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    <link>http://repositorio.cualtos.udg.mx:8080/jspui/handle/123456789/556</link>
    <description />
    <pubDate>Fri, 23 Jan 2026 01:37:40 GMT</pubDate>
    <dc:date>2026-01-23T01:37:40Z</dc:date>
    <item>
      <title>Self-Reported Periodontal Disease and Its Association with SARS-CoV-2 Infection</title>
      <link>http://repositorio.cualtos.udg.mx:8080/jspui/handle/123456789/1488</link>
      <description>Title: Self-Reported Periodontal Disease and Its Association with SARS-CoV-2 Infection
Authors: Guardado Luevanos, Israel; Bologna Molina, Ronell Eduardo; Zepeda Nuño, José Sergio; Isiordia Espinoza, Mario Alberto; Molina Frechero, Nelly; González González, Rogelio; Pérez Pérez, Mauricio; López Verdín, Sandra
Abstract: Abstract&#xD;
Introduction: Knowledge of the oral manifestations associated with SARS-CoV-2 infection, the new coronavirus causing the COVID-19 pandemic, was hindered due to the restrictions issued to avoid proximity between people and to stop the rapid spread of the disease, which ultimately results in a hyperinflammatory cytokine storm that can cause death. Because periodontal disease is one of the most frequent inflammatory diseases of the oral cavity, various theories have emerged postulating periodontal disease as a risk factor for developing severe complications associated with COVID-19. This motivated various studies to integrate questions related to periodontal status. For the present work, we used a previously validated self-report, which is a useful tool for facilitating epidemiological studies of periodontal disease on a large scale. Methodology: A blinded case-control study with participants matched 1:1 by mean age (37.7 years), sex, tobacco habits and diseases was conducted. After the diagnostic samples for SARS-CoV-2 detection were taken in an ad hoc location at Guadalajara University, the subjects were interviewed using structured questionnaires to gather demographic, epidemiological and COVID-19 symptom information. The self-reported periodontal disease (Self-RPD) questionnaire included six questions, and subjects who met the criteria with a score ≥ 2 were considered to have periodontal disease. Results: In total, 369 participants were recruited, with 117 participants included in each group. After indicating the subjects who had self-reported periodontal disease, a statistically significant difference (p value ≤ 0.001) was observed, showing that self-reported periodontal disease (n = 95, 85.1%) was higher in SARS-CoV-2-positive individuals than in controls (n = 66, 56.4%), with an OR of 3.3 (1.8–6.0) for SARS-CoV-2 infection in people with self-reported periodontal disease. Cases reported a statistically higher median of symptoms (median = 7.0, Q1= 5.5, Q3 = 10.0) than controls (p value ≤ 0.01), and cases with positive self-RPD had a significantly (p value ≤ 0.05) higher number of symptoms (median = 8.0, Q1 = 6.0, Q3 = 10.0) in comparison with those who did negative self-RPD (median = 6.0, Q1 = 5.0, Q3 = 8.0). Conclusions: According to this study, self-reported periodontal disease could be considered a risk factor for SARS-CoV-2 infection, and these individuals present more symptoms.
Description: Artículo</description>
      <pubDate>Mon, 01 Aug 2022 00:00:00 GMT</pubDate>
      <guid isPermaLink="false">http://repositorio.cualtos.udg.mx:8080/jspui/handle/123456789/1488</guid>
      <dc:date>2022-08-01T00:00:00Z</dc:date>
    </item>
    <item>
      <title>Causas del hidrops fetal: experiencia en un hospital obstétrico del Occidente de México</title>
      <link>http://repositorio.cualtos.udg.mx:8080/jspui/handle/123456789/1464</link>
      <description>Title: Causas del hidrops fetal: experiencia en un hospital obstétrico del Occidente de México
Authors: Becerra Solano, Luis Eduardo; Medina Castellanos, Marcela; Oseguera Torres, Luis Fernando; Mendoza Ruvalcaba, Sandra del Carmen; Domínguez Quezada, María Guadalupe; García Ortiz, José Elías
Abstract: Resumen &#xD;
OBJETIVO: Identificar las causas de hidrops fetal no inmunitario en un hospital obstétrico de referencia del Occidente de México. MATERIALES Y MÉTODOS: Estudio de serie de casos, con un muestreo no probabilístico por conveniencia, llevado a cabo de octubre de 2014 a septiembre de 2015 al que se incluyeron pacientes (entre las 15 y 38 semanas de embarazo), mayores de edad (en casos de menores de edad se solicitó consentimiento informado a los padres o tutores), con diagnóstico de hidrops fetal por ultrasonido obstétrico. Para el análisis estadístico se generó una base de datos en Excel y se aplicó estadística descriptiva. RESULTADOS: Se reunieron 33 embarazadas en quienes el hidrops fetal no inmunitario fue el más frecuente (n = 31) y la causa idiopática más común (n = 10) seguida por errores innatos del metabolismo, alteraciones cromosómicas y cardiacas (n = 6 de cada una). Posteriormente, las causas hematológicas (n = 4), linfáticas y sindrómicas (n = 3 de cada una), y las infecciosas y tumorales (n = 1 de cada una). En este estudio los errores innatos del metabolismo (específicamente síndrome Sly) tuvieron una frecuencia superior a la referida en la bibliografía. CONCLUSIONES: Los errores innatos del metabolismo, las anomalías cromosómicas y cardiacas fueron la segunda causa más frecuente de hidrops fetal no inmunitario. Se sugiere tener en cuenta las causas metabólicas en el enfoque diagnóstico del hidrops fetal, sobre todo para el establecimiento del tratamiento temprano. PALABRAS CLAVE: Hidrops fetal inmunitario; hidrops fetal no inmunitario; complicaciones del embarazo; síndrome Sly; Occidente de México.&#xD;
Abstract &#xD;
OBJECTIVE: To identify the causes of nonimmune fetal hydrops fetalis in an obstetric referral hospital in Western Mexico. MATERIALS AND METHODS: Case series study, with non-probabilistic sampling by convenience, carried out from October 2014 to September 2015 which included patients (between 15 and 38 weeks of pregnancy), of legal age (in cases of minors, informed consent was requested from parents or guardians), with a diagnosis of fetal hydrops fetalis by obstetric ultrasound. For statistical analysis, an Excel database was generated and descriptive statistics were applied. RESULTS: Thirty-three pregnant women were included, in whom non-immune fetal hydrops fetalis was the most frequent (94%) and idiopathic was the most common cause (n = 10), followed by inborn errors of metabolism, chromosomal and cardiac alterations (n = 6 each). This was followed by hematologic (n = 4), lymphatic and syndromic causes (n = 3 each), and infectious and tumor causes (n = 1 each). In this study, inborn errors of metabolism (specifically Sly syndrome) had a higher frequency than that reported in the literature. CONCLUSIONS: Inborn errors of metabolism, chromosomal and cardiac abnormalities were the second most frequent cause of nonimmune fetal hydrops. It is suggested that metabolic causes be taken into account in the diagnostic approach to fetal hydrops, especially for the establishment of early treatment.
Description: Artículo</description>
      <pubDate>Fri, 01 Jul 2022 00:00:00 GMT</pubDate>
      <guid isPermaLink="false">http://repositorio.cualtos.udg.mx:8080/jspui/handle/123456789/1464</guid>
      <dc:date>2022-07-01T00:00:00Z</dc:date>
    </item>
    <item>
      <title>Case Report: Whole Exome Sequencing Unveils an Inherited Truncating Variant in CNTN6 (p.Ser189Ter) in a Mexican Child with Autism Spectrum Disorder</title>
      <link>http://repositorio.cualtos.udg.mx:8080/jspui/handle/123456789/1355</link>
      <description>Title: Case Report: Whole Exome Sequencing Unveils an Inherited Truncating Variant in CNTN6 (p.Ser189Ter) in a Mexican Child with Autism Spectrum Disorder
Authors: García Ortiz, José Elías; Zarazúa Niño, Ana Itzel; Hernández Orozco, Angélica Alejandra; Reyes Oliva, Edwin A; Pérez Ávila, Carlos E.; Becerra Solano, Luis Eduardo; Galán Huerta, Kame A; Rivas Estilla, Ana María; Córdova Fletes, Carlos
Abstract: Autism spectrum disorders (ASDs) are a group of heterogeneous neurodevelopmental disorders with hundreds&#xD;
of related genes. Among these, CNTN6 (Contactin-6) has recently been associated. Herein, we describe a paternally inherited CNTN6 variant predicted in silico to be deleterious in a patient presenting with language delay, poor social interaction, stereotypic behavior, and sensory-motor and hearing problems. Additional genomic data by whole-exome sequencing (WES) suggest, however, that a concomitant pathogenic genetic background would be needed to explain the phenotype along with this CNTN6 variant.
Description: Artículo</description>
      <pubDate>Thu, 01 Jul 2021 00:00:00 GMT</pubDate>
      <guid isPermaLink="false">http://repositorio.cualtos.udg.mx:8080/jspui/handle/123456789/1355</guid>
      <dc:date>2021-07-01T00:00:00Z</dc:date>
    </item>
    <item>
      <title>Effects of SPTA1 Gene Variants on the Hematological Phenotype of Mexican Patients with Hereditary Spherocytosis</title>
      <link>http://repositorio.cualtos.udg.mx:8080/jspui/handle/123456789/1354</link>
      <description>Title: Effects of SPTA1 Gene Variants on the Hematological Phenotype of Mexican Patients with Hereditary Spherocytosis
Authors: Herrera Tirado, Isis Mariela; Espinoza Mata, Laura Lucía; Rizo De la Torre, Lourdes del Carmen; Becerra Solano, Luis Eduardo; Ibarra Cortés, Bertha; Perea Díaz, Francisco Javier
Abstract: Abstract&#xD;
Introduction: Hereditary spherocytosis (HS) is a common hereditary hemolytic anemia characterized by chronic hemolysis, increased indirect serum bilirubin, the presence of reticulocytes and spherocytes in blood smears, and great heterogeneity at the clinical, biochemical, and molecular levels. The molecular pathology of HS includes genetic variants at five genes: ANK1, EPB42, SLC4A1, SPTA1, and SPTB. Alpha spectrin (SPTA1) deficiency is the second leading cause of HS in Mexican patients.&#xD;
&#xD;
Aim: To assess the effects of five SPTA1 variants on the hematological phenotype of Mexican patients with HS.&#xD;
&#xD;
Materials and Methods: This study included a retrospective cohort of 227 biologically unrelated patients with HS. Variants c.4339-99C&gt;T and c.6531-12C&gt;T in SPTA1 were identified by the amplification-refractory mutation system polymerase chain reaction (ARMS-PCR), and variants c.5572C&gt;T, c.5992C&gt;G, and c.6794T&gt;C were identified by quantitive Real Time-Polymerase Chain Reaction (qRT-PCR) allelic discrimination. Risk tests were performed for each variant with respect to HS clinical severity.&#xD;
&#xD;
Results: The SPTA1 c.5992C&gt;G variant showed association with moderately severe HS (p = 0.006, odds ratio = 5.67, confidence interval95% = 1.6–19.9); the risk increased when the variant was in compound heterozygosity with αLELY and c.6794T&gt;C. Lower hematological levels were observed in simple αLely (c.5572C&gt;T and c.6531-12C&gt;T), and c.5992C&gt;G heterozygotes (red blood cell [RBC] p = 0.028 and 0.010; hemoglobin [Hb] p = 0.030 and 0.002; packed cell volume [PCV] p = 0.034 and 0.002 respectively), and in c.5992C&gt;G+c.6794T&gt;C compound heterozygotes (RBC p = 0.043; Hb p = 0.033; PCV p = 0.043). Additional genetic traits were observed: 15% had HS+Gilbert syndrome and 13% HS+thalassemia.&#xD;
&#xD;
Conclusion: Although most of the studied variants are considered benign, we observed significant associations with phenotypic severity. Therefore, we recommend the inclusion of these variants in molecular screening for HS.
Description: Artículo</description>
      <pubDate>Sun, 01 May 2022 00:00:00 GMT</pubDate>
      <guid isPermaLink="false">http://repositorio.cualtos.udg.mx:8080/jspui/handle/123456789/1354</guid>
      <dc:date>2022-05-01T00:00:00Z</dc:date>
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