Intrathecal morphine delivery at prepontine cistern to control refractory cancer-related pain: a case report of extensive metastatic and refractory cancer pain.

BACKGROUND: Extensive metastatic and refractory cancer pain is common, and exhibits a dissatisfactory response to the conventional intrathecal infusion of opioid analgesics. CASE PRESENTATION: The present study reports a case of an extensive metastatic esophageal cancer patient with severe intractable pain, who underwent translumbar subarachnoid puncture with intrathecal catheterization to the prepontine cistern. After continuous infusion of low-dose morphine, the pain was well-controlled with a decrease in the numeric rating scale (NRS) of pain score from 9 to 0, and the few adverse reactions to the treatment disappeared at a low dose of morphine. CONCLUSIONS: The patient achieved a good quality of life during the one-month follow-up period.

NFATc3 deficiency protects against high fat diet (HFD)-induced hypothalamus inflammation and apoptosis via p38 and JNK suppression.

Hypothalamic inflammation and apoptosis cause neural injury, playing an important role in metabolic syndrome development. Nuclear Factors of Activated T cells (NFATc3) show many physiological and pathological effects. However, the function of NFATc3 in high fat diet (HFD)-induced hypothalamus injury remains unknown. The wild type (WT) and NFATc3-knockout (KO) mice were subjected to HFD feeding for 16 weeks to examine NFATc3 function in vivo. Astrocytes isolated from WT or KO mice were cultured and exposed to fructose (Fru) in vitro. The liver damage, hypothalamus injury, pro-inflammatory markers, NF-κB (p65), Caspase-3 and mitogen-activated protein kinases (MAPKs) pathways were evaluated. NFATc3 was significantly up-regulated in hypothalamus from mice challenged with HFD, and in astrocytes incubated with Fru. Both in vivo and in vitro studies indicated that NFATc3-deletion attenuated metabolism syndrome, reduced inflammatory regulators expression, inactivated NF-κB (p65), Caspase-3 and p38/JNK signaling pathway. Of note, we identified that promoting p38 or JNK activation could rescue inflammatory response and apoptosis in NFATc3-KO astrocytes stimulated by Fru. Together, these findings revealed an important role of NFATc3 NFATc3 for HFD-induced metabolic syndrome and particularly hypothalamus injury, and understanding of the regulatory molecular mechanism might provide new and effective therapeutic strategies for prevention and treatment of hypothalamic damage associated with dietary obesity-associated neuroinflammation and apoptosis.