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Both phenoxyethanol and parabens are kinds of preservatives in cosmetics and are nominated as the restricted ingredients in cosmetics in Japanese Pharmaceutical Affairs Low. So the analytical methods for phenoxyethanol and parabens were investigated by HPLC. After adding methanol to phenoxyethanol and parabens in lotions, the testing solutions were analyzed by HPLC using the ODS column (CAPCELL PAK C18 column, 4.6 x 250 mm), the mixture either of 50 mmol/l phosphate(pH3.5) and acetonitrile (7:3) for phenoxyethanol or of 50 mmol/l phosphate buffer(pH3.5) and acetonitrile (3:2) for parabens and the detection wavelength of either 270 nm for pehnoxyethanol or 255 nm for parabens. The working curves from 0.5 to 5 micrograms/ml passed through the origin. There were no interference of peaks of phenoxyethanol and parabens from the cosmetics. Eleven lotions out of 42 lotions did not have phenoxyethanol. Phenoxyethanol in thirty-one cosmetics ranged from 0.009 to 1.043% and those average was 0.264%. Parabens, especially methylparaben, were detected in all lotions. The amounts of parabens ranged from 0.016 to 0.267% and their average was 0.120%. There were 7 kinds of lotions whose contents of phenoxyethanol and methylparaben were below 0.1%.

Domkal is one of the 19, out of 26 blocks in Murshidabad district where groundwater contains arsenic above 0.05 mg/l. Many millions of cubic meters of groundwater along with arsenic and other heavy metals are coming out from both the hand tubewells, used by the villagers for their daily needs and shallow big diameter tubewells, installed for agricultural irrigation and depositing on soil throughout the year. So there is a possibility of soil contamination which can moreover affect the food chain, cultivated in this area. A somewhat detailed study was carried out, in both micro- and macrolevel, to get an idea about the magnitude of soil contamination in this area. The mean concentrations (mg/kg) of As (5.31), Fe (6740), Cu (18.3), Pb (10.4), Ni (18.8), Mn (342), Zn (44.3), Se (0.53), Mg (534), V (44.6), Cr (33.1), Cd (0.37), Sb (0.29) and Hg (0.54) in fallow land soils are within the normal range. The mean As (10.7), Fe (7860) and Mg (733) concentrations (mg/kg) are only in higher side whereas Hg (0.17 mg/kg) is in lower side in agricultural land soils, compared to the fallow land soils. Arsenic concentrations (11.5 and 28.0 mg/kg respectively) are high in those agricultural land soils where irrigated groundwater contains high arsenic (0.082 and 0.17 mg/l respectively). The total arsenic withdrawn and mean arsenic deposition per land by the 19 shallow tubewells per year are 43.9 kg (mean: 2.31 kg, range: 0.53-5.88 kg) and 8.04 kg ha(-1) (range: 1.66-16.8 kg ha(-1)) respectively. For the macrolevel study, soil arsenic concentration decreases with increase of distance from the source and higher the water arsenic concentration, higher the soil arsenic at any distance. A proper watershed management is urgently required to save the contamination.

An investigation of total arsenic in food composites, collected from the villagers, was carried out in arsenic-affected areas of the Murshidabad district, West Bengal where the agricultural system is mostly groundwater dependent. The shallow, large-diameter tubewells installed for agricultural irrigation contain an appreciable amount of arsenic (mean 0.085 mg/l, n=6). Even the soil is arsenic-contaminated (mean 11.35 mg/kg, n=36), so some arsenic can be expected in the food chain from crops cultivated in this area. The results revealed that the individual food composite and food groups containing the highest mean arsenic concentrations (microg/kg) are potato skin (292.62 and 104), leaf of vegetables (212.34 and 294.67), arum leaf (331 and 341), papaya (196.50 and 373), rice (226.18 and 245.39), wheat (7 and 362), cumin (47.86 and 209.75), turmeric powder (297.33 and 280.9), cereals and bakery goods (156.37 and 294.47), vegetables (91.73 and 123.22), spices (92.22 and 207.60) and miscellaneous items (138.37 and 137.80) for the Jalangi and Domkal blocks, respectively. Arsenic is absorbed by the skin of most of the vegetables. The arsenic concentration in fleshy vegetable material is low (mean 2.72 microg/kg, n=45). Higher levels of arsenic were observed in cooked items compared with raw. Daily dietary intakes of arsenic (microg) from the foodstuffs for adults are 171.20 and 189.13 and for children are 91.89 and 101.63 in the Jalangi and Domkal blocks, respectively.

In order to clarify that squalene monohydroperoxide (SQOOH) correlates with changes in morphology through cytotoxicity and establish in vitro evaluation of the cytotoxicity of lipid hydroperoxide, the effect of SQOOH on cytotoxicity and morphology in normal human epidermal keratinocytes (NHEK(B)) and the Gunze three-dimensional cultured human skin model (Vitrolife-skin) was investigated. Additionally, the effect of radical scavengers (mannitol, vitamin C and (+)-catechin) on the cytotoxicity in Vitrolife-skin was studied. The level of lipid hydroperoxide (phoshatidylcholine hydroperoxide: PCOOH) in the cellular membrane was increased with the concentration of SQOOH, and the rise in cytotoxicitv in NHEK(B) was associated with changes to the cellular membrane. A concentration-dependent and protective effect on the increase in cytotoxicity and PCOOH content was observed. To clarify the effect of SQOOH on the release of cytokine from cells, IL-2 level from NHEK(B) and Vitrolife-skin were investigated. IL-2 release from the cells was enhanced by SQOOH and increased at a non-cytotoxic dose. These results suggest that the increase in lipid hydroperoxides resulting from the auto-oxidation of lipids within cellular membranes in the presence of SQOOH correlates with changes in morphology due to cytotoxicity. SQOOH enhanced the release from cells at a non-cytotoxic dose. A method for assessing the protective effect on the cytotoxicity of lipid hydroperoxides using cells would be useful for in vitro evaluation of the cytotoxicity.

Very low birth weight (VLBW) infants can be subjected to oxidative stress in the course of intensive care. We measured 8-hydroxydeoxyguanosine (8-OHdG), a biomarker of oxidative stress, and estimated the degree of oxidative stress in such infants. We also examined if the administered oxygen was related to oxidative stress. Urine samples of 50 Japanese VLBW infants [birth weights: 956.3+/-277.6g, and gestational ages: 28.0+/-2.6 weeks (mean +/- SD)] were collected on various postnatal days and 8-OHdG levels were determined using an ELISA kit. Sixteen term infants served as normal controls. As body weights at sampling increased, the average levels of urinary 8-OHdG decreased. 8-Hydroxydeoxyguanosine levels were: infants under 1000g, 29.5+/-16.4 micromol/mol creatinine (n = 24); 1000-1500g, 23.8+/-14.9 (n = 12); over 1500g, 16.1+/-8.5 (n = 14); and control, 10.9+/-7.2 (n = 16). Significant differences were found between <1000g group and > or = 1500g group (p = 0.0030), <1000g group and control (p < 0.0001), and 1000-1500g group and control (p = 0.0108). Also as postconceptional age at sampling increased, the average levels of 8-OHdG decreased. 8-Hydroxydeoxyguanosine levels were: infants before 252 days (36 weeks) of postconception: 27.4+/-15.5 micromol/mol creatinine (n = 34); after 252 days, 18.2+/-12.5 (n = 16). Differences between <252 days group and control (p < 0.0001), and <252 days group and > or = 252 days groups (p = 0.0253) were statistically significant. Among the three groups based on ambient oxygen concentration (21%, 22-29%, and > or = 30%) there was no significant difference (p = 0.417). The more premature the infants were, the more intense was the oxidative stress, hence, it is the prematurity rather than the administered oxygen which causes oxidative stress in VLBW infants. Drury et al. ["Urinary 8-hydroxydeoxyguanosine in infants and children" Free Radic. Res. 28 (1998) 423-4281 measured urinary 8-OHdG of 28 infants (24-40 weeks gestation) and found no gestation or birthweight related differences. This discrepancy seemed to be because of difference in birth weights and sampling period of the subjects.

We present theoretical evidence that the paramagnetic E' defect centers in amorphous silicon dioxide (a-SiO(2)) do not have the same microscopic structures as those well-defined in the corresponding crystalline counterparts such as alpha-quartz. We then present alternative models of some paramagnetic defects that account for the underlying experimental features of the E'-center variants in a-SiO(2). We suggest that our new model should take the place of the conventional defect model of a-SiO(2).

We here present a series of ab initio quantum-chemical calculations on clusters of atoms modeling several oxygen-deficiency-related defects in amorphous silica and illustrate how these defect centers will change their atomic configurations upon photoionization. We first give theoretical evidence that structural conversion from a neutral oxygen monovacancy to a divalent Si defect is possible, explaining the observed photoluminescence properties associated with these defects.

We reported a rare case of an occipital encephalocystocele linked by bilateral posterior horns of the lateral ventricles. The subject was a newborn girl with a large occipital cephalocele (6 x 9 cm in diameter) covered with alopetic skin. Cerebrospinal fluid leakage was not observed. The fontanel was soft, but a characteristic flat forehead was noted. Neither neurological deficits nor cardiopulmonary dysfunctions were evident at birth. Magnetic resonance images revealed that the sac contained the occipital lobes and that the cavity was linked by bilateral posterior horns. Agenesis of the corpus callosum and dysgenesis of the falx cerebri were associated. Fifteen days after birth, the cephalocele was removed surgically. Cutting sections revealed that the cephalocele contained enlarged bilateral posterior horns and cerebral hemispheres. The postoperative course was uncomplicated by hydrocephalus or infection, and the patient was discharged without any neurological deficit 22 days after surgery. Her milestone was survival; and at present 12 months after surgery, she is alive with moderate developmental retardation., (Copyright 2001 S. Karger AG, Basel)

We propose a mechanism of photostructural changes in amorphous As2S3 ( a-As2S3) on the basis of ab initio molecular orbital calculations on clusters of atoms modeling the local structure of the amorphous system. We have found that trigonal AsS3 pyramidal units can be transformed into a fivefold coordinated As site having four As-S bonds and one As-As bond via a photoionization process. This photoinduced coordination defect center exhibits a lower photoabsorption energy as compared with the usual pyramidal structure, explaining the observed photodarkening effect of a-As2S3.

We have performed ab initio quantum-chemical calculations on clusters of atoms modeling a divalent Ge defect in Ge-doped SiO (2) glasses. It has been found that the divalent Ge defect interacts with a nearby GeO (4) tetrahedron, forming complex structural units that are responsible for the observed photoabsorption band at approximately 5 eV. We have shown that these structural units can be transformed into two equivalent Ge E' centers by way of the positively charged defect center.

In order to improve the arsenic test method, we investigated the effect of temperature, solar light and masking ions on that test method. As the results, we found that the solar light gave the big damage to the colored reaction on the method. In addition, on comparing the improved method with the arsenic test method of Merckoquant kit by using the water containing 0.01 ppm arsenic as the Japanese guideline for the drinking water, the improved method gave the better analytical value than Merckoquant kit that was not sufficiently determined.

Phylogenetic relationships among 55 species of Lilium, Cardiocrinum giganteum, and Nomocharis saluenensis were inferred from nucleotide sequence variations in the internal transcribed spacer (ITS) regions of 18S-25S nuclear ribosomal DNA. The phylogeny derived from ITS sequences estimated using maximum-likelihood methods indicated that (1) most of the species construct their own clade according to the classification based on morphological features at the section level; (2) section Daurolirion is not independent of Sinomartagon, and it is appropriate to integrate two sections as Sinomartagon; (3) it is appropriate that L. henryi and L. bulbiferum are classified into subsection 6a and Sinomartagon-Daurolirion, respectively; (4) subsection 6b is much closer to Sinomartagon than subsection 6a and Archelirion, and it arose directly from Sinomartagon; and (5) Lilium is much closer to Nomocharis than Cardiocrinum. Phylogenetic estimation using sequences of the ITS region is suitable at the levels of genus, section, and most of subsection.

Background/purpose: The authors surgically treated seven of eight patients with congenital portosystemic shunt and hyperammonemia. This entity is uncommon in children., Methods: The patients included five boys and three girls with a mean age of 8 years (range, 7 months to 24 years). Preoperative symptoms included hyperammonemia. Hepatic encephalopathy was evident in five patients. Diagnosis and assessment were made by ultrasound scan, magnetic resonance imaging (MRI), angiography, and 123 I-iodoamphetamine per-rectal portal scintigraphy. Surgical banding was done for five patients and transvenous coil embolization for two. One patient was not a surgical candidate because there were no intrahepatic portal veins., Results: In four of the five patients treated using surgical banding, and in both patients who underwent coil embolizations, hyperammonemia and clinical symptoms improved soon after surgery. However, in the remaining patient, hyperammonemia worsened after surgery, and reoperation was needed because of a severe portal hypertension, possibly caused by malconformation of hepatic veins., Conclusions: For patients with congenital portosystemic shunt, early diagnosis and surgery are needed to prevent damage to central nerves caused by persistent hyperammonemia. Maldevelopment of the intrahepatic portal veins is a surgical option, if the patient has a normal liver architecture, but malconformation of hepatic veins or severe anomalies such as cardiac defects would rule out surgical intervention.

A questionnaire survey was performed in order to investigate the current status of endoscopic thoracic sympathectomy in Japan. Four hundred and twenty-nine (429) university, national or public hospitals with a minimum of 400 beds were included. A total of 248 of these hospitals responded. Among them 63 (25%) performed this procedure. The total of the cases was 1116. The number of access port and the technique for defunctioning the sympathetic chain were broadly divided into three methods. These methods were equally carried out among the departments. The clinical results were judged as satisfactory in the great majority of patients and the frequency of complications was low. On the other hand, the overall incidence of compensatory sweating remained relatively high and accumulated as the number of cases increased. But the reported frequency differed strikingly from hospital probably for lack of an objective way of quantifying following sympathectomy. Although overall complications were infrequent, the need for conventional thoracotomy to stop bleeding occurred in some cases. Therefore even this simple endoscopic operation demands the utmost surgical care, skill and experience. A few recurrences of preoperative symptoms were seen in the follow-up suggesting that all patients must be continually monitored after the operation.

In Japan, urea cycle disorders (UCDs) are one of the most frequent inborn errors of metabolism, estimated to have a prevalence of 1 per 50,000 live births. In an attempt to develop more effective treatment and enhance the quality of life, we investigated the clinical manifestations and prognosis of 216 patients with UCDs diagnosed and treated between 1978 and 1995. These included 92 cases of neonatal-onset UCD and 116 of late-onset UCD. Two cases of ornithine transcarbamylase (OTC) deficiency in males and 2 cases of argininosuccinase (AL) deficiency were diagnosed prospectively. By far the most common disorder was OTC deficiency, accounting for 2/3 of all cases. At the end of 1995, the 5-year survival rate was 22% for the neonatal-onset type and 41% for the late-onset type. Among the 20 long-term survivors with neonatal-onset UCD, 18 (90%) had moderate to severe neurodevelopmental deficits; this contrasts with 13 of 47 (28%) survivors with the late-onset type. In analysing 108 UCD cases, peak blood ammonia level during the first hyperammonaemic attack was correlated with neurodevelopmental outcome. When the concentration of blood ammonia was less than 180 mumol/L (5 times normal), there was no severe neurological damage. When the concentration of blood ammonia exceeded 350 mumol/L (10 times normal) at the first hyperammonaemic attack, the patients died or had severe neurological deficits. Our data point to the importance of early diagnosis and aggressive treatment.

Apoptosis similar to that seen in Alzheimer's disease patients was found in the brain of aged dogs by the TUNEL method of detecting in situ DNA fragmentation. Apoptosis was observed in both neurons and glial cells, and was morphologically characterized by round and swollen cytoplasm and aggregated nuclear chromatin, although these changes were slight. Neurons and astrocytes in the gray matter and oligodendrocytes in the white matter were affected. The number of ApopTag-positive brain cells increased slightly with age, but was not correlated to the number of senile plaques. A good correlation between the number of ApopTag-positive cells and the dementia index was clearly found. The present study indicates that brain cell apoptosis could account for dementia in aged dogs and suggested that aged dogs may be useful as a simplified animal model for Alzheimer's disease in man.

Ab initio molecular orbital calculations were used to determine the structure and vibrational frequencies of the cyclic glycerol trimer, which represents the region of medium-range ordering in liquid and supercooled glycerol. The calculations reproduced the experimentally observed low-frequency Raman scattering peak (or the "boson peak") at approximately50 per centimeter, which suggests that the peak results from the localized collective motions of the cooperatively hydrogen-bonded hydroxyl groups. The calculations also suggest that the fast relaxation process may result from the translational motion of each glycerol molecule in the cyclic structure. On the basis of these results, a model of the glass transition was developed.

Argininemia is an autosomal recessive disorder caused by a deficiency in the liver-type arginase enzyme. Clinical manifestations include progressive spastic diplegia and mental retardation. While the quality of life can severely deteriorate in most such patients, some do show remarkable improvement in neurological symptoms while on controlled diets. We examined the thesis that differences in clinical responses to dietary treatment are based on molecular heterogeneity in mutant arginase alleles. Genomic DNAs from 11 patients with argininemia were examined using the polymerase chain reaction, cloning, and sequencing. Nine mutations representing 21/22 mutant alleles were identified in 11 patients with argininemia, and four of these mutations were expressed in vitro to determine the severity of enzymatic defects. We found that these mutations accounted for 64% of the mutant alleles in our patients. Based on findings in vitro expression tests, the mutations can be considered either severe or moderate. Patients with at least one moderate mutant allele responded well to dietary treatment; concentrations of plasma arginine were controlled within 300 microM. In contrast, patients with two severely mutated alleles did not respond to dietary treatment and plasma arginine was over 400 microM. Argininemia is heterogeneous at the molecular level. The degree of clinical improvement during dietary treatment is reflected in the concentration of arginine in plasma, as a measure of metabolic control. Plasma arginine levels during treatment is reflected in the concentration of arginine in plasma, as a measure of metabolic control. Plasma arginine levels during treatment correlated with types of molecular defects in the arginase genes.

The purpose of the study was to test cardiac myosin light chain I (MLCI) and troponin T (TNT) as markers of myocardial damage after heart surgery. Forty-three patients undergoing cardiac surgery were arbitrarily divided into three groups according to the creatine kinase MB isoenzyme (CK-MB) levels and postoperative electrocardiogram (ECG) changes. Group 1: CK MB > 100 micrograms/l and Infarction pattern changes in ECG (Infarction): Group 2: CK-MB < 100 micrograms/l and no ECG changes (minimal myocardial damage). Group 3: CK-MB > 100 micrograms/l or non specific ECG changes (myocardial injury). MLCI levels showed strong correlations with TNT levels after the operation. The peak MLCI and TNT levels in group 1 were significantly higher than in group 2. The peak MLCI in group 1 was significantly higher than in group 3. TNT showed different patterns in the Infarction and Injury groups. The study showed that MLCI and TNT estimation could evaluate myocardial damage over several postoperative days. TNT estimation could identify myocardial damage earlier than MLCI, however MLCI could discriminate perioperative infarction better than TNT.

The purpose of the study was to test cardiac myosin light chain I (CMLCI) and troponin T (TNT) as markers on myocardial damage after heart surgery. Forty-three patients undergoing cardiac surgery were arbitrarily divided into two groups according to creatine kinase MB isoenzyme (CK-MB) levels and postoperative electrocardiogram (ECG) changes. Group 1: CK-MB > 100 micrograms/L or ECG changes (extensive myocardial damage, 42%); Group 2: CK-MB < 100 micrograms/L and no ECG changes (minimal myocardial damage, 58%). Group 1 was divided into 2 groups (Infarction and Injury groups). CMLCI levels showed strong correlations with TNT levels after the operation. The peak CMLCI and TNT levels in group 1 were significantly higher than in group 2. The peak CMLCI in the Infarction group was significantly higher than in the Injury group. TNT showed different patterns in the Infarction and Injury groups. This study showed that CMLCI and TNT estimation could evaluate myocardial damage over several postoperative days. TNT estimation could identify myocardial damage earlier than CMLCI, however CMLCI could discriminate perioperative infarction better than TNT.

The purpose of this study was to evaluate the cardiac damage by cardiac myosin light chain I after transplantation. This study included 30 patients who underwent cardiac operations and who were divided into three groups. These groups consisted of (1) control group, 15 valvular patients without coronary disease (no electrocardiography changes and creatine kinase MB isoenzyme of 100 micrograms/L or less); (2) infarction group, eight patients (six coronary bypass and two valvular patients with perioperative infarction pattern in the electrocardiography and creatine kinase MB isoenzyme of 100 micrograms/L or more; and (3) transplantation group, seven transplant patients (six heart and one heart-lung). The peak cardiac myosin light chain I value in the transplantation group (32.9 +/- 3.4 micrograms/L) was comparable to the infarction group (27.6 +/- 2.6 micrograms/L), and both of them were significantly higher than the control group (9.2 +/- 0.9 micrograms/L) (p < 0.01). Peak cardiac myosin light chain I levels in the control and transplantation groups correlated with the ischemic time (r = 0.48, p < 0.05 and r = 0.67, p < 0.05, respectively). The total dose of dopamine in the transplantation group correlated with the peak cardiac myosin light chain I (r = 0.67, p < 0.05), and with the cardiac myosin light chain I value on day 7 (r = 0.88, p < 0.01). This study suggests that circulating cardiac myosin light chain I estimations are useful to evaluate myocardial damage after transplantation during postoperative week 1.

The accurate estimation of myocardial damage is desirable for the assessment of myocardial protection and surgical treatments. The purpose of the study was to estimate myocardial damage by measuring cardiac myosin light chain I (CMLCI). Forty-nine patients undergoing cardiac surgery (for angina or valvular disease) were arbitrarily divided into four groups according to the maximum CMLCI level. Group 1: max CMLCI < 10 micrograms/L (37%); Group 2: max CMLCI 10-20 micrograms/L (39%); Group 3: max CMLCI 20-30 micrograms/L (16%); Group 4: max CMLCI > 30 micrograms/L (8%). Electrocardiogram (ECG) and serum creatine kinase MB isoenzyme (CK-MB) were conventionally used as standards of myocardial damage, and compared with CMLCI. Perioperative myocardial infarction, injury and minimum damage were determined by combinations of ECG pattern changes and CK-MB levels. The max CMLCI level was usually seen on the third postoperative day. None of the patients in group 1 had any ECG changes. The number of patients with ECG changes was much higher as the max CMLCI level increased, and evidently increased when the max CMLCI was over 20 micrograms/L. The number of patients with high CK-MB > 100 micrograms/L followed the same pattern. Furthermore, perioperative infarction was only seen when the max CMLCI was > 30 micrograms/L. The peak CMLCI level was significantly higher in the infarction group than injury and minimum damage groups. This study showed that CMLCI was able to estimate the actual extent and severity of the myocardial damage and enhanced the diagnosis of perioperative infarction.

The pharmacokinetic behavior of recombinant feline interferon produced in silkworm infected with recombinant baculovirus harboring cDNA coding for feline interferon was studied in vivo in cats. The decreasing profile of the serum interferon level after intravenous administration was fitted to a two-compartment model. The half-times of the first phase (distribution phase) and second phase (metabolic phase) were 5.0 +/- 0.5 min and 31 +/- 5 min, respectively. In the whole body autoradiogram, at 15 min after the administration, the highest radioactivity was observed in urine in the bladder, and predominant radioactivity in the kidneys, liver, thyroid gland and spleen. Almost no radioactivity was detected in the brain or fat. Three hr after administration, the highest radioactivity was recorded in the thyroid gland, urine in the bladder, intestinal contents, and gastric mucous membrane. The data obtained in this study suggest that recombinant feline interferon has similar pharmacokinetic properties to human interferons and that it is distributed primarily in the liver and kidneys, is catabolized rapidly mainly in the kidneys, and is excreted in the urine without residual accumulation in the body. It was confirmed that 2',5'-oligoadenylate synthetase activity was increased by the interferon in vivo for 3 days after an intravenous bolus injection in cats.

Five different enzymes, carbamyl phosphate synthetase I (CPS I), ornithine transcarbamylase (OTC) argininosuccinate synthetase (AS), argininosuccinate lyase (AL) and arginase (AR) play a role in urea synthesis from ammonium. The structures of cDNA of all these enzymes and those of genome DNA of some enzymes (OTC, AL, AR) have been already clarified, and using of the information, the alleles of each enzyme deficiency have been identified. Alleles are extremely heterogeneous in all enzyme deficiencies, in sharp difference from other inborn errors of metabolism, such as cystic fibrosis and hemoglobinopathies.

The effect of heparin-coated perfusion circuits on blood trauma during clinical cardiopulmonary bypass (CPB) was studied in order to find out if traumatic changes in the blood could be minimized. Twenty-four patients undergoing coronary artery bypass surgery were randomized prospectively to CPB with heparin-coated circuits (HCC) or non-coated circuits (NCC). The trauma to blood was assessed by measuring damage to blood cells by estimating red and white cell rheology changes. These were measured as red cell filtration rate (RFR) and white cell filtration rate (WFR) using standard microfiltration methods. Furthermore, changes in plasma hemoglobin (P-Hb), whole blood and plasma viscosity were simultaneously assessed. The RFR was significantly reduced in both groups during CPB by 10% in the HCC and 32% in the NCC groups (p less than 0.01). When comparing the HCC and NCC groups, a significant difference was first seen after 30 minutes of bypass (p less than 0.05) and increased at the end of CPB (p less than 0.01). Similar results were seen regarding WFR (15% and 36%, p less than 0.01). After 30 minutes of bypass, a significant difference was seen between HCC and NCC groups (p less than 0.05). Furthermore, a significant increase in P-Hb levels were seen during CPB in both patient groups. At the end of CPB, there was a significant difference in P-Hb levels (HCC 305+/-90 mg/L; NCC 455+/-78 mg/L, p less than 0.01) when comparing the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Argininemia is caused by a hereditary deficiency of liver-type arginase (E.C.3.5.3.1) and is characterized by psychomotor retardation and spastic tetraplegia. We examined findings in three Japanese patients with argininemia, by using the PCR, cloning, and sequencing procedures. We found three different mutations--G-to-A-365 in exon 4, G-to-C-703 in exon 7, and C-del-842 in exon 8--thereby leading to mutant arginase proteins of W122X, G235R, and L282FS, respectively. Patient 1 was a compound heterozygote, inheriting the allele with G-to-A-365 from his mother and the allele with G-to-C-703 from his father. Patients 2 and 3 were homozygotes of the allele with G-to-C-703 and of the allele with C-del-842, respectively. Expression tests of these mutant arginases in Escherichia coli indicated that the mutant arginase of W122X did not remain a stable product. The other two mutant arginases--G235R and L282FS--were detected by immunoblot analyses. There was no evidence of activity of the three mutant arginases expressed in E. coli. We tentatively conclude that argininemia is heterogeneous, at the molecular level.

Cold-reactive proteins, such as cold agglutinins, cryoglobulins, and cryofibrinogens, are reversibly precipitates, or gel, upon exposure to cold temperatures. Cryoglobulins are usually not of importance, but under special conditions, such as surgical hypothermia, hyperviscosity and damage in microcirculation may occur in patients with high plasma concentration of cryoglobulins. Several groups have reported their efforts to reduce further the risks of surgical hypothermia in patients with cold agglutinins, but rarely in patients with cryoglobulins. A 57-year-old woman with thoracic aneurysm, requiring replacement of the ascending aorta and the aortic arch, had mixed cryoglobulinemia (cryocrit 29%) associated with rheumatoid arthritis. Steroids therapy and preoperative plasmapheresis were performed, and cryocrit levels were decreased until 0% before operation. Systemic hypothermia (25 degrees C), hemodilution techniques during cardiopulmonary bypass, and cold crystalloid cardioplegia were successfully employed, and no clinical evidence of microcirculation damage was posed after operation.

Warfarin administered to patients with valve replacement at a dose of 0.1 mg/kg for 2 days after surgery, and blood levels of warfarin, TT, PT, HPT, total vitamin K and vitamin K1-epoxide were determined at various time intervals after the administration of the drug. The measurements were obtained from 15 patients: 8 patients with AVR, 6 patients with MVR, and 1 patient with DVR. The blood levels of warfarin reached a peak of 462 +/- 160 ng/ml 6 hours after the administration, TT, PT and HPT were 40% of the initial values 24 hours after the administration, and vitamin K1-epoxide was 1.28 +/- 0.30 ng/ml 24 hours after the administration. It is clear from the results that warfarin exhibits sufficient anticoagulant effects at a beginning dose of 0.1 mg/kg after surgery to prevent a sudden decrease in blood coagulation.

Carbamyl phosphate synthetase I (CPSI) is the first enzyme involved in urea synthesis. CPSI deficiency is an autosomal recessive disorder characterized by hyperammonemic coma in the neonatal period. To analyze the enzyme and gene structures, and to elucidate the nature of mutations in CPSI deficiency, we isolated cDNA clones encoding human liver CPSI. Oligo(dT)-primed and random primer human liver cDNA libraries in lambda gt11 were screened using 5', middle, and 3' fragments of the rat CPSI cDNA as probes. Seven positive clones covered the full-length cDNA sequence with an open reading frame encoding a precursor polypeptide of 1500 amino acids (aa) (deduced Mr, 164,828) with a putative N-terminal presequence of 38 or 39 aa, a 5'-untranslated sequence of 118 bp and a 3'-untranslated sequence of 597 bp. Comparison with the rat CPSI cDNA showed that the deduced aa sequence of the human liver CPSI precursor is 94.4% identical to the rat enzyme precursor. A molecular analysis was made of the genomic DNA from three patients with CPSI deficiency. Heterogeneity of hybridized fragments that may or may not be the cause of the deficiency was apparent on the DNA blots from tissues from one patient.

Thirty patients over 40 years of age with atrial septal defects were operated on between 1981 and 1989. They were divided into two groups according to operative technique, group A of patients with direct suture of defect (17 cases) and group B patch closure (13 cases), in order to investigate the incidence of postoperative complications. Patient age and size of defect in group B were both greater than in group A. One group A patient had pulmonary stenosis, two group B patients had mitral valvular disease and six group B patients had pulmonary hypertension. The incidence of postoperative heart failure was 29% in group A and 61% in group B and that of arrhythmia was 47% and 69% respectively, however there were no intraoperative and postoperative deaths. We concluded that, although a high incidence of postoperative complications was observed in group B, patch closure was recommended for older patients with atrial septal defect because direct suture was more likely to distort the atrial septum.

Pharmacokinetic profile and therapeutic range of plasma quinidine concentration were determined in dairy Holstein cows. Plasma half-life of intravenous quinidine was 1.28 +/- 0.492 (0.41-1.65) hr. The pattern of plasma quinidine transition after oral administration varied greatly among individuals. Total body clearance was 58.7 +/- 24.49 ml/min/kg, although renal quinidine clearance was 0.76 +/- 0.441 ml/min/kg. Therefore, the involvement of some extrarenal organ as the main site of excretion was suspected. Seven cows, diagnosed as atrial fibrillation or ventricular premature contraction, were orally administered with quinidine at various dosages. They showed plasma concentration of 2.3 +/- 1.59 mg/l when therapeutic effect was observed. Clinical signs of intoxication were observed at plasma quinidine concentrations over 10 mg/l. These results suggest the difficulty with the maintenance of effective plasma quinidine concentration by an oral or a single intravenous administration, and thus it is concluded that use of quinidine for treatment arrhythmic cows must be carefully done in order to avoid possible intoxication.

In order to examine the immune response of chickens to different population levels of mites, a microscopic slide modification of the Ouchterlony double-gel diffusion technique was adopted for examination of circulating antibody against the extract of northern fowl mite, Ornithonyssus sylviarum. Precipitating antibodies were detected in all the chickens infested with the mite. One to three clearly defined precipitation lines appeared in almost all the serum samples of infested birds. Titers of antibody correlated with population levels of the mite on chickens, and no differences in antibody development of hens and roosters were distinguished. These results suggest that the titration of precipitating antibodies appears to be useful for the assessment of mite population levels on chickens.

Experience with surgery for ruptured aneurysm of sinus of Valsalva into right atrium (Konno's type IV) in two cases was reported. The first case is a 39-year-old male developing into congestive heart failure for 5 days after the onset that was suspected of "rupture's attack". In the second case of 33-year-old male the course was slow progressing and the onset could not be identified. Mitral valve prolapse was suspected previously because of his syncope attack and infectious endocarditis. Closure of the ruptured noncoronary sinus of Valsalva with mattress suture was undertaken on both cases through the right atrium. Cardiac murmur was disappeared postoperatively on the both cases, and MR was denied in the later case. Postoperative courses were uneventful.

Atrial fibrillation (AF) is the most frequently observed arrhythmia in milking cows. About 50% of AF-affected cows have a history of ketosis, suggesting a relationship between AF and ketosis. Clinical signs of AF include a sudden decrease in milk production and an unstable appetite. Oral administration of quinidine is effective in the treatment of AF. AF in the pig has been observed only in one breeding animal. The clinical signs included anorexia and abnormal heart sounds. The AF was successfully terminated by the administration of 10 mg/kg quinidine every 8 h. AF in dogs and cats appears as a sign of cardiac failure, although AF may also be observed in large dogs without any underlying cardiac disease. Direct current defibrillation is effective in the treatment of these animals.

Mycotic cerebral aneurysm is a relatively infrequent complication of infective endocarditis. However, rupture and intra-cranial hemorrhage involves so high a mortality that few patients can be saved from this condition. We reported a 22-year-old woman with mitral regurgitation and ruptured mycotic cerebral aneurysm caused by infective endocarditis. Vegetation floating between the left atrium and the ventricle was observed by UCG. It was difficult to decide which operation should be done first, valve replacement or excision of cerebral aneurysm. To avoid further intracerebral bleeding caused by anticoagulant therapy connected with cardiotomy, the cerebral aneurysm was excised prior to the valve replacement. Mitral valve was replaced with a Björk-Shiley prosthetic valve 48 hours after the craniotomy. The postoperative course was uneventful and no neurological deficit was found. This report indicates that valve replacement surgery can be successfully performed only 48 hours after craniotomy without any bleeding complications.