Improvement in antenatal diagnosis of critical congenital heart disease implications for postnatal care and screening.

OBJECTIVE: This observational study was performed to examine the current timing and mode of diagnosis of critical congenital heart disease (CCHD), since early detection of cardiac lesions can significantly improve morbidity and mortality. METHOD: Ninety cases of CCHD in infants born in Middle Tennessee in 2009 were identified by weekly review of admissions to a single cardiac referral center. CCHD is defined as lesions requiring admission or re-admission for surgical or medical intervention within 1 month of life. RESULTS: Overall, the observed antenatal detection rate of 49% is significantly greater than published values of 25%. Hypoplastic left heart syndrome was detected in 11/11, but only 5/16 coarctations were detected. CONCLUSION: Compared to earlier reports, our study showed a doubling of the antenatal detection rate. Perhaps efforts to improve early diagnosis of CCHD could focus on antenatal ultrasound screening techniques for lesions that are missed most often as well as on postnatal screening.

Leukemia inhibitory factor deficiency modulates the immune response and limits autoimmune demyelination: a new role for neurotrophic cytokines in neuroinflammation.

The neurotrophic cytokines ciliary neurotrophic factor and leukemia inhibitory factor (LIF) play a key role in neuronal and oligodendrocyte survival and as protective factors in neuroinflammation. To further elucidate the potential of endogenous LIF in modulating neuroinflammation, we studied myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis in LIF knockout mice (LIF(-/-) mice). In the late phase of active myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis, LIF(-/-) mice exhibited a markedly milder disease course. The inflammatory infiltrate in LIF(-/-) mice was characterized by an increase in neutrophilic granulocytes early and fewer infiltrating macrophages associated with less demyelination later in the disease. In good correlation with an effect of endogenous LIF on the immune response, we found an Ag-specific T cell-priming defect with impaired IFN-gamma production in LIF(-/-) mice. On the molecular level, the altered recruitment of inflammatory cells is associated with distinct patterns of chemokine production in LIF(-/-) mice with an increase of CXCL1 early and a decrease of CCL2, CCL3, and CXCL10 later in the disease. These data reveal that endogenous LIF is an immunologically active molecule in neuroinflammation. This establishes a link between LIF and the immune system which was not observed in the ciliary neurotrophic factor knockout mouse.