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Biomedical subjects

N Hu

Publications and source records attributed to N Hu.

At least 91 records · Page 5Linked to original sources
PubMed1990

Correlation of ventricular area, perimeter, and conotruncal diameter with ventricular mass and function in the chick embryo from stages 12 to 24.

Ventricular form and function are interrelated during cardiovascular development. The study of muscle mechanics requires the real-time measurement of length, area, or volume. Because volume measures are not currently possible in the embryonic heart, we tested the hypothesis that end-diastolic (ED) and end-systolic (ES) ventricular perimeter, area, and conotruncal diameter correlate with ventricular mass and function in the stage 12 to stage 24 white Leghorn chick embryo. Video images of the contracting heart were recorded at 60 Hz on 1/2" videotape and studied with a custom image-analysis workstation. ED and ES video fields were selected by maximum and minimum ventricular area and were planimetered for epicardial ventricular perimeter, area, and conotruncal diameter. Data are reported as (mean +/- SEM, n greater than or equal to 8) and were tested by analysis of variance and regression analysis. Heart rate calculated from cycle length increased from 78 +/- 6 beats/min at stage 12 to 162 +/- 5 beats/min at stage 24. ED and ES area increased geometrically versus stage (y = 0.53 - 0.08x + 0.004x2, r = 0.96, p less than 0.001; and y = 0.60 - 0.09x + 0.004x2, r = 0.98, p less than 0.001, respectively). ED and ES perimeter and conotruncal diameter increased linearly versus stage (r = 0.95, p less than 0.001; r = 0.96, p less than 0.001; and r = 0.93, p less than 0.001; r = 0.93, p less than 0.001, respectively). Shortening fraction for each measurement increased from stage 12 to 16 or 18 then decreased.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1990

Effect of changes in circulating blood volume on cardiac output and arterial and ventricular blood pressure in the stage 18, 24, and 29 chick embryo.

We studied the hemodynamic effects of changing volume loading in the chick embryo, before autonomic innervation, to test the hypothesis that the Frank-Starling mechanism functions in the embryonic myocardium. Dorsal aortic blood velocity was measured by pulsed Doppler. Heart rate and aortic diameter were also measured to calculate cardiac output and stroke volume index. Vitelline arterial and ventricular pressures were measured with a servo-null micropressure system in stage 24 embryos. Infusing isotonic solution intravenously resulted in linear increases in stroke volume index for stages 18 (y = 388x + 6.89), 24 (y = 466x + 7.86), and 29 (y = 549x + 4.96). The slopes and intercepts were statistically the same for all three stages. Similar volume loading in stage 24 embryos initially increased mean arterial pressure linearly, but at higher loading conditions, the rate of rise lessens. Thus, volume loading resulted in a decrease in vascular resistance. Withdrawing blood from stage 24 embryos resulted in a decrease in ventricular peak systolic and end-diastolic pressures. With reinfusion of the blood, systolic and end-diastolic pressures initially rose above baseline levels and later returned to normal. We conclude that a length-tension relation is present in the preinnervated embryonic heart and that vascular resistance changes inversely with loading conditions. We speculate that these mechanisms are the primary hemodynamic control mechanism in the early chick embryo.

Animals↗
PubMed1990

[Genetic epidemiology of esophageal cancer: 10-year follow-up of 622 positive families in Yangcheng County].

Follow-up survey of 622 esophageal cancer (EC) positive families found during 1978-1979 was carried out in 1989 in a total of 5037 families. During this period (1978-1988), 35.8% of new EC deaths were found from 393 families with two or more EC deaths which accounted for only 7.8% (393/5037) of the total families. When the EC positive families were divided into three groups with 1, 2 and greater than or equal to 3 EC deaths in each, the EC deaths among offsprings of EC free parents were 6.7%, 11.1%, and 15.7% respectively. Offsprings from households with one parent died of EC belonging to family groups with 2 or greater than or equal to 3 EC deaths had different EC frequencies (9.5% versus 22.8%). In 184 families with greater than or equal to 3 EC deaths, offsprings from households with one or both parents died of EC showed also higher EC mortality (22.8% and 22.7% respectively) than those from households with EC free parents (15.7%). These results pointed to a strong tendency of familial aggregation of EC and the existence of genetically determined susceptibility to this human malignancy.

China↗
PubMed1990

Cytogenetic analysis in patients with myelodysplastic syndrome.

Forty-six patients with myelodysplastic syndrome (MDS) were studied. Chromosomal abnormalities were observed in 20 of the 46 patients (43%). Abnormalities of chromosome No. 5 occurred in 6 patients (13%); four of them had a deletion of the long arm of this chromosome [del (5q)]. Four patients had monosomy 7 (8.6%), and six patients had trisomy 8 (13%). Our results suggest that chromosomal abnormalities, deletion (5q), monosomy 7 and trisomy 8, might play important roles in the pathogenesis of MDS.

Adult↗
PubMed1990

Observations of fragile sites in patients with lymphoma and leukemia.

Chromosomal fragile sites analyses were performed in peripheral lymphocytes of 37 patients with lymphoma and 16 patients with leukemia, and also of 50 healthy individuals as controls. The results were: 1) The rates of chromosomal aberration and frequency of expression of fragile sites in patients with lymphoma and leukemia were significantly higher than those of normal controls. 2) There was a statistical association between 21 of 44 fragile sites and specific cancer breakpoints in patients with lymphoma and this was also the case with 19 of 30 fragile sites and specific cancer breakpoints in patients with leukemia. 3) Concordance between fragile sites and location of oncogenes in the diseases was established. The possible important role of fragile sites in the pathogenesis of lymphoma and leukemia is discussed.

Adolescent↗
PubMed1990

Cytogenetic analysis of 51 patients with chronic myeloid leukemia.

The Ph1 translocations were observed in 43 of the 51 patients with chronic myeloid leukemia (CML). Of the 43 patients with Ph1 chromosome, 19 (45%) had other structural abnormalities. Complex translocations were observed in 5 patients (12%). Twenty-eight patients with Ph1-positive CML have been followed up genetically.

Humans↗
PubMed1989

Effect of increased pressure on ventricular growth in stage 21 chick embryos.

We studied the effect of increased ventricular pressure on heart growth in the stage 21 (3.5-day) chick embryo. Ventricular pressure was increased by constricting the conotruncus with a loop of 10-0 nylon tied in an overhand knot. The embryos were reincubated, and physiology and cellular morphology were evaluated at successive stages of development, stages 21, 24, 27, and 29. Ventricular pressure was measured with a servo-null pressure system, and cardiac output was measured with a 20-MHz pulsed Doppler velocity meter. Ventricular and embryo dry weights were measured on an electronic microbalance, myocyte organelle composition was measured by a point counting technique, and cell growth response was measured by DNA and protein assay. The conotruncal loop increased ventricular pressure in experimental compared with control embryos, i.e., at stage 24, 2.88 +/- 0.13 vs. 1.96 +/- 0.05 (SE) mmHg (P less than 0.05), respectively, without affecting cardiac output. Ventricular dry weight increased in experimental vs. control embryos, i.e., at stage 24, 114 +/- 7 vs. 85 +/- 4 micrograms (P less than 0.05), respectively, whereas embryo weights were similar between the two groups. The difference in ventricular weights was due to myocyte hyperplasia, since organelle proportion of myofibrils and mitochondria, DNA-to-protein ratio, and myocyte area were similar in experimental voice control embryos. Thus the adjustment of myocardial mass to ventricular work occurs even during the earliest stages of embryonic development. Cardiac growth and morphogenesis are parallel but separable processes.

Animals↗
PubMed1989

Aortic impedance and hydraulic power in the chick embryo from stages 18 to 29.

Little is known about the hemodynamic properties of the rapidly expanding arterial bed during embryonic development. Using a servo-null pressure system and 20-MHz pulsed Doppler velocity meter, we recorded simultaneous dorsal aortic pressure and velocity waveforms. The waveforms were digitized at 3-msec intervals and subjected to Fourier analysis. We calculated hydraulic energy and the impedance spectrum to 10 Hz. From stages 18 to 29, heart rate (148 +/- 3 to 193 +/- 9 beats/min), systolic pressure (1.14 +/- 0.12 to 3.04 +/- 0.10 mm Hg), and mean dorsal aortic blood flow (21 +/- 2 to 214 +/- 19 mm3/min) increased. Peripheral vascular resistance (Z0: 30.4 +/- 4.8 to 6.4 +/- 0.7 dyne x sec/mm5), and the impedance moduli (Z1: 6.5 +/- 1.0 to 1.7 +/- 0.2 dyne x sec/mm5; Z2: 6.1 +/- 1.2 to 1.7 +/- 0.1 dyne x sec/mm5; Z3: 7.3 +/- 1.1 to 1.7 +/- 0.2 dyne x sec/mm5) decreased. Total hydraulic power increased from 48 +/- 7 to 2,606 +/- 96 nW, while the proportion of oscillatory energy increased from 29 +/- 2% to 65 +/- 4%. With development hydraulic load decreases, total external work increases and the dorsal aorta and embryonic vascular bed becomes more compliant. A greater proportion of total energy is expanded in pulsatile blood flow, suggesting that ventricular-arterial coupling is less efficient later in development.

Animals↗
PubMed1989

Hemodynamics of the stage 12 to stage 29 chick embryo.

The heart is the first functioning organ in the embryo and provides blood flow during cardiac morphogenesis from a muscle-wrapped tube a few cells thick to the four-chambered pump. We described the hemodynamics of the chick embryo from stage 12 (50 hours of a 21-day incubation) to stage 29 (6 days), during which the embryo weight increased 120-fold. We measured ventricular, embryo and extraembryonic vascular bed wet weights, dorsal aortic blood flow with a directional pulsed-Doppler velocity meter, and ventricular and vitelline arterial blood pressures with a servo-null micropressure system. The data are reported as mean +/- SEM. With rapid development and morphogenesis, dorsal aortic blood flow increased from 0.015 +/- 0.004 to 2.40 +/- 0.20 mm3/sec parallel to the geometric increase of wet embryo weight from 2.22 +/- 0.10 to 267.5 +/- 9.7 mg. Dorsal aortic blood flow normalized for embryo and extraembryonic weight remained relatively constant (Y = 2.13 + 0.02X, r = 0.23, SEE = 0.03). Stroke volume increased from 0.01 +/- 0.003 to 0.69 +/- 0.03 mm3, and heart rate doubled from 103 +/- 2 to 208 +/- 5 beats/min. Systolic, diastolic, and mean vitelline arterial pressure increased linearly from 0.32 +/- 0.01, 0.23 +/- 0.01, and 0.28 +/- 0.01 mm Hg at stage 12 to 2.00 +/- 0.06, 1.22 +/- 0.03, and 1.51 +/- 0.04 mm Hg, respectively, at stage 29. Ventricular peak systolic and end-diastolic pressure increased from 0.95 +/- 0.04 and 0.24 +/- 0.02 at stage 12 to 3.45 +/- 0.10 and 0.82 +/- 0.03 at stage 29, respectively. The hemodynamic waveforms were similar to those found in the four-chamber heart of the mature animal. These data are integral to understanding the interrelation of function and form during cardiac development.

Animals↗
PubMed1989

Effect of heart rate increase on dorsal aortic flow before and after volume loading in the stage 24 chick embryo.

In the stage 24 chick embryo, a paced increase in heart rate reduces stroke volume, presumably by rate-dependent decrease in passive filling. We hypothesized that rate-dependent stroke volume reduction could be abolished by volume loading. Dorsal aortic blood velocity was measured with a 20 mHz pulsed-Doppler meter from a 0.75-mm piezoelectric crystal (eight embryos), and atri-oventricular velocity was simultaneously measured from the ventricular apex (six embryos). Sinus venosus pacing (stimuli of 1 ms duration and less than 4 mA) was performed at intrinsic rate (P:I) and at 150% of intrinsic rate (P:150%I). Volume loading was performed during P:150%I by intravenous injection of 7.5 microL of chick Ringer's solution. Using atrioventricular velocity profile, stroke volume was divided into the proportion due to passive (E-phase) and active (A-phase) filling. Stroke volume was compared during P:I, P:150%I, immediately (P:150%I') and 30 s after (P:150%I") volume loading. Data (mean +/- SEM) were compared by ANOVA. During pacing, stroke volume (mm2/cycle) decreased but increased after volume loading (I, 0.43 +/- 0.03; P:I, 0.37 +/- 0.03; P:150%I, 0.19 +/- 0.03; P:150%I', 0.24 +/- 0.05; P:150%I", 0.28 +/- 0.04 (p less than 0.005). During P:150%I, E-phase filing disappeared and was not restored by volume loading, whereas, A-phase filling diminished but was restored by volume loading. In stage 24 chick embryos, rate-dependent stroke volume decrease is reversed by volume loading that restores stroke volume due to an increase in active filling but not passive filling. Thus, even at rapid heart rate, the embryonic ventricle responds to volume loading, indicating that the Frank-Starling relationship functions during tachycardia in the embryonic heart.

Animals↗
PubMed1989

[The nucleotide sequence of the chloroplast psbA gene from Solanum nigrum atrazine resistant biotype and its relevant analysis].

The psbA gene cloned in pSB135 from Solanum nigrum atrazine-resistant biotype was sequenced. It has the same nucleotide sequence as the known atrazine resistance gene from another independent biotype of S. nigrum. On the basis of the deduced amino acid sequences the secondary structure of the 32kD proteins encoded by the psbA genes were compared between atrazine-resistant and susceptible biotypes, and some indications from the protein structure comparison were discussed.

Amino Acid Sequence↗
PubMed1988

G-banded chromosome analyses of mucosal epithelium adjacent to esophageal cancer (EC)--some consistent chromosomal changes.

G-banded chromosomes of primary cultures taken from mucosal epithelium adjacent to esophageal cancer (EC) were first analyzed. Consistent chromosomal changes, i.e. marker chromosomes, appeared in 2 of seven specimens of esophageal epithelium. Some of the marker chromosomes are very similar to those found in EC8501 cell line. These results imply that the cytogenetic analyses of the mucosal epithelium adjacent to EC may detect the numerical and structural chromosome aberrations occurring at the very beginning of carcinogenesis of esophageal epithelium.

Adenocarcinoma↗
PubMed1987

Effect of heart rate increase on dorsal aortic flow in the stage 24 chick embryo.

We evaluated the effect of increased heart rate on cardiac output and stroke volume in the stage 24 chick embryo (day 4 of a 21-day incubation). Blood flow was measured with a 20 MHz pulsed-Doppler flowmeter. Heart rate was increased by pacing with square wave stimuli (1 ms duration, less than 4 mA). The sinus venosus was paced from bipolar Teflon-coated silver electrodes in eight embryos and the ventricular apex was paced in three embryos. The pacing rates were at the intrinsic heart rate (P:I); 125% of intrinsic heart rate (P:125%I); and 150% of intrinsic heart rate (P:150%I). Physiologic measurements during pacing were compared to those obtained at the control intrinsic rate (I). We also evaluated the velocity profile of atrioventricular inflow and conotruncal outflow at intrinsic rate and during sinus venosus and ventricular pacing. With sinus venosus pacing, mean dorsal aortic blood flow was similar at control (1.07 +/- 0.05 mm3/s) and P:I (1.06 +/- 0.06 mm3/s) (mean +/- SEM). However, at P:125%I and P:150%I, mean dorsal aortic blood flow decreased significantly (P:125%I, 0.88 +/- 0.05 mm3/s; P:150%I, 0.67 +/- 0.07 mm3/s) (p less than 0.05). Stroke volume per beat also decreased with increasing heart rates (I, 0.41 +/- 0.02 mm3; P:I, 0.39 +/- 0.02 mm3; P:125%I, 0.28 +/- 0.02 mm3; P:150%I, 0.18 +/- 0.02 mm3) (p less than 0.05). With rapid sinus venosus pacing, the atrioventricular blood flow velocity profile showed a rate-dependent decrease in passive ventricular filling while active filling remained the same or increased slightly.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Ventricular function and morphology in chick embryo from stages 18 to 29.

We evaluated wet and dry ventricular and embryo weights, hemodynamic parameters of ventricular function, and myocardial myocyte organelle composition in the developing chick embryo. Phasic and dP/dt ventricular pressure were measured with a servo null pressure system, and phasic, mean, and dV/dt dorsal aortic velocities were measured with a 20-MHz pulsed-Doppler meter. Ventricular and embryo weight increased geometrically with development, but at different rates, so that the ventricle-to-embryo weight ratio decreased from 0.02 to 0.001 just prior to hatching. Ventricular systolic and end-diastolic pressure increased from 1.31 +/- 0.05/0.33 +/- 0.03 mmHg at stage 18 to 3.45 +/- 0.10/0.82 +/- 0.03 mmHg at stage 29, while dP/dt increased from 23.04 +/- 1.32 to 79.55 +/- 3.69 mmHg/s over the same period. Dorsal aortic dV/dt increased from 878 +/- 17 to 2.076 +/- 65 mm/s2 from stage 18 to 29. Myocyte percent volume of myofibrils increased from 16.7 +/- 0.9% at stage 18 to 23.6 +/- 1.1% at stage 27 and diminished to 18.4 +/- 0.8% at stage 29. Mitochondrial percent myocyte volume remained constant at about 11%. These data define the parameters of normal ventricular function and morphology during embryonic development in the chick.

Animals↗
PubMed1986

Hemodynamic effects of environmental hyperthermia in stage 18, 21, and 24 chick embryos.

Environmental hyperthermia is a hazard to the poikilothermic chick embryo. We studied effects of hyperthermia on mean vitelline arterial blood pressure and mean dorsal aortic blood flow in stage 18, 21, and 24 chick embryos. The pressure was measured with a servo-null micropressure system, and the blood flow was measured with a 20 MHz pulsed Doppler flowmeter. Temperature was monitored with a needle thermoprobe positioned adjacent to the embryo. Data were obtained at 37 degrees C, after warming to 40 degrees C, and then after cooling to 37 degrees C. At stage 21, the pressure increased from 0.96 +/- 0.05 (+/- SE) to 1.04 +/- 0.06 mm Hg on warming and returned from 1.05 +/- 0.04 to 0.87 +/- 0.04 mm Hg on cooling. Pressure measurements during warming and cooling were performed in two separate groups of embryos because of technical problems. The blood flow, studied using different groups of the embryo from the pressure study, also increased from 0.65 +/- 0.06 to 0.75 +/- 0.06 mm3/s on warming and returned to 0.56 +/- 0.05 mm3/s. The heart rate increased from 173 +/- 2 to 211 +/- 3 at 40 degrees C and returned to 170 +/- 3 at 37 degrees C. Stroke volume (flow/heart rate) did not change during the temperature variation. Vascular resistance, the quotient of pressure to blood flow obtained by a ratio analysis, changed from 1.53 +/- 0.33 (median +/- 95% confidence interval) to 1.42 +/- 0.29 mm Hg/mm3/s on warming and changed to 1.60 +/- 0.32 mm Hg/mm3/s on cooling. Similar results were obtained at stages 18 and 24.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

The effect of isoproterenol on cardiovascular function in the stage 24 chick embryo.

The developing cardiovascular system of the chick embryo is susceptible to teratogenic effects of catecholamines. Yet the mechanism for the teratogenetic action is unclear. Since catecholamines affect cardiovascular physiology, we studied the acute effect of the beta-agonist isoproterenol on mean atrial pressure, heart rate, mean dorsal aortic blood flow, mean arterial pressure and vascular resistance in stage 24 chick embryos. Dorsal aortic blood velocity was measured with a 20-MHz pulsed-Doppler velocity meter and intravascular pressure was measured with a servo-null pressure system. Isoproterenol in doses of 2 X 10(-4) micrograms (2.5 micrograms/kg), 8 X 10(-4) micrograms (10 micrograms/kg), and 1.2 X 10(-3) micrograms (15 micrograms/kg) was injected intravenously in 5-microliters aliquots of chick Ringer's solution. Additional groups of embryos were treated with the beta-antagonist propranolol, and isoproterenol plus propranolol. Control embryos received 5 microliters chick Ringer's solution to assess the hemodynamic effects of a volume injection. We found that isoproterenol caused no change in mean atrial pressure, heart rate, or mean arterial pressure. However, isoproterenol caused a dose-related decrease in dorsal aortic blood flow and a 2.5-fold increase in vascular resistance. The effects of isoproterenol were blocked by propranolol, which suggested that the increase in vascular resistance was mediated by beta-receptor stimulation.

Animals↗