José María Tovar-Rodríguez

Bio: José María Tovar-Rodríguez is an academic researcher from Institute for Social Security and Services for State Workers. The author has contributed to research in topics: Cancer & Cancer screening. The author has an hindex of 4, co-authored 18 publications receiving 69 citations. Previous affiliations of José María Tovar-Rodríguez include Instituto Politécnico Nacional.

Increased Serum Levels of Inflammatory Mediators and Low Frequency of Regulatory T Cells in the Peripheral Blood of Preeclamptic Mexican Women

Abstract: Regulatory T cells (T(regs); CD4+CD25(high)Foxp3+) are critical in maintaining immune tolerance during pregnancy and uterine vascularization. In this study, we show that, in Mexican women with different preeclamptic severity levels, the number of T(regs) and the subset of CD4+CD25(high)Foxp3+ are decreased compared with those of normotensive pregnant women (NP). Moreover, a systemic inflammatory state is a pivotal feature in the pathogenesis of this disorder and could be related to hypertension and endothelial dysfunction. Likewise, we observed elevated levels of IL-6, TNF-α, and IL-8 in the serum of severe preeclamptic patients (SPE); no differences were found in the IL-1β and IL-10 levels compared with those of NP patients. An analysis of chemokines in the preeclamptic serum samples showed high levels of CXCL10, CCL2, and CXCL9. Our findings suggest that the preeclamptic state is linked with systemic inflammation and reduced numbers of T(regs).

Detección primaria del cáncer cervicouterino

Abstract: Primary cervical cancer screening Abstract Cervicouterine cancer screening with citology decrease incidence by more than 50%. The cause of this cancer is the human papilloma virus high risk, and requires a sensitive test to provide sufficient sensitivity and specificity for early detection and greater interval period when the results are negative. The test of the human papilloma virus high risk, is effective and safe because of its excellent sensitivity, negative predictive value and optimal reproducibility, especially when combined with liquid-based cytology or biomarkers with viral load, with higher

Metabolic syndrome in breast cancer

Abstract: Breast Cancer is a heterogeneous disease, progressive, currently, are classified according to in pattern of gene expression luminal A, luminal B, basal and HER-2neu + and Triple-negative, 75% to 80% have receptors positive hormonal and 15% to 20% are positive for hER-2neu and 10% to 20% are triple negative, with hormone receptor negative and HER2-neu and their diagnostic is made by exclusion, the Metabolic Syndrome is related to a higher incidence of these cancers where the insulin-leptin axisadiponectin are implicated in carcinogenesis.

Incidencia de la operación cesárea según la clasificación de Robson en el Servicio de Ginecología y Obstetricia del Hospital Gral. Dr. Fernando Quiroz Gutiérrez del Instituto de Seguridad Social al Servicio de los Trabajadores del Estado

Abstract: Introduccion El numero de cesareas en todo el mundo se ha incrementado de forma importante y nuestro pais no es la excepcion. En algunos lugares se supera el 60% de cesareas en relacion al parto vaginal. No existe una clasificacion adecuada para el analisis de este incremento. La clasificacion de los 10 grupos de Robson se basa en cuatro pilares: a) antecedentes obstetricos; b) progreso del parto; c) categoria del embarazo; y d) edad gestacional. Sugerimos utilizar la clasificacion de Robson para determinar que grupo de mujeres embarazadas contribuyen mas al total de cesareas en nuestra institucion. Metodo Estudio retrospectivo, descriptivo, transversal, observacional, de 2014 al 2016, incluyendo a todas las embarazadas con mas de 27 semanas de gestacion. Se resolvio el embarazo a 706 mujeres con un porcentaje de cesarea del 65.29%. El promedio de edad fue de 31 ± 4.2 anos, y el de la edad gestacional fue de 38.5 ± 6.7 semanas. Eran primigestas el 47%. La indicacion materna mas frecuente de cirugia fue por cesarea iterativa, y la fetal por distocia de presentacion. En cuanto a la ubicacion del mayor numero de pacientes dentro de la clasificacion de Robson, fue el grupo 5 con un 21.24%, seguido del grupo 2 con un 13.88% y del grupo 1 con un 9.6%. Conclusion La existencia de cicatriz uterina previa fue el factor determinante en la mayor parte de las cesareas. Sugerimos incidir sobre la indicacion de la primera cesarea y asi disminuir cicatrices uterinas. Introduction The increase of cesarean sections worldwide has increased significantly, our country is no exception, in some places it exceeds 60% of cesarean sections in relation to vaginal delivery, there is no adequate classification for the analysis of this increase. The classification of the 10 groups of Robson is based on four pillars: a) obstetric history; b) progress of labor; c) category of pregnancy; and d) gestational age. We suggest using Robson’s classification to determine which group of pregnant women contribute most to the total number of cesareans in our institution. Method This retrospective, descriptive, cross-sectional, observational study was conducted from 2014 to 2016, all pregnant women with more than 27 weeks’ gestation were included. Pregnancy was resolved in 706 women with a caesarean section of 65.29%, mean age was 31 ± 4.2 years, and gestational age 38.5 ± 6.7 weeks. 46.74% were primiparous. The most frequent maternal indication for surgery was by iterative cesarean section and the fetal one was due to presentation dystocia, as for the location of the patients within the Robson classification was group 5 with 21.24%, group 2 with 13.88% and the 1 with 9.6%. Conclusion The previous uterine scarring was the determining factor in most of the cesarean sections, we suggest to influence the indication of the first cesarean section and thus to avoid uterine scars.

[Giant cystic lymphangioma breast. Report of a case with 20-year follow-up and review of the literature].

Abstract: Bac kground: Lymphangiomas are congenital malformations or acquired (secondary to trauma, infection or neoplasia) in the mammary gland, are extremely rare. T...

Iconographies supplémentaires de l'article : Maternal death in the 21st century: causes, prevention, and relationship to cesarean delivery

Abstract: OBJECTIVE We sought to examine etiology and preventability of maternal death and the causal relationship of cesarean delivery to maternal death in a series of approximately 1.5 million deliveries between 2000 and 2006. STUDY DESIGN This was a retrospective medical records extraction of data from all maternal deaths in this time period, augmented when necessary by interviews with involved health care providers. Cause of death, preventability, and causal relationship to mode of delivery were examined. RESULTS Ninety-five maternal deaths occurred in 1,461,270 pregnancies (6.5 per 100,000 pregnancies.) Leading causes of death were complications of preeclampsia, pulmonary thromboembolism, amniotic fluid embolism, obstetric hemorrhage, and cardiac disease. Only 1 death was seen from placenta accreta. Twenty-seven deaths (28%) were deemed preventable (17 by actions of health care personnel and 10 by actions of non-health care personnel). The rate of maternal death causally related to mode of delivery was 0.2 per 100,000 for vaginal birth and 2.2 per 100,0000 for cesarean delivery, suggesting that the number of annual deaths resulting causally from cesarean delivery in the United States is about 20. CONCLUSION Most maternal deaths are not preventable. Preventable deaths are equally likely to result from actions by nonmedical persons as from provider error. Given the diversity of causes of maternal death, no systematic reduction in maternal death rate in the United States can be expected unless all women undergoing cesarean delivery receive thromboembolism prophylaxis. Such a policy would be expected to eliminate any statistical difference in death rates caused by cesarean and vaginal delivery.

Matrix Metalloproteinases in Normal Pregnancy and Preeclampsia.

Abstract: Normal pregnancy is associated with marked hemodynamic and uterine changes that allow adequate uteroplacental blood flow and uterine expansion for the growing fetus These pregnancy-associated changes involve significant uteroplacental and vascular remodeling Matrix metalloproteinases (MMPs) are important regulators of vascular and uterine remodeling Increases in MMP-2 and MMP-9 have been implicated in vasodilation, placentation, and uterine expansion during normal pregnancy The increases in MMPs could be induced by the increased production of estrogen and progesterone during pregnancy MMP expression/activity may be altered during complications of pregnancy Decreased vascular MMP-2 and MMP-9 may lead to decreased vasodilation, increased vasoconstriction, hypertensive pregnancy, and preeclampsia Abnormal expression of uteroplacental integrins, cytokines, and MMPs may lead to decreased maternal tolerance, apoptosis of invasive trophoblast cells, inadequate remodeling of spiral arteries, and reduced uterine perfusion pressure (RUPP) RUPP may cause imbalance between the antiangiogenic factors soluble fms-like tyrosine kinase-1 and soluble endoglin and the proangiogenic vascular endothelial growth factor and placental growth factor, or stimulate the release of inflammatory cytokines, hypoxia-inducible factor, reactive oxygen species, and angiotensin AT1 receptor agonistic autoantibodies These circulating factors could target MMPs in the extracellular matrix as well as endothelial and vascular smooth muscle cells, causing generalized vascular dysfunction, increased vasoconstriction and hypertension in pregnancy MMP activity can also be altered by endogenous tissue inhibitors of metalloproteinases (TIMPs) and changes in the MMP/TIMP ratio In addition to their vascular effects, decreases in expression/activity of MMP-2 and MMP-9 in the uterus could impede uterine growth and expansion and lead to premature labor Understanding the role of MMPs in uteroplacental and vascular remodeling and function could help design new approaches for prediction and management of preeclampsia and premature labor

Mechanisms of Endothelial Dysfunction in Hypertensive Pregnancy and Preeclampsia

Abstract: Preeclampsia is a pregnancy-related disorder characterized by hypertension and could lead to maternal and fetal morbidity and mortality. Although the causative factors and pathophysiological mechanisms are unclear, endothelial dysfunction is a major hallmark of preeclampsia. Clinical tests and experimental research have suggested that generalized endotheliosis in the systemic, renal, cerebral, and hepatic circulation could decrease endothelium-derived vasodilators such as nitric oxide, prostacyclin, and hyperpolarization factor and increase vasoconstrictors such as endothelin-1 and thromboxane A2, leading to increased vasoconstriction, hypertension, and other manifestation of preeclampsia. In search for the upstream mechanisms that could cause endothelial dysfunction, certain genetic, demographic, and environmental risk factors have been suggested to cause abnormal expression of uteroplacental integrins, cytokines, and matrix metalloproteinases, leading to decreased maternal tolerance, apoptosis of invasive trophoblast cells, inadequate spiral arteries remodeling, reduced uterine perfusion pressure (RUPP), and placental ischemia/hypoxia. RUPP may cause imbalance between the antiangiogenic factors soluble fms-like tyrosine kinase-1 and soluble endoglin and the proangiogenic factors vascular endothelial growth factor and placental growth factor, or stimulate the release of other circulating bioactive factors such as inflammatory cytokines, hypoxia-inducible factor-1, reactive oxygen species, and angiotensin AT1 receptor agonistic autoantibodies. These circulating factors could then target endothelial cells and cause generalized endothelial dysfunction. Therapeutic options are currently limited, but understanding the factors involved in endothelial dysfunction could help design new approaches for prediction and management of preeclampsia.

New Paradigm in the Role of Regulatory T Cells During Pregnancy

Abstract: Semi-allogenic fetuses are not rejected by the maternal immune system because feto-maternal tolerance induced by CD4+CD25+FoxP3+ regulatory T (Treg) cells is established during pregnancy. Paternal antigen-specific Treg cells accumulate during pregnancy, and seminal plasma priming plays an important role in expanding paternal antigen-specific Treg cells in mouse models. Although paternal-antigen specific Treg cells have not been identified in humans, recent studies suggest that antigen-specific Treg cells exist and expand at the feto-maternal interface in humans. Studies have also revealed that reduction of decidual functional Treg cells occurs during miscarriage with normal fetal chromosomal content, whereas insufficient clonal expansion of decidual Treg cells is observed in preeclampsia. In this review, we will discuss the recent advances in the investigation of mechanisms underlying Treg cell-dependent maintenance of feto-maternal tolerance.

The imbalance of Th17/Treg axis involved in the pathogenesis of preeclampsia.

Abstract: Inappropriate activation of the immune system, particularly the imbalance of T-helper type 17 (Th17)/regulatory T (Treg) cells is thought to play considerable roles in preeclampsia (PE). To investigate the probable effects of the adaptive immune system in the pathophysiology of PE, we analyzed the dynamic changes of Th17/Treg cells, cytokines profile, and transcription pattern of Th17/Treg-related genes and microRNAs (miRNAs) in 50 women suffering from PE in comparison with 50 healthy pregnant women. METHODS: Expressions of cytokines, specific transcription factors, and related miRNAs were measured by real-time polymerase chain reaction (PCR). Enzyme-linked immunosorbent assay (ELISA) was used to test the interleukin (IL)-17, IL-23, IL-6, and IL-10 and transforming growth factor β in serum and supernatant of peripheral blood mononuclear cells (PBMCs). The frequency of Th17 and Treg cells were determined by flow cytometry. RESULTS: PE patients exhibited a decreased number of Treg cells (p = 0.006), while Th17 cells were increased ( p = 0.004). Forkhead box P3 and IL-10 mRNA expressions were reduced ( p = 0.0001 and 0.0028, respectively), while expressions of retinoic acid receptor-related orphan nuclear receptor γt, IL-17, IL-23, and IL-6 were enhanced ( p < 0.0001, 0.0018, 0.0014, and 0.027, respectively). ELISA results also showed increased levels of IL-6, IL-17, and IL-23 ( p = 0.022, 0.0005, 0.0081, respectively), and decreased levels of IL-10 in the supernatant of PBMCs of PE patients compared with control group ( p = 0.0011). There was significant upregulation of miR-106b and miR-326 ( p = 0.0048 and 0.028, respectively) in PE patients in comparison with the control group. CONCLUSIONS: These findings suggest that imbalance of Th17/Treg cells, regulated possibly via microRNAs, may be involved in the pathogenesis of PE, emphasizing on the importance of these cells in feto-maternal immune cross-talk. © 2018 Wiley Periodicals, Inc.