PMC:2944667 / 35097-36005 JSONTXT

{"project":"TEST0","denotations":[{"id":"20877431-58-66-637256","span":{"begin":300,"end":304},"obj":"[\"15483108\"]"},{"id":"20877431-80-88-637257","span":{"begin":322,"end":326},"obj":"[\"14603265\"]"},{"id":"20877431-149-157-637258","span":{"begin":391,"end":395},"obj":"[\"18068248\"]"},{"id":"20877431-56-64-637259","span":{"begin":735,"end":739},"obj":"[\"18826624\"]"},{"id":"20877431-114-122-637260","span":{"begin":793,"end":797},"obj":"[\"11331082\"]"},{"id":"20877431-144-152-637261","span":{"begin":823,"end":827},"obj":"[\"19376090\"]"}],"text":"Post mortem work has also examined the levels of signaling factors in patients with depression. In frontal cortical regions, FGF ligand and receptor levels as well as BDNF receptor levels were shown to be altered in patients with depression. Findings generally show reduced expression (Evans et al., 2004; Sibille et al., 2004) but some point to upregulated receptor levels (Tochigi et al., 2008). Altered gene expression in the mature cortex may suggest a role for FGF and other important mediators of neuronal growth in mood disorders in the adult brain. However, they may also reflect a genetic defect that may have contributed to an earlier altered developmental trajectory. Parallel findings in model animal systems (Chen et al., 2008) and patients with mood disorders (Rajkowska et al., 2001; Valentine and Sanacora, 2009) suggest a role for FGF in both embryonic and mature brain functions (Figure 4)."}

{"project":"0_colil","denotations":[{"id":"20877431-15483108-637256","span":{"begin":300,"end":304},"obj":"15483108"},{"id":"20877431-14603265-637257","span":{"begin":322,"end":326},"obj":"14603265"},{"id":"20877431-18068248-637258","span":{"begin":391,"end":395},"obj":"18068248"},{"id":"20877431-18826624-637259","span":{"begin":735,"end":739},"obj":"18826624"},{"id":"20877431-11331082-637260","span":{"begin":793,"end":797},"obj":"11331082"},{"id":"20877431-19376090-637261","span":{"begin":823,"end":827},"obj":"19376090"}],"text":"Post mortem work has also examined the levels of signaling factors in patients with depression. In frontal cortical regions, FGF ligand and receptor levels as well as BDNF receptor levels were shown to be altered in patients with depression. Findings generally show reduced expression (Evans et al., 2004; Sibille et al., 2004) but some point to upregulated receptor levels (Tochigi et al., 2008). Altered gene expression in the mature cortex may suggest a role for FGF and other important mediators of neuronal growth in mood disorders in the adult brain. However, they may also reflect a genetic defect that may have contributed to an earlier altered developmental trajectory. Parallel findings in model animal systems (Chen et al., 2008) and patients with mood disorders (Rajkowska et al., 2001; Valentine and Sanacora, 2009) suggest a role for FGF in both embryonic and mature brain functions (Figure 4)."}

{"project":"2_test","denotations":[{"id":"20877431-15483108-38520533","span":{"begin":300,"end":304},"obj":"15483108"},{"id":"20877431-14603265-38520534","span":{"begin":322,"end":326},"obj":"14603265"},{"id":"20877431-18068248-38520535","span":{"begin":391,"end":395},"obj":"18068248"},{"id":"20877431-18826624-38520536","span":{"begin":735,"end":739},"obj":"18826624"},{"id":"20877431-11331082-38520537","span":{"begin":793,"end":797},"obj":"11331082"},{"id":"20877431-19376090-38520538","span":{"begin":823,"end":827},"obj":"19376090"}],"text":"Post mortem work has also examined the levels of signaling factors in patients with depression. In frontal cortical regions, FGF ligand and receptor levels as well as BDNF receptor levels were shown to be altered in patients with depression. Findings generally show reduced expression (Evans et al., 2004; Sibille et al., 2004) but some point to upregulated receptor levels (Tochigi et al., 2008). Altered gene expression in the mature cortex may suggest a role for FGF and other important mediators of neuronal growth in mood disorders in the adult brain. However, they may also reflect a genetic defect that may have contributed to an earlier altered developmental trajectory. Parallel findings in model animal systems (Chen et al., 2008) and patients with mood disorders (Rajkowska et al., 2001; Valentine and Sanacora, 2009) suggest a role for FGF in both embryonic and mature brain functions (Figure 4)."}