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A couple of weeks ago, I hinted that we would soon be publishing our 120,000th F1000 evaluation. Well, two days ago, we did just that!

The 120,000th evaluation was submitted by David Jessop of the Physiology Faculty, who highlighted a paper that could explain how stress can both exacerbate and protect against rheumatoid arthritis.

The article was written by Straub and colleagues from the University Hospital Regensburg, Germany, and published in the Brain, Behavior and Immunity journal. The authors set out to determine what role the sympathetic nervous system (SNS) plays in mediating inflammation in patients with rheumatoid arthritis. It is already known that the SNS has a pro-inflammatory influence before disease outbreak, which is converted into an anti-inflammatory one after outbreak. The authors set out to determine the influence of neuronally released neurotransmitters in mice shortly after the outbreak of RA.

David Jessop evaluated the study because they are a “very nice set of experiments that reveal a possible mechanism for the switch from pro- to anti-inflammatory influence of the SNS”. He explains that, at disease outbreak, pro-inflammatory compounds are inhibited and the anti-inflammatory compound TGF-beta is stimulated.

He continues,

… this creates an anti-inflammatory milieu during the active phase of the disease, which may play a role in controlling further progression of inflammation.

He speculates that the findings of this study

…may also provide an explanation as to how stress, which activates the SNS, can have protective or exacerbatory effects on RA depending on the timing, type and intensity of the stressor.

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The team here at F1000 would like to thank our 10,000-strong Faculty and Associate Faculty for contributing toward this 120k milestone and for making F1000 what is it today.

Congrats are also due to Yerbol, who wins an F1000 goody bag for guessing the closest publication date .