Group B streptococcus (GBS) is a major cause of severe systemic infections among the newborn. Both recurrent and maternal mastitis-associated, group B streptococcus diseases are uncommon. Persistence of GBS colonization of infants' mucous membrane is postulated to influence the pathogeneses of recurrent GBS infection. The authors describe a term infant who was treated for GBS sepsis and meningitis and then later developed recurrent GBS sepsis, without meningitis, due to feeding of infected breast milk. Randomly amplified polymorphic DNA polymerase chain reaction assay was performed to demonstrate that the GBS isolates from the first and second episode of infection and the maternal milk are identical. The authors conclude that transmission of GBS through breast milk should be considered in cases of recurrent neonatal GBS infection and bacterial culture of breast milk should be routinely performed in such cases.

Our results indicate that among our pediatric patients with INS the C1236T polymorphism in the ABCB1 gene was associated with steroid resistance, while the A6986G polymorphism in the CYP3A5 gene showed a trend of association, but did not reach statistical significance, requiring further analysis.

In CNSR, differences in stroke clinic characteristics and health care were observed among various age groups, and the old patients, receiving lower levels of stroke care, had the worst outcomes. Knowledge of the age differences in ischemic stroke may be helpful to appropriately allocate the limited health resources and to improve stroke outcomes.

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Background and AimsAgents having a positive inotropic effect on the heart are widely used for the treatment of heart failure. However, these agents have the side effect of altering heart rate. It has been established that peroxisome proliferator-activated receptor δ (PPARδ) is mediated in cardiac contraction, however the effect on heart rate is unknown. Thus, we used an agonist of PPARδ, GW0742, to investigate this issue in the present study.Methods and ResultsWe used isolated hearts in Langendorff apparatus and hemodynamic analysis in catheterized rats to measure the actions of GW0742 extra-vivo and in vivo. In diabetic rats with heart failure, GW0742 at a dose sufficient to activate PPARδ reversed cardiac contraction without changes in heart rate. In normal rats, PPARδ enhanced cardiac contractility and hemodynamic dP/dtmax significantly more than dobutamine. Both actions were diminished by GSK0660 at a dose enough to block PPARδ. However, GW0742 at the same dose failed to modify heart rate, although it did produce a mild increase in blood pressure. Detection of intracellular calcium level and Western blotting analysis showed that the intracellular calcium concentration and troponin I phosphorylation were both enhanced by GW0742.ConclusionActivation of PPARδ by GW0742 increases cardiac contractility but not heart rate. Thus, PPARδ may be a suitable target for the development of inotropic agents to treat heart failure without changing heart rate.