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Kelly Del Tredici - One of the best experts on this subject based on the ideXlab platform.
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the preclinical phase of the Pathological Process underlying sporadic alzheimer s disease
Brain, 2015Co-Authors: Heiko Braak, Kelly Del TrediciAbstract:Abnormal tau lesions (non-argyrophilic pretangle material, argyrophilic neuropil threads, neurofibrillary tangles) in select types of neurons are crucial for the pathogenesis of sporadic Alzheimer's disease. Ongoing formation of these tau lesions persists into end-stage Alzheimer's disease and is not subject to remission. The early pretangle disease phase is a focus of increasing interest because only abnormal forms of the microtubule-associated protein tau are involved at that point and, in contrast to late-stage disease when amyloid-β deposition is present, this phase is temporally closer to the prevailing conditions that induce the Pathological Process underlying Alzheimer's disease. Extracellular and aggregated amyloid-β may only be produced under Pathological conditions by nerve cells that contain abnormal tau. One potential trigger for tau protein hyperphosphorylation and conformational change in Alzheimer's disease may be the presence of a non-endogenous pathogen. Subsequently, a predictable regional distribution pattern of the tau lesions develops in phylogenetically late-appearing and ontogenetically late-maturing neurons that are connected via their axons. It is hoped that hypotheses drawn from these considerations, as well as from recent tau dissemination models, from studies of variant tau conformers, and from tau imaging will encourage the development of new preventative and disease-modifying strategies.
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are cases with tau pathology occurring in the absence of aβ deposits part of the ad related Pathological Process
Acta Neuropathologica, 2014Co-Authors: Heiko Braak, Kelly Del TrediciAbstract:and only at the same predilection sites as the tau lesions that are present in individuals with Aβ and in fully developed AD can represent possible preclinical (early) stages of the AD-related Pathological Process. In other words, an interim or transient absence of a minimum of Aβ deposits is not an adequate or compelling rationale for excluding tau-only cases from the developmental spectrum of the ADrelated Process, nor is the existence of such cases in nonaged individuals (compare Table 3 here with Table 1 in [8]) consistent with the term ‘primary age-related tauopathy.’ The authors claim that PART, in contrast to AD, is probably not APOE e4 allele-driven. However, an earlier study showing that non-demented individuals with NFT stage I pathology displayed a significantly higher APOE e4 allele frequency than controls [11] reached the opposite conclusion. That study was retrospective (cross sectional), but so were the studies in the supporting literature (13, 67, 70, 122, 150, 151) cited by Crary et al. [8], who have not incorporated into their thinking the implications of recent original findings showing that neuronal injury develops independently of Aβ in APOE e4 allele carriers [7, 13]. The fundamental question whether 3R + 4R tau-only cases and cases with 3R + 4R tau plus Aβ deposits belong to essentially different Pathological Processes cannot be resolved without identifying potentially unique mechanisms for cases with tau-only pathology, e.g., by means of experimental models of tau seeding and neuron-to-neuron transmission [12], in which tau extracts are isolated not from AD brains but from brains of individuals with autopsy-confirmed 3R + 4R tau-only lesions. Biomarkerbased research and positron emission tomography (PET) imaging of brain Aβ and of tau that can quantify abnormalities in AD-associated neurodegeneration [19] have the developmental potential to reach the point at which the presence and progression of both Pathological proteins can The current neuroPathological diagnosis of clinically suspected Alzheimer’s disease (AD) requires the presence of advanced neurofibrillary tangle (NFT) stages and of Aβ deposits in the brain [15]. Both abnormal proteins (intraneuronal forms of aggregated and hyperphosphorylated tau and extracellular Aβ) develop at different times at different predilection sites and progress gradually but inexorably during the Pathological Process by sequential spreading into previously uninvolved regions. Tau pathology develops prior to Aβ deposits [1, 5, 6]. In their position paper, Crary et al. [8] present arguments for distinguishing two Processes: an ‘AD-related Process’ and a non-AD-related ‘primary age-related tauopathy’ (PART). Both are characterized by the presence of 3R and 4R tau isoforms as well as paired helical filaments but they differ in that the first displays the combined presence of tau and Aβ pathologies, whereas the second is marked by the presence of tau pathology alone. Nevertheless, application of the criteria required to confirm neuroPathologically that the diagnosis of clinically manifest AD [15] does not warrant the disqualification of tau-only cases because the statement that “a diagnosis of AD neuropathologic changes requires at least a minimum threshold level of Aβ deposition” [8] is correct only in cases with clinically diagnosed AD but is inaccurate when applied to non-demented individuals. In the absence of Aβ deposits, tau pathology consisting of 3R and 4R isoforms that occurs in the same neuronal cell types as those known to be vulnerable to the Pathological Process underlying AD
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reply the early Pathological Process in sporadic alzheimer s disease
Acta Neuropathologica, 2013Co-Authors: Heiko Braak, Kelly Del TrediciAbstract:[7] was designated NFT stage I [8]. Gallyas-negative AT8immunopositive pretangles, described by Bancher et al. [5] and Braak et al. [6], were included in a revised staging protocol for AD [13], but subcortical and cortical “pretangle stages” (a–c, 1a, 1b) as such have been proposed only recently [10, 11, 14]. The LC is not routinely examined at autopsy for the presence of aggregated tau or other proteinopathies in children or young and middle-aged persons. We performed such a study on 42 cases under the age of 30 using AT8 immunohistochemistry and found tau aggregates in LC neurons of 38/42 (90 %) individuals [10]. The tau pathology was located only in dorsal portions of the LC that contain cortically projecting neurons [27, 43]. 41 out of 42 (98 %) cases lacked cortical Aβ deposition [10]. In a larger autopsy-based study, elobeid et al. [23] reported AT8-immunopositive tau in the LC of 25/83 (30 %) young and middle-aged cases, all without concomitant cortical Aβ deposits and all without aggregated tau in the transentorhinal region. If, as Mann and Hardy [41] speculate, the LC lesions in some of the young subjects were driven by acute lethal head injury [10], we also should have encountered at least some Aβ deposition in the brains of these individuals, inasmuch as head trauma studies performed in humans have reported the presence of transient Aβ deposits [26, 54]. Yet, this was not the case. performance of 3r and 4r immunohistochemistry can allay (or confirm) the reservations expressed by Mann and Hardy [41] regarding the absence of evidence for the different isoforms of phospho-tau in such cases. However, the presence of AT8-immunopositive tau aggregates in the LC of both relatively young cohorts makes it unlikely that all or most of the lesions seen there represent prodromal (“incidental”) pathology associated with rare non-AD tauopathies, such as corticobasal degeneration (CBD) or We are inclined to think that the riddle of the chicken or the egg (i.e., the chicken egg or simply an egg?) is too problematic to help illustrate the problem of tau and amyloid-β (Aβ). However, one can summarize our respective viewpoints in the form of “either/or” propositions: Either Aβ is present in the extracellular space at cortical predilection sites and, from there, causes tau to aggregate within coeruleus neurons, as postulated by Mann and Hardy [41]— the authors do not mention how extracellular cortical Aβ reaches the locus coeruleus (LC) to influence nerve cells there (e.g., by means of retrograde axonal transport)—“the undiscerning ‘locus chicken’ eagerly pecks at” the “bad egg (Aβ deposition).” Or involved projection cells (i.e., nerve cells containing aggregated tau) in the LC and in other nonthalamic nuclei with diffuse cortical projections [10, 29, 31, 50] cause via anterograde axonal transport the release of Aβ into the cortical extracellular space [46], where it can aggregate at local diffusion zones into diffuse amyloid plaques, as we have recently postulated [12]. In our view, the Pathological Process underlying sporadic Alzheimer’s disease (AD) develops over the course of a lifetime [11, 14]. The original staging protocol was based on the topographical distribution patterns of (1) Gallyasstained neurofibrillary changes (tangles, neuropil threads, dystrophic neurites of neuritic plaques) across six stages (NFT I–VI) and (2) Campbell–switzer-stained Aβ plaque deposition (stages A–C) in the cerebral cortex [8]. The earliest stage of cortical neurofibrillary pathology in the superficial entorhinal layer pre-α of the transentorhinal region
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the Pathological Process underlying alzheimer s disease in individuals under thirty
Acta Neuropathologica, 2011Co-Authors: Heiko Braak, Kelly Del TrediciAbstract:Brains of 42 individuals between the ages of 4 and 29 were examined with antibodies (AT8, 4G8) and silver stains for the presence of intraneuronal and extracellular protein aggregates associated with Alzheimer’s disease. Thirty-eight of 42 (38/42) cases displayed abnormally phosphorylated tau protein (pretangle material) in nerve cells or in portions of their cellular Processes, and 41/42 individuals showed no extracellular amyloid-β protein deposition or neuritic plaques—an individual with Down syndrome was the only exception. In 16/42 cases abnormal tau was found in the transentorhinal region, and in 3/42 cases this site was Gallyas-positive for isolated NFTs (NFT stage I). Of 26 cases that lacked abnormal tau in the transentorhinal region, 4 did not show pretangle material at subcortical sites. The remaining 22 of these same 26 cases, however, had subcortical lesions confined to non-thalamic nuclei with diffuse projections to the cerebral cortex, and, remarkably, in 19/22 individuals the pretangle material was confined to the noradrenergic coeruleus/subcoeruleus complex. Assuming the pretangle alterations are not transient and do not regress, these findings may indicate that the Alzheimer’s disease-related Pathological Process leading to neurofibrillary tangle formation does not begin in the cerebral cortex but, rather, in select subcortical nuclei, and it may start quite early, i.e., before puberty or in early young adulthood.
Heiko Braak - One of the best experts on this subject based on the ideXlab platform.
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the preclinical phase of the Pathological Process underlying sporadic alzheimer s disease
Brain, 2015Co-Authors: Heiko Braak, Kelly Del TrediciAbstract:Abnormal tau lesions (non-argyrophilic pretangle material, argyrophilic neuropil threads, neurofibrillary tangles) in select types of neurons are crucial for the pathogenesis of sporadic Alzheimer's disease. Ongoing formation of these tau lesions persists into end-stage Alzheimer's disease and is not subject to remission. The early pretangle disease phase is a focus of increasing interest because only abnormal forms of the microtubule-associated protein tau are involved at that point and, in contrast to late-stage disease when amyloid-β deposition is present, this phase is temporally closer to the prevailing conditions that induce the Pathological Process underlying Alzheimer's disease. Extracellular and aggregated amyloid-β may only be produced under Pathological conditions by nerve cells that contain abnormal tau. One potential trigger for tau protein hyperphosphorylation and conformational change in Alzheimer's disease may be the presence of a non-endogenous pathogen. Subsequently, a predictable regional distribution pattern of the tau lesions develops in phylogenetically late-appearing and ontogenetically late-maturing neurons that are connected via their axons. It is hoped that hypotheses drawn from these considerations, as well as from recent tau dissemination models, from studies of variant tau conformers, and from tau imaging will encourage the development of new preventative and disease-modifying strategies.
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are cases with tau pathology occurring in the absence of aβ deposits part of the ad related Pathological Process
Acta Neuropathologica, 2014Co-Authors: Heiko Braak, Kelly Del TrediciAbstract:and only at the same predilection sites as the tau lesions that are present in individuals with Aβ and in fully developed AD can represent possible preclinical (early) stages of the AD-related Pathological Process. In other words, an interim or transient absence of a minimum of Aβ deposits is not an adequate or compelling rationale for excluding tau-only cases from the developmental spectrum of the ADrelated Process, nor is the existence of such cases in nonaged individuals (compare Table 3 here with Table 1 in [8]) consistent with the term ‘primary age-related tauopathy.’ The authors claim that PART, in contrast to AD, is probably not APOE e4 allele-driven. However, an earlier study showing that non-demented individuals with NFT stage I pathology displayed a significantly higher APOE e4 allele frequency than controls [11] reached the opposite conclusion. That study was retrospective (cross sectional), but so were the studies in the supporting literature (13, 67, 70, 122, 150, 151) cited by Crary et al. [8], who have not incorporated into their thinking the implications of recent original findings showing that neuronal injury develops independently of Aβ in APOE e4 allele carriers [7, 13]. The fundamental question whether 3R + 4R tau-only cases and cases with 3R + 4R tau plus Aβ deposits belong to essentially different Pathological Processes cannot be resolved without identifying potentially unique mechanisms for cases with tau-only pathology, e.g., by means of experimental models of tau seeding and neuron-to-neuron transmission [12], in which tau extracts are isolated not from AD brains but from brains of individuals with autopsy-confirmed 3R + 4R tau-only lesions. Biomarkerbased research and positron emission tomography (PET) imaging of brain Aβ and of tau that can quantify abnormalities in AD-associated neurodegeneration [19] have the developmental potential to reach the point at which the presence and progression of both Pathological proteins can The current neuroPathological diagnosis of clinically suspected Alzheimer’s disease (AD) requires the presence of advanced neurofibrillary tangle (NFT) stages and of Aβ deposits in the brain [15]. Both abnormal proteins (intraneuronal forms of aggregated and hyperphosphorylated tau and extracellular Aβ) develop at different times at different predilection sites and progress gradually but inexorably during the Pathological Process by sequential spreading into previously uninvolved regions. Tau pathology develops prior to Aβ deposits [1, 5, 6]. In their position paper, Crary et al. [8] present arguments for distinguishing two Processes: an ‘AD-related Process’ and a non-AD-related ‘primary age-related tauopathy’ (PART). Both are characterized by the presence of 3R and 4R tau isoforms as well as paired helical filaments but they differ in that the first displays the combined presence of tau and Aβ pathologies, whereas the second is marked by the presence of tau pathology alone. Nevertheless, application of the criteria required to confirm neuroPathologically that the diagnosis of clinically manifest AD [15] does not warrant the disqualification of tau-only cases because the statement that “a diagnosis of AD neuropathologic changes requires at least a minimum threshold level of Aβ deposition” [8] is correct only in cases with clinically diagnosed AD but is inaccurate when applied to non-demented individuals. In the absence of Aβ deposits, tau pathology consisting of 3R and 4R isoforms that occurs in the same neuronal cell types as those known to be vulnerable to the Pathological Process underlying AD
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reply the early Pathological Process in sporadic alzheimer s disease
Acta Neuropathologica, 2013Co-Authors: Heiko Braak, Kelly Del TrediciAbstract:[7] was designated NFT stage I [8]. Gallyas-negative AT8immunopositive pretangles, described by Bancher et al. [5] and Braak et al. [6], were included in a revised staging protocol for AD [13], but subcortical and cortical “pretangle stages” (a–c, 1a, 1b) as such have been proposed only recently [10, 11, 14]. The LC is not routinely examined at autopsy for the presence of aggregated tau or other proteinopathies in children or young and middle-aged persons. We performed such a study on 42 cases under the age of 30 using AT8 immunohistochemistry and found tau aggregates in LC neurons of 38/42 (90 %) individuals [10]. The tau pathology was located only in dorsal portions of the LC that contain cortically projecting neurons [27, 43]. 41 out of 42 (98 %) cases lacked cortical Aβ deposition [10]. In a larger autopsy-based study, elobeid et al. [23] reported AT8-immunopositive tau in the LC of 25/83 (30 %) young and middle-aged cases, all without concomitant cortical Aβ deposits and all without aggregated tau in the transentorhinal region. If, as Mann and Hardy [41] speculate, the LC lesions in some of the young subjects were driven by acute lethal head injury [10], we also should have encountered at least some Aβ deposition in the brains of these individuals, inasmuch as head trauma studies performed in humans have reported the presence of transient Aβ deposits [26, 54]. Yet, this was not the case. performance of 3r and 4r immunohistochemistry can allay (or confirm) the reservations expressed by Mann and Hardy [41] regarding the absence of evidence for the different isoforms of phospho-tau in such cases. However, the presence of AT8-immunopositive tau aggregates in the LC of both relatively young cohorts makes it unlikely that all or most of the lesions seen there represent prodromal (“incidental”) pathology associated with rare non-AD tauopathies, such as corticobasal degeneration (CBD) or We are inclined to think that the riddle of the chicken or the egg (i.e., the chicken egg or simply an egg?) is too problematic to help illustrate the problem of tau and amyloid-β (Aβ). However, one can summarize our respective viewpoints in the form of “either/or” propositions: Either Aβ is present in the extracellular space at cortical predilection sites and, from there, causes tau to aggregate within coeruleus neurons, as postulated by Mann and Hardy [41]— the authors do not mention how extracellular cortical Aβ reaches the locus coeruleus (LC) to influence nerve cells there (e.g., by means of retrograde axonal transport)—“the undiscerning ‘locus chicken’ eagerly pecks at” the “bad egg (Aβ deposition).” Or involved projection cells (i.e., nerve cells containing aggregated tau) in the LC and in other nonthalamic nuclei with diffuse cortical projections [10, 29, 31, 50] cause via anterograde axonal transport the release of Aβ into the cortical extracellular space [46], where it can aggregate at local diffusion zones into diffuse amyloid plaques, as we have recently postulated [12]. In our view, the Pathological Process underlying sporadic Alzheimer’s disease (AD) develops over the course of a lifetime [11, 14]. The original staging protocol was based on the topographical distribution patterns of (1) Gallyasstained neurofibrillary changes (tangles, neuropil threads, dystrophic neurites of neuritic plaques) across six stages (NFT I–VI) and (2) Campbell–switzer-stained Aβ plaque deposition (stages A–C) in the cerebral cortex [8]. The earliest stage of cortical neurofibrillary pathology in the superficial entorhinal layer pre-α of the transentorhinal region
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the Pathological Process underlying alzheimer s disease in individuals under thirty
Acta Neuropathologica, 2011Co-Authors: Heiko Braak, Kelly Del TrediciAbstract:Brains of 42 individuals between the ages of 4 and 29 were examined with antibodies (AT8, 4G8) and silver stains for the presence of intraneuronal and extracellular protein aggregates associated with Alzheimer’s disease. Thirty-eight of 42 (38/42) cases displayed abnormally phosphorylated tau protein (pretangle material) in nerve cells or in portions of their cellular Processes, and 41/42 individuals showed no extracellular amyloid-β protein deposition or neuritic plaques—an individual with Down syndrome was the only exception. In 16/42 cases abnormal tau was found in the transentorhinal region, and in 3/42 cases this site was Gallyas-positive for isolated NFTs (NFT stage I). Of 26 cases that lacked abnormal tau in the transentorhinal region, 4 did not show pretangle material at subcortical sites. The remaining 22 of these same 26 cases, however, had subcortical lesions confined to non-thalamic nuclei with diffuse projections to the cerebral cortex, and, remarkably, in 19/22 individuals the pretangle material was confined to the noradrenergic coeruleus/subcoeruleus complex. Assuming the pretangle alterations are not transient and do not regress, these findings may indicate that the Alzheimer’s disease-related Pathological Process leading to neurofibrillary tangle formation does not begin in the cerebral cortex but, rather, in select subcortical nuclei, and it may start quite early, i.e., before puberty or in early young adulthood.
V A Chereshnev - One of the best experts on this subject based on the ideXlab platform.
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systemic inflammation methodological approaches to identification of the common Pathological Process
PLOS ONE, 2016Co-Authors: Natalia V Zotova, V A Chereshnev, Yu E GusevAbstract:We defined Systemic inflammation (SI) as a "typical, multi-syndrome, phase-specific Pathological Process, developing from systemic damage and characterized by the total inflammatory reactivity of endotheliocytes, plasma and blood cell factors, connective tissue and, at the final stage, by microcirculatory disorders in vital organs and tissues." The goal of the work: to determine methodological approaches and particular methodical solutions for the problem of identification of SI as a common Pathological Process. SI can be defined by the presence in plasma of systemic proinflammatory cell stress products-cytokines and other inflammatory mediators, and also by the complexity of other Processes signs. We have developed 2 scales: 1) The Reactivity Level scale (RL)-from 0 to 5 points: 0-normal level; RL-5 confirms systemic nature of inflammatory mediator release, and RL- 2-4 defines different degrees of event probability. 2) The SI scale, considering additional criteria along with RL, addresses more integral criteria of SI: the presence of ≥ 5 points according to the SI scale proves the high probability of SI developing. To calculate the RL scale, concentrations of 4 cytokines (IL-6, IL-8, IL-10, TNF-α) and C-reactive protein in plasma were examined. Additional criteria of the SI scale were the following: D-dimers>500ng/ml, cortisol>1380 or <100nmol/l, troponin I≥0.2ng/ml and/or myoglobin≥800ng/ml. 422 patients were included in the study with different septic (n-207) and aseptic (n-215) pathologies. In 190 cases (of 422) there were signs of SI (lethality 38.4%, n-73). In only 5 of 78 cases, lethality was not confirmed by the presence of SI. SI was registered in 100% of cases with septic shock (n-31). There were not significant differences between AU-ROC of CR, SI scale and SOFA to predict death in patients with sepsis and trauma.
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systemic inflammation theoretical and methodological approaches to description of general Pathological Process model part iv a dynamics of the Process
Patologicheskaia fiziologiia i èksperimental'naia terapiia, 2014Co-Authors: E Y Gusev, V A ChereshnevAbstract:Systemic inflammation (SI) as a general Pathological Process is considered as a development of cellular stress in response to systemic action of damage factors. An Acute SI is characterized by wavelike course (a changing of activation and inhibition phases); a chronic SI is characterized by successive changing of stages of its progressive development. SI may be classified into three variants which are dependened on intensity of systemic alteration as well as on condition of anti-inflammatory systems: 1) a "break" is a fulminating Process (e.g. fulminating sepsis), 2) a "caving" is a relatively gradual conversion of classical inflammation to systemic one; 3) a "sticking" is a typical chronic SI. An evolution of the acute SI is characterized by the 5 following phases: a development, hyperergic phases of the primary and the secondary phlogogenic impact, a resolution, and depressive phase. The last phase is a typical for the "break" variant and characterized by a tolerance, but not a resistance strategy to action of factors of systemic alteration. It is advisable to estimate SI with Integral Criteria (Scales), which reflect both of the development of a systemic inflammatory response and the following other particular Processes of SI: the systemic alteration, the micro thrombosis and other microcirculatory disorders, multiple organ dysfunction, and a distress of the neuroendocrine system.
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systemic inflammation theoretical and methodological approaches to description of general Pathological Process model part 3 backgroung for nonsyndromic approach
Patologicheskaia fiziologiia i èksperimental'naia terapiia, 2013Co-Authors: E Y Gusev, V A ChereshnevAbstract:Theoretical and methodological approaches to description of systemic inflammation as general Pathological Process are discussed. It is shown, that there is a need of integration of wide range of types of researches to develop a model of systemic inflammation.
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systemic inflammation theoretical and methodological approaches to description of general Pathological Process model part 2 evolution aspects
Patologicheskaia fiziologiia i èksperimental'naia terapiia, 2013Co-Authors: E Gusev, V A ChereshnevAbstract:Theoretical and methodological approaches to description of systemic inflammation as general Pathological Process are discussed. It is shown, that there is a need of integration of wide range of types of researches to develop a model of systemic inflammation.
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fundamental applied aspects of systemic inflammation in terms of physiologic and typical Pathological Process
Fiziologicheskiĭ zhurnal, 2010Co-Authors: V A Chereshnev, Gusev Eiu, N V ZotovaAbstract:The concept of systemic inflammatory response syndrome (SIRS) by sepsis as well as quality of SIRS criteria, classification, and PIRO system has been a subject to analytical criticism in terms of theory of physiologic and typical Pathological Process. It has been disclosed SIRS can be considered only as the syndrome, that solves particular clinical tasks, but not as a basic model of pathogenesis of critical states. In authors' opinion it is more correctly to discuss systemic inflammation as a typical pathologic Process that appears as a complex of one or another "resuscitation" syndrome in a clinical course.
Ferreira, Fernando A. - One of the best experts on this subject based on the ideXlab platform.
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Canine hypertrophic osteopathy: Case report
2011Co-Authors: Borin, Sofía [unesp], Crivelenti, Leandro Zuccolotto [unesp], Ortiz, Edna Gómez M. [unesp], Ferreira, Fernando A.Abstract:A case of a 11 year old Boxer dog with hypertrophic osteopathy is presented. This is an uncommon Pathological Process characterized by bilaterally symmetric and generalized periosteal proliferative in long bones and falanges
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Osteopatía hipertrófica canina: Relato de caso
2011Co-Authors: Borin Sofía, Crivelenti, Leandro Zuccolotto, Ortiz, Edna M. Gómez, Ferreira, Fernando A.Abstract:A case of a 11 year old Boxer dog with hypertrophic osteopathy is presented. This is an uncommon Pathological Process characterized by bilaterally symmetric and generalized periosteal proliferative in long bones and falanges
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CANINE HYPERTROPHIC OSTEOPATHY: CASE REPORT
'Universidad Nacional Mayor de San Marcos Vicerectorado de Investigacion', 2011Co-Authors: Borin Sofía, Zuccolotto Crivelenti Leandro, Gómez Ortiz, Edna M., Ferreira, Fernando A.Abstract:Se presenta el caso de un canino Bóxer de 11 años de edad con osteopatía hipertrófica, proceso patológico óseo de escasa presentación. Se caracteriza por osteofitosis periostales bilaterales a lo largo de las diáfisis de los huesos largos y de las falanges.A case of a 11 year old Boxer dog with hypertrophic osteopathy is presented. This isan uncommon Pathological Process characterized by bilaterally symmetric and generalizedperiosteal proliferative in long bones and falanges
Lin Wang - One of the best experts on this subject based on the ideXlab platform.
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identification of the biomarkers and Pathological Process of heterotopic ossification weighted gene co expression network analysis
Frontiers in Endocrinology, 2020Co-Authors: Shuang Wang, Jun Tian, Jianzhong Wang, Sizhu Liu, Chaojiang Shang, Jichun Yang, Lin WangAbstract:Heterotopic ossification (HO) is the formation of abnormal mature lamellar bone in extra-skeletal sites, including soft tissues and joints, which result in high rates of disability. The understanding of the mechanism of HO is insufficient. The aim of this study was to explore biomarkers and Pathological Processes in HO+ samples. The gene expression profile GSE94683 was downloaded from the Gene Expression Omnibus database. Sixteen samples from nine HO- and seven HO+ subjects were analyzed. After data preProcessing, 3,529 genes were obtained for weighted gene co-expression network analysis. Highly correlated genes were divided into 13 modules. Finally, the cyan and purple modules were selected for further study. Gene ontology functional annotation and Kyoto Encyclopedia of Genes and Genomes pathway enrichment indicated that the cyan module was enriched in a variety of components, including protein binding, membrane, nucleoplasm, cytosol, poly(A) RNA binding, biosynthesis of antibiotics, carbon metabolism, endocytosis, citrate cycle, and metabolic pathways. In addition, the purple module was enriched in cytosol, mitochondrion, protein binding, structural constituent of ribosome, rRNA Processing, oxidative phosphorylation, ribosome, and non-alcoholic fatty liver disease. Finally, 10 hub genes in the cyan module [actin related protein 3 (ACTR3), ADP ribosylation factor 4 (ARF4), progesterone receptor membrane component 1 (PGRMC1), ribosomal protein S23 (RPS23), mannose-6-phosphate receptor (M6PR), WD repeat domain 12 (WDR12), synaptosome associated protein 23 (SNAP23), actin related protein 2 (ACTR2), siah E3 ubiquitin protein ligase 1 (SIAH1), and glomulin (GLMN)] and 2 hub genes in the purple module [proteasome 20S subunit alpha 3 (PSMA3) and ribosomal protein S27 like (RPS27L)] were identified. Hub genes were validated through quantitative real-time polymerase chain reaction. In summary, 12 hub genes were identified in two modules that were associated with HO. These hub genes could provide new biomarkers, therapeutic ideas, and targets in HO.