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161.
Kai Inoue Hidenori Kabeya Michael Y. Kosoy Ying Bai George Smirnov Dorothy McColl Harvey Artsob Soichi Maruyama 《Microbial ecology》2009,57(3):534-541
To clarify the relationship between Bartonella grahamii strains and both the rodent host species and the geographic location of the rodent habitat, we have investigated 31 B. grahamii strains from ten rodent host species from Asia (Japan and China), North America (Canada and the USA), and Europe (Russia
and the UK). On the basis of multi-locus sequencing analysis of 16S rRNA, ftsZ, gltA, groEL, ribC, and rpoB, the strains were classified into two large groups, an Asian group and an American/European group. In addition, the strains
examined were clearly clustered according to the geographic locations where the rodents had been captured. In the phylogenetic
analysis based on gltA, the Japanese strains were divided into two subgroups: one close to strains from China, and the other related to strains
from Far Eastern Russia. Thus, these observations suggest that the B. grahamii strains distributed in Japanese rodents originated from two different geographic regions. In the American/European group,
B. grahamii from the North American continent showed an ancestral lineage and strict host specificity; by contrast, European strains
showed low host specificity. The phylogenetic analysis and host specificity of B. grahamii raise the possibility that B. grahamii strains originating in the North American continent were distributed to European countries by adapting to various rodent
hosts.
An erratum to this article can be found at 相似文献
162.
Davies KR McColl KA Wang LF Yu M Williams LM Crane MS 《Diseases of aquatic organisms》2010,93(1):1-15
An aquatic birnavirus, first isolated in Australia from farmed Atlantic salmon in Tasmania in 1998, has continued to be re-isolated on an infrequent but regular basis. Due to its low pathogenicity, there has been little urgency to undertake a comprehensive characterisation of this aquatic birnavirus. However, faced with possible incursions of any new aquatic birnaviruses, specific identification and differentiation of this virus from other, pathogenic, aquatic birnaviruses such as infectious pancreatic necrosis virus (IPNV) are becoming increasingly important. The present study determined the nucleic acid sequence of the aquatic birnavirus originally isolated in 1998, as well as a subsequent isolate from 2002. The sequences of the VP2 and VP5 genes were compared to that of other aquatic birnaviruses, including non-pathogenic aquatic birnavirus isolates from New Zealand and pathogenic infectious pancreatic necrosis virus isolates from North America and Europe. The deduced amino acid (aa) sequences indicate that the Australian and New Zealand isolates fall within Genogroup 5 together with IPNV strains Sp, DPL, Fr10 and N1. Thus, Genogroup 5 appears to contain aquatic birnavirus isolates from quite diverse host and geographical ranges. Using the sequence information derived from this study, a simple diagnostic test has been developed that differentiates the current Australian isolates from all other aquatic birnaviruses, including the closely related isolates from New Zealand. 相似文献
163.
Emilie Combet Aziza El Mesmari Tom Preston Alan Crozier Kenneth E.L. McColl 《Free radical biology & medicine》2010,48(6):763-771
Acid-catalyzed nitrosation and production of potentially carcinogenic nitrosative species is focused at the gastroesophageal junction, where salivary nitrite, derived from dietary nitrate, encounters the gastric juice. Ascorbic acid provides protection by converting nitrosative species to nitric oxide (NO). However, NO may diffuse into adjacent lipid, where it reacts with O2 to re-form nitrosative species and N-nitrosocompounds (NOC). In this way, ascorbic acid promotes acid nitrosation. Using a novel benchtop model representing the gastroesophageal junction, this study aimed to clarify the action of a range of water-soluble antioxidants on the nitrosative mechanisms in the presence or absence of lipids. Caffeic, ferulic, gallic, or chlorogenic and ascorbic acids were added individually to simulated gastric juice containing secondary amines, with or without lipid. NO and O2 levels were monitored by electrochemical detection. NOC were measured in both aqueous and lipid phases by gas chromatography–tandem mass spectrometry. In the absence of lipids, all antioxidants tested inhibited nitrosation, ranging from 35.9 ± 7.4% with gallic acid to 93 ± 0.6% with ferulic acid. In the presence of lipids, the impact of each antioxidant on nitrosation was inversely correlated with the levels of NO they generated (R2 = 0.95, p < 0.01): gallic, chlorogenic, and ascorbic acid promoted nitrosation, whereas ferulic and caffeic acids markedly inhibited nitrosation. 相似文献
164.
165.
166.
H. P. McColl 《New Zealand journal of zoology.》2013,40(4):355-356
Abstract Nototorchus nom. nov. and Paratorchus nom. nov. are proposed as replacement names for Nototrochus McColl, 1982 and Paratrochus McColl, 1982, which are pre-occupied in Coelenterata and Mollusca respectively. 相似文献
167.
C. Williams W.D. Neithercut M. Hossack J. Hair K.E.L. McColl 《FEMS immunology and medical microbiology》1994,9(4):273-280
Abstract The survival of Helicobacter mustelae, Proteus mirabilis, Escherichia coli and Campylobacter jejuni in the presence of urea and citrate at pH 6.0 was examined. H. mustelae , which has urease activity similar to H. pylori , had a markedly reduced survival, median 2.5% (0–78%) ( P <0.001) when incubated nder these conditions. Only 7% of the ammonia produced by H. mutelae urease activity was recovered from the buffer, a similar percentage to that previously reported with H. pylori . None of the other organisms, all of which had lower urease activity, had impaired survival under these conditions. Electron microscopical studies demonstrated extensive structural damage to H. pylori following exposure to urea and citrate at pH 6.0. This structural damage to the organisms makes it unlikely that the low recovery of ammonia was due to retention of ammonia within the bacteria and suggests that the ammonia may have been incorporated into glutamate or other amino acids. Incorporation of ammonia into these compounds would deplete the cell of the key metabolic intermediate α-ketoglutarate and could thus explain the mechanism of the urease-dependent destruction of the organism. 相似文献
168.
169.
P. McColl 《BMJ (Clinical research ed.)》1994,308(6928):550-551
170.
Karen McColl 《BMJ (Clinical research ed.)》2008,337(7662):142-144