Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Migraine attacks are characterized by unilateral throbbing, pulsating headache associated with nausea, vomiting, photophobia, phonophobia and allodynia. Peripheral sensitization is an acute, chemical-induced form of functional plasticity, which converts high-threshold nociceptors into low-threshold sensory neurons. This form of sensitization occurs when the nerve terminals (meningeal nociceptors) of the neurons of the trigeminal ganglion are soaked with the "inflammatory" soup (prostaglandin E2, bradykinin, serotonin and cytokines) along the vasculature of the cerebral dura mater. Peripheral sensitization in migraine attacks is explained clinically by intracranial hypersensitivity (the headache worsens during coughing or physical activity) and by a throbbing element in the pain of migraine (sensitized nociceptors become hyperresponsive to the otherwise innocuous and unperceived rhythmic fluctuation in intracranial pressure produced by normal arterial pulsation). The essence of central sensitization is that the second-order neurons in the trigeminocervical complex become hyperexcitable. The altered behavior of the second-order neurons is based on the increased glutamate sensistivity of the NMDA receptors and the neuronal nitric oxide synthase activity stimulated by nitric oxide. This process is explained clinically by face and scalp ollodynia and by neck stiffness (extracranial tenderness).
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PMID:[The mechanism of peripheral and central sensitization in migraine. A literature review]. 1973 14

Oxaliplatin, an anti-cancer chemotherapeutic agent used for the treatment of colorectal cancer, commonly causes gastrointestinal side-effects such as constipation, diarrhoea, nausea, and vomiting. Damage to enteric neurons may underlie some of these gastrointestinal side-effects, as the enteric nervous system (ENS) controls functions of the bowel. In this study, neuronal loss and changes to the structure and immunoreactivity of myenteric neuronal nitric oxide synthase (nNOS) neurons were examined in colonic segments from mice following exposure to oxaliplatin ex vivo and following repeated intraperitoneal injections of oxaliplatin over 3 weeks in vivo, using immunohistochemistry and confocal microscopy. Significant morphological alterations and increases in the proportion of NOS-immunoreactive (IR) neurons were associated with both short-term oxaliplatin exposure and long-term oxaliplatin administration, confirming that oxaliplatin causes changes to the myenteric neurons. Long-term oxaliplatin administration induced substantial neuronal loss that was correlated with a reduction in both the frequency and propagation speed of colonic migrating motor complexes (CMMCs) in vitro. Similar changes probably produce some symptoms experienced by patients undergoing oxaliplatin treatment.
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PMID:Effects of oxaliplatin on mouse myenteric neurons and colonic motility. 2348 39

Gastrointestinal (GI) side-effects of chemotherapy present a constant impediment to efficient and tolerable treatment of cancer. GI symptoms often lead to dose reduction, delays and cessation of treatment. Chemotherapy-induced nausea, bloating, vomiting, constipation, and/or diarrhea can persist up to 10 years post-treatment. We have previously reported that long-term 5-fluorouracil (5-FU) administration results in enteric neuronal loss, acute inflammation and intestinal dysfunction. In this study, we investigated whether the cytoprotectant, BGP-15, has a neuroprotective effect during 5-FU treatment. Balb/c mice received tri-weekly intraperitoneal 5-FU (23 mg/kg/d) administration with and without BGP-15 (15 mg/kg/d) for up to 14 days. GI transit was analyzed via in vivo serial X-ray imaging prior to and following 3, 7, and 14 days of treatment. On day 14, colons were collected for assessment of ex vivo colonic motility, neuronal mitochondrial superoxide, and cytochrome c levels as well as immunohistochemical analysis of myenteric neurons. BGP-15 did not inhibit 5-FU-induced neuronal loss, but significantly increased the number and proportion of choline acetyltransferase (ChAT)-immunoreactive (IR) and neuronal nitric oxide synthase (nNOS)-IR neurons in the myenteric plexus. BGP-15 co-administration significantly increased mitochondrial superoxide production, mitochondrial depolarization and cytochrome c release in myenteric plexus and exacerbated 5-FU-induced colonic inflammation. BGP-15 exacerbated 5-FU-induced colonic dysmotility by reducing the number and proportion of colonic migrating motor complexes and increasing the number and proportion of fragmented contractions and increased fecal water content indicative of diarrhea. Taken together, BGP-15 co-treatment aggravates 5-FU-induced GI side-effects, in contrast with our previous findings that BGP-15 alleviates GI side-effects of oxaliplatin.
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PMID:Co-treatment With BGP-15 Exacerbates 5-Fluorouracil-Induced Gastrointestinal Dysfunction. 3113 44

Gastroparesis is a disorder where the stomach empties contents too slowly into the small intestine with associated symptoms of nausea, vomiting, postprandial fullness, bloating, early satiety and/or abdominal pain. It is a well-established fact that the female gender is more susceptible to developing gastroparesis compared to males, although the significance and rationale behind this gender inequality remains an unresolved mystery. Several hypotheses have been proposed including an intrinsically slower stomach in females, elevated levels of sex steroid hormones, loss of neuronal nitric oxide (nNOS) expression, and possibly due to altered serotonergic signaling. Recently, our group investigated gender-associated differences in the number of interstitial cells of Cajal in the antral and pyloric smooth muscle of diabetic patients with severe refractory gastroparesis and found there was no significant difference between the 2 genders. Targeting these gender-specific mechanisms may lead towards future therapeutic options that might alleviate and/or prevent gastroparesis. Furthermore, a better-understanding of the sex-related differences in gastroparesis can allow medical practitioners to better tailor treatment options for their patients. This article will attempt to explain why females are more vulnerable to developing gastroparesis by examining the pathogenesis and molecular basis of gender-related factors that have been identified to play a role in the gender disparity of this entity.
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PMID:Gender-Related Differences in Gastroparesis. 3252 95