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PubMed2006

Biological enhancement of tetrachloroethene dissolution and associated microbial community changes.

A bench-scale study was performed to evaluate the enhancement of tetrachloroethene (PCE) dissolution from a dense nonaqueous phase liquid (DNAPL) source zone due to reductive dechlorination. The study was conducted in a pair of two-dimensional bench-scale aquifer systems using soil and groundwater from Dover Air Force Base, DE. After establishment of PCE source zones in each aquifer system, one was biostimulated (addition of electron donor) while the other was biostimulated and then bioaugmented with the KB1 dechlorinating culture. Biostimulation resulted in the growth of iron-reducing bacteria (Geobacter) in both systems as a result of the high iron content of the Dover soil. After prolonged electron donor addition methanogenesis dominated, but no dechlorination was observed. Following bioaugmentation of one system, dechlorination to ethene was achieved, coincident with growth of introduced Dehalococcoides and other microbes in the vicinity and downgradient of the PCE DNAPL (detected using DGGE and qPCR). Dechlorination was not detected in the nonbioaugmented system over the course of the study, indicating that the native microbial community, although containing a member of the Dehalococcoides group, was not able to dechlorinate PCE. Over 890 days, 65% of the initial emplaced PCE was removed in the bioaugmented, dechlorinating system, in comparison to 39% removal by dissolution from the nondechlorinating system. The maximum total ethenes concentration (3 mM) in the bioaugmented system occurred approximately 100 days after bioaugmentation, indicating that there was at least a 3-fold enhancement of PCE dissolution atthis time. Removal rates decreased substantially beyond this time, particularly during the last 200 days of the study, when the maximum concentrations of total ethenes were only about 0.5 mM. However, PCE removal rates in the dechlorinating system remained more than twice the removal rates of the nondechlorinating system. The reductions in removal rates over time are attributed to both a shrinking DNAPL source area, and reduced flow through the DNAPL source area due to bioclogging and pore blockage from methane gas generation.

Biodegradation, Environmental↗
PubMed2002

Risk reduction in craniofacial surgery using computer-based modeling and intraoperative immersion.

We present a two-stage concept for risk reduction in craniofacial surgery, consisting of preoperative risk modeling and intraoperative risk reduction. Preoperatively it is important to find and to visualize risk sources in order to minimize them. Our risk model is composed by superimposition of an isotropic risk potential and an anisotropic tissue field constituent. It is being applied to preoperative planning and simulation of craniofacial surgeries, for example to determine an access path with least overall risk value. In the operation room risks arise mainly from the absence of preoperative planning and simulation data in the operation field. We use a see-through head-mounted display to optimize this situation in order to allow the surgeon to maintain accuracy in the whole process of computer aided surgery. Main steps of the intraoperative immersion are optical tracking of the surgeon wearing the head-mounted display and of the patient, registration of preoperatively calculated planning data with the patient and visualization of the data within the glasses.

Computer Graphics↗
PubMed1982

Cell surface alterations of avian sarcoma virus B77-and 3,4-benzo(a)pyrene-transformed rat fibroblasts. II. Cell surface glycoproteins characterized by two-dimensional electrophoresis.

Cell surface proteins of avian sarcoma virus B77-, 3,4-benzo(a)pyrene- and spontaneously transformed rat fibroblasts were tritium-radiolabeled by mild periodate oxidation followed by tritiated sodium borohydride reduction and by galactoseoxidase/NaB3H4 technique. Radiolabeled cell surface sialoglycoproteins were analyzed by electrophoresis under denaturing conditions (SDS-PAGE), or by two-dimensional electrophoresis (isoelectric focusing, SDS-PAGE). Following major glycoproteins were quantitatively decreased on all examined transformed cells: a 220k glycoprotein with pI of approximately 6.2, a 180k glycoprotein with pI of approximately 6.0-6.2, a 110k glycoprotein (pI 6.2). A series of further sialoglycoproteins was quantitatively increased on all examined transformed cells, as follows: a markedly increased 70k glycoprotein (pI approximately 4.8) and a 120k glycoprotein (pI 5.0-5.2) increased more markedly on onco-virus-transformed and spontaneously transformed cells. Further sialogalactoprotein (28k, pI 5.8) was visualized as increased on all examined transformed cells only by galactoseoxidase/NaB3H4 technique. A 70k sialoglycoprotein was immunoprecipitated from transformed cells by the immune serum against Friend murine leukemia virus envelop glycoprotein gp70 and, to a markedly lesser extent, from untransformed cells. A similar glycoprotein, together with an another 120k glycoprotein were precipitated from transformed cells and to a minor extent from untransformed cells also by an antiserum against endogenous rat type-C virus.

Animals↗
PubMed1999

Noninvasive measurement of three-dimensional myocardial deformation with tagged magnetic resonance imaging during graded local ischemia.

The purpose of this study was to investigate the relationship between three-dimensional (3D) deformation patterns in the canine left ventricle and localized graded reductions in perfusion. Magnetic resonance (MR) tissue tagging in a clinical scanner was used to determine systolic 3D deformation throughout the left ventricle with 32-msec time resolution. Six dogs were studied at normal and reduced left anterior descending coronary artery flow levels, for a total of 14 studies. Deformation was calculated by fitting a 3D displacement field to tag displacement data from three orthogonal sets of tags and taking spatial derivatives. A novel index of 3D radial mechanical function, calculated from the 3D strain tensor components and the tissue incompressibility constraint, had a higher correlation (R = 0.94) with perfusion (colored microspheres) than any of the 3D Lagrangian finite strain tensor components or wall thickening. As a function of the fraction of baseline perfusion, it was well fit by a linear relationship for subnormal perfusion with a slope of 0.46 +/- 0.05 and an intercept of -0.156 +/- 0.026. Longitudinal strain was lost first with decreasing perfusion (48%), followed by circumferential (40%) and finally radial function (35%). The strain method detected perfusion drops as small as 20%, and early paradoxical strain transients lasting 100 msec were seen only with ischemia. 3D strain changes can be noninvasively measured throughout the left ventricle with MR tissue tagging. MR imaging-derived strain indices, unique to 3D analysis, correlate most sensitively with regional perfusion in the canine left ventricle.

Animals↗
PubMed2002

Measurement of lung tumor volumes using three-dimensional computer planning software.

PURPOSE: To examine the interclinician variation in the definition of gross tumor volume (GTV) in patients undergoing radiotherapy for non-small-cell lung cancer (NSCLC), develop methods to minimize this variation, and test these methods. METHODS AND MATERIALS: The radiotherapy planning computed tomography (CT) scans of 6 consecutive patients with NSCLC in which the radiologist was able to define and outline the GTV were used. Six oncologists independently contoured the tumors with the radiologist's markings as a guide using a three-dimensional treatment planning system. Separate contours were prepared using only mediastinal window settings and using both mediastinal and lung window settings. The volumes were calculated using the planning system software (series 1). Factors that resulted in interclinician variation were determined, and, after a 3-year interval, 5 of the 6 clinicians redefined the GTVs using a revised protocol aimed at minimizing variation (series 2). RESULTS: For series 1, the interclinician variation in the measurement of volumes ranged from 5%, in the most tightly measured tumor, to 42%, in the most variable, but was, on average, 20%. Statistically significant differences were noted among the clinicians (p = 0.002), that is, some clinicians tended to record relatively small and some relatively large volumes. The reasons for the variation among the oncologists included a tendency to include regions with a low probability of containing tumor, as if the oncologist were contouring a target volume; inclusion of adjacent atelectasis (ignoring the radiologist's outline); and variable treatment of spicules. When the exercise was repeated using the revised protocol (series 2), the degree of interclinician variation was reduced, with a range of 7-22% (average 13%). In series 2, the differences among the clinicians were not statistically significant (p = 0.25). CONCLUSION: Despite major radiologic input, significant variation occurred in the delineation of the three-dimensional GTVs of NSCLC among oncologists. Standardization of the approach with guidelines resulted in a reduction in this variation.

Analysis of Variance↗
PubMed1995

Characterisation of high-level cisplatin-resistant cell lines established from a human hepatoma cell line and human KB adenocarcinoma cells: cross-resistance and protein changes.

Human liver carcinoma cells (BEL-7404) and human KB adenocarcinoma cells were selected by stepwise increases in cisplatin. Drug sensitivity assays indicated that the IC50 value for 7404-CP7.5 cells was 49 micrograms ml-1 cisplatin, 111-fold higher than for the parental hepatoma cells. The IC50 value for KB-CP10 cells was 38 micrograms ml-1 cisplatin, which is 1152-fold higher than for the parental KB cells. The 7404-CP7.5 cells were cross-resistant to methotrexate (39 x), 5-fluorouracil (23 x) and 6-mercaptopurine (13 x), but were sensitive to drugs which are known substrates for the multidrug transporter (P-glycoprotein), including colchicine, vinblastine and actinomycin D. Similar cross-resistance patterns were observed for KB-CP10 cells. No evidence of DNA amplification or expression of the MDR1 gene was found. One-dimensional sodium dodecyl sulphate-polyacrylamide gel electrophoresis showed increases in 52 kDa protein(s) in both the soluble cytosolic and crude membrane fractions in 7404-CP(r) cells and in KB-CP(r) cells. The amount of 52 kDa protein was proportional to the degree of resistance of the 7404-CP(r) cells to cisplatin. Two-dimensional gel analysis demonstrated that two polypeptides of molecular mass 52 and 50 kDa were overexpressed in the membrane fractions in both 7404-CP20 and KB-CP20 cells. Using amino acid microsequencing and Western blotting, major 52 kDa protein was identified as the mitochondrial heat shock protein hsp60. Two-dimensional gels of [35S]methionine-labelled polypeptides showed many other changes, including reduction in soluble proteins of approximately 57 kDa molecular weight in KB-CP20 cells, and of 35 kDa in both 7404-CP20 and KB-CP20 cells. These results suggest that alterations of certain proteins occur commonly in cisplatin-resistant cells, particularly proteins of molecular weight 52 and 50 kDa.

Amino Acid Sequence↗
PubMed1998

E-Cadherin-dependent growth suppression is mediated by the cyclin-dependent kinase inhibitor p27(KIP1).

Recent studies have demonstrated the importance of E-cadherin, a homophilic cell-cell adhesion molecule, in contact inhibition of growth of normal epithelial cells. Many tumor cells also maintain strong intercellular adhesion, and are growth-inhibited by cell- cell contact, especially when grown in three-dimensional culture. To determine if E-cadherin could mediate contact-dependent growth inhibition of nonadherent EMT/6 mouse mammary carcinoma cells that lack E-cadherin, we transfected these cells with an exogenous E-cadherin expression vector. E-cadherin expression in EMT/6 cells resulted in tighter adhesion of multicellular spheroids and a reduced proliferative fraction in three-dimensional culture. In addition to increased cell-cell adhesion, E-cadherin expression also resulted in dephosphorylation of the retinoblastoma protein, an increase in the level of the cyclin-dependent kinase inhibitor p27(kip1) and a late reduction in cyclin D1 protein. Tightly adherent spheroids also showed increased levels of p27 bound to the cyclin E-cdk2 complex, and a reduction in cyclin E-cdk2 activity. Exposure to E-cadherin-neutralizing antibodies in three-dimensional culture simultaneously prevented adhesion and stimulated proliferation of E-cadherin transfectants as well as a panel of human colon, breast, and lung carcinoma cell lines that express functional E-cadherin. To test the importance of p27 in E-cadherin-dependent growth inhibition, we engineered E-cadherin-positive cells to express inducible p27. By forcing expression of p27 levels similar to those observed in aggregated cells, the stimulatory effect of E-cadherin-neutralizing antibodies on proliferation could be inhibited. This study demonstrates that E-cadherin, classically described as an invasion suppressor, is also a major growth suppressor, and its ability to inhibit proliferation involves upregulation of the cyclin-dependent kinase inhibitor p27.

Animals↗
PubMed1973

Evidence for the existence of neural mechanisms selectively sensitive to the direction of movement in space.

1. Visual sensitivity to movement in depth was measured as a function of the relative distances through which the left and right retinal images moved. This relative distance (left:right ratio) provides a sensitive cue to the direction along which a target moves in three-dimensional space.2. Gazing at a target which moved along a fixed direction in space produced a gross reduction of visual sensitivity to movements in depth along that direction. For other directions of movement, visual sensitivity was not affected.3. Sensitivity to depth movement rapidly rose almost to the preadaptation level within the first 20-60 sec after removing the adapting target, but recovery was not complete until 100-300 min had elapsed.4. Any adapting target whose left:right ratio fell within a definite range gave similar reductions of visual sensitivity to movements in depth. There were five such ranges.5. The effects of adapting to movement in depth suggest that eight mechanisms underlie depth perception. These mechanisms are ;tuned' to the direction of movement in three-dimensional space. Four mechanisms are wholly concerned with movements along directions very close to the line which cuts midway between the eyes, and do not respond to movements whose direction departs by more than 1.5 degrees from the preferred direction.6. Neural mechanisms ;tuned' to different left:right ratios could provide a physiological basis for sensing the direction in which an object moves in three-dimensional space.

Adaptation, Ocular↗
PubMed1997

Simulated car crashes and crash predictors in drivers with Alzheimer disease.

BACKGROUND: Alzheimer disease (AD) is the most common cause of dementia and can impair cognitive abilities crucial to the task of driving. Rational decisions about whether such impaired individuals should continue to drive require objective assessments of driver performance. OBJECTIVE: To measure relevant performance factors using high-fidelity driving simulation. DESIGN: We examined the effect of AD on driver collision avoidance using the Iowa Driving Simulator, which provided a high-fidelity, closely controlled environment in which to observe serious errors by at-risk drivers. We determined how such unsafe events are predicted by visual and cognitive factors sensitive to decline in aging and AD. SETTING: The University of Iowa Hospitals and Clinics, Iowa City, and the Iowa Driving Simulator. PARTICIPANTS: Thirty-nine licensed drivers: 21 with AD and 18 controls without dementia. MAIN OUTCOME MEASURES: We determined the number of crashes and related performance errors and analyzed how these occurrences were predicted by visual and cognitive factors. RESULTS: Six participants (29%) with AD experienced crashes vs 0 of 18 control participants (P = .022). Drivers with AD were more than twice as likely to experience close calls (P = .042). Plots of critical control factors in the moments preceding a crash revealed patterns of driver in-attention and error. Strong predictors of crashes included visuospatial impairment, reduction in the useful field of view, and reduced perception of 3-dimensional structure-from-motion. CONCLUSIONS: High-fidelity driving simulation provides a unique new source of performance parameters to standardize the assessment of driver fitness. Detailed observations of crashes and other safety errors provide unbiased evidence to aid in the difficult clinical decision of whether older or medically impaired individuals should continue to drive. The findings are complementary to evidence currently being gathered using techniques from epidemiology and cognitive neuroscience.

Accidents, Traffic↗
PubMed2002

Proteomic analysis of protein oxidation in Alzheimer's disease brain.

There is a growing body of evidence that oxidative stress plays a major role in Alzheimer's disease (AD) pathogenesis. Identification of oxidatively altered proteins in AD is important for understanding the relationship between protein oxidation, protein aggregation and neurodegeneration. In this communication, we report a method that can be applied to study oxidative changes of individual proteins in brain. In order to analyze protein oxidation by detection of protein-bound carbonyls, cytosolic protein extracts were derivatized with 2,4-dinitrophenylhydrazine (DNPH) and then separated by two-dimensional (2-D) gel electrophoresis. After electrotransfer to polyvinylidene difluoride (PVDF) membranes, proteins were first stained with Sypro Ruby protein stain, and then the oxidized proteins were detected with anti-dinitrophenyl (DNP) antibody. About 150 proteins and more than 100 oxidized proteins were detected and quantified in both AD and control cases by 2-D image analysis. The amount of protein-bound carbonyls was decreased for six and increased for one protein in AD. The amount of protein was increased for three proteins in AD. Furthermore, the degree of oxidation was calculated as the ratio of protein-bound carbonyls to the total amount of an individual protein. Two proteins showed a significant decrease in the degree of oxidation in AD. Our results suggest that the balance of protein oxidation and degradation is altered in AD.

Aged↗
PubMed2004

Evidence for progression in frontal cortical pathology in late-stage Huntington's disease.

Atrophy of the cerebral cortex in Huntington's disease is regionally heterogeneous and progressive, involving the entire cerebral mantle in terminal stages. Here, two areas (9 and 46) of the dorsolateral prefrontal cortex were analyzed in 11 late-stage (grades 3 or 4) Huntington's diseased patients and 8 normal control subjects. We used a 3-dimensional cell counting method to assess laminar cell density, number, and width. Reductions in overall cortical thickness in areas 9 (26%) and 46 (23%) were comparable. Area 9 exhibited loss of projection neurons in layers III (16%), V (31%), and VI (37%); these same layers were also reduced in width (25%, 34%, and 46%, respectively). In area 46, reductions in cortical width in layers II (18%) and VI (35%) were not accompanied by neuronal loss. Glial density was increased in deeper layers, reaching significance in layer VI (68%) of area 9 and in layer V (75%) of area 46; glial number was not altered. Thus, area 46 exhibited marked cortical thinning without apparent neuronal degeneration, whereas in area 9 neuronal loss was pronounced, consistent with an advanced phase of cortical pathology. Prominent involvement of corticothalamic neurons is discussed in the context of striatal loop circuitry and a possible pathologic cascade of cortical degeneration.

Adult↗
PubMed2004

Proteomic analysis of carbonylated proteins in two-dimensional gel electrophoresis using avidin-fluorescein affinity staining.

A method for detecting carbonylated proteins in two-dimensional electrophoresis (2-DE) was developed using biotinylation and avidin-fluorescein isothiocyanate (FITC) affinity staining. The method was used to examine oxidatively modified proteins associated with oxidative stress. Carbonyl formation in proteins was first examined in a model system by subjecting bovine serum albumin (BSA) and ribonuclease A (RNase A) to metal-catalyzed oxidation (MCO). Carbonyl group formation was found to occur at multiple sites along with a small amount of polypeptide chain cleavage. In vivo studies were conducted in yeast cell cultures using 5 mM hydrogen peroxide to induce oxidative stress. Biotinylation of yeast protein was accomplished during extraction at 4 degrees C in a lysis buffer containing 5 mM biotin-hydrazide. Biotin-hydrazide forms a Schiff base with a carbonyl group on an oxidized protein that is subsequently reduced before electrophoresis. Proteins were separated by either 2-DE or sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). Biotinylated species were detected using avidin-FITC affinity staining. Detection sensitivity with biotinylated proteins was five times higher than achieved by silver staining. The limit of detection with avidin-FITC staining approached 0.64 pmol of protein-associated carbonyls. Twenty carbonylated proteins were identified in the proteome of yeast following oxidative stress with hydrogen peroxide. Matrix-assisted laser desorption/ionization-mass spectrometry (MALDI-MS) analysis of tryptic peptides was used to identify peptides extracted from gels. Aconitase, heat shock protein SSA1 and SSC1, pyruvate decarboxylase isozyme 1, pyruvate kinase 1, enolase 1 and 2, phosphoglycerate kinase, fructose-bisphosphate aldorase, and glyceraldehyde-3-phosphate dehydrogenase were among the major targets of oxidative stress.

Animals↗
PubMed2005

Continuously moving table SENSE imaging.

A combination of continuously moving table imaging and parallel imaging based on sensitivity encoding (SENSE) is presented. One specific geometry is considered, where the receiver array is fixed to the MR magnet and does not move with the table, which allows for head-to-toe imaging with a small total number of coils. Sensitivity maps are defined for the enlarged virtual field of view and are composed according to the k-space sampling scheme such that established parallel reconstruction techniques are applicable to good approximation. In vivo experiments show the feasibility of this approach, and simulations determine the application range. Three-dimensional head-to-toe imaging of volunteers is performed in 77 s with a SENSE reduction factor of 2 in a virtual field of view of 1800 x 460 x 100 mm(3).

Computer Simulation↗
PubMed2004

Identification of cellular proteins modified in response to African swine fever virus infection by proteomics.

Changes in gene expression are produced in cells as a consequence of virus infections. In the present work, we used proteomic technology to globally examine African swine fever virus (ASFV)-infected Vero cells searching for infection-associated proteins in order to determine target proteins for pathogenesis studies. We studied the alterations in cellular protein profile after ASFV infection by two-dimensional electrophoresis, identifying the modified cellular proteins by matrix-assisted laser desorption/ionization peptide mass fingerprinting. A total of twelve different over-expressed cellular proteins were unambiguously identified. The most significant changes were in redox-related proteins, nucleoside diphosphate kinases, heat shock proteins, members of the Ran-Gppnhp-Ranbd1 complex and apolipoproteins. These cellular protein modifications could represent distinct roles during infection related to apoptosis and transcriptional modulation mechanisms. The present study constitutes the first attempt to understand the dynamics of ASFV-host cell interactions by proteomics.

African Swine Fever Virus↗
PubMed2004

New targets of Arabidopsis thioredoxins revealed by proteomic analysis.

Proteomics was used to search for putative thioredoxin (TRX) targets in leaves of the model plant, Arabidopsis thaliana. About forty different proteins have been found to be reduced by TRX, after TRX itself has been specifically reduced by its NADPH-dependent reductase. Twenty-one of the identified proteins were already known or recently proposed to be TRX-dependent and nineteen of the proteins were new potential targets. The identified proteins are involved in a wide variety of processes, including the Calvin cycle, metabolism, photosynthesis, folding, defense against oxidative stress and amino acid synthesis. Two proteins from the glycine cleavage complex were also identified as putative TRX targets, and a new role can be postulated in leaves for TRX in defense against herbivores and/or pathogens.

Arabidopsis↗
PubMed1999

Global protein synthesis shutdown in Autographa californica nucleopolyhedrovirus-infected Ld652Y cells is rescued by tRNA from uninfected cells.

Global protein synthesis arrest occurs in Autographa californica nucleopolyhedrovirus (AcNPV)-infected Ld652Y cells at late times postinfection (p.i.). A Lymantria dispar nucleopolyhedrovirus gene, hrf-1, precludes this protein synthesis arrest. We used in vitro translation assays to characterize the translation defect. Cell-free lysates prepared from uninfected Ld652Y cells, AcNPV-infected cells harvested at early times p.i., and cells infected with vAchrf-1, a recombinant AcNPV bearing hrf-1, all supported translation. Lysates prepared from AcNPV-infected Ld652Y cells at late times p.i. did not support translation, but activity was restored by adding small RNA species from mock-, vAchrf-1- (24 or 48 h p.i.), and AcNPV- (6 h p.i. ) infected cells. Small RNA species (24 and 48 h p.i.) from AcNPV-infected cells did not rescue translation. Assays of RNA species further fractionated by ion exchange chromatography demonstrated that tRNA rescued translation. Although specific defective tRNA species were not revealed by comparative two-dimensional gel analysis, analysis of (32)P-labeled tRNAs showed a reduction in de novo synthesis of small RNA isolated from AcNPV-infected cells compared with mock- and vAchrf-1-infected cells. This study suggests a mechanism of translation arrest involving defective or depleted tRNA species in AcNPV-infected Ld652Y cells.

Animals↗
PubMed2004

Damage-based finite-element vertebroplasty simulations.

The objectives of this study were to quantify the efficacy of vertebroplasty according to: (1) damage and (2) cement quantity (fill) and modulus. Vertebral body damage was numerically simulated using a previously validated two-dimensional finite-element model coupled with an elasto-plastic modulus reduction (EPMR) scheme. The effects of cement fill (% marrow replaced by cement, % MRC) and cement modulus on vertebral apparent modulus and trabecular bone tissue stress concentrations were parametrically assessed for four EPMR damage models (19%, 33%, 60%, and 91% modulus reduction). For this analysis, the elastic modulus of the trabecular bone tissue and marrow elements were assumed to be 10 GPa and 10 kPa, respectively. The effect of cement modulus (varied in the range 1 GPa to 9 GPa) on vertebral apparent modulus was also examined for partial fill (39% MRC) and complete fill (100% MRC) using the 33% modulus reduction damage model. In the case of polymethylmethacrylate (PMMA cement modulus = 2.16 GPa), restoration of the thoracic vertebral body (T10) apparent modulus to undamaged levels required 71% and 100% cement fill for the 19-33% and 60-91% modulus reduction damage models, respectively. Variations in cement modulus had no appreciable effect on the recovery of vertebral apparent modulus to undamaged levels for simulations of partial cement fill (39% MRC). For complete cement fill, however, a PMMA cement modulus produced approximately a 2-fold increase (82%) in vertebral apparent modulus relative to the undamaged vertebral body. Increasing the cement modulus to 9 GPa increased the vertebral apparent modulus over 2.5-fold (158%) relative to the undamaged state. The EPMR damage scheme and repair simulations performed in this study will help clinicians and cement manufacturers to improve vertebroplasty procedures.

Aged↗
PubMed2003

Proteomics for the identification of specifically oxidized proteins in brain: technology and application to the study of neurodegenerative disorders.

Proteomics offers the opportunity elucidate the complex protein interactions of cellular systems by studying the products of genes, i.e., proteins, and their structure, function and localization. The purpose of proteomics is to explain the information contained in the genome sequences in order to provide clues on cellular events, especially related to disease. Our proteomic approach has made possible the identification of specifically oxidized proteins in Alzheimer's disease (AD) brain, providing for the first time evidence on how oxidative stress plays a crucial role in AD-related neurodegeneration. This represents an example of the use of proteomics to solve biological problems related to disease. The field, which is still in its infancy, represents a very promising way to elucidate mechanism of disease at a protein level. However, the techniques that support its development present several limitations and require introduction of new tools and innovation in order to achieve a fast, reliable and sensitive method to understand normal biological processes and their regulation as well as these cellular properties in disease.

Alzheimer Disease↗