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Loss of neurons from laminas I-III of the spinal dorsal horn is not required for development of tactile allodynia in the spared nerve injury model of neuropathic pain

These models can be used to design personalized prevention and treatment strategies that address the specific molecular and biomechanical mechanisms underlying ACL injuries

Cation-chloride cotransporters in neuronal development, plasticity and disease

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Consequently, the possibility that DEHP induces precocious puberty in female offspring via interference with the IGF-1 and NKB signaling pathways necessitates more comprehensive and in-depth investigation to unravel the underlying molecular mechanisms