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Biomedical subjects

Y Nakata

Publications and source records attributed to Y Nakata.

At least 163 records · Page 9Linked to original sources

Evaluation of uptake and release of technetium-99m MIBI SPECT of pulmonary and mediastinal lesions.

We evaluated the uptake and release of Tc-99m MIBI in 7 benign and 30 malignant pulmonary and mediastinal lesions. Of the 37 patients, 13 underwent surgery; malignant involvement was examined in 21 mediastinal lymph nodes. Tl-201 SPECT was also performed in 10 patients. Tc-99m MIBI SPECT studies were performed on transverse SPECT images acquired 30 minutes and 3 hours after intravenous injection of 600 MBq of Tc-99m MIBI with three gamma camera detectors (GCA-9300A). Regions of interest were set in the area of abnormal uptake of Tc-99m MIBI and in an area of normal tissue in the contralateral lung. The uptake ratio of the lesion in the contralateral normal lung was obtained on the early image (early ratio; ER) as well as the delayed image (delayed ratio; DR). The benign lesions showed significantly lower ER (1.6 +/- 0.3) and DR (1.4 +/- 0.4) than the malignant lesions (1.9 +/- 0.5 and 1.8 +/- 0.5, respectively; both p < 0.05). There was no significant difference in the retention index (RI), calculated as RI = (DR-ER)/ER x 100. The DR obtained with Tl-201 SPECT images was significantly higher than that obtained with Tc-99m MIBI SPECT (p < 0.05). For the detection of mediastinal lymph node metastases, the early images showed sensitivity, specificity, and accuracy of 85.7%, 100%, and 95.2%, respectively, for the delayed images these values were 85.7%, 92.9%, and 90.5%, respectively. These results suggest that the uptake ratio of Tc-99m MIBI is a useful index in assessing benign or malignant pulmonary and mediastinal lesions.

Aged↗

An enzyme- linked immunosorbent assay for heparan sulfate proteoglycans.

An enzyme- linked immunosorbent assay (ELISA) for heparan sulfate proteoglycan (HSPG) was developed based on the high affinity binding profile of HSPG to lipoprotein lipase (LPL). LPL was shown to bind to precoated HSPG in dose dependent manner and was determined spectrophotometrically using specific anti- LPL antibody. This ELISA allowed to evaluate HSPG produced by PC12 cell with clear linearity at range of 10 - 500 ng/ml. Soluble chondroitin sulfate proteoglycan (CSPG) from rat brain, which was not detectable by this method, did not exhibit any inhibitory effects on affinity binding of HSPG to LPL, even if 8 times higher concentrations of CSPG to HSPG was added. The sensitivity of this ELISA was about 100 times higher than that of conventional carbazole reaction method. These findings indicated its potential usefulness of this method for measuring small amounts of HSPG capable of binding to LPL and for studying biological implications of HSPG - LPL interaction.

Animals↗

Effectiveness of an antioxidant in preventing restenosis after percutaneous transluminal coronary angioplasty: the Probucol Angioplasty Restenosis Trial.

OBJECTIVES: The Probucol Angioplasty Restenosis Trial was a prospective, randomized, controlled study that investigated the effectiveness of probucol therapy in reducing the rate of restenosis after percutaneous transluminal coronary angioplasty (PTCA). BACKGROUND: Antioxidants have an inhibitory effect on smooth muscle cell growth in experiments in vitro and in vivo, which suggests a possible pharmacologic effect on restenosis after PTCA. METHODS: One hundred one patients were randomly assigned to receive 1,000 mg/day of probucol or control (no lipid-lowering) therapy 4 weeks before PTCA. After 4 weeks of premedication, both groups underwent PTCA. Probucol was continued until follow-up angiography 24 weeks after PTCA. Angiographic results were analyzed at a core laboratory by quantitative coronary angiography. RESULTS: Dilation was successful in 46 of 50 patients in the probucol group and 45 of 51 in the control group. At follow-up angiography 24 weeks after angioplasty, angiographic restenosis occurred in 9 (23%) of 40 patients in the probucol group and 22 (58%) of 38 in the control group (p = 0.001). Minimal lumen diameter was 1.49 +/- 0.75 mm (mean +/- SD) in the probucol group and 1.13 +/- 0.65 mm in the control group (p = 0.02). Percent diameter stenosis at follow-up angiography in the probucol group was significantly lower than that in the control group (43.9% vs. 56.4%, p = 0.009). The late loss was 0.37 +/- 0.69 mm in the probucol group and 0.60 +/- 0.62 mm in the control group (p = 0.13). The loss/gain ratio was 0.32 +/- 0.74 in the probucol group and 0.56 +/- 0.81 in the control group (p = 0.059). Net gain was greater in the probucol group than in the control group (0.77 +/- 0.70 vs. 0.48 +/- 0.59 mm, p = 0.053). CONCLUSIONS: Probucol administered beginning 4 weeks before PTCA appears to reduce restenosis rates.

Aged↗

Insulin resistance is related to silent cerebral infarction in patients with essential hypertension.

Recently, hyperinsulinemia or insulin resistance has been suggested to be a risk factor for cardiovascular diseases. We evaluated the role of insulin resistance in the occurrence of silent cerebral infarction in 28 patients with essential hypertension (40 to 75 years, 157 +/- 4/89 +/- 2 mm Hg). Patients with diabetes mellitus or obesity (BMI > or = 30) were excluded. Insulin resistance was evaluated by means of constant glucose infusion rate (M value) during euglycemic-hyperinsulinemic glucose clamp test. Infarction was defined as a focal area with prolonged T1 and T2 relaxation times that was > 5 mm in diameter on brain magnetic resonance imaging. The severity of periventricular hyperlucency was evaluated by the distribution of the high intensity area. The number of silent infarctions significantly correlated only with the M value (F = 7.58, R2 = 0.23, P = .01) in multiple regression analysis using all variables: age, blood pressure, smoking history, lipid profile, levels of plasma glucose and insulin on fasting, and total amounts during 75-g OGTT. However, the severity of periventricular hyperlucency did not show a correlation with any factors. The occurrence of cerebral infarction was significantly correlated with thickening of the intima-media complex (IMC) of the common carotid artery on B-mode ultrasonography (F = 8.43, R2 = 0.25, P < .01). In conclusion, insulin resistance and thickening of IMC show a close relationship with the occurrence of silent cerebral infarction. Therefore, it may be important to improve insulin resistance for prevention of cerebral infarction in essential hypertensives.

Carotid Arteries↗

Polymorphism of angiotensin converting enzyme, angiotensinogen, and apolipoprotein E genes in a Japanese population with cerebrovascular disease.

The homozygous deletion allele of the angiotensin converting enzyme gene (ACE/DD), homozygous threonine allele of the angiotensinogen gene (AGN/TT), and the epsilon4 allele of the apolipoprotein E gene (apoE/epsilon4) are reported to be associated with ischemic heart disease. Cerebrovascular disease (CVD) is another atherosclerotic disease; and the effects of these polymorphisms on CVD have been confusing. In this study, we investigated whether ACE/DD, AGN/TT, and apoE/epsilon4 genotypes are associated with CVD and whether genetic risk is enhanced by the effect of one upon another. We ascertained these genotypes in patients with cerebral infarction (n = 55) and cerebral hemorrhage (n = 38), diagnosed by brain computed tomography. Control subjects for the infarction group and the hemorrhage group were randomly selected from 583 subjects matched for age, gender, and history of hypertension with patients. Frequency of ACE/DD genotype was higher in the patients with infarction than in the controls (chi2 = 6.1, P < .05). The AGN/TT genotype was not associated with either infarction or hemorrhage, but it increased the relative risk for cerebral infarction in the subjects with ACE/DD genotype (chi2 = 8.0, P < .01, odds ratio; 11.7, 95% confidence intervals: 1.4 to 96.0). There was no significant association between apoE/epsilon4 and CVD. These results suggest that ACE/DD predicts cerebral infarction, but not cerebral hemorrhage, and that AGN/TT enhances the risk for cerebral infarction associated with ACE/DD.

Adult↗

Echocardiographic evaluation of global left ventricular function during high thoracic epidural anesthesia.

OBJECTIVES: To assess the effects of high thoracic epidural anesthesia on left ventricular (LV) diastolic filling and systolic function in patients without heart disease. DESIGN: Prospective study. SETTING: University hospital. PARTICIPANTS: 24 ASA physical status I and II patients scheduled for elective noncardiac surgery. INTERVENTIONS: Patients received high thoracic (HTE; n = 12) or low thoracic (LTE; n = 12) epidural anesthesia. MEASUREMENT AND MAIN RESULTS: Left ventricular diastolic filling was noninvasively determined by precordial echocardiography using a pulsed Doppler technique and with a newly developed acoustic quantification (AQ) method that automatically detects endocardial borders and measures cavity area. All measurements were performed in awake premedicated patients. In the HTE group, the extent of sensory blockade of T1-T5, at the least, was induced with 2% lidocaine 5 ml. During HTE, systolic blood pressure (119 +/- 16 vs. 108 +/- 14 mmHg, p < 0.01), heart rate (73 +/- 9.8 vs. 63 +/- 6.8 beats/min, p < 0.01), cardiac output (CO; 4.5 +/- 1.1 vs. 3.8 +/- 1.2 L/min, p < 0.05), and fractional area change (50 +/- 11 vs. 37 +/- 11%, p < 0.01) decreased significantly, whereas end diastolic area (9.4 +/- 1.4 vs. 10.3 +/- 1.1 cm2, p < 0.01) and end systolic area (4.8 +/- 1.3 vs. 6.0 +/- 1.1 cm2, p < 0.05) showed a significant increase. As a result, stroke volume was kept constant (63 +/- 14 vs. 60 +/- 19 ml). Pulsed Doppler derived indices such as peak velocity during the early filling (E) and the atrial contraction (A) phases, peak early to atrial velocity ratio (E/A), and acceleration time remained unchanged. AQ derived peak dA/dt during the early diastolic (D1) and the atrial contraction phases (D2) and D1/D2 also remained unchanged. In contrast, in the LTE group, no significant differences were noted in all systolic and diastolic indices obtained by pulsed Doppler and AQ method. CONCLUSIONS: High thoracic epidural anesthesia causes a decrease in CO without changing LV ejection and diastolic filling performance in healthy subjects.

Adult↗

5-Hydroxytryptamine-facilitated release of substance P from rat spinal cord slices is mediated by nitric oxide and cyclic GMP.

The role of nitric oxide (NO) in the control of 5-hydroxytryptamine (5-HT)-induced release of substance P was investigated in rat spinal cord in vitro. 5-HT facilitated the 60 mM K(+)-evoked release of substance P-like immunoreactive materials (SPLI) from the superfused rat dorsal spinal cord slices without affecting spontaneous SPLI release. The facilitatory effect of 5-HT was significantly inhibited by ICS 205-930 or granisetron (potent and specific 5-HT3 receptor antagonists), by NG-monomethyl-L-arginine (NMMA, a NO synthase inhibitor), and by methylene blue or 1H-[1,2,4] oxadiazolo [4,3-a] quinoxaline-1-one (MB or ODQ, respectively; both are inhibitors of soluble guanylyl cyclase) and was mimicked by 2-methylserotonin (2-m-5-HT, a selective 5-HT3 receptor agonist), L-arginine (a precursor of NO), or 8-bromo-cyclic GMP. NMMA, MB, or ODQ inhibited the 2-m-5-HT-induced increase of cyclic GMP levels in the rat dorsal spinal cord slices. These data suggest that the facilitatory effect of 5-HT on the release of SPLI is mediated by the 5-HT3 receptor and that the intracellular signaling is mediated via NO by an increase in cyclic GMP production.

Animals↗

Emergence times from xenon anaesthesia are independent of the duration of anaesthesia.

Xenon (MAC = 71%) has an extremely low blood:gas partition coefficient (0.14). Therefore, we predicted that the rate of emergence from xenon anaesthesia would not be affected greatly by duration of anaesthesia. We studied 54 ASA I-II patients undergoing lower abdominal surgery who received equal MAC anaesthesia with 60% xenon, 60% nitrous oxide with 0.5% isoflurane or 60% nitrous oxide with 0.7% sevoflurane (n = 18 per group), each supplemented with extradural mepivacaine anaesthesia. Duration of anaesthesia was 58-380 min. At the end of operation, all inhalation anaesthetics were discontinued and patients were allowed to wake up while breathing oxygen spontaneously. A blinded investigator recorded the time until patients opened their eyes on command (T1), were judged ready for tracheal extubation (T2), could correctly state their name, date of birth and name of the hospital (T3), and could count backwards from 10 to 1 in less than 15 s (T4). Emergence times after xenon and nitrous oxide-sevoflurane anaesthesia did not correlate with duration of anaesthesia, whereas those from nitrous oxide-isoflurane had positive correlations. Mean emergence times from xenon anaesthesia were: T1, 3.3 (SD 1.0) min; T2, 3.6 (1.0) min; T3, 5.0 (1.1) min; and T4, 6.2 (1.7) min. These values were approximately 50% of those after nitrous oxide-sevoflurane anaesthesia (T1, 5.6 (1.4) min; T4, 10.5 (2.0) min). We conclude that xenon provided fast emergence from anaesthesia, regardless of the duration of anaesthesia.

Adult↗

Extent of resection and lymphadenectomy in early squamous cell esophageal cancer.

To decide the extent of resection and lymphadenectomy in early esophageal cancer, accurate diagnosis at the preoperative stage is essential. Because in mucosal cancer lymph node metastasis is hardly ever seen, minimal invasive surgery, by endoscopic mucosal resection is indicated. On the other hand, for submucosal cancer lymph node metastasis the rate is as high as 26-45%, therefore, standard resection and systematic lymphadenectomy is indicated, corresponding to that for advanced cancer. In Japan the 5-year survival rate after resection is 98-100% for mucosal cancer and 67-90% for submucosal cancer.

Carcinoma, Squamous Cell↗

Xenon provides faster emergence from anesthesia than does nitrous oxide-sevoflurane or nitrous oxide-isoflurane.

BACKGROUND: Xenon, an inert gas with anesthetic properties (minimum alveolar concentration [MAC] = 71%), has an extremely low blood:gas partition coefficient (0.14). Therefore, we predicted that xenon would provide more rapid emergence from anesthesia than does N2O+isoflurane or N2O+sevoflurane of equivalent MAC. METHODS: Thirty American Society of Anesthsiologists class I or II patients undergoing total abdominal hysterectomy were randomly assigned to receive 60% xenon, 60% N2O + 0.5% isoflurane, or 60% N2O + 0.70% sevoflurane (all concentrations are end-tidal: n = 10 per group). After placement of an epidural catheter, anesthesia was induced with standardized doses of midazolam, thiopental, and fentanyl. Thirty minutes later, xenon, N2O+isoflurane, or N2O+sevoflurane was started as previously assigned. These regimens were supplemented with epidural anesthesia with mepivacaine so that the mean arterial pressure and heart rate were controlled within 20% of the preoperative values. At the end of operation lasting approximately 2 h, all inhalational anesthetics were discontinued, and the patients were allowed to awaken while breathing spontaneously on an 8 l/min inflow of oxygen. A blinded investigator recorded the time until the patient opened her eyes on command (T1), was judged ready for extubation (T2), could correctly state her name, her date of birth, and the name of the hospital (T3), and could count backward from 10 to 1 in less than 15 s (T4). RESULTS: Emergence times from xenon anesthesia were: T1, 3.4 +/- 0.9 min; T2, 3.6 +/- 1 min; T3, 5.2 +/- 1.4 min; and T4, 6.0 +/- 1.6 min (mean +/- SD). These were one half to one third of those from N2O+sevoflurane (T1, 6.0 +/- 1.7 min; T4, 10.5 +/- 2.5 min) or N2O+isoflurane (T1, 7.0 +/- 1.9 min; T4, 14.3 +/- 2.8 min) anesthesia. The three groups did not differ in terms of patient demographics, the duration of anesthesia, the amount of epidural mepivacaine administered, or the postoperative pain rating. No patient could recalls intraoperative events. CONCLUSIONS: Emergence from xenon anesthesia is two or three times faster than that from equal-MAC N2O+isoflurane or N2O+sevoflurane anesthesia.

Adult↗

Fluid resuscitation and systemic complications in crush syndrome: 14 Hanshin-Awaji earthquake patients.

BACKGROUND: Crush syndrome is a form of traumatic rhabdomyolysis characterized by systemic involvement, in which acute renal failure is potentially life-threatening. METHODS: Clinical and laboratory data of 14 crush-syndrome patients transferred to a tertiary emergency department after the Hanshin-Awaji earthquake were analyzed. The patients were buried under collapsed houses for the average of 6.7 +/- 5.7 (SD) hours (range, 1 to 24 hours). They were referred to us 6 to 250 hours after the earthquake. RESULTS: Of those who arrived at our institution within 40 hours, 25% (two of eight) developed renal failure, whereas all six patients who arrived after 40 hours developed renal failure. Peak serum creatine kinase ranged from 6,677 to 134,200 U/L (51,674 +/- 41,776). Renal failure was highly associated with massive muscle damage (serum creatine kinase above 25,000 U/L) and insufficient initial fluid resuscitation (below 10,000 mL/2 days). CONCLUSIONS: Prompt and adequate, if not massive, fluid resuscitation is the key to preventing renal failure after such injury.

Creatine Kinase↗

Analysis of 2,702 traumatized patients in the 1995 Hanshin-Awaji earthquake.

BACKGROUND: This study was undertaken to define the factors that affected the final outcome of trauma patients in the Hanshin-Awaji earthquake. METHODS: Medical records of patients admitted to 95 hospitals within or surrounding the affected area during the first 15 days after the quake were reviewed. RESULTS: There were 2,702 traumatized patients. One-third of the patients were transported to hospitals in the surrounding area and had a mortality rate of 3%. The remainder, who were treated in the affected hospitals, showed a significantly higher mortality rate (8%; p < 0.05). Intensive care was provided for 513 patients, most of whom suffered from crush syndrome or from injuries to vital organs; these patients had a high mortality rate. Patients with other types of injuries had a lower mortality rate. CONCLUSION: Crush syndrome and injuries to vital organs were potentially life-threatening. We believe that early transportation of such patients to undamaged hospitals with the ability to provide intensive care would have improved the survival rate.

Abbreviated Injury Scale↗

Comparison of inhalation inductions with xenon and sevoflurane.

BACKGROUND: Xenon is an odorless gas with low blood-gas solubility coefficient and without occupational and environmental hazards. This investigation was performed to evaluate the speed of induction, and respiratory and cardiovascular reactions to inhalation induction with xenon compared to an equianesthetic concentration of sevoflurane. METHOD: Twenty-four adult ASA 1-2 patients premedicated with 0.05 mg/kg of midazolam were instructed to take vital capacity breaths of 1 minimum alveolar concentration (MAC) of either xenon or sevoflurane until they lost consciousness. Induction time, total ventilatory volume, tidal volume, respiratory rate, minute ventilation, end-tidal MAC fraction, cardiovascular parameters and oxygen saturation were recorded. The patients were interviewed on the following day to evaluate their acceptability rating of the inhalation inductions. RESULTS: Compared to equianesthetic sevoflurane, xenon produced a faster induction of anesthesia (147 +/- 59 versus 71 +/- 21 s, respectively) with smaller decreases in respiratory rate, tidal volume and minute ventilation. Both agents showed comparable cardiovascular stability and oxygen saturation during induction. One patient in the sevoflurane group had breath-holding and movements of extremities and another had only breath-holding. No patients in the xenon group experienced any complications. CONCLUSION: Xenon produced a faster induction of anesthesia without any complications than sevoflurane. Xenon had smaller decreases in tidal volume and respiratory rate during induction than sevoflurane. Xenon might offer an alternative to sevoflurane for an inhalation induction.

Adult↗

Small cell carcinoma of the kidney: case report.

An 83-year-old female diagnosed with small cell carcinoma of the kidney is reported on. The clinical picture was similar to that seen with transitional cell carcinoma of the renal pelvis. A right nephroureterectomy was performed and a histological examination revealed similar morphological features to those of small cell carcinoma of the lung. Neuroendocrine differentiation was proven by a positive immunoreaction to neuron-specific enolase. A review of the literature indicated that in the urinary tract, most of the cases of small cell carcinoma occurred in the urinary bladder, with this case being the eleventh reported case of small cell carcinoma originating in the kidney. As with many of the other cases of small cell carcinoma of the urinary tract, this patient's tumor was associated with both adenomatous and squamous differentiation. The patient died 2 months after surgery, prior to any chemotherapy administration.

Aged↗

Paroxysmal atrioventricular block induced during head-up tilt testing in an apparently healthy man.

INTRODUCTION: Prolonged asystole during head-up tilt testing has been reported, but the occurrence of paroxysmal AV block appears to be rare. METHODS AND RESULTS: A 25-year-old man with no history of syncope underwent head-up tilt testing. After 11 minutes of 80 degrees tilting, he developed syncope with paroxysmal AV block and asystole lasting 10.5 seconds. However, this response was not reproduced during a subsequent tilt test 4 weeks later. Treadmill exercise testing and Holter monitoring showed no abnormalities. Power spectral analysis of heart rate variability revealed a marked increase in sympathetic activity several minutes before the induction of paroxysmal AV block. CONCLUSION: We report a case of paroxysmal AV block that occurred during head-up tilt testing but did not recur on a subsequent test in an apparently healthy young man.

Adult↗

Association of variants in critical core promoter element of angiotensinogen gene with increased risk of essential hypertension in Japanese.

We examined the association between variants in the core promoter element 1 (AGCE1) of the human angiotensinogen gene (AGT), which acts as a critical regulator of AGT transcription, and the risk for hypertension. One hundred and eighty patients with documented essential hypertension and a family history of hypertension and 194 control subjects without hypertension were selected and frequency matched by age and sex. Genomic DNA from leukocytes was analyzed for genetic variants (position: -20 to -18) in AGCE1. The haplotype in AGCE1 was significantly associated with increased risk of essential hypertension (P<.05). The frequency of subjects with homozygous C allele at position -18(CC/C-18T) was significantly higher in case patients than in control subjects (P<.005), and the evaluated odds ratio for hypertension was 4.2 (95% confidence interval [CI]: 1.4 to 12.8, CC/C-18T versus CT/C-18T). The homozygous threonine allele at codon 235 (TT/M235T) in exon 2 of AGT was also associated with hypertension (P<.02; odds ratio, TT versus other genotypes, 1.8; 95% CI, 1.1 to 2.7). According to haplotype analysis between AGT polymorphisms, we identified linkage disequilibrium between M235T and A-20C and between M235T and C-18T. We conclude that C-18T polymorphism in AGCE1 is a genetic risk factor for essential hypertension in the Japanese and is more tightly and directly associated with hypertension than TT/M235T.

Aged↗

Serum levels of 16-dehydropregnenolone sulfate during the early neonatal period.

We have established a method for quantifying serum 16-dehydropregnenolone (3beta-hydroxy-5,16-pregnadien-20-one) sulfate (16-DHP S) by GC-MS. The levels of 16-DHP S at birth were compared in infants grouped as extremely immature (gestational age: 22-27 weeks), pre-term (gestational age: 28-36 weeks) and full-term (gestational age: 37-41 weeks). The average of the serum concentration of 16-DHP S in full-term infants was 0.172+/-0.104 micromol/l (n=10, mean+/-S.D.) which was significantly higher than the levels of the extremely immature (0.106+/-0.054 micromol/l, n=14, p<0.05) and pre-term infants (0.088+/-0.066 micromol/l, n=33, p<0.01). However, 16-DHP S in sera from normal adults (age 22-73 years, n=40) was not detected. We investigated chronological changes in serum levels of 16-DHP S during the early neonatal period. In extremely immature and pre-term infants, these levels were significantly higher at 2-7 d than those of 16-DHP S at day 0 (p<0.001). The levels at 8-18 d were still significantly higher than those at day 0 (p<0.05), but in full-term infants, these levels did not change at days 0 and 2-7. These results indicate that 16-DHP S is a steroid specific to fetuses and neonates and the involution of the fetal adrenal gland does not affect its serum levels in the early neonatal period.

Adult↗