The Politics of Metabolism: The Metabolic Syndrome and the Reproduction of Race and Racism

Biomedical researchers, government agencies, and the pharmaceutical industry increasingly use the term metabolic syndrome to define the observed co-occurrence of the major biological risk markers for heart disease, type II diabetes, and stroke. The metabolic syndrome is a new feature in what I call the politics of metabolism, or the discourses, social processes, and institutional relationships that governs the metabolism of individuals and groups. The emergence of the metabolic syndrome reflects a growing network of scientific, state, and corporate actors and institutions that are invested in studying, regulating, and profiting from control over metabolism. Drawing on insights from critical race theory, science and technology studies, and Foucauldian studies of biopower, I analyze the metabolic syndrome as a new discourse about metabolism that continually draws upon racial meanings to construct individual and group differences in different kinds of metabolic risk. The metabolic syndrome not only constitutes a new way of constructing, studying, and treating metabolic health problems, it also constitutes an emerging site for the production of racial meanings. Researchers use race in metabolic syndrome research and to study, prescribe, and label prescription drugs that may be related to the metabolic syndrome. I investigate the use of race and the metabolic syndrome in biomedical research on prescription drugs and African Americans. I develop the metaphor of killer applications to examine how prescription drugs operate in the politics of metabolism. A killer application is a superior technology that combines human and non-human elements that structure bodily practices in a wide range of social, commercial, and scientific contexts--prescription drugs have become the new killer applications in biomedicine. I argue that the search for killer applications has transformed the ways that pharmaceutical corporations study prescription drugs, metabolism, and race. I compare how drug researchers use race and the metabolic syndrome to study antipsychotics and statins in African Americans, how physicians' race-based diagnoses of schizophrenia and high cholesterol structure the prescribing patterns of antipsychotics and statins, and how scientists' assumptions about the genetic basis of racial differences in drug metabolism structure the debate about racebased drug therapies

Influenza A virus challenge models in cynomolgus macaques using the authentic inhaled aerosol and intra-nasal routes of infection

Non-human primates are the animals closest to humans for use in influenza A virus challenge studies, in terms of their phylogenetic relatedness, physiology and immune systems. Previous studies have shown that cynomolgus macaques (Macaca fascicularis) are permissive for infection with H1N1pdm influenza virus. These studies have typically used combined challenge routes, with the majority being intra-tracheal delivery, and high doses of virus (> 107 infectious units). This paper describes the outcome of novel challenge routes (inhaled aerosol, intra-nasal instillation) and low to moderate doses (103 to 106 plaque forming units) of H1N1pdm virus in cynomolgus macaques. Evidence of virus replication and sero-conversion were detected in all four challenge groups, although the disease was sub-clinical. Intra-nasal challenge led to an infection confined to the nasal cavity. A low dose (103 plaque forming units) did not lead to detectable infectious virus shedding, but a 1000-fold higher dose led to virus shedding in all intra-nasal challenged animals. In contrast, aerosol and intra-tracheal challenge routes led to infections throughout the respiratory tract, although shedding from the nasal cavity was less reproducible between animals compared to the high-dose intra-nasal challenge group. Intra-tracheal and aerosol challenges induced a transient lymphopaenia, similar to that observed in influenza-infected humans, and greater virus-specific cellular immune responses in the blood were observed in these groups in comparison to the intra-nasal challenge groups. Activation of lung macrophages and innate immune response genes was detected at days 5 to 7 post-challenge. The kinetics of infection, both virological and immunological, were broadly in line with human influenza A virus infections. These more authentic infection models will be valuable in the determination of anti-influenza efficacy of novel entities against less severe (and thus more common) influenza infections

Multidifferential study of identified charged hadron distributions in ZZ-tagged jets in proton-proton collisions at s=\sqrt{s}=13 TeV

Jet fragmentation functions are measured for the first time in proton-proton collisions for charged pions, kaons, and protons within jets recoiling against a $Z$ boson. The charged-hadron distributions are studied longitudinally and transversely to the jet direction for jets with transverse momentum 20 $< p_{\textrm{T}} < 100$ GeV and in the pseudorapidity range $2.5 < \eta < 4$. The data sample was collected with the LHCb experiment at a center-of-mass energy of 13 TeV, corresponding to an integrated luminosity of 1.64 fb$^{-1}$. Triple differential distributions as a function of the hadron longitudinal momentum fraction, hadron transverse momentum, and jet transverse momentum are also measured for the first time. This helps constrain transverse-momentum-dependent fragmentation functions. Differences in the shapes and magnitudes of the measured distributions for the different hadron species provide insights into the hadronization process for jets predominantly initiated by light quarks.Comment: All figures and tables, along with machine-readable versions and any supplementary material and additional information, are available at https://cern.ch/lhcbproject/Publications/p/LHCb-PAPER-2022-013.html (LHCb public pages

Study of the B−→Λc+Λˉc−K−B^{-} \to \Lambda_{c}^{+} \bar{\Lambda}_{c}^{-} K^{-} decay

The decay $B^{-} \to \Lambda_{c}^{+} \bar{\Lambda}_{c}^{-} K^{-}$ is studied in proton-proton collisions at a center-of-mass energy of $\sqrt{s}=13$ TeV using data corresponding to an integrated luminosity of 5 $\mathrm{fb}^{-1}$ collected by the LHCb experiment. In the $\Lambda_{c}^+ K^{-}$ system, the $\Xi_{c}(2930)^{0}$ state observed at the BaBar and Belle experiments is resolved into two narrower states, $\Xi_{c}(2923)^{0}$ and $\Xi_{c}(2939)^{0}$, whose masses and widths are measured to be $$m(\Xi_{c}(2923)^{0}) = 2924.5 \pm 0.4 \pm 1.1 \,\mathrm{MeV}, \\ m(\Xi_{c}(2939)^{0}) = 2938.5 \pm 0.9 \pm 2.3 \,\mathrm{MeV}, \\ \Gamma(\Xi_{c}(2923)^{0}) = \phantom{000}4.8 \pm 0.9 \pm 1.5 \,\mathrm{MeV},\\ \Gamma(\Xi_{c}(2939)^{0}) = \phantom{00}11.0 \pm 1.9 \pm 7.5 \,\mathrm{MeV},$$ where the first uncertainties are statistical and the second systematic. The results are consistent with a previous LHCb measurement using a prompt $\Lambda_{c}^{+} K^{-}$ sample. Evidence of a new $\Xi_{c}(2880)^{0}$ state is found with a local significance of $3.8\,\sigma$, whose mass and width are measured to be $2881.8 \pm 3.1 \pm 8.5\,\mathrm{MeV}$ and $12.4 \pm 5.3 \pm 5.8 \,\mathrm{MeV}$, respectively. In addition, evidence of a new decay mode $\Xi_{c}(2790)^{0} \to \Lambda_{c}^{+} K^{-}$ is found with a significance of $3.7\,\sigma$. The relative branching fraction of $B^{-} \to \Lambda_{c}^{+} \bar{\Lambda}_{c}^{-} K^{-}$ with respect to the $B^{-} \to D^{+} D^{-} K^{-}$ decay is measured to be $2.36 \pm 0.11 \pm 0.22 \pm 0.25$, where the first uncertainty is statistical, the second systematic and the third originates from the branching fractions of charm hadron decays.Comment: All figures and tables, along with any supplementary material and additional information, are available at https://cern.ch/lhcbproject/Publications/p/LHCb-PAPER-2022-028.html (LHCb public pages

Measurement of the ratios of branching fractions R(D∗)\mathcal{R}(D^{*}) and R(D0)\mathcal{R}(D^{0})

The ratios of branching fractions $\mathcal{R}(D^{*})\equiv\mathcal{B}(\bar{B}\to D^{*}\tau^{-}\bar{\nu}_{\tau})/\mathcal{B}(\bar{B}\to D^{*}\mu^{-}\bar{\nu}_{\mu})$ and $\mathcal{R}(D^{0})\equiv\mathcal{B}(B^{-}\to D^{0}\tau^{-}\bar{\nu}_{\tau})/\mathcal{B}(B^{-}\to D^{0}\mu^{-}\bar{\nu}_{\mu})$ are measured, assuming isospin symmetry, using a sample of proton-proton collision data corresponding to 3.0 fb${ }^{-1}$ of integrated luminosity recorded by the LHCb experiment during 2011 and 2012. The tau lepton is identified in the decay mode $\tau^{-}\to\mu^{-}\nu_{\tau}\bar{\nu}_{\mu}$. The measured values are $\mathcal{R}(D^{*})=0.281\pm0.018\pm0.024$ and $\mathcal{R}(D^{0})=0.441\pm0.060\pm0.066$, where the first uncertainty is statistical and the second is systematic. The correlation between these measurements is $\rho=-0.43$. Results are consistent with the current average of these quantities and are at a combined 1.9 standard deviations from the predictions based on lepton flavor universality in the Standard Model.Comment: All figures and tables, along with any supplementary material and additional information, are available at https://cern.ch/lhcbproject/Publications/p/LHCb-PAPER-2022-039.html (LHCb public pages

The Metabolic Fetish: Introduction to Blood Sugar: Racial Pharmacology and Food Justice in Black America

Excerpt from “Introduction” to Blood Sugar: Racial Pharmacology and Food Justice in Black America by Anthony Ryan Hatch. Minneapolis: University of Minnesota Press.Copyright 2016 by the Regents of the University of Minnesota https://www.upress.umn.edu/book-division/books/blood-sugar

Subject People Key-Topics Critical Race Theory Bibliographic Details Blackwell Encyclopedia of Sociology

Sections Critical Race Theory REFERENCES AND SUGGESTED READINGS Critical race theory refers to a historical and contemporary body of scholarship that aims to interrogate the discourses, ideologies, and social structures that produce and maintain conditions of racial injustice. Critical race theory analyzes how race and racism are foundational elements in historical and contemporary social structures and social experiences. In defining critical race theory, it is important to make a distinction between the deep historical tradition of critical theorizing about race and racism and a specific body of American legal scholarship that emerged in the 1970s and 1980s in response to the successes and failures of the Civil Rights Movement struggles for the freedom and liberation of people of color of the 1950s and 1960s. While this new school of legal thought coined the phrase &quot;critical race theory&quot; to signal a new critical analysis of the role of the law in propagating and maintaining racism, this movement is part of a broader intellectual tradition of critical theories of race and anti-racist struggle that has political roots in the work of pioneering scholar-activists like Frederick Douglass, Ida Wells-Barnett, and W. E. B. Du Bois. Using this broader framework, critical race theory can be viewed as a diagnostic body of &quot;intellectual activism&quot; scholarship that seeks to identify the pressure points for anti-racist struggle. Given the historical scope of critical race theories, this essay highlights several core themes that tie together this eclectic body of explicitly political theorizing. The first core theme deals with how critical race theories frame their two focal objects of study: race and racism. First, critical race theory understands the concept of race as a social construction that is produced as a result of the cultural and political meanings ascribed to it through social interactions and relationships across multiple levels of social organization. Since the 1600s, race has been a constitutive feature of global social, political, economic, and cultural organization. Critical race theories have demonstrated how race concepts and their accompanying racisms were foundational to the administration of colonial social systems, the rise and expansion of global capitalism, and th