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Добірка наукової літератури з теми "Structural alterations"

Автор: Grafiati

Опубліковано: 7 вересня 2022

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Статті в журналах з теми "Structural alterations"

Sugo, T., Y. Sakata, and M. Matsuda. "Structural Alterations in Hereditary Dysfibrinogens." Current Protein and Peptide Science 3, no. 3 (June 1, 2002): 239–47. http://dx.doi.org/10.2174/1389203023380648.

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Agabiti-Rosei, E., M. L. Muiesan, and G. Muiesan. "Regression of Structural Alterations in Hypertension." American Journal of Hypertension 2, no. 2 Pt 2 (February 1, 1989): 70S—76S. http://dx.doi.org/10.1093/ajh/2.2.70s.

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Tunç, T., and K. Yıldız. "Structural Alterations in Mechanically Activated Malachite." Acta Physica Polonica A 125, no. 2 (January 2014): 177–79. http://dx.doi.org/10.12693/aphyspola.125.177.

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Balek, Vladimir, and Alexandra de Koranyi. "Diagnostics of structural alterations in coal." Fuel 69, no. 12 (December 1990): 1502–6. http://dx.doi.org/10.1016/0016-2361(90)90197-x.

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Pourzal, Robin, Ralf Theissmann, Birgit Gleising, Sophie Williams, and Alfons Fischer. "Micro-Structural Alterations in MoM Hip Implants." Materials Science Forum 638-642 (January 2010): 1872–77. http://dx.doi.org/10.4028/www.scientific.net/msf.638-642.1872.

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Since the introduction of CoCrMo alloy metal-on-metal hip replacements have shown a great clinical performance. Metal-on-metal couplings produce a much lower wear rate and volume than e.g. metal-on-polyethylene. However, the particle size is significantly smaller within a nm-range. To evaluate the formation of nano-size wear particles in metal-on-metal hip replacements it is essential to understand the micro-structural changes in the sub-surface region of the CoCrMo alloy. For this study a MoM hip implant was analyzed by means of TEM. The results revealed that the good wear performance of this CoCrMo alloy is linked to a strain induced fcc  hcp phase transformation and in-situ re-crystallization under high shear stresses. The result is a nano-crystalline surface zone of ~200 to 400 nm thickness which undergoes an ongoing process of mechanical intermixing with componants of the interfacial fluid. The incorporation of organic carbon from proteins in between the nano-crystals could be visualised by EFTEM and EDS. This mechanically mixed nc-zone must be the origin of the wear particle detachment. An earlier study by Catelas et. al confirms the hypothesis of the location of wear particle detachment by analyzing the shape and chemical composition of emitted wear particles which exhibits the same size and shape of crystals observed in the nc-zone of the implant analyzed in this study.

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Siegel, Norman J., Prasad Devarajan, and Scott Van Why. "Renal Cell Injury: Metabolic and Structural Alterations." Pediatric Research 36, no. 2 (August 1994): 129–36. http://dx.doi.org/10.1203/00006450-199408000-00001.

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Chiu, Jane, Hana Farhangkhoee, Bing Ying Xu, Shali Chen, Biju George, and Subrata Chakrabarti. "PARP mediates structural alterations in diabetic cardiomyopathy." Journal of Molecular and Cellular Cardiology 45, no. 3 (September 2008): 385–93. http://dx.doi.org/10.1016/j.yjmcc.2008.06.009.

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Chong, Catherine D., Jonathan D. Plasencia, David H. Frakes, and Todd J. Schwedt. "Structural alterations of the brainstem in migraine." NeuroImage: Clinical 13 (2017): 223–27. http://dx.doi.org/10.1016/j.nicl.2016.10.023.

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Dyck, P. J., A. C. Lais, C. Giannini, and J. K. Engelstad. "Structural alterations of nerve during cuff compression." Proceedings of the National Academy of Sciences 87, no. 24 (December 1, 1990): 9828–32. http://dx.doi.org/10.1073/pnas.87.24.9828.

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FEITOSA, V., S. RECCOPIMENTEL, and A. CARDOSO. "Chromosomal analysis of : Presence of structural alterations." Cell Biology International Reports 14 (September 1990): 81. http://dx.doi.org/10.1016/0309-1651(90)90426-y.

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Дисертації з теми "Structural alterations"

Fallon, Nicholas. "Structural and functional brain alterations in fibromyalgia syndrome patients." Thesis, University of Liverpool, 2013. http://livrepository.liverpool.ac.uk/11973/.

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Fibromyalgia syndrome (FMS) is a widespread chronic pain disorder affecting 2−5% of the general population and particularly women of middle age (McBeth and Mulvey, 2012). The syndrome is frequently comorbid with a variety of clinical, functional and psychological disorders (Weir et al., 2006) and associated with a large socio-economic burden (Lachaine et al., 2010). In spite of significant previous research, the underlying aetiology and pathophysiology of FMS is not fully understood (Schmidt-Wilcke and Clauw, 2011). However, aberrant structural and functional brain alterations have been proposed as a casual or maintaining factor of the disorder (Schweinhardt et al., 2008). This thesis utilised functional and structural imaging methods and novel experimental paradigms to explore brain alterations in FMS patients. A comprehensive review of previous experimental findings was performed to identify novel research questions. EEG and MRI data for 5 unique studies was collected over two sessions. In the first study dynamic mechanical stimulation was applied to the forearm of FMS patients and healthy participants, and an ERD analysis of corresponding EEG data was performed. The results revealed that FMS patients exhibited alterations to cortical excitability during brushing stimuli which correlated with clinical measures. These findings indicate that abnormal processing of innocuous somatosensory stimulation may contribute to the pathophysiology and clinical symptom severity of FMS. Secondly, an ERP analysis of EEG data from the observation of pain and non-pain pictures was performed. FMS patients exhibited differences in ERP components and source activation patterns during observation of pain pictures relative to healthy people. Alterations to processing of observed pain occurred in parahippocampal gyrus and may relate to clinical and psychological aspects of FMS, this finding could be utilised to further understand the heterogeneity of psychological profiles of FMS patients in order to better target therapeutic interventions. The third study of the thesis describes a novel comparison of functional connectivity with resting-state network structures utilising fMRI recordings. Functional connectivity with default mode network structures was shown to be altered in FMS. This finding may reflect an ongoing time-dependent reorganisation of resting-state networks due to ongoing chronic pain. In the fourth study, a morphological analysis of subcortical structures was performed using high-resolution T1-weighted MR images. FMS patients demonstrated alterations to the morphology of the brainstem, an important structure in descending nociceptive control. Volumetric alterations in this structure correlated with clinical measures of symptom severity suggesting an important role for brainstem alterations in FMS pain symptoms. In the final study the microstructural integrity of white matter was compared between FMS patients and healthy participants. Although no significant differences were identified the findings indicate that FMS is not likely to be related to abnormal development of white matter tracts. Therefore structural alterations associated with FMS are likely to occur only in the grey matter.

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Acton, Jennifer H. "Visual field and structural alterations in age-related macular degeneration." Thesis, Aston University, 2010. http://publications.aston.ac.uk/8821/.

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The thesis investigated progression of the central 10° visual field with structural changes at the macula in a cross-section of patients with varying degrees of agerelated macular degeneration (AMD). The relationships between structure and function were investigated for both standard and short-wavelength automated perimetry (SWAP). Factors known to influence the measure of visual field progression were considered, including the accuracy of the refractive correction on SWAP thresholds and the learning effect. Techniques of assessing the structure to function relationships between fundus images and the visual field were developed with computer programming and evaluated for repeatability. Drusen quantification of fundus photographs and retro-mode scanning laser ophthalmoscopic images was performed. Visual field progression was related to structural changes derived from both manual and automated methods. Principal Findings: • Visual field sensitivity declined with advancing stage of AMD. SWAP showed greater sensitivity to progressive changes than standard perimetry. • Defects were confined to the central 5°. SWAP defects occurred at similar locations but were deeper and wider than corresponding standard perimetry defects. • The central field became less uniform as severity of AMD increased. SWAP visual field indices of focal loss were of more importance when detecting early change in AMD, than indices of diffuse loss. • The decline in visual field sensitivity over stage of severity of AMD was not uniform, whereas a linear relationship was found between the automated measure of drusen area and visual field parameters. • Perimetry exhibited a stronger relationship with drusen area than other measures of visual function. • Overcorrection of the refraction for the working distance in SWAP should be avoided in subjects with insufficient accommodative facility. • The perimetric learning effect in the 10° field did not differ significantly between normal subjects and AMD patients. • Subretinal deposits appeared more numerous in retro-mode imaging than in fundus photography.

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Wise, Toby Peter James. "Structural and neurochemical alterations in unipolar and bipolar major depression." Thesis, King's College London (University of London), 2017. https://kclpure.kcl.ac.uk/portal/en/theses/structural-and-neurochemical-alterations-in-unipolar-and-bipolar-major-depression(9951ddce-c64a-48ca-9785-426aa82483e2).html.

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Depressive disorders are common and debilitating conditions; however, current methods of diagnosis and treatment are suboptimal, largely due to a lack of understanding of the biological basis of these disorders. Neuroimaging has provided substantial insights in this area, but one particularly understudied area is the relationship between unipolar and bipolar depression. These disorders have similar symptom profiles but require different treatment strategies, making their diagnosis and management challenging for clinicians. The overarching aim of this thesis is to understand differences and similarities in the structure and neurochemistry of neurobiological systems underlying unipolar and bipolar depression. This question is addressed in three ways: Firstly meta-analyses structural neuroimaging studies looking at alterations in grey and white matter were performed to identify patterns of changes that were common or specific to either disorder. Secondly, an original investigation was carried out to identify patterns of neurochemical alteration that differ between unmedicated patients with unipolar and bipolar depression. Lastly, the appropriateness of a dimensional approach to bipolarity in depression was evaluated by looking for structural neural correlates of bipolar symptoms within patients with unip9olar and bipolar depression. The results of these studies show that although many neurobiological alterations are common to unipolar and bipolar depression, there are changes in grey matter volume that are specific to unipolar depression, and changes in white matter volume that are specific to bipolar depression. However, alterations in grey matter volume do not correlate with bipolarity when treated as a dimensional characteristic. These results contribute to our understanding of structural and neurochemical alterations in depressive disorders, and provide targets for future research into improved diagnosis of these conditions.

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Thomas, Katherine. "Alterations within the structural hierarchy of parchment induced by damage mechanisms." Thesis, Cardiff University, 2009. http://orca.cf.ac.uk/55000/.

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Collagen plays an important role in many biological tissues, including skin, which, once dried and treated, forms parchment and leather. The structural alterations that occur in collagenous materials due to X-ray radiation damage, fluctuation of relative humidity, and mechanical deformation (with a special focus on historical parchment) are the focus of this thesis. The primary aim of this thesis is to investigate major structural changes to collagen within parchment when exposed to inappropriate levels of relative humidity during conservation treatments, and cyclic-humidity during long-term storage in archives, museums and libraries. This study led to the discovery that each parchment sample reacted to the application and removal of moisture in a different way, indicating the fundamental need to treat individual parchment documents as in-homogeneous materials. This thesis investigates the changes that fibrillar collagen undergoes and describes the creation of computational models capable of reproducing the X-ray diffraction patterns for collagen. Previous structural models have been created that sufficiently account for native collagen, however, models created as part of this thesis succeed where previous models have failed in explaining the X-ray diffraction patterns collected from damaged collagen. This study provided the opportunity to contribute towards a large-scale international collaborative project on the hugely important historical resource, the Domesday Book. X-ray diffraction was used to provide unprecedented analysis of Domesday Book samples, providing a structural survey at a molecular level. This analysis produced the conclusion that the majority of samples displayed the presence of collagen axial structure, and were generally of a degraded state as a consequence of the method used to source them the samples were scrapings from the surface, which was less intact than the bulk of the parchment.

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Antonova, Elena. "Structural alterations in schizophrenia : relationship to cognitive deficits and drug response." Thesis, King's College London (University of London), 2005. https://kclpure.kcl.ac.uk/portal/en/theses/structural-alterations-in-schizophrenia--relationship-to-cognitive-deficits-and-drug-response(1dd64e90-30e8-454b-90f7-5d7ea06cf5fd).html.

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Fisher, Ashley Anne. "Chemical-Induced Post-Translational Modifications and the Consequent Structural and Functional Alterations." Diss., The University of Arizona, 2008. http://hdl.handle.net/10150/195794.

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Chemical-induced post-translational modifications (PTMs) can alter the structure of proteins, with consequences that may alter protein function, including interference with protein-protein interactions, subcellular protein compartmentalization, and disruption of cellular signaling pathways. To identify the impact of PTMs on the structure and function of protein targets in vitro and in vivo, electrophiles with known toxicity were utilized. Hydroquinone, and its thioether metabolites, cause renal proximal tubular cell necrosis and nephrocarcinogenicity in rats. The adverse effects of these chemicals are in part a result of their oxidation to 1,4-benzoquinones (BQ). Cytochrome c and caspase-7 have been studied as model proteins to identify site-specific adductions and the resulting structural and functional consequences associated with apoptosis. BQ and 2-(N-acetylcystein-S-yl)benzoquinone (NAC-BQ) preferentially bind to solvent-exposed lysine-rich regions within cytochrome c, and specific glutamic acid residues within cytochrome c are novel sites of NAC-BQ adduction. Furthermore, the microenvironment at the site of adduction governs both the initial specificity and the structure of the final adduct. Solvent accessibility and local pKa of the adducted and neighboring amino acids contribute to the selectivity of adduction. Post-adduction chemistry subsequently alters the nature of the final adduct. BQ induced PTMs in cytochrome c produce changes in the structure sufficient to inhibit its ability to initiate caspase-3 activation in native lysates, and its ability to promote Apaf-1 oligomerization into an apoptosome complex, in a purely reconstituted system.Quinone-thioether-protein adduct stability is also dependent upon physiological conditions. Adduct formation on cysteine residues under physiological conditions may be transient, whilst remaining capable of impacting cell signaling events, and of thus contributing to the toxic response elicited by these compounds. Indeed, in vitro analysis of caspase-7 revealed that cysteine residues within the protein are transiently modified with BQ, including the active site thiolate anion. In vitro and in vivo analysis of quinone-thioether adduction on caspase proteins also provided evidence that these catalytic proteins may be in vivo quinone-thioether targets, and could contribute to a mechanistic understanding of the necrotic mode of cell death initiated by quinone-thioether exposure. In summary, mass spectroscopic, molecular modeling, and biochemical approaches collectively confirm that electrophile-protein adducts produce structural changes that influence biological function. Identification of such chemical-induced PTMs on target proteins can provide critical mechanistic understanding of their role in response to environmental chemicals and the associated disease progression. Furthermore, because quinones are a well-known class of electrophilic species and the quinone moiety exits in a number of chemotherapeutic agents, identification of these PTMs will provide insight into the field of drug development and the role electrophilic drug metabolite-PTMs may play in unwanted drug-induced toxicities.

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Vascak, Michal. "STRUCTURAL AND FUNCTIONAL ALTERATIONS IN NEOCORTICAL CIRCUITS AFTER MILD TRAUMATIC BRAIN INJURY." VCU Scholars Compass, 2017. http://scholarscompass.vcu.edu/etd/4927.

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National concern over traumatic brain injury (TBI) is growing rapidly. Recent focus is on mild TBI (mTBI), which is the most prevalent injury level in both civilian and military demographics. A preeminent sequelae of mTBI is cognitive network disruption. Advanced neuroimaging of mTBI victims supports this premise, revealing alterations in activation and structure-function of excitatory and inhibitory neuronal systems, which are essential for network processing. However, clinical neuroimaging cannot resolve the cellular and molecular substrates underlying such changes. Therefore, to understand the full scope of mTBI-induced alterations it is necessary to study cortical networks on the microscopic level, where neurons form local networks that are the fundamental computational modules supporting cognition. Recently, in a well-controlled animal model of mTBI, we demonstrated in the excitatory pyramidal neuron system, isolated diffuse axonal injury (DAI), in concert with electrophysiological abnormalities in nearby intact (non-DAI) neurons. These findings were consistent with altered axon initial segment (AIS) intrinsic activity functionally associated with structural plasticity, and/or disturbances in extrinsic systems related to parvalbumin (PV)-expressing interneurons that form GABAergic synapses along the pyramidal neuron perisomatic/AIS domains. The AIS and perisomatic GABAergic synapses are domains critical for regulating neuronal activity and E-I balance. In this dissertation, we focus on the neocortical excitatory pyramidal neuron/inhibitory PV+ interneuron local network following mTBI. Our central hypothesis is that mTBI disrupts neuronal network structure and function causing imbalance of excitatory and inhibitory systems. To address this hypothesis we exploited transgenic and cre/lox mouse models of mTBI, employing approaches that couple state-of-the-art bioimaging with electrophysiology to determine the structural- functional alterations of excitatory and inhibitory systems in the neocortex.

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Halawani, Dalia. "Structural alterations in the Valosin containing protein and their mechanistic link to neurodegeneration." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=86716.

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The ubiquitin-dependent ATPase, p97, extracts ubiquitinated protein from macromolecular complexes by utilizing ATP-driven conformational changes. Consequently, p97 facilitates essential cellular quality control processes upstream of the proteasome, including endoplasmic reticulum associated degradation (ERAD) and ubiquitin fusion degradation (Ufd). Mutations in p97 are linked to an unusual muti-systemic disease (IBMPFD), involving skeletal muscle degeneration, Paget disease of bone, and fronto-temporal dementia, where the accumulation of ubiquitin-rich protein aggregates suggests impairment in p97-dependent activities. Interestingly, the accumulation of ubiquitin-rich aggregates is also well documented in common neurodegenerative diseases, such as Alzheimer Disease (AD). This thesis is focused on (i) understanding the structural and biochemical consequences of p97 mutations, and (ii) substantiating whether disruption of p97 cell biological function occurs in neurodegeneration. First, we employed a variety of biochemical and biophysical approaches to show that two p97 mutations, Arg155Pro and Ala232Glu, alter the conformational state and ATPase activity. We further demonstrated that these alterations were directly related to p97 protein aggregation in solution. Secondly, we identified p97 as a target of Caspase-6 (Casp6) proteolytic activity in AD and further demonstrated that the overexpression of a Casp6 cleaved p97 fragment compromises the ubiquitin-proteasome system (UPS). Finally, considering the role of IBMPFD-linked p97 mutations in activating caspases, we used simulation annealing modeling to provide evidence that structural defects in pathogenic p97 mutants enhanced p97 susceptibility to caspase-mediated processing. We further showed that p97 was indeed cleaved in dystrophic neurites and activated astrocytes of patients diagnosed with p97-linked fronto-temporal dementia (FTD). Collectively, this work identifies caspase-mediated cleavage of p97 as
La p97, une ATPase ubiquitine-dépendante, extrait des protéines ubiquitinées des complexes macromoléculaires en utilisant les changements conformationnels activés par l'ATP. Conséquemment, la p97 facilite les processus essentiels du contrôle-qualité cellulaire en amont du protéasome, incluant la dégradation associée au réticulum endoplasmique (ERAD) et la voie de dégradation des fusions ubiquitinées (Ufd). Les mutations dans la p97 sont liées à une maladie multisystémique inhabituelle (IBMPFD), impliquant comme effets la dégénération musculosquelettique, la maladie osseuse de Paget et la démence fronto-temporale, où l'accumulation d'aggrégats protéiques riches en ubiquitine suggère la perturbation des activités dépendantes à la p97. Il est intéressant de noter que cette accumulation d'aggrégats riches en ubiquitine est aussi bien démontrée dans les maladies neurodégénératives, telle que la maladie d'Alzheimer (MA). Cette thèse s'intéresse à (i) comprendre les conséquences structurales et biochimiques des mutations dans la p97, et (ii) confirmer si la pertubation de la fonction cellulaire biologique de la p97 s'observe dans la neurodégénération. D'abord, nous avons utilisé une variété d'approches biochimiques et biophysiques pour révéler que les deux mutations dans la p97, Arg155Pro et Ala232Glu, modifient l'état conformationnel et l'activité ATPase. Nous avons de plus démontré que ces altérations étaient directement liées à l'aggrégation protéique de la p97 en solution. Ensuite, nous avons identifié la p97 comme étant une cible de l'activité protéolytique de la Caspase-6 (Casp6) dans la MA et ainsi prouvé que la surexpression d'un fragment p97 clivé par la Casp6 compromet le système ubiquitine protéasome (UPS). Enfin, en tenant compte du rôle des mutations dans la p97 liées à l'IBMPFD dans les caspases activatrices, nous avons utilisé un modèle de simulation de l'appariement pour prouver que$

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Mellor, Russell Howarth. "Structural alterations in dermal lymphatic vessels and microvasculature in breast cancer related lymphoedema." Thesis, St George's, University of London, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.398019.

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Waqar, Tehreem. "Functional, structural and molecular alterations in the heart and kidney during diabetes mellitus." Thesis, University of Central Lancashire, 2016. http://clok.uclan.ac.uk/16733/.

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Background: Diabetes mellitus (DM) is a major metabolic disorder leading to severe long term complications including cardiomyopathy, nephropathy, retinopathy and neuropathy that are common in type 1 DM (T1DM) and type 2 DM (T2DM). Epidemiological studies have demonstrated a role of hyperglycaemia (HG) in eliciting adverse cardiac and renal outcomes including heart failure (HF), diastolic and renal dysfunction. This study investigated the effect of HG on left ventricle (LV) and kidney structural remodelling, function and underlying molecular events associated with the two organs over a period of 2 and 4 months compared to age-matched control. Methods: Molecular mechanisms underlying HG-induced remodelling changes including extracellular matrix (ECM) and myocyte apoptosis deposition, underlying cytokine induction, recapitulation of foetal genes, and transcriptional alterations that may influence the ECM and intracellular calcium [Ca2+]i handling in the LV and kidney of T1DM as well as T2DM were examined in this study. LV and kidney isolations following 2 and 4 months of the development of T1DM were used to assess the remodelling changes and underlying transforming growth factor β1 (TGFβ1) activity, gene expression profile of the ECM and calcium mediators using histological, immunohistochemical and quantitative gene expression analyses compared to age-matched Wistar control rats. Results: The results show that T1DM over 4 months can elicit severe structural and molecular changes in the LV and the kidney compared to 2 months of DM. The severity of these changes was significantly less in respective healthy age-matched control animals. The isolated ventricular cardiomyocytes from T1DM rats displayed altered cellular calcium (Ca2+) homeostasis and [Ca2+]i translating to alterations in mRNA abundance of key Ca2+ handling proteins, cardiac sarcoplasmic reticulum Ca2+ATPase 2a (SERCA2a), ryanodine receptor (RyR2), Na2+/Ca2+ exchanger, phospholamban (Plb), L-type Ca2+ channel proteins (Cav1.2 and Cav1.3), calmodulin2 (Calm2) and Ca2+/calmodulin-dependant protein kinase II delta (CaMK2d) were significantly (p < 0.05) altered in DM compared to age-matched control animals. The results showed LV and kidney remodelling in the T1DM rats with increased ECM deposition that translated into increased gene expressions of key components (collagen 1α, collagen 3α, fibronectin and elastin) and modulators i.e. MMP2 and MMP9 and their tissue inhibitor (TIMP4), connective tissue growth factor (CTGF), integrin 5α and connexin 43 (Cx43) of the ECM. Molecular derangements underlying this phenotype included increased TGFβ1 transcription and activity, recapitulation of foetal gene phenotype atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) with marked hypertrophy, underscored by caspase-3 mediated cell apoptosis. Electron microscopic analysis revealed ultrastructural alterations in LV highlighted by increased mitochondrial number and altered mitochondrial population, whereas the kidney presented with increase glomerular basement membrane thickness in T1DM compared to controls. These data clearly show that adult vs young adult, in combination with STZ-induced T1DM, can elicit severe changes to both the heart and the kidney, respectively in structural, functional and biochemical alterations. The final part of the study revealed exercise training after 2-3 months may have beneficial effects in T2DM animals compared to sedentary control rats. Ventricular myocyte and shortening were generally well preserved despite alterations in mRNA gene expression encoding a variety of cardiac muscle proteins in the exercised trained adult GK diabetic rat. LV remodelling in GK rat presented with marked hypertrophy of cardiomyocytes and increased ECM deposition that altogether translated into increased ECM components and regulators which were reversed by exercise training. Conclusions: The present results have demonstrated that T1DM, if left untreated, can lead to severe changes to both the heart and the kidney. These changes seem to occur at structural and molecular levels leading to dysfunction of the heart and kidney and the severity of the damage is enhanced over time. Data suggests that diabetic cardiomyopathy (DCM) may have possible origins in pro-fibrotic and pro-hypertrophic mechanisms. Moreover, this study demonstrates that physical exercise training continues to be one of the most valuable forms of non-pharmacological therapy in DM. Data concerning molecular signalling cascades and ECM phenotype is particularly significant as targeting features of structural remodelling may delay onset and severity of myocardial and renal complications.

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Книги з теми "Structural alterations"

Council, Surrey (England) County. Surrey structure plan 1980: Proposed first alteration : the alterations. Kingston upon Thames: The Council, 1986.

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West Sussex (England). County Planning Department. West Sussex structure plan 1980 proposed first alteration: The alterations. Chichester: West Sussex County Council, 1985.

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Council, Hampshire County. South Hampshire structure plan alterations. [Winchester]: Hampshire County Council, 1987.

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Council, Leicestershire County. Leicestershire structure plan alteration no. 2 and Rutland structure plan alteration no. 1. [Leicester]: Leicestershire County Council, 1985.

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Geyer, Hans. The pig's hoof: Its structure and alterations. Basel, Switzerland: Hoffmann-La Roche, 1986.

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Bedfordshire (England). County Planning Department. County structure plan: Alterations number 3 : policies. Bedford: Bedfordshire County Council, 1990.

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Office, Great Britain Department of the Environment and Transport West Midlands Regional. West Midlands structure plan: Proposals for alterations. Birmingham: W.M.C.C., 1986.

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Essex (England). Planning Department. Essex structure plan: Proposed 1st alteration. Chelmsford: Essex County Council, 1986.

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Council, Lincolnshire (England) County. Lincolnshire structure plan: Alteration no. 2. Lincoln: Lincolnshire County Council, 1991.

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Council, Gloucestershire County. Structure plan: First alteration, written statement. Gloucester: Gloucestershire County Council, 1992.

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Schubert, I., and R. Rieger. "Evolutionary Aspects of Structural Chromosome Aberrations." In Chromosomal Alterations, 380–94. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78887-1_36.

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Lauer, Janelle, and Marino Zerial. "Profiling Structural Alterations During Nucleotide Exchange by." In Methods in Molecular Biology, 69–89. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1346-7_6.

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Rupp, H., and R. Jacob. "Structural and functional diversity of human ventricular myosin." In Cellular and Molecular Alterations in the Failing Human Heart, 95–106. Heidelberg: Steinkopff, 1992. http://dx.doi.org/10.1007/978-3-642-72474-9_8.

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Robaire, Bernard, and Valerie Serre. "Aging Causes Structural and Functional Alterations in the Epididymis." In The Testis, 174–85. New York, NY: Springer New York, 2000. http://dx.doi.org/10.1007/978-1-4612-2106-7_16.

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Rizzoni, Damiano, Carolina De Ciuceis, Enzo Porteri, Enrico Agabiti-Rosei, and Claudia Agabiti-Rosei. "Microvascular Structural Alterations and Tissue Perfusion in Hypertension/Diabetes." In Updates in Hypertension and Cardiovascular Protection, 183–96. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-75310-2_14.

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Díez, Javier. "Structural Alterations in Arterial Stiffness: Role of Arterial Fibrosis." In Blood Pressure and Arterial Wall Mechanics in Cardiovascular Diseases, 205–13. London: Springer London, 2014. http://dx.doi.org/10.1007/978-1-4471-5198-2_17.

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Garcia, J. H., M. L. Anderson, and J. H. Halsey. "Experimental Hypoglycemia: Correlation Between EEG Abnormalities and Structural Alterations." In Cerebral Ischemia and Calcium, 44–51. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-85863-5_6.

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Shultzaberger, Ryan K., and John Dresios. "Identification of Genomic Alterations Through Multilevel DNA Structural Analysis." In Methods in Molecular Biology, 191–201. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8931-7_16.

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Tsuchihashi, Yasunari, Toshio Tani, Kyohei Maruyama, Shozo Yorioka, Katsuhiro Okada, Hiromasa Sudo, Tsukasa Ashihara, Setsuya Fujita, and Keiichi Kawai. "Structural Alterations of Mucosal Microvascular System in Human Chronic Gastritis." In Microcirculation in Circulatory Disorders, 161–69. Tokyo: Springer Japan, 1988. http://dx.doi.org/10.1007/978-4-431-68078-9_17.

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Andjelkovic, Anuska V., and Richard F. Keep. "Structural Alterations to the Endothelial Tight Junction Complex During Stroke." In Springer Series in Translational Stroke Research, 3–23. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-32337-4_1.

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Тези доповідей конференцій з теми "Structural alterations"

Shea, Christopher R., Diana Whitaker, George F. Murphy, Norah Chen, Joanne Wimberly, M. Scholz, M. E. Sherwood, Thomas J. Flotte, and Tayyaba Hasan. "Structural and functional alterations in rhodamine-123- and doxycycline-photosensitized cells." In OE/LASE '90, 14-19 Jan., Los Angeles, CA, edited by Steven L. Jacques. SPIE, 1990. http://dx.doi.org/10.1117/12.17613.

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Ramanujam, Nimmi, and J. Quincy Brown. "Physiologic, Metabolic, and Structural Alterations in Breast Cancer: Assessment via Optical Technologies." In Frontiers in Optics. Washington, D.C.: OSA, 2006. http://dx.doi.org/10.1364/fio.2006.jwc1.

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Mauad, Thais, Renata Calciolari Rossi e Silva, Raquel Annoni, Diogenes Seraphin Ferreira, and Luiz Feranado Ferraz da Silva. "Structural alterations and endothelial activation in pulmonary and bronchial vessels of asthmatics." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa3771.

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Lo, Wen, Hsin-Yuan Tan, Yuh-Ling Chang, Yen Sun, Sung-Jan Lin, Shiou-Hwa Jee, and Chen-Yuan Dong. "Demonstration of structural alterations in experimental corneal infectious model using multiphoton microscopy." In Biomedical Optics (BiOS) 2007, edited by Fabrice Manns, Per G. Soederberg, Arthur Ho, Bruce E. Stuck, and Michael Belkin. SPIE, 2007. http://dx.doi.org/10.1117/12.699468.

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Plenker, Dennis, Carina Lorenz, Miriam Bertrand, Richard Riedel, Joop de Langen, Johannes Brägelmann, Reinhard Büttner, et al. "Abstract 1920: Targeting structural RET and MET kinase alterations in lung adenocarcinoma patients." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-1920.

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Lee, Moosung, Eeksung Lee, JaeHwang Jung, Hyeonseung Yu, Kyoohyun Kim, Jonghee Yoon, Shinhwa Lee, Yong Jeong, and YongKeun Park. "Quantifying structural alterations in Alzheimer's disease brains using quantitative phase imaging (Conference Presentation)." In Quantitative Phase Imaging III, edited by Gabriel Popescu and YongKeun Park. SPIE, 2017. http://dx.doi.org/10.1117/12.2251560.

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Parolia, Abhijit, Marcin Cieslik, Shih-Chun Chu, Lanbo Xiao, Takahiro Ouchi, Yuping Zhang, Xiaoju Wang, et al. "Abstract 4497: Distinct structural classes of activating FOXA1 alterations in prostate cancer progression." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-4497.

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Sausen, Mark. "Abstract CN02-02: Comprehensive detection of structural alterations in the circulation of cancer patients." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; November 5-9, 2015; Boston, MA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1535-7163.targ-15-cn02-02.

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Jiao, X., L. Yao, E. Keating, Y. Zuo, S. Tadayyon, F. Possmayer, and RA Veldhuizen. "Ventilator Induced Lung Injury Results in Structural Alterations of the Pulmonary Surfactant Surface Film." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3840.

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Звіти організацій з теми "Structural alterations"

Cheng, Shirui, Ming Xin, Jun Zhou, Ziwen Wang, Ruirui Sun, and Fanrong Liang. Structural and functional alterations in the brain of chronic low back pain: A systematic review and multimodal meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2020. http://dx.doi.org/10.37766/inplasy2020.5.0103.

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Jackson, S. L. Alteration Zones, Structure, and Metamorphism of the Laurie Lake area. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 1989. http://dx.doi.org/10.4095/127274.

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Poulsen, K. H. Structure and Hydrothermal Alteration, Rice Lake Gold District, southeastern Manitoba. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 1989. http://dx.doi.org/10.4095/127279.

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De Almeida, Camila P. Pathological and Pathophysiological Alterations in Temporal Lobe Structures After Mild Traumatic Brain Injury. Fort Belvoir, VA: Defense Technical Information Center, January 2014. http://dx.doi.org/10.21236/ad1012808.

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Ciufo, T. J., K. Jellicoe, C. Yakymchuk, S. Lin, P. Mercier-Langevin, and N. Wodicka. Geology, structural evolution, and hydrothermal alteration of the Island gold deposit, Michipicoten greenstone belt, Ontario. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 2020. http://dx.doi.org/10.4095/323671.

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Ames, D. E., and H. L. Gibson. Geology, alteration and mineralization of the Onaping Formation, Morgan Township, Sudbury Structure, Ontario. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 2004. http://dx.doi.org/10.4095/214890.

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Wannamaker, Philip E. Structural controls, alteration, permeability and thermal regime of Dixie Valley from new-generation MT/galvanic array profiling. Office of Scientific and Technical Information (OSTI), November 2007. http://dx.doi.org/10.2172/920085.

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Lang, J. R., R. Duncan, D. R. Lentz, W. Zhang, A. Bustard, C. R. M. McFarlane, and K. G. Thorne. Geological and structural controls on hydrothermal alteration and W-Mo mineralization in the Sisson deposit, New Brunswick. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 2015. http://dx.doi.org/10.4095/296474.

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Wang, K., G. Chi, K. M. Bethune, and C. Card. Fluid composition, thermal conditions, fluid-structural relationships and graphite alteration of the Phoenix uranium deposit, Athabasca Basin, Saskatchewan. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 2015. http://dx.doi.org/10.4095/295787.

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Ames, D. E. Geology, alteration and mineralization of the Onaping Formation, Rockcut Lake area, Norman Township, Sudbury Structure, Ontario. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 2004. http://dx.doi.org/10.4095/215385.

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