Biomedical subjects

T Sakabe

Publications and source records attributed to T Sakabe.

At least 37 records · Page 2Linked to original sources

PubMed1999

Effects of graded suppression of the EEG with propofol on the neurological outcome following incomplete cerebral ischaemia in rats.

We evaluated the relation between dose and response for the neuroprotective effect of propofol in a rat model with incomplete cerebral ischaemia. For clarification of the mechanism of neuroprotection, plasma catecholamines and tumour necrosis factor-alpha levels were measured. Three doses (low, moderate and high-dose) of propofol were tested. These produced, respectively, a low amplitude, slowing and a burst-suppression pattern of electroencephalographic activity. Incomplete cerebral ischaemia was produced by right carotid artery occlusion combined with haemorrhagic hypotension (35 mmHg) for 30 min. Neurological outcome at 72 h post-ischaemia in the high-dose group was significantly better than that in both low-dose and moderate-dose groups. Propofol exhibited a trend in the dose-related attenuation of the increases in plasma adrenaline and noradrenaline during ischaemia. Tumour necrosis factor-alpha increased during and after ischaemia in all groups with no intergroup differences. The results indicate that a burst-suppression dose of propofol provides neuroprotection. The protective effect can not be completely explained by the attenuating effect on circulating catecholamines.

Anesthetics, Intravenous↗

PubMed1999

The effects of moderate hypothermia and intrathecal tetracaine on glutamate concentrations of intrathecal dialysate and neurologic and histopathologic outcome in transient spinal cord ischemia in rabbits.

UNLABELLED: The aim of the present study was to compare the effects of intrathecal tetracaine (a sodium channel blocker) with those of moderate hypothermia on glutamate concentrations of intrathecal dialysate, hindlimb motor functions, and histopathology in spinal cord ischemia. New Zealand White rabbits implanted with an intrathecal dialysis probe were assigned to one of the three groups (seven in each): control (temperature 38 degrees C), tetracaine (tetracaine 0.5%, 0.6 mL, given intrathecally 30 min before ischemia, 38 degrees C), or moderate hypothermia (32 degrees C). Spinal cord ischemia (20 min) was produced by occlusion of the abdominal aorta during isoflurane (1%) anesthesia. Glutamate concentrations significantly increased during ischemia in all groups, but the levels in the moderate hypothermia group were significantly lower than those in the control and tetracaine groups. Neurologic status (24 and 48 h after reperfusion) and histopathology (48 h) in the moderate hypothermia group were significantly better than in the other two groups. There were no significant differences between the tetracaine and control groups in either glutamate concentrations, neurologic status, or histopathology. We conclude that intrathecal tetracaine does not provide any protection against ischemic spinal cord injury, whereas moderate hypothermia does. IMPLICATIONS: Sodium channel blockers, including local anesthetics, have been shown to reduce glutamate release in brain ischemia and have a neuroprotective effect. However, in the present study, intrathecal tetracaine did not attenuate either glutamate release or the neurologic or histopathologic outcome in spinal cord ischemia, whereas moderate hypothermia did.

Anesthetics, Local↗

PubMed1999

The effects of N(G)-nitro-L-arginine-methyl ester on neurologic and histopathologic outcome after transient spinal cord ischemia in rabbits.

UNLABELLED: Little is known about the role of nitric oxide in the pathophysiology of spinal cord ischemia. We evaluated the effects of nitric oxide synthase (NOS) inhibition by N(G)-nitro-L-arginine-methyl ester (L-NAME) in rabbits whose abdominal aorta was occluded for 20 min (Experiment 1) or 25 min (Experiment 2). In Experiment 1, the L-NAME group (n = 6) received 3 mg/kg i.v. L-NAME, followed by an i.v. infusion of 3 mg x kg(-1). h(-1) until 6 h after reperfusion. Ischemia was induced 20 min after the start of L-NAME. The phenylephrine group (n = 6) received phenylephrine to maintain comparable blood pressure. The control group (n = 6) received saline. In Experiment 2, L-NAME (3 mg/kg i.v. L-NAME, followed by an i.v. infusion of 3 mg x kg(-1). h(-1) until 6 h after reperfusion) and phenylephrine groups (n = 6 each) were studied. Ischemia was induced 100 min after the start of L-NAME. Forty-eight hours after reperfusion, hindlimb motor function and histopathology of the spinal cord were examined. In Experiment 1, L-NAME and phenylephrine both improved neurologic outcome, with higher intraischemic blood pressures than saline. In Experiment 2, L-NAME worsened the neurologic and histopathologic outcome compared with phenylephrine. Attenuation of damage by L-NAME in Experiment 1 may be attributable to an intraischemic blood pressure increase. The worse outcome with L-NAME in Experiment 2 suggests that NOS inhibition exacerbates ischemic spinal cord damage. IMPLICATIONS: Nonselective inhibition of nitric oxide synthase activity has aggravating effects on the neurologic and histopathologic outcome after transient spinal cord ischemia.

Animals↗

PubMed1999

Comparative genomic hybridization of squamous cell carcinoma of the esophagus: the possible involvement of the DPI gene in the 13q34 amplicon.

We investigated copy number aberrations in 29 primary tumors and 12 cell lines of esophageal squamous cell carcinoma (ESC) using comparative genomic hybridization. In the primary tumors, the most common sites of copy number gains were 3q26.3-27 (45%), 8q24 (41%), 5p15 (38%), Xq27-28 (38%), 14q32 (31%), 11q13 (28%), and 20q13.3 (28%). High-level gains (HLGs) indicative of gene amplifications were identified at 11q13 in two cases, and in one case each at 2q33-34, 3q25-29, 5p15.1-15.2, 7q21-22, 11p11.2, 12p11.2-12, and 13q34. Recurrent losses were observed only at 9p13(17.2%). In the 12 ESC cell lines, the most common sites of HLGs were 5p15.1-15.3 (four cases), 11q13 (four cases), 8q24.1-24.2 (three cases), 20q13.2-13.3 (three cases), 3q26.3 (two cases), and 7p15-22 (two cases). Less frequent HLGs (one case each) were observed at 2p16-22, 3q25, 7p12-14, 7q21-22, 9q34, 10q21, 11p11.2, 14q13-14, 14q31-32, 15q22-26, and 17p11.2. Chromosomes and chromosome arms that showed frequent losses in the cultured lines were 18q (58%), 4 (50%), 9p (50%), and 3p (42%). These findings provide evidence for a number of previously unknown genomic aberrations in ESC, suggesting target regions for positional cloning of genes relevant to carcinogenesis in the esophagus. In particular, we identified a significant amplification of the DPI gene (TFDPI), a transcription factor that forms heterodimers with E2FI, in the single primary tumor that exhibited HLG at 13q34.

Blotting, Southern↗

PubMed1999

[Microbiological laboratories for sepsis in the 21st century].

A new concept, "SIRS (systemic inflammatory response syndrome)", introduced for the use of innovative therapies in sepsis, indicates the importance of clinically satisfying services in the laboratories. Appropriate laboratory management of the host, parasite and environment, is needed for the diagnosis, treatment and prevention of sepsis. Improvement of environmental conditions is expected to contribute to the prevention of sepsis by nosocomial infections. Another important key in the management is quality assurance in blood cultures, which involves three issues that must be improved. Concerning the first two issues, high sensitivity and low contamination, balanced procedures must be performed to ensure cost-effectiveness. Regarding the third issue, we proposed a quick return system for positive blood cultures. We need to reconsider the traditional concept of "time" in microbiological tests and employ practical measures for sepsis in clinical laboratories.

Clinical Laboratory Techniques↗

PubMed1998

The hydroxyl radical scavenger Nicaraven inhibits glutamate release after spinal injury in rats.

Neuronal degeneration after trauma is mediated in part by release of excitatory amino acids (EAAs) and oxygen free radicals (OFR). We evaluated the effect of i.v. treatment with a hydroxyl radical scavenger ((+/-)-N,N'-propylenedinicotinamide; AVS) and spinal hypothermia (33 degrees C) on spinal CSF glutamate release after spinal trauma. In a control group, spinal compression evoked at 10 min a significant increase (5-fold) in glutamate which declined over 4 h (2.1-fold). AVS treatment attenuated glutamate release but had no additive effect. These data suggest that this compound can be effective in modulating spinal excitotoxicity resulting from increased OFR synthesis and corresponding potentiation of EAA release.

Animals↗

PubMed1998

Identification of amplified DNA sequences on double minute chromosomes in a leukemic cell line KY821 by means of spectral karyotyping and comparative genomic hybridization.

Double minute chromosomes (dmin) are cytogenetic hallmarks of amplified genes. Using spectral karyotyping (SKY) and comparative genomic hybridization (CGH), we identified the origin of amplified DNA in a leukemic cell line, KY821, that harbors numerous dmin. The SKY revealed that the DNA sequences of dmin are derived from materials of chromosome 8, and CGH showed a high degree of overrepresentation only at 8q22-24, indicating that in KY821 only chromosomal material of 8q22-24, containing MYC, is amplified in dmin. An approach combining SKY with CGH should facilitate efforts to identify novel chromosomal regions of gene amplification and contribute information about genetic lesions that underly neoplastic tumors.

DNA, Neoplasm↗

PubMed1998

Postischemic reperfusion induces alpha-fodrin proteolysis by m-calpain in the synaptosome and nucleus in rat brain.

A membrane cytoskeletal protein, fodrin, is a substrate for a Ca2+-dependent protease, calpain. It remains unknown whether mu-calpain or m-calpain is involved in the proteolysis of either alpha- or beta-fodrin and in what subcellular localization during ischemia and reperfusion of the brain. To address these issues, we examined the distribution of fodrin and calpain and the activities of calpain and calpastatin (endogenous calpain inhibitor) in the same subcellular fractions. Rat forebrain was subjected to ischemia by a combination of occlusion of both carotid arteries and systemic hypotension, whereas reperfusion was induced by releasing the occlusion. Immunoblotting, activity measurement, and casein zymography did not detect the presence of mu-calpain or a significant change of m-calpain level after ischemia or reperfusion. However, casein zymography revealed a unique Ca2+-dependent protease that was eluted with both 0.18 and 0.40 M NaCl from a DEAE-cellulose column. Alpha- and beta-fodrins and m-calpain were found to be rich in the synaptosomal, nuclear, and cytosolic subfractions by immunoblotting analysis. Reperfusion (60 min) following ischemia (30 min) induced selective proteolysis of alpha-fodrin, which was inhibited by a calpain inhibitor, acetylleucylleucylnorleucinal (400 microM, 1 ml, i.v.). The mu-calpain-specific fragment of beta-fodrin was not generated during ischemia-reperfusion, supporting the possibility of the involvement of m-calpain rather than mu-calpain in the alpha-fodrin proteolysis.

Animals↗

PubMed1998

Effects of nicardipine on ventriculo-arterial coupling in humans.

The ratio of effective arterial elastance (Ea) to left ventricular elastance (Ees) is an indicator of the coupling between ventricular properties and arterial load properties. Another criterion for the coupling between an energy source and its load is the principle of economical fuel consumption, or mechanical efficiency, which is defined as the ratio of stroke work (SW) to myocardial oxygen consumption per beat (MVO2). It has been revealed that SW of ventricular contraction is maximized when Ea/Ees = 1, while mechanical efficiency is maximized when Ea/Ees = 0.5. The purpose of the present study was to investigate the ventriculo-arterial coupling during hypertension, and the effects of nicardipine on this relationship in surgical patients using Ea/Ees and SW/MVO2 as indicators. Anaesthesia was maintained with isoflurane, nitrous oxide, and fentanyl. Radial artery pressure was displayed on a polygraph, and left ventricular end-systolic and end-diastolic volumes were determined by use of transoesophageal echocardiography. Ees was calculated as MAP/(ESVI-4), where MAP is mean arterial pressure and ESVI is end-systolic volume index. Ea was calculated as the ratio of MAP to stroke volume index (SVI). Stroke work index (SWI) was calculated as the product of MAP and SVI. MVO2 was assessed by estimating the ventricular pressure-volume area index (PVAI), which is expressed as the sum of SWI and the end-systolic potential energy index. Before (baseline), and 3, 10, 20, and 30 min after i.v. nicardipine (30 micrograms kg-1), Ea/Ees and SWI/PVAI were determined in 14 surgical patients with intraoperative hypertension. Before nicardipine (during hypertension), Ea was almost equal to Ees, whereas Ea/Ees was significantly reduced to about 0.5-0.6 at 3, 10, and 20 min after nicardipine. SWI/PVAI was maximized and significantly greater than the baseline value at 3 min after nicardipine. These results suggest that, during hypertension, ventricular and arterial properties were so matched as to maximize SW at the expense of the work efficiency, whereas mechanical efficiency of ventricular contraction was maximized after nicardipine.

Adult↗

PubMed1998

Cerebrovascular CO2 reactivity during anesthesia in patients with diabetes mellitus and peripheral vascular disease.

BACKGROUND: Diabetes mellitus (DM) and systemic atherosclerosis are risk factors for stroke. Although the origins of increased risk are complex, one possibility is that cerebrovascular reactivity is impaired and does not allow the brain to compensate for aberrations in physiology. The current study tested this issue by evaluating mean blood flow velocity of the middle cerebral artery (Vmca) and carbon dioxide reactivity during anesthesia in patients with DM and peripheral vascular disease (PVD). METHODS: Fifty-two patients were observed: 20 patients with DM (the DM group), 12 patients with PVD (the PVD group), and 20 patients classified as American Society of Anesthesiologists physical status 1 or 2 (the control group). The Vmca was measured using transcranial Doppler ultrasonography during isoflurane-nitrous oxide anesthesia. After measuring baseline Vmca at a partial pressure of carbon dioxide in arterial blood (PaCO2) of 37.7 +/- 4.5 mmHg (mean +/- SD), measurements were repeated at a PaCO of 44.2 +/- 3.8 mmHg, and the carbon dioxide reactivity (absolute value: cm x s(-1) x mmHg(-1); relative value: percentage of baseline Vmca/mmHg) was calculated. RESULTS: The baseline Vmca of the DM group (51 +/- 12 cm/s) was significantly greater than those of the control group (42 +/- 6 cm/s) and the PVD group (42 +/- 13 cm/s). The absolute and relative values of carbon dioxide reactivity in the DM group (3.1 +/- 1.3 cm x s(-1) x mmHg(-1); 6.3 +/- 2.4%/mmHg) were significantly greater than or equivalent to those of the control group (2.3 +/- 0.8 cm x s(-1) x mmHg(-1); 5.3 +/- 1.7%/mmHg), respectively. In the PVD group, the baseline Vmca was equivalent to the control group, but the carbon dioxide reactivity (1.1 +/- 0.5 cm x s(-1) x mmHg(-1) 2.8 +/- 1.2%/mmHg) was significantly less. CONCLUSIONS: The patients with DM have increased baseline cerebral blood flow velocity and normal carbon dioxide reactivity during anesthesia. The patients with PVD have decreased carbon dioxide reactivity, but baseline flow velocity is maintained.

Adult↗

PubMed1998

[Changes in psychological features in patients for anesthesia and operation during perioperative period].

The purpose of this study was to assess perioperative changes in psychological features of patients receiving anesthesia and operation. Anxiety level and desire for obtaining information were evaluated in 37 patients using the Amsterdam preoperative anxiety and information scale (APAIS) at three points: before and after the preanesthetic examination, and 3 to 5 days after the operation. Anxiety scale (4-20) and information scale (2-10) scores decreased postoperatively from 9.8 +/- 3.8 to 7.3 +/- 3.4 and from 6.1 +/- 2.1 to 4.1 +/- 1.9, respectively. There was a significant but weak correlation (rs = 0.35) between the anxiety scale and information scale before the preanesthetic examination. The postoperative information scale score correlated well with preoperative anxiety scale score (rs = 0.61), and this correlation was higher than with preoperative information scale score (rs = 0.37). When patients were divided into two subgroups, namely patients with (U, n = 12) or without (non-U, n = 25) an increase in postoperative information scale score, anxiety scale score before the preanesthetic examination tended to be higher and the postoperative anxiety scale score was significantly higher in the U group than in the non-U group. We conclude that we should provide more information to the patients who have higher anxiety scale score before the preanesthetic examination regardless of their degree of desire for information.

Adult↗

PubMed1997

Mild and moderate hypothermia provide better protection than a burst-suppression dose of thiopental against ischemic spinal cord injury in rabbits.

BACKGROUND: Controversy exists over the efficacy of different methods for protecting the spinal cord against experimental ischemic injury. Therefore, the authors compared the protective effects of thiopental with those of hypothermia (35 degrees C and 32 degrees C) on hindlimb motor functions and histopathology after transient spinal cord ischemia. METHODS: Twenty-seven New Zealand white rabbits were assigned to one of the four groups: a thiopental-normothermia group (burst-suppression dose of thiopental; esophageal temperature = 38 degrees C; n = 7), a halothane-mild hypothermia group (halothane, 1%; esophageal temperature = 35 degrees C; n = 7), a halothane-moderate hypothermia group (halothane, 1%; esophageal temperature = 32 degrees C; n = 6), and a halothane-normothermia group (halothane, 1%; esophageal temperature = 38 degrees C; n = 7). The animals were then subjected to 20 min of spinal cord ischemia produced by occlusion of the aorta distal to the origin of left renal artery. Hindlimb motor function was observed for 48 h after reperfusion. Histopathology of the lumbar spinal cord also was examined. RESULTS: All animals in the halothane-mild hypothermia and halothane-moderate hypothermia groups were neurologically normal 48 h after ischemia. There was no statistical difference in the final neurologic status and histopathology between the thiopental-normothermia and halothane-normothermia groups. However, the final neurologic status and histopathology in both groups were worse than in the halothane-mild hypothermia or halothane-moderate hypothermia groups. There was a strong correlation between the final neurologic status and the numbers of normal neurons in the anterior spinal cord. CONCLUSIONS: These results suggest that mild and moderate hypothermia protects against ischemic spinal cord injury in rabbits, and a burst-suppression dose of thiopental does not offer any advantage over halothane.

Anesthetics, Intravenous↗

PubMed1997

Blood flow velocity of middle cerebral artery during prolonged anesthesia with halothane, isoflurane, and sevoflurane in humans.

BACKGROUND: It is not clear whether the increase of cerebral blood flow (CBF) produced by volatile anesthetics is maintained during prolonged anesthesia. In a previous study, the authors found that CBF equivalent, an index of flow-metabolism relationship, was stable over 3 h, suggesting no decay over time in CBF for 3 h during volatile anesthesia in humans. However, it may be possible that CBF changes in a parallel fashion to functional metabolic changes. In this study, to estimate the response of CBF to three volatile anesthetics, the authors used transcranial Doppler (TCD) ultrasonography to measure time-averaged mean velocity in the middle cerebral artery (Vmca). METHODS: Twenty-four surgical patients were randomly assigned to three groups to receive halothane, isoflurane, or sevoflurane (eight patients, each). End-tidal concentration of the selected volatile anesthetic was maintained at 0.5, 1.0, and 1.5 MAC before surgery and then at 1.5 MAC during surgery, which lasted more than 3 h. Normothermia and normocapnia were maintained. Mean arterial blood pressure was kept above 70 mmHg, using phenylephrine infusion, if necessary. TCD recordings of the Vmca were performed continuously. RESULTS: Vmca at 0.5 MAC of halothane, isoflurane, and sevoflurane was 49 +/- 19, 57 +/- 8, and 48 +/- 13 cm/s, respectively. Halothane significantly (P < 0.01) increased Vmca in a dose-dependent manner (0.5, 1.0, 1.5 MAC), whereas isoflurane and sevoflurane produced no significant dose-related changes. At 1.5 MAC for 3 h, Vmca changed significantly (P < 0.05) for the time trends, but it did not exhibit decay over time with all drugs. During burst suppression, observed electroencephalographically (EEG) on patients during isoflurane and sevoflurane anesthesia, the onset of a burst increased Vmca (approximately 5-30 cm/s), which was maintained for the duration of the burst. CONCLUSIONS: The results indicate that there was no decay in Vmca over time during prolonged (3 h) inhalation of volatile anesthetics at 1.5 MAC in humans. The fluctuation of Vmca during burst suppression on EEG at 1.5 MAC indicates that the flow-metabolism coupling occurred.

Adult↗

PubMed1996

Prognostic factors for patients with colon or rectal carcinoma treated with resection only. Five-year follow-up report.

BACKGROUND: The prognostic factors and natural history of recurrence in patients with colorectal carcinoma who underwent curative resection and no other therapy were analyzed. METHODS: The object of analysis was the potentially curative resection only subgroup in the randomized clinical trial (RCT) that we performed. Cox's proportional hazards model was used mainly to analyze recurrence rates during the first 5 years after surgery. RESULTS: The analysis was performed on a subgroup of the RCT (279 patients with colon carcinoma and 293 patients with rectal carcinoma). Five-year disease free survival rates were 76.3% and 56.5% for colon and rectal carcinomas, respectively. The prognostic factors for recurrence for colon carcinoma patients were different from those with rectal carcinoma. For colon carcinoma, only Dukes stage was significant, whereas for rectal carcinoma, Dukes stage, age, location of the tumor, and serosal and venous invasion by cancer cells were prognostic factors. Log-transformed disease free survival rates were linear in Dukes Stage B and biphasic in Dukes Stage C for both colon and rectal carcinoma. The two phases in Dukes Stage C intersected at 2.85 and 3.04 years, respectively. The annual hazard value was high for the first 3 years in both colon and rectal carcinoma. CONCLUSIONS: We conclude that follow-up of patients with colorectal carcinoma who undergo potentially curative resection is of particular importance in the first 3 years after surgery. Furthermore, the usefulness of adjuvant chemotherapy can be adequately evaluated from data yielded during this postoperative period.

Chemotherapy, Adjuvant↗

PubMed1996

Prognostic factors of colorectal cancer. Results of multivariate analysis of curative resection cases with or without adjuvant chemotherapy.

One thousand two hundred fifty-four cases (610 colonic and 644 rectal cancers resected during 2 years from 1984 and followed up for more than 5 years) were entered from 140 institutions in Japan and analyzed by means of Cox's proportional hazards model. The analyzed pathologic variables were the size and depth of invasion, Dukes' stage, venous invasion, lymphatic permeation, and other clinical features, such as the sex and age of the patient and location of the tumor. The extent of dissection, serum carcinoembryonic antigen (CEA) level, and the presence or absence of adjuvant chemotherapy were also analyzed. Adjuvant chemotherapy consisted of three arms for both colonic and rectal cancers. For colonic cancer, arm I was a combination of i.p. (intraportal) and i.v. mitomycin C (MMC) + p.o. 5-fluorouracil (5-FU); arm II was i.v. MMC + p.o. 5-FU; and arm III was surgery only. For rectal cancer, arm IV was a combination of i.a. (inferior mesenteric artery) and i.v. MMC + p.o. 5-FU; arm V was i.v. MMC + p.o. 5-FU; and arm VI was surgery only. As for the factors affecting the disease-free survival of the patient, multivariate analysis disclosed nodal involvement, venous invasion, an elevated CEA level, and the lower part of the rectum. The effect of adjuvant chemotherapy on the patient's survival was proven for rectal cancer but not for colonic cancer. We conclude that these factors should be considered in setting the stage of tumor pre- and postoperatively.

Aged↗

PubMed1996

Preservation of the ration of cerebral blood flow/metabolic rate for oxygen during prolonged anesthesia with isoflurane, sevoflurane, and halothane in humans.

BACKGROUND: In several animal studies, an increase in cerebral blood flow (CBF) produced by volatile anesthetics has been reported to resolve over time during prolonged anesthesia. It is important to investigate whether this time-dependent change of CBF takes place in humans, especially in clinical situations where surgery is ongoing under anesthesia. In this study, to evaluate the effect of prolonged exposure to volatile anesthetics (isoflurane, sevoflurane, and halothane), the CBF equivalent (CBF divided by cerebral metabolic rate for oxygen (CMRO2) was determined every 20 min during anesthesia lasting more than 4h in patients. METHODS: Twenty-four surgical patients were assigned to three groups at random to receive isoflurane, sevoflurane, or halothane (8 patients each). End-tidal concentration of the selected volatile anesthetic was maintained at 0.5 and 1.0 MAC before surgery and then 1.5 MAC for the 3 h of surgical procedure. Normothermia and normocapnia were maintained. Mean arterial blood pressure was kept above 60 mmHg, using phenylephrine infusion, if necessary. CBF equivalent was calculated every 20 min as the reciprocal of arterial-jugular venous oxygen content difference. RESULTS: CBF equivalent at 0.5 MAC of isoflurane, halothane, and sevoflurane was 21 +/- 4, 20 +/- 3, and 21 +/- 5 ml blood/ml oxygen, respectively. All three examined volatile anesthetics significantly (P<0.01) increased CBF equivalent in a dose-dependent manner (0.5, 1.0, 1.5 MAC). AT 1.5 MAC, the increase of CBF equivalent with all anesthetics was maintained increased with minimal fluctuation for 3 h. The mean value of CBF equivalent at 1.5 MAC in the isoflurane group (45 +/- 8) was significantly (P<0.01) greater than those in the halothane (32 +/- 8) and sevoflurane (31 +/- 8) groups. Electroencephalogram was found to be relatively unchanged during observation periods at 1.5 MAC. CONCLUSIONS: These results demonstrate that CBF/CMRO2 ratio is markedly increased above normal and maintained during prolonged inhalation of volatile anesthetics in humans. It is impossible to determine whether these data indicate a stable CBF or whether CBF and CMRO2 are changing in parallel during the observation period. The unchanging electroencephalographic pattern suggests that the former possibility is more likely and that the increase of CBF produced by volatile anesthetics is maintained over time without decay, which has been reported in several animal studies. It also is suggested that isoflurane possesses greater capability to maintain global CBF relative to CMRO(2) than does halothane or sevoflurane. time.)

Adult↗

PubMed1996

[Comparative clinical study of adjuvant postoperative chemotherapy (5-FU, Tegafur, 5-FU + MMC) in curatively resected cases of gastric cancer. Study Group on 5-FU Oral Adjuvant Chemotherapy in Gastric Cancer].

A multi-center collaborative study was conducted in curatively resected gastric cancer patients at Stages II and III to compare oral 5-FU (Group A), oral Tegafur (Group B) and i.v. MMC + oral 5-FU (Group C). From May 1982 to April 1985, 1,012 cases were enrolled at 55 institutions. Some 138 (13.8%) were excluded, and 874 were analyzable. In the analysis of background factors, Group B had more cases with tumor of large diameter and advanced Stage. Adverse effects were relatively mild in all groups, and there was no problem in drug tolerance. Five-year survival rate was 67.6%, 62.4% and 68.6% in Groups A, B and C, respectively, reflecting no significant difference among them. It was 85.0%, 83.0% and 81.1% in Stage II and 52.5%, 51.0% and 59.0% in Stage III of Groups A, B and C, respectively. No significant difference was found, but Stage III of Group C showed a slightly higher survival rate. Supportive clinical study will be required to assess the usefulness of MMC as an introduction therapy. We found no difference in efficacy between 5-FU and Tegafur as maintenance therapy. The life-prolongation effect of fluoropyrimidines in comparison with surgery alone should be studied separately.

Adult↗

PubMed1995

A saponin conjugated with 2,3-dihydro-2,5-dihydroxy-6-methyl-4H-pyran-4-one from Dolichos lablab.

A new 2,3-dihydro-2,5-dihydroxy-6-methyl-4H-pyran-4-one (DDMP)-conjugated saponin, lablab saponin I, was isolated from the hypocotyl of hyacinth bean (Dolichos lablab). The structure was elucidated by 1H NMR and 13C NMR spectroscopy and chemical techniques as 3-O-[alpha-L-rhamnopyranosyl- (1-->2)-beta-D-galactopyranosyl(1-->2)-beta-D-glucuronopyranosyl(1 -->)]-22-O- [2,3-dihydro-2,5-dihydroxy-6-methyl-4H-pyran-4-one(2'-->)]-3 beta, 22 beta, 24-trihy-droxyolean-12-en-28-al. SOD (superoxide dismutase)-like activity depended upon the DDMP group and the aldehyde group (C-28) of the aglycone was observed in the order of lablab saponin I > glutathione > soyasaponin beta g > maltol. The soybean saponin Bb, lacking the DDMP moiety was found not to exhibit the SOD-like activity.

Carbohydrate Conformation↗