Journal of Comparative and Physiological Psychology 1979, Vol. 93, No. 5,907-918

Contribution of Growth, Fatness, and Activity to Weight Disturbance After Septohypothalamic Cuts in Adult Hamsters Katarina Tomljenovic Borer

Nancy L. Peters

Department of Physical Education University of Michigan

University of Michigan

Robert P. Kelch Department of Pediatrics University of Michigan

Program in Human Nutrition University of Michigan

Alan C. Tsai

Susan Holder University of Michigan The mechanism responsible for weight stability in adult hamsters was investigated by (a) transecting the dorsoventrally oriented nerve pathways between the septal area and hypothalamus (SH cuts) and (b) partitioning the observed increases in the rate of weight gain into three contributory components: changes in somatic growth, in body fatness, and in energy expended as voluntary activity on horizontal disks. Between 60% and 70% of the weight increase after SH cuts was due to acquisition of lean body mass, and 30%-40% of weight increase consisted of excess body fat. After SH cuts, serum growth hormone and insulin concentrations were increased on Day 14, food intake was increased between Day 2 and Day 42, skeletal lengths were greater on Day 77, and voluntary activity levels were 84% lower on Days 10-45, relative to control hamsters. It is concluded that dorsoventrally oriented nerve pathways in the septal area are involved in the control of growth, maintenance of body fat reserves, and voluntary activity and that they contribute to the maintenance of stable body weight in adult hamsters. Around the time of puberty rodent maintenance of stable weight has commonly weight attains a stable plateau (Monteiro & been labeled a regulation, although its Falconer, 1966; Slob & Van der Werff ten mechanism is not understood. Bosch, 1975; Widdowson & McCance, 1960). The prevailing view is that regulation of This weight level is defended against upward body fat reserves (Kennedy, 1957) accounts (Cohn & Joseph, 1962) or downward (Borer for weight stability in adult mammals and & Kooi, 1975; Levitsky, Faust, & Classman, that any shifts in weight plateau represent 1976) deflections imposed by changes in the shifts in body fat stores (Keesey & Powley, available nutrient energy. Such active 1975). The neural substrate for this weightand fat-regulatory mechanism was initially This research was supported in part by Grants localized in the medial basal area of hypoRO3M29877 from the National Institute of Mental thalaniUS (MBH), because destruction of Health and PCM78-07626 from the National Science MBH led to increases in body weight, body Foundation to K. T. Borer We thank E S. Valenstein, f t (Bernardis & Frohman, 1971; Bernardis N. Radm, and B. Agranoff for the use of some equip- & „ 01 , -,n^r i-mr-i^ ir>/-«n TT ii_ • j. o ment and facilities, Mara Markovs and Sarah Browne Skelton, 1965/1966,1967; Hethermgton & for technical assistance, and Neil Rowland for com- RanSOn, 1940), and Serum insulin levels ments that helped improve the manuscript. (Bernardis & Frohman, 1971; Hales & KenN. L. Peters is now at Vanderbilt University. nedy, 1964; Hustvedt & L0V0, 1972). After it was found that comparable inAvenue, University of Michigan, Ann Arbor, Michigan creases in body weight, body tat (Falka, 48109. Liebelt, & Critchlow, 1971), and serum ihCopyright 1979 by the American Psychological Association, Inc. 0021-9940/79/9305-0907$00.75 907

908

BORER, PETERS, KELCH, TSAI, HOLDER

sulin levels (Tannenbaum, Paxinos, & Bindra, 1974) are obtained after knife cuts that partially isolate but do not destroy MBH neurons, fat-regulatory function was attributed to a longitudinal fiber system traveling through the brain stem and impinging on the MBH at the level of paraventricular (Gold, leni, & Simson, 1977), suprachiasmatic (Eng, Note 1), or anterior end of the ventromedial hypothalamic nucleus (Sclafani & Berner, 1977). Deposition of excess fat is thought to result from increased activity of the tissue lateral to MBH which promotes storage of metabolic fuels via the parasympathetic vagus nerve (Bernardis & Goldman, 1976) and is associated with, but not dependent on (King, Carpenter, Stamoutsos, Frohman, & Grossman, 1978), oversecretion of insulin. Little attention has been paid to the observation that damage to this longitudinal fiber system, unaccompanied by destruction of MBH neurons, also results in acceleration of somatic growth (Gold & Kapatos, 1975; Mitchell, Hutchins, Schindler, & Critchlow, 1973; Palka et al., 1971) and in increased secretion of growth hormone (Mitchell et al., 1973). Thus it appears that the same, or separate but overlapping, fibers inhibit fat storage and suppress somatic growth but that acceleration of growth requires the integrity of the MBH where the putative growth-hormone-releasing hormone neurons are located (Martin, 1976). The release of rapid somatic growth from the neuroendocrine inhibition following the isolation of MBH in the female rat (Gold & Kapatos, 1975, Mitchell et al., 1973; Mitchell, Smyrl, Hutchins, Schindler, & Critchlow, 1972; Palka et al., 1971), after lesions of rostral septum in the adult hamster (Borer, Kelch, White, Dolson, & Kuhns, 1977), or in response to exercise in adult hamsters (Borer & Kuhns, 1977) illustrates the fact that rodents retain the capacity for rapid ponderal and skeletal growth throughout most of their adult lifespan (Berg & Harmison, 1957; Dawson, 1925; Donaldson & Conrow, 1919) and that somatic growth can contribute to weight changes observed after different experimental manipulations. Finally, it is seldom noted in the context of energy regulation that rapid weight gain

in rodents, which follows destruction of MBH (Brooks, 1946) or isolation of MBH (Eng, Gold, & Sawchenko, 1978) and which is also seen at the time of onset of genetic obesity in Zucker rats (Stern & Johnson, 1977), is accompanied by marked reductions in energy expenditure in the form of voluntary running activity. Concomitant changes in growth, deposition of fat, and levels of voluntary activity under circumstances of disturbed weight regulation suggest that the stable body weight in adult rodents is maintained through the interaction of the following three mechanisms: one that controls the rate of somatic growth and protein synthesis, one that controls storage of energy reserves in the form of fat and glycogen, and a third one that controls diversion of energy from anabolic processes into thermoregulatory heat and energy for physical activity. In the present study we provide support for this view of weight-regulatory mechanism by delineating a longitudinal fiber system in hamster forebrain that helps maintain the weight stability in adult animals through suppression of growth and growth hormone secretion, inhibition of fat storage and insulin secretion, and facilitation of energy expenditure in the form of voluntary running activity. General Method Subjects Adult female hamsters (Mesocricetus auratus Waterhouse), weighing more than 100 g on the day of surgery, were obtained from Eagle Laboratory Animals (Farmersburg, Indiana) and Lakeview Farms (Newfield, New Jersey). Animals were housed individually in suspended wire cages at all times except during exercise when they were maintained in acrylic boxes containing a horizontal disk exerciser (Borer, 1974). Formulab Purina Chow (3.51 kcal/g), which contains 23.0% protein, 50% carbohydrate, and 6.5% fat, and water were available ad lib at all times. Some animal groups (Experiment 3) also received unlimited amounts of unshelled sunflower seeds (6.83 kcal/g), which contain 23.5% protein, 9.7% carbohydrate, and 61% fat. Animals were maintained under controlled light (12:12 hr light/dark) and temperature (20-22 °C).

Neurosurgery and Histology A horizontal septohypothalamic (SH) cut in the plane of the anterior commissure was made on both sides of the brain with a retractable wire microencephalotome

GROWTH, FATNESS, AND ACTIVITY IN ADULT HAMSTERS (Sclafani & Grossman, 1969). With the skull horizontal between bregma and lambda, the knife shaft was positioned 2.0 mm anterior to bregma, 1.6 mm lateral to the sagittal sinus, and 4.5 mm below the dura. The knife blade was extended in the anterior direction 2.5 mm and rotated medially 180°. The same procedure was followed in control-operated animals except that the knife was lowered 3.0 mm below the dura and the blade was not extended. At the end of the experiment, hamsters were anesthetized, and their brains were removed and stored in 10% formalin-saline'for histology. Coronal 80-^m sections of the brains were stained with cresyl violet. Damage associated with SH cuts was recorded on a series of diagrams of hamster brain by a procedure described elsewhere (Borer et al., 1977).

Data Analysis

909

30-

0

5 10 DAYS

15 20 26 30 35 40 AFTER SURGERY

Figure 1. Food intake of hamsters with septohypothalamic cuts (solid circles; n = 10) and hamsters with control surgery (open circles; n = 10) during the first 40 postoperative days of Experiment 1.

Standard error of the mean is used throughout to express data variability. Student's t test, two-tailed, was used in all comparisons involving two groups except that the one-tailed test was used for skeletal growth. The 2 X 2 analysis of variance was used for comparisons involving four groups.

electrolytic lesion of the rostral medial septum leads to acceleration of somatic growth and hyperphagia in adult hamsters and that this phenomenon is blocked by hypophysectomy (Borer et al., 1977). We wanted to find out whether these changes resulted from Experiment 1: SH Cuts Increase damage to neurons passing through, rather Somatic Growth, Fatness, than confined within, the rostral medial and Food Intake in Adult Hamsters septal area. The SH cuts of this study It was previously shown that a midline aimed to sever fibers interconnecting septum

225

200

-

UJ

175

150 Q O 03

125

I00|

754 25

50

DAYS

75

AFTER

0

25

50

75

SURGERY

Figure 2. Left; Mean body weight changes as a result of septohypothalamic (SH) cuts (solid circles; n = 10) or control surgery (open circles; n = 10) in Experiment 1. Right: Mean body weight changes as a function of SH cuts (solid symbols) or control surgery (open symbols) and of disk exercise (triangles) or sedentary condition (circles) in Experiment 3.

910

BORER, PETERS, KELCH, TSAI, HOLDER

and forebrain, on one hand, with hypothalamus, midbrain, and brain stem, on the other (Meibach & Siegel, 1977; Powell, 1963; Raisman, 1966). Our hypothesis was that these fibers contribute to stable weight levels in adult hamsters by maintenance of a low asymptotic rate of somatic growth and that their interruption would lead to growth similar to that after septal lesions. Method Ten pairs of female hamsters were matched by body weight and length and given either SH cuts or the control procedure. They were fed a pellet diet, and their food consumption was measured every 24 hr during the

SH

CUTS

first 42 postoperative days. To correct for the changing body size in hamsters with SH cuts (or access to exercise in Experiment 3) and to allow for comparison between experiments involving pellets only or pellets and sunflower seeds, we expressed food intake in kcal/100 g of body weight/day. These animals were sacrificed after 77 days for determination of ponderal growth, linear growth, and percentage of body fat. Brains were removed for histology before body fat determinations. Ponderal growth was monitored by daily weight measurements. Ponderal growth rate was calculated as the slope of the least squares linear regression of body weight as a function of time. Linear growth was determined from initial (day of surgery) and final (Postoperative Day 77) measurements of body length. Body length measurements were taken between the tip of the nose and the tip of the tail while extending the anes-

CONTROLS

0,0

Figure 3. Reconstruction of brain damage in septohypothalamic cut (SH) hamsters from Experiments 1 (left) and 3 (center) and in control hamsters (right). (Damage inflicted by the guide cannula in SH hamsters was similar to that seen in the control group and was omitted for sake of clarity. Heavy lines represent the location of the cut in the animal in each group that displayed the greatest increase in ponderal growth rate and in a representative control animal. Hatching defines the brain area within which damage to all animals in an experimental group was confined. Abbreviations: a, nucleus accumbens; ac, anterior commissure; F, column of the fornix, FO, fornix, FPC, precommissural fornix; GCC, genu of corpus callosum; ha, anterior hypothalamic nucleus; HI, hippocampus; hvm, ventromedial hypothalamic nucleus; LAT, lamina terminalis: pom, medial preoptic nucleus; sm, medial septal nucleus; SM, stria medullaris; TD, tract of the diagonal band of Broca; TO, optic tract; ts, triangular septal nucleus; VL, lateral ventricle; V III, third ventricle.)

GROWTH, FATNESS, AND ACTIVITY IN ADULT HAMSTERS thetized hamster on a centimeter scale. This method correlated highly (r = .958) with radiographic determinations of skeletal growth (Borer & Kuhns, 1977). The percentage of body fat was determined by direct lipid extraction of autoclaved, homogenized, freezedried carcass samples (without gut contents) with petroleum ether (Horwitz, 1970).

Results Changes in food intake as a function of SH cuts are shown in Figure 1. Both groups of animals displayed low food intake during the first postoperative day. After the first two postoperative days, the control food intake stabilized between 25 and 35 kcal/100 g/day. In contrast, by the fourth postoperative day, SH hamsters were consuming more food than the control-operated hamsters. The food intake of the two groups was averaged for Postoperative Days 4-19, 20-30, and 31-41. Differences between SH and control animals were significant in all three comparisons (42.2 ± .9 vs. 33.7 ± 1.1 kcal/100 g/day, p < .001; 36.1 ± .5 vs. 31.5 ± .7, p < .001; and 33.1 ± .5 vs. 30.7 ± .6, p < .01, respectively). The SH cuts had a significant effect on the ponderal growth rate (rate of weight gain), body size, linear growth, and percentage of body fat. After an initial 10-g weight loss over the first two postoperative days, hamsters with SH cuts gained weight more rapidly than the control hamsters over the next 74 days (Figure 2). During Postoperative Days 2-33, hamsters with SH cuts gained weight five times faster (2.1 ± .1 g/day, p < .001) than control animals (.4 ± .1 g/day). By the 77th postoperative day, SH hamsters displayed twice as much linear growth (25.3 ± .6 mm, p < .001) as control hamsters (13.1 ± 1.2 mm) and four times greater weight increments (84.3 ± 3.4 g, p < .001) than control hamsters (19.2 ± 3.2 g). On the last day of the experiment, hamsters with SH cuts were significantly fatter (17.9% ± .7%, p < .001) than the control animals (11.6% ± .7%). Twenty-nine percent of the weight difference between SH-cut and control animals could be attributed to accumulation of body fat and 71% to increases in lean body mass. Reconstruction of brain damage in SH-cut hamsters is presented in Figure 3 (left). The SH cuts separated the entire extent of sep-

911

tum and rostral thalamus from preoptic area and hypothalamus. The cut transected the vertical limb of the diagonal band of Broca, the descending columns of the fornix, and the striae medullares. Control hamsters had minor cortical and callosal damage. Experiment 2: Increases in Serum Concentrations of Growth Hormone We examined the endocrine changes associated with growth acceleration after SH cuts by measuring serum concentrations of growth hormone (GH) and insulin and concentration and content of GH in the anterior pituitary in hamsters 12 days after they received SH cuts. Method Procedure. Eighteen pairs of hamsters were matched by weight and length and given SH cuts or control surgery. Hamsters were killed by decapitation on Postoperative Day 13, 2 hr after the onset of light. To distinguish between the effects of feeding and of the knife cuts on insulin secretion, we killed the animals either after a 10-hr fast (n = 20) or in ad lib fed condition (n = 16). Trunk blood was collected in chilled glass tubes. Serum was separated from the clotted blood by centrifugation at 4° for 20 min and was stored in two aliquots at —20° for later hormone analysis. Anterior pituitaries, dissected free of the dura, were kept chilled on saline-soaked filter paper and were weighed on an analytical balance. Pituitaries were homogenized by hand in 1 ml of 1% bovine serum albumin in a .01 M phosphate-.15 M saline buffer (pH 7.6) and were stored at a 1:40 dilution at -20 °C. Hormone measurements. Serum insulin concentrations were determined by a double antibody radioimmunoassay as described previously (Borer et al., 1977). A homologous double antibody radioimmunoassay was developed for the measurement of hamster GH, as described in detail elsewhere (Borer, Kelch, Peugh, & Huseman, 1979). This assay utilizes purified hamster GH (AFP-1595-B) for iodination with 125I and as a reference preparation, and antiserum (MK-10) against purified hamster GH developed in a rhesus monkey. Assay sensitivities were 1.3 ± .3 pg for insulin and 88.2 ± 6.2 pg for hamster GH.

Results Between Day 2 and Day 13, ponderal growth rate of SH hamsters killed in fed state was 2.2 ± .4 g/day (p < .05) relative to controls (.5 ± .3 g/day). On the 13th postoperative day their serum GH concentration

912

BORER, PETERS, KELCH, TSAI, HOLDER

Table 1 Endocrine Changes 12 Days After Bilateral Septohypothalamic Cuts or Control Surgery (Experiment 2) SHcut Hormone measure Serum concentration of GH (in ng/ml) Ad lib fed 10 hr fasted Serum concentration of insulin (in ng/ml) Ad lib fed

10 hr fasted Pituitary GH (10 hr fasted) Content (in Mg/AP) Concentration (in ng/mg AP)

n

M

10 8

24.4* 9.1

9 8 8 8

Control

SE

M

SE

7.5 3.5

9 8

8.3 4.8

1.2 .6

1.1 1.5

10 8

1.9 1.8

.5 .3

2.69 656.55

8 8

7.5** 3.6 21.78 4,770.42

n

28.56 6,150.98

2.74 373.62

Note. SH = Septohypothalamic; GH = growth hormone; AP = interior pituitary. * p < .05. ** p < .001.

was three times higher (p < .05) and their serum insulin concentration was four times higher (p < .001) than in corresponding controls. The SH hamsters killed after a 10-hr fast displayed significant increases in the ponderal growth rate (2.5 ± .3 g/day, p < .001) relative to their controls (0 ± .1 g/ day) but no differences in any of the endocrine values (Table 1). Experiment 3: SH Cuts Decrease Voluntary Disk Activity and Selection of Sunflower Seeds in Adult Hamsters In this experiment we examined the levels of voluntary activity on horizontal activity devices in hamsters with SH cuts for two reasons. First, we wished to find out whether acceleration of growth following SH cuts resulted from the interference with the same neural mechanism that is blocked during exercise-induced growth in neurologically intact hamsters (Borer & Kuhns, 1977) by looking for additive or substitutive effects of exercise and SH cuts on somatic growth. For us to answer this question, activity levels of control and SH hamsters had to be equivalent. Second, we also wanted to find out whether SH cuts induced changes in activity levels. A change in voluntary activity levels after SH cuts could reflect alteration in the regulatory controls over voluntary (exercise) and involuntary (thermogenesis) routes of energy expenditure. In addition, we were mindful of reports (Marks

& Miller, 1972) that the appearance or magnitude of weight changes after ventromedial hypothalamic lesions in hamsters depends on the presence of fat in the diet. In the present experiment we, therefore, offered hamsters ad lib choice of pellets (high-carbohydrate, low-fat food) and sunflower seeds (high-fat, low-carbohydrate food). Method The experiment was a 2 X 2 factorial design, with exercise or sedentary condition and SH cuts or control surgery as the two variables applied orthogonally. Twenty-five hamsters were matched by weight and length and assigned to four groups of six or seven animals. Two groups, one SH and one control, were exposed to horizontal activity disks for 35 days starting with the seventh postoperative day, while the other two groups remained sedentary. Halfway through the experiment, activity boxes were interchanged between SH cut and control animals to balance for possible differences in the accessibility of activity disks. To assess whether differences in activity levels after SH cuts are due to a motivational change or reflect a motor deficit, we performed a test of motor ability on Postoperative Days 10 and 11. The SH hamsters (n = 13) and control animals (n = 11) were placed in a rotating drum (Wahmann wheel) with a circumference of 112 cm. The wheel was manually turned at the maximal speed that allowed the hamster to keep pace with the turns by running in the same position in the wheel. At lower speeds hamsters would outrun the wheel, and at higher wheel speeds hamsters would tumble. Food intake measurements were taken between the 7th and the 29th postoperative days. In addition to daily (Days 0-35) or biweekly (Days 36-77) weight measurements and Day 0 and Day 77 total body length measurements, we also made radiographs of the ham-

GROWTH, FATNESS, AND ACTIVITY IN ADULT HAMSTERS ster skeleton on Day 77 to determine skeletal growth according to a procedure described in detail elsewhere (Borer & Kuhns, 1977). Furthermore, after the removal of brains for histology, carcasses (without gut contents) were analyzed for fat content by the method described in Experiment 1.

Results Control hamsters generated 38,625 ± 2,093 revolutions per day, and SH-cut hamsters ran only 5,875 ± 2,474 (p < .001, Figure 4, left). The SH cuts were thus associated with an 85% decrease in voluntary activity levels. Hamsters with SH cuts ran significantly slower in the rotating drum on Day 10 (11.2 ± .9 cm/sec, p < .01) and Day 11 (14.6 ± 1.4 cm/sec, p < .001) than control hamsters (18.0 ± 1.3 and 19.5 ± 1.1 cm/sec, respectively). Since there is a negative correlation between body weight and activity levels in adult hamsters expressed by the linear regression y = —207.1 x + 52,620 (Borer & Kaplan, 1977), we wanted to see whether growth-induced increases in hamster body size can account for all of the observed differences in the activity levels between SH-cut and control hamsters. We therefore examined the activity levels of SH-cut and control hamsters in this study as a function of 10-g increments in body weight (Figure 4, right). There was no reliable correlation (r = .148) between body weight and activity level in hamsters with SH cuts. Their activity levels remained entirely out-

side the linear regression y = —248 x + 66,923.2 which described the significant relation between the body size and the activity level in the control-operated hamsters (r = -.729). The relative effects of SH cuts and exercise on somatic growth and body composition are presented in Figure 2 and Table 2. The SH cuts produced a threefold increase in the rate of weight gain between Day 7 and Day 35 after surgery (Figure 2, right) as well as significant weight increments and increases in the length of total body, skull, vertebral column of the body, humerus, and femur, and in the percentage of body fat (Table 2). On the 77th day after surgery there was a 74-g difference in the mean body weights of sedentary SH and control-operated hamsters. Forty-three percent of this difference was due to accumulation of body fat. There was a 59-g weight difference between the exercising SH and control animals on the last day of the experiment, and 37% of it was generated by body fat. To establish the possible role of a high-fat dietary choice on the manifestations of SH cuts, we compared the relative contributions of two different diets (pellets only, Experiment 1, and pellets and sunflower seeds, Experiment 3) on various measures of intake and growth in sedentary hamsters with and without SH cuts. The SH hamsters gained weight and grew longer to a significantly greater extent when fed a diet of pellets and

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100 125 150 175 200 BODY WEIGHT (g)

Figure 4. Left: Mean activity levels of septohypothalamic (SH) cut (solid circles; n = 6) and control (open circles; n = 6) hamsters during 35 days of exposure to disk exercise. Right: Activity levels of SH cut and control hamsters (same symbols as on the left) as a function of their body weight. (RPD = revolutions per day.)

914

BORER, PETERS, KELCH, TSAI, HOLDER

Table 2 Mean (± SE) Somatic Growth and Body Composition as a Function of SH Cuts and Voluntary Exercise SHcut Exercising

Sedentary

Measure Ponderal growth rate (in g/day) Weight increment (in g) Length increment (in mm) Length (in mm) Skull Vertebral column Tail Humerus Femur Body fat (%)

F(l, 21) (analysis of variance)

Control Exercising (n = 6)

Sedentary SH

E

SHX E

.86

1.94

2.5 ± .1

2.5 ± .2

1.2 ± .1

0.9 ± .1

143.86***

137.8 ±2.7

124.1 ± 3.5

78.6 ± 3.0

40.9 ± 5.0

384.75***

35.33 ± .80

30.71 ± .80 26.17 ± .83

17.17 ± 1.47 144.55***

38.33 ± .29

38.02 ± .22 37.07 ± .31

36.71 ± .27

22.38***

.82 107.70 ± 1.22 .59 33.04 ± 1.00 .31 24.36 ± .16 .27 27.27 ± .29 1.4 14.1 ± 1.4

97.35*** ns 40.31*** 26.47*** 33.97***

121.25 ±1.03 118.31 ± .46 114.28 ± 36.55 ± .39 35.43 ± 1.58 35.67 ± 26.23 ± .28 25.99 ± .08 24.99 ± 29.82 ± .30 29.26 ± .27 28.92 ± 23.0 ±1.1 24.1 ± 1.2 18.3 ±

47.57*** 10.83** 50.02***

5.29*

1.47 27.29*** ns 4.77* 14.32**** 1.23

.01

4.11 ns .47 3.65 4.33*

Note. F values are for the effects of septohypothalamic cuts (SH) and exercise (E) and their interaction. Ponderal growth rate was calculated from Day 7 to Day 35; weight and length increments, from Day 0 to Day 77. All other measurements were taken on Day 77. * p < . 0 5 . **p

Contribution of growth, fatness, and activity to weight disturbance after septohypothalamic cuts in adult hamsters.

Journal of Comparative and Physiological Psychology 1979, Vol. 93, No. 5,907-918 Contribution of Growth, Fatness, and Activity to Weight Disturbance...
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