Bruno Latours Neubestimmung der Differenz von Gesellschaft und Natur

"Ob 'die' Soziologie radikal veränderter theoretischer Grundlagen und insbesondere eines anderen Naturbegriffs bedarf, um zu einem adäquaten Verständnis der 'ökologischen Krise' zu gelangen, ist umstritten. Forderungen nach vielfältig interpretierbaren grundlegenden Kurskorrekturen stehen umweltsoziologischen Normalisierungsstrategien gegenüber. Theoretisch dominieren soziozentrische Ansätze, die die Analyse der natural-stofflichen Dimension der 'ökologischen Krise' den Naturwissenschaften überlassen, ohne deren Charakter als soziale Praxis und damit die Umkämpfheit dieser natural-stofflichen Dimension ernstzunehmen. Latours modernitätskritische 'symmetrische Anthropologie', entwickelt aus wissenschafts- und techniksoziologischen Untersuchungen, beansprucht ein radikal empirisches Programm der 'Ko-Produktion von Gesellschaft und Natur'. Beide Pole sollen demzufolge als kontingente Kristallisierungen - und nicht als gegebene Voraussetzungen - konstruktiver Prozesse aufzufassen sein sollen. In diesen Prozessen spielen Wissenschaft und Technik als 'Politik mit anderen Mitteln' die zentrale Rolle. Jeder Ansatz eines 'spezifisch Sozialen', das die menschliche Form der Vergesellschaftung kennzeichnet, wird als dem Verständnis dieser konstruktiven Prozesse hinderliche Essentialisierung abgewiesen. Latours 'symmetrische Anthropologie' verfolgt vielmehr ein postsoziologisches Programm der Untersuchung soziotechnischer Ensembles. Dieses Konzept soll schließlich auch einer Analyse ökologischer Krisenphänomene als Leitfaden dienen. Dieser Anspruch läßt sich, den produktiven Seiten der Überlegungen Latours zum Trotz, nicht halten. Nicht nur ist unklar, wie eine Erweiterung der semiologischen Wissenschafts- und Technologieanalysen die materiell-stoffliche Dimension der 'ökologischen Krise' sollte thematisieren können, sind doch jene Analysen selbst bereits dem Vorwurf ausgesetzt, die 'Materialität' von Wissenschaft und Technologie zu verfehlen. Latours Frontstellung gegen soziologische Redukdonismen erschwert die Entwicklung eines Konzeptes der 'ökologischen Krise' als ein spezifisch soziales Problem, das gesellschaftliche Ursachen hat und gesellschaftlicher Lösungen bedarf." (Autorenreferat

Influences of forested and grassland vegetation on late Quaternary ecosystem development as recorded in lacustrine sediments

Geosphere-biosphere interactions are ubiquitous features of the Earth surface, yet the development of interactions between newly exposed lithologic surfaces and colonizing plants during primary succession after glaciation are lacking temporal detail. To assess the nature, rate, and magnitude of vegetation influence on parent material and sediment delivery, we analyzed ecosystem and geochemical proxies from lacustrine sediment cores at a grassland site and a forested site in the northern United States. Over time, terrigenous inputs declined at both sites, with increasing amounts of organic inputs toward present. The similarities between sites were striking given that the grassland sequence began in the Early Holocene, and the forested sequence began after the last glacial maximum. Multiple mechanisms of chemical weathering, hydrologic transport, and changes in source material potentially contribute to this pattern. Although there were strong links between vegetation composition and nitrogen cycling at each site, it appears that changes in forest type, or from oak woodland to grassland, did not exert a large influence on elemental (K, Ti, Si, Ca, Fe, Mn, and S) abundance in the sedimentary sequences. Rather, other factors in the catchment-lake system determined the temporal sequence of elemental abundance

Metabolic insufficiency underlies intratumoral cytotoxic T cell dysfunction

T cells have the remarkable ability to recognize and remove abnormal cells with precision, a feature that is very desirable for the treatment of cancer. However, while T cells specific for tumor antigens are primed and can infiltrate tumors, they are quickly rendered dysfunctional, through both cell intrinsic and cell extrinsic mechanisms. One way that tumors cripple T cell function is through the generation of an immunosuppressive microenvironment that is chronically inflamed, hypoxic, and nutrient poor. T cell activation and subsequent generation of effector function is bioenergetically demanding, requiring large amounts of metabolic intermediates to effectively proliferate, produce cytokines, and lyse target cells. We hypothesized that T cell dysfunction in cancer is due, in part, to metabolic insufficiency caused by chronic activation in metabolically dearth conditions. Using single-cell metabolic assays and extracellular flux analysis, we show that CD8+ cytotoxic T cells that infiltrate tumors demonstrate a progressive loss of mitochondrial function and mass, concomitant with upregulation of markers that correlate with T cell exhaustion. This mitochondrial dysfunction occurs independently of coinhibitory molecule signaling and specifically in the tumor microenvironment. This results in a failure to generate an adequate pool of ATP and in inability to effectively translate effector gene transcripts. This in stark contrast to T cells responding to an acute viral infection, where activated effector T cells demonstrate increased mitochondrial mass and ATP reserve. Further, artificial induction of mitochondrial dysfunction in T cells results in upregulation of coinhibitory molecules and an ‘exhausted-like’ phenotype, suggesting that metabolic insufficiency underlies the dysfunctional phenotype in cancer. Taken together, our data support a model in which tumor-infiltrating T cells have metabolic needs that cannot be met, resulting in failed effector function and tumor growth. Our studies also suggest that modulation or reprogramming of the altered metabolism of intratumoral T cells represents a potential strategy to reinvigorate dysfunctional T cells for the immunotherapeutic treatment of cancer

Anabolism-Associated Mitochondrial Stasis Driving Lymphocyte Differentiation over Self-Renewal

Regeneration requires related cells to diverge in fate. We show that activated lymphocytes yield sibling cells with unequal elimination of aged mitochondria. Disparate mitochondrial clearance impacts cell fate and reflects larger constellations of opposing metabolic states. Differentiation driven by an anabolic constellation of PI3K/mTOR activation, aerobic glycolysis, inhibited autophagy, mitochondrial stasis, and ROS production is balanced with self-renewal maintained by a catabolic constellation of AMPK activation, mitochondrial elimination, oxidative metabolism, and maintenance of FoxO1 activity. Perturbations up and down the metabolic pathways shift the balance of nutritive constellations and cell fate owing to self-reinforcement and reciprocal inhibition between anabolism and catabolism. Cell fate and metabolic state are linked by transcriptional regulators, such as IRF4 and FoxO1, with dual roles in lineage and metabolic choice. Instructing some cells to utilize nutrients for anabolism and differentiation while other cells catabolically self-digest and self-renew may enable growth and repair in metazoa

Parent-offspring conflict over mate choice: An experimental study in China

Both parents and offspring have evolved mating preferences that enable them to select mates and children‐in‐law to maximize their inclusive fitness. The theory of parent–offspring conflict predicts that preferences for potential mates may differ between parents and offspring: individuals are expected to value biological quality more in their own mates than in their offspring's mates and to value investment potential more in their offspring's mates than in their own mates. We tested this hypothesis in China using a naturalistic ‘marriage market’ where parents actively search for marital partners for their offspring. Parents gather at a public park to advertise the characteristics of their adult children, looking for a potential son or daughter‐in‐law. We presented 589 parents and young adults from the city of Kunming (Yunnan, China) with hypothetical mating candidates varying in their levels of income (proxy for investment potential) and physical attractiveness (proxy for biological quality). We found some evidence of a parent–offspring conflict over mate choice, but only in the case of daughters, who evaluated physical attractiveness as more important than parents. We also found an effect of the mating candidate's sex, as physical attractiveness was deemed more valuable in a female potential mate by parents and offspring alike

Enforced PGC-1α expression promotes CD8 T cell fitness, memory formation and antitumor immunity.

Memory CD8 T cells can provide long-term protection against tumors, which depends on their enhanced proliferative capacity, self-renewal and unique metabolic rewiring to sustain cellular fitness. Specifically, memory CD8 T cells engage oxidative phosphorylation and fatty acid oxidation to fulfill their metabolic demands. In contrast, tumor-infiltrating lymphocytes (TILs) display severe metabolic defects, which may underlie their functional decline. Here, we show that overexpression of proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), the master regulator of mitochondrial biogenesis (MB), favors CD8 T cell central memory formation rather than resident memory generation. PGC-1α-overexpressing CD8 T cells persist and mediate more robust recall responses to bacterial infection or peptide vaccination. Importantly, CD8 T cells with enhanced PGC-1α expression provide stronger antitumor immunity in a mouse melanoma model. Moreover, TILs overexpressing PGC-1α maintain higher mitochondrial activity and improved expansion when rechallenged in a tumor-free host. Altogether, our findings indicate that enforcing mitochondrial biogenesis promotes CD8 T cell memory formation, metabolic fitness, and antitumor immunity in vivo

EFSA CEF Panel (Panel on Food Contac t Materials, Enzymes, Flavourings and Processing Aids , 2013. Scientific Opinion on Flavouring Group Evaluation 2 07 (FGE.2 07 )

International audienc

IRE1α–XBP1 controls T cell function in ovarian cancer by regulating mitochondrial activity

Tumours evade immune control by creating hostile microenvironments that perturb T cell metabolism and effector function 1?4 . However, it remains unclear how intra-tumoral T cells integrate and interpret metabolic stress signals. Here we report that ovarian cancer?an aggressive malignancy that is refractory to standard treatments and current immunotherapies 5?8 ?induces endoplasmic reticulum stress and activates the IRE1α?XBP1 arm of the unfolded protein response 9,10 in T cells to control their mitochondrial respiration and anti-tumour function. In T cells isolated from specimens collected from patients with ovarian cancer, upregulation of XBP1 was associated with decreased infiltration of T cells into tumours and with reduced IFNG mRNA expression. Malignant ascites fluid obtained from patients with ovarian cancer inhibited glucose uptake and caused N-linked protein glycosylation defects in T cells, which triggered IRE1α?XBP1 activation that suppressed mitochondrial activity and IFNγ production. Mechanistically, induction of XBP1 regulated the abundance of glutamine carriers and thus limited the influx of glutamine that is necessary to sustain mitochondrial respiration in T cells under glucose-deprived conditions. Restoring N-linked protein glycosylation, abrogating IRE1α?XBP1 activation or enforcing expression of glutamine transporters enhanced mitochondrial respiration in human T cells exposed to ovarian cancer ascites. XBP1-deficient T cells in the metastatic ovarian cancer milieu exhibited global transcriptional reprogramming and improved effector capacity. Accordingly, mice that bear ovarian cancer and lack XBP1 selectively in T cells demonstrate superior anti-tumour immunity, delayed malignant progression and increased overall survival. Controlling endoplasmic reticulum stress or targeting IRE1α?XBP1 signalling may help to restore the metabolic fitness and anti-tumour capacity of T cells in cancer hosts.Fil: Song, Minkyung. Weill Cornell Medicine; Estados UnidosFil: Sandoval, Tito A.. Weill Cornell Medicine; Estados UnidosFil: Chae, Chang-Suk. Weill Cornell Medicine; Estados UnidosFil: Chopra, Sahil. Weill Cornell Medicine; Estados UnidosFil: Tan, Chen. Weill Cornell Medicine; Estados UnidosFil: Rutkowski, Melanie R.. University of Virginia; Estados UnidosFil: Raundhal, Mahesh. Dana Farber Cancer Institute; Estados Unidos. Harvard Medical School; Estados UnidosFil: Chaurio, Ricardo A.. H. Lee Moffitt Cancer Center & Research Institute; Estados UnidosFil: Payne, Kyle K.. H. Lee Moffitt Cancer Center & Research Institute; Estados UnidosFil: Konrad, Csaba. Weill Cornell Medicine; Estados UnidosFil: Bettigole, Sarah E.. Quentis Therapeutics Inc.; Estados UnidosFil: Shin, Hee Rae. Quentis Therapeutics Inc.; Estados UnidosFil: Crowley, Michael J. P.. Weill Cornell Graduate School of Medical Sciences; Estados UnidosFil: Cerliani, Juan Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Kossenkov, Andrew V.. The Wistar Institute; Estados UnidosFil: Motorykin, Ievgen. Weill Cornell Medicine,; Estados UnidosFil: Zhang, Sheng. Weill Cornell Medicine,; Estados UnidosFil: Manfredi, Giovanni. Weill Cornell Medicine,; Estados UnidosFil: Zamarin, Dmitriy. Memorial Sloan Kettering Cancer Center; Estados UnidosFil: Holcomb, Kevin. Weill Cornell Medicine,; Estados UnidosFil: Rodriguez, Paulo C.. H. Lee Moffitt Cancer Center & Research Institute; Estados UnidosFil: Rabinovich, Gabriel Adrián. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica; ArgentinaFil: Conejo Garcia, Jose R.. H. Lee Moffitt Cancer Center & Research Institute; Estados UnidosFil: Glimcher, Laurie H.. Dana Farber Cancer Institute; Estados Unidos. Harvard Medical School; Estados UnidosFil: Cubillos-Ruiz, Juan R.. Weill Graduate School Of Medical Sciences; Estados Unidos. Weill Graduate School Of Medical Sciences; Estados Unido