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National Cancer Institute

The National Cancer Institute coordinates the United States National Cancer Program and is part of the National Institutes of Health, one of eleven agencies that are part of the U. S. Department of Health and Human Services; the NCI conducts and supports research, health information dissemination, other activities related to the causes, prevention and treatment of cancer. NCI is the oldest and has the largest budget and research program of the 27 institutes and centers of the NIH, it fulfills the majority of its mission via an extramural program that provides grants for cancer research. Additionally, the National Cancer Institute has intramural research programs in Bethesda, Maryland and at the Frederick National Laboratory for Cancer Research at Fort Detrick, in Frederick, Maryland; the NCI receives more than US$5 billion in funding each year. The NCI supports a nationwide network of 71 NCI-designated Cancer Centers with a dedicated focus on cancer research and treatment and maintains the National Clinical Trials Network.

August 5, 1937: President Franklin D. Roosevelt signed into law the National Cancer Institute Act, which established the National Cancer Institute, as a division of the Public Health Service. 1940: The first issue of the Journal of the National Cancer Institute was published. 1944: The United States Congress made the NCI an operating division of the National Institutes of Health by its passage of the Public Health Service Act. Congress amended the Public Health Service Act with the National Cancer Act of 1971, to broaden the scope and responsibilities of the NCI "in order more to carry out the national effort against cancer." 1955: NCI established the Clinical Trials Cooperative Group Program, which included several research networks that conducted cancer clinical research under the sponsorship of NCI. 1957: The first cancer, was cured with chemotherapy at NCI. 1960: NCI began funding government-supported cancer centers. 1971: President Richard Nixon converted the U. S. Army's former biological warfare facilities at Fort Detrick, Maryland, to house research activities on the causes and prevention of cancer.

1971: The National Cancer Act of 1971 declares "war on cancer," establishes the National Cancer Advisory Board, allots additional funding for cancer research. 1975: The Frederick National Laboratory for Cancer Research opened in Frederick, Maryland, as a Federally Funded Research and Development Center 1993: The NIH Revitalization Act of 1993 encourages NCI to expand its efforts in prostate cancer and other cancers which or affected women, authorized increased appropriations. 1998: Establishes the Office of Cancer Complementary and Alternative Medicine to study pseudoscientific Alternative Medicine treatments for cancer 2009: The American Recovery and Reinvestment Act of 2009 provided US$10 billion in additional funding for the NIH. 2016: The 21st Century Cures Act increased funding for biomedical research. The "Cancer Moonshot" program promised additional support for cancer research. On October 17, 2017, Norman Sharpless was sworn in as the 15th director of the National Cancer Institute. In April 2019, Sharpless left NCI to serve as the acting Commissioner of Drugs.

He returned to the institute in November 2019 as director. The NCI is divided into several centers. Center for Cancer ResearchThe CCR includes 250 internal NCI research groups in Frederick and Bethesda. Division of Cancer Epidemiology and GeneticsDCEG is divided into the Epidemiology and Biostatistics Program and the Human Genetics Program. Division of Cancer BiologyDCB oversees 2000 grants per year in the areas of cancer cell biology. "Special Research Programs" falling under the aegis of the DCB include: Physical Sciences-Oncology Network, Cancer Systems Biology Consortium, Oncology Models Forum, Barrett's Esophagus Translational Research Network, New Approaches to Synthetic Lethality for Mutant KRAS-Dependent Cancers and Cellular Characterization of Screen-Detected Lesions, Fusion Oncoproteins in Childhood Cancers, Cancer Tissue Engineering Collaborative. Division of Cancer Control and Population Sciences Division of Cancer Prevention Division of Cancer Treatment and DiagnosisDCTD supports eight research programs: The Biometric Research Program, The Cancer Diagnosis Program, The Cancer Imaging Program, The Cancer Therapy Evaluation Program, The Developmental Therapeutics Program, The Radiation Research Program, The Translational Research Program, The Office of Cancer Complementary and Alternative Medicine.

Division of Extramural ActivitiesDEA processes and supports the thousands of grant applications NCI receives each year and compiles reports on the progress of research funded by the NCI's programs. Center for Biomedical Informatics and Information Technology Center for Cancer GenomicsCCG was created in 2011 and is responsible for management of The Cancer Genome Atlas and cancer genomics initiatives. Center for Cancer Training Center for Global Health Center for Strategic Scientific InitiativesIn the 1990s, the Unconventional Innovation Program was created to integrate interdisciplinary technology research with biological applications, it was reorganized in 2004 as the CSSI. Center to Reduce Cancer Health Disparities Center for Research Strategy Coordinating Center for Clinical Trials Technology Transfer Center The NCI-designated Cancer Centers are one of the pr

Direct stiffness method

As one of the methods of structural analysis, the direct stiffness method known as the matrix stiffness method, is suited for computer-automated analysis of complex structures including the statically indeterminate type. It is a matrix method that makes use of the members' stiffness relations for computing member forces and displacements in structures; the direct stiffness method is the most common implementation of the finite element method. In applying the method, the system must be modeled as a set of simpler, idealized elements interconnected at the nodes; the material stiffness properties of these elements are through matrix mathematics, compiled into a single matrix equation which governs the behaviour of the entire idealized structure. The structure’s unknown displacements and forces can be determined by solving this equation; the direct stiffness method forms the basis for most commercial and free source finite element software. The direct stiffness method originated in the field of aerospace.

Researchers looked at various approaches for analysis of complex airplane frames. These included elasticity theory, energy principles in structural mechanics, flexibility method and matrix stiffness method, it was through analysis of these methods that the direct stiffness method emerged as an efficient method ideally suited for computer implementation. Between 1934 and 1938 A. R. Collar and W. J. Duncan published the first papers with the representation and terminology for matrix systems that are used today. Aeroelastic research continued through World War II but publication restrictions from 1938 to 1947 make this work difficult to trace; the second major breakthrough in matrix structural analysis occurred through 1954 and 1955 when professor John H. Argyris systemized the concept of assembling elemental components of a structure into a system of equations. On Nov. 6 1959, M. J. Turner, head of Boeing’s Structural Dynamics Unit, published a paper outlining the direct stiffness method as an efficient model for computer implementation.

A typical member stiffness relation has the following general form: Q m = k m q m + Q o m where m = member number m. Q m = vector of member's characteristic forces. K m = member stiffness matrix. Q m = vector of member's characteristic deformations. Q o m = vector of member's characteristic forces caused by external effects applied to the member while q m = 0. If q m are member deformations rather than absolute displacements Q m are independent member forces, in such case can be inverted to yield the so-called member flexibility matrix, used in the flexibility method. For a system with many members interconnected at points called nodes, the members' stiffness relations such as Eq. can be integrated by making use of the following observations: The member deformations q m can be expressed in terms of system nodal displacements r in order to ensure compatibility between members. This implies; the member forces Q m help to the keep the nodes in equilibrium under the nodal forces R. This implies that the right-hand-side of will be integrated into the right-hand-side of the following nodal equilibrium equations for the entire system: R = K r + R o where R = vector of nodal forces, representing external forces applied to the system's nodes.

K = system stiffness matrix, established by assembling the members' stiffness matrices k m. R = vector of system's nodal displacements that can define all possible deformed configurations of the system subject to arbitrary nodal forces R. R o = vector of equivalent nodal forces, representing all external effects other than the nodal forces which are included in the preceding nodal force vector R; this vector is established by assembling the members' Q o m. The system stiffness matrix K is square since r have the same size. In addition, it is symmetric. Once the supports' constraints are accounted for in, the nodal displacements are found by solving the system of linear equations, symbolically: r = K − 1 ( R −

Truter v Deysel

Truter and Another v Deysel is an important case in South African law, with particular resonance in the area of civil procedure and medical malpractice. It is frequently quoted or invoked for its definition of "cause of action." It was heard in the Supreme Court of Appeal by Harms JA, Zulman JA, Navsa JA, Mthiyane JA and Van Heerden JA on 24 February 2006. Counsel for the appellants was JG Dickerson SC; the case was an appeal from a decision in the Cape Provincial Division by Mlonzi AJ. The case turned on "the crisp question" of when in terms of the Prescription Act, the period of prescription commences. Deysel's claim was based on delict. Under section 12 of the Act, prescription begins to run only from the time at which creditor acquires knowledge, or is deemed to have acquired knowledge, of "the facts from which the debt arises." The creditor acquires a complete cause of action for the recovery of debt when he is in possession of the entire set of facts upon which he relies to prove his claim.

The court held. Expert opinion was rather evidence. Prescription accordingly commenced to run as soon as the creditor sustained harm, not only when he secured expert opinion that defendants' conduct was negligent; the respondent instituted action in the High Court against the appellants for damages for personal injury sustained by him as a result of the negligence of the defendants in their performance on him of certain medical and surgical procedures. The defendants raised a special plea of prescription, it appeared that, although the procedures had been performed on the plaintiff in 1993, it was only in early 2000 that he managed to secure medical opinion to the effect that the defendants had conducted themselves negligently and, for that reason, that summons was issued only in April 2000. The question which fell for determination by the High Court was the time at which the period of prescription in respect of the plaintiff's claim had commenced to run; the High Court dismissed the special plea, finding that the period of prescription had commenced running only when the plaintiff had managed to secure medical opinion to the effect that the defendants had been negligent.

Van Heerden JA held—and Harms JA, Zulman JA, Navsa JA and Mthiyane JA concurred—that, under section 11 of the Prescription Act, the plaintiff's claim was subject to a three-year extinctive period of prescription. He held, that under section 12 of the Act prescription of a debt began running when the debt became due: A debt became due when the creditor acquired knowledge of the facts from which the debt arose; the court found that, in a delictual claim, the requirements of fault and unlawfulness were not factual ingredients of the cause of action. For the purposes of prescription, "cause of action" meant every fact which it was necessary for the plaintiff to prove in order to succeed in his claim, although it did not comprise every piece of evidence, necessary to prove those facts. An expert opinion, to the effect that certain conduct had been negligent, was not itself a fact, rather, evidence; the plaintiff in the present case, to the mind of Van Heerden JA, had not lacked capacity to appreciate that a wrong had been done to him.

The running of prescription could therefore not be delayed on that ground. In accordance with the "once and for all" rule, a plaintiff's cause of action is complete as soon as he sustains some damage, not only in respect of the damage sustained, but in respect of any damage yet to be sustained; the court found that all of the facts and information in respect of the operations performed on the plaintiff by the defendants had been known, or had been accessible, to him and his legal representatives as early as 1994 or 1995. Accordingly, the appeal and the special plea had to be upheld, the decision in the Cape Provincial Division, in Deysel v Truter and Another reversed. Civil procedure in South Africa Law of South Africa Joubert Law of South Africa vol 21. Loubser Extinctive Prescription. Visser and Potgieter The Law of Damages 2 ed. Bentley v Bristol and Western Health Authority 2 Med LR. Buchner and Another v Johannesburg Consolidated Investment Co Ltd 1995 SA 215. Cape Town Municipality v Paine 1923 AD 207.

Cape Town Municipality and Another v Allianz Insurance Co Ltd 1990 SA 311. Castell v De Greef 1993 SA 501. Coetzee v SA Railways and Harbours 1933 CPD 565. Deloitte Haskins & Sells Consultants Ltd v Bowthorpe Hellerman Deutsch Ltd 1991 SA 525. Deysel v Truter and Another 2005 SA 598. Dobbie v Medway Health Authority 5 Med LR. Drennan Maud & Partners v Pennington Town Board 1998 SA 200. Evins v Shield Insurance Co Ltd 1980 SA 814. Halford v Brookes WLR 428. McKenzie v Farmers' Co-operative Meat Industries Ltd 1922 AD 16. Mkhatswa v Minister of Defence 2000 SA 1104. Nash v Eli Lilly 2 Med LR 169. Nedcor Bank Bpk v Regering van die Republiek van Suid-Afrika 2001 SA 987. Oliff v Minnie 1953 SA 1. Oslo Land Co Ltd v The Union Government 1938 AD 584. Pringle v Administrator, Transvaal 1990 SA 379. Prinsloo v Woolbrokers Federation Ltd 1955 SA 298. S v

Kiyoshi Hatanaka

Kiyoshi Hatanaka is a retired Japanese boxer, a former WBC super bantamweight champion. Hatanaka began karate at the first grade of elementary school, won the Japanese championship in the juvenile division at its sixth grade and the first grade of junior high school. In addition, he began football at the fourth grade of elementary school, was scouted by a prestigious high school, he set an interval record in the local ekiden race at the age of a junior high school student. At that time, informed from an acquaintance that a professional boxer got paid 30,000 yen per match in the amount of time, he became interested in boxing and joined Matsuda Boxing Gym, he compiled an amateur record of 26–5 before turning professional. Hatanaka made his professional debut with a first-round knockout victory in November 1984, at the age of a high school student. He won the annual Japanese boxing series, All-Japan Rookie King Tournament in the super flyweight division in March 1986. He captured the Japanese super flyweight title at the Korakuen Hall in February 1987.

In his first world title shot against WBC super flyweight champion Gilberto Román in September 1988, Hatanaka entered the ring of the Nagoya Rainbow Hall with full smile. Román floored Hatanaka in the first round, but was docked a point for a low blow late in the same round. Though Hatanaka was given a full five minutes to recover, he was hit below the belt again in the third round and took three minutes' rest; as the rounds rolled on, Román kept his pace to retain his title via a unanimous decision. Hatanaka was so nervous that he remembered nothing after the fight. After the defeat, Hatanaka decided to become a world champion from his beloved hometown of Nagoya by any means necessary, it was no longer a question of money for him. Hatanaka needed a reliable trainer, he asked Toshihide Tsutsumi three times who once worked as a trainer at Matsuda Boxing Gym, was at last accepted. He did not get anxious anymore. Hatanaka moved up two weight divisions and fought against Pedro Rubén Décima for the WBC super bantamweight title at the Nagoya International Exhibition Hall, aka Port Messe Nagoya, on February 3, 1991.

He was floored in the first round, but felt calm enough to listen to Tsutsumi's instruction between rounds. After knocking down Décima four times in the fourth round, he sent him to the canvas two more times in the seventh and eighth rounds before the referee stopped the bout. In his first defense against Daniel Zaragoza on June 14 of that year, Hatanaka was cut on the corner of his left eye from an accidental head butt in the fourth round, the referee took a point away from Zaragoza. From the seventh or eighth round, Hatanaka had triple vision in his right eye, the blood flowed into his left eye. Zaragoza was crowned the new champion via a split decision in front of 9,000 spectators at the Nagoya Rainbow Hall. In 2007, Alvaro Morales of ESPN Deportes wrote it as many Asians' consideration, "the best fight of the decade". Although Hatanaka desired a rematch with Zaragoza, he suffered from ophthalmoplegia caused by this fight, retired as a boxer after four months, he is the president of Hatanaka Boxing Gym in Nagoya.

Hatanaka Promotions has provided a boxing television program Soul Fighting on Chubu-Nippon Broadcasting. Toshihide Tsutsumi, presented with the tenth Eddie Townsend Award in 1999, serves as a trainer at that gym. List of WBC world champions List of super-bantamweight boxing champions List of Japanese boxing world champions Boxing in Japan Boxing Magazine editorial department, ed.. 日本プロボクシング史 世界タイトルマッチで見る50年. Tokyo, Japan: Baseball Magazine Sha Co. Ltd. pp. 130, 175–176, 297. ISBN 978-4-583-03695-3. Jun'ichi Hirata. "畑中清詞〜6度のダウン奪い名古屋初の王者へ〜". In Boxing Magazine editorial department; the Glorious Moments 究極の栄光・世界チャンピオン名鑑 – 日本ボクシング史に輝く41人の男たち. B. B.mook. Tokyo, Japan: Baseball Magazine Sha Co. Ltd. pp. 12, 78–79. ISBN 978-4-583-61076-4. Professional boxing record for Kiyoshi Hatanaka from BoxRec

Antiplatelet drug

An antiplatelet drug known as a platelet agglutination inhibitor or platelet aggregation inhibitor, is a member of a class of pharmaceuticals that decrease platelet aggregation and inhibit thrombus formation. They are effective in the arterial circulation, they are used in primary and secondary prevention of thrombotic cerebrovascular or cardiovascular disease. Antiplatelet therapy with one or more of these drugs decreases the ability of blood clots to form by interfering with the platelet activation process in primary hemostasis. Antiplatelet drugs can reversibly or irreversibly inhibit the process involved in platelet activation resulting in decreased tendency of platelets to adhere to one another and to damaged blood vessels' endothelium. A 2006 review states: "...low-dose aspirin increases the risk of major bleeding 2-fold compared with placebo. However, the annual incidence of major bleeding due to low-dose aspirin is modest—only 1.3 patients per thousand higher than what is observed with placebo treatment.

Treatment of 800 patients with low-dose aspirin annually for cardiovascular prophylaxis will result in only 1 additional major bleeding episode." A combination of aspirin plus an ADP/P2Y inhibitor is used in order to obtain greater effectiveness than with either agent alone. This is known as "Dual antiplatelet therapy"; the class of antiplatelet drugs include: Irreversible cyclooxygenase inhibitors Aspirin Triflusal Adenosine diphosphate receptor inhibitors Cangrelor Clopidogrel Prasugrel Ticagrelor Ticlopidine Phosphodiesterase inhibitors Cilostazol Protease-activated receptor-1 antagonists Vorapaxar Glycoprotein IIB/IIIA inhibitors Abciximab Eptifibatide Tirofiban Adenosine reuptake inhibitors Dipyridamole Thromboxane inhibitors Thromboxane synthase inhibitors Thromboxane receptor antagonists Terutroban Prevention and treatment of arterial thrombosis is essential in patients with certain medical conditions whereby the risk of thrombosis or thromboembolism may result in disastrous consequences such as heart attack, pulmonary embolism or stroke.

Patients who require the use of antiplatelet drugs are: stroke with or without atrial fibrillation, any heart surgery, Coronary Heart Disease such as stable angina, unstable angina and heart attack, patients with coronary stent, Peripheral Vascular Disease/Peripheral Arterial Disease and apical/ventricular/mural thrombus. Treatment of established arterial thrombosis includes the use of antiplatelet drugs and thrombolytic therapy. Antiplatelet drugs alter the platelet activation at the site of vascular damage crucial to the development of arterial thrombosis. Aspirin and Triflusal irreversibly inhibits the enzyme COX, resulting in reduced platelet production of TXA2. Dipyridamole inhibits platelet phosphodiesterase, causing an increase in cyclic AMP with potentiation of the action of PGI2 – opposes actions of TXA2 Clopidogrel affects the ADP-dependent activation of IIb/IIIa complex Glycoprotein IIb/IIIa receptor antagonists block a receptor on the platelet for fibrinogen and von Willebrand factor.

3 classes: Murine-human chimeric antibodies Synthetic peptides Synthetic non-peptides Epoprostenol is a prostacyclin, used to inhibit platelet aggregation during renal dialysis and is used in primary pulmonary hypertension. Thrombolytic therapy is used in myocardial infarction, cerebral infarction, and, on occasion, in massive pulmonary embolism; the main risk is bleeding. Treatment should not be given to patients having had recent bleeding, uncontrolled hypertension or a hemorrhagic stroke, or surgery or other invasive procedures within the previous 10 days. Streptokinase forms a complex with plasminogen, resulting in a conformational change that activates other plasminogen molecules to form plasmin. Plasminogen activators, tissue-type plasminogen activators are produced by recombinant technology; when considering these medications and the risk-benefit ratio in the perioperative period, one must consider the risk of stopping the medication and a clot forming versus the risk of bleeding during or after the surgery if medication is continued.

In patients with time-sensitive diseases, DAPT can be stopped 3 months after a coronary stent is placed if postponing surgery any longer would result in significant morbidity. Examples of these types of surgeries include some cancer surgery and some orthopedic surgery. Preferably 6 to 12 months of DAPT should be continued in patients having elective surgery. Bare metal stents required at least one month of DAPTBalloon angioplasty in the preoperative period - patients can proceed to surgery two weeks after the procedure. CABG: Patients may proceed with surgery as soon as they are healed from the coronary artery bypass procedure and they do not need any specific amount of time on DAPT Dentists should be aware of the risk of prolonged bleeding time in patients taking antiplatelet drugs when planning dental treatments that are to cause bleeding. Therefore, it is important for dentists to know how to assess patient's bleeding risk and how to manage them. Identify the likelihood and risk of dental treatment causing bleeding complications.

Antiplatelet drugs effect may be

The Temptations Sing Smokey

The Temptations Sing Smokey is the second studio album by The Temptations for the Motown label, released on the Gordy Records subsidiary in 1965. As its name implies, it is composed of songs written and produced by Smokey Robinson, several other members of the Miracles as well. Several of the songs are covers of songs Robinson produced for the Miracles or Mary Wells, while the rest were recorded by The Temptations. Among these are three successful hit singles, starting with "The Way You Do the Things You Do", which featured Eddie Kendricks on lead vocals; the next two songs feature lead vocals by new Temptation David Ruffin – "It's Growing" and the group's signature song, "My Girl". Not included are two singles which predate these two singles, "I'll Be in Trouble" and "Girl"; these songs would be included on The Temptin' Temptations. A third hit single, "The Way You Do the Things You Do", is present here, although it was issued on the previous Temptations album, Meet the Temptations. Side one "The Way You Do the Things You Do" 2:41 "Baby, Baby I Need You" 2:53 "My Girl" 2:45 "What Love Has Joined Together" 2:58 "You'll Lose a Precious Love" 2:35 "It's Growing" 3:00Side two "Who's Lovin' You" 2:59 "What's So Good About Goodbye" 2:40 "You Beat Me to the Punch" 2:45 "Way Over There" 3:03 "You've Really Got a Hold on Me" 3:00 " Depend on Me" 2:32Unreleased recordings from the Sing Smokey sessions: "What's Easy for Two Is So Hard for One" "Happy Landing" Both these songs have subsequently been released.

David Ruffin – vocals Eddie Kendricks – vocals Paul Williams – vocals Melvin Franklin – vocals Otis Williams – vocals Elbridge "Al" Bryant – vocals The Andantes – additional background vocals Smokey Robinson – producer, Album executive producer The Funk Brothers – instrumentation Detroit Symphony Orchestra – strings Note – There was no Billboard R&B singles chart from November 1963 until January 1965. Most discographies include R&B information from Cash Box magazine to fill in the gap in the R&B chart, as is done here with the 1964 releases. List of number-one R&B albums of 1965