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Biomedical subjects

D Wu

Publications and source records attributed to D Wu.

At least 559 records · Page 31Linked to original sources
PubMed1988

Extinction of growth hormone expression in somatic cell hybrids involves repression of the specific trans-activator GHF-1.

Growth hormone (GH) expression in pituitary-derived cells has been attributed to the presence of a positive trans-activator, GHF-1, which binds to two sites on the GH promoter. Somatic cell hybridization of non-GH-expressing L cells with pituitary-derived GH3 cells usually results in extinction of GH production. While previous studies showed that extinction occurs at the level of GH transcription, the exact mechanism remained elusive. We therefore characterized two parental cell lines and three hybrids, two of which extinguish GH expression and one in which GH is reexpressed after loss of mouse chromosomal material. Using in vivo transfections, in vitro transcription, DNAase I footprints, and immunoblotting experiments, no evidence for a direct repressor of GH transcription was found. Rather, extinction of GH expression in fibroblast x pituitary hybrids was accompanied by loss of GHF-1 protein and mRNA expression, suggesting that extinction occurs by repression of this trans-activator.

Animals↗
PubMed1988

Atrial natriuretic peptide during supraventricular tachycardia and relation to hemodynamic changes and renal function.

Changes in plasma levels of atrial natriuretic peptide (ANP) and arginine vasopressin were studied in 5 patients during and after a 30-minute period of induced supraventricular tachycardia (SVT). Immediately after the induction of SVT, plasma ANP levels began to increase, peaked at 32 minutes (+734% increase on average) and then gradually decreased. The mean plasma arginine vasopressin levels decreased during SVT, but the differences were not significant. When plasma ANP levels during SVT were compared with the simultaneously measured hemodynamic variables, a significant positive correlation (r = 0.73, p less than 0.001) was observed between plasma ANP levels and pulmonary capillary wedge pressure. Induced SVT was associated with increased urinary sodium and potassium excretion, increased urine flow and increased free water clearance. Concomitantly, glomerular filtration rate significantly increased (+77%) with an increase in filtration fraction. Although no significant change was observed in plasma renin activity, plasma aldosterone concentrations decreased during and after SVT. These results suggest that increased left atrial pressure stimulates ANP release during SVT and that increased glomerular filtration rate and decreased aldosterone secretion by ANP, in addition to the inhibition of water reabsorption by decreased arginine vasopressin, may be responsible for natriuresis and diuresis associated with SVT.

Adult↗
PubMed1988

Paired pulse pacing increases cardiac O2 consumption for activation without changing efficiency of contractile machinery in canine left ventricle.

The relation between cardiac O2 consumption (VO2) and the total mechanical energy (TME) generated by contraction was studied under paired-pulse (PP) pacing and compared with that under single-pulse pacing at the same basic rate as PP pacing and at the double-pacing rate in ten excised cross-circulated canine left ventricles (LV). TME was assessed by the systolic pressure-volume (P-V) area (PVA) defined as the area bounded by the end-systolic and end-diastolic P-V curves and the systolic P-V trajectory. The VO2-PVA relation was linear under PP pacing as well as at control and double heart rates. PP pacing increased LV contractility index Emax from 6.3 +/- 3.3 (SD) to 18.0 +/- 8.6 mmHg/(ml/100 g) and elevated markedly the VO2-PVA relation by increasing the VO2-axis intercept (or PVA-independent VO2) from 0.62 +/- 0.11 to 1.13 +/- 0.35 J.beat-1.100 g-1. However, PP pacing did not change the slope of the VO2-PVA relation at 2.24 +/- 0.53 (dimensionless). The efficiency from PVA-dependent VO2 (total VO2-PVA-independent VO2) to PVA (=TME), calculated as the reciprocal of the slope of the VO2-PVA relation, was also constant at 47 +/- 11% regardless of PP pacing. These results are similar to previous results obtained by positive inotropic interventions with catecholamines and Ca2+. We conclude that PP pacing augments the PVA-independent VO2 for activation without affecting the efficiency of the contractile machinery to generate TME from the PVA-dependent VO2.

Animals↗
PubMed1988

Scintigraphic detection of regional disruption of adrenergic neurons in the heart.

Experiments were designed to detect regional disruptions of adrenergic neurons in the hearts of living dogs. The neuron disruption was achieved by the application of phenol to the epicardium of the left ventricle. Evidence for denervation was the reduction in endogenous norepinephrine (NE) concentrations in the myocardium beneath the region of phenol treatment and toward the apex. Radiolabeled meta-iodobenzylguanidine (MIBG) acts as an analog of NE and as such is concentrated in adrenergic nerve terminals. Following phenol application, MIBG labeled with 125I was found, 20 hours after injection, to be distributed within myocardium in patterns comparable to those of NE. However, left stellectomy did not alter the distributions of NE or 125I-MIBG in the myocardium and apparently did not disrupt adrenergic innervation. MIBG labeled with 123I enabled scintigraphic images of heart neurons in the living dog 3 and 20 hours after injection; these images portrayed the regions of adrenergic neuron disruption caused by phenol treatment. Concentrations of thallium-201 depicted on scintigraphic image and of triphenyltetrazolium observed on in vitro staining demonstrated no myocardial injury. Thus scintigraphy with 123I-MIBG will display regional adrenergic denervations in the heart.

3-Iodobenzylguanidine↗
PubMed1988

Origin of sex chromosome aneuploidy.

Probabilities applicable to RFLPs are derived for the genotypes of XXY, XXX, and XO children, conditional on their mode of origin and the parental mating type, and the theory is applied to family data on the XG locus. The proportion of XXY males arising in spermatogenesis is shown to be 0.41 +/- 0.09. The large distance of XG from the centromere makes distinction between maternal meiosis I and II unreliable, but if man is like Drosophila, most of the maternal non-disjunctions arise in meiosis I, among tetrads that have undergone one or more exchanges. Data from XG show that 0.78 +/- 0.05 of XO females arise from an error involving the paternal sex chromosomes. The XG locus is virtually uninformative about the origin of XXX. Application of the theory to selected RFLPs will be much more incisive because of their large number, lack of dominance, greater heterozygosity, and distribution along the chromosome. Study of RFLPs will facilitate diagnosis of the parental origin of sex chromosome abnormalities and the comparison of recombination rates in regular and trisomic progeny of maternal mei I and mei II origin. A pseudocentromeric model that estimates map distances from exceptional progeny is applied to non-disjunction of the X chromosomes in D. melanogaster, giving good recovery of the expected map and thereby validating this approach for RFLPs in man.

Aneuploidy↗
PubMed1988

Maternal age in trisomy.

By comparison with a more general theory, data on trisomy in live births, amniocenteses, and spontaneous abortions by year of maternal age are shown to fit a logistic augmented by a proportion independent of maternal age. The frequency of trisomy increases monotonically, with no discrepancy at extremely low or high maternal age. Trisomy 16 is exceptional in that all cases appear to be age-dependent. For groups A, B, and C most trisomies arise by a process independent of maternal age. A small proportion of these trisomies and about half of trisomies for smaller chromosomes (excluding trisomies 16 and perhaps 22) originate by some process dependent on maternal (but not paternal) age and therefore presumably independent of crossingover, which in the female takes place before birth.

Abortion, Spontaneous↗
PubMed1988

Transrectal US of the seminal vesicles and ejaculatory ducts: clinical correlation.

Transrectal ultrasonography (US) provides excellent anatomic detail of pathologic changes in the seminal vesicles and ejaculatory ducts. Fifty-two patients with US findings of seminal vesicle dilatation or cysts, ejaculatory duct cysts, or seminal vesicle or ejaculatory duct calculi were given questionnaires concerning a broad spectrum of genito-urinary symptoms. Compared with age-matched controls with normal US findings, patients with calculi in the seminal vesicles or ejaculatory ducts had a significantly increased prevalence of hematospermia and ejaculatory pain (P less than .01), and patients with cystic dilatation of the seminal vesicles were more likely to have perineal pain. Large midline cysts containing calculi or debris were symptomatic and probably represent müllerian duct remnants. Small cysts of the ejaculatory ducts were asymptomatic. Transrectal US may provide clinical insight into the causes of significant genitourinary symptoms that may previously have been ascribed to chronic nonbacterial prostatitis or have been considered to be idiopathic.

Calculi↗
PubMed1988

Alternative bioassays of kinship between loci.

In this study four asymptotically equivalent estimates of kinship are derived, in the general case and for kinship between multiallelic loci. Two estimates based on chi 2 agree closely, with the Shannon estimate giving the smaller variance. The PAH, GH, GM, and HBB systems conform to a recombinational model with an evolutionary size of approximately 4,000 and a ratio of recombination to physical distance of approximately 1.4 X 10(-5) morgans/kb, as predicted on the basis of the genetic and physical lengths of the human genome. The INS and D11S12 systems have a much more rapid decline of kinship with physical distance, suggesting overlapping RFLPs (unrecognized allelism), recombinational hot spots, or selection. Sources of error in predicting kinship over small distances are discussed.

Alleles↗
PubMed1987

Pharmacokinetics and pharmacodynamic effects of aqueous diltiazem in healthy humans.

Aqueous diltiazem was given to ten healthy male volunteers in a single oral dose of 2.5 mg/kg body weight. Serum diltiazem levels were measured at various intervals up to 24 hours after administration of the drug as were blood pressure, heart rate, and PR interval. The pharmacokinetics followed a one-compartment model in six and two-compartment model in four subjects. The mean distribution half-life in the latter four subjects was 15.8 +/- 3.7 minutes (range, 10.4-18.8 min). In the ten subjects, the peak serum diltiazem level was attained in 20 to 45 minutes (mean, 32.5 +/- 9.5 min) and ranged from 136 to 701 ng/mL (mean, 332 +/- 180 ng/mL). The elimination half-life ranged from 2.8 to 4.8 hours (mean, 3.8 +/- 0.6 hr). The area under the concentration-time curve varied from 508 to 2,245 ng-hr/mL, indicating differing bioavailability. Slight but significant blood pressure reduction was seen only at one to three hours. Changes in heart rate were not significant at any measurement. Transient facial flushing, beginning at ten to 20 minutes after administration, was noted in nine subjects, reflecting the vasodilatory effect of the drug. Significant prolongation (greater than 10%) of PR intervals began at ten minutes in three, at 20 minutes in six, and at 30 minutes in one participant, and progressed to second-degree Wenckebach atrioventricular (AV) block in six subjects 20 to 60 minutes after administration and third-degree AV block in one person 45 minutes after dosing. These AV blocks resolved by the third hour without treatment, and PR prolongation resolved by the fifth to seventh hours.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Complete sinoatrial block in two patients with bradycardia-tachycardia syndrome.

Electrophysiologic studies with recordings of sinus node electrograms were performed in two patients with bradycardia-tachycardia syndrome. In both patients, the rest electrocardiogram showed apparent sinus bradycardia. Patient 1 had frequent paroxysms of atrial tachycardia with long pauses of up to 10 seconds; Patient 2 had paroxysmal atrial flutter and atrial pauses of up to 8 seconds. Multiple, repetitive, low frequency deflections, with a cycle length ranging from 730 to 960 ms in Case 1 and 570 to 750 ms in Case 2, suggestive of sinus node electrograms, were recorded at a critical area at the junction between the superior vena cava and the right atrium. These low frequency deflections had no relation to spontaneous junctional beats or the spontaneous atrial beats that showed high frequency deflections on the atrial electrogram. However, they could be suppressed by spontaneous or paced atrial beats. Pharmacologic interventions in Case 2 showed that the cycle length of the low frequency deflections shortened after administration of isoproterenol and did not change after propranolol or atropine. Thus, complete sinoatrial exit block with intact entrance conduction can occur in patients with bradycardia-tachycardia syndrome. Under such circumstances, the surface electrocardiographic manifestation of sinus bradycardia may not be of sinus origin.

Adult↗
PubMed1987

Mechanism of polyuria and natriuresis associated with paroxysmal supraventricular tachycardia.

Changes in plasma levels of atrial natriuretic peptide (ANP) and arginine vasopressin (AVP) were studied in 8 patients during a 30 min period of induced supraventricular tachycardia (SVT). The mean plasma ANP concentration increased immediately after the onset of SVT, peaked at 30 min and gradually returned to the control level. The mean plasma AVP concentration, on the other hand, was suppressed during SVT and rebounded above the control level in the post-SVT period. In 4 patients, SVT was associated with polyuria and natriuresis. The mean urine volume in these patients increased to 580% of the control and the mean urinary sodium excretion to 278% of the control, respectively. It was concluded that both a stimulation of ANP secretion and an inhibition of AVP release, elicited by an increase in atrial pressure, may be responsible for polyuria and natriuresis associated with SVT.

Adult↗
PubMed1986

Bound adenosine 5'-triphosphate formation, bound adenosine 5'-diphosphate and inorganic phosphate retention, and inorganic phosphate oxygen exchange by chloroplast adenosinetriphosphatase in the presence of Ca2+ or Mg2+.

When the heat-activated chloroplast F1 ATPase hydrolyzes [3H, gamma-32P]ATP, followed by the removal of medium ATP, ADP, and Pi, the enzyme has labeled ATP, ADP, and Pi bound to it in about equal amounts. The total of the bound [3H]ADP and [3H]ATP approaches 1 mol/mol of enzyme. Over a 30-min period, most of the bound [32P]Pi falls off, and the bound [3H]ATP is converted to bound [3H]ADP. Enzyme with such remaining tightly bound ADP will form bound ATP from relatively high concentrations of medium Pi with either Mg2+ or Ca2+ present. The tightly bound ADP is thus at a site that retains a catalytic capacity for slow single-site ATP hydrolysis (or synthesis) and is likely the site that participates in cooperative rapid net ATP hydrolysis. During hydrolysis of 50 microM [3H]ATP in the presence of either Mg2+ or Ca2+, the enzyme has a steady-state level of about one bound [3H]ADP per mole of enzyme. Because bound [3H]ATP is also present, the [3H]ADP is regarded as being present on two cooperating catalytic sites. The formation and levels of bound ATP, ADP, and Pi show that reversal of bound ATP hydrolysis can occur with either Ca2+ or Mg2+ present. They do not reveal why no phosphate oxygen exchange accompanies cleavage of low ATP concentrations with Ca2+ in contrast to Mg2+ with the heat-activated enzyme. Phosphate oxygen exchange does occur with either Mg2+ or Ca2+ present when low ATP concentrations are hydrolyzed with the octyl glucoside activated ATPase. Ligand binding properties of Ca2+ at the catalytic site rather than lack of reversible cleavage of bound ATP may underlie lack of oxygen exchange under some conditions.

Adenosine Diphosphate↗
PubMed1986

Effective termination of reentrant supraventricular tachycardia by single dose oral combination therapy with pindolol and verapamil.

We evaluated the efficacy of single oral dose combining 20 mg pindolol and 120 mg verapamil in termination of paroxysmal supraventricular tachycardia (SVT) in 12 patients with recurrent symptomatic tachycardia. All had electrically inducible SVT lasting longer than 30 minutes. Patients were administered placebo or crushed pindolol and verapamil on 2 consecutive days after tachycardia was electrically induced and allowed to sustain for 30 minutes. With placebo, SVT lasted 186 +/- 18 minutes (mean +/- SEM); five patients converted spontaneously within 121 to 180 minutes. With pindolol and verapamil, 9 of 12 patients (responders) converted to sinus rhythm within 8 to 74 minutes. The mean duration of SVT in the nine responders was 28 +/- 8 minutes compared with 168 +/- 20 minutes on placebo (p less than 0.001). Before termination, tachycardia rate on pindolol and verapamil slowed significantly from 182 +/- 5 to 164 +/- 7/min (p less than 0.05) compared with no significant change in the rate of SVT on placebo. The mean systolic blood pressure during tachycardia was 97 +/- 5 mm Hg with placebo and 101 +/- 7 mm Hg with pindolol and verapamil. Serum levels of pindolol and verapamil obtained in seven patients at time of spontaneous termination of tachycardia were 66 +/- 13 and 56 +/- 14 ng/ml, respectively. The side effects with pindolol and verapamil included lightheadedness in one patient and symptoms of rapid palpitations in three. A single oral dose of pindolol and verapamil is safe and effective in termination of acute paroxysmal SVT and may be the initial therapy of choice in selected patients.

Adult↗