Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.24.59 (MIP)
 4,906 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In myasthenia gravis (MG) the status of respiratory function has a paramount importance and a careful evaluation is recommended. The weakness of respiratory muscles has been demonstrated in several studies. However, a reliable simple method for the evaluation of this muscular group was lacking until recently, when the usefulness of the maximum respiratory pressures, expiratory (MEP) and inspiratory (MIP), was demonstrated. We evaluated with this method a series of 23 patients with a diagnosis of MG (16 females and 7 males), with a mean age of 46 years (22-68 years), clinically stable and without symptomatic dyspnea. They were distributed in: grade I (5), grade II A (12), and grade II B (6). All of them were evaluated with flow-volume curves, pletysmography, gas transfer, MEP and MIP. The resulting values were then correlated with the expected ones, a reduction greater than one SD being considered as abnormal. The results showed that respiratory function was normal without a restrictive pattern. However, the force of respiratory muscles was reduced in the following proportions of patients in the different groups: grade I: MIP 40%, MEP 60%; in grades II A and II B both MEP and MIP were reduced in 84% of patients. When a statistical comparison with the expected values was carried out it was found that MEP and MIP, considered as a group, were reduced to 53% of the expected values (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Evaluation of respiratory muscle function (maximal respiratory pressures) in myasthenia gravis]. 210 Jan 31

Patients with generalized myasthenia gravis (MG) often have associated ventilatory muscle involvement. It is not known whether patients with isolated ocular muscle involvement have identifiable involvement of their ventilatory muscles. Most studies have assessed muscle involvement by measuring muscle strength; however, we hypothesized that measures of ventilatory muscle endurance may be more sensitive tests of ventilatory muscle involvement in myasthenia gravis. We studied 17 patients with myasthenia gravis (four with ocular involvement alone and 13 with varying degrees of generalized myasthenia gravis). Spirometry, ventilatory muscle strength (maximum inspiratory and expiratory pressures (MIP and MEP)) and endurance (2 min incremental threshold loading test) were measured before and 20 min after i.m. neostigmine. We compared the results with those of 10 normal controls. We found no difference between patients with isolated ocular involvement and controls. Ocular myasthenia gravis patients did not improve after neostigmine. The patients with generalized myasthenia gravis had reduced baseline ventilatory muscle strength (MIP 67 cmH2O (70% of predicted), MEP 86 cmH2O (50% of pred) and endurance (mean maximal load achieved = 246 g, mean pressure at highest load (P) = 19.4 cmH2O) compared with controls. After neostigmine, there was a significant increase in MIP in patients with generalized myasthenia gravis and a trend towards an increased MEP. As a group, the patients with generalized myasthenia gravis did not demonstrate a change in their ventilatory muscle endurance after neostigmine; however, there was considerable interpatient variability in response. We conclude that patients with isolated ocular MG have normal ventilatory muscle strength when tested conventionally.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ventilatory muscle strength and endurance in myasthenia gravis. 758 97

In-situ hybridization with labeled oligonucleotide probes was applied to explore cytokine and chemokine mRNA expression in sections of striated muscle, the target organ in experimental autoimmune myasthenia gravis (EAMG), induced in Lewis rats by immunization with acetylcholine receptor (AChR) and complete Freund's adjuvant (CFA). A transient burst of TNF-alpha, IL-1beta and IL-6 mRNA expressing cells was detected during the early phase of EAMG. This cytokine pattern was related to muscular infiltration of macrophages. Levels of IL-4, IL-10, IFN-gamma, cytolysin and TGF-beta mRNA expressing cells were low and observed mainly during the early phase of EAMG. C-C chemokine RANTES, MCP, MIP-1alpha and MIP-2 mRNA expressing cells were not detected over the course of EAMG. The low and transient expression of cytokines in EAMG muscle tissues suggests that the immune effector responses are unlikely operated by infiltrating cells in muscle. Muscular infiltrations in EAMG are unlikely due to local accumulation of C-C chemokines.
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PMID:Cytokine and chemokine mRNA expressing cells in muscle tissues of experimental autoimmune myasthenia gravis. 987 80

The aim of this study was to examine the association of human autoimmune myasthenia gravis (MG) with two DNA polymorphisms of the chemokine receptors CCR5-Delta 32 and CCR2-64I. CCR2 and CCR5 interact primarily with the human CC family ligands CCL2 (formerly called monocyte chemoattractant protein; MCP-1), CCL3 and CCL4 (macrophage inflammatory protein-1 alpha and -1 beta; MIP-1 alpha/beta), and their main function is to recruit leukocytes from circulation into the tissues, thus playing an important role in human inflammatory disorders. A PCR-based genotyping method was used to determine the genetic variation at the CCR5 gene and an automated real-time Pyrosequencing technology was employed for the analysis of G right curved arrow A point mutation at the CCR2 gene. Results obtained from 158 patients and 272 healthy controls demonstrate no evidence of association between genetic variants of CCR2 and CCR5 with MG and its clinical manifestations. CCR2-64I and CCR5-Delta 32 genotypes are thus unlikely to be involved in protection or predisposition to MG.
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PMID:Genotypes of CCR2 and CCR5 chemokine receptors in human myasthenia gravis. 1453 4