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Título : Primary non-gestational choriocarcinoma of the uterine cervix Tipo de documento : documento electrónico Autores : Gabriel Jaime Varela Aguirre, Fecha de publicación : 2022 Títulos uniformes : International Journal of Gynecological Cancer Idioma : Inglés (eng) Palabras clave : cervix uteri gynecology pathology trophoblastic neoplasms Mención de responsabilidad : Camilo Andrés Pérez Montiel, Gabriel Jaime Varela Aguirre Referencia : Int J Gynecol Cancer. 2022 Jan;32(1):111-112. DOI (Digital Object Identifier) : 10.1136/ijgc-2021-003061 PMID : 34980664 En línea : https://ijgc.bmj.com/content/32/1/111.long Enlace permanente : https://hospitalpablotobon.cloudbiteca.com/pmb/opac_css/index.php?lvl=notice_display&id=5999 Primary non-gestational choriocarcinoma of the uterine cervix [documento electrónico] / Gabriel Jaime Varela Aguirre, . - 2022.
Obra : International Journal of Gynecological Cancer
Idioma : Inglés (eng)
Palabras clave : cervix uteri gynecology pathology trophoblastic neoplasms Mención de responsabilidad : Camilo Andrés Pérez Montiel, Gabriel Jaime Varela Aguirre Referencia : Int J Gynecol Cancer. 2022 Jan;32(1):111-112. DOI (Digital Object Identifier) : 10.1136/ijgc-2021-003061 PMID : 34980664 En línea : https://ijgc.bmj.com/content/32/1/111.long Enlace permanente : https://hospitalpablotobon.cloudbiteca.com/pmb/opac_css/index.php?lvl=notice_display&id=5999 Reserva
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Código de barras Número de Ubicación Tipo de medio Ubicación Sección Estado DD001980 AC-2022-005 Archivo digital Producción Científica Artículos científicos Disponible Sex differences in cognitive resilience in preclinical autosomal-dominant Alzheimer's disease carriers and non-carriers: Baseline findings from the API ADAD Colombia Trial / Sergio Álvarez Vallejo
Título : Sex differences in cognitive resilience in preclinical autosomal-dominant Alzheimer's disease carriers and non-carriers: Baseline findings from the API ADAD Colombia Trial Tipo de documento : documento electrónico Autores : Sergio Álvarez Vallejo, Fecha de publicación : 2022 Títulos uniformes : Alzheimer's & Dementia Idioma : Inglés (eng) Palabras clave : Alzheimer's disease autosomal-dominant Alzheimer's disease cognition neurodegeneration pathology preclinical sex differences Resumen : Introduction: Females may have greater susceptibility to Alzheimer's disease (AD)-pathology. We examined the effect of sex on pathology, neurodegeneration, and memory in cognitively-unimpaired Presenilin-1 (PSEN1) E280A mutation carriers and non-carriers. Methods: We analyzed baseline data from 167 mutation carriers and 75 non-carriers (ages 30 to 53) from the Alzheimer's Prevention Initiative Autosomal Dominant AD Trial, including florbetapir- and fludeoxyglucose-PET, MRI based hippocampal volume and cognitive testing. Results: Females exhibited better delayed recall than males, controlling for age, precuneus glucose metabolism, and mutation status, although the effect was not significant among PSEN1 mutation carriers only. APOE ε4 did not modify the effect of sex on AD biomarkers and memory. Discussion: Our findings suggest that, among cognitively-unimpaired individuals at genetic risk for autosomal-dominant AD, females may have greater cognitive resilience to AD pathology and neurodegeneration than males. Further investigation of sex-specific differences in autosomal-dominant AD is key to elucidating mechanisms of AD risk and resilience. Mención de responsabilidad : Clara Vila-Castelar, Pierre N. Tariot, Kaycee M. Sink, David Clayton, Jessica B. Langbaum, Ronald G. Thomas, Yinghua Chen, Yi Su, Kewei Chen, Nan Hu, Margarita Giraldo-Chica, Carlos Tobón, Natalia Acosta-Baena, Ernesto Luna, Marisol Londoño, Paula Ospina, Victoria Tirado, Claudia Muñoz, Eliana Henao, Yamile Bocanegra, Sergio Alvarez, Silvia Rios-Romenets, Valentina Ghisays, Dhruman Goradia, Wendy Lee, Ji Luo, Michael H. Malek-Ahmadi, Hillary D. Protas, Francisco Lopera, Eric M. Reiman, Yakeel T. Quiroz, the API ADAD Colombia Trial Group Referencia : Alzheimers Dement. 2022 Nov;18(11):2272-2282. DOI (Digital Object Identifier) : 10.1002/alz.12552 PMID : 35103388 En línea : https://alz-journals.onlinelibrary.wiley.com/doi/10.1002/alz.12552 Enlace permanente : https://hospitalpablotobon.cloudbiteca.com/pmb/opac_css/index.php?lvl=notice_display&id=6085 Sex differences in cognitive resilience in preclinical autosomal-dominant Alzheimer's disease carriers and non-carriers: Baseline findings from the API ADAD Colombia Trial [documento electrónico] / Sergio Álvarez Vallejo, . - 2022.
Obra : Alzheimer's & Dementia
Idioma : Inglés (eng)
Palabras clave : Alzheimer's disease autosomal-dominant Alzheimer's disease cognition neurodegeneration pathology preclinical sex differences Resumen : Introduction: Females may have greater susceptibility to Alzheimer's disease (AD)-pathology. We examined the effect of sex on pathology, neurodegeneration, and memory in cognitively-unimpaired Presenilin-1 (PSEN1) E280A mutation carriers and non-carriers. Methods: We analyzed baseline data from 167 mutation carriers and 75 non-carriers (ages 30 to 53) from the Alzheimer's Prevention Initiative Autosomal Dominant AD Trial, including florbetapir- and fludeoxyglucose-PET, MRI based hippocampal volume and cognitive testing. Results: Females exhibited better delayed recall than males, controlling for age, precuneus glucose metabolism, and mutation status, although the effect was not significant among PSEN1 mutation carriers only. APOE ε4 did not modify the effect of sex on AD biomarkers and memory. Discussion: Our findings suggest that, among cognitively-unimpaired individuals at genetic risk for autosomal-dominant AD, females may have greater cognitive resilience to AD pathology and neurodegeneration than males. Further investigation of sex-specific differences in autosomal-dominant AD is key to elucidating mechanisms of AD risk and resilience. Mención de responsabilidad : Clara Vila-Castelar, Pierre N. Tariot, Kaycee M. Sink, David Clayton, Jessica B. Langbaum, Ronald G. Thomas, Yinghua Chen, Yi Su, Kewei Chen, Nan Hu, Margarita Giraldo-Chica, Carlos Tobón, Natalia Acosta-Baena, Ernesto Luna, Marisol Londoño, Paula Ospina, Victoria Tirado, Claudia Muñoz, Eliana Henao, Yamile Bocanegra, Sergio Alvarez, Silvia Rios-Romenets, Valentina Ghisays, Dhruman Goradia, Wendy Lee, Ji Luo, Michael H. Malek-Ahmadi, Hillary D. Protas, Francisco Lopera, Eric M. Reiman, Yakeel T. Quiroz, the API ADAD Colombia Trial Group Referencia : Alzheimers Dement. 2022 Nov;18(11):2272-2282. DOI (Digital Object Identifier) : 10.1002/alz.12552 PMID : 35103388 En línea : https://alz-journals.onlinelibrary.wiley.com/doi/10.1002/alz.12552 Enlace permanente : https://hospitalpablotobon.cloudbiteca.com/pmb/opac_css/index.php?lvl=notice_display&id=6085 Reserva
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Código de barras Número de Ubicación Tipo de medio Ubicación Sección Estado DD001932 AC-2022-093 Archivo digital Producción Científica Artículos científicos Disponible
Título : Pituitary pathology in traumatic brain injury: a review Tipo de documento : documento electrónico Autores : Luis Vicente Syro Moreno, Fecha de publicación : 2019 Títulos uniformes : Pituitary Idioma : Inglés (eng) Palabras clave : Hypothalamic-pituitary autoimmunity (HP-A) pathology pituitary post traumatic hypopituitarism (PTHP) Traumatic brain injury (TBI) Resumen : Purpose: Traumatic brain injury most commonly affects young adults under the age of 35 and frequently results in reduced quality of life, disability, and death. In long-term survivors, hypopituitarism is a common complication. Results: Pituitary dysfunction occurs in approximately 20–40% of patients diagnosed with moderate and severe traumatic brain injury giving rise to growth hormone deficiency, hypogonadism, hypothyroidism, hypocortisolism, and central diabetes insipidus. Varying degrees of hypopituitarism have been identified in patients during both the acute and chronic phase. Anterior pituitary hormone deficiency has been shown to cause morbidity and increase mortality in TBI patients, already encumbered by other complications. Hypopituitarism after childhood traumatic brain injury may cause treatable morbidity in those survivors. Prospective studies indicate that the incidence rate of hypopituitarism may be ten-fold higher than assumed; factors altering reports include case definition, geographic location, variable hospital coding, and lost notes. While the precise pathophysiology of post traumatic hypopituitarism has not yet been elucidated, it has been hypothesized that, apart from the primary mechanical event, secondary insults such as hypotension, hypoxia, increased intracranial pressure, as well as changes in cerebral flow and metabolism may contribute to hypothalamic-pituitary damage. A number of mechanisms have been proposed to clarify the causes of primary mechanical events giving rise to ischemic adenohypophysial infarction and the ensuing development of hypopituitarism. Conclusion: Future research should focus more on experimental and clinical studies to elucidate the exact mechanisms behind post-traumatic pituitary damage. The use of preventive medical measures to limit possible damage in the pituitary gland and hypothalamic pituitary axis in order to maintain or re-establish near normal physiologic functions are crucial to minimize the effects of TBI. Mención de responsabilidad : Aydin Sav, Fabio Rotondo, Luis V Syro, Carlos A Serna, Kalman Kovacs Referencia : Pituitary. 2019 Jun;22(3):201-211 DOI (Digital Object Identifier) : 10.1007/s11102-019-00958-8 PMID : 30927184 En línea : https://link.springer.com/article/10.1007%2Fs11102-019-00958-8 Enlace permanente : https://hospitalpablotobon.cloudbiteca.com/pmb/opac_css/index.php?lvl=notice_display&id=4256 Pituitary pathology in traumatic brain injury: a review [documento electrónico] / Luis Vicente Syro Moreno, . - 2019.
Obra : Pituitary
Idioma : Inglés (eng)
Palabras clave : Hypothalamic-pituitary autoimmunity (HP-A) pathology pituitary post traumatic hypopituitarism (PTHP) Traumatic brain injury (TBI) Resumen : Purpose: Traumatic brain injury most commonly affects young adults under the age of 35 and frequently results in reduced quality of life, disability, and death. In long-term survivors, hypopituitarism is a common complication. Results: Pituitary dysfunction occurs in approximately 20–40% of patients diagnosed with moderate and severe traumatic brain injury giving rise to growth hormone deficiency, hypogonadism, hypothyroidism, hypocortisolism, and central diabetes insipidus. Varying degrees of hypopituitarism have been identified in patients during both the acute and chronic phase. Anterior pituitary hormone deficiency has been shown to cause morbidity and increase mortality in TBI patients, already encumbered by other complications. Hypopituitarism after childhood traumatic brain injury may cause treatable morbidity in those survivors. Prospective studies indicate that the incidence rate of hypopituitarism may be ten-fold higher than assumed; factors altering reports include case definition, geographic location, variable hospital coding, and lost notes. While the precise pathophysiology of post traumatic hypopituitarism has not yet been elucidated, it has been hypothesized that, apart from the primary mechanical event, secondary insults such as hypotension, hypoxia, increased intracranial pressure, as well as changes in cerebral flow and metabolism may contribute to hypothalamic-pituitary damage. A number of mechanisms have been proposed to clarify the causes of primary mechanical events giving rise to ischemic adenohypophysial infarction and the ensuing development of hypopituitarism. Conclusion: Future research should focus more on experimental and clinical studies to elucidate the exact mechanisms behind post-traumatic pituitary damage. The use of preventive medical measures to limit possible damage in the pituitary gland and hypothalamic pituitary axis in order to maintain or re-establish near normal physiologic functions are crucial to minimize the effects of TBI. Mención de responsabilidad : Aydin Sav, Fabio Rotondo, Luis V Syro, Carlos A Serna, Kalman Kovacs Referencia : Pituitary. 2019 Jun;22(3):201-211 DOI (Digital Object Identifier) : 10.1007/s11102-019-00958-8 PMID : 30927184 En línea : https://link.springer.com/article/10.1007%2Fs11102-019-00958-8 Enlace permanente : https://hospitalpablotobon.cloudbiteca.com/pmb/opac_css/index.php?lvl=notice_display&id=4256 Reserva
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Código de barras Número de Ubicación Tipo de medio Ubicación Sección Estado DD001235 AC-2019-024 Archivo digital Producción Científica Artículos científicos Disponible
Título : DICER1 gene mutations in endocrine tumors Tipo de documento : documento electrónico Autores : Luis Vicente Syro Moreno, Fecha de publicación : 2018 Títulos uniformes : Endocrine Related Cancer Idioma : Inglés (eng) Palabras clave : DICER1 endocrine tumors mutation neoplasms pathology Resumen : In this review, the importance of the DICER1 gene in the function of endocrine cells is discussed. There is conclusive evidence that DICER1 mutations play a crucial role in the development, progression, cell proliferation, therapeutic responsiveness and behavior of several endocrine tumors. We review the literature of DICER1 gene mutations in thyroid, parathyroid, pituitary, pineal gland, endocrine pancreas, paragangliomas, medullary, adrenocortical, ovarian and testicular tumors. Although significant progress has been made during the last few years, much more work is needed to fully understand the significance of DICER1 mutations. Mención de responsabilidad : Michael Solarski, Fabio Rotondo, William D Foulkes, John R Priest, Luis V Syro, Henriett Butz, Michael D Cusimano, Kalman Kovacs Referencia : Endocr Relat Cancer. 2018 Mar;25(3):R197-R208. DOI (Digital Object Identifier) : 10.1530/ERC-17-0509 PMID : 29330195 En línea : https://erc.bioscientifica.com/view/journals/erc/25/3/ERC-17-0509.xml Enlace permanente : https://hospitalpablotobon.cloudbiteca.com/pmb/opac_css/index.php?lvl=notice_display&id=4195 DICER1 gene mutations in endocrine tumors [documento electrónico] / Luis Vicente Syro Moreno, . - 2018.
Obra : Endocrine Related Cancer
Idioma : Inglés (eng)
Palabras clave : DICER1 endocrine tumors mutation neoplasms pathology Resumen : In this review, the importance of the DICER1 gene in the function of endocrine cells is discussed. There is conclusive evidence that DICER1 mutations play a crucial role in the development, progression, cell proliferation, therapeutic responsiveness and behavior of several endocrine tumors. We review the literature of DICER1 gene mutations in thyroid, parathyroid, pituitary, pineal gland, endocrine pancreas, paragangliomas, medullary, adrenocortical, ovarian and testicular tumors. Although significant progress has been made during the last few years, much more work is needed to fully understand the significance of DICER1 mutations. Mención de responsabilidad : Michael Solarski, Fabio Rotondo, William D Foulkes, John R Priest, Luis V Syro, Henriett Butz, Michael D Cusimano, Kalman Kovacs Referencia : Endocr Relat Cancer. 2018 Mar;25(3):R197-R208. DOI (Digital Object Identifier) : 10.1530/ERC-17-0509 PMID : 29330195 En línea : https://erc.bioscientifica.com/view/journals/erc/25/3/ERC-17-0509.xml Enlace permanente : https://hospitalpablotobon.cloudbiteca.com/pmb/opac_css/index.php?lvl=notice_display&id=4195 Reserva
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Código de barras Número de Ubicación Tipo de medio Ubicación Sección Estado DD000809 AC-2018-096 Archivo digital Producción Científica Artículos científicos Disponible
Título : Immunoglobulin G4 (IgG4)-Related Hypophysitis Tipo de documento : documento electrónico Autores : Luis Vicente Syro Moreno, Fecha de publicación : 2017 Títulos uniformes : Endocrine Pathology Idioma : Inglés (eng) Palabras clave : Hypophysitis IgG4 hypophysitis Neurosurgery Pathology Tuberculosis Resumen : We report two different cases of IgG4-related hypophysitis. In the first case, a pituitary lesion was accompanied by lymphocytic meningitis possibly mimicking tuberculous meningitis. The second case was unassociated with involvement of other organs. No histologic differences were noted between the two cases indicating that the morphologic features of the hypophysial lesion do not depend on the presence of other lesions. The pathogenesis of IgG4 hypophysitis is not known, and further study is necessary to explore the cause, progression, and influencing factors of this disease. Mención de responsabilidad : Fabio Rotondo, Amro Qaddoura, Luis V Syro, Jason Karamchandani, David G Munoz, Mariam J Arroyave, William P Ospina, Michael D Cusimano, Kalman Kovacs Referencia : Endocr Pathol. 2017 Dec;28(4):308-314. DOI (Digital Object Identifier) : 10.1007/s12022-016-9464-1 PMID : 28084610 En línea : https://link.springer.com/article/10.1007%2Fs12022-016-9464-1 Enlace permanente : https://hospitalpablotobon.cloudbiteca.com/pmb/opac_css/index.php?lvl=notice_display&id=4028 Immunoglobulin G4 (IgG4)-Related Hypophysitis [documento electrónico] / Luis Vicente Syro Moreno, . - 2017.
Obra : Endocrine Pathology
Idioma : Inglés (eng)
Palabras clave : Hypophysitis IgG4 hypophysitis Neurosurgery Pathology Tuberculosis Resumen : We report two different cases of IgG4-related hypophysitis. In the first case, a pituitary lesion was accompanied by lymphocytic meningitis possibly mimicking tuberculous meningitis. The second case was unassociated with involvement of other organs. No histologic differences were noted between the two cases indicating that the morphologic features of the hypophysial lesion do not depend on the presence of other lesions. The pathogenesis of IgG4 hypophysitis is not known, and further study is necessary to explore the cause, progression, and influencing factors of this disease. Mención de responsabilidad : Fabio Rotondo, Amro Qaddoura, Luis V Syro, Jason Karamchandani, David G Munoz, Mariam J Arroyave, William P Ospina, Michael D Cusimano, Kalman Kovacs Referencia : Endocr Pathol. 2017 Dec;28(4):308-314. DOI (Digital Object Identifier) : 10.1007/s12022-016-9464-1 PMID : 28084610 En línea : https://link.springer.com/article/10.1007%2Fs12022-016-9464-1 Enlace permanente : https://hospitalpablotobon.cloudbiteca.com/pmb/opac_css/index.php?lvl=notice_display&id=4028 Reserva
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