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Query: UMLS:C0022104 (
irritable bowel syndrome
)
8,033
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Functional somatic syndrome (FSS) is defined as a group of related syndromes characterized more by symptoms, suffering, and disability than by structural or functional abnormality. The diagnostic criteria and/or symptoms of FSS often overlap, and co-morbidity is commonly found among the diseases of FSS. For example, patients with
irritable bowel syndrome
often suffer from chronic pain, and a high percentage of co-morbidity can be found with fibromyalgia. Accumulating evidence indicates the presence of visceral and somatic hyperalgesia in FSS as a common feature, and the central sensitization mechanism has been suggested to play an important role in the pathophysiology of FSS. In the present article, the authors introduce the concept of FSS focusing on its possible relevance to rheumatology in terms of pain perception. A possible implication of mast cells and
proteinase-activated receptor-2
(
PAR-2
) in FSS is also reviewed.
...
PMID:Functional somatic syndrome: how it could be relevant to rheumatologists. 1756 71
Given the role of Ca
v
3.2 isoform among T-type Ca
2+
channels (T-channels) in somatic and visceral nociceptive processing, we analyzed the contribution of Ca
v
3.2 to butyrate-induced colonic pain and nociceptor hypersensitivity in mice, to evaluate whether Ca
v
3.2 could serve as a target for treatment of visceral pain in
irritable bowel syndrome
(
IBS
) patients. Mice of ddY strain, and wild-type and Ca
v
3.2-knockout mice of a C57BL/6J background received intracolonic administration of butyrate twice a day for 3 days. Referred hyperalgesia in the lower abdomen was assessed by von Frey test, and colonic hypersensitivity to distension by a volume load or chemicals was evaluated by counting nociceptive behaviors. Spinal phosphorylated ERK was detected by immunohistochemistry. Ca
v
3.2 knockdown was accomplished by intrathecal injection of antisense oligodeoxynucleotides. Butyrate treatment caused referred hyperalgesia and colonic hypersensitivity to distension in ddY mice, which was abolished by T-channel blockers and/or Ca
v
3.2 knockdown. Butyrate also increased the number of spinal phosphorylated ERK-positive neurons following colonic distension in the anesthetized ddY mice. The butyrate-treated ddY mice also exhibited T-channel-dependent colonic hypersensitivity to intracolonic Na
2
S, known to enhance Ca
v
3.2 activity, and TRPV1, TRPA1 or
proteinase-activated receptor 2
(
PAR2
) agonists. Wild-type, but not Ca
v
3.2-knockout, mice of a C57BL/6J background, after treated with butyrate, mimicked the T-channel-dependent referred hyperalgesia and colonic hypersensitivity in butyrate-treated ddY mice. Our study provides definitive evidence for an essential role of Ca
v
3.2 in the butyrate-induced colonic pain and nociceptor hypersensitivity, which might serve as a target for treatment of visceral pain in
IBS
patients.
...
PMID:Essential role of Ca
v
3.2 T-type calcium channels in butyrate-induced colonic pain and nociceptor hypersensitivity in mice. 3294 97
