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Query: UNIPROT:Q86TM3 (cage)
 29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vertebral compression fractures (VCFs) may be defined radiographically or as a clinical event. The prevalence of these fractures in women aged 50 and over has been estimated at 26% when defined as a reduction in vertebral height greater than 15%. Retrospective reviews of case records have shown a clinical detection rate of VCF in white women of 153/100,000 person years. Of these clinically detected VCFs, 84% were associated with pain. VCF may be defined as a clinical event characterised by loss of height and acute pain. The pain of acute fracture usually lasts 4 to 6 weeks with intense pain at the site of fracture. Chronic pain may also occur in patients with multiple compression fractures, height loss and low bone density but is probably due to structural changes or osteoarthritis. Radiographic VCF may not be symptomatic. The greater the deformity, the greater the likelihood of pain and disability. As height is lost, patients experience discomfort from the rib cage pressing downward on the pelvis. Patients develop a thoracic kyphosis, a lumbar lordosis, and a protuberant abdomen with prominent horizontal skinfold creases. The reduced thoracic space may result in decreased exercise tolerance and reduced abdominal space may give rise to early satiety and weight loss. Sleep disorders may also occur. Patients lose self esteem. Self care may become difficult. They are often depressed. They become fearful of further fracture. They have distorted body image and poor health perception. Patients with one vertebral fracture are at increased risk of peripheral fracture and further vertebral fracture. The aims of acute management are to reduce symptoms and mobilise the patient as quickly as possible.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The clinical consequences of vertebral compression fracture. 162 11

The reasons reduction and replacement of laboratory animals are advancing rapidly in basic biomedical research, and why in industrial toxicology progress is much slower, are analyzed. Reference is made to a previous report from our laboratory, and the general concept of the program is outlined. Encouraging developments concerning acceptance of new concepts in acute toxicity testing by various regulatory agencies are reviewed (OECD, IKS, EEC, and Bureau of Pharmaceutical Affairs, Ministry of Health and Welfare, Japan). On the basis of new concepts proposed by the British Toxicology Society, a program which attempts to evaluate acute toxicity of chemicals as far as possible without causing mortality was started. Continuous in-cage monitoring of motility of animals, regular control of general health, body weight, food and water consumption, and body temperature are used as variables. The possibilities of reducing animal use in toxicology by application of toxicological screening procedures are explained. Screening tests under development include an operant conditioning technique to detect adverse drug interactions with ethanol and a procedure for the detection of nephrotoxic properties. The successful completion of a collaborative program designed to upgrade toxicity testing with contraceptive steroids and to abolish the 7-year beagle and 10-year monkey studies is reported. The application of in vitro cytotoxicity tests for assessment of irritant and corrosive properties of chemicals is discussed and some encouraging progress on regulatory acceptance of such tests (OECD) is reported. A new test developed at the institute is described. An in vitro model for the investigation of chemically induced changes of collagen synthesis in human fibroblasts is presented. Other cell culture methods under development include a culture system of chick brain, retina, and menings cells for the study of neurotoxic chemicals and neurobehavioral teratogens, primary hepatocyte cultures for the study of drug effects on DNA and protein synthesis and ploidy, using flow cytometry, and various in vitro models for the assessment of genotoxic and tumor-promoting activities and malignant cell transformation. The problem of analgesic treatment of animals with chronic pain was investigated. Several analgesics were evaluated, and treatment modalities providing demonstrable analgesia for prolonged periods of time in mice and rats were worked out.
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PMID:Reduction and replacement of laboratory animals in toxicological testing and research. Interim report 1984-1987. 307 63

Adjuvant-induced arthritis in rats is considered as a chronic pain model. In a search for a relevant behavioural marker of the chronic pain state, we studied social interactions between an arthritic rat and a healthy partner in a neutral cage. During the test, arthritic rats emitted ultrasonic 22-28 kHz vocalizations (USV), whereas control rats did not, and showed less exploration and more immobility, but did not differ from controls in terms of social behaviours (social investigation, allogrooming). Aspirin (200 mg kg < > (en)1) or morphine (3 mg kg < > (en)1) injected intraperitoneally before the test significantly decreased USV without affecting the animals' behaviour. These results suggest that USV could be associated with affect related to aversive or painful stimuli and may constitute a behavioural marker of chronic pain in arthritic rats.
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PMID:Ultrasonic vocalization (22-28 kHz) in a model of chronic pain, the arthritic rat: effects of analgesic drugs. 873 Aug 34

In the following presentation 59 German and English articles on the use of strong opioids in chronic pain syndromes are analysed. Studies concerning the epidural, intrathecal, intracerebroventricular and transdermal application of opioids were excluded. The articles were attributed to different study levels according to their contents. The majority of articles (n=39, 66.1%) consisted of case presentations, while only 33.9% of the articles presented randomised (n=15) or non-randomised (n=5) study designs. The analgesic effect of the strong opioids morphine, buprenorphine and methadone in oral, rectal, subcutaneous and intravenous forms of application was confirmed for cancer-associated and non-cancer-associated chronic pain. Altogether there is a lack of controlled clinical studies.
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PMID:[Strong opioids for treatment of chronic pain: a meta-analysis]. 1279 98

Cage layer fatigue was first noticed after laying hens began to be housed in cages in the mid-20th century. Hens producing eggs at a high rate were most susceptible to the disease. Early research revealed that cage layer fatigue was associated with osteoporosis and bone brittleness. Severe osteoporosis leads to spontaneous bone fractures commonly in the costochondral junctions of the ribs, the keel, and the thoracic vertebrae. Vertebral fracture may damage the spinal cord and cause paralysis. Osteoporosis appears to be inevitable in highly productive caged laying hens. The condition can be made worse by metabolic deficiency of calcium, phosphorus, or vitamin D. Hens in housing systems that promote physical activity tend to have less osteoporosis and rarely manifest cage layer fatigue. Genetic selection may produce laying hens that are less prone to bone weakness. The welfare implications of osteoporosis stem from pain, debility, and mortality associated with bone fracture. The chicken has well-developed neural and psychological systems specialized to respond to pain associated with trauma and inflammation. Although studies on the chicken have not focused on pain due to bone fracture, physiological and behavioral similarities to other species allow inference that a hen experiences both acute and chronic pain from bone fracture. There is little information on osteoporosis in commercial caged layer flocks, however, evidence suggests that it may be widespread and severe. If true, most caged laying hens suffer osteoporosis-related bone fracture during the first laying cycle. Osteoporosis also makes bone breakage a serious problem during catching and transport of hens prior to slaughter. Estimates of mortality due to osteoporosis in commercial caged layer flocks are few, but range up to a third of total mortality. Many of these deaths would be lingering and attended by emaciation and possibly pain. Osteoporosis-related bone breakage during processing has reduced the marketability of spent caged laying hens, contributing to the need to develop humane on-farm killing methods to support alternative means of spent hen disposition. Overall, the evidence indicates that cage layer osteoporosis is a serious animal welfare problem. A determined effort must be made to make the laying hen no longer susceptible to the harmful effects of excessive bone loss.
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PMID:Welfare implications of avian osteoporosis. 1497 68

It is important to know the factors that will influence animal models of neuropathic pain. A good reproducibility and predictability in different strains of animals for a given test increases the clinical relevance and possible targeting. An obligatory requirement for enabling comparisons of results of different origin is a meticulous definition of the specific sensitivities of a model for neuropathic pain and a description of the test conditions. Factors influencing neuropathic pain behavior can be subdivided in external and internal factors. The most important external factors are; timing of the measurement of pain after induction of neuropathy, circadian rhythms, seasonal influences, air humidity, influence of order of testing, diet, social variables, housing and manipulation, cage density, sexual activity, external stress factors, and influences of the experimenter. The internal factors are related to the type of animal, its genetic background, gender, age, and the presence of homeostatic adaptation mechanisms to specific situations or stress. In practice, the behavioral presentations to pain depend on the combination of genetic and environmental factors such as accepted social behavior. It also depends on the use of genetic manipulation of the animals such as in transgenic animals. These make the interpretation of data even more difficult. Differences of pain behavior between in- and outbred animals will be better understood by using modern analysis techniques. Substrains of animals with a high likelihood for developing neuropathic pain make the unraveling of specific pathophysiological mechanisms possible. Concerning the effect of stress on pain, it is important to differentiate between external and internal stress such as social coping behavior. The individual dealing with this stress is species sensitive, and depends on the genotype and the social learning. In the future, histo-immunological and genetic analysis will highlight similarities of the different pathophysiological mechanisms of pain between different species and human subjects. The final objective for the study of pain is to describe the genetics of the eliciting pain mechanisms in humans and to look for correlations with the knowledge from basic research. Therefore, it is necessary to know the genetic evolution of the different mechanisms in chronic pain. In order to be able to control the clinical predictability of a putative treatment the evolutionary pharmacogenomic structure of specific transmitters and receptors must be clarified.
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PMID:Internal and external factors affecting the development of neuropathic pain in rodents. Is it all about pain? 1716 29

The mechanisms involved, and possible treatment targets, in orofacial pain due to cancer are poorly understood. The aim of the first of this two-part series is to review the involved pathophysiological mechanisms and explore their possible roles in the orofacial region. However, there is a lack of relevant research in the trigeminal region, and we have therefore applied data accumulated from experiments on cancer pain mechanisms in rodent spinal models. In the second part, we review the clinical presentation of cancer-associated orofacial pain at various stages: initial diagnosis, during therapy (chemo-, radiotherapy, surgery), and in the post-therapy period. In the present article, we provide a brief outline of trigeminal functional neuro-anatomy and pain-modulatory pathways. Tissue destruction by invasive tumors (or metastases) induces inflammation and nerve damage, with attendant acute pain. In some cases, chronic pain, involving inflammatory and neuropathic mechanisms, may ensue. Distant, painful effects of tumors include paraneoplastic neuropathic syndromes and effects secondary to the release of factors by the tumor (growth factors, cytokines, and enzymes). Additionally, pain is frequent in cancer management protocols (surgery, chemotherapy, and radiotherapy). Understanding the mechanisms involved in cancer-related orofacial pain will enhance patient management.
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PMID:Orofacial pain in cancer: part I--mechanisms. 1752 48

Persistent pain after thoracoabdominal esophageal resection is basically unexplored. The aims of the study were to define the character, intensity, and duration of pain with onset following thoracoabdominal esophageal resection and whether this pain syndrome depended on the time elapsed since the operation, the patient's physical function, and level of activity. A questionnaire was constructed that included questions about pain before surgery and at the time of the follow-up as well as the patients' physical function and activity level. The questionnaire was sent to 51 long-term survivors of thoracoabdominal esophageal resection and 46 patients responded. At the follow-up, 20 of the 46 patients had pain in the right shoulder, 17 in the left shoulder, 24 in the rib cage, and 23 in the neck/upper back. Six patients reported severe pain (VAS > 60 mm) in the rib cage. A significantly larger proportion of patients had pain after surgery than before (p < 0.001). No correlation was observed between pain and the time elapsed since surgery, nor was pain related to physical function and activity level (r(s) = 0.120-0.350). Approximately half of the patients who had undergone thoracoabdominal esophageal resection suffered from procedure-related chronic pain. These results indicate the need for focused therapeutic interventions.
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PMID:Procedure-related chronic pain after thoracoabdominal resection of the esophagus. 1992 71

Recent statistics from the World Health Organization indicate that a high percentage of people worldwide suffer from a wide variety of acute or cancer-associated chronic pain. At present, with a few exceptions, the treatment of severe pain relies upon oral administration of the mu-opioid receptor-targeting opiate morphine and its surrogates under strict clinical control. In spite of the powerful in vivo efficacy of these drugs, their long-term use is limited by antinociceptive tolerance, physical dependence, and respiratory depression that evolve. As no analgesics with moderate side effect profiles are currently available for the therapy of different types of pain and stages of cancer, considerable efforts must be made in the search for opiate substitutes. Following the recognition that endogenous peptide ligands of the opioid receptors exert striking effects in various pain models, and with the recent advances in chemical synthesis methods, research interest has steadily moved toward peptide-based compounds as potential opioid analgesics. The endomorphins are an attractive set of endogenous opioid peptides that may meet the requirements of opioid-based pain management. By virtue of their excellent mu-opioid receptor labeling and favorable analgesic properties, these tetrapeptides have gained attention in recent years as potential lead compounds. The ever-increasing number of publications in this field strongly suggests that modified analogues of endomorphins could serve as potent substitutes for opiates, with a lower propensity to induce side effects. This review surveys the main results achieved over the past decade regarding the design, radiolabeling, pharmacological characterization, and structure-activity features of a large body of endomorphin derivatives.
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PMID:Recent advances in endomorphin engineering. 2049 Nov 36

Despite the impact of chronic pain on the quality of life in patients, including changes to affective state and daily life activities, rodent preclinical models rarely address this aspect of chronic pain. To better understand the behavioral consequences of the tissue and nerve injuries typically used to model neuropathic and inflammatory pain in mice, we measured home cage and affective state behaviors in animals with spared nerve injury, chronic constriction injury (CCI), or intraplantar complete Freund's adjuvant. Mechanical hypersensitivity is prominent in each of these conditions and persists for many weeks. Home cage behavior was continuously monitored for 16 days in a system that measures locomotion, feeding, and drinking, and allows for precise analysis of circadian patterns. When monitored after injury, animals with spared nerve injury and complete Freund's adjuvant behaved no differently from controls in any aspect of daily life. Animals with CCI were initially less active, but the difference between CCI and controls disappeared by 2 weeks after injury. Further, in all pain models, there was no change in any measure of affective state. We conclude that in these standard models of persistent pain, despite the development of prolonged hypersensitivity, the mice do not have significantly altered "quality of life." As alteration in daily life activities is the feature that is so disrupted in patients with chronic pain, our results suggest that the models used here do not fully reflect the human conditions and point to a need for development of a murine chronic pain model in which lifestyle changes are manifest.
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PMID:Behavioral indices of ongoing pain are largely unchanged in male mice with tissue or nerve injury-induced mechanical hypersensitivity. 2129 96


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