1 |
Large vocabulary recognition of on-line handwritten cursive wordsSeni, Giovanni. January 1995 (has links)
Thesis (Ph. D.)--State University of New York at Buffalo, 1995. / "August, 1995." Includes bibliographical references (p. 123-136). Also available in print.
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Intelligent lexical access based on Chinese/English text queriesLam, Yat-kin., 林日堅. January 2005 (has links)
published_or_final_version / abstract / toc / Computer Science / Master / Master of Philosophy
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AUTOMATIC RECOGNITION OF PICTORIAL-PATTERNS BY DESCRIPTIVE ANALYSIS AND CLASSIFICATIONTodd, Henry Swan, 1933- January 1973 (has links)
No description available.
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4 |
Feature extraction and evaluation for cervical cell recognitionCahn, Robert L. January 1977 (has links)
No description available.
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A reexamination of the role of the hippocampus in object-recognition memory using neurotoxic lesions and ischemia in ratsDuva, Christopher Adam 11 1900 (has links)
Paradoxical results on object-recognition delayed nonmatching-to-sample (DNMS)
tasks have been found in monkeys and rats that receive either partial, ischemia-induced
hippocampal lesions or complete hippocampal ablation. Ischemia results in severe DNMS
impairments, which have been attributed to circumscribed CA1 cell loss. However,
ablation studies indicate that the hippocampus plays only a minimal role in the performance
of the DNMS task. Two hypotheses have been proposed to account for these discrepant
findings (Bachevalier & Mishkin, 1989). First, the "hippocampal interference" hypothesis
posits that following ischemia, the partially damaged hippocampus may disrupt activity in
extrahippocampal structures that are important for object-recognition memory. Second,
previously undetected ischemia-induced extrahippocampal damage may be responsible for
the DNMS impairments attributed to CA1 cell loss.
To test the "hippocampal interference" hypothesis, the effect of partial NMDAinduced
lesions of the dorsal hippocampus were investigated on DNMS performance in
rats. These lesions damaged much of the same area, the CA1, as did ischemia; but did so
without depriving the entire forebrain of oxygen, thereby reducing the possibility of
extrahippocampal damage. In Experiment 1, rats were trained on the DNMS task prior to
receiving an NMDA-lesion. Postoperatively, these rats reacquired the nonmatching rule at
a rate equivalent to controls and were unimpaired in performance at delays up to 300 s. In
Experiment 2, naive rats were given NMDA-lesions and then trained on DNMS. These
rats acquired the DNMS rule at a rate equivalent to controls and performed normally at
delays up to 300 s. These findings suggest that interference from a partially damaged
hippocampus cannot account for the ischemia-induced DNMS impairments and that they
are more likely produced by extrahippocampal neuropathology. In Experiment 3, rats from
the previous study were tested on the Morris water-maze. Compared to sham-lesioned
animals, rats with partial lesions of the dorsal hippocampus were impaired in the
acquisition of the water-maze task. Thus, subtotal NMDA-lesions of the hippocampus
impaired spatial memory while leaving nonspatial memory intact.
Mumby et al. (1992b) suggested that the ischemia-induced extrahippocampal
damage underlying the DNMS deficits is mediated or produced by the postischemic
hippocampus. To test this idea, preoperatively trained rats in Experiment 4 were subject to
cerebral ischemia followed within 1hr by hippocampal aspiration lesions. It was
hypothesized that ablation soon after ischemia would block the damage putatively produced
by the postischemic hippocampus and thereby prevent the development of postoperative
DNMS deficits. Unlike "ischemia-only" rats, the rats with the combined lesion were able to
reacquire the nonmatching rule at a normal rate and performed normally at delays up to 300
s. Thus, hippocampectomy soon after ischemia eliminated the pathogenic process that lead
to ischemia-induced DNMS deficits. Experiment 5 investigated the role of ischemiainduced
CA1 cell death as a factor in the production of extrahippocampal neuropathology.
Naive rats were given NMDA-lesions of the dorsal hippocampus followed 3 weeks later by
cerebral ischemia. If the ischemia-induced CA1 neurotoxicity is responsible for producing
extrahippocampal damage then preischemic ablation should attenuate this process and
prevent the development of DNMS impairments. This did not occur: Rats with the
combined lesion were as impaired as the "ischemia-only" rats in the acquisition of the
DNMS task. This suggests that the ischemia-induced pathogenic processes that result in
extrahippocampal neuropathology comprise more than CA1 neurotoxicity.
The findings presented in this thesis are consistent with the idea that ischemiainduced
DNMS deficits in rats are the result of extrahippocampal damage mediated or
produced by the postischemic hippocampus. The discussion focuses on three main points:
1) How might the post-ischemic hippocampus be involved in the production of
extrahippocampal neuropathology? 2) In what brain region(s) might this damage be
occurring? 3) What anatomical, molecular, or functional neuropathology might ischemia
produce in extrahippocampal brain regions? The results are also discussed in terms of a
specialized role for the hippocampus in mnemonic functions and the recently emphasized
importance of the rhinal cortex in object-recognition memory.
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6 |
A reexamination of the role of the hippocampus in object-recognition memory using neurotoxic lesions and ischemia in ratsDuva, Christopher Adam 11 1900 (has links)
Paradoxical results on object-recognition delayed nonmatching-to-sample (DNMS)
tasks have been found in monkeys and rats that receive either partial, ischemia-induced
hippocampal lesions or complete hippocampal ablation. Ischemia results in severe DNMS
impairments, which have been attributed to circumscribed CA1 cell loss. However,
ablation studies indicate that the hippocampus plays only a minimal role in the performance
of the DNMS task. Two hypotheses have been proposed to account for these discrepant
findings (Bachevalier & Mishkin, 1989). First, the "hippocampal interference" hypothesis
posits that following ischemia, the partially damaged hippocampus may disrupt activity in
extrahippocampal structures that are important for object-recognition memory. Second,
previously undetected ischemia-induced extrahippocampal damage may be responsible for
the DNMS impairments attributed to CA1 cell loss.
To test the "hippocampal interference" hypothesis, the effect of partial NMDAinduced
lesions of the dorsal hippocampus were investigated on DNMS performance in
rats. These lesions damaged much of the same area, the CA1, as did ischemia; but did so
without depriving the entire forebrain of oxygen, thereby reducing the possibility of
extrahippocampal damage. In Experiment 1, rats were trained on the DNMS task prior to
receiving an NMDA-lesion. Postoperatively, these rats reacquired the nonmatching rule at
a rate equivalent to controls and were unimpaired in performance at delays up to 300 s. In
Experiment 2, naive rats were given NMDA-lesions and then trained on DNMS. These
rats acquired the DNMS rule at a rate equivalent to controls and performed normally at
delays up to 300 s. These findings suggest that interference from a partially damaged
hippocampus cannot account for the ischemia-induced DNMS impairments and that they
are more likely produced by extrahippocampal neuropathology. In Experiment 3, rats from
the previous study were tested on the Morris water-maze. Compared to sham-lesioned
animals, rats with partial lesions of the dorsal hippocampus were impaired in the
acquisition of the water-maze task. Thus, subtotal NMDA-lesions of the hippocampus
impaired spatial memory while leaving nonspatial memory intact.
Mumby et al. (1992b) suggested that the ischemia-induced extrahippocampal
damage underlying the DNMS deficits is mediated or produced by the postischemic
hippocampus. To test this idea, preoperatively trained rats in Experiment 4 were subject to
cerebral ischemia followed within 1hr by hippocampal aspiration lesions. It was
hypothesized that ablation soon after ischemia would block the damage putatively produced
by the postischemic hippocampus and thereby prevent the development of postoperative
DNMS deficits. Unlike "ischemia-only" rats, the rats with the combined lesion were able to
reacquire the nonmatching rule at a normal rate and performed normally at delays up to 300
s. Thus, hippocampectomy soon after ischemia eliminated the pathogenic process that lead
to ischemia-induced DNMS deficits. Experiment 5 investigated the role of ischemiainduced
CA1 cell death as a factor in the production of extrahippocampal neuropathology.
Naive rats were given NMDA-lesions of the dorsal hippocampus followed 3 weeks later by
cerebral ischemia. If the ischemia-induced CA1 neurotoxicity is responsible for producing
extrahippocampal damage then preischemic ablation should attenuate this process and
prevent the development of DNMS impairments. This did not occur: Rats with the
combined lesion were as impaired as the "ischemia-only" rats in the acquisition of the
DNMS task. This suggests that the ischemia-induced pathogenic processes that result in
extrahippocampal neuropathology comprise more than CA1 neurotoxicity.
The findings presented in this thesis are consistent with the idea that ischemiainduced
DNMS deficits in rats are the result of extrahippocampal damage mediated or
produced by the postischemic hippocampus. The discussion focuses on three main points:
1) How might the post-ischemic hippocampus be involved in the production of
extrahippocampal neuropathology? 2) In what brain region(s) might this damage be
occurring? 3) What anatomical, molecular, or functional neuropathology might ischemia
produce in extrahippocampal brain regions? The results are also discussed in terms of a
specialized role for the hippocampus in mnemonic functions and the recently emphasized
importance of the rhinal cortex in object-recognition memory. / Arts, Faculty of / Psychology, Department of / Graduate
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Feature extraction and evaluation for cervical cell recognitionCahn, Robert L. January 1977 (has links)
No description available.
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Computer recognition of three-dimensional objects from optical images /Advani, Jeram Godhumal January 1971 (has links)
No description available.
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The automatic acquisition of interesting objects in a cluttered image environment /Shieh, Shang-Tsong January 1974 (has links)
No description available.
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10 |
Three-dimensional interpretation of an imperfect line drawing.January 1996 (has links)
by Leung Kin Lap. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1996. / Includes bibliographical references (leaves 70-72). / ACKNOWLEDGEMENTS --- p.I / ABSTRACT --- p.II / TABLE OF CONTENTS --- p.III / TABLE OF FIGURES --- p.IV / Chapter Chapter 1 --- Introduction --- p.1 / Chapter 1.1 --- Contributions of the thesis --- p.2 / Chapter 1.2 --- Organization of the thesis --- p.4 / Chapter Chapter 2 --- Previous Work --- p.5 / Chapter 2.1 --- An overview of 3-D interpretation --- p.5 / Chapter 2.1.1 --- Multiple-View Clues --- p.5 / Chapter 2.1.2 --- Single-View Clues --- p.6 / Chapter 2.2 --- Line Drawing Interpretation --- p.7 / Chapter 2.2.1 --- Qualitative Interpretation --- p.7 / Chapter 2.2.2 --- Quantitative Interpretation --- p.10 / Chapter 2.3 --- Previous Methods of Quantitative Interpretation by Optimization --- p.12 / Chapter 2.3.1 --- Extremum Principle for Shape from Contour --- p.12 / Chapter 2.3.2 --- MSDA Algorithm --- p.14 / Chapter 2.4 --- Comments on Previous Work on Line Drawing Interpretation --- p.17 / Chapter Chapter 3 --- An Iterative Clustering Procedure for Imperfect Line Drawings --- p.18 / Chapter 3.1 --- Shape Constraints --- p.19 / Chapter 3.2 --- Problem Formulation --- p.20 / Chapter 3.3 --- Solution Steps --- p.25 / Chapter 3.4 --- Nearest-Neighbor Clustering Algorithm --- p.37 / Chapter 3.5 --- Discussion --- p.38 / Chapter Chapter 4 --- Experimental Results --- p.40 / Chapter 4.1 --- Synthetic Line Drawings --- p.40 / Chapter 4.2 --- Real Line Drawing --- p.42 / Chapter 4.2.1 --- Recovery of real images --- p.42 / Chapter Chapter 5 --- Conclusion and Future Work --- p.65 / Appendix A --- p.67 / Chapter A. 1 --- Gradient Space Concept --- p.67 / Chapter A. 2 --- Shading of images --- p.69 / Appendix B --- p.70
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