Mid-ocean ridge unfaulting revealed by magmatic intrusions.

Mid-ocean ridges (MORs) are quintessential sites of tectonic extension1-4, at which divergence between lithospheric plates shapes abyssal hills that cover about two-thirds of the Earth's surface5,6. Here we show that tectonic extension at the ridge axis can be partially undone by tectonic shortening across the ridge flanks. This process is evidenced by recent sequences of reverse-faulting earthquakes about 15 km off-axis at the Mid-Atlantic Ridge and Carlsberg Ridge. Using mechanical models, we show that shallow compression of the ridge flanks up to the brittle failure point is a natural consequence of lithosphere unbending away from the axial relief. Intrusion of magma-filled fractures, which manifests as migrating swarms of extensional seismicity along the ridge axis, can provide the small increment of compressive stress that triggers reverse-faulting earthquakes. Through bathymetric analyses, we further find that reverse reactivation of MOR normal faults is a widely occurring process that can reduce the amplitude of abyssal hills by as much as 50%, shortly after they form at the ridge axis. This 'unfaulting' mechanism exerts a first-order influence on the fabric of the global ocean floor and provides a physical explanation for reverse-faulting earthquakes in an extensional environment.

The spreading rate dependence of the distribution of axial magma lenses along mid-ocean ridges.

Seismically imaged axial melt lenses (AMLs) are seen almost everywhere along the axis of fast-spreading ridges but at only a few localized segment centers on slow-spreading ridges. Standard models assuming that AMLs form when melt percolating upward pools where freezing produces an impermeable cap do not explain this fundamental observation. To tackle this long-standing problem, we combine a crustal density model and a thermal model with a recent mechanical model for sill formation. The mechanical model predicts that AMLs form below the axial lithosphere but only if the average density of the axial brittle lithosphere is not greater than the magma density. For standard thermal models, crustal density structures inferred from seismic velocity data and normal crustal thicknesses, AMLs are found to be stable along all of a ridge segment for spreading rates greater than about 50 mm/y. To explain slow-spreading observations, we assume that a share of the melt produced by the mantle upwelling all along a segment is focused to the segment center. Some of this melt partially crystallizes, releasing latent heat, before the evolved magma flows along the axis to build the crust away from the segment center. This "extra" heat, beyond what is supplied by the magma that builds the crust near the segment center, results in the lithosphere thin enough for stable melt lenses at the segment center. Our results are consistent with observations and offer a quantitative explanation of the marked difference in the distribution of AMLs along fast- versus slow-spreading centers.

Correlation of OPN gene expression with proliferation and apoptosis of ovarian cancer cells and prognosis of patients.

Correlation of osteopontin (OPN) gene expression with proliferation and apoptosis of ovarian cancer cells and prognosis of patients was investigated. The expression levels of OPN in 81 pairs of ovarian cancer tissues and para-carcinoma tissues obtained via surgical resection were detected using immunohistochemistry (IHC). The correlation of OPN protein expression with clinicopathological features of patients was analyzed. All patients were followed up for 3 years. The disease-free survival (DFS) and overall survival (OS) curves of patients in high/low OPN expression groups were drawn using the Kaplan-Meier method. The expression levels of OPN in normal ovarian epithelial IOSE80 cells and 5 ovarian cancer cell lines were detected via western blotting. Moreover, two cell lines with high OPN expression were interfered with lentiviral transfection technique. The effects of OPN on ovarian cancer cell proliferation and apoptosis were detected and analyzed via Cell Counting Kit-8 (CCK8) assay and flow cytometry. The positive expression rate of OPN protein in tumor tissues was higher than that in para-carcinoma tissues (P<0.05). Survival curves suggested that both DFS and OS in OPN negative group were superior to those in OPN positive group (P<0.05). Results of western blotting showed that OPN was weakly expressed in IOSE80 cells, whereas it was highly expressed in SKOV-3, COC1, A2780, HO-8910 and OVCAR-3 cells, among which the OPN protein expression levels were relatively higher in SKOV-3 and OVCAR-3 cell lines. After knockdown of OPN gene with sh-OPN, the cell proliferation rates of OVCAR-3 and SKOV-3 were significantly decreased from 48 h (P<0.05), but the apoptosis level was increased remarkably (28.2 vs. 1.3% and 25.3 vs. 3.2%), and differences were statistically significant (P<0.05). In conclusion, overexpression of OPN enhances the proliferation of ovarian cancer cells, which is an adverse factor for patient survival and prognosis.

Exercise test on the patients with normokalaemic periodic paralysis from a Chinese family with a mutation in the SCN4A gene.

BACKGROUND: Normokalaemic periodic paralysis (normoKPP) is characterized by transient and recurrent myoasthenia, and some patients also show muscle stiffness induced by cold exposure (paramyotonia congenita, PMC). It is caused by a mutation in the muscle voltage gated sodium channel alpha subunit (SCN4A) gene. Due to the diversity of the clinical manifestations of patients, it is difficult for clinicians to differentiate some of patients with atypical normoKPP from those who suffer from other periodic paralysis and nondystrophic myotonia. So far, for normoKPP there are almost no ways to assist definite diagnosis besides genetic screening. This research was designed to evaluate an exercise test (ET) in confirming the diagnosis of normoKPP and in assessing the therapeutic effectiveness of some drugs on this disease. METHODS: ET, described by McMains, was performed on six subjects from a Chinese family, including four patients with overlapping disease of normoKPP and PMC caused by a mutation of SCN4A Met1592Val that is identified by genetic analysis and two normal control members. The change of compound muscle action potential (CMAP) was recorded. Besides the family, two patients were also tested during treatments with acetazolamide. RESULTS: All patients showed a slight increase in CMAP immediately after exercise, followed by an abnormal gradual decline, which reached its nadir 25-30 minutes after exercise. CMAP amplitude dropped by more than 40% in patients but less than 23% in controls. In the patients who received treatment with acetazolamide, the change of CMAP amplitude was less than 28% and, at any fixed times, less than pretreatment values. CONCLUSIONS: The ET may be used as a predictive, easy and reliable method of diagnosing normoKPP under conditions without genetic screening help, and is an objective way to evaluate the therapeutic effectiveness. According to different response patterns, the ET may also be helpful in reducing the scope of genetic screening.