Pyridoxine Deficiency and Ethanol-induced Liver Injury

It has been suggested that pyridoxine deficiency may potentiate ethanol-induced liver injury. Our purpose was to clarify the effect of pyridoxine deficiency on ethanol-associated liver injury by comparing liver histology, serum liver enzymes, and the viability of cultured hepatocytes from pyridoxine-deficient and pyridoxine-sufficient rats that had been chronically fed ethanol-enriched diets. Our data fail to substantiate that pyridoxine-deficient animals are more susceptible to the hepatotoxic effects of ethanol than pair-fed pyridoxine-sufficient controls. Furthermore, the addition of pyridoxine to hepatocyte cultures fails to prevent in vitro cytotoxicity of added ethanol. Pyridoxine deficiency may augment ethanol-induced enhancement of hepatic urea synthesis. These data suggest that pyridoxine deficiency may contribute to the abnormal plasma amino acid profiles and nitrogen balance of chronic alcoholics, but that it does not potentiate ethanol-induced liver injury.     

Axonal transport of dopamine D1 receptors in the rat brain

Binding of a specific dopamine D₁ receptor antagonist,¹²⁵I-SCH 23982, was measured in rat brain sections by quantitative autoradiography at various time intervals, following a knife cut through the striatonigral pathway. Twenty-four hours after lesioning, accumulations of D₁ receptor binding sites were found in sagittal sections both rostral and caudal to the lesion site. No other regions studied (caudate-putamen, nucleus accumbens, olfactory tubercle, and substantia nigra pars reticulata) showed any change in D₁ receptor binding 24h after the lesion. In brain sections obtained 10 days after lesioning, only the substantia nigra pars reticulata had a significant decrease in D₁ receptors ipsilateral to the lesion. These findings suggest the possibility of a presence of bidirectional axonal transport of D₁ receptors in rat striatonigral pathway.     

Protein and fat utilization by humans as affected by calcium phosphate, calcium carbonate, and manganese gluconate supplements

The object of this study was to determine the effect of calcium carbonate or calcium phosphate supplements on dietary protein and fat utilization from low and high manganese diets. During the 63-day study, the 14 human adult subjects ate a constant laboratory controlled diet. In separate periods, subjects consumed the basal diet alone or with supplements of calcium carbonate, calcium carbonate plus manganese gluconate, calcium phosphate, or calcium phosphate plus manganese gluconate. Contrast analyses of data indicated that manganese gluconate supplementation of diets, when combined with either calcium phosphate or calcium carbonate, increased fecal losses of fat. When used as single supplements, both calcium phosphate and calcium carbonate depressed fecal fat loss in comparison with values when no supplements were used. Manganese gluconate supplements depressed fecal nitrogen losses calculated as a percentage of dry fecal weight.     

Genetic and environmental influences on cord blood serum IgE and on atopic sensitisation in infancy

It has recently been reported that cord blood serum IgE (CBsIgE) concentrations in a black Third-World cohort were significantly higher than those in a similar cohort of white and coloured newborns, and were not influenced by an atopic family history (aFH). This study reports on the 1-year follow-up of these newborns carried out to determine whether statistical differences in median CBsIgE values at birth could be found between infants in each ethnic group who subsequently developed clinical atopy in the first year of life and those who remained healthy. The infants were seen at 3, 7 and 12 months of age. At each visit a detailed history was taken from the mothers, the infants were examined clinically for the presence of atopic disease and blood was taken for immunological assay (total serum IgE by paper-disc radio-immunosorbent testing, and radio-allergosorbent testing for egg-white, cow's milk and Dermatophygoides pteronyssinus). A combination of clinical and immunological variables was assessed in order to categorise the infants into 'atopic' or 'not atopic' groups at the end of the 1-year follow-up period. The black infants who completed the study had the lowest incidence of aFH (16%), but 64% of them developed atopic disease during infancy. The median CBsIgE values for the black infants who became atopic were lower than, but not statistically different from, those for the group who remained non-atopic (P = 0.57). The white and coloured infants who completed the study had 81.6% and 30.4% incidences of aFH respectively, with 47.4% and 58.7% respectively developing atopic disease during infancy.(ABSTRACT TRUNCATED AT 250 WORDS)     

Development of bilateral asymmetry in sensory innervation to lobster claws

Sensory innervation to the paired claws of the lobster. Homarus americanus, was examined during their differentiation from a bilaterally symmetric state to an asymmetric state of a slender cutter and a stout crusher claw. This was done by estimating the total number and size distribution of axons in the second nerve root which provides most (approximately 90%) of the innervation to the claws and has few, bilaterally distributed motor axons. The paired claws which are undifferentiated and resemble each other in the 1st larval stage correspondingly have nerve roots that are bilaterally symmetric. In early juvenile (4th and 5th) stages when claw type is determined, as well as in subsequent (6th, 7th, 8th, 16th) juvenile stages when the claws gradually differentiate into cutter and crusher types, the paired homologous roots are also similar. It is only in adults that asymmetry in sensory innervation is seen with more axons in the crusher root than in its cutter counterpart. The difference in number of axons between the dimorphic claws is related to differences in surface area between the claws. Thus, bilateral asymmetry in sensory innervation is acquired by the continual but differential addition of axons to the paired claws.     

Epidemiological investigation of risk factors for campylobacter colonization in Norwegian broiler flocks.

An epidemiological investigation was conducted to identify risk factors related to hygiene and husbandry practices which determine the introduction of Campylobacter spp. into broiler chicken flocks. All 176 broiler farms in an area in southeastern Norway participated in the study. Each farm was represented by one flock selected at random during a one-year period. The flocks were examined for campylobacter colonization at slaughter, and the flock managers were subsequently interviewed about hygiene and husbandry practices. Campylobacter spp. were recovered from 32 (18%) of the flocks. The proportion of colonized flocks varied geographically and seasonally with a peak in the autumn. The following variables were found to be independently associated with an increased risk of campylobacter colonization using logistic regression analysis: (i) feeding the broilers undisinfected water (odds ratio (OR) = 3.42, P = 0.045), (ii) tending other poultry prior to entering the broiler house (OR = 6.43, P = 0.007), (iii) tending pigs before entering the house (OR = 4.86, P = 0.037), (iv) geographic region (Hedmark versus Ostfold county) (OR = 2.91, P = 0.023, (v) season (autumn versus other seasons) (OR = 3.43; P = 0.008). Presence of rats on the farm was associated with an increased risk, but this factor did not reach statistical significance (OR = 3.96, P = 0.083). Preventive measures should include disinfection of drinking water and strict hygienic routines when the farm workers enter the rearing room. The results indicate that disinfection of drinking water is the preventive measure most likely to have the greatest impact on the prevalence of campylobacter among broiler chicken flocks in the study area (population attributable fraction = 0.53).     

Concentration gradient of CSF monoamine metabolites in children and adolescents

Whether the lumbar cerebrospinal fluid (CSF) concentration gradient of monoamine metabolites found in adults is influenced by age or pubertal status was studied in 26 children ranging from 6.5 to 17.3 years of age. Homovanillic acid (HVA), 5-hydroxyindoleacetic acid (5-HIAA), and 3-methoxy-4-hydroxyphenylglycol (MHPG) were assayed by high-power liquid chromatography (HPLC) with electrochemical detection. Eight patients were prepubertal (Tanner stage I). The slopes in units of picomoles/milliliter/milliliter for regression lines for CSF monoamine metabolite concentrations versus milliliter of CSF collected were 5.07 +/- 0.65, 10.13 +/- 2.0, and 0.67 +/- 0.22 for 5-HIAA, HVA, and MHPG, respectively, for the group as a whole. Significant correlations with age, height, weight, or Tanner stage were not found for the HVA or MHPG concentration gradients. Tanner stage and 5-HIAA slope were significantly correlated. Three of eight prepubertal patients had nonsignificant 5-HIAA gradients. CSF studies in pediatric populations must control for aliquot collected, as the size of the gradient could produce differences sufficient to mimic a "positive" clinical study if the aliquots collected are not the same.