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1.
J Am Med Dir Assoc ; 15(1): 47-53, 2014 Jan.
Article in English | MEDLINE | ID: mdl-24239014

ABSTRACT

BACKGROUND: Assisted living facilities (ALFs) provide housing and care to persons unable to live independently, and who often have increasing medical needs. Disease outbreaks illustrate challenges of maintaining adequate resident protections in these facilities. OBJECTIVES: Describe current state laws on assisted living admissions criteria, medical oversight, medication administration, vaccination requirements, and standards for infection control training. METHODS: We abstracted laws and regulations governing assisted living facilities for the 50 states using a structured abstraction tool. Selected characteristics were compared according to the time period in which the regulation took effect. Selected state health departments were queried regarding outbreaks identified in assisted living facilities. RESULTS: Of the 50 states, 84% specify health-based admissions criteria to assisted living facilities; 60% require licensed health care professionals to oversee medical care; 88% specifically allow subcontracting with outside entities to provide routine medical services onsite; 64% address medication administration by assisted living facility staff; 54% specify requirements for some form of initial infection control training for all staff; 50% require reporting of disease outbreaks to the health department; 18% specify requirements to offer or require vaccines to staff; 30% specify requirements to offer or require vaccines to residents. Twelve states identified approximately 1600 outbreaks from 2010 to 2013, with influenza or norovirus infections predominating. CONCLUSIONS: There is wide variation in how assisted living facilities are regulated in the United States. States may wish to consider regulatory changes that ensure safe health care delivery, and minimize risks of infections, outbreaks of disease, and other forms of harm among assisted living residents.


Subject(s)
Assisted Living Facilities/legislation & jurisprudence , Government Regulation , Infection Control/legislation & jurisprudence , Infection Control/standards , State Government , Contract Services/legislation & jurisprudence , Contract Services/statistics & numerical data , Cross Infection/prevention & control , Disease Outbreaks/statistics & numerical data , Humans , Inservice Training/legislation & jurisprudence , Inservice Training/statistics & numerical data , Licensure/legislation & jurisprudence , Licensure/statistics & numerical data , Mandatory Reporting , Medical Staff/legislation & jurisprudence , Nursing Staff/legislation & jurisprudence , Pharmaceutical Preparations/administration & dosage , United States , Vaccination/legislation & jurisprudence , Vaccination/statistics & numerical data
3.
Naunyn Schmiedebergs Arch Pharmacol ; 372(4): 300-12, 2006 Jan.
Article in English | MEDLINE | ID: mdl-16416266

ABSTRACT

Agonists active at I1-imidazoline receptors (I1R) not only lower blood pressure but also ameliorate glucose intolerance, insulin resistance, and hyperlipidemia with long-term treatment. We sought to determine the possible mechanism for the lipid-lowering actions of imidazolines in a model of metabolic Syndrome X, the spontaneously-hypertensive obese (SHROB) rat. The acute actions of moxonidine and rilmenidine, selective I1R agonists, were compared to a specific alpha2-adrenergic receptor agonist, guanabenz, with and without selective receptor blockers. Moxonidine and rilmenidine rapidly reduced plasma triglyceride (20+/-4% and 21+/-5%, respectively) and cholesterol (29+/-9% and 27+/-9%). In contrast, the specific alpha2-adrenergic receptor agonist guanabenz failed to reduce plasma lipids. Blocking experiments showed that moxonidine's actions were mediated by I1R and not alpha2-adrenergic receptors. To evaluate a hepatic site of action, radioligand binding studies with liver plasma membranes confirmed the presence of I1R. Intraportal moxonidine reduced plasma triglycerides by 23+/-3% within 10 min. Moxonidine inhibited hepatic triglyceride secretion by 75% compared to vehicle treatment. Tracer studies with 2H2O suggested that moxonidine inhibits de novo fatty acid synthesis. Thus, activation of I1R lowers plasma lipids, with the main site of action probably within the liver to reduce synthesis and secretion of triglycerides. More selective I1R agonists might provide monotherapy for hyperlipidemic hypertension.


Subject(s)
Adrenergic alpha-2 Receptor Agonists , Adrenergic alpha-Agonists/pharmacology , Antihypertensive Agents/pharmacology , Guanabenz/pharmacology , Hyperlipidemias/drug therapy , Imidazoles/pharmacology , Liver/drug effects , Metabolic Syndrome/drug therapy , Receptors, Drug/agonists , Adrenergic alpha-2 Receptor Antagonists , Adrenergic alpha-Antagonists/pharmacology , Animals , Cell Membrane/drug effects , Cell Membrane/metabolism , Cholesterol/blood , Clonidine/pharmacology , Disease Models, Animal , Female , Hyperlipidemias/metabolism , Imidazoline Receptors , Liver/metabolism , Male , Metabolic Syndrome/metabolism , Oxazoles/pharmacology , Rats , Rats, Inbred SHR , Receptors, Drug/antagonists & inhibitors , Rilmenidine , Triglycerides/blood
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