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721.
722.
723.
Thomas S. Wilson Elizabeth M. McDowell Benjamin F. Trump 《Biotechnic & histochemistry》1983,58(4):225-229
A method is proposed for the simultaneous staining of neutral and acidic, periodate reactive and nonperiodate reactive mucosubstances, glycogen and keratin in paraffin sections. Briefly, sections are stained by the Alcian blue (pH 2.5)-PAS method, followed by a peroxidase-antiperoxidase imiminohistochemical stain for keratin. The proposed method modifies an existing method, and expands the range of polysaccharides and mucosubstances which may be demonstrated. The proposed method is easily performed within a single working day and promises to be of value in surgical pathology as well as in studies of bronchial carcinogenesis. 相似文献
724.
Flavanols from barley or hops were separated chromatographically and assayed automatically by reaction with the chromogen, 4-dimethylaminocinnamaldehyde. For separating the flavanols on Sephadex G-25, gradient elution with water-methanol mixtures was necessary. The chromogen was specific for flavanols and well suited to AutoAnalyzer methods. The method appears generally applicable in flavanol analysis of plant materials. 相似文献
725.
726.
Regeneration of hamster tracheal epithelium after mechanical injury. IV. Histochemical, immunocytochemical and ultrastructural studies 总被引:2,自引:0,他引:2
K P Keenan T S Wilson E M McDowell 《Virchows Archiv. B, Cell pathology including molecular pathology》1983,43(3):213-240
All stages of regeneration in hamster tracheal epithelium were studied following a denuding mechanical injury. At 1 h all the cells had sloughed from the wound site leaving a bare and sometimes disrupted basal lamina. Viable cells at the wound margins rapidly changed shape, flattened and migrated to cover the denuded lesion by 12 h. In addition, epithelial cells that remained viable demonstrated sublethal changes that included the rapid discharge of mucous granules from secretory cells, internalization of cilia by ciliated cells and evidence of heterophagy in both cell types. By 24 h a wave of epithelial cell divisions occurred, primarily by secretory cells. This produced a multilayered epidermoid metaplasia that was best developed at 48 h. The metaplastic epithelium was largely composed of cells with both secretory (mucous granules) and epidermoid (tonofilament bundles and numerous desmosomes) characteristics. The peroxidase-antiperoxidase (PAP) method demonstrated a few keratin-positive cells in the wound as early as 12 h post-wounding and keratin was demonstrated in more cells by 24 h. All cells in the metaplastic wound epithelium were keratin-positive by 48 h. Following 48 h some of the most superficial keratinized cells sloughed from the epithelium and the keratin content of the remaining cells began to decline. At 72 h pre-ciliated and pre-secretory cells were seen in the wound. Pre-ciliated cells were characterized by an abundant electron-lucent cytoplasm, large pale nucleus, filiform apical microvilli and evidence of ciliogenesis, similar to that seen during fetal development. Pre-ciliated cells often contained apical mucous granules, apparently carried over from the parent secretory cells. With the appearance of these columnar cells the normal mucociliary morphology was restored in small wounds by 120 h, but some persistent epidermoid metaplasia remained in the large wounds through 168 h post-wounding. These data provide further evidence for the important role of secretory cells in the histogenesis of epidermoid metaplasia and the regeneration of normal morphology following injury. The implications of these findings in understanding the histogenesis of other lesions in the tracheo-bronchial epithelium are discussed. 相似文献
727.
728.
Elizabeth M. McDowell Andrea M. DeSanti Carnell Newkirk Judy M. Strum 《Virchows Archiv. B, Cell pathology including molecular pathology》1990,59(1):231-242
The effects of vitamin A-deficiency and inflammation were studied in the conducting airways of Syrian golden hamsters. An
important goal of the study was to characterize epithelial changes that occur early in vitamin A-deficiency, that might precede
yet predispose to infection, and precipitate inflammatory changes in the lungs. Age-matched vitamin A-replete control and
vitamin A-deprived hamsters were killed at 33 days of age (preweight-plateau); at 41 days of age (weight plateau-early weight
loss); and at 48–55 days of age (prolonged weight plateau followed by weight loss). A tablet containing bromodeoxyuridine
(BrdU) was implanted subcutaneously into each hamster 7 h before it was killed. No changes were seen in the conducting airway
epithelium of vitamin A-deprived hamsters in the preweight plateau. However, labelling of secretory cells for BrdU was reduced
6–7 fold in the epithelium lining the lobar bronchus (p< 0.0002) and the bronchioles (p< 0.0001), and the proportions of ciliated cells were decreased (p<0.0001) at both airway levels in vitamin A-deficient hamsters in the weight plateau-early weight loss stage. Changes in cellular
morphology were minimal in the intrapulmonary airway epithelium at this time but a few small focal patches of epidermoid metaplasia
were seen in the tracheal epithelium. Small foci of inflammation were closely associated with the airways in the weight plateau,
and the inflammation became more widespread when the deficiency was prolonged. The results suggest that the defense of the
lungs to infection was impaired initially in the vitamin A-deficient hamsters by a widespread reduction in the numbers of
ciliated cells throughout the epithelium of the conducting airways (trachea, bronchi, bronchioles). At the foci of inflammation,
labelling of epithelial secretory cells for BrdU was greatly increased at all airway levels. A highly stratified cornifying
epidermoid metaplasia developed in the tracheal epithelium, and goblet cell metaplasia developed in the cranial portion of
the lobar bronchus, in association with submucosal inflammation. Goblet cell metaplasia appeared to be the only abnormality
that wasnot reversed when vitamin A was restored to the diet.
This is contribution no. 2911 from the Pathobiology Laboratory 相似文献