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1.

001-es BibID:BIBFORM069190
Első szerző:Alghamdi, Amani
Cím:Reduction of RPT6/S8 (a Proteasome Component) and Proteasome Activity in the Cortex is Associated with Cognitive Impairment in Lewy Body Dementia / Alghamdi Amani, Vallortigara Julie, Howlett David R., Broadstock Martin, Hortobágyi Tibor, Ballard Clive, Thomas Alan J., O'Brien John T., Aarsland Dag, Attems Johannes, Francis Paul T., Whitfield David R.
Dátum:2017
ISSN:1387-2877
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal Of Alzheimers Disease 57 : 2 (2017), p. 373-386. -
További szerzők:Vallortigara, Julie Howlett, David R. Broadstock, Martin Hortobágyi Tibor (1965-) (patológus) Ballard, Clive G. Thomas, Alan O'Brien, John Aarsland, Dag Attems, Johannes Francis, Paul T. Whitfield, David
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2.

001-es BibID:BIBFORM063502
Első szerző:Baek, Jean-Ha
Cím:Unfolded protein response is activated in Lewy body dementias / J.-H. Baek, D. Whitfield, D. Howlett, P. Francis, E. Bereczki, C. Ballard, T. Hortobágyi, J. Attems, D. Aarsland
Dátum:2016
ISSN:0305-1846
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Neuropathology And Applied Neurobiology 42 : 4 (2016), p. 352-365. -
További szerzők:Whitfield, David Howlett, David R. Francis, Paul T. Bereczki Erika Ballard, Clive G. Hortobágyi Tibor (1965-) (patológus) Attems, Johannes Aarsland, Dag
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3.

001-es BibID:BIBFORM071437
Első szerző:Bereczki Erika
Cím:Synaptic markers of cognitive decline in neurodegenerative diseases : a proteomic approach / Erika Bereczki, Rui M. Branca, Paul T. Francis, Joana B. Pereira, Jean-Ha Baek, Tibor Hortobágyi, Bengt Winblad, Clive Ballard, Janne Lehtiö, Dag Aarsland
Dátum:2017
ISSN:0006-8950
Megjegyzések:See Attems and Jellinger (doi:10.1093/brain/awx360) for a scientific commentary on this article.Cognitive changes occurring throughout the pathogenesis of neurodegenerative diseases are directly linked to synaptic loss. We used in-depth proteomics to compare 32 post-mortem human brains in the prefrontal cortex of prospectively followed patients with Alzheimer's disease, Parkinson's disease with dementia, dementia with Lewy bodies and older adults without dementia. In total, we identified 10 325 proteins, 851 of which were synaptic proteins. Levels of 25 synaptic proteins were significantly altered in the various dementia groups. Significant loss of SNAP47, GAP43, SYBU (syntabulin), LRFN2, SV2C, SYT2 (synaptotagmin 2), GRIA3 and GRIA4 were further validated on a larger cohort comprised of 92 brain samples using ELISA or western blot. Cognitive impairment before death and rate of cognitive decline significantly correlated with loss of SNAP47, SYBU, LRFN2, SV2C and GRIA3 proteins. Besides differentiating Parkinson's disease dementia, dementia with Lewy bodies, and Alzheimer's disease from controls with high sensitivity and specificity, synaptic proteins also reliably discriminated Parkinson's disease dementia from Alzheimer's disease patients. Our results suggest that these particular synaptic proteins have an important predictive and discriminative molecular fingerprint in neurodegenerative diseases and could be a potential target for early disease intervention.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Brain 141 : 2 (2018), p. 582-595. -
További szerzők:Branca, Rui M. Francis, Paul T. Pereira, Joana B. Baek, Jean-Ha Hortobágyi Tibor (1965-) (patológus) Winblad, Bengt Ballard, Clive G. Lehtiö, Janne Aarsland, Dag
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4.

001-es BibID:BIBFORM063546
Első szerző:Bereczki Erika
Cím:Synaptic proteins predict cognitive decline in Alzheimer's disease and Lewy body dementia / Erika Bereczki, Paul T. Francis, David Howlett, Joana B. Pereira, Kina Höglund, Anna Bogstedt, Angel Cedazo-Minguez, Jean-Ha Baek, Tibor Hortobágyi, Johannes Attems, Clive Ballard, Dag Aarsland
Dátum:2016
ISSN:0893-0341
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Alzheimers & Dementia 12 : 11 (2016), p. 1149-1158. -
További szerzők:Francis, Paul T. Howlett, David R. Pereira, Joana B. Höglund, Kina Bogstedt, Anna Cedazo-Minguez, Angel Baek, Jean-Ha Hortobágyi Tibor (1965-) (patológus) Attems, Johannes Ballard, Clive G. Aarsland, Dag
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5.

001-es BibID:BIBFORM020023
Első szerző:Elliott, Mark S. J.
Cím:Increased binding to 5-HT1A and 5-HT2A receptors is associated with large vessel infarction and relative preservation of cognition / Marc S. J. Elliott, Clive G. Ballard, Rajesh N. Kalaria, Robert Perry, Tibor Hortobágyi, Paul T. Francis
Dátum:2009
ISSN:0006-8950
Megjegyzések:Vascular dementia accounts for approximately 15-20% of all dementias. In addition, a significant subset of people with Alzheimer's disease have concurrent cerebrovascular disease. Vascular dementia is caused by different cerebrovascular morphological abnormalities including large artery territory infarction (multi-infarct vascular dementia) and sub-cortical ischaemic vascular dementia. Despite this distinction, there is a lack of studies examining the neurochemistry of individual vascular dementia subtypes. Serotonin is believed to play an important role in cognition, and serotonin receptors may provide a novel target for future anti-dementia therapeutics. This study aimed to determine levels of two serotonin receptors in subtypes of vascular dementia and relate any changes to cognition. We have determined, using saturation radioligand binding, the binding parameters (affinity and maximal binding) of ((3)H)-WAY 100635 binding to 5-HT(1A) receptors and ((3)H)-ketanserin binding to 5-HT(2A) receptors in post-mortem tissue from the frontal and temporal cortices of patients with either multi-infarct vascular dementia, sub-cortical ischaemic vascular dementia, mixed Alzheimer's disease/vascular dementia or stroke no dementia (SND). 5-HT(1A) and 5-HT(2A) receptor binding was significantly increased in the temporal cortex of patients with either multi-infarct vascular dementia or SND, compared to age-matched controls. 5-HT(1A) receptor maximal binding in the temporal cortex was also positively correlated with cognition as determined by Mini-Mental State Examination (MMSE) and Cambridge Assessment of Mental Health for the Elderly scores (CAMCOG). These results reveal an important distinction between the neurochemistry of multi-infarct vascular dementia/SND and sub-cortical ischaemic vascular dementia, suggesting that pharmacological manipulation of serotonin offers the possibility to develop novel therapies for stroke and multi-infarct vascular dementia patients. The results also highlight the importance of the cortical 5-HT(1A) receptor in mediating cognition.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Brain. - 132 : 7 (2009), p. 1858-1865. -
További szerzők:Ballard, Clive G. Kalaria, Rajesh N. Perry, Robert Hortobágyi Tibor (1965-) (patológus) Francis, Paul T.
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6.

001-es BibID:BIBFORM063676
Első szerző:Howlett, David R.
Cím:Regional Multiple Pathology Scores Are Associated with Cognitive Decline in Lewy Body Dementias / David R. Howlett, David Whitfield, Mary Johnson, Johannes Attems, John T. O'Brien, Dag Aarsland, Mitchell K.P. Lai, Jasinda H. Lee, Christopher Chen, Clive Ballard, Tibor Hortobágyi, Paul T. Francis
Dátum:2015
ISSN:1015-6305
Megjegyzések:Dementia with Lewy bodies (DLB) and Parkinson's disease dementia (PDD) are characterizedby the presence of ?-synuclein-containing Lewy bodies and Lewy neurites.However, both dementias also show variable degrees of Alzheimer's disease (AD) pathology(senile plaques and neurofibrillary tangles), particularly in areas of the cortex associatedwith higher cognitive functions. This study investigates the contribution of theindividual and combined pathologies in determining the rate of cognitive decline. Cortical?-synuclein, phosphorylated tau (phosphotau) and A? plaque pathology in 34 PDD and 55DLB patients was assessed semi-quantitatively in four regions of the neocortex. The declinein cognition, assessed by Mini Mental State Examination, correlated positively with thecortical ?-synuclein load. Patients also had varying degrees of senile A? plaque andphosphotau pathology. Regression analyses pointed to a combined pathology (A? plaqueplus phosphotau plus ?-synuclein-positive features), particularly in the prefrontal cortex(BA9) and temporal lobe neocortex with the superior and middle temporal gyrus (BA21,22), being a major determining factor in the development of dementia. Thus, cognitivedecline in Lewy body dementias is not a consequence of ?-synuclein-induced neurodegenerationalone but senile plaque and phosphorylated tau pathology also contribute tothe overall deficits.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Brain Pathology. - 25 : 4 (2015), p. 401-408. -
További szerzők:Whitfield, David Johnson, Mary Attems, Johannes O'Brien, John Aarsland, Dag Lai, Mitchell K.P. Lee, Jasinda H. Chen, Christopher Ballard, Clive G. Hortobágyi Tibor (1965-) (patológus) Francis, Paul T.
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7.

001-es BibID:BIBFORM051598
035-os BibID:PMID:23521156 WOS:000325608000002
Első szerző:Howlett, David R.
Cím:Clusterin associates specifically with Aβ40 in Alzheimer's disease brain tissue / David R. Howlett, Tibor Hortobágyi, Paul T. Francis
Dátum:2013
ISSN:1015-6305
Megjegyzések:Genome-wide association studies have pointed to clusterin (apolipoprotein J) as being linked to the occurrence of Alzheimer's disease (AD); studies have identified the protein as a possible biomarker. The association between clusterin and senile plaques in AD brain is well known, and clusterin levels in AD brain are 40% higher than that in control subjects. The present study investigates, immunohistochemically, the association between clusterin and Aβ peptides in AD and control cortex. A unique and specific association between clusterin and Aβ40 was observed in plaques in the cerebral cortex from AD subjects in that only plaques that contained Aβ40 showed clusterin immunoreactivity, while the many plaques with Aβ42 alone lacked clusterin labeling. Cerebrovascular Aβ in AD brain generally lacked Aβ42 but was positively labeled by both the Aβ40 and the clusterin antibodies. In control subjects, however, Aβ40 was absent from plaques, although very occasional plaques were found to be labeled by both the Aβ42 and the clusterin antibodies. Overall, in AD, but not aged control brain, clusterin was associated specifically with the Aβ40 form of Aβ in the brain. The lack of clusterin in association with Aβ42 may be a significant feature in neuronal loss and neurodegeneration in the disease state.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Alzheimer's disease
amyloid beta-protein
apolipoprotein J
biomarker
clusterin
Megjelenés:Brain Pathology. - 23 : 6 (2013), p. 623-632. -
További szerzők:Hortobágyi Tibor (1965-) (patológus) Francis, Paul T.
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8.

001-es BibID:BIBFORM016360
Első szerző:Kirvell, S. L.
Cím:Vesicular glutamate transporter and cognition in stroke : a case-control autopsy study / S. L. Kirvell, M. S. Elliott, R. N. Kalaria, T. Hortobágyi, C. G. Ballard, P. T. Francis
Dátum:2010
ISSN:0028-3878
Megjegyzések:OBJECTIVES: Vascular dementia (VaD) accounts for approximately 15%-20% of all dementias, but the relationship of progressive cognitive impairment to neurochemical changes is poorly understood. We have therefore investigated glutamatergic synaptic markers in VaD. METHODS: We used homogenates prepared from gray matter from 2 neocortical regions (Brodmann area [BA] 9 and BA 20) and Western blotting to determine the concentrations of key components of the glutamatergic neurotransmitter system, vesicular glutamate transporter 1 (VGLUT1) and excitatory amino acid transporter EAAT2 (GLT-1), and the ubiquitous synaptic protein, synaptophysin, in 73 individuals-48 patients with cerebrovascular disease with and without dementia, 10 patients with AD, and 15 controls-in a case-control design. RESULTS: VGLUT1 concentrations in BA 20 and BA 9 were correlated with CAMCOG total (Rs 0.525, p = 0.018, n = 20; Rs 0.560, p = 0.002, n = 27) and CAMCOG memory scores (Rs 0.616, p = 0.004, n = 20; Rs 0.675, p = 0.000, n = 27). VGLUT1 concentration in BA 9 differed between the different dementia groups and the stroke no dementia group (1-way analysis of variance F = 6.69, p = 0.001 and Bonferroni p < 0.01 in each case), with subjects with stroke who did not develop dementia exhibiting the highest mean value for VGLUT1. CONCLUSIONS: These data suggest that loss of glutamatergic synapses is a feature of VaD and Alzheimer disease but the preservation of synapses, in particular glutamatergic synapses, in the frontal cortex against the temporal cortex plays a role in sustaining cognition and protecting against dementia following a stroke.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Neurology. - 75 : 20 (2010), p. 1803-1809. -
További szerzők:Elliott, Mark S. J. Kalaria, Rajesh N. Hortobágyi Tibor (1965-) (patológus) Ballard, Clive G. Francis, Paul T.
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9.

001-es BibID:BIBFORM020047
Első szerző:Mulugeta, Ezra
Cím:Inflammatory mediators in the frontal lobe of patients with mixed and vascular dementia / Ezra Mulugeta, Francisco Molina-Holgado, Mark S. Elliott, Tibor Hortobagyi, Robert Perry, Rajesh N. Kalaria, Clive G. Ballard, Paul T. Francis
Dátum:2008
ISSN:1420-8008
Megjegyzések:Vascular dementia (VaD) accounts for about 20% of all dementias, and vascular risk is a key factor in more than 40% of people with Alzheimer's disease (AD). Little is known about inflammatory processes in the brains of these individuals. We have examined inflammatory mediators (interleukin (IL)-1beta, IL-1alpha, IL-6 and tumour necrosis factor alpha) and chemokines (macrophage inflammatory protein 1, monocyte chemo-attractant protein (MCP)-1 and granulocyte macrophage colony-stimulating factor) in brain homogenates from grey and white matter of the frontal cortex (Brodmann area 9) from patients with VaD (n = 11), those with concurrent VaD and AD (mixed dementia; n = 8) and from age-matched controls (n = 13) using ELISA assays. We found a dramatic reduction of MCP-1 levels in the grey matter in VaD and mixed dementia in comparison to controls (55 and 66%, respectively). IL-6 decreases were also observed in the grey matter of VaD and mixed dementia (72 and 71%, respectively), with a more modest decrease (30%) in the white matter of patients with VaD or mixed dementia. In the first study to examine the status of inflammatory mediators in a brain region severely affected by white-matter lesions, our findings highlight - in contrast to previous reports in AD - that patients at the later stage of VaD or mixed dementia have a significantly attenuated neuro-inflammatory response.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Dementia and Geriatric Cognitive Disorders. - 25 : 3 (2008), p. 278-286. -
További szerzők:Molina-Holgado, Francisco Elliott, Mark S. J. Hortobágyi Tibor (1965-) (patológus) Perry, Robert Kalaria, Rajesh N. Ballard, Clive G. Francis, Paul T.
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10.

001-es BibID:BIBFORM020018
Első szerző:Sharp, Sally I.
Cím:Choline acetyltransferase activity in vascular dementia and stroke / Sally I. Sharp, Paul T. Francis, Mark S. J. Elliott, Rajesh N. Kalaria, Natasha Bajic, Tibor Hortobagyi, Clive G. Ballard
Dátum:2009
ISSN:1420-8008
Megjegyzések:BACKGROUND/AIM: Alterations in cholinergic activity have not been systematically studied in types of cerebrovascular disease. We examined cholinergic function at postmortem, focussing on stroke and vascular dementia (VaD). METHODS: Post-mortem brain tissue was studied from 61 patients with stroke or VaD (13 infarct dementia; 8 stroke/no dementia; 11 sub-cortical ischaemic VaD, SIVD; 29 VaD and concurrent Alzheimer's disease, AD), 12 patients with AD and 23 controls. Choline acetyltransferase (ChAT) was measured in Brodmann areas (BA) 9 and 20/21. RESULTS: There were significant reductions in ChAT activity in patients with VaD and concurrent AD compared to age-matched controls (BA9: t = 2.7, p = 0.009; BA20/21: t = 4.67, p = 0.000). In patients with infarct dementia, there was a significant 27% increase in ChAT activity in BA9 (t = 2.1, p = 0.047), but not in BA20/21 (t = 1.67, p = 0.106), compared to the age-matched control group. There was no relationship between ChAT activity and cognition in the VaD patients. CONCLUSIONS: Loss of cholinergic function is only evident in VaD patients with concurrent AD. A novel increase in cholinergic activity was identified in patients with infarct dementia, which may create important new treatment opportunities.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Dementia and Geriatric Cognitive Disorders. - 28 : 3 (2009), p. 233-238. -
További szerzők:Francis, Paul T. Elliott, Mark S. J. Kalaria, Rajesh N. Bajic, Natasha Hortobágyi Tibor (1965-) (patológus) Ballard, Clive G.
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11.

001-es BibID:BIBFORM063678
Első szerző:Vallortigara, Julie
Cím:Decreased Levels of VAMP2 and Monomeric Alpha-Synuclein Correlate with Duration of Dementia / Julie Vallortigara, David Robert Edward Whitfield, William Quelch, Amani Alghamdi, David R. Howlett, Tibor Hortobágyi, Mary Johnson, Johannes Attems, John T. O'Brien, Alan J. Thomas, Clive G. Ballard, Dag Aarsland, Paul T. Francis
Dátum:2015
ISSN:1387-2877
Megjegyzések:Alpha-synuclein (?-syn) aggregations are the key pathological hallmark of dementia withLewy bodies (DLB) and Parkinson's disease dementia (PDD), but are also frequently presentin Alzheimer's disease (AD). Yet much remains unknown about the role of ?-syn in thesynapse and the wider role of synaptic dysfunction in these dementias. Changes inconcentrations of key ♭SNAP (Soluble N-ethylmaleimide Sensitive Factor AttachmentProtein) Receptor' (SNARE) proteins as a consequence of alterations in the aggregation stateof ?-syn may contribute to synaptic dysfunction in patients with DLB, PDD and AD and resultin impaired cognition. We have studied a large cohort (n=130) of autopsy confirmed DLB,PDD, AD and control brains. Using semi-quantitative western blotting we havedemonstrated significant changes across the diagnostic groups of DLB, PDD and AD in theSNARE and vesicle proteins syntaxin, Munc18, VAMP2 and monomeric ?-syn in theprefrontal cortex, with a significant reduction of Munc18 in AD patients (p<0.001). Thiscorrelated to the final MMSE score before death (p=0.016). We also identified a significantnegative correlation between the duration of dementia and the levels of the bindingpartners VAMP2 (p=0.0004) and monomeric ?-syn (p=0.0002). It is of particular note that thisassociation was identified in people with AD. Our findings may indicate that an upregulationof SNARE complex related proteins occurs in the early stages of disease as an attempt atcompensating for failing synapses, prior to widespread deposition of pathological ?-syn.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Dementia with Lewy bodies
Parkinson's disease dementia
Alzheimer's disease
Synaptic dysfunction
SNARE process
Alpha-synuclein
VAMP2
Munc18
Megjelenés:Journal Of Alzheimers Disease. - 50 : 1 (2015), p. 101-110. -
További szerzők:Whitfield, David Quelch, William Alghamdi, Amani Howlett, David R. Hortobágyi Tibor (1965-) (patológus) Johnson, Mary Attems, Johannes O'Brien, John Thomas, Alan Ballard, Clive G. Aarsland, Dag Francis, Paul T.
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12.

001-es BibID:BIBFORM062827
Első szerző:Vallortigara, Julie
Cím:Dynamin1 concentration in the prefrontal cortex is associated with cognitive impairment in Lewy body dementia / Julie Vallortigara, Sindhoo Rangarajan, David Whitfield, Amani Alghamdi, David Howlett, Tibor Hortobágyi, Mary Johnson, Johannes Attems, Clive Ballard, Alan Thomas, John O'Brien, Dag Aarsland, Paul Francis
Dátum:2014
ISSN:2046-1402
Megjegyzések:Dementia with Lewy Bodies (DLB) and Parkinson's Disease Dementia (PDD) together, represent the second most common cause of dementia, after Alzheimer's disease (AD). The synaptic dysfunctions underlying the cognitive decline and psychiatric symptoms observed throughout the development of PDD and DLB are still under investigation. In this study we examined the expression level of Dynamin1 and phospho-CaMKII, key proteins of endocytosis and synaptic plasticity respectively, as potential markers of molecular processes specifically deregulated with DLB and/or PDD. In order to measure the levels of these proteins, we isolated grey matter from post-mortem prefrontal cortex area (BA9), anterior cingulated gyrus (BA24) and parietal cortex (BA40) from DLB and PDD patients in comparison to age-matched controls and a group of AD cases. Clinical and pathological data available included the MMSE score, neuropsychiatric history, and semi-quantitative scores for AD pathology (plaques - tangles) and for ?-synuclein (Lewy bodies). Changes in the expression of the synaptic markers, and correlates with neuropathological features and cognitive decline were predominantly found in the prefrontal cortex. On one hand, levels of Dynamin1 were significantly reduced, and correlated with a higher rate of cognitive decline observed in cases from three dementia groups. On the other hand, the fraction of phospho-CaMKII was decreased, and correlated with a high score of plaques and tangles in BA9. Interestingly, the correlation between the rate of cognitive decline and the level of Dynamin1 remained when the analysis was restricted to the PDD and DLB cases, highlighting an association of Dynamin1 with cognitive decline in people with Lewy Body dementia.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:F1000Research. - 3 : 108 (2014), p. 1-11. -
További szerzők:Rangarajan, Sindhoo Whitfield, David Alghamdi, Amani Howlett, David R. Hortobágyi Tibor (1965-) (patológus) Johnson, Mary Attems, Johannes Ballard, Clive G. Thomas, Alan O'Brien, John Aarsland, Dag Francis, Paul T.
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