Smoking and mental illness: A population-based prevalence study.

CONTEXT: Studies of selected groups of persons with mental illness, such as those who are institutionalized or seen in mental health clinics, have reported rates of smoking to be higher than in persons without mental illness. However, recent population-based, nationally representative data are lacking. OBJECTIVE: To assess rates of smoking and tobacco cessation in adults, with and without mental illness. DESIGN, SETTING, AND PARTICIPANTS: Analysis of data on 4411 respondents aged 15 to 54 years from the National Comorbidity Survey, a nationally representative multistage probability survey conducted from 1991 to 1992. MAIN OUTCOME MEASURES: Rates of smoking and tobacco cessation according to the number and type of psychiatric diagnoses, assessed by a modified version of the Composite International Diagnostic Interview. RESULTS: Current smoking rates for respondents with no mental illness, lifetime mental illness, and past-month mental illness were 22.5%, 34.8%, and 41.0%, respectively. Lifetime smoking rates were 39.1%, 55.3%, and 59.0%, respectively (P<.001 for all comparisons). Smokers with any history of mental illness had a self-reported quit rate of 37.1% (P =.04), and smokers with past-month mental illness had a self-reported quit rate of 30. 5% (P<.001) compared with smokers without mental illness (42.5%). Odds ratios for current and lifetime smoking in respondents with mental illness in the past month vs respondents without mental illness, adjusted for age, sex, and region of the country, were 2.7 (95% confidence interval [CI], 2.3-3.1) and 2.7 (95% CI, 2.4-3.2), respectively. Persons with a mental disorder in the past month consumed approximately 44.3% of cigarettes smoked by this nationally representative sample. CONCLUSIONS: Persons with mental illness are about twice as likely to smoke as other persons but have substantial quit rates. JAMA. 2000;284:2606-2610.

Oxaprozin-induced fulminant hepatitis.

OBJECTIVE: To report oxaprozin-induced fulminant hepatic failure. CASE SUMMARY: A 56-year-old woman was admitted with fulminant hepatic failure. Work-up for potential etiologies was negative except for the use of oxaprozin for the preceding two months. Results of premortem liver biopsy were consistent with drug-induced hepatic injury similar to that previously reported with diclofenac. DISCUSSION: Although the literature describes elevation in hepatic transaminase concentrations associated with oxaprozin, fulminant hepatic failure has not been described previously. CONCLUSIONS: Elevations in hepatic transaminase concentrations and now fulminant hepatic failure have been shown to occur with oxaprozin, as previously seen with other nonsteroidal antiinflammatory drugs (NSAIDs). Transaminitis is a known adverse effect of NSAID use, but is usually mild and reversible with discontinuation of drug. Transaminitis may be more likely to occur in the elderly, in patients receiving concurrent potentially hepatotoxic medications, and possibly with the newer long-acting NSAIDs. The existence of fulminant hepatitis, although rare, supports the need for monitoring liver function enzymes during NSAID therapy.

Relationships between acid-base balance, serum composition and colostrum absorption in newborn calves.

Twenty-seven newborn Holstein bull calves were bottle-fed 2 litres of pooled colostrum which had been stored at -20 degrees C. Blood gas analysis before feeding showed a partially compensated respiratory acidosis in most of the calves, although they all appeared to be clinically normal. Mean venous blood pH was 7.346, carbon dioxide tension (PCO2) was 57.5 mmHg (7.6 kPa), bicarbonate was 30.6 mmol/l and base excess was 3.82 mmol/l. Mean serum IgG1 increased to 8.1 g/l after feeding colostrum. Several significant positive correlations were observed between post-absorptive serum protein, IgG1, IgM, gamma-glutamyltransferase (gamma GT) and D-xylose. Calves with either low serum albumin, high serum CK or low serum gamma GT before feeding tended to have less absorption of colostral protein. It was concluded that reduced absorption of IgG1 from colostrum is associated with hypercapnia in apparently healthy newborn calves.

Serum enzyme changes in newborn calves fed colostrum.

In 10 newborn Holstein calves, which were initially bottle-fed on pooled colostrum, there were transient increases in several serum enzymes. Within a few hours, the mean serum gamma-glutamyl transferase (gammaGT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), acid phosphatase (ACP), and lactate dehydrogenase (LDH) activities increased 62.5, 2.4, 2.0, 1.8 and 1.3 fold, respectively. In two other calves given initial feeds of enzyme-free pasteurized milk, there were similar increases in serum enzymes, except serum gammaGT. Correct interpretation of serum enzyme activities in newborn calves must take into account the normal increases which occur after feeding colostrum. Serum gammaGT was the only enzyme to increase markedly as a result of its absorption from colostrum. The other serum enzymes are presumably released from the tissues of the calf. The increased activities of serum CK observed in some newborn calves probably resulted from trauma during birth or increased muscular activity after birth.

Computer model of the absorption and distribution of colostral immunoglobulins in the newborn calf.

The transfer of immunoglobulin (Ig) isotypes (IgG1, IgG2, IgM), gamma-glutamyl transpeptidase (gamma-GT) and added D-xylose from colostrum to serum was investigated in newborn Holstein bull calves. Significant differences were observed in the time courses of the serum concentrations of these colostrum constituents following absorption from pooled colostrum. A computer model was devised to simulate the process of absorption of Ig isotypes, gamma-GT and D-xylose from colostrum in the newborn calf. A Fortran program was used to generate plots of the time course of the concentration of colostrum constituents in serum and other body fluids following a single feed of colostrum. These plots show how the changes in serum concentration of absorbed Ig isotypes, gamma-GT and D-xylose are affected by different rates of intestinal absorption, redistribution in body fluids and removal from plasma. A critical examination of data from the computer model and from the calf feeding experiments supports the view that the absorption of IgG1, IgG2 and IgM is not selective in the calf. The data were compared with earlier studies of the efficiency of the colostral transfer of Ig to the calf. In the present study the transfer efficiencies of IgG1, IgG2, IgM, gamma-GT and D-xylose were 46 per cent, 49 per cent, 47 per cent, 18 per cent and 21 per cent, respectively.

Ethanol-induced inhibition of chick brain growth.

Retarded fetal brain growth is associated with a high incidence of mental retardation among the offspring of chronic alcoholic mothers. Research using an embryonic chick model suggests that ethanol exposure suppresses fetal development including suppression of brain growth. Total brain cyclic AMP content and endogenous brain protein kinase specific activity are not altered by ethanol; however, ethanol exposure does significantly stimulate kinase catalytic activity measured in the presence of saturating amounts of exogenous cyclic AMP.

The interpretation of serum biochemistry test results in domestic animals.

The interpretation of serum biochemistry tests used in the investigation of disease was reviewed. Different methods of calculating reference ranges for biochemical constituents of serum were discussed. Reference ranges in current laboratory use were analyzed statistically to produce means and coefficients of variation.

The molecular mechanism of fetal alcohol syndrome (FAS). I. Ethanol-induced growth suppression.

Of the birth defects associated with alcohol consumption during pregnancy, in situ growth retardation resulting in neonates that are small for gestational age is the most common observation in both humans and animal models. A variety of alcohol-induced alterations in maternal, placental and/or fetal physiology have been proposed as the basis for this retarded fetal growth. The molecular mechanism(s) of this retardation, however, is obscure; and it remains to be determined whether the growth suppression is the result of the action of ethanol or its metabolites on embryonic, maternal or placental tissue. Using the embryonic chick as a model which circumvents changes in maternal and placental function, we have measured ethanol-induced growth suppression as a function of embryonic age and ethanol dosage. The data suggest that ethanol per se suppresses the rate of cell division in embryonic tissue resulting in fewer cells/embryo for a given time of gestation. The suppression of cell division is proportional to the ethanol dose and appears to be related to ethanol-induced changes in the metabolism of the prostaglandin hormones and resulting changes in the cyclic-AMP levels of the developing embryos.

The mechanisms relating to increases in plasma enzymes and isoenzymes in diseases of animals.

Changes in plasma or serum enzymes and isoenzymes are useful indicators of tissue damage in many diseases. Enzyme increases are usually related to leakage of enzymes from damaged cells. The amount of increase depends on factors such as the concentration of enzyme in the cells, the rate of leakage of enzyme from cells and the rate of clearance of enzyme from plasma. There are important species variations in the tissue concentrations and plasma clearance rates of enzymes and isoenzymes.