Observations of rift and rifted margin architecture suggest that significant spatial and temporal structural heterogeneity develops during the multiphase evolution of continental rifting. Inheritance ...is often invoked to explain this heterogeneity, such as preexisting anisotropies in rock composition, rheology, and deformation. Here, we use high‐resolution 3‐D thermal‐mechanical numerical models of continental extension to demonstrate that rift‐parallel heterogeneity may develop solely through fault network evolution during the transition from distributed to localized deformation. In our models, the initial phase of distributed normal faulting is seeded through randomized initial strength perturbations in an otherwise laterally homogeneous lithosphere extending at a constant rate. Continued extension localizes deformation onto lithosphere‐scale faults, which are laterally offset by tens of km and discontinuous along‐strike. These results demonstrate that rift‐ and margin‐parallel heterogeneity of large‐scale fault patterns may in‐part be a natural byproduct of fault network coalescence.
Key Points
Distributed normal fault networks develop from randomized initial strength perturbations
Rifted margin heterogeneity develops through fault network localization
Nontypeable Haemophilus influenzae (NTHi) causes acute exacerbation of chronic obstructive pulmonary disease (AECOPD). IL-17A is central for neutrophilic inflammation and has been linked to COPD ...pathogenesis.
We investigated whether IL-17A is elevated in NTHi-associated AECOPD and required for NTHi-exacerbated pulmonary neutrophilia induced by cigarette smoke.
Experimental studies with cigarette smoke and NTHi infection were pursued in gene-targeted mice and using antibody intervention. IL-17A was measured in sputum collected from patients with COPD at baseline, during, and after AECOPD.
Exacerbated airway neutrophilia in cigarette smoke-exposed mice infected with NTHi was associated with an induction of IL-17A. In agreement, elevated IL-17A was observed in sputum collected during NTHi-associated AECOPD, compared with samples collected before or after the event. NTHi-exacerbated neutrophilia and induction of neutrophil chemoattractants over the background of cigarette smoke, as observed in wild-type mice, was absent in Il17a(-/-) mice and in mice treated with a neutralizing anti-IL-17A antibody. Further studies revealed that IL-1 receptor (R)1 signaling was required for IL-17A-dependent neutrophilia. Moreover, deficiency or therapeutic neutralization of IL-17A did not increase bacterial burden or delay bacterial clearance.
IL-17A is induced during NTHi-associated AECOPD. Functionally, IL-1R1-dependent IL-17A is required for NTHi-exacerbated pulmonary neutrophilia induced by cigarette smoke. Targeting IL-17A in AECOPD may thus be beneficial to reduce neutrophil recruitment to the airways.
Dysfunctional innate responses of alveolar macrophages to nontypeable Haemophilus influenzae, Moraxella catarrhalis and Streptococcus pneumoniae contribute to morbidity in chronic obstructive ...pulmonary disease (COPD). Our earlier studies discovered impaired COPD alveolar macrophage responses to Toll-like receptor (TLR) ligands of nontypeable H. influenzae and provide rationale for further evaluation of TLR signaling. While the role of TLR single nucleotide polymorphisms is increasingly recognized in inflammatory diseases, TLR single nucleotide polymorphisms in COPD have only recently been explored. We hypothesized that specific TLR polymorphisms are associated with dysfunctional innate immune COPD alveolar macrophage responses and investigated polymorphisms of TLR2(Arg753Gln), TLR4(Thr399Ile; Asp299Gly), and TLR9(T1486C; T1237C).
DNA was purified from cells of 1) healthy nonsmokers (n = 20); 2) COPD ex-smokers (n = 83); 3) COPD active smokers (n = 93). DNA amplifications (polymerase chain reaction) were performed for each SNP. Alveolar macrophages from each group were incubated with nontypeable H. influenzae, M. catarrhalis and S. pneumoniae. Cytokine induction of macrophage supernatants was measured and the association with TLR single nucleotide polymorphism expression was determined.
No significant inter-group differences in frequency of any TLR SNP existed. However both TLR9 single nucleotide polymorphisms were expressed in high frequency. Among COPD ex-smokers, diminished IL-8 responsiveness to nontypeable H. influenzae, M. catarrhalis and S. pneumoniae was strongly associated with carriage of TLR9(T1237C) (p = 0.02; p = 0.008; p = 0.02), but not TLR9(T1486C). Carriage of TLR9(T1237C), but not TLR9(T1486C), correlated with diminished FEV1%predicted (p = 0.037).
Our results demonstrate a notable association of TLR9(T1237C) expression with dysfunctional innate alveolar macrophage responses to respiratory pathogens and with severity of COPD.
Extensional systems evolve through different stages due to changes in the rheological state of the lithosphere. It is crucial to distinguish ductile structures formed before and during rifting, as ...both cases have important but contrasting bearings on the structural evolution. To address this issue, we present the illustrative ductile‐to‐brittle structural history of a metamorphic core complex (MCC) onshore and offshore western Norway. Combining geological field mapping with newly acquired 3‐D seismic reflection data, we correlate two distinct onshore basement units (BU1 and BU2) to corresponding offshore basement seismic facies (SF1 and SF2). Our interpretation reveals two 40 km wide domes (one onshore and one offshore), which both show characteristic kilometer‐scale, westward plunging upright folds. The gneiss domes fill antiformal culminations in the footwall of a >100 km long, shallowly west dipping, extensional detachment. Overlying Caledonian nappes and Devonian supradetachment basins occupy saddles of the hyperbolic detachment surface. Devonian collapse of the Caledonian orogen formed dome and detachment geometries. During North Sea rifting, brittle reactivation of the MCC resulted in complex fault patterns deviating from N‐S strike dominant at the eastern margin of the rift. Around 61°N, only minor N‐S faults (<100 m throw) cut through the core of the MCC. Major rift faults (≤5 km throw), on the other hand, reactivated the detachment and follow the steep flanks of the MCC. This highlights that inherited ductile structures can locally alter the orientation of brittle faults formed during rifting.
Plain Language Summary
The mechanical behavior of the lithosphere largely determines the style of crustal deformation. Therefore, many areas go successively through different modes of extension. In the case of a thick and warm crust, extension can form ductile domes below low‐angle normal faults, so‐called metamorphic core complexes (MCCs). Onshore West Norway, we observe a MCC formed during Devonian collapse of the Caledonian orogen. Offshore, new 3‐D seismic data reveal a second dome underneath rift basins in the northern North Sea. Both domes are connected through a 100 km long extensional high strain zone, which formed during Caledonian collapse. The combination of ductile and brittle processes formed a deformation zone with nonplanar geometry, which consists of a series of domes and saddles. About 140 Myr later, Permian‐Triassic rifting formed large normal faults, which exploited the inherited weakness of the deformation zone. This brittle reactivation resulted in strongly deviating rift fault orientations around 61°N.
Key Points
Field and 3‐D seismic data constrain Devonian metamorphic core complex onshore West Norway and underneath the northern North Sea rift
Onshore‐offshore correlation reveals 100 km long detachment with nonplanar geometry
Brittle reactivation of steep detachment segments strongly deviated Permian‐Triassic rift fault orientations around 61°N
Moraxella catarrhalis causes approximately 10% of exacerbations in chronic obstructive pulmonary disease (COPD) and also colonizes the lower airway in stable patients. Little is known about the ...effects of colonization by M. catarrhalis on airway inflammation and protease-antiprotease balance, and how these changes compare to those seen during exacerbations. Since COPD is a progressive inflammatory disease, elucidating the effects of bacterial colonization and exacerbation on airway inflammation is relevant to understanding disease progression in COPD. Our aims were (1) Analyze changes in airway inflammation in colonization and exacerbation of COPD due to M. catarrhalis; (2) Explore protease-antiprotease balance in colonization and exacerbation due to M. catarrhalis. Our hypothesis were (1) Acquisition of a new strain of M. catarrhalis in COPD increases airway inflammation from baseline and alters the protease-antiprotease balance towards a more proteolytic environment; (2) These changes are greater during exacerbations associated with M. catarrhalis as compared to colonization.
Thirty-nine consecutive COPD patients with 76 acquisitions of a new strain of M. catarrhalis over a 6-year period were identified in a prospective study. Seventy-six pre-acquisition sputum supernatant samples, obtained just before acquisition of M catarrhalis, and 76 acquisition samples (34 were associated with exacerbation, 42 with colonization) were analyzed for IL-8, TNF-alpha, Neutrophil Elastase (NE) and Secretory leukocyte protease inhibitor (SLPI). Changes were compared in paired samples from each patient.
IL-8, TNF-alpha and NE were significantly elevated after acquisition of M. catarrhalis, compared to pre-acquisition samples (p =< 0.001 for all three). These changes were present in colonization (p = 0.015 for IL-8; p =< 0.001 for TNF-alpha and NE) as well as in exacerbation (p =< 0.001 for all three), compared to pre-acquisition levels. SLPI was significantly lower after acquisition (p =< 0.001), in colonization (p =< 0.001) as well as in exacerbation (p = 0.004), compared to pre-acquisition levels. SLPI levels correlated negatively with NE levels (R2 = 0.07; p = 0.001).
Acquisition of M. catarrhalis in COPD causes increased airway inflammation and worsening protease-antiprotease imbalance during exacerbations and also in colonization, even in the absence of increased symptoms. These effects could contribute to progression of airway disease in COPD.
Vibrio cholerae was found to have two sets of genes encoding TonB, ExbB and ExbD proteins. The first set (tonB1, exbB1, exbD1) was obtained by complementation of a V. cholerae tonB mutant. In the ...mutant, a plasmid containing these genes permitted transport via the known V. cholerae high‐affinity iron transport systems, including uptake of haem, vibriobactin and ferrichrome. When chromosomal mutations in exbB1 or exbD1 were introduced into a wild‐type V. cholerae background, no defect in iron transport was noted, indicating the existence of additional genes that can complement the defect in the wild‐type background. Another region of the V. cholerae chromosome was cloned that encoded a second functional TonB/Exb system (tonB2, exbB2, exbD2). A chromosomal mutation in exbB2 also failed to exhibit a defect in iron transport, but a V. cholerae strain that had chromosomal mutations in both the exbB1 and exbB2 genes displayed a mutant phenotype similar to that of an Escherichia coli tonB mutant. The genes encoding TonB1, ExbB1, ExbD1 were part of an operon that included three haem transport genes (hutBCD), and all six genes appeared to be expressed from a single Fur‐regulated promoter upstream of tonB1. A plasmid containing all six genes permitted utilization of haem by an E. coli strain expressing the V. cholerae haem receptor, HutA. Analysis of the hut genes indicated that hutBCD, which are predicted to encode a periplasmic binding protein (HutB) and cytoplasmic membrane permease (HutC and HutD), were required to reconstitute the V. cholerae haem transport system in E. coli. In V. cholerae, the presence of hutBCD stimulated growth when haemin was the iron source, but these genes were not essential for haemin utilization in V. cholerae.
Shear zones are common strain localization structures in the middle and lower crust and play a major role during orogeny, transcurrent movements and rifting alike. Our understanding of crustal ...deformation depends on our ability to recognize and map shear zones in the subsurface, yet the exact signatures of shear zones in seismic reflection data are not well constrained. To advance our understanding, we simulate how three outcrop examples of shear zones (Holsnøy - Norway, Cap de Creus - Spain, Borborema - Brazil) would look in different types of seismic reflection data using 2-D point-spread-function (PSF)-based convolution modelling, where PSF is the elementary response of diffraction points in seismic imaging. We explore how geological properties (e.g. shear zone size and dip) and imaging effects (e.g. frequency, resolution, illumination) control the seismic signatures of shear zones. Our models show three consistent seismic characteristics of shear zones: (1) multiple, inclined reflections, (2) converging reflections, and (3) cross-cutting reflections that can help interpreters recognize these structures with confidence.
•2-D seismic images of three large-scale shear zones observed in the field.•Dependency of seismic images on frequency, illumination, dip and aspect ratio.•Typical features are: (1) inclined, (2) merging, and (3) cross-cutting reflections.•Reflection junctions indicate shear zone kinematics.•Findings will help interpreters identify and map shear zones in seismic reflection data.
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