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991.
The effects of methylglyoxal bis(guanylhydrazone) on S-adenosyl-l-methionine decarboxylase (EC 4.1.1.50) activity were studied in the mouse kidney stimulated to growth by testosterone administration. The drug was found to be a potent inhibitor of the enzyme in vitro. Administration of methylglyoxal bis(guanylhydrazone) in vivo resulted in a transient inhibition followed by a strong enhancement of the enzyme activity. Dialysis of the kidney extract, to remove remaining methylglyoxal bis(guanylhydrazone), revealed a great and rapid increase in the activity of S-adenosyl-l-methionine decarboxylase. Injections of testosterone to castrated mice resulted in a marked increase in kidney weight and an accumulation of renal putrescine, spermidine and spermine. These effects of testosterone could not be blocked by simultaneous injections of methylglyoxal bis(guanylhydrazone). It appears that due to secondary effects by which the inhibition of methylglyoxal bis(guanylhydrazone) on S-adenosyl-l-methionine decarboxylase activity is circumvented the inhibitor seems to be of uncertain value in attempts to decrease selectively the in vivo levels of polyamines.  相似文献   
992.
Ducellieria chodati Teiling is an organism rarely mentioned from plankton samples. Its propagation was unknown, and all earlier authors have failed to see that it is a colourless organism. Because of its structure and some chemical reactions,Ducellieria was thought to be a member of theXanthophyceae. Many living coenobia ofD. chodati from several Austrian lakes and some steps of their reproduction have been studied: Zoospores with two unequal flagella are released. After a mobile phase they settle on coniferous pollen grains drifting in water. Inside the pollen grain, a tube or flask is developed from which zoospores are released again after one or two days. These aggregate to form newDucellieria coenobia. These observations suggest thatDucellieria chodati belongs to thePhycomycetes, perhaps to theSaprolegniales.
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993.
Gene deletion in Schizophyllum commune is hampered by a low incidence of homologous integration. As a consequence, extensive screening is required to identify a transformant with the desired genotype. To alleviate this and to facilitate the assembly of deletion plasmids, vector pDelcas was constructed. This construct has a set of restriction sites, which allows for directional cloning of the flanking sequences at both sides of a nourseothricin resistance cassette. Moreover, it contains a phleomycin resistance cassette elsewhere in the plasmid, which is used to screen for transformants with an ectopic integration of the pDelcas derivative. The use of pDelcas derivatives in combination with an improved PCR screening protocol permitted the efficient identification of S. commune deletion strains. This procedure may also function in other basidiomycetes.  相似文献   
994.
Extracellular adenosine production is crucial for host resistance against Streptococcus pneumoniae (pneumococcus) and is thought to affect antibacterial immune responses by neutrophils. However, whether extracellular adenosine alters direct host–pathogen interaction remains unexplored. An important determinant for lung infection by S. pneumoniae is its ability to adhere to the pulmonary epithelium. Here we explored whether extracellular adenosine can directly impact bacterial adherence to lung epithelial cells. We found that signaling via A1 adenosine receptor significantly reduced the ability of pneumococci to bind human pulmonary epithelial cells. A1 receptor signaling blocked bacterial binding by reducing the expression of platelet‐activating factor receptor, a host protein used by S. pneumoniae to adhere to host cells. In vivo, A1 was required for control of pneumococcal pneumonia as inhibiting it resulted in increased host susceptibility. As S. pneumoniae remain a leading cause of community‐acquired pneumonia in the elderly, we explored the role of A1 in the age‐driven susceptibility to infection. We found no difference in A1 pulmonary expression in young versus old mice. Strikingly, triggering A1 signaling boosted host resistance of old mice to S. pneumoniae pulmonary infection. This study demonstrates a novel mechanism by which extracellular adenosine modulates resistance to lung infection by targeting bacterial–host interactions.  相似文献   
995.
996.
Biological Trace Element Research - This work determines the effect nopal consumption at different maturity stages (60, 200, 400, and 600 g) as the only calcium source in bone metabolism....  相似文献   
997.
BackgroundAtrial electrical and structural remodelling in older individuals with cardiovascular risk factors has been associated with changes in surface electrocardiographic (ECG) parameters (e.g., prolongation of the PR interval) and higher risks of atrial fibrillation (AF). However, it has been difficult to establish whether altered ECG parameters are the cause or a consequence of the myocardial substrate leading to AF. This study aimed to examine the potential causal relevance of ECG parameters on risk of AF using mendelian randomisation (MR).Methods and findingsWeighted genetic scores explaining lifelong differences in P-wave duration, PR interval, and QT interval were constructed, and associations between these ECG scores and risk of AF were estimated among 278,792 UK Biobank participants (mean age: 57 years at recruitment; 19,132 AF cases). The independent genetic variants contributing to each of the separate ECG scores, and their corresponding weights, were based on published genome-wide association studies. In UK Biobank, genetic scores representing a 5 ms longer P-wave duration or PR interval were significantly associated with lower risks of AF (odds ratio [OR] 0.91; 95% confidence interval [CI]: 0.87–0.96, P = 2 × 10−4 and OR 0.94; 95% CI: 0.93–0.96, P = 2 × 10−19, respectively), while longer QT interval was not significantly associated with AF. These effects were independently replicated among a further 17,931 AF cases from the AFGen Consortium. Investigation of potential mechanistic pathways showed that differences in ECG parameters associated with specific ion channel genes had effects on risk of AF consistent with the overall scores, while the overall scores were not associated with changes in left atrial size. Limitations of the study included the inherent assumptions of MR, restriction to individuals of European ancestry, and possible restriction of results to the normal ECG ranges represented in UK Biobank.ConclusionsIn UK Biobank, we observed evidence suggesting a causal relationship between lifelong differences in ECG parameters (particularly PR interval) that reflect longer atrial conduction times and a lower risk of AF. These findings, which appear to be independent of atrial size and concomitant cardiovascular comorbidity, support the relevance of varying mechanisms underpinning AF and indicate that more individualised treatment strategies warrant consideration.

In a Mendelian randomization analysis, Parag Gajendragadkar and colleagues investigate associations between genetically-predicted EEG parameters and risk of atrial fibrillation among UK Biobank participants.  相似文献   
998.

We recently became aware of panel duplications in Supplementary Figures S6 and S7, due to pasting errors of similar flow cytometry images during figure preparation. This concerned the first two panels in the top row of Suppl. Fig S6A; second and third panel in the bottom row of Suppl. Fig S7B; and third and fourth panel in the bottom row of Suppl. Fig S7C.Furthermore, we noted a typographical error in Suppl. Fig S7B (top row, sixth plot), where the indicated percentage was wrongly given as 1.4%, instead of 1.1%. These errors did not change the results or the interpretation of the data. We deeply apologize to the scientific community for any confusion these errors may have caused. The updated appendix is published with this corrigendum.The original FlowJo analysis plots related to the affected figures are published as source data with this corrigendum. Please note that initial labelling of the experiments in these files referred to the official gene name Obfc2b informally as hSSB1, and Obfc2a‐shRNAs as ‘sh1’ and sh4’.Open in a separate windowFigure S6AOriginalOpen in a separate windowFigure S6ACorrectedOpen in a separate windowFigure S7BOriginalOpen in a separate windowFigure S7BCorrectedOpen in a separate windowFigure S7COriginalOpen in a separate windowFigure S7CCorrected  相似文献   
999.
1000.
Summary A simple method for separation of carbonic anhydrase activity into components by electrophoresis on cellulose acetate strips is described. With this method, using barbiturate buffer systems at various pH values, two main components of CAH in rat erythrocytes, and the splitting of each of these into two minor components were revealed. Two components were also observed in the CAH activity in kidney and lens homogenates, and one component in brain homogenate. A modification of Häusler's histochemical method for CAH was adapted for visualization of the electrophoretically separated bands. This rendered the evalution of the results easier than with the quantitative measurements alone. The quantitative measurement of CAH activity in electrophoretic strips corresponded with the degree of staining by the histochemical method. This among other facts supports the view of the specificity of the histochemical method used. Some examples of the histochemical staining pattern of the CAH activity in rat tissues are given.  相似文献   
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