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1.
The effect of neurotensin on submaximally-stimulated hepatobiliary and pancreatic secretion was studied in 6 healthy subjects. An intravenous infusion of neurotensin 1.4 ± 0.3 pmol/kg/min, designed to reproduce plasma neurotensin immunoreactivity levels within the physiological range, produced a significant increase in pancreatic bicarbonate output. Plasma concentrations of pancreatic polypeptide rose by 83 ± 16 pmol/l and were associated with a small reduction in trypsin, but no significant change in bilirubin outputs. 相似文献
2.
Mallela S. P. Sarma Robert S. Klein Brian A. Otter 《Nucleosides, nucleotides & nucleic acids》2013,32(1-3):369-378
Abstract The reactions of the 5-bromo-6-methyl-2′,3′-O-isopropylideneuridines 9 and 10 with a number of nucleophiles in hot DMF have been investigated. With acetate ion as the nucleophile, either the 5-acetoxy- (11,12) or the 6-acetoxymethyl- (15) products can be obtained in modest yield depending upon the exact reaction conditions. With nitrogen nucleophiles (aniline or p-methoxybenzylamine) reaction takes place at the 6-methyl carbon, whereas with sulfur nucleophiles (thiophenol, thioacetate) only the 5-substituted products are obtained. 相似文献
3.
The alkaline transition of cytochrome c is a model for protein structural switching in which the normal heme ligand is replaced by another group. Stopped flow data following a jump to high pH detect two slow kinetic phases, suggesting two rate-limiting structure changes. Results described here indicate that these events are controlled by the same structural unfolding reactions that account for the first two steps in the reversible unfolding pathway of cytochrome c. These and other results show that the cooperative folding-unfolding behavior of protein foldons can account for a variety of functional activities in addition to determining folding pathways. 相似文献
4.
A process-based carbonate budget was used to compare carbonate framework production at two reef sites subject to varying degrees
of fluvial influence in Rio Bueno, Jamaica. The turbid, central embayment was subjected to high rates of fluvial sediment
input, framework accretion was restricted to ≤30 m, and net carbonate production was 1,887 g CaCO3 m−2 year−1. Gross carbonate production (GCP) was dominated by scleractinians (97%), particularly by sediment-resistant species, e.g.
Diploria strigosa on the reef flat (<2 m). Calcareous encrusters contributed very little carbonate. Total bioerosion removed 265 g CaCO3 m−2 year−1 and was dominated by microborers. At the clear-water site, net carbonate production was 1,236 g CaCO3 m−2 year−1; the most productive zone was on the fore-reef (10 m). Corals accounted for 82% of GCP, and encrusting organisms 16%. Bioerosion
removed 126 g CaCO3 m−2 year−1 and was dominated by macroborers. Total fish and urchin grazing was limited throughout (≤20 g CaCO3 m−2 year−1). The study demonstrates that: (1) carbonate production and net reef accretion can occur where environmental conditions approach
or exceed perceived threshold levels for coral survival; and (2) although live coral cover (and carbonate production rates)
were reduced on reef-front sites along the North Jamaican coast, low population densities of grazing fish and echinoids to
some extent offset this, thus maintaining positive carbonate budgets. 相似文献
5.
Singh SM Molas JF Kongari N Bandi S Armstrong GS Winder SJ Mallela KM 《Proteins》2012,80(5):1377-1392
Muscular dystrophy (MD) is the most common genetic lethal disorder in children. Mutations in dystrophin trigger the most common form of MD, Duchenne, and its allelic variant Becker MD. Utrophin is the closest homologue and has been shown to compensate for the loss of dystrophin in human disease animal models. However, the structural and functional similarities and differences between utrophin and dystrophin are less understood. Both proteins interact with actin through their N-terminal actin-binding domain (N-ABD). In this study, we examined the thermodynamic stability and aggregation of utrophin N-ABD and compared with that of dystrophin. Our results show that utrophin N-ABD has spectroscopic properties similar to dystrophin N-ABD. However, utrophin N-ABD has decreased denaturant and thermal stability, unfolds faster, and is correspondingly more susceptible to proteolysis, which might account for its decreased in vivo half-life compared to dystrophin. In addition, utrophin N-ABD aggregates to a lesser extent compared with dystrophin N-ABD, contrary to the general behavior of proteins in which decreased stability enhances protein aggregation. Despite these differences in stability and aggregation, both proteins exhibit deleterious effects of mutations. When utrophin N-ABD mutations analogous in position to the dystrophin disease-causing mutations were generated, they behaved similarly to dystrophin mutants in terms of decreased stability and the formation of cross-β aggregates, indicating a possible role for utrophin mutations in disease mechanisms. 相似文献
6.
Mallela J Perkins R Yang J Pedigo S Rimoldi JM Shariat-Madar Z 《Biochemical and biophysical research communications》2008,374(4):635-640
The renin-angiotensin-system cascade pathway generates the vasopressor and prothrombotic hormones, angiotensin II (Ang II) and angiotensin III (Ang III) from angiotensinogen. One of the key enzymes for the generation of angiotensin 1-7 (Ang 1-7) and angiotensin 2-7 (Ang 2-7) from Ang II and III, respectively, is prolylcarboxypeptidase (PRCP). To understand the contribution of the N-terminal region to catalysis, an N-terminal truncated form, lacking 179 N-terminal residues of PRCP (rPRCP40) was constructed. The circular dichroism (CD) spectrum of rPRCP40 illustrated that it was structured with significant helical content as indicated by local minima at ∼220 and 208 nm. The main products of Ang III metabolized by rPRCP40 were Ang 2-7 plus phenylalanine as determined by LC-MS. Angiotensin I (Ang I) blocked the metabolism of Ang III by rPRCP40. These investigations showed that the C-terminal region of the rPRCP40 contributes to PRCP’s catalytic function, and provided additional experimental evidence for this suggestion. 相似文献
7.
A Puri R Sethi B Singh SK Dwivedi VS Narain RK Saran VK Puri 《Indian pacing and electrophysiology journal》2009,9(3):186-189
A 25-year-old previously asymptomatic pregnant woman at 36 weeks'' gestation was noticed to have repetitive monomorphic ventricular tachycardia. A dilated left ventricle with moderately reduced systolic function was found on echocardiographic examination. This is a very rare presentation of peripartum cardiomyopathy (PPCMP) presenting with repetitive monomorphic ventricular tachycardia. 相似文献
8.
Surinder M. Singh Swati Bandi Dinen D. Shah Geoffrey Armstrong Krishna M. G. Mallela 《PloS one》2014,9(10)
Genetic mutations in a vital muscle protein dystrophin trigger X-linked dilated cardiomyopathy (XLDCM). However, disease mechanisms at the fundamental protein level are not understood. Such molecular knowledge is essential for developing therapies for XLDCM. Our main objective is to understand the effect of disease-causing mutations on the structure and function of dystrophin. This study is on a missense mutation K18N. The K18N mutation occurs in the N-terminal actin binding domain (N-ABD). We created and expressed the wild-type (WT) N-ABD and its K18N mutant, and purified to homogeneity. Reversible folding experiments demonstrated that both mutant and WT did not aggregate upon refolding. Mutation did not affect the protein''s overall secondary structure, as indicated by no changes in circular dichroism of the protein. However, the mutant is thermodynamically less stable than the WT (denaturant melts), and unfolds faster than the WT (stopped-flow kinetics). Despite having global secondary structure similar to that of the WT, mutant showed significant local structural changes at many amino acids when compared with the WT (heteronuclear NMR experiments). These structural changes indicate that the effect of mutation is propagated over long distances in the protein structure. Contrary to these structural and stability changes, the mutant had no significant effect on the actin-binding function as evident from co-sedimentation and depolymerization assays. These results summarize that the K18N mutation decreases thermodynamic stability, accelerates unfolding, perturbs protein structure, but does not affect the function. Therefore, K18N is a stability defect rather than a functional defect. Decrease in stability and increase in unfolding decrease the net population of dystrophin molecules available for function, which might trigger XLDCM. Consistently, XLDCM patients have decreased levels of dystrophin in cardiac muscle. 相似文献
9.
A recently silenced, duplicate PgiC locus in Clarkia 总被引:1,自引:0,他引:1
Previous electrophoretic analysis showed that 17 diploid species of the
wildflower Clarkia (Onagraceae) have two cytosolic isozymes of
phosphoglucose isomerase (PGIC; EC 5.3.1.9), whereas 15 other diploid
species have a single PGIC. Molecular studies revealed that the two
isozymes in the former species are encoded by duplicate genes, PgiC1 and
PgiC2, whereas the single isozyme in the latter is always encoded by PgiC1.
Phylogenetic analysis of the nucleotide sequences implied that PgiC2 was
silenced four times independently in the genus. Here we describe a psi
PgiC2 from C. mildrediae, a species in which only PgiC1 is expressed. The
discovery of the psi PgiC2 is significant because it confirms a formal
prediction of the phylogenetic analysis. The psi PgiC2 includes 5,039
nucleotides corresponding to 18 of the 23 exons of PgiC, as well as the
intervening introns and 3' nontranslated region. The absence of an increase
of nucleotide substitutions in its "exons" suggests that the gene was
silenced recently. The present study appears to be the first to establish
that a specific duplicate gene locus regularly expressed in a group of
related plant species has been silenced in one of them. The multiple
independent silencings of PgiC2 suggest that it remained functional but
inessential in ancestral lineages. We discuss the possibility that PgiC2
may have been preserved in these lineages by selection against mutants
causing defective PGIC1- PGIC2 heterodimers.
相似文献
10.