ABSTRACT
AIMS: The present study describes a system based on PCR to distinguish tabtoxin-producing strains of Pseudomonas syringae from other Ps. syringae plant pathogens that produce chlorosis-inducing phytotoxins. METHODS AND RESULTS: Thirty-two strains of Ps. syringae and related species were examined. Two sets of PCR primers were developed to amplify genes (tblA and tabA) required for tabtoxin production. Only a PCR product of 829 bp or 1020 bp was produced in PCR reactions with the tblA or tabA primer sets, respectively, and cells from tabtoxin-producing pathovars of Pseudomonas syringae. All known non-tabtoxin producing bacterial species failed to produce an amplification product with either primer set. CONCLUSIONS: PCR of genes required for tabtoxin production is a simple, rapid and reliable method for identifying tabtoxin-producing strains of Ps. syringae. SIGNIFICANCE AND IMPACT OF THE STUDY: The protocol can effectively distinguish tabtoxin-producing strains of Ps. syringae from other Ps. syringae pathovars and Ps. syringae pv. tabaci strains from other tabtoxin-producing Ps. syringae pathovars.
Subject(s)
Dipeptides/analysis , Genes, Bacterial , Pseudomonas/chemistry , Dipeptides/genetics , Polymerase Chain Reaction , Pseudomonas/geneticsABSTRACT
We studied 143 Pi MZ heterozygous (MZ) subjects from random populations that had been examined previously for alpha 1-antitrypsin phenotype. Each Pi MZ subject was closely matched with a Pi M control subject from the same population at each of 6 centers. An expanded National Heart, Lung and Blood Institute (NHLBI) respiratory symptom questionnaire was completed by each subject. Pulmonary function tests designed to detect established as well as early obstructive airway abnormalities were administered. Multivariate analysis of the variance of data from the questionnaire and pulmonary function tests corrected for age, race, sex, and smoking history showed no significant difference (p less than 0.05) between subjects of Pi MZ and Pi M phenotype. The size of the populations studied and number of observations made for each variable were sufficient to assure that small differences could be detected with 95% power. We conclude that MZ phenotype alone carries no greater risk of developing lung disease than M phenotype.
Subject(s)
Pulmonary Emphysema/genetics , alpha 1-Antitrypsin Deficiency , Adult , Age Factors , Aged , Cross-Sectional Studies , Female , Humans , Male , Middle Aged , Phenotype , Pulmonary Emphysema/epidemiology , Pulmonary Emphysema/physiopathology , Racial Groups , Respiratory Function Tests , Sex Factors , Smoking , alpha 1-Antitrypsin/geneticsSubject(s)
Lung Diseases, Obstructive/complications , Respiratory Function Tests , alpha 1-Antitrypsin Deficiency , Female , Forced Expiratory Volume , Humans , Lung Diseases, Obstructive/diagnosis , Lung Diseases, Obstructive/genetics , Male , Maximal Midexpiratory Flow Rate , Phenotype , Risk , Smoking , Vital CapacitySubject(s)
Lung Diseases/genetics , Phenotype , alpha 1-Antitrypsin Deficiency , Female , Humans , Lung Diseases/epidemiology , Male , Middle Aged , Oklahoma , Respiratory Function Tests , SmokingABSTRACT
Both oral and intravenous TRH produce systematic alterations in brain function of depressive patients as determined by scalp-recorded computerized cerebral biopotentials (computer EEG). The computer EEG (CEEG) profiles of both formulations are not only very similar to each other, but also resemble the CEEG profiles of psychostimulant compounds (Bio-availability). As in CEEG findings, TSH plasma levels also indicate that oral TRH is indeed an active compound. Although some "antidepressive" effects were observed after both formulations, they were not present in every patient, and it was not always the case after repetitive TRH administration, nor were the effects on depressed mood too impressive. On the other hand, in almost all patients certain behavioral effects of TRH were seen which related to "life instincts" and "life performance". The increase of interest, desire and drive for work, food and sex was one of the most striking findings, particularly after intravenous TRH. This may be responsible for the "antidepressive" effects of TRH in patients in whom depression may be the result of an inhibition of "instinctive" functions.
