20 research outputs found
Lin's method for heteroclinic chains involving periodic orbits
We present an extension of the theory known as Lin's method to heteroclinic
chains that connect hyperbolic equilibria and hyperbolic periodic orbits. Based
on the construction of a so-called Lin orbit, that is, a sequence of continuous
partial orbits that only have jumps in a certain prescribed linear subspace,
estimates for these jumps are derived. We use the jump estimates to discuss
bifurcation equations for homoclinic orbits near heteroclinic cycles between an
equilibrium and a periodic orbit (EtoP cycles)
Schistosoma mansoni antigen-driven interleukin-10 production in infected asthmatic individuals
Asthmatics infected with Schistosoma mansoni have a less severe
course of asthma and an inhibition of the Th2 inflammatory response
that seems to be mediated by interleukin (IL-10). The objective of this
study was to evaluate the capacity of some S. mansoni antigens to
stimulate IL-10 production in vitro by cells of asthmatic infected
individuals. Peripheral bloods mononuclear cells were stimulated with
the S. mansoni recombinant antigens Sm22.6, Sm14, P24, and PIII
antigen. IL-10 was measured in the supernatants of cultures. As the
recombinant antigens were cloned in Escherichia coli , we blocked
contaminant endotoxin with polymyxin B added to the cultures. We
demonstrated that all antigens used drove high production of IL-10 in
S. mansoni infected individuals (n = 13, 408 ± 514 and 401 ±
383 pg/ml, 484 ± 245 pg/ml, 579 ± 468 pg/ml, respectively).
In asthmatics infected with S. mansoni (n = 21) rP24 induced higher
levels of IL-10 (565 ± 377 pg/ml) when compared to PIII, rSm14 and
rSm22.6 (184 ± 209 pg/ml; 292 ± 243 pg/ml; 156 ± 247
pg/ml, respectively). Conclusion: the S. mansoni antigens evaluated in
this study stimulated IL-10 production by cells from infected
individuals and therefore they have the potential to be used as a
modulator of the inflammatory response in asthma
<i>Lactobacillus reuteri</i> DSM 17938 Protects against Gastric Damage Induced by Ethanol Administration in Mice: Role of TRPV1/Substance P Axis
This study aimed to evaluate the effect of Lactobacillus reuteri DSM 17938 (DSM) on ethanol-induced gastric injury, and if its possible mechanism of action is related to inhibiting the transient receptor potential vanilloid type 1 (TRPV1). We evaluated the effect of supplementing 108 CFU•g body wt−1•day−1 of DSM on ethanol-induced gastric injury. DSM significantly reduced the ulcer area (1.940 ± 1.121 mm2) with 3 days of pretreatment. The effects of DSM supplementation were reversed by Resiniferatoxin (RTX), TRPV1 agonist (3 nmol/kg p.o.). Substance P (SP) (1 μmol/L per 20 g) plus 50% ethanol resulted in hemorrhagic lesions, and DSM supplementation did not reverse the lesion area induced by administering SP. TRPV1 staining intensity was lower, SP, malondialdehyde (MDA) and nitrite levels were reduced, and restored normal levels of antioxidant parameters (glutathione and superoxide dismutase) in the gastric mucosa in mice treated with DSM. In conclusion, DSM exhibited gastroprotective activity through decreased expression of TRPV1 receptor and decreasing SP levels, with a consequent reduction of oxidative stress