A 51-year-old male with cyclic neutropenia, on whom we previously reported, was admitted to our hospital with severe abdominal pain and diarrhea four years and seven months after his last hospitalization. Since then, he has received Kampo treatment at our hospital every three weeks, with good clinical results. This time, he was at first treated with Kampo daikenchuto combined with bushikobeito, which had been effective during his last hospitalization, although this time the remedy had no effect. From the viewpoint of Japanese traditional (Kampo) medicine, it was considered that the patient had severe cold syndrome. He was given uzukeishito three times a day (at 10.00, 15.00 and 20.00 hours). The dose of uzu in uzukeishito was gradually increased. Daiuzusen, in which the dose of uzu (an aconite) was 1g or 2g, was also administered five times a day due to the patient's very severe abdominal pain. On the fourth day of uzukeishito administration, the patient felt very hot and still had severe abdominal pain, although this pain was different from the previous pain, thirty minutes after daiuzusen (with 2g dose of uzu) was administered. This reaction can better be explained as mengen rather than uzu poisoning. Very soon he had a good appetite, his abdominal pain was reduced and the cycle of neutropenia was normalized. The case suggests that in cases of very severe cold syndrome, frequent and high-dose administration of aconite component medicine can be effective.

In previous studies, acute exercise might induce inflammatory cytokines from immunological cells, but it was not clear that tumor necrosis factor (TNF) -α in the liver was induced by acute exercise. In this study, we first measured the changes from acute exercise in plasma TNF-α, lipopolysaccharide (LPS), interferon (IFN) -γ and prostaglandin (PG) E2 ; from and investigated the effect of acute exercise on TNF-α expression in the liver. Then we examined the response of TNF-α to PGE2 in isolated Kupffer cells. Female Fischer 344 rats were run on a treadmill at 21 m/min for 60 min on a 15% grade. Although the portal venous plasma endotoxin concentration in the exercised group was higher than that in the resting group, plasma TNF-α was not detected in either group. In addition, plasma IFN-γ, which accelerates TNF-α production, was not detected. TNF-α mRNA expression in the liver didn't change significantly. On the other hand, plasma PGE2, which is an inhibitor of TNF-α production, markedly increased immediately after the exercise. In addition, PGE2 inhibited TNF-α production by LPS-stimulated Kupffer cells in in vitro. These results sug gest that LPS-induced TNF-α expression in rat liver is inhibited by an increase of PGE2 during acute exercise.

The present study was carried out to elucidete whether the accumulation of triglyceride (TG) in rat liver during fasting was stimulated by swimming. Male Wistar rats were divided into three groups; C: control, 24 F: 24 hour-fasted and 48 F: 48 hour-fasted. These animals were required to swim for 120 min.
In rats with both 24F and 48F, the liver glycogen contents did not change during swimming. The level of TG in rat liver was higher in 24 F and 48 F rats than the control group, and the exercise significantly affected the liver TG in each group. There was significant correlation betweem the level of TG in rat liver and the plasma free fatty acid (FFA) concentration (r=0.681, p<0.01) . However, although plasma TG did not change during exercise in each group, the TG secretion rate (TGSR) of the 48 F group was significantly lower than that of the C and 24F groups (p<0.01) .
These results provide evidence that exercise may result in the accumulation of TG in liver during fasting and suggest that the process not only depends on the surplus supply of FFA, but also inhibits very low density lipoprotein-TG secretion from liver.

Previous studies of the effect of exercise on glucose metabolism in diabetes mellitus have focused on the stimulation of glucose disposal capacity by insulin and muscle contraction. We have investigated the effects of hyperglycemia on the increase in muscle glycogen after exercise and the role of physiological saline (saline) injection under hyperglycemic conditions. Male Wistar rats weighing 100-150g (n=52) were made diabetic (DM) by injection of 90 mg/kg streptozotocin (STZ) . Glycogen content was reduced by in situ electrical stimulation of the sciatic nerve. Immediately after stimulation, the rats were injected with glucose or saline. After a 20 min recovery period, the glycogen content of the white and red gastrocnemius (WG, RG), soleus (SOL), plantaris (PL), extensor digitorum longus (EDL) and tibialis anterior (TA) was significantly increased by glucose injection in the control rats. In DM rats, the glycogen content of the TA and EDL was increased, whereas there was no change in the WG, RG, SOL and PL. These results suggest that, in hyperglycemic rats, muscle glycogen resynthesis in only fast-twitch fibers is increased by muscle contraction. However, after injection of saline, the plasma osmolality decreases significantly and glycogen resynthesis by all muscles except the SOL in diabetic rats is improved, although there is no significant increase in control rats. It is concluded that glycogenolysis and resynthesis after muscle contraction are reduced by hyperglycemia. The data suggest a possible role of saline injection in the development of glycogen resynthesis in hyperglycemia.

In this study, we investigated the effect of acute exercise on the mitochondrial structure of hepatocytes surrounding the terminal hepatic venule (zone III) in the rat liver acinus. Male SD rats were assigned to a resting group (n=8) and to running groups ran on a motor-driven treadmill for 100 min (n = 8) or did continued running beyond 100 min until exhaustion (n = 5) . Plasma guanase activity was increased with duration time of exercise. The arterial ketone body rate (AKBR) increased during the 100 min of running, but the AKBR significantly diminished with exhaustive running as compared with that for 100 min of running. Although there was no change in the mitochondrial structure of hepatocytes in the perportal area (zone I) during exhaustion, remarkable swelling was observed in that in zone III.
These results suggest that acute running affects mitochondrial structures in zone III, and that this might be a hypoxia zone during exercise.

To clarify the recovery patterns of spontaneous activity and liver damage after different stressors, female Fischer 344 rats were treated with Propionibacterium aches (P, aches) or water immersion stress before lipopolysaccharide (LPS) injection. They were then examined for wheel running activity, serum corticosterone concentration, serum alanine aminotransferase (ALT) activity, histological appearance of liver and plasma tumor necrosis factor alpha (TNF-a) concentration.
The recovery in physical activity of P. aches-treated rats was faster than that of water immersion rats. One day after the stressors, serum corticosterone cancentration and ALT activity of P. acnes-treated rats were higher than that of water immersion rats. In addition, increases in serum ALT activity and plasma TNF- a, as well as massive necrosis of the liver in P. acnes-treated rats were observed seven days after stress treatment. The P. acnes-LPS rats also showed a reduction in survival rate after 24 hours. These results suggest that P. acnes stress causes serious inflammation when stimulated by LPS. Although rapid recovery in physical activity was not inhibited by P. acnes stress, it differed from the response of water immersion stress.