Pretreatment of automobile shredder residue (ASR) for fuel utilization.

Automobile shredder residue (ASR) was pretreated to improve its quality for fuel utilization. Composition analysis revealed that ASR components could be classified into four groups: (1) urethane and textile-light fraction and combustibles containing low levels of ash and Cl; (2) plastics and rubber-light or heavy fraction and combustibles containing high levels of Cl; (3) metals and electrical wire-heavy fraction and incombustibles, and (4) particles smaller than 5.6mm with high ash contents. Based on these results, we successively performed sieving to remove particles smaller than 5.6mm, float and sink separations to reject the heavy fraction and plastics and rubber containing Cl, thermal treatment under an inert atmosphere to remove Cl derived from PVC, and char washing to remove soluble chlorides. This series of pretreatments enabled the removal of 78% of the ash and 91% of the Cl from ASR. Sieving using a 5.6-mm mesh removed a considerable amount of ash. Product quality was markedly improved after the float and sink method. Specifically, the sink process using a 1.1 g cm(-3) medium fluid rejected almost all rubber containing Cl and a large amount of PVC. The remaining Cl in char, after heating at 300 degrees C under an inert atmosphere and washing, was considered to be present as insoluble chlorides that volatilized at temperatures above 300 degrees C. Based on a tradeoff relationship between product quality and treatment cost, ASR may be utilized as a form of refuse plastic fuel or char.

400 MHz two-dimensional nuclear Overhauser spectroscopy on anesthetic interaction with lipid bilayer.

Interaction between a volatile anesthetic, methoxyflurane, and dipalmitoylphosphatidylcholine (DPPC) vesicle membrane was analyzed by nuclear Overhauser effect (NOE) difference spectroscopy and two-dimensional nuclear Overhauser spectroscopy (NOESY). The NOE difference spectra were obtained by selectively irradiating methoxy protons (hydrophobic end) of the anesthetic: a negative nuclear Overhauser effect of -2.94% was observed with the choline methyl protons of DPPC. The NOESY spectra revealed a cross-peak between the anesthetic methoxy protons and the choline methyl protons. A dipole-dipole interaction exists between the hydrophobic end of the anesthetic and the hydrophilic head group of DPPC. No other cross-peaks were observed. The anesthetic orients itself at the membrane/water interface by interacting with the hydrophilic surface of the DPPC membrane, leaving the hydrophilic end of the anesthetic molecule in the aqueous phase. The preferred residence site of dipolar volatile anesthetics is the membrane/water interface.

Interfacial preference of anesthetic action upon the phase transition of phospholipid bilayers and partition equilibrium of inhalation anesthetics between membrane and deuterium oxide.

The half-height linewidth (v 1/2) of the 1H-NMR spectra of dipalmitoylphosphatidylcholine vesicles changes abruptly at the phase transition temperature. In the absence of inhalation anesthetics, proton signals from the choline head group (hydrophilic interface) and acyl-chain tails (lipid core) change at the same temperature of 39.6 degrees C. The present study compared the effect of four inhalation anesthetics, i.e., methoxyflurane, chloroform, halothane and enflurane, upon the ligand-induced phase transition of phosphatidylcholine vesicle membranes at 37 degrees C. The anesthetics showed differential action upon the phase transition of the phospholipid vesicle membranes between the lipid core and the hydrophilic interface. The concentrations of anesthetics which induced the phase transition of the lipid core were about 2-fold greater than those required for the phase transition of the interfacial choline head groups. From the area under the proton signals of inhalation anesthetics in the NMR spectra, the maximum solubilities of methoxyflurane, chloroform and halothane in 2H2O at 37 degrees C were determined to be 0.671 . 10(-4), 2.637 . 10(-4) and 1.398 . 10(-4) (expressed as mole fractions), or 3.35, 13.17 and 6.98 mmol/1000 g 2H2O, respectively. The solubilities of the anesthetic vapor in 2H2O expressed as mole fractions according to Henry's law ere 9.586 . 10(-4), 6.432 . 10(-4) and 2.311 10(-4)/atm (1.013 . 10(5) Pa) partial pressure, respectively. The presence of phospholipid vesicles in 2H2O increased the solubility of the inhalation anesthetics. From difference between solubility in 2H2O and a dipalmitoylphosphatidylcholine vesicle suspension, the partition coefficients of methoxyflurane, chloroform and halothane between the phospholipid vesicle membranes and 2H2O were estimated. These values, calculated from the mole fractions, were 3364, 1660 and 3850, respectively at 37 degrees C.

Hydrogen bonding and anesthetic potency.

Hydrogen bond strengths in terms of the proton chemical shifts of five potent inhalation anesthetics containing acidic hydrogen were measured in cyclohexane and in methanol using the proton magnetic resonance spectroscopic method. The purpose of this study is to quantitatively compare the relative polar character of potent anesthetics. The hydrogen bond shift (delta ppm) of each anesthetic is the difference in the chemical shifts of the infinitely diluted unassociated anesthetic in cyclohexane and that of the infinitely diluted hydrogen bonded anesthetic in methanol. It was found that the hydrogen bond shifts (in delta ppm) are as follows: methoxyflurane, 0.72; chloroform, 0.75; halothane, 1.06; isoflurane, 1.38; enflurane, 1.44. There is a good correlation between the hydrogen bond shifts and the clinical potencies (minimum alveolar concentration in man). The conclusion from this study is that the acidic halogenated inhalation anesthetics are more potent if they form weaker hydrogen bonds.

Effect of moderate hypothermia on systemic and internal jugular plasma IL-6 levels after traumatic brain injury in humans.

Moderate hypothermia may reduce subsequent neuronal damage after traumatic brain injury. Interleukin (IL)-6 may have a role in the pathogenesis of traumatic neuronal damage or repair. Using the enzyme-linked immunological sorbent assay (ELISA), we serially measured IL-6 levels in plasma obtained from the radial artery (systemic) and internal jugular vein (regional) in 13 cerebral trauma patients who underwent hypothermia of 32-33 degrees C ranged from 4-9 days postinjury and 10 head-injured patients who were maintained at normothermic levels (36-37 degrees C). In both patient populations, surface cooling was used since even in the normothermic group, cooling was needed to maintain patient temperature in the normothermic range. All patients were mechanically ventilated after injection of midazolam and vecuronium. The administration of these agents were continued until the end of the study. Hypothermia was typically maintained for four days, however, in some cases based upon CT findings and/or intra-cranial pressure change, the duration was prolonged. No significant differences were found between the two groups in age, gender and Glasgow Coma Scale upon admission. Further, no differences were found in terms of the classification of computed tomography findings or the occurrence of pupillary abnormalities on admission. The patients in this study had not sustained either abdominal or thoracic trauma. Before inducing hypothermia, IL-6 levels in the arterial and internal jugular venous blood exceeded the normal range. Specifically, the internal jugular plasma levels were significantly higher than those in the arterial plasma. While IL-6 levels in the normothermic group did not decrease even at 4 days postinjury, the plasma cytokine levels fell at both sites sharply after moderate hypothermia. The cytokine suppression found in the hypothermic group continued even after rewarming in these patients showing an improved clinical course, but not in those whose condition worsened. In addition to these changes in cytokine levels, the Glasgow Outcome Scale at 6 months postinjury was significantly higher in the hypothermic group than in the normothermia group. Based on the above, this clinical study with its small patient sample size suggests the need for further prospective randomized studies to examine the role of cytokine suppression in the beneficial effects of moderate hypothermia in patients with traumatic brain injury.

Dose-dependent effects of propofol on renal sympathetic nerve activity, blood pressure and heart rate in urethane-anesthetized rabbits.

To evaluate the role of the autonomic nervous system in hemodynamic changes after propofol bolus injection, we used direct recordings of renal sympathetic nerve activity to examine the dose-dependent effects of propofol (2.5, 5, 10, and 20 mg/kg) on heart rate, mean blood pressure and renal sympathetic nerve activity in urethane-anesthetized rabbits. The animals were divided into four groups: animals with an intact neuraxis (intact group), cervical vagal nerve-sectioned animals (vagotomy group), carotid sinus and aortic-nerve sectioned animals (SAD group), and animals with SAD plus vagotomy (SADV group). Heart rate did not change significantly even after administration of 2.5 and 5 mg/kg but decreased markedly on 20 mg/kg injection in all groups. The intact and vagotomy groups had augmented renal sympathetic nerve activity with insignificant changes in mean blood pressure after 5 mg/kg injection of the agent. Insignificant changes of renal sympathetic nerve activity but a remarkable decrease of mean blood pressure appeared after 10 mg/kg propofol. Sustained hypotension in parallel with a profound depression of renal sympathetic nerve activity developed at the dose of 20 mg/kg. In SAD and SADV groups, however, dose-dependent depressions of renal sympathetic nerve activity were accompanied by decreases of mean blood pressure. These results suggest the following: (1) propofol-induced hypotensive effects are probably produced by the central-mediated sympathetic depression. (2) The baroreceptor reflex may be preserved at the lower dose of the agent. (3) Heart rate does not change significantly unless a large dose of propofol is used. The difference in effects on heart rate and on mean blood pressure may denote a greater inhibition of sympathetic vascular outflow than of the cardiac sympathetic outflow regulating cardiac rate and contractility. This hypothesis needs further clarification.

Activated cytokine production in patients with accidental hypothermia.

We have demonstrated recently that therapeutic moderate hypothermia of 32-33 degrees C, induced by surface cooling under the administration of narcotics, sedatives and muscle relaxant, suppresses cytokine production after traumatic brain injury. We present here the first documented case report of augmented cytokine production in two accidental hypothermia patients, unconscious 84- (acute immersion) and 87- (non-immersion) year-old women, whose rectal temperatures were below 28 degrees C. The victims were artificially ventilated after sedation with midazolam and buprenorphine in accordance with our protocol. Rewarming at the rate of approximately 1 degrees C/h was done by blowing forced-air with appropriate fluid resuscitation. Plasma interleukin(IL)-6 and/or IL-8 levels were measured using ELISA in the patients. In both patients, plasma IL-6 levels on admission were already elevated and the cytokine levels further increased during and after the rewarming period. In the patient with the poorer prognosis, the plasma IL-8 level on admission was not elevated remarkably but after rewarming the level rose significantly. Augmented IL-6 production in accidental hypothermia was sustained for 6 days in the patient with the poorer prognosis but not in the subject with good recovery, who was treated with anti-thrombin III in the early phase. Since the mechanisms for developing accidental hypothermia were different, simple comparisons between the two cases should be limited. But, these findings may suggest a need for testing a hypothesis whether cytokine modulation could be a therapeutic approach worthy of consideration. The results presented here also suggest that in hypothermia, changes in cytokine release may vary depending on procedures such as the anesthetic drugs used, the duration of the therapy, or the rate of rewarming from hypothermia.

Effects of halothane and supporting membrane lipids on the activity of acetylcholinesterase.

1. The activity of acetylcholinesterase in the human erythrocyte membrane was measured with and without halothane. 2. To evaluate the roles of the supporting membrane lipids, the enzyme protein was solubilized from the membrane with a surfactant, Triton X-100. 3. It is confirmed that membrane lipids alter the activation energy of the enzyme bound to the membrane, and strengthen the effects of halothane and Triton X-100 on the enzyme activity by providing a high concentration field of them around the enzyme.

The effect of volatile anesthetics on light-induced phosphorylation in spinach chloroplasts.

(1) The light-induced phosphorylation in spinach chloroplast is coupled with proton transfer. (2) We investigated the effect of volatile anesthetics (halothane, enflurane, isoflurane) on the cyclic and/or non-cyclic light-induced phosphorylation. (3) We used potassium ferricyanide as a Hill oxidant for non-cyclic phosphorylation and phenazin-methosulfate as an oxidation-reduction indicator for cyclic phosphorylation. (4) These three anesthetics inhibit the Hill reaction in light induced phosphorylation. The inhibition rate of this reaction generates concave curves with minimum values at 303 K in each of the anesthetics.

Anaesthetic mechanism--from molecular to biological aspects.

The mechanism of anaesthesia is still a black box, although many investigators have been concerned about this theme since the 19th century. It is too complex to clarify the mode of anaesthetic action, as a variety of compounds have been adopted as anaesthetics. Hill coefficients calculated from the righting reflex dose-response curve in enflurane, isoflurane sevoflurane and halothane anaesthesia in a certain strain of mice were from 14 to 56. It shows that many factors are related to the mechanisms of anaesthetic actions. In this review, we adduce from our previous studies 2 approaches to study the anaesthetic mechanism. The pharmacogenetical approach is concerned with the mode of genetics in anaesthetic sensitivities in ddN and C57BL, 2 strains of mice and their hybrids, and distributions of neurotransmitters in each mouse brain. The sensitivity rates in enflurane and isoflurane anaesthesia are both 1.4 between ddN and C57BL. The rate is highest compared with precedent data. The F1 males from ddN females x C57BL males had a significantly higher ED50 than F1 males from the reciprocal crosses for both enflurane and isoflurane, indicating that enflurane resistance and isoflurane resistance are controlled by genes on the sex (X) chromosome. In the F2 progeny, we hypothesized that 1 gene was on the X chromosome and another gene was on the autosome. Although there were several differences among ddN, C57BL and their hybrids and several anaesthetics concerning distributions of neurotransmitters, neuropeptide Y, serotonine and methionine-enkephalin in the mouse brain, the relationship to the genetical analysis has been chaotic. The physicochemical approach is concerned with the confirmation of the action site of volatile anaesthetics in phospholipid bilayer membranes. It is suspected from Overton's experiment that the action site is not in the core of lipid bilayer but on the surface of membrane. It was demonstrated by 2 methodologies. Two-dimensional nuclear Overhauser effect spectrum in H1-NMR spectra of dipalmitoyl phosphatidylcholine (DPPC) vesicle membrane in the presence of methoxyflurane revealed from the existence of the cross-peak between the methoxy-proton and the choline methyl-proton that methoxyflurane molecule interacted only to the polar head of lipid membrane at lower temperatures.(ABSTRACT TRUNCATED AT 400 WORDS)

[Relationship between three phase bone scintigram and prognosis after sympathetic blockade in reflex sympathetic dystrophy of the hand].

We attempted to correlate the changes in three phase bone scintigram (TPBS) with prognosis after sympathetic blockade in reflex sympathetic dystrophy (RSD) of the hand. Subjects were 12 patients of RSD in acute or dystrophic stage, who all had increased images on TPBS. Either intravenous regional sympathectomy with guanethidine or stellate ganglion block was performed repeatedly. We compared TPBS obtained just before and after this series of sympathetic blocks and evaluated the eventual recovery of function of the hand. In 8 patients, blood flow (phase 1) image of TPBS decreased after the blockade. Of these patients, those who showed almost normalized tracer activity not only on flow image but on blood pool (phase 2) and delayed (phase 3) image, returned to normal. But others with normalized blood flow and still increased activity in blood pool and delayed image, remained with mild contracture of the hand. These results suggest that normalization of blood pool and delayed image on TPBS is a predictor of subsequent recovery after sympathetic blockade in RSD.

[The support of postoperative renal function by ulinastatin in patients with preoperative renal dysfunction].

The principal perioperative management of patients with renal dysfunction is to prevent postoperative acute renal failure. Therefore, it is crucial to do all possible therapies by which its occurrence is prevented. We experienced three cases in which ulinastatin may have been beneficial to maintain postoperative renal function. The patients had preoperative renal dysfunction with serum Cr between 1.5 and 2.0 mg.dl-1. During the operation and for the three postoperative days, 300,000 units.day-1 of ulinastatin were administered intravenously. After the operation, serum Cr level was not elevated. Urine output and creatinine clearance increased. These three clinical cases suggest that ulinastatin may prevent the deterioration of postoperative renal function in patient with preoperative renal dysfunction.

[Acute alcoholism after ethanol fixation for ovarian chocolate cyst].

We experienced a case of acute alcoholism after ethanol fixation for ovarian chocolate cyst. A 46 year old female was scheduled for ethanol fixation for ovarian chocolate cyst. Ethanol fixation was performed with 110 ml of 99% ethanol under general anesthesia. Ethanol 70 ml was not removed. After the operation, patient did not emerge from anesthesia within 30 min. Blood alcohol concentration was 232 mg.dl-1. It is important to remove total ethanol used for ethanol fixation in anesthetic management for ethanol fixation for ovarian chocolate cyst.

[Effects of ulinastatin on rat renal energy metabolism around ischemia studied by 31P MRS].

The effects of ulinastatin (UTI) on rat renal energy metabolism during ischemia and reperfusion were studied by 31P nuclear magnetic resonance spectroscopy (31P MRS) in vivo. Rat kidney was exposed to ischemia for 30 min by clamping the abdominal aorta above the renal arteries. Pre-ischemic administration of UTI inhibited the decline of intracellular pH (pHi) during ischemia and improved the recovery of renal energy metabolism and pHi after reperfusion. This result suggests that UTI might inhibit anaerobic metabolism during renal ischemia and an improve energy metabolism during reperfusion. 31P MRS provided a unique tool to study intact cellular function continuously in noninvasive fashion, allowing assessment of metabolic function during ischemia and after reperfusion.

[A case of hysterical conversion manifested by pain in face and head].

We report a case of hysterical conversion, which was initially diagnosed as trigeminal neuralgia. The pain in the face and head which the patient complained seemed to be consistent with symptoms of trigeminal neuralgia. But it could not be relieved by repeated peripheral nerve blocks and even by Gasserian blocks. Failure to relieve pain by such blocks and concomitant hemifacial spasm with closure of the eye appeared to afford indication of microvascular decompression surgery. Injection of edrophonium before operation, for the purpose of differential diagnosis of myasthenic ptosis, made the patient free from all symptoms, i.e. facial pain, spasm, and ptosis. The diagnosis of hysterical conversion was made on this irrational episode. When we looked back the total clinical course, it was revealed that the patient's complaints and symptoms had been rather atypical, too various, and not anatomical. We also confirmed that various other episodes of this patient which had not received our attention during treatment were psychological features of hysteria, but we could not make his psychological stress clear, which had been in the background of hysterical conversion.

[Supplement of ulinastatin on renal function after cardiopulmonary bypass].

The effects of Miraclid (ulinastatin) on renal tubular function after open thorax surgery under cardiopulmonary bypass were investigated. On the 3rd day after open thorax surgery, which had lasted more than 127 min under cardiopulmonary bypass, the levels of urinary ulinastatin in the Miraclid group and control (without Miraclid) were 170 IU.mg Cr-1 and 95 IU.mg Cr-1, respectively. In the Miraclid group, 300,000 units.day-1 of Miraclid was administrated for three postoperative days. N-acetyl-beta-d-glucosaminidase in urine as a marker of tubular function rose significantly on the seventh postoperative day in the control group but not in patients with Miraclid group. These data suggested that Miraclid 300,000 units.day-1 was needed to protect renal tubular function and more than that dose was needed to prevent the deterioration of renal function after open thorax surgery after cardiopulmonary bypass lasting more than 127 min.

[Postoperative urinary ulinastatin secretion and renal function in hepatectomized patients with and without liver cirrhosis].

We compared ulinastatin secretion into urine with renal function during postoperative period in three groups, hepatectomized group with liver cirrhosis (LC(+), n = 7), hepatectomized group without liver cirrhosis (LC(-), n = 4) and subtotal gastrectomized group with normal liver function (GR, n = 7). In LC(+) group, N-acetyl-beta-D-glucosaminidase (NAG) increased above normal upper limit throughout the postoperative period. Ulinastatin (UTI) also increased but the increase was not remarkable. In LC(-) group, NAG increase but not significantly compared with the preoperative value. UTI increased from 5.8 +/- 3.0 IU.mg x Cr-1 to 30.8 +/- 16.6 IU.mg x Cr-1 and 39.9 +/- 9.0 IU. mg x Cr-1 on the 1st and 3rd postoperative day respectively. In GR group, there was no change in NAG value. UTI on the 3rd postoperative day increased significantly (from 10.0 +/- 7.7 to 75.4 +/- 39.0 IU.mg x Cr-1). A small urinary secretion of UTI and increased NAG during postoperative period in LC(+) group suggest that UTI might play an important role in postoperative renal dysfunction in patients with liver cirrhosis.

[Changes of urinary ulinastatin and serum CRP after elective surgery for gastric cancer].

Urinary ulinastatin (UTI) is elevated in various conditions, such as renal disease, myocardial infarction, neoplasm, leukemia and normal pregnancy. The purpose of the present study is to measure the change of UTI after surgery for gastric cancer and to compare with other acute phase reactants. Urine samples were collected from 7 surgical patients. UTI level was measured by radioimmunoassay and corrected by urinary level of creatinine. UTI levels began to increase from the first postoperative day and reached the maximum level on the third postoperative day. The pattern of UTI correlated with that of serum CRP levels. Meanwhile, when patient was in inflammatory condition postoperatively, UTI increased further and its pattern correlated with that of serum CRP levels. These results suggest that UTI is an acute phase reactant and a sensitive marker indicating the degree of inflammatory condition after surgery.

[Effects of ulinastatin on postoperative renal function after cardiopulmonary bypass].

The effects of ulinastatin on postoperative renal function after the open cardiac surgery under cardiopulmonary bypass (CPB) were studied. N-acetyl-beta-D-glucosaminidase in urine as a marker of tubular function and serum creatinine rose significantly after CPB in the control group but not in the ulinastatin group. Ulinastatin was considered to be effective in protection of tubular function after CPB. In patient with poor preoperative renal function, ulinastatin prevented the deterioration of postoperative renal function by protecting tubular function.

[Effects of ulinastatin on renal function after subrenal aortic cross-clamping].

Ten patients who had undergone temporary occlusion of the abdominal aorta below the origin of the renal arteries were studied to evaluate the effect of ulinastatin on the postoperative renal function after abdominal aortic cross-clamping. They were divided into two groups: ulinastatin group (ulinastatin 300,000 units.day-1 during intraoperative and postoperative three days, N = 5), control group (N = 5). In ulinastatin group, the increase of N-acetyl-beta-D-glucosaminidase on the third postoperative day was inhibited and renal function was well maintained. These results suggest that the administration of ulinastatin in perioperative day prevents postoperative renal dysfunction after abdominal aortic cross-clamping.