about
Functional decline at the aging neuromuscular junction is associated with altered laminin-α4 expression.Tick holocyclotoxins trigger host paralysis by presynaptic inhibition.Review: Neuroinflammation in intrauterine growth restriction.Loss of laminin-α4 results in pre- and postsynaptic modifications at the neuromuscular junction.Defects in synaptic transmission at the neuromuscular junction precedes motor deficits in a TDP-43Q331K transgenic mouse model of amyotrophic lateral sclerosis.Disruption to the 5-HT7 Receptor Following Hypoxia-Ischemia in the Immature Rodent Brain.Neonatal seizures are associated with redistribution and loss of GABAA α-subunits in the hypoxic-ischaemic pig.Therapeutic potential to reduce brain injury in growth restricted newbornsNeuropathology in intrauterine growth restricted newborn piglets is associated with glial activation and proinflammatory status in the brainIbuprofen Treatment Reduces the Neuroinflammatory Response and Associated Neuronal and White Matter Impairment in the Growth Restricted NewbornLoss of β2-laminin alters calcium sensitivity and voltage-gated calcium channel maturation of neurotransmission at the neuromuscular junctionSeizures Are Associated with Blood-Brain Barrier Disruption in a Piglet Model of Neonatal Hypoxic-Ischaemic Encephalopathy
P50
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P50
description
researcher ORCID ID = 0000-0001-7739-2098
@en
wetenschapper
@nl
name
Kirat K Chand
@ast
Kirat K Chand
@en
Kirat K Chand
@es
Kirat K Chand
@nl
type
label
Kirat K Chand
@ast
Kirat K Chand
@en
Kirat K Chand
@es
Kirat K Chand
@nl
prefLabel
Kirat K Chand
@ast
Kirat K Chand
@en
Kirat K Chand
@es
Kirat K Chand
@nl
P1153
56465590300
P31
P496
0000-0001-7739-2098