Fatores determinantes da near miss materna em uma unidade de terapia intensiva obstétrica: avaliação das competências profissionais da área médica

Objective: Evaluate the determinants of morbidity and mortality in an obstetric intensive care unit and professional medical skills of students/residents at a university hospital. Methods: observational cross - sectional with 492 pregnant/pue rperal women and 261 students/residents. Patients were admitted to the obstetric intensive care unit during a year, being informed about the proposals of the study and a questionnaire was applied. The analysis was performed using Microsoft Excel 2013 and G raphPad6. Chi - square tests were used to evaluate risk factors and student t test evaluates resident/students' skills concerning the cognitive test and the Mini - Cex. Results: the main risk factors to near miss were: non - white race (OR = 2.527; RR = 2.342) ; marital status(married women) (OR = 7.968; RR = 7.113) , schooling (primary) (OR = 3.177 ; RR = 2.829) , from country town (OR = 4.643 ; RR = 4.087), low income (OR = 7014 ; RR = 5.554) , gestational hypertensive disorders (OR = 16.35 ; RR = 13.27) , re alization of pre - natal (OR = 5.023 ; RR = 4.254) and C - section before labor(OR = 39.21 ; RR = 31.25). In cognitive/Mini - cex analysis were noted significant difference in the performance of students on the subject (3.75 ± 0.93, 4.03 ± 0.94 and 4.88 ± 0.35). We still observed the best performance of residents, when compared to graduation students (p < 0.01). Conclusions: the prevalence of near miss was associated with socioeconomic/clinics factors and care issues, revealing the importance of interventions to improve these indicators. In addition, we suggest a better curriculum insertion of this subject in the medical Course disciplines due the importance to avoid the near miss through of adequacy of medical education.

Pregnant Teacher

General note: Title and date provided by Bettye Lane.

Benefits for pregnant women demonstration [at Rockefeller's Office]

General note: Title and date provided by Bettye Lane.

Women demonstrate for disability payments for working pregnant women [at Rockefeller's Office]

General note: Title and date provided by Bettye Lane.

Pregnant secretary at work

Inscriptions: Verso: [stamped] Photograph by Freda Leinwand. [463 West Street, Studio 229G, New York, NY 10014].

Pregnant secretary at work

Inscriptions: Verso: [stamped] Photograph by Freda Leinwand. [463 West Street, Studio 229G, New York, NY 10014].

Pregnant secretary at work

Inscriptions: Verso: [stamped] Photograph by Freda Leinwand. [463 West Street, Studio 229G, New York, NY 10014].

Pregnant secretary at work

Inscriptions: Verso: [stamped] Photograph by Freda Leinwand. [463 West Street, Studio 229G, New York, NY 10014].

Pregnant secretary at work

Inscriptions: Verso: [stamped] Photograph by Freda Leinwand. [463 West Street, Studio 229G, New York, NY 10014].

Women at work: pregnant secretary at work

Inscription: Verso: Women at work: miscellaneous occupations. Jody Beuilacqua, CML Associates, Newton, Mass.

Régulation par l'angiotensine II de la croissance et de l'apoptose cellulaire dans la cardiomyopathie hypertensive

Mémoire numérisé par la Direction des bibliothèques de l'Université de Montréal.

Activity and expression of Na/K-ATPase in thoracic aorta of normal pregnant and experimental preeclamptic rats

Mémoire numérisé par la Direction des bibliothèques de l'Université de Montréal.

Hydrogen sulphide rescues preeclampsia-like phenotype aggravated by high sFlt-1 in placenta growth factor (PlGF) deficiency

Placenta growth factor (PlGF) deficient mice are fertile at a Mendelian ratio. Interestingly, low maternal plasma levels of PlGF are strongly associated with early onset of preeclampsia, a pregnancy hypertensive disorder characterised by high blood pressure, proteinuria and fetal growth restriction. PlGF is increasingly being recognised as an early diagnostic biomarker, but the physiological importance of PlGF in the pathogenesis of preeclampsia is unknown. We investigated whether the decreased levels of PlGF in pregnancy exacerbate the fetal growth restriction associated with preeclampsia in the presence of high sFlt-1 and the potential of hydrogen sulphide to ameliorate these effects. Pregnant PlGF−/− mice were injected with adenovirus encoding sFlt-1 (Ad-sFlt-1) at 1 × 109 pfu/ml at E10.5 and mean arterial blood pressure (MAP), biochemical and histological analysis of maternal kidney, placenta and embryos were assessed at the end of pregnancy. Ad-sFlt-1 significantly increased MAP and induced severe glomerular endotheliosis in PlGF−/− mice compared to wild-type animals. Soluble Flt-1 also significantly elevated albumin–creatinine ratio and increased levels of urinary kidney injury molecule-1, a marker for proximal tubule injury. Furthermore, sFlt-1 over expression increased fetal resorption rate in the PlGF−/− mice and promoted abnormal placental vascularisation. To determine whether placental PlGF is critical for preventing fetal growth restriction associated with preeclampsia, we generated haploinsufficient PlGF+/− placentas and embryos in dams and exposed to high sFlt-1 environment. These mothers showed reduced fetal resorption, gestational hypertension and proteinuria when compared to pregnant PlGF−/− mice. Furthermore, treatment with hydrogen sulphide-releasing agent, GYY4137, significantly reduced resorption, hypertension and proteinuria observed in Ad-sFlt-1 treated pregnant PlGF−/− mice. Our study shows that placental PlGF is a critical protective factor against the damaging effects of high sFlt-1 associated with preeclampsia and activation of the hydrogen sulphide pathway may rescue preeclampsia phenotypes even under low PlGF environment.

Hydrogen sulphide rescues preeclampsia-like phenotype aggravated by high sFlt-1 in Placenta Growth Factor (PlGF) deficiency

INTRODUCTION: Low circulating levels of placenta growth factor (PlGF) is strongly associated with the onset of preeclampsia, a maternal hypertensive disorder characterized by high blood pressure and proteinuria after 20 weeks of gestation. Although, PlGF-deficient mice are born healthy and fertile at a Mendelian ratio, the physiological importance of PlGF in the pathogenesis of preeclampsia is unclear. We hypothesised that decreased levels of PlGF in pregnancy exacerbates the fetal growth restriction associated with preeclampsia in the presence of high sFlt-1. METHODS: Pregnant PlGF-/- mice were injected with adenovirus encoding sFlt-1 (Ad-sFlt-1) at high (i) 1.5x109 pfu/ml and low (ii) 0.5x109 pfu/ml doses. Mean arterial blood pressure (MBP), biochemical and histological assessments of maternal kidney, placenta and embryos were performed. RESULTS: Ad-sFlt-1 significantly increased MBP and induced severe glomerular endotheliosis in PlGF-/- mice at E10.5 gestation compared to wild-type animals. High sFlt-1 also significantly elevated albumincreatinine ratio and increased levels of urinary kidney injury molecule-1, a marker for proximal tubule injury.At a high dose of sFlt-1, there was complete fetal resorption in the pregnant PlGF-/- mice, and even the lower dose of sFlt-1 induced severe fetal resorption and abnormal placental vascularization. Hydrogen sulphide-releasing agent, GYY4137, significantly reduced resorption, hypertension and proteinuria in Ad-sFlt-1 treated pregnant PlGF-/- mice. To determine if placental PlGF is critical for preventing fetal growth restriction associated with preeclampsia, we generated haploinsufficient PlGF+/- placentas and embryos were generated in wild-time dams and exposed to high sFlt-1 environment. This resulted in reduced fetal resorption, gestational hypertension and proteinuria when compared to pregnant PlGF-/- mice. CONCLUSIONS: Placental PlGF is a critical protective factor against the damaging effects of high sFlt-1 in preeclampsia and the hydrogen sulphide pathway may rescue preeclampsia phenotypes.