Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “instability”

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 505 records · Page 28Linked to original sources
PubMed2002

Prewavy instability of nematic liquid crystals in a high-frequency electric field.

A kind of electrohydrodynamic instability, the prewavy instability, in nematic liquid crystals is reported. The characteristic of the instability was optically investigated and discussed in comparison with some similar instabilities. Obviously the instability partially shows an isotropic feature around the nematic-isotropic transition temperature. Owing to the characteristic properties of the flow and the spatial periodicity, it should be distinguished from a previously proposed isotropic instability.

Journal Article↗
PubMed2003

Instability of convection in a fluid layer rotating about an oblique axis.

We analyze thermal convection in a fluid layer confined between isothermal horizontal boundaries at which the tangential component of the fluid stress vanishes. The layer rotates about an oblique, nearly vertical axis. Using a model set of equations for w, the horizontal planform of the vertical velocity component, and psi, a stream function related to a large-scale vertical vorticity field, we describe the instabilities of convection rolls. We show how the usual Küppers-Lortz instability, which leads to a continual precession of the roll pattern, can be suppressed by the oblique rotation vector. Of particular interest is the small-angle instability of rolls, to perturbations in the form of rolls that are almost aligned with the primary rolls; at finite Prandtl number, this instability is not prevented by the horizontal component of the rotation vector, unless this component is sufficiently strong, in which case stability is confined to small-amplitude rolls near the marginal stability boundary. A one-dimensional instability leading to amplitude-modulated rolls is unaffected by the oblique rotation. Numerical simulations of the model equations are presented, which illustrate the instabilities analyzed.

Journal Article↗
PubMed2003

Transverse instabilities in chemical Turing patterns of stripes.

We present a theoretical and experimental study of the sideband instabilities in Turing patterns of stripes. We compare numerical computations of the Brusselator model with experiments in a chlorine dioxide-iodine-malonic acid (CDIMA) reaction in a thin gel layer reactor in contact with a continuously refreshed reservoir of reagents. Spontaneously evolving Turing structures in both systems typically exhibit many defects that break the symmetry of the pattern. Therefore, the study of sideband instabilities requires a method of forcing perfect, spatially periodic Turing patterns with the desired wave number. This is easily achieved in numerical simulations. In experiments, the photosensitivity of the CDIMA reaction permits control and modulation of Turing structures by periodic spatial illumination with a wave number outside the stability region. When a too big wave number is imposed on the pattern, the Eckhaus instability may arise, while for too small wave numbers an instability sets in forming zigzags. By means of the amplitude equation formalism we show that, close to the hexagon-stripe transitions, these sideband instabilities may be preceded by an amplitude instability that grows transient spots locally before reconnecting with stripes. This prediction is tested in both the reaction-diffusion model and the experiment.

Journal Article↗
PubMed2004

Linear instability of magnetic Taylor-Couette flow with Hall effect.

The influence of the Hall effect on the linear marginal stability of a molecular hydrodynamic Taylor-Couette flow in the presence of an axial uniform magnetic field is considered. The Hall effect leads to the situation that the Taylor-Couette flow becomes unstable for any ratio of the angular velocities of the inner and outer cylinders. The instability, however, does not exist for both signs of the axial magnetic field B0. For positive shear dOmega/dR the Hall instability exists for negative Hartmann number and for negative shear dOmega/dR the Hall instability exists for positive Hartmann number. For negative shear, of course, the Hall instability combines with the magnetorotational instability, resulting in a rather complex bifurcation diagram. In this case the critical magnetic Reynolds numbers with Hall effect are much lower than without Hall effect. In order to verify the presented shear-Hall instability at the laboratory with experiments using liquid metals, one would need rather large magnetic fields ( approximately 10(7) G).

Journal Article↗
PubMed2006

Vortex core dynamics and singularity formations in incompressible Richtmyer-Meshkov instability.

Motion of a fluid interface in Richtmyer-Meshkov instability is examined as a vortex sheet with the use of Birkhoff-Rott equation. This equation coupled with an evolution equation of the strength of the vortex sheet can describe all inviscid and incompressible fluid instabilities, i.e., Kelvin-Helmholtz, Rayleigh-Taylor, and Richtmyer-Meshkov instabilities, when Atwood numbers and initial distribution of vorticities are given. With these equations, detailed motion of a vortex core in the Richtmyer-Meshkov instability is investigated. For the Kelvin-Helmholtz and Rayleigh-Taylor instabilities, it is known that the curvature of a vortex sheet diverges at a finite time t=tc. This fact indicates that the solution loses its analyticity at tc. We show that the singularity formation also occurs in the Richtmyer-Meshkov instability and at the same time, accumulation of vorticity to some points where singularities are formed develops to the roll-up of a sheet when the sheet is regularized. We investigate motion of these accumulation points, i.e., vortex cores, and present that their trajectories and the strengths depend on the Atwood numbers.

Journal Article↗
PubMed2006

Hydromagnetic instability in differentially rotating flows.

We study the stability of compressible differentially rotating flows in the presence of the magnetic field, and we show that the compressibility profoundly alters the previous results for a magnetized incompressible flow. The necessary condition of newly found instability can be easily satisfied in various flows in laboratory and astrophysical conditions and reads BsBphiOmega' not equal to 0, where Bs and Bphi are the radial and azimuthal components of the magnetic field, Omega' = d Omega/ds with s being the cylindrical radius. Contrary to the well-known magnetorotational instability that occurs only if omega decreases with s, the instability considered in this paper may occur at any sign of Omega'. The instability can operate even in a very strong magnetic field that entirely suppresses the standard magnetorotational instability. The growth time of instability can be as short as a few rotation periods.

Journal Article↗
PubMed2006

Shock-wave mach-reflection slip-stream instability: a secondary small-scale turbulent mixing phenomenon.

Theoretical and experimental research, on the previously unresolved instability occurring along the slip stream of a shock-wave Mach reflection, is presented. Growth rates of the large-scale Kelvin-Helmholtz shear flow instability are used to model the evolution of the slip-stream instability in ideal gas, thus indicating secondary small-scale growth of the Kelvin-Helmholtz instability as the cause for the slip-stream thickening. The model is validated through experiments measuring the instability growth rates for a range of Mach numbers and reflection wedge angles. Good agreement is found for Reynolds numbers of Re 2 x 10(4). This work demonstrates, for the first time, the use of large-scale models of the Kelvin-Helmholtz instability in modeling secondary turbulent mixing in hydrodynamic flows, a methodology which could be further implemented in many important secondary mixing processes.

Journal Article↗
PubMed2006

Rayleigh-Plateau and Gregory-Laflamme instabilities of black strings.

Many and very general arguments indicate that the event horizon behaves as a stretched membrane. We explore this analogy by associating the Gregory-Laflamme instability of black strings with a classical membrane instability known as the Rayleigh-Plateau instability. We show that the key features of the black string instability can be reproduced using this viewpoint. In particular, we get good agreement for the threshold mode in all dimensions and exact agreement for large spacetime dimensionality. The instability time scale is also well described within this model, as well as the dimensionality dependence. It also predicts that general nonaxisymmetric perturbations are stable. We further argue that the instability of ultraspinning black holes follows from this model.

Journal Article↗
PubMed1995

Microsatellite instability and other molecular abnormalities in human prostate cancer.

Microsatellites are highly polymorphic, short-tandem repeat sequences dispersed throughout the genome. Instability of these repeat sequences at multiple genetic loci may result from mismatch repair errors, and occurs in hereditary nonpolyposis colorectal carcinoma and certain sporadic cancers. To examine microsatellite instability during the pathogenesis of human prostate cancer, we screened 48 prostate cancer cases (20 stage B, 10 stage C and 18 endocrine therapy-resistant cancer-death cases) for replication error at 17 microsatellite marker loci on 9 chromosomes. Microsatellite instabilities were found in 7 of 48 cases (14.6%), and all 7 cases showing the instability were poorly differentiated adenocarcinomas. Moreover, microsatellite instabilities were more frequently observed in cancer-death cases (6/18, 33%) than in stage B + C cases (1/30, 3.3%). These data suggest that microsatellite instability is an important genetic change related to the progression of a subset of human prostate cancer cases. It is suggested to be associated with extensive, concurrent molecular changes including androgen receptor gene mutations, as well as frequent loss of heterozygosity at chromosomal regions 8p, 10q, and 16q.

Adenocarcinoma↗
PubMed1991

Urodynamic study of ileocystoplasty in the treatment of idiopathic detrusor instability.

Enterocystoplasty is being used with increasing frequency in the treatment of patients with idiopathic detrusor instability. We have performed a prospective clinical and urodynamic study of this procedure in 11 patients using both conventional (CMG) and ambulatory monitoring techniques (AM). Nine of 11 patients were satisfied with the symptomatic outcome, but 7 relied on clean intermittent self-catheterisation (CISC) to achieve a good result. Urodynamic studies demonstrated a significant increase in residual urine volume from 48 +/- 72 ml before to 347 +/- 298 ml after operation, but there was only a small and statistically insignificant increase in cystometric capacity. Detrusor instability, present before operation in all patients, could still be demonstrated in over half of them after operation. However, a significant decrease in the severity of instability was found after operation as assessed by an increased volume at first unstable contraction. The bladder volume before operation at which the first unstable contraction occurred was smaller in those who still had persistent instability after enterocystoplasty compared with those in whom instability could not be identified after operation. These results suggest that all patients about to undergo ileocystoplasty should be trained in the use of CISC. In selected patients with idiopathic detrusor instability refractory to other treatment, this procedure can yield satisfactory results.

Adult↗
PubMed1992

Detrusor mast cells in refractory idiopathic instability.

The diagnosis of interstitial cystitis (IC) is not usually considered in patients with idiopathic instability. Because histamine provokes detrusor contractions in vitro, we assessed detrusor mast cell counts in 29 females with refractory instability. Raised mast cell counts (greater than 28/mm2 of detrusor muscle, consistent with a histological diagnosis of IC) were found in 29% of such cases. Thus cystoscopy and bladder biopsy should be considered in patients with idiopathic instability which fails to respond to anticholinergic drugs, as alternative therapy may be useful. Patients with refractory instability and normal detrusor mast cell counts often gave a history of prolonged childhood nocturnal enuresis (55% of cases); in contrast, patients with intractable instability and abnormally high mast cell counts seldom gave such a history (12%). These trends may give some insight into the aetiology of idiopathic instability--"congenital" or acquired?

Adult↗
PubMed1988

Detrusor instability following colposuspension for urinary stress incontinence.

Sixty-two patients with genuine stress incontinence (group A) and 30 women with combined detrusor instability and genuine stress incontinence (group B) had a colposuspension operation. The proportion with symptoms of detrusor instability was significantly reduced from 24% before operation to 9% after operation in group A and from 73% to 33% in group B. Urodynamically, detrusor instability developed after surgery in 17 of the 62 patients (27%) in group A whereas only 12 of the 30 women (40%) in group B had detrusor instability after surgery. No urodynamic explanation was found to explain the effect of colposuspension in relieving the symptoms of detrusor instability in some and causing them in others. Nevertheless, it is suggested that colposuspension is helpful for most patients with combined detrusor instability and genuine stress incontinence.

Adult↗
PubMed1998

Microsatellite instability in human hepatocellular carcinoma: relationship to p53 abnormalities.

AIMS/BACKGROUND: Microsatellite instability was sought in 10 human hepatocellular carcinomas (HCCs) to determine whether defective DNA mismatch repair might be implicated in the multiple genetic alterations observed in the p53 tumor suppressor gene in some of these patients' tumors. METHODS: Genomic DNA from HCCs and adjacent nontumorous livers was subjected to PCR with primers for nine microsatellites, and PCR products were resolved in a denaturing gel. Microsatellite instability was defined as the presence of band shifts or additional bands for at least two microsatellite sequences in an HCC compared to the nontumorous liver tissue from the same patient. RESULTS: Microsatellite instability was detected in four of ten HCCs. Three of these four HCCs did not have p53 exon mutations. However, one HCC had microsatellite instability as well as multiple p53 exon mutations and multiple intron alterations. Four other patients with multiple p53 intron alterations in HCC (compared to their own nontumorous liver), three of whom also had a mutation in the exons, had no microsatellite instability. CONCLUSIONS: Defective DNA mismatch repair, as indicated by microsatellite instability, might have played a role in hepatocarcinogenesis in four of the ten patients, but in general it was not associated with p53 alterations. In one of the ten patients, defective DNA mismatch repair might have been the cause of multiple mutations in both the coding and intron sequences of the p53 gene.

Adolescent↗
PubMed2003

Up-regulation of alpha1B-adrenergic receptors with defects in G protein coupling: ligand-induced protection from receptor instability.

The biochemical basis for the unexpected agonist-induced up-regulation of the number of radioligand binding sites for two mutated alpha1B-adrenergic receptors reported previously was investigated. Up-regulation was independent of the expression vector used and was not prevented by cycloheximide or actinomycin D, eliminating several potential transcriptional mechanisms and new receptor protein synthesis. Antagonists were also able to induce up-regulation, suggesting that ligand occupancy without signal generation was sufficient to induce the increase in binding sites. Accordingly, we hypothesized that up-regulation results from ligand-induced protection from inherent instability of these mutated receptors. Studies with receptors in isolated membranes revealed that the two mutated receptors that exhibited up-regulation in intact cells also exhibited an inherent instability of their ligand binding capacity, and binding of either agonists or antagonists to these receptors could protect against the loss of binding. In contrast, the wild-type receptor and other mutated receptors that did not exhibit up-regulation in intact cells did not exhibit instability or ligand-induced protection in isolated membranes. The occurrence of instability and protection in isolated membranes for only those mutated receptors and ligands that exhibit up-regulation in intact cells provides compelling evidence that the apparent up-regulation of binding sites in intact cells results from ligand-induced protection from an inherent instability of these G protein coupling-defective receptors. Inclusion of protease inhibitors markedly reduced the loss of binding in isolated membranes, implicating membrane-localized proteolysis as the likely mechanism for the instability.

Adrenergic alpha-Agonists↗
PubMed2002

Involvement of RAD9-dependent damage checkpoint control in arrest of cell cycle, induction of cell death, and chromosome instability caused by defects in origin recognition complex in Saccharomyces cerevisiae.

Perturbation of origin firing in chromosome replication is a possible cause of spontaneous chromosome instability in multireplicon organisms. Here, we show that chromosomal abnormalities, including aneuploidy and chromosome rearrangement, were significantly increased in yeast diploid cells with defects in the origin recognition complex. The cell cycle of orc1-4/orc1-4 temperature-sensitive mutant was arrested at the G2/M boundary, after several rounds of cell division at the restrictive temperature. However, prolonged incubation of the mutant cells at 37 degrees C led to abrogation of G2 arrest, and simultaneously the cells started to lose viability. A sharp increase in chromosome instability followed the abrogation of G2 arrest. In orc1-4/orc1-4 rad9delta/rad9delta diploid cells grown at 37 degrees C, G2 arrest and induction of cell death were suppressed, while chromosome instability was synergistically augmented. These findings indicated that DNA lesions caused by a defect in Orc1p function trigger the RAD9-dependent checkpoint control, which ensures genomic integrity either by stopping the cell cycle progress until lesion repair, or by inducing cell death when the lesion is not properly repaired. At semirestrictive temperatures, orc2-1/orc2-1 diploid cells demonstrated G2 arrest and loss of cell viability, both of which require RAD9-dependent checkpoint control. However, chromosome instability was not induced in orc2-1/orc2-1 cells, even in the absence of the checkpoint control. These data suggest that once cells lose the damage checkpoint control, perturbation of origin firing can be tolerated by the cells. Furthermore, although a reduction in origin-firing capacity does not necessarily initiate chromosome instability, the Orc1p possesses a unique function, the loss of which induces instability in the chromosome.

Cell Cycle↗
PubMed2001

High-copy-number expression of Sub2p, a member of the RNA helicase superfamily, suppresses hpr1-mediated genomic instability.

We report on a novel role for a pre-mRNA splicing component in genome stability. The Hpr1 protein, a component of an RNA polymerase II complex and required for transcription elongation, is also required for genome stability. Deletion of HPR1 results in a 1,000-fold increase in genome instability, detected as direct-repeat instability. This instability can be suppressed by the high-copy-number SUB2 gene, which is the Saccharomyces cerevisiae homologue of the human splicing factor hUAP56. Although SUB2 is essential, conditional alleles grown at the permissive temperature complement the essential function of SUB2 yet reveal nonessential phenotypes. These studies have uncovered a role for SUB2 in preventing genome instability. The genomic instability observed in sub2 mutants can be suppressed by high-copy-number HPR1. A deletion mutant of CDC73, a component of a PolII complex, is also unstable for direct repeats. This too is suppressed by high-copy-number SUB2. Thus, defects in both the transcriptional machinery and the pre-mRNA splicing machinery can be sources of genome instability. The ability of a pre-mRNA splicing factor to suppress the hyperrecombination phenotype of a defective PolII complex raises the possibility of integrating transcription, RNA processing, and genome stability or a second role for SUB2.

Adenosine Triphosphatases↗
PubMed2003

Dynamic force distribution during level walking under the feet of patients with chronic ankle instability.

OBJECTIVES: To examine changes in the pattern of force transfer between the foot and the floor associated with chronically sprained ankles by measuring the peak forces and their timing under several regions of the feet during level walking. METHODS: Twelve young male subjects (mean (SD) age 21 (2) years) with recurrent ankle sprains were studied. Seven of them had unilateral and bilateral chronic instability and laxity, and five had bilateral instability. Twelve healthy men (without orthopaedic or medical disease) served as a control group. Subjects walked at their own pace along a 7 m walkway, which included a Mini-EMED pressure distribution measuring system. The variables measured were relative peak force (fraction of body weight) and relative timing (fraction of stance time). These variables were measured under six regions of interest in each foot print: heel, midfoot, medial, central, and lateral forefoot, and toes. RESULTS: (a) A significant delay to the time of peak force under the central and lateral forefoot and toes in subjects with chronic ankle instability. (b) A significant decrease in the relative forces under the heel and toes and an increase in the relative forces under the midfoot and lateral forefoot in subjects with chronic ankle instability. (c) In the patients with unilateral instability, there were no significant differences in any of the variables between the injured and non-injured foot. CONCLUSIONS: In patients with chronic ankle instability, there is a slowing down of weight transfer from heel strike to toe off, a reduced impact at the beginning and end of the stance phase, and a lateral shift of body weight.

Adult↗
PubMed1998

Allelic imbalance and microsatellite instability of the DCC gene in colorectal cancer in patients under the age of 35 using fluorescent DNA technology.

AIM: To assess allelic imbalance and microsatellite instability in the region of the "deleted in colorectal cancer" (DCC) gene on chromosome 18q using fluorescent DNA technology in colorectal cancer in patients under the age of 35. METHODS: Thirty two cases of colorectal cancer in patients under the age of 35 and with no family history of colon cancer were retrieved. DNA was extracted by standard methods, polymerase chain reaction (PCR) was performed using Cy5 labelled primers to microsatellite markers (D18S21, D18S34, and D18S58) in the DCC gene. The results were analysed using software attached to an automated DNA sequencer. RESULTS: The patients ranged in age from 17 to 35 years. Nineteen were women, all had left sided tumours (tumours distal to the splenic flexure). Twenty eight cases were either stage C or D (using the Astler Coller system). The informativity of the three markers were as follows: D18S21, 25 of 32 (78.1%); D18S34, 18 of 32 (56.25%); D18S58, 24 of 32 (75%). Allelic imbalance for the markers, after excluding homozygous and microsatellite instability cases, was: D18S21, 31.8%; D18S34, 11.7%; and D18S58, 0%. Nine cases showed allelic imbalance for both D18S21 and D18S34, yielding a combined allelic imbalance frequency of 39.1%. Ten cases showed microsatellite instability in at least one marker, with microsatellite instability seen most commonly for D18S58. Three cases showed microsatellite instability for all three markers. CONCLUSIONS: Approximately 39% of cases showed allelic imbalance for D18S21 and D18S34 markers, while microsatellite instability was found in 31.25% of cases. This figure is higher than that encountered in sporadic colorectal cancer over the age of 50, suggesting a role for the DNA repair genes in the pathogenesis of these cancers occurring under the age of 35.

Adolescent↗