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Biomedical subjects

L Keyes

Publications and source records attributed to L Keyes.

11 recordsLinked to original sources
PubMed2001

Improving preventive service delivery through office systems.

OBJECTIVE: Rates of childhood immunizations and other preventive services are lower in many practices than national goals and providers' own estimates. Office systems have been used in adult settings to improve the delivery of preventive care, but their effectiveness in pediatric practices is unknown. This study was designed to determine whether a group of primary care practices in 1 community could implement office-based quality improvement systems that would significantly improve their delivery of childhood preventive services. The study was part of a larger community-wide intervention study reported in a preceding study. METHODS: All the major providers of primary care to children in 1 community were recruited and agreed to participate (N = 8 practices). Project staff worked on-site with improvement teams in each practice to develop tailored systems to assess and improve the delivery of immunizations and screening for anemia, tuberculosis, and lead exposure. Office-based quality improvement systems typically involved some combination of chart prescreening, risk assessment forms, Post-it prompts, flow-sheets, reminder/recall systems, and patient education materials. Office systems also often involved redistributing responsibilities among office staff. RESULTS: All 8 participating practices created improvement teams. Project staff met with the practices 10 to 15 times over 12 months. After the period of office assistance, the overall rates for all preventive services except tuberculosis screening increased by amounts that were both clinically and statistically significant. Absolute percent improvements included: complete immunizations at 12 months, 7%; complete immunizations at 24 months, 12%; anemia screening, 30%; lead screening, 36%. The amount of improvement achieved varied considerably between practices. CONCLUSIONS: Office systems and the principles of quality improvement that underlie them seem to be effective in improving the delivery of childhood preventive services. Important predisposing factors may exist within practices that affect the likelihood that an individual practice will make significant improvements. prevention, immunizations, improvement, office systems, primary care.

Child↗
PubMed2001

Ability in perceiving nonnative contrasts: performance on natural and synthetic speech stimuli.

The perception of the distinction between /r/ and /l/ by native speakers of American English and of Japanese was studied using natural and synthetic speech. The American subjects were all nearly perfect at recognizing the natural speech sounds, whereas there was substantial variation among the Japanese subjects in their accuracy of recognizing /r/ and /l/ except in syllable-final position. A logit model, which additively combined the acoustic information conveyed by F1-transition duration and by F3-onset frequency, provided a good fit to the perception of synthetic /r/ and /l/ by the American subjects. There was substantial variation among the Japanese subjects in whether the F1 and F3 cues had a significant effect on their classifications of the synthetic speech. This variation was related to variation in accuracy of recognizing natural /r/ and /l/, such that greater use of both the F1 cue and the F3 cue in classifying the synthetic speech sounds was positively related to accuracy in recognizing the natural sounds. However, multiple regression showed that use of the F1 cue did not account for significant variance in natural speech performance beyond that accounted for by the F3 cue, indicating that the F3 cue is more important than the F1 cue for Japanese speakers learning English. The relation between performance on natural and synthetic speech also provides external validation of the logit model by showing that it predicts performance outside of the domain of data to which it was fit.

Adult↗
PubMed2000

Late-onset renal failure after liver transplantation: role of posttransplant alcohol use.

BACKGROUND: Late-onset renal failure is being increasingly recognized as a complication in patients undergoing liver transplantation for hepatitis C virus (HCV). However, its precise incidence, predisposing risk factors, and impact on outcome after liver transplantation, have not been defined. METHODS: The development of late-onset renal failure (defined as serum creatinine persistently >2.0 mg/dl, occurring more than 6 months posttransplant) was assessed in 120 consecutive liver transplant recipients who survived at least 6 months after transplantation. Fifty-seven percent (68/120) of the patients had undergone transplantation for liver disease due to HCV. The median follow-up was 5 years. RESULTS: Late-onset renal failure developed in 28% (33/120)of the patients. Posttransplant alcohol use (P=0.0001), posttransplant diabetes (P=0.0042), and recurrent HCV hepatitis (P=0.019) were significantly associated with late onset renal failure. In multivariate analysis, alcohol use (O.R. 10.7, 95%; CI 2.4-35.9, P=0.001) and diabetes (O.R. 2.1, 95%; CI 1.1-9.9, P=.03) were independently significant predictors of late onset renal failure. When only patients transplanted for HCV were analyzed, posttransplant alcohol use (P=0.004) was the only significant independent predictor of late-onset renal failure. HCV genotype 1b, as compared with other HCV genotypes, was associated with a higher rate of late-onset renal failure in patients with HCV; 70% of the patients with genotype 1b versus 32% of those with 1a and 33% of those with 2b, developed late onset renal failure (P=0.03). At a median follow up of 5 years, mortality in patients with HCV with late-onset renal failure was 52% as compared with 2% in those without renal failure (P=.0001). CONCLUSION: Late-onset renal failure in patients with HCV portended a grave outcome. Alcohol use was an independent predictor of late-onset renal failure in patients with HCV and represents a potentially modifiable risk factor for late-onset renal failure in these patients.

Adult↗
PubMed1998

Prolactin is an antagonist of TGF-beta activity and promotes proliferation of murine B cell hybridomas.

Prolactin (PRL) is an immunomodulator that has been demonstrated to enhance immune responses both in vitro and in vivo. Prolactin enhances the proliferative response of lymphoid cells to both nonspecific mitogens and specific antigens and increases their production of IL-2 and interferon-gamma. Studies were performed to examine whether recombinant human prolactin (r-hPRL) also acts as a growth factor for B cell hybridomas. Prolactin was able to stimulate proliferation of murine B cell hybridomas in a dose-dependent manner and enhanced their proliferation in response to IL-4, IL-5, and IL-6. This increase in proliferation resulted in an overall increase in antibody production. Studies were also undertaken to examine the effect of PRL with transforming growth factor beta (TGF-beta), an immunosuppressive cytokine. Hybridoma cell lines incubated with TGF-beta demonstrated a dose-dependent decrease in proliferation. Variability in the degree of inhibition was observed among the various hybridomas in their responsiveness to TGF-beta. The addition of r-hPRL to the cultures reversed the antiproliferative effects of TGF-beta. The mechanism by which PRL can overcome the anti-proliferative effect of TGF-beta is under investigation. These findings provide an additional rationale for using r-hPRL clinically in immunosuppressed patients in certain disease settings such as AIDS and cancer, where overexpression of TGF-beta has been implicated in disease development and progression.

Adjuvants, Immunologic↗
PubMed1998

Effect of K+ATP channel inhibition on total and regional vascular resistance in guinea pig pregnancy.

Decreased vascular resistance and vasoconstrictor response during pregnancy enables an increase in cardiac output and regional blood flow to the uterine circulation. We sought to determine whether inhibition of vascular smooth muscle ATP-sensitive potassium (K+ATP) channel activity during pregnancy increased systemic and/or regional vascular resistance and resistance response to ANG II. A total of 32 catheterized, awake, pregnant or nonpregnant guinea pigs were treated with either the K+ATP channel inhibitor glibenclamide (3.5 mg/kg) or vehicle (DMSO) (n = 8/group). In nonpregnant and pregnant animals, glibenclamide raised blood pressure and systemic, uterine, and coronary vascular resistance, diminishing cardiac output and organ blood flow. Glibenclamide produced a greater rise in coronary vascular resistance in the pregnant than nonpregnant groups and increased renal and cerebral vascular resistance in the pregnant animals only. ANG II infusion raised blood pressure and systemic and renal vascular resistance and lowered cardiac output and renal blood flow in vehicle-treated animals. Glibenclamide augmented ANG II-induced systemic vasoconstriction in the nonpregnant and pregnant groups and the rise in uteroplacental vascular resistance in the pregnant animals. We concluded that K+ATP channel activity likely modulates systemic, uterine, and coronary vascular resistance and opposes ANG II-induced systemic vasoconstriction in nonpregnant and pregnant guinea pigs. Pregnancy augments K+ATP channel activity in the uterine, coronary, renal, and cerebral vascular beds and the uteroplacental circulation during ANG II infusion. Thus increased K+ATP channel activity appears to influence regional control of vascular resistance during guinea pig pregnancy but cannot account for the characteristic decrease in systemic vascular resistance and ANG II-induced systemic vasoconstrictor response.

Angiotensin II↗
PubMed1997

Use of insulin-like growth factor I (IGF-I) and IGF-binding protein measurements to monitor feeding of premature infants.

To determine whether peptides of the insulin-like growth factor (IGF) system might be useful indicators of nutritional adequacy in premature infants, we studied 50 premature (25-34 weeks gestation) infants prospectively to define the relationship between nutrient intake and serum concentrations of IGF-I, IGF-binding protein-2 (IGFBP-2), and IGFBP-3. Each infant was monitored for at least 2 weeks. Nutrient intake was quantified from daily logs; weight was determined daily, and measurements of IGF-I, IGFBP-2, and IGFBP-3 in serum were made twice weekly. Serum IGF-I correlated strongly with length of gestation, increasing 4.03 +/- 0.95 ng/mL for each additional week of gestation (P < 0.0001) and 0.36 +/- 0.07 ng/mL day each day since birth (P < 0.0001). A higher intake of calories increased IGF-I by 0.07 +/- 0.01 ng/mL for each calorie per kg ingested over the previous 3 days (P < 0.0001). IGF-I increased quadratically as protein intake increased. For each change of 1% in calories as protein squared, IGF-I increased 0.36 +/- 0.11 ng/mL (P < 0.0001). Serum IGFBP-3 concentrations also correlated with length of gestation, increasing 25.06 +/- 11.83 micrograms/L.wk (P = 0.035) and 4.14 +/- 1.33 micrograms/.day since birth (P = 0.003). Unlike IGF-I, variation in the amount of protein supplied did not change IGFBP-3. As calorie intake increased, IGFBP-3 increased by 0.54 +/- 0.17 microgram/L for each calorie per kg consumed over the previous 3 days (P = 0.0015). In contrast to IGF-I and IGFBP-3, IGFBP-2 declined as the length of gestation increased (56.12 +/- 16.92 ng/mL.week; P = 0.001) and with each additional day of life (7.57 +/- 2.44 ng/mL.day; P = 0.003). Dietary protein, the predominant regulator of IGFBP-2, caused a decrease of 33.22 +/- 9.00 ng/mL with each percent increase in dietary calories as protein (P < 0.0003). Calorie intake had less effect on IGFBP-2 than protein intake. These results indicate that each of the three peptides studied is regulated in premature infants by nutritional intake, and that their regulatory patterns are qualitatively similar to those observed in older individuals. Measurements of these peptides in premature infants may be useful indicators of nutritional status and adequacy of nutrient intake.

Humans↗
PubMed1995

Individual and team consensus ratings of child functioning.

The authors examined agreement between interdisciplinary teams of professionals in rating the functional abilities of children with disabilities. 129 children were rated on the ABILITIES index by 72 professionals working in nine developmental evaluation centers. Independent individual ratings were made first, followed by a consensus rating. Team members had a high degree of agreement on independent ratings of abilities and limitations, with nearly 90 per cent of the ratings within one point of each other. More disagreement was associated with rating areas of behavior and communication, team experience and increased severity of disability. The team's consensus ratings were more likely to defer to the ratings of the expert in particular areas. Implications for team assessment and team functioning are discussed.

Adolescent↗
PubMed1994

Indicators of developmental and functional status of Mexican-American and Puerto Rican children.

The overall purpose of this study was to describe the developmental and functional status of young Latino children. We analyzed data from the Hispanic Health and Nutrition Examination Survey and estimated the percentages of young Mexican-American and mainland Puerto Rican children with indicators of developmental need for special services, i.e., low birth weight, use of neonatal intensive care, congenital problems, chronic conditions of developmental concern, functional limitations, and physician diagnoses of medical conditions. Estimates suggest that Puerto Rican children had substantially poorer status than Mexican-American children who, in turn, have indicators that are comparable with those reported for the general population. The difference in status between the two Latino groups merits further investigation.

Brain Damage, Chronic↗
PubMed1992

Transforming growth factor-beta (TGF-beta 1) inhibits pancreatic acinar cell growth.

Effects of transforming growth factor (TGF)-beta 1 on mouse pancreatic acinar cell growth and rapid intracellular responses to cholecystokinin (CCK) were examined in vitro. TGF-beta 1 inhibited [3H]thymidine incorporation stimulated by either the CCK analogue caerulein, epidermal growth factor, or insulin. TGF-beta 1 inhibition of growth stimulated by a maximal dose of caerulein (1 nM) was dose dependent with one-half maximal effects occurring at approximately 5 pM and maximal inhibition seen with 30 pM. In contrast to its effects on CCK-stimulated [3H]thymidine incorporation, TGF-beta 1 had no effect on CCK-stimulated increases in amylase release or intracellular Ca2+ concentration. To determine whether TGF-beta 1 might be an autocrine growth regulator, pancreatic mRNA was probed for the presence of TGF-beta 1 transcripts. TGF-beta 1 mRNA was not detected in whole pancreas but was detectable with increasing abundance over time in primary cultures of pancreatic acinar cells. The appearance of the TGF-beta 1 mRNA corresponded to the period of rapid cellular proliferation in vitro. These results suggest that TGF-beta 1 may be an autocrine growth inhibitor in the pancreas and that the inhibitory effects of TGF-beta 1 on pancreatic acinar cell growth occur at sites distal to those involved in stimulus-secretion coupling.

Animals↗
PubMed1986

Abelson virus drives the differentiation of Harvey virus-infected erythroid cells.

Abelson murine leukemia virus (A-MuLV) and Harvey murine sarcoma virus (Ha-MSV) are retroviruses carrying unrelated onc genes. However, both of these viruses are capable of stimulating the growth and differentiation of erythroid precursor cells; the target cells for both appear at the same time during fetal development and follow a similar pattern throughout ontogeny. In addition, the colonies induced by each virus are morphologically similar and synthesize the adult form of hemoglobin. However, A-MuLV-infected cells are Epo-independent, whereas Ha-MSV-infected cells are Epo-dependent. Superinfection of Ha-MSV-infected cells with A-MuLV overrides their Epo-dependency. Thus, the consequences of the infection are determined by the interaction of the different onc gene products with identical or similar erythroid cells.

Abelson murine leukemia virus↗