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Biomedical subjects

T R Patel

Publications and source records attributed to T R Patel.

At least 19 recordsLinked to original sources

A study of prenatal ultrasound and postnatal magnetic imaging in the diagnosis of central nervous system abnormalities.

Accurate prenatal diagnosis of central nervous system (CNS) abnormalities is essential in counselling parents, as they are the most common developmental abnormalities causing considerable mortality. Currently, the standard in prenatal imaging is ultrasound scanning (USS). The introduction of fast acquisition magnetic resonance imaging (MRI) has lead to increased diagnostic confidence and information available for parents. Frequently USS initially identifies CNS abnormalities as ventriculomegaly alone. However, it is known that ventriculomegaly is commonly associated with other CNS pathology, which may adversely affect the prognosis. As MRI has superior soft tissue resolution and can be used at any time postnatally, it is expected to identify disorders of myelination that may result from prenatal ventriculomegaly. This study will evaluate the role of MRI as a postnatal imaging tool in patients that had a prenatal USS diagnosis of isolated ventriculomegaly. This was a retrospective review of patient notes and scan reports. The postnatal MRI study group consisted of 9 patients that had been diagnosed initially with prenatal isolated ventriculomegaly on USS, and followed up with postnatal MRI (cases of spina bifida and Dandy-Walker malformations were excluded). Findings from the scan reports were recorded and analysed. Both MRI and prenatal USS gave the same information in 55.6 % of the patients. In the remaining 44.4 %, MRI added to the information provided by the prenatal USS. An interesting finding was that MRI missed a small fluid-filled cyst and an arachnoid cyst in 2 cases. 55.6 % of patients went on to develop other CNS abnormalities prenatally, whereas 33.3 % showed prenatal regression of VM with no other pathology. 11.1 % showed postnatal persistence of isolated VM. As USS has the advantage of being cheap and easy to perform, it will remain as the primary imaging tool in obstetric care. MRI can provide significant additional information that can affect parent counselling, prenatal intervention, and postnatal management. Postnatally, MRI can give some idea of prognosis by evaluating myelination patterns, which is not possible with USS.

Arachnoid Cysts↗

Computerized stereochronoscopy and alternation flicker to detect optic nerve head contour change.

PURPOSE/BACKGROUND: Stereochronoscopy, a technique previously explored but abandoned for glaucoma diagnosis, viewed optic nerve images acquired at separate points in time as if a stereo pair. Prior efforts to exploit this technique were impaired by a lack of superimposability for sequential optic nerve images. We investigated computerized registration techniques for aligning sequential, monoscopic optic disc images to facilitate sensitive detection of optic nerve head contour changes in glaucoma. DESIGN: Algorithm and software development. Comparisons with standard techniques. MATERIALS: Existing patient records from the Glaucoma Service, Scheie Eye Institute, University of Pennsylvania. METHODS: Two sets of optic disc photographs, separated in time by 1 to 18 years, of 25 eyes with and without glaucomatous optic disc progression were digitized. We developed custom software for accurate image alignment. Change in disc morphology was then judged by digital stereochronoscopy and user-controlled alternation flicker of superimposed, time-separated images on a computer monitor. Comparisons were made with standard stereoscopic comparison. MAIN OUTCOME MEASURE: Identification of change or no change in optic nerve head contour for images acquired at separate points in time. RESULTS: Image processing and registration permits accurate alignment of optic disc photographs. Alternation flicker of superimposed, sequential images facilitates image comparison and detection of change as indicated by change in vessel position, color, and other cues for contour change. A high concordance was found between standard stereoscopic comparison and alternation flicker. In several cases, reinspection of stereo comparison led to a revised judgment on the basis of disc changes rendered more obvious with alternation flicker. Digital stereochronoscopy was less concordant with standard techniques. CONCLUSIONS: Digital image processing techniques and alternation flicker provide a simple, sensitive, software-based method for detecting glaucomatous optic disc change.

Algorithms↗

Comparison of cerebral blood flow and injury following intracerebral and subdural hematoma in the rat.

Subdural hematomas (SDH) can induce ischemia and neuronal damage in the underlying cortex. However, the extent to which intracerebral hematomas (ICH) produce reductions in cerebral blood flow (CBF) sufficient to cause ischemic damage is uncertain. Intracranial hemorrhage was induced by the injection of 100 or 200 microl of blood into the subdural space (SDH) or into the caudate nucleus (ICH) of the rat. CBF was measured using [14C]-iodoantipyrine autoradiography at 4 h. Brain damage was measured using 2,3, 5-triphenyl tetrazolium chloride (TTC) staining at 24 h and brain edema was measured using the wet/dry weight method. Brain ion contents were measured at 24 h using a flame photometer and chloridometer. In the CBF studies, the volume of tissue perfused below the ischemic threshold (<20 ml/100 g/min) for SDH was 122+/-35 mm3 (sham: 3.3+/-1.7 mm3). Following ICH, there was a small volume of tissue perfused below the ischemic threshold 50+/-11 mm3 (sham: 3. 3+/-2.5 mm3) but this volume corresponded closely to the volume of clot (71+/-5 mm3). The extent of brain damage, measured by TTC staining, in the cerebral cortex correlated with the increasing volume of the subdural blood clot (sham: 9+/-3 mm3; 200 microl: 81+/-19 mm3; P<0.01). Conversely, minimal brain damage was detected following ICH. The injection of blood into the subdural space or into the brain parenchyma induced blood volume-dependent increases in brain water content at 24 h. Increases in brain water content after SDH, were confined to the cerebral cortex (sham: 0.1+/-0.1 g/g dry weight; 200 microl: 0.8+/-0.3 g/g dry weight; P<0.001). In contrast, increases in brain water content after ICH were predominantly in the subcortical region (sham: 0.1+/-0.1 g/g dry weight; 200 microl: 0.4+/-0.2 g/g dry weight; P<0.01). The present investigations demonstrate differences in CBF, brain injury and edema formation following SDH and ICH indicating that these conditions may require different therapeutic interventions.

Animals↗

Effect of intracerebral and subdural hematomas on energy-dependent transport across the blood-brain barrier.

Although both intracerebral and subdural hematomas induce brain edema, previous studies have indicated that they may have different cerebrovascular effects. Our own investigations have demonstrated that while subdural hematomas (SDH) are associated with ischemia this is not the case following intracerebral hematomas (ICH). Previous studies have demonstrated a decrease in energy-dependent transport of glutamine across the blood-brain barrier (BBB) following focal cerebral ischemia. The present study investigates this further by examining the effects of SDH, ICH, and intracerebral thrombin injections, an agent involved in ICH-induced injury, on blood to brain glutamine transport. The injection of 200 microL of blood into the subdural space induced a marked reduction in glutamine transport (Ki, influx rate constant) into the cerebral cortex at 4 and 24 h following SDH (sham, 105+/-4% of contralateral cortex; SDH 4 h, 63+/-5%, p<0.01; SDH 24 h, 47+/-12%, p<0.05). There were no significant changes in glutamine Ki in subcortical areas following SDH. Following ICH (200-microL clot); however, there were only modest decreases in glutamine Ki in subcortical areas (sham, 98+/-2% of right cortex; ICH 4 h, 91+/-5%, p<0.01; ICH 24 h, 91+/-2%, p<0.05). Intracerebral injection of thrombin (5U) had minimal effect on glutamine Ki, in subcortical areas, at 4 h and induced a modest decrease in transport at 24 h (sham, 98+/-2% of right cortex; thrombin 4 h, 98+/-2%; thrombin 24 h, 86+/-2%, p<0.05). The present studies demonstrate marked differences in the effects of ICH and SDH on BBB function.

Animals↗

Survival of Vibrio cholerae 01 strains in shrimp subjected to freezing and boiling.

This research was undertaken to assess the resistance of Vibrio cholerae 01 strains inoculated into white shrimp, Penaeus schimitti, to heating and freezing treatments. Shrimp samples with and without carapace were obtained from Sao Luis, Brazil. Microbial analysis revealed the presence of marine vibrios including Vibrio alginolyticus, Vibrio parahaemolyticus, and other vibrios and aerobic gram-negative and gram-positive bacteria that grew on selective medium, thiosulfate-citrate-bile salt-sucrose agar. Samples with and without carapaces were heated before inoculating with cells of V. cholerae and then one-half of the samples was stored frozen at -200 degrees C and the other one-half was heated to boiling temperatures. Viable cells of the test organism were recovered from samples without carapaces, stored under frozen conditions, after 36 days. In contrast, no living cells were recovered after 26 days from samples with carapaces. Boiling temperatures were very damaging to V. cholerae 01 in shrimp samples with and without carapaces. Total destruction of the cells occurred within 1 to 2 min of exposure to heating.

Animals↗

Effect of copper and cadmium on three Malaysian tropical estuarine invertebrate larvae.

Three species of tropical estuarine invertebrates were exposed to copper sulfate and cadmium chloride to investigate their potential as test specimens for sediment toxicity assays in the South-east Asian regions. The larvae of the reef sea urchin (Diadema setosum), the oyster (Crassostrea iradalei), and the mud crab (Scylla seratta Forskall) were used in the 48-hr assays with copper and cadmium as reference toxicants. In addition the sea urchin were tested for end point measurements at different stages of the larval development and a 60-min sperm bioassay. The study revealed that the sea urchin first cleavage, which is an assay end point and which takes place about 1 hr after fertilization, was the most sensitive stage for both toxicants, with copper being more toxic than cadmium. Sensitivity comparisons between the three invertebrate larvae revealed the mud crab zoea larvae to be most sensitive for cadmium with an LC50 value of 0.078 microgram/ml, while the sea urchin was more sensitive for copper, with EC50 values of 0.01 microgram/ml at the first cleavage stage and 0.04 microgram/ml at the pluteus larva stage. All the invertebrates tested gave responses that made them suitable test organisms for metal bioassays in the tropical estuarine environment.

Animals↗

Endothelin receptor mediated constriction and dilatation in feline cerebral resistance arterioles in vivo.

The receptors mediating the cerebrovascular actions of endothelins have been examined in feline cerebral resistance arterioles in vivo. The adventitial microapplication of the endothelin ETA receptor antagonist BQ-123 (cyclo D-aspartate-D-tryptophan-L-leucine-D-valine-L-proline) (0.1-10 microM) per se had minimal effect on cerebral resistance arterioles examined. The adventitial microapplication of endothelin-1 (10 nM) elicited a marked vasoconstriction of cerebral resistance arterioles (-29.1 +/- 1.9% from pre-injection baseline). The endothelin-1 induced vasoconstriction was attenuated, in a dose dependent manner, by the adventitial co-application of BQ-123 and endothelin-1 (estimated IC50 0.7 microM). The adventitial microapplication of the endothelin ETB receptor agonist BQ-3020 N-acetyl[Ala11,Ala15]ET-1 (6-21)) (0.001-1 microM) effected a dose dependent vasodilatation (EC50 30 nM, maximum response 25 +/- 5% from pre-injection baseline). The magnitude of the vasodilatation elicited by BQ-3020 (100 nM and 1 microM) was dependent on the pre-injection calibre of the arterioles examined. The intracarotid infusion (via the lingual artery) of BQ-3020 (0.5-500 pmol/min) had no significant effect on the calibre of cerebral resistance arterioles. These results suggest that the peptide endothelin ETB receptor agonist fails to gain access to the cerebrovascular endothelin ETB receptors following its intraluminal administration. These investigations indicate that endothelin ETA receptors mediate vasoconstriction and endothelin ETB receptors mediate vasodilatation in feline cerebral resistance arterioles in vivo.

Animals↗

The relationship between glutamate release and cerebral blood flow after focal cerebral ischaemia in the cat: effect of pretreatment with enadoline (a kappa receptor agonist).

The effect of the kappa-opioid agonist enadoline (CI-977) upon the relationship between cerebral blood flow and glutamate release was simultaneously assessed (using microdialysis and hydrogen clearance techniques respectively) at the same anatomical locus in the cerebral cortex (suprasylvian gyrus) after permanent middle cerebral artery (MCA) occlusion in halothane-anaesthetised cats. During controlled graded ischaemia, pretreatment with enadoline (0.3 mg/kg i.v. followed by continuous infusion at 0.15 mg/kg/h), initiated 30 min prior to MCA occlusion, significantly attenuated the marked increases in extracellular glutamate, aspartate and GABA observed in the focal ischaemic penumbra. The present data are consistent with the hypothesis that the neuroprotective efficacy of enadoline in focal cerebral ischaemia is due to inhibition of glutamate release in the ischaemic penumbra.

Animals↗

Failure of an endothelin antagonist to modify hypoperfusion after transient global ischaemia in the rat.

The role of endogenous endothelins in mediating postischaemic hypoperfusion after transient global ischaemia was investigated in halothane-anaesthetised rats. Pretreatment with the broad-spectrum (ET (A) and ET (B)) endothelin antagonist. Bosentan (17 micromol/kg) had minimal effect on postischaemic hypoperfusion, measured by hydrogen clearance, in the caudate nucleus and the parietal cortex in the 3 h after bilateral common carotid artery occlusion with concomitant haemorrhagic hypotension (transient global ischaemia). In a separate series of rats with CBF measured by [14C]iodoantipyrine autoradiography at 90 min after carotid occlusion with concomitant haemorrhagic hypotension, Bosentan treatment failed to significantly alter CBF in any of the 35 brain regions examined. No significant alterations in CBF, measured by hydrogen clearance, were observed after transient bilateral common carotid artery occlusion. [14C]Iodoantipyrine autoradiography at 90 min after occlusion failed to demonstrate any significant increases in CBF after transient bilateral common carotid artery occlusion in any of the 35 brain regions examined in anaesthetised rats. The failure of the broad-spectrum endothelin antagonist Bosentan, at concentrations known to inhibit the cerebrovascular effects of exogenous ET-1, provide no support for the view that endothelins have a major role in mediating acute postischaemic hypoperfusion.

Animals↗

Endothelin-mediated vascular tone following focal cerebral ischaemia in the cat.

The actions of Bosentan and PD155080, nonpeptide endothelin receptor antagonists, were examined in feline pial arterioles in situ following middle cerebral artery (MCA) occlusion to gain insight into the cerebrovascular influence of endogenous endothelins in focal cerebral ischaemia. Immediately following permanent MCA occlusion, all pial arterioles overlying the suprsylvian and ectosylvian gyri displayed marked dilatations, which were maintained in a population of vessel but differentiated into sustained constrictions in others. Perivascular subarachnoid microinjections of Bosentan (30 microM), PD155080 (30 microM), and artificial CSF (pH 7.2) were performed between 30 and 210 min following MCA occlusion. The perivascular microapplication of Bosentan (30 microM) and PD155080 (30 microM) around pial vessels overlying the suprasylvian and ectosylvian gyri, which are within the territory of the occluded MCA, elicited in increase in the calibre of postocclusion dilated and constricted pial arterioles. The perivascular microapplication of PD155080 (30 microM) around postocclusion constricted arterioles overlying the ectosylvian and suprasylvian gyri elicited an increase in the calibre of arterioles (69 +/- 49% from preinjection baseline; n = 8). The perivascular microapplication of Bosentan (30 microM) around postocclusion constricted arterioles overlying the ectosylvian and suprasylvian gyri also elicited an increase in the calibre of arterioles (68 +/- 60% from preinjection baseline; n = 13). In contrast, the microapplication of CSF (pH 7.2) elicited small reductions in pial arteriolar calibre of postocclusion constricted arterioles (-8 +/- 13% from preinjection baseline; n = 8). The perivascular microapplication of PD155080 (30 microM) around postocclusion dilated pial arterioles overlying the ectosylvian and suprasylvian gyri elicited an increase in the calibre of arterioles (11 +/- 10% from preinjection baseline; n = 38). The perivascular microapplication of Bosentan (30 microM) around postocclusion dilated arterioles elicited an increase in the calibre of arterioles (16 +/- 15% from preinjection baseline; n = 36). In contrast, the microapplication of CSF (pH 7.2) elicited small reductions in pial arteriolar calibre of postocclusion dilated arterioles (-9 +/- 6% from preinjection baseline; n = 44). Perivascular microapplication of Bosentan or PD155080 had minimal effect on the calibre of pial arterioles on the parasagittal gyrus (anterior cerebral artery territory), although these arterioles had also displayed sustained dilatation following MCA occlusion. These results indicate that contractile factors (whose effects can be reversed with endothelin receptor antagonists) constrict or impair dilatation of cortical resistance arterioles in an acute cerebral ischaemic episode.

Animals↗

Endothelin receptor antagonist increases cerebral perfusion and reduces ischaemic damage in feline focal cerebral ischaemia.

These investigations characterised the cerebrovascular effects of an endothelin ETA-receptor antagonist PD156707 in normal and ischaemic cat brain. A dose of PD156707 that inhibited the effects of exogenous endothelin-1 was established in nonischaemic cerebral resistance arterioles. Perivascular microapplication of the endothelin-receptor antagonist PD156707 (0.03-3 microM) had a minimal effect on nonischaemic pial resistance arterioles. The perivascular co-application of PD156707 and ET-1 (10 nM) effected a dose-dependent attenuation of the ET-1 vasoconstrictive response (IC50 = 0.1 microM). Intravenous administration of PD156707 (3 mumol/kg bolus + 5 mumol/kg/h infusion) attenuated the vasoconstriction elicited by perivascular ET-1 (10 nM) in normal pial arterioles (ET-1 vasoconstriction: -37 +/- 13% from preinjection baseline; after intravenous PD156707: 6 +/- 10% from preinjection baseline). In the focal ischaemia studies, cerebral perfusion was measured in the suprasylvian and ectosylvian gyri (by laser Doppler flowmetry). Occlusion of the middle cerebral artery reduced cerebral perfusion in the suprasylvian and ectosylvian gyri by approximately 50%. Intravenous administration of PD156707 (3 mumol/kg bolus + 5 mumol/kg/h infusion), initiated 30 min after middle cerebral artery occlusion, effected a progressive increase in cerebral perfusion up to preocclusion baseline levels, whereas cerebral perfusion in vehicle-treated animals did not vary from its postocclusion level. In these animals, the intravenous administration of PD156707 reduced the hemispheric volume of ischaemic damage by 45% (vehicle: 2,376 +/- 1,107 mm3; PD156707: 1,307 +/- 548 mm3; p < 0.05). Our investigations indicate that endothelin receptor antagonism may be a new therapeutic strategy for the amelioration of focal ischaemic damage.

Animals↗

AMPA receptor antagonism attenuates MK-801-induced hypermetabolism in the posterior cingulate cortex.

The effect of pretreatment with an AMPA receptor antagonist, NBQX, on MK-801-induced alterations in glucose use was examined using [14C]-2-deoxyglucose autoradiography. NBQX (7 mg/kg) had minimal effect on glucose utilisation in all anatomical regions examined. The intravenous administration of MK-801 (0.2 mg/kg) induced increases in glucose use in the limbic system and cingulate cortex. MK-801 reduced glucose utilisation in the sensory motor and auditory cortices. Pretreatment with NBQX attenuated the MK-801-induced hypermetabolism in the posterior cingulate cortex. The decreases in glucose utilisation induced by MK-801 were not exacerbated by the pretreatment with NBQX. The interaction between NBQX and MK-801 suggests a possible method of attenuating some of the adverse effects of the non-competitive NMDA receptor antagonists in the posterior cingulate cortex.

Animals↗

Therapeutic potential of endothelin receptor antagonists in experimental stroke.

This investigation demonstrates an increase in endothelin (ET)-mediated vascular tone in peri-ischemic areas after experimental focal cerebral ischemia (middle cerebral artery occlusion) in the cat. Adventitial application of the butenolide antagonist PD155080 (30 microM), after MCA occlusions resulted in marked increases in caliber of dilated (10.6 +/- 1.6% change from preinjection baseline) and constricted vessels (68.7 +/- 17.5% change from pre-injection baseline). Cerebral blood flow (measured by laser Doppler flowmetry) was reduced after MCA occlusion to 50% of preocclusion levels. Intravenous administration of PD156707 30 min after MCA occlusion restored cerebral blood flow to preocclusion baseline levels at 6 h. The volume of ischemic damage in the cerebral hemisphere after MCA occlusion was significantly reduced (by 45%) after intravenous administration of PD156707.

Animals↗

Postischemic hypoperfusion in transient global ischemia: a role for endothelins?

The role of endogenous endothelins (ETs) in mediating postischemic hypoperfusion after transient global ischemia was investigated in halothane-anesthetized rats. Pretreatment with the broad spectrum ETA and ETB antagonist bosentan (17 mumol/kg) had minimal effect on postischemic hypoperfusion, as measured by hydrogen clearance, in the caudate nucleus and the parietal cortex during 3 h after bilateral common carotid artery occlusion with concomitant hemorrhagic hypotension (transient global ischemia). In cerebral blood flow (CBF) measured by [14C]iodoantipyrine autoradiography at 90 min after carotid occlusion with concomitant hemorrhagic hypotension, bosentan treatment failed to alter CBF in any of the cerebral cortical regions examined. No changes in CBF, as measured by hydrogen clearance, were observed after transient bilateral common carotid artery occlusion. [14C]Iodoantipyrine autoradiography at 90 min post occlusion failed to demonstrate any increases in cerebral blood flow after transient bilateral common carotid artery occlusion in any of the 35 brain regions examined in anesthetized rats.

Animals↗

Effects on feline pial arterioles in situ of bosentan, a non-peptide endothelin receptor antagonist.

The cerebrovascular actions of bosentan, a novel endothelin antagonist with effects at endothelin ETA and ETB receptors, have been examined in individual pial arterioles on the cortical surface of chloralose-anaesthetised cats. Subarachnoid perivascular microapplication of bosentan (0.3-300 microM) had minimal effect on pial arteriolar calibre. Subarachnoid perivascular microapplication of endothelin (10 nM) effected a marked reduction in pial arteriolar calibre (reduced by 39.2 +/- 2.7% from baseline). This vasomotor effect of topical endothelin could be attenuated either by co-administration of bosentan (IC50 approximately 1 microM) or by the intravenous administration of bosentan (17 mumol/kg). These investigations suggest that bosentan (applied topically or systemically) may be a valuable tool in the elucidation of the functional significance of endothelins in the cerebral circulation in vivo.

Animals↗

Microbial degradation of phloroglucinol and other polyphenolic compounds.

Biodegradation of phloroglucinol (1,3,5-trihydroxybenzene) and other polyphenolic compounds by microbes may occur by aerobic and anaerobic metabolic pathways. Aerobic microbes may initiate the mineralization of phloroglucinol or other polyphenolics by either a reductive pathway, epoxide formation, or a specific hydroxylating mechanism. Cleavage of the various intermediates of phloroglucinol and polyphenolic degradation may occur by intradiol and extradiol mechanisms. The reductive pathway in contrast to other mechanisms utilized by aerobic microbes, seems both cumbersome and energy wasteful. The degradation of lignin and its associated phenolics follows an enzymatic combustion process which resembles a nonspecific enzyme-catalyzed burning. Anaerobic mineralization of phloroglucinol and its associated polyphenolics by several microbes seems to favour the reductive formation of a dihydrophloroglucinol (1,3-dioxo-5-hydroxycyclohexane), which is cleaved by a specific hydrolase. Mineralization of numerous other polyphenolic compounds by anaerobes seems to utilize phloroglucinol as a central metabolite.

Aerobiosis↗

1,3,5-Trihydroxybenzene biodegradation by Rhodococcus sp. BPG-8.

The metabolic pathway used by Rhodococcus sp. BPG-8 isolated from oil-rich soil in Newfoundland for the degradation of 1,3,5-trihydroxybenzene (phloroglucinol) as a sole source of carbon and energy was determined. Culture filtrates of cells grown on phloroglucinol detected 1,2,3,5-tetrahydroxybenzene when extracted and analyzed using gas chromatography--mass spectrometry, thin-layer chromatography, and ultraviolet spectrophotometry. Nonaromatics were either derivatized with 2,4-dinitrophenylhydrazine and compared against authentic standards by the above methods, or detected by chemical and enzymatic methods. Extracts of cells grown on phloroglucinol contained phloroglucinol hydroxylase activity, and a dioxygenase that carried out ortho-cleavage of 1,2,3,5-tetrahydroxybenzene. The extract also showed inducible activity for further metabolism of acetopyruvate leading to accumulation of formate in the supernatant. A tentative degradative pathway for phloroglucinol by Rhodococcus sp. BPG--8 is proposed.

Biodegradation, Environmental↗

Utilization of 1,3,5-trihydroxybenzene (phloroglucinol) by a soil isolate, Rhodococcus species BPG-8.

A Gram-positive bacterial strain was isolated from oil rich soil in Newfoundland and found to utilize various di- and trihydroxylated aromatic compounds as a source of carbon and energy. This bacterium exhibited rod/coccus dimorphism during its growth cycle. Chemical analysis of cell wall composition (amino acids, sugars, and fatty acids) was performed using gas chromatography-mass spectrophotometry and high pressure liquid chromatography. Comparison of both acid production and growth substrates showed complete homology with Rhodococcus erythropolis. Growth of the isolate on phloroglucinol (1,3,5 trihydroxybenzene) occurred in the pH range 5-8; with a substrate and temperature optima of 8.0 mM and 25 degrees C. The oxidation of PG was examined using whole cells as well as crude cell extracts. PG oxidation was shown to be due to an inducible enzyme system. Tentatively the isolate was identified as Rhodococcus species BPG-8 which is able to utilize phloroglucinol as the sole source of carbon and energy.

Acids↗