Consumption of reduced-fat products: effects on parameters of anti-oxidative capacity

Plasma levels of fibrinogen, factor VIIc and prothrombin fragment F1 + 2, a marker of thrombin generation in vivo, were studied in 68 subjects with serum total cholesterol (TC) levels between 135 and 349 mg/dl but without clinical evidence of cardiovascular disease and other atherosclerotic risk factors. F1 + 2 plasma levels were directly correlated with TC (p < 0.0004), low-density lipoprotein cholesterol (LDL-C; p < 0.0018) and factor VIIc (p < 0.024). Thirty-five subjects with TC greater than 249 mg/dl (median value of the whole group) showed higher levels of F1 + 2 (p < 0.0001) and fibrinogen (p < 0.0015) than those with TC lower than 249 mg/dl. In subjects with TC > 249 mg/dl and F1 + 2 > 1.2 nM (median value of the whole group), a cholesterol-lowering drug (simvastatin) was able to reduce F1 + 2 (p < 0.009) as well as TC and LDL-C. This study shows a relationship between serum cholesterol and the rate of thrombin generation supporting the hypothesis that a hypercoagulable state may occur in hypercholesterolemic subjects before the onset of clinical evidence of atherosclerotic cardiovascular disease.     

The short-term effect of a smoking prevention program for the upper graders of elementary schools--the results of intervention study for two years with quasi-experimental design

The purpose of this study was to evaluate the short-term effect of a smoking prevention program for Japanese elementary school-children in the fifth and sixth grades. The program was developed with concepts found in the Know Your Body Program and the conclusions of a National Cancer Institute-convened Expert Advisory Panel, and focused on teaching about the short-term effects of smoking and on resistance to social pressures to smoke. The study was conducted with a quasi-experimental design. An intervention group (52 boys and 54 girls) received three sessions for both the fifth grade in 1992 and the sixth grade in 1993. Moreover, the intervention group received a pre-test before the first session and a post-test after the third session in each grade. A comparison group (102 boys and 91 girls) received the same tests at the same time as the intervention group, but did not receive any program on smoking prevention. The short-term effect of the program were evaluated using the results of the pre-test in the fifth grade and of the post-test in the sixth grade in both groups. The results were as follows: 1) Remarkable short-term effects of the intervention were seen in respect to awareness of the importance of not smoking in girls, and also in the knowledge of the short-term effects of smoking in both sexes. 2) The intervention was not effective with respect to intention to smoke at the age of 20 and self-efficacy of refusing to smoke in both sexes. 3) The short-term effects were not clear in the smoking behavior in both sexes because the rates of ever smokers and of monthly smokers were almost the same for two years between the intervention group and the comparison group. 4) The smoking behaviors of children, their parents and their best friends had little influence on the results of the post-test in the sixth grade.     

Sidestream tobacco smoke exposure acutely alters human nasal mucociliary clearance

Nasal mucociliary clearance (NMC) is a biomarker of nasal mucosal function. Tobacco smokers have been shown to have abnormal NMC, but the acute effect of environmental tobacco smoke (ETS) on nonsmokers is unknown. This study evaluated acute tobacco smoke-induced alterations in NMC in 12 healthy adults. Subjects were studied on 2 days, separated by at least 1 week. Subjects underwent a 60-min controlled exposure at rest to air or sidestream tobacco smoke (SS) (15 ppm CO) in a controlled environmental chamber. One hour after the exposure, 99mTc-sulfur colloid was aerosolized throughout the nasal passage and counts were measured with a scintillation detector. Six out of 12 subjects showed more rapid clearance after smoke exposure than after air exposure, and 3/12 had rapid clearance on both days. However, substantial decreases in clearance occurred in 3/12 subjects, all of whom had a history of ETS rhinitis. In two subjects, more than 90% of the tracer remained 1 hr after tracer administration (2 hr after smoke exposure). Understanding the basis for biologic variability in the acute effect of tobacco smoke on NMC may advance our understanding of pathogenesis of chronic effects of ETS.     

Benzoquinones, a homoisoflavanone and other constitutents from Polygonatum alte-lobatum

From the rhizomes of Polygonatum alte-lobatum, two new homologous series of 1,4-benzoquinones, polygonaquinones A and B, a novel homoisoflavanone, a new gentrogenin glycoside and 13 known compounds were isolated and characterized. The structures of the new compounds were determined as two homologous series of three 2,5-dihydroxy-3-methyl-6-alkyl-1,4-benzoquinones and three 2-hydroxy-3-methyl-6-alkyl-1,4-benzoquinones, with chain lengths C21 to C23, and 4',5,7-trihydroxy-6,8-dimethylhomoisoflavanone and gentrogenin 3-O-beta-D-glucopyranosyl(1-->2)-[beta-D-xylopyranosyl(1-->3)] -beta-D-glucopyranosyl(1-->4)-beta-D-galactopyranoside.     

Expression of INK4 inhibitors of cyclin D-dependent kinases during mouse brain development

In situ hybridization of mouse embryo sections demonstrated expression of mRNAs encoding two polypeptide inhibitors (p18INK4c and p19INK4d) of cyclin D-dependent kinase (CDK) 4 and CDK6 in the central nervous system. No expression of two other INK4 members, p16INK4a and p15INK4b, was observed. The p19INK4d and p18INK4c proteins formed complexes with either CDK4 or CDK6 in a temporal pattern consistent with the results of in situ hybridization. Expression of INK4c was observed at embryonic day 13.5 in neuroepithelial zones of the developing brain, being restricted to dividing neuroblasts but absent from differentiating postmitotic neurons. In the neocortex, p18INK4c was expressed precisely at those developmental stages when neuroblasts switch from a symmetric to an asymmetric pattern of cell division with concomitant increases in their G1 interval. INK4d RNA was detected from embryonic day 11.5 onward, at higher levels than INK4c and with a distinctly different spatial and temporal pattern. Marked INK4d expression was seen in dorsal root ganglia, spinal cord, and focally throughout the brain, but primarily in postmitotic neurons. Neural expression of INK4d continued postnatally into adulthood in postmitotic cells of the dentate gyrus, the pyramidal layer of the hippocampus, and in discrete regions of the cerebral cortex, cerebellum, thalamus, and brainstem. Downregulation of p19INK4d in the dentate gyrus after kainic acid-induced seizures indicated that its expression could also be modified in nondividing cells by excitotoxic stress. Therefore, p19INK4d may contribute to maintaining the quiescent state, acting as a buffer to prevent reactivation of cyclin D-dependent kinases in terminally differentiated cells.     

Atrial fibrillation in Wolff-Parkinson-White syndrome. Development and therapy

In patients with Wolff-Parkinson-White syndrome the accessory pathway may participate in various tachyarrhythmias thereby influencing symptoms and prognosis. Atrial fibrillation occurs in 10 to 32% of patients and may have life-threatening consequences by precipitating ventricular fibrillation in patients with rapid conduction due to an accessory pathway with short anterograde refractory period (< 250 ms). Pathogenesis of atrial fibrillation in the WPW syndrome and therapeutic options are reviewed in this presentation. Spontaneous degeneration of atrioventricular reentrant tachycardia has been reported to represent the most frequent mode of initiation of atrial fibrillation during electrophysiologic study (up to 64% of episodes). Hemodynamic changes during tachycardia may lead to increased sympathetic tone, hypoxemia or increased tension of the atrial wall, thus, triggering atrial fibrillation. Induction of reentrant tachycardia during electrophysiologic study also has shown to be strongly correlated to its clinical prevalence and is inducible in up to 77% of patients with atrial fibrillation. The pathogenesis and high incidence of atrial fibrillation in patients with WPW syndrome is related to presence and functional properties of the accessory pathway. After surgical excision or catheter ablation more than 90% of patients are free of this arrhythmia. Anterograde conduction properties of the pathway appear to be more important than retrograde properties. High incidence of atrial fibrillation is related to short anterograde refractory periods, and of note, this arrhythmia is rare (3%) in patients with concealed pathways. With intracardiac recordings, Jackman et al. could demonstrate atrial fibrillation due to micro-reentry originating in accessory pathway networks.(ABSTRACT TRUNCATED AT 250 WORDS)     

Nutrition support affects the distribution and organ uptake of cachectin/tumor necrosis factor in rats

BACKGROUND: We have previously observed a potentiation of the metabolic response to cachectin/tumor necrosis factor (TNF) by total parenteral nutrition (TPN) but not in anorexic orally fed animals. We hypothesized that nutritional status might affect TNF clearance kinetics. METHODS: We compared the clearance of a bolus of labeled TNF in TPN-fed animals given sufficient nutrients to grow called weight-gaining rats (WGR) with those given 50% of the WGR called weight-losing rats (WLR) and with orally fed rats (OFR). Data were analyzed using a two-compartment open system model and by linear systems analysis. RESULTS: The data from both types of analysis indicator that although metabolic clearance was similar, WGR had a slower fractional TNF clearance rate (FCR) as well as a larger volume of distribution than WLR or OFR. Further analysis showed that an increased proportion of the total mass of TNF resided in a plasma-associated compartment in WGR compared with WLR and OFR. In addition, WGR had reduced uptake of labeled TNF by the kidney. CONCLUSION: The data suggest that nutrition support influences either the distribution of TNF or the FCR, resulting in a greater retention in the plasma-associated compartment with intact absolute removal rates. This study has important implications concerning the type of nutrition support provided to the critically ill patient because our data suggest that clinical states with increased circulating TNF levels may be adversely affected by currently available nutritional practices.     

Bovine IgG2a antibodies to Haemophilus somnus and allotype expression

AIMS/BACKGROUND: To characterise clinically a large kindred segregating retinitis pigmentosa and sensorineural hearing impairment in an autosomal dominant pattern and perform genetic linkage studies in this family. Extensive linkage analysis in this family had previously excluded the majority of loci shown to be involved in the aetiologies of RP, some other forms of inherited retinal degeneration, and inherited deafness. METHODS: Members of the family were subjected to detailed ophthalmic and audiological assessment. In addition, some family members underwent skeletal muscle biopsy, electromyography, and electrocardiography. Linkage analysis using anonymous microsatellite markers was performed on DNA samples from all living members of the pedigree. RESULTS: Patients in this kindred have a retinopathy typical of retinitis pigmentosa in addition to a hearing impairment. Those members of the pedigree examined demonstrated a subclinical myopathy, as evidence by abnormal skeletal muscle histology, electromyography, and electrocardiography. LOD scores of Zmax = 3.75 (theta = 0.10), Zmax = 3.41 (theta = 0.10), and Zmax = 3.25 (theta = 0.15) respectively were obtained with the markers D9S118, D9S121, and ASS, located on chromosome 9q34-qter, suggesting that the causative gene in this family may lie on the long arm (q) of chromosome 9. CONCLUSIONS: These data indicate that the gene responsible for the phenotype in this kindred is located on chromosome 9 q. These data, together with evidence that a murine deafness gene is located in a syntenic area of the mouse genome, should direct the research community to consider this area as a candidate region for retinopathy and/or deafness genes.