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Published: 4 June 2021
Last updated: 8 February 2022

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1

Beiko, Robert. "Bioinformatics: Hypothesis Free—Or Hypotheses Freed?" BioScience 64, no. 9 (August 8, 2014): 844–45. http://dx.doi.org/10.1093/biosci/biu126.

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2

Bashir, Josefeena. "Hypothesis Testing." Scientific Journal of India 3, no. 1 (December 31, 2018): 62–63. http://dx.doi.org/10.21276/24565644/2018.v3.i1.21.

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3

POPLACK, SHANA. "What does the Nonce Borrowing Hypothesis hypothesize?" Bilingualism: Language and Cognition 15, no. 3 (December 15, 2011): 644–48. http://dx.doi.org/10.1017/s1366728911000496.

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4

Moore, Andrew. "Hypotheses “R” Us − But What's a Hypothesis Anyway?" BioEssays 40, no. 9 (August 22, 2018): 1800137. http://dx.doi.org/10.1002/bies.201800137.

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5

Numazawa, Aibi Ivy. "Suggested Two Hypotheses on Dementia (“Anticholinergic Hypothesis” and “Cranial Skeletal Muscles Hypothesis”) and the Therapeutic Agent." Advances in Alzheimer's Disease 08, no. 02 (2019): 15–26. http://dx.doi.org/10.4236/aad.2019.82002.

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6

Yamamoto, Akihiro. "Hypothesis finding based on upward refinement of residue hypotheses." Theoretical Computer Science 298, no. 1 (April 2003): 5–19. http://dx.doi.org/10.1016/s0304-3975(02)00416-4.

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7

Heger, Tina, and Jonathan M. Jeschke. "The enemy release hypothesis as a hierarchy of hypotheses." Oikos 123, no. 6 (February 12, 2014): 741–50. http://dx.doi.org/10.1111/j.1600-0706.2013.01263.x.

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8

Spellman, Barbara A. "Hypothesis Testing: Strategy Selection for Generalising versus Limiting Hypotheses." Thinking & Reasoning 5, no. 1 (January 1999): 67–92. http://dx.doi.org/10.1080/135467899394084.

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9

Barker, Edward D., Susanna Roberts, and Esther Walton. "Hidden hypotheses in ‘hypothesis-free’ genome-wide epigenetic associations." Current Opinion in Psychology 27 (June 2019): 13–17. http://dx.doi.org/10.1016/j.copsyc.2018.07.009.

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10

Binoy, Sija. "Significance of Hypothesis in Research." Indian Journal of Holistic Nursing 10, no. 01 (November 19, 2019): 31–33. http://dx.doi.org/10.24321/2348.2133.201905.

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11

Kincaid-Smith, Priscilla. "Hypothesis." Journal of Hypertension 22, no. 6 (June 2004): 1051–55. http://dx.doi.org/10.1097/00004872-200406000-00001.

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12

Bräutigam, Katharina, Lars Dietzel, and Thomas Pfannschmidt. "Hypothesis." Plant Signaling & Behavior 5, no. 1 (January 2010): 81–85. http://dx.doi.org/10.4161/psb.5.1.10294.

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13

Shifflet, Glenn. "Hypothesis." Journal of Bisexuality 5, no. 1 (April 19, 2005): 27–37. http://dx.doi.org/10.1300/j159v05n01_03.

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14

Eger, Edmond I., Donald D. Koblin, R. Adron Harris, Joan J. Kendig, Andrew Pohorille, Michael J. Halsey, and James R. Trudell. "Hypothesis." Anesthesia & Analgesia 84, no. 4 (April 1997): 915–18. http://dx.doi.org/10.1097/00000539-199704000-00039.

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15

Eger, E. I., M. J. Halsey, R. A. Harris, D. D. Koblin, A. Pohorille, J. C. Sewell, J. M. Sonner, and J. R. Trudell. "Hypothesis." Anesthesia & Analgesia 88, no. 6 (June 1999): 1395–400. http://dx.doi.org/10.1213/00000539-199906000-00036.

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16

Azimi, Arsalan, and Arian Azimi. "Hypothesis." Anti-Cancer Drugs 28, no. 4 (April 2017): 369–75. http://dx.doi.org/10.1097/cad.0000000000000476.

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17

La Vecchia, Carlo. "Hypothesis." European Journal of Cancer Prevention 20, no. 6 (November 2011): 556. http://dx.doi.org/10.1097/cej.0b013e32834a8018.

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18

Lin, Feng Ying C., and James F. Troendle. "Hypothesis." Pediatric Infectious Disease Journal 25, no. 10 (October 2006): 884–88. http://dx.doi.org/10.1097/01.inf.0000239322.58890.94.

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19

Aviv, Abraham. "Hypothesis." Hypertension 37, no. 4 (April 2001): 1060–66. http://dx.doi.org/10.1161/01.hyp.37.4.1060.

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20

Uversky, Vladimir N. "Hypothesis." Intrinsically Disordered Proteins 1, no. 1 (January 2013): e25725. http://dx.doi.org/10.4161/idp.25725.

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21

Levin, Leonard A. "Hypothesis." Archives of Ophthalmology 126, no. 11 (November 10, 2008): 1582. http://dx.doi.org/10.1001/archopht.126.11.1582.

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22

BORDER, JOHN R. "Hypothesis:." Archives of Surgery 123, no. 3 (March 1, 1988): 285. http://dx.doi.org/10.1001/archsurg.1988.01400270019001.

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23

Hazlerigg, David G., and Gerald A. Lincoln. "Hypothesis." Journal of Biological Rhythms 26, no. 6 (November 30, 2011): 471–85. http://dx.doi.org/10.1177/0748730411420812.

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Circannual rhythms are innately timed long-term (tau ≈ 12 months) cycles of physiology and behavior, crucial for life in habitats ranging from the equator to the Poles. Here the authors propose that circannual rhythm generation depends on tissue-autonomous, reiterated cycles of cell division, functional differentiation, and cell death. They see the feedback control influencing localized stem cell niches as crucial to this cyclical histogenesis hypothesis. Analogous to multi-oscillator circadian organization, circannual rhythm generation occurs in multiple tissues with hypothalamic and pituitary sites serving as central pacemakers. Signals including day length, nutrition, and social factors can synchronize circannual rhythms through hormonal influences, notably via the thyroid and glucocorticoid axes, which have profound effects on histogenesis. The authors offer 4 arguments in support of this hypothesis: (1) Cyclical histogenesis is a prevalent process in seasonal remodeling of physiology. It operates over long time domains and exhibits tissue autonomy in its regulation. (2) Experiments in which selected peripheral endocrine signals are held constant indicate that circannual rhythms are not primarily the product of interacting hormonal feedback loops. (3) Hormones known to control cell proliferation, differentiation, and organogenesis profoundly affect circannual rhythm expression. (4) The convergence point between photoperiodic input pathways and circannual rhythm expression occurs in histogenic regions of the hypothalamus and pituitary. In this review, the authors discuss how testing this hypothesis will depend on the use of cellular/molecular tools and animal models borrowed from developmental biology and neural stem cell research.
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24

Eger, E. I., M. J. Halsey, R. A. Harris, D. D. Koblin, A. Pohorille, J. C. Sewell, J. M. Sonner, and J. R. Trudell. "Hypothesis." Anesthesia & Analgesia 88, no. 6 (June 1999): 1395–400. http://dx.doi.org/10.1097/00000539-199906000-00036.

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25

Yagil, Yoram, and Chana Yagil. "Hypothesis." Hypertension 41, no. 4 (April 2003): 871–73. http://dx.doi.org/10.1161/01.hyp.0000063886.71596.c8.

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26

Bostom, Andrew G., Dominik Steubl, and Allon N. Friedman. "Hypothesis." Transplantation Direct 3, no. 11 (November 2017): e219. http://dx.doi.org/10.1097/txd.0000000000000737.

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27

Hecht, Eric M., David C. Landy, Soyeon Ahn, WayWay M. Hlaing, and Charles H. Hennekens. "Hypothesis." Journal of Cardiovascular Pharmacology and Therapeutics 18, no. 6 (September 13, 2013): 550–54. http://dx.doi.org/10.1177/1074248413494815.

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28

Lizotte-Waniewski, Michelle, Keith Brew, and Charles H. Hennekens. "Hypothesis." Journal of Cardiovascular Pharmacology and Therapeutics 21, no. 4 (December 24, 2015): 368–71. http://dx.doi.org/10.1177/1074248415615237.

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The hypothesis that matrix metalloproteinase (MMP) inhibitors reduce risks of cardiovascular disease in humans is plausible, unproven, and difficult to test, due, in part, to differences in specificity and route of administration. Endogenous tissue inhibitors of metalloproteinases (TIMPs) are tight-binding, protein inhibitors that function in vivo and can be engineered to enhance specificity for desired targets. Nonetheless, TIMPs have been difficult to test, in part, because their secondary functions, including cell growth promotion and angiogenesis, raise concerns about side effects and they cannot be delivered orally. In contrast, doxycycline and other chemically modified tetracyclines are broad-spectrum, reversible MMP inhibitors with lower affinity but can be taken orally and have US Food and Drug Administration approval. The completed phase 2 randomized trials in humans of MMP inhibitors have methodologic limitations but generally show no significant benefits with adverse effects. At present, the principal research challenge is to achieve a better understanding of the complexities of biological functions of MMPs and subsequently to conduct large-scale phase 3 trials.
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29

Powell, Jonathan M., Emanuel Ebin, Steven Borzak, Anastasios Lymperopoulos, and Charles H. Hennekens. "Hypothesis." Journal of Cardiovascular Pharmacology and Therapeutics 22, no. 1 (July 8, 2016): 51–53. http://dx.doi.org/10.1177/1074248416644350.

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The hypothesis that paroxetine decreases morbidity and mortality in patients with heart failure (HF) is plausible but unproven. Basic research demonstrates that inhibition of G protein-coupled receptor kinase 2 (GRK2) both in vitro and in vivo in the myocardium may be beneficial. G protein-coupled receptor kinase 2 antagonism is purported to exert cardioprotective effects immediately following myocardial injury by blunting toxic overstimulation on a recently injured heart. In addition, chronic overexpression of GRK2 inhibits catecholamine induction of vital positive chronotropic and ionotropic effects required to preserve cardiac output leading to worsening of congestive HF. In cardiac-specific GRK2 conditional knockout mice, there is significant improvement in left ventricular wall thickness, left ventricular end-diastolic diameter (LVEDD), and ejection fraction (EF) compared to controls. Paroxetine is a selective serotonin reuptake inhibitor which was recently shown to have the ability to directly inhibit GRK2 both in vitro and in vivo. At physiologic temperatures, paroxetine inhibits GRK2-dependent phosphorylation of an activated G-protein-coupled receptor with a half maximal inhibitory concentration of 35 micromoles, a substantially greater affinity than for other G protein-coupled receptor kinases. In a randomized trial in mice with systolic HF and depressed EF postmyocardial infarction, those treated with paroxetine had a 30% increase in EF, improved contractility, and LVEDD and wall thickness compared to those treated with medical therapy alone. While further basic research may continue to elucidate plausible mechanisms of benefit and observational studies will contribute important relevant information, large scale randomized trials designed a priori to do so are necessary to test the hypothesis.
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30

Wang, Wenguang, Chao Liu, and Hongliang Cong. "Hypothesis." Journal of Cardiovascular Pharmacology and Therapeutics 22, no. 1 (July 7, 2016): 56–64. http://dx.doi.org/10.1177/1074248416651721.

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Calcific aortic valve disease (CAVD) is a common cardiovascular disease in the elderly individuals associated with major morbidity and mortality. The process is characterized by multiple steps: lipid infiltration, inflammation, fibrosis, and calcification. Inhibitors of proprotein convertase subtilisin/kexin type 9 (PCSK9) represent a new therapeutic category of drugs for the treatment of dyslipidemia and atherosclerotic cardiovascular disease. Monoclonal antibodies of PCSK9 can result in substantial reductions in atherogenic lipoprotein cholesterol-carrying particles, especially lipoprotein(a), and thereby hold the potential for further reducing events associated with atherosclerotic cardiovascular disease. In this article, we reviewed the clinical and experimental studies in order to find the evidence of the involvement of PCSK9 in CAVD and the potential benefits of PCSK9 monoclonal antibodies in clinical therapeutics.
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31

Alkire, Michael T., and John F. Guzowski. "Hypothesis." Anesthesiology 109, no. 5 (November 1, 2008): 768–70. http://dx.doi.org/10.1097/aln.0b013e31818aa6f2.

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32

Jahnke, U., E. H. Fischer, and E. C. Alvord. "HYPOTHESIS." Journal of Neuropathology and Experimental Neurology 44, no. 3 (May 1985): 320. http://dx.doi.org/10.1097/00005072-198505000-00049.

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33

Cerami, Anthony. "Hypothesis." Journal of the American Geriatrics Society 33, no. 9 (September 1985): 626–34. http://dx.doi.org/10.1111/j.1532-5415.1985.tb06319.x.

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34

Haas, Oskar A., and Marieke Seyger. "Hypothesis." Cancer Genetics and Cytogenetics 70, no. 2 (October 1993): 112–16. http://dx.doi.org/10.1016/0165-4608(93)90178-o.

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35

Eger, Edmond I., Donald D. Koblin, R. Adron Harris, Joan J. Kendig, Andrew Pohorille, Michael J. Halsey, and James R. Trudell. "Hypothesis." Anesthesia & Analgesia 84, no. 4 (April 1997): 915–18. http://dx.doi.org/10.1213/00000539-199704000-00039.

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36

Lindahl, Kirsten Fischer. "Hypothesis." Immunogenetics 34, no. 1 (July 1991): 1–4. http://dx.doi.org/10.1007/bf00212305.

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37

Ostrovskii, Victor, and Elena Kadyshevich. "Life Origination Hydrate Hypothesis (LOH-Hypothesis)." Life 2, no. 1 (January 4, 2012): 135–64. http://dx.doi.org/10.3390/life2010135.

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38

Harwood, Buie. "The 1995 Hypothesis + The 2015 Hypothesis." Journal of Interior Design 31, no. 2 (January 2006): xi—xxii. http://dx.doi.org/10.1111/j.1939-1668.2005.tb00406.x.

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39

Templeton, Alan R. ""Eve": Hypothesis Compatibility versus Hypothesis Testing." American Anthropologist 96, no. 1 (March 1994): 141–47. http://dx.doi.org/10.1525/aa.1994.96.1.02a00080.

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40

Ardeni, Pier Giorgio, and Brian Wright. "The Prebisch-Singer Hypothesis: A Reappraisal Independent of Stationarity Hypotheses." Economic Journal 102, no. 413 (July 1992): 803. http://dx.doi.org/10.2307/2234578.

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41

Semerdjiev, Tzvetan. "The Genetic Program - A Technocratic Hypothesis." Information & Security: An International Journal 1, no. 1 (1998): 26–45. http://dx.doi.org/10.11610/isij.0103.

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42

Imaoka, Haruki, and Tomoaki Hoshino. "1. The Dutch Hypothesis and British Hypothesis." Nihon Naika Gakkai Zasshi 102, no. 6 (2013): 1359–64. http://dx.doi.org/10.2169/naika.102.1359.

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43

Nick, Peter. "Hypothesis-driven research for hypothesis-driven application." Protoplasma 252, no. 3 (March 27, 2015): 715–16. http://dx.doi.org/10.1007/s00709-015-0806-5.

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44

Mir, Kalim U. "The hypothesis is there is no hypothesis." Trends in Genetics 16, no. 2 (February 2000): 63–64. http://dx.doi.org/10.1016/s0168-9525(99)01947-2.

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45

Christensen, Erik I., and Pierre J. Verroust. "Interstitial fibrosis: tubular hypothesis versus glomerular hypothesis." Kidney International 74, no. 10 (November 2008): 1233–36. http://dx.doi.org/10.1038/ki.2008.421.

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46

Li, Yan, and Xiaolong Pu. "Hypothesis Designs for Three-Hypothesis Test Problems." Mathematical Problems in Engineering 2010 (2010): 1–15. http://dx.doi.org/10.1155/2010/393095.

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As a helpful guide for applications, the alternative hypotheses of the three-hypothesis test problems are designed under the required error probabilities and average sample number in this paper. The asymptotic formulas and the proposed numerical quadrature formulas are adopted, respectively, to obtain the hypothesis designs and the corresponding sequential test schemes under the Koopman-Darmois distributions. The example of the normal mean test shows that our methods are quite efficient and satisfactory for practical uses.
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47

Humphreys, Lloyd G. "Attenuated hypothesis or attenuated test of hypothesis?" Intelligence 9, no. 3 (July 1985): 291–95. http://dx.doi.org/10.1016/0160-2896(85)90031-5.

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48

Brown, Lawrence D., and John I. Marden. "Complete Class Results for Hypothesis Testing Problems with Simple Null Hypotheses." Annals of Statistics 17, no. 1 (March 1989): 209–35. http://dx.doi.org/10.1214/aos/1176347012.

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49

Hipp, E. "MO-FG-206-04: Hypothesis or Hypotheses, That Is the Question." Medical Physics 43, no. 6Part31 (June 2016): 3714–15. http://dx.doi.org/10.1118/1.4957312.

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50

Hwang, Yi-Ting, Hsun-Chih Kuo, Chun-Chao Wang, and Meng Feng Lee. "Estimating the number of true null hypotheses in multiple hypothesis testing." Statistics and Computing 24, no. 3 (February 8, 2013): 399–416. http://dx.doi.org/10.1007/s11222-013-9377-5.

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