Barriers to smoking cessation initiatives for Medicaid clients in managed care.

In this paper, key barriers to providing smoking cessation services for low income individuals are illustrated using epidemiologic data from a population which was enrolled in a Medicaid managed care plan in Kansas during 1998. The Plan served 623 pregnant women who could potentially benefit from assistance in avoiding tobacco exposure. The prevalence of smoking among adult clients was 44.8%. twice the national average. Only 52.3% of adult smokers were advised by a provider to quit in the previous year. Most individuals in the client population (81.7% of the 10,733 members) were children, suggesting the importance of targeting environmental tobacco smoke exposure in order to reduce morbidity from asthma. The adult household member who needed smoking cessation services, however, was unlikely to qualify for health care benefits through Medicaid. The median length of enrollment was only 1.9 months, providing very little client contact time for tobacco control initiatives. The literature suggests that some providers may lack skills in treating tobacco as an addiction. It would be a major task for the managed care organization to train the 2,000 physicians in 68 of the 105 counties of Kansas who cared for this population. Potential solutions include improving reimbursement for smoking prevention and treatment, and developing cheaper smoking cessation services which are effective and acceptable among low-income individuals. The managed care organization could provide patient education materials and staff training for physicians and other members of the office staff.

Attitudes, values, beliefs, and practices surrounding end-of-life care in selected Kansas communities.

OBJECTIVE: This study was designed to better meet end-of-life care needs for patients and their families in rural Kansas communities. METHODS: Initially, statistical information indicated an underutilization of hospice services in rural communities. To evaluate the data, focus groups were conducted in targeted communities in order to determine attitudes, values, beliefs, and practices surrounding end-of-life care. A script was developed using established focus group protocols. Each focus group was recorded and the tapes were transcribed. Transcripts were reviewed and categorized for similarities and emerging key issues. RESULTS: Five major areas of concern were identified using this methodology. Major concerns were: (1) participants believed that control over decisions about care at the end of life is the patient's right; (2) while participants saw a need for advance directives, they avoided using them; (3) group participants believed that the patient's wishes should be given first priority and this was viewed as a patient's right; (4) there was an expressed lack of trust in the existing health care system and its providers; and (5) participants expressed more fear over the manner of death than death itself. They fear a technological death as opposed to a good death. CONCLUSIONS: The values most important to the group participants included: freedom and independence, trust, honesty, the right to information, and the importance of family. This information will be utilized in the development of programs and interventions to effect changes in end-of-life care, not only in Kansas, but also in areas with a comparable population.

An acute intratracheal selenium study: immediate effects on respiration in guinea pigs.

Pulmonary function was assessed in non-sensitized male guinea pigs (206-445 g) before and after intratracheal (ITr) treatment with saline or selenium (Se, 0.06 mg/100 g body weight) as selenium dioxide (SeO2) or seleno-L-methionine (SeM). Pulmonary functional parameters such as the respiratory rate (f), tidal volume (TV), dynamic lung compliance (Cdynl) and lung resistance (Rl) were determined using the respiratory flow (F) signal and the transpulmonary signal obtained via the intrapleural pressure (P) from the animal. Although, pulmonary dysfunction was observable with exposure to two different Se compounds, the SeO2-induced changes in f and Rl were significant (P < 0.05). Treatment with SeM did not result in alteration of any of the parameters significantly. Results indicated that acute ITr SeO2 exposure affects respiration precipitated by a significantly decreased f and an increased Rl unlike after SeM. The Cdynl did not change significantly after treatment with either of the two Se compounds. Comparing the immediate effects of the two different Se compounds on respiration, acute ITr SeO2 exposure was found to be more detrimental to pulmonary function than SeM.

Treating to meet NCEP-recommended LDL cholesterol concentrations with atorvastatin, fluvastatin, lovastatin, or simvastatin in patients with risk factors for coronary heart disease.

BACKGROUND: Our study compared use of atorvastatin, fluvastatin, lovastatin, and simvastatin for lowering low-density lipoprotein (LDL) cholesterol concentration in patients at risk for coronary heart disease (CHD). The goal was to reach the LDL cholesterol levels recommended by the National Cholesterol Education Program (NCEP). METHODS: A combined total of 344 men and women took part in this 54-week, multicenter, open-label, randomized, parallel-group, active-controlled, treat-to-target study. Patients were selected on the basis of their LDL cholesterol concentration and their risk for CHD. During treatment, doses were titrated at 12-week intervals to a maximum of 80 mg per day of atorvastatin and lovastatin, or 40 mg per day of fluvastatin and simvastatin, with colestipol added if necessary to attain the NCEP-recommended LDL cholesterol concentration. RESULTS: At the starting dose, atorvastatin decreased plasma LDL cholesterol significantly (P < .05) compared with the other reductase inhibitors, and the percentage of patients reaching target LDL cholesterol concentration at the starting dose was significantly greater in the atorvastatin group (P < .05). Overall, a significantly (P < .05) greater percentage (95%) of atorvastatin-treated patients achieved target LDL cholesterol concentration. The safety profile was similar among all reductase inhibitors tested. CONCLUSIONS: At the starting dose, a significantly (P < .05) greater percentage of atorvastatin-treated patients at risk for CHD reached the target LDL cholesterol concentration than patients with treated with other reductase inhibitors.

Guinea pig pulmonary mechanics: altered sensitivity to carbachol by cadmium and/or selenium.

Male Hartley guinea pigs (480-610 g) were treated intratracheally as follows: saline, cadmium (Cd, 0.3 mg), selenium (Se, 0.3 or 0.06 mg), or Se (0.06 mg) and Cd (0.3 mg) simultaneously. Selenium and Cd were administered as sodium selenite and cadmium chloride, respectively. Twenty-four h later, dynamic lung compliance (Cdyn) and pulmonary resistance (Rp) were measured before (baseline Cdyn and Rp) and after carbachol administration (0.0001, 0.001, 0.01, and 0.1 mumol/kg, intravenously). Results indicated a significant decrease in baseline Cdyn caused by 0.3 mg of Cd, 0.3 mg or 0.06 mg of Se, and 0.3 mg of Cd with 0.06 mg of Se (p < 0.05). A significant increase in baseline Rp due to 0.3 mg of Se was observed (p < 0.05). Carbachol decreased Cdyn significantly below baseline, evident after lower doses of carbachol, in guinea pigs pretreated with 0.3 mg of Se, whereas a significant improvement in Cdyn was seen after 0.0001 mumol/kg carbachol in the group pretreated with Se and Cd simultaneously (p < 0.05) compared with the respective baseline values of the saline-treated group. Similarly, a significant increase in Rp was observed after carbachol in groups pretreated with 0.3 mg of Cd or Se (p < 0.05). Results also indicated a significant increase in large airway constriction caused by Cd and/or Se (p < 0.05). A leftward shift in the carbachol dose-response curve indicated increased sensitivity to carbachol in Cd- and/or Sepretreated guinea pigs.

Cadmium and/or selenium effects on guinea pig lung PGE2, TXB2 and LTC4.

Male Hartley guinea pigs (480-610 g; n=5) were treated intratracheally with saline, cadmium (Cd, 0.3 mg) as cadmium chloride, selenium (Se, 0.3 or 0.06 mg) as sodium selenite or Se (0.06 mg) and Cd (0.3 mg). After 24 hours, lungs were collected and analyzed for prostaglandin (PGE2), thromboxane (TXB2) and leukotriene (LTC4) levels. Results indicated that, 0.3 mg Se and 0.06 mg Se in combination with 0.3 mg Cd increased PGE2 significantly. Selenium and Cd alone or in combination, decreased LTC4 and TXB2 significantly.

Selenium and cadmium induced pulmonary functional impairment and cytotoxicity.

Ovalbumin-sensitized (50 mg/kg, i.p.) male Hartley-guinea-pigs (550-610 g; n = 6) were treated 14 days later intratracheally with saline, cadmium (Cd 0.3 mg), selenium (Se 0.3 mg or 0.06 mg) or Se (0.06 mg) with Cd (0.3 mg). After 24 h, baseline dynamic-lung-compliance (Cdynl) and pulmonary-resistance (Rp), and percent change after ovalbumin-aerosol-challenge (10 mg/ml, 60 s) were assessed. Cadmium or Se (0.3 mg), Se (0.06 mg) and/or Cd (0.3 mg) decreased Cdynl (P < 0.05). Selenium (0.3 mg) increased Rp (P < 0.05). Ovalbumin-challenge decreased Cdynl and increased Rp in all groups. Analysis of bronchoalveolar-lavage-fluid (BALF) displayed increased activities of lactate-dehydrogenase (LDH), beta-glucuronidase (beta-G), alkaline-phosphatase (AP), and protein due to 0.3 mg Se, 0.3 mg Cd alone or with 0.06 mg Se (P < 0.05). Findings indicated that, 0.3 mg Se is more detrimental than 0.3 mg Cd to lung-dynamics despite a modest protection by 0.06 mg Se against Cd illustrated by an ameliorated Cdynl and lower protein in BALF.

Subacute exposure to cadmium chloride induces HSP-72 in rat liver.

Two groups of rats (n = 5) weighing 175-185 g were implanted (sc) with osmotic minipumps to deliver (0.5 microliter/hr) deionized water or cadmium chloride (CdCl2; 0.2 M) for 14 days. On completion of subacute treatment, liver and kidneys were collected from control and CdCl2 treated groups for analysis. We report that, subacute exposure to CdCl2 results in significant Cd accumulation in liver and kidneys, and heat-shock-protein 72 (HSP-72) induction in the liver. Results affirm a role for liver HSP-72 in Cd-toxicity.

Effect of selenium (Se) on plasma ACTH, beta-endorphin, corticosterone and glucose in rat: influence of adrenal enucleation and metyrapone pretreatment.

The effects of acute treatment (i.p.) with selenium (Se) on glucoregulation, by measuring plasma levels of adrenocorticotropic hormone (ACTH), beta-endorphin (beta-EN), corticosterone (CORT) and glucose over time, were investigated. The hormones of the hypothalamic-pituitary adrenal (HPA) axis, were measured after treating rats with saline, Se: 1.6 mg/kg, or 3.8 mg/kg. Blood samples were collected before, 30, 60 and 90 min following injection. The results show that i.p. administration of Se (both doses) induce a rise in plasma ACTH, and beta-EN (P < 0.01). Plasma CORT and glucose levels also rose sharply by 30 min (P < 0.05). Corticosterone levels were increased in a dose-dependent fashion over the ensuing hour. Bilateral adrenal demedullation resulted in the abolishment of the Se-induced rise in plasma glucose. Pretreatment with metyrapone (300 mg/kg) was found to delay the Se-induced rise in plasma glucose. The results indicate that after a Se challenge the HPA axis is activated. In addition, CORT was found to be essential in the Se-induced rise in plasma glucose.

Selenium lethality: role of glutathione and metallothionein.

Male Sprague-Dawley rats (200-300 g) were pretreated (i.p.) with diethylmaleate (DEM; 3.1 mmol/kg) or propylene glycol (PG). After 1 h, three PG and three DEM groups received saline or sodium selenite (Se: 0.8 or 1.6 mg/kg) i.p. Eighty to one hundred percent mortality occurred within 3 h after Se in DEM-pretreated groups. Except for one PG and one DEM group, which were sacrificed after 1 h, the remaining groups received saline or Se (1.6 mg/kg) 25 h after pretreatment. No mortality occurred within 3 h after Se. Liver and kidney GSH decreased at 1 h, while liver MT increased at 28 h. The changes are related to Se-induced lethality.

Effect of cadmium and/or selenium on liver mitochondria and rough endoplasmic reticulum in the rat.

This study was conducted to investigate the effect of cadmium (Cd) and/or selenium (Se) on hepatic mitochondria and rough endoplasmic reticulum (RER). Male Sprague Dawley derived rats (150-200 g) received sodium acetate (NaAc; 1.23 mg/kg), Cd (0.84 mg/kg), and/or Se (1.6 mg/kg) intraperitoneally. Livers were perfused with 2% glutaraldehyde at 48 h, 72 h, or 96 h after treatment and prepared for electronmicroscopy. Results indicate that Cd and/or Se are capable of inflicting mitochondrial and RER structural changes, and the damage by Cd alone is more severe than Se alone or with Cd.

Effect of selenium on plasma glucose of rats: role of insulin and glucocorticoids.

The effects of acute treatment (i.p.) of selenium (Se) on glucoregulation and on plasma levels of glucose, insulin and corticosterone were determined in both fed and 24-hour-fasted rats. In this experiment animals were treated with saline (control) or 1.3, 1.6 and 3.8 mg/kg doses of Se. Blood samples were collected before, 30, 60 and 90 min following injection. The results obtained show that acute intraperitoneal (i.p.) administration of Se (1.6 mg/kg or more) causes hyperglycemia in rats. It was found that Se does not change levels of plasma insulin in either fasted or fed animals. Se did, however, significantly increase the plasma levels of corticosterone in all Se-treated groups. In order to confirm the role of corticosterone and thus support the significance of adrenal glands in this hyperglycemic response, animals were subjected to bilateral adrenalectomy. Blood samples were collected before, 30, 60 and 90 min following intraperitoneal treatment with Se. The results indicate that bilateral adrenalectomy abolishes the hyperglycemic response to Se. It can be concluded that adrenal glands play a role in Se-induced hyperglycemia. The increase in corticosterone levels suggest the possibility of gluconeogenesis in contributing to this hyperglycemic response.

Effect of in vitro treatment of rat hepatocytes with selenium, and/or cadmium on cell viability, glucose output, and cellular glutathione.

The effects of cadmium as cadmium acetate and selenium as sodium selenite on glucose output, cell viability, and glutathione levels in rat hepatocytes were evaluated. Isolated hepatocytes (200 mg wet wt cells) derived from naive male Sprague--Dawley rats (210-260 g) were incubated at 37 degrees C, with sodium acetate (C2H3NaO2; NaAc) 12.5 microM, 6.3 microM, 3.2 microM; cadmium acetate (C4H6CdO4; Cd) 12.5 microM, 6.3 microM, 3.2 microM; sodium selenite (Na2SeO3; Se) 25 microM, 12.5 microM, 6.3 microM; or Se (6.3 microM) and Cd (3.2 microM). After an incubation period of 2 h, glucose output, cell viability, and reduced glutathione (GSH) levels were determined. The results obtained indicate that incubation of hepatocytes with Se (12.5 or 25 microM) or Cd (3.2, 6.3, or 12.5 microM) resulted in a significant decrease in glucose output, cell viability, and glutathione levels (P less than 0.05) when compared to those incubated with NaAc (control). Selenium in concentrations of 6.3 microM decreased glutathione levels and cell viability only. The damaging effects induced by Cd on hepatocytes were significantly greater than those induced by Se. The decrease in glutathione levels observed following Cd treatment was considerably lowered when Se was concurrently added to the incubation medium. These findings suggest that Se may in part protect against the deleterious effects of Cd on hepatocytes.

Effect of cadmium on blood glucose level in the rat.

The purpose of this study was to determine the effect of cadmium (Cd) or Cd and selenium (Se) administered simultaneously on plasma glucose level. Male Sprague-Dawley derived rats (180-300 g), maintained under controlled environmental conditions, were segregated into fed and 24-h fasted groups prior to experimentation. Each group consisted of 3 subgroups which received one of the following treatments intraperitoneally: sodium acetate (NaAc) (1.23 mg/kg), Cd (0.84 mg/kg) or a combination of Se and Cd (1.6 and 0.84 mg/kg respectively). Plasma glucose was measured before and 30, 60, 120, 180, 240, 300 or 360 min after treatment. Results indicate that both Cd and concurrent administration of Se and Cd induce hyperglycemia in fed and fasted rats.

Acute effects of cadmium and selenium on glucose output from rat liver hepatocytes using various gluconeogenic precursors.

Male Sprague-Dawley rats (250-310 g) fasted for 24 h were injected i.p. with either sodium acetate (C2H3NaO2; 1.23 mg/kg, 15 mumol/kg), cadmium acetate (C4H6CdO4; 0.84 mg/kg, 3.6 mumol/kg), sodium selenite (Na2SeO3; 1.6 mg/kg, 9.2 mumol/kg) or cadmium acetate (0.84 mg/kg, 3.6 mumol/kg) and sodium selenite (1.6 mg/kg, 9.2 mumol/kg) simultaneously. Rats were sacrificed 180 min post-treatment and hepatocytes were isolated. An average of 85% cell viability was achieved. Hepatocyte suspension (50 mg cell wt/ml, 1 ml/tube) was incubated for 180 min at 37 degrees/C with 10 mM of one of the following substrates: beta-D(-)fructose, glycerol, DL-alanine, L(+)lactic acid or pyruvic acid. Glucose concentration of the supernatant was measured by a colorimetric method. Cadmium decreased glucose output significantly (P less than 0.05), when lactic acid or alanine was used as substrate, but did significantly (P less than 0.05) increase the output when pyruvic acid, glycerol or fructose was used. Selenium alone significantly increased (P less than 0.05) hepatic glucose output only when fructose was used as substrate. Selenium and cadmium concurrently administered significantly increased (P less than 0.05) hepatic glucose output when pyruvic acid, glycerol or fructose was used as substrate as compared to sodium acetate (control), cadmium or selenium alone. These findings suggest that cadmium and selenium affect the hepatic gluconeogenic pathway and that their effects depend on the gluconeogenic precursor used.

Effect of acute and repeated selenium treatment on hepatic monooxygenase enzyme activity in male rats.

The effect of sodium selenite administered acutely or repeatedly on the biochemical components of the hepatic microsomal monooxygenase enzyme system was examined in male rats. 72 h following acute administration of selenium (2.4 mg Se/kg, i.p.), there was a significant decrease in ethylmorphine-N-demethylase activity and cytochrome P-450 levels but no change in aniline hydroxylase or NADPH cytochrome c reductase activity. Following repeated administration of selenite in the drinking water (1, 2, or 4 ppm Se) for 30 days, there was no alteration in any of the parameters measured. Following the in vitro additions of selenite to microsomes obtained from untreated rats, ethylmorphine-N-demethylase and aniline hydroxylase activities were inhibited at selenium concentrations of 10(-4) M or greater, but the inhibition achieved was less than 50%. No alterations in cytochrome P-450 levels were observed. These results indicate that selenium is a rather weak, indirect, and substrate-specific inhibitor of the hepatic monooxygenase enzyme system.

Effect of glutathione depletion on selenium lethality and hepatic drug metabolism in male rats.

Pretreatment of male rats with diethylmaleate (DEM) (3.1 mmol/kg) markedly decreased the levels of reduced glutathione in both liver (81%) and kidney (44%). Acute lethality produced by sodium selenite (0.4 to 2.4 mg Se/kg) was greatly enhanced in DEM-treated rats; however, no alterations in hepatic drug metabolism by selenium were observed.

Field observations on serological responses to vaccine strains of infectious bronchitis virus administered by coarse spray and via the drinking water.

The agar gel precipitin (AGP) and haemagglutination inhibition (HI) responses to vaccination with infectious bronchitis virus (IBV) were investigated in three flocks. The vaccines were administered by coarse spray in one large flock of commercial layers and via the drinking water in two smaller flocks of broiler breeders. In two flocks, one vaccinated by coarse spray and one vaccinated via the drinking water, the chicks had high levels of maternal antibody and failed to respond serologically to the primary vaccination at 2 to 3 weeks of age. However, a vigorous antibody response, probably due to cycling vaccine virus, was demonstrated at 6 to 7 weeks of age after the maternal antibodies had waned. By contrast the chicks in the third flock, with low levels of maternal antibody at 2 weeks, responded promptly and vigorously to the primary vaccination. Passive immunity, mediated by maternal antibodies, was thought to have inhibited the initial AGP and HI responses to vaccine in the first two flocks. Between 10 and 20 weeks, in spite of repeated vaccination, the IBV geometric mean HI titres did not increase and the number of AGP-positive sera remained low. In the densely populated group receiving the coarse spray, the AGP response was virtually absent and in those smaller groups of birds receiving water-borne vaccine only 33% became AGP-positive. As in the young chicks with passive immunity, active immunity in the older birds, associated either with deliberate vaccination or inadvertent cycling vaccine virus, was thought to have inhibited the serological responses to the second and third exposures to vaccine. There was a marked rise in the number of AGP-positive birds (84% and 68% respectively) at 25 weeks of age in two flocks. HI test results indicated that this was due to exposure to a field strain of IBV in one flock and to a cycling vaccine strain in the other. The AGP results at this time were similar in both of these flocks and this test could not be used to differentiate the responses to the different types of IBV. Only 25% of the sera were AGP-positive at 25 and 30 weeks in the third flock and therefore in such a flock any sudden rise to above 50% in the number of AGP-positive birds might be attributed to recent exposure to field or vaccine strains of IBV.