F is an important trace element for bones and teeth. The protective effect of F against dental caries is well established. Urine is the prime vehicle for the excretion of F from the body; however, the relationship between F intake and excretion is complex: the derived fractional urinary F excretion (FUFE) aids understanding of this in different age groups. The present study aimed to investigate the relationships between (1) total daily F intake (TDFI) and daily urinary F excretion (DUFE), and (2) TDFI and FUFE in 6–7-year-olds, recruited in low-F and naturally fluoridated (natural-F) areas in north-east England. TDFI from diet and toothbrushing and DUFE were assessed through F analysis of duplicate dietary plate, toothbrushing expectorate and urine samples using a F-ion-selective electrode. FUFE was calculated as the ratio between DUFE and TDFI. Pearson's correlation and regression analysis were used to investigate the relationship between TDFI and FUFE. A group of thirty-three children completed the study; twenty-one receiving low-F water (0·30 mg F/l) and twelve receiving natural-F water (1·06 mg F/l) at school. The mean TDFI was 0·076 ( sd 0·038) and 0·038 ( sd 0·027) mg/kg per d for the natural-F and low-F groups, respectively. The mean DUFE was 0·017 ( sd 0·007) and 0·012 ( sd 0·006) mg/kg per d for the natural-F and low-F groups, respectively. FUFE was lower in the natural-F group (30 %) compared with the low-F group (40 %). Pearson's correlation coefficient for (1) TDFI and DUFE was +0·22 ( P = 0·22) and for (2) TDFI and FUFE was − 0·63 ( P < 0·001). In conclusion, there was no correlation between TDFI and DUFE. However, there was a statistically significant negative correlation between FUFE and TDFI.
Thymus-deprived mice are unable to react with eosinophilia to an appropriate stimulus, but their ability to mount a neutrophil leucocytosis in response to pyogenic infection is unimpaired. It appears that thymus-processed lymphocytes are required for induction of eosinophil but not of neutrophil leucocytosis.
Effectiveness of 0.5 mg fluoride (F) milk ingestion in preventing caries has been termed only ‘moderate’. In this 3-arm partial cross-over intervention, 32 children aged 6–7 years in a non-F area were recruited and urinary F excretion (UFE) measured before and after ingestion of 0.5 or 0.9 mg F milk. Maintaining customary dietary and oral hygiene habits, children underwent a 2-week ‘wash-in’ with non-F milk, providing a 24-hour urine sample on day 4 of non-F (baseline) and F milk ingestion containing either (i) 0.5 mg or (ii) 0.9 mg F (intervention). A comparative group of thirteen 6- to 7-year-olds living in fluoridated areas provided a 24-hour urine sample on day 4 of daily non-F milk ingestion, following a 2-week non-F milk wash-in. Valid urine samples were analysed for F and UFE estimated from corrected 24-hour urine volume and F concentration. For the 24 test children providing 2 valid urine samples, mean (95% CI) change in corrected 24-hour UFE was 0.130 (0.049, 0.211) and 0.153 (0.062, 0.245) mg/day for 0.5 mg (p < 0.007) and 0.9 mg F (p < 0.001) groups, respectively. Post-intervention, mean (SD) corrected 24-hour UFE was 0.437 (0.153) mg/day and 0.420 (0.188) mg/day for the 0.5 and 0.9 mg F groups, respectively, which were lower than the WHO provisional standards (0.48–0.60 mg F/day). F milk consumption significantly increased UFE; however, the F content of 0.5 and 0.9 mg F milk may be too low to achieve WHO provisional UFE standards concomitant with optimal F exposure in children aged ≥6 years.
A women suffering from the candidiasis-endocrinopathy syndrome, developed severe myopathy in her fourth decade and died from it at the age of 37 years. Associated conditions were hypoparathyroidism, vitiligo, chronic mucocutaneous candidiasis, short stature, intellectual disability, ovarian failure and alopecia totalis. Muscle biopsy findings were non-specific with focal atrophy of type 2 fibres. Serum immunoglobulin levels were normal. The only demonstrable abnormalities of her immune system were impaired T-cell function and antibody production by B-cells (detectable to smooth muscle, mitochondria and gastric parietal cells). The T-cell abnormality may have been part of a more generalized cell defect, resulting from an unidentified genetic abnormality, whilst the circulating antibodies could have been a response to tissue damage. There was no convincing evidence of primary autoimmune damage.
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