Diagnosis of congenital/perinatal infections by neonatologists: a national survey.

OBJECTIVE: To describe the clinical approach used by neonatologists for diagnosis of congenital/perinatal infections (CPI); no such data currently exist. STUDY DESIGN: A national survey regarding the diagnosis of toxoplasma, syphilis, rubella, cytomegalovirus, and herpes simplex virus (HSV) infection in neonates. RESULT: We received 553 (11%) responses. Central nervous system calcification or hydrocephalus was the commonest trigger to pursue a CPI diagnosis (98%); maternal history was the least frequent (67%). Four hundred twenty-two (76%) used general screening such as "TORCH titer screen" (57%) or total IgG or IgM (39%). Further evaluation targeted known clinical sequelae; but cerebrospinal fluid testing was used in only 65% of those suspected of having HSV or syphilis. Fifty-six percent chose a treponemal instead of a non-treponemal test for syphilis. Multivariable analyses did not identify factors associated with the clinical diagnostic approach. CONCLUSION: We observed clinically important deviations from CPI diagnostic test recommendations in a national cohort of neonatologists.

Recent Advances in Bronchopulmonary Dysplasia: Pathophysiology, Prevention, and Treatment.

Bronchopulmonary dysplasia (BPD) is potentially one of the most devastating conditions in premature infants with longstanding consequences involving multiple organ systems including adverse effects on pulmonary function and neurodevelopmental outcome. Here we review recent studies in the field to summarize the progress made in understanding in the pathophysiology, prognosis, prevention, and treatment of BPD in the last decade. The work reviewed includes the progress in understanding its pathobiology, genomic studies, ventilatory strategies, outcomes, and therapeutic interventions. We expect that this review will help guide clinicians to treat premature infants at risk for BPD better and lead researchers to initiate further studies in the field.

PPARδ inhibits UVB-induced secretion of MMP-1 through MKP-7-mediated suppression of JNK signaling.

In the present study, we investigated the role of peroxisome proliferator-activated receptor (PPAR) δ in modulating matrix-degrading metalloproteinases and other mechanisms underlying photoaging processes in the skin. In human dermal fibroblasts (HDFs), activation of PPARδ by its specific ligand GW501516 markedly attenuated UVB-induced secretion of matrix metalloproteinase (MMP)-1, concomitant with decreased generation of reactive oxygen species. These effects were significantly reduced in the presence of PPARδ small interfering RNA and GSK0660. Furthermore, c-Jun N-terminal kinase (JNK), but not p38 or extracellular signal-regulated kinase, mediated PPARδ-dependent inhibition of MMP-1 secretion in HDFs exposed to UVB. PPARδ-mediated messenger RNA stabilization of mitogen-activated protein kinase phosphatase (MKP)-7 was responsible for the GW501516-mediated inhibition of JNK signaling. Inhibition of UVB-induced secretion of MMP-1 by PPARδ was associated with the restoration of types I and III collagen to levels approaching those in cells not exposed to UVB. Finally, in HR-1 hairless mice exposed to UVB, administration of GW501516 significantly reduced wrinkle formation and skin thickness, downregulated MMP-1 and JNK phosphorylation, and restored the levels of MKP-7, types I and III collagen. These results suggest that PPARδ-mediated inhibition of MMP-1 secretion prevents some effects of photoaging and maintains the integrity of skin by inhibiting the degradation of the collagenous extracellular matrix.