Biomedical subjects

T Tabata

Publications and source records attributed to T Tabata.

At least 73 records · Page 4Linked to original sources

PubMed1999

Effects of lipid-lowering drugs on intermediate-density lipoprotein in uremic patients.

BACKGROUND: Patients with chronic renal failure often have alterations in lipoprotein profile including elevated very-low density lipoprotein (VLDL) and intermediate density lipoprotein (IDL), and reduced high density lipoprotein (HDL) levels. Among these changes, raised IDL has been shown as an independent risk factor for atherosclerosis in hemodialysis patients. There are a limited number of studies reporting pharmacological approaches to IDL reduction in a uremic population. METHODS: We therefore summarize the effects of lipid-lowering drugs on IDL levels in patients with chronic renal failure treated by hemodialysis (HD) or continuous ambulatory peritoneal dialysis (CAPD). RESULTS: First, a nicotinic acid analog niceritrol was given to hemodialysis patients. The drug increased HDL-cholesterol by 11%, but the reductions in VLDL-, IDL- and LDL-cholesterol were not significant. Second, CAPD patients were treated with a fibric acid derivative clinofibrate, which was excreted mainly into bile unlike other drugs in this class. The fibrate resulted in a remarkable reduction in VLDL-triglycerides, although it did not reduce IDL-cholesterol. Finally, an HMG-CoA reductase inhibitor (statin) pravastatin was used in HD and CAPD patients. Pravastatin reduced IDL- and LDL-cholesterol to the same extent (by 31%). None of these treatments caused serious adverse effects. CONCLUSIONS: We propose that IDL is an important target in the management of uremic dyslipidemia. To date, statins have been shown to be suitable for this purpose, although it remains to be clarified whether such an intervention reduces the risk for atherosclerotic vascular events in the uremic population.

Cholesterol, LDL↗

PubMed1999

Coronary flow velocity immediately after reperfusion reflects myocardial microcirculation in canine models of acute myocardial infarction.

Recent reports indicate that the coronary microcirculation is sometimes injured, despite successful reperfusion in acute myocardial infarction (AMI). However, it is difficult to evaluate the coronary microcirculation immediately after reperfusion by using only angiography. The purpose of this study was to examine the relationship between the pattern of coronary blood flow velocity and myocardial microcirculatory injury immediately after reperfusion in AMI. The authors recorded the left circumflex coronary flow velocity by using the Doppler guide wire method 10 minutes after reperfusion in a canine model of AMI. In addition, myocardial contrast echocardiography was performed with the injection of contrast medium into the left circumflex coronary artery before clamping of the coronary artery and 15 minutes after release of the clamp. From these images, the ratio of the normalized gray-level postreperfusion to preclamping in the contrast-enhanced area was determined. It was compared with coronary flow velocity variables. In the 10 dogs with a diastolic-to-systolic velocity ratio (DSVR) < 4.0, this velocity ratio 10 minutes after reperfusion correlated positively (r = 0.75, p < 0.01) with the normalized gray-level ratio. However, the remaining three dogs with a DSVR > or = 4.0 markedly deviated from this pattern. Coronary flow velocities in the three dogs were characterized by a greater decrease in systolic flow velocity and occurrence of early systolic retrograde flow. Myocardial contrast echocardiographic images in these three dogs demonstrated a lower normalized gray-level ratio. In conclusion, the coronary flow velocity pattern immediately after reperfusion may reflect myocardial microcirculatory injury.

Albumins↗

PubMed1999

Possible involvement of histamine in muscular fatigue in temporomandibular disorders: animal and human studies.

As an approach to clarifying the molecular basis of pain and fatigue in muscles involved in temporomandibular disorders, we examined the activity of histidine decarboxylase (HDC), the enzyme which forms histamine, in the masseter muscles of mice. In the resting muscle, HDC activity was very low. Direct electrical stimulation of the muscle markedly elevated HDC activity. HDC activity rose within 3 hrs of the electrical stimulation, peaked at 6 to 8 hrs, and then gradually declined. Intraperitoneal injection of a small amount of interleukin-1 (IL-1) (from 1 to 10 microg/kg) produced a similar elevation of HDC activity in the masseter muscle. We also examined the effect of an antihistamine, chlorphenylamine (CP), on temporomandibular disorders in humans and compared it with that of an anti-inflammatory analgesic, flurbiprofen (FB). Two groups received one or the other of the drugs daily for 7 days, and they were asked about their signs and symptoms before and after the treatment. A positive evaluation of their treatment was made by 74% of the CP group, but by only 48% of the FB group. Although the effects of CP on the limitation of mouth-opening and on joint noise were negligible, about 50% of the CP group answered positively concerning the drug's effect on spontaneous pain or pain induced by chewing or mouth-opening. The positive evaluation for CP (50%) in relieving associated symptoms (headache or shoulder stiffness) was significantly greater than for FB (13%). FB showed effectiveness similar to but sometimes weaker than that of CP on several symptoms. On the basis of these and previous results and the known actions of histamine, we propose that the histamine newly formed following the induction of HDC activity, which is itself mediated by IL-1, may be involved in inducing pain and, possibly, stiffness in muscles in temporomandibular disorders.

Adult↗

PubMed1999

Assessment of the temporal relationship between left ventricular relaxation and filling during early diastole using pulsed Doppler echocardiography and tissue Doppler imaging.

The study investigated the temporal relationship between left ventricular (LV) relaxation and filling during early diastole. The transmitral flow (TMF) velocity by pulsed Doppler echocardiography and LV wall motion velocity by pulsed tissue Doppler imaging (TDI) were evaluated in 57 patients with various heart diseases and 33 normal controls. The patients were classified into 2 groups according to the ratio of the peak early diastolic to atrial systolic TMF velocity (E/A): (1) the high A group included 44 patients with an E/A < or = 1, and (2) the pseudonormalization group included 13 patients with an E/A > 1. The isovolumic relaxation time (IRT) from the aortic component of the second heart sound (IIA) to the onset of the E wave of the TMF was measured. The peak early diastolic velocity of the LV posterior wall (Ew) and time from the IIA to the onset of the early diastolic wave (IIA-Ewo) were determined from the LV wall motion velocity assessed by pulsed TDI. The Ew was lower in the pseudonormalization and high A groups than in the control group. The IIA-Ewo was significantly longer in the pseudonormalization and high A groups than in the control group. The time constant of the LV pressure decay at isovolumic diastole (tau) correlated negatively with the Ew, and correlated positively with the IIA-Ewo in all groups. The IIA-Ewo was equal to or shorter than the IRT in control subjects, and was longer than the IRT in patients in the pseudonormalization group. In conclusion, the temporal relationship between LV relaxation and filling during early diastole varied according to the subjects' hemodynamic status. Analysis of TMF by pulsed Doppler echocardiography and LV wall motion velocity by pulsed TDI was useful for detailed evaluation of early diastolic LV hemodynamics.

Blood Flow Velocity↗

PubMed1999

Regional left ventricular myocardial contraction abnormalities and asynchrony in patients with hypertrophic cardiomyopathy evaluated by magnetic resonance spatial modulation of magnetization myocardial tagging.

Global left ventricular (LV) pump function is generally preserved in patients with hypertrophic cardiomyopathy (HCM). However, it is unknown whether regional myocardial contractility is impaired, especially in nonhypertrophied regions. The purpose of this study was to evaluate regional LV myocardial contraction in patients with HCM using magnetic resonance (MR) spatial modulation of magnetization (SPAMM) myocardial tagging. The study group comprised 20 patients with asymmetric septal hypertrophy (HCM group) and 16 age-matched normal patients (control group), and data were collected using transthoracic M-mode and 2-dimensional echocardiography, and MR SPAMM myocardial tagging. The systolic strain ratio, maximum systolic strain velocity, and time from end-diastole to maximum systolic strain (deltaT) in the anterior, ventricular septal, inferior and lateral regions for 2 LV short-axis sections at the levels of the chordae tendineae and papillary muscles were measured at 50-ms intervals by MR myocardial tagging. The end-diastolic anterior and ventricular septal wall thicknesses and LV mass index were significantly different between the HCM and control groups. The systolic strain ratio for all 4 walls, particularly the anterior and ventricular septal regions, was significantly lower in the HCM group. In the HCM group, the maximum systolic strain velocity was significantly lower and deltaT was significantly shorter for all 4 walls, particularly the anterior and ventricular septal regions. The standard deviation for the deltaT, calculated from the deltaT for the 8 regions of the 2 LV short-axis sections, was significantly greater in the HCM group. In conclusion, regional LV myocardial contraction is impaired in both hypertrophied and nonhypertrophied regions, and systolic LV wall asynchrony occurs in patients with HCM.

Adult↗

PubMed1999

Evaluation of the hemodynamic relationship between the left atrium and left ventricle during atrial systole by pulsed tissue Doppler imaging in patients with left heart failure.

The objective of the present study was to evaluate the hemodynamic relationship between the left atrium (LA) and left ventricle (LV) during atrial systole in the presence of an elevated left ventricular end-diastolic pressure (LVEDP) and LV failure using pulsed tissue Doppler imaging (TDI). Fifty-three patients with LV systolic dysfunction and no regional LV asynergy were divided into 3 groups: relaxation failure group (RF, n=20) with a ratio of peak early diastolic to atrial systolic velocity of the transmitral flow (E/A) < or = 1; pseudonormalization group (PN, n=19) with 1 or =2. In addition, 20 normal patients (E/A > or = 1) were studied as a control group. The transmitral and pulmonary venous flow velocities were recorded by transesophageal pulsed Doppler echocardiography. The wall motion velocity patterns were recorded at the middle portion of the LV posterior wall (LVPW) and at the mitral annulus (MA) of the LVPW site in the apical LV long-axis view by transthoracic pulsed TDI. The LVEDP was significantly greater in the PN and RS groups than in the RF and control groups. The moan pulmonary capillary wedge pressure was greatest in the RS group. The percent fractional change of the LA area during atrial systole determined by 2-dimensional echocardiography was significantly lower in the RS group than in the PN group. The peak atrial systolic pulmonary venous flow velocity was significantly greater in the PN group than in the RS group. The peak atrial systolic motion velocity (Aw) at the LVPW was significantly lower in the PN and RS groups than in the RF and control groups. The Aw at the MA was significantly lower in the RS group than in the other groups. There was no significant difference in Aw between the LVPW and MA in the RS group, whereas Aw at the MA was significantly greater than that at the LVPW in the PN group. In conclusion, the measurements of Aw at the LVPW and MA can be used to noninvasively evaluate the hemodynamic relationship between the LA and LV during atrial systole in patients with LV failure.

Adult↗

PubMed1998

Induction of histidine decarboxylase in skeletal muscle in mice by electrical stimulation, prolonged walking and interleukin-1.

1. In normal non-exercised skeletal muscles in mice, the activity of histidine decarboxylase (HDC), the enzyme which forms histamine, was very low. 2. HDC activity in the quadriceps femoris muscle was markedly elevated following contractions evoked by even a few minutes of direct electrical stimulation, peaking at 8-12 h following contraction lasting 10 min, and gradually decreasing during the 24 h following contraction. The elevation in HDC activity depended on the duration and strength of stimulation. 3. Direct electrical stimulation induced a quantitatively similar elevation of HDC activity in the muscles of mast-cell-deficient mice (W/Wv mice). 4. Prolonged walking at a speed of 6 m min-1 for up to 6 h with a 30 min rest period at 3 h also elevated muscle HDC activity, the magnitude of the elevation being related to the duration of the walking. Repeated exercise (training) for several days diminished the elevation of muscle HDC activity induced by walking. In contrast, starvation augmented the elevation of muscle HDC activity induced by walking. 5. Intraperitoneal injection of interleukin-1beta (IL-1beta) also elevated muscle HDC activity in a dose-dependent manner, as little as 1 microg kg-1 of IL-1 producing a significant elevation of muscle HDC activity. 6. IL-1beta was immunohistochemically detected in normal non-exercised quadriceps femoris muscle. We could not detect a significant increase in IL-1beta after exercise in the muscle or in serum: it may be below the level of detection. 7. On the basis of these results, together with those reported previously and the known actions of histamine, we propose that an elevation of HDC activity and generation of histamine occur in skeletal muscle following muscle contraction possibly as a result of induction by IL-1beta and that the histamine may be involved in fatigue in skeletal muscle as part of a defence mechanism preventing damage to the muscle.

Animals↗

PubMed1998

Right and left ventricular wall motion velocities as diagnostic indicators of constrictive pericarditis.

The purpose of this study was to examine the usefulness of pulsed tissue Doppler imaging for diagnosing constrictive pericarditis. Motion velocities of the ventricular septum (VS) and left ventricular (LV) posterior wall along the short axis, and those of the anterior right ventricular (RV) wall, VS, and LV posterior wall along the long axis were recorded using pulsed tissue Doppler imaging in 12 patients with constrictive pericarditis, who were diagnosed by cardiac catheterization, and also in 20 normal subjects. Peak early diastolic and atrial systolic velocities (Ew and Aw, respectively) were calculated, and the time between the aortic component of the second heart sound and the peak of the early diastolic velocity (IIA-Ew) was determined. The peak Ew and II A-Ew along the short and long axes were significantly higher and shorter, respectively, in the patient group than in the normal group. In the patient group, the motion velocity of the VS along the short axis showed a "backward" motion with a sharp and marked peak velocity immediately before Ew, or a biphasic early diastolic wave; a clear "downward" motion immediately after Ew was observed in the motion velocities of the anterior RV wall, VS, and LV posterior wall along the long axis. These distinctive backward and downward motions were not observed in any of the ventricular walls of the normal subjects. In conclusion, the early diastolic RV and LV wall motion velocity patterns along the short and long axes as measured by pulsed tissue Doppler imaging provide important information for the diagnosis of constrictive pericarditis.

Adult↗

PubMed1998

Role of left atrial appendage in left atrial reservoir function as evaluated by left atrial appendage clamping during cardiac surgery.

We evaluated the role of left atrial appendage (LAA) in the left atrial (LA) reservoir function by assessing the changes in LA flow dynamics after LAA clamping during cardiac surgery. The subjects were 8 patients who had undergone coronary artery bypass grafting (CABG) and 7 who had undergone mitral valvular surgery due to mitral regurgitation. We recorded transmitral, pulmonary venous and LAA flow velocity patterns by intraoperative transesophageal pulsed Doppler echocardiography, monitoring LA pressure before and 5 minutes after LAA clamping. The maximal LAA area was significantly greater, and the peak late diastolic LAA emptying flow velocity was significantly lower before LAA clamping in the mitral regurgitation group than in the CABG group. In both groups, the peak early and late diastolic transmitral and pulmonary venous flow velocities significantly increased, and the peak second systolic pulmonary flow velocity significantly decreased during LAA clamping. There were no significant changes in heart rate and systemic systolic blood pressure during LAA clamping, whereas mean LA pressure and maximal LA dimension significantly increased in both the groups. The LA pressure-volume relation during ventricular systole shifted upward and to the left during LAA clamping, and the slope was steeper in the MR group than in the CABG group. We conclude that the LAA is more compliant than the LA main chamber, and plays an important role in LA reservoir function in the presence of LA pressure and/or volume overload.

Aged↗

PubMed1998

Evaluation of left atrial filling using systolic pulmonary venous flow velocity measurements in patients with atrial fibrillation.

BACKGROUND: The pattern of pulmonary venous flow velocity is useful for understanding the hemodynamic relationship between the left atrium and left ventricle in patients with a variety of diseases, and the systolic flow wave, in particular, is considered a clinically important parameter that reflects left atrial filling. HYPOTHESIS: The study was undertaken to determine whether systolic pulmonary venous flow velocity patterns can be used to evaluate left atrial filling in patients with atrial fibrillation. METHODS: We performed transesophageal pulsed Doppler echocardiography and cardiac catheterization in 34 patients with chronic atrial fibrillation (10 with hypertrophic cardiomyopathy, 5 with dilated cardiomyopathy, 7 with previous myocardial infarction, and 12 with isolated atrial fibrillation) and 15 normal controls in sinus rhythm. RESULTS: Mean pulmonary capillary wedge pressure, V-wave height in the pulmonary capillary wedge pressure curve, and left ventricular end-diastolic pressure were significantly higher in the hypertrophic cardiomyopathy and dilated failing heart (previous myocardial infarction and dilated cardiomyopathy) groups than in the isolated atrial fibrillation and normal groups. The peak velocity and time-velocity integral of the systolic pulmonary venous flow velocity, and percent left atrial emptying fraction were significantly lower in the dilated failing heart group than in the isolated atrial fibrillation, hypertrophic cardiomyopathy, and normal groups. The peak velocity and time-velocity integral of the systolic pulmonary venous flow velocity, percent left atrial emptying fraction, and V-wave height were comparatively constant when the preceding R-R intervals were relatively stable in the isolated atrial fibrillation group and in 4 of the 10 patients with hypertrophic cardiomyopathy. However, changes in these variables correlated with the preceding R-R interval in all patients with dilated failing hearts and in 6 of the 10 patients with hypertrophic cardiomyopathy. CONCLUSION: Transesophageal pulsed Doppler echocardiographic measurements of systolic pulmonary venous flow velocity are valid indicators of left atrial filling in patients with atrial fibrillation.

Adult↗

PubMed1998

Assessment of abnormal left atrial relaxation by transesophageal pulsed Doppler echocardiography of pulmonary venous flow velocity.

BACKGROUND: Several studies on left ventricular relaxation have been undertaken in the past; however, left atrial (LA) relaxation has not been fully evaluated. HYPOTHESIS: The purpose of this study was to assess abnormalities in LA relaxation by evaluating pulmonary venous flow velocity and interatrial septal motion using transesophageal echocardiography. METHODS: The subjects were 56 untreated patients in sinus rhythm, including 25 with previous myocardial infarction, 9 with hypertrophic cardiomyopathy, 11 with dilated cardiomyopathy, as well as 11 with chest pain syndrome as controls. Peak first systolic velocity (PVS1), peak atrial systolic velocity (PVA), and their time-velocity integrals (PVS1-I and PVA-I, respectively) were calculated from the pulmonary venous flow velocity. RESULTS: The PVS1 and PVS1-I correlated negatively with the maximum LA dimension and mean pulmonary capillary wedge pressure, and correlated positively with the amplitude of the interatrial septal motion during LA relaxation and percent fractional LA relaxation. The PVA and PVA-I did not correlate with the mean pulmonary capillary wedge pressure. There was a weak positive correlation between PVA and PVS1, and a close positive correlation between the ratio of PVA to PVS1 and mean pulmonary capillary wedge pressure. Multiple regression analysis indicated that the PVS1 was most closely related to percent fractional LA relaxation, followed by mean pulmonary capillary wedge pressure. CONCLUSION: The PVS1 determined from the pulmonary venous flow velocity is closely related to parameters of LA relaxation which may be determined by transesophageal M-mode echocardiography, and the ratio of PVA to PVS1 is useful for noninvasive evaluation of LA pressure.

Adult↗

PubMed1998

Regional left ventricular wall motion abnormalities in myocardial infarction and mitral annular descent velocities studied with pulsed tissue Doppler imaging.

We evaluated global left ventricular (LV) systolic function from mitral annular systolic motion velocities measured by pulsed tissue Doppler imaging in patients with previous myocardial infarction (MI) and LV regional wall motion abnormalities. The subject group consisted of 45 patients with wall asynergies, 3 with ischemic cardiomyopathy, 8 with dilated cardiomyopathy, and 15 healthy control subjects. The peak systolic descent velocity (Sw) and the time from the electrocardiographic Q wave to the peak of the systolic wave (Q-Sw) were measured at 6 mitral annular sites obtained from 2-dimensional apical long-axis, 4-chamber, and 2-chamber echocardiograms; these variables were compared with the LV ejection fraction (EF) calculated from the left ventriculogram. The mean Sw at the sites corresponding to the infarct regions was significantly lower and the mean Q-Sw was significantly longer in the MI groups than in the control group. The mean Sw and Q-Sw at all 6 sites in the ischemic and dilated cardiomyopathy groups were significantly lower and longer, respectively, than those of the control group. There were significant correlations between the EF and the means of the Sw and Q-Sw values at the sites corresponding to the infarct regions in the MI groups. In the ischemic and dilated cardiomyopathy groups, significant correlations existed between the EF and the means of the Sw and Q-Sw values at all 6 sites. Thus the parameters obtained from mitral annular systolic motion velocities with pulsed tissue Doppler imaging reflect LV asynergy corresponding to the infarct regions in patients with MI, and global LV systolic function may be evaluated with these parameters.

Cardiac Catheterization↗

PubMed1998

Assessment of left ventricular systolic wall motion velocity with pulsed tissue Doppler imaging: comparison with peak dP/dt of the left ventricular pressure curve.

To assess the usefulness of the tissue Doppler imaging variables for the evaluation of left ventricular (LV) systolic function, we compared variables obtained by the pulsed Doppler method with the LV ejection fraction (%EF) and the maximum value for the first derivative of LV pressure (peak dP/dt). We examined 65 patients, including 15 patients with noncardiac chest pain, 15 with ischemic heart disease, 15 with dilated cardiomyopathy, 10 with hypertensive heart disease, and 10 with asymmetric septal hypertrophic cardiomyopathy. The subendocardial systolic wall motion velocity patterns were recorded for LV posterior wall and ventricular septum in the parasternal LV long-axis view. The peak dP/dt was significantly lower in the hypertensive heart disease, hypertrophic cardiomyopathy, and dilated cardiomyopathy groups. The peak systolic velocity was lower and the time from the electrocardiographic Q wave to the peak of the systolic wave for the posterior wall was longer in the hypertensive heart disease (5.9 +/- 0.5 cm/sec and 215 +/- 21 msec, respectively), hypertrophic cardiomyopathy (6.2 +/- 0.9 cm/sec and 217 +/- 17 msec, respectively), and dilated cardiomyopathy (5.2 +/- 0.8 cm/sec and 235 +/- 26 msec, respectively) groups than in the noncardiac chest pain (7.7 +/- 0.9 cm/sec and 187 +/- 24 msec, respectively) and the ischemic heart disease (7.6 +/- 0.8 cm/sec and 184 +/- 22 msec, respectively) groups. In all groups, the peak systolic velocity and the time from the electrocardiographic Q wave to the peak of the systolic wave for the posterior wall correlated directly and inversely, respectively, with the %EF (r = 0.59, p < 0.0001; r = -0.59, p < 0.0001) and the peak dP/dt (r = 0.75, p < 0.0001; r = -0.68, p < 0.0001). Both tissue Doppler variables for the ventricular septum did not correlate with the %EF but roughly correlated with peak dP/dt. We conclude that the systolic LV wall motion velocity parameters obtained by pulsed tissue Doppler imaging may be useful for noninvasive evaluation of global LV systolic function in patients with no regional asynergy.

Cardiac Catheterization↗

PubMed1998

Left ventricular diastolic properties of hypertensive patients measured by pulsed tissue Doppler imaging.

Examination of left ventricular (LV) diastolic dysfunction in hypertensive patients has been based on parameters obtained from the transmitral flow velocity during pulsed Doppler echocardiography. However, these parameters are affected by loading conditions. We evaluated LV diastolic function along the longitudinal and transverse axes by pulsed tissue Doppler imaging (TDI) in 50 hypertensive (HT) patients and 36 age-matched healthy volunteers (N). Transmitral flow velocity was recorded by pulsed Doppler echocardiography. LV posterior wall motion velocity along the longitudinal and transverse axes also was recorded by pulsed TDI. In both groups, peak early diastolic velocity of the LV posterior wall (Ew) along the transverse axis (N: 15.8+/-5.2 cm/s, HT: 12.2+/-4.4 cm/s) was higher than that along the longitudinal axis (N: 12.7+/-3.1 cm/s, HT: 9.5+/-3.3 cm/s). Peak atrial systolic velocity of the LV posterior wall (Aw) along the longitudinal axis (N: 9.1+/-1.8 cm/s, HT: 9.7 +/-2.6 cm/s) significantly exceeded that along the transverse axis (N: 8.0+/-2.2 cm/s, HT: 8.4+/-2.4 cm/s) in both groups. The Ews were lower and the Aws were higher along both axes in the patient group than in the control group. The time intervals from the aortic component of the second heart sound to the peak of the early diastolic wave (IIA-Ews) along both the transverse (N: 142+/-18 ms, HT: 154+/-19 ms) and longitudinal (N: 151 16 ms, HT: 162+/-20 ms) axes were longer in the patient group. In 29 patients, Ews along both axes correlated negatively (transverse: r = -0.80, P < .0001; longitudinal: r = -0.71, P < .0001) and IIA-Ews correlated positively (transverse: r = 0.81, P < .0001; longitudinal: r = 0.74, P < .001) with the time constant of the LV pressure decay during isovolumic diastole. The Aws along both axes in the 24 patients without pseudonormalization in transmitral flow velocity correlated positively (transverse: r = 0.60, P < .001; longitudinal: r = 0.74, P < .0001) with the LV end-diastolic pressure. In conclusion, LV relaxation and filling along the longitudinal and transverse axes were impaired in many patients with hypertension. Pulsed TDI was useful for evaluating LV diastolic dynamics in this disease.

Aged↗

PubMed1998

Plasma leptin level and its relationship with body composition in hemodialysis patients.

Leptin is a newly found hormone secreted by adipocytes that regulates food intake, thermogenesis, and body fat. We measured plasma leptin levels in 103 patients with chronic renal failure treated by hemodialysis and 167 age- and gender-matched healthy control subjects to examine the impact of renal failure on plasma leptin levels and the influence of leptin on body composition measured by dual-energy X-ray absorptiometry. Hemodialysis patients showed a significant decrease in both body fat mass and lean body mass compared with those of the control subjects. Plasma leptin was significantly elevated in the hemodialysis group over the controls. In both groups, leptin was higher in female than male subjects, and it correlated positively with percent body fat. The subjects were divided into six categories according to percent body fat, and plasma leptin levels were compared between the two groups in the same category. Leptin of hemodialysis patients was significantly higher than that of the control subjects in the percent body fat categories of 30 or greater, whereas there was no statistically significant difference in leptin concentrations in the lower percent body fat categories. This was also true in the comparison in each gender, and leptin levels in female subjects showed a more remarkable difference between the hemodialysis and control groups in obese categories. Multiple regression analysis in all subjects indicated that plasma leptin levels were independently affected by percent body fat, plasma insulin concentration, gender, and renal failure. The positive impact of renal failure on leptin remained significant in the subjects with percent body fat of 30 or greater in the multiple regression model, whereas it was no longer significant in the remaining lean subjects. In multiple regression analysis of factors affecting fat mass index and lean mass index, leptin level was selectively associated with fat mass index, but not with lean mass index, regardless of percent body fat ranges. These results indicate that renal failure is an important factor affecting plasma leptin levels, especially in obese female subjects, and that hyperleptinemia was closely related to fat mass but not to lean body mass in hemodialysis patients.

Body Composition↗

PubMed1998

Interplay of signal mediators of decapentaplegic (Dpp): molecular characterization of mothers against dpp, Medea, and daughters against dpp.

Decapentaplegic (Dpp) plays an essential role in Drosophila development, and analyses of the Dpp signaling pathway have contributed greatly to understanding of the actions of the TGF-beta superfamily. Intracellular signaling of the TGF-beta superfamily is mediated by Smad proteins, which are now grouped into three classes. Two Smads have been identified in Drosophila. Mothers against dpp (Mad) is a pathway-specific Smad, whereas Daughters against dpp (Dad) is an inhibitory Smad genetically shown to antagonize Dpp signaling. Here we report the identification of a common mediator Smad in Drosophila, which is closely related to human Smad4. Mad forms a heteromeric complex with Drosophila Smad4 (Medea) upon phosphorylation by Thick veins (Tkv), a type I receptor for Dpp. Dad stably associates with Tkv and thereby inhibits Tkv-induced Mad phosphorylation. Dad also blocks hetero-oligomerization and nuclear translocation of Mad. We also show that Mad exists as a monomer in the absence of Tkv stimulation. Tkv induces homo-oligomerization of Mad, and Dad inhibits this step. Finally, we propose a model for Dpp signaling by Drosophila Smad proteins.

Amino Acid Sequence↗

PubMed1998

Differences in transmitral flow velocity pattern during increase in preload in patients with abnormal left ventricular relaxation.

Changes in transmitral flow (TMF) and pulmonary venous flow (PVF) velocities during increases in preload were compared in patients with a higher peak atrial systolic velocity than peak early diastolic velocity (A/E > 1) for the TMF velocity to determine differences in hemodynamic response. Fifteen patients with dilated hearts, 22 with hypertrophied hearts and 15 control patients were studied. TMF and PVF velocities were recorded by transesophageal pulsed Doppler echocardiography before and during application of lower body positive pressure. The value for peak early diastolic velocity increased, while the isovolumic relaxation time decreased with increases in preload in all groups. The value for peak atrial systolic velocity decreased in the dilated-heart group, but increased in the hypertrophied-heart and control groups. The peak second systolic and early diastolic PVF velocities increased in the dilated- and hypertrophied-heart groups, but did not change in the control group. The peak atrial systolic PVF velocity and the difference in duration of the atrial systolic PVF and TMF velocities increased in the dilated- and hypertrophied-heart groups, and its changing rate was highest in the group with dilated hearts. These results suggest that both peak early diastolic and atrial systolic TMF velocities increase during increases in preload through the Frank-Starling mechanism in hypertrophied hearts. Furthermore, the left ventricular functional reserve was lower in the dilated-heart group. Thus, TMF and PVF velocities respond differently during increases in preload, depending on the underlying heart disease.

Blood Flow Velocity↗

PubMed1998

Xenopus Smad8 acts downstream of BMP-4 to modulate its activity during vertebrate embryonic patterning.

Bone morphogenetic proteins (BMPs) participate in the development of nearly all organs and tissues. BMP signaling is mediated by specific Smad proteins, Smad1 and/or Smad5, which undergo serine phosphorylation in response to BMP-receptor activation and are then translocated to the nucleus where they modulate transcription of target genes. We have identified a distantly related member of the Xenopus Smad family, Smad8, which lacks the C-terminal SSXS phosphorylation motif present in other Smads, and which appears to function in the BMP signaling pathway. During embryonic development, the spatial pattern of expression of Smad8 mirrors that of BMP-4. We show that an intact BMP signaling pathway is required for its expression. Overexpression of Smad8 in Xenopus embryos phenocopies the effect of blocking BMP-4 signaling, leading to induction of a secondary axis on the ventral side of intact embryos and to direct neural induction in ectodermal explants. Furthermore, Smad8 can block BMP-4-mediated induction of ventral mesoderm-specific gene expression in ectodermal explants. Overexpression of Smad8 within dorsal cells, however, causes patterning defects that are distinct from those reported in BMP-4-deficient embryos, suggesting that Smad8 may interact with additional signaling pathways. Indeed, overexpression of Smad8 blocks expression of Xbra in whole animals, and partially blocks activin signaling in animal caps. In addition, Smad8 inhibits involution of mesodermal cells during gastrulation, a phenotype that is not observed following blockade of activin or BMPs in Xenopus. Together, these results are consistent with the hypothesis that Smad8 participates in a negative feedback loop in which BMP signaling induces the expression of Smad8, which then functions to negatively modulate the amplitude or duration of signaling downstream of BMPs and, possibly, downstream of other transforming growth factor-beta (TGF-beta) family ligands.

Activins↗