Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purposes of this study were: 1) to compare performance status, mood states, and level of hope between patients with cancer pain and patients without cancer pain; and 2) to determine the relationships of pain intensity and pain interference with daily life to performance status, mood states, and level of hope. A total of 233 Taiwanese cancer patients with pain and 251 without pain participated. The self report instruments consisted of the Chinese version of the Profile of Mood States (POMS) short form, the Chinese version of the Herth Hope Index, the Brief Pain Inventory-Chinese version (BPI-C), the Chinese version of the Karnorfsy Performance Scale (KPS), and a demographic questionnaire. The major findings of this study were that cancer patients with pain reported significantly lower levels of performance status and higher levels of total mood disturbance than did cancer patients who did not experience pain after controlling for sex, disease stage, and recruitment site. In addition, patients with cancer pain experienced significantly more anger, fatigue, depression, confusion, and lethargy than did patients without pain after controlling for sex, disease stage, and recruitment site. Among patients with pain, pain intensity was significantly correlated with performance status and mood state, but not with level of hope. Pain interference with daily life was significantly correlated both with performance status, mood state, and level of hope. Pain intensity and pain interference were significantly correlated with each mood state as well as with total mood disturbance. This study has demonstrated the effect of cancer pain on patients' physical, psychological, and spiritual life and has supported the multidimensional notion of the cancer pain experience in Taiwanese patients.
J Pain Symptom Manage 2003 Jan
PMID:Effect of cancer pain on performance status, mood states, and level of hope among Taiwanese cancer patients. 1256 86

Recently, an orphan G protein coupled receptor (GPCR) termed NPGPR was described. A shorter variant of this receptor lacking exon 1 was shown to have subnanomolar affinity for neuropeptide FF (NPFF), a pain modulatory peptide, and therefore was named NPFF(2) receptor. Here, we characterize the full-length cloned NPGPR and identify a novel short form lacking exon 2 with a differential pattern of mRNA abundance in several tissues and organs. The NPGPR is most similar to the recently cloned neuropeptide FF (NPFF) receptor which lacks exon 1, but also shows high homology to the orexin and neuropeptide Y (NPY) receptor families, two neuropeptides involved in food intake regulation. Therefore, we used binding studies to examine the interaction of NPFF, orexin and NPY with the NPGPR. [125I] NPFF was displaced by NPFF with an IC(50) of 14.7 +/- 8.8 nM, whereas [125I] Orexin B was displaced by Orexin B with an IC(50) of 415 +/- 195 nM. We conclude that orexins interact with the NPGPR and that the affinity of NPFF for NPGPR is approximately 100-fold lower than for the NPFF2 receptor. We postulate that NPGPR is a splice variant of the family of NPFF receptors and displays a binding profile different from the other members of the NPFF receptor family due to the presence of exon 1. In order to evaluate whether NPGPR levels are affected by the feeding status, we examined the mRNA level using real-time PCR in two feeding models, i.e. before and after diet-induced body weight increase as well as after chronic food restriction in rats. However, hypothalamic NPGPR mRNA was unchanged in both models. Therefore, our evidence does not support the hypothesis that NPGPR is involved in feeding regulation.
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PMID:Characterization of the NPGP receptor and identification of a novel short mRNA isoform in human hypothalamus. 1260 45

Most studies of pain, including chronic pain, agree that depression and pain are interrelated, although the neurobiology of this relationship remains unknown. Neuroimaging studies suggest a specific role of the prefrontal brain regions in the mechanisms of mood disorders and chronic pain. The present study examines the interrelationships between regional brain N-Acetyl aspartate (NAA) levels (as identified by in vivo proton magnetic resonance spectroscopy in the right and left dorsolateral prefrontal cortex [DLPFC], orbitofrontal cortex, cingulate and thalamus), depression (as measured by the Beck Depression Inventory), and pain (as measured by short form of the McGill Pain Questionnaire) in 10 chronic back pain (CBP) patients with depression, and compared to the relationship between regional brain NAA levels and depression in 10 normal subjects (sex and age-matched). Reduction of NAA levels was demonstrated in the right DLPFC of CBP patients with depression, as compared to the normal controls (p < 0.02, two-tailed t-test). The depression levels in CBP patients were highly correlated with NAA levels in the right DLPFC (r = -0.99, p < 0.0001), and were unrelated to the other studied regional NAA in both groups, including the right DLPFC in normal subjects (p < 10(-6); comparing the difference between r values in the right DLPFC between the two groups). The pain levels in CBP patients were also associated with the right DLPFC (r = -0.62, p < 0.05), although these relationships were much weaker as compared to depression-NAA correlations (p < 0.0001; comparing the difference between r values). The interrelationships between NAA across brain regions were examined using correlation analysis, which detected different connectivity patterns between CBP patients with depression and normal subjects. These findings provide evidence for a stronger association of prefrontal NAA to depression than to pain in CBP, which may reflect the common neurobiological substrate underlying these conditions in CBP patients. Spectroscopic brain mapping of NAA, the marker of neuronal density and function, to the depression and pain measures might be used for segregation of their circuitries in the chronic pain brain.
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PMID:Association between dorsolateral prefrontal N-acetyl aspartate and depression in chronic back pain: an in vivo proton magnetic resonance spectroscopy study. 1265 77

Through a process of subtraction cloning and differential hybridization, we previously identified several new genes whose expression was induced by peripheral inflammation. One of these coded for cystatin C, a secreted cysteine protease inhibitor in the cystatin superfamily. We hypothesized that, concurrent with increased expression in dorsal horn, increased secretion would elevate the cystatin C content in cerebrospinal fluid (CSF) during active pain states. Alterations were assessed by immunoassay and by surface enhanced laser desorption ionization (SELDI) mass spectrometry with either reverse phase or immobilized anti-cystatin C antibody surfaces using CSF from ten age-matched obstetrical patients at term. Five control subjects were scheduled for an elective caesarian section and were not in pain. Another five subjects were in labor for 8.9+/-1h and were in severe pain as assessed with a visual analog scale and the McGill short form questionnaire. The level of cystatin C as measured by immunoassay in the non-pain patients was 2.77+/-0.75 microg/ml and in the pain patients 5.36+/-0.92 microg/ml (P<0.02). The elevation occurred without significant change in total CSF protein or beta-endorphin content. The cystatin C increase also was detectable by SELDI with either raw CSF or after antibody capture. These data are consistent with our previous animal study and the idea that persistent pain induces the synthesis and release of cystatin C in dorsal spinal cord, the surplus of which overflows into the CSF.
Pain 2003 Apr
PMID:Cystatin C as a cerebrospinal fluid biomarker for pain in humans. 1267 Jun 66

A two-centred descriptive study was performed in order to describe and compare pain and health-related quality of life (HRQOL) among cancer patients, in their final stage of life. The patients were cared for by either a nurse-led palliative care team I (PCT I) or a physician-led palliative care team II (PCT II). Forty-six consecutive, stratified patients (PCT I, n = 21 and PCT II, n = 25) participated. The medical outcomes study short form 36 (SF-36) was used for evaluating HRQOL and the Pain-O-Meter for assessing pain. Patients' pain intensity, pain quality and HRQOL showed no significant difference between the two groups PCT I and PCT II. The patients from PCT I had significantly longer survival time (P = 0.017) than those from PCT II. The different composition of the teams being led by nurses or physicians is worth further research; both from the patient's and staff's viewpoint, there may also be cost-benefits worth examining.
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PMID:Pain and health-related quality of life among cancer patients in final stage of life: a comparison between two palliative care teams. 1269 66

Modulation of nociceptive transmission at the brainstem involves several neurochemical systems. The precise location and specific characteristics of nociceptive neurons activated in each system was never reported. In this study, the presence of GABA(B), mu-opioid, and neurokinin-1 (NK-1) receptors in brainstem nociceptive neurons was investigated by double-immunocytochemical detection of each receptor and noxious-evoked induction of the c-fos proto-oncogene. Noxious cutaneous mechanical stimulation significantly increased the proportions of neurons double-labelled for Fos and GABA(B) receptors in several brainstem regions, namely, the reticular formation of the caudal ventrolateral medulla (VLMlat and VLMrf), lateral reticular nucleus, spinal trigeminal nucleus, pars caudalis (Sp5C), nucleus of the solitary tract, dorsal reticular nucleus, ventral reticular nucleus, raphe obscurus nucleus and dorsal parabrachial nucleus (DPB). For mu-opioid receptors, the proportions of double-labelled neurons in noxious-stimulated animals were higher than in controls only in the VLMlat, VLMrf, Sp5C, DPB and A5 noradrenergic cell group. As for the NK-1 receptor, no significant differences were found between control and stimulated animals. According to these results, neurons expressing GABA(B), mu-opioid and NK-1 receptors at several pain control centres of the brainstem are differentially involved in processing nociceptive mechanical input. The data provide the definition of new supraspinal targets for selective modulation of nociceptive neurons in order to define better strategies of pain control.
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PMID:Noxious-evoked c-fos expression in brainstem neurons immunoreactive for GABAB, mu-opioid and NK-1 receptors. 1271 42

Sedation and tiredness are among the most frequent symptoms among cancer patients. A detailed assessment of these symptoms is necessary to evaluate therapeutic effects, such as the use of methylphenidate or comparison of different opioids. The Brief Fatigue Inventory (BFI) has been validated as a short and comprehensive instrument to assess severity of fatigue and fatigue-related impairment in cancer patients. We validated the German version of the BFI in patients with chronic cancer-related and noncancer-related pain treated in a tertiary pain center. Patients treated in the Pain Clinic of the Department of Anesthesiology completed the BFI, the minimal documentation system (MIDOS) and the short form SF-36 quality-of-life questionnaire (SF-36). Test-retest reliability was assessed with a second BFI immediately after the consultation and in a subgroup of patients after 3 to 7 days. Nineteen percent of the 117 patients were treated for cancer-related pain (C); the other patients suffered from chronic severe pain of nonmalignant origin (NC). Patients reported mean values for average fatigue of 3.9 (C) and 4.9 (NC), and for worst fatigue of 5.5 (C) and 6.2 (NC). The mean score of the 6 impairment items was 4.3 in both groups. Factor analysis led to a solution with one common factor for all nine items. Fatigue on the BFI correlated highly with 'feeling tired' in the SF-36 and with 'sedation' in MIDOS, and less with 'being worn out' in SF-36 and 'weakness' in MIDOS. Internal consistency was high, as was test-retest reliability, with a correlation of the intensity, mean scores of 0.93 and the impairment mean scores of 0.87. In conclusion, we found the German version of the BFI to be reliable and valid for cancer and noncancer patients. Minor differences were seen in the validation compared to the original version.
J Pain Symptom Manage 2003 May
PMID:Validation of the German version of the brief fatigue inventory. 1272 43

Tacrolimus is increasingly used as a baseline immunosuppressant after renal transplantation. This multicentre study assessed health-related quality of life and symptom experience in renal transplant patients on tacrolimus-based therapy, using the SF-36 and Euroqol 5 dimensions (EQ-5D) and the 'modified transplant symptom occurrence and symptom distress scale', respectively. Symptoms of depression were assessed with the short form of the Beck Depression Inventory and physical activity with the Baecke questionnaire. Overall, 350 patients with a median post-transplant status of 16.7 months were enrolled. Results revealed that patients experienced lower SF-36 scores than the general population, except in terms of bodily pain. Univariate and multivariate analyses demonstrated that a higher degree of depressive symptoms and female gender were consistently related to a health status perceived as being worse and a higher rate of symptom experience. These findings are in accordance with previous quality-of-life reports that assessed patients under various immunosuppressive therapies. Therefore, interventions, including the screening and treatment for depression and the addressing of gender-specific issues, can enhance quality of life.
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PMID:Health-related quality of life and symptom experience in tacrolimus-based regimens after renal transplantation: a multicentre study. 1274 58

Sciatic nerve section in rats evokes chronic hindlimb edema, pain behavior, and hyperalgesia, a syndrome resembling complex regional pain syndrome (CRPS II) in man. Furthermore, there is an increase in spontaneous protein extravasation in the hindpaw skin of rats after sciatic transection, similar to the increased protein extravasation observed in the edematous limbs of CRPS patients. Now we demonstrate that sciatic nerve section also generates chronic hindlimb warmth, distal articular tenderness, allodynia, and periarticular osteoporosis, sequelae of nerve injury resembling those observed in CRPS. We postulated that facilitated substance P signaling may contribute to these vascular and nociceptive abnormalities and attempted to reverse these changes with the long acting substance P receptor (NK(1)) antagonist LY303870. Hindpaw spontaneous extravasation was inhibited by LY303870. Systemic administration of LY303870 also reversed hindpaw edema and cutaneous warmth. Intrathecal, but not systemic administration of LY303870 reversed soft tissue and articular mechanical hyperalgesia in the hindpaw. Collectively, these data further support the hypothesis that the sciatic nerve transection model closely resembles CRPS and that substance P contributes to the spontaneous extravasation, edema, warmth, and mechanical hyperalgesia observed in this model.
Pain 2003 Jul
PMID:A substance P receptor (NK1) antagonist can reverse vascular and nociceptive abnormalities in a rat model of complex regional pain syndrome type II. 1285 16

Migraine headaches are often precipitated by stress and seem to involve neurogenic inflammation (NI) of the dura mater associated with the sensation of throbbing pain. Trigeminal nerve stimulation had been reported to activate rat dura mast cells and increase vascular permeability, effects inhibited by neonatal pretreatment with capsaicin implicating sensory neuropeptides, such as substance P (SP). The aim of the present study was to investigate NI, assessed by extravasation of 99-Technetium-gluceptate (99Tc-G), as well as the role of mast cells, SP and its receptor (NK-1R) in dura mater of mice in response to acute stress. Restraint stress for thirty min significantly increased 99Tc-G extravasation in the dura mater of C57BL mice. This effect was absent in W/W(v) mast cell-deficient mice and NK-1 receptor knockout mice (NK-1R-/-), but was unaltered in SP knockout mice (SP-/-). Acute restraint stress also resulted in increased dura mast cell activation in C57BL mice, but not in NK-1R-/- mice. These data demonstrate for the first time that acute stress triggers NI and mast cell activation in mouse dura mater through the activation of NK-1 receptors. The fact that SP-/- mice had intact vascular permeability response to stress indicates that some other NK-1 receptor agonist may substitute for SP. These results may help explain initial events in pathogenesis of stress-induced migraines.
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PMID:Stress-induced dura vascular permeability does not develop in mast cell-deficient and neurokinin-1 receptor knockout mice. 1286 61


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