Biología Celular y Membranas Plamáticas
Esta página contiene bibliografías específicas para los alumnos ingresantes de la Carrera de Medicina de la Universidad Nacional del Nordeste. Tema: Biología celular y membranas plasmáticas.
| Au: Quirke P; Mapstone N. ----- Ti: The new biology: histopathology. ----- So: Lancet. 354 Suppl 1:SI26-31, 1999 Jul. |
| Au: Lohse MJ. ----- Ti: New directions in pharmacology. ----- So: Lancet. 1999 Dec;354 Suppl:SIV52 |
| Au: Tournier-Lasserve E. ----- Ti: Gene therapy and beyond. ----- So: Lancet. 1999 Dec;354 Suppl:SIV22 |
| Au: Butler D. ----- Ti: All parties keen to press on with Europe-based science website. ----- So: Nature. 2000 Jan 27;403(6768):347-8 |
| Au: Reif W. ----- Ti: Linus Pauling: an inspirational and humane genius. ----- So: Lancet. 2000 Jan 29;355 (9201) :415-6 |
| Au: Dalton R. ----- Ti: DIY microarrayers promise DNA chips with everything. ----- So: Nature. 2000 Jan 20;403 (6767):234 |
| Au: Abbott A. ----- Ti: Merger of Glaxo Wellcome and SmithKline Beecham creates pharmaceutical giant. ----- So: Nature. 2000 Jan 20;403(6767):232 |
| Au: Butler D, et al. ----- Ti: Celera genome licensing terms spark concerns over 'monopoly'. ----- So: Nature. 2000 Jan 20;403(6767):231 |
| Ti: In praise of open software. ----- So: Nature. 2000 Jan 20;403(6767):229 |
| Au: Horton B. ----- Ti: From bench to bedside... research makes the translational transition. ----- So: Nature. 1999 Nov 11;402(6758):213-5 |
| Au: Butler D. ----- Ti: IBM promises scientists 500-fold leap in supercomputing power...and a chance to tackle protein structure. ----- So: Nature. 1999 Dec 16;402(6763):705-6 |
| Au: Bilder D, et al. ----- Ti: Localization of apical epithelial determinants by the basolateral PDZ protein Scribble. ----- So: Nature. 2000 Feb 10;403(6770):676-80. |
| Au: Rongo C, et al. ----- Ti: CaMKII regulates the density of central glutamatergic synapses in vivo. ----- So: Nature. 1999 Nov 11;402(6758):195-9. |
| Au: Hegde RS, et al. ----- Ti: Transmissible and genetic prion diseases share a common pathway of neurodegeneration. ----- So: Nature. 1999 Dec 16;402(6763):822-6. |
| Au: Hope J. ----- Ti: Spongiform encephalopathies. Breech-birth prions. ----- So: Nature. 1999 Dec 16;402 (6763):737, 739 |
| Au: Kell DB. ----- Ti: Revolutionary ideas come round again [letter; comment]. ----- Cm: Comment on:/Nature/1999 Jan 14;397(6715):168-71. ----- So: Nature. 397(6721):644, 1999 Feb 25. |
| Au: Dill KA. ----- Ti: Strengthening biomedicine's roots. ----- So: Nature. 400(6742):309-10, 1999 Jul 22. |
| Au: Helmer M. ----- Ti: Biophysics. Singular take on molecules [news]. ----- So: Nature. 401(6750):225-6, 1999 Sep 16. |
| Au: Santis G; Evans TW. ----- Ti: Molecular biology for the critical care physician. Part II: where are we now?. ----- So: Crit Care Med. 27(5):997-1003, 1999 May. ----- Ab: The extraordinary technical developments in molecular biology are having a profound impact in clinical medicine. The contribution of recombinant DNA technology in defining the molecular pathology of common disorders and of diagnostic molecular techniques for detection of infectious organisms are used as examples to demonstrate the clinical relevance of these developments. Finally, the potential use of DNA as a therapeutic drug (gene therapy) is addressed (Au). |
| Au: Ohkuma H; Parney I; Megyesi J; Ghahary A; Findlay JM. ----- Ti: Antisense preproendothelin-oligoDNA therapy for vasospasm in a canine model of subarachnoid hemorrhage. ----- So: J Neurosurg. 90(6):1105-14, 1999 Jun. ----- Ab: OBJECT: The purpose of this study is twofold: 1) to test antisense genetic techniques used in the prevention of cerebral vasospasm in a canine model of subarachnoid hemorrhage (SAH), targeting the endothelin-1 (ET-1) gene; and 2) to determine if fibrinolysis of subarachnoid clot with recombinant tissue plasminogen activator (rtPA) could enhance the effect of antisense treatment. METHODS: A total of 39 dogs were studied in this experiment. Placebo (six animals), rtPA (six animals), antisense preproET-1 oligodeoxynucleotide (ASOD; five animals), or rtPA plus ASOD (combined treatment; six animals) was injected into the cisterna magna 30 minutes after a second SAH was induced on the 2nd day of the experiment. The animals were observed until Day 7, when they underwent follow-up angiography and then were killed; their basilar arteries were removed for analysis. Control animals included in this study (two animals in each group) received placebo, rtPA, ASOD, or rtPA plus ASOD without induction of SAH, or rtPA with mismatched (nonsense) preproET-1 oligodeoxynucleotide following SAH. Six additional dogs were analyzed earlier following SAH. Dogs that received placebo developed severe vasospasm (51+/-8% of baseline caliber). Administration of ASOD alone resulted in a mild reduction in vasospasm (64+/-13% of baseline caliber) and rtPA alone resulted in a moderate reduction in vasospasm (81+/-5% of baseline caliber); however, the combined therapy of rtPA plus ASOD almost completely prevented vasospasm (95+/-6%, of baseline caliber), which was significantly different from all other groups (p < 0.05). Morphological analysis of the basilar arteries yielded results similar to angiography with respect to vasospasm severity. The ASOD treatment combined with rtPA resulted in reduced ET-1 expression, as demonstrated by immunohistochemical staining of the arteries, and reduced preproET-1 levels on Day 4, as measured by reverse transcription-polymerase chain reaction. Nonsense DNA sequences had no effect on the vessels. CONCLUSIONS: Antisense preproET-1 oligodeoxynucleotide treatment, when combined with clot lysis caused by rtPA, reduced vasospasm in the canine model of SAH, and this effect appeared to be related to reduced ET-1 synthesis. The results of this experiment support a causative role for ET-1 early in the course of vasospasm development in dogs. The apparent additive therapeutic effects of antisense and fibrinolytic treatments could be due to clot lysis, which allows better delivery of oligodeoxynucleotides to arteries within the subarachnoid space (Au). |
| Au: Santis G; Evans TW. ----- Ti: Molecular biology for the critical care physician part I: terminology and technology. ----- So: Crit Care Med. 27(4):825-31, 1999 Apr. ----- Ab: The past few years have seen a profound revolution in biological sciences. The enormous advances in molecular biology are providing novel insights into the etiology and treatment of human disease. These insights will undoubtedly have implications for intensive care research and practice. In this first of two articles, the basic principles and techniques of molecular biology are discussed to provide the intensive care physician with background information on the subject (Au). |
| Au: Warner LE; Garcia CA; Lupski JR. ----- Ti: Hereditary peripheral neuropathies: clinical forms, genetics, and molecular mechanisms. ----- So: Annu Rev Med. 50:263-75, 1999. ----- Ab: Hereditary peripheral neuropathies, among the most common genetic disorders in humans, are a complex, clinically and genetically heterogeneous group of disorders that produce progressive deterioration of the peripheral nerves. This group of disorders includes hereditary neuropathy with liability to pressure palsies, Charcot-Marie-Tooth disease, Dejerine-Sottas syndrome, and congenital hypomyelinating neuropathy. Our understanding of these disorders has progressed from the description of the clinical phenotypes and delineation of the electrophysiologic and pathologic features to the identification of disease genes and elucidation of the underlying molecular mechanisms (Au). |
| Au: Priori SG; Barhanin J; Hauer RN; Haverkamp W; Jongsma HJ; Kleber AG; McKenna WJ; Roden DM; Rudy Y; Schwartz K; Schwartz PJ; Towbin JA; Wilde AM. ----- Ti: Genetic and molecular basis of cardiac arrhythmias: impact on clinical management parts I and II. ----- So: Circulation. 99(4):518-28, 1999 Feb 2. ----- Ab: Genetic approaches have succeeded in defining the molecular basis of an increasing array of heart diseases, such as hypertrophic cardiomyopathy and the long-QT syndromes, associated with serious arrhythmias. Importantly, the way in which this new knowledge can be applied to managing patients and to the development of syndrome-specific antiarrhythmic strategies is evolving rapidly because of these recent advances. In addition, the extent to which new knowledge represents a purely research tool versus the extent to which it can be applied clinically is also evolving. The present article represents a consensus report of a meeting of the European Working Group on Arrhythmias. The current state of the art of the molecular and genetic basis of inherited arrhythmias is first reviewed, followed by practical advice on the role of genetic testing in these and other syndromes and the way in which new findings have influenced current understanding of the molecular and biophysical basis of arrhythmogenesis (Au). |
| Au: Claverie JM. ----- Ti: Do we need a huge new centre to annotate the human genome? ----- So: Nature. 2000 Jan 6;403(6765):12 |
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