Search PubMed⌕ Search

Biomedical subjects

M Nakajima

Publications and source records attributed to M Nakajima.

At least 253 records · Page 14Linked to original sources
PubMed1999

Effects of sevoflurane and enflurane on lower esophageal sphincter pressure and gastroesophageal pressure gradient in children.

PURPOSE: The effects of sevoflurane and enflurane on the intraluminal pressure of the lower esophagus (LE), lower esophageal sphincter (LES), and stomach were investigated in paralyzed and mechanically ventilated children under general anesthesia. METHODS: A total of 14 children, ASA physical status class I without risk factors for regurgitation, scheduled for orthopedic surgery were studied. After induction of anesthesia, we inserted a gastrointestinal pressure sensor nasally and monitored the intraluminal pressure of the LE, LES, and stomach under various concentrations of sevoflurane or enflurane with 66% nitrous oxide in oxygen prior to surgical incision. The barrier pressure (BrP), which is the difference between LES pressure and intragastric pressure, was calculated. RESULTS: Sevoflurane at 2.0 and 2.5 minimum alveolar concentration (MAC) decreased LES pressure, and enflurane at 2.0 and 2.5 MAC decreased both LES pressure and BrP in anesthetized children. The intraluminal pressure of the LE and stomach were not altered in either group. CONCLUSION: Sevoflurane and enflurane have an inhibitory effect on LES smooth muscle in anesthetized children. However, since the reduction was relatively low, even at high concentrations, these inhalation anesthetics are unlikely to influence gastroesophageal reflux during anesthesia.

Journal Article↗
PubMed1999

Diesel exhaust particulate induces airway hyperresponsiveness in a murine model: essential role of GM-CSF.

BACKGROUND: Inhaled pollutants were recently shown to be responsible for an increased incidence of airway allergic diseases, including asthma. A common feature of all forms of asthma is airway hyperresponsiveness. OBJECTIVE: Our purpose was to elucidate the effects of diesel exhaust particulate (DEP), one of the most prevalent inhaled pollutants, on airway responsiveness. METHODS: A/J and C57Bl/6 mice were used; the former are genetically predisposed to be hyperresponsive to acetylcholine, whereas the latter are not. DEP was administered intranasally for 2 weeks, after which pulmonary function was analyzed by whole-body plethysmography. RESULTS: Intranasal administration of DEP increased airway responsiveness to acetylcholine in both A/J and C57Bl/6 mice and induced displacement of ciliated epithelial cells by mucus-secreting Clara cells. The effect was mediated by M(3) muscarinic receptors. Acetylcholine-evoked bronchial constriction was reversed by administration of terbutaline, a beta(2)-adrenergic antagonist, which is also characteristic of human asthma. Intranasal administration of antibody raised against GM-CSF abolished DEP-evoked increases in airway responsiveness and Clara cell hyperplasia. The antibody raised against IL-4 also inhibited DEP-evoked increases in airway responsiveness. However, it was to a lesser extent compared with antibody against GM-CSF. In addition, DEP stimulated GM-CSF messenger RNA expression in the lung. CONCLUSION: DEP induces airway hyperresponsiveness by stimulating GM-CSF synthesis.

Acetylcholine↗
PubMed1999

A 'keyhole lesion' gunshot wound in an adipocere case.

A corpse completely converted into adipocere and showing two adjacent bone defects--a typical gunshot entrance wound and a keyhole lesion--is reported. Postmortem changes, a comminuted fracture of the cranial base, and destruction of the bullets made it impossible to determine the direction of fire through the keyhole lesion. Gunshot wounds may show various atypical forms, including keyhole lesions, and especially in old corpses, the distinction between an entrance wound and an exit wound can be very difficult, even if a careful complete autopsy is performed.

Journal Article↗
PubMed1999

Changes of cancellous bone mass in rat mandibular condyle following ovariectomy.

Changes in cancellous bone of the rat mandibular condyle following estrogen deficiency were histomorphometrically examined with 120-day-old female Fischer rats. Sixty-four animals were either ovariectomized bilaterally (ovx) or subjected to sham surgery (sham), and eight from each group were killed at 7, 14, 30, and 60 days after surgery. Seven intact animals were killed on day 0. Before killing, tetracycline and calcein were administered to all animals. Following histological observation, bone histomorphometry of the mandibular condyle was done using a confocal laser scanning microscope and an image analyzer. The sampling site was divided into two regions for analysis: (1) a "subchondral region," formed by the region connected to cartilage; and (2) a "central region," formed by the region beneath the former. The changes in these two regions were analyzed separately. In the sham group's condyle, the bone volume of the subchondral and central regions increased with the passage of time, although the bone turnover became low. This bone gain could be due to the effects of growth and the mechanical stimulus by occlusal load. In the subchondral region of the ovx group's condyle, the bone volume decreased significantly at 7 days, but recovered to reach approximately the same value as the sham group from 14 days onward. In the central region of the ovx group's condyle, the bone volume was unchanged, but revealed a significantly lower value than that of the sham group at 60 days (p < 0.01). Thus, ovariectomy inhibited bone gain, which was observed in the sham group's condyle even though there was no bone loss. On the other hand, the trabecular separation in the ovx's condyle of both the subchondral and central regions increased considerably and small marrow cavities interconnected to form a large bone marrow. Therefore, the ovx rat mandibular condyles dynamically altered their structures under the effects of estrogen deficiency and occlusal loads. Consequently, estrogen deficiency induced transient subchondral bone loss and recovery, whereas, in the central region, it inhibited bone gain. This suggests that mechanical loading modulates the normal ovx-induced bone loss found in other parts of the skeleton.

Animals↗
PubMed1999

Covalent modifications to 2'-deoxyguanosine by 4-oxo-2-nonenal, a novel product of lipid peroxidation.

Two major products (adducts A and B) from the reaction of 2-deoxyguanosine (dGuo) with 13-hydroperoxylinoleic acid were detected by liquid chromatography/mass spectrometry (LC/MS). Adducts A and B were also the major products formed enzymatically when dGuo was incubated in the presence of linoleic acid and lipoxygenase. The mass spectral fragmentation patterns of adducts A and B suggested that unique modifications to the nucleoside had been introduced. This resulted in the characterization of a novel bifunctional electrophile, 4-oxo-2-nonenal, as the principal breakdown product of linoleic acid hydroperoxide. In subsequent studies, adduct A was found to be a substituted ethano dGuo adduct that was a mixture of three isomers (A(1)-A(3)) that all decomposed to form adduct B. Adduct A(1) was the hemiacetal form of 3-(2-deoxy-beta-D-erythropentafuranosyl)-3,5,6, 7-tetrahydro-6-hydroxy-7-(heptane-2-one)-9H-imidazo[1, 2-alpha]purine-9-one. Adducts A(2) and A(3) were the diastereomers of the open chain ketone form. Adduct B was the substituted etheno dGuo adduct, 3-(2-deoxy-beta-D-erythropentafuranosyl)imidazo-7-(heptane-2 -one)-9-hydroxy[1,2-alpha]purine, the dehydration product of adducts A(1)-A(3). Identical covalent modifications to dGuo were observed when calf-thymus DNA was treated with 4-oxo-2-nonenal. These data illustrate the diversity of reactive electrophiles produced from the peroxidative decomposition of lipids and have implications in fully assessing the role of lipid peroxidation in mutagenesis and carcinogenesis.

Aldehydes↗
PubMed1999

Expression of calcium-binding protein regucalcin mRNA in the cloned rat hepatoma cells (H4-II-E) is stimulated through Ca2+ signaling factors: involvement of protein kinase C.

The expression of hepatic Ca2+-binding protein regucalcin in the cloned rat hepatoma cells (H4-II-E) was investigated. The change in regucalcin mRNA levels was analyzed by Northern blotting using rat liver regucalcin complementary DNA (0.9 kb of open reading frame). Regucalcin mRNA was expressed in H4-II-E hepatoma cells. This expression was clearly stimulated in the presence of serum (10% fetal bovine serum). Bay K 8644 (2. 5 x 10(-6) M), a Ca2+ channel agonist, significantly stimulated regucalcin mRNA expression in the absence or presence of 10% serum. Dibutyryl cyclic AMP (10(-3) M) did not have a stimulatory effect on the regucalcin mRNA expression. The presence of phorbol 12-myristate 13-acetate (PMA; 10(-6) M) or estrogen (10(-8) M) caused a significant increase in regucalcin mRNA levels in the hepatoma cells cultured in serum-free medium, while insulin (5 x 10(-9) M) or dexamethasone (10(-6) M) had no effect. Bay K 8644-stimulated regucalcin mRNA expression in the hepatoma cells was completely blocked in the presence of trifluoperazine (10(-5) M), an antagonist of calmodulin, or staurosporine (10(-7) M), an inhibitor of protein kinase C. The stimulatory effect of PMA was clearly inhibited in the presence of stauroporine. The present study demonstrates that regucalcin mRNA is expressed in the transformed H4-II-E hepatoma cells, and that the expression is stimulated through Ca2+-dependent signaling factors.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1999

Endothelin generating pathway through endothelin1-31 in human cultured bronchial smooth muscle cells.

The effects of endothelin (ET)-1(1-31) and ET-2(1-31), human chymase products of the corresponding big ETs, on the intracellular free Ca2+ concentration ([Ca2+]i) and [125I]-ET-1 binding were investigated using human cultured bronchial smooth muscle cells (BSMC). ET-1(1-31) (10(-8)M - 3 x 10(-7)M) and ET-2(1-31) (3 x 10(-8)M - 3 x 10(-6) M) caused an increase in [Ca2+]i in a concentration-dependent manner. Big ET-1 (3 x 10(-8)M - 10(-6)M) also caused this increase, but not big ET-2 at concentrations up to 10(-6)M. The [Ca2+]i increase induced by ET-1 was inhibited by both BQ123, an ET(A)-receptor antagonist, and BQ788, an ET(B)-receptor antagonist, whereas that induced by ET-3 was inhibited by BQ788 but not by BQ123. Increases in [Ca2+]i caused by ET-1(1-31), big ET-1 and ET-2(1-31) were completely inhibited by 10(-4)M phosphoramidon, a dual neutral endopeptidase (NEP)/endothelin-converting enzyme (ECE) inhibitor, and 10(-5)M thiorphan, a NEP inhibitor. Scatchard plot analyses of the saturation curves of [125I]-ET-1 and [125I]-ET-3 showed that both ET(A)- and ET(B)- receptors at the ratio of 4:1 were expressed on BSMC. ET-1(1-31), big ET-1 and ET-2(1-31) inhibited [125I]-ET-1 binding in a concentration-dependent manner, and these effects were attenuated by treatment with thiorphan. On the other hand, big ET-2 slightly inhibited the binding at a high concentration and this was not affected by thiorphan. These results suggest that ET-1(1-31), big ET-1 and ET-2(1-31) cause an increase in [Ca2+]i by being converted into the corresponding ET-1 and ET-2 by NEP, but this did not occur with big ET-2 in human BSMC. ET-2(1-31), produced by human chymase from big ET-2 might be important for the generation of ET-2 in human bronchial tissue.

Adult↗
PubMed1999

Intracerebroventricularly administered corticotropin-releasing factor inhibits food intake and produces anxiety-like behaviour at very low doses in mice.

AIM: Previous studies have demonstrated that corticotropin-releasing factor (CRF) produces behavioural, physiological and immunological responses similar to those induced by stress. However, these findings have been validated largely in laboratory rats. METHODS: We examined the effects of intracerebroventricular (i.c.v.) administration of CRF on anxiety and food intake in mice. Using the elevated-plus maze, we measured anxiety levels after i.c.v. CRF in mice. We also measured food intake for 2 h after i.c.v. CRF. RESULTS: CRF increased the normal preference for the closed arms of the maze at a very low dose of 3 pmol, indicating an anxiogenic effect. CRF powerfully suppressed food intake at the doses of 3-300 pmol for over 2 h. CONCLUSION: Our results demonstrate that i.c.v. CRF evokes anxiogenic behaviour and suppresses feeding with the same dose-response relationships in mice. CRF may thus play a role in integrating the overall responses to stress through co-ordinated actions in the brain of this species.

Animals↗
PubMed1999

Isoform selective inhibition and inactivation of human cytochrome P450s by methylenedioxyphenyl compounds.

1. A series of methylenedioxyphenyl compounds were evaluated for their inhibitory and inactivation effects on nine human cytochrome P450 (CYP) activities using microsomes from human B-lymphoblast cells expressing specific human CYP isoforms. 2. Methylenedioxyphenyl compounds which possess a bulky structure such as 1,4-benzothiazine showed substantial inhibition of S-warfarin 7-hydroxylation catalysed by CYP2C9, S-mephenytoin 4'-hydroxylation by CYP2C19, bufuralol 1'-hydroxylation by CYP2D6, and testosterone 6beta-hydroxylation by CYP3A4. Regarding ethoxyresorufin O-deethylation catalysed by CYP1A1 and benzyloxyresorufin O-dealkylation by CYP2B6, the subtle change of a substitution of the 1,4-benzothiazine structure affected the inhibition selectivity. Ethoxyresorufin O-deethylation by CYP1A2, coumarin 7-hydroxylation by CYP2A6, and chlorzoxazone 6-hydroxylation by CYP2E1 were not inhibited by almost any of the methylenedioxyphenyl compounds. The inhibitory effects of methylenedioxyphenyl compounds that possess a short chain amino group on the human CYP isoforms were not significant. 3. The methylenedioxyphenyl compounds inactivated CYP1A1 (k(inact) = 0.034 min(-1) and K(i) = 0.81 microM), CYP2C9 (k(inact) = 0.041 and 0.042 min(-1) and K(i) = 0.56 and 0.15 microM), CYP2D6 (k(inact) = 0.044-0.339 min(-1) and K(i) = 0.21-19.88 microM), and CYP3A4 (k(inact) = 0.076-0.251 min(-1) and K(i) = 0.25-0.69 microM). These results suggested that the methylenedioxyphenyl compounds investigated in this study would be potent mechanism-based inactivators of these human CYP isoforms. In contrast, CYP2B6 and CYP2C19 were not inactivated. 4. The present study suggested that the selectivity of inhibition or inactivation of human CYP isoforms by methylenedioxyphenyl compounds may vary according to the structure of the side chain.

Aryl Hydrocarbon Hydroxylases↗
PubMed1999

Activation of phenacetin O-deethylase activity by alpha-naphthoflavone in human liver microsomes.

1. The roles of different human cytochrome P450s (CYP) in phenacetin O-deethylation were investigated using human liver microsomes and recombinant proteins. Phenacetin O-deethylase (POD) activities in human liver microsomes at substrate concentrations of 10 and 500 microM were inhibited by 0.1 and 1 microM alpha-naphthoflavone and activated by 10 and 100 microM alpha-naphthoflavone. The activation of POD activity in human liver microsomes by alphanaphthoflavone was inhibited by 100 microM aniline, anti-CYP2E1 antibody, 1 microM ketoconazole and anti-CYP3A4 antibody. 2. In recombinant CYP from human B-lymphoblast cells, POD activities at a phenacetin concentration of 500 microM were detected for CYP2E1 and CYP3A4, as well as CYP1A2, CYP1A1, CYP2C19, CYP2C9 and CYP2A6. In recombinant CYP from human B-lymphoblast cells or baculovirus-infected insect cells and in reconstituted systems, a requirement of cytochrome b5 (b5) for POD activities catalysed by CYP2E1 and CYP3A4 was observed. The activation of POD activity by alpha-naphthoflavone was observed for CYP3A4, but not for CYP2E1. Co-expression of b5 with CYP3A4 enhanced the activation of POD activity by alpha-naphthoflavone. 3. In the absence of alpha-naphthoflavone, the POD activity in pooled human liver microsomes at 500 microM phenacetin was significantly inhibited (p<0.0001) by 10 microM fluvoxamine, but not by 1 microM ketoconazole. In the presence of alpha-naphthoflavone, the activity was significantly inhibited (p<0.0001) by 1 microM ketoconazole, but not by 10 microM fluvoxamine. 4. Inter-individual differences in the effects of alpha-naphthoflavone on POD activity in human liver microsomes were observed, and the involvement of CYP3A4 as well as CYP1A2 in POD activity in human liver was identified even at a low substrate concentration.

Aniline Compounds↗
PubMed1999

Genetic polymorphism in the 5'-flanking region of human CYP1A2 gene: effect on the CYP1A2 inducibility in humans.

A genetic polymorphism was identified in the 5'-flanking region of human CYP1A2 gene, and its effect on the transcriptional activation of the CYP1A2 gene was investigated. Nucleotide sequence analysis revealed the existence of a point mutation from guanine (wild type) to adenine (mutated type) at position -2964 in the gene. This point mutation was detected by a polymerase chain reaction-restriction fragment length polymorphism method using DdeI or BslI restriction enzyme, and was proven to be genetically inherited. Allele frequency in 116 Japanese subjects showed 0.77 and 0.23 for the wild and mutated types of allele, respectively. The point mutation caused a significant decrease of CYP1A2 activity measured by the rate of caffeine 3-demethylation in Japanese smokers (p<0.05). Gel retardation analysis showed the existence of protein bound to the polymorphic locus. These results suggest that this polymorphism is a causal factor of decreased CYP1A2 inducibility.

Alleles↗
PubMed1999

Design and synthesis of para-fluorophenylalanine amide derivatives as thrombin receptor antagonists.

An antagonist specific for the thrombin receptor is expected to be a remedy for thrombosis. Structure-activity studies of thrombin receptor-tethered ligand SFLLRNP have revealed the importance of the Phe-2-phenyl group in receptor recognition and the replacement of the Phe-2 by para-fluorophenylalanine [(p-F)Phe] was found to enhance its activity [Nose, T. et al. (1993) Biochem. Biophys. Res. Commun. 193, 694-699]. In order to obtain a small sized antagonist, a series of (p-F)Phe derivatives was designed and synthesized novel structural elements essential for receptor interactions being introduced at both the N and C-termini. beta-Mercaptopropionyl (betaMp) or its derivative activated by S-3-nitro-2-pyridinesulphenyl (Npys) was introduced at the N-terminus, and phenylmethyl amines were coupled to the C-terminus. All compounds were inactive when assayed for human platelet aggregation, indicating that they are not agonists. beta-Mercaptopropionyl derivatives were also inactive as antagonists. However, Npys-containing analogs were found to inhibit the agonist activity of SFLLRNP. In particular, SNpys-betaMp-(p-F)Phe-NH-R [R = -CH(C6H5)2 and -CH2-CH-(C6H5)2] potently suppressed platelet aggregation. The results suggested that (p-F)Phe can be used as a structural core to construct an effective antagonist conformation.

Amides↗
PubMed1999

Analysis of circadian blood pressure rhythm and target-organ damage in stroke-prone spontaneously hypertensive rats.

OBJECTIVE: We compared diurnal patterns of blood pressure in Wistar-Kyoto (WKY) rats, spontaneously hypertensive rats (SHR) and stroke-prone spontaneously hypertensive rats (SHRSP), and analyzed the relationship between the change in diurnal patterns of blood pressure and target-organ damage in SHRSP. MATERIALS AND METHODS: Blood pressure, heart rate and motor activity in the three groups of rats were continuously monitored by radiotelemetry, from 1100 h on the first measuring day to 1300 h on the third measuring day. The left ventricular weight and the ratio of beta-myosin heavy chain to alpha-myosin heavy chain in the cardiac left ventricle, morphological changes in the glomerular basement membrane in the kidney, 24 h urinary protein excretion and brain weights were also measured in 10-, 12- or 17-week-old SHRSP. RESULTS: The SHR circadian blood pressure rhythm exhibited a pattern which peaked during the rats' active (light-off or dark) phase, but the peak time was a little closer to the resting (light-on) phase compared with that for WKY rats. Although the circadian blood pressure rhythm for 10-week-old SHRSP was similar to that observed for SHR, the patterns in 12- and 17-week-old SHRSP were shifted further towards the resting phase. Heart and left ventricular weight increased with the progression of hypertension. The ratio of beta- to alpha-myosin heavy chain in the left ventricle was higher in 12- and 17-week-old SHRSP than in 10-week-old SHRSP. Brain weight was increased significantly in 17-week-old SHRSP compared with 10- and 12-week-old SHRSP. Increased urinary protein excretion and morphological changes in the glomerular basement membrane in the kidney were observed in 12- and 17-week-old SHRSP. CONCLUSIONS: These data suggest that SHRSP have an abnormal circadian blood pressure rhythm associated with hypertensive target-organ damage. This rat strain may therefore be a useful model in which to investigate the mechanisms responsible for the alteration in the circadian blood pressure rhythm, and to analyze the relationship between the abnormal circadian rhythm and target-organ damage.

Animals↗
PubMed1999

Pharmacological characterization of PABSA, an orally active and highly potent endothelin-receptor antagonist.

The pharmacological characterization of a nonpeptide endothelin (ET)-receptor antagonist, PABSA [(R)-(--)-2-(benzo[1,3]dioxol-5-yl)-N-(4-isopropyl-phenylsulfon yl)-2-(6-methyl-2-propylpyridin-3-yloxy)-acetamide hydrochloride] was studied. PABSA competitively inhibited the binding of [125I]-ET-1 to A7r5 cells expressing ET(A) receptors and of [125I]-ET-3 to COS cells expressing porcine ET(B) receptors with Ki values of 0.11 and 25 nM, respectively. PABSA inhibited ET(A) receptor-mediated and ET(B) receptor-mediated vasocontraction and ET(B) receptor-mediated vasorelaxation in isolated rabbit vessels with K(b) values of 0.46, 94, and 26 nM, respectively. The antagonist potency of PABSA for ET(A) receptor-mediated vasocontraction was 63- and 87-fold more potent than those of BQ-123 and bosentan, respectively, and was similar to those of TAK-044 and SB209670. Oral administration of PABSA (1-10 mg/kg) caused dose-dependent inhibition of the pressor response to exogenous ET- 1 (0.1 nmol/kg) in conscious normotensive rats. PABSA (10-100 mg/kg, p.o.) reduced blood pressure in deoxycorticosterone acetate (DOCA)-salt hypertensive rats, spontaneously hypertensive rats (SHRs), and stroke-prone spontaneously hypertensive rats (SHRSPs). The hypotensive effect of PABSA was sustained for > or =24 h in these rats. These results suggest that PABSA is a highly potent ET(A)-receptor antagonist with weak ET(B)-receptor antagonist activity. Because PABSA has a long duration of action in vivo, this antagonist should be useful in the therapy of ET-related disease.

Administration, Oral↗
PubMed1999

Effects of chronic administration of glucocorticoid on midazolam pharmacokinetics in humans.

Midazolam (MDZ) is metabolized by CYP3A. Glucocorticoids are potent inducers of CYP3A in humans. The possible interaction between intravenous MDZ and chronically administered glucocorticoids was investigated during surgery in patients. MDZ (0.2 mg/kg) was administered intravenously to 8 patients taking glucocorticoid chronically and 10 patients not taking glucocorticoid. In patients taking glucocorticoid, the AUC0-infinity and CL of MDZ was decreased to 63.9% (16.3 +/- 10.5 vs 25.5 +/- 20.7 microg x min/mL) and increased to 127.5% (16.7 +/- 10.7 vs 13.1 +/- 8.3 mL/min/kg) of that in the control group, respectively. The terminal t1/2 values of MDZ were similar in two groups. In patients taking glucocorticoid, the AUC0-infinity of 1'-hydroxymidazolam (1'-OH MDZ) was 66.7% of that in the control group (7.6 +/- 2.6 vs 11.4 +/- 9.7 microg x min/mL), and the terminal t1/2 of 1'-OH MDZ was significantly (p < 0.01) decreased (1.8 +/- 0.5 vs 3.0 +/- 0.8 hr). Accumulative urinary excretion of 1'-OH MDZ glucuronide was increased to 157.6%. These observations might be results from induction of CYP3A4 and/or UDP-glucuronosyltransferase by glucocorticoids.

Adult↗
PubMed1999

Effect of HSR-903, a new fluoroquinolone, on the concentration of theophylline in serum.

The effect of HSR-903, a new fluoroquinolone, on the concentration of theophylline in serum in healthy male volunteers was investigated. The concentration of theophylline in serum and the urinary excretion rates of theophylline on day 5 of concomitant dosing with HSR-903 tended to increase compared to those on day 4, when theophylline was given alone; however, the urinary excretion rates of 1-methyluric acid and 3-methylxanthine on day 5 of concomitant dosing with HSR-903 tended to decrease in comparison to those on day 4, when theophylline was given alone.

Adult↗
PubMed1999

Aerobic degradation of 1,1,1-trichloroethane by Mycobacterium spp. isolated from soil.

Two strains of 1,1,1-trichloroethane (TCA)-degrading bacteria, TA5 and TA27, were isolated from soil and identified as Mycobacterium spp. Strains TA5 and TA27 could degrade 25 and 75 mg. liter of TCA(-1) cometabolically in the presence of ethane as a carbon source, respectively. The compound 2,2,2-trichloroethanol was produced as a metabolite of the degradation process.

Aerobiosis↗