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As recent research by Allan Basbaum at the University of California at San Francisco has shown, with prolonged injury progressively deeper levels of pain cells in the spinal cord are activated.
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This factor binds to a protein on the pain-cell surface, a so-called receptor named TrkA, which relays the "pain" message throughout the cell.
Thanks to this less efficient, albeit still functioning, receptor, the naked mole rat still winds up with an adequate nervous system, but with fewer pain nerve cells.
Cultured sensory neurons derived from trigeminal or dorsal root ganglia have been shown to express the characteristics of "differentiated pain sensory" cells [28].
To test whether HMS could initiate gene expression associated with IVD degeneration and discogenic pain, IVD cells were cultured in HESR dishes mounted on an iris-like stretching device.
This central action accentuates the effects of these neurotransmitters in activation of endogenous pain-inhibitory systems in the brain that modulate pain-transmission cells in the spinal cord.
Recent studies, for example, suggest that a constant intake of analgesics lowers the brain's level of serotonin, a neurotransmitter that inhibits pain-conducting cells.
Endothelin 1 is a potent vasoconstrictor that has been linked to graft rejection and to inflammatory events including pain, fever, cell migration and rheumatoid arthritis.
The primary outcomes of the study are aerobic capacity (VO2peak), perceived exertion, fatigue, muscle pain, immune cell counts, lymphocyte (CD4+, CD8+, CD19+, CD16+56+) concentrations and function.
NPY has been linked to several physiological and pathological functions, such as feeding behaviour, memory processing, pain, anxiety, cell proliferation and many other processes in the central and peripheral nervous systems.
Neuroprotective effects of Ketamine attenuate the impaired cognitive behaviors resulting from pain-induced cell death in the cortical and hippocampal fields of neonatal rats.
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