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Biomedical subjects

T Phan

Publications and source records attributed to T Phan.

18 recordsLinked to original sources
PubMed1992

Contraceptive use in Vietnam: the effect of individual and community characteristics.

Data from the 1988 Vietnamese Demographic and Health Survey and the 1990 Vietnam Study of Accessibility of Contraceptives were used in this analysis to determine how selective individual and community characteristics influenced the use of modern methods of contraception in Vietnam. Although there were no significant differences in the use of contraceptives between women with a primary education and those with a higher educational attainment, the illiterate women with no formal education were significantly less likely to use modern methods of contraception. Women living in provinces with high infant mortality rates were significantly less likely to use modern methods of contraception than women in low-infant-mortality provinces. Independent of other individual and community characteristics, there were no significant differences in the use of contraception between urban and rural women.

Adolescent↗
PubMed1990

Splanchnic prostanoid production: effect of hemorrhagic shock.

The effect of hemorrhagic shock on rat splanchnic prostanoid synthesis was examined in vitro. Male rats were bled to a mean pressure of 30 mm Hg for 30 min. At that time a midline laparotomy was performed and the superior mesenteric artery (SMA) was cannulated and removed in continuity with its end organ (SV + SI). The SV + SI was perfused at 3 ml/min with oxygenated Krebs-Henseleit buffer at 37 degrees C. Venous effluent (3 ml) was collected at 15, 30, 60, 90, 120, 150, and 180 min and frozen for analysis of basal prostanoid release. Levels of 6-keto-PGF1 alpha (6-keto), PGE2, thromboxane B2 (TxB2), and PGF2 alpha were analyzed by radioimmunoassay and compared in the shock (SK) and sham-operated control (SM) animals. SK 6-keto and TxB2 increased significantly at 15 min of perfusion and then decreased to a lower baseline from 60 through 120 min of perfusion. The major prostanoid released at all time periods was 6-keto (2 to 20 times higher than other prostanoids). One-way ANOVA (pooled times) showed that 6-keto significantly increased in the SK group compared to the SM group (P less than 0.02). These data suggest that the splanchnic bed attempts to compensate for hemorrhagic shock by the marked release of the endogenous vasodilator prostacyclin. Release of the other prostanoids (including TxB2) from the splanchnic bed was modest in our model.

6-Ketoprostaglandin F1 alpha↗
PubMed1990

The effect of diabetes mellitus on aortic prostanoid synthesis and serum cholesterol levels in the rat fed a high cholesterol diet.

The effect of diabetes mellitus on serum cholesterol and aortic microsomal prostanoid synthesis was studied in cholesterol fed male Lewis rats. Normal, diabetic and diabetic rats treated with pancreatic islets were divided into three diet subgroups, control diet, control +2% cholesterol for 8 weeks and control +2% cholesterol diet for 16 weeks. Serum glucose levels were elevated three-fold in the diabetic group compared to normal. Treatment with islets restored serum glucose to normal levels in diabetic rats. The 2% cholesterol diet did not significantly alter serum glucose levels in any of the groups. Body weights in the diabetic group were significantly lower than normal or diabetic rats treated with islets. Feeding 2% cholesterol for 16 weeks significantly increased weight in normal and islet treated diabetic rats but not in the diabetic group. Aortic microsomal prostanoid synthesis was similar in all experimental groups with 6-keto-PGF1 alpha (PGI2 metabolite) being the major product synthesized in all groups. Aortic microsomal prostanoid levels were not altered by the 2% cholesterol diet. Serum cholesterol levels increased 14-fold in the diabetic group which returned to the normal level in the diabetic animals treated with islets. These data show that diabetes does not alter aortic microsomal prostanoid levels in the rat. However, diabetes significantly increased serum cholesterol levels which were reversed by islet transplantation.

Analysis of Variance↗
PubMed1990

Cytokine modulation of keratinocyte cytokines.

There is increasing evidence that epidermal cytokines may have an important role in mediating inflammatory and immune responses in the skin. A number of cell types in the epidermis are capable of secreting cytokines including keratinocytes, Langerhans cells, melanocytic cells, and even Merkle cells. Keratinocytes are the major source of cytokines in the epidermis and have been reported to secrete IL-1, IL-3, IL-6, IL-8, CSF, TNF alpha, TGF alpha, TGF beta, and PDGF. Normally these cytokines are not actively secreted by keratinocytes; however, a number of agents are capable of mediating keratinocyte cytokine production, including cytokines themselves. We examined the effect of a number of cytokines on keratinocyte IL-1, IL-6, GM-CSF, and PDGF production. It was found that these keratinocyte cytokines are all modulated by one or more cytokines, including several that keratinocytes themselves secrete. These effects appear to be mediated by high-affinity cytokine receptors on keratinocytes. We are only beginning to understand the molecular mechanisms underlying the production, regulation, and precise role of keratinocyte cytokines in normal and diseased skin; however, recent studies suggest that cytokines secreted by epidermal cells and lymphoid cells may be important modulators of keratinocyte cytokine production.

Animals↗
PubMed1985

Effect of clonidine on the activity of tryptophan hydroxylase from rat brainstem following in vivo or in vitro treatment.

In vivo administration of clonidine hydrochloride (Catapres) via tail vein injection produced a rapid increase in brainstem tryptophan hydroxylase activity assayed in vitro under subsaturating conditions of reduced pterin cofactor, 6MPH4. Enzyme activity returned to and remained at control levels about 60 min after treatment with low doses of clonidine (5 micrograms/kg). However, with higher doses of the drug (15 micrograms/kg), enzyme activity fell to below control levels for about an hour. Incubation of brainstem slices with clonidine also produced a dose-dependent increase in enzyme activity. The increase in enzyme activity appears to be mediated indirectly since it was abolished when brain catecholamine levels were depleted by pretreatment with 6-hydroxydopamine 8 days prior to clonidine treatment. The kinetic properties of tryptophan hydroxylase prepared 25 and 90 min after clonidine administration indicate that the initial increase and subsequent decrease in enzyme activity seen under these conditions may be due to changes in apparent Vmax of the enzyme.

Animals↗
PubMed1984

Histidine modification with diethylpyrocarbonate induces a decrease in the binding of an antagonist, PK 11195, but not of an agonist, RO5-4864, of the peripheral benzodiazepine receptors.

[3H]PK 11195 binding to peripheral type benzodiazepine binding sites in kidney membranes is inhibited by the histidine blocking agent diethylpyrocarbonate. This reagent irreversibly decreases the Bmax for [3H]PK 11195 without affecting the affinity. By contrast binding of [3H]RO5-4864 is not affected by diethylpyrocarbonate treatment. However RO5-4864 can protect in a concentration dependent manner the [3H]PK 11195 binding site from diethylpyrocarbonate whereas clonazepam and RO15-1788 are not active. These results suggest that PK 11195 and RO5-4864 interact with different conformational states of the receptors that RO5-4864. This is in agreement with our previous hypothesis that PK 11195 is an antagonist and RO5-4864 an agonist at the "peripheral type" benzodiazepine receptors.

Animals↗
PubMed1984

Characterization of peripheral type benzodiazepine binding sites in human and rat platelets by using [3H]PK 11195. Studies in hypertensive patients.

Peripheral type benzodiazepine binding sites have been studied in human and rat platelets and platelet membranes by using PK 11195 (1-(2-chlorophenyl)-N-methyl-N-(1-methyl propyl)-3-isoquinolinecarboxamide) as a ligand. [3H]PK 11195 binding to the intact cells and membranes is saturable, with a high affinity and presents the pharmacological specificity corresponding to the peripheral binding sites (PK 11195 greater than RO5-4864 greater than diazepam greater than clonazepam). [3H]PK 11195 affinity is not affected by cell lysis, but there is a loss of binding capacity, contrarily to RO5-4864 whose affinity is greatly diminished. For this reason [3H]RO5-4864 binding can only be demonstrated in intact cells. Furthermore opposite to RO5-4864, PK 11195 affinity is not decreased by increasing temperatures. No difference was found between binding parameters (KD and Bmax) for [3H]PK 11195 between normotensive and hypertensive subjects. The very high binding capacity of human and rat platelets (Bmax greater than pmole/10(8) cells) makes them a good biological model for studying the physiological significance of "peripheral type" benzodiazepine binding sites.

Adult↗
PubMed1984

[Methylation of erythrocyte membrane phospholipids: correlation with membrane viscosity. Study of normal and parkinsonian subjects].

Plasma membranes from erythrocytes were used to study various parameters: phospholipid methylation, viscosity and fragility. These parameters were analysed in 57 normal subjects (52 +/- 3 years old) and 14 patients with idiopathic Parkinson's disease without previous treatment (71 +/- 2 years old). No significant correlations were observed between the various parameters and sex or age in the normal group. No correlation was observed between fragility and methylation or viscosity. A statistically significant correlation was found between viscosity and phospholipid methylation. In the patients with Parkinson's disease, fragility is identical to the normal group but the viscosity is increased by 25 p. 100. The increase of viscosity is more obvious among the patients with a pure or predominantly akinetic form of the disease. These results favour the previously described correlation between phospholipid methylation and viscosity of the plasma membrane and suggest a modification of these parameters in Parkinson's disease. They also suggest that the increased viscosity observed in Parkinson patients could render the receptors inaccessible to their endogenous ligands.

Adolescent↗
PubMed1983

A subacute treatment of L-methionine induces an increase in the number of [3H]spiperone binding sites in the striatum of the rat.

A subacute treatment, 500 mg/kg I.P. twice daily during 5 days, by L-methionine provoked an increase in the Bmax of [3H]-spiperone binding in the striatum of the rat. This increase was associated to a decrease in membrane microviscosity. However in these conditions no changes were found in the [3H]-DHA, [3H]QNB bindings or in the brain dopamine sensitive adenylate cyclase activity. L-methionine treatment reduced the accumulation of Dopa after NSD 1015 and antagonized the decrease in striatal acetylcholine provoked by haloperidol. Thus L-methionine might be a new potential drug for Parkinson's disease treatment.

Animals↗
PubMed1983

[3H]spiroperidol binding on lymphocytes: changes in two different groups of schizophrenic patients and effect of neuroleptic treatment.

[3H]spiroperidol binding to lymphocytes was measured in untreated paranoid or disorganized and treated paranoid schizophrenic patients. An increase in the Bmax was detected in untreated paranoid patients but a decrease was found in the disorganized patients. No difference was detected in the KD value. Neuroleptic treatment produced a decrease in the Bmax without affecting the KD value. Such results did not comply with the down regulation but might be explained by a change in membrane viscosity as [3H]spiroperidol binding sites on lymphocytes were coupled to phospholipid methylation.

Adult↗
PubMed1983

Detection of binding sites for spiroperidol on leukemic cells: its value for the phenotype characterization of lymphoid leukemias.

The specific binding of the dopamine antagonist spiroperidol was studied in leukemic cell samples of various phenotypes. Among these only B-cell samples from chronic lymphocytic leukemias (7/7) and some "null" cell samples from acute lymphoblastic leukemias (2/7) showed specific binding. B cells from a prolymphocytic leukemia were negative as were also T-lymphoïd and non-lymphoïd leukemic cells at different stages of maturation. This pattern can be clearly correlated with the previous results obtained with normal blood cells and on cell lines. Moreover, it suggests that the detection of spiroperidol binding sites could provide a new means of distinguishing different phenotypes among B cells and early lymphoïd cells. Our results open the way to further studies which might show a correlation between spiroperidol binding sites and the new immunological markers defining subsets among non-T lymphoïd cells, as well as defining their physiological meaning.

Butyrophenones↗
PubMed1976

Effect of the fatty acid composition of ingested fats on rat liver intermediary metabolism.

The influence of a single load of medium chain triglycerides (MCT) or long chain triglycerides (LCT) on different intermediary metabolites of the rat liver was studied. Resultes showed that acetyl-CoA increased more after MCT than after LCT. MCT are more ketogenic than LCT. Mitochondrial and cytoplasmic redox state was greatly reduced after MCT. It is particularly interesting to note that MCT produced an increase in malate and citrate levels, whereas LCT had only a minor influence on these substances.

Acetoacetates↗
PubMed1975

Influence of a long or medium chain triglyceride diet on intermediary hepatic metabolism of the rat.

Two groups of rats were given, ad libitum, diets containing 20% fat for 4-5 weeks. The fat consisted of either long chain (LCT) or medium chain triglycerides (MCT). A third group of rats was given a low fat control diet. No difference in weight increase could be found between LCT and MCT rats. Total lipids and cholesterol concentrations in the plasma were the same whatever the diet. The high fat diets caused an increase in hepatic acetyl-CoA, citrate, malate and ketone body concentrations. Concentration of ketone bodies in the blood, however, decreased. No ketonuria occurred in any case. Hepatic levels of adenosine 5'-triphosphate, adenosine 5'-monophosphate and inoganic phosphate seemed higher in MCT rats than in LCT rats. The levels of these substrates were increased in both groups compared with the control group. LCT rats had hepatic (NS) and blood (HS) lactate and pyruvate concentrations below the corresponding figures for control rats. Hepatic and blood lactate concentrations in MCT rats were at least equal to or slightly higher (NS) than those of control rats. Hepatic glucose and glycogen and blood glucose concentrations were higher in rats given the high fat diet.

Acetyl Coenzyme A↗
PubMed1975

Octanoate metabolism in the isolated perfused rat liver. II. Comparison with a long chain fatty acid.

Liver of fed rats was perfused in vitro with 10 mmoles/litre lactic acid. Supplementary addition of octanoic acid (1.2 mmoles/litre) increased production of ketone bodies. By doubling the quantity of medium chain fatty acid, production of ketone bodies was doubled. Octanoic acid is as ketogenic aspalmitoleic acid if the two fatty acids are compared molecule by molecule. However, C8 : O is more ketogenic that C16: 1 when the comparison is effected on the basis of an identical number of acetyl groups. Octanoic acid increases glucose production by the liver. It was not possible to show the same phenomenon in the presence of palmitoleic acid. During oxidation of fatty acids the beta-hydroxybutyrate/acetoacetate and lactate/pyruvate ratios of the perfusion medium were increased.

Acetoacetates↗
PubMed1975

Intermediary hepatic metabolism of rat after oral medium chain triglyceride load.

Hepatic ketogenesis was studied in rats given medium chain triglycerides (MCT). Acetyl-CoA accumulated in the liver, indicating a very rapid beta-oxidation of medium chain fatty acids. Citrate level increases. Ketogenesis is strongly enhanced. Cytoplasm and particularly mitochondria are more reduced after MCT. This may explain the very high increase in hepatic malate. Under our experimental conditions, there appears to be a significant linear relationship between the hepatic acetyl-Coa level and those of total ketone bodies and malade respectively.

Acetoacetates↗