Institutionalizing Scientific Knowledge: The Social and Political Foundation of Empirical Economic Research

Scientific knowledge is an essential component of modern society. Consequently, sociologists are interested in its production process and have conducted a broad variety of studies showing how social patterns influence the definition and the boundaries of scientific knowledge. In this paper, I ask how social factors influence the transformation of a ‘normal’ field of knowledge into a ‘scientific’ one. First, I give a brief overview of the development of the sociology of scientific knowledge exploring different approaches to the social foundations and boundaries of scientific knowledge. Second, I present a case study of the transformation of empirical economic research in the 1920s from a field of knowledge produced by journalists and civil servants into a prestigious scientific domain. I use neo-institutionalist ideas to show that knowledge needs a socially legitimated organizational frame in order to count as ‘scientific’ and I examine how political needs to ‘manage the economy’ build boundaries around economic knowledge and define it as ‘scientific’ in order to control its production, distribution, and communication

Film calibration for the Skylab/ATM S-056 X-ray telescope

The sensitometry and film calibration effort for the Skylab/ATM S-056 X-ray telescope is summarized. The apparatus and procedures used are described together with the two types of flight film used, Kodak SO-212 and SO-242. The sensitometry and processing of the flight film are discussed, and the results are presented in the form of the characteristic curves and related data. The use of copy films is also discussed

Genomic Profiling Reveals Distinct Routes To Complement Resistance in Klebsiella pneumoniae.

The serum complement system is a first line of defense against bacterial invaders. Resistance to killing by serum enhances the capacity of Klebsiella pneumoniae to cause infection, but it is an incompletely understood virulence trait. Identifying and characterizing the factors responsible for preventing activation of, and killing by, serum complement could inform new approaches to treatment of K. pneumoniae infections. Here, we used functional genomic profiling to define the genetic basis of complement resistance in four diverse serum-resistant K. pneumoniae strains (NTUH-K2044, B5055, ATCC 43816, and RH201207), and explored their recognition by key complement components. More than 90 genes contributed to resistance in one or more strains, but only three, rfaH, lpp, and arnD, were common to all four strains. Deletion of the antiterminator rfaH, which controls the expression of capsule and O side chains, resulted in dramatic complement resistance reductions in all strains. The murein lipoprotein gene lpp promoted capsule retention through a mechanism dependent on its C-terminal lysine residue; its deletion led to modest reductions in complement resistance. Binding experiments with the complement components C3b and C5b-9 showed that the underlying mechanism of evasion varied in the four strains: B5055 and NTUH-K2044 appeared to bypass recognition by complement entirely, while ATCC 43816 and RH201207 were able to resist killing despite being associated with substantial levels of C5b-9. All rfaH and lpp mutants bound C3b and C5b-9 in large quantities. Our findings show that, even among this small selection of isolates, K. pneumoniae adopts differing mechanisms and utilizes distinct gene sets to avoid complement attack

Evidence of a high incidence of subclinically affected calves in a herd of cattle with fatal cases of Bovine Neonatal Pancytopenia (BNP).

BACKGROUND: Bovine Neonatal Pancytopenia (BNP) is a disease of calves characterised by bone marrow trilineage hypoplasia, mediated by ingestion of alloantibodies in colostrum. Suspected subclinical forms of BNP have been reported, suggesting that observed clinical cases may not represent the full extent of the disease. However to date there are no objective data available on the incidence of subclinical disease or its temporal distribution. This study aimed to 1) ascertain whether subclinical BNP occurs and, if so, to determine the incidence on an affected farm and 2) determine whether there is evidence of temporal clustering of BNP cases on this farm. To achieve these aims, haematological screening of calves born on the farm during one calving season was carried out, utilising blood samples collected at defined ages. These data were then analysed in comparison to data from both known BNP-free control animals and histopathologically confirmed BNP cases. An ordinal logistic regression model was used to create a composite haematology score to predict the probabilities of calves being normal, based on their haematology measurements at 10–14 days old. RESULTS: This study revealed that 15% (21 of 139) of the clinically normal calves on this farm had profoundly abnormal haematology (<5% chance of being normal) and could be defined as affected by subclinical BNP. Together with clinical BNP cases, this gave the study farm a BNP incidence of 18%. Calves with BNP were found to be distributed throughout the calving period, with no clustering, and no significant differences in the date of birth of cases or subclinical cases were found compared to the rest of the calves. This study did not find any evidence of increased mortality or increased time from birth to sale in subclinical BNP calves but, as the study only involved a single farm and adverse effects may be determined by other inter-current diseases it remains possible that subclinical BNP has a detrimental impact on the health and productivity of calves under certain circumstances. CONCLUSIONS: Subclinical BNP was found to occur at a high incidence in a herd of cattle with fatal cases of BNP

Progression of Parkinson's Disease Pathology Is Reproduced by Intragastric Administration of Rotenone in Mice

In patients with Parkinson's disease (PD), the associated pathology follows a characteristic pattern involving inter alia the enteric nervous system (ENS), the dorsal motor nucleus of the vagus (DMV), the intermediolateral nucleus of the spinal cord and the substantia nigra, providing the basis for the neuropathological staging of the disease. Here we report that intragastrically administered rotenone, a commonly used pesticide that inhibits Complex I of the mitochondrial respiratory chain, is able to reproduce PD pathological staging as found in patients. Our results show that low doses of chronically and intragastrically administered rotenone induce alpha-synuclein accumulation in all the above-mentioned nervous system structures of wild-type mice. Moreover, we also observed inflammation and alpha-synuclein phosphorylation in the ENS and DMV. HPLC analysis showed no rotenone levels in the systemic blood or the central nervous system (detection limit [rotenone]<20 nM) and mitochondrial Complex I measurements showed no systemic Complex I inhibition after 1.5 months of treatment. These alterations are sequential, appearing only in synaptically connected nervous structures, treatment time-dependent and accompanied by inflammatory signs and motor dysfunctions. These results strongly suggest that the local effect of pesticides on the ENS might be sufficient to induce PD-like progression and to reproduce the neuroanatomical and neurochemical features of PD staging. It provides new insight into how environmental factors could trigger PD and suggests a transsynaptic mechanism by which PD might spread throughout the central nervous system

Multiple constraints cause positive and negative feedbacks limiting grassland soil CO2efflux under CO2enrichment

Terrestrial ecosystems are increasingly enriched with resources such as atmospheric CO2that limit ecosystem processes. The consequences for ecosystem carbon cycling depend on the feedbacks from other limiting resources and plant community change, which remain poorly understood for soil CO2efflux, JCO2, a primary carbon flux from the biosphere to the atmosphere. We applied a unique CO2enrichment gradient (250 to 500 μL L-1) for eight years to grassland plant communities on soils from different landscape positions. We identified the trajectory of JCO2responses and feedbacks from other resources, plant diversity [effective species richness, exp(H)], and community change (plant species turnover). We found linear increases in JCO2on an alluvial sandy loam and a lowland clay soil, and an asymptotic increase on an upland silty clay soil. Structural equation modeling identified CO2as the dominant limitation on JCO2on the clay soil. In contrast with theory predicting limitation from a single limiting factor, the linear JCO2response on the sandy loam was reinforced by positive feedbacks from aboveground net primary productivity and exp(H), while the asymptotic JCO2response on the silty clay arose from a net negative feedback among exp(H), species turnover, and soil water potential. These findings support a multiple resource limitation view of the effects of global change drivers on grassland ecosystem carbon cycling and highlight a crucial role for positive or negative feedbacks between limiting resources and plant community structure. Incorporating these feedbacks will improve models of terrestrial carbon sequestration and ecosystem services

Multiple constraints cause positive and negative feedbacks limiting grassland soil CO2efflux under CO2enrichment

Terrestrial ecosystems are increasingly enriched with resources such as atmospheric CO2that limit ecosystem processes. The consequences for ecosystem carbon cycling depend on the feedbacks from other limiting resources and plant community change, which remain poorly understood for soil CO2efflux, JCO2, a primary carbon flux from the biosphere to the atmosphere. We applied a unique CO2enrichment gradient (250 to 500 μL L-1) for eight years to grassland plant communities on soils from different landscape positions. We identified the trajectory of JCO2responses and feedbacks from other resources, plant diversity [effective species richness, exp(H)], and community change (plant species turnover). We found linear increases in JCO2on an alluvial sandy loam and a lowland clay soil, and an asymptotic increase on an upland silty clay soil. Structural equation modeling identified CO2as the dominant limitation on JCO2on the clay soil. In contrast with theory predicting limitation from a single limiting factor, the linear JCO2response on the sandy loam was reinforced by positive feedbacks from aboveground net primary productivity and exp(H), while the asymptotic JCO2response on the silty clay arose from a net negative feedback among exp(H), species turnover, and soil water potential. These findings support a multiple resource limitation view of the effects of global change drivers on grassland ecosystem carbon cycling and highlight a crucial role for positive or negative feedbacks between limiting resources and plant community structure. Incorporating these feedbacks will improve models of terrestrial carbon sequestration and ecosystem services

Environmental toxins trigger PD-like progression via increased alpha-synuclein release from enteric neurons in mice

Pathological studies on Parkinson’s disease (PD) patients suggest that PD pathology progresses from the enteric nervous system (ENS) and the olfactory bulb into the central nervous system. We have previously shown that environmental toxins acting locally on the ENS mimic this PD-like pathology progression pattern in mice. Here, we show for the first time that the resection of the autonomic nerves stops this progression. Moreover, our results show that an environmental toxin (i.e. rotenone) promotes the release of alpha-synuclein by enteric neurons and that released enteric alpha-synuclein is up-taken by presynaptic sympathetic neurites and retrogradely transported to the soma, where it accumulates. These results strongly suggest that pesticides can initiate the progression of PD pathology and that this progression is based on the transneuronal and retrograde axonal transport of alpha-synuclein. If confirmed in patients, this study would have crucial implications in the strategies used to prevent and treat PDThis work was supported by the Fritz-Thyssen Foundation, theGerman Parkinson’s disease Society and by Amelia Jimenez Gomez as private dono