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101.
J L McGuire P H Brookes R F McConnell D W Hahn J P DaVanzo S A Solomon G D Turner 《Theriogenology》1975,3(1):1-13
The concentrations of plasma estrogens, progesterone, and corticosteroids and of urinary pregnanediol, pregnanetriol, ketogenic steroids, and corticosteroids were determined as indicators of ovarian and adrenal function throughout a normal sow's estrous cycle. Two broad peaks of plasma estrogen, one lasting 11–12 days during estrus and another 6-day peak period during the early part of the luteal phase were detected. Plasma progesterone was elevated during the late follicular and luteal phase. Two broad peaks of plasma corticoids appeared, one following the decrease of plasma progesterone and the second 7–14 days later. Those elevations in plasma corticoids occurred when estrogen titres were elevated. Urinary determinations generally reflected plasma findings. Estrogen levels began to rise during the follicular phase while a reasonably high progesterone level was evident. Estrogen titres never decreased to non-detectable levels. An interrelationship between adrenal function and ovarian estrogen production is suggested. 相似文献
102.
103.
Studies on the role of actin's N tau-methylhistidine using oligodeoxynucleotide-directed site-specific mutagenesis 总被引:3,自引:0,他引:3
The primary structure of all actins except that isolated from Naegleria gruberi contains a unique N tau-methylhistidine (MeHis) at position 73. This modified residue has been implicated as possibly being important for the post-translational processing of actin's amino terminus, the binding of actin to DNase I, and in the polymerization of G-actin. We have investigated the potential role of MeHis in each of these processes by utilizing site-directed mutagenesis to change His-73 of skeletal muscle actin to Arg and Tyr. Wild type and mutant actins were synthesized in vivo, using non-muscle cells transfected with mutant cDNAs, and in vitro by translating mutant RNAs synthesized using SP6 RNA polymerase in a rabbit reticulocyte lysate. We have found that actins containing Arg or Tyr at position 73 undergo amino-terminal processing, bind to DNase I-agarose, and become incorporated into the cytoskeleton of a nonmuscle cell as efficiently as wild type actin. Furthermore, using an in vitro copolymerization assay we have found that although there is no difference between the Arg mutant and the wild type actins, the Tyr mutant has a slightly greater critical concentration for polymerization. These results show that MeHis is not absolutely required for any of these processes. 相似文献
104.
Pei Dong Jessica Flores Kristine Pelton Keith R. Solomon 《Journal of cellular biochemistry》2010,111(5):1367-1374
Cholesterol is essential in establishing most functional animal cell membranes; cells cannot grow or proliferate in the absence of sufficient cholesterol. Consequently, almost every cell, tissue, and animal tightly regulates cholesterol homeostasis, including complex mechanisms of synthesis, transport, uptake, and disposition of cholesterol molecules. We hypothesize that cellular recognition of cholesterol insufficiency causes cell cycle arrest in order to avoid a catastrophic failure in membrane synthesis. Here, we demonstrate using unbiased proteomics and standard biochemistry that cholesterol insufficiency causes upregulation of prohibitin, an inhibitor of cell cycle progression, through activation of a cholesterol‐responsive promoter element. We also demonstrate that prohibitin protects cells from apoptosis caused by cholesterol insufficiency. This is the first study tying cholesterol homeostasis to a specific cell cycle regulator that inhibits apoptosis. J. Cell. Biochem. 111: 1367–1374, 2010. © 2010 Wiley‐Liss, Inc. 相似文献
105.
The output of individual neurons is dependent on both synaptic and intrinsic membrane properties. While it is clear that the response of an individual neuron can be facilitated or inhibited based on the summation of its constituent synaptic inputs, it is not clear whether subthreshold activity, (e.g. synaptic “noise”- fluctuations that do not change the mean membrane potential) also serve a function in the control of neuronal output. Here we studied this by making whole-cell patch-clamp recordings from 29 mouse thalamocortical relay (TC) neurons. For each neuron we measured neuronal gain in response to either injection of current noise, or activation of the metabotropic glutamate receptor-mediated cortical feedback network (synaptic noise). As expected, injection of current noise via the recording pipette induces shifts in neuronal gain that are dependent on the amplitude of current noise, such that larger shifts in gain are observed in response to larger amplitude noise injections. Importantly we show that shifts in neuronal gain are also dependent on the intrinsic sensitivity of the neuron tested, such that the gain of intrinsically sensitive neurons is attenuated divisively in response to current noise, while the gain of insensitive neurons is facilitated multiplicatively by injection of current noise- effectively normalizing the output of the dLGN as a whole. In contrast, when the cortical feedback network was activated, only multiplicative gain changes were observed. These network activation-dependent changes were associated with reductions in the slow afterhyperpolarization (sAHP), and were mediated at least in part, by T-type calcium channels. Together, this suggests that TC neurons have the machinery necessary to compute multiple output solutions to a given set of stimuli depending on the current level of network stimulation. 相似文献
106.
107.
Gobinath M. Subramanian N. Alagarsamy V. Nivedhitha S. Solomon Viswas Raja 《Russian Journal of Bioorganic Chemistry》2020,46(3):403-408
Russian Journal of Bioorganic Chemistry - Some new 1-substituted-4-(4-nitrophenyl)-[1,2,4]triazolo[4,3-a]quinazolin-5(4H)-ones were synthesized and screened for their H1-antihistaminic activity.... 相似文献
108.
Sean A. Parks Carlos Carroll Solomon Z. Dobrowski Brady W. Allred 《Global Change Biology》2020,26(5):2944-2955
Climate connectivity, the ability of a landscape to promote or hinder the movement of organisms in response to a changing climate, is contingent on multiple factors including the distance organisms need to move to track suitable climate over time (i.e. climate velocity) and the resistance they experience along such routes. An additional consideration which has received less attention is that human land uses increase resistance to movement or alter movement routes and thus influence climate connectivity. Here we evaluate the influence of human land uses on climate connectivity across North America by comparing two climate connectivity scenarios, one considering climate change in isolation and the other considering climate change and human land uses. In doing so, we introduce a novel metric of climate connectivity, ‘human exposure’, that quantifies the cumulative exposure to human activities that organisms may encounter as they shift their ranges in response to climate change. We also delineate potential movement routes and evaluate whether the protected area network supports movement corridors better than non‐protected lands. We found that when incorporating human land uses, climate connectivity decreased; climate velocity increased on average by 0.3 km/year and cumulative climatic resistance increased for ~83% of the continent. Moreover, ~96% of movement routes in North America must contend with human land uses to some degree. In the scenario that evaluated climate change in isolation, we found that protected areas do not support climate corridors at a higher rate than non‐protected lands across North America. However, variability is evident, as many ecoregions contain protected areas that exhibit both more and less representation of climate corridors compared to non‐protected lands. Overall, our study indicates that previous evaluations of climate connectivity underestimate climate change exposure because they do not account for human impacts. 相似文献
109.
Adipo(cyto)kines are mostly produced by adipose tissue and orchestrate the adverse
impact of excess adiposity on cardiovascular risk. Adipokines also contribute
importantly to the pathophysiology of rheumatoid arthritis. Congruent with data
reported in previous investigations, Kang and colleagues report in this issue of
Arthritis Research & Therapy that adipokine concentrations are
further associated with metabolic risk and inflammation and that the
leptin–adiponectin ratio associates with the carotid artery resistive index in
rheumatoid arthritis. Guided by evidence reported thus far on cardiovascular risk, we
discuss six reasons why careful elucidation of adipokine–cardiovascular risk
relations is needed in rheumatoid arthritis.In this issue of Arthritis Research & Therapy, Kang and colleagues
investigate whether adipokines could link inflammation, metabolic risk factors and
cardiovascular disease in rheumatoid arthritis (RA) [1]. Evidence in support of this paradigm was reported previously [2-6]. Patients with RA experience a markedly increased cardiovascular risk that is
driven by metabolic risk factors and by high-grade inflammation [7]. Kang and colleagues measured adiponectin, leptin, resistin, tumor necrosis
factor alpha and interleukin-6 concentrations and assessed the common carotid artery
intima-media thickness, resistive index (RI) and plaque presence by high-resolution
ultrasonography [1]. Concentrations of some of the adipokines related to inflammatory markers
including C-reactive protein levels and the erythrocyte sedimentation rate, and to
metabolic syndrome features.In a previous study by our group, leptin and adiponectin concentrations were not
associated with carotid intima-media thickness and plaque [3]. In addition, the leptin–adiponectin ratio and carotid RI as markers of
cardiovascular risk have not been reported in RA. For these reasons, besides the
abovementioned analyses, Kang and colleagues assessed (only) the relationship of the
leptin–adiponectin ratio with carotid RI. In univariate analysis, the
leptin–adiponectin ratio as well as age, homeostasis model assessment for insulin
resistance, waist circumference and body mass index were associated with the carotid RI.
Importantly, in multivariate analysis, only age and the leptin–adiponectin ratio
remained significantly related to the carotid RI. The leptin–adiponectin ratio may
thus provide information about the presence of subclinical cardiovascular disease beyond
that on insulin resistance as assessed by the homeostasis model of insulin resistance,
as well as adiposity extent as represented by body mass index and waist circumference in
RA.Adipo(cyto)kines comprise a vast range of disparate soluble bioactive proteins that are
mostly secreted by adipose tissue [8]. These molecules participate in biological processes that include
inflammatory responses and thereby orchestrate the adverse impact of excess adiposity on
cardiovascular risk and incident type 2 diabetes [8]. Adipokines represent both adiposity extent and biological activity. RA is a
prototypic inflammatory disease. In this context, ~200 recently reported investigations
substantiate an important involvement of adipokines in RA activity and severity [9]. By contrast, despite the contribution of adipokines to altered
cardiovascular risk in non-RA subjects and the enhanced cardiovascular risk in RA, there
is a striking paucity of reported studies on the potential role of adipokines in
atherogenesis in RA.A myriad of pertinent reasons exist why the role of adipokines in cardiovascular risk
amongst patients with RA requires thorough elucidation. First, RA can modify adipokine
production [3,9].Second, and presumably more important, the presence of autoimmunity can alter the
effects of adipokines on cardiovascular risk [3,4]. In non-RA subjects, adiponectin production decreases with increasing
adiposity and this adipokine has anti-inflammatory properties [8]. However, in RA adiponectin has marked proinflammatory properties [9]. In fact, in Kang and colleagues’ study the adiponectin concentrations
were paradoxically positively associated with the erythrocyte sedimentation rate [1]. Whereas in non-RA subjects adiponectin improves metabolic risk and also
directly inhibits atherogenesis, we reported recently that in RA, upon using
comprehensive potential confounder-adjusted analysis, adiponectin concentrations
associated paradoxically with high blood pressure [3,4] and in white but not black Africans with enhanced endothelial activation [4]. Endothelial activation mediates the very initial stages of atherosclerosis [3-6]. Whether such paradoxical relations represent altered effects mediated by RA
or a compensatory increase in adiponectin production in the presence of heightened
cardiovascular risk and in an attempt to reduce this risk needs further investigation [4].Third, conventional risk factors and disease characteristics can impact on
adipokine–atherogenesis relationships in RA [5]. Resistin concentrations thus associate independently with endothelial
activation in RA, but this relation is present only in those with, and not in those
without, traditional risk factors, abdominal obesity, joint damage as reflected by the
presence of deformed joints or prolonged disease duration [5]. This observation further supports the need for sensitivity analysis in the
present context. By contrast, interleukin-6 concentrations are more consistently
associated with endothelial activation in RA [6].Fourth, the effects of adipokines on cardiovascular risk require examination prior to
targeting the respective molecules in an attempt to reduce disease activity and severity
in RA [3]. Indeed, should the protective effect of adiponectin on cardiovascular risk
be preserved amongst patients with RA, then its blockade would be expected to further
enhance cardiovascular risk [3].Fifth, RA influences adiposity and its distribution, which also associates with
atherosclerosis in this disease [7,10].Finally, as illustrated by the disparity in adiponectin–endothelial activation
relations amongst Africans previously alluded to, population origin impacts on
adipokine–cardiovascular risk relations in RA [4].A caveat of Kang and colleagues’ study is that potential confounders were not
systematically identified. For example, gender, cardiovascular drug use, antirheumatic
agent use and the glomerular filtration rate can all influence both the concentrations
and effects of adipokines [3-6]. Nevertheless, this investigation reinforces previously reported evidence
that strongly suggests an intriguing and important involvement of adipokines in RA
atherogenesis. 相似文献
110.
Daniel E. Impoinvil Mong How Ooi Peter J. Diggle Cyril Caminade Mary Jane Cardosa Andrew P. Morse Matthew Baylis Tom Solomon 《PLoS neglected tropical diseases》2013,7(8)