Local factors affecting winter habitat use of non-native rainbow trout in a boreal stream in northern Japan

Ichthyological Research - Despite its potential use for population control, the winter ecology of nonnative fishes is still poorly understood due to the difficulty of conducting field surveys. In...     

An elevation of BUN/creatinine ratio in patients with hyperthyroidism

Blood urea nitrogen (BUN/creatinine ratio was abnormally high (24.8 +/- 0.6) in untreated hyperthyroid patients due to both increase in BUN and decrease in creatinine concentration. BUN, creatinine and BUN/creatinine ratio were all completely normalized after restoration of euthyroid status. On the other hand, BUN/creatinine ratio was slightly suppressed in hypothyroidism before treatment and it was reversed by thyroxine treatment (12.6 +/- 4.0 and 16.3 +/- 3.3, before and after treatment, respectively). An age-related increase in BUN/creatinine ratio, which was primarily due to an age-related increase in BUN, was also found in hyperthyroid subjects (21.9 +/- 2.8 vs 27.7 +/- 9.0; first vs fifth decade) and in normal controls (13.7 +/- 2.8 vs 16.0 +/- 2.9; first vs fifth decade). To elucidate reasons for abnormal increase in BUN/creatinine ratio in hyperthyroidism, measurement of cardiac output and kinetic analysis on urea nitrogen (UN) and creatinine were performed. The results indicated a marked increase in cardiac output. Serum creatine concentration was clearly increased in hyperthyroid patients. Thus, serum creatinine concentration was suppressed due to a decrease in creatinine synthesis and an increase in renal creatinine excretion. BUN was high, primarily due to an increase in UN production secondary to excessive protein catabolism together with insufficient excretion of UN.     

Kupffer cells play important roles in the metabolic degradation of a soluble anti-tumor (1 → 3)-β-d-glucan, SSG, in mice

Abstract Metabolic degradation of a soluble highly branched (1 → 3)-β- d -glucan, SSG, was examined in mice using a macrophage blocker, gadolinium chloride (GdCl₃). Intraperitoneally administered SSG distributed in the liver was slowly degraded, and after 5 weeks about 30% of the SSG became anionic. In addition, it is suggested that the metabolites would contain fewer branching points as assessed by the reactivity to limulus factor G. On the other hand, in the spleen, the molecular weight and the degree of branching of SSG were not changed for at least 5 weeks. Blockade of Kupffer cells by GdCl₃ did not significantly change the distribution ratio of SSG in the liver. However, the treatment significantly delayed the degradation of SSG. These results suggested that Kupffer cells play important roles, not in the distribution, but in the oxidative degradation of SSG in the liver. In addition, splenic macrophages did not significantly contribute to the metabolic degradation of SSG.