72 research outputs found
S100B Protein, Brain-Derived Neurotrophic Factor, and Glial Cell Line-Derived Neurotrophic Factor in Human Milk
Human milk contains a wide variety of nutrients that contribute to the fulfillment of its functions, which include the regulation of newborn development. However, few studies have investigated the concentrations of S100B protein, brain-derived neurotrophic factor (BDNF), and glial cell line-derived neurotrophic factor (GDNF) in human milk. The associations of the concentrations of S100B protein, BDNF, and GDNF with maternal factors are not well explored.To investigate the concentrations of S100B protein, BDNF, and GDNF in human milk and characterize the maternal factors associated with their levels in human milk, human milk samples were collected at days 3, 10, 30, and 90 after parturition. Levels of S100B protein, BDNF, and GDNF, and their mRNAs in the samples were detected. Then, these concentrations were compared with lactation and other maternal factors. S100B protein levels in human milk samples collected at 3, 10, 30, and 90 d after parturition were 1249.79±398.10, 1345.05±539.16, 1481.83±573.30, and 1414.39±621.31 ng/L, respectively. On the other hand, the BDNF concentrations in human milk samples were 10.99±4.55, 13.01±5.88, 13.35±6.43, and 2.83±5.47 µg/L, while those of GDNF were 10.90±1.65, 11.38±1., 11.29±3.10, and 11.40±2.21 g/L for the same time periods. Maternal post-pregnancy body mass index was positively associated with S100B levels in human milk (r = 0.335, P = 0.030<0.05). In addition, there was a significant correlation between the levels of S100B protein and BDNF (z = 2.09, P = 0.037<0.05). Delivery modes were negatively associated with the concentration of GDNF in human milk.S100B protein, BDNF, and GDNF are present in all samples of human milk, and they may be responsible for the long term effects of breast feeding
Transplantation of Specific Human Astrocytes Promotes Functional Recovery after Spinal Cord Injury
Repairing trauma to the central nervous system by replacement of glial support
cells is an increasingly attractive therapeutic strategy. We have focused on the
less-studied replacement of astrocytes, the major support cell in the central
nervous system, by generating astrocytes from embryonic human glial precursor
cells using two different astrocyte differentiation inducing factors. The
resulting astrocytes differed in expression of multiple proteins thought to
either promote or inhibit central nervous system homeostasis and regeneration.
When transplanted into acute transection injuries of the adult rat spinal cord,
astrocytes generated by exposing human glial precursor cells to bone
morphogenetic protein promoted significant recovery of volitional foot
placement, axonal growth and notably robust increases in neuronal survival in
multiple spinal cord laminae. In marked contrast, human glial precursor cells
and astrocytes generated from these cells by exposure to ciliary neurotrophic
factor both failed to promote significant behavioral recovery or similarly
robust neuronal survival and support of axon growth at sites of injury. Our
studies thus demonstrate functional differences between human astrocyte
populations and suggest that pre-differentiation of precursor cells into a
specific astrocyte subtype is required to optimize astrocyte replacement
therapies. To our knowledge, this study is the first to show functional
differences in ability to promote repair of the injured adult central nervous
system between two distinct subtypes of human astrocytes derived from a common
fetal glial precursor population. These findings are consistent with our
previous studies of transplanting specific subtypes of rodent glial precursor
derived astrocytes into sites of spinal cord injury, and indicate a remarkable
conservation from rat to human of functional differences between astrocyte
subtypes. In addition, our studies provide a specific population of human
astrocytes that appears to be particularly suitable for further development
towards clinical application in treating the traumatically injured or diseased
human central nervous system
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