Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 3 de 3
Filter
Add more filters










Database
Language
Publication year range
1.
Aust N Z J Obstet Gynaecol ; 62(6): 915-920, 2022 12.
Article in English | MEDLINE | ID: mdl-35781639

ABSTRACT

Pregnancy is a well-known risk factor of venous thromboembolism. We retrospectively reviewed case histories of 82 pregnant women who developed symptoms of venous pathology, thrombophlebitis, deep vein thrombosis (DVT) or pulmonary embolus (PE) while receiving care at our hospital. We found the VTE risk identification and documentation during their pregnancies were deficient resulting in the omission of appropriate thromboprophylaxis. Many confirmed VTE cases (antenatally or postpartum) were not on thromboprophylaxis prior to diagnosis despite having multiple risk factors. We recommend the use of a risk assessment tool by clinicians for accurate risk identification ensuring proper risk management at different stages of pregnancy.


Subject(s)
Pulmonary Embolism , Venous Thromboembolism , Female , Humans , Pregnancy , Venous Thromboembolism/etiology , Venous Thromboembolism/prevention & control , Anticoagulants/adverse effects , Retrospective Studies , Pulmonary Embolism/etiology , Pulmonary Embolism/prevention & control , Pulmonary Embolism/diagnosis , Risk Factors , Risk Assessment
3.
Dev Dyn ; 247(1): 33-46, 2018 01.
Article in English | MEDLINE | ID: mdl-28543935

ABSTRACT

Ataxia-telangiectasia (A-T) is characterized by neuronal degeneration, cancer, diabetes, immune deficiency, and increased sensitivity to ionizing radiation. A-T is attributed to the deficiency of the protein kinase coded by the ATM (ataxia-telangiectasia mutated) gene. ATM is a sensor of DNA double-strand breaks (DSBs) and signals to cell cycle checkpoints and the DNA repair machinery. ATM phosphorylates numerous substrates and activates many cell-signaling pathways. There has been considerable debate about whether a defective DNA damage response is causative of the neurological aspects of the disease. In proliferating cells, ATM is localized mainly in the nucleus; however, in postmitotic cells such as neurons, ATM is mostly cytoplasmic. Recent studies reveal an increasing number of roles for ATM in the cytoplasm, including activation by oxidative stress. ATM associates with organelles including mitochondria and peroxisomes, both sources of reactive oxygen species (ROS), which have been implicated in neurodegenerative diseases and aging. ATM is also associated with synaptic vesicles and has a role in regulating cellular homeostasis and autophagy. The cytoplasmic roles of ATM provide a new perspective on the neurodegenerative process in A-T. This review will examine the expanding roles of ATM in cellular homeostasis and relate these functions to the complex A-T phenotype. Developmental Dynamics 247:33-46, 2018. © 2017 Wiley Periodicals, Inc.


Subject(s)
Ataxia Telangiectasia Mutated Proteins/metabolism , Ataxia Telangiectasia/metabolism , Mitochondria/metabolism , Nerve Degeneration/metabolism , Oxidative Stress/physiology , Reactive Oxygen Species/metabolism , Signal Transduction/physiology , Animals , Ataxia Telangiectasia/pathology , Homeostasis/physiology , Humans , Nerve Degeneration/pathology
SELECTION OF CITATIONS
SEARCH DETAIL
...