Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “coding change”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,657 records · Page 92Linked to original sources
PubMed1985

Combination insulin/glyburide therapy in type II diabetes mellitus. Effects on lipoprotein metabolism and glucoregulation.

A randomized double-blind, placebo-controlled trial of insulin plus glyburide was carried out in 22 insulin-treated patients with poorly controlled type II diabetes mellitus. Glycemic control and lipoprotein responses were assessed for 16 weeks. Oral glucose tolerance testing was performed at weeks 0, 4, and 16. Clinical characteristics and glycemic control were similar at week 0 in the placebo/insulin group (n = 12) and the glyburide/insulin group (n = 10). Throughout the study, the dose of insulin was fixed. The placebo group had no change in any metabolic parameter throughout the protocol period. After four weeks, glyburide significantly lowered fasting blood glucose and integrated glucose areas (p less than 0.01) after oral glucose testing compared with week 0 (fasting blood glucose 225 +/- 20 mg/dl versus 286 +/- 27 mg/dl, p less than 0.02). Associated with this were mean fasting, stimulated, and integrated C-peptide levels that were significantly higher (p less than 0.02) at week 4 versus week 0. After 16 weeks, mean fasting blood glucose remained significantly lower compared with baseline values (252 +/- 25 mg/dl versus 286 +/- 27 mg/dl, p less than 0.05). Glycosylated hemoglobin (hemoglobin A1c) levels decreased significantly (p less than 0.05) at weeks 4 to 16 compared with the baseline value. Although integrated areas were no different after oral glucose, fasting and stimulated C-peptide levels were significantly higher (p less than 0.05) at week 16 versus week 0. Total cholesterol, triglycerides, low-density lipoprotein cholesterol, very-low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol did not change during the study. After the code was broken, comparisons were made between those with response to combination therapy (reduction of fasting blood glucose by at least 50 mg/dl or fasting blood glucose of 140 mg/dl or less at the end of the first week of treatment that persisted for four consecutive weeks) and those without response. Baseline clinical and laboratory characteristics were identical in both groups. Mean fasting and stimulated serum C-peptide levels after oral glucose, however, were significantly higher in the patients with response at week 4 compared with the patients without response. The mean maximal incremental C-peptide level was 1.50 +/- 0.19 ng/ml at week 0 in the patients with response compared with 0.67 +/- 0.28 ng/ml in the patients without response (p less than 0.01). Lipoproteins were not different in the two groups.(ABSTRACT TRUNCATED AT 400 WORDS)

Blood Glucose↗
PubMed1996

Accelerated evolution of crotalinae snake venom gland serine proteases.

Eight cDNAs encoding serine proteases isolated from Trimeresurus flavoviridis (habu snake) and T. gramineus (green habu snake) venom gland cDNA libraries showed that nonsynonymous nucleotide substitutions have accumulated in the mature protein-coding regions to cause amino acid changes. Southern blot analysis of T. flavoviridis genomic DNAs using two proper probes indicated that venom gland serine protease genes form a multigene family in the genome. These observations suggest that venom gland serine proteases have diversified their amino acid sequences in an accelerating manner. Since a similar feature has been previously discovered in crotalinae snake venom gland phospholipase A2 (PLA2) isozyme genes, accelerated evolution appears to be universal in plural isozyme families of crotalinae snake venom gland.

Amino Acid Sequence↗
PubMed2001

Identification of a mutation causing increased expression of the tas gene in Escherichia coli FX-11.

Studies of N-ethyl-N-nitrosourea (ENU)-induced mutagenesis with a tyrosine auxotroph of Escherichia coli revealed a new type of revertant. This mutant strain was interesting because: (i) it was not a true revertant of the nonsense (ochre) defect nor a tRNA suppressor mutation; and (ii) it was induced by ENU to greater extent in a UmuC-defective host. Genetic mapping located the probable mutation to a region of the E. coli chromosome containing a newly described gene called tas. To investigate this mutation, the upstream region of the tas gene from both wild-type and mutant cells was cloned into a promoterless lacZ expression vector and recombined onto a lambda bacteriophage. Recombinant bacteriophage were inserted into the bacterial chromosome and beta-galactosidase (betaGal) assays were performed. These assays revealed an almost three-fold greater expression of betaGal from the mutant DNA than from the wild-type DNA. Sequence analysis of the region directly upstream of the tas gene revealed a G:C to A:T transition at base number 2263 (numbering based on GenBank Accession #AE000367), located within a potential promoter site. Further sequencing indicated no other mutations within the 1454bp region analyzed; however, there were several nucleotide differences seen in our B/r strain of E. coli, when compared with the published E. coli K-12 sequence. A total of 10 base differences were discovered; one in mutH, six within a potential open reading frame (ORF-o237) and three in non-coding regions. Yet, none of the changes altered the predicted amino acid sequences. These results provide evidence of a mechanism for increased expression of the novel gene tas and support the neutral drift hypothesis for the evolution of DNA sequences.

Amino Acid Sequence↗
PubMed2002

Detection of intrasaccadic displacements and depth rotations of moving objects.

In a display with a stationary and a moving object, subjects saccaded towards one of the objects and had to detect intrasaccadic changes in position or orientation of either the saccade target or the saccade flanker. Compared to performance for stationary objects, displacement detection for translating objects was better and unaffected by saccadic status of the changed object. This pattern proved to be specific to position changes in translating objects and did not generalize to other types of motion (i.e., rotation) or to other types of intrasaccadic changes (i.e., orientation shifts). Superior transsaccadic coding of the position of a translating object was also observed in control experiments with only a single object present on each trial. Possible accounts in terms of selective attention to moving objects and perceptual relevance of object position are pitted against the data, suggesting qualitative differences in the transsaccadic representation of translating and stationary objects.

Depth Perception↗
PubMed2001

KO's and organisation of peptidergic feeding behavior mechanisms.

Feeding behavior results from complex interactions arising between numerous neuromediators, including classical neurotransmitters and neuropeptides present in hypothalamic networks. One way to unravel these complex mechanisms is to examine animal models with a deletion of genes coding for the different neuropeptides involved in the regulation of feeding. The aim of this review is to focus on feeding and body weight regulation in mice lacking neuropeptide Y (NPY), melanocortins (POMC), corticotropin-releasing hormone, melanin-concentrating hormone, or bombesin-like peptides respectively. The phenotypes, which relate to the deletion of gene coding for the peptides, rarely include changes in body weight and food intake, indicating therefore the existence of redundant mechanisms to compensate for the loss of the peptide. The phenotype is much more marked when the gene deletion is targeted towards the functioning of the peptidergic machinery, e.g. the receptors and especially the POMC and NPY receptors, as well as one subtype of bombesin receptor (BRS-3). These knockout models are also interesting when examining the role of environmental and social factors in the determination of feeding behavior. They have granted us better knowledge of all these integrated and complex mechanisms. Moreover, they are also valuable tools for pharmacological studies when specific antagonists are lacking. From the information obtained by the study of knockouts, it is possible to determine certain targets for selective drugs that could be efficient for the pharmacological treatment of obesity. However, at the present state of our knowledge, it seems necessary to target several peptides in order to get good results with weight loss. It will also be imperative to associate these multitherapies with changes in eating and behavioral habits, in order to obtain complete effectiveness and long-lasting results.

Animals↗
PubMed1994

The nature and prognostic implications of autoimmune hepatitis with an acute presentation.

To determine the nature and prognostic implications of autoimmune hepatitis with an acute presentation, 12 patients with a disease duration of 3 months or less (mean duration, 2.3 +/- 0.2 months) were compared to 14 patients with a disease duration of 12 months or more (mean duration, 15.1 +/- 0.9 months). Liver tissue specimens were graded under code for lobular, portal and architectural changes. Patients with acute and chronic presentations were indistinguishable by age, sex, human leukocyte antigen phenotype, immunoserologic markers, and biochemical indices of liver inflammation. Moderate to severe lobular hepatitis was present more frequently in patients with acute presentations (75% versus 29%, p = 0.2), but differences were not statistically significant. Bridging fibrosis and cirrhosis were seen with equal frequency in both groups (79% versus 73%). Remission, relapse, treatment failure, progression to cirrhosis, and death from hepatic failure occurred with similar frequencies in patients with acute and chronic presentations. We conclude that autoimmune hepatitis with an acute presentation is indistinguishable by clinical and laboratory features from that with a chronic presentation and it is probably a pre-existent subclinical disease that is unmasked by disease progression or an abrupt exacerbation. Lobular hepatitis is an important histologic feature regardless of disease duration. The response to corticosteroid therapy is unaffected by the perceived duration of disease prior to treatment.

Acute Disease↗
PubMed2001

Up-regulation of D3 dopaminergic receptor mRNA in the core of the nucleus accumbens accompanies the development of seizures in a genetic model of absence-epilepsy in the rat.

The basal ganglia system is thought to play a key role in the control of absence-seizures and there is ample evidence that epileptic seizures modify brain dopamine function. We recently reported that local injections of dopamine D1 or D2 agonists in the core of the nucleus accumbens suppressed absence-seizures in a spontaneous, genetic rodent model of absence-epilepsy whereas injections of D1 or D2 antagonists had aggravating effects. These findings raised the possibility that the dopaminergic system may be altered in absence-epilepsy prone rats. Therefore, we studied by in situ hybridization histochemistry the expression of pre- and postsynaptic components of the dopaminergic system in this strain of rats. When compared to non-epileptic control rats, epileptic rats displayed no change in the expression of mRNAs coding for the neuronal dopaminergic markers (tyrosine hydroxylase, membraneous and vesicular dopamine transporters). In addition, there was no difference between the two strains concerning the expression of the dopamine receptor transcripts D1, D2 and D5. In adult absence-epilepsy prone rat with an overt epileptic phenotype, however, an elevated level of D3 mRNA expression was observed in neurons of the core of the nucleus accumbens (+23% increase in silver grain density compared to non-epileptic control rats). D3 transcripts were not increased in juvenile epileptic rats without seizures. These findings suggests that up-regulation of D3 receptor mRNA is part of the epileptic phenotype in absence-epilepsy prone rats. Its localization in the core of the nucleus accumbens bears close resemblance to the dopamine-sensitive antiepileptic sites in ventral striatum and further support the involvement of ventral structures of the basal ganglia system in the control of absence-seizures.

Animals↗
PubMed1998

EMG fatigue patterns accompanying isometric fatiguing knee-extensions are different in mono- and bi-articular muscles.

OBJECTIVES AND METHODS: Isometric, fatiguing knee-extensions at 30%, 50% and 70% maximum voluntary contraction (MVC) were performed by 18 healthy human subjects. Surface electromyographic (SEMG) activity was recorded from the mono-articular vastus medialis (VM) and vastus lateralis (VL) muscles, and the bi-articular rectus femoris muscle (RF). To make the bi-articular muscle work under (1) constant and (2) similar working conditions as the two mono-articulars do, the hip was fixed in a flexed position. The root mean square (RMS) SEMG recorded during fatigue was standardized to the respective values of MVC. The mean coefficients of regression of the RMS and median frequency (MF) changes were then analyzed by multivariate analysis of variance. RESULTS: The load effect upon the muscle fatigue changes, as measured by increase in RMS EMG, differed between the bi-articular muscle and the two mono-articulars, in that the parameter dropped with maximum load for the bi-articular, whilst it remained stable or even increased for the mono-articulars. This might suggest that the mono- and bi-articular muscles have different roles in fatigue tasks where the bi-articulars function purely as mono-articulars. By contrast, such a clear dichotomy between the bi-articular RF and the two mono-articulars, VM and VL, was lacking for the fatigue parameter of MF. CONCLUSIONS: As these findings were confined to the changes in RMS EMG, different neuronal coding mechanisms for the mono- and bi-articular muscles in the central nervous system may be inferred.

Adult↗
PubMed2002

Arthropod Hox genes: insights on the evolutionary forces that shape gene functions.

Comparative studies suggest that gene duplication, changes in cis-regulatory elements and changes in protein sequence all contribute to the evolution of Hox gene functions, but the evolutionary dynamics of these changes are probably different. It seems likely that gene duplications arise as neutral changes and acquire an adaptive significance later on. By contrast, some changes in regulatory and protein-coding sequences can have immediate consequences in morphological evolution.

Animals↗
PubMed2002

Mutations of the neuronal nicotinic acetylcholine receptors and their association with ADNFLE.

Elucidating the origin of epileptic seizures represents one of the many ways by which today's scientists are approaching this devastating neurological disorder. Although epilepsies have several different origins ranging from head trauma to genetically transmissible affections, common neuronal network dysfunction can be recognised between these many forms of the disease. Thus, understanding the basic mechanisms underlying some genetically transmissible epilepsies should bring new and important knowledge that is readily applicable to other types of epilepsies. In this work we review our current knowledge of one genetically transmissible form of nocturnal epilepsy, the ADNFLE. In the light of the most recent findings obtained on five mutants of the neuronal nicotinic acetylcholine receptors associated with ADNFLE, we discuss the effects of these spontaneous genome alterations on the receptor function. The only common trait identified so far between these mutant receptors is an increase in acetylcholine sensitivity. Based on our understanding of the receptor distribution in the different brain areas, their development and the neuronal network circuitry, we hypothesise that increased acetylcholine sensitivity causes an unbalance in the fine tuning of the cortico-reticular thalamic and thalamo-cortical loops. In addition, we illustrate how spontaneous mutations in the gene coding for a receptor provoke a change in its pharmacological profile and thereby might account for the inter-individual therapeutic sensitivity.

Epilepsy, Frontal Lobe↗
PubMedDate not supplied

Identification of isobutyryl-CoA dehydrogenase and its deficiency in humans.

The acyl-CoA dehydrogenases (ACDs) are a family of related enzymes that catalyze the alpha,beta-dehydrogenation of acyl-CoA esters. Two homologues active in branched chain amino acid metabolism have previously been identified. We have used expression in Escherichia coli to produce a previously uncharacterized ACD-like sequence (ACAD8) and define its substrate specificity. Purified recombinant enzyme had a k(cat)/K(m) of 0.8, 0.23, and 0.04 (microM(-1)s(-1)) with isobutyryl-CoA, (S) 2-methylbutyryl-CoA, and n-propionyl-CoA, respectively, as substrates. Thus, this enzyme is an isobutyryl-CoA dehydrogenase. A single patient has previously been described whose fibroblasts exhibit a specific deficit in the oxidation of valine. Amplified ACAD8 cDNA made from patient fibroblast mRNA was homozygous for a single nucleotide change (905G>A) in the ACAD8 coding region compared to the sequence from control cells. This encodes an Arg302Gln substitution in the full-length protein (position 280 in the mature protein), a position predicted by molecular modeling to be important in subunit interactions. The mutant enzyme was stable but inactive when expressed in E. coli. It was also stable and appropriately targeted to mitochondria, but inactive when expressed in mammalian cells. These data confirm further the presence of a separated ACD in humans specific to valine catabolism (isobutyryl-CoA dehydrogenase, IBDH), along with the first enzymatic and molecular confirmation of a deficiency of this enzyme in a patient.

Amino Acid Metabolism, Inborn Errors↗
PubMedDate not supplied

Historical roots and future perspectives related to nursing ethics.

This article traces the evolution of the development and the refinement of the professional code from concerns about the ethical conduct of nurses to its present state as a professional code for all nurses. The importance and the relationship of the Ethics Committee of the American Nurses' Association (ANA) to the development of the code and other ANA programs and structural units is also presented. The recognized need for a code of ethics to establish nursing as a profession has been present throughout the evolution of the professional nursing organization. A distinction between ethical conduct of nurses and a code of ethics for professional nurses has been made by nursing leaders. The code has been refined to reflect nursing's changing relationship to society and the societal concerns of the times.

American Nurses' Association↗
PubMed2006

Recognition of proteins by crystallization patterns in an array of reporter solution microdroplets.

A new technique is described for specific recognition of protein analytes by observing protein-induced changes in the drying/crystallization patterns (DCP) of an array of microdroplets containing solutions of different reporter substances. Recognition is based on a difference in interaction of the protein analyte crystalline elements (planes, edges, defects, etc.) in the growing reporter crystals. Using a set of natural L-amino acids as reporters and denoting the amino acid solutions displaying substantial protein-induced changes in the DCP as "1" and those that show no or small changes as "0", a digital binary code was determined for several proteins at multiple concentrations. It was demonstrated that globular proteins can be reliably identified using this code as a "signature" when only 2-100 ng of protein was added to amino acid microdroplets.

Aerosols↗
PubMed2002

A single-base deletion in soybean flavonoid 3'-hydroxylase gene is associated with gray pubescence color.

The T locus of soybean (Glycine max (L.) Merr.) controls pubescence and seed coat color and is presumed to encode flavonoid 3'-hydroxylase (F3'H). The dominant T and the recessive t allele of the locus produce brown and gray pubescence, respectively. PCR primers were constructed based on the sequence of a soybean EST clone homologous to the F3'H gene. A putative full-length cDNA, sf3'h1 was isolated by 3' and 5' RACE. Sequence analysis revealed that sf3'h1 consists of 1690 nucleotides encoding 513 amino acids. It had 68% and 66% homology with corresponding F3'H protein sequences of petunia and Arabidopsis, respectively. A conserved amino acid sequence of F3'H proteins, GGEK, was found in the deduced polypeptide. Sequence analysis of the gene from a pair of near-isogenic lines for T, To7B (TT, brown) and To7G (tt, gray) revealed that they differed by a single C deletion in the coding region of To7G. The deletion changed the subsequent reading frame resulting in a truncated polypeptide lacking the GGEK consensus sequence and the heme-binding domain. Genomic Southern analysis probed by sf3'h1 revealed restriction fragment length polymorphisms between cultivars with different pubescence color. Further, sf3'h1 was mapped at the same position with T locus on LG3(c2). PCR-RFLP analysis was performed to detect the single-base deletion. To7B and three cultivars with brown pubescence exhibited shorter fragments, while To7G and three cultivars with gray pubescence had longer fragments due to the single-base deletion. The PCR-RFLP marker co-segregated with genotypes at the T locus in a F2 population segregating for the T locus. The above results strongly suggest that sJ3'h1 represents the T gene of soybean responsible for pubescence color and that the single-base deletion may be responsible for gray pubescence color.

Alleles↗
PubMed2006

Intramuscular electrical stimulation of facial muscles in humans and chimpanzees: Duchenne revisited and extended.

The pioneering work of Duchenne (1862/1990) was replicated in humans using intramuscular electrical stimulation and extended to another species (Pan troglodytes: chimpanzees) to facilitate comparative facial expression research. Intramuscular electrical stimulation, in contrast to the original surface stimulation, offers the opportunity to activate individual muscles as opposed to groups of muscles. In humans, stimulation resulted in appearance changes in line with Facial Action Coding System (FACS) action units (AUs), and chimpanzee facial musculature displayed functional similarity to human facial musculature. The present results provide objective identification of the muscle substrate of human and chimpanzee facial expressions- data that will be useful in providing a common language to compare the units of human and chimpanzee facial expression.

Action Potentials↗
PubMed2006

A state space analysis of emotion and flexibility in parent-child interactions.

Negative emotion has been shown to reduce flexibility in cognition and behavior. We examined interpersonal flexibility during negative emotional episodes within parent-child interactions. Fifty-five mothers and early-adolescent daughters were observed during a positive discussion, a negative (conflict) discussion, and another positive discussion. Codes of moment-to-moment changes in emotion expression were used to create state space grids from which measures of emotional valence and flexibility were derived. As expected, mean flexibility was lowest during the conflict discussion when negative emotion peaked, suggesting that interpersonal flexibility decreases with increasing negative emotion. Sub-groups identified as low or high in stress were also compared. Dyads with girls reporting more stressful events showed lower flexibility during the first positive discussion. However, dyads expressing more negative emotion during the conflict discussion were also more flexible, suggesting that flexible dyadic styles permit more negative emotion. These individual difference findings are discussed in terms of the suppression versus expression of negative emotions.

Adult↗
PubMed2002

Superficial NK1-expressing neurons control spinal excitability through activation of descending pathways.

The increase in pain sensitivity that follows injury is regulated by superficially located projection neurons in the dorsal horn of the spinal cord that express the neurokinin-1 (NK1) receptor. After selective ablation of these neurons in rats, we identified changes in receptive field size, mechanical and thermal coding and central sensitization of deeper dorsal horn neurons that are important for both pain sensations and reflexes. We were able to reproduce these changes by pharmacological block of descending serotonergic facilitatory pathways. Using Fos histochemistry, we found changes in the activation of serotonergic neurons in the brainstem as well as evidence for a loss of descending control of spinal excitability. We conclude that NK1-positive spinal projection neurons, activated by primary afferent input, project to higher brain areas that control spinal excitability--and therefore pain sensitivity--primarily through descending pathways from the brainstem.

Animals↗
PubMed1998

Comparison of reliability of manual and computer-intensive methods for radiodensity measures of alveolar bone loss.

OBJECTIVE: To compare the reliability of radiodensity measurements made from dental radiographs with manual and a novel computer-intensive methods. METHODS: As part of a prospective study of postmenopausal women, a series of seven vertical bitewing radiographs were taken of 36 patients. One of each set of radiographs was repeated. The original and the corresponding duplicate radiographs were used in this study. Radiographs were digitized at 50 microns spatial resolution and 12-bit gray-scale resolution. For the Manual Method, original and duplicate radiographs were manually cropped to improve image homology, histogram matched and mean pixel gray-scale values determined for an alveolar bone ROI within each image. For the computer-intensive method, images were put into registration with ANALYZE software (Mayo Foundation, Rochester, MINN, USA), cropped automatically, histogram matched and color-coded on the basis of the per cent difference. Alveolar bone ROIs adjacent to clinical crowns and root surfaces whose color code indicated less than a 5% change were sampled. Method error (ME) and the coefficient of variation of method error (CVME) were calculated. RESULTS: With the Manual Method the SD between original and duplicate measures was 95.21 out of 4096 gray scale values; ME = 67.32; CVME = 3.78%. For the computer-intensive method, the corresponding values were 54.74, 38.71, and 2.29%. CONCLUSIONS: The new computer-intensive method resulted in a 40% improvement over the Manual Method in the precision of radiodensity measurements.

Absorptiometry, Photon↗