Quantification 2.0? Bibliometric Infrastructures in Academic Evaluation

Due to developments recently termed as ‘audit,’ ‘evaluation,’ or ‘metric society,’ universities have become subject to ratings and rankings and researchers are evaluated according to standardized quantitative indicators such as their publication output and their personal citation scores. Yet, this development is not only based on the rise of new public management and ideas on ‘the return on public or private investment.’ It has also profited from ongoing technological developments. Due to a massive increase in digital publishing corresponding with the growing availability of related data bibliometric infrastructures for evaluating science are continuously becoming more differentiated and elaborate. They allow for new ways of using bibliometric data through various easily applicable tools. Furthermore, they also produce new quantities of data due to new possibilities in following the digital traces of scientific publications. In this article, I discuss this development as quantification 2.0. The rise of digital infrastructures for publishing, indexing, and managing scientific publications has not only made bibliometric data become a valuable source for performance assessment. It has triggered an unprecedented growth in bibliometric data production turning freely accessible data about scientific work into edited databases and producing competition for its users. The production of bibliometric data has thus become decoupled from their application. Bibliometric data have turned into a self-serving end while their providers are constantly seeking for new tools to make use of them.Peer Reviewe

Theoretical Contributions to a sociology of (e)valuation

Valuation and evaluation processes are currently a much discussed topic, in particular, in the sociology of science, in science and technology studies and in economic sociology. Phenomena such as university rankings or credit ratings are addressed in research on classification, categorization, commensuration, standardization, and quantification. However, beyond such discussions about ratings and rankings, the paper argues that valuation and evaluation processes should be furthermore understood as a substantial feature of the social. Valuation as the construction of classificatory systems through the attribution of value to objects, people and practices and evaluation as the enactment of such value-charged classificatory systems fundamentally contribute to the institutionalization of a commonly shared understanding of social reality. Focusing on conflicts about the attribution of value and the appropriateness of evaluation frameworks within everyday situations of decision-making might then help to address questions such as on institutional change

Theories of Valuation - Building Blocks for Conceptualizing Valuation between Practice and Structure

Phenomena of attributing value to objects, practices, and people, and of assessing their value have become a popular subject in sociological research. Classification, among other valuation practices, represents a central topic in these studies. Thus, the sociology of valuation is emerging as a new field that, however, lacks common ground in theorizing about its subject even though preoccupation with valuation has a long-standing history in sociology. Authors such as Durkheim, Simmel, and Dewey have interpreted valuation as more than a specific localizable phenomenon, in that valuation is a constitutive element of the fundament of the social. Discussing classical approaches to valuation and relating them to current sociological work, we identify key concepts within different theoretical approaches that need to be taken into account when theorizing valuation. We suggest five building blocks - valuation practices, value structures, valuation infrastructure, valuation situations, and reflexivity of valuation - theories of valuation need to consider for coming to terms with the multi-faceted empirical studies in the sociology of valuation

Das Personalentwicklungsparadox in der Wissenschaft

In den Debatten um eine Reform der Karrierewege im deutschen Wissenschaftssystem wird seit einigen Jahren an die Universitäten die Forderung nach einer „strategischen Personalentwicklung“ (BMBF) herangetragen. Mit dem Tenure-Track-Programm hat die Hochschulpolitik hierfür einen konkreten Anreiz gesetzt. Voraussetzung für die Teilnahme war die Vorlage eines Personalentwicklungskonzepts für das gesamte wissenschaftliche Personal. Die Universitäten mussten also, häufig erstmalig, ein ganzheitliches Konzept vorlegen. Weil an Universitäten dem Personal eine zentrale Rolle für die Leistungserbringung zukommt, sei Personalentwicklung, so die Annahme in der Hochschulmanagement-Literatur, immer auch im Interesse der Universität. Im deutschen Wissenschaftssystem ist jedoch der Verbleib des Personals unterhalb der Professur an der Universität gesetzlich auf zwölf Jahre begrenzt. Nach Ablauf dieser sogenannten Qualifikationsphase wird man entweder auf eine Professur berufen oder man scheidet aus der Wissenschaft aus. Universitäten stehen somit vor der paradoxen Aufgabe, Personalentwicklung für ein Personal zu betreiben, das nicht auf Dauer in der eigenen Organisation verbleiben wird.  Dieses Personalentwicklungsparadox wird anhand einer qualitativen Auswertung von Personalentwicklungskonzepten von 43 Hochschulen exploriert. Unter Rückgriff auf neo-institutionalistische Ansätze und ihre Problematisierung aus der Gouvernementalitätsperspektive wird der analytische Fokus auf das organisationale Selbstverhältnis von Universitäten gelegt, d.h. wie sie sich selbst als organisationaler Akteur definieren und sich so erst in die Lage versetzen, ihr Handeln mit Sinn zu versehen. Es werden vier Strategien des Umgangs mit dem Personalentwicklungsparadox empirisch rekonstruiert, die Auskunft darüber geben, wie sich Universitäten als handlungsfähig vis-à-vis ihrem Personal konstruieren

Neurodegeneration and Neuroinflammation in Parkinson’s Disease: a Self-Sustained Loop

Purpose of Review: Neuroinflammation plays a significant role in Parkinson’s disease (PD) etiology along with mitochondrial dysfunction and impaired proteostasis. In this context, mechanisms related to immune response can act as modifiers at different steps of the neurodegenerative process and justify the growing interest in anti-inflammatory agents as potential disease-modifying treatments in PD. The discovery of inherited gene mutations in PD has allowed researchers to develop cellular and animal models to study the mechanisms of the underlying biology, but the original cause of neuroinflammation in PD is still debated to date. Recent Findings: Cell autonomous alterations in neuronal cells, including mitochondrial damage and protein aggregation, could play a role, but recent findings also highlighted the importance of intercellular communication at both local and systemic level. This has given rise to debate about the role of non-neuronal cells in PD and reignited intense research into the gut-brain axis and other non-neuronal interactions in the development of the disease. Whatever the original trigger of neuroinflammation in PD, what appears quite clear is that the aberrant activation of glial cells and other components of the immune system creates a vicious circle in which neurodegeneration and neuroinflammation nourish each other. Summary: In this review, we will provide an up-to-date summary of the main cellular alterations underlying neuroinflammation in PD, including those induced by environmental factors (e.g. the gut microbiome) and those related to the genetic background of affected patients. Starting from the lesson provided by familial forms of PD, we will discuss pathophysiological mechanisms linked to inflammation that could also play a role in idiopathic forms. Finally, we will comment on the potential clinical translatability of immunobiomarkers identified in PD patient cohorts and provide an update on current therapeutic strategies aimed at overcoming or preventing inflammation in PD. © 2022, The Author(s)

Early Postnatal but Not Late Adult Neurogenesis Is Impaired in the Pitx3-Mutant Animal Model of Parkinson's Disease

The generation of new neurons in the adult dentate gyrus has functional implications for hippocampal formation. Reduced hippocampal neurogenesis has been described in various animal models of hippocampal dysfunction such as dementia and depression, which are both common non-motor-symptoms of Parkinson's disease (PD). As dopamine plays an important role in regulating precursor cell proliferation, the loss of dopaminergic neurons in the substantia nigra (SN) in PD may be related to the reduced neurogenesis observed in the neurogenic regions of the adult brain: subventricular zone (SVZ) and dentate gyrus (DG). Here we examined adult hippocampal neurogenesis in the Pitx3-mutant mouse model of PD (aphakia mice), which phenotypically shows a selective embryonic degeneration of dopamine neurons within the SN and to a smaller extent in the ventral tegmental area (VTA). Proliferating cells were labeled with BrdU in aphakia mice and healthy controls from 3 to 42 weeks of age. Three weeks old mutant mice showed an 18% reduction of proliferating cells in the DG and of 26% in the SVZ. Not only proliferation but also the number of new neurons was impaired in young aphakia mice resulting in 33% less newborn cells 4 weeks after BrdU-labeling. Remarkably, however, the decline in the number of proliferating cells in the neurogenic regions vanished in older animals (8–42 weeks) indicating that aging masks the effect of dopamine depletion on adult neurogenesis. Region specific reduction in precursor cells proliferation correlated with the extent of dopaminergic degeneration in mesencephalic subregions (VTA and SN), which supports the theory of age- and region-dependent regulatory effects of dopaminergic projections. Physiological stimulation of adult neurogenesis by physical activity (wheel running) almost doubled the number of proliferating cells in the dentate gyrus of 8 weeks old aphakia mice to a number comparable to that of wild-type mice, abolishing the slight reduction of baseline neurogenesis at this age. The described age-dependent susceptibility of adult neurogenesis to PD-like dopaminergic degeneration and its responsiveness to physical activity might have implications for the understanding of the pathophysiology and treatment of non-motor symptoms in PD

Short-term effects of amelogenin gene splice products A+4 and A-4 implanted in the exposed rat molar pulp

In order to study the short-time effects of two bioactive low-molecular amelogenins A+4 and A-4, half-moon cavities were prepared in the mesial aspect of the first maxillary molars, and after pulp exposure, agarose beads alone (controls) or beads soaked in A+4 or A-4 (experimental) were implanted into the pulp. After 1, 3 or 7 days, the rats were killed and the teeth studied by immunohistochemistry. Cell proliferation was studied by PCNA labeling, positive at 3 days, but decreasing at day 7 for A+4, whilst constantly high between 3 and 7 days for A-4. The differentiation toward the osteo/odontoblast lineage shown by RP59 labeling was more apparent for A-4 compared with A+4. Osteopontin-positive cells were alike at days 3 and 7 for A-4. In contrast, for A+4, the weak labeling detected at day 3 became stronger at day 7. Dentin sialoprotein (DSP), an in vivo odontoblast marker, was not detectable until day 7 where a few cells became DSP positive after A-4 stimulation, but not for A+4. These results suggest that A +/- 4 promote the proliferation of some pulp cells. Some of them further differentiate into osteoblast-like progenitors, the effects being more precocious for A-4 (day 3) compared with A+4 (day 7). The present data suggest that A +/- 4 promote early recruitment of osteogenic progenitors, and evidence functional differences between A+4 and A-4

Therapy-refractory Panton Valentine Leukocidin-positive community-acquired methicillin-sensitive Staphylococcus aureus sepsis with progressive metastatic soft tissue infection: a case report

We report a case of fulminant multiple organ failure including the Acute Respiratory Distress Syndrome (ARDS), haemodynamic, and renal failure due to community-acquired methicillin-sensitive Panton Valentine Leukocidin (PVL) positive spa-type 284 (ST121) Staphylococcus aureus septic shock. The patient's first clinical symptom was necrotizing pneumonia. Despite organism-sensitive triple antibiotic therapy with linezolid, imipenem and clindamycin from the first day of treatment, progressive abscess formation in multiple skeletal muscles was observed. As a result, repeated surgical interventions became necessary. Due to progressive soft tissue infection, the anti-microbial therapy was changed to a combination of clindamycin and daptomycin. Continued surgical and antimicrobial therapy finally led to a stabilisation of the patients' condition. The clinical course of our patient underlines the existence of a "PVL-syndrome" which is independent of in vitro Staphylococcus aureus susceptibility. The PVL-syndrome should not only be considered in patients with soft tissue or bone infection, but also in patients with pneumonia. Such a condition, which may easily be mistaken for uncomplicated pneumonia, should be treated early, aggressively and over a long period of time in order to avoid relapsing infection