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91.
Global ischemia caused by heart attack, pulmonary failure, near-drowning or traumatic brain injury often damages the higher brain but not the brainstem, leading to a ‘persistent vegetative state’ where the patient is awake but not aware. Approximately 30,000 U.S. patients are held captive in this condition but not a single research study has addressed how the lower brain is preferentially protected in these people. In the higher brain, ischemia elicits a profound anoxic depolarization (AD) causing neuronal dysfunction and vasoconstriction within minutes. Might brainstem nuclei generate less damaging AD and so be more resilient? Here we compared resistance to acute injury induced from simulated ischemia by ‘higher’ hippocampal and striatal neurons versus brainstem neurons in live slices from rat and mouse. Light transmittance (LT) imaging in response to 10 minutes of oxygen/glucose deprivation (OGD) revealed immediate and acutely damaging AD propagating through gray matter of neocortex, hippocampus, striatum, thalamus and cerebellar cortex. In adjacent brainstem nuclei, OGD-evoked AD caused little tissue injury. Whole-cell patch recordings from hippocampal and striatal neurons under OGD revealed sudden membrane potential loss that did not recover. In contrast brainstem neurons from locus ceruleus and mesencephalic nucleus as well as from sensory and motor nuclei only slowly depolarized and then repolarized post-OGD. Two-photon microscopy confirmed non-recoverable swelling and dendritic beading of hippocampal neurons during OGD, while mesencephalic neurons in midbrain appeared uninjured. All of the above responses were mimicked by bath exposure to 100 µM ouabain which inhibits the Na+/K+ pump or to 1–10 nM palytoxin which converts the pump into an open cationic channel.Therefore during ischemia the Na+/K+ pump of higher neurons fails quickly and extensively compared to naturally resilient hypothalamic and brainstem neurons. The selective survival of lower brain regions that maintain vital functions will support the persistent vegetative state. 相似文献
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94.
Fragmented and scrambled mitochondrial ribosomal RNA coding regions among green algae: a model for their origin and evolution 总被引:4,自引:1,他引:3
Mitochondrial ribosomal RNA coding regions in the only three green algal
taxa investigated to date are fundamentally different in that they are
continuous in Prototheca wickerhamii, but highly fragmented and scrambled
in Chlamydomonas reinhardtii and Chlamydomonas eugametos. To gain more
insight into the mode of evolution of fragmented and scrambled
mitochondrial ribosomal RNA (rRNA) genes within the green algal group, this
work (1) provides additional information on fragmentation patterns of
mitochondrial small- and large-subunit (SSU and LSU) rRNAs that strongly
supports the concept of a gradual increase in the extent of discontinuity
of mitochondrial rRNAs among chlorophycean green algae and (2) reports the
first example of fragmented and scrambled mitochondrial LSU rRNA coding
regions in a green algal taxon outside the Chlamydomonas group. The present
study (1) suggests that the scrambling of the mitochondrial rRNA coding
regions may have occurred early in the evolution of fragmented and
scrambled mitochondrial rRNA genes within the chlorophycean green algal
group, most likely in parallel with the fragmentation events, (2) proposes
recombination as a possible mechanism involved in the evolution of these
mitochondrial rRNA genes, and (3) presents a hypothetical pathway for
converting continuous mitochondrial rRNA genes into the highly fragmented
and scrambled rRNA coding regions of Chlamydomonas through a series of
recombinatorial events between short repeated sequences.
相似文献
95.
C. Brisson D. O. Azorsa L. K. Jennings S. Moog J. P. Cazenave F. Lanza 《Journal of molecular histology》1997,29(2):153-165
Summary CD9 is a 24-kDa membrane glycoprotein expressed on the surface of human platelets and potentially involved in cellular activation
and adhesion functions. This protein belongs to a recently delineated family of cell-surface antigens that span the membrane
four times, called tetraspans, and found mainly in leucocytes and tumour cells. As a first approach to clarify the function
of CD9, we used immunoelectron microscopy to determine the localization of this antigen in human platelets, and compared its
distribution with that of the GPIIb-IIIa integrin, the platelet receptor for fibrinogen. Monoclonal antibodies against CD9
(MAb7) and GPIIb-IIIa (HP1-1D) coupled to colloidal gold of different sizes (5 and 15 nm) were incubated with intact platelets
in suspension or on ultrathin sections of platelets embedded in LR white. CD9 was found in association with GPIIb-IIIa on
the inner face of ·-granule membranes. These two antigens also co-localized on pseudopods of activated platelets and in contact
regions between adjacent platelets. CD63, another member of the tetraspan family, was absent from ·-granules but was associated
with lysosomal structures. Flow cytometric analysis of platelet CD9 with a series of monoclonal antibodies revealed an increased
expression upon thrombin stimulation, confirming the presence of an intracellular granular pool. The observation that CD9
and GPIIb-IIIa are stored in the same intracellular structures and migrate to the same activation zones after platelet stimulation
lends support to previous suggestions of a close association between CD9 and GPIIb-IIIa in human platelets and of a possible
involvement of CD9 in adhesive functions of platelets.
This revised version was published online in November 2006 with corrections to the Cover Date. 相似文献
96.
97.
A ouabain-insensitive Mg2+-ATPase present in a microsomal fraction prepared from the dog submandibular gland was studied. This Mg2+-ATPase was inhibited by increasing concentrations of NaCl, KCl, RbCl and CsCl. The addition of an osmotically equal amount of sucrose was without effect. This inhibition was obtained over a pH range of from 6.3 to 8.8. The Mg2+-ATPase present in microsomes treated with NaI showed a similar inhibition. These results indicate that it is advisable to keep the ionic strength constant in solutions used to obtain (Na++K+)-ATPase activities. 相似文献
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99.
Colloc'h N Sopkova-de Oliveira Santos J Retailleau P Vivarès D Bonneté F Langlois d'Estainto B Gallois B Brisson A Risso JJ Lemaire M Prangé T Abraini JH 《Biophysical journal》2007,92(1):217-224
In contrast with most inhalational anesthetics, the anesthetic gases xenon (Xe) and nitrous oxide (N(2)O) act by blocking the N-methyl-d-aspartate (NMDA) receptor. Using x-ray crystallography, we examined the binding characteristics of these two gases on two soluble proteins as structural models: urate oxidase, which is a prototype of a variety of intracellular globular proteins, and annexin V, which has structural and functional characteristics that allow it to be considered as a prototype for the NMDA receptor. The structure of these proteins complexed with Xe and N(2)O were determined. One N(2)O molecule or one Xe atom binds to the same main site in both proteins. A second subsite is observed for N(2)O in each case. The gas-binding sites are always hydrophobic flexible cavities buried within the monomer. Comparison of the effects of Xe and N(2)O on urate oxidase and annexin V reveals an interesting relationship with the in vivo pharmacological effects of these gases, the ratio of the gas-binding sites' volume expansion and the ratio of the narcotic potency being similar. Given these data, we propose that alterations of cytosolic globular protein functions by general anesthetics would be responsible for the early stages of anesthesia such as amnesia and hypnosis and that additional alterations of ion-channel membrane receptor functions are required for deeper effects that progress to "surgical" anesthesia. 相似文献
100.
Jifeng Tang Samantha J Baldwin Jeanne ME Jacobs C Gerard van der Linden Roeland E Voorrips Jack AM Leunissen Herman van Eck Ben Vosman 《BMC bioinformatics》2008,9(1):374