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Biomedical subjects

K Satake

Publications and source records attributed to K Satake.

At least 37 records · Page 2Linked to original sources
PubMed1998

Polymorphisms of thymidine kinase gene in herpes simplex virus type 1: analysis of clinical isolates from herpetic keratitis patients and laboratory strains.

Drug-resistance of herpes simplex virus (HSV) is caused most frequently by mutation of the viral thymidine kinase (TK) gene. To elucidate the significance of detecting nucleotide changes of the TK gene for screening drug-resistant viruses, the frequency and variation of the genetic polymorphisms in the whole coding region of the TK gene were studied in 14 acyclovir-susceptible HSV type 1 (HSV-1) clinical isolates from 14 patients with epithelial herpetic keratitis. Two reference HSV-1 laboratory strains, McKrae and PH, and two acyclovir-resistant variants of the PH strain were also studied as controls. Polymerase chain reaction-single-strand conformation polymorphism (PCR-SSCP) and direct sequencing detected nucleotide differences at 24 positions, and amino acid substitutions at 12 codons in the TK gene of the examined viruses. Nucleotide diversity of 0.0029 per base (the average number of nucleotide substitutions of 3.3 per 1,131 base pairs) in the TK gene in the clinical isolates was comparable to 0.0037 per base of the whole HSV-1 genome in Japanese isolates reported previously. PCR-SSCP analysis of the acyclovir-resistant strains easily detected aberrantly shifted bands by comparing them with those of the parental strain, followed by the quick determination of mutated sequences. These results suggest that detection of nucleotide changes of the TK gene is useful for serial observation of persistent or recurrent HSV infection as observed in immunocompromised hosts, but that it is not useful for screening drug-resistant viruses from nonepidemic clinical isolates because of the comparable genetic polymorphisms in the TK gene as in the whole HSV-1 genome.

Acyclovir↗
PubMed1998

Effect of electrical stimulation of the thalamic Vim nucleus on hand tremor during stereotactic thalamotomy.

OBJECTIVE: The aim of this study was to analyze the correlation between neuronal responses in the thalamic ventralis intermedius (Vim) nucleus to peripheral, natural stimulation and the modulation of tremor by electrical stimulation during stereotactic thalamotomy. DESIGN AND METHODS: The authors studied 36 patients with hand tremor using a microelectrode. The responses of tremor to electrical stimulation were analysed electromyographically. Sixty stimulation sites were divided into three groups. RESULTS: Group A (20 sites) where responses to stretching of the contralateral forearm muscles were recorded. Group B (26 sites) where responses to stretching of the other muscles of the upper extremity were recorded. Electrical stimulation at sites in groups A and B temporarily suppressed the contralateral tremor, but the minimum current intensity to suppress tremor at sites in group A was less than that in group B. Electrical stimulation in group C (14 sites), where kinesthetic responses of contralateral lower extremity were recorded, resulted in increased amplitude of hand tremor. Selective coagulation including the area of tremor suppression resulted in abolition of the tremor in all patients. CONCLUSIONS: These results suggest that the most effective site for thalamotomy may also be suitable for chronic stimulation in the Vim nucleus.

Electric Stimulation↗
PubMed1998

Relaxant effects of NKH477, a new water-soluble forskolin derivative, on guinea-pig tracheal smooth muscle: the role of Ca2+-activated K+ channels.

1. Mechanisms underlying the bronchorelaxant action of NKH477, a newly developed water-soluble forskolin derivative, were investigated in guinea-pig isolated tracheal smooth muscle. 2. In muscles precontracted with 3 microM histamine, NKH477 (1 nM-1 microM) caused a concentration-dependent decrease of isometric tension, resulting in a complete relaxation at 300 nM. The EC550 for the relaxation was 32.6+/-4.3 nM (n=6). 3. In the presence of 30 or 90 nM iberiotoxin (IbTX), a selective blocker of the large-conductance Ca2+-activated K+ (BK(Ca)) channel, the relaxing action of NKH477 on the histamine-induced contraction was inhibited, giving rise to a parallel shift of the concentration-response curves; the EC50 of NKH477 was increased to 131.4+/-20.4 nM at 30 nM IbTX (n=4), and 125.3+/-12.2 nM at 90 nM IbTX (n=4). 4. Pretreatment of muscles with 30 mM tetraethylammonium (TEA) caused a similar rightward shift of the concentration-response curve to NKH477 with an increase of the EC50 to 139.8+/-18.4 nM (n=5). In contrast, the relaxing action of NKH477 was unaffected by 10 microM glibenclamide, an ATP-sensitive K channel blocker, or by 100 nM apamin, a blocker of small conductance Ca2+-activated K+ channels. 5. In muscles pretreated with 1 microM nifedipine, a blocker of the voltage-dependent Ca2+ channel (VDC), 30-90 nM IbTX did not affect the relaxant effects of NKH477 on the histamine-induced contraction. 6. In muscles precontracted by a K+-rich (40 mM) solution, NKH477 caused only minimal relaxation (19.8+/-1.7%, n=4) even at the highest concentration (1 microM). 7. In experiments to measure the ratio of fura-2 fluorescence signals (R(340/380)) as an index of the intracellular Ca2+ concentration ([Ca2+]i), the application of 100 nM NKH477 or 200 nM isoprenaline to the preparation precontracted by 3 microM histamine resulted in a decrease in [Ca2+]i in association with a decrease in tension. The reduction of [Ca2+]i and tension by NKH477 was 47.0+/-5.6% and 62.8+/-7.0%, respectively (n=5), and that with isoprenaline 60.6+/-7.4% and 67.4+/-6.4%, respectively (n=5). These effects of NKH477 and isoprenaline on [Ca2+]i and tension were inhibited by 30 nM IbTX. The inhibitory action of IbTX was abolished in the presence of 1 microM nifedipine. 8. These results suggest that the bronchorelaxant action of NKH477 may result, at least in part, from activation of BK(Ca) channels, which may cause a hyperpolarization of smooth muscle cell membranes and a secondary decrease in Ca2+ influx through VDCs, leading to a decrease in [Ca2+]i.

Animals↗
PubMed1998

Pancreatic surgery in Japan: historical review.

The advent of surgical techniques for the management of pancreatic cancer has had a long and varied history in the Western culture. The development of current surgical techniques and treatment modalities is based on (rooted in) techniques developed over time. Although the first written anecdotes of pancreatic resection--primarily from the 1600s through the late 1800s--did not alter the mortality of pancreatic cancer, they did pave the way for advances in surgical techniques that subsequently attained lower morbidity and mortality rates. Although there were some meager attempts at pancreatic resection in Japanese institutions before and during World War II, it was not until after the war, and particularly after the mid-1950s, that pancreatic surgery developed tremendously. The development of more radical approaches to pancreatic surgery developed tremendously. The development of more radical approaches to pancreatic resection as well as other surgical developments resulted in lower morbidity and mortality rates.

General Surgery↗
PubMed1998

A new model for pancreatitis.

Pancreatitis induced by ligation of the pancreatic duct produces morphologic similarities to human pancreatitis. This model is easily performed in big animals, but it is very difficult to perform pancreatic duct ligation in small animals. Many experimental studies of pharmaceutical treatments for pancreatitis used pancreatic duct-ligation models, but it is also difficult to evaluate the efficacy of the drugs used, because the animals used are of different species with individual differences. To overcome these problems, we ligated the main pancreatic duct of the splenic lobe by a 5.0 absorbable suture by using a surgical microscope and left the gastroduodenal lobe intact in the same rats. This model produced damaged pancreatic tissue in one part and normal pancreatic tissue in another part of the pancreas in the same animals, biochemically and histologically. We evaluated the effect of a new protease inhibitor (ONO-3404) on this preliminary model and found this new protease inhibitor demonstrated a hypertrophic effect on the damaged pancreatic tissue and the normal pancreatic tissue in the same animals. This model is also useful to study pharmaceutic treatment for pancreatic insufficiency and to study chemically induced pancreatic carcinogenesis in the damaged pancreatic tissue and the normal pancreatic tissue in the same animals.

Amylases↗
PubMed1998

Granular cell tumor of the duodenum: a case report.

Granular cell tumor (GCT) in the duodenum is an extremely rare disease: only one case has been listed in a review, to date. We reported a 47-yr-old Japanese male case with GCT of the duodenum. Clinically, melena caused by bleeding from the tumor was the only symptom. The tumor cells showed abundant, granular eosinophilic cytoplasm. Although this tumor was clinically and histologically benign, highly developed tumor microvessels were demonstrated both angiographically and histologically, suggesting malignant potential of the tumor.

Duodenal Neoplasms↗
PubMed1998

[5-fluorouracil and low-dose leucovorin as surgical adjuvant therapy from viewpoint of long-term outcome].

Biochemical modulation of 5-FU by leucovorin (LV) has been demonstrated to increase the therapeutic effect compared to single agent 5-FU in the treatment of patients (pts) with advanced colorectal cancer. The purpose of this study was to determine the effectiveness of the 5-FU + LV combination as adjuvant therapy following surgery in pts with Dukes' B, C colon cancer. Pts were entered in a stratified clinical trial comparing two different combination chemotherapeutic regimens to single agent 5-FU, given orally as a control. This report summarized the result of treatment in 61 pts who were 5-FU oral alone and 32 pts who were 5-FU (375 mg/m2) and low-dose LV (20 mg/m2) intravenously for 5 days with 5-FU oral intake. 5-FU with LV regimen was associated with an improved survival compared with the single agent 5-FU oral intake (p < 0.05). 5-FU with LV regimen resulted in less recurrence in liver and lung compared with single-agent 5-FU oral intake.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1997

Inhibitory effect of green tea extract on the process of pancreatic carcinogenesis induced by N-nitrosobis-(2-oxypropyl)amine (BOP) and on tumor promotion after transplantation of N-nitrosobis-(2-hydroxypropyl)amine (BHP)-induced pancreatic cancer in Syrian hamsters.

Epidemiologic studies have shown a lower risk of gastrointestinal cancer in green tea drinkers. In the present study, the inhibitory effect of green tea extract (GTE) on the process of pancreatic carcinogenesis induced by N-nitrosobis-(2-oxypropyl)amine (BOP) and on tumor promotion after transplantation of N-nitrosobis-(2-hydroxypropyl)amine (BHP)-induced pancreatic cancer were investigated in hamsters. In the first experiment, shortly after the initiation of pancreatic carcinogenesis by BOP, the animals in the GTE group were given GTE (0.5 mg/L) in their drinking water and the control group was given tap water. All animals were sacrificed 24 weeks later. There were no significant differences in body weight, water intake, or food consumption between the two groups during the experiments. GTE consumption was approximately 1.25 mg/day/100 g body weight during this experiment. Seven of the 13 hamsters (54%) in the control group were found to have pancreatic tumors, versus six of the 18 hamsters (33%) in the GTE group. The average number of tumors in the control group was 1.0/hamster, compared with 0.5/hamster in the GTE group. The overall incidence of macroscopic pancreatic tumors in the GTE group was about half that in the control group. The incidence of pancreatic cancer was 54% (12/13) in the control group and 44% (8/18) in the GTE group. The number of pancreatic cancers, including invasive carcinoma and carcinoma in situ, in the GTE group was 0.88/hamster, significantly lower than in the control group (1.68/hamster) (p < 0.05). The incidence of atypical ductal hyperplasia, which is thought to be an early pancreatic cancer, was also significantly lower in the GTE group than in the control group (1.50/hamster vs. 4.65/hamster) (p < 0.05). In the second experiment, 1-mm3 pieces of BHP-induced pancreatic cancer were transplanted into the back of hamsters. The control group (N = 16) was maintained on the basal diet and tap water throughout the experiment, and the GTE group (N = 16) was also maintained on the basal diet and tap water for the first 3 weeks after transplantation, when successful transplantation was confirmed and, thereafter, given tap water containing GTE (0.5 mg/L) for an additional 12 weeks. Tumor growth was similar in both groups until 11 weeks after transplantation, but inhibition of tumor growth became apparent after 11 weeks in the GTE group. At 13 weeks, the average tumor volume in the GTE group was 1.01 +/- 0.11 x 104 mm3, significantly smaller than that in the control group (1.98 +/- 0.37 x 104 mm3) (p < 0.05). The results demonstrated that GTE has an inhibitory effect on the process of pancreatic carcinogenesis and on tumor promotion of transplanted pancreatic cancer. These results suggest that GTE may come to serve as a chemopreventive and chemotherapeutic agent for pancreatic cancer.

Animals↗
PubMed1996

Amebic liver abscess.

We report eight cases of amebic liver abscess. All patients were men, and four were homosexual. Five of the eight patients had syphilis, but the four homosexual patients who were tested for HIV infection were negative. Ultrasonography (US), with or without needle aspiration, is the best method for diagnosing amebic liver abscess, and the treatment of choice is US-guided needle aspiration of the abscess followed by metronidazole therapy. Complication by other sexually transmitted diseases is another important factor affecting the treatment of this disease.

Adult↗
PubMed1996

Role of endogenous and exogenous cholecystokinin in experimental acute pancreatitis induced in rats by the duodenal loop technique.

The role of endogenous cholecystokinin (CCK) release and exogenous CCK-8 administration in the development and progression of acute pancreatitis and in the early recovery phase of acute pancreatitis were investigated in rats with closed duodenal loop (CDL)-induced pancreatitis. The subcutaneous injection of CCK-8 (2 micrograms/kg) stimulated a physiological level of pancreatic enzyme secretion in normal control rats, but did not lead to any biochemical or histological evidence of acute pancreatitis. A higher dose of CCK-8 (8 micrograms/kg), however, did produce both biochemical and histological evidence of acute pancreatitis in the normal control rats. When 2 micrograms/kg of CCK-8 was injected subcutaneously in rats 6 and 12 h after the creation of the CDL, neither the biochemical nor the histological findings of acute pancreatitis showed any progression compared with the changes in controls given no CCK-8. Serum CCK levels, measured by radio-immunoassay, increased significantly from mean levels of 5.39 pg/ml (+/- 0.95 SD) before creation of the CDL to 42.06 pg/ml (+/- 2.27 SD) 6 h after, and 41.95 pg/ml (+/- 1.88 SD) 12 h after its creation (P < 0.01). The difference between serum CCK levels at 6 and 12 h was not statistically significant. Following the release of the loop, serum CCK levels decreased gradually, especially in rats in which the loop was released 6 h after being created. Although no marked biochemical and histological changes of acute pancreatitis were observed following the administration of 2 micrograms/kg of CCK-8 to rats upon release of the loop 6 h and 12 h after its creation, a higher dose of CCK-8 (8 micrograms/kg) in these rats adversely affected both the biochemical and histological findings of acute pancreatitis. Based on these findings, it was concluded that neither endogenous CCK release, as a result of the CDL, nor physiological stimulation of the pancreas by exogenous CCK-8 administration, caused progression from edematous to hemorrhagic acute pancreatitis, and neither CCK treatment had any adverse effect on the early recovery phase of CDL-induced acute pancreatitis. A pharmacological dose of CCK, however, exacerbated the acute pancreatitis, even in the early recovery stage.

Acute Disease↗
PubMed1996

Relation between severity of magnesium deficiency and frequency of anginal attacks in men with variant angina.

OBJECTIVES: We evaluated whether the severity of magnesium deficiency was correlated with the frequency of attacks of variant angina. BACKGROUND: Magnesium deficiency may be associated with the development of variant angina. However, the relation between the activity of variant angina and magnesium deficiency remains to be elucidated. METHODS: We assessed the body magnesium status of 18 men with variant angina: Group 1 (> or = 4 attacks/week, n = 7) and Group 2 (< 4 attacks/week, n = 11). Concentrations of magnesium were determined in serum, urine, mononuclear cells and erythrocytes, and the 24-h magnesium retention rate was determined. RESULTS: Group 1 showed a higher 24-h magnesium retention rate (mean +/- SEM 63.5 +/- 7.6% vs. 24.9 +/- 2.7%, p < 0.01) and a lower intracellular concentration of magnesium in mononuclear cells and erythrocytes than did Group 2 (respectively, 156.3 +/- 13.5 vs. 212.1 +/- 6.9 fg/cell, p < 0.01; and 3.5 +/- 0.5 vs. 5.2 +/- 0.4 fg/cell, p < 0.05), demonstrating the presence of magnesium deficiency in Group 1. The 24-h magnesium retention rate and intracellular concentrations of magnesium in mononuclear cells and erythrocytes correlated well with the frequency of anginal attacks (r = 0.78, p < 0.01; r = -0.78, p < 0.01; r = -0.62, p < 0.01, respectively) for all patients. CONCLUSIONS: Data suggest that the magnesium status of men with variant angina is closely related to disease activity.

Aged↗
PubMed1996

Effects of bradykinin receptor antagonist on the release of beta-endorphin and bradykinin and on hemodynamic changes in a canine model of experimental acute pancreatitis.

Bradykinin and beta-endorphin increases during acute pancreatitis are thought to contribute to the development of hypotension and myocardial depression in acute pancreatitis. beta-Endorphin release is mediated by trypsin-like enzymes and bradykinin from the pituitary gland. This study was undertaken to investigate the effect of a long-acting bradykinin receptor antagonist on bradykinin and beta-endorphin release and on hemodynamic changes during acute pancreatitis. Pancreatitis was induced by the injection of autologous bile mixed with trypsin into the main pancreatic duct after ligation of the accessory duct. Serum bradykinin and plasma beta-endorphin levels and cardiovascular function were measured. Twelve dogs (control group) were given 10 ml/kg/h of lactate Ringer's solution intravenously beginning 1 h before the induction of pancreatitis and continuing throughout the experiments. Six dogs received an intravenous infusion of 0.6 mg/kg/h of a new bradykinin receptor antagonist, HOE 140, D-Arg-[Hyp3, Thi5, D-Tic, Oic8]-bradykinin, in lactate Ringer's solution soon after the induction of pancreatitis. Six of twelve dogs in the control group, and none of the six dogs in the bradykinin receptor antagonist group, died during the experiments. Serum bradykinin levels in both groups increased until 1 h after the induction of pancreatitis, but thereafter the levels in the bradykinin receptor antagonist group decreased gradually until 5 h after induction, and levels were significantly lower than those in the control group (p < 0.05). Plasma beta-endorphin levels in the control group increased significantly, to 291.8 pg/ml (+/- 6.6 SEM) 5 h after the induction of pancreatitis, from the mean levels of 47.8 pg/ml before the induction of pancreatitis, while the mean beta-endorphin level in the bradykinin receptor antagonist group did not increase after the induction of pancreatitis. Infusion of the bradykinin receptor antagonist improved survival rates, hypotension, myocardial depression, and plasma lactate, suggesting that the bradykinin receptor antagonist inhibited the release of bradykinin and beta-endorphin, which contributed to the clinical improvement.

Acute Disease↗
PubMed1996

Effects of a new synthetic lipid A on endogenous tumor necrosis factor production and antitumor activity against human pancreatic cancer cells.

The effects of a synthetic lipid A on tumor necrosis factor (TNF) production and antitumor activity against human pancreatic cancer cells were investigated. Lipid A (10 mg/kg) was injected into normal rats and mice and serum TNF levels were measured. Lipid A-induced inhibition of Molt 4 and MIA paca-2 cells in culture were measured by counting viable cells. Activity of lipid A against transplanted human pancreatic cancer cells (MIA paca-2, Panc-1) was examined by determining tumor volume, necrosis, and survival rate after intraperitoneal injections of lipid A (10 and 20 mg/kg) over 4 weeks. Serum TNF levels increased 80-fold in rats and 100-fold in mice after intravenous lipid A injection. Although specific tumor growth inhibition by lipid A was not observed in vitro, tumor growth was significantly inhibited, and the survival rate was improved in pancreatic cancer cell-transplanted nude mice treated with lipid A compared with controls. Synthetic lipid A induces TNF production and has antitumor activity against transplanted pancreatic cancer cells. Further studies of this lipid A as an agent for pancreatic cancer are warranted.

Animals↗
PubMed1996

Inhibitory effect of sarcophytol A on pancreatic carcinogenesis after initiation by N-nitrosobis(2-oxypropyl)amine in Syrian hamsters.

Sarcophytol A (SaA), a cembrane-type diterpene, inhibits pancreatic carcinogenesis induced by N-nitrosobis(2-oxypropyl)amine (BOP) in hamsters. The experimental groups received two injections of BOP at 70 mg/kg dose, followed 2 weeks later by a 20 mg/kg dose injection, and were fed a basal diet or 0.01 and 0.05% SaA diets starting 1 week after the second injection of BOP. Control groups were injected with normal saline and fed the basal diet or the 0.05% SaA diet. All animals were killed 30 weeks after the start of the experiments. Seventeen BOP-treated hamsters fed the basal diet developed pancreatic tumors (77.3%) while only 12 of 21 hamsters fed the 0.01% SaA diet (57.1%) and 12 of 23 hamsters fed the 0.05% SaA diet (52.2%) developed pancreatic tumors. Pancreatic lesions included ductal hyperplasia, atypical ductal hyperplasia, and carcinoma in situ. Microscopic invasive carcinoma induced by BOP and the incidence of larger pancreatic tumors in hamsters were significantly higher in hamsters fed the basal diet than in hamsters fed the SaA diet (p < 0.05). The proliferating cell nuclear antigen (PCNA) labeling index of pancreatic carcinoma in BOP-treated hamsters fed the basal diet was 41.2 +/- 13.4%, whereas BOP-treated hamsters fed 0.01 and 0.05% SaA diets yielded PCNA indexes of 26.8 +/- 8.3 and 28.4 +/- 7.0%, respectively. k-ras mutation was detected in 40% of cancers in both groups. No pancreatic tumors developed in saline-treated groups, and no differences in body weights or histological findings in their organs, including the pancreas, were observed in either group. These findings suggest that SaA not only inhibits BOP-induced pancreatic carcinogenesis in hamsters, but also provides antipromotion and antiprogression effects on these tumors, even when SaA commences 1 week after the initiation of pancreatic carcinogenesis.

Animals↗
PubMed1995

Carboxy-terminal degradation of peptides using perfluoroacyl anhydrides. A C-terminal sequencing method.

An accurate carboxy-terminal sequencing method has long been sought to complement the Edman degradation procedure for amino-terminal amino acid sequence analysis. The method presented here is a unique and simple method to partly fulfill the needs. Exposure of a polypeptide to perfluoroacyl anhydride vapor at -20 degrees C for 0.5-1 h causes sequential chemical degradation of the molecule from the C-terminus. Fast-atom-bombardment mass spectrometric analysis of the resultant mixture of C-terminally truncated molecules permits the determination of the C-terminal sequence by simple calculation of the mass differences in molecular ions. Experiments suggested that this C-terminal degradation proceeds by active intermediates such as oxazolone at the C-terminal carboxyl residues.

Acetic Anhydrides↗