Circulatory system

The circulatory system is an organ system that passes nutrients (such asamino acids, electrolytes and lymph), gases, hormones, blood cells, etc. to and from cells in the body to help fight diseases, stabilize body temperature and pH, and to maintain homeostasis.

This system may be seen strictly as a blood distribution network, but some consider the circulatory system as composed of the cardiovascular system, which distributes blood, and the lymphatic system, which returns excessfiltered blood plasma from the interstitial fluid (between cells) as lymph. While humans, as well as other vertebrates, have a closed cardiovascular system (meaning that the blood never leaves the network of arteries, veins andcapillaries), some invertebrate groups have an open cardiovascular system. The most primitive animal phyla lack circulatory systems. The lymphatic system, on the other hand, is an open system providing an accessory route for excess interstitial fluid to get returned to the blood.

Two types of fluids move through the circulatory system: blood and lymph. Lymph is essentially recycled blood plasma after it has been filtered from the blood cellsand returned to the lymphatic system. The blood, heart, and blood vessels form the cardiovascular (from Latin words meaning 'heart'-'vessel') system. The lymph, lymph nodes, and lymph vessels form the lymphatic system. The cardiovascular system and the lymphatic system collectively make up the circulatory system.

Human cardiovascular system

The main components of the human cardiovascular system are the heart, blood, andblood vessels. It includes: the pulmonary circulation, a "loop" through the lungswhere blood is oxygenated; and the systemic circulation, a "loop" through the rest of the body to provide oxygenated blood. An average adult contains five to six quarts (roughly 4.7 to 5.7 liters) of blood, which consists of plasma, red blood cells, white blood cells, and platelets. Also, the digestive system works with the circulatory system to provide the nutrients the system needs to keep the heart pumping

Pulmonary circulation

The pulmonary circulatory system is the portion of the cardiovascular system in whichoxygen-depleted blood is pumped away from the heart, via the pulmonary artery, to the lungs and returned, oxygenated, to the heart via the pulmonary vein.

Oxygen deprived blood from the vena cava, enters the right atrium of the heart and flows through the tricuspid valve (right atrioventricular valve) into the right ventricle, from which it is then pumped through the pulmonary semilunar valve into the pulmonary artery to the lungs. Gas exchange occurs in the lungs, whereby CO₂ is released from the blood, and oxygen is absorbed. The pulmonary vein returns the now oxygen-rich blood to the heart.

Systemic circulation

Systemic circulation is the portion of the cardiovascular system which transports oxygenated blood away from the heart, to the rest of the body, and returns oxygen-depleted blood back to the heart. Systemic circulation is, distance-wise, much longer than pulmonary circulation, transporting blood to every part of the body.

Coronary circulation

The coronary circulatory system provides a blood supply to the heart. As it provides oxygenated blood to the heart, it is by definition a part of the systemic circulatory system

Heart

 Human heart

The heart pumps oxygenated blood to the body and deoxygenated blood to the lungs. In the human heart there is one atrium and oneventricle for each circulation, and with both a systemic and a pulmonary circulation there are four chambers in total: left atrium, left ventricle,right atrium and right ventricle. The right atrium is the upper chamber of the right side of the heart. The blood that is returned to the right atrium is deoxygenated (poor in oxygen) and passed into the right ventricle to be pumped through the pulmonary artery to the lungs for re-oxygenation and removal of carbon dioxide. The left atrium receives newly oxygenated blood from the lungs as well as the pulmonary vein which is passed into the strong left ventricle to be pumped through the aorta to the different organs of the body.

Closed cardiovascular system

The cardiovascular systems of humans are closed, meaning that the blood never leaves the network of blood vessels. In contrast, oxygen and nutrients diffuse across the blood vessel layers and enters interstitial fluid, which carries oxygen and nutrients to the target cells, and carbon dioxide and wastes in the opposite direction. The other component of the circulatory system, the lymphatic system, is not closed.

Oxygen transportation

Main article: Blood#Oxygen transport

About 98.5% of the oxygen in a sample of arterial blood in a healthy human breathing air at sea-level pressure is chemically combined with haemoglobin molecules. About 1.5% is physically dissolved in the other blood liquids and not connected to haemoglobin. The haemoglobin molecule is the primary transporter of oxygen in mammals and many other species.

Development

The development of the circulatory system initially occurs by the process ofvasculogenesis. The human arterial and venous systems develop from different embryonic areas. While the arterial system develops mainly from the aortic arches, the venous system arises from three bilateral veins during weeks 4 - 8 of human development.

Arterial development

 Aortic arches

The human arterial system originate from the aortic arches and from the dorsal aortaestarting from week 4 of human development. Aortic arch 1 almost completely regresses except to form the maxillary arteries. Aortic arch 2 also completely regresses except to form the stapedial arteries. The definitive formation of the arterial system arise from aortic arches 3, 4 and 6. While aortic arch 5 completely regreses.

The dorsal aortae are initially bilateral and then fuse to form the definitive dorsal aorta. Approximately 30 posterolateral branches arise off the aorta and will form theintercostal arteries, upper and lower extremity arteries, lumbar arteries and the lateral sacral arteries. The lateral branches of the aorta form the definitive renal, suprarrenaland gonadal arteries. Finally, the ventral branches of the aorta consist of the vitelline arteries and umbilical arteries. The vitelline arteries form the celiac, superior andinferior mesenteric arteries of the gastrointestinal tract. After birth, the umbilical arteries will form the internal iliac arteries.

Venous development

The human venous system develops mainly from the vitelline veins, the umbilical veinsand the cardinal veins, all of which empty into the sinus venosus.

Measurement techniques

• Electrocardiogram—for cardiac electrophysiology
• Sphygmomanometer and stethoscope—for blood pressure
• Pulse meter—for cardiac function (heart rate, rhythm, dropped beats)
• Pulse—commonly used to determine the heart rate in absence of certain cardiac pathologies
• Heart rate variability -- used to measure variations of time intervals between heart beats
• Nail bed blanching test—test for perfusion
• Vessel cannula or catheter pressure measurement—pulmonary wedge pressure or in older animal experiments.

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Evolution Of Eye

Evolution of the eye

Photoreception is phylogenetically very old, with various theories of phylogenesis. The common origin (monophyly) of all animal eyes is now widely accepted as fact. This is based upon the shared anatomical and genetic features of all eyes; that is, all modern eyes, varied as they are, have their origins in a proto-eye believed to have evolved some 540 million years ago, and the PAX6 gene is considered a key factor in this. The majority of the advancements in early eyes are believed to have taken only a few million years to develop, since the first predator to gain true imaging would have touched off an "arms race". Prey animals and competing predators alike would be at a distinct disadvantage without such capabilities and would be less likely to survive and reproduce. Hence multiple eye types and subtypes developed in parallel.
Eyes in various animals show adaptation to their requirements. For example, birds of prey have much greater visual acuity than humans, and some can see ultraviolet light. The different forms of eye in, for example, vertebrates and molluscs are often cited as examples of parallel evolution, despite their distant common ancestry.

The very earliest "eyes", called eyespots, were simple patches of photoreceptor protein in unicellular animals. In multicellular beings, multicellular eyespots evolved, physically similar to the receptor patches for taste and smell. These eyespots could only sense ambient brightness: they could distinguish light and dark, but not the direction of the light source.
Through gradual change, as the eyespot depressed into a shallow "cup" shape, the ability to slightly discriminate directional brightness was achieved by using the angle at which the light hit certain cells to identify the source. The pit deepened over time, the opening diminished in size, and the number of photoreceptor cells increased, forming an effective pinhole camera that was capable of dimly distinguishing shapes.
The thin overgrowth of transparent cells over the eye's aperture, originally formed to prevent damage to the eyespot, allowed the segregated contents of the eye chamber to specialise into a transparent humour that optimised colour filtering, blocked harmful radiation, improved the eye's refractive index, and allowed functionality outside of water. The transparent protective cells eventually split into two layers, with circulatory fluid in between that allowed wider viewing angles and greater imaging resolution, and the thickness of the transparent layer gradually increased, in most species with the transparent crystallin protein.
The gap between tissue layers naturally formed a bioconvex shape, an optimally ideal structure for a normal refractive index. Independently, a transparent layer and a nontransparent layer split forward from the lens: the cornea and iris. Separation of the forward layer again formed a humour, the aqueous humour. This increased refractive power and again eased circulatory problems. Formation of a nontransparent ring allowed more blood vessels, more circulation, and larger eye sizes.

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Sinus tachycardia

Sinus tachycardia (also colloquially known as sinus tach or sinus tachy) is a heart rhythm with elevated rate of impulses originating from the sinoatrial node, defined as a rate greater than 100 beats/min in an average adult. The normal heart rate in the average adult ranges from 60–100 beats/min. Note that the normal heart rate varies with age, with infants having normal heart rate of 110–150 bpm to the elderly, who have slower normals.  

Etiology

Sinus tachycardia is usually a response to normal physiological situations, such as exercise and an increased sympathetic tone with increased catecholamine release—stress, fright, flight, anger. Other causes include:

• Fever
• Anxiety
• Dehydration
• Malignant hyperthermia
• Hypovolemia with hypotension and shock
• Anemia
• Heart failure
• Hyperthyroidism
• Mercury poisoning
• Kawasaki disease
• Pheochromocytoma
• Sepsis
• Pulmonary embolism
• Acute coronary ischemia and myocardial infarction
• Chronic pulmonary disease
• Hypoxia
• Intake of stimulants such as caffeine, nicotine, cocaine, or amphetamines
• Hyperdynamic circulation
• Electric shock
• Drug withdrawal

Symptoms                  

Tachycardia is often asymptomatic. If the heart rate is too high, cardiac output may fall due to the markedly reduced ventricular filling time. Rapid rates, though they may be compensating for ischemia elsewhere, increase myocardial oxygen demand and reduce coronary blood flow, thus precipitating an ischemic heart or valvular disease. Sinus tachycardia accompanying a myocardial infarction may be indicative of cardiogenic shock.  

ECG characteristics

• Rate: Greater than or equal to 100.
• Rhythm: Regular.
• P waves: Upright, consistent, and normal in morphology (if no atrial disease)
• P–R interval: Between 0.12–0.20 seconds and shortens with increasing heart rate
• QRS complex: Less than 0.12 seconds, consistent, and normal in morphology.

Diagnosis and differentials

Usually apparent on the EKG, but if heart rate is above 140 bpm the P wave may be difficult to distinguish from the previous T wave and one may confuse it with a paroxysmal supraventricular tachycardia or atrial flutter with a 2:1 block. Ways to distinguish the three are:

• Vagal maneuvers (such as carotid sinus massage or Valsalva's maneuver) to slow the rate and identification of P waves
• administer AV blockers (e.g., adenosine, verapamil) to identify atrial flutter with 2:1 block

Inappropriate sinus tachycardia (IST)

Also known as chronic nonparoxysmal sinus tachycardia, patients have elevated resting heart rate and/or exaggerated heart rate in response to exercise. These patients have no apparent heart disease or other causes of sinus tachycardia. IST is thought to be due to abnormal autonomic control..

 Inappropriate sinus tachycardia

Postural orthostatic tachycardia syndrome (POTS)

Usually in women with no heart problems, this syndrome is characterized by normal resting heart rate but exaggerated postural sinus tachycardia with or without orthostatic hypotension.

 Postural orthostatic tachycardia syndrome

Treatment

Not required for physiologic sinus tachycardia. Underlying causes are treated if present.

Acute myocardial infarction. Sinus tachycardia can present in more than a third of the patients with AMI but this usually decreases over time. Patients with sustained sinus tachycardia reflects a larger infarct that are more anterior with prominent left ventricular dysfunction, associated with high mortality and morbidity. Tachycardia in the presence of AMI can reduce coronary blood flow and increase myocardial oxygen demand, aggravating the situation. Beta blockers can be used to slow the rate, but most patients are usually already treated with beta blockers as a routine regimen for AMI.

Practically, many studies showed that there is no need for any treatment.

IST and POTS. Beta blockers are useful if the cause is sympathetic overactivity. If the cause is due to decreased vagal activity, it is usually hard to treat and one may consider radiofrequency catheter ablation.

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Ezetimibe

Ezetimibe   is a drug that lowers cholesterol. It acts by decreasing cholesterol absorption in the intestine. It may be used alone (marketed as Zetia or Ezetrol), when other cholesterol-lowering medications are not tolerated, or together with statins (e.g., ezetimibe/simvastatin, marketed as Vytorin and Inegy) when statins alone do not control cholesterol.

Even though ezetimibe decreases cholesterol levels, the results of two major, high-quality clinical trials (in 2008 and 2009) showed that it did not improve clinically significant outcomes, such as major coronary events, and actually made some outcomes, such as artery wall thickness, worse. Indeed, a panel of experts concluded in 2008 that it should "only be used as a last resort". In one of those studies, a head-to-head trial in 2009, a much less expensive medication (extended-release niacin) was found to be superior. Ezetimibe actually increased the thickness of artery walls (a measurement of atherosclerosis) and caused more major cardiovascular events. A more positive view of the benefits of Ezetimibe is offered by Britain's NICE statement which however was published in 2007 and may not have been updated to reflect the results of the above mentioned trials 

Pharmacology

Ezetimibe localises at the brush border of the small intestine, where it inhibits the absorption of cholesterol from the intestine. Specifically, it appears to bind to a critical mediator of cholesterol absorption, the Niemann-Pick C1-Like 1 (NPC1L1) protein on the gastrointestinal tract epithelial cells as well as in hepatocytes. In addition to this direct effect, decreased cholesterol absorption leads to an upregulation of LDL-receptors on the surface of cells and an increased LDL-cholesterol uptake into cells, thus decreasing levels of LDL in the blood plasmawhich contribute to atherosclerosis and cardiovascular events

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Hypertriglyceridemia

In medicine, hypertriglyceridemia denotes high (hyper-) blood levels (-emia) oftriglycerides, the most abundant fatty molecule in most organisms. It has been associated with atherosclerosis, even in the absence of hypercholesterolemia (highcholesterol levels). It can also lead to pancreatitis in excessive concentrations (i.e. when the triglyceride concentration is greater, and often very much greater, than 1000 mg/dl or 12 mmol/l). Very high triglyceride levels may also interfere with blood tests; hyponatremia may be reported spuriously (pseudohyponatremia).

A related term is "hyperglyceridemia" which refers to a high level of all glycerides, including monoglycerides, diglycerides and triglycerides.

Signs and symptoms  

Modestly elevated triglyceride levels do not lead to any physical symptoms. Higher levels are associated with lipemia retinalis(white appearance of the retina), eruptive xanthomas (small lumps in the skin, sometimes itchy).

Causes

• High carbohydrate diet
• Idiopathic (constitutional)
• Obesity
• Diabetes mellitus and insulin resistance - it is one of the defined components of metabolic syndrome (along with central obesity, hypertension, and hyperglycemia)
• Excess alcohol intake
• renal failure, Nephrotic syndrome
• Genetic predisposition; some forms of familial hyperlipidemia such as familial combined hyperlipidemia i.e. Type II hyperlipidemia
• Lipoprotein lipase deficiency - Deficiency of this water soluble enzyme, that hydrolyzes triglycerides in lipoproteins, leads to elevated levels of triglycerides in the blood.
• Lysosomal acid lipase deficiency or Cholesteryl ester storage disease
• Certain medications e.g. isotretinoin, estrogen, hydrochlorothiazide diuretics, beta blockers, protease inhibitors
• Hypothyroidism (underactive thyroid)
• Systemic Lupus Erythematosus
• Glycogen storage disease type 1.          

Relationship of Hypertriglyceridemia to Atherosclerosis

Since triglycerides are not a component of the atherosclerotic plaque, it is not intuitively obvious whether hypertriglyceridemia promotes atherosclerosis. Numerous studies (summarized in references ) have examined the relationship between hypertriglyceridemia and atherosclerosis with a definitive answer still not apparent. In large part, the conflicting results reflect whether various other relevant risk factors for atherosclerosis were examined and taken into account. Specifically, the following are all risk factors for atherosclerosis and all are also associated with (not necessarily in a causal way) hypertriglyceridemia:

• obesity
• diabetes and insulin resistance
• metabolic syndrome
• presence of other dyslipidemias associated themselves both with high triglycerides and atherosclerosis (e.g. mixed hyperlipidemia, low HDL (hypoalphalipoproteinemia), Familial dysbetalipoproteinemia (type III hyperlipoproteinemia), etc.)
• high levels of small, dense LDL
• high levels of apolipoprotein B (apoB)

In other words, any study purporting to demonstrate an association of hypertriglyceridemia and atheroslerosis must not only have controlled for the classic atherosclerosis risk factors but also for the more recently recognized risk factors such as insulin resistance, levels of small, dense LDL, and apoB levels. The relationship among hypertriglyceridemia, atherosclerosis, and apoB is particularly instructive. Specifically, those forms of hypertriglyceridemia associated with high levels of apoB, but not those associated with low levels of apoB, are associated with atherosclerosis             

Treatment

Treatment of hypertriglyceridemia is by restriction of carbohydrates and fat in the diet, as well as with niacin, fibrates and statins(three classes of drugs). Increased fish oil intake may substantially lower an individual's triglycerides.

Clinical practice guidelines by the National Cholesterol Education Program (NCEP) suggest that pharmacotherapy should be considered for a triglycerides level over 200 mg/dL. The guidelines state "the sum of LDL + VLDL cholesterol (termed non-HDL cholesterol [total cholesterol - HDL cholesterol]) as a secondary target of therapy in persons with high triglycerides (200 mg/dL). The goal for non-HDL cholesterol in persons with high serum triglycerides can be set at 30 mg/dL higher than that for LDL cholesterol  on the premise that a VLDL cholesterol level 30 mg/dL is normal."

Non–HDL cholesterol contains the highly atherogenic, small, dense lipoproteins that are associated with a high incidence of cardiovascular disease (CVD). Studies subsequent to the NCEP report have shown that the non–HDL cholesterol level predicts CVD in people who have diabetes. It may be superior to LDL cholesterol in this regard, and should be used as the primary lipid target in persons with diabetes

Primary prevention

Omega-3 fatty acid supplementation in the form of fish oil has been found to be effective in decreasing levels of triglycerides and all cardiovascular events by 19% to 45%.

Gemfibrozil twice daily in asymptomatic men ages 40–55 without heart disease was also found to be effective at reducing cardiac endpoints at 5 years (4.14% to 2.73%). This means that 71 people must take the treatment for five years to prevent one cardiac event (number needed to treat of 71).

Secondary prevention

A randomized controlled trial of men with known heart disease and HDL cholesterol of 40 mg/dl or less, 600 mg of gemfibrozil twice daily reduced cardiac endpoints (non-fatal myocardial infarction or death from coronary causes) at 5 years from 21.7% to 17.3%. This means that 23 patients must be treated for five years to prevent one cardiac event (number needed to treat is 23).

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Hideki Yukawa and the Pion

Once quantum electrodyamics had produced the picture of the electromagnetic force as a process of exchanging photons, the question of whether or not the other forces were also exchange forces was a natural one. In 1935, Hideki Yukawa reasoned that the electromagnetic force was infinite in range because the exchange particle was massless. He proposed that the short range strong force came about from the exchange of a massive particle which he called a meson. By observing that the effective range of the nuclear force was on the order of a fermi, a mass for the exchange particle could be predicted using the uncertainty principle. The predicted particle mass was about 100 MeV. It did not receive immediate attention since no one knew of a particle which fit that description.

In 1937 a particle of mass close to Yukawa's prediction was discovered in cosmic rays by Anderson & Neddermeyer and by Street & Stevenson in independent experiments. This particle, the muon, turned out not to interact by the strong interaction. Hans Bethe and Robert Marshak predicted that the muon could be a decay product of the particle sought. In 1947, Lattes, Muirhead, Occhialini and Powell conducted a high altitude experiment, flying photographic emulsions at 3000 meters. These emulsions revealed the pion, which met all the requirements of the Yukawa particle.


We now know that the pion is a meson, a composite particle, and the current view is that the strong interaction is an interaction between quarks, but the Yukawa theory stimulated a major advance in the understanding of the strong interaction.

Einstein talks with Hideki Yukawa, 1949 Nobel Laureate in Physics and John A. Wheeler, a Hopkins alum

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Baryons

Baryons are massive particles which are made up of three quarks in the standard model. This class of particles includes the proton and neutron. Other baryons are the lambda, sigma, xi, and omega particles. Baryons are distinct from mesons in that mesons are composed of only two quarks. Baryons and mesons are included in the overall class known as hadrons, the particles which interact by the strong force. Baryons are fermions, while the mesons are bosons. Besides charge and spin (1/2 for the baryons), two other quantum numbers are assigned to these particles: baryon number (B=1) and strangeness (S), which in the chart can be seen to be equal to -1 times the number of strange quarks included.
The conservation of baryon number is an important rule for interactions and decays of baryons. No known interactions violate conservation of baryon number.
Recent experimental evidence shows the existence of five-quark combinations which are being called pentaquarks. The pentaquark would be included in the classification of baryons, albeit an "exotic" one. The pentaquark is composed of four quarks and an antiquark, like a combination of an ordinary baryon plus a meson.

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pion

Particle	Symbol	Anti- particle	Makeup	Rest mass MeV/c2	S	C	B	Lifetime	Decay Modes
Pion	π+	π-	ud	139.6	0	0	0	2.60 x10-8	μ+νμ
Pion	π0	Self		135.0	0	0	0	0.83 x10-16	2γ

The neutral pion decays to an electron, positron, and gamma ray by the electromagnetic interaction on a time scale of about 10^-16 seconds. The positive and negative pions have longer lifetimes of about 2.6 x 10^-8 s.
The negative pion decays into a muon and a muon antineutrino as illustrated below. This decay is puzzling upon first examination because the decay into an electron plus an electron antineutrino yields much more energy. Usually the pathway with the greatest energy yield is the preferred pathway. This suggests that some symmetry is acting to inhibit the electron decay pathway.
The symmetry which suppresses the electron pathway is that of angular momentum, as described by Griffiths. Since the negative pion has spin zero, the electron and antineutrino must be emitted with opposite spins to preserve net zero spin. But the antineutrino is always right-handed, so this implies that the electron must be emitted with spin in the direction of its linear momentum (i.e., also right-handed). But if the electron were massless, it would (like the neutrino) only exist as a left-handed particle, and the electron pathway would be completely prohibited. So the suppression of the electron pathway is attributed to the fact that the electron's small mass greatly favors the left-handed symmetry, thus inhibiting the decay. Weak interaction theory predicts that the fraction of muons decaying into electrons should be 1.28 x 10^-4 and the measured branching ratio is 1.23 +/- 0.02 x 10^-4.
The pion, being the lightest meson, can be used to predict the maximum range of the strong interaction. The strong interaction properties of the three pions are identical. The connection between pions and the strong force was proposed by Hideki Yukawa. Yukawa worked out a potential for the force and predicted its mass based on the uncertainty principle from measurements of the apparent range of the strong force in nuclei.
Being composed of an up and an antidown quark, the positive pion would be expected to have a mass about 2/3 that of a proton, yet it's mass is only about 1/6 of that of the proton! This is an example of how hadron masses depend upon the dynamics inside the particle, and not just upon the quarks contained.

The pion is a meson. The π+ isconsidered to be made up of anup and an anti-down quark. The neutral pion is considered to be a combination

Pions interact with nuclei and transform a neutron to a proton or vice versa:
The pions π⁺ and π^- have spin zero and negative intrinsic parity (Rohlf Sec 17-2).

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Mesons

Mesons are intermediate mass particles which are made up of a quark-antiquark pair. Three quark combinations are called baryons. Mesons are bosons, while the baryons are fermions. Recent experimental evidence shows the existence of five-quark combinations which are being called pentaquarks.

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Microcephaly

Microcephaly is a neurodevelopmental disorder in which the circumference of the head is more than two standard deviations smaller than average for the person's age and sex. Microcephaly may be congenital or it may develop in the first few years of life. The disorder may stem from a wide variety of conditions that cause abnormal growth of the brain, or from syndromes associated with chromosomal abnormalities. Two copies of a loss-of-function mutation in one of themicrocephalin genes causes primary microcephaly.

In general, life expectancy for individuals with microcephaly is reduced and the prognosis for normal brain function is poor. The prognosis varies depending on the presence of associated abnormalities.

Causes                           

Microcephaly is a type of cephalic disorder.

A genetic factor may play a role in causing some cases of microcephaly. Relations have been found between autism, duplications of chromosomes and macrocephaly on one side. On the other side a relation has been found between schizophrenia, deletions of chromosomes and microcephaly

Microencephaly

"Microcephaly" means "small head". "Microencephaly" means "small brain". Because the size of the head is mostly determined by the size of the brain, microencephaly is implied when discussing microcephaly

Other

Microcephaly can also be associated with other conditions that are only indirectly associated with the nervous system:

• alcoholism (which can result in the fetal alcohol syndrome disability)
• diabetes
• varicella zoster virus (Chickenpox)
• rubella (German measles)
• CMV (human cytomegaovirus)
• radiation

After the dropping of atomic bombs on Hiroshima and Nagasaki, several women close to ground zero who had been pregnant at the time gave birth to children with microcephaly. A total of seven of the in utero children at Hiroshima were affected.Microcephaly prevalence was 7 out of a group of 11 pregnant women who held the distinction of surviving the blast at an distance of ≈1 km from ground zero. Due to their proximity to the bomb, the pregnant women's in utero children received a biologically significant radiation dosage that was relatively high due to the massive neutron output of the lower explosive-yielding Little Boy.Microcephaly is the only proven malformation, or congenital abnormality, found in the children of Hiroshima and Nagasaki

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The Mathematical Probability Of Life On Other Earth-Like Planets

Infinity was invented to account for the possibility that in a never-ending universe, anything can happen. Life on other Earth-like planets, for example, is possible in an infinite universe, but not probable, according to a scientist from the University of East Anglia. 

The mathematical model produced by Prof Andrew Watson suggests that the odds of finding new life on other Earth-like planets are low because of the time it has taken for beings such as humans to evolve and the remaining life span of the Earth. Structurally complex and intelligent life evolved late on Earth and this process might be governed by a small number of very difficult evolutionary steps.

Prof Watson, from the School of Environmental Sciences, takes this idea further by looking at the probability of each of these critical steps occurring in relation to the life span of the Earth, giving an improved mathematical model for the evolution of intelligent life. 

According to Prof Watson a limit to evolution is the habitability of Earth, and any other Earth-like planets, which will end as the sun brightens. Solar models predict that the brightness of the sun is increasing, while temperature models suggest that because of this the future life span of Earth will be ‘only’ about another billion years, a short time compared to the four billion years since life first appeared on the planet.

“The Earth’s biosphere is now in its old age and this has implications for our understanding of the likelihood of complex life and intelligence arising on any given planet,” said Prof Watson. 

“At present, Earth is the only example we have of a planet with life. If we learned the planet would be habitable for a set period and that we had evolved early in this period, then even with a sample of one, we’d suspect that evolution from simple to complex and intelligent life was quite likely to occur. By contrast, we now believe that we evolved late in the habitable period, and this suggests that our evolution is rather unlikely. In fact, the timing of events is consistent with it being very rare indeed.”

Prof Watson suggests the number of evolutionary steps needed to create intelligent life, in the case of humans, is four. These probably include the emergence of single-celled bacteria, complex cells, specialized cells allowing complex life forms, and intelligent life with an established language. 

“Complex life is separated from the simplest life forms by several very unlikely steps and therefore will be much less common. Intelligence is one step further, so it is much less common still,” said Prof Watson.

His model, published in the journal Astrobiology, suggests an upper limit for the probability of each step occurring is 10 per cent or less, so the chances of intelligent life emerging is low – less than 0.01 per cent over four billion years.

Each step is independent of the other and can only take place after the previous steps in the sequence have occurred. They tend to be evenly spaced through Earth’s history and this is consistent with some of the major transitions identified in the evolution of life on Earth.

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Muscle relaxant

A muscle relaxant is a drug which affects skeletal muscle function and decreases the muscle tone. It may be used to alleviate symptoms such as musclespasms, pain, and hyperreflexia. The term "muscle relaxant" is used to refer to two major therapeutic groups: neuromuscular blockers and spasmolytics. Neuromuscular blockers act by interfering with transmission at the neuromuscular end plate and have no central nervous system (CNS) activity. They are often used during surgical procedures and in intensive care and emergency medicine to cause paralysis. Spasmolytics, also known as "centrally acting" muscle relaxants, are used to alleviate musculoskeletal pain and spasms and to reduce spasticity in a variety of neurological conditions. While both neuromuscular blockers and spasmolytics are often grouped together as muscle relaxants, the term is commonly used to refer to spasmolytics only

Neuromuscular blockers

Muscle relaxation and paralysis can theoretically occur by interrupting function at several sites, including the central nervous system, myelinated somatic nerves, unmyelinated motor nerve terminals, nicotinic acetylcholine receptors, the motor end plate, and the muscle membrane or contractile apparatus. Most neuromuscular blockers function by blocking transmission at the end plate of the neuromuscular junction. Normally, a nerve impulse arrives at the motor nerve terminal, initiating an influx of calcium ions, which causes the exocytosis of synaptic vesicles containing acetylcholine. Acetylcholine then diffuses across the synaptic cleft. It may be hydrolysed by acetylcholine esterase (AchE) or bind to the nicotinic receptors located on the motor end plate. The binding of two acetylcholine molecules results in a conformational change in the receptor that opens the sodium-potassium channel of the nicotinic receptor. This allows Na⁺ and Ca²⁺ ions to enter the cell and K⁺ ions to leave the cell, causing a depolarization of the end plate, resulting in muscle contraction. Following depolarization, the acetylcholine molecules are then removed from the end plate region and enzymatically hydrolysed by acetylcholinesterase.

Normal end plate function can be blocked by two mechanisms. Nondepolarizing agents, such ase tubocurarine, block theagonist, acetylcholine, from binding to nicotinic receptors and activating them, thereby preventing depolarization. Alternatively, depolarizing agents, such as succinylcholine, are nicotinic receptor agonists which mimic Ach, block muscle contraction by depolarizing to such an extent that it desensitizes the receptor and it can no longer initiate an action potential and cause muscle contraction. These neuromuscular blocking drugs are structurally similar to acetylcholine, the endogenous ligand, in many cases containing two acetylcholine molecules linked end-to-end by a rigid carbon ring system, as in pancuronium.

Spasmolytics

The generation of the neuronal signals in motor neurons that cause muscle contractions are dependent on the balance of synaptic excitation and inhibition the motor neuron receives. Spasmolytic agents generally work by either enhancing the level of inhibition, or reducing the level of excitation. Inhibition is enhanced by mimicking or enhancing the actions of endogenous inhibitory substances, such as GABA.

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Terminology

Because they may act at the level of the cortex, brain stem or spinal cord, or all three areas, they have traditionally been referred to as "centrally acting" muscle relaxants. However, it is now known not every agent in this class has CNS activity (e.g. dantrolene), so this name is inaccurate.

Most sources still use the term "centrally acting muscle relaxant". According to MeSH, dantrolene is usually classified as a centrally acting muscle relaxant. The World Health Organization, in its ATC, uses the term "centrally acting agents",but adds a distinct category of "directly acting agents", for dantrolene. Use of this terminology dates back to at least 1973.

The term "spasmolytic" is also considered a synonym for antispasmodic

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