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Zener diode

A Zener diode is a special type of diode designed to reliably allow current to flow "backwards" (inverted polarity) when a certain set reverse voltage, known as the Zener voltage, is reached.

Zener diodes are manufactured with a great variety of Zener voltages and some are even variable. Some Zener diodes have an abrupt, heavily doped p–n junction with a low Zener voltage, in which case the reverse conduction occurs due to electron quantum tunnelling in the short distance between p and n regions − this is known as the Zener effect, after Clarence Zener. Diodes with a higher Zener voltage have lighter doped junctions which causes their mode of operation to involve avalanche breakdown. Both breakdown types are present in Zener diodes with the Zener effect predominating at lower voltages and avalanche breakdown at higher voltages.

They are used to generate low-power stabilized supply rails from a higher voltage and to provide reference voltages for circuits, especially stabilized power supplies. They are also used to protect circuits from overvoltage, especially electrostatic discharge.

History
The device is named after American physicist Clarence Zener who first described the Zener effect in 1934 in his primarily theoretical studies of breakdown of electrical insulator properties. Later, his work led to the Bell Labs implementation of the effect in form of an electronic device, the Zener diode.

Operation

A conventional solid-state diode allows significant current if it is reverse-biased above its reverse breakdown voltage. When the reverse bias breakdown voltage is exceeded, a conventional diode will conduct a high current due to avalanche breakdown. Unless this current is limited by external circuits, the diode may be permanently damaged due to overheating. A Zener diode exhibits almost the same properties, except the device is specially designed so as to have a reduced breakdown voltage, the so-called Zener voltage. By contrast with the conventional device, a reverse-biased Zener diode exhibits a controlled breakdown and allows the current to keep the voltage across the Zener diode close to the Zener breakdown voltage. For example, a diode with a Zener breakdown voltage of 3.2 V exhibits a voltage drop of very nearly 3.2 V across a wide range of reverse currents. The Zener diode is therefore well suited for applications such as the generation of a reference voltage (e.g. for an amplifier stage), or as a voltage stabilizer for low-current applications.

Another mechanism that produces a similar effect is the avalanche effect as in the avalanche diode. The two types of diode are in fact constructed in a similar way and both effects are present in diodes of this type. In silicon diodes up to about 5.6 volts, the Zener effect is the predominant effect and shows a marked negative temperature coefficient. Above 5.6 volts, the avalanche effect dominates and exhibits a positive temperature coefficient.

In a 5.6 V diode, the two effects occur together, and their temperature coefficients nearly cancel each other out, thus the 5.6 V diode is useful in temperature-critical applications. An alternative, which is used for voltage references that need to be highly stable over long periods of time, is to use a Zener diode with a temperature coefficient (TC) of +2 mV/°C (breakdown voltage 6.2–6.3 V) connected in series with a forward-biased silicon diode (or a transistor B-E junction) manufactured on the same chip. The forward-biased diode has a temperature coefficient of −2 mV/°C, causing the TCs to cancel out for a net nearly zero temperature coefficient.

It is also worth noting that the temperature coefficient of a 4.7 V Zener diode is close to that of the emitter-base junction of a silicon transistor at around -2 mV/°C, so in a simple regulating circuit where the 4.7 V diode sets the voltage at the base of an NPN transistor (i.e. their coefficients are acting in parallel), the emitter will be at around 4 V and quite stable with temperature.

Modern designs have produced devices with voltages lower than 5.6 V with negligible temperature coefficients,. Higher voltage devices have a temperature coefficient that is approximately proportional to the amount by which the breakdown voltage exceeds 5 V. Thus a 75 V diode has 10 times the coefficient of a 12 V diode.

Zener and avalanche diodes, regardless of breakdown voltage, are usually marketed under the umbrella term of "Zener diode".

Under 5.6 V, where the Zener effect dominates, the IV curve near breakdown is much more rounded, which calls for more care in choosing its biasing conditions. The IV curve for Zeners above 5.6 V (being dominated by avalanche), is much more precise at breakdown.

Construction
The Zener diode's operation depends on the heavy doping of its p–n junction. The depletion region formed in the diode is very thin (<1 μm) and the electric field is consequently very high (about 500 kV/m) even for a small reverse bias voltage of about 5 V, allowing electrons to tunnel from the valence band of the p-type material to the conduction band of the n-type material.

At the atomic scale, this tunneling corresponds to the transport of valence band electrons into the empty conduction band states; as a result of the reduced barrier between these bands and high electric fields that are induced due to the high levels of doping on both sides. The breakdown voltage can be controlled quite accurately by the doping process. Adding impurities, or doping, changes the behaviour of the semiconductor material in the diode. In the case of Zener diodes, this heavy doping creates a situation where the diode can operate in the breakdown region. While tolerances within 0.07% are available, commonly available tolerances are 5% and 10%. Breakdown voltage for commonly available Zener diodes can vary from 1.2 V to 200 V.

For diodes that are lightly doped, the breakdown is dominated by the avalanche effect rather than the Zener effect. Consequently, the breakdown voltage is higher (over 5.6 V) for these devices.

Surface Zeners
The emitter-base junction of a bipolar NPN transistor behaves as a Zener diode, with breakdown voltage at about 6.8 V for common bipolar processes and about 10 V for lightly doped base regions in BiCMOS processes. Older processes with poor control of doping characteristics had the variation of Zener voltage up to ±1 V, newer processes using ion implantation can achieve no more than ±0.25 V. The NPN transistor structure can be employed as a surface Zener diode, with collector and emitter connected together as its cathode and base region as anode. In this approach the base doping profile usually narrows towards the surface, creating a region with intensified electric field where the avalanche breakdown occurs. Hot carriers produced by acceleration in the intense field can inject into the oxide layer above the junction and become trapped there. The accumulation of trapped charges can then cause 'Zener walkout', a corresponding change of the Zener voltage of the junction. The same effect can be achieved by radiation damage.

The emitter-base Zener diodes can handle only low currents as the energy is dissipated in the base depletion region which is very small. Higher amounts of dissipated energy (higher current for longer time, or a short very high current spike) causes thermal damage to the junction and/or its contacts. Partial damage of the junction can shift its Zener voltage. Total destruction of the Zener junction by overheating it and causing migration of metallization across the junction ("spiking") can be used intentionally as a 'Zener zap' antifuse.

Subsurface Zeners
A subsurface Zener diode, also called 'buried Zener', is a device similar to the surface Zener, but the doping and design is such that the avalanche region is located deeper in the structure, typically several micrometers below the oxide. Hot carriers then lose energy by collisions with the semiconductor lattice before reaching the oxide layer and cannot be trapped there. The Zener walkout phenomenon therefore does not occur here, and the buried Zeners have stable voltage over their entire lifetime. Most buried Zeners have breakdown voltage of 5–7 volts. Several different junction structures are used.

Uses
Zener diodes are widely used as voltage references and as shunt regulators to regulate the voltage across small circuits. When connected in parallel with a variable voltage source so that it is reverse biased, a Zener diode conducts when the voltage reaches the diode's reverse breakdown voltage. From that point on, the low impedance of the diode keeps the voltage across the diode at that value.

In this circuit, a typical voltage reference or regulator, an input voltage, Uin (with + on the top), is regulated down to a stable output voltage Uout. The breakdown voltage of diode D is stable over a wide current range and holds Uout approximately constant even though the input voltage may fluctuate over a wide range. Because of the low impedance of the diode when operated like this, resistor R is used to limit current through the circuit.

In the case of this simple reference, the current flowing in the diode is determined using Ohm's law and the known voltage drop across the resistor R;
 * $$I_\text{diode} = \frac{U_\text{in} - U_\text{out}}{R}$$

The value of R must satisfy two conditions:
 * 1) R must be small enough that the current through D keeps D in reverse breakdown. The value of this current is given in the data sheet for D. For example, the common BZX79C5V6 device, a 5.6 V 0.5 W Zener diode, has a recommended reverse current of 5mA. If insufficient current exists through D, then Uout is unregulated and less than the nominal breakdown voltage (this differs from voltage-regulator tubes where the output voltage is higher than nominal and could rise as high as Uin). When calculating R, allowance must be made for any current through the external load, not shown in this diagram, connected across Uout.
 * 2) R must be large enough that the current through D does not destroy the device. If the current through D is ID, its breakdown voltage VB and its maximum power dissipation Pmax correlate as such: $$I_D V_B < P_\text{max}$$.

A load may be placed across the diode in this reference circuit, and as long as the Zener stays in reverse breakdown, the diode provides a stable voltage source to the load. Zener diodes in this configuration are often used as stable references for more advanced voltage regulator circuits.

Shunt regulators are simple, but the requirements that the ballast resistor be small enough to avoid excessive voltage drop during worst-case operation (low input voltage concurrent with high load current) tends to leave a lot of current flowing in the diode much of the time, making for a fairly wasteful regulator with high quiescent power dissipation, suitable only for smaller loads.

These devices are also encountered, typically in series with a base-emitter junction, in transistor stages where selective choice of a device centered on the avalanche or Zener point can be used to introduce compensating temperature co-efficient balancing of the transistor p–n junction. An example of this kind of use would be a DC error amplifier used in a regulated power supply circuit feedback loop system.

Zener diodes are also used in surge protectors to limit transient voltage spikes.

Noise generator
Another application of the Zener diode is using its avalanche breakdown noise (see ), which for instance can be used for dithering in an analog-to-digital converter when at a rms level equivalent to $1⁄3$ to 1 lsb or to create a random number generator.

Waveform clipper
Two Zener diodes facing each other in series clip both halves of an input signal. Waveform clippers can be used not only to reshape a signal, but also to prevent voltage spikes from affecting circuits that are connected to the power supply.

Voltage shifter
A Zener diode can be applied to a circuit with a resistor to act as a voltage shifter. This circuit lowers the output voltage by a quantity that is equal to the Zener diode's breakdown voltage.

Voltage regulator
A Zener diode can be applied in a voltage regulator circuit to regulate the voltage applied to a load, such as in a linear regulator.

title: Zener diode


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Canine distemper

Canine distemper virus (CDV) (sometimes termed "footpad disease") is a viral disease that affects a wide variety of mammal families, including domestic and wild species of dogs, coyotes, foxes, pandas, wolves, ferrets, skunks, raccoons, and felines, as well as pinnipeds, some primates, and a variety of other species. CDV does not affect humans.

In canines, CDV affects several body systems, including the gastrointestinal and respiratory tracts, the spinal cord, and the brain. Common symptoms include high fever, eye inflammation and eye/nose discharge, labored breathing and coughing, vomiting and diarrhea, loss of appetite and lethargy, and hardening of the nose and footpads. The viral infection can be accompanied by secondary bacterial infections and can eventually present serious neurological symptoms.

Canine distemper is caused by a single-stranded RNA virus of the family Paramyxoviridae (the same family of viruses that causes measles, mumps, and bronchiolitis in humans). The disease is highly contagious via inhalation. Morbidity and mortality may vary greatly among animal species, with up to 100% mortality in unvaccinated populations of ferrets. In domestic dogs, while the acute generalized form of distemper has a high mortality rate, disease duration and severity depend mainly on the animal's age, immune status, and the virulence of the infecting strain of the virus. Despite extensive vaccination in many regions, it remains a major disease in dogs and was the leading cause of infectious disease death in dogs prior to a vaccine becoming available.

Etymology
The origin of the word distemper is from Middle English distemperen, 'to upset the balance of the humors,' which is from Old French destemprer, 'to disturb,' which is from Vulgar Latin distemperare, 'to not mix properly.'

History
In Europe, the first report of CDV occurred in Spain in 1761. Edward Jenner described the disease in 1809, and French veterinarian Henri Carré determined that the disease was caused by a virus in 1905. Carré's findings were disputed by researchers in England until 1926, when Patrick Laidlaw and G.W. Dunkin confirmed that the disease was, in fact, caused by a virus.

The first vaccine against canine distemper was developed by the Italian Vittorio Puntoni. In 1923 and 1924, Puntoni published two articles in which he added formalin to brain tissue from infected dogs to create a vaccine that successfully prevented the disease in healthy dogs. A commercial vaccine was developed in 1950, yet owing to its limited use, the virus remains prevalent in many populations.

The domestic dog has largely been responsible for introducing canine distemper to previously unexposed wildlife and now causes a serious conservation threat to many species of carnivores and some species of marsupials. The virus contributed to the near-extinction of the black-footed ferret. It also may have played a considerable role in the extinction of the thylacine (Tasmanian tiger) and recurrently causes mortality among African wild dogs. In 1991, the lion population in the Serengeti, Tanzania, experienced a 20% decline as a result of the disease. The disease has also mutated into the phocid distemper virus, which affects seals.

Clinical signs
In dogs, signs of CDV vary widely, from no signs to mild respiratory signs indistinguishable from kennel cough to severe pneumonia with vomiting, bloody diarrhea, and death.

Commonly observed signs are a runny nose, vomiting and diarrhea, dehydration, excessive salivation, coughing and/or labored breathing, loss of appetite, and weight loss. If neurological signs develop, incontinence may ensue. Central nervous system signs include a localized involuntary twitching of muscles or groups of muscles, seizures with salivation, and jaw movements commonly described as "chewing-gum fits," or more appropriately as "distemper myoclonus." As the condition progresses, the seizures worsen and progress to grand mal convulsions, followed by the death of the animal. The animal may also show signs of sensitivity to light, incoordination, circling, increased sensitivity to sensory stimuli such as pain or touch, and deterioration of motor capabilities. Less commonly, they may lead to blindness and paralysis. The length of the systemic disease may be as short as 10 days, or the start of neurological signs may not occur until several weeks or months later. Those few that survive usually have a small tic or twitch of varying degrees of severity. With time, this tic usually diminishes somewhat in its severity.

Lasting signs
A dog that survives distemper can have complications afterwards. The most prevalent complication is hard pad disease, in which the skin on paw pads and skin on end of the nose thicken. Another lasting symptom that is common is enamel hypoplasia. Puppies can have damage to the enamel of teeth that are not completely formed or have not yet grown through the gums. This results from the virus killing the cells responsible for manufacturing the tooth enamel. These affected teeth tend to erode quickly.

Life-threatening complications can include nervous-system degeneration. Dogs that have been infected with distemper can have a progressive deterioration of mental abilities and motor skills. With time, the dog can develop seizures, paralysis, a reduction in sight, and incoordination. These dogs are usually humanely euthanized because of the immense pain and suffering they face.

Virology
Distemper is caused by a single-stranded RNA virus of the family Paramyxoviridae, which makes it a close relative of the viruses that cause measles in humans and rinderpest in animals.

Genetic diversity
Geographically distinct lineages of the canine distemper virus are genetically diverse. This diversity arises from mutation and, when two genetically distinct viruses infect the same cell, from homologous recombination.

Host range
Distemper, or hardpad disease in canines, affects animals in the following families and species:
 * Ailuridae (red panda)
 * Canidae (dog, fox, wolf, Chinese raccoon dog)
 * Elephantidae (Asian elephant)
 * Felidae (large cats, though not domestic cats)
 * Hyaenidae (hyena)
 * Mustelidae (ferret, mink, skunk, wolverine, marten, badger, otter)
 * Pinnipedia (seals, walrus, sea lion, etc.)
 * Primate (some) (e.g., Japanese monkey)
 * Procyonidae (raccoon, coati)
 * Ursidae (bear)
 * Viverridae (raccoon-like South Asian binturong, palm civet)

Animals in the family Felidae, including many species of large cat as well as domestic cats, were long believed to be resistant to canine distemper until some researchers reported the prevalence of canine distemper virus (CDV) infection in large felids. Both large and domestic cats are now known to be capable of infection, usually through close housing with dogs or possibly blood transfusion from infected cats, but such infections appear to be self-limiting and largely without symptoms.

In a captive population of giant pandas in China (Shanxi Rare Wild Animal Rescue and Research Center), six of 22 captive pandas were infected by CDV. All but one infected panda died; the survivor had previously been vaccinated.

Mechanism
The canine distemper virus affects nearly all body systems. Puppies from 3–6 months old are particularly susceptible. CDV spreads through aerosol droplets and through contact with infected bodily fluids, including nasal and ocular secretions, feces, and urine, 6 to 22 days after exposure. It can also be spread by food and water contaminated with these fluids. The time between infection and disease is 14 to 18 days, although a fever can appear from 3 to 6 days after infection.

The canine distemper virus tends to direct its infection toward the lymphoid, epithelial, and nervous tissues. The virus initially replicates in the lymphatic tissue of the respiratory tract. The virus then enters the blood stream and infects the respiratory, gastrointestinal, urogenital, epithelial, and central nervous systems, as well as optic nerves. Therefore, the typical pathologic features of canine distemper include lymphoid depletion (causing immunosuppression and leading to secondary infections), interstitial pneumonia, encephalitis with demyelination, and hyperkeratosis of the nose and foot pads.

The virus first appears in bronchial lymph nodes and tonsils two days after exposure. The virus then enters the bloodstream on the second or third day. A first round of acute fever tends to begin around 3–8 days after infection, which is often accompanied by a low white blood cell count, especially of lymphocytes, as well as a low platelet count. These signs may or may not be accompanied by anorexia, a runny nose, or discharge from the eye. This first round of fever typically recedes rapidly within 96 hours, and then a second round of fever begins around the 11th or 12th day and lasts at least a week. Gastrointestinal and respiratory problems tend to follow, which may become complicated with secondary bacterial infections. Inflammation of the brain and spinal cord, otherwise known as encephalomyelitis, either is associated with this, subsequently follows, or comes completely independently of these problems. A thickening of the footpads sometimes develops, and vesicular pustular lesions on the abdomen usually develop. Neurological signs are typically found in animals with thickened footpads from the virus. About half of sufferers experience meningoencephalitis. Less than 50% of the adult dogs that contract the disease die from it. Among puppies, the death rate often reaches 80%.

Diagnosis
The above signs, especially fever, respiratory signs, neurological signs, and thickened footpads, occurring in unvaccinated dogs strongly indicate CDV. However, several febrile diseases match many of the signs of the disease and only recently has distinguishing between canine hepatitis, herpes virus, parainfluenza, and leptospirosis been possible. Thus, finding the virus by various methods in the dog's conjunctival cells or foot pads gives a definitive diagnosis. In older dogs that develop distemper encephalomyelitis, diagnosis may be more difficult, since many of these dogs have an adequate vaccination history.

An additional test to confirm distemper is a brush border slide of the bladder transitional epithelium of the inside lining from the bladder, stained with Diff-Quik. These infected cells have inclusions which stain a carmine red color, found in the paranuclear cytoplasm. About 90% of the bladder cells will be positive for inclusions in the early stages of distemper.

Prevention
A number of vaccines against CDV exist for dogs (ATCvet code: and combinations) and domestic ferrets, which in many jurisdictions are mandatory for pets. Infected animals should be quarantined from other dogs for several months owing to the length of time the animal may shed the virus. The virus is destroyed in the environment by routine cleaning with disinfectants, detergents, or drying. It does not survive in the environment for more than a few hours at room temperature (20–25 °C), but can survive for a few weeks in shady environments at temperatures slightly above freezing. It, along with other labile viruses, can also persist longer in serum and tissue debris.

Despite extensive vaccination in many regions, it remains a major disease of dogs.

To prevent canine distemper, puppies should begin vaccination at 6–8 weeks of age and then continue getting the "booster shot" every 2–4 weeks until they are 16 weeks of age. Without the full series of shots, the vaccination does not provide protection against the virus. Since puppies are typically sold at the age of 8–10 weeks, they typically receive the first shot while still with their breeder, but the new owner often does not finish the series. These dogs are not protected against the virus, so are susceptible to canine distemper infection, continuing the downward spiral that leads to outbreaks throughout the world.

Treatment
No specific treatment for the CDV is known. As with measles, the treatment is symptomatic and supportive. Care is geared towards treating fluid/electrolyte imbalances, neurological symptoms, and preventing any secondary bacterial infections. Examples include administering fluids, electrolyte solutions, analgesics, anticonvulsants, broad-spectrum antibiotics, antipyretics, parenteral nutrition, and nursing care.

Outcome
The mortality rate of CDV largely depends on the immune status of the infected dogs. Puppies experience the highest mortality rate, where complications such as pneumonia and encephalitis are more common. In older dogs that develop distemper, encephalomyelitis and vestibular disease may be present. Around 15% of canine inflammatory central nervous system diseases are a result of CDV.

Epidemiology
The prevalence of canine distemper in the community has decreased dramatically due to the availability of vaccinations. However, the disease continues to spread among unvaccinated populations, such as those in animal shelters and pet stores. This provides a great threat to both the rural and urban communities throughout the United States, affecting both shelter and domestic canines. Despite the effectiveness of the vaccination, outbreaks of this disease continue to occur nationally. In April 2011, the Arizona Humane Society released a valley-wide pet health alert throughout Phoenix, Arizona.

Outbreaks of canine distemper continue to occur throughout the United States and elsewhere and are caused by many factors, including proximity to wild animals and lack of vaccinated animals. This problem is even greater within areas such as Arizona, owing to the vast amount of rural land. An unaccountable number of strays that lack vaccinations reside in these areas, so they are more susceptible to diseases such as canine distemper. These strays act as a reservoir for the virus, spreading it throughout the surrounding area, including urban areas. Puppies and dogs that have not received their shots can then be infected in a place where many dogs interact, such as a dog park.

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

title: Canine distemper


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Pressure frying

In cooking, pressure frying is a variation on pressure cooking where meat and cooking oil are brought to high temperatures while pressure is held high enough to cook the food more quickly. This leaves the meat very hot and juicy. A receptacle used in pressure frying is known as a pressure fryer. The process is most notable for its use in the preparation of fried chicken in many commercial fried chicken restaurants.

Details
Pressure frying is mostly done in industrial kitchens. Ordinary home pressure cookers are generally unsuitable for pressure frying, because they are typically designed for a maximum temperature around 121 °C (250 °F) whereas oil can reach temperatures well in excess of 160 °C (320 °F) which may damage the gasket in an ordinary pressure cooker, causing it to fail. Second-generation cookers are somewhat safer, but can still be dangerous if proper precautions, like obeying fill limits, are not taken.

title: Pressure frying