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At least 19 recordsLinked to original sources
PubMed1978

Fusion for instability and potential instability of the cervical spine in children and adolescents.

Instability and potential instability of the cervical spine in the child and adolescent not presenting as emergencies may be due to many causes. We have reviewed 30 patients treated surgically over a seven year period and have grouped them under four general headings: isolated congenital anomalies of the cervical spine, postlaminectomy instability, traumatic instability with delayed presentation, and bony or ligamentous inadequacy secondary to miscellaneous conditions. The variety of conditions permits few generalizations. However, an overview of the entire group supports the concept that abnormal motion in an immature spine or the potential for such motion should be viewed cautiously by the orthopedist, for it may herald severe neurologic compromise. When compromise has occurred, the decision to intervene is made easier. Should only increased motion or the potential for such be present, the natural history of the lesion, if available, should be the guide to treatment. If the natural history of a cervical spine lesion is not available and structural integrity is compromised with abnormal motion present, fusion is advised. Appropriate patient counseling as to the lack of an alternative, with the exception of prolonged bracing to avoid the hazards of life, is essential in this group of individuals.

Adolescent↗
PubMed2025

Human Placental Genomic Instability Predicts Adverse Pregnancy Outcomes.

Preeclampsia is a leading cause of pregnancy-related death, accounting for over 50,000 maternal and 500,000 fetal deaths worldwide each year1-4. Preeclampsia has been linked to confined placental mosaicism, which underscores a potential role of placental genomic instability in driving adverse pregnancy outcomes. Here, using bulk RNA sequencing from 59 preeclamptic and 53 normotensive pregnancies, we explored somatic genomic instability and hypoxia with respect to clinical maternal-placental-neonatal outcomes. We found that genomic instability increased the probability of delivering at an earlier gestational age with a diagnosis of preeclampsia, maternal vascular malperfusion placental lesions, and small for gestational age neonates. Notably, genomic instability and hypoxia are predictive biomarkers for all three adverse pregnancy outcomes. In an induced pluripotent stem cell-derived trophoblast stem cell model, we observed increased genomic instability in trophoblast stem cells obtained from placentas demonstrating maternal vascular malperfusion with preeclampsia. Additionally, increased genomic instability correlated with reduced extravillous trophoblast invasion, implicating a functional role for genomic instability. These findings provide promising insights into the underlying mechanisms of genomic instability in the placenta which may be useful biomarkers for early clinical diagnosis of placental injury underlying preeclampsia.

Journal Article↗
PubMed2026

Genomic instability, postoperative recurrence and therapeutic vulnerabilities in resectable non‑small cell lung cancer (Review).

Resectable non‑small cell lung cancer (NSCLC) is managed largely according to anatomical stage, pathological risk and actionable driver alterations, yet these factors do not fully explain postoperative recurrence. Genomic instability may contribute to recurrence by promoting clonal diversification, intratumoral heterogeneity, occult dissemination, persistence of residual tumor cells, and immune escape. In the present review, chromosomal instability (CIN), copy‑number complexity, whole‑genome doubling, DNA repair defects, replication stress, and extrachromosomal DNA (ecDNA) were critically evaluated using a three‑axis translational framework encompassing biological consequences, potential clinical roles, and strength of evidence. Current evidence suggests that clonal diversity and copy‑number complexity have the clearest near‑term prognostic rationale. By contrast, CIN and whole‑genome doubling are supported more strongly by evolutionary and mechanistic rather than prospective clinical evidence. Defects in DNA repair, replication stress, and ecDNA represent potential therapeutic vulnerabilities, but their clinical relevance remains to be established. To date, no treatment‑predictive biomarkers based on genomic instability have been identified for resectable NSCLC. Direct clinical evidence linking any specific genomic instability feature to the presence or longitudinal dynamics of postoperative molecular residual disease (MRD) remains limited. Postoperative circulating tumor DNA‑defined MRD provides prognostic information more directly related to residual disease but remains assay‑dependent and should not be considered a genomic‑instability phenotype. Therefore, features of genomic instability should remain investigational and should not replace established clinical, pathological, or molecular decision‑making. Their near‑term value lies in refining biological risk models and generating testable hypotheses for biomarker‑defined perioperative trials.

Humans↗
PubMed1979

[Gonarthrosis following persisting knee joint instability (author's transl)].

It is frequently assumed that persisting instability of the knee joint leads to gonarthrosis. We have reviewed recent and primary radiograms of 32 patients with old knee trauma resulting in prolonged capsular and ligamentous instability in order to study the eventual development of secondary gonarthrosis. Our results were as follows: All primarily intact joints developed gonarthrosis after an average of 46 months of permanent instability. Primarily existing gonarthrosis increased with exception of 3 cases. The tendency to develop an arthrosis seems to be proportional to the duration of instability; the type of instability apparently has no influence on the development of an instability gonarthrosis. Operative procedures having been performed prior to final stabilysing surgery obviously do not cause the development of secondary gonarthrosis. The persisting instability of the knee joint after combined discontinuation of capsule and ligaments therefore may be regarded as a prearthrotic factor.

Adult↗
PubMed2026

A system-level metastable model of cancer evolution: integrating replication stress, cell cycle deregulation and chromosomal instability.

INTRODUCTION: Cancer cell proliferation occurs within the context of persistent genomic instability. In this review, we propose the RS-CCD-CIN axis as a systems-level framework in which replication stress (RS), cell cycle deregulation (CCD) and chromosomal instability (CIN) form an interdependent triad that shapes tumour evolution. This axis represents a constrained metastable state in which genomic instability is tolerated and buffered. The objective of this review is to synthesize the current understanding of how the RS-CCD-CIN axis contributes to tumour heterogeneity, adaptability and therapy response. DISCUSSION: Evidence indicates that RS, CCD and CIN operate as a dynamic, interconnected network rather than as independent processes. Replication stress induces DNA damage and mutagenesis, while partial checkpoint disruption permits cells with unresolved lesions to proliferate. Chromosomal instability generates both structural and numerical alterations, contributing to intratumoural heterogeneity. Together, these processes facilitate adaptation to environmental and therapeutic pressures. Extrachromosomal DNA, micronuclei formation and cytosolic DNA signalling, including the cGAS-STING pathway, connect genomic instability to adaptive responses and immune modulation. Single-cell and spatial profiling reveal temporal and spatial variability in RS, CCD and CIN states, highlighting the limitations of static biomarkers. Therapeutically, targeting individual components often yields limited durability, whereas approaches that simultaneously perturb multiple aspects of the RS-CCD-CIN axis may improve clinical outcomes. CONCLUSIONS: This review highlights the RS-CCD-CIN axis as a fragile and metastable architecture that supports cancer evolution, while also being susceptible to collapse. A deeper understanding of this interconnected framework may inform the development of therapeutic strategies and enhance the management of resistance.

Humans↗
PubMedDate not supplied

Anterolateral rotary instability associated with chronic anterior cruciate insufficiency.

Patients with anterior cruciate tears identified by previous surgery were examined for anterolateral rotary instability of the knee. Twenty-four of 30 patients returning for examination had positive tests for anterolateral rotary instability using the techniques described by both Slocum and MacIntosh. The presence of anterolateral rotary instability was directly related to the attainment of full extension of the operative knee. Inherent ligamentous laxity and the degree of combined instabilities were thought to amplify the anterolateral rotary instability tests. Quadriceps rehabilitation, pes anserines transfers and semimembranosus transfers were thought not to influence anterolateral rotary instability.

Adult↗
PubMed2025

Surprisingly frequent chromosomal instability in cultivated peanut.

This study, the third in a three-part series, investigates whether chromosomal instability persists in cultivated peanut. The allotetraploid peanut (Arachis hypogaea; genome type AABB) originated from the hybridization and polyploidization of A. duranensis (AA) and A. ipaënsis (BB). Our first study established that this was an extremely narrow genetic origin, likely from a single hybridization event. This raised a paradox: how did such narrow genetics give rise to the phenotypic diversity seen in cultivated peanut? The second study addressed this, showing that a single neoallotetraploid spontaneously generates striking diversity, and that homoeologous exchanges-abundant in early generations following polyploidy-are a key mechanism in creating this diversity. In contrast to this early-generation instability, cultivated peanut is generally considered to be genetically stable, presumably due to selection. This third study tests whether residual instability still occurs in modern peanut. From a single plant of the highly selfed 'genome stock' of the cultivar 'Tifrunner', we advanced lineages through seven generations in a pollinator-free greenhouse. Among 233 plants, we identified three new large-scale chromosomal instability events: a large deletion on chromosome B01, associated with reduced pod width and seed weight, and two ABBB compositions involving chromosomes A02/B02 and A05/B05. With these observations in hand, we reinterpreted previously published data from two recombinant inbred populations. Together, these results indicate that at least 1% of pure pedigree A. hypogaea plants exhibit spontaneous large-scale chromosomal changes-a surprising frequency of instability that likely contributes to peanut's long-term adaptability and evolution.

Arachis↗
PubMed1977

Determination of sagittal instability of the knee joint.

For measuring sagittal instability in the knee joint a radiologic method has been developed which requires no complicated equipment, is easy to apply, and is relatively insensitive to the sources of error commonly associated with determination of sagittal instability, such as difference of flexion angle and changes in the projection. Measurements are made between reference points located in the femur and the tibia. The reproducibility of the method is high enough to make it suitable for testing instability before and after reconstructive surgery. By the use of constructed reference points sagittal instability can be distinguished from rotational instability.

Humans↗
PubMed1978

Demonstration of rotatory instability in injured knees by stress radiography.

Rotatory instability of injured knees may be demonstrated by stress radiography by recording the different movements of the medial and lateral tibial condyle at pull or push with the knee in 90 degrees flexion. The displacements of the condyles are expressed in millimetres, not degrees. Comparison with the healthy knee is always used. The displacement of a tibial condyle has to exceed 3.0 mm in relation to the healthy knee to be defined as pathological. If the movements of both condyles exceed the movements in the healthy knee by more than 3.0 mm in the same direction a drawer sign is present--if only one of them moves, an abnormal rotation is present. When a drawer sign is present there may still be a greater displacement of one of the tibial condyles which means a rotatory instability added to the drawer sign, designated a complex rotatory instability. All types of rotatory instabilities, simple and complex, are defined and discussed, in relation to the classification of Nicholas, Trickey and Slocum & Larson. Forty-one cases of abnormal rotation were demonstrated in this series by stress radiography. The direction of rotation and the type of instability are described and compared with the operative findings. The findings are in agreement with those of the above-mentioned authors and the experimental work of Warren et al.

Humans↗
PubMed2025

Characterization of oncohistone H2B variants in Schizosaccharomyces pombe reveals a key role of H2B monoubiquitination deficiency in genomic instability by altering gene expression.

Various amino acid substitutions commonly occur at one residue of a histone in human cancers, but it remains unclear whether these histone variants have distinct oncogenic effects and mechanisms. Our previous modeling study in the fission yeast Schizosaccharomyces pombe demonstrated that the oncohistone mutants H2BG52D, H2BD67N, and H2BP102L cause the homologous recombination defects and genomic instability by compromising H2B monoubiquitination (H2Bub). However, it is unknown whether other amino acid changes at the H2B-Gly52/Asp67/Pro102 residues influence H2Bub levels and whether they cause genomic instability by altering H2Bub-regulated gene expression. Here, we construct diverse oncomutants at the sole H2B gene htb1-Gly52/Asp67/Pro102 sites in S. pombe and study their impacts on genotoxic response, H2Bub levels, and gene expression. Interestingly, the oncomutants htb1-G52D, htb1-D67N, and htb1-P102L exclusively exhibit significant genotoxic sensitivity, reduced H2Bub levels, and altered gene expression. These defects can be rescued by restoring H2Bub levels with the deletion of the H2B deubiquitinase ubp8+. These strong genetic correlations suggest that H2Bub deficiency plays a determinant role in the genomic instability of htb1-Gly52/Asp67/Pro102 oncomutants and that the alteration of gene expression due to reduced H2Bub levels is a novel mechanism underlying the genomic instability caused by htb1-G52D, htb1-D67N, and htb1-P102L oncomutations.

Schizosaccharomyces↗
PubMed1978

Post-traumatic ligamentous instabilities of the wrist.

Dorsiflexion, palmar flexion, ulnar translocation, and dorsal carpal subluxation are four, not uncommon, post-traumatic carpal ligamentous instabilities. Palmar carpal subluxation is a theoretical possibility. Dorsiflexion and palmar flexion instabilities are named for the way the distal lunate articular surface dorsally and palmarly, respectively. Ulnar translocation, and dorsal and ventral carpal subluxations are named according to movement of the entire carpus at the radiocarpal joint. Early detection of traumatic carpal instabilities is necessary to encourage optimal treatment of these significant carpal malalignments. These and other patients with disabling wrist problems may be evaluated by a "ligamentous instability series."

Adult↗
PubMed1979

Neonatal hip instability. Reason for failure of early abduction treatment.

A series of nine children with hip joint instability in 17 hips, diagnosed neonatally, is presented. Seven had bilateral idiopathic instability and two instability secondary to arthrogryposis, one of them bilateral. After reduction seven of the children (14 hips) were treated with abduction devices, which in all cases did not lead to stability in one or both hips. In these cases arthrography revealed that closed reduction was impossible due to narrowing of the joint capsule (hour-glass shape) and the interposition of a capsular fold including the acetabular labrum. The same types of changes were seen within 1 or 2 months after birth in three hips which had had no abduction treatment before arthrography. At open reduction of 11 hips it was found that the narrowing of the capsule was caused by the tendons of the iliopsoas and rectus femoris muscles. Excision of the capsular fold (labrum) was not necessary. The femoral head was deformed and anteverted. Failure of conservative treatment can be due either to incomplete reduction or to inadequate immobilization. Our analysis has shown that the most probable reason is incomplete reduction due to interposition. An obstacle to reduction should be suspected if abduction is restricted at birth, if primary reduction is difficult and the position difficult to maintain or if instability persists after 8 weeks of treatment. On the basis of our material the incidence of such an impediment to reduction was 0.08 per thousand births in the region studied during a 5-year period.

Acetabulum↗
PubMedDate not supplied

Analysis of 100 patients with anterolateral rotatory instability of the knee.

Of 100 consecutive patients with anterolateral rotatory instability analyzed, 84 were males and the average age was 27.4 years. Over 50 per cent were injured while participating in athletics and 40 per cent were injured during daily activities. The group averaged 1.2 operations prior to diagnosis. The most frequently performed procedures were medial meniscectomy, pes anserinus transfer and medial capsular reefings. Eighty-four of 100 patients underwent surgery during the study period. Seventy-one had combined rotatory instability and 13 had anterior lateral rotatory instability alone. Sixty-six patients had articular cartilage damage. Before treating the anterolateral rotatory instability, it is necessary to identify and treat other commonly associated abnormalities.

Adolescent↗
PubMed2026

The curious case of sporadic nematode susceptibility in "Tifguard" peanut (Arachis hypogaea): seed mixture or genetic instability?

The Runner-type peanut (Arachis hypogaea L.) cultivar "Tifguard" carries an introgressed chromosomal segment on chromosome A09 from A. cardenasii that confers resistance to root-knot nematode (RKN). Despite this, a proportion of "Tifguard" plants show RKN symptoms, which could plausibly be attributed to seed mixture or outcrossing. However, recent work has shown that cultivated peanut exhibits surprisingly frequent large-scale chromosomal instability (1% to 5%); suggesting that resistance loss could arise from spontaneous structural genomic change. To test these possibilities, we grew foundation seed in an RKN-infested field and collected symptomatic and asymptomatic plants. Lineages derived by single-seed descent were genotyped using the Axiom Arachis 48K SNP array v2 and whole-genome sequencing. Symptomatic lineages lacked the A. cardenasii introgression on chromosome A09 and instead carried the complete endogenous A. hypogaea A09 region at the expected dosage. There was no evidence of large-scale homoeologous exchange, deletion, or other genomic instability affecting this chromosome. Most susceptible plants were closely related to resistant "Tifguard" but lacked the A09 introgression, with a smaller proportion assignable to known nematode-susceptible cultivars, implicating seed mixture with a possible contribution from cross-pollination rather than genomic instability. Because resistance depends on a single major-effect segment, rare events have disproportionate phenotypic impact, placing high demands on genetic purity. For important traits conferred by major loci, marker-based testing across seed-increase stages could verify trait retention directly, and is increasingly practical as marker costs decline.

Arachis↗