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161.
162.
MM El-Domyati† HM Ahmad† I Nagy† A Zahran‡ 《Journal of the European Academy of Dermatology and Venereology》2007,21(6):795-801
BACKGROUND: Chronic renal failure results in multi-organ system derangement including cardiovascular, gastrointestinal, neurological, endocrinal, blood and dermatological abnormalities. Maintenance of skin homeostasis requires a delicate balance between proliferation, differentiation and apoptosis. p53 and Bcl-2 proteins play a central role in the regulation of apoptosis. OBJECTIVE: Evaluation of the expression of apoptosis regulatory proteins p53 and Bcl-2 in apparently normal skin of patients, with chronic renal failure on maintenance haemodialysis, with respect to their role in the apoptotic process. METHODS: Biopsy specimens were obtained from 10 patients with chronic renal failure on maintenance haemodialysis, as well as seven age-matched control subjects. Computer-assisted image analysis was employed to measure epidermal thickness in H&E-stained sections. Immunoperoxidase technique was also used to demonstrate p53 and Bcl-2 proteins and the TUNEL technique for detection of apoptotic cells in these specimens. RESULTS: The mean epidermal thickness was significantly higher (P < 0.0001) in patients than controls. Meanwhile, no apoptotic cells were detected in the epidermis of patients. On the other hand, a statistically significant difference was observed in both p53 (P = 0.0001) and Bcl-2 expression (P = 0.0003) when comparing patients and controls. Expression of p53 (2.74 +/- 0.84) and Bcl-2 (3.45 +/- 1.35) proteins was higher in skin samples obtained from patients with chronic renal failure and on maintenance haemodialysis than those from control cases (0.5 +/- 0.96 and 0.8 +/- 0.6, respectively). Moreover, Bcl-2 expression in patients was observed in basal as well as squamous cell layers of skin, whereas in control subjects it was confined to the basal cell layer only. CONCLUSION: These findings suggest that an alteration in the proliferation/apoptosis balance may be present in the skin of such patients. 相似文献
163.
164.
Krimer LS; Herman MM; Saunders RC; Boyd JC; Hyde TM; Carter JM; Kleinman JE; Weinberger DR 《Cerebral cortex (New York, N.Y. : 1991)》1997,7(8):732-739
The entorhinal cortex (ERC) has been implicated in schizophrenia by a
number of studies. There is anatomical observation of neuronal heterotopias
in the rostral ERC, which is consistent with a hypothesis of
neurodevelopmental abnormalities in this disease. In view of the
significant cytoarchitectonic variation of the ERC throughout its
rostro-caudal extent, we performed a detailed subareal analysis of the
rostral two-thirds of the entorhinal cortex (ERCr) in 14 postmortem
schizophrenic brains and 14 matched controls (mean ages of 48 and 47
respectively). This systematic evaluation included both a qualitative
microscopic analysis of morphogenetic anomalies that would be consistent
with neurodevelopmental pathology and quantitative measurements of total
neuronal number, average neuronal density, laminar volume and laminar depth
from the cortical surface in cytoarchitectonically matched subareas of
schizophrenic and control brains. Parcellation of the entire ERC on the
basis of cytoarchitectonic criteria identified five distinct regions,
similar to those described in the macaque, except that in the human brain
three of the regions were further divisible into two or three subareas,
yielding nine distinct cellular compartments. Five rostral areas, prorhinal
(Pr), lateral (28L), intermediate rostral and caudal (281r and 281c), and
sulcal (28S), comprise the ERCr. Gross and microscopic examination of these
subdivisions throughout the ERCr failed to reveal laminar disorganization
in any of the schizophrenic brains. The brains also did not differ
significantly with respect to total neuronal number, total volume and
neuronal density per laminar and subareal subdivision, or laminar thickness
per entorhinal subarea. However, neuronal number and density were reduced
by 12-18% in Pr and 28L, suggesting that mild quantitative abnormalities
may exist in the ERCr and might possibly be revealed in a larger sample of
schizophrenic brains. We have failed to confirm previous reports of laminar
disorganization in the ERCr in brains of patients with schizophrenia; to
the extent that this region is implicated in schizophrenia, the structural
changes are likely to consist of more subtle cellular disturbances.
相似文献
165.
G. Hodge MM Makarious JA Charlesworth† KA Duggan 《Clinical and experimental pharmacology & physiology》1997,24(6):460-462
1. Treatment with angiotensin-converting enzyme (ACE) inhibitors slows the rate of progression of nephropathy in the spontaneously hypertensive rat (SHR) with streptozotocin-induced diabetes. Paradoxically, however, chronic ACE inhibitor therapy has been reported to be associated with induction of ACE in the plasma. We sought to determine whether induction also occurred in the glomerulus. 2. Seven days after induction of diabetes rats were randomized to receive perindopril (4mg/kg per day) in the drinking water or water alone. Blood glucoses were maintained 6–10 mmol/L by daily ultralente insulin. Rats were killed after 1 and 12 weeks of ACE inhibitor therapy and the kidneys were harvested. Angiotensin-converting enzyme activity was determined in isolated glomeruli before and after removal of perindopril and reconstitution with zinc sulphate. 3. After 1 week of ACE inhibitor therapy, glomerular ACE was significantly greater after removal of perindopril than either before its removal (P < 0.025) or in the untreated controls (P < 0.025). After 12 weeks of therapy, ACE activity was significantly lower in the perindopril-treated group than in the untreated controls (P < 0.025). There was no increase in ACE activity following removal of perindopril. 4. These studies suggest that short-term ACE inhibition is associated with induction of ACE in the glomerulus. However, there was no increase in ACE activity after removal of perindopril, suggesting that induction of synthesis of this enzyme in the glomerulus does not occur during chronic ACE inhibition. 相似文献
166.
研究发现银屑病皮损能够高度聚集原卟啉Ⅸ(PpⅨ,一种由5-ALA产生的内源性光源物质),但进行荧光诊断时却发现皮损内PpⅨ的分布存在差异,造成这种差异的原因目前尚不清楚。 相似文献
167.
168.
J Chapal D Hillaire-Buys G Bertrand D Pujalte P Petit and MM Loubatieres-Mariani 《Fundamental & clinical pharmacology》1997,11(6):537-545
Summary— Adenosine tri- and diphosphate (ATP and ADP) and their structural analogues stimulate insulin secretion from the isolated perfused rat pancreas, an effect mediated by P2Y -purinoceptor activation. Concerning the base moiety of the nucleotide, it was previously shown that purine but not pyrimidine nucleoside triphosphates were active and that substitution on purine C2 with the 2-methylthio group greatly enhanced the potency. In this study, we further analyze the consequences of ribose and polyphosphate chain modifications. Modifications in 2' and 3' position on the ribose led to a decrease in insulin response when bulky substitutions were made: indeed, 2'-deoxy ATP was similar in activity to ATP, whereas arylazido-aminopropionyl ATP (ANAPP3 ) was weakly effective and trinitrophenyl ATP (TNP-ATP) was inactive. Substitution on the /phosphorus of the triphosphate chain led to a decrease (y-anilide ATP) or no change ( y-azido ATP) in potency; the replacement of the bridging oxygen between β and /phosphorus by a peroxide group did not significantly change the activity, whereas substitution by a methylene group completely abolished stimulation of insulin secretion. As for the phosphorothioate analogues, adenosine-5'-0-(3-thiotriphosphate) (ATP)S) induced an insulin response similar to that produced by ATP, whereas adenosine-5'-0-(2-thiodiphosphate) (ADP/JS) was about 100-fold more potent than ATP, as previously shown. In conclusion, two structural features seem to have a strategic importance for increasing the insulin secretory activity of ATP analogues: substitution at the C2 position on the adenine ring of ATP and modifications of the polyphosphate chain at the level of the β phosphorus. 相似文献
169.
Suppression of intestinal polyp development by low-fat and high-fiber diet in Apc(delta716) knockout mice 总被引:1,自引:0,他引:1
Hioki K; Shivapurkar N; Oshima H; Alabaster O; Oshima M; Taketo MM 《Carcinogenesis》1997,18(10):1863-1865
Most epidemiological and animal studies show a positive correlation of the
dietary intake of fat with the incidence of colon cancer, whereas an
inverse correlation of the dietary intake of fiber. In rats fed a diet low
in fat and high in wheat bran fiber and calcium, a significant decrease was
reported in the number of azoxymethane-induced aberrant crypt foci compared
with those fed a high-fat, low-fiber and low- calcium diet. Mutations in
the human APC gene play a key role, not only in familial adenomatous
polyposis, but also in many sporadic cancers of the entire digestive tract.
We previously constructed a mouse strain Apc(delta716), carrying a
truncation mutation at codon 716 of the Apc gene, the homolog of human APC
(10). The heterozygous mice developed numerous intestinal polyps, and all
microadenomas dissected from the earliest polyps had already lost the
wild-type allele, indicating the loss of heterozygosity. Using these
Apc(delta716) knockout mice, we have investigated the effect of a low-fat
and high-fiber diet (LRD for 'low-risk' diet) on intestinal polyposis, and
compared it with that of a high-fat and low-fiber diet (HRD for 'high-risk'
diet). The mice were fed either diet for 7 weeks, and the number and size
of intestinal polyps were scored. The LRD-fed mice had fewer polyps than
the HRD-fed mice, by 36% in the small intestine and by 64% in the colon. As
for the polyp size distribution, there was no significant difference
between the HRD- and LRD-fed mice. These results indicate that LRD can
suppress intestinal polyposis compared with HRD which does not, and suggest
that its suppression is at the initiation of polyp formation. This is
likely to be due to a decreased frequency of loss of heterozygosity, rather
than a retarded growth of the polyp adenomas.
相似文献
170.
MM Abitbol 《Gait & posture》1993,1(4):189-195
Twenty children were carefully observed by using videotapes during the first 18 months of life to study the successive stages recognized in the acquisition of quadrupedal and bipedal behaviour. The different stages for the acquisition of these two modes of locomotion were intermingled and each child had its own specific sequence. But when the stages leading to quadrupedal behaviour were separated from those leading to bipedal behaviour and were placed in two separate sequences, the order of acquisition of the different phases in each sequence was identical for all children. Also, quadrupedal phases at any age can be performed for no more than 1 min, while upright stages at similar ages are performed for much longer. In view of the heavy weight of the infant's head, it is suggested that it is easier to carry the head in equilibrium over the shoulders when upright than in front of the body when on all fours. Bipedalism is, therefore, energy saving, and is selected by the child as soon as there is enough neuromuscular development to perform it. 相似文献