Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “elevational migration”

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 757 records · Page 42Linked to original sources
PubMed1980

[Creatine kinase BB sera in neonatal injury children (author's transl)].

The purpose of this study is to find, besides the determination of lactate in blood, a suitable and specific indicator of brain damage in newborn. Accordingly, we studied the total creatine kinase (CK) activity, by the method of Rosalki, and its subunit isoenzymes BB (CK BB) by fluorescence following electrophoresis on cellulose acetate. A first group (thirty newborns) without any disease represents our taest group. We havae found that the normal ranges for CK total were elevated (about 7 200 nkat/l). Electrophoresis of sera from these patients showed in addition to the normally migration isoenzyme (CK BB) was present in very small amounts, no sufficient for quantification. A second group was constituted to thirty ill newborns, with perinatal brain damage. In twenty-eight to thirty children, we find a significant correlation between the level of CK BB and brain insult. But, we have showed that it was necessary to take in consideration the time passed between the hypoxic insult and the blood puncture. Otherwise, we showed by immuno inhibition with specific antibody and by chromatography with gradient elution that identification of CK BB by electrophoresis cannot be misinterpreted. Furthermore, we demonstrated by this method, that position of CK 1 BB in blood is exactly the same that an purified human extract. This study concluded that a high level CK 1 BB in blood of newborn infants with perinatal brain damage has an accurately diagnosis value, if the blood puncture is done immediately during the severe CNS damage.

Acute Disease↗
PubMed1994

Cultures of human embryonic osteoblasts. A new in vitro model for biocompatibility studies.

Cell populations derived from human embryonic bone were isolated according to the ability of osteoblasts to migrate from bone onto glass fragments. Morphologic and biochemical assays showed (1) osteoblast-like appearance; (2) elevated alkaline phosphatase 1,25(OH)2D3 responsive activity associated with plasma membranes and matrix vesicles; (3) production of a thick extracellular matrix, mainly composed of Type I collagen, which mineralized in the presence of 10 mM beta-glycerophosphate; and (4) higher growth rate and viability when compared with their mature counterpart. Cultures of embryonic cells were challenged with particles of several biomaterials, and their effects on morphology, vitality, and osteogenic capacity of the cultured cells were tested. Stainless steel, titanium alloy, Co-Cr-Mo alloy (vitallium), carbon fiber-reinforced polybutylene terephtalate, ultra-high molecular weight polyethylene, ceramic, calcium phosphate, and hydroxyapatite did not exert any significant deleterious effects on the cultured human osteoblasts.

Alkaline Phosphatase↗
PubMed2005

Neuronal migration in the murine rostral migratory stream requires serum response factor.

The central nervous system is fundamentally dependent on guided cell migration, both during development and in adulthood. We report an absolute requirement of the transcription factor serum response factor (SRF) for neuronal migration in the mouse forebrain. Conditional, late-prenatal deletion of Srf causes neurons to accumulate ectopically at the subventricular zone (SVZ), a prime neurogenic region in the brain. SRF-deficient cells of the SVZ exhibit impaired tangential chain migration along the rostral migratory stream into the olfactory bulb. SVZ explants display retarded chain migration in vitro. Regarding target genes, SRF deficiency impairs expression of the beta-actin and gelsolin genes, accompanied by reduced cytoskeletal actin fiber density. At the posttranslational level, cofilin, a key regulator of actin dynamics, displays dramatically elevated inhibitory phosphorylation at Ser-3. Our studies indicate that SRF-controlled gene expression directs both the structure and dynamics of the actin microfilament, thereby determining cell-autonomous neuronal migration.

Actins↗
PubMed1997

Maternal serum granulocyte-colony stimulating factor in preterm birth with subclinical chorioamnionitis.

Preterm birth has been linked with intrauterine infection and inflammation. Serum and amniotic fluid markers of inflammation, such as interleukin-1 (IL-1), IL-6, and granulocyte-colony stimulating factor (G-CSF), have been associated with clinical chorioamnionitis and preterm delivery. As G-CSF regulates the production and maturation of neutrophils, we sought to determine if maternal serum G-CSF levels are elevated in patients with preterm birth with subclinical histologic chorioamnionitis. Maternal serum G-CSF levels were significantly different among five groups of women studied (P < .001, Kruskall-Wallis test), and were highest in subjects with preterm labor who delivered preterm (P < .05, Mann-Whitney U test). Among women with preterm labor who delivered preterm, maternal serum G-CSF levels were significantly higher if histologic chorioamnionitis was present than when histologic evidence of infection was not present (P = 0.04, Mann-Whitney U test). Intrauterine infection may cause a local inflammatory process and initiate preterm labor. This inflammatory response may include production of G-CSF, which would enter the circulation and stimulate the migration of neutrophils to the site of infection. Our data support this concept, as maternal serum G-CSF is elevated with subclinical infection in association with preterm birth.

Chorioamnionitis↗
PubMed2002

Thromboxane synthase inhibitors induce apoptosis in migration-arrested glioma cells.

OBJECTIVE: Because of the wide dissemination of malignant glioma cells by the time that malignant glioma is diagnosed, anti-invasive strategies that are designed to limit their further spread may be of little value unless mechanisms of the invasive cascade can be used to render invasive cells susceptible to cytoreductive treatments. We recently determined that elevated thromboxane synthase gene expression and enzymatic activity are associated with a highly migratory phenotype of glioma cells in vitro and that specific inhibitors of this enzyme block cell migration. Interference with this inherent phenotype of malignant gliomas also affects glioma cell proliferation and apoptosis. METHODS: To study the effect of thromboxane synthase inhibitors on motility, metabolic activity, and cell death, we used five human glioma cell lines, four glioblastoma-derived, low-passage cell cultures, normal human astrocytes, and fibroblasts. Motility was measured in a monolayer migration assay. Caspase activation as an early event in apoptotic cell death was assessed using a caspase 3 cleavage assay. Intracellular deoxyribonucleic acid (DNA) fragmentation was detected by enzyme-linked immunosorbent assay quantification of histone-complexed DNA. Subsequent cell death was scored by trypan blue exclusion. RESULTS: In this study, we demonstrate that the treatment of human glioma cells with the specific thromboxane synthase inhibitor furegrelate leads first to caspase activation (detectable 6 h after treatment), then to DNA fragmentation (24-48 h after treatment) and subsequent cell death. Caspase inhibitors abrogate this effect. Furthermore, the inhibition of thromboxane synthase by furegrelate increases cells' susceptibility to the induction of DNA fragmentation by camptothecin, etoposide, N,N'-bis(2-chloroethyl)-N-nitrosourea, and anti-CD95 antibodies. No induction of apoptosis was observed in normal astrocytes and fibroblasts. CONCLUSION: These data indicate that thromboxane synthase may represent a vortex of divergent signaling cascades that regulate motility and apoptosis in glioma cells. This paradigm may offer a novel perspective in the treatment of patients with malignant gliomas.

Apoptosis↗
PubMed2005

Computational analysis of biomechanical contributors to possible endovascular graft failure.

This paper evaluates numerically coupled blood flow and wall structure interactions in a representative stented abdominal aortic aneurysm (AAA) model, leading potentially to endovascular graft (EVG) failure. A total of 12 biomechanical contributors to possible EVG migration were considered. The results show that after EVG insertion for the given model, the peak AAA sac-pressure was reduced to 14.2 mmHg (11.8% of p(lumen)), and hence the maximum von Mises wall stress and wall deformation dropped by factors of 20 and 10, respectively. Thus, an EVG can significantly reduce sac pressure, mechanical stress, pulsatile wall motion, and the maximum diameter in AAAs and hence prevent AAA rupture effectively. In the absence of endoleaks, elevated sac-pressure can still be caused by fluid-structure interactions between the EVG, stagnant blood, and AAA wall. EVG migration forces vary from 1.4 to 7 N for different EVG geometries, material properties, and hemodynamic conditions. AAA-neck angle, iliac bifurcation angle, neck aorta-to-iliac diameter ratio, EVG size, aorto-uni-iliac EVG, and hypertension play important roles in generating forces potentially leading to EVG migration.

Animals↗
PubMed2026

UBE2D4 Upregulation Promotes Cuproptosis Sensitivity in Colorectal Cancer.

BACKGROUND: Cuproptosis, a copper-dependent form of regulated cell death, represents a potential therapeutic vulnerability in colorectal cancer (CRC). However, the regulatory mechanisms governing cuproptosis in CRC remain largely unknown. METHODS: UBE2D4 expression was analyzed in the TCGA-COAD cohort and validated in CRC cell lines (HCT116, HT29) and normal colon epithelial cells (FHC) by qRT-PCR and western blot. Paired CRC and adjacent normal tissues (n&#x2009;=&#x2009;5) were also examined by western blot. UBE2D4-knockdown HT29 cells were generated by transient siRNA transfection to assess cell viability (CCK-8), migration (wound healing assay), and expression of cuproptosis-related genes (DLAT, HSP70, LIAS) under copper overload conditions (elesclomol+CuSO4). RESULTS: UBE2D4 was significantly upregulated in CRC tissues and cell lines compared to normal controls. In paired clinical samples, western blot confirmed that UBE2D4 protein expression was elevated in tumor tissues, accompanied by increased DLAT, HSP70 and LIAS. Copper overload induced typical cuproptotic mitochondrial morphology and triggered a marked upregulation of UBE2D4, DLAT, and HSP70, alongside downregulation of LIAS. UBE2D4 silencing had no effect on baseline cell viability or migration but significantly rescued cells from copper-induced cytotoxicity. Genetically, UBE2D4 knockdown specifically attenuated the copper-induced elevation of DLAT, while restoring HSP70 and LIAS to near-baseline levels. CONCLUSION: These findings identify UBE2D4 as a genetically upregulated and functionally significant gene in colorectal cancer. Its upregulation correlates with altered expression of cuproptosis-related genes, particularly DLAT, suggesting that UBE2D4 expression status may represent a genetic determinant of cuproptosis sensitivity in CRC. This study provides a genetic basis for stratifying CRC patients who might benefit from copper-based therapeutic strategies.

Humans↗
PubMed2025

Migration strategies, connectivity and corridor features of the partial migrant little bustard (Tetrax tetrax) across the Iberian Peninsula.

The study of migration ecology is crucial for understanding the factors and pressures affecting migratory species. Here, we studied the migratory ecology of the little bustard (Tetrax tetrax), a steppe bird that has suffered a sharp decline over recent decades, mainly due to agricultural intensification. Using 105 adult birds tagged across the main Iberian regions where the species is present (Alentejo, Extremadura, Ebro Valley, Northern Plateau, Southern Plateau and Guadalquivir Valley), we analysed the ratio of migratory and resident birds in each population and assessed their connectivity during the three main migratory periods (summer, winter and pre-breeding). Additionally, we describe the features of the migrations recorded in terms of length, duration and day period. Our results corroborate that little bustards can be considered partial migrants across Iberia, although the proportion of residents versus migrants varied between populations: the Alentejo (94.74%) and Northern Plateau (93.75%) had the highest proportion of migrants, followed by Guadalquivir Valley (81.82%), Extremadura (65.38%), Southern Plateau (55.56%) and Ebro Valley (25.93%). Migratory connectivity varied between periods: the pre-breeding and summering migrations showed a trend to move northwards, while birds moved southwards for winter. Regarding the migratory corridors obtained from the 253 migrations identified, we found three main routes: one corridor that connects the Northern Plateau with the western part of the Southern Plateau and Extremadura, another one that connects the Southern Plateau, Extremadura, Alentejo and Guadalquivir Valley, and one corridor that concentrates migrations within the Ebro Valley, and between the Ebro Valley and the Southern Plateau. Finally, analyses showed that little bustards migrate at night through areas dominated by herbaceous cover (avoiding tree-covered land and water bodies) and of low elevation and terrain roughness. Our results highlight the importance of developing an international and inter-regional conservation strategy to protect not only the breeding and wintering quarters, but also this endangered species' migratory corridors, thus supporting the viability of the metapopulation.

Brownian bridge kernel↗
PubMed1999

Analysis of the inflammatory response induced by substance P in the mouse pleural cavity.

This study analyzes both cell migration and exudation responses elicited by substance P (SP) in the mouse pleural cavity. SP caused, 4 h after its administration into the mouse pleural cavity, a dose-related recruitment of leukocytes (ED50 = 14.2 nmol), mainly due to mononuclears. Leukocytes peaked between 2 and 4 h, being followed by a slight decay that remained elevated for up to 24 h. Exudation, although small, was significantly elevated from 2 to 96 h after. NK1 (FK 888) or NK3 (SR 142801), but not NK2 (SR 48968) tachykinin receptor antagonists, significantly inhibited cell migration. HOE 140 and NPC 17731, bradykinin B2 receptor antagonists, caused graded inhibition of cell influx (ID50s of 0.03 and 0.04 pmol), but des-Arg9-Leu8-BK, B1 receptor antagonist, had no effect. The nitric oxide inhibitors L-NOARG and L-NAME, but not D-NAME, significantly inhibited SP-induced pleurisy. Pretreatment of the animals with indomethacin, dexamethasone, terfenadine, theophylline or salbutamol produced significant inhibition of the inflammatory parameters, whereas cromolyn only inhibited exudation. These results indicate that intrapleural injection of SP in mice elicit a long-lasting inflammatory reaction that is characterized by the participation of nitric oxide, kinins, cyclooxygenase metabolites and histamine. Antiasthmatic drugs such as theophylline, salbutamol, dexamethasone, and, to a lesser extent cromolyn, also markedly inhibit this inflammatory reaction. These results provide clear evidence supporting the role played by SP in neurogenic inflammation.

Animals↗
PubMed2005

CrkI and CrkII function as key signaling integrators for migration and invasion of cancer cells.

Crk adaptor proteins play an important role during cellular signaling by mediating the formation of protein complexes. Increased levels of Crk proteins are observed in several human cancers and overexpression of Crk in epithelial cell cultures promotes enhanced cell dispersal and invasion, implicating Crk as a regulator of invasive responses. To determine the requirement of Crk for invasive signals, we targeted the CRKI/II gene by RNA interference. Consistent knockdown of CrkI/II was observed with two small interfering RNA targeting sequences in all human cancer cell lines tested. CrkI/II knockdown resulted in a significant decrease in migration and invasion of multiple malignant breast and other human cancer cell lines (MDA-231, MDA-435s, H1299, KB, and HeLa). Moreover, CrkI/II knockdown decreased cell spreading on extracellular matrix and led to a decrease in actin stress fibers and the formation of mature focal adhesions. Using immunohistochemistry, we show elevated CrkI/II protein levels in patients with breast adenocarcinoma. Together, these studies identify Crk adaptor proteins as critical integrators of upstream signals for cell invasion and migration in human cancer cell lines and support a role for Crk in metastatic spread.

Adenocarcinoma↗
PubMed1998

Invasion of cytotrophoblastic JEG-3 cells is stimulated by hCG in vitro.

Trophoblast invasion into the uterine wall is controlled by many factors. Previously, a human chorionic gonadotropin (hCG) receptor has been found to be expressed on invasive trophoblast as well as on choriocarcinoma cells implying a possible role for the hormone in trophoblast invasion. Therefore, this study examined the role of hCG in the invasion of trophoblastic (JEG-3) cells. Increasing hCG concentrations were applied in a trophoblast invasion model, JEG-3, through matrigel-coated filters. The proliferation was quantified by WST-1 cleavage assay. Cell migration was studied by examining the number of cells that had passed the uncoated porous (8-microm pore size) filters. After staining, filters were examined microscopically for cells on the underside of the membrane. A quantitative protease assay was also performed. Flow cytometric analysis of alpha5 and alpha6 integrin subunits, which are essential for interactions between cells and extracellular matrix, was performed. hCG increased significantly (P<0.01) the in vitro invasion of trophoblastic JEG-3 cells in a dose-dependent manner. Migration was also increased by hCG (P<0.01). However, cell proliferation remained unchanged. The second messenger analogue dibutyryl cAMP (db cAMP) and the cAMP elevating factor (forskolin) mimicked the effects of hCG by stimulating a dose-dependent increase of trophoblastic cell UEG-3) invasion. The collagenolytic activity of trophoblastic cells (EG-3) was increased by hCG stimulation. No changes were shown in the expression of alpha5 and alpha6 integrin subunits on JEG-3 cells. In vitro hCG is a regulatory factor of invasion and migration in trophoblastic JEG-3 cells, whereas proliferation is not influenced. The endogenous production of hCG by the trophoblast in vivo implies an autocrine control of invasion processes by hCG.

Bucladesine↗
PubMed2026

Targeting super-enhancer-driven SKIL transcription by CDK7 inhibitor THZ1 to suppress gastric cancer progression.

BACKGROUND: Gastric cancer (GC) is a lethal malignancy characterized by high incidence, mortality, and limited treatment options. Transcriptional addiction is a key cancer hallmark that drives tumor pathogenesis, making its inhibition a promising therapeutic strategy for GC. The study aims to investigate the roles and mechanisms of super-enhancer (SE)-driven oncogenic transcriptional addiction in GC progression and to identify novel targetable vulnerabilities. METHODS: We utilized cellular and animal models to assess the effects of THZ1 treatment and CDK7 knockdown on GC progression. RNA sequencing was employed to elucidate the potential molecular mechanism of THZ1 treatment. ChIP-seq was performed to establish SE landscape in GC. Integrative analysis of transcriptomic and SE profiling was used to identify THZ1-targeted oncogenic genes. Rescue experiments were conducted to confirm that THZ1 treatment suppresses GC malignant progression by targeting SE-driven SKIL transcription. RESULTS: GC cells exhibited pronounced sensitivity to THZ1 compared to normal gastric mucosa cells, and the treatment potently suppressed tumor growth and migration in both cellular and animal models. CDK7 was significantly upregulated in GC tissues, and its knockdown inhibited malignant progression in vitro and in vivo, whereas its overexpression accelerated tumor progression. Mechanistically, SE-driven oncogenic transcriptional amplification underlies GC cell susceptibility to THZ1, supported by the identification of novel oncogenic genes such as SKIL. SKIL, a key Hippo pathway regulator, was highly expressed in GC cells, and its elevated expression predicted poor patient prognosis. SKIL silencing attenuated malignant phenotypes, while its overexpression diminished THZ1&#x2019;s suppression of GC cell proliferation and migration. CONCLUSION: Our findings demonstrate that THZ1 inhibits GC progression by disrupting SE-driven oncogenic transcription, thereby offering CDK7 inhibition as a promising therapeutic intervention for GC.

Stomach Neoplasms↗
PubMed1998

Migration and acculturation among Samoans: some sources of stress and support.

Daily excretion of the stress hormone, epinephrine, has been employed to study potential stressors associated with acculturation and migration. Young men and women from Samoan communities in Hawaii (HI), American Samoa (AS) and Western Samoa (WS) which differ in exposure to American culture were included. Psychosocial factors associated with elevations in hormone excretion were assumed to be stressors, while associations with reduced excretions were assumed to be supportive or buffers. Hormone excretion levels were similar in all locations, but there were different associations which could be attributed to migration and acculturation. Among all migrants (HI) ethnic networks were apparent stressors, while a high degree of community involvement was stressful for migrant women. In sites of culture contact (HI, AS) certain adult members of the extended family were supportive, as was a superior knowledge of Samoan cultural concepts. For women in Samoa (WS, AS) community involvement was supportive. In contrast for men in WS and AS, but not in HI, being of mixed ancestry or having close family of mixed ancestry was stressful. It is concluded that hormone analysis can provide meaningful clues concerning social stressors in acculturating or migrant communities. Also that migration or acculturation do not necessarily result in increased levels of stress.

Acculturation↗
PubMed1992

The role of cell proliferation and migration in the development of a neo-intimal layer in veins grafted into arteries, in rats.

The development of a thickened (hyperplastic) fibro-cellular neo-intima is a significant event in the adaptation of a vein grafted into an artery. The histogenesis of tissues in vein grafts was explored in a rat model where the source of endothelial and smooth muscle cells was from the adjacent artery. Cell proliferation was assessed by the incorporation of tritiated thymidine and autoradiography, up to 18 months after grafting. Cell migration was detected by prelabelling in the first 5 days after grafting and sampling at later times. The proliferation of cells in the arterial media adjacent to the graft was elevated above control levels as early as 2 days after grafting; it was maximal at 3 days and returned to low levels by day 21. During the first week, prelabelled smooth muscle cells in the tunica media of the adjacent artery migrated to the subendothelial space, where they continued to proliferate to produce arterial intimal hyperplasia. The migration of endothelial and smooth muscle cells proceeded across the anastomosis to populate the vein graft neo-intima, where smooth muscle cells continued to proliferate until 28 days after grafting. Cell migration and proliferation were significant factors in the histogenesis of vein graft neo-intimal hyperplasia in this model. These processes were controlled, perhaps by local regulatory factors, to form a vein graft, the wall of which was similar in thickness and structure to that of the host artery.

Animals↗
PubMed1996

Increased monocyte chemotactic protein-1 level and activity in the peripheral blood of women with endometriosis. Le Groupe d'Investigation en Gynécologie.

OBJECTIVE: Our purpose was to evaluate monocyte chemotactic protein-1 in the peripheral blood of women with and without endometriosis. STUDY DESIGN: Fifty-seven patients with endometriosis at laparoscopy done for infertility and pelvic pain were compared with 44 fertile women with no evidence of endometriosis at tubal ligation by laparoscopy. Monocyte chemotactic protein-1 concentration in the plasma was determined by enzyme-linked immunosorbent assay and its biologic activity was evaluated by measuring monocyte chemotaxis with use of a human histiocytic cell line (U937). RESULTS: Monocyte chemotactic protein-1 concentrations (median and range of values) found in the plasma were higher in patients with endometriosis (163, 0 to 788 pg/ml) than in normal controls (0, 0 to 355 pg/ml). This elevation was significant only in the minimal stage of endometriosis (revised American Fertility Society stage I). However, increased chemotactic activity (mean number of migrating cells/mm2 +/- SEM) was found in the stages I (1240 +/- 141), II (519 +/- 30), and III-IV (523 +/- 23) of the disease compared with normal controls (205 +/- 20). A total of 35% to 44% of this activity was inhibited in the presence of an antibody specific to monocyte chemotactic protein-1. CONCLUSION: Endometriosis is associated with increased level and activity of monocyte chemotactic protein-1 in the peripheral blood. The elevation and activation of this cytokine could play a relevant role in the immunoinflammatory process associated with the disease.

Adult↗
PubMed2007

Differential regulation of cytokine release and leukocyte migration by lipopolysaccharide-stimulated primary human lung alveolar type II epithelial cells and macrophages.

Bacterial colonization is a secondary feature of many lung disorders associated with elevated cytokine levels and increased leukocyte recruitment. We hypothesized that, alongside macrophages, the epithelium would be an important source of these mediators. We investigated the effect of LPS (0, 10, 100, and 1000 ng/ml LPS, up to 24 h) on primary human lung macrophages and alveolar type II epithelial cells (ATII; isolated from resected lung tissue). Although macrophages produced higher levels of the cytokines TNF-alpha and IL-1beta (p < 0.0001), ATII cells produced higher levels of chemokines MCP-1, IL-8, and growth-related oncogene alpha (p < 0.001), in a time- and concentration-dependent manner. Macrophage (but not ATII cell) responses to LPS required activation of ERK1/2 and p38 MAPK signaling cascades; phosphorylated ERK1/2 was constitutively up-regulated in ATII cells. Blocking Abs to TNF-alpha and IL-1beta during LPS exposure showed that ATII cell (not macrophage) MCP-1 release depended on the autocrine effects of IL-1beta and TNF-alpha (p < 0.003, 24 h). ATII cell release of IL-6 depended on autocrine effects of TNF-alpha (p < 0.006, 24 h). Macrophage IL-6 release was most effectively inhibited when both TNF-alpha and IL-1beta were blocked (p < 0.03, 24 h). Conditioned media from ATII cells stimulated more leukocyte migration in vitro than conditioned media from macrophages (p < 0.0002). These results show differential activation of cytokine and chemokine release by ATII cells and macrophages following LPS exposure. Activated alveolar epithelium is an important source of chemokines that orchestrate leukocyte migration to the peripheral lung; early release of TNF-alpha and IL-1beta by stimulated macrophages may contribute to alveolar epithelial cell activation and chemokine production.

Antibodies, Blocking↗
PubMed1999

[Retrolaminar infiltration of optic nerve with intraocular tamponade following silicone oil instillation].

BACKGROUND: Eyes after intravitreal silicone oil injection may suffer various complications. We report on a patient with deep retrolaminar changes in the optic nerve after silicone oil instillation with secondary angle-closure glaucoma. PATIENT: A 69-year-old female patient with aphakic retinal detachment of the right eye was treated by pars plana vitrectomy with silicone oil injection. After 41 months the patient presented with absolute secondary angle-closure glaucoma with rubeosis iridis. The intraocular pressure was elevated up to 55 mmHg. There was a peripheral retinal detachment and a pale deeply cupped optic disc. Due to increasing pain the blind eye was enucleated. Histology showed a mainly detached retina and silicone oil occupying the vitreous cavity. The optic nerve was deeply cupped and the parenchyma presented multiple cavernous spaces of various sizes. These presumptive silicone oil bubbles reached beyond the line of surgical transection, nine millimeters behind the globe. CONCLUSION: In comparison to Schnabel's cavernous optic atrophy the vacuoles in the optic nerve in this patient were filled with silicone oil instead of acid mucopolysaccharides. A posterior migration of silicone oil into the orbital optic nerve can not be excluded, after long-term silicone oil tamponade and elevated intraocular pressure.

Aged↗
PubMed1988

A reexamination of the role of microfilaments in neurulation in the chick embryo.

Formation of wedge-shaped neuroepithelial cells, owing to the constriction of apical bands of microfilaments, is widely believed to play a major part in bending of the neural plate. Although cell "wedging" occurs during neurulation, its exact role in bending is unknown. Likewise, although microfilament bands occupy the apices of neuroepithelial cells, whether these structures are required for cell wedging is unknown. Finally, although it is known that cytochalasins interfere with neurulation, it is unknown whether they block shaping or furrowing of the neural plate, or elevation, convergence, or fusion of the neural folds. The purpose of this study was to reexamine the role of microfilaments in neurulation in the chick embryo. Embryos were treated with cytochalasin D (CD) to depolymerize microfilaments and were analyzed 4-24 hr later. CD did not prevent neural plate shaping, median neural plate furrowing, wedging of median neuroepithelial cells, or neural fold elevation. However, dorsolateral neural plate furrowing, wedging of dorsolateral neuroepithelial cells, and convergence of the neural folds were blocked frequently by CD. In addition, neural folds always failed to fuse across the midline in embryos treated with CD, and neural crest cell migration was prevented. These data indicate that only the later aspects of neurulation may require microfilaments, and that certain neuroepithelial cells, particularly those that normally wedge with median furrowing and elevation of the neural folds, become (and remain) wedge-shaped in the absence of apical microfilament bands. Thus, microfilament-mediated constriction of neuroepithelial cell apices is not the major force for median neuroepithelial cell wedging and elevation of the chick neural plate. Further studies are needed to localize the motor(s) for these processes.

Actin Cytoskeleton↗