A lead frame is formed by subjecting a frame base to a forming process, a semiconductor chip is fixed on leads formed in the lead frame and wires are provided in the semiconductor chip, and then a package which accommodates the semiconductor chip is formed; a non-conductive adhesive being provided, before the forming process, on a position on the frame base in which the leads are formed, and unnecessary portions of the frame base and the non-conductive adhesive being removed in the forming process so that the leads having a predetermined configuration and provided with the non-conductive adhesive are formed.

1. Field of the Invention
The present invention generally relates to a method of fabricating a semiconductor device and, more particularly, to a method of fabricating a semiconductor device having a Lead On Chip (LOC) construction.
Recently, in association with the high performance and high density of semiconductor devices, the chip size of a semiconductor device is increasing. Therefore, a significantly high level of fabrication technology is required in order to meet a demand for a small package size.
In this background, a semiconductor device having a Lead On Chip (LOC) construction is proposed. In a LOC semiconductor device, leads are provided on a semiconductor chip. Since such a construction allows the leads to overlap the semiconductor device in a top view, the size of a semiconductor device can be reduced.
In the semiconductor device having the LOC construction, the semiconductor chip is fixed on the leads using an adhesive. Thus, it is necessary to apply the adhesive to the leads with precision.
A second aspect of the semiconductor device having the LOC construction is that, as semiconductor devices are built with increasingly high density of constituting elements, increasingly minute formation of a circuit on the semiconductor chip is required. Accordingly, that area (hereinafter, referred to as a circuit area) on the semiconductor chip on which a circuit is formed is exposed to effects such as an external stress.
this reason, a protective film is formed on a circuit area of the semiconductor chip. For proper protection of the circuit area, a high-quality protective film forming technology is required.
2. Description of the Related Art
Conventionally, the fabrication method described below has been employed to manufacture a semiconductor device having the LOC construction.
First, a lead frame having leads is produced by blanking such that a flat base formed of a material suitable for a lead frame is cut appropriately. Subsequently, a non-conductive adhesive which also serves as a protective film is provided on leads formed in the lead frame. The semiconductor chip is secured on the leads using the non-conductive adhesive. Wiring is then done according to a predetermined design, a package is produced and the semiconductor chip is sealed. This completes a process for fabricating a semiconductor device.
Two methods described below have generally been used to provide the non-conductive adhesive on the leads.
One of the methods is film pasting. FIG. 1A shows a sheet of adhesive film 1 (protective film) formed of a non-conductive adhesive. As shown in FIG. 1B, the adhesive film 1 is die-cut to a predetermined size that corresponds to an area of a lead frame.
In a process separate from the process of cutting the adhesive film 1, a lead frame 2 having leads 3 is produced by blanking such that a base is cut appropriately. As shown in FIG. 2, the cut adhesive film 1 is fitted adhesively on the leads 3 of the lead frame 2. As a result of the process described above, the adhesive film 1 is properly provided on the leads 3.
The other of the methods that have generally been used to provide the non-conductive adhesive on the leads is printing. In the printing of the non-conductive adhesive, the lead frame 2 having the leads 3 is first produced by blanking such that a base is cut to an appropriate size. Subsequently, a mask 4 is provided on the lead frame 2 having the leads 3, whereupon, as shown in FIG. 3, a non-conductive adhesive 6 (hereinafter, simply referred to as an adhesive) which also serves as a protective film is printed on the lead frame 2 using a squeegee 5.
As shown in FIG. 4, openings 7 are formed in the mask 4 at positions that correspond to the positions of the leads 3. Accordingly, as shown in FIG. 5, by printing the adhesive 6 using the mask 4, the adhesive 6 is properly provided on the leads 3.
While FIGS. 1 through 5 show the non-conductive adhesive 6 provided on the leads 3, it is also possible to provide the non-conductive adhesive (protective film) 6 on the semiconductor chip.
FIGS. 6 and 7 show how a protective film 6b is provided on a semiconductor chip 8; and FIG. 8 shows a semiconductor device 9 fabricated by the method of FIGS. 6 and 7. In FIGS. 6 through 8, those components that correspond to the components of FIGS. 1 through 5 are designated by the same reference numerals.
The printing method as described with reference to FIG. 3 is employed in order to provide the protective film 6b on the semiconductor chip 8. In this printing method, the mask 4 is provided on the semiconductor chip 8 (which may be in a wafer state). Subsequently, as shown in FIG. 6, a protective film material 6a which forms the protective film 6b is printed on the semiconductor chip 8 using the squeegee 5.
The openings 7 are formed on the mask 4 at positions that correspond to a circuit area formed on the upper surface of the semiconductor chip 8. Therefore, as shown in FIG. 7, by printing the protective film material 6a using the mask 4 and then causing the protective film material 6a to be hardened, the protective film 6b is formed on the circuit area on the semiconductor chip 8.
As shown in FIG. 8, the semiconductor device 9 fabricated by the method of FIGS. 6 and 7 is constructed such that the semiconductor chip 8 is encapsulated in a resin package 9a. Generally, a filler is mixed in the resin package 9a.
If the protective film 6b is not formed on the semiconductor chip 8, the filler collides against the circuit area on the semiconductor chip 8, when the package is formed, thus causing a damage on the circuit formed by the microfabrication technology. Provision of the protective film 6b ensures that the circuit area on the semiconductor chip 8 is protected and prevents an unfavorable effect caused by the filler from occurring.
However, in the film pasting described above, a plurality of dies for die-cutting the adhesive film 1 are required because the adhesive films 1 having different shapes should be prepared for different lead patterns formed in the lead frame. Therefore, the film pasting method has a drawback in that it is not a general-purpose method and the cost of dies is relatively high.
When the adhesive film 1 is die-cut, waste adhesive films are produced however efficient the die-cutting process may be. The adhesive film 1 is formed of a polyimide and is relatively expensive. Therefore, wasting of the adhesive film 1 causes the cost of the product to increase.
In the printing method, the mask 4 is required for each of the lead patterns. Further, the printing method has a drawback in that, in case the lead pattern is complex or has a small pitch, bridging of the adhesive 6 or invasion thereof into the back of a lead may occur, thus preventing a subsequent wiring process and a package forming process from being performed properly.
Still another problem with the conventional printing method is that it is necessary to apply a pressure on the squeegee 5 while it is being moved on the mask 4. A pressure from the squeegee 5 is transmitted to the semiconductor chip 8. Therefore, the circuit area on the semiconductor chip 8 is scraped by the squeegee 5 via the mask 4, thus causing a stress to be built up in the circuit area. As a result, the circuit surface may be damaged even before the non-conductive adhesive 6 or the protective film 6b is formed.
Another problem with the semiconductor device having the LOC construction fabricated by the conventional method is that, since the leads 3 are provided above the circuit area, the leads 3 may come in contact with the circuit area when the leads 3 are joined with the semiconductor chip 8, thus causing a damage on the circuit area.

Method of fabricating a semiconductor device


The display device includes a display portion having a cavity portion surrounded by wall surfaces, at least one part of the wall surfaces being formed of a transparent member and forming a structural color forming surface provided with fine asperities having predetermined regularity, a liquid being hermetically sealed to have a liquid surface in the cavity portion and having a refractive index approximately equivalent to that of the transparent member, an actuator giving a disturbance to the liquid to bring the liquid into contact with the forming surface and a control unit controlling driving of the actuator to switch reflection and transmission characteristics of light when the light is incident into the forming surface, thereby controlling color display using reflected light formed by the forming surface.

The present invention relates to a display device, an image display device and an image display method, and more particularly to a display device, an image display device and a display method used for a thin image display device such as a flat panel display.
Heretofore, a liquid crystal display (LCD) device has been widely used as an image display device of an information terminal apparatus such as a personal computer or a portable information terminal (personal digital assistance: PDA) or of a car navigation system. While a liquid crystal display device using TFTs has advantages in that response speed thereof is fast and it can display a clear multicolor moving picture, the liquid crystal display device has disadvantages in that power consumption thereof is high, electric power is required for maintaining an image, a viewing angle thereof is narrow, and so on, because the liquid crystal display device requires an illumination light source such as a backlight and light utilization efficiency of the illumination light source is also low.
Therefore, image display devices according to various methods have been proposed as replacements of the liquid crystal display device. For example, a display device which switches ON/OFF of image display by use of a film boiling phenomenon of liquid has been proposed (for example, refer to JP 05-127603 A and JP 05-127604 A). Moreover, a display device which switches ON/OFF of image display in the manner in which ink is moved by use of electrocapillarity has also been proposed (for example, refer to JP 10-039799 A).
Furthermore, there has also been proposed a display device which switches ON/OFF of image display in the manner in which ink is loaded/unloaded to/from an image display unit by thermally expanding and shrinking ink in segments or mechanically driving diaphragms (for example, refer to JP 2001-042794 A). Still further, there has also been proposed a display device which switches ON/OFF of image display in the manner in which ink is moved by use of electrostatic force (for example, refer to JP 08-254962 A).
However, in each of the image display devices utilizing the film boiling phenomenon of fluid, which are disclosed in JP 05-127603 A and JP 05-127604, when color display is attempted, it is necessary to spread the respective cells of red (R), green (G), and blue (B) or the respective cells of cyan (C), magenta (M), and yellow (Y) in a horizontal direction. Accordingly, each of the image display devices has problems in that the light utilization efficiency is in principle poor and in that contrast of the device is low. Moreover, in the display device disclosed in JP 10-039799 A, the respective types of ink, which correspond to red (R), green (G), and blue (B), are compounded in the same cell, and accordingly, the light utilization efficiency is improved. However, the device involves a problem in that it is difficult to let a desired color come out after rewriting because it is difficult to separate the image into the three colors when the image display is turned off.
Furthermore, according to such a method of thermally expanding or shrinking ink, which is disclosed in JP 2001-042794 A, a thermal expansion coefficient of the ink is low, and accordingly, a volume change of the ink is as small as approximately 2% even if the ink is heated up to 300 K to 350 K. Therefore, when one attempts to secure a predetermined volume change, a considerably large reservoir tank with respect to a volume of the image display unit is necessary, leading to a problem of upsizing of the device. Moreover, according to such a method of mechanically driving the diaphragms, the structure of the device becomes complicated, leading to a problem in that downsizing of the device is inhibited. Furthermore, in the display device disclosed in JP 08-254962 A, the respective color cells corresponding to cyan (C), magenta (M), and yellow (Y) form a stacked structure. Accordingly, in order to set a certain color in a non-display state, ink corresponding to the color must be moved under the other cell. Therefore, there arise a problem of the deterioration of image quality due to step differences occurring in an array of the cells, and a problem of the movement of ink taking a long time and hence low responsiveness.

Display device, image display device and display method


This invention is a synchronization abstraction layer (SAL) providing a uniform interface to frameworks operating on sequenced flow data. It allows content developers to design and build interactive content that will operate interchangeably in different multimedia frameworks (e.g., Apple Computer, Inc.'s QuickTime™, Microsoft Corporation's NetShow™, RealNetworks, Inc.'s RealPlayer™, Sun Microsystems, Inc.'s Java™ Media Framework) and on different hardware platforms (e.g., desktop PC, Macintosh™, Television set-top boxes such as those from General Instrument Corporation and Scientific Atlanta Inc., Inc., Internet appliances such as AOL™-TV, and other appliances, e.g., a kitchen Internet radio). The uniform interface is independent of the particular framework and the platform on which the SAL is implemented, so that a single instance of content, whether created in Java™, JavaScript, VBscript, HTML, XML, or some other language, can run appropriately on different hardware, e.g., on a Television set-top and on a desktop PC.

Multimedia player frameworks have become widespread. Later versions of the most popular Internet browsers—Microsoft's Internet Explorer and Netscape's Communicator—include at least one player in the basic package. These are frameworks such as RealNetworks, Inc.'s RealPlayer™ G2 family (collectively, the "RealPlayer™"); Microsoft Corporation's Windows Media Technologies (NetShow™); Macromedia, Inc.'s Director™; Apple Computer, Inc.'s QuickTime™; and Sun Microsystems, Inc.'s Java™ Media Framework (JMF). Most of these frameworks are extensible by means of plug-ins discussed below; some, notably JMF, are extensible by means of applications built on top of the frameworks. By being extensible we mean that a particular framework supports a set of interfaces exposed for interaction with additional software modules or components.
A framework is a set of interfaces, e.g., API's and procedures, and a set of capabilities exposed for the purposes of extensibility. It need not operate on multimedia-type files, i.e., files ordered sequentially and supporting the concept of a time-line; frameworks generally need not operate on time- or otherwise-ordered data files. In the rest of this document, however, we will discuss predominantly frameworks operating on ordered data flow files. We will refer to such frameworks interchangeably as "frameworks," "extensible frameworks," "extensible data flow-based frameworks," or by similar expressions; we do not imply any difference in the particular designation used, unless otherwise indicated.
Frameworks are extended by means of extensions, for example plug-ins. Plug-ins, also referred to as extension modules, are modules or components dynamically loaded at run-time. Extensible architecture and plug-ins have been used in commercial products, the RealPlayer™ and Windows Media Technologies being two instances. They also have been described in various publications. See U.S. Pat. Nos. 5,838,906 and 5,870,559. (The specifications of these patents are incorporated by reference as if fully set forth herein.) A number of companies market plug-ins specifically for extending multimedia players.

This patent is subject to a terminal disclaimer.

Cross-platform framework-independent synchronization abstraction layer

Abstract: In one realization, the synchronization abstraction layer provides a Java™ VIRTUAL MACHINE (JVM) interface for running Java™ plug-ins for streaming media applications such as Real Networks, Inc.'s RealPlayer™, Microsoft Corporation's Windows Media Technologies (NetShow™), Apple Computer, Inc.'s QuickTime™, Sun Microsystems, Inc.'s Java™ Media Framework. The JVM interface allows third-party developers to design platform- and framework-independent plug-ins for streaming media applications.

Abstract: This invention allows content providers to use plug-ins or compatible software objects (such as Java™ applets) to build, for example, interactive streaming media content that is fully interactive but independent of the particular underlying hardware and software technologies, such as RealNetworks™ G2, Microsoft Corporation's NetShow™, a desktop PC, or a television.


Disk players for allocating pointers to the respective frames of CD data and storing the pointers in a memory, and methods of processing reproduced data of the disk player are provided. According to one aspect, a disk player includes a pointer controller, which allocates pointers to frames of recorded data read from a disk, wherein the allocation of the pointers starts from a first frame following frames having special sub-code synchronization signals and is performed in a predetermined order; a memory, which stores the frames and the allocated pointers; and a memory controller, which controls an operation of writing the data to memory. A pointer is allocated to every frame of the recorded data reproduced from the disk player, and the allocated pointers and the frame data are stored in the memory. The pointers are retrieved and the respective frame data stored in the memory are output. Therefore, the sound continuity can be maintained even in a vibration environment causing jitter.

1. Field of the Invention
The present invention relates, generally, to a disk player, and more particularly, to a disk player for allocating pointers to respective frames of CD data and storing the pointers in a memory to reproduce the CD data even in a jitter environment, and methods of processing reproduced data of the disk player.
2. Description of the Related Art
In a Compact disk (CD) player, when so-called "track jumping" occurs due to an external impact causing vibration during the disk reproduction, it is important to prevent "sound discontinuity" by ensuring continuity of PCM data. Track jumping means that a light spot of a pickup unit, which reads recorded information by tracing tracks on the disk, deviates from the tracks.
FIG. 1 is a schematic of a conventional CD player. Referring to FIG. 1, a disk 1 is driven by a spindle motor 2. The recorded information of the disk 1 is read by an optical pickup unit 3. The optical pickup unit 3 comprises an object lens 5 for focusing a laser beam as an information-read-out light spot on a signal plane of the disk 1, a polarizing beam splitter 6 for changing a direction of a reflected light beam from the disk 1, and a photo detector 7 for receiving the reflected light beam. The optical pickup unit 3 is arranged to move in a radial direction. An output current signal of the optical pickup unit 3 is converted to a voltage signal by an I/V amplifier 8. The voltage signal is subjected to a waveform-shaping process in an RF equalizer circuit 9, and then, the signal is processed by a DSP circuit 10.
The DSP circuit 10 comprises a PLL asymmetry correction circuit 11, an EFM (eight-to-fourteen modulation) demodulation circuit 12, a sub-code processing circuit 13, a RAM 14, an error correction circuit 15, a de-interleave circuit 16, a spindle servo processing unit 18, and a clock signal generator 17. The PLL asymmetry correction circuit 11 corrects a deviation of the RF signal center from the amplitude center. The EFM signal demodulation circuit 12 demodulates an EFM signal, the sub-code synchronization signal SCOR, and a sub-code signal. The demodulated sub-code signal is sent through the sub-code processing circuit 13 to a microcomputer 20, which has overall control over the system. After the EFM demodulation, the PCM data is temporarily stored in the RAM 14. The error correction circuit 15 performs an error correction based on the error correction/detection parity of the PCM data. The interleave of a CIRC (cross interleave Reed-Solomon code) is released by the de-interleave circuit 16. The clock signal generator 17 generates a system clock signal based on an oscillation output of a quartz oscillator 21, so that the DSP circuit 10 can process signals based on the system clock signal.
In the RAM 14, a reproducing clock signal, which is generated by the PLL asymmetry correction circuit 11, is used as a write-in clock signal WFCK and the system clock signal is used as a read-out clock signal RFCK. The PCM data, which is processed by the DSP circuit 10, is stored in a large capacity DRAM 23 through an ESP (electric shock proof) controller 22. The PCM data, which is stored in the DRAM 23, is read by the ESP controller 22, subjected to a filtering process in a digital filter 24 and an analog process in a D/A (digital-to-analog) converter 25, and then, output as an audio signal through left and right channels.
The DRAM 23 is used to ensure continuity of PCM data to prevent the sound discontinuity when track jumping occurs due to an external impact causing vibration during the disk reproduction. When track jumping occurs, the information-read-out light spot of the optical pickup unit 3 is returned to the point just before the occurrence of track jumping and reproduction is carried out at this point, under the control of the microcomputer 20. In addition, the PCM data stored in the DRAM 23 just before the occurrence of track jumping is linked to the PCM data obtained after reproduction under the control of the ESP controller 22.
Since the sound continuity process is carried out in units of a sub-code frame, wow, which is a variation in the pitch of the music caused by, e.g., some mechanical flaw, of the spindle motor 2 is removed in the reproducing sub-code synchronization signal SCOR to maintain the sound continuity in the time axis. The ESP controller 22 further comprises a sub-code synchronization signal generation circuit for generating a sub-code synchronization signal SCOR in which the wow of the spindle motor 22 is removed, as shown in FIG. 2.
FIG. 2 is a diagram illustrating a sub-code synchronization signal generation circuit of the conventional CD player of FIG. 1. Referring to FIG. 2, a jitter counter 28 measures the value of jitter of the write-in clock signal WFCK with reference to the read-out clock signal RFCK. The write-in clock signal WFCK is a reproduced clock signal from the disk 1 and the read-out clock signal is a fixed clock signal. An inner circumference counter 29 is provided to count 98 frames of the write-in clock signal WFCK. In an addition/subtraction unit 30, the output of the inner circumference counter 29 is added to, or subtracted from, the value of jitter measured by the jitter counter 28.
The value of jitter is subtracted from the counter output corresponding to the 98 frames of the write-in clock signal WFCK, and the reproducing sub-code synchronization signal SCOR having the wow of the spindle motor is corrected in the time axis, so that the wow in the reproducing sub-code synchronization signal SCOR can be removed and a sub-code synchronization signal GRSCOR in synchronization with the PCM data read from the DRAM 23 can be generated based on the read-out clock signal RFCK with a higher accuracy.
A match detection circuit 33 is provided to detect a match between the reproducing sub-code synchronization signal SCOR and the counter output of the inner circumference counter 29. For example, when there are two consecutive matches, a match detection signal GSS may be output. When the match detection signal GSS is sent, that is, when the reproducing sub-code synchronization signal SCOR and the counter output of the inner circumference counter 29 are consecutively matched two times, the reproducing sub-code synchronization signal GRSCOR is generated and output. As a result, an erroneous reproducing sub-code synchronization signal generated due to a scratch on the disk can be excluded and the reproducing sub-code synchronization signal GRSCOR of the optical disk player can be identified.
In the aforementioned optical disk player, the sub-code data obtained from the disk is temporarily stored in the memory, and then, the data read from the memory is finally selected by using the reproducing sub-code synchronization signal, so that the data can be reproduced by ensuring the data continuity without the sound discontinuity. Although the data is stable in a jitter environment causing vibration, a disadvantage of the conventional optical disk player is that the conventional optical disk player has a complex hardware construction.
Therefore, a need exists for a CD player with a minimum amount of hardware construction which is capable of reproducing data without sound discontinuity even in a jitter environment.

Disk player for allocating pointers to frames of CD data and storing pointers in memory and method of processing reproduced data of disk player


The number of input latching comparators in a flash analog-to-digital converter is significantly reduced by merging the input latching function into exclusive OR gates used in the converter's decoding section. A latching exclusive OR gate used for this purpose employs resonant tunneling diodes as the latching devices, with hysteresis and impedance elements connected to ensure that the gate latches in a logic state that corresponds to the input analog signal. The latching logic gates operate in a current mode, enabling updated logic states to be latched in response to a periodic clock signal.

1. Field of the Invention
This invention relates to analog-to-digital converters (ADCs), and more particularly to exclusive OR (XOR) gates and latch circuits used in flash ADCs.
2. Description of the Related Art
Flash ADCs take their name from their high conversion speed. They employ a precision voltage reference that is divided by a precision resistor divider to provide individual comparator reference voltages. As the input voltage increases the comparators switch in turn, and a decode logic network provides an appropriate digital output as a function of the state of the comparator input voltages. On a typical n-bit flash ADC, 2.sup.n-1 comparators and 2.sup.n-1 corresponding resistor taps must generally be used. An 8-bit converter would require, for example, 255 comparators and 255 resistor taps.
FIG. 1 is a block diagram of a conventional 4-bit ADC. A resistor string consisting of fourteen series resistors R1-R14 is connected between positive and negative voltage reference terminals 2 and 4. Fifteen input preamplifiers A1-A15 are provided, with each preamp inverting input receiving its input from a respective tap off the resistor string. The non-inverting preamp inputs are all connected to an input terminal 6 to receive an analog input signal that is to be converted to digital format. The output of each preamp A1-A15 is connected to a respective latching comparator, L1-L15, with a clock input 8 connected to each of the latching comparators and periodically causing them to latch the output of their respective preamps.
As the analog input signal at terminal 6 swings from its full negative to its full positive excursion, the outputs from each of the preamps toggle from 0 to 1 in turn, beginning with A15 for the most negative and progressing through A1 for the most positive input. The resultant set of digital preamp outputs is referred to as a thermometer code. With this code format, if the output of a given preamp is a logic 1, then the outputs from all of the preamps of lower bit order (vertically below the on preamp in FIG. 1) are also logic 1s.
Contingent upon the presence of a thermometer code format, the ADC's decoding logic can be greatly simplified by using a "gray-code" decoding scheme. This type of decoding logic uses XOR gates whose operation is based upon current summations. For the 4-bit ADC of FIG. 1, 7 XOR gates XOR1-XOR7 are interconnected with each other in a known fashion to produce a 4-bit digital output that is captured by four corresponding output latches L16-L19. The first rank of four XOR gates XOR1-XOR4 are current mode (CM) devices that receive thermometer code inputs from respective sets of latches L1-L15. The second and third ranks, consisting respectively of XOR5, XOR6 and of XOR7, are voltage mode (VM) devices that receive inputs from the preceding rank; their inputs do not have to be in a thermometer code format. Operating under the control of the clock input 8, the output latches yield the 4-bit digital output designated as bits B1-B4.
A limiting amplifier buffer BFR1 converts the sine wave clock signal to a square wave suitable for controlling the digital circuitry. Three more buffers BFR2, BFR3 and BFR4 in series with BFR1 provide gate delays to synchronize the clock signal at the output latches L16-L19 with the logic signals that propagate through three ranks of XOR gates. Additional buffers BFR5-BFR10 provide gate delays for connections between the decode network and the output latches that bypass one of more ranks of XOR gates.
FIG. 2 shows a current mode XOR gate that has been used in the decoding section of the FIG. 1 ADC. The gate is illustrated as having either three or five inputs. It includes a pair of resistors R15, R16 that are connected between a positive voltage bus Vcc (typically +5 volts) and the current (collector-emitter) circuits of a pair of matched npn bipolar transistors Q1, Q2. Both transistors are biased into conduction by a common bias signal Vb. The gate outputs Y and Y, corresponding to logic 1 and logic 0 outputs, are taken respectively from the R15/Q1 and the R16/Q2 junctions.
The gate inputs are supplied by respective differential transistor pairs, each of which correspond to a respective preamplifier of FIG. 1. For a three input device, in which the inputs are designated A, B and C, the most significant bit (MSB) input consists of differentially connected bipolar transistors Q3, Q4 that are biased respectively by input A and the complement of A (A). Their emitters are connected in common to a current source I1, while their collectors are connected to draw current from the current circuits of Q2 and Q1, respectively. The other input differential pairs have similar designs. The second MSB input comprises transistors Q5, Q6 and another I1 current source, while the least significant bit (LSB) input consists of differentially connected transistors Q7, Q8 and another current source I1. The inputs B and C are applied to the bases of Q5 and Q7, with complementary input signals B and C applied to the bases of Q6 and Q8, respectively. The insertion of Q1 and Q2 between R15, R16 and differential pairs Q3-Q8 allows for a higher speed operation than would be the case if the resistors were connected directly to Q3-Q8.
The connections of the differential input pairs to the transistors Q1, Q2 alternates from pair to pair. That is, whereas the differential transistors for A and A (Q3 and Q4) are connected respectively to the collectors of Q2 and Q1, the differential transistors for B and B (Q5 and Q6) are connected respectively to the collectors of Q1 and Q2, and the third differential transistor pair again alternates so that the input transistors for C and C (Q7 and Q8) are connected respectively to the collectors of Q2 and Q1, the same as for the MSB input pair.
The response of the 3-input XOR to thermometer code inputs is illustrated in the truth table of FIG. 3a. First assume that the inputs A, B and C are all at a logic 0 level (with the complementary inputs A, B and C at a logic 1 level). This is indicated on line 1 of FIG. 3a. With this input pattern, the transistors Q3, Q5 and Q7 are held OFF, while transistors Q4, Q6 and Q8 are ON. Thus, two units of current (2I1) flow through R15, and one unit of current (I1) flows through R16. With R15 and R16 having equal resistance values, this produces a voltage drop across R15 that is twice the voltage drop across R16. Subtracting these voltage drops from Vcc yields a higher voltage for output Y than for output Y; the output Y is accordingly a logic zero and its complement Y is a logic one.
If the LSB input C now goes high, as indicated on line 2 of FIG. 3a, transistor Q7 turns ON and Q8 turns OFF, and one unit of current is shifted from R15 to R16. This results in a lower voltage drop across R15 than R16, and consequently a logic 1 Y output.
The next higher input pattern, illustrated on line 3, is for input B to be high and the other inputs A and C low. However, such an input pattern violates the thermometer code pattern and accordingly no outputs from the XOR gate are given, as indicated by dashes through the I.sub.R15, I.sub.R16, Y and Y columns for this nonallowable state. The next higher input pattern, with B and C high and A low, is consistent with the thermometer code. As illustrated on line 4, this input pattern shifts one unit of current from R16 back to R15 (because of Q5 turning ON and Q6 OFF). The result is that output Y is a logic 0, while the complementary output Y is a logic 1.
The next three input patterns in progressively higher binary order, shown on lines 5-7, all violate the thermometer code pattern. The final possible input pattern, shown on line 8, is for all three inputs A, B and C to be logic 1. In this event one unit of current is shifted from R15 to R16 (compared to the line 4 pattern), with the Y output a logic 1 and the complementary Y output a logic 0.
It can be seen from an inspection of FIG. 3a that, for a gray-code input, the Y output is a logic 1 when an odd number of inputs are high, and a logic 0 when an even number of inputs are high. This satisfies the basic definition of the XOR function.
FIG. 3b presents a truth table for a five input XOR gate. In this case new differential transistor pairs Q9, Q10 and Q11, Q12, of lower bit significance than the other transistor pairs and with respective base inputs D, D and E, E, have been added to the three input case. Continuing the alternating pattern of connections, Q9 and Q10 are connected to draw current from R15 and R16, while the collectors of Q11 and Q12 are connected to draw current from R16 and R15, respectively. Three units of current (3I1) are drawn through R15 and two units (2I1) through R16 for thermometer code input patterns in which an even number of inputs are high, while two units of current are drawn through R15 and three units through R16 for thermometer code input patterns in which an odd number of inputs are high. This again satisfies the basic XOR function.
A thermometer code XOR gate requires an odd number of inputs in addition to the gray-code. If an even number of inputs is desired, the gate is implemented with the next higher odd number of inputs, and one of the inputs is forced to a constant logic 0 state. This is illustrated in FIG. 2 by replacing the Q11, Q12 transistor pair with a current source I1 that is connected directly between the R15/Q1 circuit and ground, as indicated by dashed line 9. An equivalent truth table for this gate with four effective inputs can be obtained from FIG. 3b by considering only those lines in the table for which column E is a logic 0 and the remaining columns A-D follow a thermometer code pattern.
ADCs of the type illustrated in FIG. 1 have a fairly high level of complexity and are not well adapted to the continual need for greater resolution (i.e., more bits) and higher conversion rates. To increase the operating range, the same number of circuit elements have to work at higher and higher speeds. For resolutions above 8 or 10 bits, more than one monolithic integrated circuit is usually required, and both cost and power consumption are relatively high.
Other types of ADCs have been explored in recent years, in particular folding/interpolation devices in which a certain degree of ADC decoding is performed on the analog signal prior to its being latched. Input currents are summed together and differential voltages are produced across resistor pairs, with the voltages latched by standard latching comparators. A performance limitation of the folding/interpolation approach is that each amplifier's output changes polarity multiple times as the input signal goes from its lowest to its higher value. This effectively increases the amplifier's output frequency. Since such amplifiers are limited in bandwidth, the output signal amplitude falls off at higher frequencies and their analog input bandwidth suffers compared to conventional flash ADCs. Folding/interpolation devices are disclosed, for example, in Corcoran et al., "A 400 MHz 6b ADC", IEEE International Solid-State Circuit Conference, Feb. 24, 1984, pages 294-296; van de Grift et al., "An 8b 50 MHz Video ADC with Folding and Interpolation Techniques", IEEE International Solid-State Circuits Conference, 1987, pages 94, 95, 354; and Van de Plassche, "An 8-bit 100-MHz Full Nyquist Analog-to-Digital Converter", IEEE Journal of Solid State Circuits, Vol. 23, No. 6, December 1988, pages 1334-1344.

Flash analog-to-digital converter with latching exclusive or gates


The present invention provides a chemical conversion liquid for zinc or zinc alloy bases, which contains 2-200 mmol/L of trivalent chromium ions, 1-300 mmol/L of zirconium ions and at least one component selected from among fluorine ions, a water-soluble carboxylic acid and a salt thereof, and which does not contain Co ions and hexavalent chromium ions.

A chemical conversion treatment is a technique having been utilized from the past to impart a corrosion resistance to metal surfaces. At present also, this technique is used in the surface treatments for aircrafts, construction materials, automotive parts, and so forth. Meanwhile, a coating obtained by a chemical conversion treatment represented by chromic acid/chromate chemical conversion treatment partially contains harmful hexavalent chromium.
Hexavalent chromium is restricted by the WEEE (Waste Electrical and Electronic Equipment) Directive, the RoHS (Restriction of Hazardous Substances) Directive, the ELV (End of Life Vehicles) Directive, and so forth. Chemical conversion treatment solutions using trivalent chromium instead of hexavalent chromium are actively studied for the industrialization.
Nevertheless, a trivalent chromium chemical conversion treatment solution for a zinc or zinc alloy substrate is generally supplemented with a cobalt compound to enhance the corrosion resistance.
Cobalt is one of what is called a rare metal. It cannot necessarily be said that the cobalt supply system stable because the usage and application of cobalt are increasing or the countries where cobalt is produced are limited, for example. Moreover, cobalt chloride, cobalt sulfate, cobalt nitrate, and cobalt carbonate are listed as SVHCs (Substances of Very High Concern) in REACH (Registration, Evaluation, Authorization and Restriction of Chemicals) regulation. The uses of these compounds are likely to be restricted.
Meanwhile, as environmentally-friendly chemical conversion treatment solutions for a zinc or zinc alloy substrate, several chromium-free chemical conversion treatment solutions have been reported. For example, there have been known: a treatment agent containing a compound selected from zirconium and titanium, a compound selected from vanadium, molybdenum, and tungsten, and further an inorganic phosphorus compound (Japanese Patent Application Publication No. 2010-150626); and a fluorine- and chromium-free chemical conversion treatment agent containing a compound selected from water-soluble titanium compounds and water-soluble zirconium compounds, and an organic compound having functional groups (International Publication No. WO2011/002040).
However, such chromium-free chemical conversion treatment agents are inferior to conventional cobalt-containing chemical conversion treatment agents for zinc or zinc alloys in chemical conversion treatment coating performances such as corrosion resistance. An improvement in this respect has been desired.

Trivalent chromium chemical conversion liquid for zinc or zinc alloy bases and chemical conversion coating film


The present invention provides a method for generating a timing offset signal applied to a sampling device for recovering a symbol stream from a broadcast signal by characterizing the dispersion of received signal. Preferably, the method includes steps for generating a derivative signal approximating the derivative of the symbol stream, producing a constant representative of an expected symbol stream, and multiplying the derivative signal, the constant, and a signal one of corresponding to and approximating the symbol stream to thereby generate the timing offset signal. A dispersion characterizing receiver and a digital signal processor employed therein are also described.

1. Field of the Invention
The present invention relates to timing recovery methods and apparatuses in communication systems. More specifically, the present invention relates to methods and corresponding apparatus for timing recovery based on dispersion in the received signal. Software and components for implementing the novel methods according to the present invention are also disclosed.
The instant patent application is based on Provisional Patent Application No. 60/241,274 of Oct. 17, 2000, which application is incorporated, in its entirety, by reference.
2. Description of the Related Art
In any communication system, it is necessary to synchronize the clock at the receiver with the clock at the transmitter, a process that is commonly called synchronization or timing recovery. In other words, timing recovery is the derivation of a timing signal from the received signal. Timing recovery can be accomplished by a variety of methods, two of which are discussed below.
Recent efforts in developing digital radio/video broadcasting systems, e.g., HDTV broadcasting systems, have highlighted the problem of optimal timing recovery as a significant issue in digital receiver design. More specifically, one of the features of digital media broadcasting channels is long delay spread multipath; the traditional approach to this problem, i.e., inclusion of fractionally spaced equalizers that are insensitive to timing phase in each receiver, is impractical in consumer electronics receivers and the like.
The problem of timing recovery consists of estimation of the timing frequency and the optimal timing phase. It will be appreciated that there are many methods of attacking this problem; for instance, the standard text entitled "Communication Systems Engineering," by Proakis et al. (Prentice Hall, N.J., 1994) describes several such methods. Circuitry for carrying of several of these methods will be discussed immediately below. Conventional timing recovery techniques and methods include the Early-Late Gate method, the minimum Mean-Squared-Error (MSE) method, the Maximum-Likelihood (ML) method, and the Output Energy Maximization (OEM) method. Both the Early-Late Gate and the ML methods were developed based on the assumption that there are no channel dynamics; the validity and performance of these methods are difficult to ascertain in the presence of several additional nontrivial channels, i.e., a multipath channel. On the other hand, the MSE criterion can be extended to the case where a multipath channel is present; however, due to the nature of the MSE algorithm, either a training sequence or feedback from the decision device must be employed in any practical implementation of the MSE algorithm. Since training sequences reduce the overall system throughput, and since the feedback from a decision device may be unreliable at the synchronization stage, a non-decision-directed (blind) method would be advantageous in time recovery in the presence of a multipath channel.
The output energy maximization method, which can be performed blindly, has been analyzed by D. N. Godard and reported in his article entitled "Passband Timing Recovery in All-Digital Modem Receiver" (IEEE Trans. Communications, Vol. 26, No. 5 (May 1978)). Another blind method which has not received significant attention utilizes the technique of dispersion minimization; this method is frequently referred to as employing a Constant Modulus Algorithm. This method can be implemented without a training signal. Guglielmi et al. considered the constant modulus approach to jointly optimize the combiner weights and timing offsets of a pair of received signals from two antennas. See Guglielmi et al., "Joint Clock Recovery and Baseband Combining for the Diversity Radio Channel," IEEE Trans. Communications, Vol. 44, pp. 114–117 (Jan. 1996). However, the application of the constant modulus algorithm (or the minimization of the dispersion of the received signal) heretofore has not been applied, or even proposed, as a solution for timing phase recovery for a single antenna structure subject to substantial multipath.
It should be noted here that all of the publications mentioned above are incorporated herein by reference.
FIGS. 1A, 1B and 1C illustrate three alternative circuits which can be employed for timing recovery. The circuitry of FIG. 1A, for example, includes a signal path consisting of an analog processor 10a, a sample 20a, and a digital processor 30a. The circuit also includes a voltage controlled oscillator (VCO) 40a, which controls the sampler 20a by specifying when samples of the incoming signal are to be taken. It will be appreciated from FIG. 1A that the analog processor 10a, by controlling the rate of frequency of VCO 40a, indirectly determines when the sampling instants or events will occur. In contrast, the circuit illustrated in FIG. 1B employs the digital post processor 30b, rather that analog processor 10b, to control the rate of frequency of the VCO 40b and, hence, in determining when sampling events are to occur, i.e, when sampler 20b is to be operated. In contrast to both of the figures previously discussed, in the circuit of FIG. 1C the sampling instants at sample 20c are chosen based, not on using analog processor 10c or digital processor 30c, but rather on a free running clock 50; digital post processing is employed in recovering the values of the received signal that would have occur at the optical setting instants. None of these circuits are explicitly configured for blind timing recovery.
What is needed is a method and corresponding apparatus for timing recovery that can be performed "blindly" (without a training signal). Moreover, what is needed is a method and corresponding apparatus which can be readily implemented as either an analog procedure or in digital form. It would be advantageous if the method and corresponding apparatus were robust, e.g., insensitive to clock jitter and to the effects of intersymbol interference. What is also needed is a method which advantageously can be implemented in any of the three circuit variations illustrated in FIGS. 1A–1C.

Method and apparatus for timing recovery based on dispersion characterization and components therefor


An apparatus for cooling an integrated circuit (IC) die is described. The apparatus includes an adhesion layer coated on a surface of the IC die, wherein the adhesion layer has high thermal conductivity. The apparatus also includes a heat dissipation structure affixed onto the adhesion layer. This heat dissipation structure further includes a set of discrete heat dissipation elements which are substantially mechanically isolated from each other. This set of discrete heat dissipation elements provides an extended heat dissipation surface for the IC die. Moreover, each of the set of discrete heat dissipation elements has high compliance, which allows the adhesion layer to be sufficiently thin, thereby reducing a thermal conductivity of the adhesion layer.

1. Field
The disclosed embodiments are related to integrated circuit (IC) chip cooling mechanisms. More specifically, the disclosed embodiments are related to designs of a heat dissipation structure for an IC chip.
2. Related Art
The dramatic increase in the power and speed of IC chips in computer systems, such as servers, has given rise to increasing challenges in removing the heat generated by these IC chips during system operation. Some chip cooling techniques place an IC chip inside a lidded package which interfaces with an air-cooled heat sink for heat dissipation. Other chip cooling techniques provide further improvement on the heat dissipation path (also referred to as the "thermal path") by reducing thermal resistance between the chip surface and the heat sink. For example, some techniques replace the air-cooled heat sink with a liquid-cooled cold-plate. Other techniques attempt to reduce thermal resistance by eliminating any material between the chip surface and the heat sink.
Separately, direct liquid cooling techniques which can bring coolant in direct contact with the silicon surface have been proposed. To avoid electric shorting problems associated with these techniques, a dielectric fluid can be used as the coolant. However, the limited chip surface area can limit the amount of heat that can be effectively removed by the coolant, and can also be subject to the risk of overheating and boiling the coolant. Such risk subsequently limits the effective operating power of the IC chip.
Hence, what is needed is an IC chip cooling mechanism without the above-described problems.

Heat dissipation structure for an integrated circuit (IC) chip


A method for treating type 1 diabetes in a human in need of such treatment, comprising administering to the human a biologically effective amount of at least one inhibitor of inducible nitric oxide synthase or a pro-inflammatory cytokine, wherein the inhibitor is an inhibitor of HMG-CoA reductase or a pharmaceutically acceptable salt thereof, and the inhibitor specifically inhibits the activity of HMG-CoA reductase.

1. Field of the Invention
The present invention relates generally to the treatment of conditions involving undesired or pathological levels of inducible nitric oxide synthase (iNOS), e.g. septic shock or neuroinflammatory diseases. In one important aspect, the invention relates to methods of suppressing, inhibiting or preventing the accumulation of nitric-oxide induced cytotoxicity by using inhibitors that block or suppress the induction of cytokines and/or inducible nitric oxide synthase. Another aspect of the invention is the treatment of conditions involving undesired or pathological levels of proinflammatory cytokines (i.e. TNF-α, IL-1β, IL-2, IL-6, IL-8 and/or IFN-γ) and/or iNOS. One important aspect of the invention relates to methods of suppressing, inhibiting, or preventing proinflammatory cytokines and/or iNOS induced or aggravated disorders including conditions involving the detrimental effects of inflammation (e.g. disorders such as lupus, rheumatoid arthritis, osteoarthritis, amyotrophic lateral sclerosis, and autoimmune disorders; ischemia/reperfusion; neuroinflammatory conditions such as Alzheimer's, stroke, multiple sclerosis, X-linked adrenoleukodystrophy; and the effects of aging).
2. Description of Related Art
Nitric Oxide and Proinflammatory Cytokines
Nitric oxide (NO) is a potent pleiotropic mediator of physiological processes such as smooth muscle relaxation, neuronal signaling, inhibition of platelet aggregation and regulation of cell mediated toxicity. It is a diffusible free radical which plays many roles as an effector molecule in diverse biological systems including neuronal messenger, vasodilation and antimicrobial and antitumor activities (Nathan, 1992; Jaffrey et al., 1995). NO appears to have both neurotoxic and neuroprotective effects and may have a role in the pathogenesis of stroke and other neurodegenerative diseases and in demyelinating conditions (e.g., multiple sclerosis, experimental allergic encephalopathy, X-adrenoleukodystrophy) and in ischemia and traumatic injuries associated with infiltrating macrophages and the production of proinflamatory cytokines (Mitrovic et al., 1994; Bo et al., 1994; Merrill et al., 1993; Dawson et al., 1991, Kopranski et al., 1993; Bonfoco et al., 1995). A number of pro-inflammatory cytokines and endotoxin (bacterial lipopolysaccharide, LPS) also induce the expression of iNOS in a number of cells, including macrophages, vascular smooth muscle cells, epithelial cells, fibroblasts, glial cells, cardiac myocytes as well as vascular and non-vascular smooth muscle cells. Although monocytes/macrophages are the primary source of iNOS in inflammation, LPS and other cytokines induce a similar response in astrocytes and microglia (Hu et al., 1995; Galea et al., 1992).
During inflammation, reactive oxygen species (ROS) are generated by various cells including activated phagocytic leukocytes; for example, during the neutrophil "respiratory burst", superoxide anion is generated by the membrane-bound NADPH oxidase. ROS are also believed to accumulate when tissues are subjected to inflammatory conditions including ischemia followed by reperfusion. Superoxide is also produced under physiological conditions and is kept in check by superoxide dismutates. Excessively produced superoxide overwhelms the antioxidant capacity of the cell and reacts with NO to form peroxynitrite, ONOO−, which may decay and give rise to hydroxyl radicals, −OH (Marietta, M., 1989; Moncada et al., 1989; Saran et al., 1990; Beckman et al. 1990). NO, peroxynitrite and −OH are potentially toxic molecules to cells including neurons and oligodendrocytes that may mediate toxicity through modification of biomolecules including the formation of iron-NO complexes of iron containing enzyme systems (Drapier et al., 1988), oxidation of protein sulfhydryl groups (Radi et al., 1991), nitration of proteins and nitrosylation of nucleic acids and DNA strand breaks (Wink et al., 1991).
There is now substantial evidence that iNOS plays an important role in the pathogenesis of a variety of diseases. In addition, it is now thought that excess NO production may be involved in a number of conditions, including conditions that involve systemic hypotension such as septic and toxic shock and therapy with certain cytokines. Circulatory shock of various etiologies is associated with profound changes in the body's NO homeostasis. In animal models of endotoxic shock, endotoxin produces an acute release of NO from the constitutive isoform of nitric oxide synthase in the early phase, which is followed by induction of iNOS. NO derived from macrophages, microglia and astrocytes has been implicated in the damage of myelin producing oligodendrocytes in demyelinating disorders like multiple sclerosis and neuronal death during neuronal degenerating conditions including brain trauma (Hu et al., 1995; Galea et al., 1992; Koprowski et al., 1993; Mitrovic et al., 1994; Bo et al., 1994; Merrill et al., 1993).
NO is synthesized from L-arginine by the enzyme nitric oxide synthase (NOS) (Nathan, 1992). Nitric oxide synthases are classified into two groups. One type, constitutively expressed (cNOS) in several cell types (e.g., neurons, endothelial cells), is regulated predominantly at the post-transcriptional level by calmodulin in a calcium dependent manner (Nathan, 1992; Jaffrey et al., 1995). In contrast, the inducible form (iNOS), synthesized de novo in response to different stimuli in various cell types including macrophages, hepatocytes, myocytes, neutrophils, endothelial and messangial cells, is independent of calcium. Astrocytes, the predominant glial component of brain have also been shown to induce iNOS in response to bacterial lipopolysaccharide (LPS) and a series of proinflammatory cytokines including interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ) (Hu et al., 1995; Galea et al., 1992).
Cytokines associated with extracellular signaling are involved in the normal process of host defense against infections and injury, in mechanisms of autoimmunity and in the pathogenesis of chronic inflammatory diseases. It is believed that nitric oxide (NO), synthesized by nitric oxide synthetase (NOS) mediates deleterious effects of the cytokines (Nathan, 1987; Zang et al., 1993; Kubes et al., 1991). For example, NO as a result of stimuli by cytokines (e.g., TNF-α, IL-1 and interleukin-6 (IL-6) is implicated in autoimmune diseases such as multiple sclerosis, rheumatoid arthritis, osteoarthritis. (Zang et al., 1993; McCartney-Francis et al., 1993). The NO produced by iNOS is associated with bactericidal properties of macrophages (Nathan, 1992; Stuehr et al., 1989). Recently, an increasing number of cells (including muscle cells, macrophages, keratinocytes, hepatocytes and brain cells) have been shown to induce iNOS in response to a series of proinflammatory cytokines including IL-1, TNF-α, interferon-γ (IFN-γ) and bacterial lipopolysaccharides (LPS) (Zang et al., 1993; Busse et al., 1990; Genge et al., 1995).
Signal Transduction Pathways
Mevalonate metabolites, particularly farnesyl pyrophosphate (FPP), are involved in post-translational modification of some G-proteins, including Ras (Goldstein et al., 1990; Casey et al., 1989). The inhibition of isoprenylation of Ras proteins by inhibitors of mevalonate pathway and their membrane association and transduction of signal from Ras to Raf/MAP kinase cascade (Kikuchi et al., 1994) indicates a role of mevalonate metabolites in the transduction of signal from receptor tyrosine kinases to Raf/MAP kinase cascade. Two enzymes that control the rate-limiting steps of the mevalonate pathway are 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, which catalyzes the formation of mevalonate from acetyl-CoA, and mevalonate pyrophosphate decarboxylase, which controls the use of mevalonate within the cell by converting 3-phospho-5-pyrophospho-mevalonate to isopentenyl pyrophosphate. Lovastatin, a potent inhibitor of HMG-CoA reductase, and sodium salt of phenylacetic acid (NaPA), an inhibitor of mevalonate pyrophosphate decarboxylase, are known to reduce the level of cellular isoprenoids (Castillo et al., 1991; Samid et al., 1994) and isoprenylated proteins (Repko and Maltese, 1989). No suppression of isoprenylated protein maturation in vitro by lovastatin treatment that produced 50% inhibition of sterol biosynthesis has been observed (Sinensky et al., 1991). The IC50 for inhibition of sterol synthesis is 10 nM, whereas the IC50 for inhibition of conversion of pro-p21ras to mature-p21ras is maximal at 2.6 μM (Sinensky et al., 1991). The pharmacologically attainable concentration for NaPA, however, is 1 to 5 mM (Thibault et al., 1995). HMG-CoA reductase can also be inhibited by 5-amino 4-imidazolecarboxamide ribotide (AICAR). AICAR stimulates AMP-activated protein kinase, an enzyme that inhibits acetyl-CoA carboxylase and HMG-CoA reductase (Henin et al., 1995)
LPS is shown to bind cell-surface receptor CD14 (Stefanova et al., 1993) and induce iNOS, probably via activation of NFkβ (Xie et al., 1994; Kwon et al., 1995). NFkβ is an ubiquitous multisubunit transcription factor that is activated in response to various stimuli including cytokines TNF-α, IL-1, IL-2, IL-6, viruses, LPS, DNA damaging agents and phorbol myristate acetate (PMA) (Schreck et al., 1992). Previous studies (Law et al., 1992) demonstrating the inhibition of NF-kβ activation by mevinolin and 5′-methylthioadenosine indicates a role of protein farnesylation and carboxyl methylation reactions in the activation of NF-kβ. Identification of the binding site of NF-kβ in the promoter region of the iNOS gene and that the activation of NFkβ in LPS-induced iNOS induction establishes a role of NFkβ activation in the induction of iNOS (Xie et al., 1994). Although the precise mechanism of NFkβ activation is not known at the present time, the inhibition of activation of NFkβ by inhibitors of tyrosine kinase and proteases indicates a role of phosphorylation and degradation of Ikβ in this process (Menon et al., 1993; Henkel et al., 1993).
Reactive oxygen (Schreck et al., 1992) and reactive nitrogen (Lander el al., 1993) species have been demonstrated to mediate the signal for NFkβ activation. The differential induction of NFkβ by protein phosphatase inhibitors in primary and transformed cell lines also indicates that induction of NFkβ is dependent on the dual processes of cellular redox and phosphorylation (Menon et al., 1993). The exact target of ROS that modulate cellular redox is unknown, and the lack of induction in cells in which activity of p21ras was blocked through expression of a dominant negative mutant or treatment with farnesyltransferase inhibitor indicate that direct activation of p21ras may be the central mechanism by which redox stress stimuli transmit its signal to the nucleus (Lander et al., 1995).
Ceramide Production and Apoptosis
Cytokine-mediated ceramide production is implicated in apoptosis of different cells including brain cells (Brugg et al., 1996; Wiesner and Dawson, 1996). Several studies support a role for hydrolysis of sphingomyelin as a stress-activated signaling mechanism in which ceramide plays a role in cell regulation, cell differentiation, growth suppression and apoptosis in various cell types including glial and neuronal cells (Hannun and Bell, 1989; Hannun, 1994; Kolesnick and Golde, 1994; Brugg et al., 1996; Wiesner and Dawson, 1996). Sphingomyelin is preferentially concentrated in the outer leaflet of the plasma membrane of most mammalian cells; it comprises sphingosine (a long chain sphingoid base backbone), a fatty acid, and a phosphocholine head group. Ceramide is composed of a sphingoid base with a fatty acid in amide linkage. Ceramide activates the proteases of the interleukin-converting enzyme (ICE) family (especially prICE/YAMA/CPP32), the protease responsible for cleavage of poly(A)DP-ribose polymerase (Martin et al., 1995), and that the activation of prICE by ceramide and induction of apoptosis are inhibited by overexpression of Bcl-2 (Zhang et al., 1996). Addition of exogenous ceramides or sphingomyelinase to cells induces stress-activated protein kinase-dependent transcriptional activity through the activation of c-jun (Latinis and Koretzky, 1996), and a dominant negative mutant of SEK1, the protein kinase responsible for phosphorylation and activation of stress-activated protein kinase, interferes with ceramide-induced apoptosis (Verheij et al., 1996). These observations also indicate that both Bcl-2 and stress-activated protein kinase function downstream of ceramide in the apoptotic pathway.
The signaling events in cytokine-mediated activation of sphingomyelin degradation to ceramide are poorly understood. Since the discovery of the sphingomyelin cycle, several inducers have been shown to be coupled to sphingomyelin-ceramide signaling events, including 1α,25-dihydroxyvitamin D3, radiation, antibody cross-linking, TNF-α, IFN-γ, IL-1β, nerve growth factor, and brefeldin A (Hannun and Bell, 1989; Hannun, 1994; Kolesnick and Golde, 1994; Zhang and Kolesnick, 1995; Kantey et al., 1995; Linardic et al., 1996).
The sphingomyelin pathway-associated signal transduction pathway mediates the action of several extracellular stimuli that lead to important biochemical and cellular effects (Zhang and Kolesnick, 1995; Kantey et al., 1995; Yao et al., 1995; Hannun, 1996; Lozano et al., 1994). In the case of TNF-α, the pathway is initiated by the action of TNF-α on its 55-kDa receptor, leading to phospholipase A2 activation, generation of arachidonic acid, and subsequent activation of sphingomyelinase (Jayadev et al., 1994). This pathway is initiated by the activation of two distinct forms of sphingomyelinase (SMase), a membrane-associated neutral sphingomyelinase (Chatterjee, 1993) and an acidic sphingomyelinase (Spence, 1993), which reside in the caveola and the endosomal-lysosomal compartment. Each type of SMase hydrolyzes the phosphodiester bond of sphingomyelin to yield ceramide and phosphocholine. Proinflammatory cytokines (tumor necrosis factor-α, TNF-α; interleukin-1β, IL-1β; interferon-γ, IFN-γ) and bacterial lipopolysaccharides have been shown as potent inducers of SMases. Ceramide has emerged as a second messenger molecule that is considered to mimic most of the cellular effects of cytokines and lipopolysaccharide in terminal differentiation, apoptosis, and cell cycle arrest (Zhang and Kolesnick, 1995; Kantey et al., 1995).
Sphingomyelin turnover and ceramide generation in response to TNF-α and IL-1β occurs within minutes of stimulation; however, the sequence of events linking receptor stimulation and SMase activation remains largely unknown (Hannun, 1996; Lozano et al., 1994; Jayadev et al., 1994). In a number of cell systems, interaction of TNF-α with its membrane receptors (p75 and p55) has been found to activate phospholipase A2 and to induce release of arachidonic acid from phosphatidylcholine and phosphatidylethanolamine pools. This arachidonic acid has been shown as a mediator of sphingomyelin hydrolysis in response to TNF-α (Jayadev et al., 1994). In addition, proteases have also been implicated in the pathway leading from TNF-α to the activation of SMase (Hannun, 1996; Dbaio et al., 1997) recently. On the other hand, IL-1β and TNF-α are known to induce the production of reactive oxygen species, a class of highly diffusible and ubiquitous molecules, which have been suggested to act as second messengers (Tiku et al., 1990; Lo and Cruz, 1995; Devary et al., 1991). ROS encompassing species such as superoxide, hydrogen peroxide, and hydroxyl radicals are known to regulate critical steps in the signal transduction cascade and many important cellular events including protein phosphorylation, gene expression, transcription factor activation, DNA synthesis, and cellular proliferation (Schreck et al., 1991; Sen and Packer, 1996). A recent observation has shown that glutathione or similar molecules inhibit the activity of magnesium-dependent neutral SMase in vitro (Liu and Hannun, 1997). However, surprisingly, the SH group of GSH was not required as S-methyl GSH and GSSG inhibited neutral SMase at lower concentrations than GSH (Liu and Hannun, 1997). On the other hand, N-acetylcysteine has also been found to inhibit the synthesis of ceramide in cultured rat hepatocytes through the inhibition of dihydroceramide desaturase (Michel et al., 1997).
Inflammatory Diseases
NO generated by iNOS has been implicated in the pathogenesis of inflammatory diseases. In experimental animals hypotension induced by LPS or TNF-alpha can be reversed by NOS inhibitors and reinitiated by L-arginine (Kilbourn et al., 1990). Conditions which lead to cytokine-induced hypotension include septic shock, hemodialysis (Beasley and Brenner, 1992) and IL-2 therapy in cancer patients (Hibbs et al., 1992). Studies in animal models have suggested a role for NO in the pathogenesis of inflammation and pain and NOS inhibitors have been shown to have beneficial effects on some aspects of the inflammation and tissue changes seen in models of inflammatory bowel disease (Miller et al., 1990) and cerebral ischemia and arthritis (Ialenti et al., 1993; Stevanovic-Racic et al., 1994).
Inflammation, iNOS activity and/or cytokine production has been implicated in a variety of diseases and conditions, including psoriasis (Ruzicka et al., 1994; Kolb-Bachofen et al., 1994; Bull et al., 1994); uveitis (Mandia et al., 1994); type 1 diabetes (Eisieik & Leijersfam, 1994; Kroncke et al., 1991; Welsh el at., 1991); septic shock (Petros et al., 1991; Thiemermann & Vane, 1992; Evans et al., 1992; Schilling et al., 1993); pain (Moore et al., 1991; Moore et al, 1992; Meller et al., 1992; Lee et al., 1992); migraine (Olesen et al., 1994); rheumatoid arthritis (Kaurs & Halliwell, 1994); osteoarthritis (Stadler et al., 1991); inflammatory bowel disease (Miller et al., 1993; Miller et al., 1993); asthma (Hamid et al., 1993; Kharitonov et al., 1994); Koprowski et al., 1993); immune complex diseases (Mulligan et al., 1992); multiple sclerosis (Koprowski et al., 1993); ischemic brain edema (Nagafuji et al., 1992; Buisson et al., 1992; Trifiletti et al., 1992); toxic shock syndrome (Zembowicz & Vane, 1992); heart failure (Winlaw et al., 1994); ulcerative colitis (Boughton-Smith et al., 1993); atherosclerosis (White et al., 1994); glomerulonephritis (Muhl et al., 1994); Paget's disease and osteoporosis (Lowick et al., 1994); inflammatory sequelae of viral infections (Koprowski et al., 1993); retinitis, (Goureau et al., 1992); oxidant induced lung injury (Berisha et al., 1994); eczema (Ruzica et al., 1994); acute allograft rejection (Devlin, J. et al., 1994); and infection caused by invasive microorganisms which produce NO (Chen, Y and Rosazza, J. P. N., 1994).
In the central nervous system, apoptosis may play an important pathogenetic role in neurodegenerative diseases such as iscehmic injury and white matter diseases (Thompson, 1995; Bredesen, 1995). Both X-linked adrenoleukodystrophy (X-ALD) and multiple sclerosis (MS) are demyelinating diseases with the involvement of proinflammatory cytokines in the manifestation of white matter inflammation. The presence of immunoreactive tumor necrosis factor a (TNF-α) and interleukin 1 (IL-1β) in astrocytes and microglia of X-ALD brain has indicated the involvement of these cytokines in immunopathology of X-ALD and aligned X-ALD with MS, the most common immune-mediated demyelinating disease of the CNS in man (Powers, 1995; Powers et al., 1992; McGuinnes et al., 1995; McGuiness et al., 1997). Several studies demonstrating the induction of proinflammatory cytokines at the protein or mRNA level in cerebrospinal fluid and brain tissue of MS patients have established an association of proinflammatory cytokines (TNF-α, IL-1β, IL-2, IL-6, and IFN-γ) with the inflammatory loci in MS (Maimone et al., 1991; Tsukada et al., 1991; Rudick and Ransohoff, 1992).
X-linked adrenoleukodystrophy (X-ALD), an inherited, recessive peroxisomal disorder, is characterized by progressive demyelination and adrenal insufficiency (Singh, 1997; Moser et al., 1984). It is the most common peroxisomal disorder affecting between 1/15,000 to 1/20,000 boys and manifests with different degrees of neurological disability. The onset of childhood X-ALD, the major form of X-ALD, is between the age of 4 to 8 and then death within the next 2 to 3 years. Although X-ALD presents as various clinical phenotypes, including childhood X-ALD, adrenomyeloneuropathy (AMN), and Addison's disease, all forms of X-ALD are associated with the pathognomonic accumulation of saturated very long chain fatty acids (VLCFA) (those with more than 22 carbon atoms) as a constituent of cholesterol esters, phospholipids and gangliosides (Moser et al., 1984) and secondary neuroinflammatory damage (Moser et al., 1995). The necrologic damage in X-linked adrenoleukodystrophy may be mediated by the activation of astrocytes and the induction of proinflammatory cytokines. Due to the presence of similar concentration of VLCFA in plasma and as well as in fibroblasts of X-ALD, fibroblasts are generally used for both prenatal and postnatal diagnosis of the disease (Singh, 1997; Moser et al., 1984).
The deficient activity for oxidation of lignoceroyl-CoA ligase as compared to the normal oxidation of lignoceroyl-CoA in purified peroxisomes isolated from fibroblasts of X-ALD indicated that the abnormality in the oxidation of VLCFA may be due to deficient activity of lignoceroyl-CoA ligase required for the activation of lignoceric acid to lignoceroyl-CoA (Hashmi et al., 1986; Lazo et al., 1988). While these metabolic studies indicated lignoceroyl-CoA ligase gene as a X-ALD gene, positional cloning studies led to the identification of a gene that encodes a protein (ALDP), with significant homology with the ATP-binding cassette (ABC) of the super-family of transporters (Mosser et al., 1993). The normalization of fatty acids in X-ALD cells following transfection of the X-ALD gene (Cartier et al., 1995) supports a role for ALDP in fatty acid metabolism; however, the precise function of ALDP in the metabolism of VLCFA is not known at present.
Similar to other genetic diseases affecting the central nervous system, the gene therapy in X-ALD does not seem to be a real option in the near future and in the absence of such a treatment a number of therapeutic applications have been investigated (Singh, 1997; Moser, 1995). Adrenal insufficiency associated with X-ALD responds readily with steroid replacement therapy, however, there is as yet no proven therapy for neurological disability (Moser, 1995). Addition of monoenoic fatty acid (e.g., oleic acid) to cultured skin fibroblasts of X-ALD patients causes a reduction of saturated VLCFA presumably by competition for the same chain elongation enzyme (Moser, 1995). Treatment of X-ALD patients with trioleate resulted in 50% reduction of VLCFA. Subsequent treatment of X-ALD patients with a mixture of trioleate and trieruciate (popularly known as Lorenzo's oil) also led to a decrease in plasma levels of VLCFA (Moser, 1995; Rizzo et al., 1986; Rizzo et al., 1989). Unfortunately, the clinical efficacy has been unsatisfactory since no proof of favorable effects has been observed by attenuation of the myelinolytic inflammation in X-ALD patients (Moser, 1995). Moreover, the exogenous addition of unsaturated VLCFA induces the production of superoxide, a highly reactive oxygen radical, by human neutrophils (Hardy et al., 1994). Since cerebral demyelination of X-ALD is associated with a large infiltration of phagocytic cells to the site of the lesion (Powers et al., 1992), treatment with unsaturated fatty acids may even be toxic to X-ALD patients. Bone marrow therapy also appears to be of only limited value because of the complexicity of the protocol and of insignificant efficacy in improving the clinical status of the patient (Moser, 1995).
Experimental allergic encephalomyelitis (EAE) is an inflammatory demyelinating disease of the central nervous system (CNS) that serves as a model for the human demyelinating disease, multiple sclerosis (MS). Studies have shown that the majority of the inflammatory cells constitute of T-lymphocytes and macrophages (Merrill and Benveniste, 1996). These effector cells and astrocytes have been implicated in the disease pathogenesis by secreting number of molecules that act as inflammatory mediators and/or tissue damaging agents such as nitric oxide (NO). NO is a molecule with beneficial as well as detrimental effects. In neuroinflammatory diseases like EAE, high amounts of NO produced for longer durations by inducible nitric oxide synthase (iNOS) acts as a cytotoxic agent towards neuronal cells. Previous studies have shown NO by itself or it's reactive product (ONOO−) may be responsible for death of oligodendrocytes, the myelin producing cells of the CNS, and resulting in demyelination in the neuroinflammatory disease processes (Merrill et al., 1993; Mitrovic et al., 1994).
Infiltrating T-lymphocytes in EAE produce pro-inflammatory cytokines such as IL-12, TNF-α and IFN-γ (Merrill and Benveniste, 1996). In addition to T-cells and macrophages, astrocytes have also been shown to produce TNF-α (Shafer and Murphy, 1997). Convincing evidence exists to support a role for both TNF-α and IFN-γ in the pathogenesis of EAE (Taupin et al., 1997; Villarroya et al., 1996; Issazadeh et al., 1995). Investigations with antibodies against TNF-α have shown that in mice these antibodies protect against active and adaptively transferred EAE disease (Klinkert et al., 1997). The expression of TNF-α and IFN-γ during EAE disease could result in the upregulation of iNOS in macrophage and astrocytes because TNF-α and IFN-γ have been shown to be potent inducers of iNOS in macrophages and astrocytes in culture (Xie et al., 1994). This induction of iNOS could result in the production of NO, which if produced in large amounts may lead to cytotoxic effects. Peroxynitrite (ONOO−) has been identified in both MS and EAE CNS (Hooper et al., 1997; van der Veen et al., 1997). The role of peroxynitrite in the pathogenesis of EAE is supported by the beneficial effects of uric acid, a peroxynitrite scavenger, against EAE and by a subsequent survey documenting that MS patients had significantly lower serum uric acid levels than those of controls (Hooper et al., 1998). However, aggravation of EAE by inhibitors of NOS activity (Ruuls et al., 1996) and in an animal model of iNOS gene knockout (Fenyk-Melody et al., 1998) indicate that NO may not be the only pathological mediator in EAE disease process. In addition to NO other free radicals such as reactive oxygen intermediates (O2−, H2O2, arid OH−) can also be stimulated by cytokines (Merrill and Benveniste, 1996). Reactive oxygen intermediates (ROI) and NO are believed to be key mediators of pathophysiological changes that take place during inflammatory disease process. ROI's such as superoxide anion, hydroxy radicals and hydrogen peroxide can also be stimulated by TNF-α (Merrill and Benveniste, 1996). Therefore, it is likely that both the direct modulation of cellular functions by proinflammatory cytokines and toxicity of the ROI and reactive nitrogen species may play a role in the pathogenesis of EAE disease.
Several studies on protein and/or mRNA levels in plasma, cerebrospinal fluid (CSF), brain tissue, and cultured blood leukocytes from MS patients have established an association of proinflammatory cytokines (TNF-α, IL-1 and IFN-γ) with MS (Taupin et al., 1997; Villarroya et al., 1996; Issazadeh et al., 1995). The mRNA for iNOS has also been detectable in both MS as well as EAE brains (Bagasra et al., 1995; Koprowski et al., 1993). Semiquantitative RT-PCR™ for iNOS mRNA in MS brains shows markedly higher expression of iNOS mRNA in MS brains than control brains (Bagasra et al., 1995). Analysis of CSF from MS patients has also shown increased levels of nitrite and nitrate compared with normal control (Merrill and Benveniste, 1996). Peroxynitrite, ONOO— is a strong nitrosating agent capable of nitrosating tyrosine residues of proteins to nitrotyrosine. Increased levels of nitrotyrosine have been found in demyelinating lesions of MS brains as well as spinal cords of mice with EAE (Hooper et al., 1998; Hooper et al., 1997). A strong correlation exists between CSF levels of cytokines, disruption of blood-brain barrier, and high levels of circulating cytokines in MS patients (Villarroya et al., 1996; Issazadeh et al., 1995). Increase in TNF-α and IFN-γ levels seems to predict relapse in MS and the number of circulating IFN-γ positive blood cells correlates with severity of disability. These observations support the view that in both MS and EAE, induction of proinflammatory cytokines and production of NO through iNOS play roles in the pathogenesis of these diseases.
Alzheimer's disease (AD) is the most common degenerative dementia affecting primarily the elderly population. The disease is characterized by the decline of multiple cognitive functions and a progressive loss of neurons in the central nervous system. Deposition of beta-amyloid peptide has also been associated with AD. Over the last decade, a number of investigators have noted that AD brains contain many of the classical markers of immune mediated damage. These include elevated numbers of microglia cells, which are believed to be an endogenous CNS form of the peripheral macrophage, and astrocytes. Of particular importance, complement proteins have been immunohistochemically detected in the AD brain and they most often appear associated with beta-amyloid containing pathological structures known as senile plaques (Rogers et al., 1992; Haga et al., 1993).
These initial observations which suggest the existence of an inflammatory component in the neurodegeneration observed in AD has been extended to the clinic. A small clinical study using the nonsteroidal anti-inflammatory drug, indomethacin, indicated that indomethacin significantly slowed the progression of the disease (Neurology, 43(8):1609 (1993)). In addition, a study examining age of onset among 50 elderly twin pairs with onsets of AD separated by three or more years, suggested that anti-inflammatory drugs may prevent or delay the initial onset of AD symptoms (Neurology, 44:227 (1994)).
Over the years numerous therapies have been tested for the possible beneficial effects against EAE or MS disease but with mixed results (Cross et al., 1994; Ruuls et al., 1996). Though aminoguandine (AG) has been described as a competitive inhibitor of iNOS and a suppressor of its expression (Corbett and McDaniel, 1996; Joshi et al., 1996), to date few compounds which inhibit iNOS are of potential therapeutic value have been identified. This deficiency is particularly troubling given the significant cellular damage which can arise as a result of iNOS-mediated nitric oxide toxicity, especially in chronic inflammatory disease states. There is a present need for therapeutic agents which will inhibit or even prevent cytotoxic concentrations of NO from occurring in individuals suffering from diseases and conditions to which NO toxicity or an undesired production of proinflammatory cytokines is linked.

Inhibitors of nitric oxide synthase to treat type 1 diabetes

Musc Foundation for Research Development


A transformer for reducing the electromagnetic interference (EMI) effect is disclosed. The transformer includes a bobbin; a magnetic core assembly partially sleeved by the bobbin; a first primary winding coiled around the bobbin; a secondary winding coiled on the first primary winding; and a first shielded element disposed between the first primary winding and the secondary winding for disconnecting the EMI transmission from the first primary winding to the secondary winding. The first primary winding includes a first winding portion and a second winding portion, and the first winding portion has larger EMI comparing to the second winding portion. The first winding portion of the first primary winding is adjacently disposed to the magnetic core assembly for shielding the EMI of the first primary winding by using the magnetic core assembly. The second winding portion is coiled on the first winding portion and adjacently disposed to the secondary winding for increasing the electromagnetic coupling rate of the first primary winding and the secondary winding. In addition, a power transform circuit applied in the transformer for reducing the EMI effect is also disclosed. The power transform circuit includes a switch, a power input for receiving a power signal; and a transformer electrically connected to the power input and the switch, for receiving and transforming the power signal.

Transformer is an electronic component for usually applying to various electronic apparatuses. Please refer to FIG. 1 which is a structure diagram illustrating a conventional transformer. As shown in FIG. 1, a conventional transformer 1 includes a magnetic core assembly 11, a bobbin 12, a primary winding 13 and a secondary winding (not shown in FIG. 1). The primary winding 13 and the secondary winding are coiled a winding region of the bobbin 12 by the sandwich-coiled type. That is, the primary winding 13 is separated to two portions covering the secondary winding, and the side-by-side adjacent region between the primary winding and the secondary winding are insulated by tape. Generally, the magnetic core assembly 11 is EE-core, EI-core or ER-core. The axle center 111 is disposed inside a channel 121 of the bobbin 12, for resulting in the magnetic core assembly 11 with the primary winding 13 and the secondary winding to generate the electromagnetic coupling induction for achieving the purpose of voltage transform.
Although the conventional transformer 1 certainly can achieve the effectiveness of voltage transform, there is still a problem need to be solved. When the transformer 1 is applied to a power transform circuit (not shown in FIG. 1), the primary winding 13 of the transformer 1 is electrically connected to a switch of the power transform circuit, and the current passing through the primary winding 13 is connected or broken off by controlling the switch. However, when the switch is repeatedly OFF and ON, the current passed through the primary winding 13 is changed largely. Thus, the electromagnetic interference (EMI) is generated. While the primary winding 13 is closer the switch, the EMI is the more significant. Furthermore, the generation of EMI will affect the electromagnetic coupling rate of the primary winding 13 and secondary winding and increase the leakage inductance of the transformer 1, resulting in lowering the operation efficiency of the transformer 1.
Therefore, the purpose of the present invention is to develop a transformer and a power transform circuit for reducing the effect of electromagnetic interference to deal with the above situations encountered in the prior art.

Transformer for reducing electromagnetic interference and power transform circuit applied therein


The current application is directed to methods and quantum circuits that prepare qubits in specified non-stabilizer quantum states that can, in turn, be used for a variety of different purposes, including in a quantum-circuit implementation of an arbitrary single-qubit unitary quantum gate that imparts a specified, arbitrary rotation to the state-vector representation of the state of an input qubit. In certain implementations, the methods and systems consume multiple magic-state qubits in order to carry out probabilistic rotation operators to prepare qubits with state vectors having specified rotation angles with respect to a rotation axis. These qubits are used as resources input to various quantum circuits, including the quantum-circuit implementation of an arbitrary single-qubit unitary quantum gate.

Enormous advances have been made in digital computing over the past 70 years. Crude, high-energy-consuming, vacuum-tube-based computer systems developed in the 1940s have evolved into today's personal computers, work stations, servers, and high-end distributed computer systems, based on multi-core single-integrated-circuit processors, that economically provide processing speeds, data-storage capacities, and data-transfer bandwidths that were unimaginable even 20 years ago. However, digital computing appears to be bounded by certain physical and problem-domain constraints.
With regard to physical constraints, processing speeds and data-storage capacities are generally inversely related to the minimum sizes at which transistors and other circuit elements can be fabricated within integrated circuits. Much of the exponential growth observed in computational bandwidth for various classes of computer systems can be attributed to a corresponding decrease in feature sizes within integrated circuits. There are, however, fundamental physical limits, on the order of the sizes of complex molecules, past which feature sizes cannot be further decreased, and somewhat larger feature-size limitations past which further decreases in feature sizes can be obtained only by exponentially increasing integrated-circuit cost.
With regard to problem-domain constraints, while digital computers provide the basis for practical and cost-effective solutions of many types of computational problems, there are many types and classes of computational problems that appear incapable of being addressed efficiently by digital computer systems. Examples include accurate simulation of the quantum-mechanical behavior of large molecules and aggregations of molecules and a variety of traditional numerical and computational problems, including large-integer factoring and graph-isomorphism problems.
In 1982, Richard Feynman made a suggestion for a new type of computational system based on quantum-mechanical components. He suggested that quantum computers could more efficiently address certain classes of computational problems than digital computers and, in the case of computational problems in computational chemistry and physics, provide practical approaches to computational problems that are intractable using digital computer systems. Since that time, great progress has been made in developing the theoretical foundation for quantum computing and the first quantum computers have been implemented. Various computational problems have been identified that can be addressed more efficiently by quantum computers than by classical digital computers. However, significant research and development efforts continue to be applied in order to provide practical and cost-effective general-purpose quantum-computing systems for widespread use. As one example, significant theoretical efforts are currently being applied to identify practical and cost-effective implementations of quantum circuits.

Method and system that produces non-stabilizer quantum states that are used in various quantum circuits and systems


A vehicle suspension system of a motor vehicle includes a plurality of suspension devices mounted on the vehicle with respect to right and left wheels of the vehicle, respectively, a first behavior controller that controls the motion of each of the suspension devices when a vehicle body undergoes a first behavior, and a second behavior controller that controls the motion of each of the suspension devices when the vehicle body undergoes a second behavior, independently of the first behavior controller.

1. Field of the Invention
The invention relates to a vehicle suspension system employed in a motor vehicle, such as a four-wheel vehicle, and in particular to a vehicle suspension system that includes vehicle behavior controllers that control the motion of each suspension device (e.g., hydraulic cylinder for suspension) mounted with respect to each of all right and left wheels, and is adapted to control or suppress particular types of behavior, such as bouncing, pitching and rolling, of a vehicle body.
2. Description of Related Art
An example of a vehicle suspension system of the above type is disclosed in, for example, Japanese laid-open Patent Publication No. 6-509997. In the vehicle suspension system disclosed in this publication, suspension hydraulic cylinders respectively mounted with respect to front and rear, right and left wheels of the vehicle are diagonally connected to each other by hydraulic pipes, so that the suspension system can suppress pitching and rolling of the vehicle body while assuring sufficient road-holding characteristic of the wheels on an unleveled ground.
The operating characteristics of the vehicle suspension system as shown in the above-indicated publication are determined by accumulators (e.g., gas springs) connected to and communicating with respective hydraulic pipes for connecting diagonally located cylinders, or accumulators connected to and communicating with the hydraulic pipes for connecting diagonally located cylinders and a single load distribution unit, or an actuator that includes a single load distribution unit to which the hydraulic pipes for connecting diagonally located cylinders are connected for fluid communication. With this arrangement, the operating characteristics of the suspension system cannot be individually or separately set for suppressing each type of vehicle behaviors, such as pitching and rolling, of the vehicle body. Thus, it has been difficult to set the operating characteristics of the suspension system suitable for each type of vehicle behavior.
In addition, the known vehicle suspension system as described above is constructed such that a pair of hydraulic chambers formed on the opposite sides of a piston in each of the suspension hydraulic cylinders are diagonally connected to a pair of hydraulic chambers formed in a corresponding suspension hydraulic cylinder that is located in a diagonal relationship with the above-indicated hydraulic cylinder. Namely, two ports formed in each of the suspension hydraulic cylinders are diagonally connected to two ports formed in the corresponding suspension hydraulic cylinder, to thus provide two hydraulic pipe systems. Thus, the hydraulic pipes are arranged in a complicated manner, which results in increased cost and weight of the pipes, and eventually those of the suspension system. While the vehicle suspension system as described above is able to suppress pitching and rolling of the vehicle body, the system is not able to suppress bouncing (i.e., behavior in the heaving direction) of the vehicle body.