cognitive impairment and dementia. An estimated 46.8 million individuals are currently living with dementia, with the global prevalence expected to double every 20 years. Emerging evidence suggests that ambient air pollution from traffic and other sources may be an important risk factor for cognitive decline in addition to its association with other cardiovascular and neurological outcomes.
The aim of this dissertation was to first investigate the association between long-term exposure to ambient air pollution and cognitive decline among older adults in an urban population within Northern Manhattan. I then set out to assess specific mechanisms involved in the association between long-term exposure to ambient air pollution and cognitive decline, specifically investigating the ApoE4 allele, age, and current smoking behavior as effect modifiers of the association between long-term exposure to ambient air pollution and cognitive decline.
I found evidence of an adverse effect of ambient air pollution on the cognitive functioning of older adults. Overall, exposure to higher levels of ambient air pollution was highly predictive of lower cognitive scores, but at baseline only. Contrary to the current hypothesis, limited evidence was found for an association between estimates of air pollution and trajectories of cognitive decline. The patterns of effect were similar across pollutant types and cognitive domains in this aging, urban population. I found strong evidence of effect modification by smoking status, where contrary to the hypothesis; the overall effects of ambient air pollution on cognition and cognitive decline were stronger among individuals who never smoked. The impact of effect modification by age category was most prominent in the memory and language cognitive domains. Among individuals less than 75 years old at baseline, there was a stronger association between a one IQR increase in air pollutants and cognitive domain scores at baseline as compared to individuals 75 years and older. I did not observe conclusive evidence of an association between air pollution and cognition in models stratified by APOE-4 status.
To my knowledge, this is the largest study to analyze the association of ambient air pollution on cognition and cognitive decline over time in a racially and ethnically diverse sample. These results further support the current evidence on the role of air pollution on accelerated cognitive aging and brain health.

Author: 
Erin Ryan Kulick
Subjects: 
Epidemiology
Neurosciences
Environmental health
Air--Pollution--Health aspects
Cognition--Research
Public health
Title string: 
Long-term Exposure to Ambient Air Pollution and Trajectories of Cognitive Decline in Northern Manhattan
GUID update: 
https://academiccommons.columbia.edu/catalog/ac:hhmgqnk9c1

Systematically Mapping the Epigenetic Context Dependence of Transcription Factor Binding

At the core of gene regulatory networks are transcription factors (TFs) that recognize specific DNA sequences and target distinct gene sets. Characterizing the DNA binding specificity of all TFs is a prerequisite for understanding global gene regulatory logic, which in recent years has resulted in the development of high-throughput methods that probe TF specificity in vitro and are now routinely used to inform or interpret in vivo studies. Despite the broad success of such methods, several challenges remain, two of which are addressed in this thesis.
Genomic DNA can harbor different epigenetic marks that have the potential to alter TF binding, the most prominent being CpG methylation. Given the vast number of modified CpGs in the human genome and an increasing body of literature suggesting a link between epigenetic changes and genome instability, or the onset of disease such as cancer, methods that can characterize the sensitivity of TFs to DNA methylation are needed to mechanistically interpret its impact on gene expression. We developed a high-throughput in vitro method (EpiSELEX-seq) that probes TF binding to unmodified and modified DNA sequences in competition, resulting in high-resolution maps of TF binding preferences. We found that methylation sensitivity can vary between TFs of the the same structural family and is dependent on the position of the 5mCpG within the TF binding site. The importance of our in vitro profiling of methylation sensitivity is demonstrated by the preference of human p53 tetramers for 5mCpGs within its binding site core. This previously unknown, stabilizing effect is also detectable in p53 ChIP-seq data when comparing methylated and unmethylated sites genome-wide.
A second impediment to predicting TF binding is our limited understanding of i) how cooperative participation of a TF in different complexes can alter their binding preference, and ii) how the detailed shape of DNA aids in creating a substrate for adaptive multi-TF binding. To address these questions in detail, we studied the in vitro binding preferences of three D. melanogaster homeodomain TFs: Homothorax (Hth), Extradenticle(Exd) and one of the eight Hox proteins. In vivo, Hth occurs in two splice forms: with (HthFL) and without (HthHM) the DNA binding domain (DBD). HthHM-Exd itself is a Hox cofactor that has been shown to induce latent sequence specificity upon complex formation with Hox proteins. There are three possible complexes that can be formed, all potentially having specific target genes: HthHM-Exd-Hox, HthFL-Exd-Hox, and HthFL-Exd. We characterized the in vitro binding preferences of each of these by developing new computational approaches to analyze high-throughput SELEX-seq data. We found distinct orientation and spacing preference for HthFL-Exd-Hox, alternative recognition modes that depend on the affinity class a sequence falls into, and a strong preference for a narrow DNA minor grove near Exd's N-terminal DBD. Strikingly, this shape readout is crucial to stabilize the HthHM-Exd-Hox complex in the absence of a Hth DBD and can thus be used to distinguish HthHM from HthFL isoform binding. Mutating the amino acids responsible for the shape readout by Exd and reinserting the engineered protein into the fly genome allowed us to classify in vivo binding sites based on ChIP-seq signal comparison between “shape-mutant” and wild-type Exd.
In summary, the research presented here has investigated TF binding preferences beyond sequence context by combining novel high-throughput experimental and computational methods. This interdisciplinary approach has enabled us to study binding preferences of TF complexes with respect to the epigenetic landscape of their cognate binding sites. Our novel mechanistic insights into DNA shape readout have provided a new avenue of exploiting guided protein engineering to probe how specific TFs interact with their co-factors in a cellular context, and how flanking genomic sequence helps determine which multi-TF complexes will form and which binding mode a complex adopts.

Author: 
Judith Franziska Kribelbauer
Subjects: 
Biochemistry
Bioinformatics
Biophysics
Transcription factors
Gene regulatory networks
Epigenetics
Title string: 
Systematically Mapping the Epigenetic Context Dependence of Transcription Factor Binding
GUID update: 
https://academiccommons.columbia.edu/catalog/ac:v6wwpzgmw7

Stochastic tuning of gene expression enables cellular adaptation in the absence of pre-existing regulatory circuitry

Cells adapt to familiar changes in their environment by activating predefined regulatory programs that establish adaptive gene expression states. These hard-wired pathways, however, may be inadequate for adaptation to environments never encountered before. Here, we reveal evidence for an alternative mode of gene regulation that enables adaptation to adverse conditions without relying on external sensory information or genetically predetermined cis-regulation. Instead, individual genes achieve optimal expression levels through a stochastic search for improved fitness. By focusing on improving the overall health of the cell, the proposed stochastic tuning mechanism discovers global gene expression states that are fundamentally new and yet optimized for novel environments. We provide experimental evidence for stochastic tuning in the adaptation of Saccharomyces cerevisiae to laboratory-engineered environments that are foreign to its native gene-regulatory network. Stochastic tuning operates locally at individual gene promoters, and its efficacy is modulated by perturbations to chromatin modification machinery.

Publication type: 
Author: 
Peter L. Freddolino
Jamie Siyu Yang
Amir Momen-Roknabadi
Saeed Tavazoie
Subjects: 
Gene regulatory networks
Systems biology
Gene expression
Stochastic processes
Epigenetics
Title string: 
Stochastic tuning of gene expression enables cellular adaptation in the absence of pre-existing regulatory circuitry
GUID update: 
https://academiccommons.columbia.edu/catalog/ac:cc2fqz614g

The Social Life of Health Insurance Temporality, Care, and the Politics of Financing Health in Rural Vietnam

Health insurance stands at the center of global debates on how nations can ensure equitable access to health care, especially for countries like Vietnam whose integration into the global economy has boosted economic development but intensified social inequality. When health insurance is promoted to low- to middle-income country contexts by development agencies such as the World Health Organization and the World Bank, what embedded cultural values accompany this? How do locally specific historical, political, and ethical concepts for managing vulnerability and uncertainty shape public understanding of insurance? To date, empirical research on health insurance’s impact has tended to examine its relation to health outcomes, service utilization patterns, or health care delivery rather than its cultural effects. As health insurance initiatives have expanded to at least 27 countries within the last decade, the universality of insurance’s value to local populations cannot be assumed. This ethnographic research investigates the cultural mediators and effects as a factor for understanding public responses to health insurance. It documents how this financial technology is transforming knowledge about how to care and manage health vulnerability.
With the support of international organizations, the Vietnamese government began its universal health insurance enrollment campaign in 2015. State officials, however, identify the “Vietnamese habit” of purchasing insurance only when ill as both a technical and cultural problem to achieving universal coverage. To better understand this process, I investigated how strategies to “change the mindset of citizens” were deployed by state media and personnel, and then actively resisted, incorporated, or transformed by community members. The study took place in Vinh Long Province, an agricultural area in the Mekong Delta with one of the highest uninsured rates in the country. I conducted twelve months of ethnographic research, including 60 semi-structured interviews with community members, health insurance professionals, and health care professionals; and extended participant observation in government health facilities, insurance offices, and the homes of community members.
The study analyzes the social consequences of new health insurance initiatives, the temporality of care, everyday dimensions of health care uncertainty, and their relevance to concerns within medical anthropology. I demonstrate how Vietnam’s insurance reform affected the terms through which people understood their social relations and risk subjectivities. By detailing the dynamic processes of a health insurance campaign aimed at changing health behaviors, the research reveals how financial policies are not value neutral. Rather, they reshape local moral worlds, social relations, and practices for managing uncertainty in late socialist Vietnam.

Author: 
Amy Dao
Subjects: 
Public health
Public policy (Law)
Health insurance
National health insurance
Social medicine
Title string: 
The Social Life of Health Insurance Temporality, Care, and the Politics of Financing Health in Rural Vietnam
GUID update: 
https://academiccommons.columbia.edu/catalog/ac:j3tx95x6d0

Differential Roles of PRDM16 Isoforms in Normal and Malignant Hematopoiesis

PRDM16 is a transcriptional co-regulator that is highly expressed in HSCs and required for their maintenance. It is also involved in translocations in acute myeloid leukemia (AML), myelodysplastic syndromes (MDS) and T-cell acute lymphoblastic leukemia. Prdm16 is expressed as both full-length (f Prdm16) and short-length (s-Prdm16) isoforms, the latter lacking an N-terminal PR domain homologous to SET methyltransferase domains. The roles of both isoforms in normal and malignant hematopoiesis are unclear. In chromosomal rearrangements involving PRDM16, the PR domain is deleted. Furthermore, overexpression of s-Prdm16, but not f-Prdm16, can cause leukemia in a p53-/- background predisposed to malignancy. Based on this, s-Prdm16 has been proposed as an oncogene whereas f-Prdm16 has been suggested to possess tumor suppressor activity.
The aim of this thesis was to more clearly elucidate the role of each Prdm16 isoform in normal and malignant hematopoiesis. We first showed that Prdm16 is essential for adult HSC maintenance using a conditional deletion mouse model specific for hematopoietic cells, as previous findings using an embryonic-lethal global Prdm16-/- mouse demonstrated this only in fetal liver. We then found, using a specific f-Prdm16-/- mouse model, that full-length Prdm16 is essential for HSC maintenance and induces multiple genes involved in GTPase signaling and represses inflammation. Based on a comparison of Prdm16-/- HSCs lacking both isoforms, and f-Prdm16-/- HSCs which express s-Prdm16, we were able to infer some hematopoietic properties of s-Prdm16 – namely that this isoform induces inflammatory gene expression and supports development of a Lineage-Sca1+cKit- lymphoid progenitor distinct from CLPs which predominantly differentiates into marginal zone B cells. s-Prdm16 expression alone, however, was not sufficient to maintain HSCs.
We used a mouse model of human MLL-AF9 leukemia and found that leukemia derived from Prdm16-deficient HSCs had extended latency, although expression of Prdm16 decreases during MLL-AF9 transformation and is undetectable in ex vivo leukemic cells. Forced expression of f-Prdm16 in these cells further extended leukemic latency, while forced expression of s-Prdm16 shortened latency. Gene expression profiling using RNAseq indicated that forced expression of f-Prdm16 resulted in altered respiratory metabolism of MLL-AF9 cells, whereas expression of s-Prdm16 induced a strong inflammatory gene signature, comparable to that seen in HSCs expressing only s-Prdm16. Several inflammatory cytokines and chemokines induced by s-Prdm16 are associated with MDS and with a worse prognosis in human AML. Furthermore, leukemia expressing s-Prdm16 had an elevated number of cells with abnormal nuclei, characteristic of dysplasia.
Finally, we performed an analysis of PRDM16 in human AML from the publically-available Cancer Genome Atlas dataset, containing clinical and gene expression data for 179 cases of AML. PRDM16 expression negatively correlated with overall survival, both in the entire dataset and in the NPM1 mutated and MLL¬-rearranged subsets, and s-PRDM16 exhibited a stronger correlation than f-PRDM16. HOX gene expression correlated with PRDM16 expression, suggesting that HOX genes may positively regulate PRDM16 expression in AML. In NPM1-mutant and MLL-rearranged subsets of AML, we also found that high PRDM16 expression correlated with an inflammatory gene signature, thus corroborating our findings in mouse MLL-AF9.
Our findings demonstrate distinct roles for Prdm16 isoforms in both normal hematopoiesis and AML, and identify s-Prdm16 as one of the drivers of prognostically-adverse inflammatory gene expression in leukemia.

Author: 
David Joseph Corrigan
Subjects: 
Immunology
Microbiology
Hematopoiesis
Genetic transcription--Regulation
Proteins
Title string: 
Differential Roles of PRDM16 Isoforms in Normal and Malignant Hematopoiesis
GUID update: 
https://academiccommons.columbia.edu/catalog/ac:j9kd51c5dr

Redox-Balancing Strategies in Pseudomonas aeruginosa

In natural habitats bacteria predominantly grow and survive as biofilms, which are densely populated assemblages of cells encased in self-produced matrices. Biofilms face the challenge of resource limitation due to poor substrate diffusion and consumption by cells closer to the periphery. When terminal electron acceptors for metabolism, such as oxygen, are limiting, reducing equivalents accumulate in the cell, leading to an imbalanced redox state and disruption of metabolic processes. The opportunistic pathogen Pseudomonas aeruginosa possesses various redox-balancing strategies that facilitate disposal of excess reducing power, including (i) production of phenazines, redox-active compounds that mediate extracellular electron shuttling; (ii) use of nitrate as an electron acceptor via the denitrification pathway, and (iii) fermentation of pyruvate. However, if the biofilm grows to a point where these metabolic strategies become insufficient, the community adopts a “structural” strategy: the cells collectively produce extracellular matrix to form wrinkle features, which increase surface area and oxygen availability, ultimately oxidizing (i.e., rebalancing) the cellular redox state. Though the broad physiological effects of these metabolic and structural strategies are known, details of their regulation and coordination in biofilm communities have remained elusive.
The work presented in this thesis was aimed at elucidating the (cross-)regulation and coordination of different redox-balancing strategies in biofilms of P. aeruginosa strain PA14. Studies described in Chapter 2 demonstrate novel regulatory links between phenazines and microaerobic denitrification, including a redox-mediated mechanism for control of the global transcription factor Anr, which is traditionally thought to be regulated solely by oxygen. This chapter also presents observations of the spatial segregation of denitrification enzymes in a colony biofilm, which is suggestive of metabolic specialization and substrate crossfeeding between different groups of cells.
Chapters 3 and 4 describe work examining the physiological functions and regulation of pyruvate and lactate metabolism in P. aeruginosa. These studies were motivated by pyruvate’s role as a “hub” for central metabolism, the unique structural biochemistry of the P. aeruginosa pyruvate carboxylase, and the intriguing complement of “lactate dehydrogenase” genes in P. aeruginosa. These genes include two that encode canonical and non-canonical respiration-linked L-lactate dehydrogenases. My results in Chapter 3 show that the non-canonical L-lactate dehydrogenase gene can substitute for the canonical one to support aerobic L-lactate utilization and that it is induced specifically by the L- enantiomer of lactate. This enzymatic redundancy for L-lactate utilization could be an adaptation that enhances virulence, given that host organisms (e.g. humans and plants) produce L-lactate but not D-lactate. In addition, Chapter 3 includes studies of pyruvate-lactate metabolism in the context of biofilm communities, where aerobic and anaerobic zones coexist in proximity. Evidence is provided that cells in biofilms have the potential to engage in crossfeeding of anaerobically generated D-lactate, which would constitute a new instance of bacterial multicellular metabolism. Finally, Chapter 4 shows that mutants of pyruvate carboxylase, which converts pyruvate to oxaloacetate, have a matrix-overproducing, hyperwrinkling biofilm phenotype indicative of an imbalanced cellular redox state. This result suggests that disruption of pyruvate carboxylase shunts metabolic flow through pyruvate dehydrogenase, converting pyruvate to acetyl-CoA and generating an excess of reducing power. Together, the findings presented in Chapter 3 and 4 underscore the importance of pyruvate metabolism in the contexts of redox homeostasis and community behavior.
When metabolic strategies are insufficient to balance the redox state, biofilms can ameliorate the problem of electron acceptor limitation by forming wrinkle structures, which increase the community’s surface area-to-volume ratio. Wrinkle formation depends on the production of extracellular matrix. Matrix production is also required for the formation of pellicles, biofilms that reside at air-liquid interfaces. Experiments described in Chapter 5 investigate properties of the P. aeruginosa matrix from a socio-evolutionary perspective. My results show that matrix production confers a competitive advantage in pellicle biofilms but not in colony biofilms. The evolutionary landscape of matrix production in biofilms is complex and context-specific; i.e., each microenvironment selects for a subset of phenotypes that confers fitness only in that specific microenvironment.
Chapter 6 describes the dynamic processes of pellicle formation in the gram-positive bacterium Bacillus subtilis as well as the gram-negative P. aeruginosa in a time-resolved manner. In these two distantly related species, we observed a conserved mechanism for pellicle formation that involves motility, chemotaxis and aerotaxis. These findings indicate that motility is more than just a unicellular behavior: cells collectively migrate to a microniche and initiate biofilm formation. Finally, Appendix A describes efforts to characterize proteinaceous components of the matrix isolated from P. aeruginosa PA14.
In conclusion, this work has elucidated mechanistic details of various redox-balancing strategies in P. aeruginosa, particularly from the perspective of multicellular community development.

Author: 
Yu Lin-Cheng
Subjects: 
Microbiology
Genetics
Pseudomonas aeruginosa
Biofilms
Oxidation-reduction reaction
Title string: 
Redox-Balancing Strategies in Pseudomonas aeruginosa
GUID update: 
https://academiccommons.columbia.edu/catalog/ac:m37pvmcvhn

Unsustainaburger: SDGs and the links between migrant labor, industrial livestock, and the environment

The meat-industrial-complex is a global production and consumption chain that systematically violates human rights, particularly those of workers, and degrades the environment. From food security and decent work to climate change and public health, industrial livestock operations and meat consumption patterns challenge the achievement of all 17 UN Sustainable Development Goals (SDGs) in ways that are cross-cutting and interconnected.1 In this study, interdisciplinary data about the world’s leading meat producers provide the empirical backdrop for a content analysis of the 2030 Agenda for Sustainable Development. The Declaration and Goals themselves, SDG Partnerships, Voluntary National Reviews, and other reports are analyzed to discern the degree to which issues associated with industrial meat production, and their interconnectivity, are acknowledged. The results of the content analysis demonstrate that the SDG Framework expresses less concern with the interrelated impacts of industrial meat practices than the actual gravity of those impacts demands. Like other sampled communications, the Agenda also fails to address the unique relationship between decent work and the environment, a critical linkage for successful SDG implementation. Research that explores discrepancies between global problems and the focus of international political attention is necessary for the development of public policies that are coherent and address root-causes of socio-economic inequality and environmental degradation.

Topic: 
Author: 
Iame Manucci
Subjects: 
Human rights
Migrant Labor
Factory farms
Environmental degradation
Sustainable development
Sustainable Development Goals
Title string: 
Unsustainaburger: SDGs and the links between migrant labor, industrial livestock, and the environment
GUID update: 
https://academiccommons.columbia.edu/catalog/ac:s1rn8pk0rx

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