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31.
Structure and composition of the adenovirus type 2 core. 总被引:42,自引:24,他引:18
The structure and composition of the core of adenovirus type 2 were analyzed by electron microscopy and biochemical techniques after differential degradation of the virion by heat, by pyridine, or by sarcosyl treatment. In negatively stained preparations purified sarcosyl cores reveal spherical subunits of 21.6-nm diameter in the electron microscope. It is suggested that these subunits are organized as an icosahedron which has its axes of symmetry coincident with those of the viral capsid. The subunits are connected by the viral DNA molecule. The sarcosyl cores contain the viral DNA and predominantly the arginine/alanine-rich core polypeptide VII. When sarcosyl cores are spread on a protein film, tightly coiled particles are observed which gradually unfold giving rise to a rosette-like pattern due to the uncoiling DNA molecule. Completely unfolded DNA molecules are circular. Pyridine cores consist of the viral DNA and polypeptides V and VII. In negatively stained preparations of pyridine cores the subunit arrangement apparent in the sarcosyl cores is masked by an additional shell which is probably formed by polypeptide V. In freeze-cleaved preparations of the adenovirion two fracture planes can be recognized. One fracture plane probably passes between the outer capsid of the virion and polypeptide V exposing a subviral particle which corresponds to the pyridine core. The second fracture plane observed could be located between polypeptide V and the polypeptide VII-DNA complex, thus uncovering a subviral structure which corresponds to the sarcosyl core. In the sarcosyl core polypeptide VII is tightly bound to the viral DNA which is susceptible to digestion with DNase. The restriction endonuclease EcoRI cleaves the viral DNA in the sarcosyl cores into the six specific fragments. These fragments can be resolved on polyacrylamide-agarose gels provided the sarcosyl cores are treated with pronase after incubation with the restriction endonuclease. When pronase digestion is omitted, a complex of the terminal EcoRI fragments adenovirus DNA and protein can be isolated. From this complex the terminal DNA fragments can be liberated after pronase treatment. The complex described is presumably responsible for the circularization of the viral DNA inside the virion. The nature of the protein(s) involved in circle formation has not yet been elucidated. 相似文献
32.
Christel Hintze-Podufal 《Development genes and evolution》1975,178(1):51-69
Zusammenfassung VonCerura vinula undSphinx ligustri wurden die Oenozyten im letzten Larvenstadium und in der Puppe untersucht und ihre Struktur beschrieben. Ihre Aktivitätsphasen liegen zur Zeit der beiden Häutungen (Larven- und Puppenhäutung) und im letzten Larveninstar vor der Umfärbung, einem äußerlich sichtbaren Metamorphoseschritt, und vor der Puppenhäutung im Färbungsstadium III. Sie stehen mit den Umwandlungsprozessen, die in den Raupen zu diesem Zeitpunkt stattfinden in deutlichem Zusammenhang. —2–4 Monate nach der Puppenhäutung sind in den diapausierenden Puppen noch aktive larvale Oenozyten vorhanden. — Aktivitätsphasen sind charakterisiert durch viele große und kleine Vakuolen neben kanalartigen Strukturen im Zytoplasma, stark verzweigte Kerne und weitreichende Zellaus- und-einbuchtungen.Im Vorpuppenstadium (Färbungsstadium IV) entstehen die imaginalen Oenozyten aus der Epidermis, sie werden erst kurz vor der Adulthäutung aktiv.Haemozyten, neurosekrethaltig, legen sich dicht an die Oenozyten an und dringen zwischen Zelleinfaltungen ins Innere vor.Lipide, besonders reichlich in aktiven Phasen vorhanden, konnten sowohl im Zytoplasma nachgewiesen werden, als auch ihr Übertritt aus dem Fettgewebe, das den Drüsen eng anliegt.Glykogen tritt ebenfalls in den Oenozyten auf, seine Menge steht aber in keinem merklichen. Zusammenhang mit den Zellrhythmen. Physiologische Versuche beweisen, daß die Oenozyten und auch die Prothorakaldrüsen in aktiven Phasen das Häutungs- und Metamorphosehormon abgeben. Sie lösen beide den Umfärbungsprozeß aus. Gehirne mit neurosekretorischen Zellen in aktiver Phase oder Cholesterin können die Prothorakaldrüsen und z.T. auch die Oenozyten zur Abgabe ihres Hormons anregen.
Mit dankenswerter Unterstützung durch die Deutsche Forschungsgemeinschaft. 相似文献
Changes of oenocytes and their function during metamorphosis of sphingidae and notodontidae
Summary Oenocytes of the last larval instar and the pupa ofCerura vinula andSpinx ligustri have been examined, and their structure described. The activity phases of the oenocytes at the time of both moultings, as well as during the last larval instar prior to an externally visible color change and prior to the pupal ecdysis i.e. during color change stage III) were clearly related to the process of metamorphosis, which was occurring in the larvae at this time 2–4 months after pupal ecdysis, diapausing pupae still show active larval oenocytes. Activity phases are characterized by many large and small vacuoles in addition to channel-like cytoplasmatic structures, heavily branched nuclei and extensive cell processes and infoldings of the cell membrane. In the pharate pupal stage (colour change stage IV) the imaginal oenocytes originate from the hypodermis, becoming active just prior to the adult ecdysis.Haemocytes containing neurosecretory material attach themselves to the oenocytes and enter through infoldings of the cell membrane. Lipids, which are particularly abundant during active phases, could be demonstrated in the cytoplasm as well as passing from the fatty tissue closely surrounding the glands. Glycogen was also present in the oenocytes. There was, however, no noticeable relation of these materials to the rhythm.Physiological experiments demonstrated that oenocytes as well as prothoracic glands, when active, secrete the moulting and metamorphosis hormone. Both glands initiate the process of colour change. Brain tissue, containing active neurosecretory cells, or cholesterol, may stimulate the prothoracic galnds and the oenocytes to secrete their hormone.
Mit dankenswerter Unterstützung durch die Deutsche Forschungsgemeinschaft. 相似文献
33.
Tandem repeats represent one of the most abundant class of variations in human genomes, which are polymorphic by nature and become highly unstable in a length-dependent manner. The expansion of repeat length across generations is a well-established process that results in human disorders mainly affecting the central nervous system. At least 50 disorders associated with expansion loci have been described to date, with half recognized only in the last ten years, as prior methodological difficulties limited their identification. These limitations still apply to the current widely used molecular diagnostic methods (exome or gene panels) and thus result in missed diagnosis detrimental to affected individuals and their families, especially for disorders that are very rare and/or clinically not recognizable. Most of these disorders have been identified through family-driven approaches and many others likely remain to be identified. The recent development of long-read technologies provides a unique opportunity to systematically investigate the contribution of tandem repeats and repeat expansions to the genetic architecture of human disorders. In this review, we summarize the current and most recent knowledge about the genetics of repeat expansion disorders and the diversity of their pathophysiological mechanisms and outline the perspectives of developing personalized treatments in the future.Tandem repeats represent one of the most abundant class of variations in human genomes, which are polymorphic by nature and become highly unstable in a length-dependent manner. The expansion of repeat length across generations is a well-established process that results in human disorders mainly affecting the central nervous system. At least 50 disorders associated with expansion loci have been described to date, with half recognized only in the last ten years, as prior methodological difficulties limited their identification. These limitations still apply to the current widely used molecular diagnostic methods (exome or gene panels) and thus result in missed diagnosis detrimental to affected individuals and their families, especially for disorders that are very rare and/or clinically not recognizable. Most of these disorders have been identified through family-driven approaches and many others likely remain to be identified. The recent development of long-read technologies provides a unique opportunity to systematically investigate the contribution of tandem repeats and repeat expansions to the genetic architecture of human disorders. In this review, we summarize the current and most recent knowledge about the genetics of repeat expansion disorders and the diversity of their pathophysiological mechanisms and outline the perspectives of developing personalized treatments in the future. 相似文献
34.
Dr. Christel Hintze 《Zoomorphology》1969,64(1):1-8
The larvae of Cerura vinula L. and Notodonta anceps Goeze secrete formic acid for defence. The glandular protective system which forms the acid and changes of the cell structure were studied with the light-microscope.
Mit dankenswerter Unterstützung der Deutschen Forschungsgemeinschaft. 相似文献
Mit dankenswerter Unterstützung der Deutschen Forschungsgemeinschaft. 相似文献
35.
Nb1-particles fromNitrobacter agilis were found to be highly stable and could only be disrupted by chemicals or prolonged sonication.Spectra of the Nb1-particles indicated that protein is their major component. They contain no lipid.Highly purified Nb1-particles that were electronmicroscopically free from contaminating membranes, contained 7 different proteins, as shown by sodium dodecyl sulfate-polyacrylamide gelelectrophoresis.Abbreviations SDS
sodium dodecyl sulfate
- PAGE
polyacrylamide-gelelectrophoresis
- M. W.
molecular weight
- O.D.
opitical density
- HAA
hepatitis associated antigen 相似文献
36.
Netherlands Heart Journal - 相似文献
37.
38.
39.
Ann Van Campenhout Christel M. Van Campenhout Albert R. Lagrou Begoña Manuel-y-Keenoy 《Free radical research》2013,47(10):1069-1077
Free iron is capable of stimulating the production of free radicals which cause oxidative damage such as lipid peroxidation. One of the most important mechanisms of antioxidant defense is thus the sequestration of iron in a redox-inactive form by transferrin. In diabetes mellitus, increased oxidative stress and lipid peroxidation contribute to chronic complications but it is not known if this is related to abnormalities in transferrin function. In this study we investigated the role of transferrin concentration and glycation. The antioxidant capacity of apotransferrin to inhibit lipid peroxidation by iron-binding decreased in a concentration-dependent manner from 89% at <formula>≥2 mg/ml</formula> to 42% at 0.5 mg/ml. Pre-incubation of apotransferrin with glucose for 14 days resulted in a concentration-dependent increase of glycation: 1, 5 and 13 μmol fructosamine/g transferrin at 0, 5.6 and 33.3 mmol/l glucose respectively, p<0.001. This was accompanied by a decrease in the iron-binding antioxidant capacity of apotransferrin. In contrast, transferrin glycation by up to 33.3 mmol/l glucose did not affect chemiluminescence-quenching antioxidant capacity, which is iron-independent. Colorimetric evaluation of total iron binding capacity in the presence of an excess of iron (iron/transferrin molar ratio=2.4) also decreased from 0.726 to 0.696 and 0.585 mg/g transferrin after 0, 5.6 and 33.3 mmol/l glucose, respectively, p<0.01. In conclusion, these results suggest that lower transferrin concentration and its glycation can, by enhancing the pro-oxidant effects of iron, contribute to the increased lipid peroxidation observed in diabetes. 相似文献
40.
Romain Philippe Etienne Paux Isabelle Bertin Pierre Sourdille Fréderic Choulet Christel Laugier Hana ?imková Jan ?afá? Arnaud Bellec Sonia Vautrin Zeev Frenkel Federica Cattonaro Federica Magni Simone Scalabrin Mihaela M Martis Klaus FX Mayer Abraham Korol Hélène Bergès Jaroslav Dole?el Catherine Feuillet 《Genome biology》2013,14(6):R64