Friday, December 31, 2010
AN/SPS-43
The AN/SPS-43 was a ship-based, 2-dimensional, air-search radar developed and manufactured by the American firm Westinghouse. The AN/SPS-43 was capable of providing bearing and distance information, but no altitude information. With an antenna that looked like a bedspring, it could detect the range and bearing of a target at a long range (300+ miles); the target would then be picked up by a 3-D radar such as the AN/SPS-48, which assuming the target to be hostile would present the target information to a fire-control radar like the AN/SPG-55. Operating at 0,2 GHz, the AN/SPS-43 was introduced in 1961 and, after several years of service with the US Navy, it was replaced by AN/SPS-49.
Thursday, December 30, 2010
AN/SPS-40
The AN/SPS-40 was a ship-based, long-range air search radar which was developed by Lockheed Corporation for the US Navy, and later manufactured by the firms Sperry Corporation, Westinghouse, and Norden Systems. Introduced in the 1960s, the AN/SPS-40 was a 2-Dimensional, solid state radar that provided target detection, contact bearing, and fire control system designation. It also featured low vulnerability to Anti-Radiation Missiles, imperviousness to weather clutter and chaff, and excellent range resolution for multiple missile raids. It was used on Spruance-class destroyers, Belknap-class cruisers, Leahy-class cruisers, Knox-class frigates, Bronstein-class frigates, Hamilton-class cutters, Raleigh-class amphibious transport docks and many other ship classes. The SPS-40 was replaced by the AN/SPS-49 on newer ships and on ships that received the New Threat Upgrade.
Variants: AN/SPS-40, which was the first model developed and built by Lockheed; AN/SPS-40A, which was an upgraded version produced by Sperry; AN/SPS-40B, with an integrated IFF-System; AN/SPS-40C, which had an improved tracking detection and electronic counter-countermeasures capacity; AN/SPS-40D, which was a further upgraded version of the A model manufactured by Westinghouse; AN/SPS-40E, which was a variant produced by Norden System by later cancelled by the US Navy.
Specifications for the AN/SPS-40
Type: 2D Air-search
Frequency: 400 MHz, UHF band
Performance: 200 - 250 kilowatts
Range: 230 miles (370 km)
Diameter 140" x 214"
Azimuth: 0-360°
Elevation: vertical beam width 19°
Precision: horizontal beam width 10.5°
Variants: AN/SPS-40, which was the first model developed and built by Lockheed; AN/SPS-40A, which was an upgraded version produced by Sperry; AN/SPS-40B, with an integrated IFF-System; AN/SPS-40C, which had an improved tracking detection and electronic counter-countermeasures capacity; AN/SPS-40D, which was a further upgraded version of the A model manufactured by Westinghouse; AN/SPS-40E, which was a variant produced by Norden System by later cancelled by the US Navy.
Specifications for the AN/SPS-40
Type: 2D Air-search
Frequency: 400 MHz, UHF band
Performance: 200 - 250 kilowatts
Range: 230 miles (370 km)
Diameter 140" x 214"
Azimuth: 0-360°
Elevation: vertical beam width 19°
Precision: horizontal beam width 10.5°
Wednesday, December 29, 2010
AN/SPG-51
The AN/SPG-51 is a ship-based, fire control, pulse-doppler radar which has been developed and produced by Raytheon for the US Navy to guide the RIM-66 Standard missiles. The AN/SPG-51 operates in the frequency range between 4 GHz and 10 GHz with a constant performance of 22.5 KW. It is used for targeting, tracking, and guiding surface-to-air missile on Virginia-class cruisers, California-class cruisers, and Kidd-class destroyers. The French Cassard class frigates also employs this radar. Raytheon has produced several versions: 1) AN/SPG-51A, which was the first model introduced in the 1950s; 2) AN/SPG-51B, which is a ground-based variant; 3) AN/SPG-51C, which features full automatic target tracking; 4) AN/SPG-51D, which is a tracking/illumination radar for the Standard missiles, used on Virginia-class cruisers; 5) AN/SPG-51E, which has also the capacity to guide the RIM-8 missiles.
Tuesday, December 28, 2010
ASARS-2
ASARS-2 is an advanced Synthetic aperture, high-resolution radar designed by Hughes Aircraft in the early 1980s for the US Lockheed U2 spy aircraft. This multi-mode, reconnaissance radar system is currently manufactured by Raytheon. The ASARS-2 features real time, long-range mapping capabilities. It detects and accurately locates fixed and moving ground targets, gathering detailed information, formatting the data, and transmitting high resolution images. target information is transmitted via a wideband data link to a ground station. The radar is capable of producing extremely high resolution images at long range.
The ASARS-2's high resolution capability has also been used by the American civilian community to map and assess damage from the floods along the Mississippi and Missouri rivers in 1993, the northern California floods in 1995, and the Northridge, California, earthquake in 1994. In military field, ASARS-2 was used extensively during Operation Desert Storm for target location and battle damage assessment. Raytheon is currently delivering radar upgrades under the ASARS Improvement Program (AIP), which will further enhance ASARS-2 capabilities. ASARS-2 is the foundation for current production and development radars such as HISAR, Global Hawk, and the Airborne Reconnaissance Low-Magnification (ARL-M) Crazy Hawk.
The ASARS-2's high resolution capability has also been used by the American civilian community to map and assess damage from the floods along the Mississippi and Missouri rivers in 1993, the northern California floods in 1995, and the Northridge, California, earthquake in 1994. In military field, ASARS-2 was used extensively during Operation Desert Storm for target location and battle damage assessment. Raytheon is currently delivering radar upgrades under the ASARS Improvement Program (AIP), which will further enhance ASARS-2 capabilities. ASARS-2 is the foundation for current production and development radars such as HISAR, Global Hawk, and the Airborne Reconnaissance Low-Magnification (ARL-M) Crazy Hawk.
Monday, December 27, 2010
AN/FPS-95 (Cobra Mist)
Also known under the code name of Cobra Mist, the AN/FPS-95 was an-over- the-horizon tracking radar built on the English North Sea coast in the late 1960s to overlook air and missile activity in Eastern Europe and the Western areas of the Soviet Union during the Cold War. Up to that time, the AN/FPS-95 was the most powerful and sophisticated radar of its kind. The design incorporated rather coarse spatial resolution and relied upon ultralinear wide dynamic range components and complex sygnal processing in attempting to achieve extreme subclutter visibility of 80 to 90 dB needed to separate target returns from the strong ground clutter.
Nevertheless, the detection performance of the FPS-95 was spoiled, since the actual subclutter visibility achieved was only 60 to 70 dB, the limitation being due to a noise with approximately flat amplitude-versus-Doppler frequency which appeared in all range bins containing ground clutter and aircraft returns. The experiments carried out at the site failed to determine the source of the noise, either in the equipment or in the propagation medium. The project was shut down in 1973. The site and buildings are now occupied by a broadcast transmitter for the BBC World Service.
The AN/FPS-95 antenna consisted of 18 individual strings radiating outward from a single point near the eastern shore of Orford Ness. Each string was 2,040 feet (620 m) long, supported on masts from 42 feet (13 m) to 195 feet (59 m) high, with multiple active elements hung from the strings. The strings were arranged 8 degrees 40 minutes apart, covering an arc from 19.5 to 110.5 degrees clockwise from true north. Beneath the antenna was a large wire mesh screen acting as a reflector. The mesh extended past the hub to the east. Operating the AN/FPS-95 radar took considerable pre-observation setup. To select a particular region of the sky, six adjacent antennas strings were connected to the electronics using a switch matrix hidden underground at the antenna hub. Using beam steering, the operators would select a 90 degree wide fan-shaped area to investigate.
Nevertheless, the detection performance of the FPS-95 was spoiled, since the actual subclutter visibility achieved was only 60 to 70 dB, the limitation being due to a noise with approximately flat amplitude-versus-Doppler frequency which appeared in all range bins containing ground clutter and aircraft returns. The experiments carried out at the site failed to determine the source of the noise, either in the equipment or in the propagation medium. The project was shut down in 1973. The site and buildings are now occupied by a broadcast transmitter for the BBC World Service.
The AN/FPS-95 antenna consisted of 18 individual strings radiating outward from a single point near the eastern shore of Orford Ness. Each string was 2,040 feet (620 m) long, supported on masts from 42 feet (13 m) to 195 feet (59 m) high, with multiple active elements hung from the strings. The strings were arranged 8 degrees 40 minutes apart, covering an arc from 19.5 to 110.5 degrees clockwise from true north. Beneath the antenna was a large wire mesh screen acting as a reflector. The mesh extended past the hub to the east. Operating the AN/FPS-95 radar took considerable pre-observation setup. To select a particular region of the sky, six adjacent antennas strings were connected to the electronics using a switch matrix hidden underground at the antenna hub. Using beam steering, the operators would select a 90 degree wide fan-shaped area to investigate.
Sunday, December 26, 2010
AN/FPS-35
The AN/FPS-35 was a long-range, ground-based search radar developed by Sperry Gyroscope Company and used during the Cold War. It operated between 420 and 450 MHz and had an antenna that weighed 70 tons. The FPS-35 was first deployed in 1960, but was not operational until 1962. Frequent bearing problems plagued this radar because of its massive antenna, which had a concrete tower base 80 ft high to support it.
Only twelve AN/FPS-35 radars would become operational in the US. The radar was able to detect objects 200 miles away, providing enhanced electronic countermeasures. Originally developed at the Thomasville Aircraft Control and Warning Station, in Thomasville, Alabama, all of the radars have been knocked down by the federal government, except for the one at Camp Hero on the eastern tip of Long Island, New York.
Only twelve AN/FPS-35 radars would become operational in the US. The radar was able to detect objects 200 miles away, providing enhanced electronic countermeasures. Originally developed at the Thomasville Aircraft Control and Warning Station, in Thomasville, Alabama, all of the radars have been knocked down by the federal government, except for the one at Camp Hero on the eastern tip of Long Island, New York.
AN/FPS-17
The AN/FPS-17 was a ground-based, fixed-beam, surveillance radar system. First installed at Laredo Air Force Base, Texas, the AN/FPS-17 was used to track rockets launched from White Sands, New Mexico. It was equipped with a fixed-fence antenna that stood 175 feet high and 110 feet wide. The radar transmitter sent out a VHF pulse at a frequency between 180 to 220 MHz. AN/FPS-17 units were installed in the late 1950s at Shemya Island in the Aleutians and in Turkey. The unit at Shemya subsequently was replaced by the Cobra Dane (AN/FPS-108) radar.
AN/FPS-16
The AN/FPS-16 is a C-band monopulse tracking radar used by both the US Air Force and NASA. It employs a waveguide hybrid-labyrinth comparator to develop angle track information. The comparator receives RF signals from an array of four feed horns which are located at the focal point of a 12-foot (4 m) parabolic reflector. The comparator of the AN/FPS-16 performs vector addition and subtraction of the energy received by each horn. The elevation tracking data is generated in the comparator as the difference between the sums of the top two horns. The azimuth tracking error is the difference between the sums of the two vertical horn pairs. The vectorial sums of all four horns is combined in a third channel. Three mixers with a common local oscillator, and three 30 MHz IF strips are used; one each for the azimuth, elevation, and sum signals.
The accuracy of Radar Set AN/FPS-16 is such that the position data obtained from point-source targets has azimuth and elevation angular errors of less than 0.1 milliradian (approximately 0.006 degree) and range errors of less than 5 yards (5 m) with a signal-to-noise ratio of 20 decibels or greater. The AN/FPS-16 radar system was introduced between 1958 and 1961 at the Atlantic Missile Test Range with installations including Cape Canaveral, Grand Bahama, San Salvador, Ascension and East Grand Bahama Island. The FPS-16 located on the Australian Weapons Research Establisnment Range at Woomera, in South Australia was also linked to the NASA network for Mercury and later missions. NASA Acq aid and telelmetry systems were co-located with the Australian radar. In the 1980’s WSMR started a program to move most of our FPS-16 radars from their original fixed sites into a mobile configuration. This now allows most of the radars to be moved to various sites, and when necessary throughout the world. Two radars with larger 3 Megawatt transmitters remain at fixed sites at Malone and Stallion. One other FPS-16, located at Phillips Hill, retains its original fixed site configuration.
The accuracy of Radar Set AN/FPS-16 is such that the position data obtained from point-source targets has azimuth and elevation angular errors of less than 0.1 milliradian (approximately 0.006 degree) and range errors of less than 5 yards (5 m) with a signal-to-noise ratio of 20 decibels or greater. The AN/FPS-16 radar system was introduced between 1958 and 1961 at the Atlantic Missile Test Range with installations including Cape Canaveral, Grand Bahama, San Salvador, Ascension and East Grand Bahama Island. The FPS-16 located on the Australian Weapons Research Establisnment Range at Woomera, in South Australia was also linked to the NASA network for Mercury and later missions. NASA Acq aid and telelmetry systems were co-located with the Australian radar. In the 1980’s WSMR started a program to move most of our FPS-16 radars from their original fixed sites into a mobile configuration. This now allows most of the radars to be moved to various sites, and when necessary throughout the world. Two radars with larger 3 Megawatt transmitters remain at fixed sites at Malone and Stallion. One other FPS-16, located at Phillips Hill, retains its original fixed site configuration.
Saturday, December 25, 2010
AN/APG-69
The AN/APG-69 was an X-band pulse-doppler radar developed by Emerson Electric and used in the F-5E fighter aircraft. This radar was a box-for-box replacement for the AN/APQ-153, requiring no structural wiring or cooling changes. The AN/APG-69 featured ten air-to-air and air-to-ground modes. The air-to-air modes included velocity search for long-range wide-angle searches, track-while-scan, single target track and dogfight modes that locked onto the closest target. The AN/APG-69 could guide the AIM-7 Sparrow missile, making it the first of Emerson's offerings to reach production with beyond visual range capability. The air-to-ground modes included Doppler-Beam Sharpening mapping, moving target search and track, and sea-surface-search modes. The AN/APG-69 had a look-up detection range of 30nm against a 5 square meter target.
AN/APG-67
The AN/APG-67 is a multi mode, X-band, pulse-doppler radar, which was originally developed by General Electric for the F-20 Tigershark program of the early 1980s, but today is manufactured by Lockheed Martin. The APG-67 is an active electronically, all-digital radar which features a planar phased array antenna and simplified electronics housed in three line-replaceable units, one of these being the radar "dish" itself. The entire system weighs less than 160 lb and takes up less than 1.9 cubic feet. The system broadcasts an average power of 396 watts. Offering a variety of air-to-air, air-to-ground, sea-search and mapping modes, the AN/APG-67 is compatible with most weapons used by the US Air Force in the 1980s.
In tracking mode, the AN/APG-67 can detect fighter-sized targets at up to 40 nm (75 km). In the air-to-air mode it features long-range velocity search, track-while-scan with up to ten tracked targets, and a variety of single-target-track and auto-lockon "dogfight" modes. The air-to-ground modes include real beam ground mapping, synthetic aperture radar imaging (SAR) and beacon tracking. All communications with the cockpit is handled using the MIL-STD-1553 data bus; the data bus allows the data from any of the aircraft's sensors to be shown on any of the in-cockpit displays, or sent to other aircraft using a data link.
The AN/APG-67 is fully operational 90 seconds after turn-on. Its coherent pulse-doppler processing is particularly adept at detecting targets in the "look-down" engagement which gives the pilot look-down/shoot-down capability for targets hiding in the ground clutter and sea clutter. Additionally, pilot distraction due to false alarm is minimized.
In tracking mode, the AN/APG-67 can detect fighter-sized targets at up to 40 nm (75 km). In the air-to-air mode it features long-range velocity search, track-while-scan with up to ten tracked targets, and a variety of single-target-track and auto-lockon "dogfight" modes. The air-to-ground modes include real beam ground mapping, synthetic aperture radar imaging (SAR) and beacon tracking. All communications with the cockpit is handled using the MIL-STD-1553 data bus; the data bus allows the data from any of the aircraft's sensors to be shown on any of the in-cockpit displays, or sent to other aircraft using a data link.
The AN/APG-67 is fully operational 90 seconds after turn-on. Its coherent pulse-doppler processing is particularly adept at detecting targets in the "look-down" engagement which gives the pilot look-down/shoot-down capability for targets hiding in the ground clutter and sea clutter. Additionally, pilot distraction due to false alarm is minimized.
Friday, December 24, 2010
AN/APG-66
The AN/APG-66 is a solid state, X-band, multimode radar used by US Air Force in the F-16 fighter aircraft. This radar system is composed of a transmitter, a digital signal processor, a radar computer, and an antenna. The AN/APG-66 was developed by Westinghouse in the 1970s, but it is today manufactured by Northrop Grumman. In dogfight mode, the radar is capable of scanning a 20 degrees x 20 degrees field, but in high-g maneuvers, it can scan a 40 degrees x10 degrees pattern. In lookdown mode, the AN/APG-66 has the capability of detecting a fighter-size plane at a range of 34.5 Nautical miles (55.6 kilometers). This medium range, pulse-doppler radar is also used by the U.S. Customs and Border Protection's C-550 Cessna Citation and Piper PA-42 Cheyenne II's as well as the Small Aerostat Surveillance System (SASS).
The AN/APG-66 radar had been manufactured in fourteen different variants with the APG-66(V)2, the APG-66(V)2A, and APG-66(V)3 being the most widely used. APG-66(V)2 is an upgrade of base radar, fitted with new signal processor, higher output power, improved reliability. AN/APG-66(V)2A had a new combined signal and data processor that provides seven times the speed and 20 times the memory of the older radar computer and digital signal processor line replaceable units. APG-66(V)3 has CW illumination capability, possibly for export to Taiwan. The latter is also employed in select US Navy P-3 Orion aircraft as part of a Counter Drug Update (CDU) for Counternarcotics (CN) surveillance and interdictioon operations in support of USCG.
Specifications for the AN/APG-66
Frequency: 6.2 to 10.9 GHz
Azimuth angular coverage: ±10 degrees / ± 30 degrees / ± 60 degrees
Search cone: 120 degrees × 120 degrees
Volume: 0.08 m³ to 0.102 m³ depending on configuration
Weight: 98 to 135 kg depending on configuration
The AN/APG-66 radar had been manufactured in fourteen different variants with the APG-66(V)2, the APG-66(V)2A, and APG-66(V)3 being the most widely used. APG-66(V)2 is an upgrade of base radar, fitted with new signal processor, higher output power, improved reliability. AN/APG-66(V)2A had a new combined signal and data processor that provides seven times the speed and 20 times the memory of the older radar computer and digital signal processor line replaceable units. APG-66(V)3 has CW illumination capability, possibly for export to Taiwan. The latter is also employed in select US Navy P-3 Orion aircraft as part of a Counter Drug Update (CDU) for Counternarcotics (CN) surveillance and interdictioon operations in support of USCG.
Specifications for the AN/APG-66
Frequency: 6.2 to 10.9 GHz
Azimuth angular coverage: ±10 degrees / ± 30 degrees / ± 60 degrees
Search cone: 120 degrees × 120 degrees
Volume: 0.08 m³ to 0.102 m³ depending on configuration
Weight: 98 to 135 kg depending on configuration
Thursday, December 23, 2010
AN/APG-63
The Raytheon AN/APG-63 is an all-weather multimode radar which was developed by Hughes Aircraft for the US Air Force. Used in the F-15 Eagle air superiority fighter, the AN/APG-63 is capable of detecting and tracking aircraft and small high-speed targets at distances beyond visual range down to close range, and at altitudes down to treetop level. Presently manufactured by Raytheon, the AN/APG-63 is an X-band pulse-doppler radar designed for both air-air and air-ground missions with the capability of looking up at high-flying targets and down at low-flying targets without being confused by ground clutter. The radar feeds target information into the aircraft's central computer for effective weapons delivery. For close-in dogfights, the radar automatically acquires enemy aircraft and projects this information onto the cockpit head-up display.
The latest variant of this radar is the AN/APG-63(V)3, which provides powerful, adaptable radar technology, proven performance, and tactical flexibility that F-15 pilots can rely on. It is the newest member of Raytheon’s F-15 radar family which continues a tradition of innovative, highly reliable technology. Superior situational awareness is a key benefit of this all-weather, multimode radar. Other benefits include multi-role capability, long-term support, and easy future growth options. Raytheon’s F-15 radar growth plan provides a smooth transition from one product upgrade to another. The APG-63(V)1 seamlessly integrates the APG-63(V)3’s AESA components with minimal downtime. The APG-63(V)3 provides for similarly easy future transition.
The latest variant of this radar is the AN/APG-63(V)3, which provides powerful, adaptable radar technology, proven performance, and tactical flexibility that F-15 pilots can rely on. It is the newest member of Raytheon’s F-15 radar family which continues a tradition of innovative, highly reliable technology. Superior situational awareness is a key benefit of this all-weather, multimode radar. Other benefits include multi-role capability, long-term support, and easy future growth options. Raytheon’s F-15 radar growth plan provides a smooth transition from one product upgrade to another. The APG-63(V)1 seamlessly integrates the APG-63(V)3’s AESA components with minimal downtime. The APG-63(V)3 provides for similarly easy future transition.
AN/MSQ-46
The AN/MSQ-46 Bomb Scoring Radar was an air search automatic tracking radar which operated in the 8500 to 9600 MHz frequency range. With a range of 200 nautical miles, the AN/MSQ-46 was fitted out with an 8 foot diameter fresnel lens rather than a parabolic dish. The lens provided improved low-level tracking of aircraft. Provided with an increased range capability, the AN/MSQ-46 was developed from the MSQ-39 system, and since it used a lens instead of a parabolic dish, the MSQ-46 was not affected by ground clutter, meaning returns caused by abnormalities in the earth's terrain or trees, etc.
Wednesday, December 22, 2010
AN/SPS-52
The AN/SPS-52 was a 3-D, long range air search radar which provided contact bearing, range and altitude. With medium detection probability, the AN/SPS-52C variant had four modes of operation: high angle, long range, high data rate, and MTI (Moving Target Indicator). It was capable of detecting air targets at ranges in excess of 200nm. Tilted back at an angle of 25º, its planar array antenna used frequency scanning to steer the radar beam and was capable of providing altitude on targets in excess of 100,000 feet. Then, the radar fed this data into the ship's Integrated Automated Detection and Tracking system (IADT) AN/SYS-1, which provided targeting data for the ship's fire control system. The AN/SPS-52 was used on Brooke class frigates, Charles F. Adams class destroyers, Hatakaze class destroyers, Tarawa class amphibious assault ships, Wasp class amphibious assault ships, Galveston class cruisers, Providence class cruisers and other ships. In 2004, this radar was withdrawn from service.
AN/SPS-67
The AN/SPS-67 is a solid-state, surface-search/navigation radar used by the US Navy. It is a two-dimensional, G-band radar which provides highly accurate surface and limited low-flyer detection and tracking capabilities. With a range of 104 km (56.2 nmi), the AN/SPS-67 operates in the 5450 to 5825 MHz range. It utilizes a coaxial magnetron as the transmitter output tube. The transmitter/receiver is capable of operation in several pulse width settings: a long (1.0 µsec), medium (0.25 µsec), or short (0.10 µsec) pulse mode to enhance radar performance for specific operational or tactical situations. The AN/SPS-67 was developed as a replacement for the AN/SPS-10 radar, using a more reliable antenna and incorporating standard electronic module technology for simpler repair and maintenance.
The AN/SPS-67 performs very well in rain and sea clutter, and is useful in harbor navigation, since the AN/SPS-67 is capable of detecting buoys and small obstructions without difficulty. The AN/SPS-67(V) has two other configurations, the (V)2 and (V)3. The AN/SPS-67(V)2 is identical to the AN/SPS-67(V)1 with exception of the antenna. This variant uses a standard surface search antenna. The AN/SPS-67(V)3 is ehanced from previous configurations. This radar has a signal processing unit that provides digital moving target indicator (DMTI) capability. The function of the DMTI circuitry is to automatically cancel unwanted fixed echoes (sea clutter, clouds, rain, etc.) and display only moving target signals.
The AN/SPS-67 performs very well in rain and sea clutter, and is useful in harbor navigation, since the AN/SPS-67 is capable of detecting buoys and small obstructions without difficulty. The AN/SPS-67(V) has two other configurations, the (V)2 and (V)3. The AN/SPS-67(V)2 is identical to the AN/SPS-67(V)1 with exception of the antenna. This variant uses a standard surface search antenna. The AN/SPS-67(V)3 is ehanced from previous configurations. This radar has a signal processing unit that provides digital moving target indicator (DMTI) capability. The function of the DMTI circuitry is to automatically cancel unwanted fixed echoes (sea clutter, clouds, rain, etc.) and display only moving target signals.
Blindfire Tracking Radar
The Blindfire tracking radar is a monopulse F-Band radar manufactured by Alenia Marconi Systems from 1970. Used in the Rapier missile system, the Marconi DN 181 Blindfire radar emits a very narrow "pencil" beam, tracking both the target and missile. To allow the operator to monitor the Blindfire system when it is tracking the target, the existing optical tracker is slaved to the Blindfire radar, although it is possible for the optical tracker to be manually "laid on" a second target whilst the Blindfire engages the first target. The Blindfire trailer carries its own generator unit, and a third Land Rover (a 12v winch equipped 101 FC) - the Tracking Radar Tractor (TRT) - to tow it.
The Blindfire tracking radar provides fully automatic all-weather engagement. The output is sufficiently powerful to burn through most jamming signals and the radar uses advanced frequency management techniques to evade jamming and other hostile electronic countermeasures. The system incorporates a self-surveillance reversionary mode of operation. A dedicated missile command link provides dual firing capability. Operationally, Blindfire is alerted to a potential target by an associated surveillance radar, which indicates the approximate direction of the threat. So cued, Blindfire 'immediately' swings on to this bearing and establishes target bearing, range and height. When lock-on is achieved, the target is engaged with a radar tracked missile shot. The difference between the target and missile angles are 'instantly' derived within the architecture as commands are automatically transmitted to the missile to guide it on to the target.
The Blindfire tracking radar provides fully automatic all-weather engagement. The output is sufficiently powerful to burn through most jamming signals and the radar uses advanced frequency management techniques to evade jamming and other hostile electronic countermeasures. The system incorporates a self-surveillance reversionary mode of operation. A dedicated missile command link provides dual firing capability. Operationally, Blindfire is alerted to a potential target by an associated surveillance radar, which indicates the approximate direction of the threat. So cued, Blindfire 'immediately' swings on to this bearing and establishes target bearing, range and height. When lock-on is achieved, the target is engaged with a radar tracked missile shot. The difference between the target and missile angles are 'instantly' derived within the architecture as commands are automatically transmitted to the missile to guide it on to the target.
Tuesday, December 21, 2010
Retinal Ganglion Cells
A retinal ganglion cell (RGC) is a type of neuron (nerve cell), which is situated in the retina of the eye. Forming a thin layer, retinal ganglion cells receives visual information from photoreceptors (cones and rods) via two intermediate neuron types: bipolar cells and amacrine cells. The long axons of the retinal ganglion cells join together to make up the optic nerve and transmit image-forming and non-image forming visual information from the retina to several regions in the thalamus, hypothalamus, and mesencephalon, or midbrain.
In the human retina there are about 1.2 to 1.5 million retinal ganglion cells. With about 125 million photoreceptors per retina, on average each retinal ganglion cell receives inputs from about 100 rods and cones. Based on their projections and functions, there are at least five main classes of retinal ganglion cells: 1) midget cells, which project to the parvocellular layers of the lateral geniculate nucleus; 2) parasol cells; which project to the magnocellular layers of the lateral geniculate nucleus; 3) bistratified cells, which project to the koniocellular layers of the lateral geniculate nucleus; 4) photosensitive ganglion cells, which send their axons to the suprachiasmatic nucleus (SCN) via the retinohypothalamic tract for setting and maintaining circadian rhythms; 5) other ganglion cells extend their axons to the superior colliculus for eye movements (saccades).
In the human retina there are about 1.2 to 1.5 million retinal ganglion cells. With about 125 million photoreceptors per retina, on average each retinal ganglion cell receives inputs from about 100 rods and cones. Based on their projections and functions, there are at least five main classes of retinal ganglion cells: 1) midget cells, which project to the parvocellular layers of the lateral geniculate nucleus; 2) parasol cells; which project to the magnocellular layers of the lateral geniculate nucleus; 3) bistratified cells, which project to the koniocellular layers of the lateral geniculate nucleus; 4) photosensitive ganglion cells, which send their axons to the suprachiasmatic nucleus (SCN) via the retinohypothalamic tract for setting and maintaining circadian rhythms; 5) other ganglion cells extend their axons to the superior colliculus for eye movements (saccades).
Ocular Ischemic Syndrome
Ocular ischemic syndrome (OIS) refers to the ocular signs and symptoms which result from chronic vascular insufficiency (arterial hypoperfusion) to the eye. Severe ipsilateral or bilateral carotid artery stenosis is the most common cause of ocular ischemic syndrome. The syndrome has been associated with occlusion of the common carotid artery, internal carotid artery, and less frequently the external carotid artery. Other causes include: 1) severe ophthalmic artery occlusion, due to thromboembolism; 2) giant cell arteritis; 3) Takayasu's arteritis.
Common anterior segment signs of this eye condition include advanced cataract, anterior segment inflammation, and iris neovascularization. Posterior segment signs include narrowed retinal arteries, dilated but nontortuous retinal veins, midperipheral dot-and-blot retinal hemorrhages, cotton-wool spots, and optic nerve/retinal neovascularization. The presenting symptoms include ocular pain and abrupt or gradual visual loss.
Amaurosis fugax is a form of acute vision loss caused by reduced blood flow to the eye that may be a warning sign of an impending stroke. Consequently, those with transient blurring of vision are advised to urgently seek medical attention for a thorough evaluation of the carotid artery. Those with ocular ischemic syndrome are typically between the ages of 50 and 80; twice as many men than women are affected. More than 90% of those presenting with the condition have vision loss. Patients may report a dull, radiating ache over the eye and eyebrow. Those with ocular ischemic syndrome may also present with a history of other systemic diseases including arterial hypertension, diabetes mellitus, coronary artery disease, previous stroke, and hemodialysis.
Common anterior segment signs of this eye condition include advanced cataract, anterior segment inflammation, and iris neovascularization. Posterior segment signs include narrowed retinal arteries, dilated but nontortuous retinal veins, midperipheral dot-and-blot retinal hemorrhages, cotton-wool spots, and optic nerve/retinal neovascularization. The presenting symptoms include ocular pain and abrupt or gradual visual loss.
Amaurosis fugax is a form of acute vision loss caused by reduced blood flow to the eye that may be a warning sign of an impending stroke. Consequently, those with transient blurring of vision are advised to urgently seek medical attention for a thorough evaluation of the carotid artery. Those with ocular ischemic syndrome are typically between the ages of 50 and 80; twice as many men than women are affected. More than 90% of those presenting with the condition have vision loss. Patients may report a dull, radiating ache over the eye and eyebrow. Those with ocular ischemic syndrome may also present with a history of other systemic diseases including arterial hypertension, diabetes mellitus, coronary artery disease, previous stroke, and hemodialysis.
Monday, December 20, 2010
Corneal Endothelium
The corneal endothelium is a single layer of specialized, flattened, mitochondria-rich cells that lines the posterior surface of the cornea and faces the anterior chamber of the eye. The corneal endothelium regulates fluid and solute transport across the posterior surface of the cornea and actively maintains the cornea in the slightly dehydrated state that is required for optical transparency.
The main physiological function of the corneal endothelium is to allow leakage of solutes and nutrients from the aqueous humor to the more superficial layers of the cornea while at the same time actively pumping water in the opposite direction, from the stroma to the aqueous.
Hexagonal cells of the corneal endothelium
The main physiological function of the corneal endothelium is to allow leakage of solutes and nutrients from the aqueous humor to the more superficial layers of the cornea while at the same time actively pumping water in the opposite direction, from the stroma to the aqueous.
Penetrating Keratoplasty
Penetrating keratoplasty is the surgical procedure in which a full thickness of the cornea is removed and replaced with donor tissue, using a microkeratome, which is an instrument employed for removing the cornea or a thin slice of it, creating a thin hinged flap. Penetrating keratoplasty is also used in the treatment of lattice corneal dystrophy. The aim of this eye surgery is to improve visual acuity by replacing the opaque host tissue by clear healthy donor tissue.
Penetrating Keratoplasty (Video)
Penetrating Keratoplasty (Video)
Retinal Vein Occlusion
Retinal vein occlusion (RVO) is a retinal vascular disorder in which the central vein that drains blood from the capilaries of the retina gets occluded or blocked. Since the central retinal artery and vein are the sole source of blood supply and drainage for the retina, such occlusion can lead to severe damage to the retina and blindness, due to ischemia and edema. Retinal vein occlusion is essentially an obstruction of a portion of the venous circulation that drains the retina. With blockage, a pressure build up takes place in the capillaries, leading to hemorrhages and leakage of fluid and blood. Then, this can lead to macular edema with leakage near the macula. Macular ischemia occurs when these capillaries, which supply oxygen to the retina, manifest leakage and nonperfusion. Neovascularization is the most devastating pathologic complication with the development of abnormal blood vessel growth.
Complete loss of vision in retinal vein occlusion (RVO) are due to macular edema, macular ischemia, and neovascular glaucoma. The precise pathologic event in RVO is intraluminal thrombus formation, which can be associated with the abnormalities of blood flow, its constituents, and vessels consistent with the Virchow triad. Central retinal vein occlusion has been likened to a neurovascular compartment syndrome at the site of the lamina cribrosa or closure of the final retinal vein located at the optic nerve.
There are two types of retinal vein occlusion: 1) central retinal vein occlusion, when the central retinal vein at the optic nerve gets clogged up; 2) branch retinal vein occlusion, which is an obstruction at a branch of the retinal vein. The two forms have both differences and similarities in pathogenesis and clinical presentation.
Retinal vein occlusion is usually divided into nonischemic and ischemic types. Such a distinction is relevant to the clinician, since two thirds of patients with the ischemic type develop the dreaded complications of macular edema, macular ischemia, and neovascularization that lead to blindness. Most investigators accept that these two entities represent varying degrees of the same underlying disease process. Yet, other clinicians and researchers argue that ischemic and nonischemic types are distinct clinical entities. In both types, blockage of the retinal vein occurs, but the nonischemic type is able to maintain better relative blood flow to the retina through collaterals, preventing the dreaded complications known of the ischemic type. The ischemic type of CRVO predisposes to anterior neovascularization called rubeosis irides. With this, high-pressure neovascular glaucoma develops. Neovascularization in the back of the eye can lead to vitreous hemorrhage and retinal detachments.
Visual recovery in retinal vein occlusion has been found to be highly variable, and the presenting visual acuity to be the best predictor of final visual acuity. The natural history of the nonischemic type carries a good prognosis for a return of satisfactory visual acuity. Sixty-five percent of eyes with an initial acuity of 20/40, had the same 20/40 acuity or better on final evaluation. In about 50% of patients, vision may be 20/200 or worse, of which, 79% showed deterioration in visual acuity on follow-up. In a third of patients with branch retinal vein occlusion, visual acuity ends up better than 20/40. However, almost two thirds of patients have evidence of some visual loss secondary to macular edema, macular ischemia, macular hemorrhage, and vitreous hemorrhage. Nonischemic CRVO may resolve completely without any complications in about 10% of cases. One third of patients may progress to the ischemic type, commonly in the first 6-12 months after presentation. In more than 90% of patients with ischemic CRVO, final visual acuity may be 20/200 or worse.
Complete loss of vision in retinal vein occlusion (RVO) are due to macular edema, macular ischemia, and neovascular glaucoma. The precise pathologic event in RVO is intraluminal thrombus formation, which can be associated with the abnormalities of blood flow, its constituents, and vessels consistent with the Virchow triad. Central retinal vein occlusion has been likened to a neurovascular compartment syndrome at the site of the lamina cribrosa or closure of the final retinal vein located at the optic nerve.
There are two types of retinal vein occlusion: 1) central retinal vein occlusion, when the central retinal vein at the optic nerve gets clogged up; 2) branch retinal vein occlusion, which is an obstruction at a branch of the retinal vein. The two forms have both differences and similarities in pathogenesis and clinical presentation.
Retinal vein occlusion is usually divided into nonischemic and ischemic types. Such a distinction is relevant to the clinician, since two thirds of patients with the ischemic type develop the dreaded complications of macular edema, macular ischemia, and neovascularization that lead to blindness. Most investigators accept that these two entities represent varying degrees of the same underlying disease process. Yet, other clinicians and researchers argue that ischemic and nonischemic types are distinct clinical entities. In both types, blockage of the retinal vein occurs, but the nonischemic type is able to maintain better relative blood flow to the retina through collaterals, preventing the dreaded complications known of the ischemic type. The ischemic type of CRVO predisposes to anterior neovascularization called rubeosis irides. With this, high-pressure neovascular glaucoma develops. Neovascularization in the back of the eye can lead to vitreous hemorrhage and retinal detachments.
Visual recovery in retinal vein occlusion has been found to be highly variable, and the presenting visual acuity to be the best predictor of final visual acuity. The natural history of the nonischemic type carries a good prognosis for a return of satisfactory visual acuity. Sixty-five percent of eyes with an initial acuity of 20/40, had the same 20/40 acuity or better on final evaluation. In about 50% of patients, vision may be 20/200 or worse, of which, 79% showed deterioration in visual acuity on follow-up. In a third of patients with branch retinal vein occlusion, visual acuity ends up better than 20/40. However, almost two thirds of patients have evidence of some visual loss secondary to macular edema, macular ischemia, macular hemorrhage, and vitreous hemorrhage. Nonischemic CRVO may resolve completely without any complications in about 10% of cases. One third of patients may progress to the ischemic type, commonly in the first 6-12 months after presentation. In more than 90% of patients with ischemic CRVO, final visual acuity may be 20/200 or worse.
Sunday, December 19, 2010
Lattice Corneal Dystrophy
Lattice corneal dystrophy is a type of genetic corneal dystrophy which results in protein fibers deposits in the stroma of the cornea. These abnormal fibrous protein aggregates are called amyloid. Many patients with lattice suffer from visual compromise due to these anterior stromal deposits which form lattice-shaped lines. Lattice dystrophy is usually an autosomal dominant condition and is the most common of stromal dystrophies. Like granular and Avellino dystrophy, the genetic defect of lattice dystrophy has been mapped to the BIGH3 gene on chromosome 5q.
As time go by, the lattice lines grow opaque and involve more of the stroma. They also gradually converge, giving the cornea a cloudiness that may also reduce vision. These abnormal protein fibers can accumulate under the cornea's epithelium, causing it to erode. This condition is known as recurrent epithelial erosion. Although lattice dystrophy can occur at any time in life, the condition usually arises in children between the ages of 2 and 7. By about age 40, some patients have scarring under the corneal epithelium, resulting in a haze on the cornea that can greatly obscure vision. Onset of the corneal changes usually occurs in the first decade of life, although patients may remain asymptomatic for years. Examination of the cornea in the second to third decade of life reveals branching, refractile lattice lines with intervening haze, which are observed best in retroillumination.
As time go by, the lattice lines grow opaque and involve more of the stroma. They also gradually converge, giving the cornea a cloudiness that may also reduce vision. These abnormal protein fibers can accumulate under the cornea's epithelium, causing it to erode. This condition is known as recurrent epithelial erosion. Although lattice dystrophy can occur at any time in life, the condition usually arises in children between the ages of 2 and 7. By about age 40, some patients have scarring under the corneal epithelium, resulting in a haze on the cornea that can greatly obscure vision. Onset of the corneal changes usually occurs in the first decade of life, although patients may remain asymptomatic for years. Examination of the cornea in the second to third decade of life reveals branching, refractile lattice lines with intervening haze, which are observed best in retroillumination.
Saturday, December 18, 2010
Recurrent Corneal Erosion
Recurrent corneal erosion is an eye condition in which there is a recurrent breakdown of the epithelial cells layer of the cornea. This corneal disorder is characterized by the failure of this outermost layer of the cornea to attach to the underlying Bowman's membrane. In other words, the recurrent corneal erosion is a defective adhesions and recurrent breakdowns of the corneal epithelium. The condition is excruciatingly painful because the loss of these cells results in the exposure of sensitive corneal nerves.
The corneal erosion may be seen by a doctor using the magnification of an ophthalmoscope, although usually fluorescein stain must be applied first and a blue-light used. Opticians, optometrists and ophthalmologists have use of slit lamp microscopes that allow for more thorough evaluation under the higher magnification. Mis-diagnosis of a scratched cornea is fairly common, especially in younger patients. The treatment consists of the use of therapeutic contact lens, controlled puncturing of the surface layer of the eye (Anterior Stromal Puncture) and laser phototherapeutic keratectomy (PTK). These all essentially try to allow the surface epithelium to reestablish with normal binding to the underlying basement membrane, the method chosen depends upon the location and size of the erosion.
Symptoms include recurring attacks of severe acute ocular pain, foreign-body sensation, photophobia, which is the sensitivity to bright lights, and tearing often at the time of awakening or during sleep when the eyelids are rubbed or opened. Signs of the condition include corneal abrasion or localized roughening of the corneal epithelium, sometimes with map-like lines, epithelial dots or microcyts, or fingerprint patterns.
The corneal erosion may be seen by a doctor using the magnification of an ophthalmoscope, although usually fluorescein stain must be applied first and a blue-light used. Opticians, optometrists and ophthalmologists have use of slit lamp microscopes that allow for more thorough evaluation under the higher magnification. Mis-diagnosis of a scratched cornea is fairly common, especially in younger patients. The treatment consists of the use of therapeutic contact lens, controlled puncturing of the surface layer of the eye (Anterior Stromal Puncture) and laser phototherapeutic keratectomy (PTK). These all essentially try to allow the surface epithelium to reestablish with normal binding to the underlying basement membrane, the method chosen depends upon the location and size of the erosion.
Symptoms include recurring attacks of severe acute ocular pain, foreign-body sensation, photophobia, which is the sensitivity to bright lights, and tearing often at the time of awakening or during sleep when the eyelids are rubbed or opened. Signs of the condition include corneal abrasion or localized roughening of the corneal epithelium, sometimes with map-like lines, epithelial dots or microcyts, or fingerprint patterns.
Phototherapeutic Keratectomy
Phototherapeutic keratectomy (PTK) is an eye surgical procedure in which a laser is employed to treat various ocular disorders by removing tissue from the cornea. Phototherapeutic keratectomy allows the removal of superficial corneal opacities and surface irregularities. It is similar to photorefractive keratectomy which is used for the treatment of refractive conditions. The common indications for PTK are corneal dystrophies, scars, opacities, bullous keratopathy.
Phototherapeutic Keratectomy (PTK) Versus Penetrating Keratoplasty (PK) in the Treatment of Lattice Corneal Dystrophy
Phototherapeutic keratectomy has been shown to be a successful treatment for anterior corneal lesions. Traditionally, PKP has been the primary treatment of choice for patients with lattice corneal dystrophy. Given the greater risks and costs associated with penetrating keratoplasty (surgical trauma, graft failure/ rejection/ dehiscence, infection, irregular astigmatism, chronic steroid use, and frequent clinic visits), PTK may provide a safer, cost effective and more efficacious alternative to penetrating keratoplasty (PK) in patients with anterior corneal dystrophies.
Preliminary data from ophthalmological experience suggests a role for phototherapeutic keratectomy as a primary treatment option for lattice patients, as approximately 90% of the patients treated with PTK alone achieved 20/40 or better vision and maintained this vision for four to seven years before requiring further treatment. Patients treated with PTK alone achieved equal or better visual acuity than the PK patients, had faster visual recovery, and had overall greater satisfaction and quality of life. Even though visually significant lesions typically recur in 4 to 7 years and require PTK retreatment, lattice dystrophy also recurs in transplants over a similar period of time and often requires regrafting.
Phototherapeutic Keratectomy (PTK) Versus Penetrating Keratoplasty (PK) in the Treatment of Lattice Corneal Dystrophy
Phototherapeutic keratectomy has been shown to be a successful treatment for anterior corneal lesions. Traditionally, PKP has been the primary treatment of choice for patients with lattice corneal dystrophy. Given the greater risks and costs associated with penetrating keratoplasty (surgical trauma, graft failure/ rejection/ dehiscence, infection, irregular astigmatism, chronic steroid use, and frequent clinic visits), PTK may provide a safer, cost effective and more efficacious alternative to penetrating keratoplasty (PK) in patients with anterior corneal dystrophies.
Preliminary data from ophthalmological experience suggests a role for phototherapeutic keratectomy as a primary treatment option for lattice patients, as approximately 90% of the patients treated with PTK alone achieved 20/40 or better vision and maintained this vision for four to seven years before requiring further treatment. Patients treated with PTK alone achieved equal or better visual acuity than the PK patients, had faster visual recovery, and had overall greater satisfaction and quality of life. Even though visually significant lesions typically recur in 4 to 7 years and require PTK retreatment, lattice dystrophy also recurs in transplants over a similar period of time and often requires regrafting.
Kjer's Optic Neuropathy
Also known as dominant optic atrophy, Kjer's optic neuropathy is an autosomally inherited disease that affects the optic nerves, causing reduced visual acuity and blindness beginning in childhood. Dominant optic atrophy is due to mitochondrial dysfunction mediating the death of optic nerve fibers. It was first described clinically by Batten in 1896 and named Kjer’s optic neuropathy in 1959 after Danish ophthalmologist Poul Kjer, who studied 19 families with the disease. Although Kjer's optic neuropathy is the most common autosomally inherited optic neuropathy (disease of the optic nerves), it is often misdiagnosed.
Kjer's optic neuropathy usually affects both eyes roughly symmetrically in a slowly progressive pattern of vision loss beginning in childhood. Vision testing will reveal areas of impaired visual acuity (scotomas) in the central visual fields with peripheral vision sparing and impaired color vision (color blindness). Visual acuity loss varies from mild to severe, typically ranging from 6/6 (in meters, equivalent to 20/20, ft) to 6/60 (20/200, ft) with a median value of 6/36 (roughly equivalent to 20/125 ft), corrected vision. In rare cases, vision loss is more severe. Characteristic changes of the fundus evident on examination is temporal pallor (indicating atrophy) of the optic disc and in its end stage, excavation of the optic disc, as is also seen in Leber hereditary optic neuropathy and normal tension glaucoma.
Since the onset of Kjer's optic neuropathy is insidious, symptoms are often not noticed by the patients in its early stages and are picked up by chance in routine school eye screenings. First signs of Kjer's typically present between 4–6 years of age, though presentation at as early as 1 year of age has been reported. In some cases, Dominant optic atrophy may remain subclinical until early adulthood. Progression of dominant optic atrophy varies even within the same family.
Kjer's Optic Neuropathy Pathophisiology
Vision loss in Dominant optic atrophy is due to optic nerve fiber loss from mitochondria dysfunction. Dominant optic atrophy is associated with mutation of the OPA1 gene found on chromosome 3, region q28-qter. Also, 5 other chromosomal genes are described causing optic atropy: OPA2 (x-linked), OPA3 (dominant), OPA4 (dominant), OPA5 (dominant) and OPA6 (recessive) (see OMIM 165500).
The OPA1 gene codes for a dynamin-related GTPase protein targeted to the mitochondrial inner membrane. Although the mechanism of action of the OPA1 gene product is unknown, it is likely involved in stabilization of mitochondrial membrane complexes. OPA1 has been implicated in the fusion of mitochondrial inner membranes during mitochondrial fusion events, indicating that a mitochondrial fusion dysfunction may be important in the development of OPA1 related optic atrophy. Mitochondria are subcellular structures that generate and transform energy from metabolism into discrete usable units (ATP) for the cell’s functions.
Kjer's optic neuropathy usually affects both eyes roughly symmetrically in a slowly progressive pattern of vision loss beginning in childhood. Vision testing will reveal areas of impaired visual acuity (scotomas) in the central visual fields with peripheral vision sparing and impaired color vision (color blindness). Visual acuity loss varies from mild to severe, typically ranging from 6/6 (in meters, equivalent to 20/20, ft) to 6/60 (20/200, ft) with a median value of 6/36 (roughly equivalent to 20/125 ft), corrected vision. In rare cases, vision loss is more severe. Characteristic changes of the fundus evident on examination is temporal pallor (indicating atrophy) of the optic disc and in its end stage, excavation of the optic disc, as is also seen in Leber hereditary optic neuropathy and normal tension glaucoma.
Since the onset of Kjer's optic neuropathy is insidious, symptoms are often not noticed by the patients in its early stages and are picked up by chance in routine school eye screenings. First signs of Kjer's typically present between 4–6 years of age, though presentation at as early as 1 year of age has been reported. In some cases, Dominant optic atrophy may remain subclinical until early adulthood. Progression of dominant optic atrophy varies even within the same family.
Kjer's Optic Neuropathy Pathophisiology
Vision loss in Dominant optic atrophy is due to optic nerve fiber loss from mitochondria dysfunction. Dominant optic atrophy is associated with mutation of the OPA1 gene found on chromosome 3, region q28-qter. Also, 5 other chromosomal genes are described causing optic atropy: OPA2 (x-linked), OPA3 (dominant), OPA4 (dominant), OPA5 (dominant) and OPA6 (recessive) (see OMIM 165500).
The OPA1 gene codes for a dynamin-related GTPase protein targeted to the mitochondrial inner membrane. Although the mechanism of action of the OPA1 gene product is unknown, it is likely involved in stabilization of mitochondrial membrane complexes. OPA1 has been implicated in the fusion of mitochondrial inner membranes during mitochondrial fusion events, indicating that a mitochondrial fusion dysfunction may be important in the development of OPA1 related optic atrophy. Mitochondria are subcellular structures that generate and transform energy from metabolism into discrete usable units (ATP) for the cell’s functions.
Retinal Pigment Epithelium
Retinal pigment epithelium (RPE) is the pigmented cell layer just outside the neurosensory retina that nourishes retinal visual cells, such as cones and rods, and is firmly attached to the underlying choroid (via the Bruch's membrane) and overlying retinal visual cells. The retinal pigment epithelium is composed of a single layer of hexagonal cells that are densely packed with pigment granules. At the ora serrata, the retinal pigment epithelium continues as a membrane passing over the ciliary body and continuing as the back surface of the iris. This generates the fibers of the dilator. The front end continuation of the retina is the posterior iris epithelium, which takes on pigemnt when it enter the iris.
The retinal pigment epithelium is involved in the phagocytosis of the outer segment of photoreceptor cells and it is also involved in the vitamin A cycle where it isomerizes all trans retinol to 11-cis retinal. The retinal pigment epithelium also serves as the limiting transport factor that maintains the retinal environment by supplying small molecules such as amino acid, ascorbic acid and D-glucose while remaining a tight barrier to choroidal blood borne substances. Homeostasis of the ionic environment is maintained by a delicate transport exchange system. In the eyes of albinos, the cells of this layer contain no pigment. Dysfunction of the RPE is found in Age-Related Macular Degeneration and Retinitis Pigmentosa.
The retinal pigment epithelium is involved in the phagocytosis of the outer segment of photoreceptor cells and it is also involved in the vitamin A cycle where it isomerizes all trans retinol to 11-cis retinal. The retinal pigment epithelium also serves as the limiting transport factor that maintains the retinal environment by supplying small molecules such as amino acid, ascorbic acid and D-glucose while remaining a tight barrier to choroidal blood borne substances. Homeostasis of the ionic environment is maintained by a delicate transport exchange system. In the eyes of albinos, the cells of this layer contain no pigment. Dysfunction of the RPE is found in Age-Related Macular Degeneration and Retinitis Pigmentosa.
Friday, December 17, 2010
Blood-Retinal Barrier
The blood-retinal barrier (BRB) is composed of non-fenestrated capillaries of the retinal circulation and tight-junctions between retinal epithelial cells preventing passage of large molecules from choriocapillaris into the retina. The blood-retinal barrier is part of the blood-ocular barrier that consists of specialized endothelial cells that are joined tightly together in order to prevent certain substances from entering the tissue of the retina. Diabetic retinopathy, eye damage that frequently occurs as a result of diabetes, is related to the breakdown of the blood-retinal barrier. The barrier becomes more leaky in patients with diabetic retinopathy.
The blood-retinal barrier has two components: the retinal vascular endothelium and the retinal pigment epithelium. Retinal blood vessels that are similar to cerebral blood vessels maintain the inner blood-ocular barrier. This physiological barrier comprises a single layer of non-fenestrated endothelial cells, which have tight junctions. These junctions are impervious to tracer, so many substances can impact the metabolism of the eyeball. The retinal pigment epithelium maintains the outer blood-retinal barrier.
The blood-retinal barrier has two components: the retinal vascular endothelium and the retinal pigment epithelium. Retinal blood vessels that are similar to cerebral blood vessels maintain the inner blood-ocular barrier. This physiological barrier comprises a single layer of non-fenestrated endothelial cells, which have tight junctions. These junctions are impervious to tracer, so many substances can impact the metabolism of the eyeball. The retinal pigment epithelium maintains the outer blood-retinal barrier.
Thursday, December 16, 2010
Keratomileusis
Keratomileusis is a surgical procedure to improve of the refractive state of the cornea. During this surgery a thin hinged flap of the front of the cornea is cut and lifted up. Then, the shape of the cornea is changed by using an excimer laser or other surgical device, and was developed by José Ignacio Barraquer, commonly called "the father of modern refractive surgery". A microkeratome is usually used to cut the flap, but a femtosecond laser can also be used to make the flap. Before the advent of the excimer laser, keratomileusis was performed using a cryolathe, which froze thin flaps of corneal tissue and lathe cut them much like one cuts the lens of a pair of glasses. After thawing, these reshaped flaps were placed under the front flap to correct visual improvement. LASIK is currently the only commonly performed keratomileusis procedure.
Sub Bowman's Keratomileusis (Video)
Sub Bowman's Keratomileusis (Video)
Metachromatic Leukodystrophy
Metachromatic leukodystrophy is a genetic disease which alters the normal growth and development of the myelin, which is a fatty substance that insulates and protects nerve cells axons, affecting the nerves and muscles. Metachromatic leukodystrophy is caused by a deficiency of the enzyme arylsulfatase A. When this enzyme is missing, sulfatides build up in many tissues of the body, eventually destroying the myelin sheath of the nervous system, as well as kidneys, gallbladder, and other organs. This disease gets worse over time.
There are several forms of metachromatic leukodystrophy, which are late infantile, juvenile, and adult. In the late infantile form, which is the most common form of MLD (50-60%), affected children begin having difficulty walking after the first year of life, usually at 15–24 months. Symptoms include muscle wasting and weakness, muscle rigidity, developmental delays, progressive loss of vision leading to blindness, convulsions, impaired swallowing, paralysis, and dementia. Children may become comatose. Untreated, most children with this form of MLD die by age 5.
Children with the juvenile form of MLD (onset between 3–10 years of age) usually begin with impaired school performance, mental deterioration, and dementia and then develop symptoms similar to the late infantile form but with slower progression. Age of death is variable, but normally within 10 to 15 years of symptom onset although some juveniles can live for several decades or longer after onset.
The adult form commonly begins after age 16 as a psychiatric disorder or progressive dementia. Adult-onset MLD progresses more slowly than the late infantile and juvenile forms, with a protracted course of a decade or more.
Palliative care can help with many of the symptoms and usually improves quality and longevity of life. Carriers have low enzyme levels compared to their family population but even low enzyme levels are adequate to process the body's sulfatide.
There is no cure for MLD, and no standard treatment. It is a terminal illness. Children with advanced juvenile or adult onset, and late infantile patients displaying symptoms have treatment limited to pain and symptom management.
There are several forms of metachromatic leukodystrophy, which are late infantile, juvenile, and adult. In the late infantile form, which is the most common form of MLD (50-60%), affected children begin having difficulty walking after the first year of life, usually at 15–24 months. Symptoms include muscle wasting and weakness, muscle rigidity, developmental delays, progressive loss of vision leading to blindness, convulsions, impaired swallowing, paralysis, and dementia. Children may become comatose. Untreated, most children with this form of MLD die by age 5.
Children with the juvenile form of MLD (onset between 3–10 years of age) usually begin with impaired school performance, mental deterioration, and dementia and then develop symptoms similar to the late infantile form but with slower progression. Age of death is variable, but normally within 10 to 15 years of symptom onset although some juveniles can live for several decades or longer after onset.
The adult form commonly begins after age 16 as a psychiatric disorder or progressive dementia. Adult-onset MLD progresses more slowly than the late infantile and juvenile forms, with a protracted course of a decade or more.
Palliative care can help with many of the symptoms and usually improves quality and longevity of life. Carriers have low enzyme levels compared to their family population but even low enzyme levels are adequate to process the body's sulfatide.
There is no cure for MLD, and no standard treatment. It is a terminal illness. Children with advanced juvenile or adult onset, and late infantile patients displaying symptoms have treatment limited to pain and symptom management.
Wednesday, December 15, 2010
Refractive Eye Surgery
Refractive eye surgery is any eye surgery used to improve the refractive state of the eye and decrease or eliminate dependency on glasses or contact lenses. This can include various methods of surgical remodeling of the cornea or cataract surgery. The most common methods today use excimer lasers to reshape curvature of the cornea. Successful refractive eye surgery can reduce or cure common vision disorders such as myopia, hyperopia and astigmatism.
The first experimental studies about refractive surgery were published in 1896 by Lendeer Jans Lans, an ophthalmology teacher in Holland, where he developed a theoretical work proposing penetrating corneal cuts to correct astigmatism. In 1930 the Japanese ophthalmologist Tsutomu Sato made the first practical attempt to perform such surgery in military pilots. He practiced radial cuts in the cornea to correct effects by up to 6 diopters, but this procedure was soon rejected by the medical community because of the high rate of corneal degeneration. In 1963, in the Barraquer ophthalmologic clinic (Bogotá, Colombia) Ignacio Barraquer developed the first proficient refractive surgery technique called keratomileusis, meaning corneal reshaping.
There are two surgical techniques to perform a refractive eye surgery:
1) Automated lamellar keratoplasty (ALK): The surgeon uses an instrument called a microkeratome to cut a thin flap of the corneal tissue. The flap is lifted like a hinged door, targeted tissue is removed from the corneal stroma, again with the microkeratome, and then the flap is replaced.
2) Laser Assisted In-Situ Keratomileusis (LASIK): The surgeon uses a femtosecond laser to cut a flap of the corneal tissue (usually with a thickness of 100-180 micrometres). The flap is lifted like a hinged door, but in contrast to ALK, the targeted tissue is removed from the corneal stroma with an excimer laser. The flap is subsequently replaced. Another method of creating this flap is by using a procedure called IntraLase, in which a femtosecond laser is used to create the flap. Proponents of this method assert its superiority over "traditional" LASIK, but there have been no conclusive independent studies to prove that this is a true statement.
The first experimental studies about refractive surgery were published in 1896 by Lendeer Jans Lans, an ophthalmology teacher in Holland, where he developed a theoretical work proposing penetrating corneal cuts to correct astigmatism. In 1930 the Japanese ophthalmologist Tsutomu Sato made the first practical attempt to perform such surgery in military pilots. He practiced radial cuts in the cornea to correct effects by up to 6 diopters, but this procedure was soon rejected by the medical community because of the high rate of corneal degeneration. In 1963, in the Barraquer ophthalmologic clinic (Bogotá, Colombia) Ignacio Barraquer developed the first proficient refractive surgery technique called keratomileusis, meaning corneal reshaping.
There are two surgical techniques to perform a refractive eye surgery:
1) Automated lamellar keratoplasty (ALK): The surgeon uses an instrument called a microkeratome to cut a thin flap of the corneal tissue. The flap is lifted like a hinged door, targeted tissue is removed from the corneal stroma, again with the microkeratome, and then the flap is replaced.
2) Laser Assisted In-Situ Keratomileusis (LASIK): The surgeon uses a femtosecond laser to cut a flap of the corneal tissue (usually with a thickness of 100-180 micrometres). The flap is lifted like a hinged door, but in contrast to ALK, the targeted tissue is removed from the corneal stroma with an excimer laser. The flap is subsequently replaced. Another method of creating this flap is by using a procedure called IntraLase, in which a femtosecond laser is used to create the flap. Proponents of this method assert its superiority over "traditional" LASIK, but there have been no conclusive independent studies to prove that this is a true statement.
Automated Lamellar Keratoplasty
Automated lamellar keratoplasty (ALK) is a surgical procedure in which a thin layer of the cornea is separated to create a flap, using a device called a microkeratome. The flap is then folded back, and the microkeratome removes a thin disc of corneal stroma below. The thickness and diameter of this disc determines the change in refractive error. The surgeon then places the flap back into position. This procedure can correct large amounts of myopia and hyperopia. However, the resultant change is not as predictable as with other procedures. Automated lamellar keratoplasty is used to correct vision in people with severe nearsightedness and mild degrees of farsightedness.
To perform automated lamellar keratoplasty, the eye is anesthetized and a ring is fixed to it in order to keep it properly positioned and flat. The microkeratome then makes a small incomplete flap across the cornea by cutting across it. While still attached at one side, the corneal flap is folded back to reveal a sub layer of cornea. At this point, the microkeratome is precisely readjusted to match the calculated cut depth for the patient's vision correction. The calculation is based on the patient's glasses and contact lens prescriptions. The surgeon then passes the microkeratome completely over the eye making the power cut. After the power cut, the corneal flap is laid back over the eye where it reattaches. ALK is an effective technique for very high levels of myopia and is generally used from -5.00 to -30.00 diopters of nearsightedness. Healing time from ALK is very rapid, usually in about 24 hours.
To perform automated lamellar keratoplasty, the eye is anesthetized and a ring is fixed to it in order to keep it properly positioned and flat. The microkeratome then makes a small incomplete flap across the cornea by cutting across it. While still attached at one side, the corneal flap is folded back to reveal a sub layer of cornea. At this point, the microkeratome is precisely readjusted to match the calculated cut depth for the patient's vision correction. The calculation is based on the patient's glasses and contact lens prescriptions. The surgeon then passes the microkeratome completely over the eye making the power cut. After the power cut, the corneal flap is laid back over the eye where it reattaches. ALK is an effective technique for very high levels of myopia and is generally used from -5.00 to -30.00 diopters of nearsightedness. Healing time from ALK is very rapid, usually in about 24 hours.
Leber's Hereditary Optic Neuropathy
Also known as Leber optic atrophy, Leber's hereditary optic neuropathy is a genetic disease in which retinal ganglion cells and their axons degenerate and eventually die, leading to an acute painless loss of central vision. Other minor symptoms may appear such as tremors, numbness or weakness in arms and legs, or loss of ankle reflexes. Affecting predominantly young adult males, Leber's hereditary optic neuropathy is only transmitted through the mother. This inherited disease is caused by mutations in the mitochondrial (not nuclear) genome and only the egg contributes mitochondria to the embryo. The mutations which cause Leber optic atrophy are at nucleotide positions 11778 G to A, 3460 G to A and 14484 T to C, respectively in the ND4, ND1 and ND6 subunit genes of complex I of the oxidative phosphorylation chain in mitochondria. Thus, men cannot pass on the disease to their offspring.
In Leber's hereditary optic neuropathy, both the retina and the optic nerve stop working properly, which means they stop sending signals or visual information to the occipital lobe of the brain. The rest of the eye keeps working normally, so that light enters the eye through the pupil, passing through the lens to be focused on the retina as it should. Nevertheless, even though the light is focused properly on the retina, in Leber's hereditary optic neuropathy this information is not converted into signals for the brain to process.
Without a known family history of LHON the diagnosis is difficult and usually requires a neuro-ophthalmological evaluation and/or blood testing for DNA assessment that is available only in a few laboratories. Hence the incidence is probably greater than appreciated. The prognosis for those affected is almost always that of continued very severe visual loss. Regular corrected visual acuity and perimetry checks are advised for follow up of affected individuals. There is no accepted treatment for this disease. Genetic counselling should be offered. Optical coherence tomography can be used for more detailed study of retinal nerve fiber layer thickness. Red green color vision testing may detect losses. Contrast sensitivity may be diminished. There could be an abnormal electroretinogram or visual evoked potentials. Neuron-specific enolase and axonal heavy chain neurofilament blood markers may predict conversion to affected status.
In Leber's hereditary optic neuropathy, both the retina and the optic nerve stop working properly, which means they stop sending signals or visual information to the occipital lobe of the brain. The rest of the eye keeps working normally, so that light enters the eye through the pupil, passing through the lens to be focused on the retina as it should. Nevertheless, even though the light is focused properly on the retina, in Leber's hereditary optic neuropathy this information is not converted into signals for the brain to process.
Without a known family history of LHON the diagnosis is difficult and usually requires a neuro-ophthalmological evaluation and/or blood testing for DNA assessment that is available only in a few laboratories. Hence the incidence is probably greater than appreciated. The prognosis for those affected is almost always that of continued very severe visual loss. Regular corrected visual acuity and perimetry checks are advised for follow up of affected individuals. There is no accepted treatment for this disease. Genetic counselling should be offered. Optical coherence tomography can be used for more detailed study of retinal nerve fiber layer thickness. Red green color vision testing may detect losses. Contrast sensitivity may be diminished. There could be an abnormal electroretinogram or visual evoked potentials. Neuron-specific enolase and axonal heavy chain neurofilament blood markers may predict conversion to affected status.
Tuesday, December 14, 2010
Ciliary Arteries
The ciliary arteries are the blood vessels which supply blood to the choroid, which is the vascular layer of the eyeball, the ciliary body, the iris, the conjunctiva, and the sclera. Branching off the ophthalmic artery, the ciliary arteries are divisible into three groups: 1) the long posterior; 2) short posterior; 3) the anterior.
1) The long posterior ciliary arteries are the two blood vessels which supply the iris, ciliary body and choroid. They pierce the posterior part of the sclera at some little distance from the optic nerve, running forward along either side of the eyeball, between the sclera and choroid, to the ciliary muscle, where they divide into two branches. Here the long posterior ciliary arteries form an arterial circle, the circulus arteriosus major, around the circumference of the iris, from which numerous converging branches run, in the substance of the iris, to its pupillary margin, where they form a second (incomplete) arterial circle, the circulus arteriosus minor.
2) The short posterior ciliary arteries, from six to twelve in number, arise from the ophthalmic as it crosses the optic nerve. They pass forward around the optic nerve to the posterior part of the eyeball, pierce the sclera around the entrance of the optic nerve, and supply the choroid (up to the equator of the eye) and ciliary processes. Some branches of the short posterior ciliary arteries also supply the optic disc via an anastomotic ring, the Circle of Zinn-Haller or Circle of Zinn, which is associated with the fibrous extension of the ocular tendons (Annulus of Zinn).
3) The anterior ciliary arteries are the seven blood vessels which derive from the muscular branches of the ophthalmic artery. These arteries supply the conjunctiva and sclera. They run to the front of the eyeball in company with the extraocular muscles, form a vascular zone beneath the conjunctiva, and then pierce the sclera a short distance from the cornea and end in the circulus arteriosus major. 2 Ciliary Arteries stem from each rectus muscle except the lateral rectus.
1) The long posterior ciliary arteries are the two blood vessels which supply the iris, ciliary body and choroid. They pierce the posterior part of the sclera at some little distance from the optic nerve, running forward along either side of the eyeball, between the sclera and choroid, to the ciliary muscle, where they divide into two branches. Here the long posterior ciliary arteries form an arterial circle, the circulus arteriosus major, around the circumference of the iris, from which numerous converging branches run, in the substance of the iris, to its pupillary margin, where they form a second (incomplete) arterial circle, the circulus arteriosus minor.
2) The short posterior ciliary arteries, from six to twelve in number, arise from the ophthalmic as it crosses the optic nerve. They pass forward around the optic nerve to the posterior part of the eyeball, pierce the sclera around the entrance of the optic nerve, and supply the choroid (up to the equator of the eye) and ciliary processes. Some branches of the short posterior ciliary arteries also supply the optic disc via an anastomotic ring, the Circle of Zinn-Haller or Circle of Zinn, which is associated with the fibrous extension of the ocular tendons (Annulus of Zinn).
3) The anterior ciliary arteries are the seven blood vessels which derive from the muscular branches of the ophthalmic artery. These arteries supply the conjunctiva and sclera. They run to the front of the eyeball in company with the extraocular muscles, form a vascular zone beneath the conjunctiva, and then pierce the sclera a short distance from the cornea and end in the circulus arteriosus major. 2 Ciliary Arteries stem from each rectus muscle except the lateral rectus.
Monday, December 13, 2010
Posterior Vitreous Detachment
Posterior vitreous detachment is a common eye condition in which the vitreous humor detaches from the surface of the retina. It occurs in about 75 per cent of people over the age of 65. The eyeball is filled with the vitreous humor, which is a jelly-like substance. There are millions of fine fibers intertwined within the vitreous that are attached to the surface of the retina. As we age, the vitreous slowly shrinks, and these fine fibers pull on the retinal surface. Usually the fibers break, allowing the vitreous to separate and shrink from the retina. This is a vitreous detachment.
The symptoms of vitreous detachment are flashes of light, known as photopsia, a sudden dramatic increase in the number of floaters, and a ring of floaters or hairs just to the temporal side of the central vision. Sudden detachment of the vitreous from the macular area usually causes the person to see flashes and floaters. The flashes may look like lightning or electric sparks, and the floaters may look like threads or specks. Symptoms may last days to weeks.
There is no specific treatment for vitreous detachment. Usually people find that the symptoms calm down after about six months and people do eventually get used to living with the floaters. The brain tends to adapt to the floaters and eventually is able to ignore them, so they only become a problem in very bright light. Posterior vitreous detachment does not in itself cause any permanent loss of vision. The visual acuity should remain the same as it used to be before the posterior vitreous detachment started.
The symptoms of vitreous detachment are flashes of light, known as photopsia, a sudden dramatic increase in the number of floaters, and a ring of floaters or hairs just to the temporal side of the central vision. Sudden detachment of the vitreous from the macular area usually causes the person to see flashes and floaters. The flashes may look like lightning or electric sparks, and the floaters may look like threads or specks. Symptoms may last days to weeks.
There is no specific treatment for vitreous detachment. Usually people find that the symptoms calm down after about six months and people do eventually get used to living with the floaters. The brain tends to adapt to the floaters and eventually is able to ignore them, so they only become a problem in very bright light. Posterior vitreous detachment does not in itself cause any permanent loss of vision. The visual acuity should remain the same as it used to be before the posterior vitreous detachment started.
Optic Radiation
The Optic radiation is a thick bundle of axons which lie in a fanlike pattern, going from relay neurons in the lateral geniculate body of the thalamus to the visual cortex along the calcarine fissure. Carrying visual information to the occipital lobe, the optic radiation fibers are found in each cerebral hemisphere.
Both optic radiations split into two parts on each side and travel in the following way: 1) fibers from the inferior retina, which is also called "Meyer's loop", must pass through the temporal lobe by looping around the inferior horn of the lateral ventricle, carrying information from the superior part of the visual field; 2) fibers from the superior retina, also called "Baum's loop", travel straight back through the parietal lobe to the occipital lobe in the retrolenticular limb of the internal capsule to the visual cortex, carrying information from the inferior part of the visual field.
Both optic radiations split into two parts on each side and travel in the following way: 1) fibers from the inferior retina, which is also called "Meyer's loop", must pass through the temporal lobe by looping around the inferior horn of the lateral ventricle, carrying information from the superior part of the visual field; 2) fibers from the superior retina, also called "Baum's loop", travel straight back through the parietal lobe to the occipital lobe in the retrolenticular limb of the internal capsule to the visual cortex, carrying information from the inferior part of the visual field.
Sunday, December 12, 2010
Fuchs' Corneal Dystrophy
Fuchs' corneal dystrophy is a genetic, autosomal dominant disease with high penetrance. Fuchs' dystrophy is a degenerative disorder of the corneal endothelium with accumulation of focal excrescences called guttae and thickening of Descemet’s membrane, leading to corneal edema and loss of vision. Corneal endothelial cells are the major pump cells of the cornea which allow for stromal clarity. In the Fuchs' corneal dystrophy, Descemet’s membrane is grossly thickened with accumulation of abnormal wide-spaced collagen and numerous guttae. Corneal endothelial cells in end-stage of the disease are reduced in number and appear attenuated, causing progressive stromal edema.
Progressive endothelial cell loss causes relative influx of aqueous humor into the cornea, leading to swelling (corneal stromal edema), which results in distorted vision. Eventually, the epithelium also becomes edematous, resulting in more severe visual impairment. Focal areas or blisters of epithelial edema ("bullae") may be particularly painful. At first, a person with Fuchs' dystrophy will awaken with blurred vision that will gradually clear during the day. This occurs because the cornea is normally thicker in the morning; it retains fluids during sleep that evaporate in the tear film while we are awake. As the disease worsens, this swelling will remain constant and reduce vision throughout the day.
Medical treatment includes topical hypertonic saline, the use of a hairdryer to dehydrate the precorneal tear film, and therapeutic soft contact lenses. In using a hairdryer, the patient is instructed to hold a hairdryer at an arm's length or directed across the face, to dry out the epithelial blisters. This can be done two or three times a day. Definitive treatment, however, (especially with increased corneal edema) is surgical in the form of corneal transplantation, or penetrating keratoplasty (PKP).
Progressive endothelial cell loss causes relative influx of aqueous humor into the cornea, leading to swelling (corneal stromal edema), which results in distorted vision. Eventually, the epithelium also becomes edematous, resulting in more severe visual impairment. Focal areas or blisters of epithelial edema ("bullae") may be particularly painful. At first, a person with Fuchs' dystrophy will awaken with blurred vision that will gradually clear during the day. This occurs because the cornea is normally thicker in the morning; it retains fluids during sleep that evaporate in the tear film while we are awake. As the disease worsens, this swelling will remain constant and reduce vision throughout the day.
Medical treatment includes topical hypertonic saline, the use of a hairdryer to dehydrate the precorneal tear film, and therapeutic soft contact lenses. In using a hairdryer, the patient is instructed to hold a hairdryer at an arm's length or directed across the face, to dry out the epithelial blisters. This can be done two or three times a day. Definitive treatment, however, (especially with increased corneal edema) is surgical in the form of corneal transplantation, or penetrating keratoplasty (PKP).
Saturday, December 11, 2010
Corneal Limbus
The corneal limbus is the border of the cornea where it joins the sclera. The human corneal limbus features radially oriented fibrovascular ridges known as the palisades of Vogt which contain pigment granules that are aligned with the microplicae of the epithelium. The limbus is a common site for the occurrence of corneal epithelial neoplasm.
Although it is presumed that the corneal limbus pigment granules are produced by melanocytes, the characterization of melanocytes in the limbus has not been clearly documented. Human limbal tissues has been examined by whole mounts and serial histological sections to localize epithelial cells containing melanin granules. Most of the pigmented cells observed by immunohistochemistry were K19 (+) cells in the basal limbal epithelium.
A superimposed image revealed that melanin granules were oriented towards the apex of each K19 (+) cell, acting as a pigmented cap facing the ocular surface. Melanocytes were identified by MART1, an antigen specific to melanocyte-lineage cells. Melanocytes were shown to exist as sporadic cells with dendritic processes that extend to surrounding epithelial cells.
Although it is presumed that the corneal limbus pigment granules are produced by melanocytes, the characterization of melanocytes in the limbus has not been clearly documented. Human limbal tissues has been examined by whole mounts and serial histological sections to localize epithelial cells containing melanin granules. Most of the pigmented cells observed by immunohistochemistry were K19 (+) cells in the basal limbal epithelium.
A superimposed image revealed that melanin granules were oriented towards the apex of each K19 (+) cell, acting as a pigmented cap facing the ocular surface. Melanocytes were identified by MART1, an antigen specific to melanocyte-lineage cells. Melanocytes were shown to exist as sporadic cells with dendritic processes that extend to surrounding epithelial cells.
Friday, December 10, 2010
Superheterodyne Receiver
A superheterodyne receiver is an electronic device which uses frequency mixing to convert a received signal to a fixed intermediate frequency, which can be more conveniently processed than the original radio carrier frequency. Virtually all modern radio and television receivers use the superheterodyne principle. The superheterodyne receiver has three elements: the local oscillator, a frequency mixer that mixes the local oscillator's signal with the received signal, and a tuned amplifier.
Reception starts with an antenna signal, optionally amplified, including the frequency the user wishes to tune, fd. The local oscillator is tuned to produce a frequency close to fd, fLO. The received signal is mixed with the local oscillator signal. This stage does not just linearly add the two inputs, like an audio mixer. Instead it multiplies the input by the local oscillator, producing four frequencies in the output; the original signal, the original fLO, and the two new frequencies fd+fLO and fd-fLO. The output signal also generally contains a number of undesirable mixtures as well. These are 3rd- and higher-order intermodulation products. If the mixing were performed as a pure, ideal multiplication, the original fd and fLO would also not appear; in practice they do appear because mixing is done by a nonlinear process that only approximates true ideal multiplication.
The amplifier portion of the system is tuned to be highly selective at a single frequency, fIF. By changing fLO, the resulting fd-fLO (or fd+fLO) signal can be tuned to the amplifier's fIF. In typical amplitude modulation ("AM radio" in the U.S., or MW) receivers, that frequency is 455 kHz; for FM receivers, it is usually 10.7 MHz; for television, 45 MHz. Other signals from the mixed output of the heterodyne are filtered out by the amplifier.
The original heterodyne technique was pioneered by Canadian inventor Reginald Fessenden, but it was not pursued far because local oscillators available at the time were unstable in their frequency output, and vacuum tubes were not yet available. The superheterodyne principle was revisited in 1918 by U.S. Army Major Edwin Armstrong in France during World War I. He invented this receiver as a means of overcoming the deficiencies of early vacuum tube triodes used as high-frequency amplifiers in radio direction finding equipment.
Reception starts with an antenna signal, optionally amplified, including the frequency the user wishes to tune, fd. The local oscillator is tuned to produce a frequency close to fd, fLO. The received signal is mixed with the local oscillator signal. This stage does not just linearly add the two inputs, like an audio mixer. Instead it multiplies the input by the local oscillator, producing four frequencies in the output; the original signal, the original fLO, and the two new frequencies fd+fLO and fd-fLO. The output signal also generally contains a number of undesirable mixtures as well. These are 3rd- and higher-order intermodulation products. If the mixing were performed as a pure, ideal multiplication, the original fd and fLO would also not appear; in practice they do appear because mixing is done by a nonlinear process that only approximates true ideal multiplication.
The amplifier portion of the system is tuned to be highly selective at a single frequency, fIF. By changing fLO, the resulting fd-fLO (or fd+fLO) signal can be tuned to the amplifier's fIF. In typical amplitude modulation ("AM radio" in the U.S., or MW) receivers, that frequency is 455 kHz; for FM receivers, it is usually 10.7 MHz; for television, 45 MHz. Other signals from the mixed output of the heterodyne are filtered out by the amplifier.
The original heterodyne technique was pioneered by Canadian inventor Reginald Fessenden, but it was not pursued far because local oscillators available at the time were unstable in their frequency output, and vacuum tubes were not yet available. The superheterodyne principle was revisited in 1918 by U.S. Army Major Edwin Armstrong in France during World War I. He invented this receiver as a means of overcoming the deficiencies of early vacuum tube triodes used as high-frequency amplifiers in radio direction finding equipment.
RBE2 Radar
The RBE2 is a multirole, passive electronically scanned array radar. It was developed during the 90s for the French Rafale fighter aircraft. RBE2 is an acronym for "Radar à Balayage Electronique 2". The RBE2 is capable of tracking up to 40 aircraft and engaging 8 of them. The RBE2 is also able to provide the Air-to-Ground performances that are required by the French government or potential export customers. A 90 million euros-worth contract was signed in July 2004 for the development and integration of an Active Electronically Scanned Array version of the RBE2. In July 2010, it was reported that Thales will commence deliveries of the new radar in August 2010 for use on the fourth tranche of Rafale aircraft with the first AESA-equipped squadron to become operational in 2012.
The RBE2-AA (active array) variant has been tested on both a Mystère 20, Mirage 2000 and Rafale testbed aircrafts from the Flight Test Center of the DGA (Délégation Générale pour l'Armement, the French procurement agency) and then on a Rafale. While the first tests were made with US-made transmitter/receivers, the current radar will feature parts manufactured by Thales.
The RBE2-AA (active array) variant has been tested on both a Mystère 20, Mirage 2000 and Rafale testbed aircrafts from the Flight Test Center of the DGA (Délégation Générale pour l'Armement, the French procurement agency) and then on a Rafale. While the first tests were made with US-made transmitter/receivers, the current radar will feature parts manufactured by Thales.
Thursday, December 9, 2010
AN/APQ-159
The AN/APQ-159 was a I-band/J band radar which was developed by Emmerson Electric from the APQ-153. The AN/APQ-159 was a fire control air-to-air radar system. It had four primary modes of operation, two search modes with different ranges using a simple B-Scope display, a boresight gunnery display with ranging and automatic lock-on "dogfight mode", and a similar mode used with the AIM-9 Sidewinder that calculated the missile's engagement envelope and provided cues to the pilot to fly into the envelope. Nevertheless, the radar offered no air-to-ground modes at all, nor was it capable of firing the AIM-7 Sparrow in spite of its BVR-capable range.
The AN/APQ-159 was equipped with a new planar phased array antenna, replacing the APQ-153's parabolic dish. This made the antenna smaller front-to-back and allowed it to be pointed to higher angles within the nose. It also greatly reduced the sidelobes, which improved gain and allowed the range to be greatly increased from roughly 10 nm to 20 nm. The APQ-159 had also upgraded electronics, offering increased frequency agility and dramatically improving mean time between failure (MTBF) from about 62 hours in the -153 to 125 in the latest models of the AN/APQ-159, which have actually demonstrated 150 hours MTBF in the field.
The AN/APQ-159 was manufactured in four separate models with the same radar electronics, but different displays. The APQ-159-1 and -2 models used a display that could operate in television mode to operate the AGM-65 Maverick air-to-ground missile, while the -3 and -4 lacked this capability. The difference between the odd and even numbered versions was the inclusion of a second set of displays and controls for the even-numbed versions, for use in the two seater F-5F. The APQ-159-5 version was a product improvement that further improved reliability and reduced weight to the same as the original APQ-153, making in-field upgrades much simpler. The final version was the APQ-159-7.
The AN/APQ-159 was equipped with a new planar phased array antenna, replacing the APQ-153's parabolic dish. This made the antenna smaller front-to-back and allowed it to be pointed to higher angles within the nose. It also greatly reduced the sidelobes, which improved gain and allowed the range to be greatly increased from roughly 10 nm to 20 nm. The APQ-159 had also upgraded electronics, offering increased frequency agility and dramatically improving mean time between failure (MTBF) from about 62 hours in the -153 to 125 in the latest models of the AN/APQ-159, which have actually demonstrated 150 hours MTBF in the field.
The AN/APQ-159 was manufactured in four separate models with the same radar electronics, but different displays. The APQ-159-1 and -2 models used a display that could operate in television mode to operate the AGM-65 Maverick air-to-ground missile, while the -3 and -4 lacked this capability. The difference between the odd and even numbered versions was the inclusion of a second set of displays and controls for the even-numbed versions, for use in the two seater F-5F. The APQ-159-5 version was a product improvement that further improved reliability and reduced weight to the same as the original APQ-153, making in-field upgrades much simpler. The final version was the APQ-159-7.
AN/APG-78
The AN/APG-78 is a 35 GHz, fire control radar developed by Longbow LLC for the US Army and used on the AH-64D Apache helicopter. This radar was designed for the detection, location, classification and prioritization of tactical targets in poor weather and obscured conditions. The AN/APG-78 emits a narrow, intense beam of radio waves to ensure accurate tracking information and to minimize the chance of losing track of the target. When it is in the vecinity of the target, the radar switches to the acquisition phase of operation. Once it has locked onto the target, the APG-78 radar uses AGM-114L Longbow Hellfire anti-tank missiles. It provides high performance with very low probability of intercept, and high operational availability with low support costs. With a range of 8km to 12km, it is capable of scanning an area and search for potential targets presenting to the aircrew the top 16 of 100 targets in less than 6 seconds. In addition, AN/APG-78 provides situational awareness to the Longbow Apache helicopter improving its survivability.
AN/APQ-181
The AN/APQ-181 is an all-weather, stealthy radar which operates in the Ku band. It was developed by Hughes Aircraft in the 1980s for the US Air Force and is used on B-2A Spirit bomber aircraft, entering service in 1993. The AN/APQ-181 is a low probability of intercept radar which enables the unique combination of stealth, range, payload, and precision weapons delivery capabilities. The radar, which is today manufactured by Raytheon, features a number of precision targeting modes, and also supports terrain following and terrain avoidance. The original design consists of a TWT-based transmitter with a 2-dimensional passive electronically scanned array (PESA) antenna.
As part of the radar modernization program (RMP), Raytheon has designed, built and delivered an active array, based upon an advanced T/R module design offering improved performance and reliability. The RMP is currently in flight testing of the new antenna and will enter production in summer 2007, which will replace all the electronically scanned arrays currently in the fleet with the new active arrays. The new Active Electronically Scanned Array (AESA) provides the stepping stone to additional future radar enhancements. In 2002, Raytheon was awarded a contract to develop a new, Active Electronically Scanned Array (AESA) version of the APQ-181. This upgrade will improve system reliability, and will also eliminate potential conflicts in frequency usage between the B-2 and commercial satellite systems that also use the J band.
As part of the radar modernization program (RMP), Raytheon has designed, built and delivered an active array, based upon an advanced T/R module design offering improved performance and reliability. The RMP is currently in flight testing of the new antenna and will enter production in summer 2007, which will replace all the electronically scanned arrays currently in the fleet with the new active arrays. The new Active Electronically Scanned Array (AESA) provides the stepping stone to additional future radar enhancements. In 2002, Raytheon was awarded a contract to develop a new, Active Electronically Scanned Array (AESA) version of the APQ-181. This upgrade will improve system reliability, and will also eliminate potential conflicts in frequency usage between the B-2 and commercial satellite systems that also use the J band.
Wednesday, December 8, 2010
AN/APG-65
The AN/APG-65 was an all-weather multimode airborne radar designed by Hughes Aircraft for US Navy to be used on the F/A-18 Hornet and a variety of fighter aircraft types. The APG-65 was an I-band (8 to 12 GHz) pulse-Doppler radar which was conceived for both air-to-air and air-to-surface missions. For air-to-air operations it incorporated a variety of search, track and track-while-scan modes to give the pilot a complete look-down/shoot-down capability. Air-to-surface modes included doppler beam sharpened sector and patch mapping, medium range synthetic aperture radar, fixed and moving ground target track and sea surface search. In the F/A-18, the radar was installed in a slide-out nose rack to facilitate maintenance.
The AN/APG-65 was fitted with programmable digital computers which gave it flexibility. The built-in test system provided total end-to-end radar preflight checkout and continuous monitoring. To provide maximum detection range capability against nose aspect targets, the radar also featured a velocity search, range-while-search, track-while-scan, which, when combined with an autonomous missile such as AIM-120, gave the aircraft a launch-and-leave capability, single target track, gun director and raid assessment, operating modes. The AN/APG-65 was developed in the late 1970s by Hughes, but also manufactured by Raytheon, and had been operational since 1983. From 1992, it was replaced by the AN/APG-73, which is an upgraded version of the APG-65.
The AN/APG-65 was fitted with programmable digital computers which gave it flexibility. The built-in test system provided total end-to-end radar preflight checkout and continuous monitoring. To provide maximum detection range capability against nose aspect targets, the radar also featured a velocity search, range-while-search, track-while-scan, which, when combined with an autonomous missile such as AIM-120, gave the aircraft a launch-and-leave capability, single target track, gun director and raid assessment, operating modes. The AN/APG-65 was developed in the late 1970s by Hughes, but also manufactured by Raytheon, and had been operational since 1983. From 1992, it was replaced by the AN/APG-73, which is an upgraded version of the APG-65.
Effective Radiated Power
Effective radiated power (ERP) is the product of antenna input power and antenna power gain, expressed in kilowatts. In other words, ERP is the power supplied to an antenna multiplied by the antenna gain in a given direction. If the direction is not specified, the direction of maximum gain is assumed. The type of reference antenna must be specified. The product of the power supplied to the antenna and its gain relative to a half-wave dipole in a given direction. If the direction is not specified, the direction of maximum gain is assumed.
Effective radiated power takes into consideration transmitter power output (TPO), transmission line attenuation (electrical resistance and RF radiation), RF connector insertion losses, and antenna directivity, but not height above average terrain (HAAT). ERP is typically applied to antenna systems.
Effective radiated power takes into consideration transmitter power output (TPO), transmission line attenuation (electrical resistance and RF radiation), RF connector insertion losses, and antenna directivity, but not height above average terrain (HAAT). ERP is typically applied to antenna systems.
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