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排序方式: 共有112条查询结果,搜索用时 156 毫秒
51.
Nitric oxide may be the final mediator of nonadrenergic, noncholinergic inhibitory junction potentials in the gut. 总被引:10,自引:0,他引:10
F Christinck J Jury F Cayabyab E E Daniel 《Canadian journal of physiology and pharmacology》1991,69(10):1448-1458
This study tested the hypothesis that the final mediator of nonadrenergic, noncholinergic (NANC) inhibitory junction potentials (ijps) and associated relaxation responses was nitric oxide (NO) or a related substance and not vasoactive intestinal polypeptide (VIP). We used opossum esophagus body circular muscle and canine intestine circular muscle. In both these tissues, ijps had reversal potentials near the potassium equilibrium potential, (EK); in esophagus the ijps were apamin insensitive, but in the intestine they were partially apamin sensitive. N omega-Nitro-L-arginine methyl ester (NAME) (10(-5) to 5 x 10(-4) M) abolished ijps in both tissues, an effect overcome by 10(-3) M L-arginine but not D-arginine. NAME increased input resistance of esophagus tissues in the double sucrose gap but caused no significant depolarization in the sucrose gap or in studies with microelectrodes. Contractions and basal tension were increased in both tissues by NAME. The apamin sensitive and insensitive ijp components in canine muscle were both abolished by NAME, but the time course of this abolition was different for the two components. Methylene blue (10-50 microM) with variable rapidity and extent inhibited ijps in both tissues, but L-arginine could not overcome this effect. Methylene blue, like NAME, did not depolarize detectably but enhanced the contractile activity. VIP (10(-6) M) had very small effects in both tissues, little or no hyperpolarization and increased input resistance in esophagus, these effects were not changed by NAME, and VIP did not affect ijps. We conclude that NO may be the final mediator of NANC-initiated inhibitory junction potentials in gastrointestinal circular smooth muscle. 相似文献
52.
53.
Vera Dugina Antonina Alexandrova Christine Chaponnier Jury Vasiliev Giulio Gabbiani 《Experimental cell research》1998,238(2):481
In vivo,α-smooth muscle actin (SMA) is expressedde novoand temporarily by fibroblastic cells during wound healing and correlates particularly with wound contraction. In culture, the presence of varying proportions of cells expressing and not expressing this actin isoform (α-SMA-positive and α-SMA-negative cells) is characteristic of fibroblastic populations from different tissues. It is possible that mechanisms controlling the expression of actin isoforms, and thus modulating cytoskeleton-related functions, play a major role in the organization of cell shape and motility. We have compared the cell shape as well as the cytoskeleton and focal contact organization in α-SMA-positive and α-SMA-negative rat fibroblasts from various organs (i.e., skeletal muscle, dermis, subcutaneous tissue, and lung). Within each category, i.e., α-SMA-positive or α-SMA-negative fibroblasts, no significant morphological differences were seen among populations derived from different tissues. In contrast, α-SMA-positive and α-SMA-negative fibroblasts were significantly different, independently of their origin: α-SMA-positive cells had larger average areas, higher numbers of narrow extensions at the edges, larger focal adhesions with the substratum, and a more important network of cellular fibronectin than α-SMA-negative cells. Thus, α-SMA-positive and α-SMA-negative variants naturally present in fibroblastic populations exhibit important phenotypic differences probably associated with distinct functional activities. 相似文献
54.
Unusual potassium channels mediate nonadrenergic noncholinergic nerve-mediated inhibition in opossum esophagus 总被引:7,自引:0,他引:7
Field stimulation of the circular muscle of the opossum esophagus produces a transient hyperpolarization (inhibitory junction potential, IJP) followed by an "off" depolarization. A similar nonadrenergic, noncholinergic (NANC) response in guinea pig taenia caecum has been shown to be due to an increase in the potassium ion permeability of the smooth muscle cell membrane. Double sucrose gap studies showed a decrease in resistance during the IJP, and a reversal at an estimated membrane potential of about -90 mV (4 mM K+). The reversal potential was dependent on the extracellular potassium concentration, shifting to -75 mV when the potassium in the superfusion medium was increased to 10 mM. The IJP in the opossum esophageal circular smooth muscle is therefore like the IJP of the guinea pig taenia caecum in that it is probably due to a selective increase in potassium ion permeability. Potassium conductance blocking agents, tetraethylammonium chloride (TEA, 20 mM) and 4-aminopyridine (4-AP, 5 mM) both caused a depolarization of the smooth muscle cell membrane, but TEA increased the membrane resistance, whereas 4-AP did not affect the membrane conductance in a consistent way. A decrease in IJP amplitude owing to these agents was not apparent. Apamin (10 microM) did not affect the membrane potential, the membrane resistance, or the IJP. Quinine (0.1 mM) produced effects quantitatively similar to those of TEA. Quinine (1 mM) did abolish the IJP, however, this was likely due to a blockade of impulse transmission of the intramural nerves.(ABSTRACT TRUNCATED AT 250 WORDS) 相似文献
55.
An attempt is made to compare the conditions for the general error-optimality of linear systems developed by Kalman with the
conditions for feasibility of linear models of neuromuscular and physiological control systems. Models of three actual physiological
systems are tested for both the above criteria. Theoretical analysis presented here shows that there are no simple relationships
between the two sets of conditions. Analysis carried out on the physiological systems models suggests the need for a general
set of conditions for other optimality criteria, such as time and energy minimization, similar to Kalman's condition for error
minimization. 相似文献
56.
Sites and mechanisms of action of neuropeptides on canine gastric motility differ in vivo and in vitro 总被引:5,自引:0,他引:5
Motilin, pentagastrin and substance P (SP), injected intra-arterially into the canine gastric corpus in vivo increased the amplitude of contractions by an action dependent on activation of cholinergic nerves; i.e. atropine or tetrodotoxin (TTX) completely blocked the responses to motilin and pentagastrin and increased the ED50 of SP. TTX and atropine were not equally effective in increasing the ED50 for SP in vivo and the effect of combining them depended on the order of their addition. Both were much more effective than the SP analog D-Pro2, D-Trp7,9 SP (DSP) which appeared to be a weak antagonist of actions dependent on neural activity. In strips from the same region in vitro no receptors dependent on cholinergic nerve activation could be demonstrated for any peptide; i.e., all were atropine- and TTX-insensitive. Motilin, as expected in the absence of such receptors caused no contractile response in vitro. SP, also as predicted, caused contractions suggesting that a smooth muscle receptor, independent of nerve activation was present. However contrary to expectation pentagastrin induced an atropine and TTX-insensitive increase in the amplitude and frequency of contractions. These results show that 1) the most sensitive sites of action of a number of excitatory peptides depend on cholinergic nerve function in vivo; 2) such sites or the nerve activity on which they depend cannot be demonstrated in vitro; 3) SP has an additional site of action on smooth muscle demonstrable in vivo and in vitro, but motilin does not; 4) pentagastrin has only an action dependent on nerve function in vivo, but manifests an action independent of nerve function in vitro. We conclude that sites and mechanisms of action of peptides cannot be assumed to be identical in vivo and in vitro. Actions dependent on nerves are often lost in vitro and not all smooth muscle actions can be demonstrated in vivo. 相似文献
57.
Turki Abujamel Jennifer L. Cadnum Lucy A. Jury Venkata C. K. Sunkesula Sirisha Kundrapu Robin L. Jump Alain C. Stintzi Curtis J. Donskey 《PloS one》2013,8(10)
Background
Clostridium difficile is an anaerobic, spore-forming bacterium that is the most common cause of healthcare-associated diarrhea in developed countries. A significant proportion of patients receiving oral vancomycin or metronidazole for treatment of Clostridium difficile infection (CDI) develop recurrences. However, the period of vulnerability to re-establishment of colonization by C. difficile after therapy is not well defined.Principal Findings
In a prospective study of CDI patients, we demonstrated that most vancomycin-treated patients maintained inhibitory concentrations of vancomycin in stool for 4 to 5 days after therapy, whereas metronidazole was only detectable during therapy. From the time of elimination of the antibiotics to 14 to 21 days after therapy, a majority of stool suspensions supported growth of C. difficile and deep 16S rRNA sequencing demonstrated persistent marked alteration of the indigenous microbiota. By 21 to 28 days after completion of CDI treatment, a majority of stool suspensions inhibited growth of C. difficile and there was evidence of some recovery of the microbiota.Conclusions
These data demonstrate that there is a vulnerable period for re-establishment of C. difficile colonization after CDI treatment that begins within a few days after discontinuation of treatment and extends for about 3 weeks in most patients. 相似文献58.
Jane M. M. Natividad Christina L. Hayes Jean-Paul Motta Jennifer Jury Heather J. Galipeau Vivek Philip Clara L. Garcia-Rodenas Hiroshi Kiyama Premysl Bercik Elena F. Verdu 《Applied and environmental microbiology》2013,79(24):7745-7754
The intestinal microbiota is a key determinant of gut homeostasis, which is achieved, in part, through regulation of antimicrobial peptide secretion. The aim of this study was to determine the efficiency by which members of the intestinal microbiota induce the antimicrobial peptide REGIII and to elucidate the underlying pathways. We showed that germfree mice have low levels of REGIII-γ in their ileum and colon compared to mice with different intestinal microbiota backgrounds. Colonization with a microbiota of low diversity (altered Schaedler flora) did not induce the expression of REGIII-γ as effectively as a complex community (specific pathogen free). Monocolonization with the probiotic Bifidobacterium breve, but not with the nonprobiotic commensal Escherichia coli JM83, upregulated REGIII-γ expression. Induction of REGIII-γ by B. breve was abrogated in mice lacking MyD88 and Ticam1 signaling. Both live and heat-inactivated B. breve but not spent culture medium from B. breve induced the expression of REGIII-α, the human ortholog and homolog of REGIII-γ, in human colonic epithelial cells (Caco-2). Taken together, the results suggest that REGIII-γ expression in the intestine correlates with the richness of microbiota composition. Also, specific bacteria such as Bifidobacterium breve NCC2950 effectively induce REGIII production in the intestine via the MyD88-Ticam1 pathway. Treatment with this probiotic may enhance the mucosal barrier and protect the host from infection and inflammation. 相似文献
59.
Spartak N. Litvinchuk Glib O. Mazepa Rosa A. Pasynkova Abdusattor Saidov Toszhiddin Satorov Yuriy A. Chikin Dmitriy A. Shabanov Angelica Crottini Leo J. Borkin Jury M. Rosanov Matthias Stöck 《Journal of Zoological Systematics and Evolutionary Research》2011,49(3):233-239
We studied the distribution of Palearctic green toads (Bufo viridis subgroup), an anuran species group with three ploidy levels, inhabiting the Central Asian Amudarya River drainage. Various approaches (one‐way, multivariate, components variance analyses and maximum entropy modelling) were used to estimate the effect of altitude, precipitation, temperature and land vegetation covers on the distribution of toads. It is usually assumed that polyploid species occur in regions with harsher climatic conditions (higher latitudes, elevations, etc.), but for the green toads complex, we revealed a more intricate situation. The diploid species (Bufo shaartusiensis and Bufo turanensis) inhabit the arid lowlands (from 44 to 789 m a.s.l.), while tetraploid Bufo pewzowi were recorded in mountainous regions (340–3492 m a.s.l.) with usually lower temperatures and higher precipitation rates than in the region inhabited by diploid species. The triploid species Bufo baturae was found in the Pamirs (Tajikistan) at the highest altitudes (2503–3859 m a.s.l.) under the harshest climatic conditions. 相似文献
60.
A. C. Povey F. Jury W. M. Dippnall A. E. Smith S. Thomson B. Mackness M. Mackness P. Durrington N. M. Cherry 《Biomarkers》2007,12(2):188-202
Previously we reported that in sheep dippers exposed to organophosphates the frequency of paraoxonase (PON1) polymorphisms differed between those with or without self-reported ill health. We have now examined whether polymorphisms in other genes involved in xenobiotic metabolism alter disease risk in this population. There were elevated but non-significant risks associated with the CYP2D6 WT genotype (odds ratio (OR) 1.47, 95% CI 0.83-2.60), or a GSTP1*B or *C allele (OR 1.37, 95% CI 0.88-2.01) or being GSTM1*2/GSTT1*2 homozygous (OR 1.61, 95% CI 0.74-3.48). Similar results were generally obtained after the exclusion of subjects to obtain a more homogenous case-referent population: for double null GSTM1 and GSTT1 homozygotes the OR was 2.06 (95% CI 0.85-2.04). In those also likely to have been exposed to diazinon, risks associated with a GSTP1*B or *C allele (OR 1.82, 95% CI 0.92-3.63) or a GSTM1*2/GSTT1*2 homozygous (OR 2.60, 95% CI 0.72-10.42) were elevated but not to a significant extent. Risk associated with PON1 genotype and phenotype varied with CYP2D6 and GSTP1 genotype but not consistently with a priori hypotheses. Further work is necessary to delineate more clearly pathways of organophosphate activation and non-PON1 pathways of detoxification and to confirm whether CYP and GST polymorphisms alter disease risk in populations exposed to organophosphates. 相似文献