Comparison of six-month outcome of coronary artery stenting in patients <65, 65-75, and >75 years of age

We studied 1,238 patients receiving 1,880 coronary stents. In-hospital outcomes were divided by age into <65 years (n = 747, group 1), 65 to 75 years (n = 326, group 2), and >75 years (n = 165, group 3). Procedural success was 97.2%, 95.1%, and 98.8% in groups 1, 2, and 3, respectively (p = NS). There was 1 death (group 1). Myocardial infarction occurred in 1.2%, 2.8%, and 1.8%, bypass surgery occurred in 0.9%, 1.8%, and 1.2%, and repeat balloon angioplasty in 0.3%, 0.6%, and 0% of patients in groups 1, 2, and 3, respectively (p = NS for all comparisons). Vascular complications occurred in 2.8%, 4.9%, and 6.1% in groups 1, 2, and 3, respectively (p <0.05). Six-month follow-up of patients was divided by age: <65 years (n = 564, group 1); 65 to 75 years (n = 221, group 2); and >75 years (n = 122, group 3). Event-free survival was 94.5%, 90.5%, and 89.3% for groups 1, 2, and 3, respectively (p = NS). Death occurred in 0.4%, 0.5%, and 1.6%; myocardial infarction occurred in 1.2%, 2.3%, and 1.6%, and target vessel revascularization in 4.3%, 8.6%, and 7.4% for groups 1, 2, and 3, respectively (p = NS for all comparisons). Thus, coronary stenting produced favorable in-hospital and 6-month outcomes in all 3 age groups. Age itself should not preclude patients from undergoing coronary stenting.     

Review of autologous and allogeneic blood transfusion practices in patients undergoing radical hysterectomy

We investigated the short-term recuperation of bone mass during skeletal reloading after a period of unloading in young rats. One hind limb of 4-week-old rats was either unloaded irreversibly by sciatic neurectomy, or unloaded reversibly by external fixation. Other animals were sham-operated. After 9 days, the fixation-unloaded limbs were reloaded for 1-3 weeks and were compared with the hind limbs of age-matched unloaded (neurectomized) and sham-operated controls. Cortical and cancellous bone mass was measured using ashing and histomorphometry. Cortical bone mass (expressed as femoral dry and ash weight and tibial cortical bone area) was reduced in both unloaded groups and was accompanied by production of hypomineralized bone, as shown by a reduction in the percent ash of the dry weight. Cancellous bone mass (expressed as bone area and surface at the tibial metaphysis) was also reduced in both unloaded groups. Cortical bone mass deficit was greater in the fixation group than in the neurectomy group. Thereafter it increased in the neurectomy group despite a normal longitudinal growth rate, but returned to age-matched values in the reloaded group by 3 weeks. The changes in tibial cancellous bone mass were more pronounced but followed a similar pattern and normalized by 2 weeks. These data demonstrate that total unloading produced by external fixation causes a greater degree of bone mass deficit than partial unloading (produced by neurectomy); the rate of bone loss during unloading in the rat hind limb is more rapid than its recovery during reloading; and cancellous bone recuperates during the reloading phase faster than does cortical bone.     

Reliability and validity of a self-efficacy instrument for protective sexual behaviors

Alzheimer's disease (AD) is one of the most frequent causes of dementia in the aged. The elucidation of the pathomechanisms of this neurodegenerative disease with age, as the only risk factor for the majority of cases, is in the centre of the efforts of molecular and cellular neurobiology in preclinical research. Various findings point to the involvement of the amyloid beta protein (A beta) in the pathogenesis and progression of AD. Precipitated A beta aggregates are found in the brain of AD patients post mortem in the so-called plaques, a major histopathological hallmark of this progressive destructive disease. A beta can be toxic to cultivated neuronal cells only in its aggregated fibril form. After interaction with the neuronal cell membrane, these aggregates can induce intracellular oxidative events and can lead to the release of so-called free radicals. This is just one important finding for the involvement of oxidative events in the nerve cell degeneration in AD supporting the oxidative stress hypothesis. Furthermore, different neurochemical methods revealed many additional traits and scars of oxidative reactions in the brain of AD patients. Inflammatory events also seem to take part in the generation of an oxidative environment and therefore in nerve cell death as well. In addition, various age-dependent pathophysiological changes can increase neuronal vulnerability. Different antioxidants can protect cultivated neurons against A beta toxicity, but also against other oxidative stressors relevant to the disease. Besides the classical lipophilic antioxidant vitamin E, the female sex hormone oestrogen could also play an important neuroprotective role as an antioxidant, as was shown recently. Oestrogen, oestrogen derivatives, but also other potential free radical scavengers could block the accumulation of oxidative events on the long run and could, therefore, possibly slow down or prevent progressive nerve cell death of AD, which occurs over decades. If future clinical trials using antioxidants as neuroprotectants in AD would also support the oxidative stress hypothesis of the aetiopathogenesis of AD, antioxidants identified in the laboratory could then find their way more and more into the clinical treatment of Alzheimer's dementia.     

Consequences of prolonged inhalation of ozone on F344/N rats: collaborative studies. Part XIII. A comparison of changes in the tracheobronchial epithelium and pulmonary acinus in male rats at 3 and 20 months

A limitation of the NTP/HEI Collaborative Ozone Project conducted with F344/N rats at the Battelle Pacific North-west Laboratories in Richland, WA (1991-1993) was that the study used only one time point (20 months) to examine the chronic effects of exposure to ozone. Issues the design of that study could not address were (1) the status of cellular differentiation at earlier time points during the course of ozone exposure; (2) whether changes that appeared to be compensatory after 20 months of exposure were due to ozone, or were aspects of the natural aging process in rats; (3) the inability to define adequately which effects were related specifically to the prolonged duration of exposure; and (4) how and what changes brought about by the natural aging process may have overridden or confounded a clear definition of the effects of exposure to ozone at ambient concentrations (e.g., 0.12 parts per million [ppm]), which are of most concern with long-term exposure to this pollutant. The present study examined the effects of a 3-month exposure to ozone under conditions identical to those of the 20-month NTP/HEI Collaborative Ozone Project. In our facilities at the University of California, Davis, we exposed 42 male F344/N rats to either filtered air or 0.12 or 1.0 ppm ozone. After 3 months of exposure to 1.0 ppm ozone, changes in the distribution of superoxide dismutase (SOD) in the copper-zinc (Cu-Zn) form were shown by a pattern of reduced staining in terminal bronchioles and the centriacinar region; and the manganese (Mn) form of SOD was elevated within the centriacinar region. Further analysis by transmission electron microscopy and immunogold labeling confirmed that Mn SOD was elevated within epithelial type II cells immediately distal to the bronchiole-alveolar duct, junction (BADJ). The trachea, three major bronchi, and a short-length and long-length airway path relative to the trachea were examined by morphometric techniques. The pulmonary acini arising from each of these two paths were also examined morphometrically as a function of distance into the alveolar duct. Cellular changes occurring in each of these anatomical regions after 3 months of exposure were analyzed and compared to the changes noted after the 20-month ozone exposures. We found significant increases in the volume density of nonciliated epithelial cells lining the trachea and caudal bronchi as well as in the proximal and terminal bronchioles of the cranial region at a concentration of 1.0 ppm ozone after both 3 and 20 months of exposure. Remodeling of the centriacinar region, particularly within the cranial region of the lungs after exposure to 1.0 ppm ozone, was statistically significant at both 3 and 20 months. No statistically significant effects were noted following exposure to 0.12 ppm ozone for either 3 or 20 months. An important finding was that age did not influence the effect of ozone on the lungs of rats. We conclude that long-term exposure to ozone, rather than the effects of aging, lead to significant alterations of epithelial cell populations lining the airways and centriacinar region of the lung. Marked cellular changes were noted after exposure to 1.0 ppm ozone, but not to 0.12 ppm.     

Inhibitors of sterol synthesis. Chemical synthesis of 7 alpha-ethyl and 16 alpha-ethyl derivatives of delta 8(14)-15-oxygenated sterols and their effects on 3-hydroxy-3-methylglutaryl coenzyme A reductase in CHO-K1 cells

Three-dimensional data representing biological structures can be derived using several methods, including serial section reconstruction, optical sectioning, and tomography. The investigation, comprehension, and communication of structural relationships to others is greatly facilitated by computer-based visualization procedures. We describe SYNU, a suite of programs developed for interactive investigation of three-dimensional structure and for the production of high-quality three-dimensional images and animations. We illustrate the capabilities of SYNU in applications to biological data obtained by confocal light microscopy, serial section, and high-resolution electron microscopy from investigations at the cellular, subcellular, and molecular levels.     

Multidisciplinary care in the management of childhood cancer

Curing the child with cancer at the least cost in terms of short- and long-term morbidity remains a major challenge in paediatric medicine. The effective use of high doses of chemotherapy requires supportive care involving many disciplines. This review considers the interactions between the various groups involved in both early and late care of these patients.     

Effect of environmental tobacco smoke on LDL accumulation in the artery wall

BACKGROUND: Previous research has shown that exposure to environmental tobacco smoke (ETS) increases the risk of atherosclerosis. To test the hypothesis that exposure to ETS increases LDL accumulation in the artery wall, we developed a model to measure the rate of LDL accumulation in individually perfused rat carotid arteries after the artery had been perfused with plasma taken from rats exposed to ETS (ETS-plasma). METHODS AND RESULTS: Rats were exposed to ETS in a chamber in which steady-state sidestream smoke was continuously circulating. After exposure, blood from the animals was collected. Carotid arteries from unexposed rats were perfused first with normal plasma containing fluorescently labeled LDL. Then the same arteries (10 arteries from five rats) were perfused with ETS-plasma plus fluorescently labeled LDL. Photometric measurements were made during perfusion of the arteries with fluorescently labeled LDL, and rate of LDL accumulation (mV/min) and lumen volume (mV) (volume of fluorescently labeled LDL solution) were determined. Perfusion with ETS-plasma increased the rate of LDL accumulation (mean +/- SEM, 6.9 +/- 1.8 mV/min) compared with control (1.6 +/- 0.40 mV/min, P < or = .02). LDL accumulation was primarily dependent on LDL interaction with ETS-plasma rather than the interaction of ETS-plasma with the artery wall. Also, ETS-plasma significantly increased lumen volume (43.3 +/- 5.1 mV) compared with control (35.1 +/- 4.4 mV, P < or = .005). CONCLUSIONS: Exposure to ETS acutely increased LDL accumulation in perfused arteries. Repeated exposure to ETS may represent important early events in atherogenesis.     

The effect of carbohydrate source on nitrogen capture in dairy cows on pasture

The objective of this study was to determine if feeding carbohydrate supplements with faster degradation rates than corn to dairy cows grazing ryegrass would improve nitrogen capture, milk production, and components. Treatments were grain supplements based on: 1) corn (CORN), 2) barley and molasses (BM), or 3) citrus pulp and molasses (CM). For BM and CM, the diet composition was the same as that of CORN except that a portion of the corn was replaced with barley and molasses or citrus pulp and molasses, respectively, on a dry matter basis. Cows grazed ryegrass (Lolium multiflorum Lam.) pasture. Yield of milk, 3.5% fat-corrected milk, energy-corrected milk, and milk fat, as well as milk fat percentage, were not different among treatments. True milk protein percentage was higher for CORN (2.81%) compared with CM (2.70%), but was not different for BM (2.77%). However, true milk protein yield was not different among treatments. Milk urea N was higher for BM (11.43 mg/dL) compared with both CORN and CM (average: 9.95 mg/dL). There were no differences among CORN, BM, and CM treatments for overall BUN (average: 10.60 mg/dL). At 0400 h, however, cows on CORN had higher BUN than cows on CM (11.43 vs. 9.96 mg/dL), but there were no differences between CORN and BM (average: 11.21 mg/dL) or BM and CM (average: 10.48 mg/dL), and there were no differences among treatments at other time points. The CM diet might have shown more advantage if the pasture crude protein content was higher. Partial replacement of corn with citrus pulp for grazing cows should be further studied using pasture with higher crude protein content. Although cows receiving CM and BM did not produce more milk than cows on CORN, if barley or citrus pulp is less expensive than corn, they may be viable replacements for a portion of the corn supplement for grazing cows.