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Original Studies |
Carbohydrate and Lipid Metabolism Research Unit, Departments of Medicine, Nuclear Medicine, and Chemical Pathology, University of the Witwatersrand Medical School, Parktown 2193, South Africa; and the Department of Internal Medicine, University of Goteborg, Sahlgren’s Hospital (P.-A.J., P.N.L.), S-41345 Goteborg, Sweden
Address all correspondence and requests for reprints to: M. T. van der Merwe, M.D., Department of Endocrinology, Johannesburg General Hospital, Private Bag X39, Parktown 2000, South Africa. E-mail: 014jhp{at}chiron.wits.ac.za
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Abstract |
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In the postabsorptive state, the plasma glucose and insulin levels of the black men and white men were similar. The black men had higher plasma free fatty acids (825 ± 97 vs. 439 ± 58 µmol/L; P < 0.005), glycerol (99.5 ± 5.1 vs. 54.1 ± 3.3 µmol/L; P < 0.0001), and lactate (1056 ± 95 vs. 729 ± 45 µmol/L; P < 0.01). Interstitial glycerol concentrations in the black and white men were 227 vs. 163 µmol/L (P < 0.01) and 230 vs. 162 µmol/L (P < 0.05) in the abdominal and femoral regions. The adipose tissue blood flow rate was higher in the black men in the abdominal (7.9 ± 0.9 vs. 3.1 ± 0.5 mL/100 g·min; P < 0.01) and femoral area (5.2 ± 0.6 vs. 2.8 ± 0.3; P < 0.01). Interstitial lactate concentrations in black and white men were 1976 vs. 1364 µmol/L (P < 0.004) and 1953 vs. 1321 µmol/L (P < 0.004) in the abdominal and femoral regions, respectively. Glycerol release was higher in black men vs. white men for abdominal (0.21 ± 0.02 vs. 0.14 ± 0.02 µmol/100 g·min; P < 0.02) and femoral (0.22 ± 0.02 vs. 0.15 ± 0.01; P < 0.05) areas.
Postprandially, black men had higher plasma glucose levels [1 h, 9.6 ± 0.4 vs. 8.2 ± 0.5 mmol/L (P < 0.05); 2 h, 8.9 ± 0.4 vs. 7.2 ± 0.4 mmol/L (P < 0.01)], but lower plasma insulin levels [1 h, 173 ± 13 vs. 264 ± 48 pmol/L (P < 0.05); 2 h, 136 ± 20 vs. 209 ± 34 pmol/L (P < 0.05)]. Plasma free fatty acid, lactate, and glycerol levels remained higher in the black men. After 1 h, lactate release was higher in the black men vs. that in the white men for abdominal (20.5 ± 1.6 vs. 14.7 ± 2.5 µmol/100 g·min; P < 0.05) and femoral (15.6 ± 1.1 vs. 12.1 ± 1.8; P < 0.03) areas.
We conclude that the black men, who are relatively insulinopenic postprandially, have a brisker lipolysis and also release more lactate from sc fat tissue than white men. These differences in adipose tissue metabolism may be related to differences in the lipid profiles and glucose metabolism previously documented in these ethnic groups.
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Introduction |
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Subjects and Methods |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Nine black and nine white normal male volunteers were studied
according to an identical protocol and by the same research team. They
were lean, fit, manual laborers and were matched for age, BMI, and
waist/hip ratio (Table 1
). The men all
had normal renal and liver function, with no documented metabolic
diseases. The subjects followed a diet very similar in composition, but
some minor differences in dietary habits could not be excluded as no
definitive dietary analysis was performed. More importantly, weight was
kept at a stable level for 3 months before the investigations. None of
the men smoked, and they were not allowed to consume alcohol for 7 days
before the investigation. The black men (BM) are of pure ancestral
history, with a less than 4% genetic admixture (10, 11, 12). The men all
gave informed consent, and the study was approved by the committee for
research on human subjects of the Universities of the Witwatersrand and
Goteborg.
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The investigations were started at 0700 h after a 9-h overnight fast. No vigorous exercise was allowed for 12 h before the test.
Body composition analyses
This was performed first thing in the morning with bioelectrical impedance analysis (6). The Bodystat machine (Bodytrach Pty. Ltd., Stellenbosch, South Africa) was used to assess the body composition for fat and muscle tissue (kg; percentage). The bioimpedance equations are standard and based on the South African and Swedish populations as a whole [FFM (kg) = aH2/z + bH2/wt + cH + d age +e: H(height); wt (body mass); z (whole body impedance and a, b, c, d, and e are regression coefficients, validated by the Dunn Nutrition Center, University of Cambridge, Cambridge, UK].
Microdialysis and blood tests
The patients were studied in the supine position in a room kept at 25 C. One polyethylene catheter was inserted iv in the forearm and placed under a heating pad to ensure sampling of arterialized venous blood (13). At the onset of the study we measured fasting plasma glucose, insulin, FFA, glycerol, and lactate levels. Two microdialysis catheters (0.4 by 30 mm, F4HPS, 5000 mol wt cut-off, Fresenius, Hamburg, Germany) were inserted into sc adipose tissue, 5 cm lateral to the umbilicus and at the level of the midfemur. The insertion was performed through a fine cannula (Jelco 16SDD, Criticon, Johannesburg, South Africa) (14), and the inlet nylon tubing of the microdialysis catheter was connected to a precision pump (CMA/100, Carnegie Medicine, Stockholm, Sweden). No local anesthetic was required. For initial equilibration, the microdialysis catheters were perfused for 60 min at a rate of 2.5 µL/min with an isotonic saline solution containing 2.5 mmol/L glucose, 25 µmol/L glycerol, and 250 µmol/L lactate to prevent depletion of tissue concentrations (14).
In vivo calibration for the microdialysis catheters
The equilibration calibration technique has been described in detail previously (14). Briefly, known concentrations of the compound to be measured in the interstitial space are added to the perfusate. In this study, four different concentrations of glycerol (0–300 µmol/L) and lactate (0–750 µmol/L) and a standard concentration of glucose (2.5 mmol/L) were added to the perfusate. Two 10-min samples were collected for each perfusion concentration until equilibration was reached, and after the oral glucose tolerance test (OGTT) the samples were collected at 15-min intervals at the final concentrations of the perfusate. The net changes in glycerol and lactate concentrations in the outgoing dialysate were calculated. The linear relationship between the concentrations of glycerol and lactate in the ingoing perfusate and the net changes in these concentrations in the outgoing dialysate could then be used to calculate the absolute interstitial concentrations for these substances by means of regression analyses by determining the point of no net influx of substrate into perfusate (14).
OGTT
A standard OGTT at 1.25 g/kg was performed at approximately 1400 h. Arterialized postprandial blood samples were taken at four time points over the next 2 h.
Subcutaneous adipose tissue blood flow
This was used to determine lactate and glycerol release per
100 g adipose tissue/min. An injection of 3–6 megabecquerels
(mol/L) 133Xe in 0.1 mL sterile saline was given 5 mm under
the skin in the sc adipose tissue, contralateral to the two
microdialysis sites. After 60 min, xenon clearance was monitored at 20
frames/min for a period of 180 min, of which 120 min were post-OGTT.
The energy window was set at 80 kiloelectron volts (±10%). The
initial number of counts per site was about 10,000 in the 3-min
missing period to enable reliable measurements for 3–4 h. The
Elscint 415 ECT 
-camera was used for acquisition of the data, with
the detector placed at 30–50 cm from the 133Xe depot
(frame size, 128 x 128 pixels; zoom factor, 1; Collimator
(General Electric, Haifa, Israel), low energy, general purpose).
The counts were plotted on a logarithmic-linear diagram as a function
of time. The adipose tissue blood flow rate (ATBF) was then calculated
with the equation: ATBF = 
x K x 100,
where is the tissue to blood partition coefficient for xenon at
equilibrium, and K is the slope of the washout curve.
Experimental values of K were estimated as:
(lny1 - lny2)
x t-1, where y1 and
y2 are the counting rates on two occasions
(>25-min interval), and t is time in minutes between these
registrations (least squares regression analysis on the data for the
desired interval). A mean value of 10.0 mL/g was used for the partition
coefficient (14). In addition, this value of 10 mL/g was chosen for
both the abdominal and femoral areas in both groups of men (15), and it
is unlikely that a significant difference in cell size would exist
between the ethnic groups at such a low BMI. Control experiments have
previously shown a 24% mean relative error of 133Xe
clearance measured at two corresponding sites (16).
Biochemical analyses
Glucose was measured with an enzymatic colorimetric method
(GOD-PAP, Roche Molecular Biochemicals, Mannheim,
Germany), and insulin levels were determined with an
enzyme-amplified sensitivity immunoassay (EASIA-Medgenix Diagnostics,
Freunus, Belgium; normal range, 13.8–172.5 pmol/L). FFA levels
were measured with the Half-Micro test (Roche Molecular Biochemicals). The glycerol contents in adipose tissue dialysate
and plasma were determined with a radiometric phosphorous method (17, 18). Glycerokinase was obtained from Roche Molecular Biochemicals, and [-32P]ATP was purchased from
New England Nuclear (Boston, MA). Plasma lactate was analyzed within 14
days according to a fluorometric method described by Loomis (19). The
specimens were centrifuged within the hour, and the serum was stored at
-70 C until analyzed in a single batch to avoid interassay
variation.
Estimation of glycerol and lactate release
According to Fick’s principle, arterialized venous plasma (A)
and capillary venous plasma concentrations of lactate and glycerol (V)
and plasma flow rate (Q) were entered into the equation: (V -
A) x Q x (1 - hematocrit x 10-2)
(µmol/100 g·min). Conversion of interstitial (I) to venous (V)
lactate and glycerol levels was performed using the equation: V =
I - A x (1 - e-PS/Q) + A, where PS is
the permeability surface product area (adopted to be 
5 mL/100
g·min for glycerol and lactate) (20, 21). Each 30-min period
represents the mean calculated amount of release over that period of
time.
Statistical analysis
Data are expressed as the mean ± SEM. Significance for multiple samples was established by one-way ANOVA. Statistical significance of parametric data was assessed by Student’s paired and unpaired t tests. Nonparametric data (e.g. blood flow, tissue levels, and release values) were assessed by signed rank test for paired samples.
Absolute interstitial levels were calculated by linear regression analysis with the least squares method, and linear correlations were tested with Pearson’s correlation coefficient. Results were deemed significant at P < 0.05.
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Results |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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The clinical characteristics of the patients are shown in Table 1
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There was no significant difference between the age (29.2 ± 1.6
vs. 28.1 ± 2.0 yr), the BMI (21.0 ± 0.5
vs. 21.9 ± kg/m2), or the waist/hip ratio
(0.86 ± 0.01 vs. 0.86 ± 0.01) in the BM compared
to the white men (WM). The BM were significantly lighter than the WM
(61.5 ± 2.8 vs. 78.6 ± 2.8 kg; P
< 0.005). This was accounted for by the taller stature of the
Caucasians (169 ± 19 vs. 187 ± 18 cm;
P < 0.0005), resulting in a greater number of
kilograms of lean body mass in the WM (52.3 ± 2.2 vs.
68.1 ± 2.1; P < 0.0005). However, the fat mass
both in kilograms (9.3 ± 0.9 vs. 10.5 ± 0.9) and
as a percentage (13.5 ± 1.2 vs. 15.0 ± 1.4) as
well as the percent lean body mass (86.5 ± 1.2% vs.
85.0 ± 1.5%) was no different between the two groups. The mean
blood pressure, heart rate, and respiratory rate (125/78, 66/min, and
12–14 beats/min) were comparable in both groups. This was performed
initially at 30-min intervals and later at hourly intervals.
Postabsorptive biochemical measurements (Table 2)
The BM had higher postabsorptive plasma FFA (825 ± 97 vs. 439 ± 58 µmol/L; P < 0.005), glycerol (99.5 ± 5.1 vs. 54.1 ± 3.3 µmol/L; P < 0.0001), and lactate (1056 ± 95 vs. 729 ± 45 µmol/L; P < 0.01) values. In contrast, they had similar fasting plasma glucose (4.6 ± 0.1 vs. 4.7 ± 0.1 mmol/L) and insulin (31.7 ± 2.1 vs. 36.6 ± 4.8 pmol/L) levels.
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During the OGTT, the glucose levels in the BM were significantly
higher from 30–120 min [BM vs. WM; 30 min, 8.5 ± 0.6
vs. 6.4 ± 0.4 mmol/L (P < 0.01); 60
min, 9.6 ± 0.4 vs. 8.2 ± 0.5 mmol/L
(P < 0.05); 90 min, 9.7 ± 0.3 vs.
7.3 ± 0.4 mmol/L (P < 0.0009); 120 min, 8.9
± 0.4 vs. 7.2 ± 0.4 mmol/L (P <
0.01)]. In contrast, the insulin values were lower in the BM compared
to the WM from 1–2 h post-OGTT [BM vs. WM; 30 min,
116 ± 30 vs. 151 ± 26 pmol/L (P
= NS); 60 min, 174 ± 14 vs. 264 ± 48 pmol/L
(P < 0.05); 90 min, 144 ± 21 vs.
232 ± 48 pmol/L (P < 0.05); 120 min, 136 ±
20 vs. 209 ± 35 pmol/L (P < 0.05)].
The postprandial plasma FFA, glycerol, and lactate levels are shown in
Fig. 2. By 120 min, the significantly
higher fasting FFA values in the BM had decreased by 83% (by ANOVA,
P < 0.0001) to a level of 142 ± 34 µmol/L and
by 87% (by ANOVA, P < 0.0001) in the WM to a level of
52 ± 13 µmol/L (BM vs. WM, P <
0.05). At 30 min there was an inverse correlation between the high FFA
and low insulin levels in the BM (r = 0.7; P <
0.01). The plasma glycerol results showed a similar pattern and also
decreased from a significantly higher fasting value in the BM (by
ANOVA, P < 0.0001) to a level of 30 ± 3.0
µmol/L in the BM and a level of 20 ± 4 µmol/L in the WM (by
ANOVA, P < 0.0001; BM vs. WM,
P < 0.005). For all of the illustrated time points,
both the FFA and glycerol values remained at a higher level in the BM
(Fig. 2). In contrast, the plasma lactate levels increased
significantly (by ANOVA, P < 0.01) in both groups (120
min; BM vs. WM, 1489 ± 83 vs. 924 ±
58 µmol/L; P < 0.001), but strikingly so in the BM
by 30 min post-OGTT (BM vs. WM, 1476 ± 94
vs. 731 ± 40 µmol/L; P < 0.0001).
The plasma lactate levels remained at a higher level in the BM group
for the duration of the postprandial period (Fig. 2).
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The BM started off with a significantly higher blood flow in the
postabsorptive state in both the abdominal area (7.9 ± 0.9
vs. 3.1 ± 0.5 mL/100 g•min; P <
0.005) and the femoral area (5.2 ± 0.6 vs. 2.8 ±
0.3 mL/100 g•min; P < 0.006). The higher flow rate
in the sc adipose tissue of BM persisted in the postprandial period for
up to at least 1 h in the femoral area (BM vs. WM,
8.8 ± 0.6 vs. 4.9 ± 0.9 mL/100 g·min;
P < 0.05) and possibly for up to 2 h in the
abdominal area (BM vs. WM, 8.0 ± 0.6 vs.
5.1 ± 0.8 mL/100 g•min; P < 0.01). However,
both groups of men showed a significant response to the vasodilatory
effect of the glucose load and increased their blood flow in both
regions post-OGTT, more so in the abdominal areas (Table 3).
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After the ingestion of glucose, a significant increase of between
14–24% was noted in the interstitial lactate concentrations of both
groups, reaching a maximum concentration at 60 min in the BM in the
abdominal area (fasting, 1956 ± 136; 1 h, 2328 ± 119
µmol/L; P < 0.05) and the femoral area (fasting,
1933 ± 134; 1 h, 2206 ± 167 µmol/L;
P < 0.05). Maximum concentrations were reached at 120
min in the WM in the abdominal area (fasting, 1364 ± 114; 2
h, 1827 ± 140 µmol/L; P < 0.01) and femoral
area (fasting, 1321 ± 98; 2 h, 1762 ± 135 µmol/L;
P < 0.01; Fig. 3). For
both groups these interstitial lactate levels were significantly higher
than the plasma lactate levels, as was apparent from the
interstitial-arterial differences in lactate values (Fig. 4). When calculating the lactate release,
we were able to demonstrate a higher sc lactate release in the BM
vs. the WM in both the abdominal and femoral regions at 30
min [14.1 ± 1.4 vs. 8.9 ± 1.8 µmol/kg•min
(P < 0.04) and 15.2 ± 2.1 vs.
9.9 ± 1.8 µmol/kg•min (P < 0.05)] and 60
min post-OGTT [20.5 ± 1.6 vs. 14.7 ± 2.5
µmol/kg•min (P < 0.05) and 15.6 ± 1.1
vs. 12.1 ± 1.8 µmol/kg•min (P <
0.03); Fig. 3]. The interstitial glycerol concentrations were higher
in the BM vs. WM, both during the postabsorptive state
[abdominal, 227 ± 12 vs. 163 ± 19 µmol/L
(P < 0.01); femoral, 230 ± 12 vs.
162 ± 17 µmol/L (P < 0.05)] and for up to 30
min post-OGTT [abdominal, 179 ± 15 vs. 128 ± 15
µmol/L (P < 0.03); femoral, 186 ± 14
vs. 121 ± 17 µmol/L (P < 0.01);
Fig. 5]. The amount of sc glycerol
released in micromoles per kg/min was also higher in the BM vs. the WM
in the postabsorptive state and for up to 30 min post-OGTT (Fig. 5).
This was the case for both the abdominal and femoral regions [fasting,
0.21 ± 0.02 vs. 0.14 ± 0.02 µmol/kg•min
(P < 0.02) and 0.22 ± 0.02 vs.
0.15 ± 0.01 µmol/kg•min (P < 0.05); at 30
min, 0.23 ± 0.02 vs. 0.13 ± 0.02 µmol/kg•min
(P < 0.01) and 0.20 ± 0.01 vs.
0.13 ± 0.02 µmol/kg•min (P < 0.05)].
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Discussion |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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The WM disposed of an oral glucose load more effectively than the BM by secreting more insulin. This serves to confirm previous observations of relative insulinopenia in normoglycemic lean black South Africans (5, 6) as a somewhat unique phenotype of Africa (22). A putative reduction in ß-cell mass might be linked to transient periods of protein-energy malnutrition in the fetal period and early human life (23, 24, 25). In addition, alterations in the key insulin-sensitive enzymes of glycolysis and gluconeogenesis during perineonatal malnutrition predispose toward an insulin-resistant liver (26).
The shorter stature of the BM may represent an inherent difference in the height outcome of the two populations, or it could be a reflection of growth stunting during infancy and adolescence, as previously reported by Cameron et al. (27, 28). Importantly, the percent fat masses of the two groups were comparable. The oral glucose load was calculated so as to specifically compensate for the lower lean body mass in the BM. The higher glucose levels after the OGTT in the BM can therefore be regarded as the result of the insulinopenia and not the lower lean body mass, which, when corrected for surface area, would be the same as that in the WM.
In the BM the relationship between insulin levels, and FFA and glycerol levels is intriguing. In the postabsorptive state, the BM, compared to the WM, have higher FFA levels and release more glycerol for a similar insulin level. This would be indicative of postabsorptive adipose tissue resistance to the antilipolytic effect of insulin in the BM (29). The higher glycerol release may have been enhanced by the brisker ATBF observed in the BM, but would not entirely explain the significantly higher interstitial-arterial difference in glycerol values in the BM during the postabsorptive period. In addition, Karlsson et al. recently showed, using denervated adipose tissue, that the antilipolytic effect of insulin is the main regulator of lipolysis before and during an OGTT (30). This was further supported by our finding of a higher amount of glycerol produced per 100 g sc adipose tissue in the relatively insulinopenic BM at 30 min post-OGTT. Systemically elevated FFA levels induce insulin resistance in most tissues involved with glucose homeostasis (31, 32). We have recently demonstrated in vivo and in vitro insulin resistance in obese urban women from South Africa (33) (E.P. Buthelezi, M.-T. van der Merwe, I.P. Gray, N.J. Crowther, P.N. Lönnroth; manuscript in preparation). One of the recently described mechanisms for this resistance is an increase in the flux of fructose-6-phosphate into the hexosamine pathway (34) as well as an alteration in both insulin secretion and (35, 36, 37) hepatic degradation (38). Furthermore, Pei et al. have previously shown that an increase in adipose tissue lipolysis, leading to increases in ambient FFA and glycerol concentrations, correlated independently with resistance to insulin-mediated glucose disposal by muscle (39). The magnitude of this resistance to the action of insulin on muscle can be substantially induced in a significant proportion of lean individuals, to a level comparable to that found in noninsulin-dependent diabetics (40, 41). During the postprandial state, the levels of insulin in both BM and WM were sufficient to significantly decrease lipolysis, as it far exceeds the half-maximal suppressive effect of insulin on lipolysis (42). Insulin concentrations in both groups were also sufficient to suppress hormone-sensitive lipase enzyme activity, causing a drop in FFA levels (43). This would explain, to a large extent, the similar percent decrease in postprandial FFA concentrations in the two groups.
The factors that modulate lactate production by adipocytes in vivo remain largely unknown. Previous measurements with microdialysis in sc adipose tissue have shown that adipose tissue is a significant source of lactate production (44, 45), and is proportional to the amount of adipose tissue mass (9). Lactate production has important physiological and pathophysiological implications in the control of whole body metabolism; as a gluconeogenic precursor, lactate may stimulate hepatic glucose-6-phosphate synthesis (46) and, hence, hepatic glucose production and/or glycogen synthesis (47, 48). As a potential energy fuel, lactate may compete with glucose for its oxidation in peripheral tissue (49). It has also been concluded by Henry et al. that both hyperinsulinemia and hyperglycemia will stimulate glucose conversion to lactate in adipocytes (50).
In the BM, the higher postabsorptive values for plasma lactate, interstitial adipose tissue lactate, and lactate release suggest an associated insulin resistance as previously described by Lovejoy et al. (51). Abnormalities, similar to those found in obesity, such as elevated basal lactate levels, are seen in lean hypertensives (52) and insulin-dependent diabetics (53), conditions that are associated with insulin resistance. The present data on lactate metabolism obtained in the lean BM will need validation in further prospective studies in the obese black population, with their higher incidence of type 2 diabetes. Lactate release from an expanded adipose tissue mass will contribute to an impaired ability of insulin to inhibit hepatic glucose production (54).
In the postprandial state, approximately 50% of glucose taken up by muscle is completely oxidized; 35% is stored, presumably as glycogen, and 15% is released as lactate and alanine (for hepatic glycogen synthesis) (55). During conditions of insulinopenia as well as hyperglycemia, increased production rates of lactate by muscle tissue will prevail (56, 57, 58). This raises the possibility of a reduced glucose oxidation rate in the muscle tissue of BM, with an increased amount of lactate released post-OGTT. The higher postprandial lactate production per 100 g sc adipose tissue in the BM may also have been enhanced by the higher sc blood flow in the BM vs. WM. This was apparent from the decrease in the interstitial-arterial differences in lactate levels in the BM postprandialy compared to the increase in the levels found in the WM. Furthermore, this decrease in the interstitial-arterial differences in the BM indicates an additional source of lactate production other than just the sc adipose tissue. The source is most likely to be muscle, as the mean amount of visceral fat in BM measured by computed tomography scan according to the method we previously described (7), was small: 22.1 cm2 at the level of L4/5.
The brisker ATBF observed in the BM in the postprandial state could have been caused by a higher degree of hyperglycemia induced by the glucose load and by the higher lactate levels in the postabsorptive state (9, 20, 58). The independent contributions of either hyperinsulinemia or glucose metabolism to increase sc blood flow after glucose ingestion remain controversial (9, 48, 59). In view of the higher level of glycemia achieved in our BM in the presence of lower insulin levels compared to that in the WM, we would favor a glycemia-induced increase in blood flow.
In summary, we can conclude that there is adipose tissue insulin resistance as well as relative insulinopenia described in lean black South African men (previously also reported in larger groups). The inevitable high plasma FFA level may be of importance in the development of insulin resistance as well as for a diminished insulin secretion (35, 36, 37). This will have to be studied in more detail in the future in this group, but if found to be the case, it could well play an important role in the pathogenesis of noninsulin-dependent diabetes mellitus, the incidence of which is increasing within the African population (60). In addition, the BM have higher postabsorptive and postprandial plasma and interstitial lactate levels and greater lactate release from sc adipose tissue. The influence this may have on hepatic gluconeogenesis in this black population needs to be clarified.
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Acknowledgments |
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Footnotes |
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Received December 1, 1998.
Revised April 19, 1999.
Accepted April 27, 1999.
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References |
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