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Lung cancer single intramedullary metastasis vs delayed radionecrosis. A case report.

The neuroradiology journal

Conforti R, Tagliatatela G, De Cristoforo M, Di Costanzo A, Scuotto A, Sanpaolo S, Dericoloso A, Cirillo S.
PMID: 24207155
Neuroradiol J. 2009 Aug 29;22(4):458-63. doi: 10.1177/197140090902200417. Epub 2009 Aug 29.

Intramedullary metastases are rare, accounting for 0.9-5% of spinal metastases. Radiation myelopathy is considered one of the most distressing complications of radiotherapy. In both cases symptoms are aspecific, and there are no characteristic neuroradiologic findings. We describe a case...

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Conforti R, Tagliatatela G, De Cristoforo M, et al. Lung cancer single intramedullary metastasis vs delayed radionecrosis. A case report. Neuroradiol J. 2009;22(4):458-63doi: 10.1177/197140090902200417.
Conforti, R., Tagliatatela, G., De Cristoforo, M., Di Costanzo, A., Scuotto, A., Sanpaolo, S., Dericoloso, A., & Cirillo, S. (2009). Lung cancer single intramedullary metastasis vs delayed radionecrosis. A case report. The neuroradiology journal, 22(4), 458-63. https://doi.org/10.1177/197140090902200417
Conforti, R, et al. "Lung cancer single intramedullary metastasis vs delayed radionecrosis. A case report." The neuroradiology journal vol. 22,4 (2009): 458-63. doi: https://doi.org/10.1177/197140090902200417
Conforti R, Tagliatatela G, De Cristoforo M, Di Costanzo A, Scuotto A, Sanpaolo S, Dericoloso A, Cirillo S. Lung cancer single intramedullary metastasis vs delayed radionecrosis. A case report. Neuroradiol J. 2009 Aug 29;22(4):458-63. doi: 10.1177/197140090902200417. Epub 2009 Aug 29. PMID: 24207155.
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Molecular pathophysiology and pharmacology of the voltage-sensing module of neuronal ion channels.

Frontiers in cellular neuroscience

Miceli F, Soldovieri MV, Ambrosino P, De Maria M, Manocchio L, Medoro A, Taglialatela M.
PMID: 26236192
Front Cell Neurosci. 2015 Jul 15;9:259. doi: 10.3389/fncel.2015.00259. eCollection 2015.

Voltage-gated ion channels (VGICs) are membrane proteins that switch from a closed to open state in response to changes in membrane potential, thus enabling ion fluxes across the cell membranes. The mechanism that regulate the structural rearrangements occurring in...

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Miceli F, Soldovieri MV, Ambrosino P, et al. Molecular pathophysiology and pharmacology of the voltage-sensing module of neuronal ion channels. Front Cell Neurosci. 2015;9:259doi: 10.3389/fncel.2015.00259.
Miceli, F., Soldovieri, M. V., Ambrosino, P., De Maria, M., Manocchio, L., Medoro, A., & Taglialatela, M. (2015). Molecular pathophysiology and pharmacology of the voltage-sensing module of neuronal ion channels. Frontiers in cellular neuroscience, 9259. https://doi.org/10.3389/fncel.2015.00259
Miceli, Francesco, et al. "Molecular pathophysiology and pharmacology of the voltage-sensing module of neuronal ion channels." Frontiers in cellular neuroscience vol. 9 (2015): 259. doi: https://doi.org/10.3389/fncel.2015.00259
Miceli F, Soldovieri MV, Ambrosino P, De Maria M, Manocchio L, Medoro A, Taglialatela M. Molecular pathophysiology and pharmacology of the voltage-sensing module of neuronal ion channels. Front Cell Neurosci. 2015 Jul 15;9:259. doi: 10.3389/fncel.2015.00259. eCollection 2015. PMID: 26236192; PMCID: PMC4502356.
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Role of Magnetic Resonance Imaging in Duane's Retraction Syndrome: Presence of the Abducens Nerve Depending on Type. A Clinical-Anatomical Study.

The neuroradiology journal

Taglialatela G, Conforti R, Notaro M, Cotticelli L, Caranci F, Cirillo S.
PMID: 24148725
Neuroradiol J. 2010 Dec;23(6):704-6. doi: 10.1177/197140091002300610. Epub 2010 Dec 23.

This study correlated anatomical findings and clinical evidence in Duane's Retraction Syndrome using brain MRI. The study included 11 patients with different types of Duane's Retraction Syndrome (DRS). Each patient underwent brain MRI. The VI(th) nerve was absent in...

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Taglialatela G, Conforti R, Notaro M, et al. Role of Magnetic Resonance Imaging in Duane's Retraction Syndrome: Presence of the Abducens Nerve Depending on Type. A Clinical-Anatomical Study. Neuroradiol J. 2010;23(6):704-6doi: 10.1177/197140091002300610.
Taglialatela, G., Conforti, R., Notaro, M., Cotticelli, L., Caranci, F., & Cirillo, S. (2010). Role of Magnetic Resonance Imaging in Duane's Retraction Syndrome: Presence of the Abducens Nerve Depending on Type. A Clinical-Anatomical Study. The neuroradiology journal, 23(6), 704-6. https://doi.org/10.1177/197140091002300610
Taglialatela, G, et al. "Role of Magnetic Resonance Imaging in Duane's Retraction Syndrome: Presence of the Abducens Nerve Depending on Type. A Clinical-Anatomical Study." The neuroradiology journal vol. 23,6 (2010): 704-6. doi: https://doi.org/10.1177/197140091002300610
Taglialatela G, Conforti R, Notaro M, Cotticelli L, Caranci F, Cirillo S. Role of Magnetic Resonance Imaging in Duane's Retraction Syndrome: Presence of the Abducens Nerve Depending on Type. A Clinical-Anatomical Study. Neuroradiol J. 2010 Dec;23(6):704-6. doi: 10.1177/197140091002300610. Epub 2010 Dec 23. PMID: 24148725.
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Neurotoxic tau oligomers after single versus repetitive mild traumatic brain injury.

Brain communications

Bittar A, Bhatt N, Hasan TF, Montalbano M, Puangmalai N, McAllen S, Ellsworth A, Carretero Murillo M, Taglialatela G, Lucke-Wold B, Logsdon A, Rosen C, Turner RC, Kayed R.
PMID: 31608324
Brain Commun. 2019;1(1):fcz004. doi: 10.1093/braincomms/fcz004. Epub 2019 Jun 28.

Mild traumatic brain injury accounts for the majority of head injuries and has been correlated with neurodegeneration and dementia. While repetitive mild traumatic brain injury is highly correlated to neurodegeneration, the correlation of a single mild traumatic brain injury...

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Bittar A, Bhatt N, Hasan TF, et al. Neurotoxic tau oligomers after single versus repetitive mild traumatic brain injury. Brain Commun. 2019;1(1):fcz004doi: 10.1093/braincomms/fcz004.
Bittar, A., Bhatt, N., Hasan, T. F., Montalbano, M., Puangmalai, N., McAllen, S., Ellsworth, A., Carretero Murillo, M., Taglialatela, G., Lucke-Wold, B., Logsdon, A., Rosen, C., Turner, R. C., & Kayed, R. (2019). Neurotoxic tau oligomers after single versus repetitive mild traumatic brain injury. Brain communications, 1(1), fcz004. https://doi.org/10.1093/braincomms/fcz004
Bittar, Alice, et al. "Neurotoxic tau oligomers after single versus repetitive mild traumatic brain injury." Brain communications vol. 1,1 (2019): fcz004. doi: https://doi.org/10.1093/braincomms/fcz004
Bittar A, Bhatt N, Hasan TF, Montalbano M, Puangmalai N, McAllen S, Ellsworth A, Carretero Murillo M, Taglialatela G, Lucke-Wold B, Logsdon A, Rosen C, Turner RC, Kayed R. Neurotoxic tau oligomers after single versus repetitive mild traumatic brain injury. Brain Commun. 2019;1(1):fcz004. doi: 10.1093/braincomms/fcz004. Epub 2019 Jun 28. PMID: 31608324; PMCID: PMC6777515.
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Distinct epilepsy phenotypes and response to drugs in KCNA1 gain- and loss-of function variants.

Epilepsia

Miceli F, Guerrini R, Nappi M, Soldovieri MV, Cellini E, Gurnett CA, Parmeggiani L, Mei D, Taglialatela M.
PMID: 34778950
Epilepsia. 2022 Jan;63(1):e7-e14. doi: 10.1111/epi.17118. Epub 2021 Nov 14.

A wide phenotypic spectrum of neurological diseases is associated with KCNA1 (Kv1.1) variants. To investigate the molecular basis of such a heterogeneous clinical presentation and identify the possible correlation with in vitro phenotypes, we compared the functional consequences of...

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Miceli F, Guerrini R, Nappi M, et al. Distinct epilepsy phenotypes and response to drugs in KCNA1 gain- and loss-of function variants. Epilepsia. 2021;63(1):e7-e14doi: 10.1111/epi.17118.
Miceli, F., Guerrini, R., Nappi, M., Soldovieri, M. V., Cellini, E., Gurnett, C. A., Parmeggiani, L., Mei, D., & Taglialatela, M. (2022). Distinct epilepsy phenotypes and response to drugs in KCNA1 gain- and loss-of function variants. Epilepsia, 63(1), e7-e14. https://doi.org/10.1111/epi.17118
Miceli, Francesco, et al. "Distinct epilepsy phenotypes and response to drugs in KCNA1 gain- and loss-of function variants." Epilepsia vol. 63,1 (2022): e7-e14. doi: https://doi.org/10.1111/epi.17118
Miceli F, Guerrini R, Nappi M, Soldovieri MV, Cellini E, Gurnett CA, Parmeggiani L, Mei D, Taglialatela M. Distinct epilepsy phenotypes and response to drugs in KCNA1 gain- and loss-of function variants. Epilepsia. 2022 Jan;63(1):e7-e14. doi: 10.1111/epi.17118. Epub 2021 Nov 14. PMID: 34778950.
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Neurological risks and benefits of cytokine-based treatments in coronavirus disease 2019: from preclinical to clinical evidence.

British journal of pharmacology

Pignataro G, Cataldi M, Taglialatela M.
PMID: 33512003
Br J Pharmacol. 2021 Jan 29; doi: 10.1111/bph.15397. Epub 2021 Jan 29.

Immunodeficiency and hyperinflammation are responsible for the most frequent and life-threatening forms of coronavirus disease 2019 (COVID-19). Therefore, cytokine-based treatments targeting immuno-inflammatory mechanisms are currently undergoing clinical scrutiny in COVID-19-affected patients. In addition, COVID-19 patients also exhibit a wide...

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Pignataro G, Cataldi M, Taglialatela M. Neurological risks and benefits of cytokine-based treatments in coronavirus disease 2019: from preclinical to clinical evidence. Br J Pharmacol. 2021;doi: 10.1111/bph.15397.
Pignataro, G., Cataldi, M., & Taglialatela, M. (2021). Neurological risks and benefits of cytokine-based treatments in coronavirus disease 2019: from preclinical to clinical evidence. British journal of pharmacology, . https://doi.org/10.1111/bph.15397
Pignataro, Giuseppe, et al. "Neurological risks and benefits of cytokine-based treatments in coronavirus disease 2019: from preclinical to clinical evidence." British journal of pharmacology vol. (2021). doi: https://doi.org/10.1111/bph.15397
Pignataro G, Cataldi M, Taglialatela M. Neurological risks and benefits of cytokine-based treatments in coronavirus disease 2019: from preclinical to clinical evidence. Br J Pharmacol. 2021 Jan 29; doi: 10.1111/bph.15397. Epub 2021 Jan 29. PMID: 33512003.
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REV1-Polζ maintains the viability of homologous recombination-deficient cancer cells through mutagenic repair of PRIMPOL-dependent ssDNA gaps.

Molecular cell

Taglialatela A, Leuzzi G, Sannino V, Cuella-Martin R, Huang JW, Wu-Baer F, Baer R, Costanzo V, Ciccia A.
PMID: 34508659
Mol Cell. 2021 Oct 07;81(19):4008-4025.e7. doi: 10.1016/j.molcel.2021.08.016. Epub 2021 Sep 10.

BRCA1/2 mutant tumor cells display an elevated mutation burden, the etiology of which remains unclear. Here, we report that these cells accumulate ssDNA gaps and spontaneous mutations during unperturbed DNA replication due to repriming by the DNA primase-polymerase PRIMPOL....

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Taglialatela A, Leuzzi G, Sannino V, et al. REV1-Polζ maintains the viability of homologous recombination-deficient cancer cells through mutagenic repair of PRIMPOL-dependent ssDNA gaps. Mol Cell. 2021;81(19):4008-4025.e7doi: 10.1016/j.molcel.2021.08.016.
Taglialatela, A., Leuzzi, G., Sannino, V., Cuella-Martin, R., Huang, J. W., Wu-Baer, F., Baer, R., Costanzo, V., & Ciccia, A. (2021). REV1-Polζ maintains the viability of homologous recombination-deficient cancer cells through mutagenic repair of PRIMPOL-dependent ssDNA gaps. Molecular cell, 81(19), 4008-4025.e7. https://doi.org/10.1016/j.molcel.2021.08.016
Taglialatela, Angelo, et al. "REV1-Polζ maintains the viability of homologous recombination-deficient cancer cells through mutagenic repair of PRIMPOL-dependent ssDNA gaps." Molecular cell vol. 81,19 (2021): 4008-4025.e7. doi: https://doi.org/10.1016/j.molcel.2021.08.016
Taglialatela A, Leuzzi G, Sannino V, Cuella-Martin R, Huang JW, Wu-Baer F, Baer R, Costanzo V, Ciccia A. REV1-Polζ maintains the viability of homologous recombination-deficient cancer cells through mutagenic repair of PRIMPOL-dependent ssDNA gaps. Mol Cell. 2021 Oct 07;81(19):4008-4025.e7. doi: 10.1016/j.molcel.2021.08.016. Epub 2021 Sep 10. PMID: 34508659; PMCID: PMC8500949.
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Age dependence of retinal vascular plexus attenuation in the triple transgenic mouse model of Alzheimer's disease.

Experimental eye research

Nazari HK, Karimaghaei C, van der Merwe R, Montalbano M, Taglialatela G, Vargas G, Zhang W, Motamedi M.
PMID: 34896306
Exp Eye Res. 2021 Dec 10;214:108879. doi: 10.1016/j.exer.2021.108879. Epub 2021 Dec 10.

The influence of Alzheimer's disease (AD) progression and severity on the structural and functional integrity of the cerebral vasculature is well recognized. The retina is an extension of the brain; thus, changes in retinal vascular features may serve as...

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Nazari HK, Karimaghaei C, van der Merwe R, et al. Age dependence of retinal vascular plexus attenuation in the triple transgenic mouse model of Alzheimer's disease. Exp Eye Res. 2021;214:108879doi: 10.1016/j.exer.2021.108879.
Nazari, H. K., Karimaghaei, C., van der Merwe, R., Montalbano, M., Taglialatela, G., Vargas, G., Zhang, W., & Motamedi, M. (2021). Age dependence of retinal vascular plexus attenuation in the triple transgenic mouse model of Alzheimer's disease. Experimental eye research, 214108879. https://doi.org/10.1016/j.exer.2021.108879
Nazari, Hossein K, et al. "Age dependence of retinal vascular plexus attenuation in the triple transgenic mouse model of Alzheimer's disease." Experimental eye research vol. 214 (2021): 108879. doi: https://doi.org/10.1016/j.exer.2021.108879
Nazari HK, Karimaghaei C, van der Merwe R, Montalbano M, Taglialatela G, Vargas G, Zhang W, Motamedi M. Age dependence of retinal vascular plexus attenuation in the triple transgenic mouse model of Alzheimer's disease. Exp Eye Res. 2021 Dec 10;214:108879. doi: 10.1016/j.exer.2021.108879. Epub 2021 Dec 10. PMID: 34896306.
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Age dependence of retinal vascular plexus attenuation in the triple transgenic mouse model of Alzheimer's disease.

Experimental eye research

Nazari HK, Karimaghaei C, van der Merwe R, Montalbano M, Taglialatela G, Vargas G, Zhang W, Motamedi M.
PMID: 34896306
Exp Eye Res. 2021 Dec 10;214:108879. doi: 10.1016/j.exer.2021.108879. Epub 2021 Dec 10.

The influence of Alzheimer's disease (AD) progression and severity on the structural and functional integrity of the cerebral vasculature is well recognized. The retina is an extension of the brain; thus, changes in retinal vascular features may serve as...

Cite
Nazari HK, Karimaghaei C, van der Merwe R, et al. Age dependence of retinal vascular plexus attenuation in the triple transgenic mouse model of Alzheimer's disease. Exp Eye Res. 2021;214:108879doi: 10.1016/j.exer.2021.108879.
Nazari, H. K., Karimaghaei, C., van der Merwe, R., Montalbano, M., Taglialatela, G., Vargas, G., Zhang, W., & Motamedi, M. (2021). Age dependence of retinal vascular plexus attenuation in the triple transgenic mouse model of Alzheimer's disease. Experimental eye research, 214108879. https://doi.org/10.1016/j.exer.2021.108879
Nazari, Hossein K, et al. "Age dependence of retinal vascular plexus attenuation in the triple transgenic mouse model of Alzheimer's disease." Experimental eye research vol. 214 (2021): 108879. doi: https://doi.org/10.1016/j.exer.2021.108879
Nazari HK, Karimaghaei C, van der Merwe R, Montalbano M, Taglialatela G, Vargas G, Zhang W, Motamedi M. Age dependence of retinal vascular plexus attenuation in the triple transgenic mouse model of Alzheimer's disease. Exp Eye Res. 2021 Dec 10;214:108879. doi: 10.1016/j.exer.2021.108879. Epub 2021 Dec 10. PMID: 34896306.
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Age dependence of retinal vascular plexus attenuation in the triple transgenic mouse model of Alzheimer's disease.

Experimental eye research

Nazari HK, Karimaghaei C, van der Merwe R, Montalbano M, Taglialatela G, Vargas G, Zhang W, Motamedi M.
PMID: 34896306
Exp Eye Res. 2021 Dec 10;214:108879. doi: 10.1016/j.exer.2021.108879. Epub 2021 Dec 10.

The influence of Alzheimer's disease (AD) progression and severity on the structural and functional integrity of the cerebral vasculature is well recognized. The retina is an extension of the brain; thus, changes in retinal vascular features may serve as...

Cite
Nazari HK, Karimaghaei C, van der Merwe R, et al. Age dependence of retinal vascular plexus attenuation in the triple transgenic mouse model of Alzheimer's disease. Exp Eye Res. 2021;214:108879doi: 10.1016/j.exer.2021.108879.
Nazari, H. K., Karimaghaei, C., van der Merwe, R., Montalbano, M., Taglialatela, G., Vargas, G., Zhang, W., & Motamedi, M. (2021). Age dependence of retinal vascular plexus attenuation in the triple transgenic mouse model of Alzheimer's disease. Experimental eye research, 214108879. https://doi.org/10.1016/j.exer.2021.108879
Nazari, Hossein K, et al. "Age dependence of retinal vascular plexus attenuation in the triple transgenic mouse model of Alzheimer's disease." Experimental eye research vol. 214 (2021): 108879. doi: https://doi.org/10.1016/j.exer.2021.108879
Nazari HK, Karimaghaei C, van der Merwe R, Montalbano M, Taglialatela G, Vargas G, Zhang W, Motamedi M. Age dependence of retinal vascular plexus attenuation in the triple transgenic mouse model of Alzheimer's disease. Exp Eye Res. 2021 Dec 10;214:108879. doi: 10.1016/j.exer.2021.108879. Epub 2021 Dec 10. PMID: 34896306.
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Neuroimmunomodulation by calcineurin in aging and Alzheimer's disease.

Aging and disease

Reese LC, Taglialatela G.
PMID: 22396864
Aging Dis. 2010 Dec;1(3):245-53. Epub 2010 Sep 09.

Alzheimer's disease (AD) is a progressive, age-related neurodegenerative disorder which first manifests as profound memory dysfunction. The majority of cases are idiopathic, although advanced age is the greatest risk factor for AD. Recent evidence suggests that pre-fibrillar soluble amyloid-beta...

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Reese LC, Taglialatela G. Neuroimmunomodulation by calcineurin in aging and Alzheimer's disease. Aging Dis. 2010;1(3):245-53
Reese, L. C., & Taglialatela, G. (2010). Neuroimmunomodulation by calcineurin in aging and Alzheimer's disease. Aging and disease, 1(3), 245-53.
Reese, Lindsay C, and Taglialatela, Giulio. "Neuroimmunomodulation by calcineurin in aging and Alzheimer's disease." Aging and disease vol. 1,3 (2010): 245-53.
Reese LC, Taglialatela G. Neuroimmunomodulation by calcineurin in aging and Alzheimer's disease. Aging Dis. 2010 Dec;1(3):245-53. Epub 2010 Sep 09. PMID: 22396864; PMCID: PMC3295036.
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KCNQ2 encephalopathy: Features, mutational hot spots, and ezogabine treatment of 11 patients.

Neurology. Genetics

Millichap JJ, Park KL, Tsuchida T, Ben-Zeev B, Carmant L, Flamini R, Joshi N, Levisohn PM, Marsh E, Nangia S, Narayanan V, Ortiz-Gonzalez XR, Patterson MC, Pearl PL, Porter B, Ramsey K, McGinnis EL, Taglialatela M, Tracy M, Tran B, Venkatesan C, Weckhuysen S, Cooper EC.
PMID: 27602407
Neurol Genet. 2016 Aug 22;2(5):e96. doi: 10.1212/NXG.0000000000000096. eCollection 2016 Oct.

OBJECTIVE: To advance the understanding of KCNQ2 encephalopathy genotype-phenotype relationships and to begin to assess the potential of selective KCNQ channel openers as targeted treatments.METHODS: We retrospectively studied 23 patients with KCNQ2 encephalopathy, including 11 treated with ezogabine (EZO)....

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Millichap JJ, Park KL, Tsuchida T, et al. KCNQ2 encephalopathy: Features, mutational hot spots, and ezogabine treatment of 11 patients. Neurol Genet. 2016;2(5):e96doi: 10.1212/NXG.0000000000000096.
Millichap, J. J., Park, K. L., Tsuchida, T., Ben-Zeev, B., Carmant, L., Flamini, R., Joshi, N., Levisohn, P. M., Marsh, E., Nangia, S., Narayanan, V., Ortiz-Gonzalez, X. R., Patterson, M. C., Pearl, P. L., Porter, B., Ramsey, K., McGinnis, E. L., Taglialatela, M., Tracy, M., Tran, B., Venkatesan, C., Weckhuysen, S., & Cooper, E. C. (2016). KCNQ2 encephalopathy: Features, mutational hot spots, and ezogabine treatment of 11 patients. Neurology. Genetics, 2(5), e96. https://doi.org/10.1212/NXG.0000000000000096
Millichap, John J, et al. "KCNQ2 encephalopathy: Features, mutational hot spots, and ezogabine treatment of 11 patients." Neurology. Genetics vol. 2,5 (2016): e96. doi: https://doi.org/10.1212/NXG.0000000000000096
Millichap JJ, Park KL, Tsuchida T, Ben-Zeev B, Carmant L, Flamini R, Joshi N, Levisohn PM, Marsh E, Nangia S, Narayanan V, Ortiz-Gonzalez XR, Patterson MC, Pearl PL, Porter B, Ramsey K, McGinnis EL, Taglialatela M, Tracy M, Tran B, Venkatesan C, Weckhuysen S, Cooper EC. KCNQ2 encephalopathy: Features, mutational hot spots, and ezogabine treatment of 11 patients. Neurol Genet. 2016 Aug 22;2(5):e96. doi: 10.1212/NXG.0000000000000096. eCollection 2016 Oct. PMID: 27602407; PMCID: PMC4995058.
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