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)

CASE. Timmy was born at 32 weeks of gestation after an uncomplicated pregnancy until there was a spontaneous rupture of the membranes and preterm labor associated with chorioamnionitis. A 2-month hospitalization in the neonatal intensive care unit (NICU) was associated with pneumonia, a Grade II intraventricular hemorrhage, chronic lung disease, and a slow weight gain in the nursery. He was discharged to home with plans for ongoing care by his pediatrician. The primary care pediatrician attended a multidisciplinary conference with the NICU staff and Timmy's parents. At the time of discharge from the nursery, at 38 weeks postconceptual age, Timmy still required oral diuretics and supplemental oxygen, as well as other medications such as iron. Timmy's respiratory rates were between 40 and 60 breaths per minute at rest, with mild intercostal retractions. He was discharged with a cardiorespiratory monitor. The discharge examination revealed mild to moderate symmetrical hypotonia with intact deep tendon reflexes, shoulder girdle weakness, and a mild head lag. Timmy would regard a human face and a bright object and would follow them briefly. He became active and would thrash his extremities with minimal tactile, bright light, or auditory stimulation. Typically, he settled slowly with swaddling and a pacifier. Nursing was slow to develop; he was currently receiving one half of his calories at the breast and the remainder of his calories from bottle-feeding of fortified expressed breast milk. As she prepared for the first office visit with Timmy and his parents, the pediatrician asked herself, "What can I do to enhance the developmental outcome for this child?"
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PMID:"What can I do to enhance the development of a premature infant with chronic lung disease?". 1079 83

In recent years the greatest progress in our understanding of pneumoconioses, other than those produced by asbestos, silica, and coal, has been in the arena of metal-induced parenchymal lung disorders. Inhalation of metal dusts and fumes can induce a wide range of lung pathology, including airways disorders, cancer, and parenchymal diseases. The emphasis of this update is on parenchymal diseases caused by metal inhalation, including granulomatous disease, giant cell interstitial pneumonitis, chemical pneumonitis, and interstitial fibrosis, among others. The clinical characteristics, epidemiology, and pathogenesis of disorders arising from exposure to aluminum, beryllium, cadmium, cobalt, copper, iron, mercury, and nickel are presented in detail. Metal fume fever, an inhalation fever syndrome attributed to exposure to a number of metals, is also discussed. Advances in our knowledge of antigen-specific immunologic reactions in the lung are particularly evident in disorders secondary to beryllium and nickel exposure, where immunologic mechanisms have been well characterized. For example, current evidence suggests that beryllium acts as an antigen, or hapten, and is presented by antigen-presenting cells to CD4+ T cells, which possess specific surface antigen receptors. Other metals such as cadmium and mercury induce nonspecific damage, probably by initiating production of reactive oxygen species. Additionally, genetic susceptibility markers associated with increased risk have been identified in some metal-related diseases such as chronic beryllium disease and hard metal disease. Future research needs include development of biologic markers of metal-induced immunologic disease, detailed characterization of human exposure, examination of gene alleles that might confer risk, and association of exposure data with that of genetic susceptibility.
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PMID:Inorganic dust pneumonias: the metal-related parenchymal disorders. 1093 87

Pasteurella haemolytica serovar A1 is the causative agent of acute fibrinohemorrhagic pneumonia also known as shipping fever. Many pathogens, including P. haemolytica, survive in their respective hosts through the up-regulation of an iron acquisition system. In this study we identified, purified and characterized a 35-kDa periplasmic iron-regulated protein. The N-terminal sequence of the iron-regulated protein ANEVNVYSYRQP YLIEPMLK was identical to the deduced amino acid sequence of the ferric binding protein, FbpA, of P. haemolytica. Growth of P. haemolytica in a synthetic medium (RPMI-1640), without iron and supplemented with 50 gM 2,2' dipyridyl, facilitated the expression, isolation and purification of the native P. haemolytica FbpA. The protein was purified to homogeneity by using ammonium sulfate precipitation followed by CM-Sepharose ion exchange chromatography. SDS-PAGE showed a single band with a molecular weight of 35,369. Isoelectric focusing showed multiple bands with pIs of 5.5, 5.6, 5.8, and one major band with pI of 6.4. The molecular weight obtained by electrospray mass spectrometry was 35,822. Equilibrium velocity ultracentrifugation established that the protein existed as a monomer under native conditions with an apparent molecular weight of 33,795. Analysis of secondary structure of FbpA by circular dichroism showed 42.1% alpha helical structure. This protein is the second periplasmic iron-regulated protein described for P. haemolytica.
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PMID:Purification and characterization of the Pasteurella haemolytica 35 kilodalton periplasmic iron-regulated protein. 1106 79

Malnutrition increases morbidity and mortality and affects physical growth and development, some of these effects resulting from specific micronutrient deficiencies. While public health efforts must be targeted to improve dietary intakes in children through breast feeding and appropriate complementary feeding, there is a need for additional measures to increase the intake of certain micronutrients. Food-based approaches are regarded as the long-term strategy for improving nutrition, but for certain micronutrients, supplementation, be it to the general population or to high risk groups or as an adjunct to treatment must also be considered. Our understanding of the prevalence and consequences of iron, vitamin A and iodine deficiency in children and pregnant women has advanced considerably while there is still a need to generate more knowledge pertaining to many other micronutrients, including zinc, selenium and many of the B-vitamins. For iron and vitamin A, the challenge is to improve the delivery to target populations. For disease prevention and growth promotion, the need to deliver safe but effective amounts of micronutrients such as zinc to children and women of fertile age can be determined only after data on deficiency prevalence becomes available and the studies on mortality reduction following supplementation are completed. Individual or multiple micronutrients must be used as an adjunct to treatment of common infectious diseases and malnutrition only if the gains are substantial and the safety window sufficiently wide. The available data for zinc are promising with regard to the prevention of diarrhea and pneumonia. It should be emphasized that there must be no displacement of important treatment such as ORS in acute diarrhea by adjunct therapy such as zinc. Credible policy making requires description of not only the clinical effects but also the underlying biological mechanisms. As findings of experimental studies are not always feasible to extrapolate to humans, the biology of deficiency as well as excess of micronutrients in humans must continue to be investigated with vigour.
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PMID:Micronutrient deficiency in children. 1150 11

Mannheimia haemolytica (previously known as Pasteurella haemolytica) is a weakly hemolytic, gram-negative coccobacillus that is an opportunistic pathogen of cattle, sheep and other ruminants. In stressed, immunocompromised animals, the organism causes a fibrinous, necrotic pneumonia, commonly called "shipping fever". In the United States, economic losses due to shipping fever pneumonia surpass the combined cost of all other diseases of cattle. M. haemolytica, which is a member of the family Pasteurelleaceae, includes twelve serotypes (A1, A2, A5-A9, A12-14, A16 and A17) based on capsular antigen typing. Worldwide, serotypes A1 and A2 predominate, though all serotypes can cause disease. Serotype A1 causes pasteurellosis in cattle and has been the subject extensive study, while serotype A2 causes disease in sheep and is less-well characterized. Potential virulence factors of M. haemolytica have been identified and characterized by gene cloning and DNA sequence analysis. These factors include a ruminant-specific leukotoxin, an anti-phagocytic capsule, lipopolysaccharide, iron-regulated outer membrane proteins, lipoproteins, a sialoglycoprotease, a neuraminidase and two potential immunoglobulin proteases. Unlike the well-characterized leukotoxin, little is known about the expression of these other virulence factors. Attempts to dissect the mechanisms of M. haemolytica pathogenesis have been hindered by the lack of a robust genetic system for mutation of the organism, though new tools for genetic manipulation of M. haemolytica have been developed. Expression plasmids and operon fusion plasmids have been created and a series of antibiotic resistance cassettes useful for site-specific recombination have been constructed. It is anticipated that use of these tools for gene expression and mutagenesis, in combination with the soon to be released genomic sequence of a serotype A1 organism, will aid in understanding the molecular mechanisms of pathogenesis of M. haemolytica and will help to drive development of new vaccines to prevent shipping fever.
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PMID:Molecular genetic analysis of virulence in Mannheimia (pasteurella) haemolytica. 1153 7

The leukotoxin of Mannheimia haemolytica is an important virulence factor that contributes to much of the pathology observed in the lungs of animals with bovine shipping fever pneumonia. We believe that identification of factors that regulate leukotoxin expression may provide insight into M. haemolytica pathogenicity. The DNA sequence upstream of the leukotoxin operon is divergently shared by P(lapT), which transcribes an arginine permease gene. The intergenic region contains several elements that are potential sites for transcriptional modulation of the promoters. We have developed plasmid-borne chloramphenicol acetyltransferase (cat) operon fusions, as well as lktC::cat chromosomal fusions, to study transcription initiation in M. haemolytica. Using these genetic tools, we have identified cis-acting sequences and environmental conditions that modulate transcription of the leukotoxin and lapT promoters. By deletion analysis, promoters were shown to rely on sequences upstream of their -10 and -35 regions for full activity. Direct repeats of the sequence TGT-N(11)-ACA and a static bend region caused by phased adenine tracts were necessary for full activation of P(lkt). A computer-generated model of the promoter's structure shows how DNA bending brings the repeat sequences within close proximity to the P(lkt) RNA polymerase, and we hypothesize that these repeats are a binding site for an activator of leukotoxin transcription. The lktC::cat operon fusion was also used to demonstrate that, like that of other RTX toxins, leukotoxin transcription is environmentally regulated. Roles for iron deprivation and temperature change were identified.
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PMID:Use of operon fusions in Mannheimia haemolytica to identify environmental and cis-acting regulators of leukotoxin transcription. 1155 65

We describe here a case report of a patient with acute lymphocytic leukemia in whom hepatic gallium-67 (Ga-67) uptake was suppressed. The patient was hospitalized with increasing dyspnea. In Ga-67 scintigraphy, there was no hepatic uptake, although other physiological uptake was clearly observed. In addition, the scintigraphy showed increased accumulation in the right lung consistent with infection. We considered possible reasons for these findings. The patient had no history of chemotherapy or blood transfusion, and his iron metabolism was almost normal. He was not receiving any medication which might reduce hepatic blood flow. Blood chemistry suggested normal hepatic and renal function. The patient died from pneumonia 6 weeks later. The autopsy revealed extensive infiltration of the right lung with Bacillus cereus (B. cereus). Metabolic acidosis and/or iron utilization of B. cereus may induce both increased Ga-67 accumulation in the infected lesion and suppressed uptake in the liver, but these mechanisms could not explain normal physiological uptake in the other organs. This case warranted the further study of the hepatic Ga-67 uptake mechanism.
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PMID:Inexplicable suppression of hepatic uptake of gallium-67, a case report. 1157 65

Although iron supplementation is considered beneficial for groups at risk for anemia, concern has been raised that it could be harmful during human immunodeficiency virus (HIV) infection. Studies suggest: (1) faster HIV disease progression in thalassemia major patients receiving inadequate doses of iron-chelating drug; (2) higher mortality among patients receiving iron supplementation with dapsone compared with aerosolized pentamidine for prophylaxis against Pneumocytis carinii pneumonia; (3) higher iron stores and mortality among patients with haptoglobin Hp 2-2 phenotype; and (4) shorter survival among patients with high bone marrow iron deposition. These studies largely involved men in developed countries. Among HIV-infected pregnant women in Africa with a high prevalence of iron deficiency, no relationship was found between indicators of iron status and HIV disease severity. The available data do not contraindicate the current practice of iron supplementation in developing countries where there is a high prevalence of both HIV infection and iron deficiency.
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PMID:Iron supplementation during human immunodeficiency virus infection: a double-edged sword? 1160 73

In June 2000, the WHO warned that the level of resistance to drugs used to treat common infectious diseases is now reaching a crisis point. If world governments do not control infections better in order to slow down the development of drug resistance, entire populations could be wiped out by superbugs against which there is no efficient treatment. Development of resistance is due to both underuse and overuse of drugs, and strategies have been worked out, to slow down the development of resistance for instance by the Norwegian Ministry of Health and Social Affairs. The present article deals with an old principle, mainly developed behind the Iron Curtain, which is now attracting renewed attention in the west: the application of bacterial viruses (bacteriophages) in the fight against bacteria. According to clinical trials in Eastern Europe, mostly uncontrolled, phages have been used successfully in treatments against antibiotic-resistant bacteria, for instance in suppurative wound infections, gastroenteritis, sepsis, osteomyelitis and pneumonia. These encouraging data are supported by recent findings in well-controlled animal models demonstrating that phages can rescue animals from a variety of fatal infections. The present review discusses possible advantages and limitations of phage treatment in humans.
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PMID:[Bacteria-killing viruses, Stalinists and "superbugs"]. 1187 46

The impact of laser therapy in the multimodality treatment for pneumonia on the serum levels of trace elements and microcirculation was studied. A total of 105 patients with pneumonia were examined. The patients were divided into 2 groups: 1) 68 patients received laser therapy and 2) 37 patients took drug therapy alone. There was a more substantial reduction in the permeability of cellular membranes, a significant increase in the serum levels of iron and chromium, better circulation at the expense of a vascular component. The above changes highly correlated with laboratory data and external respiratory function parameters.
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PMID:[Serum concentrations of trace elements and microcirculation during laser therapy for pneumonia]. 1189 97


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