How did the cardiovascular system evolve?

How did the cardiovascular system evolve?

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How has evolution created our blood, lungs and the heart?

We can't exist without blood, which transports the oxygen to all areas of our body. However, the blood needs a lung, which gives it the oxygen to transport. The blood also needs something which lets it flow through the whole body, which are our veins. And in order to allow the blood to flow through our veins, an organ is needed to pump the blood, which is our heart. We also need a brain which controls all that, and the brain in turn needs the blood in order to function right.

Evolution makes very slow steps… "it just doesn't jump". So, How did evolution manage to create all that?

While others have addressed the big picture aspects of your question, I think it would be useful to look at the specifics.

Have a look at the heart (or more accurately, the hearts) of the earthworm:

They're nothing more than veins with some pumping muscles wrapped around them. It seems almost a stretch to call them hearts, they are shaped so different from what we think of as a heart proper.

Also, note the earthworm's lungs, or rather, lack of them. It doesn't have any! Why not? It doesn't need them. It gets enough oxygen through its skin via osmosis. It's only larger organisms that need dedicated systems to concentrate oxygen from the surrounding environment.

So, the worm has a simpler system (no chambered heart, no lungs) that works.

All vertebrates descended from a common ancestor that was very similar to this earthworm. It had simple hearts, and no lungs. You can follow the evolution of the human heart through fish heart:

which is a more sophisticated pumping vessel with two chambers.

Amphibians evolved from fish, reptiles from amphibians, and mammals from reptiles. In this diagram, you will find that the heart becomes more sophisticated and efficient in each:

So, this should give you a good idea of the evolution of the human heart from simpler, working system. I won't take the time to draw out the evolution of blood vessels or lungs; maybe someone else will, or you can google them yourself, the information is readily out there. But they all follow the same pattern: gradual, incremental improvements on working, simpler systems.

This kind of question was raised in a book called "Darwin's Black Box" by Michael Behe, who is a biochemistry professor in the U.S. - he calls this 'irreducible complexity' (IC). For example, the blood clotting cascade system where you have a large number of components that are all apparently essential for the process.

Now I have to say I find the idea that this is a problem very unconvincing, to say the least. However, it's a reasonable question to ask; how does a system of interdependent elements evolve, if we assume that no part can change gradually without the whole system breaking?

There are - at least - two major problems with this. Firstly, the assumption that you can't change any part of such a system has mostly turned out to be false. Secondly, systems would obviously evolve from other, simpler systems which are just as effective.

Say I start out with three elements in my system (three proteins, for example). They are all essential as each requires the other to function properly. Now I introduce another protein to the system and make it dependent on only one of the existing proteins. Is this system IC? No, we can remove the new protein and the whole thing still works. Gradually, we make the other parts of the system dependent on the new protein and suddenly we have an 'IC' system.

In other words, the 'problem' lies in imagining that you have to go from nothing to a complete working mousetrap. What seems more likely is that elements of a system are changed one by one, and that the system evolves through a series of states where you could point to some element and claim that it is essential.

One final point to note is that no multicellular organism is born whole in one step. The processes that an embryo goes through are conceptually similar (though not exactly ) to evolution in that you can have different organs developing at different times, or simpler versions of them that can work together as a simpler system.

To make this a little less abstract, consider the earthworm example given in the top answer. It has just a simple heart(s) and blood vessels - it doesn't seem that difficult, therefore to add in some lungs. Here's a trivial diagram:

The lines here are interactions between the organs - the heart pumps blood through the vessels, and the lungs (if any) oxygenate the blood. We evolve from the simpler system (1) to the more complex system (2) just by adding another element.

However, the difficulty with some systems is that the interactions between the parts are dependencies. A very simple example could be proteins that activate/deactivate other proteins (by phosphorylation, say). Then we could theoretically get a situation like this:

Here, the final system (4) looks like it is 'irreducibly' complex because you can't remove any of (A, B, C, D) without breaking the cycle. However, at each step, we only added or removed one dependency. This also shows the importance of redundancy in biological systems. If you knock out either C or D from system (3) then it still works.

This is a good question, but it has a vast scope, as you're talking about the progression of millions of different living animals over hundreds of millions of years, none of which are still alive, so we have to make inferences based on what we observe in their surviving offspring.

That means if you want to learn how 'intermediate' (say, not-quite-lungs, not-quite-heart, not-quite-brain) body systems could function, you'd first need to learn about the biology of lots of other animals. Not all animals have lungs or hearts or nervous systems. Not all animals have blood.

More to the point, though, the key factor is that several hundred million years is a really, really, really long time. It's such a long time that it's well outside any typical human scale of comprehension. Consider the entirety of your life experience thus far and everything you've seen change. In comparison to how long the evolutionary process has been operating, your life's span has been on the order of a millisecond out of a day.

Simpler forms developed to handle simpler requirements. Take planarians, for instance, which are thin and small enough that they can receive their oxygen supply by diffusion straight through their surface. Now imagine a slightly bigger animal that needs a slightly more sophisticated system to oxygenate their internal regions well. A muscle with an aberrant, autonomous twitch would be enough to stir/circulate more oxygenated fluids through the body. Past that, any little accident that facilitates this (e.g. some cells bind to oxygen a little better, the muscle twitches a little stronger or more regularly, etc.) is another form closer to what we see today.

A good question, indeed, and not easy to answer (or grasp). I'll give a very simplified answer. Bear in mind that the processess I'll describe are REALLY complex.

You have to think way before blood, brains, etc. Billions of years ago, organic molecules were formed in the planet. These organic molecules started to """join""". Millions of years latter, simple cells which didn't even have a nucleus were formed. Some millions of years latter, cells with nucleus started to form. Latter, these cells started to agreggate, turning into colonies of unicellular individuals. In time, these colonies turned into multicellular individuals, but with all cells being equal to one another. After that, cells in one organism started to differentiate into some functions (digestive and neural, for example). Slowly, more complex organisms were formed, as the cells which formed these organisms started to differentiate and form various kinds of tissues, which, through millions of years, developed into more and more complex organisms. Think of Cnidarians, for example. They are very "simple" (I use "simple" as a proxy for "not complex") beings. They have no circulatory system. A circulatory system developed in latter groups: the first, "simple" circulatory system appeared in Nematodeans (if I'm not mistaken). But it was really "simple". With time, other, more complex, circulatory systems started to originate due to various evolutionary pressures. The same applies to every type of cell, tissue or organ you can think about in any organism: complex organisms are the result of millions of years of simpler organisms which generated more complex organisms, by really little steps.

I hope you get the idea of what I'm trying to say. For really grasping all this, you have to study a lot of evolution, because it is a hard concept for us to deeply understand.

Lab 6: Circulatory Systems

  • Contributed by Susan Burran and David DesRochers
  • Associate Professor (Biology) at Dalton State College
  • Sourced from GALILEO Open Learning Materials

Most animals are complex multicellular organisms that require a mechanism for transporting nutrients throughout their bodies and removing waste products. The circulatory system has evolved over time from simple diffusion through cells in the early evolution of animals to a complex network of blood vessels that reach all parts of the human body. This extensive network supplies the cells, tissues, and organs with oxygen and nutrients, and removes carbon dioxide and waste, which are byproducts of respiration and other cellular activities.

Circulatory systems differ significantly throughout the Animal Kingdom. In all vertebrate organisms, as well as some invertebrates, this is a closed-loop system, in which the blood is not free in a cavity. In a closed circulatory system, blood is contained inside blood vessels and circulates unidirectionally from the heart around the systemic circulatory route, then returns to the heart again. As opposed to a closed system, arthropods&mdashincluding insects, crustaceans, and most mollusks&mdashhave an open circulatory system. In an open circulatory system, the blood is not enclosed in the blood vessels but is pumped into a cavity called a hemocoel and is called hemolymph because the blood mixes with the interstitial fluid.

Phylum Porifiera

All animals are multicellular, meaning that they have different types of cells. The simplest animals living today that represent multicellularity are commonly known as sponges (Phylum Porifera). Sponges are filter feeders in marine environments that have very porous bodies, allowing for the constant circulation of nutrient-containing water. Interestingly, the feeding cells of sponges (known as choanocytes, Fig. 3) closely resemble the morphology of choanoflagellates (Fig. 1). These specialized cells have flagella that trap food particles within them (similar to choanoflagellates) and either digest the particles or shuttle the food to other cells. This differentiation of cell types makes sponges multicellular. Unlike sponges, choanoflagellate cells do not share food particles. While members of Porifera have a few different cells, those cells are not separated from each other by membranes. In this regard, it is said that sponges do not have “true” tissues. All other animals have true tissues. Sponges are radically different from all other animals. They have an asymmetrical body plan (Fig. 4) and lack nerves and muscles, whereas all other animals have symmetry and contain nerves and muscles.

Figure 3. Cross section of a sponge. The digestive layer of sponges contain choanocytes, which capture food particles with their flagella and entrap the food in the collars of the cells.

Figure 4. Asymmetry. Sponges also differ from all other animals in that they have an asymmetrical body plan and do not have nerves, muscles, a digestive or a circulatory system. Radial Symmetry. Cnidarians (i.e. jelly fish) and Ctenophorans (box jellies) have radial symmetry, consisting of many planes of symmetry. Bilateral Symmetry. Most animals are bilaterally symmetrical, consisting of two symmetrical halves.

Electrical activity

The vertebrate heart is myogenic (rhythmic contractions are an intrinsic property of the cardiac muscle cells themselves). Pulse rate varies widely in different vertebrates, but it is generally higher in small animals, at least in birds and mammals. Each chamber of the heart has its own contraction rate. In the frog, for example, the sinus venosus contracts fastest and is the pacemaker for the other chambers, which contract in sequence and at a decreasing rate, the conus being the slowest. In birds and mammals, where the sinus venosus is incorporated into the right atrium at the sinoauricular node, the latter is still the pacemaker and the heartbeat is initiated at that point. Thus, the evolutionary history of the heart explains the asymmetrical pattern of the heartbeat.

In the frog each contraction of the heart begins with a localized negative charge that spreads over the surface of the sinus venosus. In lower vertebrates, the cardiac muscle cells themselves conduct the wave of excitation. In birds and mammals, however, special conducting fibres (arising from modified muscle cells) transmit the wave of excitation from the sinoauricular node to the septum between the auricles, and then, after a slight delay, down between and around the ventricles. The electrical activity of the heart can be recorded the resulting pattern is called an electrocardiogram.

The Institute for Creation Research

The creationist sees the incredible detail of the living world as part of God&rsquos plan, purpose, and special design. Indeed, the various systems (e.g., digestive, muscular, circulatory, endocrine, etc.) of the human body working together is called homoeostasis, meaning the body is designed to maintain itself in a state of stable, healthy equilibrium.

The endocrine system is a complex arrangement of ductless glands that secrete hormones into the bloodstream. Hormones are regulatory substances (i.e., chemical messengers such as insulin and prolactin) produced by specially designed cells and are effective in low concentrations. As you read this article, dozens of hormones are flowing in your bloodstream&mdashand these hormones are designed to impact only the cells that have special receptor molecules on their surfaces. If the matching receptor molecules are not on a given cell&rsquos surface, the corresponding hormones do not affect that cell. Most of these receptor molecules are called G protein coupled receptors. God designed them to &ldquosense&rdquo molecules (such as hormones or odors) outside the cell and activate special pathways inside the cell, resulting in a specific response.

The endocrine system is nothing short of fantastically complicated, and scientists are learning more about it every day. With each function and pathway elucidated, evolutionary explanations make less and less sense.

A 2013 zoology textbook by Stephen Miller and John Harley discussed the &ldquoevolution of endocrine systems.&rdquo With students and the public being overwhelmed daily with &ldquothe fact of evolution,&rdquo the authors committed just 220 words to endocrine system evolution! They wrote, &ldquoEndocrine systems could only arise following the evolution of circulatory systems that could carry hormones.&rdquo 2 And they did not discuss &ldquothe evolution of circulatory systems&rdquo at all. They have, however, an evolution-based diagram that shows the &ldquophylogenetic [evolutionary] trends in the circulatory systems of animals&rdquo (Figure 26.6). 3 To the left of the diagram are black solid lines connecting the major groups of animals (e.g., mammals, birds, crocodilians, most reptiles, etc.). At the point where the solid lines meet one another, the name of the ethereal transitional animal is absent. To the right of these major animal groups is listed the kind of heart each group supposedly had. But these charts and descriptions do not address circulatory system evolution.

Returning to endocrine systems evolution, the authors simply wrote &ldquothat endocrine systems arose multiple times.&rdquo But they do not discuss how endocrine systems actually evolved. They do appeal to &ldquoa shared set of basic signal transduction mechanisms involved in paracrine communication [a type of cell-to-cell communication] in ancestral animals,&rdquo but this is hardly an explanation. 2 How exactly did this intricate cell-to-cell communication evolve? &ldquoBasic signal transduction&rdquo is an oxymoron, since transduction is incredibly complex. Readers are invited to look this up online or in a recent physiology text, but they will not be able to find the names of these &ldquoancestral animals&rdquo since they do not exist.

Miller and Harley also used two well-worn words that are ubiquitous in evolutionary literature and explain nothing: &ldquoover time.&rdquo Darwinists often use generous portions of &ldquotime&rdquo to gloss over macroevolutionary problems&mdashbut this is not evidence for evolution. The zoology student is left knowing less about endocrine system evolution than he or she did before reading those cryptic 220 words.

The similarities of function and structure of vertebrate circulatory systems (including hearts) and endocrine systems reflect that they all have the same wonderful Creator. Truly, His amazing work is &ldquoclearly seen&rdquo in all of His creation (Romans 1:20).

  1. Even more surprising, this statement can be made regarding virtually every biological system in people and animals.
  2. Miller, S. and J. Harley. 2013. Zoology, 9th ed. New York: McGraw Hill, 479.
  3. Ibid, 487.

* Mr. Sherwin is Research Associate, Senior Lecturer, and Science Writer at the Institute for Creation Research.

Cite this article: Sherwin, F. 2013. Endocrine System Evolution: A Textbook Example? Acts & Facts. 42 (9): 15.

How did the cardiovascular system evolve? - Biology

Blood circulates through a network of vessels throughout the body to provide individual cells with oxygen and nutrients and helps dispose of metabolic wastes. The heart pumps the blood around the blood vessels.

Functions of blood and circulation:

  • Circulates OXYGEN and removes Carbon Dioxide.
  • Provides cells with NUTRIENTS.
  • Removes the waste products of metabolism to the excretory organs for disposal.
  • Protects the body against disease and infection.
  • Clotting stops bleeding after injury.
  • Transports HORMONES to target cells and organs.
  • Helps regulate body temperature.


Blood is made up of about 45% solids (cells) and 55% fluids (plasma). The plasma is largely water, containing proteins, nutrients, hormones, antibodies, and dissolved waste products.

General types of blood cells: (each has many different sub-types)

ERYTHROCYTES (red cells) are small red disk shaped cells. They contain HAEMOGLOBIN, which combines with oxygen in the lungs and is then transported to the body's cells. The haemoglobin then returns carbon dioxide waste to the lungs. Erythrocytes are formed in the bone marrow in the knobby ends of bones. LEUKOCYTES (white cells) help the body fight bacteria and infection. When a tissue is damaged or has an infection the number of leukocytes increases. Leukocytes are formed in the small ends of bones. Leukocytes can be classed as granular or non granular. There are three types of granular leukocytes (eosinophils, neutrophils, and basophils), and three types of non-granular (monocytes, T-cell lymphocytes, and B-cell lymphocytes). See also the lymphatic system. THROMBOCYTES (platelets) aid the formation of blood CLOTS by releasing various protein substances. When the body is injured thrombocytes disintegrate and cause a chemical reaction with the proteins found in plasma, which eventually create a thread like substance called FIBRIN. The fibrin then "catches" other blood cells which form the clot, preventing further loss of blood and forms the basis of healing.

Blood vessels

Simplified diagram of the circulatory system. Image Source: ARTERIES carry oxygenated blood away from the heart. They are thick hollow tubes which are highly ELASTIC which allows them to DILATE (widen) and constrict (narrow) as blood is forced down them by the heart. Arteries branch and re-branch, becoming smaller until they become small ARTERIOLES which are even more elastic. Arterioles feed oxygenated blood to the capillaries. The AORTA is the largest artery in the body, taking blood from the heart, branching into other arteries that send oxygenated blood to the rest of the body. CAPILLARIES distribute the nutrients and oxygen to the body's tissues and remove deoxygenated blood and waste. They are extremely thin, the walls are only one cell thick and connect the arterioles with the venules (very small veins). VENULES (very small veins) merge into VEINS which carry blood back to the heart. The vein walls are similar to arteries but thinner and less elastic. Veins carry deoxygenated blood towards the lungs where oxygen is received via the pulmonary capillaries. The PULMONARY Veins then carries this oxygenated blood back to the heart.
Image source:

The heart

The heart is a hollow muscular organ which beats over 100,000 times a day to pump blood around the body's 60,000 miles of blood vessels. The right side of the heart receives blood and sends it to the lungs to be oxygenated, while the left side receives oxygenated blood from the lungs and sends it out to the tissues of the body. The Heart has three layers the ENDOCARDIUM (inner layer), the EPICARDIUM (middle layer), and MYOCARDIUM (outer layer). The heart is protected by the PERICARDIUM which is the protective membrane surrounding it.

The heart has FOUR CHAMBERS, in the lower heart the right and left Ventricles, and in the upper heart the right and left Atria. In a normal heart beat the atria contract while the ventricles relax, then the ventricles contract while the atria relax. There are VALVES through which blood passes between ventricle and atrium, these close in such a way that blood does not backwash during the pauses between ventricular contractions. The right and left ventricles are divided by a thick wall (the VENTRICULAR SEPTUM), babies born with "hole in the heart" have a small gap here, which is a problem since oxygenated and deoxygenated can blood mix. The walls of the left ventricle are thicker as it has to pump blood to all the tissues, compared to the right ventricle which only pumps blood as far as the lungs.

The spleen

This is a large flat oval organ located below the diaphragm, it's main function is to STORE BLOOD. The size of the spleen can vary, for example it may enlarge when the body is fighting infection also it's size tends to decrease with age. It is a non-vital organ and it is possible to survive after removal of the spleen.

Perinicious anaemia is a Vitamin B12 deficiency resulting in a reduction in number of erythrocytes.

Aplastic anemia is a failure of the bone marrow to produce the enough red blood cells.

Septicaemia - bacterial toxins in blood.

Roots, suffixes, and prefixes

Most medical terms are comprised of a root word plus a suffix (word ending) and/or a prefix (beginning of the word). Here are some examples related to the Integumentary System. For more details see Chapter 4: Understanding the Components of Medical Terminology

component meaning example
CARDIO- heart echocardiogram = sound wave image of the heart.
CYTE- cell thrombocyte = clot forming cell.
HAEM- blood haematoma - a tumour or swelling filled with blood.
THROMB- clot, lump thrombocytopenia = deficiency of thrombocytes in the blood
ETHRO- red ehtrocyte = red blood cell
LEUKO- white leukocyte = white blood cell
SEP, SEPTIV- toxicity due to micro-organismssepticaemia
VAS- vessel / duct cerebrovascular = blood vessels of the cerebrum of the brain.
HYPER- excessive hyperglycaemia = excessive levels of glucose in blood.
HYPO- deficient / below hypoglycaemia = abnormally low glucose blood levels.
-PENIA deficiency neutropenia = low levels of neutrophilic leukocytes.
-EMIA condition of blood anaemia = abnormally low levels of red blood cells.

Cancer Focus

Overview of Haematological Malignancies The most common haematological malignancy is leukaemia - cancer of the white blood cells. There are many types of leukaemia Acute types progress rapidly, while Chronic types develop more slowly. Leukaemia is often accompanied by anaemia because the red oxygen carrying cells in the blood are crowded out by the cancerous white cells. There are a number of malignancies and disorders affecting other types of blood cells.

Internet Resources for Leukaemia Acute Lymphoblastic Leukaemia (ALL) Acute lymphoblastic leukaemia (also known as acute lymphocytic leukaemia or ALL) is a disease where too many immature lymphocytes (a type of white blood cell) are found in the blood and bone marrow. Symptoms can include persistent fever, weakness or tiredness, achiness in the bones or joints, or swollen lymph nodes. Adult ALL and its treatment is usually different to childhood ALL. Almost a third of adult patients have a specific chromosome translocation "Philadelphia Positive" ALL.

Internet Resources for Acute Lymphoblastic Leukaemia Acute Myeloid Leukaemia (AML) Acute myeloid leukemia (AML) is a disease in which too many immature granulocytes (a type of white blood cell) are found in the blood and bone marrow. There are a number of subtypes of AML including acute myeloblastic leukemia, acute promyelocytic leukemia, acute monocytic leukemia, acute myelomonocytic leukemia, erythroleukemia, and acute megakaryoblastic leukemia.

Internet Resources for Acute Myeloid Leukaemia Other Types of Leukaemia Chronic Lymphocytic Leukaemia
Chronic Myelogenous Leukaemia
Hairy Cell Leukaemia

Internet Resources for Leukaemia Childhood Leukaemia Childhood leukaemias tend to have different characteristics and treatments compared to adult leukaemias. There is a "childhood peak" of Acute Lymphoblastic Leukaemia, there is a lower proportion of Acute Myeloid Leukaemias compared to adult patients. Clinical prognostic factors include age, White Blood Cell count (WBC) at presentation, and Central Nervous System (CNS) involvement. Infants less than 1 year and adolescents over 10 years of age, WBC greater than 50,000, or CNS involvement are associated with a less favourable prognosis.

Internet Resources for Childhood Leukaemia Other Haematological Malignancies - Lymphomas These are covered in the chapter on the Lymphatic System - Myelodysplastic Syndromes Myelodysplastic syndromes, sometimes called "pre-leukaemia" are a group of diseases in which the bone marrow does not produce enough normal blood cells. Common symptoms are anaemia, bleeding, easy bruisability, and fatigue. These Myelodysplastic syndromes can occur in all age groups but are more common in people aged over 60. Myelodysplastic syndromes may develop spontaneously or be secondary to treatment with chemotherapy / radiotherapy. There is an association with Myelodysplastic syndromes and acute myeloid leukaemia. - Myeloproliferative Disorders Myeloproliferative disorders are diseases in which too many blood cells are made by the bone marrow, there are 4 main types of myeloproliferative disorders: chronic myelogenous leukaemia, polycythemia vera, agnogenic myeloid metaplasia, and essential thrombocythemia. Chronic myelogenous leukaemia is where an excess of granulocytes (immature white blood cells) are found in the blood and bone marrow. Polycythemia vera is where red blood cells become too numerous often resulting in a swelling of the spleen. Agnogenic myeloid metaplasia is a condition in which certain blood cells do not mature properly, this may result in a swelling of the spleen and anaemia. Essential thrombocythemia is a disease in which the body produces excessive numbers of platelets (cells in the blood that make it clot) which impedes the normal circulation of blood. - Aplastic Anaemia Anaplastic Anemia is not a cancer. AA is a rare disease in which the bone marrow is unable to produce adequate blood cells leading to pancytopenia (deficiency of all types of blood cells). AA may occur at any age, but there is a peak in adolescence / early adulthood, and again in old age. Slightly more males than females are diagnosed with AA, also the disease is more common in the Far East. Patients successfully treated for aplastic anemia have a higher risk of developing other diseases later in life, including cancer. - Fanconi Anaemia Fanconi Anaemia is not a cancer, it is a rare disorder found in children that involves the blood and bone marrow. The symptoms include severe aplastic anemia, hypoplasia of the bone marrow, and patchy discoloration of the skin. Recent research has shown an association between Fanconi anaemia and leukaemia. - Waldenstrom's Macroglobulinemia This is a rare malignant condition, involving an excess of beta-lymphocytes (a type of cell in the immune system) which secrete immunoglobulins (a type of antibody). WM usually occurs in people over sixty, but has been detected in younger adults. Internet Resources for Haematological Malignancies French-American-British (FAB) Classification Scheme Leukaemia can be classified using the French-American-British (FAB) criteria. for cell morphology:
L1 - ALL: small lymphoid cells, regular nuclei
L2 - ALL: large lymphoid cells, irregualr nuclei
L3 - ALL: large homogeneous cells with prominent nucleolus
M1 - Myeloblastic leukemia without maturation
M2 - Myeloblastic leukemia with maturation
M3 - Promyelocytic leukemia
M4 - Myelomonocytic leukemia
M5 - Monocytic leukemia
M6 - Erythroleukemia
M7 - Megakaryoblastic leukemia
M0 - AML with minimal differentiation CNS Prophylaxis Leukaemia can sometimes spread to the spinal cord and brain (Central Nervous System). Intrathecal chemotherapy (injection into the fluid around the spine) may be given to combat or prevent CNS relapse. Blood Counts Blood counts are done to test the number of each of the different kinds of cells in the blood. This may be an aid to diagnosis or done to monitor toxicity after each course of chemotherapy. The next course of chemotherapy may be delayed until white cells, neutrophils, and platelets have recovered to a safe level. Cardiotoxicity Cardiotoxicity (damage to the heart) is associated with certain anti cancer drugs, especially Adriamycin. As such the total dose of these drugs may be limited to reduce the risk of cardiotoxicity. Echocardiagram An Echocardiogramis where an image of the heart is formed when high frequency sound waves are reflected from the muscles of the heart. An echocardiogram may be done before treatment starts to establish a baseline from which to compare future tests. Metastases through the cardivascular system The network of blood vessels reach all parts of the body and may provide one of the routes for cancer cells to spread to secondary sites.

Related Abbreviations and Acronyms

AA Anaplastic Anaemia
ALL Acute lymphoblastic leukaemia
AML Acute Myeloid leukaemia
ANC Absolute neutrophil count
ANLL Acute non-lymphatic leukaemia
ASH American Society for Hematology
B-ALL B-cell Acute Lymphoblastic Leukaemia
BP Blood pressure
CALGB Cancer and Leukemia Group B (USA)
cALL Common ALL
CGL Chronic Granulocytic Leukaemia
CHF Congestive heart failure
CLL Chronic lymphocytic Leukaemia
CML Chronic myeloid leukaemia
CMML chronic myelomonocytic leukemia
CPR Cardio pulmonary resuscitation
CVA Cardiovascular Accident (stroke)
CVC Central venous catheters
ECG Electrocardiogram - heart scan
FAB French American and British classification scheme for leukaemia
FBC Full Blood Count
G-CSF Granulocyte colony stimulating factor promotes production of white blood cells
GM-CSF Granulocyte and macrophage colony stimulating factor
Hb Haemoglobin
HCL Hairy Cell Leukaemia
HD Hodgkin's Disease (lymphoma)
HTLV Human T-cell leukemia-lymphoma virus
IV Intravenous - into a vein
LVEF Left Ventricular Fjection Fraction - a heart function test
LVSF Left Ventricular Shortening Fraction - a heart function test
MM Multiple Myeloma
RBC Red blood cell / red blood count
WBC White blood cell count
WCC White cell count

Further Resources (4 links)

SEER, National Cancer Institute
Part of a SEER training module for cancer registry staff.

WebAnatomy, University of Minnesota
Test your anatomy knowledge with these interactive questions. Includes different question types and answers.

Human Anatomy - Heart circulatory system

The Circulatory System

Paul Andersen
Paul Andersen surveys the circulatory system in humans. He begins with a short discussion of open and closed circulatory systems and 2,3, and 4-chambered hearts. He describes the movement of blood through the human heart and the blood vessels. He discusses the major components of blood and the cause of a heart attack.

Brainy mammals

By 360 million years ago, our ancestors had colonised the land, eventually giving rise to the first mammals about 200 million years ago. These creatures already had a small neocortex – extra layers of neural tissue on the surface of the brain responsible for the complexity and flexibility of mammalian behaviour. How and when did this crucial region evolve? That remains a mystery. Living amphibians and reptiles do not have a direct equivalent, and since their brains do not fill their entire skull cavity, fossils tell us little about the brains of our amphibian and reptilian ancestors.

What is clear is that the brain size of mammals increased relative to their bodies as they struggled to contend with the dinosaurs. By this point, the brain filled the skull, leaving impressions that provide tell-tale signs of the changes leading to this neural expansion.

Timothy Rowe at the University of Texas at Austin recently used CT scans to look at the brain cavities of fossils of two early mammal-like animals, Morganucodon and Hadrocodium, both tiny, shrew-like creatures that fed on insects. This kind of study has only recently become feasible. “You could hold these fossils in your hands and know that they have answers about the evolution of the brain, but there was no way to get inside them non-destructively,” he says. “It’s only now that we can get inside their heads.”

Rowe’s scans revealed that the first big increases in size were in the olfactory bulb, suggesting mammals came to rely heavily on their noses to sniff out food. There were also big increases in the regions of the neocortex that map tactile sensations – probably the ruffling of hair in particular – which suggests the sense of touch was vital too (Science, vol 332, p 955). The findings fit in beautifully with the widely held idea that early mammals were nocturnal, hiding during the day and scurrying around in the undergrowth at night when there were fewer hungry dinosaurs running around.

After the dinosaurs were wiped out, about 65 million years ago, some of the mammals that survived took to the trees – the ancestors of the primates. Good eyesight helped them chase insects around trees, which led to an expansion of the visual part of the neocortex. The biggest mental challenge, however, may have been keeping track of their social lives.

If modern primates are anything to go by, their ancestors likely lived in groups. Mastering the social niceties of group living requires a lot of brain power. Robin Dunbar at the University of Oxford thinks this might explain the enormous expansion of the frontal regions of the primate neocortex, particularly in the apes. “You need more computing power to handle those relationships,” he says. Dunbar has shown there is a strong relationship between the size of primate groups, the frequency of their interactions with one another and the size of the frontal neocortex in various species.

Besides increasing in size, these frontal regions also became better connected, both within themselves, and to other parts of the brain that deal with sensory input and motor control. Such changes can even be seen in the individual neurons within these regions, which have evolved more input and output points.

All of which equipped the later primates with an extraordinary ability to integrate and process the information reaching their bodies, and then control their actions based on this kind of deliberative reasoning. Besides increasing their overall intelligence, this eventually leads to some kind of abstract thought&colon the more the brain processes incoming information, the more it starts to identify and search for overarching patterns that are a step away from the concrete, physical objects in front of the eyes.

Which brings us neatly to an ape that lived about 14 million years ago in Africa. It was a very smart ape but the brains of most of its descendants – orang-utans, gorillas and chimpanzees – do not appear to have changed greatly compared with the branch of its family that led to us. What made us different?

It used to be thought that moving out of the forests and taking to walking on two legs lead to the expansion of our brains. Fossil discoveries, however, show that millions of years after early hominids became bipedal, they still had small brains.

We can only speculate about why their brains began to grow bigger around 2.5 million years ago, but it is possible that serendipity played a part. In other primates, the “bite” muscle exerts a strong force across the whole of the skull, constraining its growth. In our forebears, this muscle was weakened by a single mutation, perhaps opening the way for the skull to expand. This mutation occurred around the same time as the first hominids with weaker jaws and bigger skulls and brains appeared (Nature, vol 428, p 415).

Once we got smart enough to innovate and adopt smarter lifestyles, a positive feedback effect may have kicked in, leading to further brain expansion. “If you want a big brain, you’ve got to feed it,” points out Todd Preuss of Emory University in Atlanta, Georgia.

He thinks the development of tools to kill and butcher animals around 2 million years ago would have been essential for the expansion of the human brain, since meat is such a rich source of nutrients. A richer diet, in turn, would have opened the door to further brain growth.

Primatologist Richard Wrangham at Harvard University thinks that fire played a similar role by allowing us to get more nutrients from our food. Eating cooked food led to the shrinking of our guts, he suggests. Since gut tissue is expensive to grow and maintain, this loss would have freed up precious resources, again favouring further brain growth.

Mathematical models by Luke Rendell and colleagues at the University of St Andrews in the UK not only back the idea that cultural and genetic evolution can feed off each other, they suggest this can produce extremely strong selection pressures that lead to “runaway” evolution of certain traits. This type of feedback might have played a big role in our language skills. Once early humans started speaking, there would be strong selection for mutations that improved this ability, such as the famous FOXP2 gene, which enables the basal ganglia and the cerebellum to lay down the complex motor memories necessary for complex speech.

“Cultural and genetic evolution can feed off each other, leading to ‘runaway’ evolution”

The overall picture is one of a virtuous cycle involving our diet, culture, technology, social relationships and genes. It led to the modern human brain coming into existence in Africa by about 200,000 years ago.

Evolution never stops, though. According to one recent study, the visual cortex has grown larger in people who migrated from Africa to northern latitudes, perhaps to help make up for the dimmer light up there (Biology Letters, DOI&colon 10.1098/rsbl.2011.0570).

Coronavirus and the Heart

Lung injury and acute respiratory distress syndrome have taken center stage as the most dreaded complications of COVID-19, the disease caused by the new coronavirus, SARS-CoV-2. But heart damage has recently emerged as yet another grim outcome in the virus's repertoire of possible complications.

COVID-19 is a spectrum disease, spanning the gamut from barely symptomatic infection to critical illness. Reassuringly, for the large majority of individuals infected with the new coronavirus, the ailment remains in the mild-to-moderate range.

Yet, a number of those infected develop heart-related problems either out of the blue or as a complication of preexisting cardiac disease. A report from the early days of the epidemic described the extent of cardiac injury among 41 patients hospitalized with COVID-19 in Wuhan, China: Five, or 12 percent, had signs of cardiovascular damage. These patients had both elevated levels of cardiac troponin—a protein released in the blood by the injured heart muscle—and abnormalities on electrocardiograms and heart ultrasounds. Since then, other reports have affirmed that cardiac injury can be part of coronavirus-induced harm. Moreover, some reports detail clinical scenarios in which patients’ initial symptoms were cardiovascular rather than respiratory in nature.

How does the new coronavirus stoke cardiac damage?

The ways in which the new coronavirus provokes cardiac injury are neither that new nor that surprising, according to Harvard Medical School physician-scientists Peter Libby and Paul Ridker . The part that remains unclear is whether SARS-CoV-2 is somehow more virulent toward the heart than other viruses.

Libby and Ridker, who are practicing cardiologists at Brigham and Women’s, say COVID-19-related heart injury could occur in any several ways.

First, people with preexisting heart disease are at a greater risk for severe cardiovascular and respiratory complications from COVID-19. This is hardly a surprise. Research has shown that infection with the influenza virus poses a more severe threat for people with heart disease than those without cardiac problems. Research also shows that heart attacks can actually be brought on by respiratory infections such as the flu.

Second, people with previously undiagnosed heart disease may be presenting with previously silent cardiac symptoms unmasked by the viral infection. In people with existing heart-vessel blockages, infection, fever and inflammation can destabilize previously asymptomatic fatty plaques inside the heart vessels. Fever and inflammation also render the blood more prone to clotting, while also interfering with the body’s ability to dissolve clots—a one-two punch akin to throwing gasoline on smoldering embers.

“It’s like one big stress test for the heart,” said Ridker, who is the Eugene Braunwald Professor of Medicine at Brigham and Women’s Hospital.

Third, some people may experience heart damage that mimics heart attack injury even if their arteries lack the fatty, calcified flow-limiting blockages known to cause classic heart attacks. This scenario, called myocardial infarction type 2, can occur when the heart muscle is starved for oxygen, which in the case of COVID-19 may be triggered by a mismatch between oxygen supply and oxygen demand. Fever and inflammation accelerate heart rate and increase metabolic demands on many organs, including the heart. That stress is compounded if the lungs are infected and incapable of exchanging oxygen and carbon dioxide optimally. This impaired gas exchange can further diminish oxygen supply to the heart muscle.

Finally, there is a subset of people with COVID-19—some of them previously healthy and with no underlying cardiac problems—who develop fulminant inflammation of the heart muscle as a result of the virus directly infecting the heart. This type of inflammation could lead to heart rhythm disturbances and cardiac muscle damage as well as interfere with the heart’s ability to pump blood optimally.

The propensity of certain viruses to attack the heart muscle and cause viral myocarditis is well known, Libby said, adding that the most notorious viral offender has been the Coxsackie B virus. Nonetheless, a recent case report from Italy underscores the notion that the new coronavirus could also infect the heart and affect heart muscle function in healthy adults even after the acute phase of the infection has resolved and even in the absence of lung damage.

“There are definitely some people who develop acute fulminant myocarditis—in which the virus infects the heart muscle itself or the cells within the heart—and causes a horrible inflammatory reaction,” said Libby, who is also the Mallinckrodt Professor of Medicine at Brigham and Women’s Hospital. “This can be life threatening, and it can happen in people who don't have any preexisting risk factors.”

Libby and Ridker, however, say this out-of-the-blue scenario in otherwise healthy individuals is likely rare relative to the overall number of people with COVID-19 who experience heart problems.

The frenemy within

For Ridker and Libby, who have studied the immune pathways of cardiovascular disease for decades, the cardiac involvement in COVID-19 is yet another striking example of the widespread effects of inflammation on multiple organs and systems.

Inflammation is a critical defense response during infection, but it has a dark side. Infections can set off a cascade of immune signals that affect various organs.

Libby and Ridker hypothesize that any infection in the body—a festering boil, an injured joint, a virus—can become a source of inflammation that activates the release of inflammatory proteins known as cytokines and calls up armies of white blood cells and other messenger molecules that, in an effort to fight the infection, disrupt normal processes. When these inflammatory molecules reach the welcoming soil of a fatty deposit in the blood vessel wall—one that is already studded with resident inflammatory white blood cells—the cytokines can boost the local inflammatory response and trigger a heart attack.

“Our work has shown that cytokines can impinge on these cells in the plaque and push it through a round of further activation,” Libby said.

The inflammatory chemicals released during infection can also induce the liver to ramp up the production of important proteins that defend the body from infection. These proteins, however, make the blood more prone to clotting, while also reducing the secretion of natural clot-dissolving substances. The tiny clots that may form can clog the small blood vessels in the heart and other organs, such as the kidneys, depriving them of oxygen and nutrients and setting the stage for the multisystem failure that can occur in acute infection.

Thus, immune-mediated injury to the heart and other organs could be collateral damage because of the body’s overwhelming systemic immune response—a condition known as cytokine storm , which is marked by the widespread release of cytokines that can cause cellular demise, tissue injury and organ damage.

COVID-19 and blood pressure medications

SARS-CoV-2 invades human cells by latching its spike protein onto the ACE2 receptor found on the surface of cells in the airways, lungs, heart, kidneys and blood vessels. The ACE2 protein is an important player in the renin-angiotensin-aldosterone system, which regulates blood vessel dilation and blood pressure. Two classes of drugs widely used to treat high blood pressure and heart disease—ACE inhibitors and angiotensin receptor blockers—interact with the ACE2 receptor. A possible concern related to COVID-19 stems from the notion that these blood pressure medications could increase the number of ACE2 receptors expressed on cells, possibly creating more molecular gates for the virus to enter. Some experts have wondered whether the use of such drugs could render people who take them more susceptible to infection . Conversely, others have postulated that the abundance of ACE2 receptors may enhance cardiovascular function, exercising a protective effect during infection.

The answer is far from clear, but a recent review suggests these medicines may play a dual role in COVID-19—on the one hand, enhancing susceptibility to infection and, on the other, protecting the heart and ameliorating lung damage from the disease.

Libby and Ridker cautioned that patients who take such life-saving medications should stay on them or at least have a careful discussion with their cardiologists. This is because these drugs have clear and well-established benefits in hypertension and certain forms of heart disease, while their propensity to make humans more susceptible to SARS-CoV-2 remains speculative for the time being .

But what remains speculative today will crystalize in the weeks and months to come, Ridker and Libby said, because the science is moving forward rapidly, with new papers coming out daily and a growing pool of patients to draw observations from.

“In 12 to 18 months we're going to have a great deal of information, but right now our job is to, number one, keep people from getting COVID-19 by strict adherence to now-familiar containment measures,” Libby said. “Then, we need to get people who get the disease through this acute phase.”

The need for rigorous randomized trials done quickly and effectively is acute, they said. Until the evidence from these trials begins to coalesce, clinicians will have to navigate the uncharted territory of delivering cardiac care in the time of pandemic with caution but also with resolve.

“We don't have the comfort of our usual databases, so we have to rely on our clinical skills and judgment. But we have to do so in all humility because often data don’t bear out our logical preconceptions,” Libby said. “Yet, we must act.”

Mind & Body Articles & More

According to new research, happiness isn’t just a state of mind. It affects your heart rate, your body chemistry, and it could contribute to substantial physical health benefits over time.

British researchers Andrew Steptoe, Jane Wardle, and Michael Marmot asked 228 volunteers, ages 45-59, to rate their levels of happiness over a workday and a leisure day, and monitored their blood pressure and heart rate regularly. Volunteers also gave saliva samples and completed a mental stress test. Study results showed that people with higher happiness ratings not only had a lower heart rate, but also had lower levels in their saliva of cortisol, a hormone associated with stress, and less concentration in their blood of a plasma that’s connected to heart disease.

While some of the differences between happier individuals and their less happy counterparts were small, the researchers point out the potential impact of these seemingly minor variations over an extended period of time. “If differences of this magnitude are elicited in everyday life when people are exposed to daily hassles and challenges,” they write, “the result could be a marked difference in cardiovascular disease risk.” They also note that lower levels of cortisol are related to reduced long-term risk of abdominal obesity, type II diabetes, hypertension, and immune system problems.

For years, research has shown that reducing depression, stress, anxiety, and other negative states decreases the risk of heart disease and other maladies. This study has gone a step further by linking a positive emotional state to physical health benefits. Indeed, when the researchers measured their participants’ levels of psychological distress, they found that the physical health benefits of happiness occurred independent of whether or not participants showed any signs of depression or another negative state. This suggests that there may be a distinct biology of happiness that carries its own set of health benefits, beyond the benefits of simply not being depressed.

Honors Bio

Honors Biology is a course for motivated, college-bound 9th graders that involves group learning, audio-visual aids such as animations and DVD’s, on-line lessons, lecture, portfolio assignments and hands-on laboratory methods of teaching. A wide range of biological topics is covered in accordance with the Sunshine State Standards. Emphasis will be on the major themes that guide our study of life, chief among them being Interactions Within Systems and the modern Theory of Evolution by Natural Selection. The course is 36 weeks in length.

Add to my Remind system. For Pre-IB classes (1st and 3rd period) Text @g6k69e to 81010

For Honors classes (4th, 5th and 7th period) Text @6ghf42 to 81010

An End of Course (EOC) exam will count 30% of the final grade in the class. This exam comes from the state and will have only multiple choice questions on it, and they are quite difficult. Grading of the test will be on a curve based on how all students in the state and county perform on it. There are documents in each quarter’s section below that have all the objectives that will be tested as well as practice tests from other states. The tests from Tennessee may be most helpful as they were made by the same publisher that will make our state tests.

Here are the standards, along with a timeline for when we will cover each:Biology Pacing Guide 2015-2016

Here is a link to the Florida Virtual School they have provided an extensive list of practice questions. A pdf copy of this test is also in the EOC folder.

Here is a good review website from Escambia County:

The good news is that last year, not only did all of our honors students pass the test, but almost all got an A or a B. BUT…what they did last year doesn’t help you, so get ready to work like they did.

Your grade in Biology will be calculated using weighted percent categories as follows:

These percentages are subject to change by marking period as determined by the Biology Department. You will be notified of any changes to the grading weighted percent categories.

There are no retests on unit tests. Here is the test remediation policy. Quarter-Semester test policy

Late Work Policy:

Late work will not be accepted. Assignments will not be accepted after they are collected at the beginning of the class period on the day they are due.

If it is a long term assignment, such as extra credit or the pedigree project, work must be received by the beginning of your class on that due date whether you are in class or not. If you are absent for any reason, the work still needs to be to me. A friend can bring it, you can email it to me or send it by Remind message, but I need to have it. No one gets extra time for long term assignments. There will be no exceptions to this.

Absences & Make-Up Work: From the St. Johns County School District Student Code of Conduct 2017-2018

Excused Absences:

When a student is absent from school with an excused absence, the student shall be responsible for all work and assignments missed during the student’s absence. The student shall make arrangements with teachers for “make-up” work and will complete it within a reasonable time frame (as determined by the school) upon the student’s return to schools. Coursework, test, and quizzes can be made up at 100% credit.

Unexcused Absences:

When a student has an unexcused absence, it is the responsibility of the student to complete all coursework, tests, and quizzes and turn them in to the appropriate teacher. A student shall have one day to complete and turn in the work for each day the student is absent (i.e., in the event of a 3 day absence, the student has 3 days to complete and turn in the assignments) and may only earn 50% credit. Tests and quizzes can be made up at 100% credit. There is no expectation that the student’s teacher or teachers will recreate lessons, lectures, or labs for an unexcused absence.

Unexcused absence without parental knowledge/consent, or absence from class without a written excuse from a teacher/administrator will result in NO CREDIT for coursework, tests, and quizzes missed during the absence.

If a student is absent on the day work is assigned, the student will have 5 days from the day they return to turn in the work. If a student is absent only on the day the work is due, one day after it is assigned, they should have the work with them to turn in on the day they return to class. If the assignment is one the student had several days to complete then that assignment is due on the due date whether the student is in school or not a student needs to have the assignment delivered by another student, a parent, or they can email the assignment directly to the instructor by the beginning of class on the due date.No assignments will be accepted after they are collected at the beginning of class on the day they are due.

These guidelines are in place to prevent students from gaining an unfair advantage by getting extra time to complete assignments.

If a student is absent the day of a test, they will be expected to take it the day they return. If a student is absent the day before a test, the student will still be required to take the test the day they return to class, provided that no new material was taught the day they were absent. In class review does not count as new material taught.

Course Materials & Supplies:

  • You are expected to have writing paper and a writing utensil with you every day.
  • Markers, colored pencils, glue sticks, rulers, scissors, and highlighters are provided but you may bring your own if you prefer.
  • The following supplies are not required but would greatly benefit the class if you were to bring them in J:
    • Tissues
    • Paper Towels

    Class powerpoint notes can be accessed through my website below. To print notes to use in class in a way to SAVE INK AND PAPER, find “Print what?” on the print screen and then select “Handouts” from the drop down menu. This will bring up an option just to the right of “Handouts” that allows you to select “Slides per page”. I would suggest three slides per page because this gives you room to take notes as well. Then, to save color ink, find the “Color/gray scale” box and choose “Pure black and white” from the drop down menu. This will save lots of paper and color ink.

    Our before school study sessions are now famous! Come with specific questions, quiz each other, use the whiteboard to sketch, outline, diagram, etc. Get help…it really works. Come any day, with friends or alone, any time before school starts.

    Here are some bits of wisdom about this course:

    1. I know that almost every teacher stresses the importance of keeping up on a day to day basis in their class. I would hate for you to find out the hard way that it is actually true for this class. Talk to and listen to someone you know who has been in this class. If you don’t have a direct assignment, you always have the assignment to look over the day’s notes.

    2. Study by testing yourself!! Read the article in the handouts folder called NY Times Study By Testing for details. Experiments has shown this to be a VERY POWERFUL technique.

    3. Come early. In 2008, I taught this class first period, and several students would come in early and use the whiteboard to sketch out/outline/diagram things that they were trying to understand. They would question each other and ask me about things they couldn’t figure out. What I now call the Copenhaver Technique after its main practitioner is a GREAT way to digest material. In a pinch it can also pass for a social life.

    Take all the notes you can in class. THIS MAY WELL BE YOUR BIGGEST TRANSITION FROM MIDDLE SCHOOL!! You are going to sit there for 45 minutes anyway, why not engage yourself in the listening, decision making (what to write, what not to write) and the visual and kinesthetic confrontation of the material you get when you take notes? It doesn’t take an Einstein to realize that you will come out much better if you engage yourself instead of just listening passively, and it doesn’t take any extra time. It is the biggest no-brainer there is, yet few students do it those that do live a happier life.

    • Review your notes every day. This does take extra time, but it really isn’t much. Add things you didn’t have time to write while they are still fresh on your mind, correct things you wrote by mistake, put a question mark beside something you don’t understand and come in the next morning and ask about it. When you are done reviewing that day’s notes (should only take 3-5 minutes), go back and skim over the previous notes for the current section we are doing. This will take very little time, and the repetition will be invaluable. You will be amazed when you get to test day and you really don’t have to study because you have gone over everything so many times. The total amount of time you have spent on a section will be the same as if you crammed the night before the exam, but YOU WILL DO MUCH BETTER ON THE TEST by spreading out the time and getting more repetition. I regretted not starting to do this until I got to college because IT WORKS. Imagine – EQUAL TIME and BETTER RESULTS: what a deal!

    Please be curious, don’t be afraid to ask questions, and I hope you have a great year at PVHS.

    What to bring to class: textbook, notebook. I suggest a one or two inch three ring binder with a pocket or two that you can keep handouts and graded papers in, along with math paper, graph paper (this is mandatory for graphing exercises), pens, pencils, brains.

    Metacognition and the Feynman Technique
    Here is a video explaining the Feynman Technique, a way to test yourself as a method of learning: This is a very powerful technique try it! I constantly use it in class.

    Careful though. You must confront the material, and your lecture videos or textbook is vital. Not only are you learning biology, you are learning how to be an independent learner. Watch this video from Mr. Anderson, a biology teacher at Bozeman High School. You will be watching several of his videos this year here he speaks to what we all want to know – how best to know. Metacognition

    Video lectures

    Here is a link I just found that has all the Bozeman’s: When assigned a Bozeman video to watch, link to this site, choose the right category (Biology, AP Biology, etc.), and link to the proper video.
    And here is a link to Hank Green’s Crash Course Biology: You can choose Mr. Anderson (Bozeman) or Hank.

    Here is a list, by unit, of the videos to watch at home. Remember to either take notes or compose a Top 5 Concepts/Facts list for each video.

    If you prefer to read the text, corresponding textbook (Modern Biology) are listed beside each video in red.

    Here is the on-line access to the book:

    Quarter 1
    General Handouts

    Nature of Science/Scientific Method

    Bozeman – Scientific Method:

    Basic Chemistry and Water

    Scales: Unit 2-Biochemistry Scale Tracker These also contain the next unit’s scales

    Bozeman – Chemistry, Unit 4 Bonding: Chemical Bonds, Ionic and Covalent pp. 30 – 38

    Crash Course: That’s Why Carbon Is a Tramp

    Bozeman – Biology – Unit 2: Chemistry of Life – Water a Polar Molecule If this link doesn’t work, search for it in You Tube. pp. 38-42

    Crash Course: Water – Liquid Awesome

    Bozeman: Chemistry, Unit 11 Acid Base Chemistry: Acids, Bases and pH pp. 43-44

    Here is a link I just found that has all the Bozeman’s: When assigned a Bozeman video to watch, link to this site, choose the right category (Biology, AP Biology, etc.), and link to the proper video.

    And here is a link to Hank Green’s Crash Course Biology: You can choose Mr. Anderson (Bozeman) or Hank.

    Bozeman – Biology – Introduction: Scientific Method

    Bozeman: Biology, Unit 2 Chemistry of Life: Molecules of Life pp. 51-53

    Bozeman: Biology, Unit 2 Chemistry of Life: Carbohydrates pp. 55-56
    Bozeman: Biology, Unit 2 Chemistry of Life: Lipids pp. 59-60
    Bozeman: Biology, Unit 2 Chemistry of Life: Proteins pp. 56-57
    Crash Course: Biological Molecules – You Are What You Eat

    Bozeman: Biology, Unit 3 Cells: Enzymes p. 54,57

    Bozeman: ATP: Adenosine Triphosphate

    Here is a link I just found that has all the Bozeman’s: When assigned a Bozeman video to watch, link to this site, choose the right category (Biology, AP Biology, etc.), and link to the proper video.
    And here is a link to Hank Green’s Crash Course Biology: You can choose Mr. Anderson (Bozeman) or Hank.

    Bozeman: Biology, Unit 3 Cells: A Tour of the Cell pp. 74-90

    Bozeman: Why Are Cells Small?

    Thinkwell Plant and Animal Cell: (for cell size) pp. 72-73
    Bozeman: Biology, Unit 3 Cells: Cell Membranes pp. 77-78
    Microscope tutorial:

    Bozeman: Cell Organelles
    Crash Course: Eukaryopolis – The City of Animal Cells
    Crash Course: Plant Cells

    Parts of the cell Good for review
    Bozeman: Biology, Unit 3 Cells: Endosymbiosis p. 290

    Bozeman: Biology, Unit 3 Cells: Transport Across Cell Membranes pp. 96-106 Crash Course: In Da Club – Membranes and Transport
    diffusion and osmosis (optional) Sodium Potassium Pump (optional)
    Practice Tests:
    Cells Practice Test 2 Questions 45, 47, 51-53, 57, 58, 60 – 69, 71 – 72

    Molecular Genetics: DNA Structure and function

    Here is a link I just found that has all the Bozeman’s:
    When assigned a Bozeman video to watch, link to this site, choose the right category (Biology, AP Biology, etc.), and link to the proper video.
    And here is a link to Hank Green’s Crash Course Biology: You can choose Mr. Anderson (Bozeman) or Hank.

    Bozeman: Biology, Unit 4: Genetics: What is DNA? pp. 192-210 basic structure and function

    Bozeman: Biology, Unit 4: Genetics: DNA and RNA Part 1 Experiments, structure, Pr. syn., Gen. eng. transformation pp. 192-210

    Bozeman: Biology, Unit 4: Genetics: DNA and RNA part 2 a bit more detail than Part 1 Watch 0:00 – 3:40 for replication. 3:40 to end for protein synthesis

    Crash Course: DNA – Structure and Replication

    Hippocampus: link to website , select Biology for AP from the left side, then watch: Replication Overview and The Mechanism

    DNA: Protein Synthesis – Transcription and Translation

    Bozeman: Biology, Unit 4: Genetics: Transcription and Translation pp. 204-210

    Bozeman: Biology, Unit 4: Genetics: DNA and RNA part 2 a bit more detail than Part 1 Watch 0:00 – 3:40 for replication. 3:40 to end for protein synthesis

    Crash Course: DNA, Hot Pockets and the Longest Word Ever

    Hippocampus: RNA Structure and Function, The Transcription of DNA to RNA: Summary, Decoding RNA, The Mechanism of Translation

    Cloning: click on Cloning at the bottom of the page pp. 268-269

    Bozeman: Biology – Unit 6: Microorganisms and Fungi Viral Replication pp.485-488

    Cell Division: Mitosis and Meiosis

    Bozeman: Biology, Unit 3 Cells: Mitosis pp. 154-159
    Crash Course: Mitosis – Splitting Up Is Complicated

    Bozeman: Biology, Unit 3 Cells : Meiosis pp. 161-164
    Crash Course: Meiosis – Where Sex Starts
    Thinkwell: Mitosis vs. Meiosis:
    Optional: BozemanBiologyMitosisandMeiosisSimulation

    Here is a link I just found that has all the Bozeman’s: When assigned a Bozeman video to watch, link to this site, choose the right category (Biology, AP Biology, etc.), and link to the proper video.

    And here is a link to Hank Green’s Crash Course Biology: You can choose Mr. Anderson (Bozeman) or Hank.

    Bozeman: Biology, Unit 4: Genetics: Mendelian Genetics pp. 172-186
    Crash Course: Heredity
    Thinkwell – Dihybrid Crosses:
    Bozeman: Biology, Unit 4: Genetics: Beginner’s Guide to Punnett Squares
    Bozeman: Biology, Unit 4: Genetics:Advanced Genetics 3:10 – 7:45 for multiple alleles and polygenic traits pp. 242-244
    Multiple Alleles:

    Chromosomal Heredity: Beyond Mendel

    Bozeman: Biology, Unit 4: Genetics: Advanced genetics 0:00 – 3:10 for linked genes, 7:45 – 10:45 for sex-linked traits pp. 234-238
    Non-disjunction: p. 239
    Pedigree Analysis 1: pp. 241-243
    Pedigree Analysis 2:

    Quarter 2 Review questions . Remember, this test will have quarter 1 questions on it also see those practice questions at the end of Quarter 1 section above.

    Also, MAKE SURE you use these practice questions from the Escambia site: Here is a good review website from Escambia County:

    Here is a link I just found that has all the Bozeman’s:
    When assigned a Bozeman video to watch, link to this site, choose the right category (Biology, AP Biology, etc.), and link to the proper video.
    And here is a link to Hank Green’s Crash Course Biology: You can choose Mr. Anderson (Bozeman) or Hank.
    Bozeman – Biology, Unit 5 Evolution – Evidence for Evolution pp. 302-307
    Crash Course: Evolution – It’s A Thing
    Bozeman – Biology, Unit 5 Evolution – Radiocarbon Dating
    Bozeman – Biology, Unit 5 Evolution – Evidence for Evolution II
    Whale video:
    Bozeman – Biology, Unit 5 Evolution – Natural Selection pp. 297-301
    Crash Course: Natural Selection
    Bozeman – Biology, Unit 5 Evolution – Examples of Natural Selection pp. 308-309

    Bozeman – Five fingers of Biology
    Bozeman – Biology, Unit 5 Evolution – Microevolution pp. 317-320
    Crash Course: Population Genetics – When Darwin Met Mendel
    Bozeman – Biology, Unit 5 Evolution – Solving Hardy Weinberg Problems
    Khan HardyWeinberg:
    Bozeman – Biology, Unit 5 Evolution – Genetic Drift p. 322
    Bozeman – Biology, Unit 5 Evolution – Selection pp. 324-325
    Bozeman – Biology, Unit 5 Evolution – Essential Characteristics of Life
    Bozeman – Biology, Unit 5 Evolution – Cladograms pp. 341-345
    Bozeman – Biology, Unit 5 Evolution – Speciation and Extinction pp. 326-330
    Bozeman – Biology, Unit 5 Evolution – Speciation
    Crash Course: Speciation – Of Ligers & Men
    Bozeman – Biology, Unit 5 Evolution- Evolution Continues

    Origin of Life, Classification

    Here is a link I just found that has all the Bozeman’s:

    When assigned a Bozeman video to watch, link to this site, choose the right category (Biology, AP Biology, etc.), and link to the proper video.

    You can choose Mr. Anderson (Bozeman) or Hank.

    Bozeman – Biology, Unit 5 Evolution – Abiogenesis pp. 279-281

    Bozeman – Biology, Unit 5 Evolution- Origin of Life Scientific Evidence pp. 282-290

    Bozeman – Biology, Unit 1 Introduction: Three Domains of Life pp. 337-339, 347-348

    Crash Course: Taxonomy – Life’s Filing System pp. 348-350

    Here is a link I just found that has all the Bozeman’s:

    When assigned a Bozeman video to watch, link to this site, choose the right category (Biology, AP Biology, etc.), and link to the proper video.

    You can choose Mr. Anderson (Bozeman) or Hank.

    Bozeman: Biology – Unit 7 Plants Plant Structure pp. 584-586, 602

    Bozeman: Biology – Unit 7 Plants Plant Nutrition and Transport p. 597

    Crash Course: Vascular Plant = Winning

    Bozeman: Biology – Unit 7 Plants Plants

    Crash Course: The Plants and the Bees – Plant Reproduction

    Energetics (Photosynthesis and Respiration)

    Here is a link that has all the Bozeman’s: When assigned a Bozeman video to watch, link to this site, choose the right category (Biology, AP Biology, etc.), and link to the proper video.
    And here is a link to Hank Green’s Crash Course Biology: You can choose Mr. Anderson (Bozeman) or Hank

    Bozeman – Biology – Unit 3 – Cellular Respiration pp. 130-135, 135-144

    Bozeman – Biology – Unit 3 Anaerobic Respiration pp. 130-135
    Crash Course: ATP and Respiration
    Bozeman Photosynthesis: pp. 112-124
    Crash Course: Photosynthesis
    Khan Academy Optionals

    Quarter 3 practice questions. This test will have ONLY quarter 3 questions on it.

    ECOLOGY: Pick either the Bozemans or Hippocampus…or both!!

    Ecology 1: Community Ecology, Cycles, Succession


    Here is a link I just found that has all the Bozeman’s:
    When assigned a Bozeman video to watch, link to this site, choose the right category (Biology, AP Biology, etc.), and link to the proper video.

    And here is a link to Hank Green’s Crash Course Biology:
    This is a different link than the other Crash Course one. It is his Ecology section. You can choose Mr. Anderson (Bozeman) or Hank.

    Hippocampus: link to website , select Biology for AP from the left side, then choose either the Populations and

    Ecology (P&E) section or the Ecosystems (E) section and go to the subsections as listed below.

    Bozeman: Biology – Unit 10: Ecology Ecosystems – Population size, Food webs *Just look at the Food Web part

    Hippocampus, P&E, Community Ecology pp. 366-369

    Crash Course: Ecosystem Ecology – Links In The Chain

    Crash Course: Ecological Succession – Change Is Good

    Bozeman: Biology – Unit 10: Ecology Environmental Matter Exchange (Water and Carbon cycles)

    Hippocampus, E, Energy Flow and the Water Cycle pp. 371-374

    Crash Course: The Hydrologic and Carbon Cycles – Always Recycle!

    Ecology 2: Conservation, Aquatic systems, Population Dynamics

    Bozeman: Biology – Unit 10: Ecology Communities Diversity, Population growth

    Hippocampus, P&E, The Natural Setting, Population Ecology pp. 359-363, 383-392

    Crash Course: Population Ecology – The Texas Mosquito Mystery

    Bozeman: Biology – Unit 10: Ecology Populations Human Impact

    Hippocampus, E, Conservation Biology pp. 441-444, 446-452

    Crash Course: 5 Human Impacts on the Environment

    Bozeman: Biology – Unit 10: Ecology Ecosystem Change Global climate change pp. 408-410, 435-437, 440-1

    Bozeman: Biology – Unit 10: Ecology Biodiversity pp. 438-9

    Crash Course: Conservation and Restoration Ecology

    Here is a link I just found that has all the Bozeman’s:
    When assigned a Bozeman video to watch, link to this site, choose the right category (Biology, AP Biology, etc.), and link to the proper video.

    And here is a link to Hank Green’s Crash Course Biology:
    You can choose Mr. Anderson (Bozeman) or Hank.

    Bozeman: Biology, Unit 11 – Human Body Circulatory System pp. 932-944

    Crash Course: Circulatory and Respiratory Systems

    Bozeman: Biology, Unit 11 – Human Body Immune system pp. 956-972

    Crash Course: Your Immune System – Natural Born Killers

    Bozeman: Biology, Unit 11 – Human Body The Reproductive System pp. 1048-1057

    Crash Course: The Reproductive System – How Gonads Go

    Crash Course: The Nervous System

    Crash Course: The Digestive System

    and here are some math ones, all from Bozeman:

    Here is a link I just found that has all the Bozeman’s:
    When assigned a Bozeman video to watch, link to this site, choose the right category (Biology, AP Biology, etc.), and link to the proper video.

    Bozeman – Statistics and Graphing – Unit 2 – A Beginner’s Guide To Graphing Data

    Bozeman – Statistics and Graphing – Unit 1 – Statistics for Science

    Bozeman – Statistics and Graphing – Unit 1 – Chi-squared Test

    Bozeman – Biology – Unit 5 Evolution – Solving Hardy-Wienberg problems

    Bozeman – Biology – Unit 4 Genetics – Probability in Genetics

    EOC Test Prep

    Here are the instructions for your Study Island assignment: Study Island Review Guide

    Here is the site:

    Here is a breakdown of # of questions by topic: Question Breakdown 2013 EOC

    Here are the standards, along with a timeline for when we will cover each:Biology Pacing Guide 2015-2016

    Here is a link to the Florida Virtual School they have provided an extensive list of practice questions. A pdf copy of this test is also in the EOC folder.

    Here is a good review website from Escambia County:

    Here are some practice tests besides the Study Island ones if you want to go the extra mile. sorry, but most don’t have keys. The EOC Practice Test Pearson and the Virtual School Practice Test are Florida EOC-specific, but the ones from the other states are not, so realize that you might run into a few questions on topics that won’t be on our test.