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Biomedical subjects

M Ash

Publications and source records attributed to M Ash.

At least 19 recordsLinked to original sources
PubMed2001

Measuring shortages of hospital nurses: how do you know a hospital with a nursing shortage when you see one?

Lack of clarity in definitions of shortages of hospital registered nurses may cause problems for effective policy making, particularly if different measures for identifying a nurse shortage lead to different conclusions about which hospitals and regions are experiencing a shortage. The authors compared different methods of identifying hospitals and regions with a shortage of registered nurses, including both relatively subjective measures (e.g., a hospital administrator's report of a nurse shortage) and more objective measures (e.g., number of registered nurses per inpatient year). Associations were strongest between self-reported shortage status and nursing vacancy rates and weaker for self-reported shortage status and registered nurses per inpatient year and overall regional supply of nurses. Different definitions of nursing shortage are not equally reliable in discriminating between hospitals and regions with and without nursing shortages. When faced with reports sounding an alarm about a hospital nursing shortage, policy makers should carefully consider the definition of shortage being used.

Catchment Area, Health↗
PubMed2001

Hospital registered nurse shortages: environmental, patient, and institutional predictors.

OBJECTIVE: To examine the characteristics of acute-care hospitals that report registered nurse shortages when a widespread shortage exists and when a widespread shortage is no longer evident. DATA SOURCE: Secondary data from the American Hospital Association's Nursing Personnel Survey from 1990 and 1992 were used. The study population was all acute-care hospitals in the United States. STUDY DESIGN: Outcome variables included whether a hospital experienced a shortage in 1990, when many hospitals reported a nursing shortage, or whether a hospital reported a shortage in both 1990 and 1992. Predictor variables included environmental, patient, and institutional characteristics. Associations between predictor and outcome variables were investigated using probit analyses. PRINCIPAL FINDINGS: Location in the South, a high percentage of nonwhite county residents, a high percentage of patients with Medicaid or Medicare as payer, a higher patient acuity, and use of team or functional nursing care delivery consistently predicted hospitals reporting shortages both when there was a widespread shortage and when there was no widespread shortage. CONCLUSIONS: Although some characteristics under the direct control of hospitals, such as nursing care delivery model, are associated with their reporting a shortage of nurses, shortage is also strongly associated with broader population characteristics such as minority communities and a public insurance payer mix. Awareness of these broader factors may help inform policies to improve the distribution of nurse supply.

Aged↗
PubMed1998

Effects of a myofunctional appliance on orofacial muscle activity and structures.

The aim of the study was to examine the effect of an oral shield treatment on orofacial muscle activity and facial morphology in children with lip and/or tongue dysfunction. The sample consisted of 7 girls and 2 boys, 7 to 12 years old. EMG recordings with and without the shield in situ were obtained when the shield was placed, and 3, 6, and 12 months later. Lateral cephalograms were obtained at the initial and 1-year stages. The lip muscles showed dominant activity when the subjects were sucking on an empty straw and during swallowing; this was strongest during the first 3 months. The mentalis, buccinator, and digastric muscles generally showed weaker activity. The anterior temporal muscle showed dominant activity during maximal clench, but after the 3-month stage a significant decrease was noted. After 1 year of treatment, no significant changes in overjet or overbite were observed. Most of the craniofacial growth changes were normal for the age group. The results indicate that treatment with an oral shield caused a decrease in orofacial muscle activity during oral functions. Although there was a slight average retraction of the maxillary incisors, the change in position was not statistically significant.

Cephalometry↗
PubMed1997

Placental leptin: an important new growth factor in intrauterine and neonatal development?

BACKGROUND: Leptin, the protein product of the ob gene, is produced by the adipocyte and seems to function as a link between adiposity, satiety, and activity. Leptin has also been found to be necessary for pubertal development, conception, and pregnancy in mice, and is increased in prepubertal children, independent of adiposity, suggesting a role in childhood growth and development. This study investigated 100 mother/newborn pairs to determine the role of leptin in neonatal development. Placental tissue was assayed for leptin mRNA to evaluate it as a source of leptin production in utero. METHODS: One hundred mother/newborn pairs were enrolled in this study. Radioimmunoassay was performed for leptin on maternal venous and newborn cord blood. Leptin concentrations were measured in 43 children in Tanner stages 1 and 2 as a control group. Placental tissue was obtained from five mothers and assayed for leptin mRNA by reverse transcription/polymerase chain reaction (RT/PCR). Human placental cell lines JAR and JEG-3 were also assayed for leptin mRNA expression. RESULTS: Leptin was present in all newborns studied at a mean concentration of 8.8 ng/mL (+/-9.6 standard deviations). Leptin concentrations in cord blood correlated with newborn weight (r = .51), body mass index (BMI) (r = .48), and arm fat (r = .42). There was no correlation between leptin and insulin. When statistically covarying for adiposity for newborns and Tanner stages 1 and 2 children, newborns had greater concentrations of leptin (mean, 10.57 ng/mL) than children (mean, 3.04 ng/mL). Leptin was present in all mothers at a mean value of 28.8 ng/mL (+/-22.2 standard deviations). Leptin concentration correlated with prepregnancy BMI (r = .56), BMI at time of delivery (r = .74), and arm fat (r = .73). Maternal leptin correlated with serum insulin (r = .49). There was no correlation between maternal and newborn leptin concentrations. Thirteen percent of newborns had higher leptin concentrations than their mothers. Placental tissue from five separate placentas expressed leptin mRNA at comparable or greater levels than adipose tissue. Two human trophoblastic placental cell lines, JAR and JEG-3, also expressed leptin mRNA. CONCLUSIONS: The correlation between leptin and adiposity found in children and adults was also found in newborns. Serum leptin concentrations in newborns were increased more than three-fold compared with children in Tanner stages 1 and 2 when controlling for adiposity, suggesting that leptin concentrations in the newborn are not explained by adiposity alone. Maternal leptin concentrations correlated with measures of adiposity at delivery but did not correlate with newborn adiposity or leptin. Leptin mRNA was expressed both in placental tissue and in two human placental cell lines. These data suggest that leptin has a role in intrauterine and neonatal development and that the placenta provides a source of leptin for the growing fetus.

Adipose Tissue↗
PubMed1995

Hyperinsulinemia inhibits hepatic peroxisomal beta-oxidation in rats.

Studies show that insulin deficiency enhances peroxisomal enzyme activities. It is not known, however, whether hyperinsulinemia exerts the opposite effect on peroxisomes. Male Sprague-Dawley rats were infused with normal saline, glucose or galactose for 7 days. Only glucose caused an increase in serum insulin levels. The increase in insulin secretion, in response to glucose, was blocked with diazoxide. Data show an inverse relationship between serum insulin levels and hepatic peroxisomal beta-oxidation (r2 = 0.90, p < 0.01). While hyperinsulinemic rats had diminished peroxisomal beta-oxidation, lowering serum insulin restored peroxisomal enzyme activity to normal levels. These effects were independent of blood glucose levels (r2 = 0.35). In addition to decreasing peroxisomal beta-oxidation, hyperinsulinemia was accompanied by accelerated animal mortality, an effect which was also prevented by lowering serum insulin levels. Peroxisomal deficit may be a potentially lethal consequence of hyperinsulinemia.

Animals↗