6 research outputs found
Caracterização patogĂȘnica, fisiolĂłgica e morfolĂłgica de Pseudocercospora musae
- Author
- BENDEZU J. M.
- COCHRANE V.W.
- CORDEIRO Z.J.M.
- DANTAS B.
- DEL PELOSO M.C.
- FOURĂ E.
- GRIFFIN D.H.
- HAWKER L.E.
- HAWKER L.E.
- LILLY V.G.
- MARIA MENEZES
- McGAHAN M.W.
- MEDINA J.C.
- NAGEL C.M.
- QUEIROZ F.M.
- REGINA C.T. ROSA
- RIBEIRO Z.M.A.
- SILVA M.F.
- SIMMONDS N.W.
- STAVELY J.R.
- STOVER R.H.
- STOVER R.H.
- STOVER R.H.
- STOVER R.H.
- STOVER R.H.
- STOVER R.H.
- VIEIRA G.M.
- WARDLAW C. W.
- Publication venue
- 'FapUNIFESP (SciELO)'
- Publication date
- Field of study
New insights into the genetic etiology of Alzheimer's disease and related dementias
- Author
- Aaltonen L.
- Aaltonen V.
- Aarsland Dag
- Aavikko M.
- Abalos M.S.
- Abdelnour Carla
- Abner E.
- Abraham R.
- Adams H.
- Adams P.M.
- Adarmes-GĂłmez A.
- Adarmes-GĂłmez A.D.
- Aguilera N.
- Aguilera N.
- Aguirre A.
- Ahmad S.
- Akinyemi R.O.
- Al-Chalabi A.
- AlarcĂłn-MartĂn Emilio
- Albert M.S.
- Albin R.L.
- Alcolea Daniel
- Alegret Montserrat
- Ali M.
- Allen M.
- Allende I.R.
- Alonso M.D.
- Alonso M.D.
- Alvarez I.
- Alvarez L.
- Amer-Ferrer G.
- Amin N.
- Amouyel Philippe
- Anastasiou A.
- Anastasiou C.
- Andrade V.
- Andreassen Ole A.
- Andreoni S.
- Antequera M.
- Antikainen R.
- Antonell A.
- Anttonen V.
- AntĂșnez C.
- Aparicio H.J.
- Apostolova L.G.
- Appollonio I.
- Arcaro M.
- Archetti S.
- Armstrong N.J.
- Arnold S.E.
- Arosio B.
- Arvas M.
- Assogna F.
- Asthana S.
- Athanasiu L.
- Atwood C.S.
- Auge F.
- Auranen A.
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- Awaisa G.
- Ayres G.
- Bacha J.I.
- Bahadori M.
- Bahrami S.
- Bailly H.
- Baldwin C.T.
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- Barber R.C.
- Barnes L.L.
- Barral S.
- Barral S.
- Bass N.
- Bass N.J.
- Bastiani P.
- Bayer A.
- Beach T.G.
- Becker J.T.
- Becker J.T.
- Becker T.
- Beecham G.W.
- Beekly D.
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- Beiser A.
- Belezhanska D.
- Bellenguez CĂ©line
- Below J.E.
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- Publication venue
- Publication date
- 01/01/2022
- Field of study
Characterization of the genetic landscape of Alzheimer's disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/'proxy' AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE Δ4 allele
Avaliação de meios de cultura no crescimento micelial e esporulação de Alternaria brasiliensis
- Author
- Publication venue
- 'FapUNIFESP (SciELO)'
- Publication date
- Field of study
Inheritance of resistance to races 69 and 453 of Colletotrichum lindemuthianum in the common bean
- Author
- Balardin - R. S.
- Balardin R. S.
- Balardin R. S.
- Carlos Alberto Scapim
- ClĂĄudia Thomazella
- Cruz C.D.
- CĂĄrdenas F.
- Del Peloso M. J.
- Fouilloux G.
- Fukuda W. M. G.
- Gonçalves-Vidigal M. C.
- Gonçalves-Vidigal M. C.
- Gonçalves-Vidigal M. C.
- Habgood H.
- Juliana P. Poletine
- Kelly J. D.
- Lucas Silvério
- M.C. Gonçalves-Vidigal
- Mastenbroek C.
- Mathur R. S.
- McRostie G. P.
- Menezes J. R.
- Menezes J. R.
- Muhalet C. S.
- Paradela Filho O.
- Pastor-Corrales M. A.
- Pastor-Corrales M. A.
- Pastor-Corrales M. A.
- Pedro S. Vidigal Filho
- Schwartz H. F.
- Vieira C.
- Young R. A.
- Young R. A.
- Young R. A.
- Publication venue
- Instituto de Tecnologia do ParanĂĄ (Tecpar)
- Publication date
- 01/01/2000
- Field of study
The cultivars, AB 136 and G 2333 both resistant to Colletotrichum lindemuthianum races 69 and 453, were crossed with the cultivars Michelite and Perry Marrow (susceptible to both races), with Dark Red Kidney and Cornell 49242 (resistant to both races) and F1 and F2 generations were obtained. Plants were inoculated using a spore suspension at 1.2 x 10(6) concentration. The reaction of F1 and F2 populations showed that Dark Red Kidney, Cornell 49242 and AB 136 cultivars had the dominant genes A (Co-1), Are (Co-2) and Co-6, respectively, was conferring resistance to races 69 and 453. The segregation data obtained from F2 populations indicated that G 2333 carried two dominant resistance genes Co-5 gene and another one Co-7 for 69 and 453 races. The dominant genes in G 2333 and its resistance to C. lindemuthianum race could be transferred to provide anthracnose resistance to susceptible cultivars relatively easy.<br>Os cultivares AB 136 e G 2333 ambos resistentes Ă s raças 69 e 453 de Colletotrichum lindemuthianum foram cruzados com os cultivares Michelite e Perry Marrow (suscetĂveis Ă ambas as raças) e com Dark Red Kidney e Cornell 49242 (resistentes Ă ambas as raças) e, obtidas as geraçÔes F1 e F2. As plantas foram inoculadas com uma suspensĂŁo de esporos, utilizando-se uma concentração de 1,2 x 10(6) esporos/ml de ĂĄgua. As reaçÔes das populaçÔes F1 e F2 evidenciaram que os cultivares Dark Red Kidney; Cornell 49242 e AB 136 possuem, respectivamente, os genes dominantes A (Co-1) Are (Co-2) e Co-6, os quais conferiram a resistĂȘncia Ă s raças 69 e 453. Os dados de segregação obtidos nas populaçÔes F2 indicaram que G 2333 carrega os genes dominantes de resistĂȘncia Co-5 e Co-7. Os genes dominantes presentes em G 2333 e sua resistĂȘncia Ă s raças de C. lindemuthianum, poderĂŁo serem transferidos para cultivares suscetĂveis com relativa facilidade
New insights into the genetic etiology of Alzheimer's disease and related dementias
- Publication venue
- Publication date
- 01/01/2022
- Field of study
Characterization of the genetic landscape of Alzheimer's disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/'proxy' AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE Δ4 allele. © 2022. The Author(s)
New insights into the genetic etiology of Alzheimerâs disease and related dementias
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/2022
- Field of study
Characterization of the genetic landscape of Alzheimerâs disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/âproxyâ AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE Δ4 allele. © 2022, The Author(s)