Dc Power Supply Design

Abstract: The main aim of this assignment is to design a pre amplifier circuit with an NPN transistor to be used in a simple public address (PA) system. The pre amplifier is fed from a microphone that produces an average output voltage of 10 mV rms. The amplifier is to operate over a frequency range of 300 Hz to 5 kHz and should have an adjustable volume control. The expected gain of the amplifier is 100.First we are going to design an amplifier for given specifications, model the operation of the circuit using h-parameter and r-parameter model, use computer aided design software to analyze the circuit performance and demonstrate the working of the circuit by hardware implementation. Then, we will plot the frequency response of the circuit and analyze the effect of the emitter bypass capacitor. Finally we will compare the mid-band gain, bandwidth and lower cutoff frequency obtained from the simulation result and the hardware implementation with the designed values. Chapter 1Introduct ion: Bipolar Junction Transistor (BJT) is a three terminal device with three regions (Emitter, Base and Collector) and two PN junctions (Emitter-Base junction and Base-Collector junction). Since there are two junctions that means there are four possible ways of biasing a transistor. If both junctions are forward biased then the transistor will operate in the saturation region. If both junctions are reverse biased then the transistor will operate in the cut of region. These two conditions of operation are used when the transistor is needed to work as a switch.To use a transistor as an amplifier, the emitter base junction should be forward biased and the collector base junction should be reverse biased. Amplifier is an electronic circuit that can amplify signals applied to its input terminal. If an AC signal is given to a transistor amplifier it will produce an AC base current. This AC base current will produce a much larger AC collector current since IC=? IB. The AC collector current produces an AC voltage across the load resistor RL, thus producing an amplified, but inverted, reproduction of the AC input voltage in the active region of operations.DC load line is a sloping straight line connecting all the operating points of a transistor biasing drawn on the output characteristics of the transistor and the intersection point gives the Quiescent point (Q-point). A prober Q-point should be in the middle of the DC load line. Selecting a good Q-point prevents the transistor from going into the cutoff or the saturation region and gives more stability. A fixed bias (i. e. base bias) circuit or a voltage divider bias circuit can be used for this assignment but a voltage divider circuit is more efficient.The main disadvantage in a fixed bias circuit is that ? ac depends on temperature, which means ? ac is not stable. And when ? ac changes, IC will change(IC=? IB) and VCE will change. The changes in IC and VCE make the Q-point unstable. Whereas in voltage divider bias c ircuit, IC is independent of ? ac and hence the Q-point is more stable. Voltage divider bias is widely used because reasonably good stability reached with a single power supply. Chapter 2 Problem Description: The problem is to design and fabricate a pre amplifier circuit with an NPN transistor to be used in a simple public address (PA) system.The input of the pre amplifier circuit is taken from a microphone that produces an average output voltage of 10 mV rms. The amplifier is to operate over a frequency range of 300 Hz to 5 kHz. Also, it should have an adjustable volume control. The expected voltage gain of the amplifier is 100. Design Specifications: Voltage gain = 100 Lower cut off frequency = 300Hz Vin = 10mV (rms) RL = 10k? DC power supply = 10V to 15V Type of transistor – NPN We will begin our assignment by selecting a suitable transistor. Then we will decide on a DC voltage supply and assume a prober Q-point (IC, VCE) to carry out the design.We will start the design by calculating the values of Resistors RC and RE and the voltage divider resistors R1 and R2. After that we will calculate the values of the two coupling capacitors (C1 and C2) and the emitter bypass capacitor (CE) for the required cut off frequency. After finishing the mathematical model we will simulate the circuit using OrCAD to analyze the circuit performance. Then, after finishing the simulation, we will assemble the circuit using approximate values of the calculated ones. Finally, we will compare the simulation results with the hardware results.The results we will be focusing on are the voltage gain, the cutoff frequency and the Bandwidth. Chapter 3 Circuit Diagram and Design: Av = 100 FL = 300Hz Av = 100 FL = 300Hz Figure 1 – Circuit Diagram Step1 – Selection of Transistor, Supply Voltage (VCC) and Collector Current (IC): The selected transistor should have a minimum current gain (? ) that is equal to or greater than the desired voltage gain. Therefore, we will us e Q2N2222 in this assignment. Since the output voltage swing is not specified in this assignment, we will choose 12V as our voltage supply. We will choose IC as 4 mA. Transistor: Q2N2222Supply Voltage: VCC = 12 V Collector Current: IC = 4 mA * To carry out the design we need to draw the dc equivalent circuit. Figure 2 – DC Equivalent Circuit Step2 – Design of Collector Resistor (RC) and Emitter Resistor (RE): VCE = 50% VCC = 50% ? 12 = 6 V VE = 10% VCC = 10% ? 12 = 1. 2 V VRC = VCC – VE – VCE = 12 – 6 – 1. 2 = 4. 8 V RC = VRCIC = 4. 8 V4 mA = 1. 2 k? RE = VEIE = VEIC = 1. 2 V4 mA = 300 ? , since IC ? IE Step3 – Design of Voltage Divider R1 and R2: ? = 100 (data sheet) R2 = ? RE10= 100? 30010 = 3 k? VB = VBE + VE = 0. 7 + 1. 2 = 1. 9 V VB = VCCR2R1+R2 R1 = VCCR2VB+R2 = 100? 3k1. +3k = 16 k? * Now we need to draw the ac equivalent circuit. Figure 3 – AC Equivalent Circuit Step4 – Design of RE1 and RE2: RE = RE1 + RE2 Rout = Rc || RL = 1. 2? 101. 2+10= 1 k? r'e = 26mIE = 26mIC = 6. 5 ? AV = Routr'e+RE1 r'e+RE1= RoutAv = 1k100 = 10 ? RE1 =10 – r'e = 10 – 6. 5 = 3. 5 ? RE2 = RE – RE1 = 300 – 3. 5 = 296. 5 ? Step5 – Design of Coupling Capacitors C1 and C2: hie = Rin (base) = ? (r'e+RE1) = 100 ? (3. 5 + 6. 5) = 1 k? Rin (tot) = R1 || R2 || Rin (base) = 1116+13+11 = 716. 4 ? XC1 = Rin(tot)10 = 716. 410 = 71. 64 ? C1 = 12? fLXC1 = 12 300? 71. 64 = 7. 4  µF XC2 = RC + RL = 1. 2 + 10 = 11. k? C2 = 12? fLXC2 = 12 300? 11200 = 47. 4 nF Step6 – Design of Bypass Capacitor CE: R’S = R1 || R2 = 16. 09? 316. 09+3 = 2. 5 k? Re = RE2 ||{ R’S ? + (r'e+RE1)} = 296. 5 ||{ 2500 100+ (6. 5+3. 5)} = 296. 5? 35296. 5+35 = 31. 3 ? XCE = Re10 = 31. 310 = 3. 13 ? CE = 12? fLXCE = 12 300? 3. 13 = 169. 5  µF Av = 100 FL = 300Hz Av = 100 FL = 300Hz Figure 4 – Circuit Diagram with values Simulation Results: With CE: Mid-band gain, AV = 99. 8 Lower Cutoff Frequency, FL = 334 Hz Higher Cutoff Frequency, FH = 20. 6 MHz Bandwidth, BW = FH – FL = 20. 6 M – 334 = 20. 6 MHz Without CE: Mid-band gain, AV = 3. 5Lower Cutoff Frequency, FL = 305 Hz Higher Cutoff Frequency, FH = 46 MHz Bandwidth, BW = FH – FL = 46 M – 305 = 46 MHz (Circuit Diagram and Frequency Response are enclosed along with this report) Chapter 4 Hardware Fabrication and Testing Details: During circuit assembling process we tried to find the nearest values to the calculated ones. These are the values we used: RC = 1. 2 k? we selected1. 2 k? RE1 = 3. 5 ? we selected4. 5 ? RE2 = 296. 5 ? we selected270 ? R1 = 16 k? we selected15 k? R2 = 3 k? we selected2. 2 k? C1 = 7. 4  µF we selected10  µF C2 = 47. 4 nF we selected47 nF CE = 169. 5  µF we selected147  µF Procedure: . Assembled the circuit on a breadboard and connected a DC power supply of 12V. 2. Applied a sine wave of 10 mV amplitude and 100 Hz frequency to the input. 3. Observed the output waveform in the CRO and noted down the amplitude. 4. Increased the input signal frequency in steps, without changing its amplitude, and noted down the output amplitude at each step. 5. Calculated the voltage gain of the amplifier by the equation, AV = Vout/Vin found the voltage gain in dB by the equation, AV (dB) = 10 log (AV). 6. Plotted the frequency response curve and found the frequencies (fL and fH) for which the gain reaches 0. 07 of mid band gain. 7. Found the frequency range between fL and fH which gives the bandwidth of the amplifier. Hardware Results: With CE: Frequency (Hz)| Vout (mV)| AV| AV (dB)| log f| 100| 182| 18. 2| 25. 20| 2. 0| 500| 662| 66. 2| 36. 42| 2. 7| 1 k| 750| 75. 0| 37. 50| 3. 0| 5 k| 784| 78. 4| 37. 89| 3. 7| 10 k| 786| 78. 6| 37. 91| 4. 0| 50 k| 786| 78. 6| 37. 91| 4. 7| 100 k| 786| 78. 6| 37. 91| 5. 0| 500 k| 786| 78. 6| 37. 91| 5. 7| 1 M| 786| 78. 6| 37. 91| 6. 0| 2 M| 784| 78. 4| 37. 89| 6. 3| 5 M| 770| 77. 0| 37. 73| 6. 7| 10 M| 728| 72. 8| 37. 24| 7. 0| 50 M| 344| 34. 4| 30. 73| 7. 7| 100 M| 182| 18. 2| 25. 0| 8. 0| Mid-band gain, AV = 78. 6 Lower Cutoff Frequency, FL = 2. 6 B = 398 Hz Higher Cutoff Frequency, FH = 7. 35 B = 17. 78 MHz Bandwidth, BW = FH – FL = 17. 78 M – 398 = 17. 78 MHz Without CE: Frequency (Hz)| Vout (mV)| AV| AV (dB)| log f| 100| 12| 1. 2| 1. 58| 2. 0| 500| 32| 3. 2| 10. 10| 2. 7| 1 k| 36| 3. 6| 11. 13| 3. 0| 5 k| 38| 3. 8| 11. 60| 3. 7| 10 k| 38| 3. 8| 11. 60| 4. 0| 50 k| 38| 3. 8| 11. 60| 4. 7| 100 k| 38| 3. 8| 11. 60| 5. 0| 500 k| 38| 3. 8| 11. 60| 5. 7| 1 M| 38| 3. 8| 11. 60| 6. 0| 2 M| 38| 3. 8| 11. 60| 6. 3| 5 M| 38| 3. 8| 11. 60| 6. 7| 10 M| 36| 3. 6| 11. 13| 7. 0| 50 M| 26| 2. 6| 8. 0| 7. 7| 100 M| 18| 1. 8| 5. 10| 8. 0| Mid-band gain, AV = 78. 6 Lower Cutoff Frequency, FL = 2. 55 B = 356 Hz Higher Cutoff Frequency, FH = 7. 6 B = 39. 81 MHz Bandwidth, BW = FH – FL = 39. 81 M – 356 = 39. 81 MHz (Frequency responses of the circuit with and without CE are enclosed along with this report) (Frequency responses of the circuit with and without CE are enclosed along with this report) Chapter 5 Discussion and Conclusion: * First of all, there are several ways and various methods to design a common emitter amplifier or so-called RC coupled amplifier that are completely different than the one we used.We did not choose this method because it is the best method, actually, there is no such a thing called the best method. There are simple ways and there are more accurate ways. It depends on the primary assumptions, the design specifications and the thumb rules used. Simply, the method we used achieved the design requirements and accomplished desired results. * An Amplifier is a circuit that is capable of amplifying signals applied to its input terminal. The main component in any amplifier circuit is usually a transistor.Since the transistor configuration we used is a common emitter configuration, the circuit is called a Common Emitter Amplifier. Unlike other configurat ions, CE amplifier exhibit high voltage gain and high current gain. Generally, the process of a common emitter amplifier can be explained in three steps. First, the AC input signal produces an AC base current. Then, This AC base current will produce a much larger AC collector current since IC=? IB. After that, The AC collector current produces an AC voltage across the load resistor RL, thus producing an amplified, but inverted, reproduction of the AC input voltage. To use a transistor as an amplifier it should be operated in the active region (linear region). To set a transistor in the active region both junctions, Emitter-Base junction and Base-Collector junction, should be forward biased. Since changes in in temperature and other factors during the amplification process may drive the transistor into the cutoff or the saturation region, the Q-point should be in the middle of the active region to enhance the stability of the amplifier. * We preferred using a voltage divider bias cir cuit over other biasing circuits because in this kind of biasing circuits, IC is independent of ? nd therefore the Q-point is more stable. Voltage divider bias circuit is widely used because of the good stability reached with a single power supply. * C1 and C2 are called coupling capacitors. They pass ac from one side to another and block dc from appearing at the output side. In addition to that, C1 act as a high pass filter on the input signal and its value must be chosen so that it does not attenuate the frequencies which are to be amplified. Similarly, C2 also must be prevented from attenuating the output signal. * The bypass capacitor CE provides an effective short to the ac signal round the emitter resistor RE2, thus keeping only RE1 seen by the ac signal between the emitter and ground. Therefore, with the bypass capacitor, the gain of the amplifier is maximum and equal to AV=Routr'e+RE1 . Without the bypass capacitor, both RE1 and RE2 are seen by the ac signal between the emit ter and ground and effectively add to r'e in the voltage gain formula. Hence, AV=Routr'e+RE1+RE2 . * r'e is a dynamic resistor that depends on temperature. If AV was dependent only on r'e, and RE1 was not there (i. e. AV=Routr'e ), AV will be unstable over changes in temperature because when r'e increases, the gain decreases and vice versa.In order to minimize the effect of r'e without reducing the voltage gain to its minimum value we partially bypassed the total emitter resistance RE. This is known as swamping which is a compromise between having a bypass capacitor across RE and not having a bypass capacitor at all. RE1 should be at least ten times greater than r'e to minimize the effect of it. In our design RE1 is less than r'e and hence it will not do anything other than slightly reducing the gain to be about 100. In other words, in our design RE1 is somehow useless. * At lower frequencies, a capacitor will act as an open circuit.At higher frequencies, a capacitor will act as a s hort circuit. That is because the capacitive reactance is inversely proportional to the frequency (XC=1/2? fC). In an RC coupled amplifier circuits, at lower frequencies, more voltage drops across C1 and C2 because their reactance is very high. This higher signal voltage drop reduces the voltage gain of the amplifier. Similarly, at lower frequencies, the reactance of the bypass capacitor (CE) increases and this reactance in parallel with RE1 create an impedance that reduces the voltage gain.This is why RC coupled amplifier circuits have less voltage gain at lower frequencies than they have at higher frequencies. However, at higher frequencies, the reactance of the internal transistor junction capacitance goes down and when it becomes small enough, a portion of the output signal voltage is fed back out of phase with the input, thus effectively reducing the voltage gain. * Our hardware implementation results and simulation results were different. Obviously, that is because we did not find the exact values for our design. There was a notable difference between the design values and the values we have selected, especially for R2.The cutoff frequency (fL=398 Hz) is somehow acceptable but the mid band gain (AV=78. 6) is a little bit less than the desired one. Increasing the value of R2 could have solved the problem. It could have increased the voltage gain and reduced the cutoff frequency. * One of the aims of the design is to have an adjustable volume control. There are several ways to do this. One of them, and I think it’s the best, is by using a variable resistor in place of RE1 (i. e. a 100 ? variable resistor). Basically, this resistor is inversely proportional to the voltage gain (AV=Routr'e+RE1 ).Reducing the value of RE1 will increase the voltage gain, thereby increasing the volume and vice versa. References: 1. Theodore F. Bogart, Jefferey S. Beasley and Guilermo Rico (2004). Electronic Devices and Circuits. India: Pearson Education, Inc. 2. Thomas L . Floyd (2005). Electronic Devices. 7th ed. India: Pearson Education, Inc. 3. HyperPhysics  (2004)  Common Emitter Amplifier,[online] Available at: http://hyperphysics. phy-astr. gsu. edu/hbase/electronic/npnce. html [Accessed: 20th Nov 2011]. 4. Scribd  (2006)  Common Emitter Amplifier,  [online] Available at: http://www. cribd. com/doc/27767944/Common-Emitter-Amplifier [Accessed: 25th Nov 2011]. 5. Visionics  (2005)  RC Coupled Amplifier,  [online] Available at: http://www. visionics. ee/curriculum/Experiments/RC%20Ampr/RC%20Coupled%20Amplifier1. html [Accessed: 1st Nov 2011]. 6. SSIT  (2006)  Analog Electronic Circuits,  [online] Available at: http://www. ssit. edu. in/dept/assignment/aeclabmanual. pdf [Accessed: 5th Nov 2011]. 7. Edutalks  (2007)  RC Coupled Amplifier,  [online] Available at: http://www. edutalks. org/electronics%20lab%20manual%201. pdf [Accessed: 7th Nov 2011].

Delving into macbeth essays

Delving into macbeth essays Macbeths character and the changes he undergoes can be traced throughout the events of Shakespeares The Tragedy of Macbeth. He begins the play as a good man who has just taken up the reputation of a valiant man who has done well for his country. However, with one single act of killing the king, he brings about his downfall. Macbeths deterioration in morality and plagued feelings of guilt and fear dominate his character as he stumbles towards his death. Macbeth is first introduced as a nobleman who had just saved Scotland from the Norwegian king and successfully subdued two rebellions. He is portrayed as brave Macbeth, one who has valiantly killed many enemies, whose sword smoked with bloody execution, and is even associated with the goddess of war, Belonas Bridegroom. Such successes won over favor from the king and a promising future. The positive image that Macbeth is presented through is quickly challenged, and his ambitious nature to aspire to become king is revealed after he hears the prophecies of the witches that he would become Thane of Cawdor and even king. The first prophecy, of being Thane of Cawdor was immediately fulfilled after the witches left Macbeth, which led him to believe that it was possible for him to become king. This reveals that Macbeth may possibly have longed for the throne, but had never seriously considered it, but with some encouragement, he is ready to seize the position of the king. However Macbeth is revealed as an innately good man through his soliloquy in contemplating the murder of the king. Such horrible imaginings are so atrocious to him that he feels smothered in surmise, and unable to function normally throughout the day. Despite the effects of the horrid thoughts of murder that plague Macbeth, he is found to be continually lost in the contemplation of murder. He himself is ashamed of such thoughts, henc...

15 Color Terms

15 Color Terms 15 Color Terms 15 Color Terms By Mark Nichol Words describing the qualities of color can confuse because they sometimes but not always overlap or are even interchangeable. Here’s a roster of color terms with definitions. 1. Cast: a change in appearance or color by adding one color over another; also, multiple senses of assigning, depositing, directing, shaping, spreading, turning, or twisting 2. Chroma: a combination of hue and saturation (see definitions below), or synonymous with saturation 3. Chromaticity: the quality of color based on wavelength and purity 4. Coloration: the condition of coloring, as in skin tone, an arrangement of colors, or the choice or use of colors 5. Colorway: a color or arrangement of colors 6. Contrast: the degree of difference in colors or light and dark, or their juxtaposition 7. Hue: color, gradation of color, or the characteristic that distinguishes one color from another 8. Pigmentation: coloration caused by the presence of a pigment, a substance that produces a color (or black and white) in a material 9. Saturation: purity of color; also, the state of being thoroughly wet, or heavy infiltration 10. Shade: a color produced by a mixture that includes black dye or pigment, or a color somewhat distinct from another, or, as a verb, to produce such a color; also, various meanings associated with the blocking or minimizing of light 11. Tincture: synonymous with color; also, a trace in a mixture 12. Tinge: color spread or stained over another color, or, as a verb, to spread or stain one color over another; also, a figurative sense of a light touch or effect, or, as a verb, to touch or effect lightly 13. Tint: a pale or slight coloration, or lighter or darker variations of a color, or, as a verb, to produce such an effect; also, a slight difference, or hair dye 14. Tone: a quality of color, or a shade, tint, or value (see definitions) 15. Value: the lightness or darkness of a color, or the difference in lightness and darkness Want to improve your English in five minutes a day? Get a subscription and start receiving our writing tips and exercises daily! Keep learning! Browse the Vocabulary category, check our popular posts, or choose a related post below:Comma After i.e. and e.g.The Difference Between "will" and "shall"The Uses of â€Å"The†

Law and Human Trafficking Essay Example | Topics and Well Written Essays - 2000 words

Law and Human Trafficking - Essay Example The immigration laws that should prevent trafficking are not stringent thereby, creating the conducive environment that encourages human trafficking (Theresa 275). This has increased the cases of Unaccompanied Alien Children (UAC). Human trafficking has also been on the rise because some of the officers working at the immigration offices and the Office of Refugee and Resettlement (ORR) are also involved in the evil act of human trafficking because of the huge profits that accrue to them from the sale of the children and the adults. This as noted by the US house Judiciary chairman Rep. Bob Goodlatte, makes over 90% of the UACs cases not being presented to the courts for justice to be sought for the victims (Theresa 275). It is, therefore, important to note that human trafficking has become a crisis because of the laxity in the enforcement of the trafficking laws, not in the absence of the laws.United Nations Definition of Human Trafficking  Human trafficking is considered a serious crime and gross violation of human rights, therefore United Nations have been in the forefront in trying to assist the United States and the affected countries in preventing human trafficking through the implementation of the Trafficking in Persons Protocol. This aims at preventing, suppressing and punishers the traffickers (Shelley 115). According to the United Nations definition of Human Trafficking, Article 3, of the Trafficking in Persons Protocol provides the definition of Human Trafficking as â€Å"recruitment, transportation.

Roles, Relationships and Responsibilities in Lifelong learning Essay

Roles, Relationships and Responsibilities in Lifelong learning - Essay Example The religious teachings must not be aimed at spreading the lessons of a particular religion to influence the idea, thoughts and beliefs of the learners. Such acts of religious teaching are prohibited by the law. The teachings of different religion and faith are, however, not prohibited. The teaching of religious education should not be biased and should give equal respect to the faith and belief of all the religions. The regulatory requirements although imposes limitations on the schools to impart religious education on a particular belief or faith but allows flexibility to the teaching of religious education in the terms of the time and process of exploration of religious ideas and beliefs for dissemination to the learners. The codes of practice for teaching of religious education offers liberty to the teachers of religious education to engage into teaching of as many religious lessons and faith to the students but disallows confinement or stress on a particular religion. Thus the r ole of teachers is very important in developing a non-biased environment during the process of teaching. There is ample scope of questions related to values of life in religious teaching. The codes of practice allow teachers to address such question in an effective manner in order to impart complete teachings in the field of religious education. ... The promotion of equality and valuation of diversity in religious teachings is a key area of responsibility for the teachers. The teachers should be responsible in imparting the religious beliefs of all faith to learners. The strength of religious teachings lies in the inclusive aspect of the field. The teachers are responsible for non-discrimination of primary or specific religion among the vast field of religious ideas and beliefs. The learners should have the freedom to question on any aspect of religion keeping due respect to the teachings of other religions as well. The students irrespective of their notions on different religions and culture should be treated equally by the teachers. The students should have the freedom to raise the queries on the subject. The teachers should distribute equal emphasis to the teachings of all religion in order to attain equality in religious teachings. The weakness factor is presented by the aspect of diversity in religious teaching. Thus the te acher also has the responsibility of managing diversity in religious teachings. The teacher should be able to value diversified ideas and beliefs of different religions. The fundamentals of various religious faiths should be clearly explained to the learners. The responsibilities of the teacher demand avoidance of any bias and value the diversified ideas by developing a comprehensive study of religious teachings. These are the factors that influence the responsibility of the teachers in achieving equality and valuing diversity in religious teachings (Gravells and  Simpson, p.56). Evaluation of roles and responsibilities in the Lifelong learning The evaluation of roles and

Community Communication Essay Example | Topics and Well Written Essays - 1000 words

Community Communication - Essay Example He wondered such, because of the diffusion of cities created due to the stage of industrial revolution and unsettled west. Another scholar that set out to find the relation between community and communication was Gabriel Tarde in the 1980s. According to him, public opinion is a means of collective community which is controlled and arranged by the media (Katz, 1991). Furthering the previous thought, Bowes (1997) confirms that this relationship further gained strength in the 1920s and thus has now become indivisible. According to this study, for a collective action, communication between citizens and individuals is an important function for initiating a combined action, with the collective action being stimulated and expressed through the media. Of course, when it comes to finding the relation between these two variables, it is obvious to understand the definition of community. According to Hillary (1955), community can be explained in 94 ways. However, three essential components can b e found in the explanation of this variable. Beginning with a person involved in a specific community contact, the author mentioned geographic area as the second component with the common ties completing the collection. Bracht (1990) also revolves around the same concept of community. According to this study, a community can be explained as a cluster of individuals that share the same ethics, ideals and institutions. Further adding to the definitions, the author explained interpersonal relationships, culture and social groups as the interdependent basic components. Therefore, the above mentioned components work collectively towards a common good. This means that these components are a food for the community that are intellectual and conscious in nature and is thus a highly necessary requirement Dewey (1946). Bell and Newby (1971) added more to the definition and stated that communities have nowadays adopted a virtual nature. According to this study, the idea of a physical space has currently adopted a less physical approach of communication. Nonetheless, the relation between community and communication remains intact. Where traditionally the use of broadcast and print media was at its peak, the introduction of the computer based era and the enhancement of development and interactive media have positively worked towards eliminating the geographical constraints in communication. The virtual temperament of the media used two basic tools; the internet and direct broadcast satellites. Therefore, it becomes imperative to mention at this stage that after adopting the virtual mode, the communication media not simply aid the traditional community, rather it aids to the change in the entire definition of it (Bowes, 1997). According to Berrigan (May 1979), there is always the risk of importance in considering communication. That is, it is the author’s firm belief that although communication media is an effective tool in affecting the community, the role of the med ia is highly exaggerated. The study also stated that the media revolves around precedence in its importance. For the role of communication to be effective, it must be understood that it can never work alone. The media, in spite of its role in not the only factor that can bring changes to the community, the organizational, social and political structures also play a vital role that need to be identified. As the international communication association (May 2012) states; as our perceptions regarding the organizational, personal and social communities are undergoing massive changes, the boundaries and peripheries are becoming

Treating Alzheimers Disease with Vitamin A, C E (ACE)

Treating Alzheimers Disease with Vitamin A, C E (ACE) ACE Alzheimers: An adjuvant strategy of treating Alzheimers disease with Vitamin A, C E (ACE) ABSTRACT Alzheimers disease (AD) is a chronic and slowly progressing neurodegenerative disorder which has become a major concern with regards to health, worldwide. This disorder is characterised by progressive dementia and cognitive decline. Pathologically, AD is characterised by the presence of AÃŽÂ ² plaques and tau neurofibrils. However, literature has shown that oxidative stress is one of the most important risk factor behind the cause of AD. Oxidative stress often leads to production of Reactive Oxygen Species (ROS), which further increases structural and functional abnormalities in neurons of the brain, which subsequently, presents as dementia and cognitive decline. In order, to curb the oxidative stress, antioxidants can be of great help. There have been many evidences that supports the use of antioxidants in the treatment for AD. Vitamins A, C and E are an example of antioxidants that can be used as adjuvants in the treatment of AD. This article will focus on current literature and will present forward the evidence based advantages of using Vitamin A, C and E as an adjuvant treatment for AD. Keywords: Antioxidants, ACE, Adjuvant therapy. INTRODUCTION A clinical psychiatrist and neuroanatomist, Alois Alzheimer, reported A peculiar severe disease process of the cerebral cortex to the 37th Meeting of South-West German Psychiatrists in Tubingen, thus marking the discovery of one of the most interesting pathologies in medicine Alzheimers disease. His invention was based on the observations in one his patient named Auguste D, suffering from profound memory loss, unfounded suspicions about her family, and additional worsening psychological changes. Her post mortem findings further revealed dramatic shrinkage of the brain and abnormal deposits in and encircling the nerve cells [1]. AD has proven to be a significant public health issue, as it consumes a major amount of heath budget in developed as well as developing countries. AD has become one of the leading causes of dementia in patients less than 65 years, other causes being Lewy body dementia (LBD), frontotemporal dementia (FTD), vascular dementia (VaD) and alcohol associated dementia [2]. United States alone has documented a $200 billion annual expenditure on patients affected by AD. Moreover, one person develops Alzheimers dementia every 68 seconds emphasizing the incidence of the disease [3]. Dementia can be defined as a chronic progressive disorder marked by memory deficits, personality changes, and impaired reasoning. Results from population-based studies have shown a significant relationship between the certain risk factors and development of AD. Increased risk was shown with an increase in age, fewer years of education, and head trauma. Genetic factors do contribute to the early development of AD increased risk with mutations on chromosome 21 (cases of downs syndrome) as it carries the amyloid precursor protein, the presence of apolipoprotein E epsilon 4 allele and the presenilin 1 and 2 genes. The strongest factor identified till date are the apolipoprotein E genes located on chromosome 19 which exists in three forms ÃŽÂ µ2, ÃŽÂ µ3, and ÃŽÂ µ4. ÃŽÂ µ2 has been found to reduce the risk, ÃŽÂ µ3 is found to be neutral whereas ÃŽÂ µ4 has been associated with a tremendous increase in risk as well as early development of symptoms (Figure 1) [4]. Chromosome Genes 21 AMYLOID PRECURSOR PROTEIN 19 APOLIPOPROTEIN E 14 PRESENILIN 1 1 PRESENILIN 2 Figure 1. Genetic factors causing a risk to develop Alzheimers Ad is difficult to differentiate from other causes of dementia like LBD, FTD and Vad [5]. It may present with dysfunction of various fields such as vision, touch voluntary movements, personality deficits and judgemental disorders depending upon the area of the brain affected [6].The National Institute of Neurological and Communicative Disorders and Stroke and the Alzheimers disease and Related Disorders Association (NINCDS/ADRDA) has proposed a diagnostic criteria for differentiating between AD and other known causes of dementia. In compliance with NINCDS/ADRDA , AD is diagnosed if: (I) Cognitive functions decline progressively over a period of time including/ not including memory impairment or (Ia) Inability to understand language and verbal commands (aphasia); (Ib) Loss of ability to accomplish tasks due to incoordination of muscles (apraxia); (Ic) Failure to recognise previously known objects and loss of ability to use them(agnosia); (Id) Unable to plan, organise and execute dail y chores; (II) All above mentioned under I do get progressively deteriorated with time; (III) Other known causes of dementia as well as cognitive deterioration must be eliminated [6,7]. Neurofibrillatory tangles and extracellular amyloid plaques have been the initial histopathological findings associated with AD. Recently several other features have been recognised which include degeneration of neuronal synapses, aneuploidy and loss of neurons in the hippocampus. Despite the recent inventions, presence of extracellular amyloid plaques and intracellular NFT have been taken into account as the main histopathological criteria for establishment of AD [8]. Among all the different hypothesis, AÃŽÂ ² cascade has been the most accepted. Previously, a mutation in beta-Amyloid Precursor Protein (APP), which contributes to the normal function of neurons and cerebral development, was thought to be the sole culprit since the accumulation of AÃŽÂ ² proteins had lead to the pathogenesis of AD [9]. Eventually, mutated presenilin genes (both 1 and 2) have been discovered to play a role in the formation of AÃŽÂ ² pools [10]. But the exact mechanism underlying how AÃŽÂ ² a ggregation contributes to the pathophysiology of AD largely remains unclear. Formerly, toxicity of neurons was believed to be caused by intracellular plaques. But recent data has suggested the role of intracellular AÃŽÂ ² proteins, which do not become sequestered into the extracellular plaques, as the toxic triggers stimulating the progression of AD [11]. Recently, it has also been shown that intracellular accumulation of AÃŽÂ ² proteins precedes the formation of extracellular AÃŽÂ ² protein plaques and NFT formation [12]. The role of intracellular AÃŽÂ ² protein in the progression of AD has also been demonstrated in recent experiments on transgenic mice. Results of these experiments indicate that increased deposits of AÃŽÂ ² proteins within the cells are associated with accelerated cell death [13]. Other important causative factors in the development of AD include oxidative stress and Reactive Oxygen Species (ROS) [14]. Susceptibility to oxidative damage is due to several factors which include relatively lower levels of antioxidants, significantly higher levels of polyunsaturated fatty acids, (these fatty acids rapidly fall prey to ROS), the presence of metallic ions and high oxygen utilisation [15]. Oxidation have been prove to be fatal for several constituents of the cells including carbohydrates, lipids, proteins, RNA and DNA [16]. Indirect mechanisms do play a vital role in the damaging process. Oxidation has been proven to accelerate the expression of inducible nitric oxide (iNOS) and accentuate the activity of neuronal NOS (nNOS). This leads to increased production of nitric oxide (NO). NO is known to interact with super oxide anions thus forming a highly reactive peroxynitrite anion. These transient molecules exerts their effects mainly on sulfhydryl groups of cells. [17 ]. The entire process has been depicted in figure 2. Figure 2. Nitric Oxide Pathogenesis In addition to the indirect mechanisms, oxidative stress alters the protein structure. Impaired proteins are known to accelerate oxidative damage, thus proven to be interrelated. ROS causes the protein to be oxidised leading to a modified structure and causing them to be dimerized and aggregated [18]. Thus the oxidised protein which is both structurally and functionally abnormal gather as inclusions within the cytoplasm of the neurons, seen in the form of NFT (tau aggregates) and AÃŽÂ ² plaques [19]. Alternatively, AÃŽÂ ² plaques can also lead to the increased production of ROS. The entire process has been depicted in figure 3. OXIDATION ALTERED PROTEIN STRUCTURE CYTOPLASMIC INCLUSIONS DIMERISATION AGGREGATION Figure 3.Displaying Correlation between Oxidation and Protein Dimerization, thus forming a Vicious Cycle AÃŽÂ ² (1-42) is an abundant species of AÃŽÂ ² proteins seen in AD [20]. AÃŽÂ ² (1-42) peptides is known for its toxicity which can be attributed to a residue of methionine at position 35 [21]. Oxidation of methionine contributes to the formation of methionine sulfoxide, which generally leads to irreversible oxidation and subsequently, forming methionine sulfone [22]. Methionine sulfoxide reductase (MSR) can even help the reduction of methionine sulfoxide into methionine [23]. However, the activity of MSR is also observed to be impaired in AD [24]. Methionine peroxide plays an important role in oxidative stress and toxicity caused by AÃŽÂ ² (1-42) peptides. The lone-pair of electrons present on the S atom of methionine undergoes oxidation of one atom and as a result, sulfuranyl radicals (MetS.+) are generated [21,25]. Sulfuranyl radicals are known to trigger the generation of other ROS like sulfoxides and superoxides by interacting with molecular oxygen [26]. The reason behind this intense oxidative damage could be attributed to the relative absence or decreased function of different antioxidant mechanisms of the body. Glutathione is one of the major antioxidant which can protect the brain tissues by causing detoxification of damaging ROS [27]. One of the main reasons of increase in oxidative stress in AD is the decreased glutathione levels in the brain [28]. The other members of the cellular antioxidant mechanism which plays a pivotal role includes Superoxide Dismutase (SOD) and Catalase (CAT). SOD is an antioxidant which is responsible for converting toxic superoxide ions into far less toxic hydrogen peroxide [29]. CAT evolves this reaction in to one step further and turns hydrogen peroxide into water [30]. Investigations have revealed that the levels of SOD and CAT decline in patients with AD [31]. Glutathione reductase (GR) and Glutathione peroxidase (GPx) represent the other crucial parts of the cellular defence mechanism which acts against oxidative stress. GPx is responsible for the metabolism of hydrogen peroxide and lipid hydroperoxides [32] and GR accelerates the reaction which helps in the regeneration of Glutathione (GSH) [33]. In total, the combination of an oxidative stress with above mentioned cellular defence mechanism against ROS, leads to the pathogenesis of AD. The pathogenesis of Alzheimers disease is mentioned in Figure 4. Figure 4. Pathogenesis of Alzheimers disease (MG : Microglia ; AS: Astrocyte; AP: Amyloid protein beta; NFT: Neurofibrillary tangles) ACE ALZEIHMERS: VITAMIN A, C E (ACE) THERAPY   Ã‚   ROLE OF VITAMIN A Vitamin A and beta carotene have been shown to have multiple benefits for people suffering from AD. Various studies have found that patients suffering from AD have significantly lower levels of Vitamin A level and beta carotene in their CSF as well as blood [34]. The development of neurodegenerative disorders has shown to be influenced by Vitamin A and beta-carotene. Vitamin A plays an active role in neuronal development both in early life and in the adult nervous system. It protects and assists in the regeneration of neurons during recovery from neurodegeneration [35]. Inhibition of formation and destabilization of AÃŽÂ ² fibrils is an additional effect of Vitamin A and beta-carotene [35]. Since oligomerization of AÃŽÂ ² fibrils is an important mechanism contributing to neuronal toxicity in AD, Vitamin A supplementation has been shown to decrease the aggregation and oligomerization of AÃŽÂ ²40 and AÃŽÂ ²42 fibrils [36]. It has also been shown that Vitamin A and beta carotene decrease the decline of cognitive function in AD. Moreover, higher levels of these vitamins have been associated with better memory performance and spatial learning in these patients [3436]. ROLE OF VITAMIN C Various studies both in vivo and in vitro have shown to have significant effect in the brain due to decreased levels of vitamin C. Decreased plasma levels despite adequate intake in patients further confirmed the belief of protective effects of vitamin C in the spectrum of neurodegenerative diseases [37]. Hence, it can be proved that oxidative stress induces damage in AD and protection against this stress is offered to a certain degree by antioxidant vitamins. The progression of AD is altered by Vitamin C by interfering with various different aspects of pathology. Numerous studies, both in-vivo and in vitro, have shown that Vitamin C can decrease oxidative stress. The structural progression of AD is prevented by Vitamin C by hindering the oligomerization of AÃŽÂ ² peptides [38]. Brain injury induces oxidative stress and reduces the level of antioxidants like vitamin C and SOD. Vitamin C supplementation improves the level of SOD, which consecutively helps to decrease oxidative stress and subsequent brain injury [39]. It has been suggested that even without additional supplementation, a normal intake of Vitamin C can have a neuroprotective effect in patients with AD. Cognitive decline in AD patients has shown to decrease is patients taking adequate Vitamin C [40]. In addition, results from a prospective observational study (n=4740) over a period of 3 years have shown that additional supplementation with antioxidant vitamins like vitamin C and E may be associated with both decreased incidence and prevalence of AD [41]. ROLE OF VITAMIN E Vitamin E represents a cluster of 8 antioxidants composed of 4 tocotrienols and 4 tocopherols. It has been reported that there is a greater risk of neurodegenerative disorders like AD and Mild Cognitive Impairment (MCI) with lower plasma levels of vitamin E. Additionally, the level of vitamin E metabolic products (5-nitro-ÃŽÂ ³-tocopherol etc.) is shown to increase significantly in AD and MCI [42]. Deficiency of Vitamin E can lead to the damage and destruction of neurons and has been implicated in cases of cerebellar atrophy [43]. Vitamin E is a potent antioxidant which can delay the progression of AD at several levels. Increased oxidative stress induced by AÃŽÂ ² plaques is known to be a risk factor for neuronal death and ensuing brain injury in AD. Vitamin E behaves like a scavenger for these free radicals and therefore, is neuroprotective. [44]. Vitamin E also provides protection against AD via various other methods. For example, the 12-lipoxygenase pathway leads to glutamate-induced neuronal cell death by inflammation. Vitamin E can reduce this inflammation induced neuronal death [45]. Furthermore, consumption of vitamin E has been linked with the regeneration of SOD, levels of which are shown to decline in AD [39]. Among the different forms of vitamin E, the greatest degree of protection against AD is provided by ÃŽÂ ±-tocopherols and ÃŽÂ ³-tocopherols [46]. A population-based cohort study of 5395 individuals was conducted to evaluate the efficacy of dietary supplementation of antioxidants to provide protection against AD. Among all the antioxidants used, results showed that the most significant degree of protection (p=0.02) against dementia and AD was provided by Vitamin E [47]. Moreover, supplementation of 30 International Units of alpha-tocopherols can act as a valuable adjuvant in the treatment of various neurodegenerative diseases, including AD [48]. Conclusion Alzheimers disease represents one of the most significant age-related neurodegenerative disorders. 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