ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • Rats  (4)
  • Biological Clocks/genetics/*physiology  (2)
  • American Association for the Advancement of Science (AAAS)  (6)
Collection
Publisher
  • American Association for the Advancement of Science (AAAS)  (6)
  • 1
    Publication Date: 1999-06-26
    Description: Regulation of circadian period in humans was thought to differ from that of other species, with the period of the activity rhythm reported to range from 13 to 65 hours (median 25.2 hours) and the period of the body temperature rhythm reported to average 25 hours in adulthood, and to shorten with age. However, those observations were based on studies of humans exposed to light levels sufficient to confound circadian period estimation. Precise estimation of the periods of the endogenous circadian rhythms of melatonin, core body temperature, and cortisol in healthy young and older individuals living in carefully controlled lighting conditions has now revealed that the intrinsic period of the human circadian pacemaker averages 24.18 hours in both age groups, with a tight distribution consistent with other species. These findings have important implications for understanding the pathophysiology of disrupted sleep in older people.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Czeisler, C A -- Duffy, J F -- Shanahan, T L -- Brown, E N -- Mitchell, J F -- Rimmer, D W -- Ronda, J M -- Silva, E J -- Allan, J S -- Emens, J S -- Dijk, D J -- Kronauer, R E -- MO1-RR02635/RR/NCRR NIH HHS/ -- P01-AG09975/AG/NIA NIH HHS/ -- R01-GM53559/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Jun 25;284(5423):2177-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Circadian, Neuroendocrine, and Sleep Disorders Section, Division of Endocrinology, Department of Medicine, Harvard Medical School, Brigham and Women's Hospital, 221 Longwood Avenue, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10381883" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Aging/*physiology ; Biological Clocks/genetics/*physiology ; Body Temperature ; Circadian Rhythm/genetics/*physiology ; Darkness ; Female ; Humans ; Hydrocortisone/blood ; Light ; Male ; Melatonin/blood ; Middle Aged ; Sleep
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 2
    Publication Date: 2001-09-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Czeisler, C A -- Dijk, D J -- Kronauer, R E -- Brown, E N -- Duffy, J F -- Allan, J S -- Shanahan, T L -- Rimmer, D W -- Ronda, J M -- Mitchell, J F -- Silva, E J -- Emens, J S -- New York, N.Y. -- Science. 2000 May 19;288(5469):1174-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Circadian, Neuroendocrine, and Sleep Disorders Section, Division of Endocrinology, Department of Medicine, Harvard Medical School, Brigham and Women's Hospital, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11536927" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Clocks/genetics/*physiology ; Chronobiology Phenomena ; Circadian Rhythm/genetics/*physiology ; Darkness ; Humans ; Sleep
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 3
    Publication Date: 1990-10-12
    Description: The amyloid beta protein is deposited in the brains of patients with Alzheimer's disease but its pathogenic role is unknown. In culture, the amyloid beta protein was neurotrophic to undifferentiated hippocampal neurons at low concentrations and neurotoxic to mature neurons at higher concentrations. In differentiated neurons, amyloid beta protein caused dendritic and axonal retraction followed by neuronal death. A portion of the amyloid beta protein (amino acids 25 to 35) mediated both the trophic and toxic effects and was homologous to the tachykinin neuropeptide family. The effects of the amyloid beta protein were mimicked by tachykinin antagonists and completely reversed by specific tachykinin agonists. Thus, the amyloid beta protein could function as a neurotrophic factor for differentiating neurons, but at high concentrations in mature neurons, as in Alzheimer's disease, could cause neuronal degeneration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yankner, B A -- Duffy, L K -- Kirschner, D A -- AG08572/AG/NIA NIH HHS/ -- NS01240/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1990 Oct 12;250(4978):279-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2218531" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amyloid beta-Peptides/antagonists & inhibitors/*pharmacology ; Animals ; Cells, Cultured ; Embryo, Mammalian ; Hippocampus/cytology ; Molecular Sequence Data ; Neurons/*cytology/drug effects ; *Neurotoxins ; Peptide Fragments/pharmacology ; Rats ; Tachykinins/*pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 4
    Publication Date: 1981-06-05
    Description: Long-term potentiation of the hippocampal slice preparation results in an increase in the incorporation of labeled valine into the proteins destined for secretion into the extracellular medium. Double-labeling methods established that the increased secretion of the labeled proteins was limited to the potentiated region of a slice; incorporation of labeled valine was increased in the hippocampus if potentiation was through the Schaffer collaterals and in the dentate if potentiation was through the perforant path. Controls for nonspecific stimulation showed no changes. There appears to be a link between long-term potentiation and the metabolic processes that lead to protein synthesis in the hippocampal slice system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duffy, C -- Teyler, T J -- Shashoua, V E -- New York, N.Y. -- Science. 1981 Jun 5;212(4499):1148-51.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7233208" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carbon Radioisotopes ; Electric Stimulation ; Hippocampus/*metabolism/physiology ; In Vitro Techniques ; Kinetics ; Nerve Tissue Proteins/*biosynthesis/secretion ; Rats ; Tritium ; Valine
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 5
    facet.materialart.
    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1979-05-11
    Description: 2-Deoxy-[14C]glucose metabolism was examined in brains of hypoxic, normotensive rats by autoradiography, which revealed alternating cortical columns of high and low metabolism. Activity in white matter was increased severalfold over that in adjacent gray matter. The columns were anatomically related to penetrating cortical arteries with areas between arteries demonstrating higher rates of metabolism. The results suggest the presence of interarterial tissue oxygen gradients that influence regional glucose metabolism. The relatively greater sensitivity of white matter metabolism to hypoxia may lead to an understanding of white matter damage in postanoxic leukoencephalopathy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pulsinelli, W A -- Duffy, T E -- New York, N.Y. -- Science. 1979 May 11;204(4393):626-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/432667" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anoxia/*metabolism/physiopathology ; Brain/*metabolism ; Cerebral Cortex/metabolism ; Cerebrovascular Circulation ; Deoxyglucose/metabolism ; Glucose/*metabolism ; Male ; Phosphorylation ; Rats
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 6
    Publication Date: 1979-06-08
    Description: Kindling is an experimental model of epilepsy in which periodic brain stimulation induces the progressive development of electrical and behavioral seizures. A kindling-induced electrical seizure (afterdischarge) in the rat hippocampus produces prolonged neuronal supersensitivity to microiontophoretically applied acetylcholine after a latency of 40 to 60 minutes. Neuronal acetylcholine supersensitivity is correlated with the further progression of kindling. A larger hippocampal after-discharge is elicited by a subsequent kindling stimulus delivered in the presence of acetylcholine supersensitivity, but not by one delivered before the onset of the supersensitivity. The results suggest that alteration of synaptic sensitivity to acetylcholine may contribute to kindling and epileptogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burchfiel, J L -- Duchowny, M S -- Duffy, F H -- New York, N.Y. -- Science. 1979 Jun 8;204(4397):1096-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/36660" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/*pharmacology ; Animals ; Electric Stimulation ; Epilepsy/physiopathology ; Glutamates/pharmacology ; Hippocampus/drug effects/*physiology ; Neurotransmitter Agents/pharmacology ; Rats ; Synaptic Transmission ; Time Factors ; gamma-Aminobutyric Acid/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...