Why Leaves Change Color?

hy Leaves Change Color?
image of leaf
The Splendor of Autumn

Every autumn we revel in the beauty of the fall colors. The mixture of red, purple, orange and yellow is the result of chemical processes that take place in the tree as the seasons change from summer to winter.

During the spring and summer the leaves have served as factories where most of the foods necessary for the tree’s growth are manufactured. This food-making process takes place in the leaf in numerous cells containing chlorophyll, which gives the leaf its green color. This extraordinary chemical absorbs from sunlight the energy that is used in transforming carbon dioxide and water to carbohydrates, such as sugars and starch.

Along with the green pigment are yellow to orange pigments, carotenes and xanthophyll pigments which, for example, give the orange color to a carrot. Most of the year these colors are masked by great amounts of green coloring.
Chlorophyll Breaks Down

But in the fall, because of changes in the length of daylight and changes in temperature, the leaves stop their food-making process. The chlorophyll breaks down, the green color disappears, and the yellow to orange colors become visible and give the leaves part of their fall splendor.

At the same time other chemical changes may occur, which form additional colors through the development of red anthocyanin pigments. Some mixtures give rise to the reddish and purplish fall colors of trees such as dogwoods and sumacs, while others give the sugar maple its brilliant orange.

The autumn foliage of some trees show only yellow colors. Others, like many oaks, display mostly browns. All these colors are due to the mixing of varying amounts of the chlorophyll residue and other pigments in the leaf during the fall season.
Other Changes Take Place

As the fall colors appear, other changes are taking place. At the point where the stem of the leaf is attached to the tree, a special layer of cells develops and gradually severs the tissues that support the leaf. At the same time, the tree seals the cut, so that when the leaf is finally blown off by the wind or falls from its own weight, it leaves behind a leaf scar.

Image of trees changing colors in the fall

Most of the broad-leaved trees in the North shed their leaves in the fall. However, the dead brown leaves of the oaks and a few other species may stay on the tree until growth starts again in the spring. In the South, where the winters are mild, some of the broad-leaved trees are evergreen; that is, the leaves stay on the trees during winter and keep their green color.
Only Some Trees Lose Leaves

Most of the conifers – pines, spruces, firs, hemlocks, cedars, etc. – are evergreen in both the North and South. The needle- or scale-like leaves remain green or greenish the year round, and individual leaves may stay on for two to four or more years.
Weather Affects Color Intensity

Temperature, light, and water supply have an influence on the degree and the duration of fall color. Low temperatures above freezing will favor anthocyanin formation producing bright reds in maples. However, early frost will weaken the brilliant red color. Rainy and/or overcast days tend to increase the intensity of fall colors. The best time to enjoy the autumn color would be on a clear, dry, and cool (not freezing) day.

Enjoy the color, it only occurs for a brief period each fall.

Life Cycle of A Mosquito (Practical IX Class Biology)

Objective

Our objective is to study the life cycle of a mosquito.

The Theory

The mosquitoes are a family of small, midge-like flies. Like all flies, mosquitoes go through four stages in their life – egg, larva, pupa, and adult. We call this as the life cycle.  Each of these stages is morphologically different from the other, with even the habitat of each stage differing. The first three stages – egg, larva and pupa are largely aquatic, whereas the adult stage is aerial.

Mosquito Life cycle

We will now look at the four distinct stages of development in the life cycle of a mosquito.

Stage 1 – Egg

The eggs are laid one at a time and they float on the surface of the water. Normally the eggs are white when first deposited, then darken to near black within a day. They hatch in one to three days depending on the temperature. Eggs left on moist soil can last for up to a year, until the ground is flooded again, before hatching.

In the case of Culex and Culiseta species, 200-300 eggs are stuck together in rafts. Anopheles and Aedes species do not make egg rafts but lay their eggs separately. Culex, Culiseta, and Anopheles lay their eggs on water while Aedes lay their eggs on damp mud. The eggs generally do not hatch until the place is flooded. Most eggs hatch into larvae within 48 hours. When the larvae are ready to hatch, they use a small temporary ‘tooth’ on their head to break open the egg along a suture that was made by it.

Stage 2 – Larva

Mosquito larvae, commonly called ‘wigglers’ or ‘wrigglers’, live in water from 7 to 14 days depending on the water temperature. Larvae swim either through propulsion with their mouth brushes, or by jerky movements of their entire bodies, giving them the common name of ‘wigglers’. The larva begins to feed on bacteria and decaying organic matter on the water surface, soon after they hatch out of eggs. They spend most of their time hanging upside down at the surface, sucking in oxygen through the siphon. The siphon is located at the base of their abdomen and is similar to a snorkel. Brushes that are located in front of their mouths collect the food. Anopheles larvae do not have a siphon and they lay parallel to the water surface. The larval stage lasts for a few days to a few weeks, during which the larvae shed several layers of their outer skin, called moulting. This allows further growth.

Stage 3 – Pupa

After the larvae have completed moulting, they become pupae. This is the stage in which they undergo metamorphosis to become an adult mosquito. The pupal stage is a resting, non-feeding stage. Mosquito pupae are commonly called ‘tumblers’. The pupa is lighter than water and therefore floats at the surface. The mosquito pupa is comma-shaped. The head and thorax are merged into a cephalothorax, with the abdomen curving around underneath. At one end of these curved bodies is the large head and at the other end is the flippers used for swimming. They must take in oxygen from time to time through two breathing tubes known as ‘trumpets’. After a few days or longer, depending on the temperature and other circumstances, the pupa rises to the water surface, the dorsal surface of its cephalothorax splits, and the adult mosquito emerges.

Stage 4 – Adult

The newly emerged adult rests on the surface of the water for a short time to allow itself to dry and harden its parts. Also, the wings have to spread out and dry properly before it can fly.

Adult mosquitoes have a head with two large compound eyes, a thorax, a pair of scaled wings and six jointed legs. They also have antennae and a proboscis. Adult mosquitoes mate within the first few days after emerging from the pupal stage.

It is the carbon dioxide that we exhale, and the lactic acid from our sweat that combine to make us smell like a mosquito buffet. Mosquitoes can pick up these smells from 100 feet, and they can also feel our body heat and notice movements.

Only female mosquitoes have the mouth parts necessary for sucking blood. When biting with their proboscis, they stab two tubes into the skin, one is an anti-coagulant to keep the blood flowing and is a mild painkiller that helps them escape detection, the other helps to suck blood. They use the blood not for their own nourishment but as a source of protein for their eggs. For food, both males and females eat nectar and other plant sugars.

Some interesting mosquito facts

  • There are over 2500 different species of mosquitoes.
  • The feeding habits of mosquitoes are quite unique in that it is only the adult females that feed on blood. The male mosquitoes feed only on plant juices.
  • Mosquitoes must have water in which to complete their life cycle.
  • Most female mosquitoes need to feed on animal blood before they can develop eggs.
  • A female can produce up to 500 eggs before she finally dies.
  • Mosquitoes don’t travel more than a mile from the place where they were hatched.
  • The length of life of the adult mosquito usually depends on factors like – temperature, humidity, sex of the mosquito and time of the year.
  • Once mosquitoes emerge from their pupal cocoons and take flight, male mosquitoes last less than a week and the females’ maybe a couple of months.

Learning Outcomes

  1. Students understand the different stages of a Mosquito life cycle.
  2. Students get to know different types of Mosquitoes and the diseases spread by them.
  3. Students understand the differences in each stage of the mosquito life cycle through the animated demonstrations.

Stress Mastery

What is the “fight or flight response?”

This fundamental physiologic response forms the foundation of modern day stress medicine. The “fight or flight response” is our body’s primitive, automatic, inborn response that prepares the body to “fight” or “flee” from perceived attack, harm or threat to our survival.

What happens to us when we are under excessive stress?

When we experience excessive stress—whether from internal worry or external circumstance—a bodily reaction is triggered, called the “fight or flight” response. Originally discovered by the great Harvard physiologist Walter Cannon, this response is hard-wired into our brains and represents a genetic wisdom designed to protect us from bodily harm. This response actually corresponds to an area of our brain called the hypothalamus, which—when stimulated—initiates a sequence of nerve cell firing and chemical release that prepares our body for running or fighting.

What are the signs that our fight or flight response has been stimulated (activated)?

When our fight or flight response is activated, sequences of nerve cell firing occur and chemicals like adrenaline, noradrenaline and cortisol are released into our bloodstream. These patterns of nerve cell firing and chemical release cause our body to undergo a series of very dramatic changes. Our respiratory rate increases. Blood is shunted away from our digestive tract and directed into our muscles and limbs, which require extra energy and fuel for running and fighting. Our pupils dilate. Our awareness intensifies. Our sight sharpens. Our impulses quicken. Our perception of pain diminishes. Our immune system mobilizes with increased activation. We become prepared—physically and psychologically—for fight or flight. We scan and search our environment, “looking for the enemy.”

When our fight or flight system is activated, we tend to perceive everything in our environment as a possible threat to our survival. By its very nature, the fight or flight system bypasses our rational mind—where our more well thought out beliefs exist—and moves us into “attack” mode. This state of alert causes us to perceive almost everything in our world as a possible threat to our survival. As such, we tend to see everyone and everything as a possible enemy. Like airport security during a terrorist threat, we are on the look out for every possible danger. We may overreact to the slightest comment. Our fear is exaggerated. Our thinking is distorted. We see everything through the filter of possible danger. We narrow our focus to those things that can harm us. Fear becomes the lens through which we see the world.

We can begin to see how it is almost impossible to cultivate positive attitudes and beliefs when we are stuck in survival mode. Our heart is not open. Our rational mind is disengaged. Our consciousness is focused on fear, not love. Making clear choices and recognizing the consequences of those choices is unfeasible. We are focused on short-term survival, not the long-term consequences of our beliefs and choices. When we are overwhelmed with excessive stress, our life becomes a series of short-term emergencies. We lose the ability to relax and enjoy the moment. We live from crisis to crisis, with no relief in sight. Burnout is inevitable. This burnout is what usually provides the motivation to change our lives for the better. We are propelled to step back and look at the big picture of our lives—forcing us to examine our beliefs, our values and our goals.

What is our fight or flight system designed to protect us from?

Our fight or flight response is designed to protect us from the proverbial saber tooth tigers that once lurked in the woods and fields around us, threatening our physical survival. At times when our actual physical survival is threatened, there is no greater response to have on our side. When activated, the fight or flight response causes a surge of adrenaline and other stress hormones to pump through our body. This surge is the force responsible for mothers lifting cars off their trapped children and for firemen heroically running into blazing houses to save endangered victims. The surge of adrenaline imbues us with heroism and courage at times when we are called upon to protect and defend the lives and values we cherish.

What are the saber tooth tigers of today and why are they so dangerous?

When we face very real dangers to our physical survival, the fight or flight response is invaluable. Today, however, most of the saber tooth tigers we encounter are not a threat to our physical survival. Today’s saber tooth tigers consist of rush hour traffic, missing a deadline, bouncing a check or having an argument with our boss or spouse. Nonetheless, these modern day, saber tooth tigers trigger the activation of our fight or flight system as if our physical survival was threatened. On a daily basis, toxic stress hormones flow into our bodies for events that pose no real threat to our physical survival.

Once it has been triggered, what is the natural conclusion of our fight or flight response?

By its very design, the fight or flight response leads us to fight or to flee—both creating immense amounts of muscle movement and physical exertion. This physical activity effectively metabolizes the stress hormones released as a result of the activation of our fight or flight response. Once the fighting is over, and the threat—which triggered the response—has been eliminated, our body and mind return to a state of calm.

Has the fight or flight response become counterproductive?

In most cases today, once our fight or flight response is activated, we cannot flee. We cannot fight. We cannot physically run from our perceived threats. When we are faced with modern day, saber tooth tigers, we have to sit in our office and “control ourselves.” We have to sit in traffic and “deal with it.” We have to wait until the bank opens to “handle” the bounced check. In short, many of the major stresses today trigger the full activation of our fight or flight response, causing us to become aggressive, hypervigilant and over-reactive. This aggressiveness, over-reactivity and hypervigilance cause us to act or respond in ways that are actually counter-productive to our survival. Consider road rage in Los Angeles and other major cities.

It is counterproductive to punch out the boss (the fight response) when s/he activates our fight or flight response. (Even though it might bring temporary relief to our tension!) It is counterproductive to run away from the boss (the flight response) when s/he activates our fight or flight response. This all leads to a difficult situation in which our automatic, predictable and unconscious fight or flight response causes behavior that can actually be self-defeating and work against our emotional, psychological and spiritual survival.

Is there a cumulative danger from over-activation of our fight or flight response?

Yes. The evidence is overwhelming that there is a cumulative buildup of stress hormones. If not properly metabolized over time, excessive stress can lead to disorders of our autonomic nervous system (causing headache, irritable bowel syndrome, high blood pressure and the like) and disorders of our hormonal and immune systems (creating susceptibility to infection, chronic fatigue, depression, and autoimmune diseases like rheumatoid arthritis, lupus, and allergies.)

To protect ourselves today, we must consciously pay attention to the signals of fight or flight.

To protect ourselves in a world of psychological—rather than physical—danger, we must consciously pay attention to unique signals telling us whether we are actually in fight or flight. Some of us may experience these signals as physical symptoms like tension in our muscles, headache, upset stomach, racing heartbeat, deep sighing or shallow breathing. Others may experience them as emotional or psychological symptoms such as anxiety, poor concentration, depression, hopelessness, frustration, anger, sadness or fear.

Excess stress does not always show up as the “feeling” of being stressed. Many stresses go directly into our physical body and may only be recognized by the physical symptoms we manifest. Two excellent examples of stress induced conditions are “eye twitching” and “teeth-grinding.” Conversely, we may “feel” lots of emotional stress in our emotional body and have very few physical symptoms or signs in our body.

By recognizing the symptoms and signs of being in fight or flight, we can begin to take steps to handle the stress overload. There are benefits to being in fight or flight—even when the threat is only psychological rather than physical. For example, in times of emotional jeopardy, the fight or flight response can sharpen our mental acuity, thereby helping us deal decisively with issues, moving us to action. But it can also make us hypervigilant and over-reactive during times when a state of calm awareness is more productive. By learning to recognize the signals of fight or flight activation, we can avoid reacting excessively to events and fears that are not life threatening. In so doing, we can play “emotional judo” with our fight or flight response, “using” its energy to help us rather than harm us. We can borrow the beneficial effects (heightened awareness, mental acuity and the ability to tolerate excess pain) in order to change our emotional environment and deal productively with our fears, thoughts and potential dangers.

A public health agency in Finland is using an interesting approach to shock teens into not smoking

The Tobacco Body website features an interactive image of a man and a woman. Users zoom in and out of their body parts to observe the effects smoking has on a male and female body.

This is a new campaign by the Cancer Society of Finland, whose objective, according to the website of their ad agency, is to use this as a tool to show teenagers “to think critically about smoking.” The idea is to move beyond the black lungs, gooey tar and damaged livers, and use technology to “make the shock effect more shocking.”

And pretty shocking it is. Before-lady and Before-man are indeed much better-looking than After-lady and the After-man.

The strategy employed is clear: teens today don’t care about lungs, livers and cancer, or if they do, the constant exposure to such warnings has rendered them ineffective. What they do care about is appearances. So let’s show them how ugly smoking makes them.

On one hand you can’t argue with facts: smoking does give you spots, increase your testosterone levels, give you bad breath and unhealthy hair, yellow your teeth and nails, etc. Fact-wise there’s not much to dispute in the Tobacco Body website. But how advisable is it to resort to telling teenagers what is beautiful/popular/acceptable and what is not, even if it is towards the noble cause of telling them to not smoke?

Sample these snippets taken from the website:

[Man & Woman] “Dear Smoker, we’re sorry to inform you that according to nail fashion experts, nicotine yellow is not this season’s colour.”

[Woman] “Hey non-smoking girl, you are on a wonder-diet and you don’t even know it! Your body shape is closer to the average, whereas research shows that smokers weigh more and are rounder around the abdominal area.”

[Woman] “The non-smoking woman is less-likely to have as much hair growing on her arms as a smoker.”

[Woman] “The non-smoking woman usually has no additional hairs growing under her nose… No need for a five-bladed special razor.”

[Man & Woman] “Smokers have bad breath. As many as 20 per cent of people have ended relationships because of smoking. In Burn Magazine’s interviews several celebrities reveal they prefer kissing non-smokers.”

[Man & Woman] “A weary face is not a popular one: out of the 100 most popular profile pictures in a dating service only 2 were pictures of smokers.”

Basically, the Cancer Society of Finland is telling youngsters that smoking makes you hairy, fat, yellow-toothed and gives you bad breath. I found it slightly bothersome how features that are quite normal in several healthy teenagers, like rounded abdomens and hair on arms (for women), was being grouped with those which are blatantly undesirable and unhealthy, like yellowing teeth, bad breath and damaged lungs.

I wondered if this ad could be sending negative body image messages to kids who are naturally fat or hairy – are they implying that these kids are not as desirable?

But the more I thought about it the harder I realised it was to completely buy into that line of reasoning. Because, as a friend pointed out, this may be a case where the end could perhaps justify the means.

It was different in the case of the Dove ‘You’re more beautiful than you think you are’ campaign which also used a similar strategy to sell their product. They too inadvertently (?) went about setting definitions for beauty. The glaring difference of course was that Dove, at the end of the day, was trying to sell us soap under the guise of the noble motive of wanting women to feel good about themselves.

In the case of Tobacco Body, there’s no such deception. As questionable as their strategy might be, we can probably be sure that all this campaign wants is for teenagers to say no to smoking. They are, after all, the Cancer Society of Finland.

ScreenHunter_15 Oct. 18 13.27

http://tobaccobody.fi/

Life Cycle of the Malaria Parasite

lifecycleWeb

  1. A female Anopheles mosquito carrying malaria-causing parasites feeds on a human and injects the parasites in the form of sporozoites into the bloodstream. The sporozoites travel to the liver and invade liver cells.
  2. Over 5-16 days*, the sporozoites grow, divide, and produce tens of thousands of haploid forms, called merozoites, per liver cell. Some malaria parasite species remain dormant for extended periods in the liver, causing relapses weeks or months later.
  3. The merozoites exit the liver cells and re-enter the bloodstream, beginning a cycle of invasion of red blood cells, asexual replication, and release of newly formed merozoites from the red blood cells repeatedly over 1-3 days*. This multiplication can result in thousands of parasite-infected cells in the host bloodstream, leading to illness and complications of malaria that can last for months if not treated.
  4. Some of the merozoite-infected blood cells leave the cycle of asexual multiplication. Instead of replicating, the merozoites in these cells develop into sexual forms of the parasite, called male and female gametocytes, that circulate in the bloodstream.
  5. When a mosquito bites an infected human, it ingests the gametocytes. In the mosquito gut, the infected human blood cells burst, releasing the gametocytes, which develop further into mature sex cells called gametes. Male and female gametes fuse to form diploid zygotes, which develop into actively moving ookinetes that burrow into the mosquito midgut wall and form oocysts.
  6. Growth and division of each oocyst produces thousands of active haploid forms called sporozoites. After 8-15 days*, the oocyst bursts, releasing sporozoites into the body cavity of the mosquito, from which they travel to and invade the mosquito salivary glands. The cycle of human infection re-starts when the mosquito takes a blood meal, injecting the sporozoites from its salivary glands into the human bloodstream .

The Mechanism of Muscle Contraction

1) The sequence of events leading to contraction is initiated somewhere in the central nervous system, either as voluntary activity from the brain or as reflex activity from the spinal cord.

(2) A motor neuron in the ventral horn of the spinal cord is activated, and an action potential passes outward in a ventral root of the spinal cord.

(3) The axon branches to supply a number of muscle fibers called a motor unit, and the action potential is conveyed to a motor end plate on each muscle fiber.

(4) At the motor end plate, the action potential causes the release of packets or quanta of acetylcholine into the synaptic clefts on the surface of the muscle fiber.

(5) Acetylcholine causes the electrical resting potential under the motor end plate to change, and this then initiates an action potential which passes in both directions along the surface of the muscle fiber.

(6) At the opening of each transverse tubule onto the muscle fiber surface, the action potential spreads inside the muscle fiber.

(7) At each point where a transverse tubule touches part of the sarcoplasmic reticulum, it causes the sarcoplasmic reticulum to release Ca++ ions.

(8) The calcium ions result in movement of troponin and tropomyosin on their thin filaments, and this enables the myosin molecule heads to “grab and swivel” their way along the thin filament. This is the driving force of muscle contraction.

Contraction is turned off by the following sequence of events:

(9) Acetylcholine at the neuromuscular junction is broken down by acetylcholinesterase, and this terminates the stream of action potentials along the muscle fiber surface.

(10) The sarcoplasmic reticulum ceases to release calcium ions, and immediately starts to resequester all the calcium ions that have been released.

(11) In the absence of calcium ions, a change in the configuration of troponin and tropomyosin then blocks the action of the myosin molecule heads, and contraction ceases.

(12) In the living animal, an external stretching force, such as gravity or an antagonistic muscle, pulls the muscle back to its original length.

Pituitary Gland – Endocrine System.

In vertebrate anatomy, the pituitary gland, or hypophysis, is an endocrine gland about the size of a pea and weighing 0.5 grams (0.018 oz) in humans. It is a protrusion off the bottom of the hypothalamus at the base of the brain, and rests in a small, bony cavity (sella turcica) covered by a dural fold (diaphragma sellae). The posterior pituitary gland is functionally connected to the hypothalamus by the median eminence via a small tube called the pituitary stalk, (also called the infundibular stalk or the infundibulum). The pituitary gland sits in the hypophysial fossa, situated in the sphenoid bone in the middle cranial fossa at the base of the brain. The pituitary gland secretes nine hormones that regulate homeostasis.

Anatomy

The pituitary gland is a pea-sized gland that sits in a protective bony enclosure called the sella turcica. It is composed of three lobes: anterior, intermediate, and posterior. In many animals, these three lobes are distinct. However, in humans, the intermediate lobe is but a few cell layers thick and indistinct; as a result, it is often considered part of the anterior pituitary. In all animals, the fleshy, glandular anterior pituitary is distinct from the neural composition of the posterior pituitary. It belongs to the diencephalon.

Anterior

Main article: Anterior pituitary

The anterior pituitary arises from an invagination of the oral ectoderm and forms Rathke’s pouch. This contrasts with the posterior pituitary, which originates from neuroectoderm.

Endocrine cells of the anterior pituitary are controlled by regulatory hormones released by parvocellular neurosecretory cells in the hypothalamus. The latter release regulatory hormones into hypothalamic capillaries leading to infundibular blood vessels, which in turn lead to a second capillary bed in the anterior pituitary. This vascular relationship constitutes the hypothalamo-hypophyseal portal system. Diffusing out of the second capillary bed, the hypothalamic releasing hormones then bind to anterior pituitary endocrine cells, upregulating or downregulating their release of hormones.

The anterior pituitary is divided into anatomical regions known as the pars tuberalis, pars intermedia, and pars distalis. It develops from a depression in the dorsal wall of the pharynx (stomodial part) known as Rathke’s pouch.

Posterior

Main article: Posterior pituitary

The posterior lobe develops as an extension of the hypothalamus. The magnocellular neurosecretory cells of the posterior side possess cell bodies located in the hypothalamus that project axons down the infundibulum to terminals in the posterior pituitary. This simple arrangement differs sharply from that of the adjacent anterior pituitary, which does not develop from the hypothalamus. The release of pituitary hormones by both the anterior and posterior lobes is under the control of the hypothalamus, albeit in different ways.

Intermediate lobe

Although rudimentary in humans (and often considered part of the anterior pituitary), the intermediate lobe located between the anterior and posterior pituitary is important to many animals. For instance, in fish, it is believed to control physiological color change. In adult humans, it is just a thin layer of cells between the anterior and posterior pituitary. The intermediate lobe produces melanocyte-stimulating hormone (MSH), although this function is often (imprecisely) attributed to the anterior pituitary.

The intermediate lobe is, in general, not well developed in tetrapods, and is entirely absent in birds.

Variations among vertebrates

The pituitary gland is found in all vertebrates, but its structure varies between different groups.

The division of the pituitary described above is typical of mammals, and is also true, to varying degrees, of all tetrapods. However, only in mammals does the posterior pituitary have a compact shape. In lungfishes, it is a relatively flat sheet of tissue lying above the anterior pituitary, and, in amphibians, reptiles, and birds, it becomes increasingly well developed. The intermediate lobe is, in general, not well developed in tetrapods, and is entirely absent in birds.

Apart from lungfishes, the structure of the pituitary in fish is generally different from that in tetrapods. In general, the intermediate lobe tends to be well developed, and may equal the remainder of the anterior pituitary in size. The posterior lobe typically forms a sheet of tissue at the base of the pituitary stalk, and in most cases sends irregular finger-like projection into the tissue of the anterior pituitary, which lies directly beneath it. The anterior pituitary is typically divided into two regions, a more anterior rostral portion and a posterior proximal portion, but the boundary between the two is often not clearly marked. In elasmobranchs there is an additional, ventral lobe beneath the anterior pituitary proper.

The arrangement in lampreys, which are among the most primitive of all fish, may indicate how the pituitary originally evolved in ancestral vertebrates. Here, the posterior pituitary is a simple flat sheet of tissue at the base of the brain, and there is no pituitary stalk. Rathke’s pouch remains open to the outside, close to the nasal openings. Closely associated with the pouch are three distinct clusters of glandular tissue, corresponding to the intermediate lobe, and the rostral and proximal portions of the anterior pituitary. These various parts are separated by meningial membranes, suggesting that the pituitary of other vertebrates may have formed from the fusion of a pair of separate, but associated, glands.

Most armadillos also possess a neural secretory gland very similar in form to the posterior pituitary, but located in the tail and associated with the spinal cord. This may have a function in osmoregulation.

There is a structure analogous to the pituitary in the octopus brain.

Hormones secreted

Anterior

The anterior pituitary synthesizes and secretes the following important endocrine hormones:

Somatotrophins:

  • Growth hormone (also referred to as ‘Human Growth Hormone’, ‘HGH’ or ‘GH’ or somatotropin), released under influence of hypothalamic Growth Hormone-Releasing Hormone (GHRH), (also known as growth-hormone-releasing factor (GHRF)); inhibited by hypothalamic somatostatin

Thyrotrophins:

  • Thyroid-stimulating hormone (TSH), released under influence of hypothalamic Thyrotropin-releasing hormone (TRH) (or TRF); inhibited by somatostatin

Corticotropins:

  • Adrenocorticotropic hormone (ACTH), released under influence of hypothalamic Corticotropin-Releasing Hormone (CRH), (or CRF)
  • Beta-endorphin, released under influence of hypothalamic Corticotropin-Releasing Hormone (CRH)or (CRF)[5]

Lactotrophins:

  • Prolactin (PRL), also known as ‘Luteotropic’ hormone (LTH), whose release is inconsistently stimulated by hypothalamic TRH, oxytocin, vasopressin, vasoactive intestinal peptide, angiotensin II, neuropeptide Y, galanin, substance P, bombesin-like peptides (gastrin-releasing peptide, neuromedin B and C), and neurotensin, and inhibited by hypothalamic dopamine.[6]

Gonadotropins:

  • Luteinizing hormone (also referred to as ‘Lutropin’ or ‘LH’).
  • Follicle-stimulating hormone (FSH), both released under influence of Gonadotropin-Releasing Hormone (GnRH)

These hormones are released from the anterior pituitary under the influence of the hypothalamus. Hypothalamic hormones are secreted to the anterior lobe by way of a special capillary system, called the hypothalamic-hypophysial portal system.

Posterior

The posterior pituitary synthesizes and secretes the following important endocrine hormones:

Magnocellular Neurons:

  • Antidiuretic hormone (ADH, also known as vasopressin and AVP, arginine vasopressin), the majority of which is released from the supraoptic nucleus in the hypothalamus
  • Oxytocin, most of which is released from the paraventricular nucleus in the hypothalamus. Oxytocin is one of the few hormones to create a positive feedback loop. For example, uterine contractions stimulate the release of oxytocin from the posterior pituitary, which, in turn, increases uterine contractions. This positive feedback loop continues throughout labour.

Intermediate

The intermediate lobe synthesizes and secretes the following important endocrine hormone:

  • Melanocyte–stimulating hormones (MSHs), although this function is often (imprecisely) attributed to the anterior pituitary. These are sometimes called “intermedins,” as these are released by the pars intermedia.

Functions

Hormones secreted from the pituitary gland help control the following body processes:

  • Growth (Excess of HGH can lead to gigantism and acromegaly.)
Compared with the hand of an unaffected person (left), the hand of someone with acromegaly (right) is enlarged.
  • Blood pressure
  • Some aspects of pregnancy and childbirth including stimulation of uterine contractions during childbirth
  • Breast milk production
  • Sex organ functions in both males and females
  • Thyroid gland function
  • The conversion of food into energy (metabolism)
  • Water and osmolarity regulation in the body
  • Water balance via the control of reabsorption of water by the kidneys
  • Temperature regulation
  • Pain relief

Diseases involving the pituitary gland

Main article: Pituitary disease

Some of the diseases involving the pituitary gland are:

  • Hyperpituitarism, the increased (hyper) secretion of one or more of the hormones normally produced by the pituitary gland.
  • Hypopituitarism, the decreased (hypo) secretion of one or more of the hormones normally produced by the pituitary gland. If there is decreased secretion of most pituitary hormones, the term panhypopituitarism (pan meaning “all”) is used.
  • Pituitary tumours.
  • Pituitary adenomas, noncancerous tumors that occur in the pituitary gland.

What was the Human Genome Project?

The Human Genome Project (HGP) was the international, collaborative research program whose goal was the complete mapping and understanding of all the genes of human beings. All our genes together are known as our “genome.”

The HGP was the natural culmination of the history of genetics research. In 1911, Alfred Sturtevant, then an undergraduate researcher in the laboratory of Thomas Hunt Morgan, realized that he could – and had to, in order to manage his data – map the locations of the fruit fly (Drosophila melanogaster) genes whose mutations the Morgan laboratory was tracking over generations. Sturtevant’s very first gene map can be likened to the Wright brothers’ first flight at Kitty Hawk. In turn, the Human Genome Project can be compared to the Apollo program bringing humanity to the moon.

The hereditary material of all multi-cellular organisms is the famous double helix of deoxyribonucleic acid (DNA), which contains all of our genes. DNA, in turn, is made up of four chemical bases, pairs of which form the “rungs” of the twisted, ladder-shaped DNA molecules. All genes are made up of stretches of these four bases, arranged in different ways and in different lengths. HGP researchers have deciphered the human genome in three major ways: determining the order, or “sequence,” of all the bases in our genome’s DNA; making maps that show the locations of genes for major sections of all our chromosomes; and producing what are called linkage maps, complex versions of the type originated in early Drosophila research, through which inherited traits (such as those for genetic disease) can be tracked over generations.

The HGP has revealed that there are probably about 20,500 human genes. The completed human sequence can now identify their locations. This ultimate product of the HGP has given the world a resource of detailed information about the structure, organization and function of the complete set of human genes. This information can be thought of as the basic set of inheritable “instructions” for the development and function of a human being.

The International Human Genome Sequencing Consortium published the first draft of the human genome in the journal Nature in February 2001 with the sequence of the entire genome’s three billion base pairs some 90 percent complete. A startling finding of this first draft was that the number of human genes appeared to be significantly fewer than previous estimates, which ranged from 50,000 genes to as many as 140,000.The full sequence was completed and published in April 2003.

Upon publication of the majority of the genome in February 2001, Francis Collins, the director of NHGRI, noted that the genome could be thought of in terms of a book with multiple uses: “It’s a history book – a narrative of the journey of our species through time. It’s a shop manual, with an incredibly detailed blueprint for building every human cell. And it’s a transformative textbook of medicine, with insights that will give health care providers immense new powers to treat, prevent and cure disease.”

The tools created through the HGP also continue to inform efforts to characterize the entire genomes of several other organisms used extensively in biological research, such as mice, fruit flies and flatworms. These efforts support each other, because most organisms have many similar, or “homologous,” genes with similar functions. Therefore, the identification of the sequence or function of a gene in a model organism, for example, the roundworm C. elegans, has the potential to explain a homologous gene in human beings, or in one of the other model organisms. These ambitious goals required and will continue to demand a variety of new technologies that have made it possible to relatively rapidly construct a first draft of the human genome and to continue to refine that draft. These techniques include:

Of course, information is only as good as the ability to use it. Therefore, advanced methods for widely disseminating the information generated by the HGP to scientists, physicians and others, is necessary in order to ensure the most rapid application of research results for the benefit of humanity. Biomedical technology and research are particular beneficiaries of the HGP.

However, the momentous implications for individuals and society for possessing the detailed genetic information made possible by the HGP were recognized from the outset. Another major component of the HGP – and an ongoing component of NHGRI – is therefore devoted to the analysis of the ethical, legal and social implications (ELSI) of our newfound genetic knowledge, and the subsequent development of policy options for public consideration.

What Is Sickle Cell Anemia?

Sickle cell anemia  is the most common form of sickle cell disease (SCD). SCD is a serious disorder in which the body makes sickle-shaped red blood cells. “Sickle-shaped” means that the red blood cells are shaped like a crescent.

Normal red blood cells are disc-shaped and look like doughnuts without holes in the center. They move easily through your blood vessels. Red blood cells contain an iron-rich protein called hemoglobin (HEE-muh-glow-bin). This protein carries oxygen from the lungs to the rest of the body.

Sickle cells contain abnormal hemoglobin called sickle hemoglobin or hemoglobin S. Sickle hemoglobin causes the cells to develop a sickle, or crescent, shape.

Sickle cells are stiff and sticky. They tend to block blood flow in the blood vessels of the limbs and organs. Blocked blood flow can cause pain and organ damage. It can also raise the risk for infection.

Normal Red Blood Cells and Sickle Cells

Figure A shows normal red blood cells flowing freely in a blood vessel. The inset image shows a cross-section of a normal red blood cell with normal hemoglobin. Figure B shows abnormal, sickled red blood cells blocking blood flow in a blood vessel. The inset image shows a cross-section of a sickle cell with abnormal (sickle) hemoglobin forming abnormal strands.

Figure A shows normal red blood cells flowing freely in a blood vessel. The inset image shows a cross-section of a normal red blood cell with normal hemoglobin. Figure B shows abnormal, sickled red blood cells blocking blood flow in a blood vessel. The inset image shows a cross-section of a sickle cell with abnormal (sickle) hemoglobin forming abnormal strands.

Overview

Sickle cell anemia is one type of anemia. Anemia is a condition in which your blood has a lower than normal number of red blood cells. This condition also can occur if your red blood cells don’t contain enough hemoglobin.

Red blood cells are made in the spongy marrow inside the larger bones of the body. Bone marrow is always making new red blood cells to replace old ones. Normal red blood cells live about 120 days in the bloodstream and then die. They carry oxygen and remove carbon dioxide (a waste product) from your body.

In sickle cell anemia, the abnormal sickle cells usually die after only about 10 to 20 days. The bone marrow can’t make new red blood cells fast enough to replace the dying ones.

Sickle cell anemia is an inherited, lifelong disease. People who have the disease are born with it. They inherit two genes for sickle hemoglobin—one from each parent.

People who inherit a sickle hemoglobin gene from one parent and a normal gene from the other parent have a condition called sickle cell trait.

Sickle cell trait is different than sickle cell anemia. People who have sickle cell trait don’t have the disease. Like people who have sickle cell anemia, people who have sickle cell trait can pass the sickle hemoglobin gene to their children.