Víctor Javier Lara-Díaz
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Víctor Javier Lara-Díaz has a total of 103 co-authors. Here are the top co-authors by number of shared publications:
- Fabiola Castorena-Torres
Tecnologico de Monterrey, Escuela de Medicina y Ciencias de la Salud, Ave. Morones Prieto 3000, Monterrey, N.L, Mexico
5 shared publications - Mario René Alcorta-García
Hospital Regional Materno Infantil, Servicios de Salud de Nuevo León, OPD, Ciudad Guadalupe, N.L., Mexico
4 shared publications - Víctor Arízaga-Ballesteros
Tecnológico de Monterrey, Escuela de Medicina. Programa Multicéntrico de Residencias Médicas, Neonatología
3 shared publications - Alberto López-Reyes
Laboratorio de Gerociencias, Dirección General, Departamento de Reconstrucción Articular, Instituto Nacional de Rehabilitación Luis Guillermo Ibarra Ibarra, Secretaría de Salud, Mexico City, Mexico
2 shared publications - Claudia N. López-Villaseñor
Hospital Regional Materno Infantil, Servicios de Salud de Nuevo León, OPD, Ciudad Guadalupe, N.L., Mexico
2 shared publications - Inma Castilla-Cortázar
Fundación de Investigación HM Hospitales, Madrid, Madrid
2 shared publications
Latest Publications
- Open Access
- 2 July 2025
- Published by Royal Society of Chemistry (RSC) in Food & Function
- Vol. 16 (14) , 5900-5916
Analysis of human colostrum reveals differential co-occurrence networks of metabolites, microbiota and cytokines in maternal obesity
Breastmilk is essential for neonatal development, particularly in seeding the gut microbiota and modulating the immune system. This proof-of-concept study explores the systemic nature of colostrum and the influence of maternal obesity on co-occurrences of colostrum bioactives. Using 16S-rRNA sequencing, untargeted metabolomics, and cytokine quantification, we analyzed co-occurring elements in the colostrum of mothers with normal weight (18.5 < BMI < 25) or obesity (BMI > 30). We identified 5 different co-occurrence networks, characterized by positive correlations of taxonomically related bacteria. Our integrative analysis reveals that Aeromonadaceae, Xanthomonadaceae and Staphylococcaceae negatively correlate with pro-inflammatory cytokines TNF-α, IL-6, and IL-12p70 in the colostrum of mothers with obesity (WO). Additionally, lipid mediators, including 15-HEDE and LysoPC (16:00), were associated with cytokines IL-10 and IL-8 and microbiota taxa Burkholderiaceae, Beijerinckiaceae and Planococcaceae – first reported in the colostrum of mothers WO. Our findings suggest a pervasive regulation of bioactives in the colostrum of mothers WO. This may have implications for distinctive neonatal intestine development.
- 2 July 2025
- Published by Royal Society of Chemistry (RSC) in Food & Function
- Vol. 16 (14) , 5900-5916
Open AccessAnalysis of human colostrum reveals differential co-occurrence networks of metabolites, microbiota and cytokines in maternal obesity
Breastmilk is essential for neonatal development, particularly in seeding the gut microbiota and modulating the immune system. This proof-of-concept study explores the systemic nature of colostrum and the influence of maternal obesity on co-occurrences of colostrum bioactives. Using 16S-rRNA sequencing, untargeted metabolomics, and cytokine quantification, we analyzed co-occurring elements in the colostrum of mothers with normal weight (18.5 < BMI < 25) or obesity (BMI > 30). We identified 5 different co-occurrence networks, characterized by positive correlations of taxonomically related bacteria. Our integrative analysis reveals that Aeromonadaceae, Xanthomonadaceae and Staphylococcaceae negatively correlate with pro-inflammatory cytokines TNF-α, IL-6, and IL-12p70 in the colostrum of mothers with obesity (WO). Additionally, lipid mediators, including 15-HEDE and LysoPC (16:00), were associated with cytokines IL-10 and IL-8 and microbiota taxa Burkholderiaceae, Beijerinckiaceae and Planococcaceae – first reported in the colostrum of mothers WO. Our findings suggest a pervasive regulation of bioactives in the colostrum of mothers WO. This may have implications for distinctive neonatal intestine development.
- Open Access
- 18 May 2022
- Published by SPIE-Intl Soc Optical Eng in Journal of Biomedical Optics
- Vol. 27 (05) , 056003-19
COVID-19 classification using thermal images
Significance: There is a scarcity of published research on the potential role of thermal imaging in the remote detection of respiratory issues due to coronavirus disease-19 (COVID-19). This is a comprehensive study that explores the potential of this imaging technology resulting from its convenient aspects that make it highly accessible: it is contactless, noninvasive, and devoid of harmful radiation effects, and it does not require a complicated installation process. Aim: We aim to investigate the role of thermal imaging, specifically thermal video, for the identification of SARS-CoV-2-infected people using infrared technology and to explore the role of breathing patterns in different parts of the thorax for the identification of possible COVID-19 infection. Approach: We used signal moment, signal texture, and shape moment features extracted from five different body regions of interest (whole upper body, chest, face, back, and side) of images obtained from thermal video clips in which optical flow and super-resolution were used. These features were classified into positive and negative COVID-19 using machine learning strategies. Results: COVID-19 detection for male models [receiver operating characteristic (ROC) area under the ROC curve (AUC) = 0.605 95% confidence intervals (CI) 0.58 to 0.64] is more reliable than for female models (ROC AUC = 0.577 95% CI 0.55 to 0.61). Overall, thermal imaging is not very sensitive nor specific in detecting COVID-19; the metrics were below 60% except for the chest view from males. Conclusions: We conclude that, although it may be possible to remotely identify some individuals affected by COVID-19, at this time, the diagnostic performance of current methods for body thermal imaging is not good enough to be used as a mass screening tool.
- 18 May 2022
- Published by SPIE-Intl Soc Optical Eng in Journal of Biomedical Optics
- Vol. 27 (05) , 056003-19
Open AccessCOVID-19 classification using thermal images
Significance: There is a scarcity of published research on the potential role of thermal imaging in the remote detection of respiratory issues due to coronavirus disease-19 (COVID-19). This is a comprehensive study that explores the potential of this imaging technology resulting from its convenient aspects that make it highly accessible: it is contactless, noninvasive, and devoid of harmful radiation effects, and it does not require a complicated installation process. Aim: We aim to investigate the role of thermal imaging, specifically thermal video, for the identification of SARS-CoV-2-infected people using infrared technology and to explore the role of breathing patterns in different parts of the thorax for the identification of possible COVID-19 infection. Approach: We used signal moment, signal texture, and shape moment features extracted from five different body regions of interest (whole upper body, chest, face, back, and side) of images obtained from thermal video clips in which optical flow and super-resolution were used. These features were classified into positive and negative COVID-19 using machine learning strategies. Results: COVID-19 detection for male models [receiver operating characteristic (ROC) area under the ROC curve (AUC) = 0.605 95% confidence intervals (CI) 0.58 to 0.64] is more reliable than for female models (ROC AUC = 0.577 95% CI 0.55 to 0.61). Overall, thermal imaging is not very sensitive nor specific in detecting COVID-19; the metrics were below 60% except for the chest view from males. Conclusions: We conclude that, although it may be possible to remotely identify some individuals affected by COVID-19, at this time, the diagnostic performance of current methods for body thermal imaging is not good enough to be used as a mass screening tool.
- Open Access
Insights into the trafficking of human leukocytes to colostrum evidences a modulation of the B lymphocyte compartment in obesity
Breastmilk is a dynamic fluid which initial goal is to provide the most adapted nutrition to the neonate. Additional functions have been recently attributed to breastmilk, with the evidence of a specific microbiota and the presence of a variety of components of the immune system, such as cytokines and leukocytes. The composition of breastmilk varies through time, according to the health status of mother and child, and altogether contributes to future health of the infant. Obesity is a rising condition worldwide, that creates a state of systemic, chronic inflammation including leukocytosis. Here, we asked whether colostrum, the milk produced within the first 48 h post-partum, would contain a distinct leukocyte composition depending on the body mass index (BMI) of the mother. We applied a panel of 6 antibodies plus viability marker to the peripheral blood and colostrum obtained from obese (BMI > 30) and lean (BMI < 25) mothers to characterize 10 major leukocyte subpopulations using flow cytometry. While lymphoid cells were otherwise unaffected by their tissue of origin, the phenotypes of granulocyte and monocyte populations significantly contrasted between blood and colostrum, including variations in morphology and surface expression of CD45 and CD16. These differences recapitulated across groups, which suggests a generalized cell-specific phenotype alteration caused by trafficking to colostrum. The B lymphocyte compartment was significantly reduced in obese colostrum and these cells did not exhibit enhanced CD16 shedding in this tissue, unlike B lymphocytes from lean mothers’ colostrum. This is the first exhaustive characterization of major leukocyte subsets in obese mothers’ colostrum, and the first report of leukocyte subpopulations from Latin-American women’s colostrum. This pioneering study is a steppingstone to further investigate active immunity in human breastmilk.
Open AccessInsights into the trafficking of human leukocytes to colostrum evidences a modulation of the B lymphocyte compartment in obesity
Breastmilk is a dynamic fluid which initial goal is to provide the most adapted nutrition to the neonate. Additional functions have been recently attributed to breastmilk, with the evidence of a specific microbiota and the presence of a variety of components of the immune system, such as cytokines and leukocytes. The composition of breastmilk varies through time, according to the health status of mother and child, and altogether contributes to future health of the infant. Obesity is a rising condition worldwide, that creates a state of systemic, chronic inflammation including leukocytosis. Here, we asked whether colostrum, the milk produced within the first 48 h post-partum, would contain a distinct leukocyte composition depending on the body mass index (BMI) of the mother. We applied a panel of 6 antibodies plus viability marker to the peripheral blood and colostrum obtained from obese (BMI > 30) and lean (BMI < 25) mothers to characterize 10 major leukocyte subpopulations using flow cytometry. While lymphoid cells were otherwise unaffected by their tissue of origin, the phenotypes of granulocyte and monocyte populations significantly contrasted between blood and colostrum, including variations in morphology and surface expression of CD45 and CD16. These differences recapitulated across groups, which suggests a generalized cell-specific phenotype alteration caused by trafficking to colostrum. The B lymphocyte compartment was significantly reduced in obese colostrum and these cells did not exhibit enhanced CD16 shedding in this tissue, unlike B lymphocytes from lean mothers’ colostrum. This is the first exhaustive characterization of major leukocyte subsets in obese mothers’ colostrum, and the first report of leukocyte subpopulations from Latin-American women’s colostrum. This pioneering study is a steppingstone to further investigate active immunity in human breastmilk.
- Open Access
High Iodine Urinary Concentration Is Associated with High TSH Levels but Not with Nutrition Status in Schoolchildren of Northeastern Mexico
According to the Iodine Global Network, Mexico is considered a country with adequate national iodine intake (297 mg/L), but some regions have not been studied. We aimed to evaluate urinary iodine concentration (UIC) and its association with thyroid stimulating hormone (TSH) levels and the nutritional status in 307 children (aged 5 to 11 years) from three elementary schools of Monterrey, northern Mexico. UIC in spot urine samples and capillary TSH levels were measured to assess thyroid function, in addition to weight, height, body mass index (BMI), and waist circumference (WC). We found a median UIC of 442 mg/L and a significant association between UIC and TSH levels by logistic regression when data were adjusted for (1) age and sex; (2) age, sex, and WC; and (3) age, sex, and weight status. UIC values were higher in 7-year-old children compared to 11-year-old children. High prevalences of overweight/obesity (41%) and WC >90 pctl (22%) were observed. This study identified higher UIC levels in children than those previously reported in the country. The UIC showed a positive and significant correlation between TSH levels in the three models evaluated. More studies are needed to assess the causes and possible outcomes of high UIC levels.
Open AccessHigh Iodine Urinary Concentration Is Associated with High TSH Levels but Not with Nutrition Status in Schoolchildren of Northeastern Mexico
According to the Iodine Global Network, Mexico is considered a country with adequate national iodine intake (297 mg/L), but some regions have not been studied. We aimed to evaluate urinary iodine concentration (UIC) and its association with thyroid stimulating hormone (TSH) levels and the nutritional status in 307 children (aged 5 to 11 years) from three elementary schools of Monterrey, northern Mexico. UIC in spot urine samples and capillary TSH levels were measured to assess thyroid function, in addition to weight, height, body mass index (BMI), and waist circumference (WC). We found a median UIC of 442 mg/L and a significant association between UIC and TSH levels by logistic regression when data were adjusted for (1) age and sex; (2) age, sex, and WC; and (3) age, sex, and weight status. UIC values were higher in 7-year-old children compared to 11-year-old children. High prevalences of overweight/obesity (41%) and WC >90 pctl (22%) were observed. This study identified higher UIC levels in children than those previously reported in the country. The UIC showed a positive and significant correlation between TSH levels in the three models evaluated. More studies are needed to assess the causes and possible outcomes of high UIC levels.
- 4 November 2020
- Published by Frontiers Media SA in Experimental Biology and Medicine
- Vol. 246 (6) , 695-706
Prenatal indole-3-carbinol administration activates aryl hydrocarbon receptor-responsive genes and attenuates lung injury in a bronchopulmonary dysplasia model
Hyperoxia−hypoxia exposure is a proposed cause of alveolar developmental arrest in bronchopulmonary dysplasia in preterm infants, where mitochondrial reactive oxygen species and oxidative stress vulnerability are increased. The aryl hydrocarbon receptor (AhR) is one of the main activators of the antioxidant enzyme system that protects tissues and systems from damage. The present study aimed to determine if the activation of the AhR signaling pathway by prenatal administration of indole-3-carbinol (I3C) protects rat pups from hyperoxia–hypoxia-induced lung injury. To assess the activation of protein-encoding genes related to the AhR signaling pathway (Cyp1a1, Cyp1b1, Ugt1a6, Nqo1, and Gsta1), pup lungs were excised at 0, 24, and 72 h after birth, and mRNA expression levels were quantified by reverse transcription-quantitative polymerase chain reaction assays (RT-qPCR). An adapted Ratner's method was used in rats to evaluate radial alveolar counts (RACs) and the degree of fibrosis. The results reveal that the relative expression of AhR-related genes in rat pups of prenatally I3C-treated dams was significantly different from that of untreated dams. The RAC was significantly lower in the hyperoxia–hypoxia group (4.0 ± 1.0) than that in the unexposed control group (8.0 ± 2.0; P < 0.01). When rat pups of prenatally I3C-treated dams were exposed to hyperoxia–hypoxia, an RAC recovery was observed, and the fibrosis index was similar to that of the unexposed control group. A cytokine antibody array revealed an increase in the NF-κB signaling cascade in I3C-treated pups, suggesting that the pathway could regulate the inflammatory process under the stimulus of this compound. In conclusion, the present study demonstrates that I3C prenatal treatment activates AhR-responsive genes in pup’s lungs and hence attenuates lung damage caused by hyperoxia–hypoxia exposure in newborns.
- 4 November 2020
- Published by Frontiers Media SA in Experimental Biology and Medicine
- Vol. 246 (6) , 695-706
Prenatal indole-3-carbinol administration activates aryl hydrocarbon receptor-responsive genes and attenuates lung injury in a bronchopulmonary dysplasia model
Hyperoxia−hypoxia exposure is a proposed cause of alveolar developmental arrest in bronchopulmonary dysplasia in preterm infants, where mitochondrial reactive oxygen species and oxidative stress vulnerability are increased. The aryl hydrocarbon receptor (AhR) is one of the main activators of the antioxidant enzyme system that protects tissues and systems from damage. The present study aimed to determine if the activation of the AhR signaling pathway by prenatal administration of indole-3-carbinol (I3C) protects rat pups from hyperoxia–hypoxia-induced lung injury. To assess the activation of protein-encoding genes related to the AhR signaling pathway (Cyp1a1, Cyp1b1, Ugt1a6, Nqo1, and Gsta1), pup lungs were excised at 0, 24, and 72 h after birth, and mRNA expression levels were quantified by reverse transcription-quantitative polymerase chain reaction assays (RT-qPCR). An adapted Ratner's method was used in rats to evaluate radial alveolar counts (RACs) and the degree of fibrosis. The results reveal that the relative expression of AhR-related genes in rat pups of prenatally I3C-treated dams was significantly different from that of untreated dams. The RAC was significantly lower in the hyperoxia–hypoxia group (4.0 ± 1.0) than that in the unexposed control group (8.0 ± 2.0; P < 0.01). When rat pups of prenatally I3C-treated dams were exposed to hyperoxia–hypoxia, an RAC recovery was observed, and the fibrosis index was similar to that of the unexposed control group. A cytokine antibody array revealed an increase in the NF-κB signaling cascade in I3C-treated pups, suggesting that the pathway could regulate the inflammatory process under the stimulus of this compound. In conclusion, the present study demonstrates that I3C prenatal treatment activates AhR-responsive genes in pup’s lungs and hence attenuates lung damage caused by hyperoxia–hypoxia exposure in newborns.
- Open Access
- 1 June 2020
- Published by Springer Nature in Molecular and Cellular Pediatrics
- Vol. 7 (1) , 1-12
Modulation of CYP2E1 metabolic activity in a cohort of confirmed caffeine ingesting pregnant women with preterm offspring
Background: To ascertain interactions of caffeine ingestion, food, medications, and environmental exposures during preterm human gestation, under informed consent, we studied a cohort of Mexican women with further preterm offspring born at ≤ 34 completed weeks. At birth, blood samples were taken from mothers and umbilical cords to determine caffeine and metabolites concentrations and CYP1A2 (rs762551) and CYP2E1 (rs2031920, rs3813867) polymorphisms involved in caffeine metabolism. Results: In 90 pregnant women who gave birth to 98 preterm neonates, self-informed caffeine ingestion rate was 97%, laboratory confirmed rate was 93 %. Theobromine was the predominant metabolite found. Consumption of acetaminophen correlated significantly with changes in caffeine metabolism (acetaminophen R2 = 0.637, p = 0.01) due to activation of CYP2E1 alternate pathways. The main caffeine source was cola soft drinks. Conclusion: Environmental exposures, especially acetaminophen ingestion during human preterm pregnancy, can modulate CYP2E1 metabolic activity.
- 1 June 2020
- Published by Springer Nature in Molecular and Cellular Pediatrics
- Vol. 7 (1) , 1-12
Open AccessModulation of CYP2E1 metabolic activity in a cohort of confirmed caffeine ingesting pregnant women with preterm offspring
Background: To ascertain interactions of caffeine ingestion, food, medications, and environmental exposures during preterm human gestation, under informed consent, we studied a cohort of Mexican women with further preterm offspring born at ≤ 34 completed weeks. At birth, blood samples were taken from mothers and umbilical cords to determine caffeine and metabolites concentrations and CYP1A2 (rs762551) and CYP2E1 (rs2031920, rs3813867) polymorphisms involved in caffeine metabolism. Results: In 90 pregnant women who gave birth to 98 preterm neonates, self-informed caffeine ingestion rate was 97%, laboratory confirmed rate was 93 %. Theobromine was the predominant metabolite found. Consumption of acetaminophen correlated significantly with changes in caffeine metabolism (acetaminophen R2 = 0.637, p = 0.01) due to activation of CYP2E1 alternate pathways. The main caffeine source was cola soft drinks. Conclusion: Environmental exposures, especially acetaminophen ingestion during human preterm pregnancy, can modulate CYP2E1 metabolic activity.
- 1 December 2018
- Published by Elsevier in Sensors and Actuators B: Chemical
- Vol. 276, 429-436
Aluminium valving and magneto-balloon mixing for rapid prediction of septic shock on centrifugal microfluidic platforms
- 1 December 2018
- Published by Elsevier in Sensors and Actuators B: Chemical
- Vol. 276, 429-436
Aluminium valving and magneto-balloon mixing for rapid prediction of septic shock on centrifugal microfluidic platforms
- 14 April 2017
- Published by Taylor & Francis in Fetal and Pediatric Pathology
- Vol. 36 (5) , 345-346
To the Editor: Concerning Kaya et al.
- 14 April 2017
- Published by Taylor & Francis in Fetal and Pediatric Pathology
- Vol. 36 (5) , 345-346
To the Editor: Concerning Kaya et al.
- Open Access
- 26 January 2017
- Published by Springer Nature in Journal of Physiology and Biochemistry
- Vol. 73 (2) , 245-258
IGF-1 modulates gene expression of proteins involved in inflammation, cytoskeleton, and liver architecture
Even though the liver synthesizes most of circulating IGF-1, it lacks its receptor under physiological conditions. However, according to previous studies, a damaged liver expresses the receptor. For this reason, herein, we examine hepatic histology and expression of genes encoding proteins of the cytoskeleton, extracellular matrix, and cell-cell molecules and inflammation-related proteins. A partial IGF-1 deficiency murine model was used to investigate IGF-1’s effects on liver by comparing wild-type controls, heterozygous igf1+/−, and heterozygous mice treated with IGF-1 for 10 days. Histology, microarray for mRNA gene expression, RT-qPCR, and lipid peroxidation were assessed. Microarray analyses revealed significant underexpression of igf1 in heterozygous mice compared to control mice, restoring normal liver expression after treatment, which then normalized its circulating levels. IGF-1 receptor mRNA was overexpressed in Hz mice liver, while treated mice displayed a similar expression to that of the controls. Heterozygous mice showed overexpression of several genes encoding proteins related to inflammatory and acute-phase proteins and underexpression or overexpression of genes which coded for extracellular matrix, cytoskeleton, and cell junction components. Histology revealed an altered hepatic architecture. In addition, liver oxidative damage was found increased in the heterozygous group. The mere IGF-1 partial deficiency is associated with relevant alterations of the hepatic architecture and expression of genes involved in cytoskeleton, hepatocyte polarity, cell junctions, and extracellular matrix proteins. Moreover, it induces hepatic expression of the IGF-1 receptor and elevated acute-phase and inflammation mediators, which all resulted in liver oxidative damage.
- 26 January 2017
- Published by Springer Nature in Journal of Physiology and Biochemistry
- Vol. 73 (2) , 245-258
Open AccessIGF-1 modulates gene expression of proteins involved in inflammation, cytoskeleton, and liver architecture
Even though the liver synthesizes most of circulating IGF-1, it lacks its receptor under physiological conditions. However, according to previous studies, a damaged liver expresses the receptor. For this reason, herein, we examine hepatic histology and expression of genes encoding proteins of the cytoskeleton, extracellular matrix, and cell-cell molecules and inflammation-related proteins. A partial IGF-1 deficiency murine model was used to investigate IGF-1’s effects on liver by comparing wild-type controls, heterozygous igf1+/−, and heterozygous mice treated with IGF-1 for 10 days. Histology, microarray for mRNA gene expression, RT-qPCR, and lipid peroxidation were assessed. Microarray analyses revealed significant underexpression of igf1 in heterozygous mice compared to control mice, restoring normal liver expression after treatment, which then normalized its circulating levels. IGF-1 receptor mRNA was overexpressed in Hz mice liver, while treated mice displayed a similar expression to that of the controls. Heterozygous mice showed overexpression of several genes encoding proteins related to inflammatory and acute-phase proteins and underexpression or overexpression of genes which coded for extracellular matrix, cytoskeleton, and cell junction components. Histology revealed an altered hepatic architecture. In addition, liver oxidative damage was found increased in the heterozygous group. The mere IGF-1 partial deficiency is associated with relevant alterations of the hepatic architecture and expression of genes involved in cytoskeleton, hepatocyte polarity, cell junctions, and extracellular matrix proteins. Moreover, it induces hepatic expression of the IGF-1 receptor and elevated acute-phase and inflammation mediators, which all resulted in liver oxidative damage.