Application of AIS Technology to Forest Mapping

Concerns about environmental effects of large scale deforestation have prompted efforts to map forests over large areas using various remote sensing data and image processing techniques. Basic research on the spectral characteristics of forest vegetation are required to form a basis for development of new techniques, and for image interpretation. Examination of LANDSAT data and image processing algorithms over a portion of boreal forest have demonstrated the complexity of relations between the various expressions of forest canopies, environmental variability, and the relative capacities of different image processing algorithms to achieve high classification accuracies under these conditions. Airborne Imaging Spectrometer (AIS) data may in part provide the means to interpret the responses of standard data and techniques to the vegetation based on its relatively high spectral resolution

Roles of circadian clocks in cancer pathogenesis and treatment

Circadian clocks are ubiquitous timing mechanisms that generate approximately 24-h rhythms in cellular and bodily functions across nearly all living species. These internal clock systems enable living organisms to anticipate and respond to daily changes in their environment in a timely manner, optimizing temporal physiology and behaviors. Dysregulation of circadian rhythms by genetic and environmental risk factors increases susceptibility to multiple diseases, particularly cancers. A growing number of studies have revealed dynamic crosstalk between circadian clocks and cancer pathways, providing mechanistic insights into the therapeutic utility of circadian rhythms in cancer treatment. This review will discuss the roles of circadian rhythms in cancer pathogenesis, highlighting the recent advances in chronotherapeutic approaches for improved cancer treatment

Circadian Rhythms and the Treatment of Rheumatoid Arthritis

Circadian clocks are ubiquitous biological timing systems that drive roughly 24 rhythms of our behavior (e.g., sleep/wake, feeding/fasting cycles) and physiology (e.g., metabolism, hormonal system, immune functions) through daily adjustments to environmental day and night cycles. Besides the rhythmic regulation of physiological processes, the circadian clockwork has been increasingly recognized to determine the daily variation in pathological symptoms and severity, particularly in autoimmune diseases including Rheumatoid Arthritis (RA). RA is a chronic inflammatory disease caused by the body’s immune system attacking its own tissues and joints, resulting in major symptoms such as joint pain and stiffness. In most RA patients, the autoimmune symptoms are pronounced in the morning and are mediated by circadian rhythms of leukocyte recruitment to inflamed tissues, release of pro-inflammatory cytokines (e.g., IL-6, TNF-α), and immune-modulatory hormone levels (e.g., glucocorticoid, melatonin). With the growing knowledge of the circadian etiology of RA clinical symptoms, here, we will briefly discuss recently established chronotherapeutic concepts as well as approaches to improve outcomes of RA treatment

Regulated cationic channel function in Xenopus oocytes expressing Drosophila big brain

Copyright © 2002 Society for NeuroscienceBig brain (bib) is a neurogenic gene that when mutated causes defects in cell fate determination during Drosophila neurogenesis through an unknown mechanism. The protein Big Brain (BIB) has sequence identity with the major intrinsic protein family that includes the water- and ion-conducting aquaporin channels. We show here that BIB expressed heterologously in Xenopus oocytes provides a voltage-insensitive, nonselective cation channel function with permeability to K+ > Na+ tetraethylammonium. The conductance, activated in response to endogenous signaling pathways in BIB-expressing oocytes, is decreased after treatment with 20 µM insulin and is enhanced with 10 µM lavendustin A, a tyrosine kinase inhibitor. Western blot analysis confirms that BIB is tyrosine-phosphorylated. Both tyrosine phosphorylation and the potentiating effect of lavendustin A are removed by partial deletion of the C terminus (amino acids 317-700). Current activation is not observed in control oocytes or in oocytes expressing a nonfunctional mutant (BIB E71N) that appears to be expressed on the plasma membrane by confocal microscopy and Western blotting. These results indicate that BIB can participate in tyrosine kinase-regulated transmembrane signaling and may suggest a role for membrane depolarization in the neurogenic function of BIB in early development.Gina M. Yanochko and Andrea J. Yoo

Redox-active Vitamin C Suppresses Human Osteosarcoma Growth by Triggering Intracellular ROS-Iron-Calcium Signaling Crosstalk and Mitochondrial Dysfunction

Pharmacological vitamin C (VC) has gained attention for its pro-oxidant characteristics and selective ability to induce cancer cell death. However, defining its role in cancer has been challenging due to its complex redox properties. In this study, using a human osteosarcoma (OS) model, we show that the redox-active property of VC is critical for inducing non-apoptotic cancer cell death via intracellular reactive oxygen species (ROS)-iron-calcium crosstalk and mitochondrial dysfunction. In both 2D and 3D OS cell culture models, only the oxidizable form of VC demonstrated potent dose-dependent cytotoxicity, while non-oxidizable and oxidized VC derivatives had minimal effects. Live-cell imaging showed that only oxidizable VC caused a surge in cytotoxic ROS, dependent on iron rather than copper. Inhibitors of ferroptosis, a form of iron-dependent cell death, along with classical apoptosis inhibitors, were unable to completely counteract the cytotoxic effects induced by VC. Further pharmacological and genetic inhibition analyses showed that VC triggers calcium release through inositol 1,4,5-trisphosphate receptors (IP3Rs), leading to mitochondrial ROS production and eventual cell death. RNA sequencing revealed down-regulation of genes involved in the mitochondrial electron transport chain and oxidative phosphorylation upon pharmacological VC treatment. Consistently, high-dose VC reduced mitochondrial membrane potential, oxidative phosphorylation, and ATP levels, with ATP reconstitution rescuing VC-induced cytotoxicity. In vivo OS xenograft studies demonstrated reduced tumor growth with high-dose VC administration, concomitant with the altered expression of mitochondrial ATP synthase (MT-ATP). These findings emphasize VC's potential clinical utility in osteosarcoma treatment by inducing mitochondrial metabolic dysfunction through a vicious intracellular ROS-iron-calcium cycle

Potential Role of the Circadian Clock in the Regulation of Cancer Stem Cells and Cancer Therapy

Circadian rhythms, including sleep/wake cycles as well as hormonal, immune, metabolic, and cell proliferation rhythms, are fundamental biological processes driven by a cellular time-keeping system called the circadian clock. Disruptions in these rhythms due to genetic alterations or irregular lifestyles cause fundamental changes in physiology, from metabolism to cellular proliferation and differentiation, resulting in pathological consequences including cancer. Cancer cells are not uniform and static but exist as different subtypes with phenotypic and functional differences in the tumor microenvironment. At the top of the heterogeneous tumor cell hierarchy, cancer stem cells (CSCs), a self-renewing and multi-potent cancer cell type, are most responsible for tumor recurrence and metastasis, chemoresistance, and mortality. Phenotypically, CSCs are associated with the epithelial-mesenchymal transition (EMT), which confers cancer cells with increased motility and invasion ability that is characteristic of malignant and drug-resistant stem cells. Recently, emerging studies of different cancer types, such as glioblastoma, leukemia, prostate cancer, and breast cancer, suggest that the circadian clock plays an important role in the maintenance of CSC/EMT characteristics. In this review, we describe recent discoveries regarding how tumor intrinsic and extrinsic circadian clock-regulating factors affect CSC evolution, highlighting the possibility of developing novel chronotherapeutic strategies that could be used against CSCs to fight cancer

Novel function of C5 protein as a metabolic stabilizer of M1 RNA

AbstractEscherichia coli RNase P is a ribonucleoprotein composed of a large RNA subunit (M1 RNA) and a small protein subunit (C5 protein). We examined if C5 protein plays a role in maintaining metabolic stability of M1 RNA. The sequestration of C5 protein available for M1 RNA binding reduced M1 RNA stability in vivo, and its reduced stability was recovered via overexpression of C5 protein. In addition, M1 RNA was rapidly degraded in a temperature-sensitive C5 protein mutant strain at non-permissive temperatures. Collectively, our results demonstrate that the C5 protein metabolically stabilizes M1 RNA in the cell

Transient thermo-structural analysis of an insulated space structure

Thesis (M.S.)--Massachusetts Institute of Technology, Dept. of Aeronautics and Astronautics, 1995.Includes bibliographical references (leaves 96-99).by Yool A. Kim.M.S

Thermal creak induced dynamics of space structures

Thesis (Ph.D.)--Massachusetts Institute of Technology, Dept. of Aeronautics and Astronautics, 1999.Includes bibliographical references (p. 151-154).Space structures may be subjected to a continually changing thermal environment due to Earth eclipse transients and changes in the spacecraft orientation. During the transient thermal state, components in a structure may experience different amounts of thermal strain due to temperature gradients or coefficient of thermal expansion (CTE) mismatches. Such differential thermal strain can result in stress build-up, especially in statically indeterminate structures. If a nonlinear element, such as a friction dependent joint, is present, stress in the element builds up until the maximum load that can be sustained by friction is reached, at which point the element slips and releases some of the stored elastic energy. Such a nonlinear release mechanism will induce impulsive broadband and possibly high frequency loading to the system, in response to low frequency thermal excitations. This phenomenon is referred to as thermal creak. Nonlinear joints with freeplay, tensioning cables and pulleys, and other structural components that depend on friction and allow relative motion are all examples of potential creak elements that are common in space structures. An analytical and experimental investigation of the thermal creak phenomenon is presented. A generic model of a thermal creak element is developed to understand the mechanism and to identify the key parameters. The model captures the thermoelastic response, the friction behavior, and the dynamic response of a system. Key parameters that govern the response and quantify the parameters correlated with the energy storage, energy release and energy propagation are identified. The dynamic response is parametrically studied to qualitatively understand the range of behaviors. Two laboratory experiments were conducted to demonstrate thermal creak and to correlate with the model behavior. The first experiment, a joint characterization, focused on the local thermal creak response and the friction behavior. The model is shown to capture the nonlinear creak response over a range of loading conditions and trends seen in the experiment. The second experiment, a set of thermal tests on a representative deployable structure, investigated the structural response due to thermal creak. Thermal creak events were observed and the resulting dynamics were characterized. The results from the ground experiments and an on-orbit flight experiment conducted by Jet Propulsion Laboratory are used to assess the model and its applicability. The developed model and the experimental results provide a tool for developing thermal creak analysis techniques and mitigation strategies.by Yool A. Kim.Ph.D

Future change in ocean productivity: Is the Arctic the new Atlantic?

One of the most characteristic features in ocean productivity is the North Atlantic spring bloom. Responding to seasonal increases in irradiance and stratification, surface phytopopulations rise significantly, a pattern that visibly tracks poleward into summer. While blooms also occur in the Arctic Ocean, they are constrained by the sea-ice and strong vertical stratification that characterize this region. However, Arctic sea-ice is currently declining, and forecasts suggest this may lead to completely ice-free summers by the mid-21st century. Such change may open the Arctic up to Atlantic-style spring blooms, and do so at the same time as Atlantic productivity is threatened by climate change-driven ocean stratification. Here we use low and high-resolution instances of a coupled ocean-biogeochemistry model, NEMO-MEDUSA, to investigate productivity. Drivers of present-day patterns are identified, and changes in these across a climate change scenario (IPCC RCP 8.5) are analyzed. We find a globally significant decline in North Atlantic productivity (> ?20%) by 2100, and a correspondingly significant rise in the Arctic (> +50%). However, rather than the future Arctic coming to resemble the current Atlantic, both regions are instead transitioning to a common, low nutrient regime. The North Pacific provides a counterexample where nutrients remain high and productivity increases with elevated temperature. These responses to climate change in the Atlantic and Arctic are common between model resolutions, suggesting an independence from resolution for key impacts. However, some responses, such as those in the North Pacific, differ between the simulations, suggesting the reverse and supporting the drive to more fine-scale resolutions