Search PubMed⌕ Search

Biomedical subjects

T Nguyen

Publications and source records attributed to T Nguyen.

At least 199 records · Page 11Linked to original sources
PubMed1998

Analytic treatment of resolution precision in electronically collimated SPECT imaging involving multiple-interaction gamma rays.

The widely applied single-interaction analytic expression characterizing the energy resolution component of the angular resolution precision for an electronically collimated point source is extended to include multiple-interaction Compton scatter sequences as well as sequences terminated by photoelectric absorption. The analytic formulation is developed using the statistical variance of the mean for components comprising composite, multivariate resolution precision estimators. It is demonstrated that enhanced resolution precision in the incident interaction scatter angle is attained when use is made of information from multiple interactions. An improvement in the resolution precision of up to approximately 40% is observed for triple Compton scatter. Comparison of the analytic estimates with Monte Carlo/chi-square results shows good agreement.

Chi-Square Distribution↗
PubMed1998

Penetration of natural prostaglandins and their ester prodrugs and analogs across human ocular tissues in vitro.

The objective of this study was to assess the corneal and scleral permeabilities of natural prostaglandins as well as their prodrugs and analogs through human cornea and sclera in vitro. The "apparent permeability coefficients" (Papp) of natural prostaglandins (PGF2alpha, PGD2 and PGE2), ester prodrugs of PGF2alpha (1-isopropyl PGF2alpha, 11-pivaloyl PGF2alpha and 11,15-dipivaloyl PGF2alpha) and four analogs (16-m-chlorophenoxy tetranor PGF2alpha, 17-phenyl trinor PGF2alpha, 17-phenyl trinor PGE2 and AH 13205) were measured using modified Ussing perfusion chambers and quantitative high performance liquid chromatography. Our results indicate that the corneal penetration of natural prostaglandins (PGs) is poor (the Papp values ranged from 1.65 x 10(-6) to 2.38 x 10(-6) cm/sec), while the PGF2alpha prodrugs showed higher corneal penetration than PGF2alpha. The 11-pivaloyl ester of PGF2alpha penetrated the cornea faster than both 1-isopropyl ester and the lipophilic 11,15-dipivaloyl ester. The PG analogs also showed poor corneal penetration (Papp values ranged from 0.696 x 10(-6) to 1.49 x 10(-6) cm/sec) except for AH 13205. All compounds tested showed good scleral penetration (Papp values ranged from 6.90 x 10(-6) to 17.1 x 10(-6) cm/sec) except PGF2alpha 11,15-dipivaloyl (Papp = 1.22 x 10(-6) cm/sec). The penetration profiles correlated well with tissue uptake ratios (ratio of final tissue concentration to initial dose) for all compounds except 11,15-dipivalate PGF2alpha. All ester prodrugs (but not the PGs and analogs) underwent corneal first-pass metabolism. The study results demonstrate that transcleral absorption may play a significant role in the ocular absorption of these compounds.

Cornea↗
PubMed1998

A genetic analysis of interactions with Spc110p reveals distinct functions of Spc97p and Spc98p, components of the yeast gamma-tubulin complex.

The spindle pole body (SPB) in Saccharomyces cerevisiae functions as the microtubule-organizing center. Spc110p is an essential structural component of the SPB and spans between the central and inner plaques of this multilamellar organelle. The amino terminus of Spc110p faces the inner plaque, the substructure from which spindle microtubules radiate. We have undertaken a synthetic lethal screen to identify mutations that enhance the phenotype of the temperature-sensitive spc110-221 allele, which encodes mutations in the amino terminus. The screen identified mutations in SPC97 and SPC98, two genes encoding components of the Tub4p complex in yeast. The spc98-63 allele is synthetic lethal only with spc110 alleles that encode mutations in the N terminus of Spc110p. In contrast, the spc97 alleles are synthetic lethal with spc110 alleles that encode mutations in either the N terminus or the C terminus. Using the two-hybrid assay, we show that the interactions of Spc110p with Spc97p and Spc98p are not equivalent. The N terminus of Spc110p displays a robust interaction with Spc98p in two different two-hybrid assays, while the interaction between Spc97p and Spc110p is not detectable in one strain and gives a weak signal in the other. Extra copies of SPC98 enhance the interaction between Spc97p and Spc110p, while extra copies of SPC97 interfere with the interaction between Spc98p and Spc110p. By testing the interactions between mutant proteins, we show that the lethal phenotype in spc98-63 spc110-221 cells is caused by the failure of Spc98-63p to interact with Spc110-221p. In contrast, the lethal phenotype in spc97-62 spc110-221 cells can be attributed to a decreased interaction between Spc97-62p and Spc98p. Together, these studies provide evidence that Spc110p directly links the Tub4p complex to the SPB. Moreover, an interaction between Spc98p and the amino-terminal region of Spc110p is a critical component of the linkage, whereas the interaction between Spc97p and Spc110p is dependent on Spc98p.

Calmodulin-Binding Proteins↗
PubMed1998

Reduced periinfarction mortality as a result of long-term therapy with captopril but not hydralazine or propranolol in spontaneously hypertensive rats.

Hypertension and left ventricular hypertrophy (LVH) are known to increase susceptibility to ventricular arrhythmias during and before myocardial ischemia and to increase the risk of periinfarction mortality. Although regression of LVH has been advocated as a therapeutic goal, little evidence exists to suggest that it can reduce periinfarction mortality, and if it does, by which mechanisms it may do this. In this study, we evaluated the effects of control of systemic arterial blood pressure, of regression of myocardial hypertrophy, and of cardiac fibrosis on the susceptibility to ventricular arrhythmias and periinfarction mortality in the spontaneously hypertensive rat (SHR) model of hypertension and LVH. After 12 weeks of treatment, captopril and hydralazine reduced systolic blood pressure to 93 +/- 14 and 126 +/- 13 mm Hg, respectively, as compared with 193 +/- 12 mm Hg, p < 0.05, in the untreated control SHR group. The decrease with propranolol (to 185 +/- 12 mm Hg) was of borderline significance. There was a significant decrease in inducibility of ventricular arrhythmias by programmed electrical stimulation with captopril (5%; p < 0.05). One hour after infarction, there was a trend toward reduced mortality in the rats treated with hydralazine, 9.5% (p = 0.20 vs. control; p = 0.10 vs. propranolol), and captopril, 5% (p = 0.08 vs. control; p = 0.010 vs. propranolol). However, only captopril reduced 3-h postinfarction mortality (40%; p = 0.022) compared with 72% in the control group. The results showed a significant decrease of the left ventricular weight/body weight ratio in the rats treated with hydralazine (2.6 +/- 0.2 mg/g; p < 0.05) and captopril (2.2 +/- 0.2 mg/g; p < 0.05) compared with the control group (2.8 +/- 0.2 mg/g). An assessment of cardiac fibrosis indicated that captopril decreased the volume percentage of collagen the most (2.01 +/- 0.53; p < 0.05), followed by propranolol (2.29 +/- 0.64; p < 0.05) and hydralazine (2.92 +/- 0.58; p < 0.05) versus controls (3.23 +/- 0.61). This study suggests that regression of myocardial hypertrophy or long-term normalization of arterial systolic blood pressure or both are the major determinants of very early mortality (within 1 h after infarction) and that later mortality (3 h after infarction) may be the result of a more complex interplay of regression of myocardial hypertrophy and fibrosis and of control of blood pressure.

Animals↗
PubMed1998

The superoxide synthases of rose cells . Comparison Of assays

In an effort to identify the enzymatic mechanism responsible for the synthesis of reactive oxygen species produced during the hypersensitive response, preparations of rose (Rosa damascena) cell plasma membranes, partially solubilized plasma membrane protein, and cytosol were assayed for the NADH- and NADPH-dependent synthesis of superoxide using assays for the reduction of cytochrome c (Cyt c), assays for the reduction of nitroblue tetrazolium, and assays for the chemiluminescence of N,N'-dimethyl-9,9'-biacridium dinitrate (lucigenin). Each assay ascribed the highest activity to a different preparation: the Cyt c assay to cytosol, the nitroblue tetrazolium assay to plasma membrane, and the lucigenin assay to the partially solubilized plasma membrane protein (with NADH). This suggests that no two assays measure the same set of enzymes and that none of the assays is suitable for comparisons of superoxide synthesis among different cell fractions. With the plasma membrane preparation, the presence of large amounts of superoxide-dismutase-insensitive Cyt c reductase confounded attempts to use Cyt c to measure superoxide synthesis. With the partially solubilized membrane protein, direct reduction of lucigenin probably contributed to the chemiluminescence. Superoxide synthesis detected with lucigenin should be confirmed by superoxide-dismutase-sensitive Cyt c reduction.

Journal Article↗
PubMed1998

Periodontal repair in dogs: effect of recombinant human transforming growth factor-beta1 on guided tissue regeneration.

This study evaluated alveolar bone and cementum regeneration following surgical implantation of recombinant human transforming growth factor-beta1 (rhTGF-beta1) in conjunction with guided tissue regeneration (GTR). Supraalveolar, critical size, periodontal defects were surgically created around the 3rd and 4th mandibular premolar teeth in right and left jaw quadrants in 5 beagle dogs. Alternate jaw quadrants in consecutive animals received rhTGF-beta1, in a CaCO3/hydroxyethyl starch carrier with GTR, or carrier with GTR alone (control). 20 microg of rhTGF-beta1 in buffer solution was incorporated into approximately 0.8 ml of carrier for each defect scheduled to receive rhTGF-beta1. Animals were sacrificed at week 4 postsurgery and tissue blocks were harvested and processed for histometric analysis. Clinical healing was generally uneventful. Minor membrane exposures were observed. Defects with membrane exposure displayed an inflammatory infiltrate underneath the membrane. Bone regeneration of trabecular nature, apparent in all animals, was generally limited to the very apical aspect of the defects. Cementum regeneration was limited without obvious differences between experimental conditions. Comparing rhTGF-beta1, to control defects, statistically significant differences were found for area (1.8+/-0.4 and 1.3+/-0.6 mm2, respectively; p<0.05) and density (0.3+/-0.1 and 0.2+/-0.03, respectively; p<0.05) of alveolar bone regeneration. Observed differences are small and represent a clinically insignificant potential for enhanced regeneration in this preclinical model. Within the limitations of study, it may be concluded that rhTGF-beta1 has a restricted potential to enhance alveolar bone regeneration in conjunction with GTR.

Alveolar Bone Loss↗
PubMed1998

[Prevalence of depressive disorders in early puerperium].

OBJECTIVE: The aims of this investigation were to detect the prevalence and influencing factors of early postpartal depressive disorders in a large hospital sample. METHODS: By means of an interview we acquired information on sociodemographic data, physical and psychiatric anamnesis, obstetric and psychological variables. The German version of the Edinburgh Postnatal Depression Scale (EPDS) served to determine the depressive disorder of our patients. The interview was carried out on 1,250 women at the maternity ward 5 days after delivery. RESULTS: According to the results of the German validation of the EPDS, 254 (20.3%) women at the maternity ward had an at least mild depressive disorder. A comparison between nondepressed women (n = 996, 79.7%) and depressed women (n = 254, 20.3%) revealed the following risk factors for the development of an early postpartal depressive disorder: higher subjective burden of childbirth, higher trait anxiety, poorer couple compatibility, lower job satisfaction and lower social status. Of all the obstetric variables previous abortions, elevated pregnancy risks, low weight of the newborn at delivery and cesarean section were of significant influence. CONCLUSIONS: Early postpartal depressive disorder appears in 20% of all women 5 days after delivery. According to previous studies this group seems to be at highest risk for developing a later postpartum depression. Considering the psychosocial and obstetric risk factors, preventive psychotherapeutic interventions at the maternity ward are indicated.

Adult↗
PubMed1998

Effects of the AT1 antagonist HR 720 in comparison to losartan on stimulated sympathetic outflow, blood pressure, and heart rate in pithed spontaneously hypertensive rats.

It has been demonstrated in isolated organs that angiotensin II mediates catecholamine release via presynaptically located AT1 receptor subtypes. In the present study, the relevance of AT1-mediated noradrenaline and adrenaline release in a whole-animal model, which reflects the peripherally sympathetic system (pithed rat), was investigated. Furthermore, the effects of a new AT1 antagonist, HR 720, are demonstrated with respect to its pre- and postsynaptic actions in comparison to the AT1 antagonist losartan. Dose-response curves to angiotensin II of blood pressure show a tenfold higher potency for HR 720 to compete for angiotensin II, thereby decreasing the maximum effects when compared with losartan. The electrically induced sympathetic outflow resulted in a dose-dependent increase after angiotensin II infusions. It could markedly be reduced with both AT1 antagonists, whereby HR 720 again was ten times more potent than losartan. Neither with HR 720 nor with losartan an agonistic activity could be demonstrated. The results indicate an AT1 receptor subtype mediated release of catecholamines in a whole-animal model. HR 720 is ten times more potent than the AT1 antagonist losartan and acts in a noncompetitive manner.

Angiotensin I↗
PubMed1998

Self-reported fears in Hispanic youth with mental retardation: a preliminary study.

There is a paucity of research on the frequency, intensity, and content of fears experienced by Hispanic (or Latino) American youth with mental retardation. We assessed fears experienced by 48 Hispanic youth with mental retardation (ages 10 to 21 years) using the Fear Survey for Children With and Without Mental Retardation. Although differences were found in the content of fears across age and gender groups, the number and intensity of fears did not differ. Promising evidence of the validity of this survey instrument was attained by its significant correlations with the Revised Children's Manifest Anxiety Scale. Implications for future research were discussed.

Adolescent↗
PubMed1998

Effect of vitamin D receptor gene alleles on bone loss in early rheumatoid arthritis.

OBJECTIVE: Rheumatoid arthritis (RA) is a polygenic disease characterized by localized joint destruction and generalized osteoporosis resulting in increased fracture risk. The pathogenetic mechanisms that determine the severity of generalized bone loss in RA are poorly understood. Polymorphisms in the vitamin D receptor (VDR) gene have been described as a significant determinant of bone turnover and mass. In this prospective study we describe VDR gene allele effects on bone loss in patients with early RA. METHODS: We recruited 232 patients with early RA. Bone mineral density measurements were repeated in 167 patients. Serial clinical and laboratory measures were recorded during the period of followup. DNA extraction, polymerase chain reaction amplification, and restriction fragment length polymorphism analysis of VDR alleles were performed using standard techniques. Presence of the Taq restriction site for both alleles was denoted "tt", and absence "TT". RESULTS: In women with RA the tt genotype group lost bone more rapidly than subjects with TT genotype at both the lumbar spine (-0.1 vs -4.9% p.a, respectively; p < 0.05) and femoral neck (-3.9 vs -9.6%, respectively; p < 0.01). The effect was independent of other disease characteristics. CONCLUSION: The presence of the VDR gene "t" allele in female patients with RA was associated with accelerated bone loss.

Alleles↗
PubMed1998

Osteoclastic activation is the principal mechanism leading to secondary osteoporosis in rheumatoid arthritis.

OBJECTIVE: To use clinical measures and biochemical markers of bone turnover to investigate mechanisms of generalized bone loss in early rheumatoid arthritis (RA). METHODS: We studied 232 patients with RA of less than 2 years' duration and 72 healthy controls using serial dual x-ray absorptiometry scanning of lumbar spine and hips. Patients attended the clinic for clinical and laboratory assessment with storage of serum, urine, and plasma at each visit. Change in bone mineral density (BMD) was calculated for patients and controls and compared with baseline and mean serial values of bone markers over the same intervals. Serum was assayed for procollagen I carboxyterminal propeptide (PICP) and skeletal alkaline phosphatase (sALP); urine for pyridinoline and deoxypyridinoline corrected for creatinine; and plasma for interleukin 1 (IL-1) and IL-6. RESULTS: Patients lost bone significantly faster than controls at all sites (p < 0.01 for all). At first visit patients had significantly lower PICP levels than controls (p < 0.05) and sALP correlated with initial BMD in both patients (p < 0.01, r > 0.35, all sites) and controls (p < 0.0001, r > 0.50, all sites). We rescanned 167 patients at one year and 121 patients at 2 years. Mean urinary pyridinoline and deoxypyridinoline levels correlated strongly with BMD change at all sites, were increased in patients with active disease (p < 0.005), and correlated closely with mean C-reactive protein (CRP) (p < 0.005, r > 0.41 for both). CONCLUSION: This study suggests that osteoclastic activation, rather than suppression of bone formation, is the dominant process leading to bone loss in early RA. Although urinary pyridinoline and deoxypyridinoline were excellent markers of BMD change, CRP was found to be best overall. This provides a rational approach for selecting and treating patients with RA to reduce their established longterm risk of osteoporotic fracture.

Absorptiometry, Photon↗
PubMed1998

Definitive cure of recurrent prosthetic endocarditis using silver-coated St. Jude Medical heart valves: a preliminary case report.

Despite progress in the area of antimicrobial treatment and the surgical use of homografts, prosthetic valve endocarditis (PVE) remains one of the most dangerous complications following heart valve replacement. We present the case of a patient treated for acute endocarditis which affected the mitral valve and who developed recurrent PVE and native aortic valve endocarditis. After multiple valve surgery, the infection was controlled following aortic and mitral valve replacement using silver-coated prostheses. The St. Jude Medical (SJM) mechanical heart valve Masters Series with Silzone coating is intended to protect heart valve patients against microbial infection. The Silzone coating is formed by an ion beam-assisted deposition process that incorporates silver into the sewing cuff of the SJM heart valve. It has also been suggested that silver treatment may improve the healing characteristics of the heart valve sewing cuff. This technology may be a valuable option to prevent or cure PVE, in addition to homografts. Although the present patient is an isolated case, it was encouraging to find not only a well-healed mitral valve silver-coated prosthesis but also no persistent or recurrent infection during a nine-month follow up.

Adult↗
PubMed1998

Modifications of arterial blood flow to the hand after carpal tunnel release.

Any surgical procedure is followed by an inflammatory reaction, associated with arteriolar dilatation and increased capillary permeability. The normal evolution is in most cases a progressive decrease of the inflammatory signs. Some patients however, particularly after orthopedic trauma affecting the extremities, develop algodystrophy, initially characterized by arterial vasodilatation and low capillary flow. In an effort to better understand the normal phenomena seen after uncomplicated hand surgery, the authors have evaluated the postoperative arterial blood flow using the Duplex flowmetry ultrasound technique in 13 patients operated for carpal tunnel syndrome, who did not subsequently develop algodystrophy. After measurement of the transverse section of the ulnar and radial arteries, and longitudinal measurement of the mean velocimetry, the arterial blood flow was calculated. The measurements were done 1, 2 and 4 weeks after the operative procedure. The study demonstrated a moderate (15%-30%) but significant increase in the arterial blood flow to the hand, related to arterial dilatation of the vessels and to an increase in blood velocimetry.

Adult↗
PubMed1997

A cluster of four novel human G protein-coupled receptor genes occurring in close proximity to CD22 gene on chromosome 19q13.1.

In our search for novel human galanin receptor (GALR) subtypes, human genomic DNA was PCR amplified using sets of degenerate primers based on conserved sequences in human and rat GALR. The sequence of one of the subcloned PCR products revealed homology to a sequence in the 3' region of the human CD22 gene following a BLAST search of GenBank's database. A search for open reading frames (ORF) in the non-coding CD22 sequence resulted in identification of two novel putative intronless genes, GPR40 and GPR41. The recent submission of sequence overlapping the downstream CD22 sequence revealed a possible polymorphic insert containing a third intronless gene, GPR42, sharing 98% amino acid identity with GPR41, followed by a fourth intronless gene, GPR43. Thus, the GPR40, GPR41, GPR42, and GPR43 genes, respectively, occur downstream from CD22, a gene previously localized on chromosome 19q13.1. The four putative novel human genes encode new members of the GPCR family and share little homology with GALR.

Amino Acid Sequence↗
PubMed1997

Binding properties of neuroligin 1 and neurexin 1beta reveal function as heterophilic cell adhesion molecules.

beta-Neurexins and neuroligins are plasma membrane proteins that are displayed on the neuronal cell surface. We have now investigated the interaction of neurexin 1beta with neuroligin 1 to evaluate their potential to function as heterophilic cell adhesion molecules. Using detergent-solubilized neuroligins and secreted neurexin 1beta-IgG fusion protein, we observed binding of these proteins to each other only in the presence of Ca2+ and in no other divalent cation tested. Only neurexin 1beta lacking an insert in splice site 4 bound neuroligins, whereas neurexin 1beta containing an insert was inactive. Half-maximal binding required 1-3 microM free Ca2+, which probably acts by binding to neuroligin 1 but not to neurexin 1beta. To determine if neurexin 1beta and neuroligin 1 can also interact with each other when present in a native membrane environment on the cell surface, we generated transfected cell lines expressing neuroligin 1 and neurexin 1beta. Upon mixing different cell populations, we found that cells aggregate only if cells expressing neurexin 1beta are mixed with cells expressing neuroligin 1. Aggregation was dependent on Ca2+ and was inhibited by the addition of soluble neurexin 1beta lacking an insert in splice site 4 but not by the addition of neurexin 1beta containing an insert in splice site 4. We conclude that neurexin 1beta and neuroligin 1 (and, by extension, other beta-neurexins and neuroligins) function as heterophilic cell adhesion molecules in a Ca2+-dependent reaction that is regulated by alternative splicing of beta-neurexins.

Animals↗
PubMed1997

Astroglial ciliary neurotrophic factor mRNA expression is increased in fields of axonal sprouting in deafferented hippocampus.

Evidence that ciliary neurotrophic factor promotes axonal sprouting and regeneration in the periphery raises the possibility that this factor is involved in reactive axonal growth in the brain. In situ hybridization was used in the present study to determine whether ciliary neurotrophic factor mRNA expression is increased in association with axonal sprouting in deafferented adult rat hippocampus. In untreated rats, ciliary neurotrophic factor cRNA labeling density was high in the olfactory nerve, pia mater, and aspects of the ventricular ependyma and was relatively low within areas of white matter (fimbria, internal capsule) and select neuronal fields (hippocampal cell layers, habenula). After an entorhinal cortex lesion, hybridization was markedly increased in fields of anterograde degeneration, including most prominently the ipsilateral dentate gyrus outer molecular layer and hippocampal stratum lacunosum moleculare. Labeling in these fields was increased by 3 days postlesion, was maximal at 5 days, and returned to normal levels by 14 days. Double labeling demonstrated that, in both control and experimental tissue, ciliary neurotrophic factor mRNA was colocalized with glial fibrillary acidic protein immunoreactivity in astroglia, but it was not colocalized with markers for oligodendrocytes or microglia. These results demonstrate that astroglial ciliary neurotrophic factor expression is increased in fields of axonal and terminal degeneration and that increased expression is coincident with 1) increased insulin-like growth factor-1 and basic fibroblast growth factor expression and 2) the onset of reactive axonal growth. The synchronous expression of these glial factors in fields of deafferentation suggests the possibility of additive or synergistic interactions in the coordination of central axonal growth.

Afferent Pathways↗