Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Superprecipitation (SP) of artificial actomyosin, obtained by hybridization of Straub actin from the human myocardium with myosin of normal animal hearts was studied. Actin was prepared from the myocardium of persons who died of congestive heart failure and various non-cardiac diseases, as well as of infants whose death resulted from toxic pneumonia complicated or not with heart failure. It was shown that, in the control hybrid actomyosin, the substitution of normal Straub actin by that from the failing heart resulted in decrease of both the rate and extent of SP. The conclusion was made that both changes in myosin properties and Straub actin underlie the reduced contractility of the myofibrillar protein system in acute and congestive heart failure.
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PMID:Superprecipitation of hybrid actomyosin containing pathologic actin from failing hearts of adults and infants. 402 5

Many patients mechanically ventilated for acute respiratory failure, are treated with medication that includes a combination of cortico-steroids and non-depolarizing neuromuscular-blocking agents (NNBa). A third of them can be expected to develop delayed neuromuscular damage, which may be severe and prolonged. We describe a 50-year-old man who suffered from acute myeloid leukemia and was ventilated due to pneumonia. He was treated with pancuronium and cortico-steroids, and during recovery suffered quadriparesis that lasted several months. Typically this damage is purely motor and is accompanied by absent tendon-reflexes, sometimes with elevated creatine-kinase. Muscle biopsy usually shows deletion and degeneration of thick myosin filaments. The phenomenon is related to the duration of NNBa treatment, and probably results from an adverse synergistic effect on muscle tissue of the cortico-steroids and cortico-steroid-like NNBa given the immobilized patient. Awareness of this adverse effect of steroids and pancuronium, the use of passive mobilization, shortening the use of NNBa and early rehabilitation would minimize disability due to this phenomenon.
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PMID:[Prolonged neuromuscular damage following corticosteroids and muscle relaxants]. 1097 26

Critical Illness Polyneuropathy (CIP) and Myopathy (CIM), either singly or in combination, are a common complication of critical illness. Both disorders may lead to severe weakness and require mechanical ventilation. CIP, as initially described by Bolton et al., in 1984, is a sensorimotor polyneuropathy that is often a complication of sepsis and multiorgan failure. In Japan, Horinouchi et al., first reported a case in 1994. CIM has been referred to by a number of different terms (acute quadriplegic myopathy, thick filament myopathy, acute necrotizing myopathy of intensive care, rapidly evolving myopathy with myosin-deficiency fibers) in the literature. A variety of serious problems (e.g., pneumonia, severe asthma, and lung or liver transplantation) and the concomitant use of high-dose intravenous corticosteroids and nondepolarizing neuromuscular blocking agents predispose to CIM. In Japan, Kawada et al., reported a first case as acute quadriplegic myopathy in 2000. There is no specific treatment for CIP and CIM. Minimizing the use of corticosteroids and nondepolarizing neuromuscular blocking agents in a critical illness setting may prove helpful in preventing the occurrence of these disorders. The prognosis is directly related to the age of the patient and the seriousness of the underlying illness.
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PMID:[Critical illness polyneuropathy and myopathy]. 1515 69

With better survival of critically ill patients, 'de novo' arising neuromuscular complications like critical illness myopathy or polyneuropathy have been increasingly observed. Prolonged hospitalization not only imposes risks like pneumonia or thrombosis on patients but also represents a real budget threat to modern intensive-care medicine. Clinical symptoms like muscle weakness and weaning failure are common to critical illness myopathy and critical illness polyneuropathy and do not allow for distinction. Specific therapies are not yet available, and the quest for the pathomechanisms has proved more complicated than anticipated. Especially for critical illness myopathy, multiple sites of disturbances to the excitation-contraction coupling cascade are possible causes of muscle weakness. The present review summarizes the epidemiological, clinical and diagnostic features of critical illness myopathy and then focuses on current concepts of the presumed pathomechanisms of critical illness myopathy. Sepsis was shown to be a major cause of critical illness myopathy and special emphasis will be placed on how sepsis and inflammatory mediators influence (i) the membrane excitability at the level of voltage-gated ion channels and (ii) the intracellular protein signalling that results in selective loss of myosin protein content and muscle wasting. For (i), critical illness myopathy represents a new type of acquired channelopathy affecting the inactivation properties of Na+ channels. For (ii), both protein proteolysis and protein build up at the transcriptional level seem to be involved. Findings from different studies are put into a common context to propose a model for cytokine-mediated failure of muscle in severe sepsis. This can open a series of new possible trials to test specific therapeutic strategies in the future.
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PMID:Critical illness myopathy: sepsis-mediated failure of the peripheral nervous system. 1828 21

B-1 cells play an important role in the outcome of infection in schistosomiasis, pneumonia and experimental filariasis. However, no information exists regarding status of B-1 cells in clinical manifestations of human filariasis. We investigated the levels of B-1 cells from the total B cells by flow cytometry. Significantly low levels of B-1 cells and IgM antibodies were detected against a wide variety of autoantigens in microfilariae carriers as compared to endemic controls and patients with chronic pathology. A positive correlation was found between IgM antibodies to actin and ss-DNA. Absorption of plasma with soluble actin, myosin and lipopolysaccharides (LPS) resulted in significant removal of antifilarial antibodies. Affinity-purified anti-ss-DNA antibodies were found to be reactive to filarial antigens and various autoantigens. Further, a positive correlation was found between polyreactive antibodies and B-1 cells in filarial-infected human subjects. After antifilarial treatment, levels of IgM antibodies to ss-DNA, actin, LPS and filarial antigen increased significantly indicating a role of polyreactive naturally occurring antibodies in filarial infection. Our findings add to the existing evidence that the B-cell defect in BALB.Xid mice account for susceptibility to murine filarial infection and indicate an important role for these antibodies in providing host protection against filarial infection.
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PMID:Bancroftian filariasis: circulating B-1 cells decreased in microfilaria carriers and correlate with immunoglobulin M levels. 2449 28