ABSTRACT
OBJETIVO: Los objetivos principales son describir la práctica de la ventilación mecánica en un periodo de 18 años en México y estimar los cambios en la mortalidad de los pacientes críticos con ventilación mecánica invasiva (VMI). DISEÑO: Subanálisis retrospectivo de un estudio prospectivo y observacional en 1998, 2004, 2010 y 2016. ÁMBITO: Unidades de Cuidados Intensivos (UCI) de México. PARTICIPANTES: Pacientes adultos que ingresaron consecutivamente en la UCI, durante un mes y que recibieron VMI durante más de 12 h o ventilación mecánica no invasiva durante más de una hora. El seguimiento se realizó hasta 28 días después de la inclusión. INTERVENCIONES: Ninguna. VARIABLES DE INTERÉS: Edad, sexo, gravedad al ingreso estimada por el SAPS II, parámetros de la gasometría arterial diaria, variables de tratamiento y complicaciones, fecha y estado al alta de la UCI y del hospital. RESULTADOS: Se incluyó a 959 pacientes en 81 UCI. El volumen corriente (VC) ha disminuido significativamente tanto en pacientes con criterios de SDRA (de 8,5 ml/kg de peso estimado en 1998 a 6 ml/kg en 2016; p < 0,001) como en enfermos sin SDRA (de 9 ml/kg de peso estimado en 1998 a 6ml/kg en 2016; p < 0,001). La estrategia ventilatoria protectora (definida como VC < 6 ml/kg o < 8 ml/kg y una presión meseta < 30 cmH2O) fue: 19% en 1998, 44% en 2004, 58% en 2010 y 75% en 2016 (p < 0,001). La mortalidad ajustada en UCI a lo largo de los 4 periodos fue: en 2004, oportunidad relativa (OR) 1,05 (IC 95%: 0,73-1,72; p = 0,764); en 2010, OR 1,68 (IC 95%: 1,13-2,48; p = 0,009); en 2016, OR 0,85 (IC 95%: 0,60-1,20; p = 0,368). CONCLUSIONES: La práctica clínica de la VMI en las UCI de México se ha modificado a lo largo de un periodo de 18 años. El cambio más significativo es la estrategia ventilatoria basada en VC bajos. Estos cambios no se han asociado a cambios significativos en la mortalidad
OBJECTIVE: The main study objectives were to describe the practice of mechanical ventilation over an 18-year period in Mexico, and estimate changes in mortality among critical patients subjected to invasive mechanical ventilation (IMV). DESIGN: A retrospective subanalysis of a prospective observational study conducted in 1998, 2004, 2010 and 2016 was carried out. SETTING: Intensive Care Units (ICUs) in Mexico. PARTICIPANTS: Adult patients consecutively enrolled in the ICU during one month and who underwent IMV for more than 12hours or noninvasive mechanical ventilation for more than one hour. Follow-up was performed up to a maximum of 28 days after inclusion. INTERVENTIONS: None. PRINCIPAL VARIABLES OF INTEREST: Age, sex, severity upon admission as estimated by SAPS II, parameters of daily arterial blood gases, treatment and complication variables, date and status at discharge from the ICU and from hospital. RESULTS: A total of 959 patients were included in 81 ICUs. Tidal volume (vt) decreased significantly both in patients with acute respiratory distress syndrome (ARDS) criteria (estimated 8.5 ml/kg b.w. in 1998 to 6 ml/kg in 2016; P < 0.001) and in patients without ARDS (estimated 9 ml/kg b.w. in 1998 to 6 ml/kg in 2016; P < 0.001). The ventilatory protective strategy (defined as vt < 6 ml/kg or < 8 ml/kg and a plateau pressure < 30 cmH2O) was: 19% in 1998, 44% in 2004, 58% in 2010 and 75% in 2016 (P < 0.001). The adjusted mortality rate in ICU over the 4 periods was: in 2004, odds ratio (OR) 1.05 (95% confidence interval, 95% CI: 0.73-1.72; P = 0.764); in 2010, OR 1.68 (95% CI: 1.13-2.48; P = 0.009); in 2016, OR 0.85 (95%CI: 0.60-1.20; P = 0.368). CONCLUSIONS: The clinical practice of IMV in Mexican ICUs has been modified over a period of 18 years. The most significant change is the ventilatory strategy based on low vt. These changes have not been associated with significant changes in mortality
Subject(s)
Humans , Male , Middle Aged , Respiration, Artificial/methods , Evidence-Based Medicine , Hospital Mortality , Respiration, Artificial/trends , Mexico , Retrospective Studies , Prospective Studies , Analysis of Variance , Odds Ratio , Risk Factors , Respiratory Distress Syndrome/epidemiology , Positive-Pressure RespirationABSTRACT
OBJECTIVE: The main study objectives were to describe the practice of mechanical ventilation over an 18-year period in Mexico, and estimate changes in mortality among critical patients subjected to invasive mechanical ventilation (IMV). DESIGN: A retrospective subanalysis of a prospective observational study conducted in 1998, 2004, 2010 and 2016 was carried out. SETTING: Intensive Care Units (ICUs) in Mexico. PARTICIPANTS: Adult patients consecutively enrolled in the ICU during one month and who underwent IMV for more than 12hours or noninvasive mechanical ventilation for more than one hour. Follow-up was performed up to a maximum of 28 days after inclusion. INTERVENTIONS: None. PRINCIPAL VARIABLES OF INTEREST: Age, sex, severity upon admission as estimated by SAPS II, parameters of daily arterial blood gases, treatment and complication variables, date and status at discharge from the ICU and from hospital. RESULTS: A total of 959 patients were included in 81 ICUs. Tidal volume (vt) decreased significantly both in patients with acute respiratory distress syndrome (ARDS) criteria (estimated 8.5ml/kg b.w. in 1998 to 6ml/kg in 2016; P<0.001) and in patients without ARDS (estimated 9ml/kg b.w. in 1998 to 6ml/kg in 2016; P<0.001). The ventilatory protective strategy (defined as vt < 6ml/kg or < 8ml/kg and a plateau pressure < 30cmH2O) was: 19% in 1998, 44% in 2004, 58% in 2010 and 75% in 2016 (P<0.001). The adjusted mortality rate in ICU over the 4 periods was: in 2004, odds ratio (OR) 1.05 (95% confidence interval, 95%CI: 0.73-1.72; P=0.764); in 2010, OR 1.68 (95%CI: 1.13-2.48; P=0.009); in 2016, OR 0.85 (95%CI: 0.60-1.20; P=0.368). CONCLUSIONS: The clinical practice of IMV in Mexican ICUs has been modified over a period of 18 years. The most significant change is the ventilatory strategy based on low vt. These changes have not been associated with significant changes in mortality.
ABSTRACT
Arsenic, a metalloid and naturally occurring element, is one of the most abundant elements in the earth's crust. Water is contaminated by arsenic through natural sources (underground water, minerals and geothermal processes) and anthropogenic sources such as mining, industrial processes, and the production and use of pesticides. Humans are exposed to arsenic mainly by drinking contaminated water, and secondarily through inhalation and skin contact. Arsenic exposure is associated with the development of vascular disease, including stroke, ischemic heart disease and peripheral vascular disease. Also, arsenic increases the risk of tumors of bladder, lungs, kidneys and liver, according to the International Agency for Research on Cancer and the Food and Drug Administration. Once ingested, an estimated 70-90% of inorganic arsenic is absorbed by the gastrointestinal tract and widely distributed through the blood to different organs, primarily to the liver, kidneys, lungs and bladder and secondarily to muscle and nerve tissue. Arsenic accumulates in the organs, especially in the liver. Its excretion mostly takes place through urination. The toxicokinetics of arsenic depends on the duration of exposure, pathway of ingestion, physicochemical characteristics of the compound, and affected biological species. The present review outlines of arsenic toxic effects focusing on different cancer types whit highest prevalence's by exposure to this metalloid and signaling pathways of carcinogenesis.
Subject(s)
Arsenic/toxicity , Carcinogens/toxicity , Environmental Exposure/adverse effects , Environmental Pollutants/toxicity , Neoplasms/chemically induced , Animals , Arsenic/pharmacokinetics , Carcinogens/pharmacokinetics , Environmental Pollutants/pharmacokinetics , Environmental Pollution , Humans , Neoplasms/genetics , ToxicokineticsABSTRACT
Complex congenital heart disease (CHD) affects cardiac blood flow, generating a pressure overload in the compromised ventricles and provoking hypertrophy that over time will induce myocardial dysfunction and cause a potential risk of imminent death. Therefore, the early diagnosis of complex CHD is paramount during the first year of life, with surgical treatment of patients favoring survival. In the present study, we analyzed cardiac tissue and plasma of children with cardiac hypertrophy (CH) secondary to CHD for the expression of 11 miRNAs specific to CH in adults. The results were compared with the miRNA expression patterns in tissue and blood of healthy children. In this way, we determined that miRNAs 1, 18b, 21, 23b, 133a, 195, and 208b constitute the expression profile of the cardiac tissue of children with CHD. Meanwhile, miRNAs 21, 23a, 23b, and 24 can be considered specific biomarkers for the diagnosis of CH in infants with CHD. These results suggest that CH secondary to CHD in children differs in its mechanism from that described for adult hypertrophy, offering a new perspective to study the development of this pathology and to determine the potential of hypertrophic miRNAs to be biomarkers for early CH.
Subject(s)
Cardiomegaly/genetics , Heart Defects, Congenital/genetics , MicroRNAs/genetics , Biomarkers/analysis , Biopsy , Child , Child, Preschool , Female , Heart Defects, Congenital/complications , Heart Ventricles/pathology , Humans , Infant , Infant, Newborn , Male , MicroRNAs/analysis , TranscriptomeABSTRACT
The main objective of this study was to create a postnatal model for cardiac hypertrophy (CH), in order to explain the mechanisms that are present in childhood cardiac hypertrophy. Five days after implantation, intraperitoneal (IP) isoproterenol (ISO) was injected for 7 days to pregnant female mice. The fetuses were obtained at 15, 17 and 19 dpc from both groups, also newborns (NB), neonates (7-15 days) and young adults (6 weeks of age). Histopathological exams were done on the hearts. Immunohistochemistry and western blot demonstrated GATA4 and PCNA protein expression, qPCR real time the mRNA of adrenergic receptors (α-AR and ß-AR), alpha and beta myosins (α-MHC, ß-MHC) and GATA4. After the administration of ISO, there was no change in the number of offsprings. We observed significant structural changes in the size of the offspring hearts. Morphometric analysis revealed an increase in the size of the left ventricular wall and interventricular septum (IVS). Histopathological analysis demonstrated loss of cellular compaction and presence of left ventricular small fibrous foci after birth. Adrenergic receptors might be responsible for changing a physiological into a pathological hypertrophy. However GATA4 seemed to be the determining factor in the pathology. A new animal model was established for the study of pathologic CH in early postnatal stages.
ABSTRACT
The aim of this study was to determine the histomorphological changes that occurred in response to two treatments for oestrus synchronization in three different regions of the gilt's uterine tubes epithelium: the ampulla (AMP), ampulla-isthmic junction (AIJ) and isthmus (IST). Nine prepuberal gilts were divided into three groups (n = 3): (1) eCG 400 IU and hCG 200 IU (eCG/hCG), (2) progesterone agonist (P4) and (3) control group. The number of secretory cells (stained with periodic acid-Schiff reaction or PAS-positive cells) decreased in the AMP in the P4 treated group when compared to the control group, whereas, no difference was observed in the number of PAS-negative cells in the AMP of the three groups. A significant decrease in the number of PAS-positive cells was observed in the AIJ and IST of the P4 treated group when compared to the eCG/hCG and control groups. An increase in the number of PAS-negative cells was observed in the AIJ and IST in the P4 treated group. The epithelium height in the AMP and AIJ was increased in the eCG/hCG group when compared to the control and P4 groups. In this last group, we observed a reduced height compared with the other two groups for the AIJ. In the IST, there were no significant changes in the epithelium height of the control or the other two groups (eCG/hCG and P4). The epithelial cells of the P4 treated group had the least amount of cytoplasmic granules and the lowest intensity of PAS staining in the AMP, AIJ and IST. Animals treated with eCG/hCG showed an intermediate number of cytoplasmic granules and intensity in all regions evaluated. These data show that P4 treatment for synchronization induces a significant (P < 0.001) decrease of PAS-positive cells and staining intensity of cytoplasmic granules in the different regions studied and an increased number of PAS-negative cells in the AIJ and IST epithelium. Moreover, eCG/hCG treatment increased the height of the epithelium in the AMP and AIJ, while in this last region, the P4 treatment decreased the epithelium height. These results show that synchronization treatments with P4 and in a smaller proportion with eCG/hCG can modify the amount of PAS-positive and PAS-negative cells, and the epithelium height. This has influence in the secretory activity of the epithelium and possibly alters the fluid microenvironment of the gilt's uterine tube. The biological impact of regional variations in the epithelial cells of the gilt's uterine tube needs further investigation to understand the implications that the reproductive processes can have in the uterine tube.
