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At least 919 records · Page 51Linked to original sources
PubMed1985

Reversibility of phorbol diester-induced macrophage spreading.

Phorbol 12-myristate 13-acetate and phorbol 12, 13-dibutyrate induced spreading of mouse macrophages with 50% effective concentrations of 3 nM and 35 nM, respectively. Macrophages treated with 100 or 1000 nM phorbol 12, 13- dibutyrate showed a time related decrease in spreading after washout. Spreading induced by 1, 10, or 100 nM phorbol 12-myristate 13-acetate was irreversible; however, washed phorbol 12,13-dibutyrate-treated cells respread after a second exposure to this compound. Washout of 3[H]phorbol diesters corroborated these observations in that 5% of 3H-phorbol 12-myristate 13-acetate and only 0.1% 3[H]phorbol, 12,13-dibutyrate remained associated with washed cells. Since phorbol 12-myristate 13 acetate is much more lipophilic than phorbol 12,13-dibutyrate, the reversibility of phorbol diester-induced macrophage spreading may depend upon the lipophilicity of the derivative utilized.

Animals↗
PubMed1993

Metastatic disease of the ureter: patterns of tumoral spread and radiologic findings.

The radiographic and sectional imaging features (ultrasound [US], computed tomography [CT], and magnetic resonance imaging [MRI]) of ureteral obstruction due to metastatic disease are reviewed. The radiologic findings depend on the pattern of the tumoral spread: hematogenous submucosal/mucosal metastasis, hematogenous adventitia metastases spreading along periureteral vessels, scirrhous metastatic spread along periureteral vessels, or metastatic spread into lymph nodes with perinodal desmoplastic reaction. Solitary or multiple extraluminal obstructions without substantial displacement of the ureter are characteristic. CT is the examination of choice for morphological analysis. Together with the patient's history and clinical data, a presumptive diagnosis of ureteral obstruction caused by metastatic disease can be made.

Adult↗
PubMed1982

Differential specificity of substrate-attached lectins stimulating spreading of GH3-cells under serum-free, hormone-supplemented culture conditions.

Most mammalian cells are capable of growth in culture only when they are supplied with an appropriate substrate to which they can adhere and spread. To prepare suitable substrates different lectins were attached onto polystyrene tissue-culture dishes after coating with polylysine. GH3-cells (a pituitary-tumor-cell line) were seeded into the culture dishes containing serum-free, hormone-supplemented medium. When succinylated Concanavalin A (s-Con A), which binds specifically to mannose residues, is attached to the surface an extraordinary spreading of GH3-cells is induced within 15 to 20 min after seeding. Other lectins with a different sugar-binding specificity are less effective in inducing cell spreading. However, the cell spreading depends not only on the substrate-attached lectins but also on the hormones used in the proliferation-culture of GH3-cells. Both types of molecules found in the microenvironment of a cell, the matrix-fixed sugar-binding proteins and the diffusive hormones, are responsible for the regulation of the behaviour of the mammalian cell. It is suggested that the interaction of the cell-surface carbohydrates with the plasma-membrane-bound lectins of contiguous cells plays a central role in such processes, especially in in-vivo.

Animals↗
PubMed1988

Carbohydrate moieties of the basal lamina: their role in attachment and spreading of basal corneal epithelial cells.

Three lectins, Wheat germ agglutinin, succinyl Concanavalin A and Ricinus communis agglutinin were used to block specific sugar moieties in the basal lamina. Corneal epithelial basal cells were plated onto freshly denuded basal lamina. Attachment was studied by quantifying the adherence of prelabeled cells and by examining attachment sites using transmission electron microscopy. Spreading was examined using scanning electron microscopy. Attachment of the cells occurred within 15 min and spreading was apparent after 45 min. Both Wheat germ agglutinin and beta-N-acetylglucosaminidase inhibited cellular attachment. Succinyl Concanavalin A and Ricinus Communis agglutinin permitted attachment, but inhibited extensive cellular spreading. The results indicate that the attachment of basal cells is dependent on N-acetylglucosamine residues, and spreading is mediated by alpha methylmannoside, glucose, and galactose residues.

Animals↗
PubMed1990

Spread of vesicular stomatitis virus along the visual pathways after retinal infection in the mouse.

Vesicular stomatitis virus (VSV) was injected into the left eyeball of 3-week-old mice and it infected the retinal ganglion cells. The infection spread rapidly along the visual pathways to the postsynaptic neurons in the contralateral superior collicle (SC) and lateral geniculate body (LGB). The distributional pattern of the viral immunoreactivity indicated an anterograde axonal transport of the infectious material. A subsequent spread to the ganglion cells of the right retina further indicated retrograde axonal VSV transport. Within the retina the infection spread from the ganglion cells to the pigment epithelium. Although a transneuronal spread of the VSV infection was observed, no VSV budding from or uptake in synaptic membranes was demonstrated ultrastructurally in the retina or the superior collicle. In the retina virions budded from the perikaryal and dendritic plasma membranes of the ganglion cells as well as from the nerve cell bodies of the inner and outer nuclear layers, but not from the receptor segments. In the superior collicle budding was also observed from the plasma membranes of nerve cell bodies and dendrites. In contrast, the intraocular injection of Sendai virus caused a limited retinal ganglion cell infection, with no further propagation in the retina or to the SC or LGB.

Animals↗
PubMed1989

Control of an epidemic spread of a multi-resistant strain of Acinetobacter calcoaceticus in a hospital.

The spread of a multi-resistant glucose-acidifying Acinetobacter calcoaceticus strain in a community hospital was studied. After admission of a colonized patient to the hospital the strain was found in clinical specimens from ICU patients and subsequently from several of these patients after transfer to medical wards. Environmental specimens from the ICU and medical wards were analysed in order to investigate the mode of spread of the strain. Isolates of A. calcoaceticus were screened by their antibiotic resistance pattern. In addition, the cell envelope protein electrophoretic profiles were used as epidemiological markers. The multi-resistant acinetobacters all had the same protein profile. To prevent spread of the epidemic strain strict hygienic measures were enforced, e.g. scrupulous cleaning of the room after discharge of any colonized patient and increased attention to the hand hygiene of the medical and nursing staff. Furthermore, the use of antibiotics was restricted. Although this strain was only eradicated with difficulty in the affected patients, it did not spread throughout the hospital. Colonization of patients with the multi-resistant micro-organism was predominantly localized to the ICU.

Acinetobacter↗
PubMed1992

Spread and distribution of 5-ASA colonic foam and 5-ASA enema in patients with ulcerative colitis.

Rectal treatment with enemas, foams, and suppositories is the most efficient method of delivering an adequate quantity of locally active drugs to the distal colon. In a pilot study carried out by colonoscopy in four patients, it was observed that 4 g 5-ASA in 20 ml foam spread up or beyond the splenic flexure and more extensively than 2 g 5-ASA in 10 ml foam. Therefore we have undertaken a study in order to compare by scintigraphy the colonic distribution of 4 g 5-ASA foam versus 4 g 5-ASA in 100 ml liquid enemas in 10 patients with ulcerative colitis using a crossover randomized design. Both preparations were labeled with 100 MBq [99mTc]sulfur colloid before administration. Anterior scans were taken at intervals for 4 hr. Activity, expressed as a percentage of total radioactivity, was measured in the rectum, sigmoid, descending, transverse, and ascending colon. Six patients had the same extent of spread with the two formulations; in three patients with foam and in one patient with enema a greater spread was observed. The foam reached the upper limit of disease in all cases, while enema failed in two cases. The maximum spread with foam was observed within 30 min in nine of 10 patients compared with seven of 10 after enema. Compared to enema, foam distributes more uniformly and seems to persist longer in the descending and sigmoid colon. The 5-ASA colonic foam shows some more favorable characteristics than enema for the local treatment of left-sided ulcerative colitis.

Administration, Topical↗
PubMed1980

Cleavability of hemagglutinin determines spread of avian influenza viruses in the chorioallantoic membrane of chicken embryo.

The spread of infection in the chorioallantoic membrane (CAM) has been analysed with pathogenic and non-pathogenic avian influenza A viruses. After allantoic inoculation of pathogenic strains, high titers of infectious virus were found in the allantoic fluid, and virus growth could be demonstrated by immunohistology and electron microscopy in the allantoic epithelium, the mesenchyma, and in the chorionic epithelium. By the same route of inoculation, non-pathogenic strains yielded also higher titers of infectious virus in the allantoic fluid, but virus replication was restricted to the allantoic epithelium and did not occur in the other cell layers. After chorionic inoculation of pathogenic strains, replication occurred in all layers of the CAM, and infectious virus was released into the allantoic fluid. However, when the chorionic epithelium was infected with a non-pathogenic strain, infection did not spread beyond the site of inoculation. These differences in virus spread are based on differential activation of the hemagglutinin by proteolytic cleavage. The hemagglutinin of pathogenic strains is cleaved in cells of each layer, whereas the hemagglutinin of non-pathogenic strains is cleaved only in the allantoic epithelium. In epithelial cells, virus budding occurred nearly exclusively at the apical side of the cell surface, but this polarization of virus maturation was found with both pathogenic and nonpathogenic strains, indicating that it does not account for the differences in virus spread and, thus, in pathogenicity.

Allantois↗
PubMedDate not supplied

Attachment, spreading and growth in vitro of highly malignant and low malignant murine fibrosarcoma cells.

Highly malignant cell lines and low-malignant cell lines isolated from three different methylcholanthrene-induced murine fibrosarcomas were examined for their ability to attach to plastic dishes and collagen-coated dishes under serum-free conditions and in the presence of serum. Most of the cells from the three highly malignant lines attached and spread under all conditions. By 72 h, there was a significant increase in the number of cells indicating that at least some of the cells had undergone division (even in the absence of serum). In contrast, fewer of the cells from the three low-malignant lines attached and spread on the plastic or collagen substrates in the absence of serum or in the presence of 0.1 per cent serum. However, when 15 micrograms laminin per dish was added along with the low-malignant cells, they then attached and spread on the plastic and collagen-coated dishes. Previous studies have indicated that the highly malignant lines express cell surface antigens that cross-react with laminin while the low-malignant cell lines do not. We speculate that the differences between the high- and low-malignant cells in the expression of cell surface laminin-like antigens contribute to the dissimilarities in attachment and spreading capacity. These differences may also contribute to the dissimilarity between these cells in malignant potential.

Animals↗
PubMed1987

Mechanism of direct spread of abdominal neuroblastoma: CT demonstration and clinical implications.

Neuroblastoma, a malignant tumor of neural crest origin, is the most common extracranial solid tumor in children. In 1971 Evans et al. introduced a clinical staging for neuroblastoma. Over sixty percent of patients present with neuroblastoma beyond stage I. Despite more aggressive therapy there has been only minimal improvement in survival. Since 1978, all patients with neuroblastoma have had CT scanning as part of their initial evaluation at our institution. Children with abdominal neuroblastoma beyond stage I form the basis of this report. Selected cases illustrating the permeative nature of neuroblastoma and the mechanism of direct abdominal spread by CT scanning are presented. The tumor originates in the retroperitoneum and spreads to the abdominal aorta where it gains access to the subperitoneal space via the celiac axis and superior mesenteric artery. These vessels course from the aorta to their ultimate destination within their peritoneal folds. These folds form the interconnecting space (subperitoneal space) between the retroperitoneum and the peritoneal organs. Such scanning is extremely sensitive in detecting neuroblastoma with early infiltration into adjacent tissues and contiguous spread through abdominal spaces. The clinical implications of the permeative nature of neuroblastoma and the mechanism of contiguous abdominal spread are discussed.

Abdominal Neoplasms↗
PubMed1986

Retrograde spread of 5-aminosalicylic acid enemas in patients with active ulcerative colitis.

In an attempt to know the exact retrograde spread of high-dosage 5-aminosalicylic acid enemas, we have studied eight patients with active left-sided colitis, by adding a small amount of barium sulfate to the enemas and by checking the spread radiologically after 15 minutes, 1 hour, and 6 hours. Four grams of 5-aminosalicylic acid in 100-ml enemas and 4 gm in 200-ml enemas were used. The same experiment was repeated in a subsequent attack, with enemas labeled with technetium-99m and checked by scintiscans in five of these patients. We always have observed a volume-dependent spread of enemas but, interestingly, in the patients studied with technetium-99m there was always a wider spread than that which was detected with barium enemas. In all five patients, 100-ml enemas reached the splenic flexure. In two patients with total colitis, a progression of 100-ml technetium-99m enemas was performed in the transverse colon, but the maximum opacity remained in the left side. We can conclude that 4 gm of 5-aminosalicylic acid in 100-ml enemas can be suitable for treating patients with left-sided colitis, and will represent a valid addition for patients with more extensive colitis.

Adult↗
PubMed1985

Substrate influences human epidermal melanocyte attachment and spreading in vitro.

Previous culture systems for melanocytes have employed serum-supplemented medium and uncoated plastic dishes, prohibiting examination of possible substrate influences on cellular morphology and function. We now report, using a sensitive serum-free system and a quantitative procedure for evaluating cellular morphology, that modification of the plating surface affects human epidermal melanocyte attachment rate and subsequent morphology in vitro. Melanocytes attach and spread more rapidly on surfaces coated with fibronectin or Type I/III collagen or on surfaces previously conditioned by human keratinocytes, dermal fibroblasts, melanocytes, or melanoma cells than do melanocytes on untreated control surfaces. Type IV collagen and laminin, although minimally beneficial for cell attachment, do support a characteristic melanocyte morphology that differs from that seen either on the other coated surfaces or on uncoated plastic controls. Addition of fetal bovine serum at the time of inoculation has no appreciable effect on attachment but markedly improves cell spreading on untreated surfaces, while addition of nerve growth factor with or without serum to this system fails to affect cell attachment or spreading. Our data establish that human epidermal melanocytes are indeed capable of responding morphologically to substrate signals. The ability of several biochemically unrelated surfaces to enhance melanocyte attachment rate and spreading suggests that melanocytes have surface receptors with a variety of specificities. This work is relevant to the development of improved culture systems for melanocytes in vitro and to understanding melanocyte behavior in vivo.

Cell Adhesion↗
PubMed1989

Mycoplasma provides for the spreading of opossum kidney cells in a serum-free, defined medium.

During the course of investigating the growth and differentiation of opossum kidney cells in serum-free medium, it was observed that a mycoplasma contamination (M. hyorhinis) contributed to the spreading of cells. Contaminated cells, seeded on collagen-coated plates, spread out and grew to confluency in Dulbecco's modified eagle's medium/Ham's F12 nutrient mixture containing insulin, transferrin, sodium selenite, and bovine serum albumin fraction V. In addition, differentiated characteristics, including parathyroid hormone-inhibitable, sodium-dependent phosphate transport, were expressed by these cells grown in this medium. After the infection was eradicated, the contamination-free cells would not spread out and proliferate in the same serum-free medium as they had done in the presence of mycoplasma. Normal cellular development, however, was attained after cells were plated in serum-free medium that included fetuin. Cells once again spread out, grew to confluency, and were able to express their differentiated characteristics.

Animals↗
PubMed1990

Spreading of wheat germ agglutinin-induced erythrocyte contact by formation of spatially discrete contacts.

The time dependence of agglutination and cell-cell contact spreading in human erythrocytes exposed to wheat germ agglutinin (WGA) was characterized by light and electron microscopy. Cells (3 x 10(7)/mL) had a threshold lectin concentration in the range of 0.6-2.0 micrograms/mL for initial cell contact. Spreading was essentially completed within 60 and 2 min in undisturbed and gently agitated suspensions, respectively. The cells in large WGA agglutinates retained features of their initial disk form in contrast to the convex outlines of polycation or polyethylene glycol-induced agglutinates. Spreading of contact area was accompanied by development of a pattern of discrete contact regions separated by a distance of the order of 1 micron. Freeze fracture electron microscopy and studies with ferritin-labeled WGA showed no significant aggregation of intramembrane particles or specific lectin receptors under conditions when contact spreading occurred. It is argued that flow stress effects on cells in suspended agglutinates give rise to a situation where opposite membranes, at the leading edge of cell contact, are separated by a thin aqueous layer. When this intercellular water layer exceeds a critical length, it becomes unstable. The layer breaks up by surface wave development to form an array of intracellular water spaces. Formation of the aqueous spaces causes opposite membrane regions to move synchronously toward each other. Lectin molecules crosslink the wave crests to give spatially periodic contact points.

Cell Communication↗
PubMed2000

Calcium mobilization is required for spreading in human osteoblasts.

Adhesion-induced changes in intracellular calcium concentration ([Ca2+]i) were measured in populations of human osteoblasts spreading on bone matrix proteins. In cells spreading on collagen type I, fibronectin, or laminin, average values for [Ca2+]i were found to increase approximately 2x over baseline and then decline. The speed with which [Ca2+]i increased and declined was dependent upon the matrix protein on which the cells were plated but was generally complete within 1 hour from the time of plating. Calcium mobilization was found to be due to influx of calcium across the osteoblast plasma membrane and was integrin dependent. Carboxyamido triazole (CAI), a specific inhibitor of nonvoltage-dependent calcium channels, or BAPTA-AM, a chelator of intracellular calcium, inhibited osteoblast adhesion and spreading on collagen type I, fibronectin and laminin in a dose-dependent manner. In conclusion, these results demonstrate that calcium mobilization is induced upon integrin-ligand contact and that calcium influx is required for cell adhesion and spreading.

Calcium↗
PubMed2002

Vertical evolution and intragenic spread of lichen-fungal group I introns.

One family within the Euascomycetes (Ascomycota), the lichen-forming Physciaceae, is particularly rich in nuclear ribosomal [r]DNA group I introns. We used phylogenetic analyses of group I introns and lichen-fungal host cells to address four questions about group I intron evolution in lichens, and generally in all eukaryotes: 1) Is intron spread in the lichens associated with the intimate association of the fungal and photosynthetic cells that make up the lichen thallus? 2) Are the multiple group I introns in the lichen-fungi of independent origins, or have existing introns spread into novel sites in the rDNA? 3) If introns have moved to novel sites, then does the exon context of these sites provide insights into the mechanism of intron spread? and 4) What is the pattern of intron loss in the small subunit rDNA gene of lichen-fungi? Our analyses show that group I introns in the lichen-fungi and in the lichen-algae (and lichenized cyanobacteria) do not share a close evolutionary relationship, suggesting that these introns do not move between the symbionts. Many group I introns appear to have originated in the common ancestor of the Lecanorales, whereas others have spread within this lineage (particularly in the Physciaceae) putatively through reverse-splicing into novel rRNA sites. We suggest that the evolutionary history of most lichen-fungal group I introns is characterized by rare gains followed by extensive losses in descendants, resulting in a sporadic intron distribution. Detailed phylogenetic analyses of the introns and host cells are required, therefore, to distinguish this scenario from the alternative hypothesis of widespread and independent intron gains in the different lichen-fungal lineages.

Ascomycota↗
PubMed2006

Incurable esophageal cancer: patterns of tumor spread and therapeutic consequences.

BACKGROUND: The aim of the study was to determine if the two histologic tumor types in esophageal cancer exhibit different behavior at advanced tumour stages and require a differentiated therapy. PATIENTS AND METHODS: From November 1997 to December 2003, 268 patients presented with esophageal carcinoma. Esophagectomy was contraindicated in 88 (32.8%) patients (75 men, 13 women) with a median age of 64.7 (42-83) years. Fifty-six (63.6%) had squamous cell carcinoma; adenocarcinoma was identified in 31 (35.2%). RESULTS: The causes of incurable disease were non-resectable distant metastases in 32 (36.4%) patients, local tumor spread in 25 (28.4%), and general operative risk in 19 (21.5%). Surgical intervention was contraindicated in 7 patients because of a combination of general inoperability and local tumor spread, or the presence of distant metastases at the time of diagnosis (4 patients declined to undergo surgery and in one patient esophageal resection and reconstruction was technically not possible). The incurability rate for squamous cell carcinoma was 44.6% because of the presence of local tumor spread, compared to a rate of 12.4% for adenocarcinoma. Adenocarcinomas with proven hematogenic metastases were characterized by a higher incurability rate (64.5% vs. 21.4%) (P=0.0014). The prevalence of technical causes of inoperability or of poor general condition was similar in both patient groups (P>0.05). The median 1-year survival rates estimated (Kaplan-Meier) were 36.5% for patients with squamous cell carcinoma and 23.7% for patients with adenocarcinoma (P=0.051). Therapeutic measures had a significant influence on the prognosis: patients without tumor-specific therapy survived 3.4 (0-24) months; those with radiochemotherapy 10.6 (0-25) months; those with radiotherapy 11.0 (0-65) months; and those with chemotherapy 16.5 [0-16.5] months (log-rank test: P=0.0229). In the multivariate analysis, the therapeutic measures (P=0.0126) and tumor localization (P=0.0474) proved significant for prognosis, but were not the cause of incurability (P=0.0948). CONCLUSIONS: The histologic tumor type does not represent an independent prognostic factor in patients with incurable disease. Rather, the prognosis is dependent on the suitability of the induction of tumor-specific therapeutic measures. These are also recommended in patients with incurable disease after consideration of the extent of tumor spread, provided the performance of the selected measures is justified by the general condition of the patient and the expected prognosis.

Adenocarcinoma↗
PubMed2003

A mathematical model of cell-to-cell spread of HIV-1 that includes a time delay.

We consider a two-dimensional model of cell-to-cell spread of HIV-1 in tissue cultures, assuming that infection is spread directly from infected cells to healthy cells and neglecting the effects of free virus. The intracellular incubation period is modeled by a gamma distribution and the model is a system of two differential equations with distributed delay, which includes the differential equations model with a discrete delay and the ordinary differential equations model as special cases. We study the stability in all three types of models. It is shown that the ODE model is globally stable while both delay models exhibit Hopf bifurcations by using the (average) delay as a bifurcation parameter. The results indicate that, differing from the cell-to-free virus spread models, the cell-to-cell spread models can produce infective oscillations in typical tissue culture parameter regimes and the latently infected cells are instrumental in sustaining the infection. Our delayed cell-to-cell models may be applicable to study other types of viral infections such as human T-cell leukaemia virus type 1 (HTLV-1).

CD4-Positive T-Lymphocytes↗