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1.
David T. Dunn Damayanti Poddar Beryl E. Serjeant Graham R. Serjeant 《British journal of haematology》1989,72(3):434-438
The pregnancy related changes in fetal haemoglobin (HbF) have been observed in 152 pregnancies in 125 women with homozygous sickle cell (SS) disease and related to steady state levels in the same individual. Statistically significant increases in the first and second trimesters, were followed by significant falls below steady state levels in the third trimester and postpartum period. Although these corresponded to a mean increase of 0.7% and a mean decrease of 1.6%, much greater changes occurred in some individuals. Mean levels had not returned to steady state values 1 year after delivery. The hormonal changes in pregnancy appear to have profound effects on HbF level in SS disease, the mechanisms of which require further study. 相似文献
2.
Two cases of acute polymyosotis associated with W. bancrofti , presented with generalised painful swelling and weakness of the muscles. These patients had elevated muscle enzymes, a myopathic EMG pattern, inflammatory myopathy on biopsy and W. bancrofti in the peripheral blood smear. The clinical, improvement of the disorder and total clearance of microfilariae was obtained with the combination therapy of steroid and diethyl-carbamazine in comparison with steroid alone. 相似文献
3.
This review of the current scenario of celiac disease (CD) in India covers both pediatric and adult CD. CD is primarily reported from northern India with isolated case reports from the rest of the country. CD cases among Indian children are associated with multiple DR3-DQ2 haplotypes. Delay in diagnosis is contributed by multiple factors including atypical presentations. Use of serological tests, IgA EMA and anti-tTG antibodies, along with modified ESPGHAN criteria provides a definitive diagnosis of CD. Dietary management is often difficult due to non-availability of labeled and marketed gluten-free foods. A majority of children with CD show normalization of nutrition, substantial improvement in growth parameters and attainment of healthy percentile curves on gluten-free diet. Small bowel histology remarkably improves but does not normalize even after 2-3 years on gluten-free diet. The true burden of the disease should be addressed by large epidemiological studies. 相似文献
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Tirthadipa Pradhan-Sundd Silvia Liu Sucha Singh Minakshi Poddar Sungjin Ko Aaron Bell Jonathan Franks Ian Huck Donna Stolz Udayan Apte Sarangarajan Ranganathan Kari Nejak-Bowen Satdarshan P. Monga 《The American journal of pathology》2021,191(5):885-901
Hepatocytes are highly polarized epithelia. Loss of hepatocyte polarity is associated with various liver diseases, including cholestasis. However, the molecular underpinnings of hepatocyte polarization remain poorly understood. Loss of β-catenin at adherens junctions is compensated by γ-catenin and dual loss of both catenins in double knockouts (DKOs) in mice liver leads to progressive intrahepatic cholestasis. However, the clinical relevance of this observation, and further phenotypic characterization of the phenotype, is important. Herein, simultaneous loss of β-catenin and γ-catenin was identified in a subset of liver samples from patients of progressive familial intrahepatic cholestasis and primary sclerosing cholangitis. Hepatocytes in DKO mice exhibited defects in apical-basolateral localization of polarity proteins, impaired bile canaliculi formation, and loss of microvilli. Loss of polarity in DKO livers manifested as epithelial-mesenchymal transition, increased hepatocyte proliferation, and suppression of hepatocyte differentiation, which was associated with up-regulation of transforming growth factor-β signaling and repression of hepatocyte nuclear factor 4α expression and activity. In conclusion, concomitant loss of the two catenins in the liver may play a pathogenic role in subsets of cholangiopathies. The findings also support a previously unknown role of β-catenin and γ-catenin in the maintenance of hepatocyte polarity. Improved understanding of the regulation of hepatocyte polarization processes by β-catenin and γ-catenin may potentially benefit development of new therapies for cholestasis.A hallmark of epithelial cells is polarization, which is achieved by the orchestration of external cues, such as cellular contact, extracellular matrix, signal transduction, growth factors, and spatial organization.1 Hepatocytes in the liver show a unique polarity by forming several apical and basolateral poles within a cell.2 The apical poles of adjacent hepatocytes form a continuous network of bile canaliculi into which bile is secreted, whereas the basolateral membrane domain forms the sinusoidal pole, which secretes various components, such as proteins or drugs, into the blood circulation.3 Loss of hepatic polarity has been associated with several cholestatic and developmental disorders, including progressive familial intrahepatic cholestasis (PFIC) and primary sclerosing cholangitis (PSC).4,5 Although the molecular mechanisms governing hepatocyte polarity have been extensively studied in the in vitro systems, there is still a significant gap in our understanding of how polarity is established within the context of tissue during development or maintained during homeostasis.6,7 Similarly, the molecular pathways contributing to hepatic polarity are not entirely understood, and a better comprehension of hepatic polarity regulation is thus warranted.Previous studies have confirmed the role of hepatocellular junctions, such as tight and gap junctions, in the maintenance of hepatocyte polarity.8,9 Studies done in vitro and in vivo have shown that loss of junctional proteins, such as zonula occludens protein (ZO)-1, junctional adhesion molecule-A, and claudins, lead to impairment of polarity and distorted bile canaliculi formation.10, 11, 12, 13 In addition, proteins involved in tight junction assembly, such as liver kinase B1, are also involved in polarity maintenance.14 Among adherens junction proteins, various in vitro cell culture models have confirmed the role of E-cadherin in the regulation of hepatocyte polarity, possibly through its interaction with β-catenin.15,16 However, there is a lack of an in vivo model to study the role of adherens junction proteins in hepatocyte polarity and their misexpression contributing to various liver diseases.β-Catenin plays diverse functions in the liver during development, regeneration, zonation, and tumorigenesis.17, 18, 19 The relative contribution of β-catenin as part of the adherens junction is challenging to study because like in other tissues, γ-catenin compensates for the β-catenin loss in the liver.20,21 To address this redundancy, we previously reported a hepatocyte-specific -catenin and γ-catenin double-knockout (DKO) mouse model was reported.22 Simultaneous deletion of β-catenin and γ-catenin in mice livers led to cholestasis, partially through the breach of cell-cell junctions. However, more comprehensive understanding of the molecular underpinnings of the phenotype is needed.In the current study, prior preclinical findings of dual β-catenin and γ-catenin loss were extended to a subset of PFIC and PSC patients. In vivo studies using the murine model with hepatocyte-specific dual loss of β-catenin and γ-catenin showed complete loss of hepatocyte polarity compared to the wild-type controls (CONs). Loss of polarity in DKO liver was accompanied by epithelial-mesenchymal transition (EMT), activation of transforming growth factor (TGF)-β signaling, and reduced expression of hepatocyte nuclear factor 4α (HNF4α). Our findings suggest that β-catenin and γ-catenin and in turn adherens junction integrity, are critical for the maintenance of hepatocyte polarity, and any perturbations in this process can contribute to the pathogenesis of cholestatic liver disease. 相似文献
6.
Sen R Chakrabarti S Sengupta B De M Haldar A Poddar S Gajra B Talukder G Sengupta S 《Hemoglobin》2005,29(4):277-280
Five hundred and thirteen unrelated subjects belonging to various tribes of West Bengal, Arunachal Pradesh and Assam in Eastern India, were screened for the presence of alpha-thalassemia (thal) gene deletion(s) as a possible cause of unexplained anemia (Hb < 11 g/dL and/or MCH <28 pg, MCV < 78 fL). As reported earlier, beta-globin gene mutant alleles were found with a frequency of up to 20% in some tribes. In the present study, alpha-globin gene deletion alleles were found in 18% of subjects from West Bengal, 3.9% from Arunachal Pradesh and 3.84% from Assam tribesmen. Coexistence of alpha- and beta-globin gene abnormalities was observed in up to 18% of some tribal groups. The high inbreeding rate and lack of appropriate medical care make these populations particularly vulnerable. 相似文献
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Rishi Bolia Aditya Kapoor Surender Kumar Yachha Ujjal Poddar 《Scandinavian journal of gastroenterology》2018,53(7):803-808
Introduction: We assessed cardiac function (CF) in celiac disease (CD) patients and the effect of gluten-free diet (GFD) on CF.Methods: Prospective evaluation of CF using conventional and tissue doppler echocardiography in 50 CD patients (age 4.2?±?1.1 years) at diagnosis and after a year of GFD (group 1), 100 CD children (group 2; 47 compliant and 53 non-compliant) in follow-up and 25 healthy controls.Results: Untreated CD (n?=?50) children had larger left ventricle end diastolic dimension (35.33?±?0.87 vs. 32.90?±?0.91 mm; p?=?.04), reduced (<55%) left ventricular ejection fraction (20% vs. 0%; p?=?.01) and a higher (>0.6) myocardial performance index (MPI, 66% vs. 0%; p ≤ .01) as compared to controls. Re-evaluation after one year with good dietary compliance showed changes in isovolumic relaxation time (72.5?±?4.2 vs. 50.62?±?2.69; p?=?.0001) and deceleration time (121.05?±?10.1 vs. 99.87?±?8.5; p?=?.02), reflecting improved cardiac diastolic function. GFD compliant patients had lower MPI than non-compliant (0.60?±?.03 vs. 0.66?±?.08; p?=?.04), reflecting improvement in load-independent echocardiographic parameters.Conclusions: Subclinical cardiac dysfunction is common in CD children at diagnosis. Improvementin echocardiographic parameters occurs with GFD and non-compliant children continue to havepersistent cardiac dysfunction. 相似文献
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