Análisis de la perspectiva de los vendedores ambulante sobre el posible contagio de Covid-19

La pandemia de COVID-19 ha impactado grandemente a la salud y economía de todas las sociedades a nivel global. Sin embargo, dentro de una comunidad, no todos sus sectores socioeconómicos se afectaron por igual. Analizaremos como esta pandemia fue percibida y manejada de manera diferente por dos sectores importantes de la población mexicana: vendedores ambulantes y trabajadores formales. En dos estudios científicos se demostró que el 82.6% de los vendedores ambulantes prefirieron exponerse a la enfermedad, en contraste con un 18.4% de los trabajadores formales. Además, los vendedores ambulantes mostraron tener 7 veces menos temor a morir por COVID-19, o tener hasta 16 veces menos preocupación por el incremento de las infecciones de la pandemia. Es importante contemplar este tipo de actitudes que determinan el comportamiento de la gente, que en consecuencia pueden incidir de forma negativa a las estrategias propuestas para el combate a la pandemia. Por ello, posiblemente las recomendaciones realizadas en países desarrollados no necesariamente serían efectivas en países subdesarrollados. Es por eso que analizar el entorno socioeconómico y las necesidades de cada población es importante para así poder diseñar estrategias específicas ante crisis mundiales, como la pandemia de COVID-19

The phenotype, psychotype and genotype of bruxism

Abstract. Bruxism is a jaw muscle activity that involves physio-pathological, psycho-social, hereditary and genetic factors. The purpose of this study was to determine the associations between self-reported bruxism, anxiety, and neuroticism personality trait with the rs6313 polymorphism in the gene HTR2A. A sample of 171 subjects of both sexes (14-53 years of age) was included. The control group (group 1, n=60) exhibited no signs or symptoms of bruxism. The case group had signs and symptoms of bruxism (n=112) and was subdivided into group 2, bruxism during sleep (n=22); group 3, awake bruxism (n=44); and group 4 combined bruxism (n=46). As diagnostic tools, the Self-Reported Bruxism Questionnaire (SBQ), the Beck Anxiety Inventory (BAI) and the Eysenck Personality Questionnaire Revised-Abbreviated (EPQR-A) were used. HTR2A (rs6313) SNPs were determined by qPCR for all the participants. The packages SPSS, maxLik and EPI-INFO were used for data analysis. The combined bruxism group reported higher scores in bruxism symptoms, mean = 32.21; anxiety symptoms, mean = 14.80; and neuroticism, mean = 3.26. Combined bruxism was associated with a higher degree of neuroticism (OR=15.0; CI 1.52-148.32) and anxiety in grade 3-moderate (OR=3.56; CI 1.27-10.03), and grade 4-severe (OR=8.40; CI 1.45-48.61), as determined using EPISODE computer software. Genotypic homogeneity analysis revealed no significant differences in allele frequency (P=0.612) among the four groups. The population was in Hardy-Weinberg equilibrium (maxLik package). In conclusion, the three instruments confirm traits of bruxism, anxiety and neuroticism in individuals with bruxism. These data were ratified when the sample was divided by genotypic homogeneity. On the other hand, there was no significant difference between the groups in the SNPs rs6313 from the HTR2A gene

Current model systems for the study of preeclampsia

Preeclampsia (PE) is a pregnancy complex disease, distinguished by high blood pressure and proteinuria, diagnosed after the 20th gestation week. Depending on the values of blood pressure, urine protein concentrations, symptomatology, and onset of disease there is a wide range of phenotypes, from mild forms developing predominantly at the end of pregnancy to severe forms developing in the early stage of pregnancy. In the worst cases severe forms of PE could lead to systemic endothelial dysfunction, eclampsia, and maternal and/or fetal death. Worldwide the fetal morbidity and mortality related to PE is calculated to be around 8% of the total pregnancies. PE still being an enigma regarding its etiology and pathophysiology, in general a deficient trophoblast invasion during placentation at first stage of pregnancy, in combination with maternal conditions are accepted as a cause of endothelial dysfunction, inflammatory alterations and appearance of symptoms. Depending on the PE multifactorial origin, several in vitro, in vivo,andin silico models have been used to evaluate the PE pathophysiology as well as to identify or test biomarkers predicting, diagnosing or prognosing the syndrome. This review focuses on the most common models used for the study of PE, including those related to placental development, abnormal trophoblast invasion, uteroplacental ischemia, angiogenesis, oxygen deregulation, and immune response to maternal–fetal interactions. The advances in mathematical and computational modeling of metabolic network behavior, gene prioritization, the protein–protein interaction network, the genetics of PE, and the PE prediction/classification are discussed. Finally, the potential of these models to enable understanding of PE pathogenesis and to evaluate new preventative and therapeutic approaches in the management of PE are also highlighted

Anti‑inflammatory drugs and uterine cervical cancer cells: Antineoplastic effect of meclofenamic acid

Uterine cervical cancer (UCC) is one of the main causes of cancer-associated mortality in women. Inflammation has been identified as an important component of this neoplasia; in this context, anti-inflammatory drugs represent possible prophylactic and/or therapeutic alternatives that require further investigation. Anti-inflammatory drugs are common and each one may exhibit a different antineoplastic effect. As a result, the present study investigated different anti-inflammatory models of UCC in vitro and in vivo. Celecoxib, sulindac, nimesulide, dexamethasone, meclofenamic acid, flufenamic acid and mefenamic acid were tested in UCC HeLa, VIPA, INBL and SiHa cell lines. The cytotoxicity of the drugs was evaluated in vitro. Celecoxib, sulindac, nimesulide, mefenamic acid and flufenamic acid presented with slight to moderate toxicity (10–40% of cell death corresponding to 100 µM) in certain cell lines, while meclofenamic acid exhibited significant cytotoxicity in all essayed cell lines (50–90% of cell death corresponding to 100 µM). The meclofenamic acid was tested in murine models (immunodeficient and immunocompetent) of UCC, which manifested a significant reduction in tumor growth and increased mouse survival. It was demonstrated that of the evaluated anti-inflammatory drugs, meclofenamic acid was the most cytotoxic, with a significant antitumor effect in murine models. Subsequent studies are necessary to evaluate the clinical utility of this drug

A promising novel formulation for articular cartilage regeneration: Preclinical evaluation of a treatment that produces SOX9 overexpression in human synovial fluid cells

Osteoarthritis (OA) is a chronic disorder of synovial joints, in which there is progressive softening and disintegration of the articular cartilage. OA is the most common form of arthritis, and is the primary cause of disability and impaired quality of life in the elderly. Despite considerable medical necessity, no treatment has yet been proven to act as a disease‑modifying agent that may halt or reverse the structural progression of OA. The replacement of the joint with a prosthesis appears to be the best option in the advanced stages of the disease. A formulation (BIOF2) for cartilage regeneration has been recently developed. The present study evaluated the effects of BIOF2 on gene expression in human cell cultures, followed by efficacy trials in three OA animal models. Human synovial fluid cells that were exposed to the formulation exhibited increased transcription factor SOX‑9 (SOX9; chondrogenic factor) expression, and decreased mimecan (mineralization inducer) and macrophage‑stimulating protein receptor (osteoclastogenic factor) expression. The intra‑articular application of BIOF2 in the animal models significantly increased cartilage thickness from 12 to 31% at 28 days, compared with articular cartilage treated with saline solution. The articular area and number of chondrocytes additionally increased significantly, maintaining an unaltered chondrocyte/mm2 proportion. Evaluation of the histological architecture additionally displayed a decrease in the grade of articular damage in the groups treated with BIOF2. In conclusion, BIOF2 has proven to be effective for treating OA in animal models, most likely due to SOX9 overexpression in articular cells

Adenovirus 5 produces obesity and adverse metabolic, morphological, and functional changes in the long term in animals fed a balanced diet or a high‑fat diet: a study on hamsters

Adenovirus 5 (Ad-5) infection is a common cause of acute respiratory infections and the main vector used in gene therapy. There are few studies on the relationship of Ad-5 to obesity. In the present study, we evaluated the chronic effects of Ad-5 infection on golden (Syrian) hamsters fed either a balanced diet (BD) or a high-fat diet (HFD). After a single inoculation with Ad-5 (1 × 107 pfu), the body weight of the animals was measured weekly. Medium-term (22 weeks) serum biochemical analyses and long-term (44 weeks) liver morphology, adiposity, and locomotive functionality (movement velocity) assessments were carried out. In the animals fed the BD, adenovirus infection produced hyperglycemia and hyperlipidemia. In the long term, it produced a 57% increase in epididymal pad fat and a 30% body weight gain compared with uninoculated animals. In addition, morphological changes related to non-alcoholic fatty liver disease (NAFLD) were observed. The animals fed the HFD had similar but more severe changes. In addition, the hamsters presented an obesity paradox: at the end of the study, the animals that had the most morphological and functional changes (significantly reduced movement velocity) had the lowest body weight. Despite the fact that an HFD appears to be a more harmful factor in the long term than adenovirus infection alone, infection could increase the severity of harmful effects in individuals with an HFD. Epidemiological studies are needed to evaluate the effect of adenovirus as a precursor of chronic liver and cardiovascular diseases, including the chronic effects of gene therapy

Circulating levels of specific members of chromosome 19 microRNA cluster are associated with preeclampsia development

Purpose: To perform serum microRNA expression profiling to identify members of chromosome 19 miRNA cluster involved in preeclampsia development. Methods: Serum chromosome 19 miRNA cluster microRNA expression profiling was evaluated at 12, 16, and 20 gestational weeks and at the time of preeclampsia diagnosis, in women who developed preeclampsia (WWD-PE; n = 16) and controls (n = 18) using TaqMan low density array plates. Results: A total of 51 chromosome 19 microRNA cluster members were evaluated. The circulating hsa-miRs 512-3p, 518f3p, 520c-3p, and 520d-3p, were differentially expressed between groups (P < 0.05). Compared with controls, serum levels of hsa-miR-518f-3p at 20 GW were useful for identifying WWD-Mild-PE (P = 0.035) and WWD-Severe-PE(P = 0.007). Conclusions: Serum hsa-miRs 512-3p, 518f-3p, 520c-3p, and 520d-3p, are differentially expressed between WWD-PE and controls and their role in the development of preeclampsia should be investigated further

Molecular cloning of the myo-inositol oxygenase gene from the kidney of baboons

Abstract. The enzyme myo-Inositol oxygenase (MIOX) is also termed ALDRL6. It is a kidney‑specific member of the aldo‑keto reductase family. MIOX catalyzes the first reaction involved in the myo‑inositol metabolism signaling pathway and is fully expressed in mammalian tissues. MIOX catalyzes the oxidative cleavage of myo‑Inositol and its epimer, D-chiro-Inositol to D-glucuronate. The dioxygen-dependent cleavage of the C6 and C1 bond in myo‑Inositol is achieved by utilizing the Fe2+/Fe3+ binuclear iron center of MIOX. This enzyme has also been implicated in the complications of diabetes, including diabetic nephropathy. The MIOX gene was amplified with reverse transcription‑polymerase chain reaction from baboon tissue samples, and the product was cloned and sequenced. MIOX expression in the baboon kidney is described in the present study. The percentages of nucleotide and amino acid similarities between baboons and humans were 95 and 96%, respectively. The MIOX protein of the baboon may be structurally identical to that of humans. Furthermore, the evolutionary changes, which have affected these sequences, have resulted from purifying forces. Key words: animal models, gene expression, kidney, myo-inositol oxygenase, Old World monke

Animal Models of Rheumatoid Arthritis

Autoimmunity is a condition in which the host organizes an immune response against its own antigens. Rheumatoid arthritis (RA) is an autoimmune disease of unknown etiology, characterized by the presence of chronic inflammatory infiltrates, the development of destructive arthropathy, bone erosion, and degradation of the articular cartilage and subchondral bone. There is currently no treatment that resolves the disease, only the use of palliatives, and not all patients respond to pharmacologic therapy. According to RA multifactorial origin, several in vivo models have been used to evaluate its pathophysiology as well as to identify the usefulness of biomarkers to predict, to diagnose, or to evaluate the prognosis of the disease. This chapter focuses on the most common in vivo models used for the study of RA, including those related with genetic, immunological, hormonal, and environmental interactions. Similarly, the potential of these models to understand RA pathogenesis and to test preventive and therapeutic strategies of autoimmune disorder is also highlighted. In conclusion, of all the animal models discussed, the CIA model could be considered the most successful by generating arthritis using type II collagen and adjuvants and evaluating therapeutic compounds both intra-articularly and systemically