VIRGINIA SEDENO MONGE

Dr. VIRGINIA SEDENO MONGE

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Research Focus & Metrics

Academic Career Length

17Years (2010-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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Emmanuel Rojas MoralesEmmanuel Rojas Morales
Emmanuel Rojas Morales
Gerardo Santos-LopezGerardo Santos-Lopez
Gerardo Santos-Lopez
SHSamuel Hernández-Cabañas
Samuel Hernández-Cabañas
RARaúl Arcega-Revilla
Raúl Arcega-Revilla
Nora Hilda Rosas-MurrietaNora Hilda Rosas-Murrieta
Nora Hilda Rosas-Murrieta
VMVIRGINIA SEDENO MONGE
VIRGINIA SEDENO MONGE
The participation of proinflammatory cytokines in the progression of Multiple Sclerosis (MS) has been well documented. Cytokines activate the JAK-STAT pathway, in which the suppressors of cytokine signaling (SOCS) exert a negative feedback. This paper analyzes the levels of SOCS5 and SOCS7 transcripts, quantified by RT-qPCR, in MS patients, and the concentrations of proinflammatory cytokines, IFN-γ, IL17, and IL6, determined by ELISA. Samples of peripheral blood were obtained from MS patients in the relapsing–remitting phase, treated with IFN-β or glatiramer acetate (GA), and from healthy individuals. SOCS7 mRNA was significantly higher in patients treated with GA (1.36 ± 0.23) than in those treated with IFN-β (0.65 ± 0.1). Regarding gender, the level of SOCS5 and SOCS7 transcripts were similar between MS and healthy females; in MS males, the level of SOCS7 transcripts were significantly lower (0.59 ± 0.03) than in healthy males (1.008 ± 0.05). Plasmatic levels of IFN-γ were significantly higher in MS patients (60 pg/mL, range 0–160) than in healthy subjects (0 range, 0–106). The same pattern was observed in MS patients treated with IFN-β (68 pg/mL, range 0–160) compared to patients treated with GA (51 pg/mL, range 0–114), and in MS females (64 pg/mL, range 0–161) compared to healthy females (0, range 0–99). We hypothesize that the increase in SOCS7 transcription in patients treated with GA could partially explain the action mechanism of this drug, while the increase in the concentration of IFN-γ in MS patients could help elucidate the immunopathology of the disease.

18 September 2010 in Virology Journal
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VMVIRGINIA SEDENO MONGE
VIRGINIA SEDENO MONGE
Gerardo Santos-LopezGerardo Santos-Lopez
Gerardo Santos-Lopez
RRRosa del Carmen Rocha-Gracia
Rosa del Carmen Rocha-Gracia
DMDaniel Meléndez-Mena
Daniel Meléndez-Mena
ARAlberto Ramírez-Mata
Alberto Ramírez-Mata
JRJulio Reyes-Leyva
Julio Reyes-Leyva
Background: Interferon (IFN)-α receptor 1 (ifnar1) and suppressor of cytokine signaling 1 (socs1) transcription levels were quantified in peripheral blood mononuclear cells (PBMC) of 59 patients infected with hepatitis C virus (HCV) and 17 non-infected individuals. Samples were obtained from patients infected with HCV that were either untreated or treated with IFN-α2 plus ribavirin for 1 year and divided into responders and non-responders based on viral load reduction 6 months after treatment. Ifnar1 and socs1 transcription was quantified by real-time RT-PCR, and the fold difference (2-ΔΔCT) with respect to hprt housekeeping gene was calculated. Results: Ifnar1 transcription increased significantly in HCV-infected patients either untreated (3.26 ± 0.31), responders (3.1 ± 0.23) and non-responders (2.18 ± 0.23) with respect to non-infected individuals (1 ± 0.34; P = 0.005). Ifnar1 transcription increased significantly (P = 0.003) in patients infected with HCV genotypes 1a (4.74 ± 0.25) and 1b (2.81 ± 0.25) but not in 1a1b (1.58 ± 0.21). No association was found of Ifnar1 transcription with disease progress, initial viral load or other clinical factors. With respect to socs1 transcription, values were similar for non-infected individuals (1 ± 0.28) and untreated patients (0.99 ± 0.41) but increased in responders (2.81 ± 0.17) and non-responder patients (1.67 ± 0.41). Difference between responder and non-responder patients was not statistically significant. Socs1 transcription increased in patients infected with HCV genotypes 1a and 1b (2.87 ± 0.45 and 2.22 ± 0.17, respectively) but not in 1a1b (1.28 ± 0.40). Socs1 transcript was absent in three patients infected with HCV genotype 1b. A weak correlation between ifnar1 and socs1 transcription was found, when Spearman's correlation coefficient was calculated. Conclusion: Our results suggest that HCV infection may up-regulate ifnar1 transcription. HCV genotypes differ in their capacity to affect ifnar1 and socs1 transcription, as well as in the ability to evade the antiviral response.

1 January 2020 in Archivos Latinoamericanos de Nutrición
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VMVIRGINIA SEDENO MONGE
VIRGINIA SEDENO MONGE
EPEduardo A Fabre Palacios
Eduardo A Fabre Palacios
CGCristina López García
Cristina López García
MJMaría de Lourdes Meza Jiménez
María de Lourdes Meza Jiménez
La alimentación influye en la mejora de la sintomatología de cualquier enfermedad, incluida la esclerosis múltiple (EM),la cual, se caracteriza por un proceso inflamatorio crónico, autoinmune del sistema nervioso central generando situaciones como inflamación, alteraciones; digestivas y mentales, discapacidad, y fatiga. El propósito de la presente revisión fue identificar la evidencia científica sobre los aspectos nutricionales que mejoran la progresión de EM. La metodología consistió en la búsqueda de literatura, en bases de datos electrónicas, referente a nutrición y esclerosis múltiple, principalmente entre los años 2015-2020. Entre los resultados de los aspectos nutricionales que mostraron eficacia en mejorar la progresión de EM, se encuentran el zinc, vitamina D, fibra, probióticos, aceite de pescado y de oliva, cacao, cúrcuma, y salmón. Existen evidencias del papel inmunomodulador del Zn y de la vitamina D en la inhibición de la producción de citocinas proinflamatorias. Niveles bajos de ambos componentes se asocian con mayor riesgo de padecer EM. Otros componentes de interés nutricional son la fibra y probióticos; producen ácidos grasos de cadena corta, con propiedades antiinflamatorias. La primera se conoce por su papel en la motilidad gastrointestinal y los segundos por su acción celular y molecular en procesos inflamatorios, y modulación del microbioma, por mencionar algunos. Los aspectos nutricionales antes mencionados pueden contribuir a modular la inflamación y mejorar la fatiga. Finalmente, este documento genera un panorama importante para continuar con la investigación referente a la influencia de la alimentación en pacientes con EM. Diet influences the improvement of the symptoms of any disease, including multiple sclerosis (MS), which is characterized by a chronic, autoimmune inflammatory process of the central nervous system generating situations such as inflammation, mental and digestive alterations, disability and fatigue. The aim of this review was to identify the scientific evidence on the nutritional aspects that improve the progression of MS. The methodology consisted of searching literature, in electronic databases, referring to nutrition and multiple sclerosis, mainly between the years 2015-2020. The results of the nutritional aspects that showed effectiveness in improving the progression of MS, are zinc, vitamin D, fiber, probiotics, fish oil and olive oil, cocoa, turmeric and salmon. There is evidence of the immunomodulatory role of Zn and vitamin D in inhibiting the production of proinflammatory citokines. Low levels of both components are associated with an increased risk of MS. Other components of nutritional interest are fiber and probiotics; they produce short chain fatty acids, with anti-inflammatory properties. The first is known for its role in gastrointestinal motility and the second one for its cellular and molecular actions in inflammatory processes and the microbiome modulation, to name a few. The nutrition aspects mentioned above, can contribute to modulate inflammation and improve fatigue. Finally, this paper creates an important perspective to continue the investigation concerning the influence of diet in MS patients.