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Nutrient Metabolism

Study of Diet-Induced Changes in Lipoprotein Metabolism in Two Strains of Golden-Syrian Hamsters^1,2

Cardiovascular Nutrition Laboratory and ^* Comparative Biology Unit, Jean Mayer U.S. Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, Boston, MA

³To whom correspondence should be addressed. E-mail: Alice.Lichtenstein{at}Tufts.edu.

	ABSTRACT

TOP ABSTRACT MATERIALS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
The objective of this study was to characterize two strains of Golden-Syrian hamsters for use in the study of diet-induced changes in lipoprotein metabolism. In Experiment 1, the time course and response to dietary saturated fat was investigated for serum lipoprotein profiles and aortic lesion formation in Golden-Syrian hamsters from Charles River Laboratories, Wilmington, MA (CR) and Bio Breeders, Watertown, MA (F₁B). Hamsters were fed a nonpurified diet containing 10 g/100 g saturated fat and 0.1 g/100 g dietary cholesterol. After 12 wk, CR hamsters had significantly lower serum total and non-HDL cholesterol (TC and nHDL-C) levels, but higher aortic cholesteryl ester (CE) than the F₁B hamsters (P < 0.05). In Experiment 2, CR hamsters were fed a nonpurified diet containing 10 g/100 g saturated fat and 0.1, 0.5 or 1 g/100 g dietary cholesterol. After 10 wk of dietary intervention, TC and nHDL-C levels were significantly higher in the 0.5 and 1.0 g/100 g cholesterol groups than in the 0.1 g/100 g cholesterol group. These levels declined after 20 wk of dietary intervention in all groups, potentially reflecting the toxic effect of high cholesterol intakes. CR hamsters fed a 10 g/100 g saturated fat containing 0.1 g/100 g dietary cholesterol for 10 wk appear to be a good model for investigating diet-induced change in plasma lipids.

KEY WORDS: • Golden-Syrian hamsters • dietary cholesterol • saturated fat • butter • coconut oil • serum lipids and lipoproteins • aortic cholesteryl ester

The Golden-Syrian hamster has been used as a model with which to study lipid metabolism and diet-induced atherosclerosis since the early 1980s (1). Advantages of this animal model compared with others of comparable size include the presence of LDL receptor–mediated and cholesteryl ester transfer protein (CETP)³ activities (2–5). However, a major consideration when utilizing this model is that breeding laboratories produce different strains of hamsters that respond differently to dietary perturbations (4,6). Among four commonly used breeding laboratories in the United States, Trautwein et al. (6) found differences in plasma lipoprotein levels and hepatic and biliary lipids. Two of these suppliers, Charles River Laboratories (Wilmington, MA) and Bio Breeders (Watertown, MA) are still producing hamsters for research use. Bio Breeders produces inbred hamsters that are reported to have a characteristic phenotype of hyperlipidemia and develop atherosclerotic lesions when fed a high saturated fat diet (7), whereas Charles River Laboratories produces outbred hamsters that have been reported to have a smaller rise in plasma total cholesterol levels and limited lesion formation relative to hamsters from Bio Breeders (8).

There is a high degree of variability among hamster studies in response to dietary perturbations as assessed by monitoring lipoprotein profiles and atherosclerotic lesion formation (8–18). It is difficult to determine the cause of this variability solely from data in the literature due to heterogeneity in strains of hamsters used, and variability in study designs, methodology and format of reported data. Discrepancies among studies may be due to strain-specific differences in the dietary perturbation, drift in animal phenotype, response over time or other as yet unknown factors.

To address these issues, we conducted two experiments to characterize two strains of hamsters currently available to study diet-induced changes in lipoprotein metabolism, the Golden-Syrian hamsters from Charles River Laboratories (CR; Wilmington, MA) and Bio Breeders (F₁B; Watertown, MA). In Experiment 1, the time course and response to dietary fat of serum lipid variables and aortic lipid composition were investigated in both strains of hamsters. In Experiment 2, the effect of dietary cholesterol amount on serum lipids, lipoproteins and aortic lipid composition, and temporal response was investigated in CR hamsters.

	MATERIALS AND METHODS

TOP ABSTRACT MATERIALS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
Animals and diets.

    Experiment 1. Eight-wk-old male CR and F₁B Golden-Syrian hamsters (n = 24/group) were housed individually in stainless steel suspended rodent cages with free access to modified rodent sterilizable diet (Harlan Teklad, Madison, WI) and water for a 2-wk acclimation period. The hamsters were kept in AAALAC-accredited facilities, in an environmentally controlled atmosphere (temperature 23°C, 45% relative humidity) with 15 air changes of 100% fresh HEPA-filtered air per hour and a reverse 10-h:14-h light:dark cycle (19). The health status of the hamsters was monitored daily. After the acclimation period, each strain of hamster was weighed, ear-punched and randomly assigned to one of two experimental diets, resulting in 4 groups. One group from each strain (n = 12) was fed a nonpurified diet (6.25 g fat/100 g diet, no cholesterol; Harlan Teklad 7014 modified rodent diet) (Table 1). The second group from each strain (n = 12) was fed a high saturated fat nonpurified diet [10 g butter/100 g diet, 0.1 g cholesterol/100 g diet (Sigma #C-8503 95% pure; St. Louis, MO); Harlan Teklad]. The hamsters were housed 4 hamsters/cage (71 cm x 28 cm x 18 cm) and fed the experimental diets for 12 wk. Before initiating the experimental diet period and every 2 wk thereafter, body weights were recorded and blood was collected from the retroorbital sinus under isoflurane anesthetization after16–18 h of food deprivation. During wk 12, hamsters were food deprived for 16–18 h, blood samples collected and then the hamsters were killed by terminal exsanguination from the abdominal aorta under isoflurane anesthesia. The hearts were immediately perfused with PBS and removed from the body. Aortae were cleaned of adventitia within 12 h, weighed, flash frozen in liquid nitrogen and stored at -80°C.

Serum lipid and lipoprotein analysis.

Serum was separated from RBC by centrifugation at 1100 x g at 4°C and assayed for total and HDL cholesterol (TC, HDL-C), and fasting triglyceride (TG) levels on a Hitachi 911 automated analyzer (Roche Diagnostics, Indianapolis, IN) using enzymatic reagents. The assays are standardized through the Lipid Standardization Program of the CDC, Atlanta, GA. Non-HDL cholesterol (nHDL-C) was computed as the difference between TC and HDL-C.

Aorta lipid extraction and measurement of cholesteryl ester (CE).

Lipids were extracted from aortae using the method of Folch et al. (21). Chemical analysis of lipid extracts was preformed using the method of Carr et al. (22). CE levels were calculated as the difference between TC and free cholesterol (FC). TC, FC and CE were recorded as µg/mg wet weight of aorta.

Statistical analysis.

All data are reported as means ± SD. In Experiment 1, two-way ANOVA was used to determine differences between diet and strain (SAS, Cary, NC). In Experiment 2, two-way ANOVA was used to test the differences between dietary cholesterol composition and length of time the diets were consumed, 10 and 20 wk. The Student-Newman-Keuls test was used for post-hoc analysis. Differences were considered significant at P 0.05.

	RESULTS

TOP ABSTRACT MATERIALS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
Experiment 1.

F₁B hamsters had lower body weights than CR hamsters at baseline, but gained more weight during the 12-wk experimental period (Table 1). Hamsters fed the high fat diet, independent of strain, gained significantly more weight than hamsters fed the nonpurified diet.

Plasma lipid levels (TC, nHDL-C, HDL-C, TG, P = 0.001, 0.002, 0.003, 0.033, respectively) decreased over the 12-wk period when the hamsters were fed nonpurified diet in the F₁B but not in the CR hamsters (Fig. 1). This difference between species was not apparent over the 12-wk period, when the hamsters were fed the butter diet. In fact, the response was greater in the F₁B hamsters. Hence, it is unlikely that the differences observed in the nonpurified diet groups were due to the faster growth rate of the F₁B compared with the CR strain. Differences in TC:HDL-C ratios followed a pattern similar to nHDL-C levels in both species of hamsters, increasing with saturated fat feeding.

View larger version (21K): [in this window] [in a new window]   FIGURE 1 Time course for body weights (A) total cholesterol (TC) (B), non-HDL cholesterol (nHDL-C) (C), HDL-C (D) and fasting triglycerides (TG) (E) in Charles River (CR) and Bio Breeders (F1B) Golden-Syrian hamsters fed a nonpurified diet or butter/dietary cholesterol–enriched nonpurified diets for 12 wk. Values are means ± SD. CR nonpurified diet, n = 8; CR butter diet, n = 12; F1B nonpurified diet, n = 12; F1B butter, n = 10. To convert TC, nHDL-C, HDL-C to mmol/L, divide by 38.65. To convert TG to mmol/L, divide by 88.54.

The pattern of change in TC and nHDL-C levels over the 12-wk diet period was different in the two strains of hamsters when the high fat diet was fed (Fig. 1). The CR hamsters TC and nHDL-C levels reached a plateau at 4 wk, whereas the F₁B hamster levels continued to increase throughout the feeding period. This difference in response resulted in higher TC and nHDL-C levels at the end of the 12-wk period in the F₁B hamsters compared with the CR hamsters. HDL-C levels peaked somewhat earlier than TC and nHDL-C levels and remained relatively constant and similar in both hamster strains; at the 12-wk time point, however, there was an unexplained decline in HDL-C levels in both species. TG levels of food-deprived hamsters tended to be higher (P = 0.29) in the F₁B hamsters after 4 wk of consuming the high fat diet and were significantly higher than those of the CR hamsters at the 12-wk time point. Fasting TG levels in both CR and F₁B declined slightly between wk 10 and 12. The difference between strains appeared to be accentuated by a greater decrease in fasting TG in the CR hamsters.

Aortic CE concentrations of CR and F₁B hamsters did not differ after the nonpurified diet was fed for 12 wk (Fig. 2). In contrast, the aortic CE levels were significantly higher in the CR than F₁B hamsters after the high fat diet was consumed for that same period of time.

View larger version (15K): [in this window] [in a new window]   FIGURE 2 Aortic cholesterol ester concentration in Charles River (CR) and Bio Breeders (F1B) Golden-Syrian hamsters consuming the nonpurified and butter diets. Dots represent aortic cholesteryl ester (µg/mg wet weight) in individual hamsters. CR 1 = Charles River nonpurified diet, CR 2 = Charles River butter diet, F1B 1 = Bio Breeders nonpurified diet, F1B 2 = Bio Breeders butter diet. Lines represent group means ± SD, n = 8, n = 12, n = 12, n = 10, respectively. Means without a common letter differ, P < 0.05. To convert µg/mg to µmol/g, divide by 0.651.

Because plasma lipid levels stabilized by wk 12, fasting TG levels were within the near physiologic range for humans and dietary modification–induced aortic lesion formation, the CR hamster strain was chosen for subsequent work. The focus of Experiment 2 was to assess the effect of dietary cholesterol and temporal changes on blood lipid levels and aortic CE accumulation over a longer period of time, 20 wk. Plotted separately in Figure 3 are the data for hamsters killed at 10 and 20 wk. Hamsters fed the diet containing the lowest level of cholesterol (0.1 g/100 g) had higher body weights after both 10 (P = 0.005) and 20 (P = 0.004) wk than hamsters fed the intermediate (0.5 g/100 g) and highest (1 g/100 g) levels of cholesterol. Gross inspection of the livers indicated that enlarged, pale and mottled livers were associated with the intermediate and highest levels of cholesterol at both 10 and 20 wk, suggesting hepatotoxicity.

View larger version (27K): [in this window] [in a new window]   FIGURE 3 Time course of body weights over 10 wk (a) and 20 wk (b) in Charles River (CR) Golden-Syrian hamsters consuming a high saturated fat diet (10 g coconut oil/100 g diet) enriched with varying amounts of dietary cholesterol for 10 and 20 wk. Values are means ± SD, n = 16 (10 wk), n = 8 (20 wk). Within a panel, diet groups without a common letter differ, P < 0.05.

Similar to what was observed in Experiment 1, CR hamsters fed a diet containing 0.1 g/100 g dietary cholesterol for 10 wk had a 0.8-fold increase in the TC:HDL-C ratio relative to baseline. The higher cholesterol diets, 0.5 and 1.0 g/100 g dietary cholesterol, caused a 1.3-fold and twofold increase in TC:HDL-C ratio at 10 wk, respectively, suggesting that the hamsters responded to dietary cholesterol in a dose-dependent manner. After 20 wk, TC:HDL-C ratios declined in these two groups of hamsters, reflecting changes observed primarily in nHDL-C levels.

The level of cholesterol in the diet had a significant effect on aortic CE at 10 wk (Table 4). The amount of aortic CE increased proportionally with the level of dietary cholesterol. A similar pattern was not seen in the hamsters fed the diets for 20 wk, most likely reflecting the deterioration of lipoprotein metabolism due to hepatotoxicity.

	DISCUSSION

TOP ABSTRACT MATERIALS AND METHODS RESULTS DISCUSSION LITERATURE CITED

Initially, in Experiment 1, F₁B hamsters weighed less than CR hamsters, yet they had higher TC and nHDL-C levels, reflecting differences in strain (4,6). At the end of the saturated fat intervention period, the body weights of the two strains did not differ. However, with respect to serum lipid levels, the F₁B hamsters had significantly higher fasting TG and HDL-C levels. These data are consistent with earlier observations comparing the two strains of hamsters (6–8,15). Nevertheless, high saturated fat feeding resulted in more aortic CE accumulation in CR than F₁B hamsters. Diminished lesion formation may be a result of the outbreeding of the original inbred F₁B strain over the years as documented by others, or an as yet unknown intraspecies difference (9,12,16,23).

In Experiment 1, plasma lipid and lipoprotein levels stabilized by wk 4 of the12-wk saturated fat feeding period in CR hamsters, but continued to rise throughout the study period in the F₁B hamsters. Nevertheless, under our experimental setting and diet conditions, the aortae in the CR hamsters sustained significantly more atherosclerotic lesion formation as assessed by aortic CE content than the F₁B hamsters, suggesting higher sensitivity to the circulating lipoproteins. On the basis of lipoprotein response and aortic lesion formation, we chose to study CR hamsters for subsequent work.

In Experiment 2, we investigated the effect of the amount of dietary cholesterol on temporal changes in plasma lipoprotein levels and aortic CE accumulation. Although dietary cholesterol significantly increased TC:HDL-C ratios, the magnitude of the effect on aortic CE accumulation was smaller than might have been anticipated from this change. Furthermore, TC:HDL-C ratios declined in the 0.5 and 1.0 g/100 g dietary cholesterol groups after 20 wk. This last-mentioned observation is likely attributable to the toxic effects of the higher levels of cholesterol in the diet. Visual inspection of livers suggested that cholesterol infiltration may have altered apolipoprotein synthesis and impeded hepatic lipoprotein metabolism. This observation was somewhat unexpected because it was reported previously that hamsters fed 3 g/100 g dietary cholesterol for 10 mo had a 17-fold increase in serum TC, and plaques covering 30% of the lumen in the aortic arch (1). Furthermore, Parker et al. (24) reported no toxicity in hamsters fed 0.8 g/100 g dietary cholesterol for 10 wk. The data from the current investigation suggest that results from feeding very high levels of dietary cholesterol to hamsters, which resulted in hepatotoxicity, have limited relevance to understanding the pathophysiology of atherosclerosis in humans.

There are limitations to the current work. Two different types of saturated fat were used to induce changes in lipoprotein metabolism and aortic CE accumulation, butter and coconut oil. Although the response to the butter diet was of a smaller magnitude than to the coconut oil diet, the pattern of response and the relationship between plasma nHDL-C and aortic CE were similar. There is no evidence that this difference would alter the response of the hamsters in a way that would preclude assessing their suitability for use as an animal model of diet-induced lesion formation. The response of either strain of hamster to dietary perturbations intended to simulate a proatherogenic state in humans did not result in a lipoprotein pattern similar to that of humans. However, there are features of the system that will allow for an investigation of the mechanisms underlying the diet-induced changes.

Although the use of the hamster as a model has limited utility in expanding our understanding of the diet/disease relationship in humans, it does afford the unique opportunity to explore underlying mechanisms that could not otherwise be addressed due to ethical concerns. Within the narrow focus of the current work, the CR hamsters consuming a diet containing 0.1 g/100 g dietary cholesterol for 10 wk comprise an acceptable model for investigating the mechanisms of diet-induced changes in lipoprotein metabolism and aortic lesion development.

	ACKNOWLEDGMENTS

	FOOTNOTES

 
¹ Supported by grant HL 54727 from the National Institutes of Health, Bethesda, MD and the U.S. Department of Agriculture, under agreement No. 58–1950-9–001. Supported in part by grant T32 DK62032–11 from the National Institutes of Health, Bethesda, MD (S.E.D).

² Any opinions, findings, conclusion, or recommendations expressed in this publication are those of the author(s) and do not necessarily reflect the view of the U.S. Department of Agriculture.

⁴ Abbreviations used: F₁B, Bio Breeders hamsters; CR, Charles River Laboratories hamsters; CE, cholesteryl ester; CETP, cholesteryl ester transfer protein; FC, free cholesterol; HDL-C, HDL cholesterol; nHDL-C, non-HDL cholesterol; TC, total cholesterol; TG, triglycerides.

Manuscript received 2 July 2003. Initial review completed 23 July 2003. Revision accepted 10 September 2003.

	LITERATURE CITED

TOP ABSTRACT MATERIALS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 

1. Nistor, A., Bulla, A., Filip, D. A. & Radu, A. (1987) The hyperlipidemic hamster as a model of experimental atherosclerosis. Atherosclerosis 68:159-173.[Medline]

2. Chen, J., Song, W. & Redinger, R. N. (1996) Effects of dietary cholesterol on hepatic production of lipids and lipoproteins in isolated hamster liver. Hepatology 24:424-434.[Medline]

3. Remillard, P., Shen, G., Milne, R. & Maheux, P. (2001) Induction of cholesteryl ester transfer protein in adipose tissue and plasma of the fructose-fed hamster. Life Sci. 69:677-687.[Medline]

4. Trautwein, E. A., Liang, J. & Hayes, K. C. (1993) Cholesterol gallstone induction in hamsters reflects strain differences in plasma lipoproteins and bile acid profiles. Lipids 28:305-312.[Medline]

5. Ahn, Y. S., Smith, D., Osada, J., Li, Z., Schaefer, E. J. & Ordovas, J. M. (1994) Dietary fat saturation affects apolipoprotein gene expression and high density lipoprotein size distribution in golden Syrian hamsters. J. Nutr. 124:2147-2155.

6. Trautwein, E. A., Liang, J. & Hayes, K. C. (1993) Plasma lipoproteins, biliary lipids and bile acid profile differ in various strains of Syrian hamsters Mesocricetus auratus. Comp. Biochem. Physiol. Comp. Physiol. 104:829-835.[Medline]

7. Terpstra, A. H., Holmes, J. C. & Nicolosi, R. J. (1991) The hypocholesterolemic effect of dietary soybean protein vs. casein in hamsters fed cholesterol-free or cholesterol-enriched semipurified diets. J. Nutr. 121:944-947.

8. Kowala, M. C., Nunnari, J. J., Durham, S. K. & Nicolosi, R. J. (1991) Doxazosin and cholestyramine similarly decrease fatty streak formation in the aortic arch of hyperlipidemic hamsters. Atherosclerosis 91:35-49.[Medline]

9. El-Swefy, S., Schaefer, E. J., Seman, L. J., van Dongen, D., Sevanian, A., Smith, D. E., Ordovas, J. M., El-Sweidy, M. & Meydani, M. (2000) The effect of vitamin E, probucol, and lovastatin on oxidative status and aortic fatty lesions in hyperlipidemic-diabetic hamsters. Atherosclerosis 149:277-286.[Medline]

10. Wilson, T. A., Nicolosi, R. J., Lawton, C. W. & Babiak, J. (1999) Gender differences in response to a hypercholesterolemic diet in hamsters: effects on plasma lipoprotein cholesterol concentrations and early aortic atherosclerosis. Atherosclerosis 146:83-91.[Medline]

11. Nicolosi, R. J., Wilson, T. A., Rogers, E. J. & Kritchevsky, D. (1998) Effects of specific fatty acids (8:0, 14:0, cis-18:1, trans-18:1) on plasma lipoproteins, early atherogenic potential, and LDL oxidative properties in the hamster. J. Lipid Res. 39:1972-1980.[Abstract/Free Full Text]

12. Pitman, W. A., Osgood, D. P., Smith, D., Schaefer, E. J. & Ordovas, J. M. (1998) The effects of diet and lovastatin on regression of fatty streak lesions and on hepatic and intestinal mRNA levels for the LDL receptor and HMG CoA reductase in F₁B hamsters. Atherosclerosis 138:43-52.[Medline]

13. Robins, S. J., Fasulo, J. M., Patton, G. M., Schaefer, E. J., Smith, D. E. & Ordovas, J. M. (1995) Gender differences in the development of hyperlipemia and atherosclerosis in hybrid hamsters. Metabolism 44:1326-1331.[Medline]

14. Otto, J., Ordovas, J. M., Smith, D., van Dongen, D., Nicolosi, R. J. & Schaefer, E. J. (1995) Lovastatin inhibits diet induced atherosclerosis in F₁B golden Syrian hamsters. Atherosclerosis 114:19-28.[Medline]

15. Kowala, M. C., Mazzucco, C. E., Hartl, K. S., Seiler, S. M., Warr, G. A., Abid, S. & Grove, R. I. (1993) Prostacyclin agonists reduce early atherosclerosis in hyperlipidemic hamsters. Octimibate and BMY 42393 suppress monocyte chemotaxis, macrophage cholesteryl ester accumulation, scavenger receptor activity, and tumor necrosis factor production. Arterioscler. Thromb. 13:435-444.[Abstract/Free Full Text]

16. Vinson, J. A., Teufel, K. & Wu, N. (2001) Red wine, dealcoholized red wine, and especially grape juice, inhibit atherosclerosis in a hamster model. Atherosclerosis 156:67-72.[Medline]

17. Carr, T. P., Cai, G., Lee, J. Y. & Schneider, C. L. (2000) Cholesteryl ester enrichment of plasma low-density lipoproteins in hamsters fed cereal-based diets containing cholesterol. Proc. Soc. Exp. Biol. Med. 223:96-101.[Abstract/Free Full Text]

18. Foxall, T. L., Shwaery, G. T., Stucchi, A. F., Nicolosi, R. J. & Wong, S. S. (1992) Dose-related effects of doxazosin on plasma lipids and aortic fatty streak formation in the hypercholesterolemic hamster model. Am. J. Pathol. 140:1357-1363.[Abstract]

19. Smith, D., Pedro-Botet, J., Cantuti-Castelvetri, I., Shukitt-Hale, B., Schaefer, E. J., Joseph, J. & Ordovas, J. M. (2001) Influence of photoperiod, laboratory caging and aging on plasma lipid response to an atherogenic diet among F₁B hamsters. Int. J. Neurosci. 106:185-194.[Medline]

20. Nicolosi, R. (1997) Dietary fat saturation effects on low-density-lipoprotein concentrations and metabolism in various animal models. Am. J. Clin. Nutr. 65:1617S-1627S.[Abstract/Free Full Text]

21. Folch, M., Lees, B. & Sloan-Stanley, G. H. (1957) A simple method for the isolation and purification of total lipids from animal tissues. J. Biol. Chem. 226:497-509.[Free Full Text]

22. Carr, T. P., Andresen, C. J. & Rudel, L. L. (1993) Enzymatic determination of triglyceride, free cholesterol, and total cholesterol in tissue lipid extracts. Clin. Biochem. 26:39-42.[Medline]

23. Nicolosi, R. J., Wilson, T. A. & Krause, B. R. (1998) The ACAT inhibitor, CI-1011 is effective in the prevention and regression of aortic fatty streak area in hamsters. Atherosclerosis 137:77-85.[Medline]

24. Parker, R. A., Sabrah, T., Cap, M. & Gill, B. T. (1995) Relation of Vascular Oxidative Stress, Alpha-Tocopherol, and Hypercholesterolemia to Early Atherosclerosis in Hamsters. Arterioscler. Thromb. 15:349-358.[Abstract/Free Full Text]

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This Article Abstract Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Dorfman, S. E. Articles by Lichtenstein, A. H. Search for Related Content PubMed PubMed Citation Articles by Dorfman, S. E. Articles by Lichtenstein, A. H.