Platelets called thrombocytes, are a component of blood whose function is to react to bleeding from blood vessel injury by clumping, thereby initiating a blood clot. Platelets have no cell nucleus: they are fragments of cytoplasm that are derived from the megakaryocytes of the bone marrow, which enter the circulation. Circulating unactivated platelets are biconvex discoid structures, 2–3 µm in greatest diameter. Activated platelets have cell membrane projections covering their surface. Platelets are found only in mammals, whereas in other vertebrates thrombocytes circulate as intact mononuclear cells. On a stained blood smear, platelets appear as dark purple spots, about 20% the diameter of red blood cells; the smear is used to examine platelets for size, qualitative number, clumping. The ratio of red blood cells to platelets in a healthy adult ranges from 1:10 to 1:20. One major function of platelets is to contribute to hemostasis: the process of stopping bleeding at the site of interrupted endothelium.

They gather at the site and unless the interruption is physically too large, they plug the hole. First, platelets attach to substances outside the interrupted endothelium: adhesion. Second, they turn on receptors and secrete chemical messengers: activation. Third, they connect to each other through receptor bridges: aggregation. Formation of this platelet plug is associated with activation of the coagulation cascade, with resultant fibrin deposition and linking; these processes may overlap: the spectrum is from a predominantly platelet plug, or "white clot" to a predominantly fibrin, or "red clot" or the more typical mixture. Some would add the subsequent retraction and platelet inhibition as fourth and fifth steps to the completion of the process and still others would add a sixth step, wound repair. Platelets participate in both innate and adaptive intravascular immune responses; the platelet cell membrane has receptors for collagen. Following the rupture of the blood vessel wall, the platelets are exposed and they adhere to the collagen in the surrounding connective tissue.

Low platelet concentration is called thrombocytopenia, is due to either decreased production or increased destruction. Elevated platelet concentration is called thrombocytosis, is either congenital, reactive, or due to unregulated production: one of the myeloproliferative neoplasms or certain other myeloid neoplasms. A disorder of platelet function is a thrombocytopathy. Normal platelets can respond to an abnormality on the vessel wall rather than to hemorrhage, resulting in inappropriate platelet adhesion/activation and thrombosis: the formation of a clot within an intact vessel; this type of thrombosis arises by mechanisms different from those of a normal clot: namely, extending the fibrin of venous thrombosis. An arterial thrombus may obstruct blood flow, causing downstream ischemia, or may obstruct it, causing downstream tissue death. Platelet concentration is measured either manually using a hemocytometer, or by placing blood in an automated platelet analyzer using electrical impedance, such as a Coulter counter.

The normal range for platelets in healthy Caucasians is 150,000 to 450,000 per cubic millimeter. Or 150–450 × 109 per liter; the normal range has been confirmed to be the same in the Spanish populations. The number of platelets varies across individuals; the normal physiologic range is 200000 to 500000 per microliter of blood. Since they contain receptors for thrombopoietin, a higher number of platelets binds more of the protein. There is stimulation for more production of thrombopoietin in the liver and kidneys; this is the basis for production of more thrombopoietin and, as a result, more platelets in the bloodstream during the blood clotting process. In a first approximation, the platelet shape can be considered similar to oblate spheroids, with a semiaxis ratio of 2 to 8; this approximation is used to model the hydrodynamic and optical properties of a platelet population, as well as to restore the geometric parameters of individual measured platelets by flow cytometry. More accurate biophysical models of the platelet surface morphology, which model its shape from first principles, make it possible to obtain a more realistic platelet geometry in a calm and activated state Structurally the platelet can be divided into four zones, from peripheral to innermost: Peripheral zone – is rich in glycoproteins required for platelet adhesion and aggregation.

For example, GPIb/IX/X. Sol-gel zone – is rich in microtubules and microfilaments, allowing the platelets to maintain their discoid shape. Organelle zone – is rich in platelet granules. Alpha granules contain clotting mediators such as factor V, factor VIII, fibronectin, platelet-derived growth factor, chemotactic agents. Delta granules, or dense bodies, contain ADP, serotonin, which are platelet-activating mediators. Membranous zone – contains membranes derived from megakaryocytic smooth endoplasmic reticulum organized into a dense tubular system, responsible for thromboxane A2 synthesis; this dense tubular system is connected to the surface platelet membrane to aid thromboxane A2 release. Megakaryocyte and platelet production is regulated by thrombopoietin, a hormone produced in the kidneys and liver; each megakaryocyte produces between 1,000 and 3,000

Airborne Interception radar, Mark VIII, or AI Mk. VIII for short, was the first operational microwave-frequency air-to-air radar, it was used by Royal Air Force night fighters from late 1941 until the end of World War II. The basic concept, using a moving parabolic antenna to search for targets and track them remained in use by most airborne radars well into the 1980s. Low-level development began in 1939 but was sped after the introduction of the cavity magnetron in early 1940; this operated at 9.1 cm wavelength, much shorter than the 1.5 m wavelength of the earlier AI Mk. IV. Shorter wavelengths allowed it to use much more directional antennas. Mk. IV was blinded by the reflections off the ground from its wide broadcast pattern, which made it impossible to see targets flying at low altitudes. Mk. VIII could avoid this by keeping the antenna pointed upward, allowing it to see any aircraft at or above its own altitude; the design was just beginning to mature in late 1941. A prototype version, the Mk.

VII, entered service on the Bristol Beaufighter in November 1941. A small number of these were sent to units across the UK to provide coverage at low altitudes while Mk. IV equipped aircraft operated at higher altitudes. After a small run of the improved Mk. VIIIA, the definitive Mk. VIII arrived in early 1942, offering higher power as well as a host of electronic and packaging upgrades, it arrived just as production rates of the De Havilland Mosquito began to improve displacing the Beaufighter units in RAF squadrons. Mk. VIII equipped; the Mk. VIII spawned a number of variants, notably the AI Mk. IX which included a lock-on feature to ease interceptions. A series of events, including a deadly friendly fire incident, so delayed the Mk. IX that it never entered service. During the late-war period, many UK aircraft adopted the US SCR-720 under the name AI Mk. X; this worked on the same general principles as the Mk. VIII, but used a different display system. Development of the basic system continued, the Mk.

IX would briefly re-appear in advanced form as the AI.17 during the 1950s. The seminal Daventry Experiment of 1935 proved the basic concept of radar was feasible and led to the rapid formation of the Air Ministry Experimental Station at Bawdsey Manor to develop them; the AMES team's primary concern was the development and deployment of the Chain Home system, providing early warning for raids approaching the UK. As the team grew, the work diversified, by 1938 there were a number of teams working on other projects as well. One of the first of these side efforts came about due to Henry Tizard's concerns about the potential effectiveness of Chain Home, he believed that the Luftwaffe would suffer so stiffly at the hands of the RAF's ground-controlled intercept system that they would switch to the night bombing role. At night, a pilot could see a target at 1,000 yards, an accuracy the Dowding system could not provide. Tizard's concerns were brought up by Robert Watson-Watt at a round-table meeting at the Crown and Castle pub.

"Taffy" Bowen offered to take up development of a new system able to be installed in aircraft to close the distance between CH direction and visual range at night. Due to the physics of radio transmission, antennas have to be about as long as the wavelength of the radio signal to achieve reasonable gain; the half-wave dipole, with two poles each about one-quarter the length of the signal, is a common solution. CH operated at anywhere from 10 m to 50 m depending on the version, meaning antennas would have to be at least 5 to 10 metres long, which made it impractical for use on an aircraft. Bowen started development of a new system operating at shorter wavelengths, first at 6.7 m following work by the British Army, finally settling on 1.5 m, the practical limit of available technology. This became known as Airborne Interception radar, was the primary focus of Bowen's work from 1936 to 1940. While testing an early 1.5 m set the team failed to detect any aircraft, but picked out large objects like cranes and ships at nearby wharves.

Further experiments demonstrated the ability to pick up ships at sea, leading to a live demonstration where the team was able to track down Royal Navy capital ships in terrible weather. This led to immediate interest on behalf of RAF Coastal Command which saw this as a way to find enemy ships and U-Boats, by the British Army, interested in using the radars to direct fire against shipping in the English Channel. Work on the system for AI use ended, it was not until 1939, with war looming, that the team once again returned to AI work. Compared to the successful and rapid development of the anti-shipping radars, the team found themselves facing a continual stream of problems in air-to-air settings. There were two primary problems, a lack of maximum range that made finding the targets difficult, a lack of minimum range that made it difficult for the pilot to see the target before it became invisible to the radar. Like Chain Home, the AI radar sent out a powerful pulse semi-directionally, lighting up the entire sky in front of it.

Echoes from aircraft would be received on multiple directional antennas, by comparing the signal strength from each one, the direction of the target could be determined. However, this meant that the signal reached the ground and reflected off it, producing a return so powerful that it overwhelmed the receiver no matter where the antenna was positioned. Since this signal had to travel to the ground and back, it produced a line on the display at an indicated range e

Hollywood-Monster is a 1987 horror comedy film directed by Roland Emmerich, about a film crew working in a haunted mansion. Emmerich's third film, it starred Jill Whitlow, Paul Gleason and Tim McDaniel. A co-production between West Germany and the United States, the film was released theatrically in Germany on June 25, 1987, it would be released on video cassette in the United States on February 7, 1990, by M. C. E. G. Virgin Home Entertainment. In 2001, the film was released on DVD by Image Entertainment. Two cousins and Warren, live together in Hollywood. Fred, an aspiring horror-movie director with developed skills in SFX and animatronics tries to shoot his first movie in their house, but Warren, who plays the main male protagonist, keeps on flirting with Laurie, the main actress; when she can't stand it anymore, the project is over, the bills are pilling up. Out of the blue, Warren is called out to the reading of his grandfather's testament; the boys end up with an old clock, inhabited with the spirit of Warren, Karl's grandfather's deformed butler.

The benevolent spirit, having appeared to Fred in the night, as well as showing him a flashback of the day he and Warren's grandfather Karl died, which Karl poisoned himself, sealing himself in the basement with all his money to prevent his family from getting any, the butler dies falling down stairs. The dream inspires Fred in making a new script for which he builds an animatronic version of the butler, whose spirit inhabits; the butler and the boys will help each other as they face a new problem the son of Warren's grandfather's partner who managed to swindle Warren. It will all end in a race against the clock in an old house basement, a fight against a demented ghost armor, as the movie pays homage to the late 50-to-70's Sci Fi B movies. Jason Lively as Warren McCloud Tim McDaniel as Fred Jill Whitlow as Laurie Sanders Leonard Lansink as Karl Paul Gleason as Stan Gordon Ian MacNaughton as Frederick McCloud Chuck Mitchell as Mr. Rosenbaum Julian Curry as Lawyer Cynthia Frost as Secretary Andreas Kovac-Zemen as Pawn Shop Owner Toby Kaye as Laurie's Girlfriend Larry Pennell as Bum Ernie Lively as Production Manager Hollywood Monster on IMDb Hollywood-Monster at Rotten Tomatoes