A New Measure of Misfit for Covariance Structure Models

Various fit indices exist in structural equation models. Most of these indices are related to the noncentrality parameter (NCP) of the chi-square distribution that the involved test statistic is implicitly assumed to follow. Existing literature suggests that few statistics can be well approximated by chi-square distributions. The meaning of the NCP is not clear when the behavior of the statistic cannot be described by a chi-square distribution. In this paper we define a new measure of model misfit (MMM) as the difference between the expected values of a statistic under the alternative and null hypotheses. This definition does not need to assume that the population covariance matrix is in the vicinity of the proposed model, nor does it need for the test statistic to follow any distribution of a known form. The MMM does not necessarily equal the discrepancy between the model and the population covariance matrix as has been assumed in existing literature. Bootstrap approaches to estimating the MMM and a related quantity are developed. An algorithm for obtaining bootstrap confidence intervals of the MMM is constructed. Examples with practical data sets contrast several measures of model misfit. The quantile-quantile plot is used to illustrate the unrealistic nature of chi-square distribution assumptions under either the null or an alternative hypothesis in practice.

     

Regression of severe atherosclerotic plaque in patients with mild elevation of LDL cholesterol

BACKGROUND: Intensive risk factor reduction in patients with dyslipidemias and coronary atherosclerosis has been shown to result in alterations in coronary artery morphology and reduced clinical events. However, the impact of such interventions in populations with relatively normal levels of low-density lipoproteins (LDL) is unclear. METHODS: To test the hypothesis that intensive risk factor reduction results in angiographic regression in patients with only mildly elevated levels of LDL, 14 patients with angiographically proven coronary atherosclerosis were entered into the University of California Davis Coronary Artery Disease Regression Program and intensively treated with pharmacologic and nonpharmacologic interventions for 2 years. Quantitative angiography was performed prior to and after 2 years of therapy to determine changes in coronary artery diameter. RESULTS: As a result of this program, dietary fat intake was reduced by 58% and LDL fell from 120 +/- 7 mg/dL to 104 +/- 6 mg/dL (p = 0.05). The average diameter of the measured arterial locations (including all 53 stenoses and 292 nondiscrete regions) on study entry was 2.74 +/- 0.05 mm. After 24 months, there was a net increase in arterial diameter (regression) of +0.05 +/- 0.04 mm to 2.81 +/- 0.05 mm (p = 0.01). While there was no significant change in the average diameter of discrete stenoses, all 8 lesions > or = 50% initial diameter narrowing regressed, with a mean diameter change of + 0.2 mm. Conversely, only 1 of 8 mild lesions < or = 20% regressed, while 4 progressed. Intermediate lesions (20% to 50%, n = 37) had balanced progression and regression. CONCLUSIONS: When examined as a continuous variable, there was a significant linear correlation between initial lesion severity (% stenosis) and the extent of regression (mm). Therefore, risk factor reduction (dietary therapy, exercise, psycho-social counseling, and lipid lowering therapy) in patients with only mild dyslipidemia results in angiographic regression of more severe lesions (> 50% initial stenosis), but does not prevent progression of mild lesions (< 20%). These findings demonstrate that intensive risk factor reduction in patients with only mild elevation of lipids beneficially influences the morphology of the most severe lesions.     

Determination of molecular weight distributions of tert-octylphenol ethoxylate surfactant polymers by laser desorption Fourier transform ion cyclotron resonance mass spectrometry and high-performance liquid chromatography

Triton polymers are commercial surfactants whose molecular weight distributions are conventionally determined by means of high-performance liquid chromatography (HPLC). However, in the case of the important octylphenol ethoxylates [p-C8H17-C6H4-O-(CH2CH2O)n-H], HPLC cannot resolve individual oligomers of high molecular weight Triton surfactants (e.g., greater than 2000 u or so; u = unified atomic mass unit). In this paper, we show that laser desorption Fourier transform ion cyclotron resonance mass spectrometry (LD/FT/ICR/MS) provides a simple and accurate measure of such Triton surfactant molecular weight distributions up to at least 3500 u, based on a single-shot laser pulse measurement of a few seconds duration. Comparison of LD/FT/ICR/MS and HPLC molecular weight distributions of low molecular weight surfactants shows that laser desorption/ionization produces minimal fragmentation and thus offers an accurate measure of the relative abundances of the neutral oligomers, without the need for prior chromatographic separation of the components. Moreover, for all Triton polymer molecular weight distributions (700-3000 u), LD/FT/ICR/MS provides much more highly resolved profiles of oligomer relative abundances. Finally, LD/FT/ICR/MS reveals the presence of poly(ethylene oxide) side products of the polymerization process, which are not observed by HPLC with conventional ultraviolet absorption detection.     

Renal length in sickle cell disease: observations from a cohort study

Renal length has been measured by ultrasound in 237 subjects with homozygous sickle cell (SS) disease, 147 with sickle cell-hemoglobin C (SC) disease, and in 78 age-matched controls with a normal hemoglobin (AA) genotype. As expected, renal length increased with age in all genotypes but mean length was significantly greater in SS disease compared with SC disease (mean difference 4.3 mm after adjustment for height) and significantly greater in both genotypes than in AA controls (SS/AA difference 9.2 mm, SC/AA difference 5.0 mm after adjustment for height). Examination of relationships between renal length and some hematological indices (hemoglobin, fetal hemoglobin, reticulocyte counts, alpha thalassemia status) in SS or SC disease showed only a significant negative correlation with hemoglobin and positive correlation with reticulocyte count in SS disease. Further analysis suggested that the stronger relationship was between renal length and high reticulocyte count. The mechanism of renal enlargement is unknown although glomerular hypertrophy and increased renal blood volume are likely contributors.     

A conservation principle and its effect on the formulation of Na-Ca exchanger current in cardiac cells

In the rat the exact role of vagal fibers and the interaction between the extrinsic and intrinsic neural system in distention-induced gastrin release are still a matter of debate. Accordingly, the aim of the present study was to examine the contribution of afferent and efferent vagal fibers as well as intrinsic neurons on gastrin response to gastric distention. In anesthetized rats graded gastric distention by 5, 10 and 15 ml saline for 20 min caused a significant volume-dependent increase of plasma gastrin levels by 12+/-6 pg/ml (5 ml saline, n = 8, P =0.05), 26+/-7 pg/ml (10 ml saline, n = 10, P < 0.05) and 37+/-7 pg/ml (15 ml saline, n = 8, P < 0.01 ), respectively. To examine the role of the extrinsic vagal innervation, gastrin response to distention was studied in anesthetized rats after bilateral truncal vagotomy (n = 9) or selective afferent vagotomy following pretreatment with capsaicin (n = 6). Stimulation of gastrin release by 10 ml distention in sham-operated control rats was reversed to an inhibition after truncal vagotomy (26+/-7 vs. -11+/-4 pg/ml; P<0.05) and capsaicin-treatment (37+/-18 vs. -34+/-11 pg/ml; P<0.05). A contribution of cholinergic mechanisms to this vagovagal-mediated stimulation of distention-induced gastrin release was excluded, since atropine (100 microg/kg/h; n = 8) further augmented distention-stimulated gastrin release. Since bombesin/gastrin-releasing peptide (GRP)-neurons contribute to vagally stimulated gastrin secretion, we have examined gastrin response to distention in the presence of the specific bombesin-receptor antagonist D-Phe6-BN(6-13)OMe (400 microg/kg/h: n = 10). This bombesin-antagonist completely reduced distention-stimulated gastrin release in vivo. In contrast, distention of the isolated, extrinsically denervated stomach significantly decreased gastrin release by 13+/-5 pg/min (5 ml saline, n = 8, P < 0.05), 28+/-8 pg/min (10 ml saline, n = 11, P < 0.05) and 35+/-10 pg/min (15 ml saline, n = 8, P < 0.01), respectively, without changing the activity of bombesin/GRP-neurons. Distention-induced decrease of gastrin release was attenuated to 50 percent by atropine (10(-7) M: n = 10) or tetrodotoxin (TTX) (10(-6) M; n = 10), respectively. These data demonstrate, that in anesthetized rats distention-stimulated gastrin secretion depends on the activation of a vagovagal reflex and intrinsic bombesin/GRP-neurons. In contrast distention of the isolated rat stomach inhibits gastrin release in part via intrinsic cholinergic pathways and other as yet unknown mechanisms.     

Cervical esophageal web associated with a patch of heterotopic gastric mucosa

Cervical esophageal webs are a relatively common finding on esophograms. We report a web resulting from the squamocolumnar junction produced by heterotopic gastric mucosa. The clinical significance of this lesion is discussed and the importance of differentiating it from Barrett's esophagus is stressed.     

Electron-beam CT scanning for detection of coronary calcification and prediction of coronary heart disease

Electron-beam or ultrafast computerized tomographic (CT) scanning provides a convenient and sensitive means of detecting coronary calcification, which is an early index of atherosclerosis. The procedure has strong negative predictive power for the presence of coronary artery disease, but a limited ability to predict disease severity. However, preliminary indications are that it is as good or better than conventional risk factors in this respect. Although further validation is needed before electron-beam CT can be regarded as an established method of detecting presymptomatic coronary atherosclerosis, the procedure has potential in this context.     

Allergy and depression: A neurochemical threshold model of the relation between the illnesses.

Empirical studies suggest a very high prevalence of atopic disorder in people with depression. Research indicates that individuals with allergy have cholinergic hyperresponsiveness and beta-adrenergic hyporesponsiveness in the autonomic nervous system. Evidence is reviewed that similar imbalances in CNS cholinergic–adrenergic activity play a causal role in depression behaviors. It is hypothesized that the allergic state or allergic reactions can accentuate cholinergic–adrenergic activity imbalances in the CNS of a small subgroup of people at risk for endogenous depression thereby producing depression symptomatology. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

A broadly cross-protective monoclonal antibody binding to Escherichia coli and Salmonella lipopolysaccharides

During the last decade, episodes of sepsis have increased and Escherichia coli has remained the most frequent clinical isolate. Lipopolysaccharides (LPS; endotoxin) are the major toxic and antigenic components of gram-negative bacteria and qualify as targets for therapeutic interventions. Molecules that neutralize the toxic effects of LPS are actively investigated. In this paper, we describe a murine monoclonal antibody (MAb; WN1 222-5), broadly cross-reactive and cross-protective for smooth (S)-form and rough (R)-form LPS. As shown in enzyme-linked immunosorbent assay and the passive hemolysis assay, WN1 222-5 binds to the five known E. coli core chemotypes, to Salmonella core, and to S-form LPS having these core structures. In immunoblots, it is shown to react with both the nonsubstituted core LPS and with LPS carrying O-side chains, indicating the exposure of the epitope in both S-form and R-form LPS. This MAb of the immunoglobulin G2a class is not lipid A reactive but binds to E. coli J5, an RcP+ mutant which carries an inner core structure common to many members of the family Enterobacteriaceae. Phosphate groups present in the inner core contribute to the epitope but are not essential for the binding of WN1 222-5 to complete core LPS. Cross-reactivity for clinical bacterial isolates is broad. WN1 222-5 binds to all E. coli clinical isolates tested so far (79 blood isolates, 80 urinary isolates, and 21 fecal isolates) and to some Citrobacter, Enterobacter, and Klebsiella isolates. This pattern of reactivity indicates that its binding epitope is widespread among members of the Enterobacteriaceae. WN1 222-5 exhibits biologically relevant activities. In vitro, it inhibits the Limulus amoebocyte lysate assay activity of S-form and R-form LPS in a dose-dependent manner and it neutralizes the LPS-induced release of clinically relevant monokines (interleukin 6 and tumor necrosis factor). In vivo, WN1 222-5 blocks endotoxin-induced pyrogenicity in rabbits and lethality in galactosamine-sensitized mice. The discovery of WN1 222-5 settles the long-lasting controversy over the existence of anti-core LPS MAbs with both cross-reactive and cross-protective activity, opening new possibilities for the immunotherapy of sepsis caused by gram-negative bacteria.