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51.
BACKGROUND & AIMS: The majority of patients with celiac sprue experience diarrhea before diagnosis. There have been no studies of the prevalence or causes of chronic diarrhea in these patients after treatment with a gluten-free diet. METHODS: Seventy-eight patients with celiac sprue (59 women and 19 men) treated with a gluten-free diet for at least 12 months were surveyed about their bowel habits. Those with chronic diarrhea, defined as passage of loose stools three or more times per week for 6 months, underwent an extensive diagnostic evaluation to determine its cause. RESULTS: Sixty-two of the 78 patients (79%) experienced diarrhea before treatment, and 13 (17%) had chronic diarrhea (of lesser severity) after treatment. The causes of diarrhea in 11 patients consenting to this study were microscopic colitis, steatorrhea secondary to exocrine pancreatic insufficiency, dietary lactose or fructose malabsorption, anal sphincter dysfunction causing fecal incontinence, and the irritable bowel syndrome. Only 1 patient had antigliadin antibodies detected in serum or small intestinal villous atrophy. CONCLUSIONS: After treatment of celiac sprue with a gluten-free diet, chronic diarrhea persists in a substantial percentage of patients. Although ongoing gluten ingestion is one possible cause, other causes may be more frequent. Therefore, diagnostic investigation of diarrhea in celiac sprue after treatment seems warranted. (Gastroenterology 1997 Jun;112(6):1830-8) 相似文献
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NJ Gogtay KD Kamtekar SS Dalvi SS Mehta AR Chogle U Aigal NA Kshirsagar 《BMC infectious diseases》2006,6(1):16-4
Background
The WHO recommends that adults with uncomplicated P. falciparum successfully treated with a blood schizonticide receive a single dose of primaquine (PQ) 45 mg as a gametocytocidal agent. An earlier pilot study suggested that 75 mg of bulaquine (BQ), of which PQ is a major metabolite, may be a useful alternate to PQ. 相似文献54.
Theoharis C. Theoharides Bodi Zhang Duraisamy Kempuraj Michael Tagen Magdalini Vasiadi Asimenia Angelidou Konstantinos-Dionysios Alysandratos Dimitris Kalogeromitros Shahrzad Asadi Nikolaos Stavrianeas Erika Peterson Susan Leeman Pio Conti 《Proceedings of the National Academy of Sciences of the United States of America》2010,107(9):4448-4453
The peptide substance P (SP) has been implicated in inflammatory conditions, such as psoriasis, where mast cells and VEGF are increased. A relationship between SP and VEGF has not been well studied, nor has any interaction with the proinflammatory cytokines, especially IL-33. Here we report that SP (0.1–10 μM) induces gene expression and secretion of VEGF from human LAD2 mast cells and human umbilical core blood-derived cultured mast cells (hCBMCs). This effect is significantly increased by coadministration of IL-33 (5–100 ng/mL) in both cell types. The effect of SP on VEGF release is inhibited by treatment with the NK-1 receptor antagonist 733,060. SP rapidly increases cytosolic calcium, and so does IL-33 to a smaller extent; the addition of IL-33 augments the calcium increase. SP-induced VEGF production involves calcium-dependent PKC isoforms, as well as the ERK and JNK MAPKs. Gene expression of IL-33 and histidine decarboxylase (HDC), an indicator of mast cell presence/activation, is significantly increased in affected and unaffected (at least 15 cm away from the lesion) psoriatic skin, as compared with normal control skin. Immunohistochemistry indicates that IL-33 is associated with endothelial cells in both the unaffected and affected sites, but is stronger and also associated with immune cells in the affected site. These results imply that functional interactions among SP, IL-33, and mast cells leading to VEGF release contribute to inflammatory conditions, such as the psoriasis, a nonallergic hyperproliferative skin inflammatory disorder with a neurogenic component. 相似文献
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Asadi S Zhang B Weng Z Angelidou A Kempuraj D Alysandratos KD Theoharides TC 《International journal of immunopathology and pharmacology》2010,23(4):1015-1020
HgCl2 is a known environemental neurotoxin, but is also used as preservative in vaccines as thimerosal containing ethyl mercury covalently linked to thiosalicylate. We recently reported that mercury choloride (HgCl(2)) can stimulate human mast cells to release vascular endothelial growth factor (VEGF), which is also vasoactive and pro-inflammatory. Here we show that thimerosal induces significant VEGF release from human leukemic cultured LAD2 mast cells (at 1 microM 326 ± 12 pg/106 cells and 335.5 ± 12 pg/106 cells at 10 microM) compared to control cells (242 ± 21 pg/106 cells, n=5, p less than 0.05); this effect is weaker than that induced by HgCl2 at 10 microM (448 ± 14 pg/106 cells) (n=3, p less than 0.05). In view of this finding, we hypothesize that the thiosalicylate component of thimerosal may have an inhibitory effect on VEGF release. Thimerosal (10 microM) added together with the peptide Substance P (SP) at 2 microM, used as a positive control, reduced VEGF release by 90 percent. Methyl thiosalicylate (1 or 10 microM) added with either SP or HgCl2 (10 microM) inhibited VEGF release by 100 percent, while sodium salicylate or ibuprofen had no effect. Pretreatment for 10 min with the flavonoid luteolin (0.1 mM) before HgCl2 or thimerosal compeletly blocked their effect. Luteolin and methyl thiosalicylate may be useful in preventing mercury-induced toxicity. 相似文献
57.
Enhanced transcription factor DNA binding and gene expression induced by arsenite or arsenate in renal slices 总被引:5,自引:4,他引:1
Although the kidney represents a target for the accumulation and toxicity
of arsenic, little is known about the molecular targets of arsenic in this
organ. Therefore, these studies were designed to examine the molecular
impact of arsenite [As(III)] and arsenate [As(V)] at low (nanomolar)
concentrations. Precision-cut rabbit renal cortical slices were challenged
with As(III) or As(V) for up to 8 h. Neither form of the metal induced
overt cytotoxicity as assessed by intracellular K+ levels over this time
period at concentrations from 0.01-10 microM. In addition, no alterations
in the expression of Hsp 60, 70, or 90 were observed. However, induction of
heme oxygenase-1 (Hsp 32) was seen following a 4-h challenge with As(III),
but not with As(V). As(III) and As(V) induced DNA binding of AP-1 at 2- and
4-h exposure; following a 6-h exposure there was no difference. Although no
alteration in the DNA binding activity of ATF-2 was induced by As(III) or
As(V), both forms enhanced the DNA binding activity of Elk-1. Enhanced DNA
binding activity of AP-1 and Elk-1 correlated with increased gene
expression of c-fos, but not c-jun, at 2 h. c-myc gene expression was also
induced by As(III) and As(V), albeit at a later time point (6 h). These
results suggest that acute arsenic challenge, by either As(III) or As(V),
is associated with discrete alterations in the activity of signaling
pathways and gene expression in renal tissue.
相似文献
58.
59.
Strom TM; Hortnagel K; Hofmann S; Gekeler F; Scharfe C; Rabl W; Gerbitz KD; Meitinger T 《Human molecular genetics》1998,7(13):2021-2028
Wolfram syndrome is an autosomal recessive disorder characterized by
juvenile diabetes mellitus, diabetes insipidus, optic atrophy and a number
of neurological symptoms including deafness, ataxia and peripheral
neuropathy. Mitochondrial DNA deletions have been described in a few
patients and a locus has been mapped to 4p16 by linkage analysis.
Susceptibility to psychiatric illness is reported to be high in affected
individuals and increased in heterozygous carriers in Wolfram syndrome
families. We screened four candidate genes in a refined critical linkage
interval covered by an unfinished genomic sequence of 600 kb. One of these
genes, subsequently named wolframin, codes for a predicted transmembrane
protein which was expressed in various tissues, including brain and
pancreas, and carried loss-of- function mutations in both alleles in
Wolfram syndrome patients.
相似文献
60.