Who gets lupus

Anyone can get lupus. About 9 out of 10 adults with lupus are women ages 15 to 45. African-American women are three times more likely to get lupus than white women. Lupus is also more common in Latina, Asian, and Native American women. Men are at a higher risk before puberty and after age 50. 

Despite an increase in lupus in men in these age groups, two-thirds of the people who have lupus before puberty and after age 50 are women.

Lupus affects young women most More than 90 percent of people with lupus are women between the ages of 15 and 45. African-American, Latina, Asian, and Native American women are at greater risk of getting lupus than white women.

African-Americans and Latinos tend to get lupus at a younger age and have more severe symptoms, including kidney problems. African-Americans with lupus also have more problems with seizures, strokes, and dangerous swelling of the heart muscle. Latina patients have heart problems as well. Scientists believe that genes play a role in how lupus affects these ethnic groups.

Apart from genetic factors, lupus can be more severe for people who aren't getting the care they need. studies have shown that people with lupus who have a lower household income, lower level of education, or less of a support system tend to do worse with the disease. For some people with lupus, severe symptoms of the disease leave them unable to work, which may result in low income and lack of health insurance. These factors make it hard for a person with lupus to get the right treatment or sometimes even diagnosis that they need.

SOURCE:

womenshealth.gov

KINDS OF LUPUS

Systemic lupus erythematosus, or SLE,makes up about 70 percent of all cases of lupus. SLE can be Mild or severe and can affect various parts of the body. Common symptoms include fatigue, hair loss, sensitivity to the sun (photosensitivity), painful and swollen joints, unexplained fever, skin rashes, and kidney problems. In general the diagnosis of lupus is based on both physical symptoms and lab results.

Cutaneous(kyoo-TAY-nee-uhss) lupus erythematosus can be limited to the skin or seen in those with SLE. “Cutaneous” means “skin.” Symptoms may include rashes/lesions, hair loss, vasculitis (swelling of the blood vessels), ulcers, and photosensitivity. A doctor will remove a small piece of the rash or sore and look at it under a microscope to tell if someone has skin lupus and what form it is. There are two major kinds of cutaneous lupus

Discoid(DISS-koid) lupus erythematosus,also called DLE, mainly affects the skin. The discoid rash usually begins as a red raised rash that becomes scaly or changes color to a dark brown. These rashes often appear on the face and scalp, but other areas may also be affected. Many people with DLE have scarring. Sometimes DLE causes sores in the mouth or nose. A doctor will remove a small piece of the rash or sore and look at it under a microscope to tell if someone has DLE. If you have DLE, there is a small chance that you will later get SLE. Currently there is no way to know if someone with DLE will get SLE.

Subacute cutaneous lupus erythematosus,makes up 10 percent of lupus cases. About 50 percent of the time, people with subacute cutaneous lupus also have SLE. Subacute cutaneous lupus causes skin lesions on parts of the body exposed to sun. These lesions do not cause scars.

Drug-induced lupusis a form of lupus caused by certain medicines. The symptoms of drug-induced lupus are like those of systemic lupus, but only rarely affect major organs. Symptoms can include joint pain, muscle pain, and fever, and are mild for most people. Most of the time, the disease goes away when the medicine is stopped. However, not everyone who takes these drugs will get drug-induced lupus.

The drugs most commonly connected with drug-induced lupus are used to treat other chronic conditions, such as seizures, high blood pressure, or rheumatoid arthritis. Examples include procainamide  (Pronestyl, Procanbid); hydralazine (Apresoline; also, hydralazine is an ingredient in Apresazide and BiDil); phenytoin (Dilantin); etanercept (Enbrel); and adalimumab (Humira).

Neonatal lupusis a rare disease in infants that is caused by certain antibodies from the mother. These antibodies can be found in mothers who have lupus. But it is also possible for an infant to have neonatal lupus even though the mother is healthy. However, in these cases the mother will often develop symptoms of lupus later in life. At birth, an infant with neonatal lupus may have a skin rash, liver problems, or low blood cell counts, but these symptoms disappear completely after several months and have no lasting effects. Infants with neonatal lupus can also have a rare but serious heart defect. With proper testing, physicians can now identify most at-risk mothers, and the infant can be treated at or before birth. Most infants of mothers with lupus are healthy.

SOURCE
womenshealth.gov

Lupus

Lupus (LOO-puhss) is a chronic, autoimmune (aw-toh-ih-MYOON) disease. It can harm any part of the body (skin, joints, and/or organs inside the body). Chronic means that the signs and symptoms last longer than six weeks and often for many years. In lupus, something goes wrong with your immune system, which is the part of the body that fights off viruses, bacteria, and other germs (“foreign invaders,” like the flu). Normally your immune system makes proteins called antibodies that protect the body from these invaders. Autoimmune means your immune system cannot tell the difference between these invaders and your body's
healthy tissues (“auto” means “self”). In lupus, your immune system creates auto antibodies (AW-toh-AN-teyebah-deez), which sometimes attack and destroy healthy tissue. These auto antibodies add to inflammation, pain, and damage in parts of the body.

When people talk about “lupus,” they usually mean systemic lupus erythematosus (ur-uh-thee-muh-TOH-suhss), or SLE. This is the most common type of lupus. It is hard to guess how many people in the U.S. have lupus, because the symptoms are so different for every person. Sometimes it is not diagnosed. The Lupus Foundation of America thinks that about 16,000 new cases are reported across the country each year.

Although lupus can affect almost any organ system, the disease, for most people, affects only a few parts of the body. For example, one person with lupus may have swollen knees and fever. Another person may be tired all the time or have kidney trouble. Someone else may have rashes. Over time, more symptoms can develop.

Normally, lupus develops slowly, with symptoms that come and go. Women who get lupus most often have symptoms and are diagnosed between the ages of 15 and 45. But the disease also can happen in childhood or later in life.

For some people, lupus is a mild disease. But for others, it may cause severe problems. Even if your lupus symptoms are mild, it is a serious disease that needs constant monitoring and treatment. It can harm your organs and put your life at risk if untreated.

KINDS OF LUPUS

SOURCE

womenshealth.gov

Does how much you eat affect how long you live?

Your body needs food to survive. However, the very process of extracting energy from food metabolizing food creates stress on your body. Overeating creates even more stress on the body. That’s part of the reason why it can lead to a shorter lifespan and serious health problems common among older people, including cardiovascular disease and type 2 diabetes.

Calorie restriction, an approach primarily used in a research setting, is more tightly controlled than normal 

healthy eating or dieting. It is commonly defined by at least a 30 percent decrease in calorie consumption from the normal diet with a balanced amount of protein, fat, vitamins, and minerals. In the 1930s, Investigators found that laboratory rats and mice lived up to 40 percent longer when fed a calorie restricted diet, compared to mice fed a normal diet. Since that time, scientists observed that calorie restriction increased the lifespan of many other animal models, including yeast, worms, flies, some strains of mice, and maybe even nonhuman primates. In addition, when started at an early age or as a young adult, calorie restriction was found to increase the health span of many animal models by delaying onset of age-related disease and delaying normal age-related decline. 

Two studies of calorie restriction in nonhuman primates have had intriguing results. In a study conducted at NIA, monkeys fed a calorie-restricted diet had a notably decreased and/or delayed onset of age-related 

diseases, compared to the control group of “normal” eaters. In a University of Wisconsin study supported by NIA, calorie-restricted rhesus monkeys had three times fewer age related diseases compared to the control 

group. The Wisconsin study also found that rhesus monkeys on a restricted diet had fewer age-related Deaths compared to their normal fed controls. In 2007, when the findings from the study conducted at NIA were published, it was too early to determine whether calorie restriction had any effects on lifespan. Research in primates continues.

Despite its apparent widespread acceptance, calorie restriction does not increase lifespan in all animals. In studies of non-laboratory (wild) mice, researchers found that on average, calorie restriction did not have any effect on lifespan. Some of the calorie-restricted mice actually lived shorter than average lives. This may be due to differences in the genetics of the wild mice. A 2010 NIA-funded study provides further evidence that genetics may play a role in whether or not calorie restriction will have a positive effect on longevity. Looking at 42 closely related strains of laboratory mice, researchers found that only about a third of the strains on a calorie-restricted diet had an increase in longevity. One-third of the strains of mice on a calorie-restricted diet had a shortened lifespan, and the other third had no significant difference in lifespan compared to mice on a normal diet.

While animal studies are ongoing, researchers are also exploring calorie restriction in humans to test its safety and practicality, as well as to see if it will have positive effects on health. Participants in a 2002 pilot of the Comprehensive Assessment of Long-term Effects of  Reducing Intake of Energy (CALERIE) study had, after 1 year, lowered their fasting glucose, total cholesterol, core body temperature, body weight, and fat. At the cellular level, they had better functioning mitochondria and reduced DNA damage. However, in terms of practicality, scientists observed that adapting and adhering to the regimen could be difficult. A longer-term trial is underway. 

Given that ample studies have demonstrated mostly positive effects of calorie restriction in many organisms, today’s scientific studies focus on finding the mechanisms and pathways by which calorie restriction works. Researchers are also studying compounds that might act the same way in the body, mimicking the benefits of 

calorie restriction. A wide range of possible mechanisms for calorie restriction are being investigated. Some scientists are exploring the possibility that metabolizing fewer calories results in less oxidative damage to the cells. Other scientists are looking at how the relative scarcity of nutrients caused by calorie restriction might 

induce heat shock proteins and other defense mechanisms that allow the body to better withstand other stresses and health problems. Some researchers wonder if the effects of calorie restriction are controlled by the brain and nervous system. In one NIA-conducted study, calorie restriction increased the production 

of brain-derived neurotrophic factor, or BDNF, a protein that protects the brain from dysfunction and degeneration, and supports increased regulation of blood sugar and heart function in animal models. Still other studies indicate calorie restriction may influence hormonal balance, cell senescence, or gene expression. It is likely that calorie restriction works through a combination of these mechanisms, and others yet to be identified. 

There is an intriguing overlap between the pathways that control normal aging and those that scientists think may be pertinent to calorie restriction. The most relevant are the sirtuins and mTOR (mammalian target 

of rapamycin) pathways as discussed on page 16. In several, but not all cases, disrupting these pathways means the organism no longer responds positively to calorie restriction. These two pathways have been important for identifying at least two compounds that may mimic the effects of calorie restriction: resveratrol and rapamycin. 

Resveratrol, found naturally in grapes, wine, and nuts, activates the sirtuin pathway. It has been shown to increase the lifespan of yeast, flies, worms, and fish. In 2006, NIA researchers, in collaboration with university scientists funded by NIA, reported on a study comparing mice fed a standard diet, a high fat-and-calorie diet, or a high fat-and-calorie diet supplemented with resveratrol beginning at middle age. Resveratrol appeared to lessen the negative effects of the high fat-and-calorie diet, both in terms of lifespan and disease. In a 2008 follow-up study, investigators found that resveratrol improved the health of aging mice fed a standard diet. It prevented age- and obesity-related decline in heart function. Mice on resveratrol had better bone health, reduced cataract formation, and enhanced balance and motor coordination compared to non-treated mice. In addition, resveratrol was found to partially mimic the effects of calorie restriction on gene expression profiles of liver, skeletal muscle, and adipose (fatty) tissue in the mice. However, the compound did not have an impact on the mice’s overall survival or maximum lifespan. These findings suggest that resveratrol does not affect all aspects of the basic aging process and that there may be different mechanisms for health versus lifespan. Research on resveratrol continues in mice, along with studies in nonhuman 

primates and people.

Rapamycin, another possible calorie restriction mimetic, acts on the mTOR pathway. This compound’s main clinical use is to help suppress the immune system of people who have had an organ transplant so that 

the transplant can succeed. A study by NIA’s Interventions Testing Program, as discussed on page 7, reported in 2009 that rapamycin extended the median and maximum lifespan of mice, likely by inhibiting the mTOR pathway. Rapamycin had these positive effects even when fed to the mice beginning at early-old age (20 months), suggesting that an intervention started later in life may still be able to increase longevity. Researchers are now looking at rapamycin’s effects on health span and if there are other compounds that 

may have similar effects as rapamycin on the pathway.

Scientists do not yet know how resveratrol, rapamycin, and other compounds that demonstrate effects similar to calorie restriction will influence human aging. Learning more about these calorie restriction mimetic s, and the mechanisms and pathways underlying calorie restriction, may point the way to future healthy aging therapies.

SOURCE:

1. LINK1

Does stress really shortens life

Biological stress begins with the very basic processes in the body that produce and use energy. We eat foods and we breathe, and our body uses those two vital elements (glucose from food and oxygen from the air) to produce energy, in a process known as metabolism. You may already think of metabolism as it pertains to eating“. My metabolism is fast, so I can eat dessert," or “My metabolism has slowed down over the years, so I’m gaining weight.” Since metabolism is all about energy, it also encompasses breathing, 

circulating blood, eliminating waste, controlling body temperature, contracting muscles, operating the brain and nerves, and just about every other activity associated with living.

These everyday metabolic activities that sustain life also create “metabolic stress,” which, over time, results in damage to our bodies. Take breathing—obviously, we could not survive without oxygen, but oxygen is a catalyst for much of the damage associated with aging because of the way it is metabolized inside our cells. Tiny parts of the cell, called mitochondria, use oxygen to convert food into energy. While mitochondria are extremely efficient in doing this, they produce potentially harmful byproducts called oxygen free radicals. A variety of environmental factors, including tobacco smoke and sun exposure, can produce them, too. The oxygen free radicals react with and create instability in surrounding molecules. This process, called oxidation, occurs as a chain reaction: the oxygen free radical reacts with molecule “A” causing molecule “A” to become unstable; molecule “A” attempts to stabilize itself by reacting with neighboring molecule “B”; then molecule “B” is unstable and attempts to become stable by reacting with neighboring molecule “C”; and so on. This process repeats itself until one of the molecules becomes stable by breaking or rearranging itself, instead of 

passing the instability on to another molecule. 

Some free radicals are beneficial. The immune system, for instance, uses oxygen free radicals to destroy bacteria and other harmful organisms. Oxidation and its by-products also help nerve cells in the brain communicate. But, in general, the outcome of free radicals is damage (breaks or rearrangements) to 

other molecules, including proteins and DNA. Because mitochondria metabolize oxygen, they are particularly prone to free radical damage. As damage mounts, mitochondria may become less efficient, progressively 

generating less energy and more free radicals.

Scientists study whether the accumulation of oxidative (free radical) damage in our cells and tissues over time might be responsible for many of the changes we associate with aging. Free radicals are already implicated in many disorders linked with advancing age, including cancer, atherosclerosis, cataracts, and neurodegeneration.

Fortunately, free radicals in the body do not go unchecked. Cells use substances called antioxidants to counteract them. Antioxidants include nutrients, such as vitamins C and E, as well as enzyme proteins produced naturally in the cell, such as superoxide dismutase (SOD), catalase, and glutathione peroxidase. 

Many scientists are taking the idea that antioxidants counter the negative effects of oxygen free radicals a step further. Studies have tested whether altering the antioxidant defenses of the cell can affect the lifespan of animal models. These experiments have had conflicting results. NIA-supported researchers found that inserting extra copies of the SODgene into fruit flies extended the fruit flies’ average lifespan by as much as 30 percent. Other researchers found that immersing roundworms in a synthetic form of SOD and catalase extended their lifespan by 44 percent. However, in a comprehensive set of experiments, increasing or 

decreasing antioxidant enzymes in laboratory mice had no effect on lifespan. Results from a limited number of human clinical trials involving antioxidants generally have not supported the premise that adding antioxidants to the diet will support longer life. Antioxidant supplementation remains a topic of continuing investigation.

SOURCE:

LINK1

What happens when DNA becomes damaged?

The impact of age, of course, is not limited to organisms. You drive a brand new car off the lot, and ideally it’s in perfect working condition. But by the time it reaches the 100,000 mile mark, the car doesn’t run quite 

like it used to. Or, that lovely walking path you discovered when you first moved into your home has now become weathered, the weeds are overgrown, and some of the asphalt has buckled. 

Like the car and the walking path, over time your DNA accumulates damage. That’s normal. Our DNA suffers millions of damaging events each day. Fortunately, our cells have powerful mechanisms to repair damage and, by and large, these mechanisms remain active and functional through old age. However, over time, some damage will fail to be repaired and will stay in our DNA. Scientists think this damage and a decrease in the body’s ability to fix itself may be an important component of aging. Most DNA damage is harmless for example, small errors in DNA code, called mutations, are harmless. Other types of DNA damage, for example, when a DNA strand breaks, can have more serious ramifications. Fixing a break in a DNA strand is a complex operation and it is more likely the body will make mistakes when attempting this repair mistakes that could shorten lifespan. 

Another kind of DNA damage build-up occurs when a cell divides and passes its genetic information on to its two daughter cells. During cell division, the telomere, a stretch of DNA at each end of a chromosome that doesn’t encode any proteins but instead protects the protein-encoding part of the DNA, becomes shorter. 

When the telomere becomes too short, it can no longer protect the cell’s DNA, leaving the cell at risk for serious damage. In most cells, telomere length cannot be restored. Extreme telomere shortening triggers an SOS response, and the cell will do one of three things: stop replicating by turning itself off, becoming what is known as senescent; stop replicating by dying, called apoptosis; or continue to divide, becoming abnormal and potentially dangerous. 

Scientists are interested in senescent cells because, although they are turned off, they still work on many levels. For instance, they continue to interact with other cells by both sending and receiving signals. However, senescent cells are different from their earlier selves. They cannot die, and they release molecules that lead to an increased risk for diseases, particularly cancer. 

The relationship among cell senescence, cancer, and aging is an area of ongoing investigation. When we are young, cell senescence may be critical in helping to suppress cancer. Senescence makes the cell stop replicating when its telomeres become too short, or when the cell cannot repair other damage to its DNA. Thus, senescence prevents severely damaged cells from producing abnormal and perhaps cancerous daughter cells. However, later in life, cell senescence may actually raise the risk of cancer by releasing certain molecules that make the cells more vulnerable to abnormal function. 

Consider fibroblasts, cells that divide about 60 times before turning off. Normally, fibroblasts hold skin and other tissues together via an underlying structure, a scaffold outside the cell, called the extracellular matrix. The extracellular matrix also helps to control the growth of other cells. When fibroblasts turn off, they emit molecules that can change the extracellular matrix and cause inflammation. This disturbs the tissue’s function and contributes to aging. At the same time, the breakdown of the extracellular matrix may contribute to increased risk of cancer with age. 

Learning why on a biological level cell senescence goes from being beneficial early in life to having Detrimental effects later in life may reveal some important clues about aging. 

SOURCE:

1. LINK1

Immune system plays an essential role in the heart.

The embryonic macrophages in the heart promote healing after injury, A new research has revealed that immune system plays an essential role in the heart's response to injury. Now, researchers says that two major pools of immune cells are at work in the heart. Both belong to a class of cells known as macrophages. One appears to promote healing, while the other likely drives ignition which is detrimental to long-term heart function.

Macrophages have long been thought of as a single type of cell, the author said. Our study shows really many different types of macrophages that originate in different places in the body. Some are protecting and can help blood vessels grow and reborn tissue. Others are unhealthy and can bring to harm.

Actually, the heart is one of the few organs with a association of macrophages formed in the embryo and maintained into adults. The heart, brain and liver are the only organs that contain large numbers of macrophages that arise in the yolk sac, in very early stages of arises, and they think these macrophages tend to be protective. Healthy hearts maintain this population of embryonic macrophages, as well as a smaller pool of adult macrophages derived from the blood. But during cardiac stress such as high BP, not only were more adult macrophages recruited from the blood and brought to the heart, they actually replaced the embryonic macrophages.

The study is published in the journal Immunity. (ANI)

Industrial control system

Industrial control system(ICS) is a general term that encompasses several types of control systems, including supervisory control and data acquisition (SCADA) systems, distributed control systems (DCS), and other smaller control system configurations such as skid-mounted Programmable Logic Controllers (PLC) often found in the industrial sectors and critical infrastructures. ICSs are typically used in industries such as Electrical, water, oil and gas, chemical, transportation, pharmaceutical, pulp and paper, food and beverage, and discrete manufacturing (e.g., automotive, aerospace, and durable goods.) These control systems are critical to the operation of the U.S. critical infrastructures that are often highly interconnected and mutually dependent systems. It is important to note that approximately 90 percent of the nation's critical infrastructures are privately owned and operated. Federal agencies also operate many of the industrial processes mentioned above; other examples include air traffic control and materials handling (e.g., Postal Service mail handling.) This section provides an overview of SCADA, DCS, and PLC systems, including typical architectures and components. Several diagrams are presented to depict the network connections and components typically found on each system to facilitate the understanding of these systems. The diagrams in this section do not address security and the diagrams in this section do not represent a secure architecture.

SOURCE:
NIST Guide to Supervisory and Data Acquisition-SCADA and Industrial Control Systems Security (2007)

DCSs

DCSs are used to control industrial processes such as electric power generation, oil and gas refineries, water and wastewater treatment, and chemical, food, and automotive production. DCSs are integrated as a control architecture containing a supervisory level of control overseeing multiple, integrated subsystems that are responsible for controlling the details of a localized process.  Product and process control are usually achieved by deploying feed back or feed forward control loops whereby key product and/or process conditions are automatically maintained around a desired set point. To accomplish the desired product and/or process tolerance around a specified set point, specific programmable controllers (PLC) are employed in the field and proportional, integral, and/or differential settings on the PLC are tuned to provide the desired tolerance as well as the rate of self-correction during process upsets. DCSs are used extensively in process-based industries. 

SCADA

SCADA (supervisory control and data acquisition)systems are highly distributed systems used to control geographically dispersed assets, often scattered over thousands of square kilometers, where centralized data acquisition and control are critical to system operation. They are used in distribution systems such as water distribution and wastewater collection systems, oil and gas pipelines, electrical power grids, and railway transportation systems. 

A SCADA control center performs centralized monitoring and control for field sites over long-distance communications networks, including monitoring alarms and processing status data. Based on information received from remote stations, automated or operator-driven supervisory commands can be pushed to remote station control devices, which are often referred to as field devices. Field devices control local operations such as opening and closing valves and breakers, collecting data from sensor systems, and 

monitoring the local environment for alarm conditions. 

SVURESET ELECTRICAL AND ELECTRONICS SYLLABUS

 

Unit I

Electric Circuits and Fields: Network graph, KCL, KVL, node and mesh analysis, transient response 

of dc and ac networks; sinusoidal steady-state analysis, resonance, basic filter concepts;  ideal current and voltage sources, Thevenin's, Norton's and Superposition and Maximum Power Transfer theorems, two -port networks, three phase circuits; Gauss Theorem, electric field and potential due to point, line, plane  and  spherical  charge  distributions;  Ampere's  and  Biot-Savart's  laws;  inductance;  dielectrics; capacitance.

Signals  and  Systems:  Representation  of  continuous  and  discrete-time  signals;  shifting  and  scaling 

operations;  linear,  time-invariant  and  causal  systems;  Fourier  series  representation  of  continuous 

periodic signals; sampling theorem; Fourier, Laplace and Z transforms.

Unit II

Electrical Machines:  Single phase transformer  -  equivalent circuit, phasor diagram, tests, regulation and  efficiency;  three  phase  transformers  -  connections,  parallel  operation;  auto -transformer;  energy conversion principles; DC machines - types, windings, generator characteristics, armature reaction and commutation, starting and speed control of motors; three phase induction motors  -  principles, types, performance  characteristics,  starting  and speed control;  single  phase  induction  motors; Synchronous machines -  performance, regulation and parallel operation of generators, motor starting, characteristics and applications; servo and stepper motors.

Unit III

Power Systems:  Basic power generation concepts; transmission line models and performance; cable performance, insulation; corona and radio interference; distribution systems; per-unit quantities; bus impedance  and  admittance  matrices;  load  flow;  voltage  control;  po wer  factor  correction; economic operation; symmetrical components; fault analysis; principles of over-current, differential and distance protection; solid state relays and digital protection; circuit breakers; system stability concepts,  swing curves and equal area criterion; HVDC transmission and FACTS concepts

Unit IV

Control Systems: Principles of feedback; transfer function; block diagrams; steady-state errors; Routh and Niquist techniques; Bode plots; root loci; lag, lead and lead-lag compensation; state space model; state Transition matrix, controllability and observability.

Electrical  and  Electronic  Measurements:  Bridges  and  potentiometers;  PMMC,  moving iron, dynamometer  and  induction  type  instruments;  measurement  of  voltage,  current,  power,  energy  and power factor; instrument transformers; digital voltmeters and multimeters; phase, time and frequency

measurement; Q-meters; oscilloscopes; potentiometric recorders; error analysis.

Unit V

Analog and Digital Electronics: Characteristics of diodes, BJT, FET; amplifiers - biasing, quivalent circuit  and  frequency  response; oscillators and feedback amplifiers; operational  amplifiers - Characteristics and applications; simple active filters; VCOs and timers; combinational and sequential logic circuits; multiplexer;  Schmitt  trigger;  multi-vibrators;  sample  and  hold  circuits;  A/D  and D/A converters; 8-bit microprocessor basics, architecture, programming and interfacing.

Power  Electronics  and  Drives:  Semiconductor  power  diodes,  transistors,  thyristors,  triacs,  GTOs, 

MOSFETs  and  IGBTs  - static  characteristics  and  principles  of  operation; triggering  circuits; phase 

control rectifiers; bridge converters - fully controlled and half controlled; principles of choppers and inverters; basis concepts of adjustable speed dc and ac drives 

Why industries are using Capacitor Banks

This phase difference can take two basics forms. 

• The current can “lag” the voltage when an inductive load (i.e., motors, magnetic HID ballasts) is used or
• The current can “lead” the voltage when a capacitive load(i.e., computers, electronic fluorescent ballasts) is used. 

When the current is out of phase with the voltage,the power utility has to supply more volt-amperes(VA) for a given wattage (W). Certain customers, such as industrial companies, may have to pay an additional charge if their power factor is too low which is why many industrial applications have banks of capacitors. These capacitors correct the poor power factor caused by the motors. This is also how manufacturers have been able to take a product that is inductive in nature, such as a magnetic HID ballast with a normal power factor, and include a “power factor correcting” capacitor to give the ballast a high power factor. 

REFERENCE:

LINK 1

What is power factor?

This is a very involved subject that will be dealt with in terms of field application and typical questions from end-users. Power factor is characteristic of alternating current (AC) circuits. Always a value between (0.0) and (1.0), the higher the number the greater/better the power factor. Circuits containing only heating elements (filament lamps, strip heaters, cooking stoves, etc.) have a power factor of 1.0. 

Other circuits containing inductive or capacitive elements (ballasts, motors, personal computer, etc.) usually have a power factor below 1.0. Normal power factor ballasts (NPF) typically have a value of (0.4) - (0.6). Ballasts with a power factor greater than (0.9) are considered high power factor ballasts (HPF). The significance of power factor lies in the fact that utility companies supply customers with volt-amperes, but bill them for watts. The relationship is (watts = volts x amperes x power factor). It is clear that power factors below 1.0 require a utility to generate more than the minimum volt-amperes necessary to supply the power (watts). This increases generation and transmission costs. Good power factor is considered to be greater than 0.85 or 85%.

Utilities may impose penalties on customers who do not have good power factors on their overall buildings.

Watts, or real power, is what a customer pays for. VARS is the extra“ power ” transmitted to compensate for a power factor less than 1.0. The combination of the two is called "apparent" power (VA or volt-amperes). Consider this popular analogy to clarify the relationship between real and apparent power.

We all know a glass of draft beer generally has a "head" on it. Let's say your favorite pub institutes a new policy -you only pay for the beer, not the foam. While the foam is just aerated beer, it is not really usable in that form. If the glass of beer is half foam, you pay half the price. This is the same principle as electricity generation - the consumer only pays for the beer (real power), not the foam (the "VARS" mentioned above).

Reference links:

REFER ONE