Estrada Mena, Francisco Javier
Main Affiliation
Preferred name
Estrada Mena, Francisco Javier
Official Name
Estrada Mena, Francisco Javier
ORCID
0000-0002-0833-3630
Researcher ID
AAI-2437-2020
Scopus Author ID
57192982524
32 results
Now showing 1 - 10 of 32
- Some of the metrics are blocked by yourconsent settings
Item type:Publication, Novel genome-wide associations for age-related macular degeneration in the sarcoglycan-sarcospan protein complex(2020) ;Asaf Calderon, Andrea Michelle ;Dewan, Andrew ;Ramírez, Israel ;Zepeda-Palacio, ClaudiaPalacio, ClaudiaPurpose : Since the advent of genomic approaches, many chromosomal regions and polymorphisms have been associated with age-related macular degeneration (AMD). However, most of the disease variability might not be still captured by current researched genetic markers due to power issues. We have evidence that at least one component of the sarcoglycan-sarcospan protein complex (Sg-Sspn) gene is associated with increased odds of geographic atrophy (GA) AMD. Moreover, the retina of the knocked-out mouse model for the Sg-Sspn phenotypically resembles GA. Here, we aimed to explore the genome-wide association of the Sg-Sspn complex gene regions with AMD.2 19 - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Preparation of Mouse Embryonic Eye Sections for Routine Histology(Springer US, 2026); ; Ramírez-Sánchez, Israel7 - Some of the metrics are blocked by yourconsent settings
Item type:Publication, nef/long terminal repeat quasispecies from HIV type 1-infected Mexican patients with different progression patterns and their pathogenesis in hu-PBL-SCID mice(2000) ;Gómez-Román, Víctor Raúl ;Vásquez, Joel A. ;Basualdo, Maria Del Carmen; Soler, CarmenTo examine the genetic features of the long terminal repeat (LTR) derived from six HIV-1-infected individuals enrolled in the Mexico City Cohort, we cloned and sequenced a 505-bp fragment of the proviral LTR from their peripheral blood mononuclear cells (PBMCs). All patients harbored HIV-1 LTR quasispecies corresponding to the B subtype. Three patients with high CD4+ T cell counts (>500/mm3) presented LTR sequences with point mutations in the TAR bulge. The LTR sequence from a patient classified as a long-term nonprogressor (LTNP) presented the most frequent naturally occurring length polymorphism (MFNLP) and two substitutions in the TAR region that were predicted to result in two alternative secondary RNA structures. A novel 18-bp deletion, which eliminates part of the putative binding site for the nuclear factor of activated T cells (NFAT-1), was identified in the overlapping nef/LTR sequence derived from a patient progressing to AIDS. This deletion coincides with the ability of this virus to consistently replicate at low levels in vivo (viral load <500 RNA copies/ml) and in vitro (unsuccessful virus isolation). On one occasion, when virus isolation was successful, the 18-bp deletion was no longer evident and LTR sequences with intact NFAT-1-binding sites were observed. Inoculation of hu-PBL-SCID mice with viruses from several Mexican patients resulted in differential CD4+ T cell depletion patterns 15 days postinfection, which agree with the in vivo CD4+ T cell count data from each patient. © AIDS Research and Human RetrovirusesScopus© Citations 11 2 12 - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Development of muscle atrophy and loss of function in a Gulf-War illness model: underlying mechanisms(2020) ;Ramírez-Sánchez, Israel ;Navarrete-Yañez, Viridiana ;Garate-Carrillo, Alejandra ;Loredo Mendoza, María LiliaGulf War illness (GWI) afflicts military personnel who served during the Persian Gulf War and is notable for cognitive deficits, depression, muscle pain, weakness, intolerance to exercise, and fatigue. Suspect causal agents include the chemicals pyridostigmine (PB), permetrim (PM) and N,N-diethyl-m-toluamide (DEET) used as protectants against insects and nerve gases. No pre-clinical studies have explored the effects on skeletal muscle (SkM). Young male rats were provided PB, PM and DEET at equivalent human doses and physical restraint (to induce stress) for 3 weeks followed a 3-week recovery. GWI gastrocnemius weight was ~ 35% lower versus controls, which correlated with decreases in myofiber area, limb strength, and treadmill time/distance. In GWI rats, SkM fiber type relative abundance changed towards slow type I. Muscle wasting pathway proteins were upregulated while those that promote growth decreased as did mitochondrial endpoints and muscle ATP levels. Proteomic analysis of SkM also documented unique alterations in mitochondrial and metabolic pathways. Thus, exposure to GWI chemicals/stress adversely impacts key metabolic pathways leading to muscle atrophy and loss of function. These changes may account for GWI Veterans symptoms.1Scopus© Citations 11 11 - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Significant Association Between Variant in SGCD and Age-Related Macular Degeneration(2018) ;Luna-Angulo, Alexandra ;Zenteno, Juan Carlos ;Rendon, Álvaro ;Cortes-Ballinas, Liliana GuadalupeJiménez-Collado, DavidCFH and HTRA1 genes are traditional markers of increased risk of age-related macular degeneration (AMD) across populations. Recent findings suggest that additional genes-for instance, in the dystrophin-associated protein complex-might be promising markers for AMD. Here, we performed a case-control study to assess the effect of SGCD single nucleotide polymorphisms (SNPs), a member of this protein family, on AMD diagnosis and phenotype. We performed a case-control study of an under-studied population from Hispanics in Mexico City, with 134 cases with 134 unpaired controls. Cases were 60 years or older (Clinical Age-Related Maculopathy Staging (CARMS) grade 4⁻5, as assessed by experienced ophthalmologists following the American Association of Ophthalmology (AAO) guidelines), without other retinal disease or history of vitreous-retinal surgery. Controls were outpatients aged 60 years or older, with no drusen or retinal pigment epithelium (RPE) changes on a fundus exam and a negative family history of AMD. We examined SNPs in the SGCD gene (rs931798, rs140617, rs140616, and rs970476) by sequencing and real-time PCR. Genotyping quality checks and univariate analyses were performed with PLINK v1.90b3.42. Furthermore, logistic regression models were done in SAS v.9.4 and haplotype configurations in R v.3.3.1. After adjusting for clinical covariates, the G/A genotype of the SGCD gene (rs931798) significantly increases the odds of being diagnosed with AMD in 81% of cases (1.81; 95% CI 1.06⁻3.14; p = 0.031), especially the geographic atrophy phenotype (1.82; 95% CI 1.03⁻3.21; p = 0.038) compared to the G/G homozygous genotype. Moreover, the GATT haplotype in this gene (rs931798, rs140617, rs140616, and rs970476) is associated with lower odds of AMD (adjusted odds ratio (OR) 0.13; 95% CI 0.02⁻0.91; p = 0.041). SGCD is a promising gene for AMD research. Further corroboration in other populations is warranted, especially among other Hispanic ethnicities.Scopus© Citations 3 1 1 - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Machine learning method to establish the connection between age related macular degeneration and some genetic variations(2016); ;Zenteno, Juan Carlos; ;Miralles-Pechuán, LuisMedicine research based in machine learning methods allows the improvement of diagnosis in complex diseases. Age related Macular Degeneration (AMD) is one of them. AMD is the leading cause of blindness in the world. It causes the 8.7% of blind people. A set of case and controls study could be developed by machine-learning methods to find the relation between Single Nucleotide Polymorphisms (SNPs) SNP_A, SNP_B, SNP_C and AMD. In this paper we present a machine-learning based analysis to determine the relation of three single nucleotide SNPs and the AMD disease. The SNPs SNP_B, SNP_C remained in the top four relevant features with ophthalmologic surgeries and bilateral cataract. We aim also to determine the best set of features for the classification process. © Springer International Publishing AG 2016.2 16Scopus© Citations 2 - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Pharmacological Treatments and Therapeutic Targets in Muscle Dystrophies Generated by Alterations in Dystrophin-Associated Proteins(2024) ;Alexandra Luna-Angulo ;Carlos Landa-Solís ;Rosa Elena Escobar-Cedillo; Laura Sánchez-Chapul<jats:p>Muscular dystrophies (MDs) are a heterogeneous group of diseases of genetic origin characterized by progressive skeletal muscle degeneration and weakness. There are several types of MDs, varying in terms of age of onset, severity, and pattern of the affected muscles. However, all of them worsen over time, and many patients will eventually lose their ability to walk. In addition to skeletal muscle effects, patients with MDs may present cardiac and respiratory disorders, generating complications that could lead to death. Interdisciplinary management is required to improve the surveillance and quality of life of patients with an MD. At present, pharmacological therapy is only available for Duchene muscular dystrophy (DMD)—the most common type of MD—and is mainly based on the use of corticosteroids. Other MDs caused by alterations in dystrophin-associated proteins (DAPs) are less frequent but represent an important group within these diseases. Pharmacological alternatives with clinical potential in patients with MDs and other proteins associated with dystrophin have been scarcely explored. This review focuses on drugs and molecules that have shown beneficial effects, mainly in experimental models involving alterations in DAPs. The mechanisms associated with the effects leading to promising results regarding the recovery or maintenance of muscle strength and reduction in fibrosis in the less-common MDs (i.e., with respect to DMD) are explored, and other therapeutic targets that could contribute to maintaining the homeostasis of muscle fibers, involving different pathways, such as calcium regulation, hypertrophy, and maintenance of satellite cell function, are also examined. It is possible that some of the drugs explored here could be used to affordably improve the muscular function of patients until a definitive treatment for MDs is developed.</jats:p>16Scopus© Citations 2 - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Genetic analysis of Mexican hairless pig populations(2001) ;Lemus-Flores, C. ;Ulloa-Arvizu, Raúl; Alonso, R. A.The main Creole pig population in Mexico, the hairless Mexican pig, remains as an unimproved and endangered genetic resource. In order to learn more about the genetic characteristics of this pig population, we assessed the allele frequency of 10 microsatellite loci in 177 unrelated hairless pigs from seven regions at Mexico and in 111 pigs of four commercial breeds (Landrace, Large White, Hampshire, and Duroc). Genetic diversity in each population was estimated by the unbiased average heterozygosity and the allele number. Nei's standard genetic distances and a neighbor-joining dendrogram were used to reveal the genetic relationships among these populations. In this report, we present data showing that the level of the genetic diversity in Mexican hairless pigs is high compared with previous reports, and that they belong to a genetic lineage divergent from commercial breeds. Furthermore, Mexican hairless pigs seem to have developed several genetically distinct lines associated with their geographic location. We conclude that the Mexican Creole pig populations may be a reservoir of genetic diversity that is important to preserve and evaluate as a source of new alleles for the future improvement of commercial pig lines.Scopus© Citations 58 1 17 - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Assessment of CFH and HTRA1 polymorphisms in age-related macular degeneration using classic and machine-learning approaches(2020); ;Antonio-Aguirre, Bani; ;Palacio-Pastrana, ClaudiaCFH: and HTRA1 are pivotal genes driving increased risk for age-related macular degeneration (AMD) among several populations. Here, we performed a hospital-based case-control study to evaluate the effects of three single nucleotide polymorphisms (SNPs) among Hispanics from Mexico. Materials and methods: 122 cases and 249 controls were genotyped using Taqman probes. Experienced ophthalmologists diagnosed AMD following the American Association of Ophthalmology guidelines. We studied CFH (rs1329428, rs203687) and HTRA1 (rs11200638) SNPs thoroughly by logistic regression models (assuming different modes of inheritance) and machine learning-based methods (ML). HTRA1: rs11200638 is the most significant polymorphism associated with AMD in our studied population. In a multivariate regression model adjusted for clinically and statistically meaningful covariates, the A/G and A/A genotypes increased the odds of disease by a factor of 2.32 and 7.81, respectively (P < .05) suggesting a multiplicative effect of the polymorphic A allele. Furthermore, this observation remains statistically meaningful in the allelic, dominant, and recessive models, and ML algorithms. When stratifying by phenotype, this polymorphism was significantly associated with increased odds for geographic atrophy (GA) in a recessive mode of inheritance (12.4, p < .05). Conclusions: In sum, this work supports a strong association between HTRA1 genetic variants and AMD in Hispanics from Mexico, especially with GA. Moreover, ML was able to replicate the results of conventional biostatistics methods unbiasedly. © 2020 Taylor & Francis Group, LLC.1Scopus© Citations 2 14 - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Lack of Delta-Sarcoglycan (Sgcd) Results in Retinal Degeneration(2019) ;Peralta-Ildefonso, Martha Janneth; ;Ramírez-Sánchez, Israel; Age-related macular degeneration (AMD) is the leading cause of central vision loss and severe blindness among the elderly population. Recently, we reported on the association of the SGCD gene (encoding for δ-sarcoglycan) polymorphisms with AMD. However, the functional consequence of Sgcd alterations in retinal degeneration is not known. Herein, we characterized changes in the retina of the Sgcd knocked-out mouse (KO, Sgcd−/−). At baseline, we analyzed the retina structure of three-month-old wild-type (WT, Sgcd+/+) and Sgcd−/− mice by hematoxylin and eosin (H&E) staining, assessed the Sgcd-protein complex (α-, β-, γ-, and ε-sarcoglycan, and sarcospan) by immunofluorescence (IF) and Western blot (WB), and performed electroretinography. Compared to the WT, Sgcd−/− mice are five times more likely to have retinal ruptures. Additionally, all the retinal layers are significantly thinner, more so in the inner plexiform layer (IPL). In addition, the number of nuclei in the KO versus the WT is ever so slightly increased. WT mice express Sgcd-protein partners in specific retinal layers, and as expected, KO mice have decreased or no protein expression, with a significant increase in the α subunit. At three months of age, there were no significant differences in the scotopic electroretinographic responses, regarding both a- and b-waves. According to our data, Sgcd−/− has a phenotype that is compatible with retinal degeneration. © 2019 by the authors. Licensee MDPI, Basel, Switzerland.2Scopus© Citations 7 24
