253 research outputs found
Schwinger's Dynamical Casimir Effect: Bulk Energy Contribution
Schwinger's Dynamical Casimir Effect is one of several candidate explanations
for sonoluminescence. Recently, several papers have claimed that Schwinger's
estimate of the Casimir energy involved is grossly inaccurate. In this letter,
we show that these calculations omit the crucial volume term. When the missing
term is correctly included one finds full agreement with Schwinger's result for
the Dynamical Casimir Effect. We have nothing new to say about sonoluminescence
itself except to affirm that the Casimir effect is energetically adequate as a
candidate explanation.Comment: 6 pages. Uses LaTeX with RevTeX package in two-column forma
Pharmacokinetics of C1-inhibitor protein in patients with acute myocardial infarction
OBJECTIVES: C1-inhibitor protein (C1-INH) purified from pooled human plasma is used for the treatment of patients with hereditary angioedema. Recently, the beneficial effects of high-dose C1-INH treatment on myocardial ischemia or reperfusion injury have been reported in various animal models and in humans. We investigated the pharmacokinetic behavior of C1-INH in patients with acute myocardial infarction to calculate the amount of C1-INH required for optimal efficacy. METHODS: Twenty-two patients received an intravenous loading dose, followed by 48 hours of continuous infusion of C1-INH. Changes in the endogenous production of C1-INH were evaluated in 16 control patients with acute myocardial infarction. A 2-compartment model was used to estimate the fractional catabolic rate constant (FCR), transcapillary escape rate constant (TER), and extravascular return rate constant (ERR) of C1-INH. Software designed to analyze and fit measured data to unknown parameters in a system of differential equations was used to fit the experimental data against the 3-parameter model. RESULTS: With fixed TER and ERR values (0.014 h(-1) and 0.018 h(-1), respectively), 20 of the 22 cases yielded well-determined FCR values, and simultaneous fitting resulted in a median FCR of 0.011 h(-1) (95% confidence interval, 0.010 to 0.012 h(-1)) versus 0.025 h(-1) as reported in healthy control patients. Simultaneous estimation of TER, ERR, and FCR demonstrated weakly defined TER and ERR values, whereas the median FCR value remained unchanged. The use of a 2-compartment model resulted in a significantly better fit compared with the 1-compartment model. Physiologic explanations are offered for discrepancies in the literature. CONCLUSIONS: Dose calculation of C1-INH in patients treated with massive doses of C1-INH requires turnover parameters that differ from those found in healthy subjects, possibly because of suppression of continuous C1-INH consumption by target protease
Pharmacokinetics of C1-inhibitor in patients with acute myocardial infarction
Nederlands Tijdschrift voor Klinische Chemie 27(2),69(2002) -- Nederlandse Vereniging voor Klinische Chemie en Laboratoriumgeneeskunde --
Economic Issues in Funding and Supplying Public Sector Information
BACKGROUND: Cerebrospinal fluid (CSF) biomarkers are increasingly being used for diagnosis of Alzheimer's disease (AD). OBJECTIVE: We investigated the influence of CSF intralaboratory and interlaboratory variability on diagnostic CSF-based AD classification of subjects and identified causes of this variation. METHODS: We measured CSF amyloid-beta (Abeta) 1-42, total tau (t-tau), and phosphorylated tau (p-tau) by INNOTEST enzyme-linked-immunosorbent assays (ELISA) in a memory clinic population (n = 126). Samples were measured twice in a single or two laboratories that served as reference labs for CSF analyses in the Netherlands. Predefined cut-offs were used to classify CSF biomarkers as normal or abnormal/AD pattern. RESULTS: CSF intralaboratory variability was higher for Abeta1-42 than for t-tau and p-tau. Reanalysis led to a change in biomarker classification (normal vs. abnormal) of 26% of the subjects based on Abeta1-42, 10% based on t-tau, and 29% based on p-tau. The changes in absolute biomarker concentrations were paralleled by a similar change in levels of internal control samples between different assay lots. CSF interlaboratory variability was higher for p-tau than for Abeta1-42 and t-tau, and reanalysis led to a change in biomarker classification of 12% of the subjects based on Abeta1-42, 1% based on t-tau, and 22% based on p-tau. CONCLUSIONS: Intralaboratory and interlaboratory CSF variability frequently led to change in diagnostic CSF-based AD classification for Abeta1-42 and p-tau. Lot-to-lot variation was a major cause of intralaboratory variability. This will have implications for the use of these biomarkers in clinical practice
Generalized glycogen storage and cardiomegaly in a knockout mouse model of Pompe disease
Glycogen storage disease type II (GSDII; Pompe disease), caused by
inherited deficiency of acid alpha-glucosidase, is a lysosomal disorder
affecting heart and skeletal muscles. A mouse model of this disease was
obtained by targeted disruption of the murine acid alpha-glucosidase gene
(Gaa) in embryonic stem cells. Homozygous knockout mice (Gaa -/-) lack Gaa
mRNA and have a virtually complete acid alpha-glucosidase deficiency.
Glycogen-containing lysosomes are detected soon after birth in liver,
heart and skeletal muscle cells. By 13 weeks of age, large focal deposits
of glycogen have formed. Vacuolar spaces stain positive for acid
phosphatase as a sign of lysosomal pathology. Both male and female
knockout mice are fertile and can be intercrossed to produce progeny. The
first born knockout mice are at present 9 months old. Overt clinical
symptoms are still absent, but the heart is typically enlarged and the
electrocardiogram is abnormal. The mouse model will help greatly to
understand the pathogenic mechanism of GSDII and is a valuable instrument
to explore the efficacy of different therapeutic interventions
Injury markers predict time to dementia in subjects with MCI and amyloid pathology
OBJECTIVES: Alzheimer disease (AD) can now be diagnosed in subjects with mild cognitive impairment (MCI) using biomarkers. However, little is known about the rate of decline in those subjects. In this cohort study, we aimed to assess the conversion rate to dementia and identify prognostic markers in subjects with MCI and evidence of amyloid pathology. METHODS: We pooled subjects from the VU University Medical Center Alzheimer Center and the Development of Screening Guidelines and Criteria for Predementia Alzheimer's Disease (DESCRIPA) study. We included subjects with MCI, an abnormal level of ÎČ-amyloid(1-42) (AÎČ(1-42)) in the CSF, and at least one diagnostic follow-up visit. We assessed the effect of APOE genotype, CSF total tau (t-tau) and tau phosphorylated at threonine 181 (p-tau) and hippocampal volume on time to AD-type dementia using Cox proportional hazards models and on decline on the Mini-Mental State Examination (MMSE) using linear mixed models. RESULTS: We included 110 subjects with MCI with abnormal CSF AÎČ(1-42) and a mean MMSE score of 26.3 ± 2.8. During a mean follow-up of 2.2 ± 1.0 (range 0.4-5.0) years, 63 subjects (57%) progressed to AD-type dementia. Abnormal CSF t-tau (hazard ratio [HR] 2.3, 95% confidence interval [CI] 1.1-4.6, p = 0.03) and CSF p-tau (HR 3.5, 95% CI 1.3-9.2, p = 0.01) concentration and hippocampal atrophy (HR 2.5, 95% CI 1.1-5.6, p = 0.02) predicted time to dementia. For subjects with both abnormal t-tau concentration and hippocampal atrophy, HR was 7.3 (95% CI 1.0-55.9, p = 0.06). Furthermore, abnormal CSF t-tau and p-tau concentrations and hippocampal atrophy predicted decline in MMSE score. CONCLUSIONS: In subjects with MCI and evidence of amyloid pathology, the injury markers CSF t-tau and p-tau and hippocampal atrophy can predict further cognitive decline
Towards a definition of sarcopenia--results from epidemiologic studies
The age-related loss of muscle mass, also called sarcopenia, is receiving increasing attention in aging research. While the concept is frequently being used in research settings and introduced to clinical settings, thus far no consensus on its definition has been established. This article provides an overview of the history of sarcopenia definitions proposed in the literature thus far. It will describe the methodology used to develop the cutpoints for low muscle mass (or strength) in large epidemiological studies, how sarcopenia based on these cutpoints relates to functional outcomes, and the advantages and disadvantages of the different definitions. This overview will contribute to the current need to develop a consensus definition of sarcopenia which can be used in all relevant settings. The Journal of Nutrition, Health & Aging©
The composition of the protosolar disk and the formation conditions for comets
Conditions in the protosolar nebula have left their mark in the composition
of cometary volatiles, thought to be some of the most pristine material in the
solar system. Cometary compositions represent the end point of processing that
began in the parent molecular cloud core and continued through the collapse of
that core to form the protosun and the solar nebula, and finally during the
evolution of the solar nebula itself as the cometary bodies were accreting.
Disentangling the effects of the various epochs on the final composition of a
comet is complicated. But comets are not the only source of information about
the solar nebula. Protostellar disks around young stars similar to the protosun
provide a way of investigating the evolution of disks similar to the solar
nebula while they are in the process of evolving to form their own solar
systems. In this way we can learn about the physical and chemical conditions
under which comets formed, and about the types of dynamical processing that
shaped the solar system we see today.
This paper summarizes some recent contributions to our understanding of both
cometary volatiles and the composition, structure and evolution of protostellar
disks.Comment: To appear in Space Science Reviews. The final publication is
available at Springer via http://dx.doi.org/10.1007/s11214-015-0167-
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