Intestinal inorganic phosphate transport and its regulation have not been studied in fish. In this study, we initially characterized the mechanisms of intestinal inorganic phosphate transport in rainbow trout (Oncorhynchus mykiss) then determined the effects of dietary phosphorus concentrations on intestinal inorganic phosphate uptake, plasma inorganic phosphate, and intestinal luminal inorganic phosphate concentrations. In 11-g trout, the saturable mechanism of brushborder inorganic phosphate uptake had a Kt= 1.2 mmol l(-1) and a Vmax = 0.22 nmol mg(-1) min(-1), while the diffusive component had a Kd = 0.012 min(-1). Similar kinetic constants were obtained from 51-g trout, suggesting that development or size had little effect on transport. Tracer inorganic phosphate (1.18 mmol l(-1)) uptake was almost completely inhibited (>95%) by 20 mmol l(-1) unlabeled inorganic phosphate. Inorganic phosphate uptake (0.2 mmol l(-1)) was strongly inhibited (approximately 75% inhibition) by phosphonoformic acid, a competitive inhibitor of mammalian inorganic phosphate transport, as well as by the absence of Na+ (approximately 90% inhibition). Northern blot and reverse transcription-polymerase chain reaction indicated that the intestinal inorganic phosphate transporter in trout is not related to the cloned Na+ inorganic phosphate-II transporter of winter flounder. Intestinal luminal and plasma inorganic phosphate concentrations each increased with dietary P concentrations. Intestinal inorganic phosphate, but not proline, absorption rates decreased with dietary phosphorus concentrations. As in mammals and birds, a Na-dependent inorganic phosphate carrier that is tightly regulated by diet is present in trout small intestine.

Year-by-year, there has been an increasing number of literature on hypospadias, and most of them are mainly focused on two aspects, namely surgical techniques and aetiology, including the molecular mechanism and associated environmental factors. Surgical techniques and nursing levels are being continuously improved. However, in stark contrast, the study of aetiology still lags behind. Up to now, there is still no consensus on the aetiology of hypospadias, including the molecular mechanism and associated environmental factors. To obtain an overall and latest result on the aetiology, we reviewed published literature regarding the aetiology of hypospadias including the molecular mechanism and associated environmental factors in PubMed in the last 5 years. Thirty-seven studies on the aetiology of hypospadias including molecular mechanism and associated environmental factors were found, of which 25 were about associated environmental factors, and they were described according to the aspects of chemicals, parental characteristics, nutrition and hormones. The remaining studies were about the hormone-dependent phase of molecular mechanism, namely androgen-related genes and oestrogen-related genes. Furthermore, the various points of view were classified and discussed in detail.

Gastric acid secretion was measured in 20 infants aged 6-438 days. The values for the basal acid output and that after stimulation with 6 mug/kg pentagastrin subcutaneously were found to be related to age, body weight and body surface area. But these correlations were not comparable to those in adults. Standard values for different age groups in childhood must therefore be established. Furthermore, the results indicate parietal-cell immaturity during the first six months of life. Measurement of fasting serum-gastrin concentration by radioimmunoassay in 74 infants, aged 1-438 days, and 154 adults as controls revealed a high serum-gastrin level in infants, with an exponential decrease during the first year of life. Despite comparable pH values in gastric juice at one year of life, the gastrin concentrations were higher than those in adults (at a statistically significant level). On the other hand, normal serum-gastrin concentrations were found in ten pregnant women just before delivery. The results suggest a negative feed-back mechanism between gastric-acid secretion and fasting serum-gastrin levels, but such mechanism probably being limited by extragastric gastrin secretion.

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