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1.
Am J Emerg Med ; 46: 550-555, 2021 08.
Article in English | MEDLINE | ID: mdl-33279330

ABSTRACT

BACKGROUND AND OBJECTIVES: Lack of mental health resources, such as inpatient psychiatric beds, has increased frequency and duration of boarding for mental health patients presenting to U.S. emergency departments (EDs). The purpose of this study is to describe characteristics of mental health patients with an ED length of stay of one week or longer and to identify barriers to their disposition. METHODS: This study was conducted in an academic ED in which emergency psychiatric evaluations and care are provided by a Psychiatric Emergency Services (PES) team contained within the Department of Emergency Medicine. Prolonged boarding was defined as an ED length of stay of 7 days or more. Pediatric, adult, and geriatric mental health patients with prolonged ED boarding from January 1 to August 31, 2019 were included. This study includes prospective data collection of the boarding group and retrospective identification and data collection of a comparison group of non-barding patients over the same 8-month period to compare patient characteristics and outcomes for each group. RESULTS: Between January 1 and August 31, 2019, the PES team completed 2,745 new assessments of mental health patients, of whom 39 met criteria for prolonged ED boarding. The following characteristics were associated with boarding: child (8%), male (64%), having Medicaid (49%) or both Medicaid and Medicare (18%), and having either a neurodevelopmental (15%) or neurocognitive disorder (15%) with a median stay of 18 days. Barriers to discharge included being declined from all state inpatient psychiatric hospitals (69%), declined from community living environments (21%), or declined from both (10%). The most common ED non-boarding patients were: Caucasian (64%), have a diagnosis of unspecified mental disorder (including suicidal ideation) or other specified mental disorder (59%) and have private insurance (42%) with a median stay of 1 day. CONCLUSION: In this study of mental health patients with prolonged ED stays, the primary barrier to disposition was the lack of patient acceptance to inpatient psychiatric hospitals, community settings, or other housing. Early identification of potential prolonged boarding, quality treatment and care for those patients, and effective case management, may resolve the ongoing challenges of boarding within the ED.


Subject(s)
Bed Occupancy , Emergency Service, Hospital , Hospitalization , Mental Disorders , Patient Transfer , Adolescent , Adult , Age Factors , Aged , Assisted Living Facilities , Child , Child, Preschool , Emergency Services, Psychiatric , Female , Group Homes , Hospital Bed Capacity , Hospitals, Psychiatric , Hospitals, State , Housing , Humans , Infant , Male , Medicaid , Medicare , Middle Aged , Mood Disorders , Neurocognitive Disorders , Neurodevelopmental Disorders , Patient Discharge , Psychotic Disorders , Retrospective Studies , Schizophrenia , Sex Factors , Substance-Related Disorders , United States , Young Adult
2.
Elife ; 92020 09 10.
Article in English | MEDLINE | ID: mdl-32909945

ABSTRACT

The umbilical artery lumen closes rapidly at birth, preventing neonatal blood loss, whereas the umbilical vein remains patent longer. Here, analysis of umbilical cords from humans and other mammals identified differential arterial-venous proteoglycan dynamics as a determinant of these contrasting vascular responses. The umbilical artery, but not the vein, has an inner layer enriched in the hydrated proteoglycan aggrecan, external to which lie contraction-primed smooth muscle cells (SMC). At birth, SMC contraction drives inner layer buckling and centripetal displacement to occlude the arterial lumen, a mechanism revealed by biomechanical observations and confirmed by computational analyses. This vascular dimorphism arises from spatially regulated proteoglycan expression and breakdown. Mice lacking aggrecan or the metalloprotease ADAMTS1, which degrades proteoglycans, demonstrate their opposing roles in umbilical vascular dimorphism, including effects on SMC differentiation. Umbilical vessel dimorphism is conserved in mammals, suggesting that differential proteoglycan dynamics and inner layer buckling were positively selected during evolution.


Subject(s)
Aggrecans/metabolism , Myocytes, Smooth Muscle , Umbilical Arteries , ADAMTS1 Protein/metabolism , Animals , Cell Differentiation/physiology , Female , Humans , Mice, Transgenic , Myocytes, Smooth Muscle/cytology , Myocytes, Smooth Muscle/metabolism , Myocytes, Smooth Muscle/physiology , Parturition/physiology , Pregnancy , Umbilical Arteries/cytology , Umbilical Arteries/metabolism , Umbilical Arteries/physiology
3.
Nat Commun ; 10(1): 953, 2019 02 27.
Article in English | MEDLINE | ID: mdl-30814516

ABSTRACT

Although hundreds of cytosolic or transmembrane molecules form the primary cilium, few secreted molecules are known to contribute to ciliogenesis. Here, homologous secreted metalloproteases ADAMTS9 and ADAMTS20 are identified as ciliogenesis regulators that act intracellularly. Secreted and furin-processed ADAMTS9 bound heparan sulfate and was internalized by LRP1, LRP2 and clathrin-mediated endocytosis to be gathered in Rab11 vesicles with a unique periciliary localization defined by super-resolution microscopy. CRISPR-Cas9 inactivation of ADAMTS9 impaired ciliogenesis in RPE-1 cells, which was restored by catalytically active ADAMTS9 or ADAMTS20 acting in trans, but not by their proteolytically inactive mutants. Their mutagenesis in mice impaired neural and yolk sac ciliogenesis, leading to morphogenetic anomalies resulting from impaired hedgehog signaling, which is transduced by primary cilia. In addition to their cognate extracellular proteolytic activity, ADAMTS9 and ADAMTS20 thus have an additional proteolytic role intracellularly, revealing an unexpected regulatory dimension in ciliogenesis.


Subject(s)
ADAMTS Proteins/metabolism , ADAMTS9 Protein/metabolism , Cilia/metabolism , Cilia/ultrastructure , ADAMTS Proteins/deficiency , ADAMTS Proteins/genetics , ADAMTS9 Protein/deficiency , ADAMTS9 Protein/genetics , Animals , Cell Line , Endocytosis , Gene Knockout Techniques , Humans , Mice , Mice, Knockout , Mice, Transgenic , Microscopy, Electron, Scanning , Models, Biological , Mutation , Neural Tube Defects/embryology , Neural Tube Defects/genetics , Neural Tube Defects/metabolism , Proteolysis , Signal Transduction , Versicans/genetics , Versicans/metabolism , Yolk Sac/embryology , Yolk Sac/metabolism
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