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Biostatistics

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REVIEW QUESTIONS AND EXERCISES 405<br />

Rat<br />

Diet<br />

HW/BW<br />

(g/100 g)<br />

LW/BW<br />

(g/100 g)<br />

KW/BW<br />

(g/100 g)<br />

SW/BW<br />

(g/100 g)<br />

Ceruloplasmin<br />

(mg/dl)<br />

6 0.00249 0.00589 0.00463 0.00126 35.30<br />

7 0.00284 0.00773 0.00550 0.00187 39.00<br />

8 PF 0.00227 0.00788 0.00481 0.00217 28.00<br />

9 0.00254 0.00697 0.00513 0.00189 34.20<br />

10 0.00279 0.00900 0.00514 0.00171 45.20<br />

11 0.00247 0.00919 0.00469 0.00159 34.60<br />

12 0.00254 0.00829 0.00520 0.00144 39.00<br />

13 CuA 0.00280 0.00906 0.00507 0.00169 37.10<br />

14 0.00249 0.00917 0.00491 0.00155 33.40<br />

15 0.00268 0.01191 0.00560 0.00165 37.30<br />

nd, no data.<br />

Source: Data provided courtesy of Corrie B. Allen.<br />

63. Hughes et al. (A-66) point out that systemic complications in acute pancreatitis are largely responsible<br />

for mortality associated with the disease. They note further that proinflammatory cytokines, particularly<br />

TNFa, may play a central role in acute pancreatitis by mediating the systemic sequelae. In their research<br />

they used a bile-infusion model of acute pancreatitis to show amelioration of disease severity as well as<br />

an improvement in overall survival by TNFa inhibition. Experimental material consisted of adult male<br />

Sprague-Dawley rats weighing between 250 and 300 grams divided into three groups: untreated (bile<br />

solution infused without treatment); treated (bile solution infused preceded by treatment with<br />

polyclonal anti TNFa antibody); and sham (saline infused). Among the data collected were the<br />

following hematocrit (%) values for animals surviving more than 48 hours:<br />

Sham Untreated Treated<br />

38 56 40<br />

40 60 42<br />

32 50 38<br />

36 50 46<br />

40 50 36<br />

40 35<br />

38 40<br />

40 40<br />

38 55<br />

40 35<br />

36<br />

40<br />

40<br />

35<br />

45<br />

Source: Data provided courtesy of<br />

Dr. A. Osama Gaber.<br />

64. A study by Smarason et al. (A-67) was motivated by the observations of other researchers that sera<br />

from pre-eclamptic women damaged cultured human endothelial cells. Subjects for the present study<br />

were women with pre-eclampsia, matched control women with normal pregnancies, and nonpregnant

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