For the Sciences They Are A‐Changin’: A Response to Commentaries on Núñez et al.’s (2019) “What Happened to Cognitive Science?”

A recent issue of Topics in Cognitive Science featured 11 thoughtful commentaries responding to our article “What happened to cognitive science?” (Núñez et al., 2019). Here, we identify several themes that arose in those commentaries and respond to each. Crucial to understanding our original article is the fundamental distinction between multidisciplinary and interdisciplinary endeavors: Cognitive science began (and has stayed) as multidisciplinary but has failed to move on to form a cohesive interdisciplinary field. We clarify and elaborate our original argument and reiterate the importance of a data‐driven evaluation of the current status of the field, which exhibits a marked disciplinary imbalance, a lack of a coherent conceptual core, and a striking absence of a consistent curriculum in the institutions that grant degrees in this domain. Half a century after the creation of cognitive science, it may now be a good time to revisit goals and visions for how to best approach the ever‐fascinating scientific study of the mind(s).     

The impact of low-dose versus high-dose antibiotic prophylaxis regimens on surgical site infection rates after cesarean delivery

Archives of Gynecology and Obstetrics - The objective of this study was to determine if high-dose antibiotic prophylaxis with cefazolin decreases the risk of surgical site infection (SSI) after a...     

Gelingt das Screening von Schwangeren auf HIV,Syphilis und Hepatitis B in Deutschland? Eine Analyse auf Basis von Routinedaten

Bundesgesundheitsblatt - Gesundheitsforschung - Gesundheitsschutz - Infektionen in der Schwangerschaft sind weltweit eine der führenden Ursachen für erhöhte Morbidität und...     

Mycobacterium abscessus Complex Identification with Matrix-Assisted Laser Desorption Ionization–Time of Flight Mass Spectrometry

We determined that the Vitek MS Plus matrix-assisted laser desorption ionization–time of flight mass spectrometry using research-use-only (RUO) v.4.12 and in vitro-diagnostic (IVD) v.3.0 databases accurately identified 41 Mycobacterium abscessus subsp. abscessus and 13 M. abscessus subsp. massiliense isolates identified by whole-genome sequencing to the species but not the subspecies level, from Middlebrook 7H11 and Burkholderia cepacia selective agars. Peak analysis revealed three peaks potentially able to differentiate between subspecies.     

Microglial responses after phagocytosis: Escherichia coli bioparticles,but not cell debris or amyloid beta,induce matrix metalloproteinase-9 secretion in cultured rat primary microglial cells

Upon infection or brain damage, microglia are activated to play roles in immune responses, including phagocytosis and soluble factor release. However, little is known whether the event of phagocytosis could be a trigger for releasing soluble factors from microglia. In this study, we tested if microglia secrete a neurovascular mediator matrix metalloproteinase-9 (MMP-9) after phagocytosis in vitro. Primary microglial cultures were prepared from neonatal rat brains. Cultured microglia phagocytosed Escherichia coli bioparticles within 2 hr after incubation and started to secrete MMP-9 at around 12 hr after the phagocytosis. A TLR4 inhibitor TAK242 suppressed the E. coli-bioparticle-induced MMP-9 secretion. However, TAK242 did not change the engulfment of E. coli bioparticles in microglial cultures. Because lipopolysaccharides (LPS), the major component of the outer membrane of E. coli, also induced MMP-9 secretion in a dose–response manner and because the response was inhibited by TAK242 treatment, we assumed that the LPS-TLR4 pathway, which was activated by adhering to the substance, but not through the engulfing process of phagocytosis, would play a role in releasing MMP-9 from microglia after E. coli bioparticle treatment. To support the finding that the engulfing step would not be a critical trigger for MMP-9 secretion after the event of phagocytosis in microglia, we confirmed that cell debris and amyloid beta were both captured into microglia via phagocytosis, but neither of them induced MMP-9 secretion from microglia. Taken together, these data demonstrate that microglial response in MMP-9 secretion after phagocytosis differs depending on the types of particles/substances that microglia encountered.