Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0006277 (bronchitis)
 6,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A workshop in which 17 practicing scientists participated was intended to address primarily people who use or could use biotechnology in their work and was confined to five techniques. Endonuclease fingerprinting and mapping involved cleaving nucleic acid with a specific restriction enzyme and separating the nucleic acid fragments by electrophoresis. Field and vaccine isolates of Pasteurella multocida could be distinguished; Salmonella enteritidis could be divided into three groups; chlamydia could be grouped into seven groups; and vaccinia, quail pox, and fowl pox could be clearly distinguished. Preparation of nucleic acid probes involved producing large amounts of labeled oligonucleotides, usually of unknown sequence. Successful probes had been made for infectious bursal disease virus, avian influenza virus, Newcastle disease virus, and infectious bronchitis virus. In Southern, Northern, and dot blotting, either DNA or RNA fragments were placed on or transferred to a solid substrate and probed. The procedure was able to detect infectious bursal disease virus, infectious bronchitis virus, Mycoplasma gallisepticum, and Marek's disease virus. In situ hybridization involved applying a labeled probe to frozen or fixed sections or to intact cells. In Polymerase chain reaction, two primers, some distance apart, were annealed to a denatured target DNA. Repeated cycles of DNA synthesis with a thermostable polymerase, denaturing, and reannealing resulted in great amplification of a rare sequence. After 30 cycles, a rare gene sequence could be amplified more than 10(6) times. It was used successfully to detect minute quantities of influenza virus and infectious bursal disease virus, and the process was used to facilitate DNA sequencing of coccidiosis gene segments.
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PMID:Practical application of nucleic acid techniques to avian disease problems. 255 97

Totals of 58,661,000 acute respiratory disease (ARD) cases, 1,376,651 bronchitis and pneumonia complications, and 93,042 deaths from influenza, bronchitis, pneumonia or chronic pulmonary affection were notified during 11 years of ARD surveillance from 1975 to 1986. All ARD seasons started with the first phase in September-December; this increase in morbidity was caused chiefly by adenoviruses, parainfluenza viruses, rhinoviruses and M. pneumoniae. Second wave of ARD morbidity occurring in January-April used to be explosive and was associated with an influenza epidemic in 9 of the 11 seasons; only in 1978/79 and 1984/85 the ARD epidemics were caused by adenoviruses and especially RSV, the share of influenza being minimal. Pneumonia and bronchitis excesses occured during epidemics caused by M. pneumoniae in 1975/76, 1980/81 and 1985/86. Particularly high mortality excesses occurred in 1976, 1977 and 1983 during epidemics elicited by a new drift variants of influenza A(H3N2). Identification of viral agent of M. pneumoniae attempted in 5474 ARD cases was successful at 37.4%. The respective contributions of parainfluenza viruses, adenoviruses, influenza A virus and RSV to overall aetiologically identified morbidity were 14.2, 13.9, 13.8, and 12.0%. Mixed infections (2-3 agents identified simultaneously) accounted for 14.6% of cases. Type B influenza virus, rhinoviruses, enteroviruses and herpes simplex virus contributed only by 5.6-7.8%. In ordinary seasons the share of M. pneumoniae in aetiologically identified ARD morbidity was 0.6-3.8%; this agent displayed predominance at 5-year cycles, when accounting for 20.5-38.9% of cases. The most frequently detected agents in individual age groups were as follows: in preschool children parainfluenza (18.6%), RSV (16.6%), and adenoviruses (17.4%); in school children M. pneumoniae (26%), influenza A and B (10.2 and 14.7% respectively), and adenoviruses (10.7%); in adolescents and young adults influenza type A (20.2%), M. pneumoniae (15.0%), and rhinoviruses (13.3%); in adults above 25 years age influenza A virus (38%), and other respiratory viruses at a frequency lower than 10% each.
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PMID:Occurrence and aetiology of acute respiratory diseases: results of a longterm surveillance programme. 256 74

The aim of this study was to determine the viral agents associated with acute lower respiratory infections (ALRI) in young children. During a 2-yr period, 204 nasopharyngeal aspirates (NPA) from children under 4 yr of age living in an orphanage and exhibiting febrile ALRI were studied by both indirect immunofluorescence (IIF) and isolation in four cell lines. NPA cell smears as well as tissue culture cells exhibiting cytopathic effect (CPE) or hemadsorption were stained by IIF for respiratory syncytial virus (RSV), adenovirus, influenza A and B, and parainfluenza 1 and 3. Viral etiology was demonstrated in 21.2% of acute respiratory infection cases. The most frequently detected virus was RSV (53.5% of viral positive diagnoses), followed by unidentified viruses (18.6%), adenovirus (13.9%), influenza A (7%), and parainfluenza 3 (4.7%). The most common clinical entities were: bronchitis, 46.1%; pneumonia, 24%; bronchiolitis, 22%; and multifocal pneumonia, 8%. Malnourishment was found in 56% of children with ALRI, whereas 50% was found among total orphanage population. The 3 to 8-month-old age group accounted for half of all ALRI cases. Viral etiology was shown for 26.5% of patients with pneumonia, 22% with bronchitis, and 16% with bronchiolitis. RSV and adenovirus occurred in fall and winter, while parainfluenza 3 was detected in early spring. In the two fatal cases observed, histologic lesions were compatible with adenovirus infection, but this virus could be isolated from the lung in only one case.
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PMID:Viral etiology in acute lower respiratory infections in children from a closed community. 267 3

A study was undertaken to examine 320 patients with seasonal fevers occurred in June to September. These included fever of unknown etiology, acute respiratory virus diseases, pneumonias, bronchitis, enterovirus diseases, and serous meningitis. Serological tests revealed that in 20 (6.3%) of them the viruses of the complex in California encephalitis (Tyagin's virus or antigenically related virus) contributed to the etiology of the disease. Major clinical symptoms of the disease were defined in this group of patients. The disease appeared as neuroinfections (serous meningitis), influenza-like conditions (fever, symptoms of intoxication), occasionally, infiltrative changes in the lung. Thus, the viruses of the antigen complex of California encephalitis makes an etiological contribution to infectious abnormalities.
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PMID:[Significance of viruses of antigen complex of California encephalitis in pathology]. 268 61

Data are given on the changes in the hemostatic system in 42 patients with uncomplicated influenza and in complications (pneumonia, bronchitis, aggravation of ischemic heart disease). In the acute period of the disease they were characterized by hypercoagulation which was most pronounced in patients with influenza complicated by pneumonia. In cases of aggravation of ischemic heart disease functional platelet activity during convalescence decreases but the plasma link of hemostasis remains activated and fibrinolytic blood activity inhibited. Functional platelet activity in dynamics of the disease increases which should be taken into consideration in pathogenetic therapy.
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PMID:[Hemostatic changes in various clinical courses of influenza]. 277 42

The authors submit an aetiological and epidemiological analysis of the influenza epidemic which occurred in the CSR between the 4th and 14th week of 1986 and was caused by the influenza virus subtype A/H3N2/ and type B. The epidemic affected a total of 27.1% of the population, in the age group of 0-5 years 63.7%, in the age group 6-14 years 52.7% and in the age group above 15 years 17.1%. In the course of the epidemic 77,458 cases of pneumonia and bronchitis were reported and 1,412 deaths with the diagnosis influenza, bronchitis, pneumonia and chronic affection of the lungs. The authors analyze also specific indicators of the activation of influenza viruses and reach the conclusion that serological evidence of the circulation of influenza viruses in the population was detected already in the third quarter of 1985, the first isolations were made six weeks before the influenza epidemic. Activation of the influenza viruses is indicated already during the pre-epidemic period by some non-specific indicators which include the rising number of patients with acute respiratory affections in surgeries and the rising number of children absent from nurseries and nursery schools on account of these diseases. The most sensitive non-specific indicator is the rising number of patients with respiratory diseases in surgeries of the First aid medical service.
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PMID:[Specific and nonspecific indicators of activation of influenza viruses before an epidemic caused by influenza viruses subtype A/H3N2 and type B in Czechoslovakia in 1986]. 292 Mar 98

Respiratory specimens and blood were collected from all infants and children admitted with acute respiratory illness to a paediatric unit in Christchurch from May to November (late autumn, winter and spring) 1983, to define the viral aetiological agents involved. A virus or Mycoplasma pneumoniae was identified in 160 (50%) of 317 children studied by the rapid indirect immunofluorescence, virus culture and/or serological techniques. Aetiological agents were detected in 71% of children with bronchiolitis, 57% with pneumonia, 53% with bronchitis, 40% with laryngotracheitis (croup), and 45% with upper respiratory tract illness. Respiratory syncytial virus was the most frequently identified virus, confirming the importance of this virus as a cause of respiratory illness requiring hospitalisation of young children in Christchurch. An epidemic due to influenza A/Dunedin/7/83 (HINI) and A/New Caledonia/4/83 (HINI) viruses occurred during the study period.
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PMID:Acute respiratory tract infections of children in hospital: a viral and Mycoplasma pneumoniae profile. 299 30

Oligonucleotide-directed mutagenesis was used to construct chimeric cDNAs that encode the extracellular and transmembrane domains of the vesicular stomatitis virus glycoprotein (G) linked to the cytoplasmic domain of either the immunoglobulin mu membrane heavy chain, the hemagglutinin glycoprotein of influenza virus, or the small glycoprotein (p23) of infectious bronchitis virus. Biochemical analyses and immunofluorescence microscopy demonstrated that these hybrid genes were correctly expressed in eukaryotic cells and that the hybrid proteins were transported to the plasma membrane. The rate of transport to the Golgi complex of G protein with an immunoglobulin mu membrane cytoplasmic domain was approximately sixfold slower than G protein with its normal cytoplasmic domain. However, this rate was virtually identical to the rate of transport of micron heavy chain molecules measured in the B cell line WEHI 231. The rate of transport of G protein with a hemagglutinin cytoplasmic domain was threefold slower than wild type G protein and G protein with a p23 cytoplasmic domain, which were transported at similar rates. The combined results underscore the importance of the amino acid sequence in the cytoplasmic domain for efficient transport of G protein to the cell surface. Also, normal cytoplasmic domains from other transmembrane glycoproteins can substitute for the G protein cytoplasmic domain in transport of G protein to the plasma membrane. The method of constructing precise hybrid proteins described here will be useful in defining functions of specific domains of viral and cellular integral membrane proteins.
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PMID:Cytoplasmic domains of cellular and viral integral membrane proteins substitute for the cytoplasmic domain of the vesicular stomatitis virus glycoprotein in transport to the plasma membrane. 301 9

The lateral mobility of the vesicular stomatitis virus spike glycoprotein (G protein) and various mutant G proteins produced by site-directed mutagenesis of the G cDNA has been measured. Fluorescence recovery after photobleaching results for the wild type G protein in transfected COS-1 cells yielded a mean diffusion coefficient (D) of 8.5 (+/- 1.3) X 10(-11) cm2/s and a mean mobile fraction of 75% (+/- 3%). Eight mutant proteins were also examined: dTM14, lacking six amino acids from the transmembrane domain; TA2, lacking an oligosaccharide in the extracellular domain; QN2, possessing an extra N-linked oligosaccharide in the extracellular domain; CS2, possessing a serine instead of a cysteine at residue 489 in the cytoplasmic domain, preventing palmitate addition to the glycoprotein; TMR-stop, lacking the entire cytoplasmic domain except an arginine at residue 483; and three chimeric proteins, G mu, G23, and GHA, containing in place of the 29 amino acid wild type cytoplasmic domain the cytoplasmic domains from the surface IgM from the spike protein of the infectious bronchitis virus or from the hemagglutinin protein of the influenza virus, respectively. The mean D for the mutant proteins varied over a relatively small range, with the slowest mutant, G23, exhibiting a value of 11.3 (+/- 1.4) X 10(-11) cm2/s and the fastest mutant, GHA, having a D of 28.6 (+/- 4.5) X 10(-11) cm2/s. The mean mobile fraction similarly varied over a small range, extending from 55 to 68%. None of the mutations resulted in the more rapid diffusion characteristic of membrane proteins embedded in artificial bilayers. Therefore, it appears that the cytoplasmic and transmembrane domains themselves contribute little to restraining the lateral mobility of this integral membrane protein when expressed in transfected cells.
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PMID:Effects of mutations in three domains of the vesicular stomatitis viral glycoprotein on its lateral diffusion in the plasma membrane. 303 31

Virological and immunological studies on 53 patients with chronic obstructive bronchitis at the clinical stage of fading exacerbation were conducted. A high percentage of active viral infection (43%), persistence of viruses (25%) and virus-specific components (ribonucleoprotein in influenza) in the cells of brush biopsy bronchial mucosa specimens was characteristic for these patients. The respiratory-syncytial virus was the most common persisting virus (11%). A high percentage of association (72%) of respiratory viruses (influenza, adenoviruses) and pneumonia Mycoplasma contributed to an increase in a period of an infective process. The utmost decrease in indices of cellular immunity (natural killer cell activity, T-cell and phagocytosis function) was detected in a group of patients with a prolonged (over 4 months) virus persistence.
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PMID:[Characteristics of viral infections in patients with chronic obstructive bronchitis]. 311 90


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