In a noisy environment, the larger receptive fields became narrower, whereas the sharply tuned receptive fields got broader. (C) 2009 Elsevier Ireland Ltd. All rights reserved.”
“Results
of several studies show that some DC populations are susceptible to HIV. Modulation of DCs by HIV infection, in particular interference of the antigen-presenting function of DCs, selleck chemicals llc is a key aspect in viral pathogenesis and contributes to viral evasion from immunity because the loss of the DC function engenders some impairment effects for a proliferation of CTL responses, which play an important role in the immune response to HIV. As described herein, we use a simple mathematical model to examine virus-immune dynamics over the course of HIV infection in the context of the immune impairment effects. A decrease of the DC number and function during the course of HIV-1 infection
selleck kinase inhibitor is observed. Therefore, we simply assumed that the immune impairment rate increases over the HIV infection. Under the assumption, four processes of the disease progression dynamics of our model are classifiable according to their virological properties. It is particularly interesting a typical disease progression presents a “”risky threshold’ and an “”immunodeficiency threshold”. Regarding the former, the immune system might collapse when the impairment rate of HIV exceeds a threshold value (which corresponds to a transcritical bifurcation point). For the latter, the immune system always collapses when the impairment rate exceeds the value (which corresponds to a saddle-node bifurcation point). To test our theoretical framework, we investigate the existence and distribution of these thresholds in 10 patients. (C) 2009 Elsevier Ltd. All rights reserved.”
“Evidence are that inhibition of cyclooxygenase 2 STI571 mw (COX-2) enhances endocannabinoid signaling, indicating a crosstalk between
these two eicosanoid pathways. Aspirin, a non-selective COX inhibitor, acetylates COX-2 with generation of a lipoxygenase (LOX) substrate, whose end product is the 15-epi-lipoxin A(4) (15-epi-LXA(4)), an aspirin-triggered lipoxin. Our objective was to investigate whether 15-epi-LXA(4) would potentiate in vivo effects of the endocannabinoid anandamide (AEA). Catalepsy was selected as a behavioral parameter and tested 5 min after AEA injection in all experiments. AEA induced close-dependent (200 pmol/2 mu l, i.c.v.) catalepsy. A sub-dose of AEA (110 pmol/2 mu l, i.c.v.) was potentiated by aspirin (300 mg/kg, p.o.) via a 5-LOX-dependent step. The cataleptic effect induced by the interaction between sub-doses of 1 5-epi-LXA(4) (0.01 pmol/2 mu l, i.c.v.) and AEA (10 pmol/2 mu l, i.c.v.) was prevented by the cannabinoid CB1 receptors antagonist SR141716A (1 mg/kg, i.p.), but not by the antagonist of lipoxin ALX receptors Boc-2 (10 mu g/kg, i.p.).