We studied the role of FGF-2 on regulation of neurogenesis and cell loss in the granule cell layer (GCL) of the hippocampal dentate gyrus after experimental traumatic brain injury (TBI). In both FGF-2 -/-and FGF-2 +/+ mice subjected to controlled cortical impact, the number of dividing cells labeled with BrdU, injected on posttrauma days 6 through 8, increased at 9 days after TBI, and the number of BrdU-positive cells colabeled with neuron-specific nuclear antigen significantly increased at 35 days. However, in injured FGF-2 -/-mice, BrdU-positive cells and BrdU-positive neurons (days 9, 35) were fewer compared with FGF-2 +/+ mice. There was also a decrease in the volume of the GCL and the number of GCL neurons after TBI in both FGF-2 -/-and FGF-2 +/+ mice, but the decrease in both was greater in FGF-2 -/-mice at 35 days. Overexpression of FGF-2 by intracerebral injection of herpes simplex virus-1 amplicon vectors encoding this factor increased numbers of dividing cells (day 9) and BrdU-positive neurons (day 35) significantly in C57BL/6 mice. Furthermore, the decrease in GCL volume was also attenuated. These results suggest that FGF-2 upregulates neurogenesis and protects neurons against degeneration in the adult hippocampus after TBI, and that FGF-2 supplementation via gene transfer can reduce GCL degeneration after TBI.

Our study findings show no difference in PSM rates, complication rates or intermediate-term renal functional outcomes between patients with unimpaired renal function who underwent SAC vs those who underwent MAC. When expected WIT is low, the routine use of SAC may not be necessary. Further studies will need to determine the role of SAC in patients with a solitary kidney or with significantly impaired renal function.

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