Microprocessor and Interfacing Essay Example for Free

Microprocessor and Interfacing Essay Peripherals and Interfacing PIO 8255 The parallel input-output port chip 8255 is also called as programmable peripheral input-output port. The Intel’s 8255 is designed for use with Intel’s 8-bit, 16-bit and higher capability microprocessors. It has 24 input/output lines which may be individually programmed in two groups of twelve lines each, or three groups of eight lines. The two groups of I/O pins are named as Group A and Group B. Each of these two groups contains a subgroup of eight I/O lines called as 8-bit port and another subgroup of four lines or a 4-bit port. Thus Group A contains an 8-bit port A along with a 4-bit port. C upper. PIO 8255 †¢ The port A lines are identified by symbols PA0-PA7 while the port C lines are identified as PC4-PC7. Similarly, GroupB contains an 8-bit port B, containing lines PB0-PB7 and 4-bit port C with lower bits PC0- PC3. The port C upper and port C lower can be used in combination as an 8-bitport C. †¢ Both the port C are assigned the same address. Thus one may have either three 8-bit I/O ports or two 8-bit and two 4-bit ports from 8255. All of these ports can function independently either as input or as output ports. This can be achieved by programming the bits of an internal register of 8255 called as control word register ( CWR ). PIO 8255 †¢ The internal block diagram and the pin configuration of 8255 are shown in fig. †¢ The 8-bit data bus buffer is controlled by the read/write control logic. The read/write control logic manages all of the internal and external transfers of both data and control words. †¢ RD, WR, A1, A0 and RESET are the inputs provided by the microprocessor to the READ/ WRITE control logic of 8255. The 8-bit, 3-state bidirectional buffer is used to interface the 8255 internal data bus with the external system data bus. PIO 8255 †¢ This buffer receives or transmits data upon the execution of input or output instructions by the microprocessor. The control words or status information is also transferred through the buffer. †¢ The signal description of 8255 are briefly presented as follows : †¢ PA7-PA0: These are eight port A lines that acts as either latched output or buffered input lines depending upon the control word loaded into the control word register. †¢ PC7-PC4 : Upper nibble of port C lines. They may act as either output latches or input buffers lines. PIO 8255 This port also can be used for generation of handshake lines in mode 1 or mode 2. †¢ PC3-PC0 : These are the lower port C lines, other details are the same as PC7-PC4 lines. †¢ PB0-PB7 : These are the eight port B lines which are used as latched output lines or buffered input lines in the same way as port A. †¢ RD : This is the input line driven by the microprocessor and should be low to indicate read operation to 8255. †¢ WR : This is an input line driven by the microprocessor. A low on this line indicates write operation. PIO 8255 †¢ CS : This is a chip select line. If this line goes low, it enables the 8255 to respond to RD and WR signals, otherwise RD and WR signal are neglected. †¢ A1-A0 : These are the address input lines and are driven by the microprocessor. These lines A1-A0 with RD, WR and CS from the following operations for 8255. These address lines are used for addressing any one of the four registers, i. e. three ports and a control word register as given in table below. †¢ In case of 8086 systems, if the 8255 is to be interfaced with lower order data bus, the A0 and A1 pins of 8255 are connected with A1 and A2 respectively. RD 0 0 0 0 RD 1 1 1 1 RD X 1 WR 1 1 1 1 WR 0 0 0 0 WR X 1 CS 0 0 0 0 CS 0 0 0 0 CS 1 0 A1 0 0 1 1 A1 0 0 1 1 A1 X X A0 0 1 0 1 A0 0 1 0 1 A0 X X Input (Read) cycle Port A to Data bus Port B to Data bus Port C to Data bus CWR to Data bus Output (Write) cycle Data bus to Port A Data bus to Port B Data bus to Port C Data bus to CWR Function Data bus tristated Data bus tristated Control Word Register PIO 8255. †¢ D0-D7 : These are the data bus lines those carry data or control word to/from the microprocessor. †¢ RESET : A logic high on this line clears the control word register of 8255. All ports are set as input ports by default after reset. Block Diagram of 8255 (Architecture) ( cont.. ) †¢ 1. 2. 3. 4. †¢ It has a 40 pins of 4 groups. Data bus buffer Read Write control logic Group A and Group B controls Port A, B and C Data bus buffer: This is a tristate bidirectional buffer used to interface the 8255 to system databus. Data is transmitted or received by the buffer on execution of input or output instruction by the CPU. Control word and status information are also transferred through this unit. †¢ Block Diagram of 8255 (Architecture) ( cont.. ) Read/Write control logic: This unit accepts control signals ( RD, WR ) and also inputs from address bus and issues commands to individual group of control blocks ( Group A, Group B). †¢ It has the following pins. a) CS Chipselect : A low on this PIN enables the communication between CPU and 8255. b) RD (Read) A low on this pin enables the CPU to read the data in the ports or the status word through data bus buffer. †¢ Block Diagram of 8255 (Architecture) ( cont.. ) WR ( Write ) : A low on this pin, the CPU can write data on to the ports or on to the control register through the data bus buffer. ) RESET: A high on this pin clears the control register and all ports are set to the input mode e) A0 and A1 ( Address pins ): These pins in conjunction with RD and WR pins control the selection of one of the 3 ports. †¢ Group A and Group B controls : These block receive control from the CPU and issues commands to their respective ports. c) Block Diagram of 8255 (Architecture) ( cont.. ) †¢ Group A PA and PCU ( PC7 -PC4) †¢ Group B PCL ( PC3 PC0) †¢ Control word register can only be written into no read operation of the CW register is allowed. a) Port A: This has an 8 bit latched/buffered O/P and 8 bit input latch. It can be programmed in 3 modes mode 0, mode 1, mode 2. b) Port B: This has an 8 bit latched / buffered O/P and 8 bit input latch. It can be programmed in mode 0, mode1. Block Diagram of 8255 (Architecture). c) Port C : This has an 8 bit latched input buffer and 8 bit out put latched/buffer. This port can be divided into two 4 bit ports and can be used as control signals for port A and port B. it can be programmed in mode 0. Modes of Operation of 8255 (cont.. ) †¢ These are two basic modes of operation of 8255. I/O mode and Bit Set-Reset mode (BSR). †¢ In I/O mode, the 8255 ports work as programmable I/O ports, while in BSR mode only port C (PC0-PC7) can be used to set or reset its individual port bits. †¢ Under the I/O mode of operation, further there are three modes of operation of 8255, so as to support different types of applications, mode 0, mode 1 and mode 2. Modes of Operation of 8255 (cont.. ) †¢ BSR Mode: In this mode any of the 8-bits of port C can be set or reset depending on D0 of the control word. The bit to be set or reset is selected by bit select flags D3, D2 and D 1 of the CWR as given in table. I/O Modes : a) Mode 0 ( Basic I/O mode ): This mode is also called as basic input/output mode. This mode provides simple input and output capabilities using each of the three ports. Data can be simply read from and written to the input and output ports respectively, after appropriate initialisation. D3 0 0 0 0 1 1 1 1 D2 0 0 1 1 0 0 1 1 D1 0 1 0 1 0 1 0 1 Selected bit s of port C D0 D1 D2 D3 D4 D5 D6 D7 BSR Mode : CWR Format PA 8 2 5 5 PCU PCL PA6 PA7 PC4 PC7 PC0-PC3 PB PB0 PB7 8 2 5 5 PA PCU PCL PB PA PC PB0 PB7 All Output Port A and Port C acting as O/P. Port B acting as I/P Mode 0 Modes of Operation of 8255 (cont.. ) †¢ 1. The salient features of this mode are as listed below: Two 8-bit ports ( port A and port B )and two 4-bit ports (port C upper and lower ) are available. The two 4-bit ports can be combinedly used as a third 8-bit port. Any port can be used as an input or output port. Output ports are latched. Input ports are not latched. A maximum of four ports are available so that overall 16 I/O configuration are possible. All these modes can be selected by programming a register internal to 8255 known as CWR. 2. 3. 4. †¢ Modes of Operation of 8255 (cont.. †¢ The control word register has two formats. The first format is valid for I/O modes of operation, i. e. modes 0, mode 1 and mode 2 while the second format is valid for bit set/reset (BSR) mode of operation. These formats are shown in following fig. D7 1 D6 X D5 X D4 X D3 D2 D1 D0 0- Reset 0-for BSR mode Bit select flags D3, D2, D1 are from 000 to 111 for bits PC0 TO PC71- Set I/O Mode Control Word Register Format and BSR Mode Control Word Register Format PA3 PA2 PA1 PA0 RD CS GND A1 A0 PC7 PC6 PC5 PC4 PC0 PC1 PC2 PC3 PB0 PB1 PB2 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 0 39 38 37 36 35 34 33 32 31 30 29 28 27 26 25 24 23 22 21 PA4 PA5 PA6 PA7 WR Reset D0 D1 D2 D3 D4 D5 D6 D7 Vcc PB7 PB6 PB5 PB4 PB3 8255A 8255A Pin Configuration = D0-D7 CS RESET 8255A A0 A1 RD PA0-PA7 PC4-PC7 PC0-PC3 PB0-PB7 Vcc WR GND Signals of 8255 3 Group A control 1 D0-D7 Data bus Buffer 8 bit int data bus 4 Group A Port A(8) PA0-PA7 Group A Port C upper(4) Group B Port C Lower(4) PC7-PC4 PC0-PC3 2 RD WR A0 A1 RESET CS Block Diagram of 8255 READ/ WRITE Control Logic Group B control PB7-PB0 Group B Port B(8) D7 D6 D5 Mode for Port A D4 PA D3 PC U D2 Mode for PB D1 PB D0 PC L Mode Set flag 1- active 0- BSR mode Group A 1 Input PC u 0 Output 1 Input PA 0 Output 00 mode 0 Mode 01 mode 1 Select of PA 10 mode 2 Group B PCL PB Mode Select 1 Input 0 Output 1 Input 0 Output 0 mode- 0 1 mode- 1 Control Word Format of 8255 Modes of Operation of 8255 (cont.. ) b) Mode 1: ( Strobed input/output mode ) In this mode the handshaking control the input and output action of the specified port. Port C lines PC0-PC2, provide strobe or handshake lines for port B. This group which includes port B and PC0-PC2 is called as group B for Strobed data input/output. Port C lines PC3-PC5 provide strobe lines for port A. This group including port A and PC3-PC5 from group A. Thus port C is utilized for generating handshake signals. The salient features of mode 1 are listed as follows: Modes of Operation of 8255 (cont.. ) 1. 2. 3. 4. Two groups group A and group B are available for strobed data transfer. Each group contains one 8-bit data I/O port and one 4-bit control/data port. The 8-bit data port can be either used as input and output port. The inputs and outputs both are latched. Out of 8-bit port C, PC0-PC2 are used to generate control signals for port B and PC3-PC5 are used to generate control signals for port A. he lines PC6, PC7 may be used as independent data lines. Modes of Operation of 8255 (cont.. ) †¢ The control signals for both the groups in input and output modes are explained as follows: Input control signal definitions (mode 1 ): †¢ STB( Strobe input ) If this lines falls to logic low level, the data available at 8-bit input port is loaded into input latches. †¢ IBF ( Input buffer full ) If this signal rises to logic 1, it indicates that data has been loaded into latches, i. e. it works as an acknowledgement. IBF is set by a low on STB and is reset by the rising edge of RD input. Modes of Operation of 8255 (cont.. ) †¢ INTR ( Interrupt request ) This active high output signal can be used to interrupt the CPU whenever an input device requests the service. INTR is set by a high STB pin and a high at IBF pin. INTE is an internal flag that can be controlled by the bit set/reset mode of either PC4 (INTEA) or PC2(INTEB) as shown in fig. †¢ INTR is reset by a falling edge of RD input. Thus an external input device can be request the service of the processor by putting the data on the bus and sending the strobe signal. Modes of Operation of 8255 (cont.. Output control signal definitions (mode 1) : †¢ OBF (Output buffer full ) This status signal, whenever falls to low, indicates that CPU has written data to the specified output port. The OBF flip-flop will be set by a rising edge of WR signal and reset by a low going edge at the ACK input. †¢ ACK ( Acknowledge input ) ACK signal acts as an acknowledgement to be given by an output device. ACK sig nal, whenever low, informs the CPU that the data transferred by the CPU to the output device through the port is received by the output device. Modes of Operation of 8255 (cont.. ) †¢ INTR ( Interrupt request ) Thus an output signal that can be used to interrupt the CPU when an output device acknowledges the data received from the CPU. INTR is set when ACK, OBF and INTE are 1. It is reset by a falling edge on WR input. The INTEA and INTEB flags are controlled by the bit set-reset mode of PC 6and PC2 respectively. 1 0 1 0 Input control signal definitions in Mode 1 1/0 X X X 1 X X X X 1 1 X D7 D6 D5 D4 D3 D2 D1 D0 1 Input 0 Output For PC6 PC7 PA0 PA7 INTEA PC4 PC5 STBA IBFA D7 D6 D5 D4 D3 D2 D1 D0 PB0 PB7 INTEB PC 2 PC1 STBB IBFB PC3 RD PC6 PC7 INTRA I/O PC0 INTR A Mode 1 Control Word Group A I/P RD Mode 1 Control Word Group B I/P STB IBF INTR RD DATA from Peripheral Mode 1 Strobed Input Data Transfer WR OBF INTR ACK Data OP to Port Mode 1 Strobed Data Output Output control signal definitions Mode 1 1 0 1 0 1/0 X X X 1 X X X X 1 0 X D7 D6 D5 D4 D3 D2 D1 D0 1 Input 0 Output For PC4 PC5 PA0 PA7 INTEA PC7 PC6 OBF ACKA D7 D6 D5 D4 D3 D2 D1 D0 PB0 PB7 INTEB PC PC2 1 OBFB ACKB PC3 WR PC4 PC5 PC0 INTRA I/O INTRB Mode 1 Control Word Group A Mode 1 Control Word Group B Modes of Operation of 8255 (cont.. ) †¢ Mode 2 ( Strobed bidirectional I/O ): This mode of operation of 8255 is also called as strobed bidirectional I/O. This mode of operation provides 8255 with an additional features for communicating with a peripheral device on an 8-bit data bus. Handshaking signals are provided to maintain proper data flow and synchronization between the data transmitter and receiver. The interrupt generation and other functions are similar to mode 1. †¢ In this mode, 8255 is a bidirectional 8-bit port with handshake signals. The RD and WR signals decide whether the 8255 is going to operate as an input port or output port. Modes of Operation of 8255 (cont.. ) †¢ 1. 2. 3. 4. 5. The Salient features of Mode 2 of 8255 are listed as follows: The single 8-bit port in group A is available. The 8-bit port is bidirectional and additionally a 5-bit control port is available. Three I/O lines are available at port C. ( PC2 PC0 ) Inputs and outputs are both latched. The 5-bit control port C (PC3-PC7) is used for generating / accepting handshake signals for the 8-bit data transfer on port A. Modes of Operation of 8255 (cont.. ) †¢ Control signal definitions in mode 2: †¢ INTR (Interrupt request) As in mode 1, this control signal is active high and is used to interrupt the microprocessor to ask for transfer of the next data byte to/from it. This signal is used for input ( read ) as well as output ( write ) operations. †¢ Control Signals for Output operations: †¢ OBF ( Output buffer full ) This signal, when falls to low level, indicates that the CPU has written data to port A. Modes of Operation of 8255 (cont.. ) ACK ( Acknowledge ) This control input, when falls to logic low level, acknowledges that the previous data byte is received by the destination and next byte may be sent by the processor. This signal enables the internal tristate buffers to send the next data byte on port A. †¢ INTE1 ( A flag associated with OBF ) This can be controlled by bit set/reset mode with PC6 . †¢ Control signals for input operations : †¢ STB (Strobe inp ut ) A low on this line is used to strobe in the data into the input latches of 8255. Modes of Operation of 8255 (cont.. ) †¢ IBF ( Input buffer full ) When the data is loaded into input buffer, this ignal rises to logic ‘1’. This can be used as an acknowledge that the data has been received by the receiver. †¢ The waveforms in fig show the operation in Mode 2 for output as well as input port. †¢ Note: WR must occur before ACK and STB must be activated before RD. WR OBF INTR ACK STB IBF Data bus RD Mode 2 Bidirectional Data Transfer Data from 8085 Data towards 8255 Modes of Operation of 8255 (cont.. ) †¢ The following fig shows a schematic diagram containing an 8-bit bidirectional port, 5-bit control port and the relation of INTR with the control pins. Port B can either be set to Mode 0 or 1 with port A( Group A ) is in Mode 2. Mode 2 is not available for port B. The following fig shows the control word. †¢ The INTR goes high only if either IBF, INTE2, STB and RD go high or OBF, INTE1, ACK and WR go high. The port C can be read to know the status of the peripheral device, in terms of the control signals, using the normal I/O instructions. D7 1 D6 1 D5 X D4 X D3 X D2 1/0 D1 1/0 D0 1/0 1/0 mode Port A mode 2 Port B mode 0-mode 0 1- mode 1 PC2 PC0 1 Input 0 Output Port B 1- I/P 0-O/P Mode 2 control word PC3 PA0-PA7 INTR INTE 1 PC7 PC6 OBF ACK STB IBF 3 I/O INTE 2 RD WR PC4 PC5 Mode 2 pins

Capital Punishment Must Be Put To Death Essay -- Capital Punishment, De

Capital punishment, better known as the death penalty, has been around for centuries. Like all elements of modern society, the death penalty has evolved over the course of many years. Initially, the death penalty was administered by a royal court or monarchy through brutal stoning. Since then, the guillotine, noose, electric chair, and [currently] lethal injection have all been tools created to administer the death penalty here in the United States. Before the act of actually ending the criminal’s life is performed he or she waits on death row during the course of any court proceedings. In America, death row is the term given to the section of a prison reserved for inmates awaiting trial concerning the death penalty. The term â€Å"death row† is figurative. Due to extensive court proceedings, individuals on death row may await trial or sentencing for months or years. There is no way to determine how long an inmate will stay on death row. However, research has shown that extensive periods of time on death row lowers inmates’ mental capacities and capabilities, and deteriorates their physical health at alarming rates. Inmates on death row have no one to comfort them, to care for them, or to visit them. Jack Alderman is the longest serving death row American prisoner with over thirty-three years prior to his execution. In the state of Georgia on September 16, 2008 Alderman was executed by lethal injection. He was convicted for his part in the murder of his wife Barbara Alderman. Although the â€Å"U.S. Supreme Court declared the death penalty unconstitutional† (Swarns 1 of 3), the issue has gone back to trial and reinstated. The death penalty is legal rhetoric that is based on heightened emotions and revenge. The â€Å"justice† system that determin... ... Works Cited Hawkins, Steven W. â€Å"It is Immoral and Ineffective†. World and I Sept. 2002: 247 General OneFile. Web. 1 Nov. 2011. â€Å"Death Penalty is violation of human Rights: L:aws are not Meant to Punish Anyone but to Bring Change.† DNA (Daily News and Analysis). 11 Oct. 2009. General OneFile. Web. 1 Nov. 2011 Lafevere, Patricia. â€Å"Group Urges Legislator to Scrap Death Penalty. (Nation)†. National Catholic Reporter 28 Dec. 2001 General OneFile. Web. 1 Nov. 2011. Swarns, Christina. â€Å"The Uneven Scale of Capital Justice: How Race and Class Affect Who Ends Up on Death Row†. The American Prospect. 15.7 (2004): A14+. Gale Opposing Viewpoints in Context. Web. 1 Nov. 2011 â€Å"Top 10 Pros and Cons: Should the Death Penalty be Allowed?† deathpenalty.procon.org N.p. n.d. Web. 3 Nov. 2011

Diabetes Type 1: Stem Cell Research

Stem cell therapy involves the direct transplant of islet cells to potential areas in the pancreas that have the ability to store and facilitate the differentiation of beta cells in the body. Such treatment is currently under progressive study in terms of its effectiveness and the possibility of fortifying the islet transplant’s resistance to autoimmune attacks antibodies. We discuss the actual procedures and different alternatives of stem cell therapy for DMT1 patients. The discussion covers the potential problems being confronted by such treatment, such as stem cell scarcity, autoimmune attacks against the islet transplants, etc.Lastly, discussion also covers the potential alternatives of the treatment, specifically (1) human embryonic stem cells, (2) cultured stem cells and (3) potential xenogeneic resources. In the conclusion, we have found several problems currently being faced by stem cell therapy. These problems include the scarcity of available islet grafts or transpla nts and the autoimmune risks that can dramatically hinder to the success of the therapy. However, various studies are currently being explored in order to obtain potential alternatives, such as xenogeneic stem cell resources, embryonic or progenitor alternatives, etc.Furthermore, we discover different methodologies in stem cell culturing and preparation techniques that confront the immunity problems most especially in post-transplant phase. These include the usage of different immuno-suppressing drugs, such as gastrin, etc. 2. Introduction 1. 1 . Type 1 Diabetes DMT1 is essentially the absence or severe insufficiency of insulin due to the autoimmune (e. g. CD4 interleukin attacks, cellular necrosis, macrophagial reactions, etc. ), environmental or viral destruction of beta cells (e. g. iral infections from mumps, etc. ) or insulin-secreting cells in the pancreas. Although, autoimmune reasons are the most commonly associated etiology that cause DMT1 condition. Apparently, the body an tibodies, specifically interleukins and minor interferons, recognize the antigenicity present on pancreatic islets as foreign substances, which consequently triggers autoimmune responses. The prevalence of DMT1 in United States is approximately 1 in 2500 for the age group of 5 years old, which 1 in 300 for every 20 years of age group.Although the most considerable nature of DMT1 is its autoimmune nature, prevalence of DMT1 in United States and European nations largely depends on two causations: (1) genetics and (2) lifestyle. According to the EURODIAB collaborative study, a registry involving 44 countries in Europe, states an annually increasing rate of DMT1 with approximately 3 to 4%, with a larger increase in some central and eastern European countries . The prevalence of DMT1 among 191 World Health Organization (WHO) member states and for all age groups worldwide is estimated to be 2. % in 2000 and 4. 4% in 2030 . DMT1’s beta cell destruction does not only consider the neg ative effects towards insulin production. Deficiency in insulin can directly lead to moderate to severe hyperglycemia that can further trigger problems, especially in (1) neural systems, (2) peripheral and central vascular regions, (3) cardiac and (4) kidney areas. Vascular complications among DMT1 are associated to different cellular dysfunctions, such as Endothelial Progenitor Cells (EPC) that induce metabolic stress and vascular angiogenicity especially when the cells are decreased.The primary principle that explains the metabolic and cardiovascular dangers of this illness is the increased of tonicity in the blood or also known as fluid hypertonicity. Due to the increased surge of blood glucose levels, fluids, such as blood, lymph, interstitial fluid, etc. , become thicker than its normal viscosity. With this fluid condition, the circulation exerts tremendous vascular and hyperosmolar pressure from major vessels to minor arterioles and veinuoles. Eventually, the prolonged pressur e can lead to various complications, such as eye retinopathy, nephronic damage, nerve ending necrosis, etc.The common treatment being prescribed among DMT1 patients is the continuous administration of insulin injectables in order to fill in the body’s insulin requirements. This is done to temporarily replace or fill in the insulin insufficiency of the body. However, insulin therapy and maintenance are lifetime measures that require continuous commitment, which can greatly interfere in the person’s self-esteem and lifestyle progression. To resolve these potential emotional and psychosocial damages of the temporary insulin therapy, permanent treatments, such as stem cell implants, autoimmune suppressors, etc. are currently being studied with hopes of permanently curing the disease. Stem cell studies have carefully focused in determining the potential strategies in order to induce beta cell differentiation and cellular regeneration, especially among those damaged or destr oyed islet cells. Clearly, with cellular differentiation and regeneration s the goal of stem cell treatment, vast numbers of research discussed in the latter part of the studies have intensively focused their explorations in the disease’s autoimmune nature.Modern studies of beta cells have always been associated to the macrophagial and lymphocytic activities of T-cell mediated antibodies, such as CD4+CD25+, CD+ T-cells, etc. Most studies are determined in configuring the possible strategies of resolving, preventing and/or countering the DMT1’s autoimmune response on both original islets and implant islet grafts. In animal trials, most commonly rodents, autoimmune elements of the disease are somehow resisted when significant dosage of immune-inhibiting drugs (e. g. nfliximab, daclizumab and sirolimus, etc. ) are applied on the islet implants prior to the commencement of stem cell implantation.Several studies (e. g. Gastrin applicationetc. ) have found promising strategi es that can immunize the transplant grafts and possibly the original islets themselves from the autoimmune destruction rendered by the disease; although, modern science has not yet considered the safe applicability and effectiveness among human trials due to the conflicts encountered by the studies, such variations of drug responses or autoimmune actions. On the other hand, the signs and symptoms of DMT1 and DMT2 are both related to the two principal components of diabetes: (1) hyperglycemia and (2) hypoinsulinemia.DMT1 commonly presents its condition with the classic manifestations of polydipsia, polyphagia and polyuria . Physiologically, the three principal signs of DMT1 are extremely integrated and fostered by the body’s sympathetic natural response. For example, due to the hyperglycemic state of the body, the satiety centers of the brain triggers polydipsia in order for the body to increase its fluid intake aiming to dilute the tonicity or increased blood glucose levels. In the process, the body increases the fluid contents in the blood increasing as well the kidney workload in processing urinary output; therefore, producing polyuria.Consequently, fluid loss also causes significant electrolyte losses and glucose malabsorption that trigger body weakness. In order to compensate, the body triggers polyphagia that aims to increase food consumption. The three latter manifestations are considered the cardinal or principal manifestations of DMT1 common to all patients. Weight loss, fatigue, blurred vision, pruritis and muscle wastage are the secondary symptoms that follow with the continuous manifestations of DMT1 cardinal signs .The secondary complications of DMT1 can further aggravate if the physiological hyperglycemia and other associated signs and symptoms are not resolved. Tertiary complications involve severe manifestations that can be fatal in nature, such as diabetic ketoacidosis and possibly diabetic coma. 1. 2. Causes of DMT1 DMT1 has three poten tial origins that are currently under extensive study, namely (1) chronic autoimmune destruction of beta cells, (2) environmental destruction of beta cells that is commonly viral in nature, and (3) genetic abnormality in beta cells and/or insulin receptors .The autoimmune etiology of DMT1, as discussed earlier, involves the activity of interleukin-1 protein cytokine that principally triggers the immunologic response of CD4+ T cells against beta cells. The autoimmune nature has proven the relationship between beta cell destruction and islets’ inflammation due to interleukin invasion; however, studies have not yet determined the principal source of this cytokine production . The issues surrounding the autoimmune proposition in the DMT1 condition is the communicating element/s induced by the disease that activates antibodies’ response against the islet cells.As of the recent studies, no specific communicating agent has been discovered linking both DMT1 condition and its a utoimmune reaction towards islet cells; although, there are numerous evidences that reveal the exact autoimmune attacks against pancreatic islet cells, most significantly on the beta cells. Meanwhile, viral causations have also been associated to the occurrence of DMT1. Common viruses, such as mumps, rubella and coxsackie, have been associated to the destruction of beta cells, which eventually triggers the chronic drop of insulin production .Cytokine-interferon alpha (IFN-alpha) has been associated with the occurrence of DMT1 with hypothetical viral origin. According to clinical reports, IFN-alpha is brought by environmental viruses (enteroviruses) that trigger immune-mediated beta cell destruction. Significantly, therapeutic agents targeting IFN-a may potentially be beneficial in the prevention of type 1 diabetes and autoimmunity . Lastly, genetic abnormalities min beta cell progenitors and cellular differentiations are also becoming part of the controversial cause of DMT1.The idea of genetic causation of DMT1 involves the reduced activity of embryonic progenitors in pancreatic endothelial, which consequently lessens the cellular differentiation of beta cells. With small beta cell count in the body, insulin production becomes insufficient causing cellular tension for insulin production. Prolonged state of hypoinsulinemia or complete absence of insulin in the blood usually results to DMT1 complications. Islet transplantation or stem cell therapy considers the destroyed islet areas that need replacement.According to Rother and Harlan, if patients with greater body mass indices and/or with insulin resistance were also considered for an islet transplant, the 3,000 transplantable islet preparations presently achievable would likely be sufficient to restore euglycemia to fewer than 1,000 patients per year, or less than 0. 1% of patients with T1DM, or approximately 0. 005% of those with either form of diabetes. Despite of the technological advancements of stem cells and islet transplants, most parts of DMT1 condition and autoimmune functionalities are still left undetermined.The scarcity of islet stem cells is not the only problems being faced by islet transplant therapy but also the impending variations of autoimmune activities of the body. Controlled experiments have been conducted on both rodents and primates; however, the results most of the time vary when applied to human samples. Although, such islet therapy have already been applied to human sample and proven to cause independent insulin production; although, medical issues, such as alternative stem cell or islet graft sources, risk of anaphylactic rejections, etc, are still being studies extensively.Therefore, scarcity and further study of the procedure are necessary to further the application of islet stem cell therapy among DMT1 patients. 1. 3. Therapy for DMT1 Stem cell transplant of islets of langerhans, specifically the ß -cells, is now considered as alternative treatment in tr eating Diabetes Mellitus Type 1 (DMT1); although, not all DMT1 patients are applicable candidates of stem cell therapy. Antigenicity testing and severity of DMT1 manifestations as well as autoimmune response to the treatment are usually evaluated before considering stem cell transplant.Through the process of genetic engineering, the autoimmune response of DMT1 towards the islet cells can now be countered by replacing the cellular necrosis of ß-cells. The study explores the different sections of ß–cells stem cell transplant, particularly on (1) the actual procedure, (2) allogeneic and xenogeneic possibilities, (3) the actual condition of DMT1 and (4) the pathophysiological principles involved in the process of disease progress and stem cell therapy.The case of DMT1 is autoimmune by nature wherein the body acts negatively to the islet cells by recognizing these cells as a form of foreign objects. Theoretically, the body’s macrophages and interleukins are alarmed by the foreign or abnormal structuring of islet antigens, which probably resulted due to the extensive response of the cells thriving within high insulin-needing environment. In response, the body’s immunologic centers trigger macrophagial and anti-body mediators (e. g. GAD65 Ab – Glutamic Acid Decarboxylase Antibodies, Iinsulinoma Antigen 2, etc. attacking and destroying the body’s own pancreatic tissues . During these conditions, islet cells chronically declines in number as macrophagial actions subdue and destroy both progenitor cells in the pancreas and those differentiated islet cells, which include the beta cells. With the destruction of progenitor cells, the rate of cellular differentiations for further beta cells and other islet cell types (e. g. alpha cells, etc. ) decline leaving the body deficient of these endocrine hormones.Furthermore, as the existing and pre-existing beta cells die due to autoimmune damages, the capacity of the islet cells to regener ate also decline, which eventually decreases the number of existing beta cells within the islets. Theoretically, According to Xu, Wang and Hou (2008), as the body’s insulin requirement heightens and prolonged, the remaining beta cells experience physiological stress in insulin production, which, if not prevented, can lead to a negative feedback mechanism wherein insulin production complete shuts off its production.DMT1 patients experience decreased and/or absence of insulin production, and usually peaks between early adolescence (10 to 14 years of age) to middle adulthood (30 and above) . Pancreas manifests lymphocytic infiltration and destruction of islets of langerhans, which consequently causes depletion of insulin production. During the past few decades, studies on islet transplantation through mesenchymal stem cells (MSC) have shown to improve the metabolic conditions of DMT1 patients. However, the performances and study results using MSC remains to be questionable.Trans -differentiation of MSCs into insulin-producing cells (IPCs) is considered the principal concept of the therapy; however, other reports have negated these results claiming that it is too difficult to assume and determine the timing and extent of improvement by only analyzing the effects through trans-differentiation. Cellular differentiation and self renewal can greatly vary depending on various conditions, such as existing drug therapies, immunologic sensitivity, duration of the illness, other existing disorder including complications dealt by DMT1, etc.Similar to other beta-stimulating treatments, MSC is considered growth factor stimulant of the surrounding beta cells, which aids in the mechanism of self duplication rather than cellular proliferation. According to Xu, Wang and Hou (2008), â€Å"MSCs transplantation into diabetic animals may prevent apoptosis of injured pancreatic beta cells and enhance regeneration of endogenous progenitor cells through paracrine actions† ( e. g. angiogenic, cytoprotective, anti-inflammatory, mitogenic and anti-apoptotic effects, etc. ). MSC studies are still on the process of development along with animal trials.MSC therapy alternative is process for treating principally the occurrence of hyperglycemia in DMT1; however, the process remains an assumption and currently being studied. In the study of Ezquer, Ezquer and Parrau (2008), MSC procedure has been detected to also contribute to tissue regeneration (e. g. bones, cartilage, infracted heart, brain and kidney). In the study, a test subject with streptozotocin (STZ)-induced type 1 diabetes (C57BL/6 mice) has shown significant cellular neogenesis on pancreatic and renal function as well structure.Somehow, MSC has triggered a potential role of becoming a promising alternative as pancreatic progenitor cells that possess the capacity to initiate cellular differentiations. After the subject received a 0. 5 x 10(6) MSCs via ex vivo expansion, the sample has shown significa nt reduction in blood glucose levels and euglycemic values after a month. With MSC acting as the islet’s alternative progenitor cells, beta cell differentiation can progress to the development of other beta cells, which if continued can trigger cellular regeneration among produced existing beta cells.According to final conclusions of Ezquer, Ezquer and Parrau (2008), â€Å"MSC administration resulted in beta-pancreatic islets regeneration and prevented renal damage in diabetic animals. † This evidence shows the possibility of using MSC in initiating both cellular differentiation and self-duplication. Altthough, Xu, Wang and Hou (2008) still consider this process as an experimental alternative therapy for DMT1 condition. However, the study sample did not consider the potential effects of human autoimmune responses against these MSC grafts.Autoimmune responses can risk the success of graft transplant considering the increased antigenicity present among these islet transp lants, which is a considerable issue that arises in the results of their study. Meanwhile in the study of Feng, De-quan and Yan-hua (2008), they have focused on MSCs derived from human umbilical cord blood (UCB) in order to facilitate cellular transdifferentiation into beta cell alternatives via in vitro. In the study, UCB samples are obtained, while presenting MSCs are isolated for analysis via flow cytometer.In the process, islet-cellular differentiation has been induced for 15 days with or without extracellular matrix gel. This extracellular matrix gel provides an enriched environment that nourishes cellular requirements aiding in their differentiation and consequent self-duplication. With the help of chemiluminescent immunoassay system (CIS) in detecting glucose activity and insulin response, the studied found out that insulin positive cells (25. 2 ±3. 4%; UCB n=42) within ECM gel have produced functional islet proteins after 9 days of pancreatic differentiation.Considering th e feasible environment setup by ECM, the possibility of creating a zone wherein autoimmune reactions are considered nullified has also become one of the propositions that theoretically explained the results of the study. According to the conclusion of their study, MSC can actually differentiate into islet like cells in vitro and ECM gel. Fortunately, with the advent of modern technology and introduction of somatic stem cell transplant, the depletion of ß–cells can now be replaced with new generating ß–cells through stem cell implantation.In 1990, Scharp et al. has brought reports of success in the process of transplanting islet cells to patients with DMT1 through the process of improved islet isolation techniques (developed by Ricordi, Lacy and Finke et al. 1988) . Isolation techniques aim in discovering alternative progenitor sources of progenitor cells that possess the capacity to differentiate into insulin-producing cells that can serve as essential alternativ e for beta cells.Aside from pancreatic progenitor cells, the study has also discovered potential sources in the kidney, liver, bone marrow and other vital organs of the body. Isolation techniques usually require individualized culturing of islet transplants prior to the actual therapy. With the introduction of ß–cells implantation, different forms of islet transplant (e. g. billiary installation of islet cells, xenogeneic sources of islets, etc. ) have been considered throughout the process of stem cell therapy. On the other hand, certain reaction problems produced during the process (e. . anaphylactic response, incompatible cellular transplant, insulin-sensory impairment, etc. ) have also been observed in throughout the process of therapy. Despite of the potential therapeutic permanence of islet transplant therapy against DMT1 condition, most medical specialists (Kabelitz, Geissler and Soria, 2008; Xu, Wang and Hou, 2008) consider this treatment as last resort therapy for severe cases of DMT1. Stem cell therapy is not yet considered as a general treatment applicable for all sorts of DMT1 conditions.According to Kabelitz, Geissler and Soria (2008), the concepts in the cellular treatment of DMT1 are (1) the replacement of islet cells by islet-like cells derived from embryonic or adult stem cells, and (2) promotion and establishment of immunological tolerance of islet cells towards self-antigens through regulatory T cells and/or tolerance-promoting monocyte-derived cells. Studies have explored possible ways in dealing with the confronting problems of the procedures, such as scarcity, autoimmune sensitivity, etc.In the preceding sections of the discussion, the two concepts are further explained considering the possibility of merging the two procedures in order to attain maximum efficiency in the DMT1 cellular therapy. 3. Modern Techniques in Treatments of DMT1 1. 1 Islet Cell Transplant The principal concept of stem cell therapy is the harvesting of pot ential and/or adult health cells that are transferred to failing or degenerating organs. As for DMT1 conditions, islet transplantation, specifically on ß–cells implantation, is the most impressive treatment that shows promising permanent cure for islets’ autoimmune degradation.According to Hussain and Theise, â€Å"stem-cell therapy here implies the replacement of diseased or lost cells from progeny of pluripotent or multipotent cells. † According to Haller, Viener and Wasserfall et al (2008), UCB-derived MSCs are significant autologous progenitor inducers that can initiate cellular self duplication or regeneration. In their study using 12 autologous UCB infusions, preliminary results show significant slowing of endogenous loss of beta cell degradation among DMT1 children subjects.Aside from the slowing of hyperglycemic actions induced by DMT1, Keymeulen (2008) has proposed the possibility of actually blocking or preventing the autoimmune destruction of beta cells in DMT1 conditions. In the study, Keymeulen (2008) proposes the short-term humanized anti-T-cell antibody treatment that aim to inhibit the t-cell activities and preserve the residual beta-cells for at least 18 months in order to induce cellular regeneration and stabilize metabolic control of the body over the rising glucose levels.By applying Anti-Thymocyte-Globulin, tacrolimus and mycophenolate mofetil to a non-uremic C peptide negative DMT1 patient, marked decrease in autoimmune activities has risen to more than 80%. Another principle of stem cell transplant in islet cell therapy is biologic differentiation wherein a pool of undifferentiated precursors (e. g. Human Islet-derived Precursor Cells or hIPCs, etc. in pancreas appears to be a series of stem cell that further differentiate to islet-endocrine cellular population: (1) Glucagon-producing alpha-cells, (2) insulin-producing beta-cells, (3) somatostatin-producer in Delta cell, (4) pancreatic polypeptide secreting cells . Both of these cellular somas act as the cellular surrogate of ß–cells that shall replace the depleted or damaged cellular source in the pancreas . Cellular differentiation holds the key in inducing growth to the depleted beta cells in the islet of langerhans.According to the study of Abdi, Fiorina and Adra (2008), islet transplantation (ppluripotent stromal cells) provides great potential for diversifying the cellular lineage even with postnatal damaged tissues. The study of of Abdi, Fiorina and Adra (2008) support the idea of cellular renewal and differentiation giving more emphasis on the mesodermal origin. In such case, the study introduces the concept similar to other studies (e. g. immuno suppression of T-cell activity, increasing beta cell antigenitcity resistance, etc. wherein the introduction of MSCs or islet transplant pluripotent cells may induce an immunomodulatory effect, which eventually facilitates cellular regeneration. The study of Seissler and Schott (20 08) also supports the idea of cellular differentiation and self-renewal; however, they have questioned the capacity of supporting the cellular capabilities of stem cells derived from adult pancreas or non-pancreas. During cellular differentiation of endocrine tissue, precursor cells secrete multiple hormones prior to final maturation of differentiated cells that secret single classification of hormone.Most of these hormones are actual growth hormones that enhance cellular differentiations and regeneration. Although these actions are most of the time slow-phased and are very much vulnerable to immunologic attacks, some studies (e. g. Piper, Brickwood and Turnpenny, 2004; Lai, Schneider and Kidszun, 2005) suggest that once islet cells have regained its stable cellular disposition, which can varies depending on the prevailing physiological atmosphere (e. g. decreased immune activity, prolonged hypoinsulinemia, etc. , the cellular proliferation and restorative scheme can pursue more rap idly than its common phasing. In the process of islet transplant, beta cells are produced as part of the general cellular differentiation produced by broad cellular differentiations . According to Rosenburg, Lipsett and Yoon et al (2004), once islet cell quantity have increased to a stable position and the environment requires extensive insulin production, autoimmune response of the body against these cells are seen to decline dramatically.Once islets have differentiated from progenitor populations, the cells migrate towards the surrounding exocrine tissues. With the help of angiogenesis resulted by vascularization of islet’s arteriolar blood flow, specific cells present in the islet progenitors, beta cell progenitor, increase its differentiation phase, which consequently increases the number of beta cells present in the pancreas . As beta cells increase, the body’s glucose-perception also enhances considering the increased quantity of glucose sensing beta cells.The di fferentiated beta cells react against the decreased body insulin levels by producing insulin, which further stimulate beta cell’s massive proliferation in islets of langerhans . Upon stimulation of cellular differentiation under insulin deficient environment, islet transplant may significantly continue with its differentiation and regeneration schemes without the heightened danger of autoimmune attacks. This theoretical physiology can serve as the actual basis for considering the value of restoring stable beta cell count within the body.However, the conflict that needs resolution is the safety of islet grafts upon its initial stage of transplant. Differentiation of beta cells is the primary target of islet stem cell therapy among DMT1 patients. These cells are highly specialized cell type, phylogenetically developed, and regulators of glucose homeostasis in higher forms of organisms. However, some studies suggest (Montanya, 2004; Vinik, Rosenberg and Pittinger, 2004; Hermann, Margreiter and Hengster, 2007) the inverse relationship present between cellular proliferation and differentiation of islet implanted stem cells.The most common problem that arises during post-transplant phase is the decreased differentiation of beta cells, which, in some cases, are not enough to fill in the body’s insulin requirements . However, Dor, Brown and Martinez (2004) assert that Beta cells, during post-stem cell therapy, do not base the production of additional beta cells in the rate of differentiation; rather, beta-cells proliferate through the process of self-duplication .This is considered as an argument in the idea proposed in the latter section wherein it proposes the nullity in achieving cellular stability in both differentiation and regeneration once specific rate of beta cells are reached in the process. Although the proposed theory does not entirely in-distant with the latter, the argument suggests that beta cell proliferation solely derives from the pre-e xisting beta cells obtained via transplant, which further proliferates via the process of cellular regeneration and not entirely differentiation.As for the critique, cellular differentiation is regarded as of little importance due to its low contribution in cellular proliferation. According to Dor, Brown and Martinez (2004), â€Å"Our analysis shows that pre-existing beta-cells, rather than pluripotent stem cells, are the major source of new beta-cells during adult life and after pancreatectomy in mice†¦ These results suggest that terminally differentiated beta-cells retain a significant proliferative capacity in vivo and cast doubt on the idea that adult stem cells have a significant role in beta-cell replenishment. Xunrong, Hua and Soo (2005) support the argument through their study indicating the process of autoimmune blockage (Transforming Growth Factor-TGF-[beta]1) rather than the concept of cellular differentiation brought by stem-cell therapy . In the study, they have m ention the capacity of growth factors, such as TGF, to provide temporary autoimmune suppression that blocks the hazardous effects of this bodily responses.With increased angiogenesis or vascularization, the newly introduced cells (beta cells) can rapidly and freely proliferate as long as adequate oxygenation from rapid blood supply is present, and autoimmune suppression is being facilitated by the growth factors. According to Xunrong, Hua and Soo (2005), â€Å"Syngeneic islet grafts failed by day 17 in all untreated mice, whereas Ad-hTGF- [beta]1 therapy prolonged survival of islet grafts. Our data demonstrate that systemic TGF-[beta]1 gene therapy blocks islet destructive autoimmunity, facilitates islet regeneration, and cures diabetes in diabetic NOD mice†.TGF-[beta]1 possesses the functions of temporarily blocking the autoimmune response against the transplanted islet graft as well as triggering cellular regeneration channeled through self-duplication. Considering the argu ments propose by the two latter studies, this study still concludes the essential contributions of cellular differentiations brought by pre-existing progenitor cells from stem transplant or original sources; since, these component holds the appropriate physiological distribution of islet cell re-categorization and reproduction. 1. 2 Stem Cell TransplantationContrary to the concept of cellular differentiation and proliferation, post-stem cell transplant on islet cell is said to induce aggressive self-renewal due to the presence of significant growth components (e. g. TGF-[beta] 1, hemo-erythropoetin,etc. ) that enhance pre-existing beta cell proliferation and protect the cells from autoimmune attacks. Through the use of a DNA analog-based lineage-tracing technique , the study has found that precursor cells do not actually contribute to further differentiation of adult beta cells, and not even during acute beta cell regeneration.Rather, beta cells are being produced through self-renew al or duplication wherein a programmed cell division occurs through a refractory period preventing excessive or massive beta cell proliferation. Although, as argued by various studies (Lee, Grossman and Chong, 2008; Gershengorn, Anandwardhan and Wei, 2004), theoretically, differentiation rate usually surges during the initial phase of cellular implantation; however, once the cellular count of these differentiated cells stabilize, self-renewal or cellular regeneration of the existing beta or islet differentiated cells follow.Thus, explaining the inverse relationship between beta-cell proliferation and differentiation. Current studies in both allogeneic and xenogeneic stem cell sources are now being studied with marked emphasis on autoimmunity reversal or even autoimmunity tolerance. According to Lee, Grossman and Chong (2008), â€Å"stem cells from hematopoietic sources, such as bone marrow and fetal cord blood, pancreas, intestine, liver, and spleen, promise either new sources of i slets or may function as stimulators of islet regeneration†.Through stem cell introduction of pancreatic cells, specifically islets of langerhans, the adult human beta cells pre-existing in the stem cell transplant exhibit hormonal expression . Contrary to the concept of cellular proliferation, stem cell transplant essentially increases beta-cell resistance to autoimmune destruction of DMT1, which consequently facilitates the proliferation of beta cell in the islets of langerhans.According to various studies (Linning and Madkuhar, 2004; Strobel, Yuval and Stirman, et al. 006), aggressive beta cell self-duplication is the actual cause of beta cell proliferation whether by implantation of TGF-[beta] 1- induced islet cells or the traditional islet replacement. Implanted islet progenitors, when cultured, expresses 1% of endocrine cell proliferation during the first 48 hours up to 6% after five days . According to Rosenberg, Lipset and Yoon (2004), increasing the mass of beta cells after the event of post-immune destruction induces a 175-amino acid pancreatic acinar cell protein called, Islet Neogenesis-Associated Protein (INGAP) peptide, which acts as a stimulator of beta cell mass stimulator.INGAP peptide, similar to TGF-Beta growth factor, triggers cellular neogenesis enabling the rapid rate of cellular regeneration after significant results from cellular differentiation. The production of INGAP protein is commonly cited during post-phase of islet transplant. However, according to Lai, Irina and Eugen et al. (2008), gene modification present in cell transplantation process is problem considering the extensive cellular processes involved in the adaptation and transplant reception.Although, applications of several viral vectors (e. g. adenovirus-associated vectors, etc. have proven to be successful, but hESC is considered a more potent alternative due to its feasibility for genetic manipulation and self-renewal. During the mass replication of beta cells, the small portion of the cells stops in the process of neogenesis, while other beta cells are reserved for continuous replication at a very slow phase. After this scenario, the counter-attack of autoimmunity is usually expected; hence, treatment regimen that suppresses immunologic reaction on islet grafts are usually being instilled to the transplant sample prior to the therapy.This procedure increases the resistance of the graft cells against the autoimmune reactions triggered by the body. With a disorder such as DMT1, the chances of beta cell recovery become lesser due to the persistent autoimmune destruction of beta cells . The decreased capacity cellular replication in the adult beta cell is very much limited to result in a significant regeneration rate following autoimmune damages . Likewise, chronically increased metabolic requirements, such as increased insulin demand, can cause beta cells’ incapacity to fully cope in the given physiologic environment.This gives the appro priate rationale for implanting islet cells in the area of depleting beta cell in order for the progenitors to differentiate and proliferate mass beta cells in the area. According to the study of Urban, Kiss and Kovacs et al. (2008), hematopoetin centers of the body, such as bone marrow, may harbor cells that can actually influence the self-duplication of beta cells. Such concept is greatly associated to the principle of angiogenesis implying the value of appropriate oxygenation in the area of developing cellular clusters.In the study, sex-mismatched bone marrow cells (BMCs) and syngeneic or allogeneic MSCs are administered to a mice sample with streptozotocin induced DMT1, and consequently led to the rapid tissue regeneration after a single injection of a mixture of 10(6) BMCs per 10(5) MSCs. Other agents that can forcefully differentiate beta cells during post-islet transplant are INGAP (Rosenberg, Lipset and Yoon et al. , 2004; Weir, Toschi and Inanda et al. , 2004), GLP-1 and GL P-1 receptor agonist exendin-4 (Li et al. , 2004), betacellulin and activin A (Brubaker and Drucker, 2004), and the combination of EGF and Gastrin (Rooman and Bouwens, 2004) .These agents can actually force the cellular differentiation providing immediate and ensured processing new beta cells with much more lessened risks of being attacked by immunologic elements. Betacellulin, Activin A and Gastrin are the common immuno-suppressants being applied to most controlled studies on islet transplants today due to its availability and decreased result variations; although, some studies still explore the applicability and effectiveness of these agents in the process of triggering cellular differentiation.Meanwhile, Melleoul (2006) suggests that cellular differentiation of beta cell during post-islet transplant is controlled by series of genetic activators and transcription factors . Its absence in mice and humans during embryogenic to postnatal development may actually lead to pancreatic ag enesis. After such condition, cellular differentiation becomes restricted principally to ß cells wherein cellular regulation of genetic expression in ß cell-specific genes occurs.Furthermore, such condition facilitates the mediation of the glucose effect on insulin gene transcription, which shows that any exposure of ß cells to high glucose even with short period of time can actually stimulates insulin gene expression. However, chronic exposure to high glucose levels can actually trigger negative effects, such as alteration in ß-cell functions and gene transcription. PDX-1 transcription breaks down upon exposure to chronic hyperglycemia, while stimulation of beta activity is seen during acute hyperglycemia.Such genetic modifications can actually enhance the survivability of islet transplants within a new host considering the autoimmune function being rendered by continuous DMT1-induced CD4 immunoglobulins. According to Phillips and Tang (2008), using cellular, molecular and gene manipulation strategies, each islet transplant can actually be guarded or attain enhanced resistance even with the hostile environment directing immune rejection, inflammation, hypoxia and apoptosis.Genetic engineering provides cellular modification for constructing gene sequences. Considering the conflict existing in mass beta cell replication and autoimmune destruction, high quantities of beta cell replication during post-islet transplant has been associated to the reduced impact of autoimmune damage. With the help of CTL antagonists in terms of restricting T-cell activity, the regenerative capacity and neogenesis of ß-cells are expected to progress through forced-differentiation therapies.Initial activities between autoaggressive Cytotoxic T-lymphocytes (CTL) and beta cells are terminal event leading to cellular agenesis of ß-cell, which consequently affects both progenitor beta cells and those potential self-replicating beta cells from the pool of potential ß-c ell replenishment . Progression of CTL is unlikely to be stopped; hence, the only appropriate idea of treating the pathogenesis of DMT1 is the replenishment of beta cells that have been damaged throughout the ongoing autoimmune attacks.According to Dor (2006), progenitor cells present in the pancreas, specifically on pancreatic ducts, acini, islets of Langerhans, and other parts of the body (e. g. bone marrow, spleen, etc. ) are even more potent source of beta differentiation . However, these progenitor cells provide variable cellular differentiation rate that can compromise the process of stem cell therapy especially if the non-ideal progenitor cell source are used in the procedure.To compensate, most studies have explored the possibility of using embryonic-obtained stem cells that contain the most feasible progenitor cells aside from the ideal pancreatic progenitors. Although beta cells are differentiated from progenitor cells during embryonic phase of pancreatic development, the progenitors (marked by expression of neurogenin 3 and the paired box protein Pax-4) are seen to disappear upon birth . Such disappearance actually implicates a significant process that are undergoing with beta cells, which actually trigger fundamental change in their mode of maintenance and expansion.The cellular process begins from the embryonic progenitor-cell-based differentiation and further progress to massive self-regeneration. In the study of Nagaoka, Fukuda and Hashizume (2008), betacellulin (BTC) is analyzed as another potential growth factor that can induce progenitor-cell-based differentiation and cellular self-duplication. BTC possesses ErbB receptor tyrosine kinases that induces differentiation and cellular mitosis, especially among acinar-derived AR42J cells, transforming these cells into insulin-producing or beta functioning cells. As supported by Parnaud, Bosco and Berney et al. 2008), BTC-induced purified beta cells within allogeneic islet transplant graft enhanced by ECM have yielded a population of 91. 4 ±2. 8%. Nagaoka, Fukuda and Hashizume (2008) mention that BTC â€Å"independently and preferentially binds to two type I tyrosine kinase receptors, the EGF receptor (ErbB1) and ErbB4†. Significantly, BTC induced graft transplants are seen to contain mutant protein that promotes the rapid differentiation of pancreatic acinar AR42J cells to insulin-producing cells, which is actually the opposite with AR42J cells that contain wild-type BTC protein.Rapid differentiation is not entirely beneficial in nature as this can cause hyperplasia. According to Min Cho, Lim and Yoo et al. (2008), BTC, together with Nicotinamide sustained PDX1 expressions, actually induced cellular differentiation C-peptide proteins; although, insulin mRNA is found to be very low. 4. New Advances in Stem Cell Research The theory between stem cell differentiations versus beta cell progenitor self-duplication still coincide the need to restore pre-existing beta cell p ool from the ongoing damage made by the autoimmune CTL.Stem cell is still an important consideration in replenishing these depleted resources. However, due to the extensive problem on stem cell donors and sources, stem cell therapy is not yet considered part of an ideal DMT1 treatment. According to Korsgren, Lundgren and Felldin (2008), new alternatives for stem cell therapy are currently being explored with aims of determining other contributing components that induce cellular graft survivability and reduction of immunoresponse against DMT1 mediated antibodies.During the process of transplantation, the isolated islets transplant grafts are induced to embolise the liver after its introduction via the hepatic portal vein, which is a procedure that is unique in the area of stem cell implantation. However, such procedure is only an example of low efficacy procedure. A novel view on the engraftment of intraportally transplanted islets is presented that could explain the low efficacy of the procedure. As supported by Rother and Harlan (2004), and Hardikar (2004), only 750 patients have already been treated using allogeneic islet transplants since 1974 despite of the billions of DMT1 cases worldwide.Various alternatives have been proposed in order to counter such scarcity, specifically: (1) embryogenic blastocyst and post-natal resources, (2) culturing of stem cells, and (3) stem cell grafting using xenogeneic resource (e. g. umbilical cord, etc). The isolation of human embryonic stem (hES) cells has been introduced as a potential prospect for filling in the scarcity of beta cells, specifically through islet transplantation . Embryonic stem cells are harvested from blastocysts, while adult stem cells are from postnatal organisms.The process involves (1) the culturing and plating of embryoid bodies in insulin-transferrin-selenium-fibronectin medium, (2) supplementation and maintenance using N2, B27, and basic fibroblast growth factor (bFGF), (3) lowering of glucose c oncentration to reduce the physiological pressure on premature beta cell, (4) bFGF is withdrawn to prevent excessive growth stimulation, and (5) nicotinamide addition . Counteracting transcription-polymerase chain reaction found out an enhanced cellular expression of pancreatic genetic chains within the site of cellular differentiated cells.Using the Immunofluorescence and in situ hybridization analysis, the findings have revealed a significantly increased percentile range of insulin-expressing cells within the cellular clusters. According to the study of Xia, Ayala and Thiede et al. (2008), hESCs, with the help of drug-inducing transgene expression (in vitro and in vivo) forms >95% purity level, which significantly implies the high possibility of regulating genetic expression of hESCs. After the islet transplantation, genetic expression of the cells remained stable and regulated with the help of an orally administered drug.Although, according to Chung and Stainer (2008), cellular o rigins that regulate pancreatic B cell induction and genetic expression is not yet fully understood. Differentiation of embryonic stem (ES) cells to islet phenotype, identification and utilization of pancreatic precursor/stem cell from adult sources, and the cultivation of new islets from adult stem cells obtained from various tissue types or directly form other terminally differentiated cell types are the common areas being covered by islet transplant or stem cell research for DMT1 immunogenetics research .In such case, cultured embryogenic or adult somatic islet cells are transferred from its original placement to appropriate locations in the body of a DMT1 patient. Human Embryonic Stem Cell (HESCs) or ES possesses the capacity to continuously differentiate to cells that express both endoderm and pancreatic progenitor function, such as Foxa2, Sox17, Pdx1, and some islet endocrine hormones (e. g. beta cells) . According to Kroon, Martinson and Kadoya et al (2008), cellular therapy for DMT1 requires the renewal of human beta cells and not entirely the replacement of the degraded ones.In order to induce regeneration, pancreatic endoderm must be stimulated through the use cellular mediated glucose-responsive endocrine cells present within hESCs. The hESC-derived insulin-producing islet-like clusters (ILCs) comprises of 2 to 8% of human C-peptide-positive cells, glucagon-positive and somatostatin-positive cells. The study has detected a content of 70 ng of insulin/mug of DNA being produced through these hESC-derived ILCs, which is statistically higher than the innate fetal islets.In addition, cellular differentiation of hESCs induces the formation of Embryoid Bodies (EBs) that stimulate the gene expressions of POU5F1, nestin, FOXA2, ONECUT1, NEUROD1, PAX6, and insulin as long as the glucose environment is within 25mM levels . In the essence, implantation of hESCs in autoimmune-damaged islets can mobilize the islet cell differentiation through genetically expresse d progenitors from the islet transplant medium. Furthermore, continuous genetic expression is expected since the body’s glucose levels also influence the cellular differentiation of beta cells.Stem cells derived from hESCs places markers of development for endoderm, pancreatic and ß-cell development, glucose sensing, and production of mature insulin . Meanwhile, most studies have also centered in protein-based cellular communication involved during cellular differentiation phase after stem cell implants have been introduced. According to Kroon, Martinson and Kadoya (2008), therapeutic tests using a mice sample with 3000 transplanted human islet cells indicate that hESC derived pancreatic endoderm can actually aid in antibody resistance.In the study’s conclusion, they have pointed the definitive evidence proving the capacity of hESCs in generating glucose-responsive and insulin secreting implanted cells. Interestingly, in the study of Yu, Vodyanik and Smuga-Otto et a l (200), hESCs are found to be programmed by specific four genes, OCT4, SOX2, NANOG, and LIN28, which actually determines the pluripotent capacity of the embryonic stem cells and the characteristic of cellular differentiation. Although, the study concludes that the genetic mapping and processes involved within these newly discovered hESC genes are still in the process of intensive studies.Implanted stem cells actually integrate their needed functions for initiating the mechanism of glucose responsive regulation present as pre-proinsulin mRNA and expression of insulin C-peptide in vitro (Clark, Yochem and Axelman, 2007). Following transplantation into mice, cells become insulin and C-peptide immunoreactive and produce plasma C-peptide in response to glucose. The results of the study suggest that embryonic germ cell derivatives (e. g. ILCs, etc. ) may eventually function as a potent insulin producing cells .The use of islet-derived or stem cell therapy using embryonic cells remain exp erimental due to the challenges of cellular differentiation. Currently, the problems being faced by the treatment is the availability of stem cells that can possess the appropriate capacity to induce cellular differentiation and regeneration. According to the mentioned studies, simple cellular implantation is not entirely enough due to the greater risks imposed by the body’s physiological reaction against islet grafts.Hence, another issue arises in determining the best anti-immunity function or tolerance enhancer of islet graft transplants; although, latter studies have already discovered potential enhancers that can disregard or at least lessen the impact of cellular degradation brought by DMT1 immunity. Lastly, new advances of genetic modification techniques that shall increase cellular differentiation and renewal rates are already in the process of development. 5. Discussion In the research of Froud, Ricordi and Baidal, islet stem cells are cultured under steroid-free immu nosuppression and are transplanted to 16 DMT1 samples.The cultured islet stem cells have undergone a period of in vitro culture-process with heightened necrosis resistance through TNF- a (Tumor Necrosis Factor) blockade that aim to improve islet engraftment and provide alternative to fresh human islet transportation. The results of the study suggest that the implantation of cultured human islet allografts cause a reproducible insulin independence in all subjects under the series immunosuppressant infusions (a. intial Infliximab infusion, b. daclizumab and c. irolimus maintenance), comparable to that of freshly transplanted islets (Edmonton protocol) .In the absence of supplemental infusions (nfliximab, daclizumab and sirolimus), the results of the study have incurred 11/14 (79%) subjects that produced insulin independence at 1 year, while other 6/14 (43%) samples have gained this capacity after 18 months. Surprisingly, the same test subjects have maintained their insulin independenc e until 33  ± 6 month span. Furthermore, the findings have observed that patients are able to maintain their graft function while under the immunosuppressing infusions.According to the results, 8 out of 14 patients have suffered chronic partial graft losses that are likely immunological in nature considering that 5 of these already received supplemental infusions. Currently, 11 out of 14 subjects are in the receiving immunosuppressing infusions, and 8 (73%) of these are already manifesting insulin independence. The study significantly demonstrates the possibility of withholding the immunologic response upon exposure to certain immunosuppressant (e. g. nfliximab, daclizumab and sirolimus, etc. ).Although, the study has not mentioned the possible side effects and complications that such infusion can provide towards the body as a whole. However, since the stem cells are the only ones infused with these immunosuppressants, the chances of systemic immunosuppression are less likely as l ong as the dosage infused with the stem cells remain appropriate and feasible to the body’s normal function. In another culture study brought by Pinzon, Lakey and Brand (2005), they have used the combination of epidermal growth factor (EFG) and gastrin in order to induce beta cell neogenesis specifically on pancreatic exocrine duct cells .These growth factors also carry the risk of triggering extensive cellular neoplasia over-cellular multiplication; although, studies have already found drug induced techniques that can contain the cellular differentiation and regeneration upon introduction within the body system. In the study, human islet cells are placed under four weeks culture study in a serum-free medium with EGF (0. 3  µg/ml) as the control variable and gastrin content of 1. 0  µg/ml.Beta cells have shown significant increase in cultures with the combined medium of EGF and gastrin (+118%), while +81% for cultures with EGF alone. The EGF-gastrin culture has been obser ved again for the next four weeks, but without the said combination. Impressive results have shown beta cells progressive increase in quantity for the culture previously infused with both EGF and gastrin (+232%). Comparing these results from the latter discussed studies, EGF and gastrin have actually trigger cellular differentiation and self-duplication due to their growth factor properties.In the study of Suarez-Pinzon and Rabinovitch (2008), gastrin growth factor combined with epidermal growth factor (EGF) can actually restore pancreatic islet beta-cell mass and even reverse hyperglycemia even in the absence of immunotherapy in mice samples with artificially induced-DMT1. Reversal of hyperglycemia is most likely due to the increase in insulin production that counters the effects of DMS1. With the appropriate amounts of insulin secretion in the blood, the glucose tonicity will consequently be absorbed by the cells granted that the diabetic anomaly does not consider the insulin rece ptor functionalities within cellular surfaces.In the study, EGF dose of 10 microg/kg and gastrin dose of 30 microg/kg via intraperitoneally have been administered to 10 sample DMT1 mice. In terms of glucose levels, the samples have shown a marked decline from blood glucose of 23 +/- 2 mmol/L to 12 mmol/L within 36 days of individual EGF administration, while 19 days in individual gastrin administration. When combined, the decline in the samples’ glucose levels is already present within 11 days.In addition, the cellular islet counts have increased from 13. 0 +/- 0. x 10(5) cells to 29 +/- 2 x 10(5)cells, and considering the marked decrease of surrounding CD45+ leukocytes have also been observed. Therefore, such combination (EGF plus Gastrin) is confirmed to reduce blood glucose levels, prevent autoimmune activity of DMT1 mediated CD4 cells and increase cellular differentiation. Lastly, aside from hESC’s and cultured islet transplants, another potential source of stem ce lls currently being studied is from animals, known as xenogeneic sources . Pig islets are considered the best option available for xenogeneic transplants.According to Rother and Harlan (2004), such potential alternative are now being studied for different considered potentials, such as: Pig islets have been considered as potential source of islet stem cells aside from human source (a) The fact that humans had been treated with pig insulin for more than 60 years (b) Favorable husbandry — in that the species has large litters with offspring that attain adult size rapidly and with relatively robust islet numbers (c) The fact that pig islets respond to glucose in the same physiological glucose range as human islets (d) Existence of suitable societal-cultural relationship between the speciesDespite of the potential capacity of pig islets in acting as alternative stem cell resource, studies (Hering, Wijkstrom and Graham et al. , 2006; Rood, Buhler and Bottino, 2006) have identified its increased immuno-response towards CTL and autoimmune attacks initiated by DMT1 disease. Autoimmune attacks are the principal conflict considered in the process of islet transplantation wherein even if the graft has been successfully implanted, the risk of failure in the procedure is still considered possible considering the effects of autoimmunity triggered by increased antigenicity in the graft transplant.In one study, acute rejection caused the death of two macaque samples through cellular rejection mediated by CD4+ and CD*+ T cells and macrophages . In order to increase the effectiveness of xenografts after post-transplant phase, different culture infusions have been studied to prolong the life of pig islets xenografts. CD4 antibodies are usually being activated upon detecting significant system foreign antigens, which are usually introduced by bacteria, virus or any material that enters the body systems.In this principle, researchers (Kirchhof, Shibata and Wikkstrom et al. 004) have pointed their assumptions in the possible presence of antigens within xenotransplanted islet grafts. In addition, cellular infusions are considered to be at great risk due to the potential intrusion of incompatible antigens that might induce transplant rejection, and eventually autoimmune degradation of transplanted islet cells in the body. This condition is currently under extensive analysis and consideration since even with successful islet transplant, autoimmune response due to heightened cellular antigenicity can still pose the failure of the stem cell therapy.Due to this genetic dilemma, some studies (Kirchhof, Shibata and Wikkstrom et al. 2004; Komoda, S. Miyagawa and T. Omori et al. , 2004) have focused in determining the potential drug enhancers that can improve transplant antigenicity, especially among xenogeneic sources. First, with the infusion of islets from N-acetylglucosaminyltransferase-III (GnT-III) transgenic pigs, pig islet’s xenoantigenicity have significantly declined prolonging the survival of islets for the next five days of culture study. In another study, pig islets subjected for xenotransplantation are tested with alginate encapsulation.The transplant to tested in a primate, specifically a monkey-Cynomolgus maccacus . Adult pig islets encapsulated in alginate under optimal conditions (n=7) or not (n=5) are transplanted under the kidney capsule of the non-diabetic primate sample. Meanwhile, additional samples have received empty capsules (n=1) and non-encapsulated pig islets (n=2) as controls . The results of the study show the rapid inviability of non-encapsulated and encapsulated islets with no alginate and not in optimal condition.Implanted pig islets under optimum alginate encapsulation showing significant prolonged islet survival for as long as six months. However, despite of the experimental success, the study still regards the conflicts encountered by the processes (e. g. variations of graft antigenicity, etc). 6 . Conclusion DMT1 is a condition manifested by increased and frequent manifestations of hyperglycemia caused by the insufficient production or depleted insulin levels. The most universally recognized cause of beta cell destruction is the autoimmune etiology caused by CD4 interleukins, and other associate antibodies.The aims of the therapy are the induction of cellular differentiation while facilitating as well the renewal of the existing and pre-existing beta cells in the islet graft transplant or in the remaining original islets. However, the principal conflict of the procedure is the interference caused by the autoimmune reaction of the body towards the transplanted islet grafts; although, recent studies have continuously explored different possibilities of suppressing autoimmune responses and forcing cellular activities.Stem cell therapy is a potential prospect for permanently treating the condition of DMT1 considering the main concept involved in its pathogenesis – destru ction of beta cell or insulin producing cells. The processes, physiology and pathological considerations in the stem cell therapy of islet transplant involve the criticality of autoimmune response towards the islet transplant.The controversy of such treatment is the effectiveness of implanting whether the islet cells containing stem cells based on the concept of cellular differentiation or islet cells with pre-existing beta cells based on the concept of cellular self-renewal. Despite of the argument between the two perspectives involve, another main issue arises, specifically the scarcity of stem cell from allogeneic donors. According to the approximated statistics, only 750 cased of DMT1 have successfully obtained the stem cell transplant of islet cells considering the billions of other DMT1 patients existing.In order to resolve such scarcity, various forms of stem cell resources have been proposed and are currently under extensive studies, specifically (1) human embryonic stem cel ls, (2) cultured islet stem cells, and (3) xenogeneic sources specifically the pig islet stem cells. According to most studies, autoimmune damage progress if cell count of beta cells is introduced insufficiently to the recipient body; although, stem cell therapy is nearing towards its potential of being a significant cure as beta cell replacement and insulin producer.

Decision Analysis Task 2 Essay - 897 Words

Shuzworld Task 2 Charlene Taylor WGU 000345193 Shuzworld Task 2 I was asked to provide a distribution pattern that minimizes shipping costs and provides adequate availability and demand. I used transportation modeling to solve this problem. Transportation modeling is â€Å"an interactive procedure that finds the least costly means of moving products from a series of sources to a series of destinations† (Heizer Render, 2011). This tool is used to determine the best distribution pattern for multiple locations. It is best for this problem because it allows for us to determine how many products can be held at each location to give Shuzworld the lowest shipping costs. The original setup had an optimal shipping cost of $13,600. It had 1300†¦show more content†¦Machine 1 had a reliability of 84%, Machine 2’s reliability was 91%, and Machine 3 had a reliability of 99%. The first possible setup, and ultimately the recommended setup, was to backup Machine 1. This led to an overall reliability of 84%. Backing up Machine 2 on ly gave a reliability of 82%. Backing up Machine 3 only gave a reliability of 76%. Therefore the recommendation is to backup Machine 1 and increase the reliability to 88%. The next task is to provide the optimum number of shoelaces to order, using appropriate cost balancing. The economic order quantity (EOQ) is the order amount that allows for an optimum level of materials at the lowest cost possible. There is a demand ofr 300,000 shoelaces per year. The setup cost is $125 per order. There is a $.10 holding cost per unit. The optimal order quantity recommended is 27,386.13 shoelaces per order, with a maximum inventory of 27,386.13. This means that we will order just the amount of shoelaces needed to fulfill current production orders. The average inventory is 13,693.06 shoelaces. There will be approximately 10.95 orders per year. The annual setup cost is $1,369.31, and the annual holding cost is $1,369.31. 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