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#incremental_learning #learning
Five basic skills of incremental reading

Incremental reading requires skills that you will perfect only over months and years of use. This overview will only help you master the basic skills and help you make a start with incremental reading. The 5 basic skills are:

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Incremental learning - SuperMemo Help
seem complex at first. However, once you master it, you will begin a learning process that will surpass your expectations. You will be surprised with the volume of data your memory can process and retain! See this simple demo at YouTube. <span>Five basic skills of incremental reading Incremental reading requires skills that you will perfect only over months and years of use. This overview will only help you master the basic skills and help you make a start with incremental reading. The 5 basic skills are: importing articles to SuperMemo reading articles and decomposing articles into manageable pieces converting most important pieces of knowledge into question-answer material review of the material to ensure good recall handling of the unavoidable overflow of information Skill 1: Importing articles Five article import methods Initially, you may limit your imports to a simple copy&paste of individual articles. Later, you will want to mas




Augmenting Long-term Memory
#SRS #anki #has-images #incremental #memory #reading

Augmenting Long-term Memory

Michael Nielsen | Y Combinator Research | July 2018

Related Resources
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By Michael Nielsen

One day in the mid-1920s, a Moscow newspaper reporter named Solomon Shereshevsky entered the laboratory of the psychologist Alexander Luria. Shereshevsky's boss at the newspaper had noticed that Shereshevsky never needed to take any notes, but somehow still remembered all he was told, and had suggested he get his memory checked by an expert.

Luria began testing Shereshevsky's memory. He began with simple tests, short strings of words and of numbers. Shereshevsky remembered these with ease, and so Luria gradually increased the length of the strings. But no matter how long they got, Shereshevsky could recite them back. Fascinated, Luria went on to study Shereshevsky's memory for the next 30 years. In a book summing up his research** Alexander Luria, “The Mind of a Mnemonist”, Harvard University Press (1968)., Luria reported that:

[I]t appeared that there was no limit either to the capacity of S.'s memory or to the durability of the traces he retained. Experiments indicated that he had no difficulty reproducing any lengthy series of words whatever, even though these had originally been presented to him a week, a month, a year, or even many years earlier. In fact, some of these experiments designed to test his retention were performed (without his being given any warning) fifteen or sixteen years after the session in which he had originally recalled the words. Yet invariably they were successful.

Such stories are fascinating. Memory is fundamental to our thinking, and the notion of having a perfect memory is seductive. At the same time, many people feel ambivalent about their own memory. I've often heard people say “I don't have a very good memory”, sometimes sheepishly, sometimes apologetically, sometimes even defiantly.

Given how central memory is to our thinking, it's natural to ask whether computers can be used as tools to help improve our memory. This question turns out to be highly generative of good ideas, and pursuing it has led to many of the most important vision documents in the history of computing. One early example was Vannevar Bush's 1945 proposal** Vannevar Bush, As We May Think, The Atlantic (1945). for a mechanical memory extender, the memex. Bush wrote:

A memex is a device in which an individual stores all his books, records, and communications, and which is mechanized so that it may be consulted with exceeding speed and flexibility. It is an enlarged intimate supplement to his memory.

The memex vision inspired many later computer pioneers, including Douglas Engelbart's ideas about the augmentation of human intelligence, Ted Nelson's ideas about hypertext, and, indirectly, Tim Berners-Lee's conception of the world wide web** See, for example: Douglas Engelbart,

...
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#incremental_learning #learning
Typical learning at school puts an emphasis on a few areas of knowledge and neglects all the remaining areas. A medical student may spend a few months mastering anatomy, while gradually forgetting his biochemistry material in the meantime (or the other way round). At the same time, he or she will not find time to study important issues of the day that will always depend on a given person in a given context. With blinkers imposed by the heavy load of school material, the student may never find time, for example, to figure out what incremental learning is. Narrow horizons and narrow perspectives only make it harder to further rationalize the selection of the learning material.
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e video collection, and read a few articles in subjects related to a forthcoming exam. In other words, all areas of knowledge keep growing in parallel in proportion to interests and importance. <span>Typical learning at school puts an emphasis on a few areas of knowledge and neglects all the remaining areas. A medical student may spend a few months mastering anatomy, while gradually forgetting his biochemistry material in the meantime (or the other way round). At the same time, he or she will not find time to study important issues of the day that will always depend on a given person in a given context. With blinkers imposed by the heavy load of school material, the student may never find time, for example, to figure out what incremental learning is. Narrow horizons and narrow perspectives only make it harder to further rationalize the selection of the learning material. Incremental learning is the opposite of the irrational school system learning in which a heavy focus is put on just a few areas of knowledge in a semester (at the cost of other, equally




Perseverance Powers Student Growth Designed from the ground up to meet the high expectations of Mathematics Standards, Into Math is the only solution built to track, predict, and propel growth for all your students in kindergarten through grade 12.
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#has-images

START UNKNOWN INTO MATH EXAMPLES ADD TO

A problem in which the change (what is added to the start) and result (the outcome of performing the action) are given in the problem. The start is not known and is what the students determine. 4 Some horses are in the field. Then 8 more horses come to the field. Now there are 11 horses in the field. How many horses were in the field to start? ■ + 8 = 11 Example from Lesson 14.2, Task 4 • Additional Lessons 14.4, M14 Review, 15.1, M15 Review TAKE FROM A problem in which the change (what is taken from the start) and result (the outcome of performing the action) are given in the problem. The start is not known and is what the students determine. 2 José has some baseball cards. He gives 8 cards to Elena. Now José has 9 baseball cards. How many baseball cards did José have to start? ■ - 8 = 9 Example from Lesson 14.2, Task 3 • Additional Lessons 14.3, M14 Review, 15.2, M15 Review

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#Bacteriologie #Bacteriology #Clinical #Clinique #MDB-Tularemia #MDB-Tularemie #Maladies-infectieuses-et-tropicales #Tularemia
Francisella tularensis is a gram-negative pathogen primarily of animals and occasionally of humans. The disease is now recognized as tularemia in most areas of the world, but it has been called rabbit fever, deer fly fever, Francis disease, and market men’s disease in the United States; wild hare disease (yato-byo) and Ohara disease in Japan; and water-rat trappers’ disease in Russia
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Tularemia has been so intimately linked to investigators in the United States that it has been referred to as “the first American disease” or an “A m e r i c a n a c h i e v e m e nt.” 2,3 However, its history is notable for important contributions from other areas of the world, including Japan and the former Soviet Union.
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Hare-associated illness compatible with tularemia has been known in Japan since 1818, and perhaps the earliest written description of a patient with unmistakable tularemia was provided by Soken Honma in 1837.4
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Credit for recognizing the clinical syndromes and identifying the organism belongs to American workers. In 1911, while evaluating possible plague outbreaks after the San Francisco earthquake of 1906, McCoy described a plague-like illness then prevalent in ground squirrels. With Chapin, he successfully cultured the causative bacteria in 1912.5 They named it Bacterium tularense because their discovery occurred in Tulare County, California
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In 1914, the first case with bacteriologic confirmation was reported in a patient from Ohio with an ocular infection.7,8
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In 1919, Dr. Edward Francis linked the deer fly as the vector of disease while recovering an unusual organism in the blood of febrile patients from Millard County, Utah, who also had suppurative lymphadenopathy9; he subsequently coined the human disease tularemia to emphasize the frequently accompanying bacteremia.10
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In Japan, Ohara had described a rabbit-associated febrile disease in 1926.12 He subsequently, transmitted the illness to his wife by rubbing rabbit hearts over her hand, and he recovered an organism from her lymph nodes13; Francis and Moore later showed that this Japanese organism was identical to B. tularense.14
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Francisella organisms are small, aerobic, catalase-positive, pleomorphic, gram-negative coccobacilli that are nonmotile and non–spore forming. They are more uniformly rod-shaped during logarithmic growth, during which they tend to exhibit bipolar staining with Gram or Giemsa methods; this staining pattern accentuates a coccoidal appearance, measuring 0.2 × 0.2 μm.
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{"exception-message":"unterminated string literal (unnamed script#7)","exception-type":"EvaluatorException"}
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Wild-type strains possess an electron-transparent, lipid-rich capsule. Loss of the capsule may lead to loss of serum resistance and virulence, but may not diminish viability or survival within neutrophils.13 The capsule had traditionally been thought to be directly neither toxic nor immunogenic, though recent studies have suggested that bacterial lipoproteins may interfere with neutrophil apoptosis by way of Toll-like receptor (TLR) mechanisms, and therefore foster local tissue destruction.16
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Francisella spp. belong to the Gammaproteobacteria class in the family Francisellaceae and include the human pathogens F. tularensis, F. philomiragia, and F. hispaniensis; the fish pathogens F. noatunensis subsp. orientalis and F. halioticida; and environmental isolates of F. guangzhouensis.
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Francisella traditionally has been categorized by growth characteristics, biochemical reactions, and virulence properties (Table 2 27.1). The three Francisella spp. potentially pathogenic for humans are F. tularensis, F. philomiragia, and F. hispaniensis.19–21 Although all three have been associated with human disease, only the tularensis and holarctica subspe- cies of F. tularensis are relatively common.
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F. tularensis subsp. tularensis (nearctica), also referred to as type A, is found almost exclusively in North America and is the most virulent species. Although previously thought to be restricted to North America, F. tularen si s subsp. tularensis has been isolated in Europe and its identity verified using molecular techniques.22
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F. tularensis subsp. holarctica (palaearctica), also referred to as type B, is found predominantly in Asia, Australia, and Europe but also in North America; it is less virulent in humans and of low virulence in rabbits.
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The F. tu la ren si s live vaccine strains are derived from F. tul ar en si s subsp. holarctica (see later under “Vaccination”)
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F. tularensis subsp. novicida is of low virulence and only rarely causes human infection, mainly in patients who are immunosuppressed.23 Although previously classified as a separate species, its reclassification as a subspecies of F. tularensis was proposed based on a high degree of genetic similarity to F. tul ar en si s .19,24 However, this has been controversial, and some authori- ties feel it should remain a separate Francisella species based on phe- notypic as well as genomic differences.20,23
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[unknown IMAGE 7677643721996] #Bacteriologie #Bacteriology #Clinical #Clinique #MDB-Tularemia #MDB-Tularemie #Maladies-infectieuses-et-tropicales #Tularemia #has-images
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Strains isolated in Japan have been designated F. tu la re ns is subsp. holarctica biovar japonica, but their differentiation from other F. tularensis subsp. holarctica strains by traditional phenotypic testing was not possible.21
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A fourth subspecies, F. tul ar ens is subsp. mediasiatica, has been found only in sparsely settled regions in Central Asia and Russia.20,25,26 An absence of human infection reports suggests that if capable of infecting, it would have low virulence
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F. ph i l om i ra g i a was previously called Ye r s i n i a p hi l o m i ra g i a . Reclassified because it shared the unique fatty acid profile of the Francisella spp. and substantial DNA relatedness to this genus, it does have some unique biochemical features (see Ta bl e 227.1) and DNA hybridization patterns that distinguish it from F. tu l a re n si s .
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F. ph i lo mi ra g i a is of low pathogenicity for humans, although it has been isolated from muskrats and a dog.20,27,28 It is naturally found in brackish and salt water, and in liquid media it may form biofilms and interact with free-living amebas.29 All strains originally tested produced β-lactamase and were most susceptible to aminoglycosides, cefoxitin, cefotaxime, fluoroquinolones, tetracycline, and chloramphenicol. However, an infection caused by F. philomiragia resistant to cefazolin and cefotaxime has been reported.30 The most active agents against six strains in a standardized broth microdilution assay were the aminoglycosides and the fluoroquinolones.31
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The complete genome of F. philomiragia has been sequenced, and it encodes a class A carbapenemase.28,32
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The taxonomy of Francisella has been complicated because biochemi- cal reactions may be variable, weak, or delayed and also in part because of the different terms given to organisms isolated in different areas of the world.
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Molecular typing has identified three genotypes of F. tularensis subsp. tularensis (designated A1a, A1b, and A2) and at least 10 genotypes of F. tu l ar en si s subsp. holarctica.39
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Genomic analyses have indicated that there was a common F. tularensis ancestor for clonal subspecies evolution, that F. tularensis subsp. novicida is the oldest, and that F. tu l ar e ns i s subsp. tularensis appeared before F. tu la re nsi s subsp. holarctica, which is the youngest.40
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. tu l ar e ns is requires cysteine or cystine (or another sulfhydryl source) for growth and therefore will not grow using most routine solid media or gram-negative selective media such as MacConkey or eosin methylene blue agars. It may be recovered with the use of glucose cysteine blood agar, thioglycollate broth, chocolate agar suitable for gonococcal growth, modified Thayer-Martin medium, buffered charcoal-yeast agar, or cysteine heart agar with 9% chocolatized sheep blood.20,21
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Blood agar may support the growth of some F. tularensis isolates on initial plating but not on subpassage.41
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A novel brain heart infusion supple- mented with 2% Vitox, 10% Fildes, and 1% histidine (BVFH) broth has been described as facilitating the early growth of F. t ul are n si s compared to customary media formulations.42
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Some strains of F. tularensis lack an overt requirement for cysteine or enriched medium for growth, and clinically significant strains of Francisella have been reported that do not show the expected fastidious growth characteristics.21
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rancisella should be suspected, however, whenever a slowly growing, small, and poorly staining gram-negative coccobacillus is isolated on chocolate agar and grows poorly or not at all on blood agar. Visible colonies take 2 to 5 days to appear. Incubation at 35°C is optimal, with or without an atmosphere of increased carbon dioxide.
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Virtually all F. tularensis strains are positive for β-lactamase, and a weak class A β-lactamase native to F. tularensis has been identified.43
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The recovery of F. tularensis from contaminated specimens may be facilitated by plating onto antibiotic-containing media known to support the growth of F.tularensis.20
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Antisera can distinguish between F. tularensis subsp. tularensis and F. tularensis subsp. novicida but not between F. tu laren si s subsp. tularensis and F. t ul ar en si s subsp. holarctica; strains within subspecies do not have antigenic differences detectable by antisera
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It is important to note that automated laboratory identification systems should not be used for the identification of Francisella because they may generate aerosols and commonly misidentify F. tularensis as Haemophilus or Aggregatibacter species.41
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Differentiation of Francisella from other bacteria can be accomplished using direct fluorescent antibody (DFA) staining, slide agglutination, polymerase chain reaction (PCR) assay, matrix-assisted laser desorption/ ionization time-of-flight (MALDI-TOF) sequencing, or cellular fatty acid composition analysis.20,44
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F. tularensis produces no known exotoxins, but many components of the Francisella envelope contribute to its pathogenicity, though questions remain about many putative virulence factors.33,44,45
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The lipopolysac- charide (LPS) from the live vaccine strain of F. tularensis possesses at least 1000-fold less endotoxin activity than the LPS from Escherichia coli.46 This is in part because F. tularensis LPS has a different structure composed primarily of the O antigen that makes the capsule and lacks many of the traditional LPS incitatory endotoxin components.
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The capsule can also block both immunoglobulin M (IgM) and complement binding with C3.48 Many of these features are believed to contribute both to immune activation and evasion
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Unlike other gram-negative bacteria, it is less recognized by TLR4 and does not bind to LPS-binding protein.33,45,49
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Genome sequencing has detected genes homologous to those from other bacteria that encode type IV pili in F. tularensis subspp. tularensis, holarctica, and novicida; and type IV pili assembly contributes to virulence in murine models.52
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Host immune responses are directed against numerous cell wall antigens, including membrane proteins, LPS, and carbohydrates, but previously it was not possible to identify dominant antigens. Proteomic analysis using serum from donors who have had tularemia or who have been immunized with the live vaccine strain has identified a large number of F. tularensis protein antigens and found possible immunodominant antigens.55 These include many cytoplasmic and membrane proteins, as well as hypothetical proteins of unknown localization
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Phenotypic correlates of virulence have included the capsule and citrulline ureidase activity.
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he contribution of citrulline ureidase to virulence is unclear. There are pathogenic isolates that do not possess this activity.
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Mechanisms for iron acquisition are present in F. tularensis, and their disruption attenuates in vitro intracellular growth and organism virulence in a mouse model.62
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Although deletion of acpA, acpB, acpC, and hap from F. tu l ar ens is subsp. novicida results in a mutant strain that is impaired in its ability to survive within macrophages and to escape from the phagosome, deletion of acpA and the combination of acpA, acpB, and acpC deletions do not alter the virulence of F. tu la re n si s type A strain Schu S4.60,61
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Genomic and proteomic analyses have the potential to more specifi- cally identify virulence factors in F. tularensis.57,63 F. tularensis contains a cluster of genes involved in virulence, the Francisella pathogenicity island (FPI). There are two copies of the FPI in F. tularensis subsp. tularensis and F. t ul are n sis subsp. holarctica and one copy in F. tul ar ensi s subsp. novicida; although largely identical, the FPI from F. tularensis subsp. tularensis differs from that in the other subspecies.64,65 The FPI contains 19 genes required for murine virulence and intracellular growth in macrophages, including iglABCD and pdpABCD. FPI regulation involves at least six proteins that regulate many FPI genes, and some also regulate non-FPI genes.66,67
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Within macrophage cytosol the organism depends on host amino acids as the gluconeogenic sources for metabolism.68
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Several endosymbiotic bacteria of ticks have been classified within the Francisellaceae family on the basis of 16S ribosomal gene sequence data. These include Wolbachia (Francisella) persica, an endosymbiont found in Rocky Mountain wood ticks (termed Dermacentor andersoni symbiont), and symbiont B of the soft tick Ornithodoros moubata.21
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