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D Tran

Publications and source records attributed to D Tran.

At least 91 records · Page 5Linked to original sources
PubMed1992

The field topography of ERG components in man--I. The photopic luminance response.

A technique of multi-input systems analysis is used to explore the field topography of ERG responses to local luminance modulation. Variations in amplitude and wave form are studied within the central 23 degrees. Outside the fovea, the amplitude appears to follow a simple power law rx as a function of eccentricity r where x is approximately -2/3. The largest inter-subject variability is found in the fovea. Some nasal-temporal asymmetry is observed in all subjects with higher response densities in the temporal field outside the blind spot. The topography of the luminance response shares all these properties with the density of retinal cones.

Electrophysiology↗
PubMed1991

Asymmetric distribution of phosphoinositides and phosphatidic acid in the human erythrocyte membrane.

The distribution of phosphoinositides and phosphatidic acid (PA) between the outer and inner layers of the human erythrocyte membrane was investigated by using two complementary methodologies: hydrolysis by phospholipase A2 (PLA2) and immunofluorescence detection with monoclonal antibodies against polyphosphoinositides. The contents of phosphatidylinositol 4,5-bisphosphate (PIP2), phosphatidylinositol 4-phosphate (PIP) and PA were decreased by 15-20% after 60 min incubation with PLA2, while that of phosphatidylinositol (PI) was increased. Studies with 32P-labelled cells revealed that PLA2 treatment led to indirect effects on the metabolism of these phospholipids. Therefore, the asymmetric distribution of phosphoinositides and PA was inferred from the data obtained in ATP-depleted erythrocytes. In these cells with arrested phosphoinositide metabolism, the asymmetric distribution of the major phospholipids was maintained: PLA2 hydrolyzed approx. 20% of PI, PIP2 and PA (but no PIP) indicating their localization in the outer layer of the membrane. This finding was confirmed by immunofluorescence studies with antibodies specific to each phosphoinositide. External addition of anti-PIP2 but not anti-PIP gave a positive reaction both in control and in ATP-depleted erythrocytes. A pretreatment of cells with PLA2 led to a decrease in the intensity of anti-PIP2 staining. These results demonstrate that significant fractions of PIP2, PI and PA are localized on the outer surface of the erythrocyte membrane.

Adenosine Triphosphate↗
PubMed1989

Mechanisms of polyethylene glycol 400 permeability of perfused rat intestine.

Abnormal permeability to polyethylene glycol 400 (PEG 400) has been demonstrated in various disorders with defective intestinal barrier functions. To understand the basic mechanisms of PEG 400 permeability, we compared PEG 400 permeation in different segments of the intestine and studied the kinetics and influence of intraluminal factors on PEG 400 absorption in vivo in perfused intestinal segments of the rat. The permeation rate of PEG 400 was dependent on the luminal concentration (y = 12.99x + 3.5; r = 0.97), indicating that passive movement is the mechanism involved in PEG 400 absorption. Changing the perfusate pH from 6 to 7.4 or modifying the unstirred water layer resistance by changing luminal flow rate did not affect PEG 400 absorption. When luminal osmolarity was varied from 0.225 to 0.6 osmol/L, higher osmolarity decreased both water and PEG 400 absorption (p greater than 0.01). The relationship between PEG 400 and water absorption at different osmolarities was linear (y = 0.9x + 5.7; r = 0.98). At a luminal osmolarity of 0.3 osmol/L 43% of PEG 400 permeation was mediated by passive diffusion and 57% was mediated by solvent drag. Increasing water absorption by decreasing luminal osmolarity resulted in proportional increase of PEG 400 permeation through solvent drag or convection. The solvent drag reflection coefficient (sigma f) for PEG 400 permeation of the jejunum was 0.1. Taurocholic acid (10 mM) alone or with oleic acid (2.5 mM) did not affect PEG 400 absorption. Permeabilities of 1 mM PEG 400 and water were similar in jejunum and ileum but were markedly increased in the colon (p greater than 0.01). These studies demonstrate that PEG 400 is absorbed by both passive diffusion and by solvent drag, with the latter accounting for a greater fraction of the absorptive drive under normal conditions. Polyethylene glycol 400 uses aqueous pathways for its permeation across the intestinal epithelium.

Animals↗
PubMed1989

Anti-idiotypic antibodies to a monoclonal antibody raised against anti-müllerian hormone exhibit anti-müllerian biological activity.

Polyclonal anti-idiotypic antibodies were raised to three monoclonal antibodies to bovine anti-Müllerian hormone, and purified by affinity chromatography. All anti-idiotypes inhibited binding of labelled anti-Müllerian hormone to the monoclonal antibody against which they were directed; in addition, the anti-idiotypes directed against a non-zoospecific monoclonal antibody inhibited binding of labelled anti-Müllerian hormone to a monoclonal antibody raised against human testicular AMH, indicating that the idiotype against which these anti-idiotypes are directed recognizes a conserved epitope on the anti-Müllerian hormone molecule. These anti-idiotypes, but not those directed against other monoclonals, exhibit hormone-like activity in a bioassay for anti-Müllerian activity, and we suggest that they may act as antibodies against the anti-Müllerian hormone receptor.

Animals↗
PubMed1989

The persistent Müllerian duct syndrome: a molecular approach.

A rare form of male pseudohermaphroditism is characterized by the persistence of Müllerian derivatives in phenotypic males. To determine the etiology of this syndrome, we studied the expression of anti-Müllerian hormone (AMH) in six boys, including three brothers, with the persistent Müllerian duct syndrome. All except one presented with an inguinal hernia containing the Müllerian derivatives, and in two boys the hernial sac contained the contralateral testis. AMH was normally expressed in the testicular tissue of two patients, as shown by bioassay of anti-Müllerian activity and immunocytochemistry. The testicular tissue of the other patients had no detectable bioactive or immunoreactive AMH, yet they expressed AMH mRNA with a normal transcription initiation site and in the amount expected for their age. These results prove the heterogeneity of the persistent Müllerian duct syndrome and suggest that it may sometimes involve peripheral insensitivity to AMH.

Animals↗
PubMed1988

Anti-müllerian hormone in sheep follicles.

The purpose of this work was to study anti-Müllerian hormone (AMH) secretion during ovarian development in sheep before and after birth. We used avidinbiotin immunocytochemistry and a monoclonal antibody specific for ruminant AMH. Only granulosa cells have an immunoreactivity; this immunoreactivity was influenced by animal age and by the degree of follicular development. In the fetus, no immunoreactivity was detected in somatic cells of ovigerous cords at 70 days post-coitum (p.c.) or in primordial and growing follicles at 100 and 120 days p.c. A faint reaction was only seen occasionally in a few cells belonging to preantral follicles at 120 days p.c. AMH was never detected in primordial follicles in ovaries of 144 days p.c., at birth, at 8, 97, 145 days post-natal or in adult ovaries. A faint reaction, elicited in small growing follicles, increased with follicle size to become more intense in antral follicles. Immunoreactivity was strongly positive in granulosa cells, especially in those lining the antral cavity and close to the oocyte, whereas there was little or no reactivity in peripheral cells near the basal membrane. Follicles without AMH reactivity were found at all times and their number decreased with age.

Aging↗
PubMed1988

Anti-müllerian hormone and freemartinism: inhibition of germ cell development and induction of seminiferous cord-like structures in rat fetal ovaries exposed in vitro to purified bovine AMH.

In 13 and 14-day old fetal rat ovaries maintained 3 to 10 days in organ culture, purified bovine anti-Müllerian hormone (AMH) (1.5 to 3 micrograms/ml) induced a characteristic freemartin effect. Gonadal volume and germ cell number were significantly reduced, compared to control ovaries cultured in anhormonal medium, and epithelial cells with large clear cytoplasm linked by interdigitations differentiated in the gonadal blastema. These cells resembling rat fetal Sertoli cells became polarized and formed seminiferous cord-like structures delineated by a basal membrane containing laminin and fibronectin as is the case of testicular seminiferous cords at the first step of their differentiation. These data indicate that AMH is probably the testicular factor responsible for the morphological modifications of bovine freemartin gonads and suggest that this hormone could also be involved in normal morphological differentiation of the testis. In contrast, in fetal rat ovaries, AMH did not trigger the testosterone production which occurs in freemartin gonads at an early stage of the gestation.

Animals↗
PubMed1988

Effect of isoflurane and enflurane on the electrocorticogram of epileptic patients.

We studied the effect of inhaled anesthetic agents on the electrocorticogram (ECoG) in four epileptic patients during nondominant right hemisphere temporal lobectomy while they received 70% nitrous oxide in oxygen (70% N2O/O2) alone, 70% N2O/O2 with 0.5 to 1.5% isoflurane, or 70% N2O/O2 with 2% enflurane. The mean frequency of epileptiform spikes decreased during use of isoflurane, but not enflurane, compared with use of 70% N2O/O2 alone. Enflurane produced paroxysms of synchronous high-voltage spikes. The mean number of electrodes exhibiting spike activity decreased with isoflurane use and increased with enflurane use compared with use of 70% N2O/O2 alone. This preliminary study suggests that isoflurane can suppress epileptogenic tissue and that both isoflurane and enflurane can distort the ECoG, confounding accurate identification of the seizure focus. When used judiciously, however, enflurane may be a potent synchronizer and activator of the epileptogenic focus, making it easier to identify.

Action Potentials↗
PubMed1987

Ligands internalized through coated or noncoated invaginations follow a common intracellular pathway.

Cholera toxin (CT) represents a class of ligands that binds preferentially to noncoated pits on the cell surface. In the present study, we have investigated the mechanism of endocytosis of this class of ligand and compared it to the classic coated pit mechanism. When either CT coupled to colloidal gold particles (CT-gold) or 125I-labeled CT were incubated with 3T3 L1 fibroblasts at 4 degrees C, both ligands bound in a preferential fashion to small noncoated pits on the cell surface. CT-gold surface-labeled cells were then incubated at 22 degrees C. The labeled ligand progressively moved into noncoated vesicles and a tubulovesicular compartment composed of a network of tubules and vesicles closely associated with multivesicular bodies but distinct from the Golgi complexes. The ligand next passed into multivesicular bodies. By contrast, alpha 2-macroglobulin (alpha 2m)-gold initially localized preferentially to coated pits and subsequently to coated vesicles and tubulovesicular structures before associating with multivesicular bodies. To directly compare the intracellular pathway followed by CT-gold to that followed by alpha 2m-gold, CT-gold (7 nm) was coincubated with alpha 2m-gold (15 nm). By 10 min of incubation at 22 degrees C, up to 66% of tubulovesicular units contained both ligands when analyzed in serial sections. Subsequently, both ligands were colocalized in multivesicular bodies. We conclude that CT-gold endocytosed via noncoated vesicles and alpha 2m-gold endocytosed through coated vesicles subsequently associate with the same tubulovesicular units, multivesicular bodies, and lysosomes.

Animals↗
PubMed1987

Neutrophil accumulation in experimental myocardial infarcts: relation with extent of injury and effect of reperfusion.

The effects of reperfusion on the myocardial accumulation of neutrophils and their role in the extent of injury were investigated in a canine preparation with a 3 hr coronary occlusion followed by 21 hr of reperfusion. The left anterior descending coronary artery (LAD) was permanently occluded in group 1 and reperfused after 3 hr in four others (groups 2 to 5). All but group 5 received lidocaine (1 mg/min over 8 hr). A critical stenosis was produced and left in place at reperfusion only in group 2. In groups 1 and 2, 111In-labeled autologous neutrophils were injected at the time of coronary occlusion. Group 4 animals were rendered leukopenic 2 hr before the coronary ligature and throughout the experiment by injection of an antineutrophil rabbit serum. Quantification of the radioactivity by digitized scintigraphy of the heart slices revealed an 80% (p less than .05) increase in neutrophil accumulation in the infarct region after reperfusion (group 2) as compared with permanent occlusion (group 1). Gamma counting of myocardial tissue samples showed that the neutrophil accumulation ratio in the subendocardial central zone of the infarct was increased five times (p less than .05) by reperfusion, whereas no difference was evident in the subepicardium. Infarct size and myocardial area at risk were not statistically different among the five groups. However LAD flow in the leukopenic group (group 4) was significantly higher (p less than .05) 30 min after reperfusion (40.0 +/- 5 ml/min) when compared with the preocclusion value (21.7 +/- 4 ml/min). In contrast, in a parallel experiment without leukopenia (group 3), LAD flow after reperfusion did not differ from the preocclusion value.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Immunocytochemical detection of anti-müllerian hormone in Sertoli cells of various mammalian species including human.

An immunocytochemical method, based on the use of a polyclonal antibody raised against purified bovine anti-Müllerian hormone (AMH), was used to detect AMH in Sertoli cell cytoplasm of various mammalian species, including human. Immunopurification of antiserum by AMH-affinity chromatography, although not mandatory, leads to better results and increased sensitivity. In human testicular tissue, AMH is detectable up to 6 years of age. In rats, AMH production is initiated at 13 days post coitum, peaks between 15 and 17 days, and is no longer detectable 1 week after birth. The reaction is strongest in Sertoli cells of calves, sheep, goats, and pigs, species characterized by a high degree of development of the rough endoplasmic reticulum. It is fainter in human, rat, rabbit, and cat Sertoli cells, in which the rough endoplasmic reticulum is not as abundant. This correlation is not unexpected, in view of the localization of reaction product in this cytoplasmic organelle. Preliminary results indicate that there may be a relationship between the amount of immunoreactive AMH present in testicular biopsies of intersex patients and the degree of regression of the Müllerian duct on the ipsilateral side. This may help to elucidate whether persistence of Müllerian ducts results from lack of testicular production of AMH or from peripheral resistance of the Müllerian primordia to the hormone.

Animals↗
PubMed1987

Purified bovine AMH induces a characteristic freemartin effect in fetal rat prospective ovaries exposed to it in vitro.

To determine whether anti-Müllerian hormone (AMH) is responsible for the gonadal lesions observed in bovine genetic females united by placental anastomoses to male twins (freemartins), prospective ovaries of fetal rats were exposed to purified bovine AMH in vitro. In cultures initiated at 14 days p.c. and maintained 3 to 10 days, AMH consistently induced a characteristic 'freemartin effect', namely reduction of gonadal volume, germ cell depletion and differentiation, in the gonadal blastema, of epithelial cells with large clear cytoplasm linked by interdigitations, resembling rat fetal Sertoli cells. These cells tend to become polarized and form cords, delineated by a continuous basal membrane containing laminin and fibronectin. Such structures, resembling developing seminiferous cords, were not detected in control ovarian cultures. These data strongly suggest that AMH is the testicular factor responsible for triggering the morphological abnormalities of freemartin gonads.

Animals↗
PubMed1987

Immunocytochemical study of anti-Müllerian hormone in sheep ovarian follicles during fetal and post-natal development.

Anti-Müllerian hormone (AMH) was detected in perinatal and postnatal sheep ovaries, using avidin-biotin immunohistochemistry with a monoclonal antibody specific for ruminant AMH. Immunoreactivity was limited to granulosa cells, and was influenced both by the degree of follicular development, and by the age of the animal. In the fetus, only the most advanced follicles exhibited a faint immunoreactivity at 120 days gestation, and no reaction was observed in younger animals. Immediately before and after birth, primordial follicles were still negative, but a faint reaction was elicited in young growing follicles, increasing with follicle size. Strong immunoreactivity was visible in antral follicles, especially in the innermost granulosa cell layers, close to the oocyte and lining the antral cavity.

Animals↗
PubMed1987

Effect of barbiturate coma on glucose utilization in normal brain versus gliomas. Positron emission tomography studies.

Glucose utilization by normal and neoplastic cerebral tissue can be measured in humans using positron emission tomography (PET) with fluorine-18-labeled 2-deoxy-D-glucose (FDG). Malignant gliomas are known to exhibit hypermetabolic glucose consumption compared to normal brain. Barbiturate-sensitive cerebral glucose utilization is coupled to neuronal activity, and lesions lacking neuronal activity should be relatively insensitive to barbiturate suppression of glucose utilization. In a study to examine this phenomenon, three patients with cerebral gliomas underwent FDG-PET while awake and during deep barbiturate coma. Cerebral glucose utilization was measured in normal brain, tumor, and a homologous, non-neoplastic control site in the contralateral hemisphere. A glucose utilization ratio for tumor/control tissue was calculated. The mean reduction of glucose utilization during barbiturate coma was: gray matter 67%, white matter 47%, basal ganglia 66%, thalamus 57%, cerebellar cortex 55%, tumor 32%, and the contralateral control site 64%. The mean tumor glucose utilization ratio was 1.48:1 in the awake state and 2.69:1 during barbiturate coma. The changes in gray matter, basal ganglia, thalamus, cerebellar cortex, and tumor/control tissue ratio were significant (p less than 0.05). In one patient, deep tumor invasion not evident on computerized tomography, magnetic resonance imaging, or baseline FDG-PET was apparent during barbiturate-enhanced FDG-PET scanning. The study findings suggest that gliomas resist suppression of glucose utilization by barbiturates; this supports the hypothesis that barbiturates reduce neuronal metabolism by blocking synaptic activity. This differential effect on normal brain and gliomas enhances the capability to assess the extent of neoplastic tissue in brain and may represent the basis for novel therapeutic strategies.

Adult↗
PubMed1986

Persistence of müllerian ducts in male rabbits passively immunized against bovine anti-müllerian hormone during fetal life.

A female rabbit was immunized against purified bovine AMH and mated. Booster injections were given at Day 8 of pregnancy to ensure a high titer of anti-AMH antibodies at the time the rabbit fetal testis begins to produce AMH. In three consecutive litters, the immunized female produced a total of 12 males, 9 of which had persistent Müllerian duct derivatives. No other significant abnormalities were detected in these animals, which were compared to the offspring of a control saline-injected female. In particular, testicular morphology was normal in most animals, and serum FSH levels did not differ from controls. This experimental model lends no support to the hypothesis that AMH controls extra-Müllerian events of male sex differentiation, nor that of the existence of a regulatory mechanism for synthesis of AMH by Sertoli cells, but it does not definitely exclude these possibilities, inasmuch as our tentative conclusions are based upon study of only one immunized female.

Animals↗
PubMed1986

Monoclonal antibodies raised against bovine anti-müllerian hormone: bovine, ovine, and caprine hormones share a set of identical epitopes.

Monoclonal antibodies (Mabs) have been raised against purified bovine anti-Müllerian hormone (bAMH) in an effort to obtain nonzoospecific reagents. Although the majority of the resulting hybridomas resembled those obtained previously insofar as they recognized only bovine, ovine and caprine AMH, four others, all immunoglobulin Ms, were directed against an epitope shared with AMH of other species, namely rabbit, pig and cat. Both the zoospecific and the conserved epitopes were located close to the site required for biological activity. It is suggested that the similarity between the immunogenic characteristics of bovine, ovine and caprine AMH is in some way related to the fact that AMH in these species is disseminated in the blood stream and may produce freemartinism.

Animals↗
PubMed1985

Insulin receptors and bioresponses in a human liver cell line (Hep G-2).

A newly developed human hepatoma cell line, designated Hep G-2, expresses high-affinity insulin receptors meeting all the expected criteria for classic insulin receptors. 125I-insulin binding is time-dependent and temperature-dependent and unlabeled insulin competes for the labeled hormone with a half-maximal displacement of 1-3 ng/ml. This indicates a Kd of about 10(-10) M. Since Scatchard analysis of the binding data results in a curvilinear plot and unlabeled insulin accelerates the dissociation of bound hormone, these receptors exhibit the negative cooperative interactions characteristic of insulin receptors in many other cell and tissue types. Proinsulin and des(Ala, Asp)-insulin compete for 125I-insulin binding with 4% and 2%, respectively, of the potency of insulin. Anti-(insulin receptor) antibody competes fully for insulin binding. The two insulin-like growth factors, multiplication-stimulating activity and IGF-I are 2% as potent as insulin against the Hep G-2 insulin receptor. Furthermore, Hep G-2 cells respond to insulin in several bioassays. Glucose uptake, glycogen synthase, uridine incorporation into RNA and acetate incorporation into lipid are all stimulated to varying degrees by physiological concentrations of insulin. In addition, these cells 'down-regulate' their insulin receptor, internalize 125I-insulin and degrade insulin in a manner similar to freshly isolated rodent hepatocytes. This is the first available human liver cell line in permanent culture in which both insulin receptors and biological responses have been carefully examined.

Cell Line↗