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A Takasu

Publications and source records attributed to A Takasu.

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

Lipopolysaccharide-induced desensitization to pancreatic edema formation in rat cerulein pancreatitis.

Previously we reported that prior administration of lipopolysaccharide (LPS) mitigates subsequently produced cerulein (Cn) pancreatitis. To clarify the mechanism further, the pathological features of Cn pancreatitis were examined in detail after treating rats with very low doses of LPS. LPS pretreatment reduced the formation of pancreatic edema during Cn pancreatitis in a dose- and time-dependent manner. In contrast, the elevation of serum amylase and the histological findings, including acinar cell vacuolization and infiltration of inflammatory cells, were not affected. The lowest dose of LPS, 500 ng/kg, was sufficient to inhibit pancreatic edema formation completely. LPS at a dose of 5 microg/kg was fully effective when it was given from 30 min to 12 h before the induction of pancreatitis. Pretreatment with tumor necrosis factor-alpha (TNF-alpha) inhibited the pancreatic edema in a manner similar to that of LPS. Moreover, the inhibitory effect of LPS was partially attenuated by the administration of anti-TNF-alpha antibody before the injection of LPS. Actinomycin D (0.5 mg/kg) abolished the effect of LPS, whereas cycloheximide (0.5 mg/kg) given alone reduced pancreatic edema formation during pancreatitis. From these results, it was concluded that very low doses of LPS can induce, partially via TNF-alpha, a state refractory to pancreatic edema formation during Cn pancreatitis, and this phenomenon seems to be regulated at the transcriptional level.

Animals↗
PubMed1998

Low doses of lipopolysaccharide upregulate acinar cell apoptosis in cerulein pancreatitis.

We have reported previously that administration of a sublethal low dose of lipopolysaccharide (LPS; 50 microg/kg) prior to the induction of cerulein (Cn) pancreatitis mitigates the pathological course. To clarify the mechanism, we examined apoptosis in the pancreas using the same model. Apoptosis was evaluated by terminal deoxynucleotidyl transferase mediated dUTP-biotin nick end labeling (TUNEL) and transitional electron microscopy. LPS pretreatment at a dose of 50 microg/kg increased remarkably the incidence of acinar cell apoptosis in Cn pancreatitis rats compared with LPS-untreated Cn pancreatitis rats. Apoptosis was observed selectively in acinar cells but was not shown in endocrine cells or ductal epithelial cells. Infiltration of inflammatory cells was scarcely observed. These acinar cells showed the characteristic morphological features of apoptosis by electron microscopy. Administration of LPS at a dose of 50 microg/kg alone caused acinar cell apoptosis but the incidence was much lower than that in the LPS-pretreated Cn pancreatitis rats. The TUNEL labeling was significantly increased depending on the dose of LPS and on the interval between the administration of LPS and that of Cn. These results suggest that the pathological features of acute pancreatitis might be modified by the presence of nonfatal endotoxemia through the induction of acinar cell apoptosis.

Animals↗
PubMed1998

[Anesthesia for tracheobronchial stent insertion].

We experienced nine cases of general anesthesia for tracheobronchial stent insertion. As far as possible, we anesthetized the patients under spontaneous respiration with inhalation anesthesia, depending on the types of the tracheobronchial stent (Dumon stent or expandable metallic stent), or respiratory status of the patient. Having experienced a case requiring PCPS (percutaneous cardiopulmonary support) to recover from severe ventilatory insufficiency due to tracheal perforation, we, in advance, inserted 18- or 20-gage cannulas into the femoral artery and vein for PCPS standby, and could manage general anesthesia safely for tracheobronchial stent insertion.

Adult↗
PubMed1997

Gallbladder emptying and cholecystokinin and pancreatic polypeptide responses to a liquid meal in patients with diabetes mellitus.

To investigate gallbladder motility and its regulation in patients with diabetes mellitus (DM), we examined the gallbladder response to an intraduodenal test meal by measuring the temporal course of plasma cholecystokinin (CCK) and pancreatic polypeptide (PP) levels. Eighteen patients with type 2 DM and 7 healthy subjects (controls) were enrolled. The gallbladder volume was calculated by the sum-of-cylinders method from ultrasonographic images, and plasma CCK and PP were measured by radioimmunoassays. No significant difference was found in either the gallbladder response or in the CCK response between patients with DM and controls. However, the fasting plasma PP level of patients with DM was more than tenfold higher than that of controls. The integrated PP response (IPPR) of patients with DM to the test meal was 8.3-fold higher than that of controls. When patients with DM were grouped according to whether they had been treated with insulin or not, the fasting plasma PP of patients with DM without insulin treatment was significantly higher than the level in those treated with insulin. These results suggest that overproduction of PP-like immunoreactive substance(s) may occur in patients with DM, but the high plasma PP immunoreactivity does not appear to be related to the fasting gallbladder volume or to gallbladder emptying and filling.

Adult↗
PubMed1997

Effect of an endothelin-1 antagonist, BQ-485, on cerebral oxygen metabolism after complete global cerebral ischemia in dogs.

Endothelin-1 (ET-1) plays an important role in the physiologic or pathophysiologic regulation of cerebral circulation. To evaluate the effects of the newly synthesized ETA receptor-selective antagonist, BQ-485 (N-perhydroazepin-l-ylcarbonyl-Leu-D-Trp-D-Trp-OH), on the cerebral metabolism of oxygen during the delayed cerebral hypoperfusion that follows global cerebral ischemia, we occluded the ascending aorta and caval veins of 10 beagle dogs for 12.5 min. The animals were randomized into two groups. BQ-485 was given directly into the carotid artery at 0.03 mg/kg per min for 30 min, starting 15 min after reperfusion in the treatment group (n = 5). Isotonic saline was infused in the control group (n = 5). A fiberoptic catheter was inserted into the superior sagittal sinus to monitor its oxygen saturation (SssO2) continuously. Arterial O2 content (CaO2), and sagittal sinus O2 content (CssO2) were monitored before and at 0.5, 1, 2, 4, 6 and 8 h after the ischemic insult. BQ-485 significantly prevented the expected decrease in SssO2 and increase in the cerebral O2 utilization coefficient at 4, 6 and 8 h after the ischemic insult (P < 0.05). Thus, BQ-485 ameliorated the mismatch between O2 supply and demand in the delayed hypoperfusion phase. We conclude that ET may be involved in the pathogenesis of delayed cerebral hypoperfusion after cardiac arrest.

Analysis of Variance↗
PubMed1997

Analysis of the substrate binding site and carboxyl terminal region of vacuolar H+-pyrophosphatase of mung bean with peptide antibodies.

Vacuolar H+-translocating inorganic pyrophosphatase is a single-protein enzyme and uses a simple substance as an energy donor. Functional domains of the enzyme were investigated by using antibodies specific to peptides corresponding to the putative substrate-binding site (DVGADLVGKVE) in the hydrophilic loop and the carboxyl terminal part. The antibody to the former peptide clearly reacted with the pyrophosphatases of different plant species, and strongly inhibited the hydrolytic activity of the purified enzymes and the proton pumping activity of membrane vesicles. These results indicate that the sequence functions as an actual substrate-binding site and is a common motif. The antibody to the carboxyl terminal part reacted only to the mung bean enzyme, suppressing its hydrolytic and proton pumping activities. The results suggest that the carboxyl terminus is exposed to the cytosol and is close to the catalytic site. H+-Pyrophosphatase hydrolyzed triphosphate and tetraphosphate at low rates. Phytic acid, myo-inositol hexaphosphate, inhibited the enzyme even in the presence of Mg2+. The concentration for 50% inhibition was 0.15 mM. The inhibition of H+-PPase by dicyclohexyldiimide was partly reversed by Mg2+. The catalytic site and the membrane topology of the enzyme are discussed.

Amino Acid Sequence↗
PubMed1996

Effect of mild hypothermia on ischemia-induced release of endothelin-1 in dog brain.

Endothelin-1 (ET-1) plays an important role in the physiologic or pathophysiologic regulation of cerebral circulation. To evaluate the effect of mild hypothermia on the cerebral concentration of ET-1 and on the cerebral metabolism of oxygen after complete global cerebral ischemia, we occluded the ascending aorta and caval veins of 9 dogs for 15 min. A fiberoptic catheter was inserted into the sagittal sinus to monitor venous oxygen saturation (S(SO)2) continuously. Blood samples were collected 30 min before and 30 min, 1 h, 2 h, 4 h and 6 h after the ischemic insult. Concentrations of ET-1 were assayed in the blood of the sagittal sinus and abdominal aorta. Before, during and after the aortic occlusion, we compared findings in a normothermic control Group 1 (pulmonary artery temperature 38.5 degrees C) (n = 4) with those in the mildly hypothermic Group 2 (pulmonary artery temperature 34.0 degrees C) (n = 5) by surface cooling induced before and maintained during and after ischemia for 6 h. Following ischemia, the plasma concentration difference of ET-1 (sagittal sinus--arterial) was significantly decreased in Group 2 (P < 0.05). Differences in S(SO)2 between the two groups were not statistically significant. Mild hypothermia reduced the ET-1 release in the cerebral circulation but did not improve cerebral oxygen metabolism after complete cerebral ischemia. Findings indicated that the decrease in ET-1 induced by mild hypothermia contributes to the improvement of the cerebral microcirculation after ischemia.

Animals↗
PubMed1996

[An immunohistochemical study of proliferating cell nuclear antigen (PCNA) and MIB-1 in epithelial hyperplasia and dysplasia of the vocal cords].

We investigated the proliferative activities in epithelial hyperplasia and dysplasia of the human vocal cords as precancerous lesions, using immunohistochemical staining with anti-PCNA and MIB-1 (anti-Ki-67) monoclonal antibody. The series for this study consisted of nine patients with hyperplasia, 12 with mild dysplasia, ten with moderate dysplasia, eight with severe dysplasia, eight with vocal cord polyps, and 14 with invasive squamous cell carcinoma. The following results were obtained: 1) The mean PCNA labeling index was 1.12 +/- 1.05 (MEAN +/- STD%) in polyp, 4.88 +/- 2.02 in hyperplasia, 2.76 +/- 1.76 in mild dysplasia, 3.80 +/- 2.03 in moderate dysplasia, 6.12 +/- 3.01 in severe dysplasia, and 19.07 +/- 10.37 in invasive cancer. 2) The mean MIB-1 positive rates were 5.50 +/- 2.47 (MEAN +/- STD%) in polyp, 13.08 +/- 6.86 in hyperplasia, 16.55 +/- 7.34 in mild dysplasia, 15.94 +/- 6.73 in moderate dysplasia, 21.43 +/- 8.16 in severe dysplasia, and 41.48 +/- 14.05 in invasive cancer. In cases of hyperplasia, dysplasia and invasive cancer, PCNA labeling index values and MIB-1 positive rates increased in proportion to the histological atypical grade increasing. Some lesions which recurred or progressed to cancer were found show high expression of PCNA and MIB-1. In cancer cases, there was no significant correlation between the PCNA labeling index, MIB-1 positive rates and either the degree of tumor cell differentiation or the T-classification. There was a positive correlation between the PCNA labeling index and MIB-1 positive rates among all cases. In this study, those cases showing a high PCNA labeling index and/or MIB-1 positive rates may indicate the possibility of recurrence or progression to malignancy in precancerous lesions of the vocal cords.

Aged↗
PubMed1995

Combined continuous monitoring of systemic and cerebral oxygen metabolism after cardiac arrest.

Cerebral oxygenation was assessed in 8 patients in cardiac arrest during the 24 h after resuscitation, by continuous fiber-optic monitoring of jugular bulb venous oxygen saturation (SjO2), in conjunction with continuous monitoring of mixed venous oxygen saturation (SvO2). Three patients survived and 5 died. SjO2 and SvO2 patterns were compared between surviving and non-surviving patients with regard to their prognostic and therapeutic implications. The mean SjO2 of the survivors (67%) was significantly lower than that of the non-survivors (80%) (P < 0.001), whereas the corresponding SvO2 value was higher in the survivor group (74%) than in the non-survivor group (64%) (P < 0.001). Three of the non-survivors died of brain death within 5 days after resuscitation, and then the others died of respiratory or cardiovascular failure without recovering from deep coma. The high SjO2 of the non-survivors suggests that an inability of damaged neurons to use oxygen may be an indicator of poor neurological outcome in resuscitated patients after cardiac arrest. When SjO2 was < 45%, Sv-O2 was extremely low, reflecting cardiovascular failure after resuscitation. SjO2 may thus serve to warn of deterioration in cardiopulmonary function and serve as a predictor of outcome in cardiac arrest survivors.

Brain↗
PubMed1995

Role of endothelin-1 in the failure of cerebral circulation after complete global cerebral ischemia.

The role of endothelin-1 (ET-1) in the failure of cerebral circulation after cardiac arrest is unknown. We evaluated the effect of complete global cerebral ischemia that was induced on the plasma ET-1 concentration in 5 dogs, by occluding the ascending aorta and caval veins for 15 min. A fiberoptic catheter was inserted into the sagittal sinus for the continuous monitoring of venous oxygen saturation. Blood samples were collected before and at 0.5, 1, 2, 4, and 6 h after the ischemic insult. The ET-1 concentration in the sagittal sinus and abdominal aorta was assayed. Complete global cerebral ischemia resulted in a significant 3-fold increase in the sagittal sinus concentration of ET-1 (P < 0.01) that was associated with a significant decrease in the sagittal sinus venous oxygen saturation (P < 0.01); the arterial ET-1 concentration remained unchanged. The difference between arterial and venous ET-1 concentrations during the hypoperfusion phase subsequent to the ischemic insult may result from an increased secretion of ET-1 by the cerebrovasculature and a decrease in the clearance of ET-1 in the cerebral circulation. The result suggests that ET-1 may contribute to the failure of cerebral circulation after cardiac arrest.

Animals↗
PubMed1993

Folimycin (concanamycin A), an inhibitor of V-type H(+)-ATPase, blocks cell-surface expression of virus-envelope glycoproteins.

Folimycin (concanamycin A) inhibited syncytium formation without affecting glycoprotein synthesis. Excretion of the glycoprotein (G protein) of vesicular stomatitis virus into the medium was blocked. Inaccessibility of the cell-associated viral G protein to protease added extracellularly indicates that cell-surface expression of the viral G protein is blocked by folimycin. The viral G protein accumulated intracellularly in the presence of folimycin electrophoresed a little faster than the control mature one excreted to the medium. Glycopeptides derived from the viral G protein bound to concanavalin A-agarose and were endo H-sensitive. Taken together these results indicate that processing of N-glycosidic oligosaccharide is incomplete in the presence of folimycin and suggest that intracellular trafficking is arrested before reaching at the latest to the trans Golgi compartments.

Animals↗
PubMed1991

Gd-DTPA-enhanced MR imaging of cryptococcal meningoencephalitis.

This report describes magnetic resonance (MR) imaging of biopsy-proved cryptococcal central nervous system (CNS) infection in a 31-year-old HIV negative man. Initial MR imaging revealed multi-focal Gd-DTPA enhancement and showed more lesions than contrast enhanced CT. The lesions regressed after antifungal therapy. MR imaging aids in diagnosis as well as helps to monitor the response to the pharmacological therapy of cryptococcal meningoencephalitis and possibly provides valuable insights into the pathophysiology of this condition.

Adult↗
PubMed1991

[A case of emphysematous cystitis with familial amyloidosis].

This is a report of the thirteenth known case in Japan of emphysematous cystitis. A 70-year-old man visited our hospital because of pollakisuria and macrohematuria on November 21, 1989. The patient had been known to have familiar amyloid polyneuropathy for the previous 3 years. Urinalysis showed marked hematopyuria. The residual urine was 216 cc, and urine cultures yielded 10,000,000 colonies of Escherichia coli per ml. Laboratory studies revealed systemic inflammatory findings, but no diabetic change. A plain X-ray film of the abdomen and an excretory urogram (DIP) showed small linear and round gas collections in the bladder shadow. A CT scan revealed multiple gas locules within the bladder wall. A diagnosis of emphysematous cystitis was established. The patient was given antibiotics, and there was striking clinical improvement. Histological examination of the endoscopically obtained biopsy specimen of the bladder revealed amyloidosis. We believe that this patient had a cystitis emphysematosa precipitated neurogenic bladder due to amyloid polyneuropathy and amyloidosis of the bladder.

Aged↗
PubMed1988

Transcatheter embolization in the treatment of massive bleeding due to maxillofacial injury.

Thirty-one cases of massive bleeding due to blunt maxillofacial injuries were treated by several procedures. Blind techniques, such as nasal and/or oral packing or ligation of external carotid artery, failed to achieve hemostasis in 13 of the 18 cases (72.2%) in which they were employed before 1984. Since then, carotid angiography has documented the location of the bleeding in 12 of the 13 cases (92.3%) in which it was employed. Each of the four cases in which extravasation was visualized from the external carotid artery was successfully treated by transcatheter embolization. We conclude that selective, angiographically guided embolization can reliably achieve hemostasis in a high proportion of patients with maxillofacial injury who are in danger of exsanguination from the branches of the external carotid artery.

Adult↗