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)

We have previously found that tissue type and urokinase type plasminogen activators (tPA and uPA) are induced in dorsal root ganglia (DRG) neurons after peripheral axotomy and that tPA plays crucial roles in generating neuropathic pain. Here we examined whether the plasminogen activator inhibitor-1 and -2 (PAI-1 and PAI-2) mRNA, endogenous inhibitors of tPA and uPA, are induced in the DRG following sciatic nerve transection. L4 and L5 DRG sections were examined using in situ hybridization histochemistry. The results showed that both PAI-1 and PAI-2 mRNA were up-regulated in DRG neurons within 1 day, and peaked at 1-3 days, after injury. Reduction of these mRNA was observed from 7 days after injury. The precise expression patterns of PAI-1 and PAI-2 mRNA at 3 days after axotomy revealed that PAI-1 mRNA was observed in predominantly small neurons, while much of the PAI-2 mRNA was expressed in large neurons. Double-labeling analysis of these mRNAs with activated transcription factor 3, known as an injury marker, revealed that most PAI-1 and PAI-2 mRNAs was induced in injured neurons. Co-expression of PAI-1, 2 with tPA and uPA in DRG neurons suggests that these inhibitors may act in an autocrine manner to modulate extracellular proteolytic activity after nerve injury.
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PMID:Induction of plasminogen activator inhibitor-1 and -2 in dorsal root ganglion neurons after peripheral nerve injury. 1578 Apr 77

Recently much attention has been directed toward novel treatment alternatives for refractory angina pectoris. Refractory angina is persistent stable class III or IV angina despite maximally tolerated medical treatment in patients with end-stage coronary artery disease. Transmyocardial laser revascularization (TMLR), gene therapy, intermittent urokinase therapy, enhanced external balloon counterpulsation, and spinal cord stimulation have all been employed to treat refractory angina pectoris. TMLR and gene therapy are invasive open-chest procedures that have yielded controversial results. Intermittent urokinase and enhanced external balloon counterpulsation studies have limited follow-up times and require multiple clinic visits for treatment. Spinal cord stimulation has a proven short- and long-term efficacy and cost-effectiveness in the treatment of refractory angina. When compared to coronary artery bypass grafting (CABG), it has been shown to decrease the frequency of anginal attacks and consumption of short-acting nitrates to the same extent in refractory angina. Spinal cord stimulation's safety profile has also been well established and it can be used concurrently with cardiac pacemakers or MRI systems, provided the proper precautions are taken. Since spinal cord stimulation is a minimally invasive procedure with a favorable efficacy and safety profile, it should be considered as a valid treatment alternative after medical management has failed in refractory angina prior to implementing invasive modalities such as TMLR or gene therapy.
Pain Pract 2001 Jan
PMID:Spinal cord stimulation: a comparison of efficacy versus other novel treatments for refractory angina pectoris. 1712 82

We report a case of blindness due to occlusion of the ophthalmic artery following injection of autologous fat into the glabellar region for cosmetic surgery. A 30-year-old woman underwent aspiration of autologous fat from her gluteal region and injection of it into her breasts, nose, and glabellar area. At the time of injection into the glabellar area, she suffered nausea, pain, and visual loss in her right eye. She consulted an ophthalmologist. The first examination revealed that her right eye had loss of light perception, widespread retinal whitening, and obstruction of the retinal vessels of the fundus. It was suspected that she had occlusion of the central retinal artery, and drip infusion of urokinase and hyperbaric oxygen therapy were implemented. Since no improvement was seen, she was referred to Shinshu University hospital. Fundoscopy showed remarkable edema of the entire right retina and whitened retinal vessels. Fluorescein angiography showed no filling of the right retinal arterioles. Cerebral angiography showed complete obstruction of the right ophthalmic artery at its bifurcation. Subsequent administration of urokinase and corticosteroid had no effect. We considered that occlusion of the ophthalmic artery happened when autologous fat was injected into the glabellar area.
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PMID:[A case of ophthalmic artery obstruction following autologous fat injection in the glabellar area]. 1730 92

Between January 2000 and June 2003, 70 patients (63 men and 7 women) with acute-on-chronic lower limb vascular occlusion underwent thrombolysis with 1 million units of urokinase. Forty-eight patients had unilateral and 22 had bilateral involvement; 9 had gangrenous changes. The mean age was 47 +/- 9 years, 73% were smokers, and 13% had diabetes. The definition of a good response was either return of distal pulses or a warm limb and relief of pain at rest. Fifty-three (76%) patients (including 5 with gangrenous changes) had symptomatic improvement with thrombolysis (group 1), and 17 (24%) did not respond (group 2). All 70 patients (including 7 who later required amputation) underwent surgical intervention with a polytetrafluoroethylene interposition graft or arterioplasty. A good response to surgical treatment was found in significantly more patients (49/53, 92%) in group 1 compared to group 2 (7/17, 41%). Claudication distance after 6 months of follow-up improved in a significantly higher percentage of patients in group 1 (85%) than group 2 (38%). Preoperative thrombolysis improved the outcome and predicted the result of arterial surgery.
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PMID:Urokinase thrombolysis in acute-on-chronic vascular occlusion of lower limb. 1791 Oct 68

Antiphospholipid syndrome (APS) is an autoimmune disease, and its most critical pathologic process is thrombosis, which may explain most of the clinical features. Acute management of thrombosis involves immediate anticoagulation. Acute proximal venous thrombosis can be managed with thrombolytic therapy to reduce the long-term complications of the postthrombotic syndrome (pain, swelling, skin discoloration, or ulceration) and perform recanalization of occluded vessels. However, thrombolytic therapies are associated with high risks of bleeding. To our knowledge, this is the first report of epidural hematoma mimicking transverse myelitis after catheter-directed thrombolysis in a patient with primary APS. A 42-year-old male was admitted with sudden onset pain and swelling on left lower extremity. Venography demonstrated multiple thrombi on superficial femoral vein, common femoral vein, common iliac vein, and external iliac vein. Laboratory tests indicated the presence of IgM anticardiolipin antibody. He was diagnosed with primary APS with multiple venous thrombi. He was treated with urokinase (200,000/h) as thrombolytic therapy. After 1 day, he complained both leg weakness and urinary dysfunction. T1- and T2-weighted magnetic resonance images of spine showed about 8 cm-sized mass, suggesting hematoma on the posterior epidural space at thoracolumbar area. Despite the successful evacuation of hematoma, neurologic symptoms persisted and he is now receiving aspirin, warfarin, and physical therapy.
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PMID:Epidural hematoma mimicking transverse myelitis in a patient with primary antiphospholipid syndrome. 1807 36

Of the estimated 565,650 people in the U.S. who will die of cancer in 2008, almost all will have metastasis. Breast, prostate, kidney, thyroid and lung cancers metastasize to the bone. Tumor cells reside within the bone using integrin type cell adhesion receptors and elicit incapacitating bone pain and fractures. In particular, metastatic human prostate tumors express and cleave the integrin A6, a receptor for extracellular matrix components of the bone, i.e., laminin 332 and laminin 511. More than 50% of all prostate cancer patients develop severe bone pain during their remaining lifetime. One major goal is to prevent or delay cancer induced bone pain. We used a novel xenograft mouse model to directly determine if bone pain could be prevented by blocking the known cleavage of the A6 integrin adhesion receptor. Human tumor cells expressing either the wildtype or mutated A6 integrin were placed within the living bone matrix and 21 days later, integrin expression was confirmed by RT-PCR, radiographs were collected and behavioral measurements of spontaneous and evoked pain performed. All animals independent of integrin status had indistinguishable tumor burden and developed bone loss 21 days after surgery. A comparison of animals containing the wild type or mutated integrin revealed that tumor cells expressing the mutated integrin resulted in a dramatic decrease in bone loss, unicortical or bicortical fractures and a decrease in the ability of tumor cells to reach the epiphyseal plate of the bone. Further, tumor cells within the bone expressing the integrin mutation prevented cancer induced spontaneous flinching, tactile allodynia, and movement evoked pain. Preventing A6 integrin cleavage on the prostate tumor cell surface decreased the migration of tumor cells within the bone and the onset and degree of bone pain and fractures. These results suggest that strategies for blocking the cleavage of the adhesion receptors on the tumor cell surface can significantly prevent cancer induced bone pain and slow disease progression within the bone. Since integrin cleavage is mediated by Urokinase-type Plasminogen Activator (uPA), further work is warranted to test the efficacy of uPA inhibitors for prevention or delay of cancer induced bone pain.
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PMID:The role of alpha 6 integrin in prostate cancer migration and bone pain in a novel xenograft model. 1895 75

Chronic refractory angina pectoris is a clinical entity characterized by a persistent thoracic pain, despite pharmacological therapy (Canadian Cardiovascular Society functional class 3-4); the patients show a severe, diffuse coronary atherosclerosis not amenable to myocardial revascularization at coronary angioplasty or bypass grafting. This clinical entity which is becoming ever more frequent is a cause of a poor quality of life necessitating repeated hospitalization. Many therapeutic alternatives have been proposed for the treatment of these patients, but results were inconclusive. In this review their pathophysiological background, clinical efficacy, safety and complications are analyzed. Data concerning spinal cord stimulation, upper thoracic sympathectomy, high thoracic epidural analgesia, chronic-intermittent urokinase administration, enhanced external counterpulsation and transmyocardial laser revascularization are presented. Finally, the main research directions in this particular field are reported.
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PMID:[Non-pharmacological, non-conventional therapy of chronic refractory angina pectoris]. 1939 5

(1) The signs of infection of implanted port catheters are inflammation along the course of a central catheter, oozing or signs of an abscess of the pocket in which the port is implanted. Catheter-related venous thrombosis should be suspected in the event of pain, oedema, local swelling, a palpable venous cord and development of superficial collateral circulation; (2) The rapid appearance of local signs and symptoms at the time of injection suggests extravasation of the injected drug; (3) Catheter patency should be checked with normal saline, never using too much force if resistance is encountered. If there is a thrombotic occlusion, the catheter can often be unblocked with heparin, or if not, with urokinase. There is only a moderate risk of bleeding if these agents are used carefully.
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PMID:Identifying complications of central venous catheters: infection, thrombosis, occlusion. 1974 62

A 37-year-old man with known intravenous drug abuse presented in the surgical ambulatory care unit with acute leg ischemia after accidental intra-arterial injection of dissolved flunitrazepam tablets into the right femoral artery. A combination of anticoagulation, vasodilatation, and local selective and superselective thrombolysis with urokinase was performed to salvage the leg. As a result of the severe ischemia-induced pain, the patient had to be monitored over the complete therapy period on the intensive care unit with permanent administration of intravenous fluid and analgetics. We describe the presenting symptoms and the interventional technique, and we discuss the recent literature regarding the management of accidental intra-arterial injection of dissolved flunitrazepam tablets.
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PMID:Successful thrombolysis and spasmolysis of acute leg ischemia after accidental intra-arterial injection of dissolved flunitrazepam tablets. 2155 63

Opioids including morphine are commonly used in pain management during and after cancer surgery but have been linked to a variety of pro- and anti-tumor effects. In the present study the effect of morphine administration on the localization and growth of breast tumor cells in lungs and the level of extracellular matrix (ECM) proteases were investigated. In a mouse syngeneic model of intravenously inoculated breast cancer cells, morphine administration led to a reduction in the localization and growth of tumors in the lungs and a reduction in circulating matrix metalloproteinase-9 (MMP-9) and urokinase-like plasminogen activator (uPA). To model the involvement of non-malignant cells of the tumor microenvironment in the changes we observed in the level of proteases, we co-cultured breast cancer cells with macrophages, endothelial cells and fibroblasts. We found a significant elevation of matrix proteases as well as matrix protease inhibitors in co-cultures of breast cancer cells with macrophages or endothelial cells. Interestingly, morphine treatment of these co-cultures reduced the level of MMP-9 and increased its endogenous inhibitor, TIMP-1, thereby altering the proteolytic profile. Morphine affected the level of enzymes in co-cultures but not in cells grown individually. This suggests that anti-tumor effects of morphine observed in our in vivo model could be mediated at least in part through modulation of paracrine communication between cancer cells and non-malignant cells in the tumor microenvironment.
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PMID:Morphine and breast tumor metastasis: the role of matrix-degrading enzymes. 2407 19


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