Monoidal 2-structure of Bimodule Categories

We define a notion of tensor product of bimodule categories and prove that with this product the 2-category of C-bimodule categories for fixed tensor C is a monoidal 2-category in the sense of Kapranov and Voevodsky. We then provide a monoidal-structure preserving 2-equivalence between the 2-category of C-bimodule categories and Z(C)-module categories (module categories over the center). For finite group G we show that de-equivariantization is equivalent to tensor product over category Rep(G) of finite dimensional representations. We derive Rep(G)-module fusion rules and determine the group of invertible irreducible Rep(G)-module categories extending earlier results for abelian groups.Comment: 40 pages, minor errors corrected, references added. To appear in J. Algebr

State-based components made generic

Genericity is a topic which is not sufficiently developed in state-based systems modelling, mainly due to a myriad of approaches and behaviour models which lack unification. This paper adopts coalgebra theory to propose a generic notion of a state-based software component, and an associated calculus, by quantifying over behavioural models specified as strong monads. This leads to the pointfree, calculational reasoning style which is typical of the so-called Bird-Meertens school.(undefined

Self-Managed Working Time and Employee Effort: Theory and Evidence

This paper theoretically and empirically examines the impact of self-managed working time (SMWT) on employee effort. As a policy of increased worker autonomy, SMWT can theoretically increase effort via intrinsic motivation and reciprocal behaviour, but it can also lead to a decrease of effort due to a loss of control. Based on German individual-level panel data, we find that SMWT employees exert higher effort levels than employees with fixed working hours. Even after accounting for observed and unobserved characteristics there remains a modest positive effect. This effect is largely driven by employees who are intrinsically motivated, suggesting that intrinsic motivation is complementary to SMWT. However, reciprocal work intensification does not seem to be an important channel of providing extra effort

TLR2 and TLR4 mediate differential responses to limb ischemia through MyD88-dependent and independent pathways.

The danger signal HMGB1 is released from ischemic myocytes, and mediates angiogenesis in the setting of hindlimb ischemia. HMGB1 is a ligand for innate immune receptors TLR2 and TLR4. While both TLR2 and TLR4 signal through myeloid differentiation factor 88 (MyD88), TLR4 also uniquely signals through TIR-domain-containing adapter-inducing interferon-β (TRIF). We hypothesize that TLR2 and TLR4 mediate ischemic myocyte regeneration and angiogenesis in a manner that is dependent on MyD88 signaling.Mice deficient in TLR2, TLR4, MyD88 and TRIF underwent femoral artery ligation in the right hindlimb. Laser Doppler perfusion imaging was used to assess the initial degree of ischemia and the extent of perfusion recovery. Muscle regeneration, necrosis and fat replacement at 2 weeks post-ligation were assessed histologically and vascular density was quantified by immunostaining. In vitro, endothelial tube formation was evaluated in matrigel in the setting of TLR2 and TLR4 antagonism.While control and TLR4 KO mice demonstrated prominent muscle regeneration, both TLR2 KO and TRIF KO mice exhibited marked necrosis with significant inflammatory cell infiltrate. However, MyD88 KO mice had a minimal response to the ischemic insult with little evidence of injury. This observation could not be explained by differences in perfusion recovery which was similar at two weeks in all the strains of mice. TLR2 KO mice demonstrated abnormal vessel morphology compared to other strains and impaired tube formation in vitro.TLR2 and TRIF signaling are necessary for muscle regeneration after ischemia while MyD88 may instead mediate muscle injury. The absence of TLR4 did not affect muscle responses to ischemia. TLR4 may mediate inflammatory responses through MyD88 that are exaggerated in the absence of TLR2. Additionally, the actions of TLR4 through TRIF may promote regenerative responses that are required for recovery from muscle ischemia

Assessment of the formation of vascular structures following hind limb ischemia.

<p>(A) Vascular density was quantified by the number of CD31 structures per HPF in control, TLR2 KO and TLR4 KO mice two weeks following femoral artery ligation (black bars). Vessel area was also measured (gray bar) (N = 4 per group; *P<0.05 versus control and TLR4 KO). (B) Number of SMA staining vessels per HPF 2 weeks (N = 4 per group; *P = 0.003 vs. control and TLR4 KO).</p

Skeletal muscle responses to hind limb ischemia at 2 weeks following femoral artery ligation.

<p>(A) Representative sections of tibialis anterior muscle from control C57B6, TLR2 KO, TLR4 KO, MyD88 KO and TRIF KO mice were stained with H&E. Arrow represents regenerating muscle fiber with centrally located nucleus. Arrowhead depicts areas of fat replacement. Asterisk indicates necrotic muscle fiber, characterized by eosinophilia, loss of muscle architecture and inflammatory infiltrate. (B) Hemorrhage into ischemic tissue was seen in TLR2KO mice (double arrow). Scale bar = 50 µm. (C) Erythrocytes (orange) are seen outside of vasculature (green) in TLR2KO mice. Red box demonstrates area of magnification shown in images below originals. Scale bar = 25 µm.</p

Necrosis, fat replacement and muscle regeneration in control, TLR2 KO, and TLR4 KO mice two weeks following femoral artery ligation.

<p>Quantification of area was performed on 4–5 non-overlapping images per section with 3 sections per animal. Results are presented as % of total muscle area (mean ± SEM; *P<0.03 vs. control and TLR4 KO, **P<0.05 vs. control and TLR4 KO).</p