Magnitude Of Shortening Research Articles

Thick slides dominated by regular-wavelength folds and thrusts in biosiliceous sediments on the Vema Dome offshore of Norway

Three-dimensional seismic reflection data image four submarine slides on the flanks of the Vema Dome in the Vøring Basin. Each one covers an area of ~ 30 km 2, is several hundred metres thick, and hosted in biosiliceous sediments. The topography the upper surface of each slide consists of a series of regular-wavelength arcuate ridges (and associated troughs), perpendicular to the dip of the slope, that correspond to internal fold and thrust structures. Thrusts probably propagated retrogressively based upon the observation that fold amplitudes decrease upslope. The slides lack clearly defined head-scarps, and the magnitude of shortening accommodated by the folding indicates short transport distances. The spatial co-location of the slides on the flanks of the Vema Dome is interpreted as that they were in part initiated due to the increased dip on the flanks of the dome cause by differential uplift during the Late Miocene (6–8 Ma). These slides have three particularly unusual characteristics in comparison to other submarine slides: a relatively low ratio of length to thickness, are dominated by regular spaced folds and thrusts, and short translational distances. We attribute these characteristics to deep detachments that resulted from the inherent ability of biosiliceous sediments to maintain a cohesive framework and resist failure during early burial (burial depths < 75 m).

Congenital Fibular Deficiency

Congenital longitudinal deficiency of the fibula is the most common lower extremity congenital deficiency, with a broad spectrum of severity and subsequent reconstructive treatment. Published classification schemes do not accurately predict reconstructive treatment currently in practice. We reviewed all medical records of patients with a dominant deformity of congenital fibular deficiency who were managed at our institution between 1971 and 2005. We assessed the impact of limb-length inequality, foot deformity, bilateral extremity involvement, and extent of fibular preservation on the treatment of the limb deficiency. One hundred and four patients (including twenty-two with bilateral congenital fibular deficiency) with 126 affected extremities had adequate radiographs to be included in the study. Femoral shortening was noted in seventy (85.4%) of eighty-two patients with unilateral limb involvement. Limb-length discrepancy prior to any treatment remained proportional in forty-seven (82.5%) of fifty-seven patients during an average duration of follow-up of ten years and ten months (range, two years to fifteen years and six months). Limb salvage with foot preservation was deemed feasible in thirty-eight (97.4%) of thirty-nine five-rayed feet, thirty (81.1%) of thirty-seven four-rayed feet, twenty (48.8%) of forty-one three-rayed feet, and one of nine feet having fewer than three rays. Twenty-two (41.5%) of fifty-three limbs with an absent or vestigial fibula were not treated with amputation. Of the twenty-two patients with bilateral fibular deficiency, twelve (54.5%) had preservation of both feet, three (13.6%) had unilateral amputation, and seven (31.8%) had bilateral amputation. We propose a simplified classification for congenital fibular deficiency based on the clinical status of the foot and the magnitude of limb shortening as a percentage of the contralateral limb on radiographs. This classification may be effectively applied in infancy to allow the physician and family to anticipate the extent of deformity at maturity and to estimate the amount of treatment required to reconstruct this limb deformity. This system more accurately predicted the management of patients with fibular deficiency who were managed at our institution over the past three decades .

Reverse Remodeling With Left Ventricular Assist Devices

Over the last 2 decades, numerous advancements in medical therapies have improved patient outcomes in heart failure (HF). However, a significant number of patients still progress to end-stage HF, in which treatment options are largely limited to cardiac transplantation. As patient demands for transplant continue to exceed the supply of available organs, mechanical assist devices—specifically, the left ventricular assist device (LVAD)—were initially introduced as a bridge to cardiac transplantation. LVADs have 2 important beneficial effects. First, LVADs are placed in parallel to the native left ventricle (LV), causing pressure and volume unloading of the LV. Second, LVADs restore cardiac output and subsequent perfusion to the organs. As a result of these 2 effects, it became evident that some patients had actual improvement in LV function after LVAD placement. The term reverse remodeling was used to describe the improvement in myocardial function that was observed in patients with a seemingly end-stage disease. With reverse remodeling, a new hope for the treatment of HF was born—using LVADs as a bridge to recovery; however, to date, this promise has largely been unrealized. This probably is reflective of the fact that the sequela of mechanical ventricular unloading are quite complex and appear to involve the engagement of competing biological pathways including regression of cardiomyocyte hypertrophy as well as progressive cell atrophy. Although the promise of ventricular recovery still persists, its actualization will await a more comprehensive dissection of these competing biological processes. This review will discuss the beneficial clinical effects of LVAD support as well as review what is known about the cellular and molecular response to mechanical unloading and mechanisms of reverse remodeling. Key research findings have been summarized in the Table. View this table: Table. Summary of Research of LVAD Support on Clinical Effects and the Cellular and Molecular Changes That May Contribute to Reverse …

Small-Conductance Calcium-Activated Potassium Channel and Recurrent Ventricular Fibrillation in Failing Rabbit Ventricles

Fibrillation/defibrillation episodes in failing ventricles may be followed by action potential duration (APD) shortening and recurrent spontaneous ventricular fibrillation (SVF). We hypothesized that activation of apamin-sensitive small-conductance Ca(2+)-activated K(+) (SK) channels is responsible for the postshock APD shortening in failing ventricles. A rabbit model of tachycardia-induced heart failure was used. Simultaneous optical mapping of intracellular Ca(2+) and membrane potential (V(m)) was performed in failing and nonfailing ventricles. Three failing ventricles developed SVF (SVF group); 9 did not (no-SVF group). None of the 10 nonfailing ventricles developed SVF. Increased pacing rate and duration augmented the magnitude of APD shortening. Apamin (1 μmol/L) eliminated recurrent SVF and increased postshock APD(80) in the SVF group from 126±5 to 153±4 ms (P<0.05) and from 147±2 to 162±3 ms (P<0.05) in the no-SVF group but did not change APD(80) in nonfailing group. Whole cell patch-clamp studies at 36°C showed that the apamin-sensitive K(+) current (I(KAS)) density was significantly larger in the failing than in the normal ventricular epicardial myocytes, and epicardial I(KAS) density was significantly higher than midmyocardial and endocardial myocytes. Steady-state Ca(2+) response of I(KAS) was leftward-shifted in the failing cells compared with the normal control cells, indicating increased Ca(2+) sensitivity of I(KAS) in failing ventricles. The K(d) was 232±5 nmol/L for failing myocytes and 553±78 nmol/L for normal myocytes (P=0.002). Heart failure heterogeneously increases the sensitivity of I(KAS) to intracellular Ca(2+), leading to upregulation of I(KAS), postshock APD shortening, and recurrent SVF.

Assessing uncertainties in balanced cross sections

Balanced structural cross sections are models that are fit to incomplete data. The models are under-constrained with respect to any particular two-dimensional line-length model, but enough data generally exists to yield a well-constrained area balance solution. Furthermore, the area balance encompasses all possible line-length solutions. Therefore, where the primary objective of section balancing is the determination of horizontal shortening magnitude, area balancing provides an analytical solution. We use this analytical solution to develop a comprehensive, robust analysis of the uncertainty in shortening estimates resulting from cross-section balancing. The analytical solution allows us to propagate errors formally on the input parameters — stratigraphic thicknesses, depth to decollement, eroded hanging wall cutoffs — through the equations and produce the resulting uncertainty on the magnitude of shortening. Balanced cross sections from the Subandean belt of the Central Andes are used to demonstrate the relative importance of stratigraphy and eroded hanging wall cutoffs in the contribution to the overall error.

Building a New Heart From Old Parts

See related article, pages 1374–1386 The prevailing dogma in cardiac biology for almost a century has been that the adult mammalian heart is a terminally differentiated organ. According to this paradigm, a 100-year-old human heart is comprised of a population of cardiomyocytes that are as old as the individual. Over the last decade, work from the laboratory of Piero Anversa and others has challenged this dogma.1 Cardiac biologists are now confronted with an alternative conceptual framework proposing the heart as a dynamic, self-renewing organ, capable of cardiomyocyte turnover throughout life. Heart disease is the leading cause of death in the developed world. A major reason for this is that the adult mammalian heart has limited regenerative capacity following injury. The default healing response to myocyte loss in the adult mammalian heart (eg, following myocardial infarction) involves replacement of myocytes with fibrous, noncontractile scar tissue. The consequent loss of contractile units compromises cardiac function and ultimately leads to heart failure. Absence of regeneration in the adult mammalian heart contrasts with the impressive regenerative potential of lower vertebrates, such as urodele amphibians and teleost fish, which are capable of regenerating significant portions of ventricular myocardium following injury.2,3 Although studies in adult rodents and humans suggest that some myocyte repopulation occurs after myocardial infarction,4,5 this response is clearly limited and incapable of circumventing large-scale myocyte loss, fibrosis, and ultimately organ failure. Cardiomyocyte loss accompanies aging. The heart undergoes a series of structural and morphological changes during normal aging that are characterized by cardiomyocyte loss (through apoptosis, necrosis, and autophagy) and hypertrophy of remaining viable myocytes, as well as interstitial and perivascular fibrosis.6 Aging also renders the heart more susceptible to major cardiovascular events.6 Therefore, studies investigating the physiological turnover and aging of myocytes are …

Late Cenozoic tectonic deformation across the northern foreland of the Chinese Tian Shan

To understand the reactivation and intensified uplift of the Tian Shan range in the Cenozoic, the age of development of the associated series of anticlinal belts formed in the southern and northern foreland basins must be constrained. To estimate the shortening magnitude and rates in the northern foreland basin, we provide here regional structural analysis based on identified growth strata dated with existing magnetostratigraphy, together with balanced cross sections from interpreted seismic data. These results indicate that three paralleled rows of anticlinal belts have developed sequentially from south to north accommodating a total shortening of ∼15 km at the location of the structurally restored seismic section provided here. These three belts present different structural deformational styles with the southern (Qingshuihe) anticline as a basement-involved fold, the middle (Huoerguosi) anticline as a fault-bend fold and the northern (Anjihai) anticline as a fault-propagation fold. Growth strata inferred from seismic profiles start stratigraphically far below growth strata observed on the outcrop. The latter coincide with accelerated folding of the anticlinal belts at ∼6 Ma for the southern, ∼2 Ma for the middle ∼1 Ma for the northern. Our results imply that the northern Tian Shan foreland rates of deformation were lower until late Miocene and increased in more recent times to values in line with GPS-derived rates.

Myocardial adenosine A1-receptor-mediated adenoprotection involves phospholipase C, PKC-ε, and p38 MAPK, but not HSP27

Adenosine via an adenosine A(1) receptor (A(1)R) is a negative feedback inhibitor of adrenergic stimulation in the heart, protecting it from toxic effects of overstimulation. Stimulation of the A(1)R results in the activation of G(i) protein, release of free Gbetagamma-subunits, and activation/translocation of PKC-epsilon to the receptor for activated C kinase 2 protein at the Z-line of the cardiomyocyte sarcomere. Using an anti-Gbetagamma peptide, we investigated the role of these subunits in the A(1)R stimulation of phospholipase C (PLC), with the premise that the resulting diacylglycerol provides for the activation of PKC-epsilon. Inositol 1,4,5-triphosphate release was an index of PLC activity. Chlorocyclopentyl adenosine (CCPA), an A(1)R agonist, increased inositol 1,4,5-triphosphate production by 273% in mouse heart homogenates, an effect absent in A(1)R knockout hearts and inhibited by anti-Gbetagamma peptide. In a second study, p38 MAPK and heat shock protein 27 (HSP27), found by others to be associated with the loss of myocardial contractile function, were postulated to play a role in the actions of A(1)R. Isoproterenol, a beta-adrenergic receptor agonist, increased the Ca(2+) transient and sarcomere shortening magnitudes by 36 and 49%, respectively. In the rat cardiomyocyte, CCPA significantly reduced these increases, an action blocked by the p38 MAPK inhibitor SB-203580. While CCPA significantly increased the phosphorylation of HSP27, this action was inhibited by isoproterenol. These data indicate that the activation of PKC-epsilon by A(1)R results from the activation of PLC via free Gbetagamma-subunits released upon A(1)R-induced dissociation of G(i)alphabetagamma. Attenuation of beta-adrenergic-induced contractile function by A(1)R may involve the activation of p38 MAPK, but not HSP27.

Timing and magnitude of shortening within the inner fore arc of the Japan Trench

New structural data and kinematic modeling provide evidence for Plio‐Quaternary, inner fore‐arc shortening inboard of the Japan Trench, northeastern Honshu, accommodated by the Futaba fault, a high‐angle, basement‐involved fault that bounds the Abukuma massif on the east. Significant throw along the Futaba fault associated with exhumation of the massif is implied by a regionally extensive footwall syncline, the absence of Neogene sediments in the hanging wall, and high relief in the hanging wall adjacent to the fault. Kinematic fault‐related fold modeling best reproduces fold geometry with 2.0–3.1 km of dip slip along a 40°–55° west dipping reverse fault. At the southern tip of the fault, tephra horizons of known age within units that predate and postdate deformation bracket the onset of deformation to 3.95–5.6 Ma and are used to calculate an average slip rate of 0.5–0.7 mm/yr, a throw rate of 0.3–0.5 mm/yr, and a shortening rate of 0.3–0.5 mm/yr. The northeastern Japan subduction zone is viewed as a classic example of an erosive margin, where offshore subsidence records have been used to argue for Neogene basal erosion of the upper plate. Tectonic erosion rates have been estimated from reconstructions of the paleomargin that assume no upper plate deformation and temporally constant fore‐arc taper. Evidence presented here for Neogene fore‐arc shortening, however, suggests that the upper plate is deformable and implies that that offshore subsidence records may reflect a combination of tectonic erosion and upper plate shortening.

Contractile Function is Altered by Regulation of HO-1 Activity in Single Adult Rat Cardiomyocytes

Heme oxygenase-1 (HO-1) is a membrane protein upregulated in response to oxidative stress that confers cardioprotection. The therapeutic potential of HO-1 can be assessed by examining cardiomyocytes survival and function using cobalt protoporphyrin (CoPP) or tin protoporphyrin (SnPP) to increase or inhibit HO-1 activity, respectively. Whether altered HO-1 function affects cardiomyocyte contractility, however, is unknown. Thus, we determined the effects of CoPP (n=11), SnPP (n=15), or PBS (control, n=15) on in vitro single intact adult cardiomyocyte contraction and relaxation using video microscopy and calcium imaging (IonOptix) at 0.5, 1 and 2Hz. At 0.5Hz there was no difference in the rate or magnitude of shortening between groups, and all cells had similar fractional shortening (FS) normalized to peak calcium (FS/Ca2+). FS/Ca2+ was, however, greater at 1Hz and 2Hz in SnPP-treated cells, while CoPP- and PBS-treated cells maintained similar FS/Ca2+ relationships across frequencies (p<0.05). Intriguingly, while SnPP-treated cells increased contraction at faster pacing, only 53% of those cells contracting at 0.5Hz beat synchronously at 1Hz, compared to 100% of CoPP-treated cells and 80% of PBS-treated cells. This difference became more pronounced at 2Hz, as only 26% of SnPP-treated cells and 60% of PBS treated cells able to follow stimulation, while 100% of CoPP-treated cells continued to beat synchronously. Similarly, although time to 90% relaxation was not different between groups at 0.5Hz, it was significantly faster in CoPP- vs. SnPP-treated cells at 2Hz (p<0.05). These results suggest that increasing HO-1 activity via CoPP treatment maintains cell viability under stress, while SnPP- induced HO-1 inhibition reduces survivability at higher pacing frequencies. The mechanisms behind this action are unknown, but may be partially due to HO-1-induced calcium desensitization of the myofilament. Supported by NSF GRFP (SGN) and NIH HL086709 (MA, MR).

Timing and magnitude of shortening within the inner fore arc of the Japan Trench

Timing and magnitude of shortening within the inner fore arc of the Japan Trench

Force depression in single myofibrils

Force depression after active shortening has been observed in different muscle preparations. It has been assumed that force depression is caused by the development of sarcomere length nonuniformities after shortening. However, this hypothesis has never been investigated in a preparation where individual sarcomere lengths could be directly measured. Here, we investigated force depression in single myofibrils (n = 11) and tracked simultaneously the changes in individual sarcomere lengths (n = 60) before, during, and after shortening and after a purely isometric contraction performed at the final length. Shortening produced force depression in all myofibrils (mean +/- SE; 30.9 +/- 3.9%). During shortening, all sarcomeres shortened, but not by the same amount. Sarcomere lengths were nonuniform, with the same mean SD before (0.11 +/- 0.06 microm) and after shortening (0.11 +/- 0.06 microm) and after a purely isometric contraction at the final length (0.10 +/- 0.05 microm). Furthermore, greater shortening magnitudes were found for sarcomeres that were long in the initial isometric configuration. Nonuniformities of half-sarcomere lengths were also the same before (SD = 0.13 microm) and after (SD = 0.14 microm) shortening. We conclude from these results that the development of sarcomere (or half-sarcomere) length nonuniformities does not play a major role in force depression. Rather, force depression seems an intrinsic property of individual (half-) sarcomeres and muscle contraction.

New thermochronometric constraints on the rapid Palaeogene exhumation of the Cordillera Darwin complex and related thrust sheets in the Fuegian Andes

AbstractThermal modelling of new fission‐track and (U–Th–Sm)/He data from the Fuegian Andes reveals rapid cooling (∼12–48 °C Ma−1) during the middle and late Eocene followed by slow cooling (∼1.5 °C Ma−1) to the Recent. We interpret the rapid cooling as a result of exhumation from contractional uplift within the crystalline interior of the orogen. This interpretation is consistent with independent evidence of Eocene shortening, flexural subsidence and provenance changes in the study area, and is approximately coeval with marine geochemical evidence of the onset of Drake Passage opening. In light of the Palaeogene history of Nazca‐South American plate convergence and the differences in shortening magnitudes and exhumation histories between the Fuegian and Patagonian Andes, our data support Eocene development of the Patagonian orocline, which also provides a plausible explanation for early opening of Drake Passage.

Transient lower oesophageal sphincter relaxation in achalasia: everything but LOS relaxation

In conducting clinical high-resolution oesophageal pressure topography (HROPT) studies we observed that after subjects sat upright between series of supine and upright test swallows, they frequently had a transient lower oesophageal sphincter relaxation (TLOSR). When achalasia patients were studied in the same protocol, they exhibited a similar HROPT event leading to the hypothesis that achalasics had incomplete TLOSRs. We reviewed clinical HROPT studies of 94 consecutive non-achalasics and 25 achalasics. Studies were analyzed for a TLOSR-like event during the study and, when observed, that TLOSR-like event was characterized for the degree and duration of distal oesophageal shortening, the degree of LOS relaxation, associated crural diaphragm (CD) inhibition, oesophageal pressurization and upper oesophageal sphincter (UOS) relaxation. About 64/94 (68%) non-achalasics and 15/24 (63%) of achalasics had a pressure topography event after the posture change characterized by a prolonged period of distal oesophageal shortening and/or LOS relaxation. Events among the non-achalasics and achalasics were similar in terms of magnitude and duration of shortening and all were associated with CD inhibition. Similar proportions had associated non-deglutitive UOS relaxations. The only consistent differences were the absence of associated LOS relaxation and the absence of HROPT evidence of reflux among the achalasics leading us to conclude that their events were incomplete TLOSRs. Achalasic patients exhibit a selective defect in the TLOSR response suggesting preservation of all sensory, central and efferent aspects of the requisite neural substrate with the notable exception of LOS relaxation, a function of inhibitory (nitrergic) myenteric plexus neurons.

Constraining neotectonic orogenesis using an isostatically compensated model of transpression

Current models of transpression allow upward flow of material to compensate for shortening in the horizontal plane. We present an isostatically compensated model of transpression, where material is allowed to flow both upwards to create topographic relief and downwards to form a crustal root. Our model also incorporates the effects of erosion to more accurately examine the developing topography in orogenic systems. The modeling results suggest that topographic relief and crustal root thickness developed in transpressional orogens are most dependent on the magnitude of shortening, the initial thickness of the crust, and the density contrast between the crust and mantle. In contrast, the rate of convergence and final width of the deformed zone are relatively unimportant parameters in this model. Application to the Alpine fault system in New Zealand, a well-constrained active transpressional plate boundary, shows good agreement between topography-based model estimates of shortening and those derived from plate reconstructions. Application of our model to the Central Range fault zone in Trinidad suggests 2 ± 1 km of neotectonic shortening. The strain analysis approach presented here may be useful for isolating the effects of modern deformation in a region that has reactivated an ancient contractional belt.

Mechanisms of enhanced arrhythmogenicity of regional ischemia in the hypertrophied heart

The coexistence of cardiac hypertrophy (H) and ischemia (I) can create a particularly arrhythmogenic substrate. Most studies investigate the effects of global I on H. However, global I is not a good surrogate model of the clinical situation. The purpose of this study was to investigate the electrophysiological effects of regional I superimposed on H using optical mapping of membrane voltage. We investigated the guinea pig model of left ventricular H (LVH) induced by suprarenal banding of abdominal aorta. Twelve hearts with or without LVH were mounted in a Langendorff preparation, and regional I was induced by 20 minutes of ligation of the left anterior descending artery. Left ventricle epicardial action potential duration (APD) was significantly prolonged in the LVH group compared with controls. I significantly shortened APD in the I risk zone in both groups, but the percentages of APD shortening (28% vs. 40%) and the magnitudes of shortening (57 +/- 18 vs. 105 +/- 32 ms) were greater in the LVH group. The greater dispersion of repolarization (DR) across the border of the I zone resulted in arcs of functional conduction block and circulating wave fronts. Tachycardia-dependent APD alternans developed more often in the LVH group, and the area of alternans versus the area of the I zone was significantly larger. Ventricular tachyarrhythmias (VTs) developed in all 12 hearts with LVH including six non-self-terminating VTs, compared with four control hearts with self-terminating VT. Regional I superimposed on LVH resulted in greater DR at the border between the I and non-I zones as well as in a greater tendency to develop APD alternans. Both arrhythmogenic mechanisms correlated with an increased incidence of VT.

Paleogene building of the Bolivian Orocline: Tectonic restoration of the central Andes in 2‐D map view

Using available information on the magnitude and age of tectonic shortening, as well as paleomagnetically determined tectonic rotations, we have run a series of 2‐D map view restorations of the central Andes. Neogene shortening in the foreland belt induced only slight orogenic curvature of the central Andes. The constraints on the ages of the large observed fore‐arc rotations (average of 37° counterclockwise in southern Peru and 29° clockwise in northern Chile) indicate that the Bolivian Orocline formed during the Eocene‐Oligocene as a consequence of differential shortening focused in the Eastern Cordillera. To minimize local block rotations along the fore arc, the restoration that best fits the central Andean rotation pattern requires about 400 km of total (Paleogene plus Neogene) shortening near the Arica bend. This value corresponds to the upper bound of estimates of maximum horizontal shortening for the central Andes. Along‐strike variations in horizontal shortening in the back arc induced bending of the continental margin, block rotations with fore‐arc along‐strike extension, and/or orogen‐parallel transport of upper crustal material toward the symmetry axis of the orocline.

Muscular force production after concentric contraction

The steady-state force following active shortening does not reach the maximum isometric force associated with the final length. Isolated extensor digitorum longus and soleus muscles from mice (NMRI strain) were used to investigate the force produced by a muscle, and some parameters hypothetically influencing this shortening-induced force depression. The muscles were pre-stimulated at fixed length, shortened and then held isometrically to give maximum post-shortening forces, before de-stimulation. The shortening magnitude was 0.18, 0.36 or 0.72 mm (about 2–7% of optimal length), time of shortening was chosen as 0.03, 0.06 and 0.12 s, and final length as + 0.72 , 0 and - 0.72 mm , related to optimal length. The mechanical work during active shortening was evaluated by integrating the product of force and shortening velocity over the shortening period. The results show a positive correlation between the force depression and the mechanical work, whereas the force depression was not correlated to the velocity of shortening. Depression of the passive force component was also observed following all stimulations. Experiments show that the fully stimulated redevelopment of isometric force following concentric contraction follows a time function similar to the creation of force when isometric muscle is initially stimulated. The conclusion is that the isometric force development after active shortening can be well described by an asymptotic force which is decided by the produced work, and the initial isometric time constant.

Geometric, kinematic, and erosional history of the central Andean Plateau, Bolivia (15–17°S)

Latitudinal changes in topography, climate, and thrust belt geometry in the central Andes have led to conflicting hypotheses that climate or tectonics exert a first‐order control on orogen evolution. The relative roles of climate and tectonics in the evolution of the Andean orogen are difficult to quantify because of a lack of detailed observations for both the long‐term deformation and erosion history of the Andean fold‐thrust belt. We contribute to the resolution of this problem by presenting a sequentially restored, balanced cross section based on new mapping across the northern Bolivia portion of the thrust belt (15–17°S). The timing and magnitude of exhumation across the cross section are determined by synthesizing 10 new and ∼70 previously published mineral cooling ages. Once balanced and restored, the section was sequentially forward modeled using stratigraphic and cooling age constraints. Results indicate the Eastern Cordillera (EC) records the highest magnitudes of shortening (123 km or 55%). The Interandean zone (IA) has shortened 48 km or 30%. In both the EC and IA individual thrust sheets are tightly folded and have minor offsets of 1–5 km. The Subandes (SA) has multiple levels of detachments allowing for thrust sheets with relatively large offsets (6–17 km). Total shortening in the SA is 66 km or 40%. Total magnitude of shortening for the entire fold‐thrust belt in this region is 276 km (40%). New apatite and zircon fission track cooling ages in conjunction with published ages indicate two phases of rapid exhumation; an earlier phase from ∼40 to 25 Ma in the EC and one prior to ∼25 Ma in the IA, followed by distributed exhumation of the entire fold‐thrust belt from ∼15–0 Ma. Combined exhumation estimates from the balanced cross section and thermochronology suggest ∼9–11 km of exhumation in the EC, ∼5–9 km in the IA, and ∼3–4 km in the SA. Long‐term shortening rates are 7 mm/a for the EC and IA and 4–8 mm/a for the SA. The SA shortening rates are based on a ∼15–0 Ma or 8–0 Ma deformation window. By linking cooling ages to location and magnitude of shortening, we suggest an ∼10–17 Ma pause or a dramatic deceleration in the rate of deformation and propagation of the fold‐thrust belt between 25 and ∼15 or 8 Ma.

Strain and rotation rate from GPS in Tibet, Anatolia, and the Altiplano

Deformation measured by regional GPS networks in continental plateaus reflects the geologic and tectonic variability of the plateaus. For two collisional plateaus (Tibet and Anatolia) and one noncollisional (the Altiplano), we analyze the regional strain and rotation rate by inverting GPS velocities to calculate the full two‐dimensional velocity gradient tensor. To test the method, we use gridded velocities determined from an elastic block model for the eastern Mediterranean/Middle East region and show that to a first order, the deformation calculated directly from the GPS vectors provides an accurate description of regional deformation patterns. Principal shortening and extension rate axes, vertical axis rotation, and two‐dimensional (2‐D) volume strain (dilatation) are very consistent with long‐term geological features over large areas, indicating that the GPS velocity fields reflect processes responsible for the recent geologic evolution of the plateaus. Differences between geological and GPS descriptions of deformation can be attributed either to GPS networks that are too sparse to capture local interseismic deformation, or to permanent deformation that accrues during strong earthquakes. The Altiplano has higher internal shortening magnitudes than the other two plateaus and negative 2‐D dilatation everywhere. Vertical axis rotation changes sign across the topographic symmetry axis and is due to distributed deformation throughout the plateau. In contrast, the collisional plateaus have large regions of quasi‐rigid body rotation bounded by strike‐slip faults with the opposite rotation sense from the rotating blocks. Tibet and Anatolia are the mirror images of each other; both have regions of positive dilatation on the outboard sides of the rotating blocks. Positive dilatation in the Aegean correlates with a region of crustal thinning, whereas that in eastern Tibet and Yunnan province in China is associated with an area of vertical uplift. Rollback of the Hellenic trench clearly facilitates the rotation of Anatolia; rollback of the Sumatra–Burma trench probably also enables rotation about the eastern syntaxis of Tibet.