Spatiotemporal trafficking of HIV in human plasmacytoid dendritic cells defines a persistently IFN-α–producing and partially matured phenotype
Meagan P. O’BrienOlivier ManchesRachel Lubong SabadoSonia Jimenez BarandaYaming WangI. MarieLinda RolnitzkyMartin MarkowitzDavid M. MargolisDavid LevyNina Bhardwaj
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Objective
To classify the high-resolution CT (HRCT) phenotypes of COPD, and to investigate the clinical characteristics of various phenotypes and the relationship with airway inflammation.
Methods
Chest HRCT and pulmonary function tests were performed in 84 COPD patients. The patients were classified into 3 phenotypes according to the visual HRCT findings. Exhaled breath condensate was gathered from 30 patients and the interleukin (IL)-6 level was measured by ELISA.
Results
The COPD patients were classified into 3 phenotypes: Phenotype A, absence of emphysema, with or without bronchial wall thickening (n=34); Phenotype E, emphysema without bronchial wall thickening (n=23); and Phenotype M, emphysema with bronchial wall thickening (n=27). The 3 phenotypes of COPD showed different characteristics in several aspects. Patients with phenotype A showed a higher body mass index [(25.1±4.4) kg/m2vs phenotype E (22.5±4.1) kg/m2 and phenotype M (21.3±3.4) kg/m2,F=6.732, P<0.01]. The prevalence of patients with milder dyspnea was lower in phenotype A compared with others (15/34) vs phenotype E (2/23) and phenotype M (6/27), χ2 =9.097, P<0.05. The patients who complained of severe expectoration in phenotype E were fewer than those in other groups (0/23) vs phenotype A (2/34) and phenotype M (4/27), χ2=8.702, P<0.05. The FEV1/FVC and FEV1% in phenotype M [(53±14)% and (51±25)%] were significantly lower as compared with those in other phenotypes [ (67±11)% and (72±24)% in phenotype A, and (53±14)% and (52±26)% in phenotype E], F=10.252, F=6.508, P<0.01. The ratio of inspiratory capacity to total lung capacity (IC/TLC) in phenotype A was higher [phenotype A (41±17)%, phenotype E (33±13)%, phenotype M (28±13)%, F=5.964, P<0.01], while the ratio of residual volume to total lung capacity (RV/TLC) was lower [phenotype A (37±9)%, phenotype E (44±10)%, phenotype M (45±8)%, F=6.954, P<0.01]. Patients with different phenotypes showed various levels of IL-6 in exhaled breath condensate [phenotype A (19.9±6.3) ng/L, phenotype E (16.7±2.1) ng/L, phenotype M (25.6±4.4) ng/L, F=7.749, P<0.01].
Conclusion
Various morphological phenotypes of COPD based on HRCT showed different clinical characteristics and airway inflammation.
Key words:
Pulmonary disease, chronic obstructive; Tomography, X-ray computed; Respiratory function tests; Interleukin-6
Air trapping
Clinical phenotype
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The envelope (E) glycoprotein of JEV is the major antigen to elicit neutralizing antibody (NAb) against JEV infection. In order to develop a rapid and safe neutralization assay system for evaluation of the JEV vaccine strains, we constructed JEV-pseudotyped viruses with JEV env genes (Nakayama-NIH, Beijing-1). The titers of JEV-pseudotyped viruses with NK and BJ strains were 4.0×104 IFU/ml and 1.3×105 IFU/ml in Vero cell cultures, respectively. We have analyzed the neutralization activity of immunized mouse sera with JEV-NK and JEV-BJ pseudotyped viruses. The neutralizing antibody titers of NK and BJ (50% reduction of virus) were about 1:10,000 at each immunized sera. Compared with conventional plaque reduction neutralization test (PRNT), the method using JEV-pseudotyped virus has desirable advantages such as more rapid, easier, and non-biohazardous. This neutralization assay system might be useful to evaluate NAb activity against JEV vaccine strains or vaccine candidates.
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In two brothers treated for severe pulmonary emphysema, was demonstrated an alpha-1-antitrypsin deficiency associated with a ZZ phenotype (Pi system). The authors carried out a genetic study of the family including 60 members spread over 4 generations. In all, were demonstrated 4 subjects of phenotype ZZ, 29 of phenotype MZ, 3 of phenotype MS ; one subject had a phenotype SZ and 23 members of this family had normal levels of alpha-1-antitrypsin and were of phenotype MM. The disease was transmitted in all cases as an autosomic codominant. The interest of a study of the phenotype in alpha-1-antitrypsin deficiency is emphasized together with the practical steps to be taken on discovery of a subject with the allele responsible for a reduction in serum levels of alpha-1-antitrypsin.
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Summary 1. Many organisms respond to threats such as stress and predation by expressing a defended phenotype (phenotypic plasticity) or inducing the expression of a defended phenotype in offspring (transgenerational phenotypic plasticity). While defended phenotypes can increase resistance to a predator or stress, in the absence of the inducing agent defended phenotypes often have poorer performance. Producing a defended phenotype unnecessarily has been termed a phenotype‐environment mismatch. 2. Most studies have focused on the benefits of a defended phenotype along a single environmental gradient (i.e. the presence/absence of the inducing agent) but in nature, organisms must face conditions that vary across a number of environmental gradients simultaneously. By focusing on the costs and benefits of a defended phenotype in a single dimension alone we risk underestimating the strength and likelihood of phenotype‐environment mismatches. 3. For the marine bryozoan Bugula neritina , we examined the performance of individuals with an induced, defended phenotype (pollution resistance) relative to individuals with an undefended phenotype across a number of different environments. We found that individuals with the defended phenotype were more sensitive to osmotic stress, but surprisingly, were less susceptible to predation than individuals with the undefended phenotype. 4. Our findings suggest that the costs and benefits associated with expressing a defended phenotype are more complex than previously realized because the full consequences of induced phenotypes are only unmasked when performance in multiple environments is examined.
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ABSTRACT . In an earlier note in Science the authors described a multizoned, six-phenotype system of rabbit serum esterases and showed that the atropinesterase and cocainesterase activity of rabbit serum are properties of that system. Phenotypes A and AF exhibited both activities. Phenotypes F, P, and S exhibited cocainesterase activity alone, whereas the serum of rabbits of phenotype M was incapable of hydrolyzing either substrate. Isozyme zone A, found only in phenotypes A and AF, is synonymous with atropinesterase. Isozyme zone S, common to phenotypes A, AF, F, P, and S, but lacking in phenotype M, is synonymous with cocainesterase.
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Inbred strain
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Phenotypes exhibited by microorganisms can be useful for several purposes, e.g., ethanol as an alternate fuel. Sometimes, the target phenotype maybe required in combination with other phenotypes, in order to be useful, for e.g., an industrial process may require that the organism survive in an anaerobic, alcohol rich environment and be able to feed on both hexose and pentose sugars to produce ethanol. This combination of traits may not be available in any existing organism or if they do exist, the mechanisms involved in the phenotype-expression may not be efficient enough to be useful. Thus, it may be required to genetically modify microorganisms. However, before any genetic modification can take place, it is important to identify the underlying cellular subsystems responsible for the expression of the target phenotype.In this paper, we develop a method to identify statistically significant and phenotypically-biased functional modules. The method can compare the organismal network information from hundreds of phenotype expressing and phenotype non-expressing organisms to identify cellular subsystems that are more prone to occur in phenotype-expressing organisms than in phenotype non-expressing organisms. We have provided literature evidence that the phenotype-biased modules identified for phenotypes such as hydrogen production (dark and light fermentation), respiration, gram-positive, gram-negative and motility, are indeed phenotype-related.Thus we have proposed a methodology to identify phenotype-biased cellular subsystems. We have shown the effectiveness of our methodology by applying it to several target phenotypes. The code and all supplemental files can be downloaded from (http://freescience.org/cs/phenotype-biased-biclusters/).
Model Organism
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We describe the second patient with the de novo p.Arg377Trp variant in ACTL6A (Actin-like 6A) (MIM#604958) and a phenotype reminiscent a disorder of the BRG1-associated factor (BAF) complex, including dysmorphic facies and acral malformations. So far, only three patients with ACTL6A variants and neurodevelopmental delay have been reported but the specific p.Arg377Trp mutation seems to correlate with a distinctive phenotype well-fitting a BAFopathy, which lacks in individuals carrying different mutations. This could suggest an emergent genotype-phenotype correlation among the ACTL6A-related phenotype.
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Pedigree chart
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