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The marble goby, Oxyeleotris marmorata, considered a freshwater fish, was able to hypoosmoregulate successfully during 14 days of acclimation to seawater (30 per thousand) following 6 days of progressive increase in salinity. In seawater, there were slight perturbations in plasma osmolality and ionic concentrations, and significant increases in contents of some free amino acids, which presumably acted as osmolytes, in tissues. The muscle glutamine content increased significantly during seawater acclimation, and the activity and the protein abundance of glutamine synthetase increased significantly in the liver of fish exposed to seawater for 14 days. Exposure to seawater for 14 days also resulted in branchial osmoregulatory acclimation. There were significant increases in the activity and the protein abundance of gill Na(+)/K(+)-ATPase, and protein abundance of gill Na(+):K(+):2Cl(-) cotransporter (NKCC). Immunofluorescence microscopy of branchial Na(+)/K(+)-ATPase-immunoreactive cells revealed that exposure to seawater led to increases in protein expression of apical cystic fibrosis transmembrane receptor-like chloride channel and basolateral NKCC. Overall, our results indicate that juvenile marble goby can acclimate to brackish water and subsequently to seawater, and prompt future studies on the effects of salinity on its growth and development which may have important application to the Asian marble goby aquaculture industry.

The objective of this study was to examine postprandial nitrogen metabolism and excretion in the juvenile marble goby, Oxyeleotris marmorata (30–80 g), fed a high protein diet (cod fish fillet). Feeding led to only a slight increase in plasma ammonia concentration and had no significant effect on the ammonia content in the brain of juvenile O. marmorata during the subsequent 24 h. Unlike other fishes, juvenile O. marmorata could apparently avoid postprandial ammonia toxicity, and as a result there was no increase in the brain glutamine content, which decreased significantly instead at certain post-feeding time point. Since no prominent increases in tissue glutamine and urea contents were observed after feeding despite its ability to detoxify ammonia to glutamine during emersion and its possession of a full complement of hepatic ornithine-urea cycle enzymes, it can be concluded that only a moderate amount of ammonia was produced after feeding. Traditionally, it has been accepted that excess amino acid would be degraded in the liver through transdeamination which involves the deamination of glutamate catalyzed by glutamate dehydrogenase (GDH). However, we report for the first time that glutamate content in liver and intestine of juvenile O. marmorata increased to 10.8 µmol g − 1 and 3.3 µmol g − 1 , respectively, 6 h post-feeding. These results indicate that the rate of glutamate catabolism in the liver was lower than the total rate of glutamate released directly from protein degradation and produced indirectly from other amino acids through transamination. Indeed, feeding led to significant increases in hepatic GDH amination activity and intestinal GDH activity, in both amination and deamination directions, in juvenile O. marmorata . Thus, there could be an increase in the capacity of the liver, and perhaps the intestine, to produce and retain glutamate after feeding. As a result, only 33% of the ingested nitrogen was excreted during the 24-h post-feeding period, with 67% being retained for somatic growth. Results obtained from this study can be useful for designing re-circulating aquaculture systems for juvenile marble goby, and they offer insights into mechanisms that can be induced by feeding to retain ingested nitrogen.

The African sharptooth catfish Clarias gariepinus lives in freshwater, is an obligatory air-breather, and can survive on land during drought. The objective of this study was to elucidate the mechanism of acute ammonia toxicity in C. gariepinus, and to examine whether methionine sulfoximine [MSO; an inhibitor of glutamine synthetase (GS)] or MK801 [an antagonist of N-methyl d-aspartate type glutamate (NMDA) receptors] had protective effects against acute ammonia toxicity in this fish. After 48 h of exposure to a sublethal concentration (75 mmoll(-1)) of environmental ammonia, the brain glutamine and ammonia contents in C. gariepinus increased to 15 micromol g(-1) and 4 micromol g(-1), respectively. Thus, C. gariepinus detoxified ammonia to glutamine and could tolerate high levels of glutamine in its brain. After C. gariepinus was injected intraperitoneally with a sublethal dose of ammonium acetate (CH(3)COONH(4); 8 micromol g(-1) fish) followed with emersion, brain ammonia and glutamine contents increased continuously during the subsequent 24-h period, reaching 7 and 18 micromol g(-1), respectively, at hour 24. These results suggest that when confronted with acute ammonia toxicity, the survival of C. gariepinus was crucially determined by its high tolerance of ammonia and high capacity to detoxify ammonia to glutamine in the brain. For fish injected with a sublethal dose of CH(3)COONH(4) (10 micromol g(-1) fish) followed with immersion, there were transient but significant increases in brain ammonia and glutamine contents, which peaked at hour 2 (4 micromol g(-1)) and hour 6 (6 micromol g(-1)), respectively. From these results, it can be deduced that C. gariepinus accumulated glutamine in preference to ammonia in its brain. By contrast, for fish injected with a lethal dose (20 micromol g(-1) fish) of CH(3)COONH(4) followed with immersion, the brain ammonia content increased drastically to 10 micromol g(-1) after 30 min, while the brain glutamine content remained relatively low at 5 micromol g(-1). Therefore, it can be concluded that increased synthesis and accumulation of glutamine in the brain was not the major cause of death in C. gariepinus confronted with acute ammonia toxicity. The determining factor of acute ammonia toxicity appeared to be the rate of ammonia build-up in the brain. MK801 (2 microg g(-1) fish) had no protective effect on C. gariepinus injected with a lethal dose of CH(3)COONH(4) (20 micromol g(-1) fish) indicating that activation of NMDA receptors might not be involved. By contrast, the prior administration of MSO (100 microg g(-1) fish) reduced the mortality rate from 100% to 80% and at the same time prolonged the time of death significantly from 27 min to 48 min. However, the protective effect of MSO was apparently unrelated to the inhibition of glutamine synthetase and prevention of glutamine accumulation in the brain. Instead, MSO affected activities of glutamate dehydrogenase and alanine aminotransferase and suppressed the rate of ammonia build up in the brain of fish injected with a lethal dose of CH(3)COONH(4).

This is a prospective study of wound healing after extractions in patients who had radiation therapy for nasopharyngeal cancer. From 40 patients who fulfilled all the study criteria were extracted a total of 155 teeth. The demographic data were analysed, checking for factors that might affect the healing process after extraction. Wound healing was divided into three groups: normal wound healing, delayed healing and osteoradionecrosis. Logistic regression was used to analyse possible relationships. There was a low complication rate: 5.8% and 1.9% of extractions showed delayed healing and osteoradionecrosis, respectively. The age of the patient at time of extraction was the only significant factor that influenced the occurrence of delayed healing. It was observed that localized radiation absorption was considerably different from the total radiation dose. In conclusion, postradiation extractions have a low risk of complications and the results point to age as a factor that may influence wound healing.

Summary Purpose An earlier phase II trial of paclitaxel in patients with metastatic nasopharyngeal carcinoma (NPC) demonstrated a response rate of 22%. Hence we proceeded to study the combination of paclitaxel and carboplatin in these patients. Patients and methods The 21-day regimen was as follows: i.v. paclitaxel 175 mg/m2 over three hours preceded by standard premedications, followed by i.v. carboplatin dosed at AUC of six infused over one hour. Only chemotherapy-naive patients with histological diagnoses of undifferentiated carcinoma of the nasopharynx, systemic metastases and radiologically measurable lesions were eligible. Results Thirty-two patients were accrued to this study. Twenty patients (62%) had at least two sites of metastasis. The main grade 3–4 toxicity was neutropenia (31%). Nine patients (28%) developed neutropenic sepsis, which caused the demise of one of them. Twenty-four patients (75%) responded to treatment, with one (3%) attaining a complete response. The median time to progression of disease was seven months and the median survival was 12 months. At one year, 52% of the patients were alive. Conclusions The combination of paclitaxel and carboplatin is an active regimen in NPC. Its convenience of administration and good tolerability make it an attractive alternative regimen to consider for patients with metastatic disease.