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11.
Partial 18S rRNA sequences of five chelicerate arthropods plus a
crustacean, myriapod, insect, chordate, echinoderm, annelid, and
platyhelminth were compared. The sequence data were used to infer phylogeny
by using a maximum-parsimony method, an evolutionary-distance method, and
the evolutionary-parsimony method. The phylogenetic inferences generated by
maximum-parsimony and distance methods support both monophyly of the
Arthropoda and monophyly of the Chelicerata within the Arthropoda. These
results are congruent with phylogenies based on rigorous cladistic analyses
of morphological characters. Results support the inclusion of the
Arthropoda within a spiralian or protostome coelomate clade that is the
sister group of a deuterostome clade, refuting the hypothesis that the
arthropods represent the "primitive" sister group of a protostome coelomate
clade. Bootstrap analyses and consideration of all trees within 1% of the
length of the most parsimonious tree suggest that relationships between the
nonchelicerate arthropods and relationships within the chelicerate clade
cannot be reliably inferred with the partial 18S rRNA sequence data. With
the evolutionary-parsimony method, support for monophyly of the Arthropoda
is found in the majority of the combinations analyzed if the coelomates are
used as "outgroups." Monophyly of the Chelicerata is supported in most
combinations assessed. Our analyses also indicate that the
evolutionary-parsimony method, like distance and parsimony, may be biased
by taxa with long branches. We suggest that a previous study's inference of
the Arthropoda as paraphyletic may be the result of (a) having two few
arthropod taxa available for analysis and (b) including long-branched taxa.
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12.
S Vamsee Raju Jody H Tate Sandra KG Peacock Ping Fang Robert A Oster Mark T Dransfield Steven M Rowe 《Respiratory research》2014,15(1):18
Background
Cigarette smoking causes Chronic Obstructive Pulmonary Disease (COPD), the 3rd leading cause of death in the U.S. CFTR ion transport dysfunction has been implicated in COPD pathogenesis, and is associated with chronic bronchitis. However, susceptibility to smoke induced lung injury is variable and the underlying genetic contributors remain unclear. We hypothesized that presence of CFTR mutation heterozygosity may alter susceptibility to cigarette smoke induced CFTR dysfunction. Consequently, COPD patients with chronic bronchitis may have a higher rate of CFTR mutations compared to the general population.Methods
Primary human bronchial epithelial cells derived from F508del CFTR heterozygotes and mice with (CFTR+/-) and without (CFTR+/+) CFTR heterozygosity were exposed to whole cigarette smoke (WCS); CFTR-dependent ion transport was assessed by Ussing chamber electrophysiology and nasal potential difference measurements, respectively. Caucasians with COPD and chronic bronchitis, age 40 to 80 with FEV1/FVC < 0.70 and FEV1 < 60% predicted, were selected for genetic analysis from participants in the NIH COPD Clinical Research Network’s Azithromycin for Prevention of Exacerbations of COPD in comparison to 32,900 Caucasian women who underwent prenatal genetic testing. Genetic analysis involved an allele-specific genotyping of 89 CFTR mutations.Results
Exposure to WCS caused a pronounced reduction in CFTR activity in both CFTR (+/+) cells and F508del CFTR (+/-) cells; however, neither the degree of decrement (44.7% wild-type vs. 53.5% F508del heterozygous, P = NS) nor the residual CFTR activity were altered by CFTR heterozygosity. Similarly, WCS caused a marked reduction in CFTR activity measured by NPD in both wild type and CFTR heterozygous mice, but the severity of decrement (91.1% wild type vs. 47.7% CF heterozygous, P = NS) and the residual activity were not significantly affected by CFTR genetic status. Five of 127 (3.9%) COPD patients with chronic bronchitis were heterozygous for CFTR mutations which was not significantly different from controls (4.5%) (P = NS).Conclusions
The magnitude of WCS induced reductions in CFTR activity was not affected by the presence of CFTR mutation heterozygosity. CFTR mutations do not increase the risk of COPD with chronic bronchitis. CFTR dysfunction due to smoking is primarily an acquired phenomenon and is not affected by the presence of congenital CFTR mutations. 相似文献13.
We investigated the protective effect of vitamin D against liver damage caused by carbon tetrachloride (CCl4). Twenty-four male rats were divided into four equal groups: G1, untreated controls; G2, administered CCl4; G3, administered both CCl4 and vitamin D for 10 weeks; G4, administered CCl4 for 10 weeks and vitamin D for 12 weeks. At the end of experiment, intracardiac blood samples were taken and liver samples were removed. Hepatic damage due to CCl4 was assessed using biochemistry and histopathology. Glutathione (GSH) levels decreased, while malondialdehyde (MDA) levels increased in liver tissues of G2. Alanine transaminase (ALT), alkaline phosphatase (ALP), and gamma-glutamyl-transaminase (GGT) levels increased, while albumin (ALB) levels decreased. Hepatocyte degeneration, lobular disorder, sinusoid dilation, focal necrotic areas, hyperemia, and glycogen loss were observed. Hepatic fibrosis was observed around portal areas and central veins. Bridging fibrous septa were formed between portal veins. By immunohistochemistry, both matrix metalloproteinase-9 (MMP-9) and desmin reactivity were increased. All aspects of liver damage were at least partially prevented in rats treated with vitamin D. Vitamin D appears to act as an antioxidant and anti-fibrotic to protect the rat liver against damage. 相似文献