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1.
Front Pediatr ; 10: 883185, 2022.
Article in English | MEDLINE | ID: mdl-35844759

ABSTRACT

Passive transplacental immunity is crucial for neonatal protection from infections. Data on the correlation between neonatal immunity to SARS-CoV-2 and protection from adverse outcomes is scarce. This work aimed to describe neonatal seropositivity in the context of maternal SARS-CoV-2 infection, seropositivity, and neonatal outcomes. This retrospective nested case-control study enrolled high-risk pregnant women with a SARS-CoV-2 RT-PCR positive test who gave birth at the Instituto Nacional de Perinatología in Mexico City and their term neonates. Anti-SARS-CoV-2 IgG antibodies in maternal and cord blood samples were detected using a chemiluminescent assay. In total, 63 mother-neonate dyads (mean gestational age 38.4 weeks) were included. Transplacental transfer of SARS-CoV-2 IgG occurred in 76% of neonates from seropositive mothers. A positive association between maternal IgG levels and Cycle threshold (Ct) values of RT-qPCR test for SARS-CoV-2 with neonatal IgG levels was observed. Regarding neonatal outcomes, most seropositive neonates did not require any mechanical ventilation, and none developed any respiratory morbidity (either in the COVID-19 positive or negative groups) compared to 7 seronegative neonates. Furthermore, the odds of neonatal respiratory morbidity exhibited a tendency to decrease when neonatal IgG levels increase. These results add further evidence suggesting passive IgG transfer importance.

2.
Synapse ; 76(9-10): 1-16, 2022 08.
Article in English | MEDLINE | ID: mdl-35709361

ABSTRACT

Cadmium (Cd) is a heavy metal classified as a carcinogen whose exposure could affect the function of the central nervous system. Studies suggest that Cd modifies neuronal morphology in the hippocampus and affects cognitive tasks. The oxidative stress pathway is proposed as a mechanism of toxicity. However, this mechanism is not precise yet. This study aimed to evaluate the effect of Cd administration on oxidative stress markers in the male rat's hippocampus. Male Wistar rats were divided into (1) control (drinking water) and (2) treatment with Cd (32.5 ppm of cadmium chloride (CdCl2 ) in water). The Cd was administered for 2, 3, and 4 months. The results show that the oral administration of CdCl2 increased the concentration of Cd in plasma and hippocampus, and this response is time-dependent on its administration. Likewise, it caused an increase in lipid peroxidation and nitrosative stress markers. Moreover, it increased reactive astrogliosis and antioxidant enzyme activity. Consequently, the progression of the oxidative response exacerbated neurodegeneration in hippocampal cells. Our results suggest that Cd exposure induces a severe oxidative response that contributes critically to hippocampal neurodegeneration. It is suggested that exposure to Cd increases the risk of developing neurological diseases, which contributes to a decrease in the quality of life of the human and the environment in which it lives.


Subject(s)
Antioxidants , Cadmium , Animals , Antioxidants/pharmacology , Cadmium/metabolism , Cadmium/toxicity , Cadmium Chloride/metabolism , Cadmium Chloride/toxicity , Hippocampus/metabolism , Humans , Lipid Peroxidation , Male , Oxidative Stress , Quality of Life , Rats , Rats, Wistar
3.
J Nutr Biochem ; 83: 108416, 2020 09.
Article in English | MEDLINE | ID: mdl-32554223

ABSTRACT

The main characteristic of brain aging is an exacerbated inflammatory and oxidative response that affects dendritic morphology and the function of the neurons of the prefrontal cortex (PFC) and the hippocampus. This consequently causes memory loss. Recently, the use of the Goji berry (Lycium barbarum) as an antioxidant extract has provided neuroprotection and neuroplasticity, however, its therapeutic potential has not been demonstrated in aging conditions. The objective of this study was to evaluate the effect of Goji administration on memory recognition, as well as the changes in the dendritic morphology of the PFC and Hippocampus pyramidal neurons in old rats. Goji (3 g/kg) was administrated for 60 days in 18-month-old rats. After the treatment, recognition memory was evaluated using the new object recognition task (NORt). The changes in the neuron morphology of the PFC and hippocampus pyramidal neurons in old rats were evaluated by Golgi-cox stain and immunoreactivity for synaptophysin, glial fibrillary acidic protein (GFAP), caspase-3, 3-nitrotyrosine (3-NT) and nuclear factor erythroid 2-related factor 2 (Nrf2). The rats treated with Goji showed a significant increase in dendritic morphology in the PFC and hippocampus neurons, a greater immunoreactivity to synaptophysin and a decrease in reactive astrogliosis and also in caspase-3, in 3-NT and in Nrf2 in these brain regions was also observed. Goji administration promotes the plasticity processes in the PFC and in the hippocampus of old rats, critical structures in the brain aging process.


Subject(s)
Aging/drug effects , Hippocampus/drug effects , Lycium/chemistry , Neuronal Plasticity/drug effects , Plant Extracts/administration & dosage , Prefrontal Cortex/drug effects , Aging/genetics , Aging/metabolism , Animals , Antioxidants/administration & dosage , Brain/drug effects , Brain/metabolism , Brain/physiopathology , Caspase 3/genetics , Caspase 3/metabolism , Hippocampus/metabolism , Hippocampus/physiopathology , Humans , Male , NF-E2 Transcription Factor/genetics , NF-E2 Transcription Factor/metabolism , Neurons/drug effects , Neurons/metabolism , Prefrontal Cortex/metabolism , Prefrontal Cortex/physiopathology , Rats , Rats, Sprague-Dawley
4.
Synapse ; 74(9): e22153, 2020 09.
Article in English | MEDLINE | ID: mdl-32190918

ABSTRACT

Metabolic syndrome (MS) is a health problem that is characterized by body fat accumulation, hypertension, dyslipidemia, and hyperglycemia; recently, it has been demonstrated that MS also damages memory processes. The first-line drug in the treatment of MS and type 2 diabetes mellitus is metformin, which is an antihyperglycemic agent. This drug has been shown to produce neuroprotection and to improve memory processes. However, the mechanism involved in this neuroprotection is unknown. A 90-day administration of metformin improved the cognitive processes of rats with MS as evaluated by the novel object recognition test, and this finding could be explained by an increase in the neuronal spine density and spine length. We also found that metformin increased the immunoreactivity of synaptophysin, sirtuin-1, AMP-activated protein kinase, and brain-derived neuronal factor, which are important plasticity markers. We conclude that metformin is an important therapeutic agent that increases neural plasticity and protects cognitive processes. The use of this drug is important in the minimization of the damage caused by MS.


Subject(s)
Hippocampus/drug effects , Hypoglycemic Agents/pharmacology , Metabolic Syndrome/physiopathology , Metformin/pharmacology , Neuronal Plasticity , Neuroprotective Agents/pharmacology , Recognition, Psychology , AMP-Activated Protein Kinase Kinases , Animals , Brain-Derived Neurotrophic Factor/metabolism , Hippocampus/metabolism , Hippocampus/physiology , Hypoglycemic Agents/administration & dosage , Hypoglycemic Agents/therapeutic use , Male , Metabolic Syndrome/drug therapy , Metabolic Syndrome/metabolism , Metformin/administration & dosage , Metformin/therapeutic use , Neuroprotective Agents/administration & dosage , Neuroprotective Agents/therapeutic use , Protein Kinases/metabolism , Rats , Rats, Wistar , Sirtuin 1/metabolism , Synaptophysin/metabolism
5.
Neurochem Res ; 44(2): 485-497, 2019 Feb.
Article in English | MEDLINE | ID: mdl-30673958

ABSTRACT

Cadmium (Cd) is a toxic metal and classified as a carcinogen whose exposure could affect the function of the central nervous system. There are studies that suggest that Cd promotes neurodegeneration in different regions of the brain, particularly in the hippocampus. It is proposed that its mechanism of toxicity maybe by an oxidative stress pathway, which modifies neuronal morphology and causes the death of neurons and consequently affecting cognitive tasks. However, this mechanism is not yet clear. The aim of the present work was to study the effect of Cd administration on recognition memory for 2, 3 and 4 months, neuronal morphology and immunoreactivity for caspase-3 and 9 in rat hippocampi. The results show that the administration of Cd decreased recognition memory. Likewise, it caused the dendritic morphology of the CA1, CA3 and dentate gyrus regions of the hippocampus to decrease with respect to the time of administration of this heavy metal. In addition, we observed a reduction in the density of dendritic spines as well as an increase in the immunoreactivity of caspase-3 and 9 in the same hippocampal regions of the animals treated with Cd. These results suggest that Cd affects the structure and function of the neurons of the hippocampus, which contribute to the deterioration of recognition memory. Our results suggest that the exposure to Cd represents a critical health problem, which if not addressed quickly, could cause much more serious problems in the quality of life of the human population, as well as in the environment in which they develop.


Subject(s)
Apoptosis/drug effects , Cadmium/pharmacology , Hippocampus/drug effects , Memory/drug effects , Neurons/drug effects , Animals , Cadmium/administration & dosage , Dendrites/drug effects , Dendritic Spines/drug effects , Dentate Gyrus/drug effects , Hippocampus/metabolism , Male , Neurons/metabolism , Rats, Wistar
6.
Acta Ortop Mex ; 23(6): 366-75, 2009.
Article in Spanish | MEDLINE | ID: mdl-20377003

ABSTRACT

INTRODUCTION: The production of scientific health publications is ever increasing and it is therefore essential to evaluate their quality as well as their repercussion and visibility in the scientific community, so that they can be included and indexed in the various national and international databases. The Information Center for Public Health Decisions (CENIDSP) at the National Public Health Institute (INSP) has produced since 1992 a CD ROM under the name Artemisa (articles on health information published in Mexico). In 2005 it included the full version of 56 journals which were rigorously evaluated and met the selection and evaluation criteria for inclusion. OBJECTIVE: Describe the selection criteria and the evaluation process followed in 2005 to choose the biomedical journals included in Artemisa. METHODOLOGY: It consists of a description of the universe of journals to be included according to the guidelines established and of the first stage of the evaluation (journal and article format). Based on the results, journals were selected for the second stage, which consisted of evaluating the content of the articles randomly selected. RESULTS: Twenty-one journals were included in the first stage, 19 of which were selected for the second stage. A total of 274 articles were selected for peer review by the Mexican Health Journals Evaluation System (SERM@S), with the participation of 64 evaluators. The final result of the second stage was satisfactory to all of them. CONCLUSION: The evaluation of biomedical journals conducted by CENIDSP has led to maintaining a quality standard of the biomedical publications in Mexico.


Subject(s)
Periodicals as Topic/standards , Academies and Institutes , Guidelines as Topic , Humans , Mexico , Peer Review
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