15.8. 1977
Specialia
s c r i b e d c o m b i n a t i o n t e s t e n a b l e s us to r e j e c t t h e h y p o t h e s i s t h a t t h e fish s i m p l y s w i m s f o r w a r d o n s o u n d . D i r e c t i o n a l h e a r i n g has b e e n s h o w n a t l e a s t for t h e coarse d i s c r i m i n a t i o n of b e a r i n g s 180 ~ a p a r t . This a b i l i t y alone h a s (already) biological m e a n i n g . I t is q u i t e p r o b a b l e t h a t t h e orfe possesses a m u c h b e t t e r a n g u l a r resolution. W e did n o t t e s t t h i s d i r e c t l y o w i n g to t h e risk of a n o t h e r act of willful h i n d e r i n g 'S in t h e field. V o n F r i s c h a n d D i j k g r a a f x9 a n d R e i n h a r d t ~~ h a v e b e e n u n a b l e t o s h o w acoustic localization in O s t a r i o p h y s i , e x c e p t w h e n t h e fish were w i t h i n a d m r a n g e f r o m t h e sources. W e t e n t a t i v e l y a t t r i b u t e t h e i r n e g a t i v e r e s u l t s t o i n a d e q u a t e qualities of t h e a p p l i e d s o u n d fields (too few l o w - f r e q u e n c y c o m p o n e n t s ?). Since in our e x p e r i m e n t s t h e r e was n o c o r r e l a t i o n b e t w e e n t h e p o l a r i t y of t h e acoustic p r e s s u r e a t t h e o n s e t of t h e s o u n d s a n d t h e l o c a t i o n of t h e sources, we c o n c l u d e t h a t t h e d i s c r i m i n a t i o n c a n n o t be b a s e d on d e t e c t i o n of t h e initial p o l a r i t y of t h e acoustic p r e s s u r e : a s e n s o r y a b i l i t y d e m o n s t r a t e d b y P i d d i n g t o n ~x for goldfish. W e t h i n k t h a t in o u r experim e n t a phase analysis between acoustic pressure and p a r t i c l e d i s p l a c e m e n t s as s h o w n for cod. *z e x p l a i n s t h e d i s c r i m i n a t i o n of o p p o s i t e l y t r a v e l l i n g waves.
1
2
The authors gratefully acknowledge the efforts of Mr M. Kleisma in the conduction of preliminary laboratory and field experiments. We thank Dr J. Ringelberg for making available to us the field facilities of the Limnological Laboratory, University of Amsterdam. Dr E. Meelis, Institute of Theoretical Biology, Leyden, has Checked the applied statistics. D.R. Nelson and S. H. Gruber, Science 142, 975 (1963).
3 4 5
1063
17
D.R. Nelson, Bull. Mar. Sci. 17, 741 (1968). A. Banner, Bull. Mar. Sei. 22, 251 (1972). A.A. Myrberg, Jr, S. J. Ha, S. Walewski and J. C. Banbury, Bull. Mar. Sei. 22, 926 (1972). A.A. Myrberg, Jr, C. R. Gordon arid A. P. Klimley, in: Sound reception in Fish, p. 209. Elsevier, Amsterdam 1976. A. Schui~f and A. D. Hawkins, Sound reception in fish. Elsevier, Amsterdam 1976. O. Sand and P. S. Enger, in: J. Sehwartzkopff, Mecbanoreception, p. 223. Ed. J: Schwartzkopff. Abh. Rhein.-~,Vestf. Akad. Wiss. 53 (1974). A. Schuijf, J. W. Baretta and J. T. Wildsehut, Neth. J. Zool. 22, 81 (1972). A. Schuijf and M. E. Siemelink, Experientia 30, 773 (1974). K. Olsen, in: Sound reception in Fish, p. 259. Elsevier, Amsterdam 1976. A. Schuijf, J. eomp. Physiol. 98, 307 (1975). O. Sand, J. exp. Biol. 60, 881 (1974). R . J . A . Buwalda and J. van der Steen, Experientia (in press). The observations stopped abruptly after our subject had disappeared being exchanged by someone, otherwise we certainly would have decided to make additional observations, particularly with tail stimulations. J. Oosterhoff, Math. Centre Tracts 28. Math. Centrum, Amsterdam. 4 4 Ix = Z mlC,/N, a 2 = ~ m,n,Cl(Ni-C~)/{N~(Ni-1)}
18
i=l i=l Let the value of pl and p~ under Ho be ~i. If we accept Hi then
6 7 8 9 10 11 12 13 14 15
16
19 20 21 22
we have pi > ~l > p~. The expected number of correct choices is mpi + n(1-p~) > mz~l + n(1-ni). K. yon Friscb and S. Dijkgraaf, Z. vergl. Physiol. 22, 641 (1935). F. Reinhardt, Z. vergl. Physiol. 22, 570 (1935). R.W. Piddington, J. exp. Biol. 56, 403 (1972). A. Schuijf and R. J. A. Buwalda, J. comp. Physiol. 98, 333 (1975).
H i g h density lipoproteins in i s c h a e m i c h e a r t disease 1 I. C. O n o n o g b u 2
Department o/ Biochemistry, University o/Nigeria, Nsukka (Nigeria), 21 December 1976 Summary. H i g h d e n s i t y l i p o p r o t e i n cholesterol c o n c e n t r a t i o n s were s i g n i f i c a n t l y lower in ischaemic h e a r t disease p a t i e n t s t h a n in h e a l t h y s u b j e c t s w h e n age a n d s e x - m a t c h e d . This difference was, h o w e v e r , n o t o b s e r v e d in t h e older age g r o u p ( > 60 years). I s c h a e m i c h e a r t disease d u e to c o r o n a r y atherosclerosis ( o b s t r u c t i o n of t h e c o r o n a r y a r t e r y as a result of lipid d e p o s i t i o n in t h e a r t e r i a l wall) is a m a j o r w o r l d p r o b l e m a t t h e p r e s e n t t i m e 3, 4. T h e r e are m a n y risk f a c t o r s for i s c h a e m i c h e a r t disease. H y p e r c h o l e s t e r o l a e m i a 5,s a n d h y p e r t r i g l y c e r i d a e m i a ~ are k n o w n to be a s s o c i a t e d w i t h i s c h a e m i c h e a r t disease. T h e role of l i p o p r o t e i n s in t h e aeti01ogy of i s c h a e m i c h e a r t disease has, h o w e v e r , n o t b e e n fully explored. R e c e n t l y it h a s b e e n i n d i c a t e d t h a t h i g h d e n s i t y l i p o p r o t e i n is an a n t i a t h e r o g e n i c a g e n t 8. The m o d e of a c t i o n of h i g h d e n s i t y l i p o p r o t e i n as an a n t i a t h e r o g e n i c a g e n t is not, h o w e v e r , c o m p l e t e l y u n d e r s t o o d . S u g g e s t i o n s h a v e , a t a n y r a t e , b e e n m a d e as to t h e m e a n s b y which high density lipoprotein could act a s a n antia t h e r o g e n i c agent. One of t h e s e ~ believes t h a t h i g h d e n s i t y l i p o p r o t e i n h a s t h e a b i l i t y t o solubilize e x o g e n o u s c h o l e s t e r o l in a d d i t i o n to its o w n c h o l e s t e r o l c o n t e n t , t h u s p r e v e n t i n g i n f l u x of c h o l e s t e r o l i n t o t h e arterial wall. T h e localization of ApoA-1 in a t h e r o s c l e r o t i c lesions 1~ m a y also i n d i c a t e t h a t h i g h d e n s i t y l i p o p r o t e i n has t h e a b i l i t y t o t r a n s p o r t lipids f r o m t h e a r t e r i a l wall to t h e plasma. A n o t h e r m o d e of a c t i o n of h i g h d e n s i t y l i p o p r o t e i n is b e l i e v e d 11 t o be due t o its a b i l i t y to i n h i b i t u p t a k e a n d d e g r a d a t i o n of low d e n s i t y l i p o p r o t e i n , a n d d e p r e s s n e t
i n c r e m e n t in cell sterol c o n t e n t . L o w d e n s i t y l i p o p r o t e i n is t h e m a i n carrier of c h o l e s t e r o l a n d i n h i b i t i o n of its d e g r a d a t i o n m a y p r e v e n t a c c u m u l a t i o n of cholesterol in t h e arterial wall. Material and methods. H e a l t h y subjects. T h e s e were m a d e u p of 99 w h i t e B r i t i s h - b o r n m e n a n d w o m e n b e t w e e n t h e ages of 20 a n d 69 y e a r s living in t h e L o n d o n area. S u b j e c t s were selected on t h e basis of a b s e n c e of clinical or E C G 1
Acknowledgment. This investigation was supported by a grant from University of Nigeria, Nsukka. 2 I am grateful to Prof. Barry Lewis, St. Thomas Hospital Medical School, London, for his expert advice. 3 A. Keys, Atherosclerosis 22, 149 (1975). 4 B. Lewis, Lancet 7, 141 (1974). 5 W.B. Kannel, T. R. Dawber, G. D. Friedman, W. E. Glonnon and P. M. McNamara, Ann. int. Med. 6J, 888 (1964). 6 E. Nikkila and A. Aro, Lancet 7, 954 (1973). 7 L.A. Carlson and L. E. Bottiger, Lancet 1,865 (1972). 8 G.J. Miller and N. E. Miller, Lancet 1, 16 (1975). 9 S.L. Hsia, Y. Chao, C. H. Hennekens and W. B. Reader, Lancet 2, 1000 (1975). 10 H . F . Hoff, C. L. Heideman, R. L. Jackson, R. J. Bayardo, H. Kim and A. M. Gotto, Circulation Res. 37, 72 (1975). 11 T. E. Carew, T. Koschinsky, S. B. Hayes and D. Steinberg, Lancet 7, 1315 (1976).
1064
Specialia
e v i d e n c e of i s c h a e m i c h e a r t disease (IHD) f r o m h i s t o r y or clinical e x a m i n a t i o n . S u b j e c t s were e x c l u d e d on g r o u n d s of cirrhosis, r e n a l failure, clinically e v i d e n t e n d o c r i n e disease, c o n g e s t i v e h e a r t failure a n d m a l i g n a n t disease. I s c h a e m i c h e a r t disease p a t i e n t s . Those were m a d e u p of 50 w h i t e B r i t i s h - b o r n m e n a n d w o m e n (20-69 years) w h o were i s c h a e m i c h e a r t disease p a t i e n t s w h o were a t t e n d i n g t h e c a r d i a c clinic a t H a m m e r s m i t h H o s p i t a l , L o n d o n . F a s t i n g (12-14 h) b l o o d s a m p l e s were collected f r o m t h e 2 g r o u p s of s u b j e c t s . S e r u m w a s s e p a r a t e d b y low s p e e d centrifugation. High density lipoprotein separation by precipitation and cholesterol and triglyceride analyses b y Technicon A u t o a n a l y s e r were d o n e b y t h e m e t h o d s d e s c r i b e d in a n earlier p a p e r x~.
Table 1 HDL cholesterol HDL triglyceride (rag/100 ml) Males Control
n=57
56 -6 12 (mean 4- SD) Ischaemic heart disease n = 35 46 4- 11 T-value 4.01 p-value < 0.001 Females Control n =42 70 4- 22 Ischaemic heart disease n = 15 51 -64-21 T-value 2.99 p-value
Specialia
s c r i b e d c o m b i n a t i o n t e s t e n a b l e s us to r e j e c t t h e h y p o t h e s i s t h a t t h e fish s i m p l y s w i m s f o r w a r d o n s o u n d . D i r e c t i o n a l h e a r i n g has b e e n s h o w n a t l e a s t for t h e coarse d i s c r i m i n a t i o n of b e a r i n g s 180 ~ a p a r t . This a b i l i t y alone h a s (already) biological m e a n i n g . I t is q u i t e p r o b a b l e t h a t t h e orfe possesses a m u c h b e t t e r a n g u l a r resolution. W e did n o t t e s t t h i s d i r e c t l y o w i n g to t h e risk of a n o t h e r act of willful h i n d e r i n g 'S in t h e field. V o n F r i s c h a n d D i j k g r a a f x9 a n d R e i n h a r d t ~~ h a v e b e e n u n a b l e t o s h o w acoustic localization in O s t a r i o p h y s i , e x c e p t w h e n t h e fish were w i t h i n a d m r a n g e f r o m t h e sources. W e t e n t a t i v e l y a t t r i b u t e t h e i r n e g a t i v e r e s u l t s t o i n a d e q u a t e qualities of t h e a p p l i e d s o u n d fields (too few l o w - f r e q u e n c y c o m p o n e n t s ?). Since in our e x p e r i m e n t s t h e r e was n o c o r r e l a t i o n b e t w e e n t h e p o l a r i t y of t h e acoustic p r e s s u r e a t t h e o n s e t of t h e s o u n d s a n d t h e l o c a t i o n of t h e sources, we c o n c l u d e t h a t t h e d i s c r i m i n a t i o n c a n n o t be b a s e d on d e t e c t i o n of t h e initial p o l a r i t y of t h e acoustic p r e s s u r e : a s e n s o r y a b i l i t y d e m o n s t r a t e d b y P i d d i n g t o n ~x for goldfish. W e t h i n k t h a t in o u r experim e n t a phase analysis between acoustic pressure and p a r t i c l e d i s p l a c e m e n t s as s h o w n for cod. *z e x p l a i n s t h e d i s c r i m i n a t i o n of o p p o s i t e l y t r a v e l l i n g waves.
1
2
The authors gratefully acknowledge the efforts of Mr M. Kleisma in the conduction of preliminary laboratory and field experiments. We thank Dr J. Ringelberg for making available to us the field facilities of the Limnological Laboratory, University of Amsterdam. Dr E. Meelis, Institute of Theoretical Biology, Leyden, has Checked the applied statistics. D.R. Nelson and S. H. Gruber, Science 142, 975 (1963).
3 4 5
1063
17
D.R. Nelson, Bull. Mar. Sci. 17, 741 (1968). A. Banner, Bull. Mar. Sei. 22, 251 (1972). A.A. Myrberg, Jr, S. J. Ha, S. Walewski and J. C. Banbury, Bull. Mar. Sei. 22, 926 (1972). A.A. Myrberg, Jr, C. R. Gordon arid A. P. Klimley, in: Sound reception in Fish, p. 209. Elsevier, Amsterdam 1976. A. Schui~f and A. D. Hawkins, Sound reception in fish. Elsevier, Amsterdam 1976. O. Sand and P. S. Enger, in: J. Sehwartzkopff, Mecbanoreception, p. 223. Ed. J: Schwartzkopff. Abh. Rhein.-~,Vestf. Akad. Wiss. 53 (1974). A. Schuijf, J. W. Baretta and J. T. Wildsehut, Neth. J. Zool. 22, 81 (1972). A. Schuijf and M. E. Siemelink, Experientia 30, 773 (1974). K. Olsen, in: Sound reception in Fish, p. 259. Elsevier, Amsterdam 1976. A. Schuijf, J. eomp. Physiol. 98, 307 (1975). O. Sand, J. exp. Biol. 60, 881 (1974). R . J . A . Buwalda and J. van der Steen, Experientia (in press). The observations stopped abruptly after our subject had disappeared being exchanged by someone, otherwise we certainly would have decided to make additional observations, particularly with tail stimulations. J. Oosterhoff, Math. Centre Tracts 28. Math. Centrum, Amsterdam. 4 4 Ix = Z mlC,/N, a 2 = ~ m,n,Cl(Ni-C~)/{N~(Ni-1)}
18
i=l i=l Let the value of pl and p~ under Ho be ~i. If we accept Hi then
6 7 8 9 10 11 12 13 14 15
16
19 20 21 22
we have pi > ~l > p~. The expected number of correct choices is mpi + n(1-p~) > mz~l + n(1-ni). K. yon Friscb and S. Dijkgraaf, Z. vergl. Physiol. 22, 641 (1935). F. Reinhardt, Z. vergl. Physiol. 22, 570 (1935). R.W. Piddington, J. exp. Biol. 56, 403 (1972). A. Schuijf and R. J. A. Buwalda, J. comp. Physiol. 98, 333 (1975).
H i g h density lipoproteins in i s c h a e m i c h e a r t disease 1 I. C. O n o n o g b u 2
Department o/ Biochemistry, University o/Nigeria, Nsukka (Nigeria), 21 December 1976 Summary. H i g h d e n s i t y l i p o p r o t e i n cholesterol c o n c e n t r a t i o n s were s i g n i f i c a n t l y lower in ischaemic h e a r t disease p a t i e n t s t h a n in h e a l t h y s u b j e c t s w h e n age a n d s e x - m a t c h e d . This difference was, h o w e v e r , n o t o b s e r v e d in t h e older age g r o u p ( > 60 years). I s c h a e m i c h e a r t disease d u e to c o r o n a r y atherosclerosis ( o b s t r u c t i o n of t h e c o r o n a r y a r t e r y as a result of lipid d e p o s i t i o n in t h e a r t e r i a l wall) is a m a j o r w o r l d p r o b l e m a t t h e p r e s e n t t i m e 3, 4. T h e r e are m a n y risk f a c t o r s for i s c h a e m i c h e a r t disease. H y p e r c h o l e s t e r o l a e m i a 5,s a n d h y p e r t r i g l y c e r i d a e m i a ~ are k n o w n to be a s s o c i a t e d w i t h i s c h a e m i c h e a r t disease. T h e role of l i p o p r o t e i n s in t h e aeti01ogy of i s c h a e m i c h e a r t disease has, h o w e v e r , n o t b e e n fully explored. R e c e n t l y it h a s b e e n i n d i c a t e d t h a t h i g h d e n s i t y l i p o p r o t e i n is an a n t i a t h e r o g e n i c a g e n t 8. The m o d e of a c t i o n of h i g h d e n s i t y l i p o p r o t e i n as an a n t i a t h e r o g e n i c a g e n t is not, h o w e v e r , c o m p l e t e l y u n d e r s t o o d . S u g g e s t i o n s h a v e , a t a n y r a t e , b e e n m a d e as to t h e m e a n s b y which high density lipoprotein could act a s a n antia t h e r o g e n i c agent. One of t h e s e ~ believes t h a t h i g h d e n s i t y l i p o p r o t e i n h a s t h e a b i l i t y t o solubilize e x o g e n o u s c h o l e s t e r o l in a d d i t i o n to its o w n c h o l e s t e r o l c o n t e n t , t h u s p r e v e n t i n g i n f l u x of c h o l e s t e r o l i n t o t h e arterial wall. T h e localization of ApoA-1 in a t h e r o s c l e r o t i c lesions 1~ m a y also i n d i c a t e t h a t h i g h d e n s i t y l i p o p r o t e i n has t h e a b i l i t y t o t r a n s p o r t lipids f r o m t h e a r t e r i a l wall to t h e plasma. A n o t h e r m o d e of a c t i o n of h i g h d e n s i t y l i p o p r o t e i n is b e l i e v e d 11 t o be due t o its a b i l i t y to i n h i b i t u p t a k e a n d d e g r a d a t i o n of low d e n s i t y l i p o p r o t e i n , a n d d e p r e s s n e t
i n c r e m e n t in cell sterol c o n t e n t . L o w d e n s i t y l i p o p r o t e i n is t h e m a i n carrier of c h o l e s t e r o l a n d i n h i b i t i o n of its d e g r a d a t i o n m a y p r e v e n t a c c u m u l a t i o n of cholesterol in t h e arterial wall. Material and methods. H e a l t h y subjects. T h e s e were m a d e u p of 99 w h i t e B r i t i s h - b o r n m e n a n d w o m e n b e t w e e n t h e ages of 20 a n d 69 y e a r s living in t h e L o n d o n area. S u b j e c t s were selected on t h e basis of a b s e n c e of clinical or E C G 1
Acknowledgment. This investigation was supported by a grant from University of Nigeria, Nsukka. 2 I am grateful to Prof. Barry Lewis, St. Thomas Hospital Medical School, London, for his expert advice. 3 A. Keys, Atherosclerosis 22, 149 (1975). 4 B. Lewis, Lancet 7, 141 (1974). 5 W.B. Kannel, T. R. Dawber, G. D. Friedman, W. E. Glonnon and P. M. McNamara, Ann. int. Med. 6J, 888 (1964). 6 E. Nikkila and A. Aro, Lancet 7, 954 (1973). 7 L.A. Carlson and L. E. Bottiger, Lancet 1,865 (1972). 8 G.J. Miller and N. E. Miller, Lancet 1, 16 (1975). 9 S.L. Hsia, Y. Chao, C. H. Hennekens and W. B. Reader, Lancet 2, 1000 (1975). 10 H . F . Hoff, C. L. Heideman, R. L. Jackson, R. J. Bayardo, H. Kim and A. M. Gotto, Circulation Res. 37, 72 (1975). 11 T. E. Carew, T. Koschinsky, S. B. Hayes and D. Steinberg, Lancet 7, 1315 (1976).
1064
Specialia
e v i d e n c e of i s c h a e m i c h e a r t disease (IHD) f r o m h i s t o r y or clinical e x a m i n a t i o n . S u b j e c t s were e x c l u d e d on g r o u n d s of cirrhosis, r e n a l failure, clinically e v i d e n t e n d o c r i n e disease, c o n g e s t i v e h e a r t failure a n d m a l i g n a n t disease. I s c h a e m i c h e a r t disease p a t i e n t s . Those were m a d e u p of 50 w h i t e B r i t i s h - b o r n m e n a n d w o m e n (20-69 years) w h o were i s c h a e m i c h e a r t disease p a t i e n t s w h o were a t t e n d i n g t h e c a r d i a c clinic a t H a m m e r s m i t h H o s p i t a l , L o n d o n . F a s t i n g (12-14 h) b l o o d s a m p l e s were collected f r o m t h e 2 g r o u p s of s u b j e c t s . S e r u m w a s s e p a r a t e d b y low s p e e d centrifugation. High density lipoprotein separation by precipitation and cholesterol and triglyceride analyses b y Technicon A u t o a n a l y s e r were d o n e b y t h e m e t h o d s d e s c r i b e d in a n earlier p a p e r x~.
Table 1 HDL cholesterol HDL triglyceride (rag/100 ml) Males Control
n=57
56 -6 12 (mean 4- SD) Ischaemic heart disease n = 35 46 4- 11 T-value 4.01 p-value < 0.001 Females Control n =42 70 4- 22 Ischaemic heart disease n = 15 51 -64-21 T-value 2.99 p-value
