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Introduction: The heterocyclic compound 4‐hydroxy‐(2,2,6,6‐Tetramethylpiperidin‐1‐yl)oxyl (TEMPOL) has a protective effect on neurological function in brain tissues damaged by ischemia and hypoxia. This study explored the effects of TEMPOL pretreatment on postoperative cognitive function in aged rats under sevoflurane anesthesia, focusing on inflammatory response and oxidative stress. Methods: Sixty male rats were divided into normal control (C), sevoflurane anesthesia (S), TEMPOL pretreatment (T), and sevoflurane anesthesia + TEMPOL pretreatment (ST) groups (15 per group). Groups T and ST rats received continuous intraperitoneal TEMPOL (100 mg/kg) for 3 days, while groups C and S rats were injected with 0.9% saline. After pretreatment, groups S and ST received 3% sevoflurane anesthesia. Results: Rats in group S exhibited a longer swimming distance, longer escape latency, lower frequency of platform crossing, and shorter dwell time in the targeted quadrant than those in groups C and T. Rats in group ST exhibited a shorter swimming distance, shorter escape latency, higher frequency of platform crossing, and longer dwell time in the targeted quadrant than those in group S. The expressions of interleukin‐6, tumor necrosis factor‐α, inducible nitric oxide synthase, and Ym1/2 messenger ribonucleic acid were higher in groups S and ST rats than in groups C and T rats and lower in group ST rats than in group S rat (p <.05). Superoxide dismutase (SOD), total antioxidant capacity (T‐AOC), and glutathione peroxidase (GSH‐Px) were lower, while malondialdehyde (MDA) was higher in groups S and ST rats than in groups C and T rats (p <.05). Group ST showed higher SOD, T‐AOC, and GSH‐Px, and lower MDA than group S (p <.05). Conclusions: TEMPOL pretreatment attenuated postoperative cognitive impairment induced by sevoflurane anesthesia in aged rats. This may be attributed to the downregulation of NR2B‐CREB‐BDNF pathway, reducing the inflammatory response and oxidative stress damage in hippocampal tissue. [ABSTRACT FROM AUTHOR]

Oceanic transform faults connect spreading centers and are imprinted with previous tectonic events. However, their tectonic interactions are not well understood due to limited observations. The Discovery transform fault system at 4°S, East Pacific Rise (EPR), represents a young transform system, offering a unique opportunity to study the interplay between faulting and other tectonic events at an early phases of an oceanic transform system. Discovery regularly hosts M5–6 characteristic earthquakes, and the seafloor north of Discovery includes a 35 km‐long rift zone that records a complex history of rifting, faulting and volcanism, suggesting that the transform faults likely interact with regional tectonic activity. We apply a machine‐learning enabled workflow to locate 21,391 earthquakes recorded during a 1‐year ocean bottom seismometer experiment in 2008. Our results indicate that seismicity on the western Discovery fault is separated into seven patches with distinct aseismic and seismic slip modes. Additionally, we observe a patch of off‐fault seismicity near where seafloor abyssal hills intersect the rift zone. This seismicity may have been caused by varying opening rates as spreading rate decreases from north to south in the rift zone. Our findings suggest that the Discovery system is still evolving, and that system equilibrium has not been reached between rifting and faulting. These results reflect the complex yet rarely observed interactions between fault slip, plate rotation, and rifting which are likely ubiquitous at oceanic transform systems. Plain Language Summary: Oceanic transform faults are major plate boundaries connecting mid‐ocean ridges. Despite their important role in plate tectonics, their interactions with adjacent mid‐ocean ridges and surrounding oceanic plates are not well understood. The Discovery transform fault system at 4°S, East Pacific Rise, is a young oceanic transform system formed approximately 1 My ago, offering a unique opportunity to study the interplay between faulting and other tectonic events at an early phase of an OTF. Discovery faults have quasi‐periodical magnitude (M) 5–6 earthquakes. Using ocean bottom seismometer data recorded over 1 year, we find that seismicity of the western Discovery fault can be grouped into seven patches, indicating division of alternating slip modes that either releases tectonic strain by M > 5 earthquakes or creep steadily. North of the western Discovery fault, a ∼10 km wide rift zone, abundant seamounts, and abyssal hills form an interactive tectonic complex. We observe a patch of off‐fault seismicity coinciding with seafloor abyssal hills near their intersection with the rift zone. This off‐fault seismicity indicates ongoing deformation within the oceanic plate and possible spatial variations in rifting rates. Our results suggest that the Discovery system is still evolving with rifting and faulting accommodating plate spreading simultaneously. Key Points: The western Discovery transform fault has seven patches that are likely dominated by alternating seismic and aseismic slip modesMachine‐learning method helps to identify off‐fault seismicity along abyssal hills, indicating ongoing deformation within the oceanic plateThe Discovery transform system is young and still evolving, forming an interactive system with faulting, rifting, and plate rotation [ABSTRACT FROM AUTHOR]

Closely spaced, multi‐strand ridge transform faults (RTFs) accommodate relative motions along fast spreading mid‐ocean ridges. However, the relations between RTFs and plate spreading dynamics are poorly understood. The Quebrada system is one of the most unique RTF systems at the East Pacific Rise, consisting of four transform faults connected by three short intra‐transform spreading centers (ITSCs). We use seven‐months of ocean bottom seismograph data to study the Quebrada system, and find abundant earthquakes unevenly distributed among three active faults. We identify two deep, diffuse seismicity clouds at the inside corners of the ITSC‐transform fault intersections, and one seismically active fracture zone. The observations suggest a complex regional plate‐motion pattern, including possible heterogeneous rotations within the Quebrada system. Evolution of multi‐strand RTFs may have resulted from a strong three‐dimensional local thermal and fluid effects, while the RTFs may have also regulated regional tectonics, forming an intricate feedback system. Plain Language Summary: Mid‐ocean ridge transform faults (RTFs) are plate boundaries that offset adjacent mid‐ocean ridges. At fast spreading mid‐ocean ridges, such as the East Pacific Rise (EPR), closely spaced, multi‐strand RTFs are often connected by two or more short intra‐transform spreading centers (ITSCs). However, physical processes accommodating plate spreading along such multi‐strand RTF systems and the inter‐relations between the fault system and the tectonic dynamics are not well understood. Quebrada is one of such multi‐strand RTFs at the EPR. We utilize seven‐month seismic data from ocean bottom seismographs of a 2008 experiment to investigate the seismotectonics of the region. We find intriguing, abundant seismicity on one of the fracture zones, contradicting the traditional view that fracture zones are seismically quiescent. Further, we identify two diffuse seismicity clouds penetrating the uppermost mantle at the inside corners of the ITSC‐transform fault intersections, implying complex interactions among ITSCs, transform faults, and their surrounding structure. From these observations, we infer that there are rotational motions within the Quebrada fault system, which have caused slip along the fracture zone and facilitated fluid circulations to produce deep, diffuse seismicity. We speculate that there is a complex feedback system between the multi‐strand RTFs and local three‐dimensional tectonic processes. Key Points: Four segments of Quebrada transform system show significantly different seismic intensitiesOne fracture zone segment appears to be seismogenic indicating local plate rotationDeep clouds of seismicity extend into the uppermost mantle at spreading center‐ transform fault intersections [ABSTRACT FROM AUTHOR]

Summary: Seed aging tolerance and rapid seedling growth are important agronomic traits for crop production; however, how these traits are controlled at the molecular level remains largely unknown. The unaged seeds of two independent maize DEHYDRATION‐RESPONSIVE ELEMENT‐BINDING2A mutant (zmdreb2a) lines, with decreased expression of GRETCHEN HAGEN3.2 (ZmGH3.2, encoding indole‐3‐acetic acid [IAA] deactivating enzyme), and increased IAA in their embryo, produced longer seedling shoots and roots, than the null segregant (NS) controls. However, the zmdreb2a seeds, with decreased expression of RAFFINOSE SYNTHASE (ZmRAFS) and less raffinose in their embryo, exhibit decreased seed aging tolerance, than the NS controls. Overexpression of ZmDREB2A in maize protoplasts increased the expression of ZmGH3.2, ZmRAFS genes and that of a Rennila LUCIFERASE reporter (Rluc) gene, which was controlled by either the ZmGH3.2‐ or ZmRAFS‐promoter. Electrophoretic mobility shift assays and chromatin immunoprecipitation assay quantitative polymerase chain reaction showed that ZmDREB2A directly binds to the DRE motif of the promoters of both ZmGH3.2 and ZmRAFS. Exogenous supplementation of IAA to the unaged, germinating NS seeds increased subsequent seedling growth making them similar to the zmdreb2a seedlings from unaged seeds. These findings provide evidence that ZmDREB2A regulates the longevity of maize seed by stimulating the production of raffinose while simultaneously acting to limit auxin‐mediated cell expansion. [ABSTRACT FROM AUTHOR]

Gravity, magnetic, and bathymetry data collected along a continuous 1,400‐km‐long spreading‐parallel flow line across the Mid‐Atlantic Ridge indicate significant tectonic and magmatic fluctuations in the formation of oceanic crust over a range of time scales. The transect spans from 28 Ma on the African Plate to 74 Ma on the North American plate, crossing the Mid‐Atlantic Ridge at 35.8°N. Gravity‐derived crustal thicknesses vary from 3–9 km with a standard deviation of 1.0 km. Spectral analysis of bathymetry and residual mantle Bouguer anomaly show a diffuse power at >1 Myr and concurrent peaks at 390, 550, and 950 kyr. Large‐scale (>10 km) mantle thermal and compositional heterogeneities, variations in upper mantle flow, and detachment faulting likely generate the >1 Myr diffuse power. The 550‐ and 950‐kyr peaks may reflect the presence of magma solitons and/or regularly spaced ~7.7 and 13.3 km short‐wavelength mantle compositional heterogeneities. The 390‐kyr spectral peak corresponds to the characteristic spacing of faults along the flow line. Fault spacing also varies over longer periods (>10 Myr), which we interpret as reflecting long‐lived changes in the fraction of tectonically versus magmatically accommodated extensional strain. A newly discovered off‐axis oceanic core complex (Kafka Dome) found at 8 Ma on the African plate further suggests extended time periods of tectonically‐dominated plate separation. Fault spacing negatively correlates with gravity‐derived crustal thickness, supporting a strong link between magma input and fault style at mid‐ocean ridges. Key Points: We conducted one of the longest continuous geophysical surveys along a 74‐Myr spreading‐parallel flow line across the Mid‐Atlantic RidgeSpectral densities of bathymetry and gravity data show concurrent peaks at 390‐, 550‐, and 950‐kyr periods and diffuse power at >1 MyrA negative correlation between fault spacing and gravity‐derived crustal thickness suggests a link between magma input and fault style [ABSTRACT FROM AUTHOR]

Objective Sclerostin plays a major role in regulating skeletal bone mass, but its effects in articular cartilage are not known. The purpose of this study was to determine whether genetic loss or pharmacologic inhibition of sclerostin has an impact on knee joint articular cartilage. Methods Expression of sclerostin was determined in articular cartilage and bone tissue obtained from mice, rats, and human subjects, including patients with knee osteoarthritis (OA). Mice with genetic knockout (KO) of sclerostin and pharmacologic inhibition of sclerostin with a sclerostin-neutralizing monoclonal antibody (Scl-Ab) in aged male rats and ovariectomized (OVX) female rats were used to study the effects of sclerostin on pathologic processes in the knee joint. The rat medial meniscus tear (MMT) model of OA was used to investigate the pharmacologic efficacy of systemic Scl-Ab or intraarticular (IA) delivery of a sclerostin antibody-Fab (Scl-Fab) fragment. Results Sclerostin expression was detected in rodent and human articular chondrocytes. No difference was observed in the magnitude or distribution of sclerostin expression between normal and OA cartilage or bone. Sclerostin-KO mice showed no difference in histopathologic features of the knee joint compared to age-matched wild-type mice. Pharmacologic treatment of intact aged male rats or OVX female rats with Scl-Ab had no effect on morphologic characteristics of the articular cartilage. In the rat MMT model, pharmacologic treatment of animals with either systemic Scl-Ab or IA injection of Scl-Fab had no effect on lesion development or severity. Conclusion Genetic absence of sclerostin does not alter the normal development of age-dependent OA in mice, and pharmacologic inhibition of sclerostin with Scl-Ab has no impact on articular cartilage remodeling in rats with posttraumatic OA. [ABSTRACT FROM AUTHOR]

The article discusses a study which found that sclerostin antibody therapy promoted bone formation and increased bone mass and strength in a rat model of postmenopausal osteoporosis. The researchers identified a sclerostin neutralizing monoclonal antibody (Scl-AbII) via a cell culture model. Scl-AbII treatment in the animal model showed robust anabolic effects.