Biomedical subjects
Publications and source records attributed to M Ray.
Among undergraduates in a carefully controlled design, 9 students who took notes studied longer than groups of 30 and 17 who did not. No differences were observed on test scores, retention interval, comprehension scores, or reading rate. Whether students expected multiple-choice or free-recall testing, strategies were similar, suggesting study oriented to rote learning.
New information is revealed concerning the frequency of expression and distribution of aphidicolin-induced fragile sites in eight leukaemic patients, namely, four chronic myeloid leukaemic patients (CML), three acute lymphocytic leukaemic (ALL) patients, and one acute myeloid leukaemic (AML) patient. The cytogenetic data demonstrate a statistically significant (p less than 10(-6] increase in the frequency of aphidicolin-induced fragile sites in seven of the eight leukaemic patients compared with healthy age-matched and sex-matched controls. The chromosomal band locations of the aphidicolin-induced fragile sites from 400 metaphase spreads of these leukaemic patients reveal a nonrandom distribution in the karyotype. Some aphidicolin-induced fragile sites in these leukaemic patients were located at chromosome bands known to be induced specifically by folic acid, distamycin A, bromodeoxyuridine or azacytidine. The cross-induction of fragile sites in the leukaemic patients may be indicative of shared molecular homology in the sequence composition of nonrandom chromosomal DNA.
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Leishmania donovani is a protozoal pathogen that belongs to the kinetoplastida order. Unlike in other eucaryotic systems, the first three enzymes of the de novo pyrimidine biosynthetic pathway are not components of a multifunctional protein system. The three enzyme activities in the crude extract were separated on a Sephacryl S-200 column. Aspartate carbamoyltransferase (EC 2.1.3.2) has been purified to apparent homogeneity. The enzyme has an approximate molecular weight of 135,000 and seems to be a tetramer of equivalent subunits of molecular weight 35,000. The enzyme shows strictly hyperbolic kinetics with both the substrates under a variety of conditions and is not inhibited by nucleotide phosphates. Km for carbamyl phosphate is 3.1 x 10(-4) M and for aspartate is 7.6 x 10(-3) M. Apparently, the enzyme has no regulatory role in pyrimidine biosynthesis. N-(Phosphonoacetyl)-L-aspartic acid is a powerful competitive inhibitor (Ki = 5 x 10(-7) M) for this enzyme with carbamyl phosphate as substrate. This inhibitor completely inhibits the growth of the vector form of organism at 60 microM and significantly affects the growth of the pathogenic form in a macrophage assay system. The potency of the inhibitor is comparable with allopurinol which is undergoing human clinical trial as an antileishmanial drug.
We present a girl with ring chromosome 16. Clinical abnormalities included developmental delay, short stature, and minor facial anomalies. Analysis of the glutamate-pyruvate transaminase (GPT) phenotype suggests the possible exclusion of the GPT locus expressed in erythrocytes (GPT) from the very distal p13 region of chromosome 16.
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To examine the relation between ethanol-induced microvascular and absorptive changes, we have investigated the effect of 16,16-dimethyl prostaglandin E2 on the jejunal intraluminal plasma albumin loss (which was taken as a measure of microvascular changes) and the inhibition of water, sodium, and glucose transport caused by intraluminal ethanol. A group of 8 dogs received intravenously 16,16-dimethyl prostaglandin E2 at a dose of 0.1 microgram/kg as a bolus followed by 0.05 microgram/kg.hour for 2 h (prostaglandin-treated group). A second group of 8 dogs received no 16,16-dimethyl prostaglandin E2 (untreated group). In each dog of both groups, one jejunal segment was perfused with an ethanol-free solution (control segment) and an adjacent segment was perfused with the same solution containing 6% (wt/vol) ethanol (ethanol-perfused segment). The albumin loss (mg/g dry gut wt.90 min, mean +/- SE) by the control and the ethanol-perfused segments was 0.76 +/- 0.23 and 8.29 +/- 1.27, respectively, in the untreated group, and 0.66 +/- 0.23 and 4.81 +/- 0.67, respectively, in the prostaglandin-treated group. The ethanol-induced increase in albumin loss was significant in both groups, but was significantly lower (p less than 0.05) in the prostaglandin-treated group than in the untreated group. Intraluminal ethanol depressed net water, sodium, and glucose transport by 74%, 52%, and 22%, respectively, in the untreated group, and by 92%, 65%, and 38%, respectively, in the prostaglandin-treated group. The magnitude of this depression did not differ significantly between the two groups. As 16,16-dimethyl prostaglandin E2 attenuated the ethanol-induced plasma albumin loss, but not the inhibition of water, sodium, or glucose transport, we conclude that the microvascular and the absorptive changes produced by ethanol are not mediated by the same mechanism.
The amniotic band syndrome (ABS) refers to the infrequent occurrence of congenital deformities presumably due to fetal entanglement in strands of ruptured amniotic sac. The most commonly associated anomalies include amputations, constriction bands, syndactyly, craniofacial defects, club feet, and cleft lip. We present a typical case and short literature review of ABS. The infant reported also had a connective tissue nevus and a cutaneous striated muscle hamartoma.
Chorionic villi sampling (CVS) has become a first trimester alternative to amniocentesis for prenatal diagnosis. The cytogenetic findings in 150 experimental samples are presented. The ages of the mothers ranged from 12 to 35 years, but the majority of them were 18 and 19 years of age. Various parameters of culturing and processing the samples in order to improve the method, were investigated. Short term incubation for 48 h was the method routinely employed in processing the biopsies for cytogenetic analysis. In the first series of 100 cases one mosaic case (46,XX/45,X), one Robertsonian translocation (13;14), one marker chromosome and one fragment were found. The foetal tissues were not analysed for chromosomes. In the second series of 50 samples, one case of mosaicism was found in the chorionic villi (46,XX/47,XX, 18q-), but this abnormality was absent in the foetal tissue. One variant inv(9) was observed in the foetal tissue as well as in the chorionic villi. In all other cases the karyotypes from the chorionic villi samples matched those of the corresponding foetal samples. There was no maternal contamination in this series of 50 samples. The discrepancies in the cytogenetic results from other investigators are discussed.
The mechanism of cardio-inhibitory effects of sodium deoxycholate (DOC) was investigated by studying its effects on the contractility, action potentials (APs) and ultrastructure of guinea pig atrial preparations. DOC (10(-7)-10(-4) M) caused reversible negative ino- (NIE) and chrono-tropy in spontaneously beating (SBA) and NIE in electrically driven left (EDA) atria. At higher doses (greater than or equal to 1.10(-3) M) DOC caused irreversible inhibition of contractions. Atropine (10(-7)-10(-4) M) failed to inhibit both the reversible and irreversible effects of DOC. The NIE due to lower doses of DOC (less than or equal to 1.10(-4) M) was inhibited by higher [Ca2+]0, isoprenaline (10(-6)-10(-4) M), and noradrenaline (10(-6)-10(-5) M), which did not alter the dose of DOC required for the irreversible and complete NIE. In lower doses (10(-7)-10(-4) M) DOC caused a reversible inhibition of the AP durations at -20 and -40 mV (APD20 and APD40, respectively), but increased the AP duration at 90% repolarisation (APD90). At higher doses (greater than 5.10(-4) M) it caused an irreversible membrane depolarization, reduction in APD20 and APD40, and complete cessation of electrical activity. The ultrastructural changes in atria treated with 1.10(-4) M DOC were characterized by poorly delineated glycocalyx and at greater than 1.10(-3) M by disruption of sarcolemma and sarcoplasmic reticulum and swelling disruption of mitochondria. Taken together these observations show that DOC caused reversible and irreversible inhibition of atrial contractions at low (10(-7)-10(-4) M) and high (greater than 5.10(-4) M) concentrations, respectively, by different mechanisms. The former effect is due to inhibition of Ca2+ channel activity and the latter due to its detergent property causing removal of subcellular components.
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The method reported here for determining pyrazinamide and its metabolites (2-pyrazinoic acid, 5-hydroxypyrazinamide, 5-hydroxypyrazinoic acid and pyrazinuric acid) consists of diluting urine or acid deproteinisation of serum followed by chromatography on a cation-exchange column. The column length and the detection system (ultraviolet or fluorimetry) allow for a very good separation of the different compounds; the sensitivity of the method makes it suitable for pharmacokinetic studies.
An enzyme which oxidizes aminoacetone to methylglyoxal has been purified from the particulate fraction of goat liver. Polyamines, such as spermidine and spermine, are also good substrates for this enzyme. The pH optimum for aminoacetone oxidation was found to be 8.2. The apparent Km values of the enzyme for aminoacetone and spermidine were 0.009 and 0.095 mM, respectively. The subunit molecular weight of the enzyme was 93,000 as determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The apparent molecular weight of the native enzyme was 186,000 by gel filtration. The enzyme is highly sensitive to carbonyl group reagents. The enzyme is not inhibited by monoamine and diamine oxidase inhibitors.
Mercury is a major environmental pollutant and a proven teratogen in man and animals. Its teratogenicity and effects on fetal chromosomes were investigated in mice. Various dose levels of methylmercuric chloride (MMC) were administered via an intragastric tube to pregnant ICR Swiss/Webster mice on day 9 of gestation. On day 18 of gestation the animals were killed and the fetuses were removed. Fetal lung and liver tissues were processed for cytogenetic studies. Fetuses were also fixed in Bouin's solution for subsequent teratological examination by using Wilson's technique. Mercury levels were determined in maternal blood and randomly selected fetuses. One fetus from each litter was processed for skeletal staining with Alizarin Red S. A significant increase in embryonic deaths and resorptions was observed at all dose levels. The incidence of fetal anomalies was significantly increased following maternal treatment with 10, 15, or 20 mg/kg of MMC. Maternal weight between day 9 and day 18 of gestation decreased significantly. The LD50 of MMC in pregnant mice was determined to be 20 mg/kg of body weight; the LD100 was 30 mg/kg. A significant difference was observed between the mean fetal weights at the various dose levels. Levels of mercury were found to be significantly higher in treated animals and fetuses, and increased in a dose-related manner. The levels of mercury were significantly higher in the fetuses than in the mothers at the same dosage, indicating a correlation between the levels of mercury in maternal mice and corresponding higher levels in their fetuses. Cytogenetic studies revealed significant clumping of chromosomes in metaphase at all dose levels and the frequency of clumping increased as dosage increased. The euploidy number (2n = 40) of chromosomes per cell did not vary between the treatment groups and control groups. The frequency of nucleolus-organizing regions per cell did not change significantly between the treatment groups and the control. The frequency of sister chromatid exchanges increased significantly as the dosage increased.
The recovery times and the state of postoperative awakening were studied after anaesthesia with propofol or enflurane. The forty patients who were to undergo surgery for cold thyroid nodules were divided into two homogeneous groups which were similar in age, sex, weight and length of surgery. In one group, induction was carried out with propofol, fentanyl, pancuronium bromide, and maintained with 9 mg X kg-1 X h-1 propofol. In the other group, this was done with thiopentone, fentanyl, pancuronium bromide, followed by 0.8% enflurane. Repeat injections of fentanyl were given as required. The time between stopping giving the anaesthetic drug and eye opening was measured, as well as the performance in memorizing and sorting numbers; these two tests were carried out before and 2 h after surgery. The overall results did not show any differences between the two groups in recovery time or quality of awakening. In the propofol group, recovery time and quality were better than in the enflurane group if the patient was less than 50 years old or surgery lasted less than 100 min. In the propofol group, there were significant correlations between recovery time and age (r = 0.83), and between recovery time and duration of surgery (r = 0.87). The doses of this new product should therefore be modified according to the age of the patient and the length of surgery.
We describe a family where four brothers show the rare heritable folate sensitive autosomal fragile site (FSAFS) at 19p13 when cells were grown in TC199. Two of the brothers are schizophrenic while one brother is mentally retarded with autistic-like features. The clinical significance of this fragile site however is still unknown.
Varying dose levels of methylmercuric chloride (MMC), 1000 ppm (5 mg through 15 mg/kg of body weight), were administered via an intragastric tube to pregnant ICR Swiss/Webster mice on day 9 of gestation. The animals were killed on gestational day 18 and the fetuses removed. Fetal lung sections were processed for light and electron microscopy. A group of animals treated with physiological saline in a similar manner served as the controls. The fetal lungs from treated animals were hypoplastic and retarded in development. The severity of pulmonary changes increased with the dose-levels of MMC. Vacuolation and lysis of mitochondria were seen in fetal lungs. Mitochondrial damage increased in severity with dose-level of methylmercuric chloride.