Sandra Guzmán-Silahua

Dr. Sandra Guzmán-Silahua

Universidad de Guadalajara, Guadalajara, Jalisco, Mexico
orcid

Research Focus & Metrics

Academic Career Length

5Years (2022-Present)

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

Representative Publications

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5 August 2024 in Healthcare
Verified
Journal Article
Open access
PDF file
PRPatricia Anaid Romero-Garcia
Patricia Anaid Romero-Garcia
Sergio Ramírez-PérezSergio Ramírez-Pérez
Sergio Ramírez-Pérez
JMJorge Javier Miguel-González
Jorge Javier Miguel-González
SGSandra Guzmán-Silahua
Sandra Guzmán-Silahua
JCJavier Adan Castañeda-Moreno
Javier Adan Castañeda-Moreno
SRSimón Quetzalcoatl Rodríguez-Lara
Simón Quetzalcoatl Rodríguez-Lara
While research on complementary and alternative medicine (CAM) for the general population is expanding, there remains a scarcity of studies investigating the efficacy and utilisation of CAM practices, specifically in the paediatric population. In accordance with the World Health Organization (WHO), the prevalence of the parental utilisation of CAM in their dependents is estimated to reach up to 80%. This literature review identified broad, heterogeneous, and inconclusive evidence regarding CAM’s applications and effectiveness, primarily attributed to variance in sociodemographic factors and differences in national healthcare systems. Additionally, the review identified a lack of consensus and polarised positions among mainstream professionals regarding the mechanisms of action, applications, and effectiveness of CAM. This narrative review presents varied results concerning the efficacy of most CAM therapies and their applications; however, some evidence suggests potential benefits for acupuncture, yoga, tai chi, and massage in improving physical and mental health. Moreover, the available evidence indicates that meditation may enhance mental health, while reiki may only influence patients’ perceptions of comfort. In light of the intricate and multifaceted nature of herbal medicine, it is imperative to assess its efficacy on a case-by-case basis, taking into account the specific compounds and procedures involved. This comprehensive review serves as a valuable resource for health professionals, offering guidance for personalised healthcare approaches that consider the values and beliefs of patients, thereby facilitating integrated, evidence-based practices aimed at enhancing the quality of healthcare services and patient satisfaction.

30 May 2025 in Cells
Verified
Journal Article
Open access
PDF file
YVYarielis Ivette Vázquez-Galán
Yarielis Ivette Vázquez-Galán
SGSandra Guzmán-Silahua
Sandra Guzmán-Silahua
WTWalter Ángel Trujillo-Rangel
Walter Ángel Trujillo-Rangel
SRSimón Quetzalcoatl Rodríguez-Lara
Simón Quetzalcoatl Rodríguez-Lara
Shock is a life-threatening condition characterized by inadequate tissue perfusion leading to systemic hypoxia and metabolic failure. Ischemia/reperfusion (I/R) injury exacerbates shock progression through oxidative stress and immune dysregulation, contributing to multi-organ dysfunction. This narrative review synthesizes current evidence on the interplay between I/R injury, oxidative stress, and immune modulation in shock states. We analyze the classification of shock, its progression, and the molecular pathways involved in ischemic adaptation, inflammatory responses, and oxidative injury. Shock pathophysiology is driven by systemic ischemia, triggering adaptive responses such as hypoxia-inducible factor (HIF) signaling and metabolic reprogramming. However, prolonged hypoxia leads to mitochondrial dysfunction, increased reactive oxygen species (ROS) and reactive nitrogen species (RNS) production, and immune activation. The transition from systemic inflammatory response syndrome (SIRS) to compensatory anti-inflammatory response syndrome (CARS) contributes to immune imbalance, further aggravating tissue damage. Dysregulated immune checkpoint pathways, including CTLA-4 and PD-1, fail to suppress excessive inflammation, exacerbating oxidative injury and immune exhaustion. The intricate relationship between oxidative stress, ischemia/reperfusion injury, and immune dysregulation in shock states highlights potential therapeutic targets. Strategies aimed at modulating redox homeostasis, controlling immune responses, and mitigating I/R damage may improve patient outcomes. Future research should focus on novel interventions that restore immune balance while preventing excessive oxidative injury.

17 December 2024 in Diagnostics
Verified
Journal Article
Open access
PDF file
DMDaniela Anahí Méndez-Cobián
Daniela Anahí Méndez-Cobián
SGSandra Guzmán-Silahua
Sandra Guzmán-Silahua
DGDiana García-Hernández
Diana García-Hernández
JCJulian Conde-Sánchez
Julian Conde-Sánchez
YBYaocihuatl Castañeda Borrayo
Yaocihuatl Castañeda Borrayo
ANArnulfo Hernan Nava-Zavala
Arnulfo Hernan Nava-Zavala
Background: Gaucher disease (GD) is a rare autosomal recessive disorder caused by mutations in the GBA1 gene that lead to a deficiency in the glucocerebrosidase gene. This deficiency results in the accumulation of glucocerebrosides in macrophages, primarily affecting the liver, spleen, and bone marrow. Focusing on the Mexican population, this study aims to review GD’s epidemiology, clinical manifestations, and treatment options to enhance early diagnosis and optimize treatment outcomes. Methods: This study is a comprehensive literature review analyzing epidemiological data, clinical presentations, and current therapeutic approaches for Gaucher disease, including enzyme replacement therapy (ERT) and substrate reduction therapy (SRT). Conclusions: Early diagnosis and individualized treatment, primarily through enzyme replacement therapy, significantly improve the prognosis of patients with Gaucher disease, particularly type 1. Continued research is required to enhance therapeutic approaches for the neuropathic types and better understand the disease’s epidemiology in Mexico. These efforts will contribute to improved clinical outcomes and quality of life for patients.

Verified
Journal Article
Open access
PDF file
SBSonia Guadalupe Barreno-Rocha
Sonia Guadalupe Barreno-Rocha
SGSandra Guzmán-Silahua
Sandra Guzmán-Silahua
SRSinaí-Del-Carmen Rodríguez-Dávila
Sinaí-Del-Carmen Rodríguez-Dávila
GGGuadalupe Estela Gavilánez-Chávez
Guadalupe Estela Gavilánez-Chávez
EMErnesto Germán Cardona Muñoz
Ernesto Germán Cardona Muñoz
ANArnulfo Hernan Nava-Zavala
Arnulfo Hernan Nava-Zavala
One of the main groups of lipids is phospholipids, which are mainly involved in forming cell membranes. Neoplastic processes such as cell replication have increased lipid synthesis, making tumor cells dependent on this synthesis to maintain their requirements. Antiphospholipid antibodies attack phospholipids in the cell membranes. Three main types of antiphospholipid antibodies are recognized: anti-β2 glycoprotein I (anti-β2GP-I), anticardiolipin (aCL), and lupus anticoagulant (LA). These types of antibodies have been proven to be present in hematological neoplasms, particularly in LH and NHL. This review on antiphospholipid antibodies in hematological neoplasms describes their clinical relationship as future implications at the prognostic level for survival and even treatment.

6 August 2023 in Healthcare
Verified
Journal Article
Open access
PDF file
SBSonia Guadalupe Barreno-Rocha
Sonia Guadalupe Barreno-Rocha
SGSandra Guzmán-Silahua
Sandra Guzmán-Silahua
EMErnesto German GERMAN Cardona Muñoz
Ernesto German GERMAN Cardona Muñoz
MZMaria G Zavala-Cerna
Maria G Zavala-Cerna
DGDavid Eduardo Muñoz Gaytan
David Eduardo Muñoz Gaytan
ANArnulfo Hernan Nava-Zavala
Arnulfo Hernan Nava-Zavala
(1) Background: Non-Hodgkin Lymphoma is a neoplasm that can significantly compromise the immune system, but timely assessment can change the patient outcome. In cancer, the activation of the immune system could lead to the secretion of autoantibodies. (2) Methods: A retrospective cohort study was performed from 2017 to 2019 in patients with Non-Hodgkin Lymphoma diagnosed with a biopsy. (3) Results: We included 39 patients who were newly diagnosed, untreated, and without any autoimmune disease previously reported. Thirty patients had the presence of autoantibodies (antiphospholipid antibodies, anti-cytoplasmic neutrophils antibodies, antinuclear antibodies), and nine were without autoantibodies. There were no statistical differences among groups regarding clinical, demographic, staging, and prognosis characteristics. Also, there were no differences in the outcomes of the patients after finishing chemotherapy and one year after initiating treatment. (4) Conclusions: Further investigations must be conducted regarding an extended panel of autoantibodies because the panel of autoantibodies in this study did not show a relationship between the presence and the clinical outcome of the patients.

25 March 2025 in Preprints.org
Verified
Preprint
Open access
PDF file
YVYarielis Ivette Vázquez-Galán
Yarielis Ivette Vázquez-Galán
SGSandra Guzmán-Silahua
Sandra Guzmán-Silahua
WTWalter Ángel Trujillo-Rangel
Walter Ángel Trujillo-Rangel
SRSimón Quetzalcoatl Rodríguez-Lara
Simón Quetzalcoatl Rodríguez-Lara
Shock is a life-threatening condition characterized by inadequate tissue perfusion, leading to systemic hypoxia and metabolic failure. Ischemia-reperfusion (I/R) injury exacerbates shock progression through oxidative stress and immune dysregulation, contributing to multi-organ dysfunction. This narrative review synthesizes current evidence on the interplay between I/R injury, oxidative stress, and immune modulation in shock states. We analyze the classification of shock, its progression, and the molecular pathways involved in ischemic adaptation, inflammatory responses, and oxidative injury. Shock pathophysiology is driven by systemic ischemia, triggering adaptive responses such as hypoxia-inducible factor (HIF) signaling and metabolic reprogramming. However, prolonged hypoxia leads to mitochondrial dysfunction, increased reactive oxygen species (ROS) and reactive nitrogen species (RNS) production, and immune activation. The transition from systemic inflammatory response syndrome (SIRS) to compensatory anti-inflammatory response syndrome (CARS) contributes to immune imbalance, further aggravating tissue damage. Dysregulated immune checkpoint pathways, including CTLA-4 and PD-1, fail to suppress excessive inflammation, exacerbating oxidative injury and immune exhaustion. The intricate relationship between oxidative stress, ischemia-reperfusion injury, and immune dysregulation in shock states highlights potential therapeutic targets. Strategies aimed at modulating redox homeostasis, controlling immune responses, and mitigating I/R damage may improve patient outcomes. Future research should focus on novel interventions that restore immune balance while preventing excessive oxidative injury.