q fever/phosphatase

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Neutrophile alkaline phosphatase changes in tularemia, sandfly fever, Q fever and noninfectious fevers.

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Acute Q fever pneumonia: a review of 80 hospitalized patients.

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OBJECTIVE To emphasize epidemiologic, clinical, or radiologic characteristics whose detection could lead to an early diagnosis and to enhance therapeutic efficacy. METHODS Eighty hospitalized patients from 1982 to 1996. METHODS The diagnosis of Q fever infection was serologically confirmed in all

Ribosomal protein phosphorylation induced during Q fever or by lipopolysaccharide: in vitro translation is stimulated by infected liver ribosomes.

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Q fever, as well as the lipopolysaccharide prepared from the rickettsial agent Coxiella burnetii, stimulates the phosphorylation of guinea pig liver ribosomal protein S6. In vitro mRNA and ribosome-dependent rabbit reticulocyte lysate translation systems reconstituted with ribosomes and mRNAs from

Coxiella burnetii acid phosphatase inhibits the release of reactive oxygen intermediates in polymorphonuclear leukocytes.

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Coxiella burnetii, the etiological agent of Q fever, is a small, Gram-negative, obligate intracellular bacterium. Replication of C. burnetii during infection has been shown to be increased by decreasing oxidative stress using p47(phox -/-) and iNOS(-/-) mice in vivo and by pharmacologic inhibitors

[Liver involvement in Q fever and Mediterranean boutonneuse fever. Comparative study].

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Rickettsia spp. infections produce hepatic damage with transaminases elevation and biological signs of cholostasis. Classical biochemical tests of hepatic function were analyzed and compared in 8 patients with Q Fever (QF) and 7 with Boutonneuse Mediterranean Fever (BMF). Liver enlargement was

Phosphorylation-dephosphorylation of nuclear proteins during infection (Q fever).

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The proposal that gene expression may be regulated by phosphorylation of nonhistone chromatin proteins was tested by studying increased transcription resulting from Q fever. Certain liver nuclear phosphoprotein kinase and phosphatase activities were altered after guinea pigs were infected with

Pathophysiologic features of Q fever-infected guinea pigs.

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Guinea pigs infected with 9-mile phase I strain of Coxiella burnetii had increased blood glucose concentrations; alkaline phosphatase (ALP), glutamic-oxalacetic transaminase (GOT), alpha-hydroxybutyrate dehydrogenase (alpha-HBDH), and creatine phosphokinase (CPK) activities; and bilirubin value.

Acid phosphatase activity in Coxiella burnetii: a possible virulence factor.

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High-speed supernatant fluids derived from sonicated Coxiella burnetii contained considerable acid phosphatase activity when assayed by using 4-methylumbelliferylphosphate; they also contained a factor that blocked superoxide anion production by human neutrophils stimulated with formyl-Met-Leu-Phe.

Chemical and biochemical changes in subcellular fractions of guinea pig liver during infection with Coxiella burneti.

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Livers of uninfected guinea pigs and of guinea pigs infected with Coxiella burneti were fractionated into smooth endoplasmic reticulum, rough endoplasmic reticulum (RER), pellet, and cell sap fractions. The ribonucleic acid (RNA) and protein of each fraction were determined, and the phosphorylase,

A Coxiella burnetii gene encodes a sensor-like protein.

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Two-component regulatory systems play important roles in the adaptive responses of many bacteria to environmental changes. The sensor proteins of these systems are highly conserved near their C-termini. We exploited this feature to isolate a gene encoding a putative sensor component from the

Coxiella burnetii exhibits morphological change and delays phagolysosomal fusion after internalization by J774A.1 cells.

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Coxiella burnetii, the etiological agent of Q fever, is an obligate intracellular bacterium proliferating within the harsh environment of the phagolysosome. Mechanisms controlling trafficking to, and survival of pathogens within, the phagolysosome are unknown. Two distinct morphological variants

Systemic infections affecting the liver. Some cause jaundice, some do not.

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The patient who has clinical jaundice, abnormal results on liver function tests, or both presents a difficult diagnostic challenge. Many infectious diseases affect the liver, and the extent of involvement determines the degree of clinically apparent jaundice. Some diseases that affect the liver

Enzyme-linked immunosorbent fluorescence assay and high-pressure liquid chromatography for analysis of humoral immune responses to Coxiella burnetti proteins.

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A microtiter enzyme-linked immunosorbent fluorescence assay based on alkaline phosphatase conjugate and 4-methylumbelliferyl phosphate as fluorogenic substrate was developed and adapted to quantitatively analyze immunoglobulin G subclass 1 (IgG1) and IgG2 responses of vaccinated and infected cattle

The liver in boutonneuse fever.

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Hepatic lesions were studied for the first time in 13 cases of boutonneuse fever (Mediterranean exanthematous fever). The glutamic-oxalacetic transaminases were raised in eight patients, the glutamic-pyruvic transaminases showed an increase in 10 patients, alkaline phosphatases in seven of the 10

Molecular pathogenesis of Coxiella burnetii in a genomics era.

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The agent of acute and chronic Q fever, Coxiella burnetii, occupies a unique niche among intracellular pathogens. The mechanisms the organism employs to cause disease are unclear but involve persistence in a parasitophorous vacuole and the subsequent host response. Studies designed to model

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