Reducing alcohol intake.

Alcohol is second in importance only to smoking as a proved cause of cancer. The risk associated with excessive alcohol consumption can be reduced by adopting national and local population based policies. The population approach is aimed at reducing the level of consumption across the whole population, which contains many modest drinkers. Underlying this approach is the fact that a larger proportion of the total morbidity and mortality attributed to alcohol in a population occurs in modest drinkers, even though individually they are at lower risk. This approach should be complemented by risk reduction initiatives in primary care, focused on high risk individuals. Several studies have shown the efficacy of brief interventions by general practitioners in patients with excessive alcohol consumption. Brief interventions, taking 5 to 10 minutes, use simple assessments to identify those at risk and provide information and advice. Evidence exists that general practitioners underuse opportunities to identify and advise patients about excessive drinking.     

The possible protective effect of cysteine during acute alcohol intoxication]

In the experimental conditions used, cysteine administered per os together with ethanol reduces the blood alcohol levels, but does not modify significantly the rate of alcohol oxidation. No effect of cysteine administration is however observed when ethanol is injected intraperitoneally. Cysteine addition in vitro enhances ethanol consumption by liver slices and reduces at the same time 14CO2 production from [2-14C] ethanol. This effect is only observed with a high cysteine/ethanol molar ratio. The changes in the blood alcohol level resulting from cysteine administration do not appear to result from such an interaction with ethanol oxidation, but seem to be due to a delayed ethanol absorption from the gastrointestinal tract.     

Association of paternal alcohol use with gestational age and birth weight.

Paternal alcohol use has been associated with a number of adverse reproductive outcomes in laboratory animals and there is one epidemiologic report of a detrimental effect on infant birth weight. To expand the epidemiologic evidence, data from the Child Health and Development Studies were analyzed. Data collected from the onset of prenatal care in 10,232 women enrolled in the Kaiser Foundation Health Plan and residing in the San Francisco East Bay area between June 1959 and September 1966 were available, including information on the mother's report of paternal alcohol consumption and a number of potential confounders. Pregnancy outcomes included preterm delivery (< 37 weeks completed gestation), moderately low birth weight (1,501-2,500 g), very low birth weight (< or = 1,500 g), small-for-gestational-age (< 10th percentile of weight for gestational age), and mean birth weight. Paternal alcohol use, analyzed in intervals from 0 to 2.0 or more drinks per day, showed no association with any of the outcomes of interest. Adjusted prevalence odds ratios ranged from 0.7 to 1.5, with no indication of a monotonic dose-response gradient. Mean birth weight was also virtually unrelated to paternal alcohol use. Compared with the earlier report, this population had a very modest level of alcohol consumption. Nonetheless, within the range that was studied there appears to be no association between paternal alcohol use and birth outcome.     

The effect of pregnancy on paternal skin allograft survival

Elucidation of maternal-fetal tolerance mechanisms clarifies the role of regulatory T cells (Treg) in transplant tolerance. This study aim to investigate the effect of pregnancy on paternal skin allograft survival. Flow cytometry techniques, mixed lymphocytes reaction (MLR), PCR, real-time PCR and skin transplantation were key methods. Treg increased significantly from 4.2% before pregnancy to peak at 6.8% day 8 after pregnancy. Both heme oxygenase-1 (HO-1) and indoleamine 2,3-dioxygenase (IDO) mRNA express high in placenta while low in spleen (P<0.05). Although Treg increased during pregnancy, and splenocytes from the pregnant mice showed lower MLR response toward the paternal stimulator, single time pregnancy showed no significant protective effect on paternal skin allograft survival in the tested condition.     

The possible mode of action of iproniazid. I. Differential luteolytic effect of iproniazid before and after the establishment of placental adolescence.

Iproniazid, a very specific monoamine oxidase inhibitor, at a dose level of 200 mg/kg body weight induced luteolysis and caused lysis of deciduomata as well as resorption of the established embryos. Exogenous replacement of prolactin, a most consistent stimulant of the endocrine functioning of corpus luteum, or progesterone absolutely reversed the adversity developed following iproniazid injection. Moreover, failure of iproniazid even at a higher dose level in the deviation of the normal sequence of pregnancy after the establishment of placental adolescence strongly tempting to suggest that iproniazid could only show its luteolytic effect when the hypothalamic-pituitary complex is exclusively involved in the maintennance of pregnancy.     

The esterases of Drosophila. I. The anodal esterases and their possible role in eclosion

The ontogeny of esterase activity was analyzed electrophoretically throughout the development of Drosophila pseudoobscura. The major adult enzyme form, Esterase 5, and several minor components, showed no important developmental variation. A group of several rapidly migrating (anodal) esterases, in contrast, accumulated maximum activity during late pupal stages, but was completely absent in newly emerged adults. This disappearance was not the result of some rapid inactivation, for subsequent to eclosion these enzymatic forms could be fully recovered from the discarded pupal case. Of the four additional Drosophila species examined, all but one displayed a similar pattern of ontogenesis. The possible role of these pupa-specific esterases is discussed.     

The effect of paternal investment on female fertility intention in South Korea

Life history theory views reproduction as an outcome of resource allocation. The allocation of resources such as parental investments of time, energy and material resources involves trade-offs between number of offspring and timing of reproduction. Within the framework of mammalian parental investment, the outstanding feature of human reproduction is the high level of paternal care. Although empirical evidence suggests that human paternal investment may have evolved as a reproductive strategy to reduce infant and child mortality rates, the effects of actual paternal investment, including allocating time to child care, on female reproductive decisions have received relatively little attention. We examined the trade-off from two perspectives using a representative sample of married South Korean women aged 20–44 in 2005 (n=977). First, paternal investment in domestic labor, including child care and housework, was expected to be associated with women's preference regarding future reproduction. Second, relative paternal investment was expected to increase women's preference for future reproduction, especially among employed women. We found that increased paternal investment in child care and housework remarkably enhanced women's intention to have a second child, especially among employed women. In addition, although family members provide a low percentage of child care in South Korea, such help is likely to be a useful resource for second childbirth among employed women. Somewhat expectedly, older age and longer time since first birth had negative effects on women's second-child intention. There is growing evidence that, in the lowest fertility societies, paternal investment may be an essential resource for promoting future reproductive behavior of women, especially employed women.     

Reexamination of paternal age effect in Down's syndrome

Summary The recent discovery that the extra chromosome in about 30% of cases of 47, trisomy 21 is of paternal origin has revived interest in the possibility of paternal age as a risk factor for a Down syndrome birth, independent of maternal age. Parental age distribution for 611 Down's syndrome 47,+21 cases was studied. The mean paternal age was 0.16 year greater than in the entire population of live births after controlling for maternal age. There was no evidence for a significant paternal age effect at the 0.05 level. For 242 of these Down's syndrome cases, control subjects were selected by rigidly matching in a systematic manner. Paternal age was the variable studied, with maternal age and time and place of birth controlled. There was no statistically significant association between paternal age and Down's syndrome. After adjustment for maternal age, these two studies were not consistent with an increase of paternal age in Down's syndrome.     

Reexamination of paternal age effect in Down's syndrome

Summary Paternal age distribution for 1279 cases of Down's syndrome born in 1952–1968 was compared with the corresponding distribution for the general population, corrected for the maternal age as well as for the year of birth of the patients. Although there was no difference in the mean paternal age, the two distributions differed significantly, largely due to the excess of fathers aged 55 years and over and to the deficit of those aged 40–44 years in the patients born to mothers aged 30 years and over. The overall pattern of the relative incidence of Down's syndrome with advancing paternal age, with maternal age controlled, seems consistent with the hypothesis proposed by Stene et al. (1977). It increased from 0.8 for fathers aged 20–24 years slowly up to 1.2 for those aged 45–49 years, though with an intermediate drop to 0.8 at the age of 40–44 years, and then sharply to 2.4 for those aged 55 years and over. This rising pattern of the relative incidence with paternal age was essentially the same for the patients born in 1952–1960 and for those born in 1961–1968, although the slope was less steep in the latter than in the former group.This paper is dedicated to Professor Heinrich Schade in honor of his 70th birthday     

No paternal effect on monozygotic twinning in the Swedish Twin Registry.

Previous research has provided evidence for a genetic effect in monozygotic twinning, indicated by an increased risk for monozygotic women to have monozygotic offspring. However, since the biological mechanism for this trait is unknown, it is not clear if there exists a paternal inheritance. In this study we investigated twin pregnancies in offspring born in 1941-1996 to male twins in the Swedish Twin Registry and population controls born in 1926-1980. In total 4,225,331 offspring, of which 89,286 were twins, were studied. There was neither an increase in the probability for monozygotic men to have like-sexed twin offspring risk ratio (RR = 0.95; 95% CI = 0.77-1.13) nor an increase in the estimated number of monozygotic twin births. Thus, there is no evidence for a paternal effect on monozygotic twinning, suggesting that the gene(s) increasing the liability for division of the embryo are expressed in the mother and not in the fertilised egg.     

The effect of alcohol on zinc absorption

Two methods of intestinal perfusion are described and used to study the effecs of alcohol on zinc absorption in the rat small intestine. The first method used perfusion of the lumen of the rat small intestinein situ without interruption of the vascular supply. During perfusion with a zinc-containing medium (with and without alcohol), alcohol was found to have no effect on net zinc uptake from the lumen of the intestine. However, there were significantly higher serum zinc concentrations recorded in the rats perfused wih the zinc and alcohol, 28.8 μmol/L, when compared with a group perfused without alcohol, 19.1 μmol/L (P < 0.01). The second method used simultaneous perfusion of the lumen of the rat small intestine, with constant-rate perfusion of the vascular bed with an artificial blood supply. In this experiment with a zinc-containing medium, with and without alcohol, there was no difference noted in zinc absorption from the lumen of the intestine, or release into the artificial blood supply. Therefore, in conclusion, alcohol does not appear to directly influence zinc absorption by the mucosal cells of the small intestine.     

Biogeochemistry of billabong sediments. I. The effect of macrophytes

SUMMARY.

• 1 We examined the effects of an emergent macrophyte (Eleocharis sphacelata R. Br., Cyperaceae) and a submerged macrophyte (Vallisneria gigantea Graeb., Hydrocharitaceae) on the biogeochemistry of the sediments of a billabong in south-eastern Australia.
• 2 Sediments from an E. sphacelata bed had significantly lower concentrations of exchangeable phosphorus than did sediments from a nearby bare area or a V. gigantea bed, but neither macrophyte had a measureable effect on their sediment's exchangeable ammonium content.
• 3 The redox potential in the upper 10cm of E. sphacelata sediments was about 100 mV higher than that of bare sediments, or of sediments colonized by V. gigantea.
• 4 There were few consistent differences between vegetated and bare sediments in terms of the activity of extracellular enzymes, such as α-amylase, protease, β-d glucosidase, lipase or alkaline phosphatase. Rates of alkaline phosphatase activity (235–306μmol (g dry wt)^?1 day^?1) were markedly higher than those commonly reported for sediments or soils.
• 5 Rates of gas release were higher from bare sediments (21–93 ml m^?2 h^?1) than from E. sphacelata or V. gigantea sediments (17–23 and 21-24ml m^?2 h^?1, respectively). Gas bubbles consisted mainly of methane (26–66%) and nitrogen (15–68%). Rates of methane ebullition varied from 5 to 60ml m^?2 h^?1.
• 6 In-vitro methanogenesis was most rapid in samples of the upper flocculent sediment. Methanogenesis was slower in V. gigantea sediments than in bare area or E. sphacelata sediments, but was markedly accelerated by additions of acetate and/or H₂/CO₂ in all sites.
• 7 Profiles of total extractable fatty acids and phospholipid fatty acids demonstrated that material derived from higher plants dominated the sediment organic matter in all sites. Bacteria were also a significant component of sediment organic matter, as fatty acids for which bacteria can be assumed the sole source accounted for 18–30% of total fatty acid content. Biomarkers for sulphate-reducing bacteria (Desulfobacter spp.) were detected, and for type II methanotrophic bacteria.

     

Influence of paternal age, smoking, and alcohol consumption on congenital anomalies

The potential effects of paternal exposures on fetal development are of great public and scientific concern, yet few epidemiologic studies have examined this association. Single live births from 1959 to 1966 among 14,685 Kaiser Foundation Health Plan members who participated in the Child Health and Development Studies were analyzed to assess the impact of paternal age, cigarette smoking, and alcohol consumption on the occurrence of birth defects in the offspring. Prevalence odds ratios for anomalies identified by age 5 were analyzed, contrasting exposed to unexposed fathers with adjustment for maternal age, race, education, smoking, and alcohol use. Advanced paternal age was associated with increased risk of preauricular cyst, nasal aplasia, cleft palate, hydrocephalus, pulmonic stenosis, urethral stenosis, and hemangioma. Father's cigarette smoking was more common among children with cleft lip +/- cleft palate, hydrocephalus, ventricular septal defect, and urethral stenosis. Alcohol use by the father was most positively related to the offspring's risk of ventricular septal defect. For both smoking and alcohol use, inverse associations were more common than positive associations. These data generally do not indicate strong or widespread associations between paternal attributes and birth defects. However, because of this study's imprecision, limited ability to isolate defects most likely to be of paternal origin, and the identification of several suggestive associations with age and smoking, further study of this issue would be of value.     

Rat liver alcohol dehydrogenase. I. Purification and characterization

Alcohol dehydrogenase was purified in 14 h from male Fischer-344 rat livers by differential centrifugation, (NH4)2SO4 precipitation, and chromatography over DEAE-Affi-Gel Blue, Affi-Gel Blue, and AMP-agarose. Following HPLC more than 240-fold purification was obtained. Under denaturing conditions, the enzyme migrated as a single protein band (Mr congruent to 40,000) on 10% sodium dodecyl sulfate-polyacrylamide gels. Under nondenaturing conditions, the protein eluted from an HPLC I-125 column as a symmetrical peak with a constant enzyme specific activity. When examined by analytical isoelectric focusing, two protein and two enzyme activity bands comigrated closely together (broad band) between pH 8.8 and 8.9. The pure enzyme showed pH optima for activity between 8.3 and 8.8 in buffers of 0.5 M Tris-HCl, 50 mM 2-(N-cyclohexylamino)ethanesulfonic acid (CHES), and 50 mM 3-(cyclohexylamino)-1-propanesulfonic acid (CAPS), and above pH 9.0 in 50 mM glycyl-glycine. Kinetic studies with the pure enzyme, in 0.5 M Tris-HCl under varying pH conditions, revealed three characteristic ionization constants for activity: 7.4 (pK1); 8.0-8.1 (pK2), and 9.1 (pK3). The latter two probably represent functional groups in the free enzyme; pK1 may represent a functional group in the enzyme-NAD+ complex. Pure enzyme also was used to determine kinetic constants at 37 degrees C in 0.5 M Tris-HCl buffer, pH 7.4 (I = 0.2). The values obtained were Vmax = 2.21 microM/min/mg enzyme, Km for ethanol = 0.156 mM, Km for NAD+ = 0.176 mM, and a dissociation constant for NAD+ = 0.306 mM. These values were used to extrapolate the forward rate of ethanol oxidation by alcohol dehydrogenase in vivo. At pH 7.4 and 10 mM ethanol, the rate was calculated to be 2.4 microM/min/g liver.