714 research outputs found
Information Processing in the Visual System: David H. Hubel, Nobel Laureate Physiology or Medicine 1981
No full textDavid H. Hubel is the John Enders University Professor of Neurobiology at Harvard Medical School. Born in Canada of American parents, he grew up in Montreal, graduated from McGill Medical School, and received training in neurology at the Montreal Neurological Institute and Johns Hopkins Hospital. He began research in vision at the Walter Reed Army Institute of Research, and then returned to Johns Hopkins in the laboratory of Stephen Kuffler, where he began a collaboration with Torsten Wiesel that was to last over twenty years and which led, in 1981, to their receiving the Nobel Prize in Medicine or Physiology. I invited Dr. Hubel to the Unit for Neurovisual Disorders, Department of Neurology at the Massachusetts General Hospital to record an audio clip superimposed on a video tape recorded by Hubel in his laboratory during an experiment on a cat. The video shows a sequence of examples of the intracellular recordings going from one cell type to another in the lateral genicular body of the cat and then in various types of neurons in the primary visual cortex.EYE, BRAIN AND VISION David H. Hubel When we look out at the world, more than 100 million receptors in the retina are bombarded by photons of light. These receptors - rods and cones - translate light energy into electrical signals that are carried back through the retina to the brain. How does the brain make sense of these signals? How do we process this staggering influx of information into a coherent image rich in form, color, depth and movement? For thirty years, David H. Hubel has been close to the center of research into these questions. By intricate study of the physiology of the brain down to the level of single cells, he and his colleagues have learned how visual information is reorganized and analyzed, in stage after stage of increasing complexity. In this book we learn how scientists are constructing a wiring diagram of the visual path; we discover what is known about the structure and function of each stage in the pathway, from the light receptors in the retina, through the peanut-size clusters of cells known as the lateral geniculate bodies, to the striate cortex - the first of many higher areas devoted to vision and the part of the brain that is now best understood. We are also introduced to the remarkable geometric patterns that result from the surprising tendency of cells with related functions to be organized in sheets, columns, blobs, and stripes. Dr. Hubel examines the mechanisms by which we perceive color, depth, and movement, and the function of the fibers connecting the two halves of the brain. He describes how the visual circuits develop before birth, and discusses the unexpected consequences of visual deprivation early in life. He brings us to the edge of current knowledge with glimpses of higher visual areas known as areas 18, V4, and MT. And he explores the tasks scientists face in deciphering the many remaining mysteries of vision and of the workings of the human brain. From the back flap of the dust jacket published in 1988 Scientific American Library, a division of HPHLP, New Yorkcurriculum_fellow; IC-A4g-visual-association-area
The Prize: An Interview with David H. Hubel Nobel Laureate Physiology or Medicine 1981
No full textNormalScintillating scotomaDavid H. Hubel is the John Enders University Professor of Neurobiology at Harvard Medical School. Born in Canada of American parents, he grew up in Montreal, graduated from McGill Medical School, and received training in neurology at the Montreal Neurological Institute and Johns Hopkins Hospital. He began research in vision at the Walter Reed Army Institute of Research, and then returned to Johns Hopkins in the laboratory of Stephen Kuffler, where he began a collaboration with Torsten Wiesel that was to last over twenty years and which led, in 1981, to their receiving the Nobel Prize in Medicine or Physiology. I invited Dr. Hubel to the Unit for Neurovisual Disorders, Department of Neurology at the Massachusetts General Hospital to record an audio clip superimposed on a video tape recorded by Hubel in his laboratory during an experiment on a cat. The video shows a sequence of examples of the intracellular recordings going from one cell type to another in the lateral genicular body of the cat and then in various types of neurons in the primary visual cortex.EYE, BRAIN AND VISION David H. Hubel When we look out at the world, more than 100 million receptors in the retina are bombarded by photons of light. These receptors - rods and cones - translate light energy into electrical signals that are carried back through the retina to the brain. How does the brain make sense of these signals? How do we process this staggering influx of information into a coherent image rich in form, color, depth and movement? For thirty years, David H. Hubel has been close to the center of research into these questions. By intricate study of the physiology of the brain down to the level of single cells, he and his colleagues have learned how visual information is reorganized and analyzed, in stage after stage of increasing complexity. In this book we learn how scientists are constructing a wiring diagram of the visual path; we discover what is known about the structure and function of each stage in the pathway, from the light receptors in the retina, through the peanut-size clusters of cells known as the lateral geniculate bodies, to the striate cortex - the first of many higher areas devoted to vision and the part of the brain that is now best understood. We are also introduced to the remarkable geometric patterns that result from the surprising tendency of cells with related functions to be organized in sheets, columns, blobs, and stripes. Dr. Hubel examines the mechanisms by which we perceive color, depth, and movement, and the function of the fibers connecting the two halves of the brain. He describes how the visual circuits develop before birth, and discusses the unexpected consequences of visual deprivation early in life. He brings us to the edge of current knowledge with glimpses of higher visual areas known as areas 18, V4, and MT. And he explores the tasks scientists face in deciphering the many remaining mysteries of vision and of the workings of the human brain. From the back flap of the dust jacket published in 1988 Scientific American Library, a division of HPHLP, New Yorkcurriculum_fello
W. Maxwell Cowan to David H. Hubel, February 25, 1972
No full textAttached is a list of people to whom the letter was sentAbout creating a cumulative index for the Journal of Comparative NeurologyCorrespondenc
Migraine Visual Aura: A Discussion with Nobel Laureate David H. Hubel
No full textNormalMigraine/PET Study: https://collections.lib.utah.edu/details?id=188606Scintillating scotomaI am greatly indebted to the Nobel Laureate, David Hubel for his permission to publish his description of his migraine aura. The recording was made fortuitously at the time that I invited David to the Unit for Neuro-Visual Disorders to record an audio clip describing the experiments in the cat that led him and Torsten Wiesel to win the 1981 Nobel Prize in Medicine or Physiology. Hubel and Wiesel used microelectrodes and modern electronics to detect the activity of individual visual neurons, using cats as their subjects. (The cats were not harmed by these experiments; indeed, their purring created vibration problems.) Thanks to the work of Hubel and Wiesel, the visual cortex has become the best known part of the brain. Review ID 947-3 The Prize, David Hubel, Nobel Laureate Physiology or Medicine 1981.In this recording, you will hear David Hubel describing his migraine visual aura. He had no history of migraine headache. All the episodes of visual aura were headache free The interview is unique and remarkable because the world\u27s most expert visual physiologist and Nobel Laureate found it difficult to describe what he sees during an aura. Hubel speculates on what may be happening in the visual cortex to generate the characteristic spread of the arc of a scintillating scotoma. We also briefly discussed an observation by Woods et al who described a patient who, during positron emission tomography (PET), fortuitously had an attack of migraine. The PET study showed a reduction in blood flow that started in the occipital cortex and spread slowly forward to the temporal and parietal lobes bilaterally. The observed pattern of "spreading oligemia", is illustrated on video tape courtesy of J.C. Mazziotto, M.D., Ph.D. et al (ID41-1).Functional MRI (fMRI) performed during spontaneous visual aura in migraineurs has shown moderate focal reductions in cerebral blood flow and volume in the occipital lobe during the aura. The occipital lobe perfusion deficit corresponded anatomically with the reported visual field disturbance and with the side of the subsequent headache.Review ID 41-1Cortical spreading depression (CSD) has been suggested to underlie migraine visual aura. However, it has been challenging to test this hypothesis in human cerebral cortex. Data from functional MRI studies in the visual cortex strongly suggest that an electrophysiological event such as CSD does in fact generate visual aura in migraine. Visual aura are characterized by a wave of cerebral hypoperfusion-oligemia that passes across the cortex at the characteristically slow rate of 2 to 6 mm per minute. Richards suggested that in migraineurs the cortical neurons activated by the leading edge of CSD are sensitive ‘line detectors\u27. His reasoning was based on Hubel and Wiesel\u27s concept of neurons as ‘feature detectors\u27, which in turn was suggested by the results of recording the intracellular activity of single neurons in the primary visual cortex of the cat and monkey brain in response to specific visual stimuli. Richards calculated that the cortical distance for each teichoptic line was 1.2 mm, five times larger than the known diameter of individual orientation columns in the monkey and so he argued that the scale discrepancy suggested that the orientation columns alone were not responsible for the phenomena. Increased activity within lattice-like, long range excitatory connections in different layers of V1, V2 and V4 are considered better anatomical candidates for the generation of visual aura. The trigger to provoke visual aura is unknown. In a study of visual processing in migraine subjects with aura, Wray et al found that the migraineurs response time in the low-level tasks was better than normal controls. The data suggests that migraineurs process visual signals to the primary visual cortex [Area V1] more rapidly than non-migraineurs and that Area V1, between attacks of visual aura, may be hypersensitive to visual stimuli.In a related disorder, known as hemiplegic migraine, linkage analysis studies have localized the responsible gene to chromosome 19 in one third of families; in other families the gene has localized to chromosome 1; and yet in other families no linkage has been found. The gene on chromosome 19 codes for a voltage-gated calcium channel protein, which raises the provocative possibility that other forms of migraine are also due to an ion channel disorder. In migraine with and without aura, an underlying genetic factor is implicated, although it is expressed in a recognizable mendelian pattern (autosomal dominant) in a relatively small number of families. The puzzle is how this genetic fault is translated periodically into a regional neurologic deficit, unilateral headache or both.Patients with episodic migraine visual aura without headache do not require treatment.1. Afridi SK, Giffin NJ, Kaube H, Friston KJ, Ward NS, Frackowiak RSJ, Goadsby PJ. A Positron Emission Tomographic Study in Spontaneous Migraine. Arch Neurol 2005;62:1270-1275. http://www.ncbi.nlm.nih.gov/pubmed/16087768 2. Afridi SK, Matharu MS, Lee L, Kaube H, Friston KJ, Frackowiak RSJ, Goadsby PJ. A PET study exploring the laterality of brainstem activation in migraine using glyceryl trinitrate. Brain 2005;128:932-939. http://www.ncbi.nlm.nih.gov/pubmed/15705611 3. Afridi SK, Goadsby PJ. Neuroimaging of migraine. Curr Pain Headache Rep 2006;10:221-224. Review. http://www.ncbi.nlm.nih.gov/pubmed/18778577 4. Cutrer FM, Sorensen AG, Weisskoff RM, Ostergaard L, Sanchez del Rio M, Lee EJ, Rosen BR, Moskowitz MA.. Perfusion-weighted imaging defects during spontaneous migraine aura. Ann Neurol 1998, 43:25-31. http://www.ncbi.nlm.nih.gov/pubmed/9450765 5. Goadsby PJ, Hargreaves R. Refractory migraine and chronic migraine: pathophysiological mechanisms. Headache 2008;48:1399-1405. http://www.ncbi.nlm.nih.gov/pubmed/19006557 6. Goadsby PJ. Calcitonin gene-related peptide (CGRP) antagonists and migraine: is this a new era? Neurology 2008;70:1300-1301. http://www.ncbi.nlm.nih.gov/pubmed/18413584 7. Hadjikhani N, Sanchez del Rio M, Wu O, Schwartz D, Bakker D, Fischl B, Kwong KK, Cutrer FM, Rosen BR, Tootell RBH, Sorensen AG, Moskowitz MA. Mechanisms of migraine aura revealed by functional MRI in human visual cortex. Proc Natl Acad Sci USA 2001;98:4687-4692. http://www.ncbi.nlm.nih.gov/pubmed/11287655 8. Hubel DH, Wiesel TN. Receptive fields and functional architecture of monkey striate cortex. J Physiol (Lond) 1968; 195:215-243. http://www.ncbi.nlm.nih.gov/pubmed/4966457 9. Hubel DH, Wiesel TN. Sequence regularity and geometry of orientation columns in the monkey striate cortex. J Comp Neurol 1974a; 158:267-293. http://www.ncbi.nlm.nih.gov/pubmed/4436456 10. Hubel DH, Wiesel TN. Uniformity of monkey striate cortex: a parallel relationship between field size, scatter and magnification factor. J Comp Neurol 1974b; 158:295-305. http://www.ncbi.nlm.nih.gov/pubmed/4436457 11. Lashley KS. Patterns of cerebral integration indicated by the scotomas of migraine. Arch Neurol Psychiatry 1941; 46:331-339. 12. Lauritzen M. Pathophysiology of the migraine aura: the spreading depression theory. Brain 1994;117:199-210. http://www.ncbi.nlm.nih.gov/pubmed/7908596 13. Leao AAP. Spreading depression of activity in cerebral cortex. J Neurophysiol 1944, 7:379-390. http://www.ncbi.nlm.nih.gov/pubmed/20268874 14. Olesen J, Larsen B, Lauritzen M. Focal hyperemia followed by spreading oligemia and impaired activation of rCBF in classic migraine. Ann Neurol 1981;9:344-352. http://www.ncbi.nlm.nih.gov/pubmed/6784664 15. Richards W. The fortification illusions of migraines. Sci Am 1971; 224(5): 88-96. http://www.ncbi.nlm.nih.gov/pubmed/5552581 16. Woods RP, Jacoboni M and Mazziotta JC. Bilateral spreading cerebral hypoperfusion during spontaneous migraine headache. New Eng J Med 1994; 331:1689-1692. http://www.ncbi.nlm.nih.gov/pubmed/7969360 17. Wray SH, Mijovic-Prelec D, Kosslyn SM. Visual processing in migraineurs. Brain. 1995 Feb;118 ( Pt 1):25-35. http://www.ncbi.nlm.nih.gov/pubmed/7895008IC-E10fii4-aura-without-headach
David H. Hubel to Viktor Hamburger, March 7, 1982
No full textHandwritten letter, 1 pageThank you note for letterCorrespondenc
Supplementary material from David Hunter Hubel. 27 February 1926 - 22 September 2013
No full textDavid Hunter Hubel - curriculum vita
Supplementary material from David Hunter Hubel. 27 February 1926 - 22 September 2013
No full textDavid Hunter Hubel - Bibliograph
Early onset preeclampsia is characterized by altered placental lipid metabolism and a premature increase in circulating FABP4
No full textPreeclampsia is a pregnancy-associated disorder that manifests as a sudden increase in maternal blood pressure accompanied by proteinuria. Because the placenta is a key organ in preeclampsia, we used proteomic and lipidomic analyses to compare placentae from preeclamptic and gestational age matched control pregnancies. Fatty acid binding protein 4 (FABP4), enoyl-CoA dehydrogenase and delta-3,5-delta-2,4-dienoyl-CoA isomerase had altered abundance in preeclamptic placentae compared to controls. FABP4 placental protein and RNA and plasma levels were all increased in early-onset preeclampsia (prior to 28 weeks gestation) compared to controls (6-fold, 3.3-fold and 3.5-fold respectively). After 28 weeks, FABP4 protein in control placenta and plasma increased to the same concentrations as in preeclampsia. Total tetracosapentaenoic acid in preeclamptic placentae was decreased to 0.6 of control levels before 28 weeks. The data indicate a disruption of fatty acid transport and metabolism in the placenta in early onset preeclampsia that is reflected in the maternal plasma
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