Class U5a or aplastic uterus with rudimentary (functional) cavity characterized by the presence of bi- or unilateral functional horn, Class U5b or aplastic uterus without rudimentary (functional) cavity characterized either by the presence of uterine remnants or by full uterine aplasia.
Two possible explanations of this complex uterine anomaly can be given: (i) Müllerian 'duplication' at the level of the uterine body responsible for the presence of the two functional rudimentary horns or (ii) aplasia of the mid part of the uterus combined with a fusion defect of the upper part.
We introduce compact model-based representations of q-Horn theories, analyze the structure of functional dependencies in q-Horn theories, and show that every minimal functional dependency in a q-Horn theory Σ can be expressed either by a single term or by a single clause.
Finally, even if spatial artifacts, registration inaccuracies, signal dropout, physiological noise, and partial volume averaging effects were minimized, it may be that functional connectivity between dorsal horns is more variable if the automated selection of gray matter sub-regions (step #14) isolate signals from different laminae within dorsal horns (Ruscheweyh and Sandkühler, 2002).
This paper studies functional dependencies in q-Horn theories, and discusses their use in knowledge condensation.
Importantly, the new sprouted terminals form functional connections with dorsal horn neurons, such that cells that normally only respond to inputs from the damaged nerves now respond to intact inputs from adjacent body areas.
The seed voxel is selected in the right ventral horn in C5, and exhibits functional connectivity with the contralateral ventral horn in the same slice as well as adjacent slices.
Other unfamiliar names can be found at Mondo Cane, which has devoted part of its stand to a dense display of small functional objects in brass, leather, horn and wood by the Austrian designers Carl Auböck (1900-57) and his son, Carl Jr. (1924-93).
Chemokines released from primary afferent central terminals could exert either direct activation of superficial dorsal horn neurons via functional chemokine receptor expression or indirect sensitization via activation of microglia and astrocytes that subsequently release nociceptive mediators.
The initial phase, neurogenic pain, is occurred by C-fiber activation produced by direct stimulation of nociceptive neurons; while the second phase, inflammatory pain, is caused by local tissue inflammation and also by functional changes in the dorsal horn of the spinal cord [ 22, 24].
Studies of inflammatory and neuropathic pain models in animals demonstrate extensive structural and functional alterations in the dorsal horn of the spinal cord that represent a relatively specific degeneration of the inhibitory interneurone system, leading to central sensitization and increases in pain-related behaviours (for review see [ 122]).
