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VEHICLE DYNAMICS AND CONTROL
VEHICLE DYNAMICS AND CONTROL
Advanced Methodologies
SHAHRAM AZADI
Associate Professor, Faculty of Mechanical Engineering,
K.N. Toosi University of Technology, and Vehicle Advanced
Technologies Deputy Manager, Automotive Industries
Research and Innovation Center, Tehran, Iran
REZA KAZEMI
Professor, Faculty of Mechanical Engineering, K.N. Toosi
University of Technology, Tehran, Iran
Notices
Knowledge and best practice in this field are constantly changing. As new research and experience
broaden our understanding, changes in research methods, professional practices, or medical
treatment may become necessary.
Practitioners and researchers must always rely on their own experience and knowledge in evaluating
and using any information, methods, compounds, or experiments described herein. In using such
information or methods they should be mindful of their own safety and the safety of others, including
parties for whom they have a professional responsibility.
To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors, assume
any liability for any injury and/or damage to persons or property as a matter of products liability,
negligence or otherwise, or from any use or operation of any methods, products, instructions, or
ideas contained in the material herein.
Library of Congress Cataloging-in-Publication Data
A catalog record for this book is available from the Library of Congress
British Library Cataloguing-in-Publication Data
A catalogue record for this book is available from the British Library
ISBN: 978-0-323-85659-1
I dedicate this book to my dear wife, Vida, who has always encouraged me in
this way.
Shahram Azadi
This book is dedicated to my dearest wife, Atousa, and my two children,
Kimia and Kiana, who have all been the source of my perseverance.
Reza Kazemi
xi
Foreword
xiii
xiv Foreword
It is hoped that this book will provide a unified and balanced treatment and a
useful perspective on the enterprise of an advanced approach to vehicle
dynamics and control as well as emphasize the common links and connec-
tions that exist between layers of vehicle dynamics and control problems.
The first five chapters are related to passenger car topics, and the other
chapters deal with articulated vehicles.
The main contents are excerpts from many postgraduate theses, books,
and articles that have been compiled from various sources; at the end of each
chapter, a list of references is provided to inform and refer the readers. We
hope the reader enjoys this book and, more importantly, finds this work
educational.
We hope that the sincere efforts of all those involved in preparing this
book will be noticed. Because there is no perfect work, we ask all experts
to help us with their feedback to correct any defects and improve the book’s
quality in future editions. Please feel free to inform us if you spot a typo or
other error. Our email addresses are listed below:
xvii
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CHAPTER 1
1.1 Introduction
Modern vehicles include several control systems responsible for a wide
variety of control tasks. A review of past control systems reveals that the
controller was individually designed and implemented on the vehicle. How-
ever, with modern advancements in electronic systems, remarkable progress
has been made in analyzing, transferring, and transmitting data in the digital
field. Therefore, this industry is witnessing the emergence of novel tech-
niques and ideas in integrating control systems to improve the overall vehicle
performance and optimize costs. Currently, vehicles are equipped with
many control systems, which increases their complexity.
The most commonly presented solution is the use of hierarchical con-
trol structures, in the sense that all control commands are computed using
a single central algorithm, and the key to control integration is the coor-
dination of subsystem performance. According to the definition presented
in [1], the integrated vehicle dynamics control can be considered respon-
sible for combining and coordinating all the control subsystems affecting
the vehicle’s dynamics behavior to improve performance, safety, and com-
fort while reducing costs.
Chassis control systems follow two main objectives: handling and ride
comfort. These systems are divided into active and passive classes. Seat belts
and airbags are common passive systems. Passive systems usually reduce the
damage from accidents, whereas active systems prevent the occurrence of
accidents. On the other hand, active systems primarily avoid some of the
vehicle’s unwanted events, such as wheel locking, traction dissipation, or
excessive changes in the roll and yaw angles, which can result in the loss
of vehicle control by the driver. In other words, in the case of incorrect vehi-
cle behavior, these systems either fully take control of the vehicle or partic-
ipate with the driver in the vehicle’s control until the vehicle behavior is
corrected [2].
In summary, the reasons for the tendency toward integration are the
following:
▪ Diversity of control systems
▪ Diversity in the technology and requirements of each system
▪ Independent performance of these systems
▪ Undesired effects of these systems on each other.
Handling and ride comfort have an inverse relationship, such that an
improvement in one leads to a loss in the other. For example, to improve
vehicle handling, it is preferable to increase the damping ratio and stiffness
of the dampers, which decreases the ride comfort [3]. According to these
discussions and the fact that control systems usually improve only one of
these two parameters, a significant role integration can combine the systems
related to these parameters. Several techniques have been developed to reach
integrated control of the chassis. These techniques can be divided into the
following two groups:
▪ Multivariable control
▪ Hierarchical control.
In this chapter, we used a hierarchical control system. The advantages of
hierarchical control include the following:
▪ Facilitation of designing control subsystems
▪ Control of the complexities by taking them into account in the lower
control layers
▪ Preference for more tasks and workload.
conditions, especially road input. It is worth mentioning that the ride com-
fort is important under normal conditions, and the system must act in such a
way that the passenger does not become tired under normal driving
conditions.
In this chapter, self-tuning regulator (STR) adaptive optimal control is
selected to explain the control structure by introducing the optimal control
strategy and the recursive least squares (RLS) error estimator. The self-
tuning regulator adaptive control strategy is used to design the ESP (elec-
tronic stability program). The algorithm used to design the ABS is simple
and consists of several logical conditions. Moreover, an optimal control
strategy has been used to design the ASS. Finally, the integration algorithm
utilized will be introduced.
Adaptive control is defined as a control scheme with adjustable param-
eters and a mechanism for adapting the parameters. The reasons for using this
strategy include the following:
▪ Changes in the process dynamics
▪ Changes in the properties of the system disturbance
▪ Engineering efficiency and simplicity of use
▪ Various adaptive control ideas
▪ Gain scheduling.
In the STR structure, the controller is updated by estimating the parameters.
The self-tuning in this controller means that the controller parameters are
tuned automatically to attain the desired state; see Fig. 1.2 [5].
In the STR method, we update the structure of the controller, but we
also update the desired state in the design of the ESP. The STR method will
4 Vehicle dynamics and control
assist the optimal control method in the proposed algorithm. The RLS
method has been employed to estimate the system parameters. The combi-
nation of these two methods will provide us with a self-tuning adaptive
controller that updates in each step with changes in the system parameters.
As will be discussed, significant and wide changes in the lateral stiffness
of the tires make it impossible to obtain the desired results using only
optimal control. Because changes in the parameters affecting the system
vibrations are slight, the LQR control strategy is used alone in the design
of the ASS.
2 3 2 C 3
Cαr + Cαf Cαr lr + Cαf lf
v " # αf
6 x7 0
A¼6
m v m v 7 1 ,E ¼ 4 t 7
6 m
4 Cαr lr + Cαf lf Cαr lr 2 + Cαf lf 2 5, B ¼ Cαf lf 5 (1.3)
t x t x
Izz
Izz vx Izz vx Izz
where Cαf and Cαr are the turning constants of the front and rear tires,
respectively. To this end, we use the bicycle model in the form of Eq. (1.4);
8 1
>
< ay ¼ m Fyf + Fyr
>
t
(1.4)
>
> 1
: r_ ¼ Fy lf Fyr lr + Mz
Izz f
In Eq. (1.4), the values of ay and r_ are readily determined using the exist-
ing sensors. Moreover, Mz is the output of this system. As mentioned before,
Fyf and Fyr are the parameters that must be estimated. The last equation can
be written in the form of Eqs. (1.5) and (1.6) to use the RLS method.
2 3
ay
yðtÞ ¼ 4 Mz 5 (1.5)
r_
Izz
F
θðt Þ ¼ yf (1.6)
Fyr
After determining the lateral forces and obtaining the slip angle values
from the above relationships, the lateral stiffness values can be determined.
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Horse 0·2 lb. per 100 lb. live weight.
Ass and Mule 0·16 lb. „„
Cow and Sheep 1·0 lb. „„
Goat 1·2 lb. „„
Pig 0·3 lb. „„
Rabbit 2·0 lb. „„
In the leaves of the male common Yew Moss found 0·082 per
cent. of Taxine, or less than one-half the quantity found by Thorpe
and Stubbs.
Symptoms. The Yew is irritant and narcotic, and the poison is not
cumulative, but on the other hand rapidly effective, so that animals
may die apparently suddenly, no previous symptoms having been
observed.
When small quantities only have been taken the closest attention
is necessary to discern the symptoms, which simply consist in a little
excitement with a slight rise in temperature.
With larger (but not fatal) quantities the first symptom,
excitement, is more pronounced and is followed by nausea, and
(where possible) vomiting. There is a pronounced slackening of
respiration and circulation, the pulse being small, slow, and difficult
to perceive, and the movement of the flanks very slow; sensibility is
diminished. There is a fall in temperature, the skin and extremities
being cold. The head is lowered, the eyes are closed and there is
decubitus. In some cases pregnant animals have aborted. In the
horse there are muscular tremors and frequent urination. In cattle
and sheep rumination is suspended and there is more or less
pronounced tympanites, with eructation, nausea, and sometimes
vomiting. Pigs bury the head in the litter and sleep, their sleep being
interrupted from time to time by nausea and groaning; or the
animals rise, stagger about, and lie down again.
With fatal quantities the foregoing symptoms may be followed by
coma, with death in two hours or more after the poisoning, but more
generally and usually in horses, asses, and mules (but also in cattle)
there is no period of coma, the excitement is less pronounced and
often unobserved, and death appears very sudden. The animals
stop, shake their heads, respiration is modified, there is falling, and
death (sometimes with convulsions) results from cessation of the
heart’s action (Cornevin).
The symptoms given by Müller are roaring, torpidity, stupefaction,
laboured breathing, convulsions and death in from ten minutes to an
hour in the worst cases; or where the course of poisoning is slower,
there is salivation, nausea, vomiting, bloating, retardation of pulse
and respiration, great giddiness and stupefaction, diabetes and
hæmaturia.
The rapidity of the poisoning is confirmed by cases noted in the
veterinary journals. Lander shows that the effects often only appear
in cattle when chewing the cud; whilst quietly chewing, they drop as
if shot. In some examples the animal died while eating the plant, or
was found to have fallen and died suddenly and without evidence of
a struggle. The animal in some cases will stop suddenly whilst
working, start blowing and trembling, stagger, fall on its haunches,
then on its side, and die quietly. Death occurs in about five minutes
with symptoms resembling apoplexy. A colt died after 16 or 17
hours; the plant was taken on a full stomach, but paralysis of the
alimentary system with stoppage of digestion immediately ensued.
In the case of pheasants there was acute inflammation of the
small intestines (Tegetmeier).
REFERENCES.
4, 16, 49, 73, 81, 84, 100, 128, 130, 141, 144, 161,
170, 189, 190, 205, 213, 239, 240, 256.
AROIDEÆ.
Cuckoo Pint (Arum maculatum L.). The well-known Cuckoo Pint,
or Lords and Ladies, is to be regarded as highly poisonous, and
children have died from eating the berries. Animals have
exceptionally eaten the plant, but no record of death has been
found, as it does not appear to be taken in sufficient quantity.
Cornevin records that pigs have eaten the roots, and suffered in
consequence, though the results were not fatal. All parts of the plant
are poisonous, though the virulence is lost on drying. The plant is
acrid, and emits a disagreeable smell when bruised. In Gerarde’s
Herball the following passage occurs: “The most pure and white
starch is made from the rootes of the Cuckowpint; but most hurtfull
for the hands of the laundresse that hath the handling of it, for it
choppeth, blistereth, and maketh the hands rough and rugged, and
withall smarting.” In Dorset the tuber-like corms have been
macerated in water, dried and powdered, and eaten under the name
Portland Sago or Portland Arrowroot, the poisonous property being
dissipated.
Toxic Principle. The Cuckoo Pint does not seem to have received
much attention in this connection, but the poisonous principle is
believed to be a Saponin.
Symptoms. The juice acts as an irritant when in contact with the
mucous membrane. When a pig has eaten several roots rich in sap,
the mouth and tongue redden and tumefy, there is salivation, and
swallowing is difficult on account of the inflammation at the back of
the mouth. Introduced in small quantity into the digestive tract it
acts as an irritant and purgative, and sometimes causes vomiting.
Severe intestinal pains, excitement, some muscular contraction of
the limbs, rocking of the head, and superpurgation with tenesmus
are also symptoms which have been observed. The intestinal pains
continue for some days and the appetite is small. Cornevin states
that animals never take a sufficient quantity to cause fatal poisoning,
but according to Lander, if a dangerous quantity is taken,
convulsions, exhaustion, and death from shock may possibly follow
the foregoing symptoms.
A case in which a horse was poisoned through a wound being
washed with a decoction of arum leaves is cited by Müller. There was
much local swelling, trembling, and rapid breathing, and the heart
beat strongly; the animal died on the third day.
REFERENCES.
73, 190.
LILIACEÆ.
Herb Paris (Paris quadrifolia L.). Owing to its habitat—damp
woods—it is unlikely that stock will eat this plant, but it may be
possible where fields border open woods in which it grows. No
records of stock poisoning have been met with, but cases of
poisoning in man are recorded, one due to eating a considerable
number (30 to 40) of the berries, and symptoms of poisoning in a
child four years of age who had eaten a few berries. In smaller
quantities they are very poisonous to poultry. All parts are stated to
be poisonous, especially the berries. Fatal poisonings are nil, or very
rare if recorded.
Toxic Principle. Walz isolated the glucoside Paridin; and Esser
states that the toxic property is due to a Saponin,—the bitter irritant
glucoside Paristyphnin (C38H64O18), which is convertible into Paridin
(C16H28O7 + 2H2O) and sugar.
Symptoms. The plant is emetic, purgative, intensely acrid, and
narcotic. Poisoning up to the present only appears to have been
recorded in fowls, the symptoms being intense local inflammation,
narcotic effects, vomiting, colic, diarrhœa, stupefaction, convulsions,
and paralysis (Müller).
REFERENCES.
Its effect when mixed with flour was also referred to by Gerarde
(1597): “The new bread wherein Darnell is, eaten hot, causeth
drunkenness; in like manner doth beere or ale wherein the seede is
fallen, or put into the mault.”
Before the seeding stage is reached Darnel seems to be quite
suitable as a food for stock, only the seed or grain being poisonous,
and this not invariably so. The chief danger perhaps is that the grain
may not be thoroughly removed from cereal grains, and may thus
find its way into bread or cereal stock foods. Though it has caused
many cases of human poisoning, fatal results seem to be rare: Dr.
Taylor could record no fatal case up to 1859. Darnel mixed with
barley caused the poisoning of pigs (Veterinarian, 1842). Johnson
and Sowerby (1861) state that Darnel has in several cases proved
fatal to horses and sheep. The same authorities quote a case in
which 80 inmates of Sheffield Workhouse were attacked by violent
vomiting and purging from the use of oatmeal containing Darnel. At
the Veterinary School at Lyons a horse was killed by giving it 2
kilogrammes (4·4 lb.) of Darnel. Cornevin concluded that the
amounts of Darnel necessary to kill certain animals would be as
follows:—
4, 16, 73, 81, 106, 128, 130, 141, 190, 203, 204,
205, 213, 233, 235, 254.
EQUISETACEÆ.
Horsetails (Equisetum sp.). A very great deal has been written
on the subject of Equisetosis or Equisetum poisoning, and even at
the present day opinion is divided as to which species are poisonous
and to what extent. From the time of Linnæus there has been
uncertainty as to the species, which has generally been given as E.
arvense. Two German papers, by Weber and Lohmann respectively,
published by the German Agricultural Society in 1903 and 1904,
have done much to remove doubt on the matter, but cannot be said
to have settled the question absolutely. These two papers seem to
have been overlooked by some recent writers on the subject, but
Lohmann’s appears to be the most authoritative paper yet written.
Both are referred to below.
It seems to be definitely proved that certain species of Equisetum
really are poisonous, hesitating statements notwithstanding. Chesnut
and Wilcox state that there are cases of poisoning of both horses
and sheep by E. arvense in the United States, though they are not
common, and the opinion is expressed that “the plant, if deleterious,
is evidently so only on account of its harsh scouring action in the
mouth and intestinal tract.” On the other hand Rich and Jones record
poisoning of horses by E. arvense in hay, but while adding that
horses seem to develop a depraved appetite for the weed, they state
that they have no evidence that horses grazing upon the green plant
are poisoned. Güssow’s experience has been that cattle do not suffer
any inconvenience at all from this species, or only very slight
disturbance of the digestive organs, but that horses are
conspicuously subject to fatal poisoning by it. Examination of hay on
which a considerable number of poisoned horses were fed revealed
in every case the presence of E. arvense. When the food was
changed, horses, if not too seriously affected, made rapid recovery.
(Treatment suggested is to change to easily digested food, give a
sharp purgative, and follow by small doses of nux vomica three
times a day.) Pammel says that in recent years a disease of horses in
Vermont has been attributed to hay and fodder containing the weed;
that it is proved by experiment that when ingested in sufficient
quantity E. arvense is capable of causing fatal poisoning in horses,
and is at times the cause of extensive losses; and that young horses
are most susceptible, while grain-fed horses are less susceptible
than others. He adds that sheep are supposed to be slightly
affected, but cattle eat hay in which it occurs in large proportion
with impunity.
Coming to the two German reports, it is stated by Weber (1903)
that E. palustre contains a specific poison for cattle and other
ruminants, but sheep and goats are able, owing to their fine
muzzles, to separate it in fodder, and hence suffer less. Horses and
pigs, he says, seem to suffer very little. Young animals and stock,
from districts where the species does not occur, suffer more than
those from places where it occurs—the latter appearing to learn
early to avoid it.
Lohmann conducted feeding experiments with guinea-pigs with E.
arvense, E. palustre, E. pratense, E. sylvaticum, E. maximum, and E.
heleocharis (not British). He also fed E. arvense and E. palustre to
horses, cattle, sheep, pigs, and geese in considerable quantities for
many days on end; and made experiments with aconitic acid on
guinea-pigs and horses. The feeding experiments with guinea-pigs
showed that of the species named only E. palustre and to a less
extent E. sylvaticum are poisonous plants (to guinea-pigs). With the
large domestic animals the experiments showed E. arvense to be a
harmless plant, and E. palustre to be really injurious to cattle but
avoided by other stock. Lohmann considers that the many
statements in the literature agree in part with this result, and that
the divergent observations may be traced to various causes, among
which perhaps an abnormal chemical composition of the weed fed
plays a principal part.
In this connection, however, the American results must be
carefully borne in mind, and E. arvense must not too hastily be
regarded as blameless.
Toxic Principle. It was for some years believed that the apparent
toxic symptoms induced by Horsetails were due to Silica or to
Aconitic acid—the latter a substance found by Matz and Ludwig. The
conclusion come to by Weber, however, was that the poisoning by E.
palustre is of an organic character, not due to silica. The young
shoots, which contain little silica, were found in general to be much
more poisonous than the old plants, which contain much silica. It
was long since found by Wiggers that dried plants of E. palustre
contained 8·88 per cent. of silica, but all species contain this
substance in greater or less degree, and it varies considerably in
amount, even in the same species. The feeding experiments
conducted by Lohmann, with certain species of Equisetum, and the
observed symptoms of illness after the consumption of some of
them, particularly E. palustre, serve to show that the ill effects are
neither to be attributed to greater or less digestibility, nor to the
silica present. Neither are the aconitic acid and other organic
substances, in part found in previous investigations, responsible for
the poisoning. However, an active compound named Equisetine, a
substance belonging to the alkaloid group, was isolated; this occurs
usually, perhaps only, in E. palustre, at any rate in sufficient quantity
to be dangerous to animals. Lohmann then, following up the
investigations of Paucerzynski, Matz, Meyer, Weber and others,
ascertained definitely that E. palustre contains an alkaloidal nerve
poison, to which the name Equisetine was given, and the
experiments were held to decide that this is the poisonous substance
in this species. (As stated above, E. arvense was held to be
harmless.)
Symptoms. At first, excitement and anxiety, followed by
uncertainty of movement, reeling and staggering; paralysis of hind
limbs at least, falling, possibly general paralysis, insensibility to
external irritants, unconsciousness, and coma. Pulse accelerated,
appetite at first normal, but in course of time great disturbance of
nutrition; sugar in the urine. Course sometimes very acute, death
occurring in a few hours, but sometimes protracted (two to eight
days), and at times even chronic (one to several weeks).
In cattle, after excessive eating, continuous diarrhœa is
characteristic, with paralysis; while, if the food be persisted with,
cachexia and hydræmia combined with weakness bordering on
paralysis make their appearance (Friedberger and Fröhner, via
Pammel). In addition to cachexia, Pott also mentions colic, stoppage,
bloody urination, abortion, and loss of teeth.
Young animals appear to succumb sooner than older ones, while
grain-fed animals are more resistant than others. Referring to E.
arvense Pammel says it produces paralysis of the rear extremities,
and when death occurs spasms are noted. In relation to the
poisoning of horses by the same species in hay Rich and Jones note
unthriftiness, the animal appearing thin and the muscles wasted. In
from two to five weeks, according to the age of the horse and the
manner of feeding, the animal begins to lose control of the muscles,
and there is swaying and staggering, though the eye is bright and
the appetite good. If the plant is regularly ingested the horse loses
the power of standing, becomes nervous, struggles to rise, the legs
become more or less rigid, and at times all the muscles of the body
seem convulsed. Even in this condition one well-nursed patient lived
two weeks. The horses are generally willing to eat, although unable
to rise, but become sore and tired from struggling, finally dying from
exhaustion. Life is much prolonged by turning from side to side three
or four times in twenty-four hours, thus preventing congestion. The
pulse is slow till near the end, when it is rapid and weak; the
temperature is below normal at first, but when the animal is down
there is fever; the extremities are usually cold; and the lining
membrane of the mouth, nose, and eye becomes pale.
Of Equisetum sp. Stebler and Schroeter say that they induce
diarrhœa in cattle, which become poor, and in cows the milk yield is
checked or ceases. Weber also refers to the effect on milk yield of E.
palustre, which he says causes the milk of affected cows to become
watery, poor in fat, and gives rise to a greasy, unappetising butter,
while the yield may soon quite fail.
REFERENCES.
2, 20, 57, 111, 176, 203, 204, 213, 220, 221, 222, 237, 260, 261.
FILICES.
Bracken (Pteris aquilina L.). The Bracken, Brake Fern, or “Fern” is
of very considerable importance to farmers for four reasons: (1) It is
a most pernicious weed; (2) it forms an excellent litter for stock and
treads down into good manure; (3) it is said to have been
successfully converted into silage; but (4) it has been accused of
poisoning cattle.
In regard to possible poisonous properties, it must be said that the
facts are at present somewhat uncertain, but a number of
authorities clearly regard the Bracken as poisonous. (a) Müller
(1897) records the poisoning of horses which ate it for some weeks
with chaff—and some died. (b) Chesnut and Wilcox (1901) say that
cases of poisoning of horses and cattle have been reported from
England and a few localities in the United States. (c) Pott states that
when eaten in quantity by cattle Bracken causes hæmaturia, and in
horses nervous symptoms (brain trouble), sometimes with fatal
effects. (d) Pammel also remarks on the believed poisonous
character of this plant. (e) In view of its suspected poisonous
character feeding experiments were conducted by the Board of
Agriculture and Fisheries with a large quantity of Bracken, but the
results were negative, yielding no experimental proof of the plant
being poisonous. One animal—a heifer—consumed 60 lb. of Bracken
between Aug. 14 and Aug. 20, and after two meals containing about
30 lb. of Bracken showed only symptoms of indigestion. After the 60
lb. there were no symptoms of illness. It has been thought possible
that the so-called Bracken poisoning is due to Potentilla Tormentilla
(q.v.).
In 1893 Storrar dealt with the question and expressed the view
that any disorder due to Bracken was probably not a toxic effect but
a digestive trouble simply (Jour. Comp. Path., 1893).
Toxic Principle. Continental authorities say that Bracken contains
the poisonous Pteritannic acid, which is identical with the Filicic acid
of the Male Fern (Aspidium filix-mas).
Symptoms. In the cases of horses which died Müller gives the
symptoms as timidity, slower movement or action, loss of balance,
dilated pupils, reddening followed by yellowing of the conjunctivæ,
and slowing of the pulse.
Pammel notes Bracken as an astringent and anthelmintic, and also
says it causes enteritis, spasms, and paralysis.
REFERENCES.
1, 4, 13, 16, 35, 57, 81, 82, 128, 154, 161, 203, 242, 251.
CHAPTER VII
PLANTS SUSPECTED OF BEING POISONOUS.
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