No abstract

Our results suggest that both in vivo T(1rho) and T(2) relaxation times increase with the degree of cartilage degeneration. T(1rho) relaxation time may be a more sensitive indicator for early cartilage degeneration than T(2). The ability to detect early cartilage degeneration prior to morphologic changes may allow us to critically monitor the course of OA and injury progression, and to evaluate the success of treatment to patients with early stages of OA.

The goal of this MR-imaging study was to quantify vertebral bone marrow fat content and composition in diabetic and non-diabetic postmenopausal women with fragility fractures and to compare them with non-fracture controls with and without type-2 diabetes mellitus. Sixty-nine postmenopausal women (mean age 63±5 years) were recruited. Thirty-six patients (47.8%) had spinal and/or peripheral fragility fractures. Seventeen fracture patients were diabetic. Thirty-three women (52.2%) were non-fracture controls. Sixteen women were diabetic non-fracture controls. To quantify vertebral bone marrow fat content and composition, patients underwent MR-spectroscopy (MRS) of the lumbar spine at 3 Tesla. Bone mineral density (BMD) was determined by dual-energy X-Ray-absorptiometry (DXA) of the hip and lumbar spine (LS) and quantitative computed tomography (QCT) of the LS. To evaluate associations of vertebral marrow fat content and composition with spinal and/or peripheral fragility fractures and diabetes, we used linear regression models adjusted for age, race, and spine vBMD by QCT. At the LS, non-diabetic and diabetic fracture patients had lower vBMD than controls and diabetics without fractures (p=0.018; p=0.005). However, aBMD by DXA did not differ between fracture and non-fracture patients. After adjustment for age, race, and spinal vBMD, the prevalence of fragility fractures was associated with -1.7% lower unsaturation levels (confidence interval [CI] -2.8% to - 0.5%, p=0.005) and +2.9% higher saturation levels (CI 0.5% to 5.3%, p=0.017). Diabetes was associated with -1.3% (CI -2.3% to -0.2%, p=0.018) lower unsaturation and +3.3% (CI 1.1% to 5.4%. p=0.004) higher saturation levels. Diabetics with fractures had the lowest marrow unsaturation and highest saturation. There were no associations of marrow fat content with diabetes or fracture. Our results suggest that altered bone marrow fat composition is linked with fragility fractures and diabetes. MRS of spinal bone marrow fat may therefore serve as a novel tool for BMD-independent fracture risk assessment.

The developmental plasticity of plants relies on the remarkable ability of the meristems to integrate nutrient and energy availability with environmental signals. Meristems in root and shoot apexes share highly similar molecular players but are spatially separated by soil. Whether and how these two meristematic tissues have differential activation requirements for local nutrient, hormone, and environmental cues (e.g., light) remain enigmatic in photosynthetic plants. Here, we report that the activation of root and shoot apexes relies on distinct glucose and light signals. Glucose energy signaling is sufficient to activate target of rapamycin (TOR) kinase in root apexes. In contrast, both the glucose and light signals are required for TOR activation in shoot apexes. Strikingly, exogenously applied auxin is able to replace light to activate TOR in shoot apexes and promote true leaf development. A relatively low concentration of auxin in the shoot and high concentration of auxin in the root might be responsible for this distinctive light requirement in root and shoot apexes, because light is required to promote auxin biosynthesis in the shoot. Furthermore, we reveal that the small GTPase Rho-related protein 2 (ROP2) transduces light-auxin signal to activate TOR by direct interaction, which, in turn, promotes transcription factors E2Fa,b for activating cell cycle genes in shoot apexes. Consistently, constitutively activatedROP2plants stimulate TOR in the shoot apex and cause true leaf development even without light. Together, our findings establish a pivotal hub role of TOR signaling in integrating different environmental signals to regulate distinct developmental transition and growth in the shoot and root.

Purpose:To longitudinally evaluate cartilage matrix changes by using magnetic resonance (MR) imaging T1 r (T1 relaxation time in rotating frame) and T2 quantifi cation and to study the relationship between meniscal damage and cartilage degeneration in anterior cruciate ligament (ACL)-reconstructed knees. Materials and Methods:This was an institutional review board-approved, HIPAAcompliant study. Informed consent was obtained. Twelve patients with acute ACL injuries were imaged with 3.0-T MR imaging at baseline (after injury and prior to ACL reconstruction) and 1 year after ACL reconstruction. Ten age-matched healthy subjects were studied as controls. Cartilage T1 r and T2 were quantifi ed in full thickness, superfi cial, and deep layers of defi ned subcompartments at baseline and follow-up in ACL-injured knees and were compared with measures acquired in matched regions of control knees. Meniscal lesions were graded by using modifi ed subscores of the Whole-Organ Magnetic Resonance Imaging Score system. Results:T1 r values of the posterolateral tibial cartilage in ACLinjured knees were signifi cantly elevated at baseline compared with T1 r values of control knees and were not fully recovered at 1-year follow-up. T1 r values of weight-bearing medial femorotibial cartilage in ACL-injured knees were signifi cantly elevated at 1-year follow-up compared with those of control knees. No signifi cant differences in T2 values between ACL-injured and control knees were found. Patients with lesions in the posterior horn of the medial meniscus showed a greater increase of T1 r and T2 from baseline to follow-up in adjacent cartilage than patients without lesions in the medial meniscus. Conclusion:Quantitative MR imaging T1 r and T2 enable detection of changes in the cartilage matrix of ACL-reconstructed knees as early as 1 year after ACL reconstruction.q RSNA, 2010

For T 1 quantification, a three-dimensional (3D) acquisition is desired to obtain high-resolution images. Current 3D methods that use steady-state spoiled gradient-echo (SPGR) imaging suffer from high SAR, low signal-to-noise ratio (SNR), and the need for retrospective correction of contaminating T 1 effects. In this study, a novel 3D acquisition scheme-magnetization-prepared angle-modulated partitioned-k-space SPGR snapshots (3D MAPSS)-was developed and used to obtain in vivo T 1 maps. Transient signal evolving towards the steady-state were acquired in an interleaved segmented elliptical centric phase encoding order immediately after a T 1 magnetization preparation sequence. Noninvasive early detection of cartilage degeneration in osteoarthritis (OA) is of increasing clinical importance. Magnetic resonance imaging (MRI) has been widely used for detecting and monitoring cartilage injuries (1). Recent developments in high field MR (such as the availability of clinical systems with a field strength of 3 T) have further enhanced image spatial resolution and signal-to-noise ratio (SNR) (2). However, conventional MRI is limited to providing primarily morphologic changes of cartilage. Since damage to the collagen-proteoglycan (PG) matrix in cartilage occur early in the course of OA, imaging markers that can probe biochemical changes are essential for early detection of cartilage degeneration. Recent developments in this active field include delayed gadolinium enhanced MRI of cartilage (dGEMRIC) (3-5), T 2 (6 -10), and T 1 (11-16) relaxation time quantification.The T 1 parameter describes the spin-lattice relaxation in the rotating frame (17). It reflects the slow motion interactions between motion-restricted water molecules and their local macromolecular environment. The extracellular matrix (ECM) in articular cartilage provides a motionrestricted environment for water molecules. Changes to the ECM therefore may be reflected in measurements of T 1 . T 1 relaxation rate (1/T 1 ) has been shown to decrease linearly with decreasing PG content in ex vivo bovine patellae (11) and in trypsinized cartilage (18). In vivo studies have also shown increased cartilage T 1 values for patients with OA (19,20).Current T 1 quantification techniques are based on either two dimensional (2D) fast spin echo (FSE) (21), spiral imaging (16), echo planar imaging (EPI) (22), or 3D gradient echo sequences (20,23). Compared with 2D methods, 3D imaging is free from artifacts caused by slice cross-talk. Therefore 3D sequences can generally have a thinner slice thickness, and consequently may provide a more accurate assessment of cartilage degeneration. High-resolution MRI is particularly attractive in the context of OA, in which cartilage becomes very thin-on the order of or less than 1 mm. Furthermore, a 3D acquisition is desired due to the non-slice-selective nature of the T 1 preparation pulses (spin-lock pulses). A 3D T 1 mapping technique has been developed based on a steady-state spoiled gradient echo (SPGR) imaging sequence (23) and has s...

PIP2;1 is an integral membrane protein that facilitates water transport across plasma membranes. To address the dynamics of Arabidopsis thaliana PIP2;1 at the single-molecule level as well as their role in PIP2;1 regulation, we tracked green fluorescent protein-PIP2;1 molecules by variable-angle evanescent wave microscopy and fluorescence correlation spectroscopy (FCS). Single-particle tracking analysis revealed that PIP2;1 presented four diffusion modes with large dispersion of diffusion coefficients, suggesting that partitioning and dynamics of PIP2;1 are heterogeneous and, more importantly, that PIP2;1 can move into or out of membrane microdomains. In response to salt stress, the diffusion coefficients and percentage of restricted diffusion increased, implying that PIP2;1 internalization was enhanced. This was further supported by the decrease in PIP2;1 density on plasma membranes by FCS. We additionally demonstrated that PIP2;1 internalization involves a combination of two pathways: a tyrphostin A23-sensitive clathrin-dependent pathway and a methyl-b-cyclodextrin-sensitive, membrane raft-associated pathway. The latter was efficiently stimulated under NaCl conditions. Taken together, our findings demonstrate that PIP2;1 molecules are heterogeneously distributed on the plasma membrane and that clathrin and membrane raft pathways cooperate to mediate the subcellular trafficking of PIP2;1, suggesting that the dynamic partitioning and recycling pathways might be involved in the multiple modes of regulating water permeability.

Although seed germination is a major subject in plant physiological research, there is still a long way to go to elucidate the mechanism of seed germination. Recently, functional genomic strategies have been applied to study the germination of plant seeds. Here, we conducted a proteomic analysis of seed germination in rice (Oryza sativa indica cv. 9311) - a model monocot. Comparison of 2-DE maps showed that there were 148 proteins displayed differently in the germination process of rice seeds. Among the changed proteins, 63 were down-regulated, 69 were up-regulated (including 20 induced proteins). The down-regulated proteins were mainly storage proteins, such as globulin and glutelin, and proteins associated with seed maturation, such as "early embryogenesis protein" and "late embryogenesis abundant protein", and proteins related to desiccation, such as "abscisic acid-induced protein" and "cold-regulated protein". The degradation of storage proteins mainly happened at the late stage of germination phase II (48 h imbibition), while that of seed maturation and desiccation associated proteins occurred at the early stage of phase II (24 h imbibition). In addition to alpha-amylase, the up-regulated proteins were mainly those involved in glycolysis such as UDP-glucose dehydrogenase, fructokinase, phosphoglucomutase, and pyruvate decarboxylase. The results reflected the possible biochemical and physiological processes of germination of rice seeds.