Respiratory system

The respiratory system (also respiratory apparatus, ventilatory system) is a biological system consisting of specific organs and structures used for gas exchange in animals and plants. The anatomy and physiology that make this happen varies greatly, depending on the size of the organism, the environment in which it lives and its evolutionary history. In land animals the respiratory surface is internalized as linings of the lungs. Gas exchange in the lungs occurs in millions of small air sacs; in mammals and reptiles these are called alveoli, and in birds they are known as atria. These microscopic air sacs have a very rich blood supply, thus bringing the air into close contact with the blood. These air sacs communicate with the external environment via a system of airways, or hollow tubes, of which the largest is the trachea, which branches in the middle of the chest into the two main bronchi. These enter the lungs where they branch into progressively narrower secondary and tertiary bronchi that branch into numerous smaller tubes, the bronchioles. In birds the bronchioles are termed parabronchi. It is the bronchioles, or parabronchi that generally open into the microscopic alveoli in mammals and atria in birds. Air has to be pumped from the environment into the alveoli or atria by the process of breathing which involves the muscles of respiration.
In most fish, and a number of other aquatic animals (both vertebrates and invertebrates) the respiratory system consists of gills, which are either partially or completely external organs, bathed in the watery environment. This water flows over the gills by a variety of active or passive means. Gas exchange takes place in the gills which consist of thin or very flat filaments and lammelae which expose a very large surface area of highly vascularized tissue to the water.
Other animals, such as insects, have respiratory systems with very simple anatomical features, and in amphibians even the skin plays a vital role in gas exchange. Plants also have respiratory systems but the directionality of gas exchange can be opposite to that in animals. The respiratory system in plants includes anatomical features such as stomata, that are found in various parts of the plant.
Mammals.
Anatomy.
In humans and other mammals, the anatomy of a typical respiratory system is the respiratory tract. The tract is divided into an upper and a lower respiratory tract. The upper tract includes the nose, nasal cavities, sinuses, pharynx and the part of the larynx above the vocal folds. The lower tract (Fig. 2.) includes the lower part of the larynx, the trachea, bronchi, bronchioles and the alveoli.
The branching airways of the lower tract are often described as the respiratory tree or tracheobronchial tree (Fig. 2). The intervals between successive branch points along the various branches of "tree" are often referred to as branching "generations", of which there are, in the adult human about 23. The earlier generations (approximately generations 0–16), consisting of the trachea and the bronchi, as well as the larger bronchioles which simply act as air conduits, bringing air to the respiratory bronchioles, alveolar ducts and alveoli (approximately generations 17–23), where gas exchange takes place. Bronchioles are defined as the small airways lacking any cartilagenous support.
The first bronchi to branch from the trachea are the right and left main bronchi. Second only in diameter to the trachea (1.8 cm), these bronchi (1 -1.4 cm in diameter) enter the lungs at each hilum, where they branch into narrower secondary bronchi known as lobar bronchi, and these branch into narrower tertiary bronchi known as segmental bronchi. Further divisions of the segmental bronchi (1 to 6 mm in diameter) are known as 4th order, 5th order, and 6th order segmental bronchi, or grouped together as subsegmental bronchi.
Compared to the 23 number (on average) of branchings of the respiratory tree in the adult human, the mouse has only about 13 such branchings.
The alveoli are the dead end terminals of the "tree", meaning that any air that enters them has to exit via the same route. A system such as this creates dead space, a volume of air (about 150 ml in the adult human) that fills the airways after exhalation and is breathed back into the alveoli before environmental air reaches them. At the end of inhalation the airways are filled with environmental air, which is exhaled without coming in contact with the gas exchanger.
Ventilatory volumes.
The lungs expand and contract during the breathing cycle, drawing air in and out of the lungs. The volume of air moved in or out of the lungs under normal resting circumstances (the resting tidal volume of about 500 ml), and volumes moved during maximally forced inhalation and maximally forced exhalation are measured in humans by spirometry. A typical adult human spirogram with the names given to the various excursions in volume the lungs can undergo is illustrated below (Fig. 3):
Not all the air in the lungs can be expelled during maximally forced exhalation. This is the residual volume of about 1.0-1.5 liters which cannot be measured by spirometry. Volumes that include the residual volume (i.e. functional residual capacity of about 2.5-3.0 liters, and total lung capacity of about 6 liters) can therefore also not be measured by spirometry. Their measurement requires special techniques.
The rates at which air is breathed in or out, either through the mouth or nose, or into or out of the alveoli are tabulated below, together with how they are calculated. The number of breath cycles per minute is known as the respiratory rate.
Mechanics of breathing.
In mammals, inhalation at rest is primarily due to the contraction of the diaphragm. This is an upwardly domed sheet of muscle that separates the thoracic cavity from the abdominal cavity. When it contracts the sheet flattens, (i.e. moves downwards as shown in Fig. 7) increasing the volume of the thoracic cavity. The contracting diaphragm pushes the abdominal organs downwards. But because the pelvic floor prevents the lowermost abdominal organs moving in that direction, the pliable abdominal contents cause the belly to bulge outwards to the front and sides, because the relaxed abdominal muscles do not resist this movement (Fig. 7). This entirely passive bulging (and shrinking during exhalation) of the abdomen during normal breathing is sometimes referred to as "abdominal breathing", although it is, in fact, "diaphragmatic breathing", which is not visible on the outside of the body. Mammals only use their abdominal muscles during forceful exhalation (see Fig. 8, and discussion below). Never during any form of inhalation.
As the diaphragm contracts, the rib cage is simultaneously enlarged by the ribs being pulled upwards by the intercostal muscles as shown in Fig. 4. All the ribs slant downwards from the rear to the front (as shown in Fig. 4); but the lowermost ribs "also" slant downwards from the midline outwards (Fig. 5). Thus the rib cage's transverse diameter can be increased in the same way as the antero-posterior diameter is increase by the so-called pump handle movement shown in Fig. 4.
The enlargement of the thoracic cavity's vertical dimension by the contraction of the diaphragm, and its two horizontal dimensions by the lifting of the front and sides of the ribs, causes the intrathoracic pressure to fall. The lungs' interiors are open to the outside air, and being elastic, therefore expand to fill the increased space. The inflow of air into the lungs occurs via the respiratory airways (Fig. 2). In health, these airways begin with the nose. It is possible to begin with the mouth, which is the backup breathing system. However, chronic mouth breathing leads to, or is a sign of, illness. They end in the microscopic dead-end sacs called alveoli, which are always open, though the diameters of the various sections can be changed by the sympathetic and parasympathetic nervous systems. The alveolar air pressure is therefore always close to atmospheric air pressure (about 100 kPa at sea level) at rest, with the pressure gradients that cause air to move in and out of the lungs during breathing rarely exceeding 2–3 kPa.
During exhalation the diaphragm and intercostal muscles relax. This returns the chest and abdomen to a position determined by their anatomical elasticity. This is the "resting mid-position" of the thorax and abdomen (Fig. 7) when the lungs contain their functional residual capacity of air (the light blue area in the right hand illustration of Fig. 7), which in the adult human has a volume of about 2.5–3.0 liters (Fig. 3). Resting exhalation lasts about twice as long as inhalation because the diaphragm relaxes passively more gently than it contracts actively during inhalation.
The volume of air that moves in "or" out (at the nose or mouth) during a single breathing cycle is called the tidal volume. In a resting adult human it is about 500 ml per breath. At the end of exhalation the airways contain about 150 ml of alveolar air which is the first air that is breathed back into the alveoli during inhalation. This volume air that is breathed out of the alveoli and back in again is known as dead space ventilation, which has the consequence that of the 500 ml breathed into the alveoli with each breath only 350 ml (500 ml - 150 ml = 350 ml) is fresh warm and moistened air. Since this 350 ml of fresh air is thoroughly mixed and diluted by the air that remains in the alveoli after normal exhalation (i.e. the functional residual capacity of about 2.5–3.0 liters), it is clear that the composition of the alveolar air changes very little during the breathing cycle (see Fig. 9). The oxygen tension (or partial pressure) remains close to 13-14 kPa (about 100 mm Hg), and that of carbon dioxide very close to 5.3 kPa (or 40 mm Hg). This contrasts with composition of the dry outside air at sea level, where the partial pressure of oxygen is 21 kPa (or 160 mm Hg) and that of carbon dioxide 0.04 kPa (or 0.3 mmHg).
During heavy breathing (hyperpnea), as, for instance, during exercise, inhalation is brought about by a more powerful and greater excursion of the contracting diaphragm than at rest (Fig. 8). In addition the "accessory muscles of inhalation" exaggerate the actions of the intercostal muscles (Fig. 8). These accessory muscles of inhalation are muscles that extend from the cervical vertebrae and base of the skull to the upper ribs and sternum, sometimes through an intermediary attachment to the clavicles. When they contract the rib cage's internal volume is increased to a far greater extent than can be achieved by contraction of the intercostal muscles alone. Seen from outside the body the lifting of the clavicles during strenuous or labored inhalation is sometimes called clavicular breathing, seen especially during asthma attacks and in people with chronic obstructive pulmonary disease.
During heavy breathing, exhalation is caused by relaxation of all the muscles of inhalation. But now, the abdominal muscles, instead of remaining relaxed (as they do at rest), contract forcibly pulling the lower edges of the rib cage downwards (front and sides) (Fig. 8). This not only drastically decreases the size of the rib cage, but also pushes the abdominal organs upwards against the diaphragm which consequently bulges deeply into the thorax (Fig. 8). The end-exhalatory lung volume is now well below the resting mid-position and contains far less air than the resting "functional residual capacity". However, in a normal mammal, the lungs cannot be emptied completely. In an adult human there is always still at least 1 liter of residual air left in the lungs after maximum exhalation.
The automatic rhythmical breathing in and out, can be interrupted by coughing, sneezing (forms of very forceful exhalation), by the expression of a wide range of emotions (laughing, sighing, crying out in pain, exasperated intakes of breath) and by such voluntary acts as speech, singing, whistling and the playing of wind instruments. All of these actions rely on the muscles described above, and their effects on the movement of air in and out of the lungs.
Although not a form of breathing, the Valsalva maneuver involves the respiratory muscles. It is, in fact, a very forceful exhalatory effort against a tightly closed glottis, so that no air can escape from the lungs. Instead abdominal contents are evacuated in the opposite direction, through orifices in the pelvic floor. The abdominal muscles contract very powerfully, causing the pressure inside the abdomen and thorax to rise to extremely high levels. The Valsalva maneuver can be carried out voluntarily, but is more generally a reflex elicited when attempting to empty the abdomen during, for instance, difficult defecation, or during childbirth. Breathing ceases during this maneuver.
Gas exchange.
The primary purpose of the respiratory system is the equalizing of the partial pressures of the respiratory gases in the alveolar air with those in the pulmonary capillary blood (Fig. 11). This process occurs by simple diffusion, across a very thin membrane (known as the blood–air barrier), which forms the walls of the pulmonary alveoli (Fig. 10). It consists of the alveolar epithelial cells, their basement membranes and the endothelial cells of the alveolar capillaries (Fig. 10). This blood gas barrier is extremely thin (in humans, on average, 2.2 μm thick). It is folded into about 300 million small air sacs called alveoli (each between 75 and 300 µm in diameter) branching off from the respiratory bronchioles in the lungs, thus providing an extremely large surface area (approximately 145 m2) for gas exchange to occur.
The air contained within the alveoli has a semi-permanent volume of about 2.5-3.0 liters which completely surrounds the alveolar capillary blood (Fig. 12). This ensures that equilibration of the partial pressures of the gases in the two compartments is very efficient and occurs very quickly. The blood leaving the alveolar capillaries and is eventually distributed throughout the body therefore has a partial pressure of oxygen of 13-14 kPa (100 mmHg), and a partial pressure of carbon dioxide of 5.3 kPa (40 mmHg) (i.e. the same as the oxygen and carbon dioxide gas tensions as in the alveoli). As mentioned in the section above, the corresponding partial pressures of oxygen and carbon dioxide in the ambient (dry) air at sea level are 21 kPa (160 mmHg) and 0.04 kPa (0.3 mmHg) respectively.
This marked difference between the composition of the alveolar air and that of the ambient air can be maintained because the functional residual capacity is contained in dead-end sacs connected to the outside air by fairly narrow and relatively long tubes (the airways: nose, pharynx, larynx, trachea, bronchi and their branches down to the bronchioles), through which the air has to be breathed both in and out (i.e. there is no unidirectional through-flow as there is in the bird lung). This typical mammalian anatomy combined with the fact that the lungs are not emptied and re-inflated with each breath (leaving a substantial volume of air, of about 2.5-3.0 liters, in the alveoli after exhalation), ensures that the composition of the alveolar air is only minimally disturbed when the 350 ml of fresh air is mixed into it with each inhalation. Thus the animal is provided with a very special "portable atmosphere", whose composition differs significantly from the present-day ambient air. It is this portable atmosphere (the functional residual capacity) to which the blood and therefore the body tissues are exposed – not to the outside air.
The resulting arterial partial pressures of oxygen and carbon dioxide are homeostatically controlled. A rise in the arterial partial pressure of CO2 and, to a lesser extent, a fall in the arterial partial pressure of O2, will reflexly cause deeper and faster breathing till the blood gas tensions in the lungs, and therefore the arterial blood, return to normal. The converse happens when the carbon dioxide tension falls, or, again to a lesser extent, the oxygen tension rises: the rate and depth of breathing are reduced till blood gas normality is restored.
Since the blood arriving in the alveolar capillaries has a partial pressure of O2 of, on average, 6 kPa (45 mmHg), while the pressure in the alveolar air is 13-14 kPa (100 mmHg), there will be a net diffusion of oxygen into the capillary blood, changing the composition of the 3 liters of alveolar air slightly. Similarly, since the blood arriving in the alveolar capillaries has a partial pressure of CO2 of also about 6 kPa (45 mmHg), whereas that of the alveolar air is 5.3 kPa (40 mmHg), there is a net movement of carbon dioxide out of the capillaries into the alveoli. The changes brought about by these net flows of individual gases into and out of the alveolar air necessitate the replacement of about 15% of the alveolar air with ambient air every 5 seconds or so. This is very tightly controlled by the monitoring of the arterial blood gases (which accurately reflect composition of the alveolar air) by the aortic and carotid bodies, as well as by the blood gas and pH sensor on the anterior surface of the medulla oblongata in the brain. There are also oxygen and carbon dioxide sensors in the lungs, but they primarily determine the diameters of the bronchioles and pulmonary capillaries, and are therefore responsible for directing the flow of air and blood to different parts of the lungs.
It is only as a result of accurately maintaining the composition of the 3 liters of alveolar air that with each breath some carbon dioxide is discharged into the atmosphere and some oxygen is taken up from the outside air. If more carbon dioxide than usual has been lost by a short period of hyperventilation, respiration will be slowed down or halted until the alveolar partial pressure of carbon dioxide has returned to 5.3 kPa (40 mmHg). It is therefore strictly speaking untrue that the primary function of the respiratory system is to rid the body of carbon dioxide “waste”. The carbon dioxide that is breathed out with each breath could probably be more correctly be seen as a byproduct of the body's extracellular fluid carbon dioxide and pH homeostats
If these homeostats are compromised, then a respiratory acidosis, or a respiratory alkalosis will occur. In the long run these can be compensated by renal adjustments to the H+ and HCO3− concentrations in the plasma; but since this takes time, the hyperventilation syndrome can, for instance, occur when agitation or anxiety cause a person to breathe fast and deeply thus causing a distressing respiratory alkalosis through the blowing off of too much CO2 from the blood into the outside air.
Oxygen has a very low solubility in water, and is therefore carried in the blood loosely combined with hemoglobin. The oxygen is held on the hemoglobin by four ferrous iron-containing heme groups per hemoglobin molecule. When all the heme groups carry one O2 molecule each the blood is said to be “saturated” with oxygen, and no further increase in the partial pressure of oxygen will meaningfully increase the oxygen concentration of the blood. Most of the carbon dioxide in the blood is carried as bicarbonate ions (HCO3−) in the plasma. However the conversion of dissolved CO2 into HCO3− (through the addition of water) is too slow for the rate at which the blood circulates through the tissues on the one hand, and through alveolar capillaries on the other. The reaction is therefore catalyzed by carbonic anhydrase, an enzyme inside the red blood cells. The reaction can go in both directions depending on the prevailing partial pressure of CO2. A small amount of carbon dioxide is carried on the protein portion of the hemoglobin molecules as carbamino groups. The total concentration of carbon dioxide (in the form of bicarbonate ions, dissolved CO2, and carbamino groups) in arterial blood (i.e. after it has equilibrated with the alveolar air) is about 26 mM (or 58 ml/100 ml), compared to the concentration of oxygen in saturated arterial blood of about 9 mM (or 20 ml/100 ml blood).
Control of ventilation.
Ventilation of the lungs in mammals occurs via the respiratory centers in the medulla oblongata and the pons of the brainstem. These areas form a series of neural pathways which receive information about the partial pressures of oxygen and carbon dioxide in the arterial blood. This information determines the average rate of ventilation of the alveoli of the lungs, to keep these pressures constant. The respiratory center does so via motor nerves which activate the diaphragm and other muscles of respiration.
The breathing rate increases when the partial pressure of carbon dioxide in the blood increases. This is detected by central blood gas chemoreceptors on the anterior surface of the medulla oblongata. The aortic and carotid bodies, are the peripheral blood gas chemoreceptors which are particularly sensitive to the arterial partial pressure of O2 though they also respond, but less strongly, to the partial pressure of CO2. At sea level, under normal circumstances, the breathing rate and depth, is determined primarily by the arterial partial pressure of carbon dioxide rather than by the arterial partial pressure of oxygen, which is allowed to vary within a fairly wide range before the respiratory centers in the medulla oblongata and pons respond to it to change the rate and depth of breathing.
Exercise increases the breathing rate due to the extra carbon dioxide produced by the enhanced metabolism of the exercising muscles. In addition passive movements of the limbs also reflexively produce an increase in the breathing rate.
Information received from stretch receptors in the lungs limits tidal volume (the depth of inhalation and exhalation).
Responses to low atmospheric pressures.
The alveoli are open (via the airways) to the atmosphere, with the result that alveolar air pressure is exactly the same as the ambient air pressure at sea level, at altitude, or in any artificial atmosphere (e.g. a diving chamber, or decompression chamber) in which the individual is breathing freely. With expansion of the lungs the alveolar air occupies a larger volume, and its pressure falls proportionally, causing air to flow in through the airways, till the pressure in the alveoli is again at the ambient air pressure. The reverse happens during exhalation. This "process" (of inhalation and exhalation) is exactly the same at sea level, as on top of Mt. Everest, or in a diving chamber or decompression chamber.
However, as one rises above sea level the density of the air decreases exponentially (see Fig. 14), halving approximately with every 5500 m rise in altitude. Since the composition of the atmospheric air is almost constant below 80 km, as a result of the continuous mixing effect of the weather, the concentration of oxygen in the air (mmols O2 per liter of ambient air) decreases at the same rate as the fall in air pressure with altitude. Therefore, in order to breathe in the same amount of oxygen per minute, the person has to inhale a proportionately greater volume of air per minute at altitude than at sea level. This is achieved by breathing deeper and faster (i.e. hyperpnea) than at sea level (see below).
There is, however, a complication that increases the volume of air that needs to be inhaled per minute (respiratory minute volume) to provide the same amount of oxygen to the lungs at altitude as at sea level. During inhalation the air is warmed and saturated with water vapor during its passage through the nose passages and pharynx. Saturated water vapor pressure is dependent only on temperature. At a body core temperature of 37 °C it is 6.3 kPa (47.0 mmHg), irrespective of any other influences, including altitude. Thus at sea level, where the ambient atmospheric pressure is about 100 kPa, the moistened air that flows into the lungs from the trachea consists of water vapor (6.3 kPa), nitrogen (74.0 kPa), oxygen (19.7 kPa) and trace amounts of carbon dioxide and other gases (a total of 100 kPa). In dry air the partial pressure of O2 at sea level is 21.0 kPa (i.e. 21% of 100 kPa), compared to the 19.7 kPa of oxygen entering the alveolar air. (The tracheal partial pressure of oxygen is 21% of [100 kPa – 6.3 kPa] = 19.7 kPa). At the summit of Mt. Everest (at an altitude of 8,848 m or 29,029 ft) the total atmospheric pressure is 33.7 kPa, of which 7.1 kPa (or 21%) is oxygen. The air entering the lungs also has a total pressure of 33.7 kPa, of which 6.3 kPa is, unavoidably, water vapor (as it is at sea level). This reduces the partial pressure of oxygen entering the alveoli to 5.8 kPa (or 21% of [33.7 kPa – 6.3 kPa] = 5.8 kPa). The reduction in the partial pressure of oxygen in the inhaled air is therefore substantially greater than the reduction of the total atmospheric pressure at altitude would suggest (on Mt Everest: 5.8 kPa "vs." 7.1 kPa).
A further minor complication exists at altitude. If the volume of the lungs were to be instantaneously doubled at the beginning of inhalation, the air pressure inside the lungs would be halved. This happens regardless of altitude. Thus, halving of the sea level air pressure (100 kPa) results in an intrapulmonary air pressure of 50 kPa. Doing the same at 5500 m, where the atmospheric pressure is only 50 kPa, the intrapulmonary air pressure falls to 25 kPa. Therefore, the same change in lung volume at sea level results in a 50 kPa difference in pressure between the ambient air and the intrapulmonary air, whereas it result in a difference of only 25 kPa at 5500 m. The driving pressure forcing air into the lungs during inhalation is therefore halved at this altitude. The "rate" of inflow of air into the lungs during inhalation at sea level is therefore twice that which occurs at 5500 m. However, in reality, inhalation and exhalation occur far more gently and less abruptly than in the example given. The differences between the atmospheric and intrapulmonary pressures, driving air in and out of the lungs during the breathing cycle, are in the region of only 2–3 kPa. A doubling or more of these small pressure differences could be achieved only by very major changes in the breathing effort at high altitudes.
All of the above influences of low atmospheric pressures on breathing are accommodated primarily by breathing deeper and faster (hyperpnea). The exact degree of hyperpnea is determined by the blood gas homeostat, which regulates the partial pressures of oxygen and carbon dioxide in the arterial blood. This homeostat prioritizes the regulation of the arterial partial pressure of carbon dioxide over that of oxygen at sea level. That is to say, at sea level the arterial partial pressure of CO2 is maintained at very close to 5.3 kPa (or 40 mmHg) under a wide range of circumstances, at the expense of the arterial partial pressure of O2, which is allowed to vary within a very wide range of values, before eliciting a corrective ventilatory response. However, when the atmospheric pressure (and therefore the partial pressure of O2 in the ambient air) falls to below 50-75% of its value at sea level, oxygen homeostasis is given priority over carbon dioxide homeostasis. This switch-over occurs at an elevation of about 2500 m (or about 8000 ft). If this switch occurs relatively abruptly, the hyperpnea at high altitude will cause a severe fall in the arterial partial pressure of carbon dioxide, with a consequent rise in the pH of the arterial plasma. This is one contributor to high altitude sickness. On the other hand, if the switch to oxygen homeostasis is incomplete, then hypoxia may complicate the clinical picture with potentially fatal results.
There are oxygen sensors in the smaller bronchi and bronchioles. In response to low partial pressures of oxygen in the inhaled air these sensors reflexively cause the pulmonary arterioles to constrict. (This is the exact opposite of the corresponding reflex in the tissues, where low arterial partial pressures of O2 cause arteriolar vasodilation.) At altitude this causes the pulmonary arterial pressure to rise resulting in a much more even distribution of blood flow to the lungs than occurs at sea level. At sea level the pulmonary arterial pressure is very low, with the result that the tops of the lungs receive far less blood than the bases, which are relatively over-perfused with blood. It is only in the middle of the lungs that the blood and air flow to the alveoli are ideally matched. At altitude this variation in the ventilation/perfusion ratio of alveoli from the tops of the lungs to the bottoms is eliminated, with all the alveoli perfused and ventilated in more or less the physiologically ideal manner. This is a further important contributor to the acclimatatization to high altitudes and low oxygen pressures.
The kidneys measure the oxygen "content" (mmol O2/liter blood, rather than the partial pressure of O2) of the arterial blood. When the oxygen content of the blood is chronically low, as at high altitude, the oxygen-sensitive kidney cells secrete erythropoietin (EPO) into the blood. This hormone stimulates the red bone marrow to increase its rate of red cell production, which leads to an increase in the hematocrit of the blood, and a consequent increase in its oxygen carrying capacity (due to the now high hemoglobin content of the blood). In other words, at the same arterial partial pressure of O2, a person with a high hematocrit carries more oxygen per liter of blood than a person with a lower hematocrit does. High altitude dwellers therefore have higher hematocrits than sea-level residents.
Other functions of the lungs.
Local defenses.
Irritation of nerve endings within the nasal passages or airways, can induce a cough reflex and sneezing. These responses cause air to be expelled forcefully from the trachea or nose, respectively. In this manner, irritants caught in the mucus which lines the respiratory tract are expelled or moved to the mouth where they can be swallowed. During coughing, contraction of the smooth muscle in the airway walls narrows the trachea by pulling the ends of the cartilage plates together and by pushing soft tissue into the lumen. This increases the expired airflow rate to dislodge and remove any irritant particle or mucus.
Respiratory epithelium can secrete a variety of molecules that aid in the defense of the lungs. These include secretory immunoglobulins (IgA), collectins, defensins and other peptides and proteases, reactive oxygen species, and reactive nitrogen species. These secretions can act directly as antimicrobials to help keep the airway free of infection. A variety of chemokines and cytokines are also secreted that recruit the traditional immune cells and others to the site of infections.
Surfactant immune function is primarily attributed to two proteins: SP-A and SP-D. These proteins can bind to sugars on the surface of pathogens and thereby opsonize them for uptake by phagocytes. It also regulates inflammatory responses and interacts with the adaptive immune response. Surfactant degradation or inactivation may contribute to enhanced susceptibility to lung inflammation and infection.
Most of the respiratory system is lined with mucous membranes that contain mucosa-associated lymphoid tissue, which produces white blood cells such as lymphocytes.
Prevention of alveolar collapse.
The lungs make a surfactant, a surface-active lipoprotein complex (phospholipoprotein) formed by type II alveolar cells. It floats on the surface of the thin watery layer which lines the insides of the alveoli, reducing the water's surface tension.
The surface tension of a watery surface (the water-air interface) tends to make that surface shrink. When that surface is curved as it is in the alveoli of the lungs, the shrinkage of the surface decreases the diameter of the alveoli. The more acute the curvature of the water-air interface the greater the tendency for the alveolus to collapse. This has three effects. Firstly the surface tension inside the alveoli resists expansion of the alveoli during inhalation (i.e. it makes the lung stiff, or non-compliant). Surfactant reduces the surface tension and therefore makes the lungs more compliant, or less stiff, than if it were not there. Secondly, the diameters of the alveoli increase and decrease during the breathing cycle. This means that the alveoli have a greater tendency to collapse (i.e. cause atelectasis) at the end of exhalation that at the end of inhalation. Since surfactant floats on the watery surface, its molecules are more tightly packed together when the alveoli shrink during exhalation. This causes them to have a greater surface tension-lowering effect when the alveoli are small than when they are large (as at the end of inhalation, when the surfactant molecules are more widely spaced). The tendency for the alveoli to collapse is therefore almost the same at the end of exhalation as at the end of inhalation. Thirdly, the surface tension of the curved watery layer lining the alveoli tends to draw water from the lung tissues into the alveoli. Surfactant reduces this danger to negligible levels, and keeps the alveoli dry.
Pre-term babies who are unable to manufacture surfactant have lungs that tend to collapse each time they breathe out. Unless treated, this condition, called respiratory distress syndrome, is fatal. Basic scientific experiments, carried out using cells from chicken lungs, support the potential for using steroids as a means of furthering development of type II alveolar cells. In fact, once a premature birth is threatened, every effort is made to delay the birth, and a series of steroid injections is frequently administered to the mother during this delay in an effort to promote lung maturation.
Contributions to whole body functions.
The lung vessels contain a fibrinolytic system that dissolves clots that may have arrived in the pulmonary circulation by embolism, often from the deep veins in the legs. They also release a variety of substances that enter the systemic arterial blood, and they remove other substances from the systemic venous blood that reach them via the pulmonary artery. Some prostaglandins are removed from the circulation, while others are synthesized in the lungs and released into the blood when lung tissue is stretched.
The lungs activate one hormone. The physiologically inactive decapeptide angiotensin I is converted to the aldosterone-releasing octapeptide, angiotensin II, in the pulmonary circulation. The reaction occurs in other tissues as well, but it is particularly prominent in the lungs. Angiotensin II also has a direct effect on arteriolar walls, causing arteriolar vasoconstriction, and consequently a rise in arterial blood pressure. Large amounts of the angiotensin-converting enzyme responsible for this activation are located on the surfaces of the endothelial cells of the alveolar capillaries. The converting enzyme also inactivates bradykinin. Circulation time through the alveolar capillaries is less than one second, yet 70% of the angiotensin I reaching the lungs is converted to angiotensin II in a single trip through the capillaries. Four other peptidases have been identified on the surface of the pulmonary endothelial cells.
Vocalization.
The movement of gas through the larynx, pharynx and mouth allows humans to speak, or "phonate". Vocalization, or singing, in birds occurs via the syrinx, an organ located at the base of the trachea. The vibration of air flowing across the larynx (vocal cords), in humans, and the syrinx, in birds, results in sound. Because of this, gas movement is vital for communication purposes.
Temperature control.
Panting in dogs, cats, birds and some other animals provides a means of reducing body temperature, by evaporating saliva in the mouth (instead of evaporating sweat on the skin).
Clinical significance.
Disorders of the respiratory system can be classified into several general groups:
Disorders of the respiratory system are usually treated by a pulmonologist and respiratory therapist.
Where there is an inability to breathe or an insufficiency in breathing a medical ventilator may be used.
Exceptional mammals.
Horses.
Horses are obligate nasal breathers which means that they are different from many other mammals because they do not have the option of breathing through their mouths and must take in air through their noses.
Elephants.
The elephant is the only mammal known to have no pleural space. Rather, the parietal and visceral pleura are both composed of dense connective tissue and joined to each other via loose connective tissue. This lack of a pleural space, along with an unusually thick diaphragm, are thought to be evolutionary adaptations allowing the elephant to remain underwater for long periods of time while breathing through its trunk which emerges as a snorkel.
In the elephant the lungs are attached to the diaphragm and breathing relies mainly on the diaphragm rather than the expansion of the ribcage.
Birds.
The respiratory system of birds differs significantly from that found in mammals. Firstly, they have rigid lungs which do not expand and contract during the breathing cycle. Instead an extensive system of air sacs (Fig. 15) distributed throughout their bodies act as the bellows drawing environmental air into the sacs, and expelling the spent air after it has passed through the lungs (Fig. 18). Birds also do not have diaphragms or pleural cavities.
Bird lungs are smaller than those in mammals of comparable size, but the air sacs account for 15% of the total body volume, compared to the 7% devoted to the alveoli which act as the bellows in mammals.
Inhalation and exhalation are brought about by alternately increasing and decreasing the volume of the entire thoraco-abdominal cavity (or coelom) using both their abdominal and costal muscles. During inhalation the muscles attached to the vertebral ribs (Fig. 17) contract angling them forwards and outwards. This pushes the sternal ribs, to which they are attached at almost right angles, downwards and forwards, taking the sternum (with its prominent keel) in the same direction (Fig. 17). This increases both the vertical and transverse diameters of thoracic portion of the trunk. The forward and downward movement of, particularly, the posterior end of the sternum pulls the abdominal wall downwards, increasing the volume of that region of the trunk as well. The increase in volume of the entire trunk cavity reduces the air pressure in all the thoraco-abdominal air sacs, causing them to fill with air as described below.
During exhalation the external oblique muscle which is attached to the sternum and vertebral ribs anteriorly, and to the pelvis (pubis and ilium in Fig. 17) posteriorly (forming part of the abdominal wall) reverses the inhalatory movement, while compressing the abdominal contents, thus increasing the pressure in all the air sacs. Air is therefore expelled from the respiratory system in the act of exhalation.
During inhalation air enters the trachea via the nostrils and mouth, and continues to just beyond the syrinx at which point the trachea branches into two primary bronchi, going to the two lungs (Fig. 16). The primary bronchi enter the lungs to become the intrapulmonary bronchi, which give off a set of parallel branches called ventrobronchi and, a little further on, an equivalent set of dorsobronchi (Fig. 16). The ends of the intrapulmonary bronchi discharge air into the posterior air sacs at the caudal end of the bird. Each pair of dorso-ventrobronchi is connected by a large number of parallel microscopic air capillaries (or parabronchi) where gas exchange occurs (Fig. 16). As the bird inhales, tracheal air flows through the intrapulmonary bronchi into the posterior air sacs, as well as into the "dorso"bronchi, but not into the "ventro"bronchi (Fig. 18). This is due to the bronchial architecture which directs the inhaled air away from the openings of the ventrobronchi, into the continuation of the intrapulmonary bronchus towards the dorsobronchi and posterior air sacs. From the dorsobronchi the inhaled air flows through the parabronchi (and therefore the gas exchanger) to the ventrobronchi from where the air can only escape into the expanding anterior air sacs. So, during inhalation, both the posterior and anterior air sacs expand, the posterior air sacs filling with fresh inhaled air, while the anterior air sacs fill with "spent" (oxygen-poor) air that has just passed through the lungs.
During exhalation the pressure in the posterior air sacs (which were filled with fresh air during inhalation) increases due to the contraction of the oblique muscle described above. The aerodynamics of the interconnecting openings from the posterior air sacs to the dorsobronchi and intrapulmonary bronchi ensures that the air leaves these sacs in the direction of the lungs (via the dorsobronchi), rather than returning down the intrapulmonary bronchi (Fig. 18). From the dorsobronchi the fresh air from the posterior air sacs flows through the parabronchi (in the same direction as occurred during inhalation) into ventrobronchi. The air passages connecting the ventrobronchi and anterior air sacs to the intrapulmonary bronchi direct the "spent", oxygen poor air from these two organs to the trachea from where it escapes to the exterior. Oxygenated air therefore flows constantly (during the entire breathing cycle) in a single direction through the parabronchi.
The blood flow through the bird lung is at right angles to the flow of air through the parabronchi, forming a cross-current flow exchange system (Fig. 19). The partial pressure of oxygen in the parabronchi declines along their lengths as O2 diffuses into the blood. The blood capillaries leaving the exchanger near the entrance of airflow take up more O2 than do the capillaries leaving near the exit end of the parabronchi. When the contents of all capillaries mix, the final partial pressure of oxygen of the mixed pulmonary venous blood is higher than that of the exhaled air, but is nevertheless less than half that of the inhaled air, thus achieving roughly the same systemic arterial blood partial pressure of oxygen as mammals do with their bellows-type lungs.
The trachea is an area of dead space: the oxygen-poor air it contains at the end of exhalation is the first air to re-enter the posterior air sacs and lungs. In comparison to the mammalian respiratory tract, the dead space volume in a bird is, on average, 4.5 times greater than it is in mammals of the same size. Birds with long necks will inevitably have long tracheae, and must therefore take deeper breaths than mammals do to make allowances for their greater dead space volumes. In some birds (e.g. the whooper swan, "Cygnus cygnus", the white spoonbill, "Platalea leucorodia", the whooping crane, "Grus americana", and the helmeted curassow, "Pauxi pauxi") the trachea, which some cranes can be 1.5 m long, is coiled back and forth within the body, drastically increasing the dead space ventilation. The purpose of this extraordinary feature is unknown.
Reptiles.
The anatomical structure of the lungs is less complex in reptiles than in mammals, with reptiles lacking the very extensive airway tree structure found in mammalian lungs. Gas exchange in reptiles still occurs in alveoli however. Reptiles do not possess a diaphragm. Thus, breathing occurs via a change in the volume of the body cavity which is controlled by contraction of intercostal muscles in all reptiles except turtles. In turtles, contraction of specific pairs of flank muscles governs inhalation and exhalation.
Amphibians.
Both the lungs and the skin serve as respiratory organs in amphibians. The ventilation of the lungs in amphibians relies on positive pressure ventilation. Muscles lower the floor of the oral cavity, enlarging it and drawing in air through the nostrils into the oral cavity. With the nostrils and mouth closed, the floor of the oral cavity is then pushed up, which forces air down the trachea into the lungs. The skin of these animals is highly vascularized and moist, with moisture maintained via secretion of mucus from specialised cells, and is involved in cutaneous respiration. While the lungs are of primary organs for gas exchange between the blood and the environmental air (when out of the water), the skin's unique properties aid rapid gas exchange when amphibians are submerged in oxygen-rich water.
Some amphibians have gills, either in the early stages of their development (e.g. tadpoles of frogs), while others retain them into adulthood (e.g. some salamanders).
Fish.
Oxygen is poorly soluble in water. Fully aerated fresh water therefore contains only 8–10 ml O2/liter compared to the O2 concentration of 210 ml/liter in the air at sea level. Furthermore, the coefficient of diffusion (i.e. the rate at which a substances diffuses from a region of high concentration to one of low concentration, under standard conditions) of the respiratory gases is typically 10,000 faster in air than in water. Thus oxygen, for instance, has a diffusion coefficient of 17.6 mm2/s in air, but only 0.0021 mm2/s in water. The corresponding values for carbon dioxide are 16 mm2/s in air and 0.0016 mm2/s in water. This means that when oxygen is taken up from the water in contact with a gas exchanger, it is replaced considerably more slowly by the oxygen from the oxygen-rich regions small distances away from the exchanger than would have occurred in air. Fish have developed gills deal with these problems. Gills are specialized organs containing filaments, which further divide into lamellae. The lamellae contain a dense thin walled capillary network that exposes a large gas exchange surface area to the very large volumes of water passing over them.
Gills use a countercurrent exchange system that increases the efficiency of oxygen-uptake from the water. Fresh oxygenated water taken in through the mouth is uninterruptedly "pumped" through the gills in one direction, while the blood in the lamellae flows in the opposite direction, creating the countercurrent blood and water flow (Fig. 22), on which the fish's survival depends.
Water is drawn in through the mouth by closing the operculum (gill cover), and enlarging the mouth cavity (Fig. 23). Simultaneously the gill chambers enlarge, producing a lower pressure there than in the mouth causing water to flow over the gills. The mouth cavity then contracts inducing the closure of the passive oral valves, thereby preventing the back-flow of water from the mouth (Fig. 23). The water in the mouth is, instead, forced over the gills, while the gill chambers contract emptying the water they contain through the opercular openings (Fig. 23). Back-flow into the gill chamber during the inhalatory phase is prevented by a membrane along the ventroposterior border of the operculum (diagram on the left in Fig. 23). Thus the mouth cavity and gill chambers act alternately as suction pump and pressure pump to maintain a steady flow of water over the gills in one direction. Since the blood in the lamellar capillaries flows in the opposite direction to that of the water, the consequent countercurrent flow of blood and water maintains steep concentration gradients for oxygen and carbon dioxide along the entire length of each capillary (lower diagram in Fig. 22). Oxygen is, therefore, able to continually diffuse down its gradient into the blood, and the carbon dioxide down its gradient into the water. Although countercurrent exchange systems theoretically allow an almost complete transfer of a respiratory gas from one side of the exchanger to the other, in fish less than 80% of the oxygen in the water flowing over the gills is generally transferred to the blood.
In certain active pelagic sharks, water passes through the mouth and over the gills while they are moving, in a process known as "ram ventilation". While at rest, most sharks pump water over their gills, as most bony fish do, to ensure that oxygenated water continues to flow over their gills. But a small number of species have lost the ability to pump water through their gills and must swim without rest. These species are "obligate ram ventilators" and would presumably asphyxiate if unable to move. Obligate ram ventilation is also true of some pelagic bony fish species.
There are a few fish that can obtain oxygen for brief periods of time from air swallowed from above the surface of the water. Thus Lungfish possess one or two lungs, and the labyrinth fish have developed a special "labyrinth organ", which characterizes this suborder of fish. The labyrinth organ is a much-folded suprabranchial accessory breathing organ. It is formed by a vascularized expansion of the epibranchial bone of the first gill arch, and is used for respiration in air.
This organ allows labyrinth fish to take in oxygen directly from the air, instead of taking it from the water in which they reside through use of gills. The labyrinth organ helps the oxygen in the inhaled air to be absorbed into the bloodstream. As a result, labyrinth fish can survive for a short period of time out of water, as they can inhale the air around them, provided they stay moist.
Labyrinth fish are not born with functional labyrinth organs. The development of the organ is gradual and most juvenile labyrinth fish breathe entirely with their gills and develop the labyrinth organs when they grow older.
Invertebrates.
Arthropods.
Some species of crab use a respiratory organ called a branchiostegal lung. Its gill-like structure increases the surface area for gas exchange which is more suited to taking oxygen from the air than from water. Some of the smallest spiders and mites can breathe simply by exchanging gas through the surface of the body. Larger spiders, scorpions and other arthropods use a primitive book lung.
Insects.
Most insects breath passively through their spiracles (special openings in the exoskeleton) and the air reaches every part of the body by means of a series of smaller and smaller tubes called 'trachaea' when their diameters are relatively large, and 'tracheoles' when their diameters are very small. The tracheoles make contact with individual cells throughout the body. They are partially filled with fluid, which can be withdrawn from the individual tracheoles when the tissues, such as muscles, are active and have a high demand for oxygen, bringing the air closer to the active cells. This is probably brought about by the buildup of lactic acid in the active muscles causing an osmotic gradient, moving the water out of the tracheoles and into the active cells. Diffusion of gases is effective over small distances but not over larger ones, this is one of the reasons insects are all relatively small. Insects which do not have spiracles and trachaea, such as some Collembola, breathe directly through their skins, also by diffusion of gases.
The number of spiracles an insect has is variable between species, however, they always come in pairs, one on each side of the body, and usually one pair per segment. Some of the Diplura have eleven, with four pairs on the thorax, but in most of the ancient forms of insects, such as Dragonflies and Grasshoppers there are two thoracic and eight abdominal spiracles. However, in most of the remaining insects, there are fewer. It is at the level of the tracheoles that oxygen is delivered to the cells for respiration.
Insects were once believed to exchange gases with the environment continuously by the simple diffusion of gases into the tracheal system. More recently, however, large variation in insect ventilatory patterns has been documented and insect respiration appears to be highly variable. Some small insects do not demonstrate continuous respiratory movements and may lack muscular control of the spiracles. Others, however, utilize muscular contraction of the abdomen along with coordinated spiracle contraction and relaxation to generate cyclical gas exchange patterns and to reduce water loss into the atmosphere. The most extreme form of these patterns is termed discontinuous gas exchange cycles.
Molluscs.
Molluscs generally possess gills that allow gas exchange between the aqueous environment and their circulatory systems. These animals also possess a heart that pumps blood containing hemocyanin as its oxygen-capturing molecule. Hence, this respiratory system is similar to that of vertebrate fish. The respiratory system of gastropods can include either gills or a lung.
Plants.
Plants use carbon dioxide gas in the process of photosynthesis, and exhale oxygen gas as waste. The chemical equation of photosynthesis is 6 CO2 (carbon dioxide) and 6 H2O (water), which in the presence of sunlight makes C6H12O6 (glucose) and 6 O2 (oxygen). Photosynthesis uses electrons on the carbon atoms as the repository for the energy obtained from sunlight. Respiration is the opposite of photosynthesis. It reclaims the energy to power chemical reactions in cells. In so doing the carbon atoms and their electrons are combined with oxygen forming CO2 which is easily removed from both the cells and the organism. Plants use both processes, photosynthesis to capture the energy and oxidative metabolism to use it.
Plant respiration is limited by the process of diffusion. Plants take in carbon dioxide through holes, known as stomata, that can open and close on the undersides of their leaves and sometimes other parts of their anatomy. Most plants require some oxygen for catabolic processes (break-down reactions that release energy). But the quantity of O2 used per hour is small as they are not involved in activities that require high rates of aerobic metabolism. Their requirement for air, however, is very high as they need CO2 for photosynthesis, which constitutes only 0.04% of the environmental air. Thus, to make 1 g of glucose requires the removal of all the CO2 from "at least" 18.7 liters of air at sea level. But inefficiencies in the photosynthetic process cause considerably greater volumes of air to be used.


Lingual artery

The lingual artery arises from the external carotid artery between the superior thyroid artery and facial artery. It can be located easily in the tongue.
Structure.
The lingual artery first branches off from the external carotid artery. It runs obliquely upward and medialward to the greater horns of the hyoid bone.
It then curves downward and forward, forming a loop which is crossed by the hypoglossal nerve. It then passes beneath the digastric muscle and stylohyoid muscle running horizontally forward, beneath the hyoglossus. This takes it through the sublingual space. Finally, ascending almost perpendicularly to the tongue, it turns forward on its lower surface as far as the tip of the tongue, now called the deep lingual artery (profunda linguae).
Branches.
The lingual artery gives 4 main branches: the deep lingual artery, the sublingual artery, the suprahyoid branch, and the dorsal lingual branch.
Deep lingual artery.
The deep lingual artery (or ranine artery) is the terminal portion of the lingual artery after the sublingual artery is given off. As seen in the picture, it travels superiorly in a tortuous course along the under (ventral) surface of the tongue, below the longitudinalis inferior, and above the mucous membrane.
It lies on the lateral side of the genioglossus, the main large extrinsic tongue muscle, accompanied by the lingual nerve. However, as seen in the picture, the deep lingual artery passes inferior to the hyoglossus (the cut muscle on the bottom) while the lingual nerve (not pictured) passes superior to it (for a comparison, the hypoglossal nerve, pictured, passes superior to the hyoglossus). At the tip of the tongue, it is said to anastomose with the artery of the opposite side, but this is denied by Hyrtl. In the mouth, these vessels are placed one on either side of the frenulum linguæ.
Sublingual artery.
The sublingual artery arises at the anterior margin of the hyoglossus, and runs forward between the genioglossus and mylohyoid muscle to the sublingual gland.
It supplies the gland and gives branches to the mylohyoideus and neighboring muscles, and to the mucous membrane of the mouth and gums.
One branch runs behind the alveolar process of the mandible in the substance of the gum to anastomose with a similar artery from the other side; another pierces the mylohyoideus and anastomoses with the submental branch of the facial artery.
Function.
The lingual artery supplies the tongue. It also supplies the palatine tonsils.


Ascandra contorta

Ascandra contorta is a species of calcareous sponge belonging to the family Clathrinidae.
This is a whitish sponge which appears as a mass of irregular, convoluted tubes. It is very similar to "Clathrina clathrus" but usually differs in colour ("C. clathrus" is usually yellow) and by the presence of terminal oscula on vertical tubes (absent in "C. clathrus"). When viewed microscopically, the spicule structure of the two species is very different, "A. contorta" possessing two-pointed "diactines" and four-pointed "tetractines" as well as the three-pointed "triactines" which "C. clathrus" is exclusively made up of.
This sponge is found on north-eastern Atlantic coasts from the Arctic to the Mediterranean, usually on rocks at depths of 10–30 m, but occasionally in shallower water.


Scottish Birds


Total body surface area

Total body surface area (TBSA) is an assessment of injury to or disease of the skin, such as burns or psoriasis.
In adults, the Wallace rule of nines can be used to determine the total percentage of area burned for each major section of the body.
In burn cases that involve partial body areas, or when dermatologists are evaluating the Psoriasis Area and Severity Index (PASI) score, the patient's palm can serve a reference point roughly equivalent to 1% of the body surface area.
For children and infants, the Lund and Browder chart is used to assess the burned body surface area. Different percentages are used because the ratio of the combined surface area of the head and neck to the surface area of the limbs is typically larger in children than that of an adult.
Typical values for common groups of humans follow. (Due to rounding, values may not add to 100%.)


Alan Solem

George Alan Solem (21 June 1931 – 26 March 1990), known professionally as Alan Solem, was an American malacologist, a biologist who studied mollusks.
He was one of the most renowned land snail experts of his time and had earned a reputation for his comprehensive revisions of mainly terrestrial pulmonates. He worked on land snails from all regions of the world but became particularly known for his revisions of land snails from Australasia and various Pacific Islands.
He named many taxa, amongst them about 350 species of Australian land snails, and several genera.
Some species named by him are:


Dewlap

A dewlap is a longitudinal flap of skin that hangs beneath the lower jaw or neck of many vertebrates. While the term is usually used in this specific context, it can also be used to include other structures occurring in the same body area with a similar aspect, such as those caused by a double chin or the submandibular vocal sac of a frog. In a more general manner, the term refers to any pendulous mass of skin, such as a fold of loose skin on an elderly person's neck, or the wattle of a bird. Dewlaps can be considered as a "caruncle", defined as "a small, fleshy excrescence that is a normal part of an animal's anatomy".
Mammals.
Many mammals such as dogs, rabbits and moose possess dewlaps. In zebu cattle, the dewlap is colloquially known as the "briefcase folds". The dewlap is also found on female rabbits, such as the New Zealand white rabbit. While pregnant, the female rabbit will pluck fur from the dewlap to line a nest for her babies. Although these masses can be referred to as dewlaps, they are formed by stored fat. The dewlap is also seen in both sexes of moose.
Reptiles and birds.
Many reptiles have dewlaps, most notably the anole family of lizard, which have large skin dewlaps they can extend and retract. The anole family has been found to have enhanced vision for color and depth perception. This family is able to see dewlap coloration from a far distance, giving the dewlap use and importance. These dewlaps are usually of a different color from the rest of their body and, when enlarged, make the lizard seem much bigger than it really is. The dewlap is primarily used when indicating territorial boundaries and for males to attract females during the mating season. Studies have found that the pigments generating this color are pterins and carotenoids. These two pigments are the most easily seen through the anole's eyes. Pterin and carotenoid pigments are located throughout the tissue of the dewlap, creating yellow and red hues. Lizards usually accompany their dewlap movement with head bobs and other displays. The dewlap moves through extension and contraction. The muscles creating this movement are known as the ceratohyoid muscles connected to the hyoid apparatus. These muscles controlling movement of the dewlap are around the throat and larynx. This is also where the motorneurons, the neurons signaling the dewlap movement, are found. Though much uncertainty resides around the purpose of these displays, the color of the dewlap and the head bobs are thought to be a means of contrasting background noise.
Many birds also have dewlaps, such as domestic chickens, some cracids and some guans.


Thulinius

Thulinius is a genus of water bear or moss piglet, a tardigrade in the class Eutardigrada.


Habrotrocha

Habrotrocha is a genus of bdelloid rotifers.


Hermann von Maltzan

Hermann Friedrich Freiherr von Maltzan (18 December 1843, Rostock – 19 February 1891, Berlin) was a German malacologist known for his work in the field of conchology.
A former law student at the University of Rostock, in 1864–65 he undertook an extended scientific journey to France, Spain, Italy and Egypt; a trip in which he collected numerous zoological specimens and expanded his malacological knowledge. In 1879, he traveled to Portugal, where he conducted extensive zoological research in the Algarve region. Afterwards, he continued his research in western Africa (especially French Senegambia), followed by travels to Greece, Crete and Asia Minor. After his return to Germany, he took up residence in Darmstadt and later Berlin (since 1885).
In 1866 he founded the "Maltzan`sches Naturhistorisches Museums für Mecklenburg" ("Maltzaneum"), a natural history museum that the present-day "Müritzeum", located near the city of Waren, traces its origins to.
He was the binomial author of numerous malacological species, including several within the land snail genus, "Xerocrassa".


List of introduced mammal species

This list of introduced mammal species includes all the species of mammal introduced to an area without regard to that territory being or not being their native area of occupation or the success of that re-introduction or introduction to the area. This practice has been harmful in many areas, although some introductions are made with the aim of preserving mammal species. Following the name of the mammal, a brief description of where they were introduced is included.


Monogononta

Monogononta is a class of rotifers, found mostly in freshwater but also in soil and marine environments. They include both free-swimming and sessile forms. Monogononts generally have a reduced corona, and each individual has a single gonad, which gives the group its name. Males are generally smaller than females, and are produced only during certain times of the year, with females otherwise reproducing through parthenogenesis.
Their mastax is not designed for grinding. They produce mictic and amictic eggs. The class contains 1,570 species.


Nicobar treeshrew

The Nicobar treeshrew ("Tupaia nicobarica") is a treeshrew species within the Tupaiidae. It is endemic to the Nicobar Islands where it inhabits the islands' rain forests. It is threatened by habitat loss.
Although previously listed as an endangered species, the Nicobar treeshrew is now commonly found in its appropriate habitats.
The Nicobar treeshrew was first described by Johann Zelebor in 1868.
Habitat.
The Nicobar treeshrew only occupies the Indian Islands of Great Nicobar and Little Nicobar and can be found on the highest points of these two islands, 640 m above sea level.


Serket (journal)

"Serket, The Arachnological Bulletin of the Middle East and North Africa", is a biannual peer-reviewed scientific journal on arachnology. It was established in August 1987 in Egypt, taking its name from the ancient Egyptian for a scorpion.
Abstracting and indexing.
The journal is abstracted and indexed in:


Zone of polarizing activity

The zone of polarizing activity (ZPA) is an area of mesenchyme that contains signals which instruct the developing limb bud to form along the anterior/posterior axis. Limb bud is undifferentiated mesenchyme enclosed by an ectoderm covering. Eventually, the limb bud develops into bones, tendons, muscles and joints. Limb bud development relies not only on the ZPA, but also many different genes, signals, and a unique region of ectoderm called the apical ectodermal ridge (AER). Research by Saunders and Gasseling in 1948 identified the AER and its subsequent involvement in proximal distal outgrowth. Twenty years later, the same group did transplantation studies in chick limb bud and identified the ZPA. It wasn't until 1993 that Todt and Fallon showed that the AER and ZPA are dependent on each other.
Patterning.
Patterning along the limb bud requires signals from many sources. Specifically, proteins called transcription factors (TF) help control the rate at which a gene is transcribed. The limb bud expresses a TF called ALX4 at the anterior part of the mesoderm, with the TF HOXB8 being expressed at the posterior portion. The Alx4 region, the medial region, and the Hox8 expressing area meet at a proximal area where the AER develops. The ZPA forms where the Hox8 region joins the AER.
These regions are dependent on signaling in order for the appropriate induction events to occur. The AER expresses FGF8 which induces Shh expression in the posterior mesoderm. Shh then stimulates FGF4 to be expressed in the posterior part of the AER. After these events, there is a co-dependence between FGF-4 and Shh for their subsequent expression and maintenance. Additionally, Wnt7a is expressed in the dorsal ectoderm, is needed to maintain the FGF and Shh signaling.
Apical ectodermal ridge.
Saunders and Gasseling published data in the Journal of Experimental Biology in 1948, showing that reference marks inserted near the rim of the apical border of the wing bud are dispersed throughout the whole forearm of the wing. This led them to believe that the apical ectoderm may play a role in forming parts of the wing. To test this, they removed apical ectoderm from wing buds which yielded deformed wings. When they removed dorsal ectoderm, normal wings formed. These results showed that the cells of the apical ectoderm have a precise fate to form specific regions of the wing.
Sonic hedgehog.
In 1968, Saunders and Gasseling did transplantation studies using tissue from chick limb bud. Removing cells from the posterior region of the limb, they transplanted them to the anterior region and noticed that extra digits formed in the anterior area and these digits were mirror images to the normal ones. This posterior mesenchyme was the ZPA, which is now known to express the protein sonic hedgehog (Shh). One hypothesis is that at high concentrations, this unknown morphogen causes mesenchyme to form on the posterior side, while low concentrations induces meshenchyme to form on the anterior end. Identifying this morphogen was the next crucial step.
The first hypothesis came from Tickle et al. who showed that when retinoic acid is placed in the anterior margin of the limb bud, mirror image duplications result. However, concentrations of retinoic acid that cause mirror image duplications induce high levels of a downstream gene, retinoic acid receptor Beta, which is not seen in the posterior region. It is now known that endogenous retinoic acid acts permissively prior to limb bud initiation to allow the budding process to begin, and that the specific morphogen, hypothesized to be Shh, is normally expressed independently of retinoic acid in the posterior region of the limb bud. By looking at signaling homologs of other organisms, the segmentation gene of "Drosophila", hedgehog, served as a viable candidate.
The idea that Shh is required for proper ZPA signaling and anterior/posterior limb formation needed to be tested. Riddle et al. took Saunders and Gasselings findings to the next step and proved that Shh is the morphogen within the ZPA that is required for anterior posterior patterning. By isolating the Shh gene and implanting it into the anterior limb bud, mirror image digit duplications formed.
Isolation was conducted by designing PCR primers that correspond to sequences of Shh that are conserved in "Drosophila" and mouse and involved in limb bud formation. The clone was then used as a template to screen a cDNA library from stage 22 limb bud RNA. The group ectopically expressed the gene by taking advantage of a retroviral vector to insert the cDNA into chick cells. There are unique types of this retroviral vector that only infect specific strains of avian species. Therefore, this group used a retroviral vector termed RCAS-E, which lacks a type E envelope protein, and is able to infect certain chick embryo fibroblasts with Shh.
Results showed digit duplications, with the most common being 4-3-3-4, with digit 2 missing. Though there was variability, it was clearly consistent with anterior to posterior positional patterning. Variations were due to the amount of tissue grafted, and the location of the graft. These findings indicate that Shh could substitute for the function of the ZPA. Thus Shh is sufficient for ZPA action.
Mediators.
Shh may be a critical signal regulating ZPA function, but the genes involved in Shh signaling are under the control of several other factors that are needed for ZPA maintenance and function including Hand2 and Hoxb-8. Retinoic acid, an important signaling molecule needed throughout embryogenesis, acts through the Hox genes. It was originally postulated that retinoic acid acts to induce the Hoxb-8 gene, but this hypothesis has not been supported by genetic studies in mouse embryos lacking retinoic acid synthesis that still express Hoxb-8 in the limb. Hoxb-8 signaling is active in the early embryo, beginning at the posterior end of the lateral plate mesoderm and extending to the anterior region. As Hoxb-8 spreads to more anterior regions, Shh is induced in the area that will become the ZPA. Shh is only induced in the anterior region because of signals from the AER. Experiments done by Heikinheimo et al. show that when the AER is removed, beads that express FGF are sufficient to induce Shh signaling in the ZPA. Thus, the likely signaling factor from the AER is FGF.
Additionally when the AER is removed, Shh is no longer expressed, and the ZPA can no longer be maintained. Acting in a positive feedback mechanism, FGF-4 is expressed near the ZPA. FGF-4 acts to maintain Shh expression, while Shh acts to maintain FGF-4 expression. At the same time, Wnt-7a is expressed in the dorsal ectoderm, and provides further positive feedback to FGF-4 and Shh. Without this system, limbs and digits are either significantly reduced or missing.
Downstream signals.
The downstream targets that are activated in response to Shh pose another challenge. Genes that are targets of Shh signaling encode factors that lead to the formation of the autopod, stylopod and zeugopod.
Activation of Gli zinc-finger transcription factors occurs through the Hedgehog signaling pathway. There are three Gli factors that are essential for limb development: Gli1, Gli2 and Gli3. Without Shh, Gli2 and Gli3 are processed to a repressor form and travel to the nucleus to repress the Shh response. But when Shh is present, unprocessed Gli2 and Gli3 are able to pass into the nucleus and stimulate expression of Shh target genes, including Gli1. Studies in mice show that Gli3 knockouts have polydactyly digits. Fundamentally, Shh acts to remove repression of Gli3. When Shh diffuses from the ZPA, it predominates in the posterior region of the limb bud, activating Gli3 in the posterior region, while the repressor is still active in the anterior region. This leads to activation of other genes such as Hox genes, FGF genes and BMP genes in the posterior region, setting up digit patterning. BMP, plays a role in limb morphology, specifically, digit positioning, but the specific regulation of BMP is unclear.
In particular, the Hox genes A and D are likely to be controlled by Shh within the ZPA. Three phases of activation of the Hox genes results in patterning of the limb parallel to the expression of the Hox genes in a nested pattern. Activation of these genes results in a new limb axis that ultimately results in digit development, possibly interpreting gene expression to assign digit identity. Overall, the molecular ZPA requires input for several signaling centers, but acts as an organizer itself, inducing anterior-posterior pattering of the chick limb bud.


Henry Ford (Michigan legislator)

Henry Ford (February 11, 1825June 20, 1894) was a Michigan politician.
Early life.
Ford was born on February 11, 1825 in Monroe, New York.
Career.
Ford moved to Michigan in 1867 to oversee the erection of the Lawton Iron Works. From 1868 to 1869, Ford served as village president of Lawton, Michigan. He served as village president again in 1879. On November 2, 1880, Ford was elected to the Michigan Senate where he represented the 12th district from January 1, 1881 to December 31, 1882. Ford had also served as justice of the peace.
Personal life.
At some point in his life, Ford married a woman named Catherine. Together they had two children. Ford married Florence A. Smith on January 18, 1882 in Lawton.
Death.
Ford died on June 20, 1894 of heart failure.


Weberian apparatus

The Weberian apparatus is an anatomical structure that connects the swim bladder to the auditory system in fishes belonging to the superorder Ostariophysi. When it is fully developed in adult fish, the elements of the apparatus are sometimes collectively referred to as the Weberian ossicles. The presence of the structure is one of the most important and phylogenetically significant distinguishing characteristics of the Ostariophysi. The structure itself consists of a set of minute bones that originate from the first few vertebrae to develop in an embryonic ostariophysan. These bones grow to physically connect the auditory system, specifically the inner ear, to the swim bladder. The structure acts as an amplifier of sound waves that would otherwise be only slightly perceivable by the inner ear structure alone.
Structural anatomy and function.
The generalized structure of the Weberian apparatus is akin to a skeletal complex of bones and ossicles that are physically connected to the labyrinth auditory complex anteriorly and the anteriormost region of the swim bladder posteriorly. The entire structure is derived from skeletal elements of the first four vertebrae. The involved elements include: the supraneural bones of the skull; modified neural arch bones, specifically the paired claustra and the scaphia; the intercalarium and the lateral processes; the tripus; the os suspensorium from the fourth vertebra; the parapophysis of vertebra number five including the vertebra itself, plus the vertebra's corresponding pleural rib. In addition, a structure composed of fused neural spines form the dorsalmost part of the Weberian apparatus. Together, the structure interacts anteriorly with the lagenar otolith set within the skull and posteriorly with the swim bladder via the pleural rib. Postero-ventrally, it is the tripus, the os suspensorium and the third rib that interact directly with the anterior chamber of the swim bladder.
The Weberian apparatus functions by transmitting auditory signals straight from the gas bladder, through the Weberian ossicles and then straight into the labyrinth structures of the inner ear. The structure essentially acts as an amplifier of sound waves that would otherwise be only slightly perceivable by the inner ear structure alone. With the added function of the swim bladder as a resonating chamber, signals are amplified to noticeable levels.
Embryology.
Embryonic analysis of Weberian apparatuses of the taxon "Brycon" has shed some light on the development of the structure itself. The Weberian apparatus elements form from the fully distinguishable first five vertebrae of the individual. The supraneural starts as an element of the skull. The claustra and the scaphia develop from expanded elements of the neural arch of the first vertebra (V1). From the second vertebra (V2), the intercalarum and the vertebra's lateral process are reduced and clump together. The plural rib (R1) of the third vertebra (V3) shrinks and moves somewhat ventrally, forming the tripus from a vertebral parapophysis fusing with the pleural rib. The os suspensorium bone of the fourth vertebra (V4) somewhat retains its shape, developing from the pleural rib of the vertebra (R2). The remaining elements of the fifth vertebra (V5), the parapophysis and the articulating rib (R3), including the vertebra itself form the posterior structure of the Weberian apparatus. The neural spines of the first four vertebrae fuse and compress, forming one of the major structures of the apparatus.
Study of the embryology of the Weberian apparatus has since been conducted on various other ostariophysan species, the outcomes of which have resulted in various interpretations of the development (and thus the homology) of the structures that form the structure. Specific studies have been done on the Weberian apparatuses of a few select taxa, including "Danio rerio", "Rhaphiodon vulpinus" and "Corydoras paleatus".
Evolutionary history.
The earliest recorded incidence of a Weberian apparatus is from the fossil fish "Santanichthys diasii" dating from the Early Cretaceous of Northeastern Brazil. In the aforementioned taxon, the Weberian apparatus is fairly developed; there is a distinguishable intercalarium and a tripus which articulate with the second and third vertebrae respectively. A scaphium can be seen in at least two specimens. The neural arch of the third vertebra has already broadened, almost similar to that of modern ostariophysans. The claustrum, an element in modern apparati, is noticeably absent from the Weberian apparatus of "S. diasii". Only the first four vertebrae are involved in the Weberian apparatus of "Santanichthys"; There are no signs of involvement from the elements of the fifth vertebra unlike in modern otophysans. An important feature within the formation of the Weberian apparatus, which is a synapomorphy of the Otocephala, is the attachment of the anterior Pleural cavity(rib) to the Swim bladder. Another crucial feature is the anterior otophysic diverticula of the swim bladder and contacting the inner ear, seen in extant Clupeiformes. There is also a relationship between the interossicular ligament and the swim bladder that it originated from the swim bladder diverticulum. This was shown by comparing the fiber of the ligament and the tunica externa of the swim bladder that have the same histological composition of elastin and icthyocoll (a specific type I collagen).
Etymology.
The Weberian apparatus is named after the German anatomist and physiologist Ernst Heinrich Weber (1795 – 1878). The apparatus was first described in detail by Weber. Only four bones were identified, specifically the claustrum, scaphium, intercalarium and tripus. Together, these elements were hypothesized to play a part in auditory functions. Over the years, other functions have been proposed and discarded. Hydrostatic regulation was one of the early alternative suggestions for the function of the apparatus.


Chlamyphorinae

Chlamyphorinae is a subfamily of South American armadillos in the family Chlamyphoridae. Members of this subfamily, the fairy armadillos, are largely fossorial and have reduced eyes and robust forearms with large claws for digging.
Taxonomy.
The subfamily has two monotypic genera:
Phylogeny.
Chlamyphorinae is the sister group of Tolypeutinae (giant, three-banded and naked-tailed armadillos), as shown below.


Surfactant metabolism dysfunction

Surfactant metabolism dysfunction is a condition where pulmonary surfactant is insufficient for adequate respiration. Surface tension at the liquid-air interphase in the alveoli makes the air sacs prone to collapsing post expiration. This is due to the fact that water molecules in the liquid-air surface of alveoli are more attracted to one another than they are to molecules in the air. For sphere-like structures like alveoli, water molecules line the inner walls of the air sacs and stick tightly together through hydrogen bonds. These intermolecular forces put great restraint on the inner walls of the air sac, tighten the surface all together, and unyielding to stretch for inhalation. Thus, without something to alleviate this surface tension, alveoli can collapse and cannot be filled up again. Surfactant is essential mixture that is released into the air-facing surface of inner walls of air sacs to lessen the strength of surface tension. This mixture inserts itself among water molecules and breaks up hydrogen bonds that hold the tension. Multiple lung diseases, like ISD or RDS, in newborns and late-onsets cases have been linked to dysfunction of surfactant metabolism.
Surfactant is a mixture of 90% phospholipids and 10% other proteins, produced by epithelial type II cells in the alveolar. This mixture is made and packaged into lysosomally- derived structures called lamellar bodies. Lamellar bodies are then secreted into the liquid-air interphase surface of alveolar through membrane fusion initiated by influx of Ca2+. Released pulmonary surfactant acts as a protective layer to prevent alveolar from collapsing due to surface tension. Furthermore, surfactants also contains some innate immune components to defend against pulmonary infections. Surfactant is classified into two types of proteins, hydrophilic proteins that are responsible for innate immune system, and hydrophobic proteins that carry out physical functions of pulmonary surfactant. Surfactant metabolism dysfunction involves mutations or malfunctions of those hydrophobic proteins that lead to ineffective surfactant layer to protect alveolus integrity. SP-B and SP-C are the two hydrophobic surfactant proteins that participate in its physical functions; these proteins are encoded by SFTPB and SFTPC genes on chromosomes 2 and 8 respectively. Thus, mutations on these genes produce incomplete or nonfunctioning SP-B and SP-C proteins and lead to lung diseases.
Both SP-B and SP-C are synthesized in epithelial type II cells as large precursor proteins (proSP-B and proSP-C) and subsequently cleaved by proteolytic enzymes at both amino and carboxyl termini to produce functional mature proteins. proSP-B and proSP-C are first made in the endoplasmic reticulum of epithelial type II cell, they are then translocated through Golgi apparatus to multivesicular bodies for delivery to lamellar bodies. During this transition, proteolytic processing begins to cleave precursor proteins. Once multivescular body reaches the membrane of lamellar body, both membranes fuse together so that processed proteins can be transported into lamellar body, where last steps of maturation for both SP-B and SP-C occur. When lamellar body is ready to be secreted, exocytosis is initiated through influx of Ca2+, and lamellar membrane fuses with plasma membrane to release surfactant phospholipid contents into the surface of the cell. SP-B and SP-C are responsible to carry out adsorption of the lipid monolayer at the liquid-air interphase to prevent post expiration atelectasis. Used surfactant phospholipid materials are taken up into epithelial type II cells by pulmonary macrophages.
Another important protein that contributes to outcome of surfactant metabolism dysfunction is ABCA3, a transmembrane phospholipid transporter in lamellar body. ABCA3 has two ATP binding sites in the cytoplasmic domain to power phospholipid transportation through ATP hydrolysis. ABCA3 is synthesized in endoplasmic reticulum and transported through Golgi apparatus to the membrane of lamellar body. Once inserted into the membrane, ABCA3 can help deliver surfactant lipids into the lumen of lamellar body, and create tightly packed internal environment of surfactant lipids and surfactant proteins. Mutations in ABCA3 cause failure in lamellar body synthesis and result in decreased production of surfactant, along with deficiency of SP-B and SP-C.
Cause.
Surfactant metabolism dysfunction describes a group of dysfunctions caused by different mutations in surfactant related genes.Severe deficiency of pulmonary surfactant due to disturbed metabolism of any of these proteins can lead to some form of interstitial lung disease in newborns and adults. These conditions share similar pathophysiology and overlapping phenotypes because surfactant gene products interactively communicate and control one another. Thus, dysfunction of a surfactant protein, or relating protein, generates deficiencies of others.
SFTPB mutations.
Most disease-causing mutations in SFTPB result in a complete lack of mature SP-B protein . Lung disease is inherited in an autosomal recessive manner, requiring mutations in both alleles. Surfactant produced by infants with SP-B deficiency is abnormal in composition and does not function normally in lowering surface tension.
More than 40 different mutations along the length of SFTPB gene have been accounted for in surfactant metabolism dysfunction. SFTPB mutations are inherited in autosomal recessive fashion, loss-of-function mutation on both alleles are required for full expression of disease. About 2/3 or 60%-70% of those accounted disease-causing alleles come from a frameshift mutation, called 121ins2, on exon 4 of SFTPB gene, which also accounts for ~65% of US cases. The rest of the mutated alleles come from nonsense, missense, splice-site mutations, and other possible insertion and deletion mutations throughout the entire gene. These mutations cause total absence or loss-of-function of SP-B and lead to imbalance in surfactant homeostasis. Since SP-B has a major role in surfactant biogenesis and spreading of surfactant and lipid layer, any disruption to existence of SP-B results in ineffective respiration and lethal pulmonary conditions at birth. Pathology manifestation in full-term infant resembles characteristics of newborn with Respiratory Distress Syndrome. Imaging of epithelial type II cells with SP-B deficiency shows immature lamellar bodies without tightly packed membranes, but rather with loose and unorganized membranes. The ratio of phospholipid-protein also decreases with abnormal phospholipids. In addition, surfactant collected from SP-B deficiency epithelial type II cells is not as effective in lowering surface tension and creating film as normal surfactant. Immunohistochemical features of SP-B deficiency show decreased levels of proSP-B and SP-B proteins, along with increased presence of immuno protein SP-A and partially processed intermediate peptides of proSP-C. Appearance of partially processed proSP-C shows significance of mature SP-B in biogenesis and processing of SP-C. Absences of both proSP-B and SP-B proteins are observed in frameshift and nonsense mutations of SFTPB, while low level of proSP-B is detected in missense, in-frame deletionof insertion mutations. However, these mutations prevent proSP-B from fully mature into SP-B, resulting in deficiency of SP-B and surfactant.
SFTPC mutations.
Familial cases of SP-C dysfunction are inherited in an autosomal dominant pattern, although the onset and severity of lung disease are highly variable, even within the same family.
More than 40 distinct mutation variations in SFTPC gene have also been described in patients. Wild-type SP-C proteins are embedded inside the phospholipid bilayer of epithelial type II cell and function to generate and maintain monolayer of surfactant on alveolar surface. Individuals with mutated SFTPC genes tend to manifest lung diseases in late childhood or adulthood. Mutated alleles are inherited in autosomal dominant fashion, although de novo mutations can also cause sporadic emergence of diseases. The age of onset and severity vary significantly among patients with SFTPC mutations, some only manifest symptoms in fifth or sixth decade. Most of these mutations are missense, but there have been recordings of frameshift, splice-site mutations, together with small insertions or deletions along the carboxyl terminal of SFTPC. Mutations in SFTPC gene are thought to prevent proSP-C peptides from being fully processed into mature SP-C proteins. ProSP-C proteins tend to self-accumulate along the secretory pathway, due to high hydrophobic nature, and may activate cellular destruction response. SFTPC mutations cause proSP-C proteins to aggregate and misfold during secretory process. These folded proteins trigger unfolded protein response (UPR) and cellular apoptosis to get rid of clusters of mutated peptides. Patients with SP-C dysfunction show lack of mature SP-C in epithelial type II cells and up-regulation of UPR. SFTPC mutation with highest occurrence frequency is substitution of threonine for isoleucine in codon 73, termed I73T, found in more than 25% of patients with SP-C related disorders. Staining of proSP-C shows diffuse staining strictly in cytoplasm and accumulation of immunoreactive substances surrounding the nucleus. Evaluation of diseases related to SFTPC mutations show association with chronic parenchymal lung disease.
ABCA3 mutations.
Mutations in ABCA3 appear to be the most common cause of genetic surfactant dysfunction in humans. The mutations result in a loss of or reduced function of the ABCA3 protein, and are inherited in an autosomal recessive manner .
There are more than 150 different mutations throughout ABCA3 gene with various allelic heterogeneity, making it the biggest class of genetic cause of surfactant dysfunction.Like SP-B deficiency, ABCA3 mutations are inherited in autosomal recessive trait. Mutations of ABCA3 consist of missense, nonsense, frameshift, splice-cite, insertion or deletion. These mutations are classified into two types of ABCA3 mutations, those that preclude normal trafficking of ABCA3 from ER to lamellar membrane, and those that affect ATP-binding ability of ABCA3 needed for phospholipid transportation. Due to its roles in lamellar body biogenesis and maturation of surfactant proteins, epithelial type II cells with altered ABCA3 exhibit premature lamellar bodies and damaged maturation of SP-B/SP-C. Surfactant samples from patients with ABCA3 deficiency do not lower surface tension as effectively. Affected surface tension ability results from incomplete formation of lamellar bodies, due to lack of lipid influx by ABCA3. Immunostaining of SP-B in ABCA3 patients show decreased level of mature SP-B and impaired process of proSP-B to SP-B, thus, confirming why ABCA3 dysfunction leads to severe surfactant metabolism dysfunction.
Diagnosis.
Types.
Non-invasive genetic testing can be used to infer possible interstitial lung disorders caused by surfactant metabolism dysfunction. Although these sequencing tests can take up to several weeks, which may not be so useful in case of acute respiratory problems in newborns. Overlapping phenotypes of surfactant metabolism dysfunction and other interstitial lung diseases make it hard to propose definitive diagnosis for surfactant disorders. Overall testings, family history, external factors, and clinical presentations should all be considered to diagnose surfactant metabolism dysfunction. Testing for surfactant metabolism dysfunction should be considered for newborns with diffuse lung disease or hypoxemia, especially in families with history of neonatal lung diseases or ILD in adults. Neonatal and adult onset lung diseases with unfound causes should also be tested early for surfactant dysfunction. ABCA3 and SP-B dysfunctions manifest in newborns and progress aggressively within the first few months of life, thus, testing for ABCA3 and SP-B disorders should preclude those for SP-C, especially when infants are showing symptoms of ILD or diffuse lung disease. Distinctions between SP-B and ABCA3 are ABCA3 tends to occur in families with neonatal lung disease history, and SP-B testing almost unneeded in older children. Late on-set conditions with inheritance in dominant fashion should infer SP-C dysfunction. Antibodies against proSP-B, proSP-C, SP-B, SP-C, and ABCA3 have been thoroughly developed, which makes detection for these proteins highly accessible and accurate. Immuno staining of each of these type of surfactant dysfunction differs in absence and presence of specific proteins and propeptides, thus immunohistochemisty can help decipher which type of deficiency is being dealt with. In addition, hypothyroidism can cause damaged production of NKX2.1 proteins, which can lead to insufficient transcription of multiple surfactant proteins.
Treatment.
Neonates with surfactant metabolism dysfunctions, especially those with SP-B disorder, only have lung transplantation as one possible choice of treatment. Children with lung transplant due to surfactant metabolism dysfunction perform on similar level to those with transplant for due to other reasons. Some less severe cases of ABCA3 dysfunctions manifest in late childhood or adult hood are due to missense mutations that result in semi-sufficient levels of active surfactant, while SP-C clinical presentation varies greatly depending on level of penetration of the mutated alleles.


Paraloxoceras

Paraloxoceras is a genus of straight shelled, orthoconic nautiloid cephalopods, now extinct, that lived during the Early Carboniferous. Fossils have been found in Europe and central Asia; the type, "P. konincki", named by Flower, came from Belgium.
The shell of "Paraloxoceras" is slightly depressed, with straight sutures. Septa are fairly close spaced. The siphuncle is located about half way between the center and the venter with segments that are broadly expanded into the chambers. As typical for the subfamily, "Paraloxoceras" contains organic endosiphuncular deposits penetrated by a canal system similar to that found in actinocerids but differs in the having a protoconch characteristic of the pseudorthocerids. During grow of the animal the shell expands dorsally with the distance between the dorsum and siphuncle increasing while the separation between the venter and siphuncle remains at a more or less constant.
Related genera include "Pseudactinoceras", "Macroloxoceras", and "Eusthenoceras".


Pleocola limnoriae

Pleocola limnoriae is a species of tardigrades. It is the only species of the genus Pleocola, which belongs to the family Styraconyxidae. The species and genus were named by Alexandre Cantacuzène in 1951. It has been found in the North Atlantic Ocean, type locality Roscoff, Brittany, France. It was discovered living in commensalism on the isopod "Limnoria lignorum".