Scaling up prevention and control of noncommunicable diseases in the WHO Eastern Mediterranean Region.

Surveillance is an essential component in the campaign to prevent and control noncommunicable diseases (NCDs), both globally and in the Eastern Mediterranean Region (EMR). In order to address the increasing burden from these diseases, countries must first evaluate their own systems and see what steps need to be taken to improve preparedness. Therefore, the WHO Regional Office for the Eastern Mediterranean in Cairo, Egypt, conducts country capacity surveys on a regular basis to compare each Member State's NCD provision to the Framework for Action to implement the UN Political Declaration (2011).

Brief, low frequency stimulation of rat peripheral C-fibres evokes prolonged microglial-induced central sensitization in adults but not in neonates.

The sensitization of spinal dorsal horn neurones leads to prolonged enhancement of pain behaviour and can be evoked by intense C-fibre stimulation, tissue inflammation and peripheral nerve injury. Activation of central immune cells plays a key role in establishing pain hypersensitivity but the exact nature of the afferent input that triggers the activation of microglia and other glial cells within the CNS, remains unclear. Here intense but non-damaging, electrical stimulation of intact adult rat C-fibres for 5 min at 10 Hz induced central sensitization characterized by significant decreases in mechanical withdrawal thresholds 3, 24 and 48 h later.

Origins, actions and dynamic expression patterns of the neuropeptide VGF in rat peripheral and central sensory neurones following peripheral nerve injury.

Background: The role of the neurotrophin regulated polypeptide, VGF, has been investigated in a rat spared injury model of neuropathic pain. This peptide has been shown to be associated with synaptic strengthening and learning in the hippocampus and while it is known that VGFmRNA is upregulated in dorsal root ganglia following peripheral nerve injury, the role of this VGF peptide in neuropathic pain has yet to be investigated.

Results: Prolonged upregulation of VGF mRNA and protein was observed in injured dorsal root ganglion neurons, central terminals and their target dorsal horn neurons.

Developmental changes in the fidelity and short-term plasticity of GABAergic synapses in the neonatal rat dorsal horn.

The lower thresholds and increased excitability of dorsal horn neurons in the neonatal rat suggest that inhibitory processing is less efficient in the immature spinal cord. This is unlikely to be explained by an absence of functional GABAergic inhibition because antagonism of gamma-aminobutyric acid (GABA) type A receptors augments neuronal firing in vivo from the first days of life. However, it is possible that more subtle deficits in GABAergic signaling exist in the neonate, such as decreased reliability of transmission or greater depression during repetitive stimulation, both of which could influence the relative excitability of the immature spinal cord.

Nerve injury induces robust allodynia and ectopic discharges in Nav1.3 null mutant mice.

Changes in sodium channel activity and neuronal hyperexcitability contribute to neuropathic pain, a major clinical problem. There is strong evidence that the re-expression of the embryonic voltage-gated sodium channel subunit Nav1.3 underlies neuronal hyperexcitability and neuropathic pain.