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71.
Das B Rudra S Yadav A Ray A Rao AV Srinivas AS Soni A Saini S Shukla S Pandya M Bhateja P Malhotra S Mathur T Arora SK Rattan A Mehta A 《Bioorganic & medicinal chemistry letters》2005,15(19):4261-4267
Novel oxazolidinones were synthesized containing a number of substituted five-membered heterocycles attached to the 'piperazinyl-phenyl-oxazolidinone' core of eperezolid. Further, the piperazine ring of the core was replaced by other diamino-heterocycles. These modifications led to several compounds with potent activity against a spectrum of resistant and susceptible gram-positive organisms, along with the identification of ranbezolid (RBx 7644) as a clinical candidate. 相似文献
72.
Short-term zinc deficiency in diet induces increased oxidative stress in testes and epididymis of rats 总被引:5,自引:0,他引:5
Nair N Bedwal S Prasad S Saini MR Bedwal RS 《Indian journal of experimental biology》2005,43(9):786-794
In order to determine the effects of Zinc deficient diet on oxidative stress in testis and epididymis, various parameters viz: total proteins, lipid peroxidation, hydroperoxides, antioxidant capacity and enzymatic activities are evaluated in rats fed on zinc deficient diet for 2, 4 and 6 weeks. Total proteins, water and lipid solouble antioxidant capacity decreased while lipid peroxidation (TBARS) and hydroperoxides concentration increased in testes, caput and cauda epididymis except in 2ZD (testes) where hydroperoxides revealed a significant decrease. GSH decreased in testes and caput and cauda epididymis. GPx and gamma-GT activities increased in testes and caput and cauda epididymis of zinc deficient rats. Further, GST increased in testes but exhibited decreases after 2 and 4 weeks and an increase after 6 weeks in caput and cauda epididymis of zinc deficient rats. GR activities decreased in testes but it increased in caput and cauda epididymis of zinc deficient rats. Thus, zinc deprivation results in increased sensitivity to oxidative stress. All these may have been as a consequence of increased ROS generation and/or decreased zinc dependent antioxidant processes. 相似文献
73.
Saini HK Xu YJ Arneja AS Tappia PS Dhalla NS 《Journal of cellular and molecular medicine》2005,9(4):818-839
The development of atherosclerotic plaque is a highly regulated and complex process which occurs as a result of structural and functional alterations in endothelial cells, smooth muscle cells (SMCs), monocytes/macrophages, T-lymphocytes and platelets. The plaque formation in the coronary arteries or rupture of the plaque in the peripheral vasculature in latter stages of atherosclerosis triggers the onset of acute ischemic events involving myocardium. Although lipid lowering with statins has been established as an important therapy for the treatment of atherosclerosis, partially beneficial effects of statins beyond decreasing lipid levels has shifted the focus to develop newer drugs that can affect directly the process of atherosclerosis. Blockade of renin angiotensin system, augmentation of nitric oxide availability, reduction of Ca(2+) influx, prevention of oxidative stress as well as attenuation of inflammation, platelet activation and SMC proliferation have been recognized as targets for drug treatment to control the development, progression and management of atherosclerosis. A major challenge for future drug development is to formulate a combination therapy affecting different targets to improve the treatment of atherosclerosis. 相似文献
74.
Ranta H Oksanen A Hokkanen T Bondestam K Heino S 《International journal of biometeorology》2005,49(3):146-151
Masting, the intermittent production of large crops of flowers by a plant population, is a common feature among trees in boreal and temperate forests. The pollen of many broadleaved trees causes allergic diseases, which are major causes of increasing health-care costs in industrialised countries. As the prevalence and severity of allergic diseases are connected with the concentrations of airborne pollen, an universal model predicting the intensity of the coming flowering would be a valuable tool for pollen information services, and ultimately for allergic people and allergologists. We investigated whether a resource budget model created in Japan explains the fluctuations in the annual pollen sums of Betula-species in north European data sets (10–12 years at 4 sites, 20 years at 10 sites). Using the shorter data sets, the model explained 76–92% of the annual fluctuations at five study sites. Using the 20-year data set, the percentage for southern Finland was much lower, only 48%, compared with the 85% of the 12-year data set. The annual pollen sums have been higher during the 1990s than in the 1980s, which may explain the ineffectiveness of the model, while applied to the 20-year data set. Our results support the resource budget model: the masting of birch species is regulated by weather factors together with the system of resource allocation among years. The model can serve pollen information service. However, only the 10 most recent years should be used to avoid interference from trends in changing vegetation and/or climate. 相似文献
75.
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77.
Saini S Koirala S Floess E Mears PJ Chemla YR Golding I Aldridge C Aldridge PD Rao CV 《Journal of bacteriology》2010,192(24):6477-6481
FliZ is an activator of class 2 flagellar gene expression in Salmonella enterica. To understand its role in flagellar assembly, we investigated how FliZ affects gene expression dynamics. We demonstrate that FliZ participates in a positive-feedback loop that induces a kinetic switch in class 2 gene expression. 相似文献
78.
Saini HK Dhalla NS 《American journal of physiology. Heart and circulatory physiology》2006,291(6):H2790-H2800
Although the Na(+)/H(+) exchanger (NHE) is considered to be involved in regulation of intracellular Ca(2+) concentration ([Ca(2+)](i)) through the Na(+)/Ca(2+) exchanger, the exact mechanisms of its participation in Ca(2+) handling by cardiomyocytes are not fully understood. Isolated rat cardiomyocytes were treated with or without agents that are known to modify Ca(2+) movements in cardiomyocytes and exposed to an NHE inhibitor, 5-(N-methyl-N-isobutyl)amiloride (MIA). [Ca(2+)](i) in cardiomyocytes was measured spectrofluorometrically with fura 2-AM in the absence or presence of KCl, a depolarizing agent. MIA increased basal [Ca(2+)](i) and augmented the KCl-induced increase in [Ca(2+)](i) in a concentration-dependent manner. The MIA-induced increase in basal [Ca(2+)](i) was unaffected by extracellular Ca(2+), antagonists of the sarcolemmal (SL) L-type Ca(2+) channel, and inhibitors of the SL Na(+)/Ca(2+) exchanger, SL Ca(2+) pump ATPase and mitochondrial Ca(2+) uptake. However, the MIA-induced increase in basal [Ca(2+)](i) was attenuated by inhibitors of SL Na(+)-K(+)-ATPase and sarcoplasmic reticulum (SR) Ca(2+) transport. On the other hand, the MIA-mediated augmentation of the KCl response was dependent on extracellular Ca(2+) concentration and attenuated by agents that inhibit SL L-type Ca(2+) channels, the SL Na(+)/Ca(2+) exchanger, SL Na(+)-K(+)-ATPase, and SR Ca(2+) release channels and the SR Ca(2+) pump. However, the effect of MIA on the KCl-induced increase in [Ca(2+)](i) remained unaffected by treatment with inhibitors of SL Ca(2+) pump ATPase and mitochondrial Ca(2+) uptake. MIA and a decrease in extracellular pH lowered intracellular pH and increased basal [Ca(2+)](i), whereas a decrease in extracellular pH, in contrast to MIA, depressed the KCl-induced increase in [Ca(2+)](i) in cardiomyocytes. These results suggest that NHE may be involved in regulation of [Ca(2+)](i) and that MIA-induced increases in basal [Ca(2+)](i), as well as augmentation of the KCl-induced increase in [Ca(2+)](i), in cardiomyocytes are regulated differentially. 相似文献
79.
Muscle damage with a lack of regeneration, manifests itself in several life-threatening diseases, including cancer cachexia, congestive heart failure, AIDS and sepsis. Often misdiagnosed as a condition simply of weight loss, cachexia is actually a highly complex metabolic disorder involving features of anorexia, anaemia, lipolysis and insulin resistance. A significant loss of lean body mass arises from such conditions, resulting in wasting of skeletal muscle. Unlike starvation, the weight loss seen in chronic illnesses arises equally from loss of muscle and of fat. The cachectic state is particularly problematic in cancer, typifying poor prognosis and often lowering responses to chemotherapy and radiation treatment. More than half of cancer patients suffer from cachexia, and strikingly, nearly one-third of cancer deaths are related to cachexia rather than the tumour burden. In considering this disorder, we are faced with a conundrum; how is it possible for uncontrolled growth to prevail in the tumour, in the face of unrestrained tissue loss in our muscles? Consistently, the catabolic state has been associated with a shift in the homeostatic balance between muscle synthesis and degradation mediated by the actions of growth factors and cytokines. Indeed, tumour necrosis factor-alpha (TNF-alpha) levels are raised in several animal models of cachectic muscle wasting, whereas the insulin-like growth factor (IGF) system acts potently to regulate muscle development, hypertrophy and maintenance. This concept of skeletal muscle homeostasis, often viewed as the net balance between two separate processes of protein synthesis and degradation has however changed. More recently, the view is that these two biochemical processes are not occurring independently of each other but in fact are finely co-ordinated by a web of intricate signalling networks. This review, therefore, aims to discuss data currently available regarding the mechanisms of degeneration and regeneration with specific emphasis on the potential and controversial cross-talk which may exist between anabolic growth factors (e.g. IGF-I) and catabolic cytokines (e.g. TNF-alpha). Also importantly, the potential impact at a cellular level of exercise, diet and age will be addressed. Finally, the ability to 'hi-jack' signalling pathways traditionally believed to be for growth and survival or death will be reviewed. It is anticipated that such a review will highlight significant gaps in our knowledge of the cachectic state as well as provide caution with regards to therapeutics suggesting total block on inflammatory processes such as that associated with TNF-alpha action. 相似文献
80.
M. Kumar O. P. Luthra V. Chawla L. Chaudhary N. Saini A. Poonia R. Kumar A. P. Singh 《Biologia Plantarum》2006,50(4):755-758
A set of 104 wheat recombinant inbred lines (RILs) obtained from a cross between parents resistant (HD 29) and susceptible
(WH 542) to karnal bunt (KB) (caused by Neovossia indica) were screened and used to identify random amplified polymorphic DNA (RAPD) markers linked with resistance to karnal bunt
as these would allow indirect marker assisted selection of KB resistant genotypes. The two parents were analysed with 92 RAPD
primers. A total of 65 primers proved functional by giving scorable polymerase chain reaction (PCR) products. Of these, 21
(32 %) primers detected polymorphism between the two parental genotypes. Using these primers, bulked segregant analysis was
carried out on two bulk DNAs, one obtained by pooling DNA from 10 KB resistant RILs and the other similarly derived by pooling
10 KB susceptible RILs. One marker, OPM-20 showed apparent association with resistance to KB. This was confirmed following
selective genotyping of individual RILs included in the bulks. 相似文献