Signaling pathway networks mined from human pituitary adenoma proteomics data

Abstract Background We obtained a series of pituitary adenoma proteomic expression data, including protein-mapping data (111 proteins), comparative proteomic data (56 differentially expressed proteins), and nitroproteomic data (17 nitroproteins). There is a pressing need to clarify the significant signaling pathway networks that derive from those proteins in order to clarify and to better understand the molecular basis of pituitary adenoma pathogenesis and to discover biomarkers. Here, we describe the significant signaling pathway networks that were mined from human pituitary adenoma proteomic data with the Ingenuity pathway analysis system. Methods The Ingenuity pathway analysis system was used to analyze signal pathway networks and canonical pathways from protein-mapping data, comparative proteomic data, adenoma nitroproteomic data, and control nitroproteomic data. A Fisher's exact test was used to test the statistical significance with a significance level of 0.05. Statistical significant results were rationalized within the pituitary adenoma biological system with literature-based bioinformatics analyses. Results For the protein-mapping data, the top pathway networks were related to cancer, cell death, and lipid metabolism; the top canonical toxicity pathways included acute-phase response, oxidative-stress response, oxidative stress, and cell-cycle G2/M transition regulation. For the comparative proteomic data, top pathway networks were related to cancer, endocrine system development and function, and lipid metabolism; the top canonical toxicity pathways included mitochondrial dysfunction, oxidative phosphorylation, oxidative-stress response, and ERK/MAPK signaling. The nitroproteomic data from a pituitary adenoma were related to cancer, cell death, lipid metabolism, and reproductive system disease, and the top canonical toxicity pathways mainly related to p38 MAPK signaling and cell-cycle G2/M transition regulation. Nitroproteins from a pituitary control related to gene expression and cellular development, and no canonical toxicity pathways were identified. Conclusions This pathway network analysis demonstrated that mitochondrial dysfunction, oxidative stress, cell-cycle dysregulation, and the MAPK-signaling abnormality are significantly associated with a pituitary adenoma. These pathway-network data provide new insights into the molecular mechanisms of human pituitary adenoma pathogenesis, and new clues for an in-depth investigation of pituitary adenoma and biomarker discovery.</p

Genetic Algorithms-Based Parameter Optimization of a Non-Destructive Damage Detection Method

Abstract ⎯ Non-destructive testing (NDT) is an important area of research, dealing with diagnostic and monitoring the health of structures and structural components and preventing catastrophic failures. One of the recently developed NDT techniques is the method of strain energy mode shapes that allows the determination of changes in structural integrity from changes in the vibrational response of a structure. Normally, application of the strain energy mode shape method requires knowing the state of a structure before it was damaged, which limits the range of the method’s applicability. A modification of the strain energy method has been developed at West Virginia University. The modified (non-baseline) method does not require knowledge of the undamaged state of a structure (baseline). It has been theoretically proven tha

An Automated Damage Detection System for Armored Vehicle Launched Bridge

This paper presents an overview of an automated damage detection system for the Armored Vehicle Launched Bridge (AVLB). The system utilizes a non-contact laser vibrometer mounted on a computer-controlled robotic gantry as the measurement sensor. Acquired data is automatically processed to obtain strain energy mode shapes, which are used as the damage indicator. The analysis of the strain energy mode shapes is performed by a fuzzy expert system. This system was successfully tested on a full-scale AVLB with different damage scenarios

NON-BASELINE DAMAGE DETECTION FROM CHANGES IN STRAIN ENERGY MODE SHAPES. EXPERIMENTS ON ARMORED VEHICLE LAUNCHED BRIDGE

ABSTRACT. There are several existing methods for damage detection based on identifying changes in strain energy mode shapes. Most of these methods require knowing strain energy mode shapes for a structure without damage in order to establish a baseline for damage detection. Usually, the mode shapes from the structure under test should be compared to the baseline mode shapes to identify and locate damage. However, these methods of damage detection are not very suitable for application on structures where baseline mode shapes cannot be readily obtained, for example, structures with preexisting damage. Conventional methods, like building a finite element model of a structure to be used as a baseline might be an expensive and time-consuming task that can be impossible for complex structures. A new (non-baseline) method for the extraction of localized changes (damage peaks) from strain energy mode shapes based on Fourier analysis of the strain energy mode shapes has been developed and analytically proved for the cases of a pinned-pinned and a free-free beam. The new method looks for characteristic changes in the power spectrum of the strain energy mode shapes in order to locate and identify damage. The analytical results have been confirmed both by the finite element model and impact testing experiments on a free-free aluminum beam, including single and multiple damage scenarios. This paper presents results of testing the non-baseline method on a complex structure – Armored Vehicle Launched Bridge, which consists of loosely coupled hinged beams with variable cross-section. The results of testing confirm applicability of the non-baseline method to damage detection in complex structures and highlight certain particularities of its use

Development and Field-Testing of a Hand-Held Ultrasonic Monitoring Device

The effective life of timber bridges is often shortened by decay of timber components and failure of timber connections. Consequently, periodic inspections must be carried out to identify potential problems. Reliable methods for in-situ assessment of the strength and degradation rate in terms of strength loss over a period of time are essential for maintenance and rehabilitation of wooden bridges. A nondestructive technique such as ultrasonic measurement and testing has been found to be more accurate than the conventional practice of visual inspection for assessing the condition of wooden members. Ultrasonic measurements have shown considerable promise in determining the stiffness and strength of wood members by identifying the presence of defects such as knots and decay [1,2,3]. Experimental results have shown significant differences between the velocities of ultrasonic signals in defect-free areas and areas with knots, decays, and other localized defects [4]. Halabe et al. [5,6] has shown that frequency domain signal amplitude and wave attenuation measurements, when used in conjunction with time domain velocity measurements, can be much more accurate and reliable than simply using velocity measurements in predicting stiffness and condition of wood. Use of simple parameters such as area under FFT amplitude plots or power spectral density plots can greatly simplify comparison of various signals in the field.</p

Glial influences on neuron survival and regeneration in the CNS environment

Inflammation plays important role in limiting neuronal survival and axonal regeneration. Meanwhile, microglia and astrocytes are key players in mediating inflammation in CNS. Controlling inflammation thus is a crucial step in promoting neural survival and axonal regeneration. In our recent experiments, we have established an in vitro model to study inflammatory response in the CNS after ischemic (glucose and oxygen deprived)/hypoxic (oxygen deprived) injury. Methods: E-16 cortical neurons from rats were seeded on ischemic/hypoxic-injured glial cells, isolated from 1-day old rat brains, and co-cultured for 7 days. Using MAP2 immunocytochemistry, neuronal survival and neurite outgrowth were assessed by cell counts and image analysis (Neurolucider). Results: Our data suggest that small amount of inflammation (0.5 hr of ischemic treatment on glial cells) promotes neuronal survival and neurite extension. However, in longer ischemic/hypoxic-treated groups (>2hrs), both neuronal survival and neurite extension were decreased. Neurotrophic factors (NTF) are believed to modulate microglia, and glial cells have been known to release NTFs. However, detail mechanism on the regulation of NTFs by glial cells has not been fully understood. Our hypothesis is that the release of cytokines from the glial cells as a response to inflammation will decrease NTFs release, which leads to a decrease of neuronal survival and neurite extension. This abstract is sponsored by The Hong Kong Society of Neuroscience. Supported by the Hong Kong Regional Grant Council and The University of Hong Kong