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nPoint Inc cumulative probability distribution
Cumulative Probability Distribution, supplied by nPoint Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Article Title: Precise Estimation of Cosmological Parameters Using a More Accurate Likelihood Function
Article Snippet: From the Sklar’s theorem [15], one can relate any npoint cumulative probability distribution (CDF) to onepoint CDFs as Prob(x1 ≤ x̂1, x2 ≤ x̂2, .



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Statistical tests and significance threshold used for each experiment in each experimental series

Journal: eNeuro

Article Title: Developmental Nicotine Exposure Alters Synaptic Input to Hypoglossal Motoneurons and Is Associated with Altered Function of Upper Airway Muscles

doi: 10.1523/ENEURO.0299-19.2019

Figure Lengend Snippet: Statistical tests and significance threshold used for each experiment in each experimental series

Article Snippet: First, the IEI and amplitude of all sEPSCs/mEPSCs from all cells within an age or treatment group were used to construct a cumulative probability distribution using Prism (GraphPad Software, Inc.; For example, see , ).

Techniques: In Vivo, In Vitro, Transmission Assay

DNE alters the modulation of glutamatergic sEPSCs in response to an acute nicotine challenge but only in cells from pups aged P3–P5. Cumulative probability distributions of glutamatergic sEPSC IEIs in control and DNE cells, at baseline and during acute nicotine challenge. At P1–P2 ( A , B ), acute nicotine challenge with 0.5 μM nicotine (black dashed lines) caused a left shift, toward shorter IEIs, of glutamatergic sEPSCs in both control and DNE cells [control, p = 0.049 ( A ) DNE, p < 0.0001 ( B )]. In cells from P3–P5 animals ( C , D ), acute nicotine challenge caused a left shift, toward shorter IEIs in control cells ( p < 0.0001; C ), but the distribution shifted to the right, toward longer IEIs in the DNE cells ( p = 0.012; D ). Arrows indicate the direction of the shift with acute nicotine challenge and indicates significant differences with K–S test (see Materials and Methods). Dotted gray lines indicate the 95% confidence intervals of each curve.

Journal: eNeuro

Article Title: Developmental Nicotine Exposure Alters Synaptic Input to Hypoglossal Motoneurons and Is Associated with Altered Function of Upper Airway Muscles

doi: 10.1523/ENEURO.0299-19.2019

Figure Lengend Snippet: DNE alters the modulation of glutamatergic sEPSCs in response to an acute nicotine challenge but only in cells from pups aged P3–P5. Cumulative probability distributions of glutamatergic sEPSC IEIs in control and DNE cells, at baseline and during acute nicotine challenge. At P1–P2 ( A , B ), acute nicotine challenge with 0.5 μM nicotine (black dashed lines) caused a left shift, toward shorter IEIs, of glutamatergic sEPSCs in both control and DNE cells [control, p = 0.049 ( A ) DNE, p < 0.0001 ( B )]. In cells from P3–P5 animals ( C , D ), acute nicotine challenge caused a left shift, toward shorter IEIs in control cells ( p < 0.0001; C ), but the distribution shifted to the right, toward longer IEIs in the DNE cells ( p = 0.012; D ). Arrows indicate the direction of the shift with acute nicotine challenge and indicates significant differences with K–S test (see Materials and Methods). Dotted gray lines indicate the 95% confidence intervals of each curve.

Article Snippet: First, the IEI and amplitude of all sEPSCs/mEPSCs from all cells within an age or treatment group were used to construct a cumulative probability distribution using Prism (GraphPad Software, Inc.; For example, see , ).

Techniques: Control

Cumulative probability distributions of glutamatergic mEPSC IEIs in control and DNE cells, at baseline and during acute nicotine challenge. In cells from animals aged P1–P2 ( A , B ), acute nicotine challenge with 0.5 μM nicotine (black dashed lines) caused a left shift, toward shorter IEIs, of glutamatergic mEPSCs in both control ( p < 0.0001; A ) and DNE cells ( p < 0.0001; B ). In cells from animals aged P3–P5 ( C , D ), acute nicotine challenge caused a significant left shift of glutamatergic mEPSCs in control cells ( p = 0.004; C ), but there was no change in the distribution of IEIs in DNE cells ( p = 0.066; D ). Arrows indicate the direction of the shift with acute nicotine challenge and indicates significant differences with K–S test (see Materials and Methods). Dotted gray lines indicate the 95% confidence intervals of each curve.

Journal: eNeuro

Article Title: Developmental Nicotine Exposure Alters Synaptic Input to Hypoglossal Motoneurons and Is Associated with Altered Function of Upper Airway Muscles

doi: 10.1523/ENEURO.0299-19.2019

Figure Lengend Snippet: Cumulative probability distributions of glutamatergic mEPSC IEIs in control and DNE cells, at baseline and during acute nicotine challenge. In cells from animals aged P1–P2 ( A , B ), acute nicotine challenge with 0.5 μM nicotine (black dashed lines) caused a left shift, toward shorter IEIs, of glutamatergic mEPSCs in both control ( p < 0.0001; A ) and DNE cells ( p < 0.0001; B ). In cells from animals aged P3–P5 ( C , D ), acute nicotine challenge caused a significant left shift of glutamatergic mEPSCs in control cells ( p = 0.004; C ), but there was no change in the distribution of IEIs in DNE cells ( p = 0.066; D ). Arrows indicate the direction of the shift with acute nicotine challenge and indicates significant differences with K–S test (see Materials and Methods). Dotted gray lines indicate the 95% confidence intervals of each curve.

Article Snippet: First, the IEI and amplitude of all sEPSCs/mEPSCs from all cells within an age or treatment group were used to construct a cumulative probability distribution using Prism (GraphPad Software, Inc.; For example, see , ).

Techniques: Control