You'll never sail among the Islands of Langerhans or drift lazily down the aqueduct of Sylvius. And don't expect to stroll along the banks of Hunter's Canal, or watch the sun go down behind McBurney's point, explore the Fissure of Rolando or ride through the Tunnel of Corti. You'll never trundle the Bundle of Vicq d' Azyr, or pillow your head no Passavant's Cushion, or vacation in Wernicke's Centre. Nor will you wall under the Palmar Arch, or Loop the Loop of Henle. And you may travel the whole world over and never gaze down upon Pacchionian depression or stand in the shadow of the Pyramids of Malpighi. Because - they are parts of the human body!!!!

Iron is critical to a number of
synthetic and enzymatic
processes. Most of the body iron
is part of the hemoglobin
molecule where iron serves a key
role in oxygen transport. Iron is
recycled and thus conserved by
the body. Daily intake ( 1 mg ) s
balanced against small daily
losses (1 mg ).
The amounts shown in the Fe
Cycle Card are in mg of iron lost
or gained per day. They were
derived in the following manner.
The average blood volume in a
70 kg man is 5,000 ml.
There are 150 grams of
hemoglobin in each liter of
blood, therefore there are 750 g
of hemoglobin in the body.
Each gram of hemoglobin
contains approximately 3.3 mg of
iron or 2475 mg of iron in the
body.
Dividing the 2475 mg total by the
120 day average RBC lifespan
results in the iron needed per
day or 20.6 mg iron/day.
Hemoglobin Fe 2200 mg
Ferritin & Hemosiderin 1000 mg
Myoglobin Fe 300 mg
Other Fe (cytochromes; enzymes) 100 mg
Total Body Iron 3600 mg
An average adult in the U.S. on a
2,500 calorie diet ( 6 mg of
iron/1,000 kcal) ingests 15 mg of
iron daily. Only 5-10 % or about
1.0 mg of dietary iron is
absorbed as ferrous iron (Fe++),
mainly in the duodenum and
upper jejunum where the pH is
low. The mucosal cells oxidize the
ferrous iron to ferric iron
, which is then
complexed with apoferritin to
form ferritin. Some of the ferritin
is transported out of the mucosal
cell into the plasma bound to
transferrin. Thus bound, iron can
be transported to the bone
marrow or iron storage sites
where it is stored as either
ferritin or hemosiderin.

Most cells have transferrin
receptors (CD 71) to which iron
ladden transferrin binds. The
receptor-transferrin-iron
complex is then incorporated
into the cytosol by endocytosis.
In red cells the endocytotic
vacuole fuses with a lysozyme,
where at an acid pH the iron (Fe+
+) is released from transferrin
and transported to mitochondria
where it is incorporated into
heme, the ferrous iron complex
of protoporphyrin IX.
Fe
Although iron is utilized in
virtually all cells, the bulk of body
iron is found in erythrocytes with
lesser amounts in myoglobin.
Large amounts of iron are
required during growth periods
in infant, childhood and teenage
years.
Transferrin carries iron to the
bone marrow where it is
accepted into RBCs via a
transferrin receptor (CD71) and
incorporated into heme for use
in hemoglobin.
Not all erythrocytes develop and
mature successfully. Some die in
the marrow and their iron is
salvaged by macrophages. This
failure to mature resulting in
death in the marrow is known as
ineffective erythropoiesis.

Normally only small amounts of
iron are lost daily as hair, skin,
urinary bladder,and
gastrointestinal cells are shed.
This amount can easily be
replaced by dietary intake.
With bleeding, larger amounts of
iron can be lost. The most
common normal blood losses are
due to menstruation and
pregnancy.

Glucose is by far the most
common carbohydrate and classified as a monosaccharide,
an aldose, a hexose, and is a reducing sugar. It is also known
as dextrose, because it is dextrorotatory (meaning that as
an optical isomer is rotates plane
polarized light to the right and also an origin for the D
designation. Glucose is also called blood sugar as it circulates in the blood at a
concentration of 65-110 mg/mL of blood.
Glucose is initially synthesized by chlorophyll in plants using carbon dioxide from the air and
sunlight as an energy source. Glucose is further converted to
starch for storage.

Ring Structure for Glucose:

Up until now we have been
presenting the structure of
glucose as a chain. In reality, an
aqueous sugar solution contains
only 0.02% of the glucose in the
chain form, the majority of the
structure is in the cyclic chair
form.
Since carbohydrates contain both
alcohol and aldehyde or ketone
functional groups, the straight-
chain form is easily converted
into the chair form - hemiacetal
ring structure. Due to the
tetrahedral geometry of carbons
that ultimately make a 6
membered stable ring , the -OH
on carbon #5 is converted into
the ether linkage to close the
ring with carbon #1. This makes
a 6 member ring - five carbons
and one oxygen.
Steps in the ring closure
(hemiacetal synthesis):
1. The electrons on the alcohol
oxygen are used to bond the
carbon #1 to make an ether (red
oxygen atom).
2. The hydrogen (green) is
transferred to the carbonyl
oxygen (green) to make a new
alcohol group (green).
The chair structures are always
written with the orientation
depicted on the left to avoid
confusion.
Hemiacetal Functional Group:
Carbon # 1 is now called the
anomeric carbon and is the
center of a hemiacetal functional
group. A carbon that has both an
ether oxygen and an alcohol
group is a hemiacetal.

Glucose in the Chair Structures:

The position of the -OH group on
the anomeric carbon (#1) is an important distinction for carbohydrate chemistry. The Beta position is defined as
the -OH being on the same side of the ring as the C # 6. In the
chair structure this results in a horizontal projection.
The Alpha position is defined as the -OH being on the opposite
side of the ring as the C # 6. In the chair structure this results in a downward projection.
The alpha and beta label is not
applied to any other carbon -
only the anomeric carbon, in this
case # 1.

As the heart undergoes
depolarization and
repolarization, electrical currents
spread throughout the body
because the body acts as a
volume conductor. The electrical
currents generated by the heart
are commonly measured by an
array of electrodes placed on the
body surface and the resulting
tracing is called an
electrocardiogram (ECG, or EKG).
By convention, electrodes are
placed on each arm and leg, and
six electrodes are placed at
defined locations on the chest.
These electrode leads are
connected to a device that
measures potential differences
between selected electrodes to
produce thecharacteristic ECG
tracings.
Some of the ECG leads are bipolar
leads (e.g., standard limb leads)
that utilize a single positive and a
single negative electrode
between which electrical
potentials are measured.
Unipolar leads (augmented leads
and chest leads) have a single
positive recording electrode and
utilize a combination of the other
electrodes to serve as a
composite negative electrode.
Normally, when an ECG is
recorded, all leads are recorded
simultaneously, giving rise to
what is called a 12-lead ECG.

General Description
As the heart undergoes
depolarization and
repolarization , the electrical
currents that are generated
spread not only within the heart,
but also throughout the body.
This electrical activity generated
by the heart can be measured by
an array of electrodes placed on
the body surface. The recorded
tracing is called an
electrocardiogram (ECG, or EKG).
A "typical" ECG tracing is shown
to the right. The different waves
that comprise the ECG represent
the sequence of depolarization
and repolarization of the atria
and ventricles. The ECG is
recorded at a speed of 25 mm/
sec, and the voltages are
calibrated so that 1 mV = 10 mm
in the vertical direction.
Therefore, each small 1-mm
square represents 0.04 sec (40
msec) in time and 0.1 mV in
voltage. Because the recording
speed is standardized, one can
calculate the heart rate from the
intervals between different
waves.
P wave
The P wave represents the wave
of depolarization that spreads
from the SA node throughout the
atria, and is usually 0.08 to 0.1
seconds (80-100 ms) in
duration. The brief isoelectric
(zero voltage) period after the P
wave represents the time in
which the impulse is traveling
within the AV node (where the
conduction velocity is greatly
retarded) and the bundle of
His. Atrial rate can be calculated
by determining the time interval
between P waves. Click here to
see how atrial rate is calculated.
The period of time from the
onset of the P wave to the
beginning of the QRS complex is
termed the P-R interval, which
normally ranges from 0.12 to
0.20 seconds in duration. This
interval represents the time
between the onset of atrial
depolarization and the onset of
ventricular depolarization. If the
P-R interval is >0.2 sec, there is
an AV conduction block, which is
also termed a first-degree heart
block if the impulse is still able to
be conducted into the ventricles.
QRS complex
The QRS complex represents
ventricular
depolarization. Ventricular rate
can be calculated by determining
the time interval between QRS
complexes. Click here to see how
ventricular rate is calculated.
The duration of the QRS complex
is normally 0.06 to 0.1 seconds.
This relatively short duration
indicates that ventricular
depolarization normally occurs
very rapidly. If the QRS complex
is prolonged (> 0.1 sec),
conduction is impaired within
the ventricles. This can occur
with bundle branch blocks or
whenever a ventricular foci
(abnormal pacemaker site)
becomes the pacemaker driving
the ventricle. Such an ectopic foci
nearly always results in impulses
being conducted over slower
pathways within the heart,
thereby increasing the time for
depolarization and the duration
of the QRS complex.
The shape of the QRS complex in
the above figure is idealized. In
fact, the shape changes
depending on which recording
electrodes are being used. The
shape will also change when
there is abnormal conduction of
electrical impulses within the
ventricles. The figure to the right
summarizes the nomenclature
used to define the different
components of the QRS complex.
ST segment
The isoelectric period (ST
segment) following the QRS is
the time at which the entire
ventricle is depolarized and
roughly corresponds to the
plateau phase of the ventricular
action potential. The ST segment
is important in the diagnosis of
ventricular ischemia or hypoxia
because under those conditions,
the ST segment can become
either depressed or elevated.
T wave
The T wave represents
ventricular repolarization and is
longer in duration than
depolarization (i.e., conduction of
the repolarization wave is slower
than the wave of
depolarization). Sometimes a
small positive U wave may be
seen following the T wave (not
shown in figure at top of page).
This wave represents the last
remnants of ventricular
repolarization. Inverted or
prominent U waves indicates
underlying pathology or
conditions affecting
repolarization.
Q-T interval
The Q-T interval represents the
time for both ventricular
depolarization and repolarization
to occur, and therefore roughly
estimates the duration of an
average ventricular action
potential. This interval can range
from 0.2 to 0.4 seconds
depending upon heart rate. At
high heart rates, ventricular
action potentials shorten in
duration, which decreases the Q-
T interval. Because prolonged Q-
T intervals can be diagnostic for
susceptibility to certain types of
tachyarrhythmias, it is important
to determine if a given Q-T
interval is excessively long. In
practice, the Q-T interval is
expressed as a "corrected Q-T
( QTc)" by taking the Q-T interval
and dividing it by the square root
of the R-R interval (interval
between ventricular
depolarizations). This allows an
assessment of the Q-T interval
that is independent of heart
rate. Normal corrected Q-Tc
intervals are less than 0.44
seconds.
There is no distinctly visible wave
representing atrial repolarization
in the ECG because it occurs
during ventricular
depolarization. Because the
wave of atrial repolarization is
relatively small in amplitude (i.e.,
has low voltage), it is masked by
the much larger ventricular-
generated QRS complex.
ECG tracings recorded
simultaneous from different
electrodes placed on the body
produce different characteristic
waveforms.

Donnan equilibrium (which can
also be referred to as the Gibbs-
Donnan equilibrium) describes
the equilibrium that exists
between two solutions that are
separated by a membrane. The
membrane is constructed such
that it allows the passage of
certain charged components
(ions) of the solutions. The
membrane, however, does not
allow the passage of all the ions
present in the solutions and is
thus a selectively permeable
membrane.
Donnan equilibrium is named
after Frederick George Donnan ,
who proved its existence in
biological cells. J. Willard Gibbs
had predicted the effect some 30
years before.
The impermeability of the
membrane is typically related to
the size of the particular ion. An
ion can be too large to pass
through the pores of the
membrane to the other side. The
concentration of those ions that
can pass freely though the
membrane is the same on both
sides of the membrane. As well,
the total number of charged
molecules on either side of the
membrane is equal.
A consequence of the selective
permeability of the membrane
barrier is the development of an
electrical potential between the
two sides of the membrane. The
two solutions vary in osmotic
pressure, with one solution
having more of a certain type
(species) or types of ion that
does the other solution.
As a result, the passage of some
ions across the membrane will
be promoted. In bacteria , for
example, the passage of
potassium across the outer
membrane of Gram-negative
bacteria occurs as a result of an
established Donnan equilibrium
between the external
environment and the periplasm
of the bacterium. The potassium
enters in an attempt to balance
the large amount of negative ion
inside the cell. Since potassium is
freely permeable, it will tend to
diffuse out again. The inward
movement of sodium corrects
the imbalance. In the absence of
a Donnan equilibrium, the bulky
sodium molecule would not
normally tend to move across the
membrane and an electrical
potential would be created.

Various intrinsic, neural, and
hormonal factors act to influence
the rhythm control and impulse
conduction within the heart. The
rhythmic control of the cardiac
cycle and its accompanying
heartbeat relies on the regulation
of impulses generated and
conducted within the heart.
Regulation of the cardiac cycle is
also achieved via the autonomic
nervous system. The sympathetic
and parasympathetic divisions of
the autonomic system regulate
heart rhythm by affecting the
same intrinsic impulse
conducting mechanisms that lie
within the heart in opposing
ways.
Cardiac muscle is self-contractile
because it is capable of
generating a spontaneous
electrochemical signal as it
contracts. This signal induces
surrounding cardiac muscle
tissue to contract and a wave-
like contraction of the heart can
result from the initial contraction
of a few localized cardiac cells.
The cardiac cycle describes the
normal rhythmic series of cardiac
muscular contractions. The
cardiac cycle can be subdivided
into the systolic and diastolic
phases. Systole occurs when the
ventricles of the heart contract
and diastole occurs between
ventricular contractions when
the right and left ventricles relax
and fill. The sinoatrial node (S-A
node) and atrioventricular node
(AV node) of the heart act as
pacemakers of the cardiac cycle.
The contractile systolic phase
begins with a localized
contraction of specialized cardiac
muscle fibers within the sino-
atrial node. The S-A node is
composed of nodal tissue that
contains a mixture of muscle and
neural cell properties. The
contraction of these fibers
generates an electrical signal that
then propagates throughout the
surrounding cardiac muscle
tissue. In a contractile wave
originating at the S-A node, the
right atrium muscle contracts
(forcing blood into the right
ventricle) and then the left atrium
contracts (forcing blood into the
left ventricle).
Intrinsic regulation is achieved
by delaying the contractile signal
at the atrioventricular node. This
delay also allows the complete
contraction of the atria so that
the ventricles receive the
minimum amount of blood to
make their own contractions
efficient. A specialized type of
neuro-muscular cells, named
Purkinje cells, form a system of
fibers that covers the heart and
which conveys the contractile
signal from S-A node (which is
also a part of the Purkinje system
or subendocardial plexus).
Because the Purkinje fibers are
slower in passing electrical
signals (action potentials) than
are neural fibers, the delay allows
the atria to finish their
contractions prior to ventricular
contractions. The signal delay by
the AV node lasts about a tenth
(0.1) of a second.
The contractile signal then
continues to spread across the
ventricles via the Purkinje system.
The signal travels away from the
AV node via the bundle of His
before it divides into left and
right bundle branches that travel
down their respective ventricles.
Extrinsic control of the heart rate
and rhythm is achieved via
autonomic nervous system (ANS)
impulses (regulated by the
medulla oblongata) and specific
hormones that alter the
contractile and or conductive
properties of heart muscle. ANS
sympathetic stimulation via the
cervical sympathetic chain
ganglia acts to increase heart
rate and increase the force of
atrial and ventricular
contractions. In contrast,
parasympathetic stimulation via
the vagal nerve slows the heart
rate and decreases the vigor of
atrial and ventricular
contractions. Sympathetic
stimulation also increases the
conduction velocity of cardiac
muscle fibers. Parasympathetic
stimulation decreases
conduction velocity.
The regulation in impulse
conduction results from the fact
that parasympathetic fibers
utilize acetylcholine, a
neurotransmitter hormone that
alters the transmission of an
action potential by altering
membrane permeability to
specific ions (e.g., potassium ions
[K+]). In contrast, sympathetic
postganglionic neurons secrete
the neurotransmitter
norepinephrine that alters
membrane permeability to
sodium (Na+) and calcium ions
(Ca2+).
The ion permeability changes
result in parasympathetic
induced hypopolarization and
sympathetic induced
hyperpolarization.
Additional hormonal control is
achieved principally by the
adrenal glands (specifically the
adrenal medulla) that release
both epinephrine and
norepinephrine into the blood
when stimulated by the
sympathetic nervous system. As
part of the fight or flight reflex,
these hormones increase heart
rate and the volume of blood
ejected during the cardiac cycle.
The electrical events associated
with the cardiac cycle are
measured with an
electrocardiogram (EKG).
Disruptions in the impulse
conduction system of the heart
result in arrhythmias.
Variations in the electrical system
can lead to serious, even
dangerous, consequences. When
that occurs an artificial electrical
stimulator, called a pacemaker,
must be implanted to take over
regulation of the heartbeat. The
small pacemaker can be
implanted under the skin near
the shoulder and long wires
from it are fed into the heart and
implanted in the heart muscle.
The pacemaker can be regulated
for the number of heartbeats it
will stimulate per minute. Newer
pacemakers can detect the need
for increased heart rate when
the individual is under exertion
or stress and will respond.

Enzyme catalysis is a topic of
fundamental importance in
organic, bio-organic and
medicinal chemistry. This new
edition of a very popular
textbook provides a concise
introduction to the underlying
principles and mechanisms of
enzyme and coenzyme action
from a chemical perspective.
Whilst retaining the overall
structure of the first edition –
preliminary chapters describe the
basic principles of enzyme
structure and catalysis moving
through to detailed discussions
of the major classes of enzyme
processes in the later chapters –
the book has been thoroughly
updated to include information
on the most recent advances in
our understanding of enzyme
action. A major feature of the
second edition is the inclusion of
two-colour figures of the active
sites of enzymes discussed in the
text, in order to illustrate the
interplay between enzyme
structure and function. Problems,
with outline answers, at the end
of each chapter give the student
the chance to the check their
understanding of the material.
As a concise but comprehensive
account, Introduction to Enzyme
and Coenzyme Chemistry will
continue to prove invaluable to
both undergraduate and
postgraduate students of
organic, bio-organic and
medicinal chemistry.

Universities in Bangladesh
Bangladeshi universities are
mainly categorized into three
different types - Public,
government owned and
subsidized universities, Private,
private sector owned universities
and International, mainly
operated and funded by
international organizations such
as OIC. Currently xx public, yy
private and zz international
universities are operating their
activities in Bangladesh.
University of Dhaka is the oldest
university of the country
established in 1921. Bangladeshi
universities are affiliated with the
University Grants Commission
(UGC), a commission created
according to the Presidential
Order (P.O. No 10 of 1973) of the
Government of People's Republic
of Bangladesh.
Universities in Bangladesh play
very important role in the over all
development of the country. This
is evident form the fact that the
students and teachers of the
Dhaka University which was
established in the year 1921, was
at the forefront of the national
liberation struggle that led to the
independence of the country.
There are at present 54 private
Universities in Bangladesh.
The University Grant Commission
of Bangladesh would in fact be
responsible for supervising and
maintaining the quality of
education in all the public and
private Universities of
Bangladesh, as it is the statutory
apex body in the field of higher
education in Bangladesh.