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PubMed1992

Cancer volume and site of origin of adenocarcinoma in the prostate: relationship to local and distant spread.

Biologic aggressive behavior in adenocarcinoma of the prostate is proposed to be a direct function of cancer volume. In an autopsy series, distant metastasis was found only in cancers that had both volume greater than 5 cc and areas of poor differentiation (Gleason grades 4 and 5). In subsequent study of over 200 radical prostatectomy specimens, cancers were found to originate both in the peripheral zone (PZ) and in the normally small anteromedial transition zone (TZ) where benign nodular hyperplasia also develops. Anatomic TZ and PZ cancers were nearly equivalent to clinical stage A and B cancers, respectively. Transition zone cancers showed much less capsule penetration and seminal vesicle invasion than PZ cancers of comparable volume because the TZ boundary provided a barrier to cancer spread through the PZ. In PZ carcinomas, capsule penetration depended largely on facilitated spread along perineural spaces, and its distribution was determined by the location of superior and inferior nerve pedicles. Capsule penetration, seminal vesicle invasion, and positive surgical margins were all strongly correlated with cancer volume. Tumors smaller than 4 cc had all morphologic variables favorable; tumors larger than 12 cc tended to have all variables unfavorable. Lymph node metastasis in radical prostatectomy cases was most strongly predicted by a combination of cancer volume plus percentage of high-grade tumor. Cancers with more than 3.2 cc of grade 4 and/or 5 component showed a 100-fold increase in proportion of cases with nodal spread.

Adenocarcinoma↗
PubMed1983

Antianginal drug trapidil (Rocornal) inhibits spreading of platelets and formation of surface-bound thrombi-like aggregates.

Effects of an antianginal drug trapidil (Rocornal) on platelet interaction with a surface coated with fibrillar calf skin collagen (CSC) have been studied by scanning electron microscopy. Gel filtered human platelets were incubated with the CSC substrate in the absence or in the presence of soluble inducers of platelet activity: arachidonic acid (AA), stable analogue of prostaglandin (PG) endoperoxides, U46619, and thrombin. In the absence of soluble inducers, trapidil does not alter the total number of adherent platelets. At the same time, trapidil inhibits the shape change of adherent platelets, induced by the CSC substrate, increasing the percentage of discoid and decreasing the percentage of spread platelets. It was demonstrated earlier (1) and in the present study that soluble inducers of platelet activity stimulate massive spreading of platelets and formation of surface-bound thrombi-like aggregates on the CSC substrate. Trapidil completely prevents the effects of the exogenous AA and U46619 on platelet-substrate interactions, but inhibits the AA-stimulated synthesis of thromboxane A2 (TXA2) in platelets by 40-50% only. Trapidil also blocks platelet aggregation in suspension, spreading and formation of surface-bound aggregates induced by low, but not high, concentrations of thrombin. Possible sites of trapidil action are discussed.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1989

Phorbol ester stimulates platelet spreading and thrombi-like aggregate formation on the surface of immobilized type V collagen.

We have studied the effect of the tumor-promoting phorbol ester, 4 beta-phorbol-12 beta-myristate-13 a-acetate (PMA), and of the stable prostaglandin endoperoxide analogue U46619 on the interaction of human blood platelets with surfaces coated with monomeric human type V collagen (CV) and on free calcium concentration in platelet cytoplasm. It was shown by scanning electron microscopy that native resting platelets sparingly attach to CV and fail to spread or aggregate on the collagenous substrate in the absence of PMA and U46619. Addition of 0.15-1.5 nM PMA or 1.5 microM U46619 stimulates platelet spreading and formation of multilayer (thrombi-like) platelet aggregates on the per se non-thrombogenic type V collagen substrate. It was further demonstrated using the fluorescent indicator quin2 that U46619 (0.1 microM) increases cytoplasmic free calcium concentration from basal level (100-120 nM) up to 600 nM, whereas PMA (0.75-15 nM) exerts only a minor effect, increasing free calcium level by 30-40 nM. These results indicate that the tumor-promoting phorbol ester PMA induces massive platelet spreading and aggregation on surfaces coated with non-thrombogenic type V collagen via activation of protein kinase C with little or no apparent change in free cytoplasmic calcium.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1994

Nitric oxide donors inhibit platelet spreading on surfaces coated with fibrinogen but not with fibronectin.

We have studied the effect of nitric oxide (NO) on the interaction of washed human platelets with fibrinogen or fibronectin adsorbed on glass. Platelet contacts were visualized by interference reflection microscopy at 37 degrees C in Tyrode's solution. The areas of spread platelets were measured, using digital video image processing techniques, at times up to 30 minutes after initial surface platelet contact. On fibrinogen spreading was inhibited by NO donors in the order of potency: S-nitroso-acetylpenicillamine > sodium nitroprusside > S-nitroso-glutathione. The inhibitory action of NO donors was prevented by Oxy-haemoglobin, confirming that this inhibition was due to the release of NO. In contrast, NO donors had virtually no effect on platelet spreading on fibronectin. Platelet adhesion to fibrinogen is mediated by GP IIb IIIa and the vitronectin receptor (VNR), while that to fibronectin is via GP IIb IIIa, VNR, Ic IIa and VLA-6. Our results thus indicate that NO inhibits adhesion mediated by GP IIb IIIa and/or VNR but not by the two other receptors. The mechanism of this receptor-specific inhibition of platelet adhesion remains to be elucidated.

Adsorption↗
PubMed1982

Release of 6-keto-prostaglandin F1 alpha and thromboxane B2 from mouse peritoneal macrophages during their adhesion and spreading on a glass surface.

The release of 6-keto-prostaglandin F1 alpha (6KF1 alpha) and of thromboxane B2 (TXB2) from cells were investigated using mouse peritoneal exudate cells (PECs) and non-cultured peritoneal macrophages. They were prepared by adhesion to glass dishes and incubated for 1 hr at 37 degrees C in 5% CO2 in air. Both the percentage of spreading macrophages and the release of 6KF1 alpha and TXB2 increased in proportion to the incubation time. 6KF1 alpha and TXB2 were released from the macrophages, not from the non-coated glass dishes, the spreading of macrophages was hardly detected and lower amounts of 6KF1 alpha and TXB2 were released from these cells compared with cells incubated in non-treated glass dishes. These findings suggest that adhesion with the correlated spreading of macrophages on glass dishes serve as a considerable physical factor for the release of 6KF1 alpha and TXB2.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

V factor (tumor volume) and T factor (FIGO classification) in the assessment of cervix cancer prognosis: the risk of lymph node spread.

An attempt was made by investigation of the operative specimens from 98 patients suffering from epidermoid carcinoma of the cervix to assess the relationship between lymphatic spread on one hand and tumor volume and anatomical stage on the other hand. Within the same anatomical stage the risk of lymphatic spread is more important as the tumor volume increases. The reverse is also true. Within the same volume the risk of lymphatic spread increases when cancer extends beyond the "cervix-parametrium" barrier. The anatomical classification based on the T factor deserves to be retained, classification which some wanted to replace by another one based exclusively on the V factor.

Carcinoma, Squamous Cell↗
PubMed1985

Blockade of peripheral beta-adrenergic receptors fails to suppress the cerebral spread of an engram in mice.

Using bitemporal injections of puromycin, we have reported observations interpreted to indicate that a systemic injection of (-)-propranolol (50 micrograms/kg) drastically suppressed the spread of an engram in mice from the hippocampalentorhinal area to widespread cerebral areas. The present experiments were made with a non-selective, irreversible beta-adrenergic receptor antagonist that fails to cross the blood-brain barrier in order to test the possibility that the propranolol-induced blockade of peripheral beta-receptors might contribute to its effect on engram spread. Prolonged blockade of peripheral receptors by the irreversible antagonist had no effect on engram spread, suggesting that propranolol's effect was centrally mediated.

Animals↗
PubMed1995

Effect of chemical sympathectomy on the neural spread of pseudorabies virus in mice.

To investigate the routes of neural spread of pseudorabies (Aujeszky's disease) virus (PRV), the effects of chemical sympathectomy by 6-hydroxydopamine (6-OHDA) on clinical signs and viral spread in mice inoculated intraocularly with PRV were examined. Similar to non-treated mice, the treated mice developed pruritus as a major clinical sign, followed by peracute death, but the time of death tended to be slightly delayed in about half of the treated mice. On immunohistological examination, viral antigens in treated mice were found to be markedly reduced in all the ipsilateral retinae; they were detected diffusely in the forebrain area with a localization in the mammillary area. In the treated mice, viral antigens were also reduced in the ipsilateral trigeminal nerve ganglia as well as in its central nuclei. These findings indicate that both the sympathetic nervous system and the trigeminal nervous system play an important role in the neural spread of PRV. Possible involvement of the dopaminergic nervous system, particularly in the eye, as the main site of viral growth was discussed.

Animals↗
PubMed1995

Immunohistochemical analysis of pseudorabies virus spread through neurons innervating the eyeball.

Pseudorabies virus (PRV) was inoculated intraocularly into BALB/c mice, and the distribution pattern of cells positive for several neurotransmitters and viral antigens in the eyeball, trigeminal nerve ganglia, and superior cervical ganglia was examined immunohistochemically to clarify the neural route of the virus spread. In the eyeball, substance P (SP)- and calcitonin gene-related peptide (CGRP)-positive cells were detected in the ipsilateral iris and ciliary body, neuropeptide tyrosine (NPY)-positive cells were detected in the choloid membrane, and tyrosine hydroxylase (TH)-positive cells were detected in the ipsilateral inner nuclear layer of the retina; all these cells contained viral antigens. In the superior cervical ganglia, viral antigen-positive cells containing TH or NPY were found at bilateral sites. In the trigeminal nerve ganglia, viral antigen-positive cells containing SP or CGRP were found at bilateral sites. These findings indicated that the SP- and CGRP-positive ganglion cells of the trigeminal nerve ganglia innervating the iris or ciliary body, and the NPY-positive ganglion cells of the superior cervical ganglia innervating the iris, ciliary body, and choroid membrane served as the route for the virus spread. These findings also suggested that dopaminergic neurons, such as the TH-positive retinal cells and TH-positive ganglion cells of the superior cervical ganglia, served as the route for virus spread.

Animals↗
PubMed1983

Characterization of lizard venom hyaluronidase and evidence for its action as a spreading factor.

Hyaluronidase was isolated from the lizard (Heloderma horridum horridum) crude venom. The chemical properties were characterized and compared to the same enzyme from other sources. The enzyme was found to be a single polypeptide chain with a molecular weight of 63,000 daltons. It possesses an isoelectric point and pH optimum of 5.0, and was observed to be extremely temperature sensitive. The role of hyaluronidase as a spreading factor which serves to aid in the diffusion of toxins has been suspected for a long time; yet no experimental proof has been offered until now. It was shown that hyaluronidase promotes the spread of the hemorrhagic area in mice when injected with hemorrhagic toxin. Thus experimental evidence is supplied for the first time that the enzyme plays a role as a "spreading factor" in the toxic action of venom.

Amino Acids↗
PubMed1987

The initiation and spread of epileptiform bursts in the in vitro hippocampal slice.

We recorded spontaneous synchronized epileptiform bursts from hippocampal slices from guinea pig using an array of 16 extracellular electrodes placed over the stratum pyramidale of CA2 and CA3. The slices were made epileptogenic with the GABA antagonist picrotoxin (or occasionally penicillin). We found that spontaneous bursts always originate at a discrete focus at or near CA2. These bursts spread smoothly and uniformly across CA3 at an average velocity of 0.13 m/s. This velocity is slower than the conduction velocity of the Schaffer collaterals or mossy fibers. Picrotoxin produced afterdischarges following the initial primary burst, and these afterdischarges were found to originate and spread in a fashion nearly identical to the primary burst. These results indicate that CA2 is a unique region which must possess unusual cellular and/or synaptic connectivity properties which result in a decreased threshold for initiation of epileptiform activity. We consider several hypothetical patterns of local synaptic connectivity in the light of these results, and we discuss the possible role of residual inhibition in limiting the spread of synchronized discharges.

Animals↗
PubMed1993

Two neurotropic viruses, herpes simplex virus type 1 and mouse hepatitis virus, spread along different neural pathways from the main olfactory bulb.

Several neurotropic viruses enter the brain after peripheral inoculation and spread transneuronally along pathways known to be connected to the initial site of entry. In this study, the pathways utilized by two such viruses, herpes simplex virus type 1 and mouse hepatitis virus strain JHM, were compared using in situ hybridization following inoculation into either the nasal cavity or the main olfactory bulb of the mouse. The results indicate that both viruses spread to infect a unique and only partially overlapping set of connections of the main olfactory bulb. Both quantitative and qualitative differences were observed in the patterns of infection of known primary and secondary main olfactory bulb connections. Using immunohistochemistry for tyrosine hydroxylase combined with in situ hybridization, it was shown that only herpes simplex virus infected noradrenergic neurons in the locus coeruleus. In contrast, both viruses infected dopaminergic neurons in the ventral tegmental area, although mouse hepatitis virus produced a more widespread infection in the A10 group, as well as infecting A8 and A9. The results suggest that differential virus uptake in specific neurotransmitter systems contributes to the pattern of viral spread, although other factors, such as differences in access to particular synapses on infected cells and differences in the distribution of the cellular receptor for the two viruses, are also likely to be important. The data show that neural tracing with different viruses may define unique neural pathways from a site of inoculation. The data also demonstrate that two viruses can enter the brain via the olfactory system and localize to different structures, suggesting that neurological diseases involving disparate regions of the brain could be caused by different viruses, even if entry occurred at a common site.

Animals↗
PubMed1980

Effects of nocodazole, a new synthetic microtubule inhibitor, on movement and spreading of mouse peritoneal macrophages.

Colchicine treatment enhances movement and suppresses spreading of mouse peritoneal macrophages. The effects of colchicine could result either from disruption or cytoplasmic microtubules or from other actions of colchicine on mammalian cell processes. Nocodazole is a new synthetic microtubule inhibitor that is structurally dissimilar to colchicine and is therefore unlikely to share with colchicine any common action besides of inhibition of microtubule assembly. Nocodazole was shown here to have activities similar to colchicine on macrophage migration and spreading. This supports the idea of a direct relationship between disruption of cytoplasmic microtubules and macrophage migration and spreading.

Animals↗
PubMed1989

Fractal spreading growth of Serratia marcescens which produces surface active exolipids.

An irregular fiord-like outline of a S. marcescens colony expanding on a hard agar medium was shown to be fractal which promised an extremely long array of outermost cells. For the analysis of such spreading growth, mutants defective in production of surface active exolipids (serawettin W1 and W3) and flagella-less mutants were isolated. The fractal spreading growth was found to be correlated with serrawettin production. Furthermore, serrawettin-less mutants demonstrated spreading growth when purified serrawettin W1 or W3 were supplied exogenously.

Mutation↗
PubMedDate not supplied

Head and neck carcinoma: detection of extraorgan spread with MR imaging and CT.

A retrospective analysis of the Magnetic resonance (MR) and CT findings in 18 untreated carcinomas of the oral cavity (7), oropharynx (2), hypopharynx (7), and larynx (2) was performed to assess the accuracy in evaluating extraorgan tumor spread and nodal involvement. Surgical and pathologic correlation was available for 13 primary tumors and nodal status was analyzed in 18. Nine primary tumors had extraorgan extension. MR had a tendency to be superior to CT in predicting tumor invasion of the cartilage and muscle. Sensitivity, specificity and accuracy for extraorgan spread of primary tumors were 89%, 100% and 92%, respectively, for MR and 78%, 75% and 77% for CT. Accuracy for nodal classification (83%) and carotid invasion (94%) of MR was equal to that of CT. CT was more sensitive than MR for demonstrating necrosis within the nodes and vice versa for detecting retropharyngeal nodes. MR imaging is a useful radiologic modality in evaluating extraorgan tumor spread and nodal levels of the head and neck carcinomas.

Adult↗
PubMed1988

Idiotypic spreading promotes the production of pathogenic autoantibodies.

We propose that a major immunoregulatory abnormality in murine and human autoantibody-mediated disease is idiotypic spreading. By this mechanism, B cells with the genetic information to produce immunoglobulin (Ig) bearing certain public idiotypes (Ids) are selectively upregulated, probably by Id-recognizing helper T cells. The model in which we are testing the hypothesis is systemic lupus erythematosus (SLE) in humans and NZB/NZW F1 (BW) female mice. Recent experiments have shown that the number of public Ids expressed on the Ig of nephritic BW mice is quite restricted. IdX is the dominant Id on serum Ig; IdGN1 and IdGN2 are also common. All three Ids were initially derived from spontaneous antibodies to DNA. Together the three are present on 85% of the total Ig repertoire. Such restriction suggests idiotypic spreading. In glomerular Ig deposits from nephritic BW mice, IdGN1 and IdGN2 are found on 45% of the total Ig: IdX is present in minute amounts. Furthermore, suppression of IdGNs by administration of anti-IdGN1 to BW mice resulted in significant delay in the onset of nephritis, but the IdGNs escaped from control and eventually caused a fatal nephritis. Finally, studies of glomerular Ig deposits in renal biopsies of patients with SLE have shown that IdGN2 dominates such Ig, being present in 76% of renal biopsies from SLE patients and in 6% from patients with non-lupus immune nephritis. Therefore, we have concluded that IdGN1 and IdGN2 are markers of nephritogenic subsets of autoantibodies and are probably the products of idiotypic spreading most likely to cause disease. Finally, after a review of recent experiments suggesting the dominance of autoreactive, Mossman Type 2 T helper cells in nephritic BW mice, it is hypothesized that autoreactive, IdGN-recognizing helper T cells may be central to the sustained upregulation of pathogenic autoantibodies in murine and human SLE.

Animals↗
PubMed2004

Pleural perfusion thermo-chemotherapy under VATS: a new less invasive modality for advanced lung cancer with pleural spread.

BACKGROUND: We conducted a trial of a new less invasive, locoregional modality for lung cancer with pleural spread. This study was planned to investigate the feasibility, safety, and pharmacokinetics of pleural perfusion thermochemotherapy (PPTC) under video-assisted thoracoscopic surgery (VATS) and its modified method with a short perfusion time for preventing heat damage to the lung during the procedure. METHODS: Seventeen patients, 59 to 79 years old, underwent surgical resection of the primary lesions and PPTC under VATS without thoracotomy. All had pleural spread with malignant effusion due to lung cancer proven before the treatment. PPTC consists of irrigating the pleural space with 42 degrees C saline solution containing cisplatin (200 mg/m(2)) using a devised circuit. The time for perfusion was two hours in 10 patients (group L), and one hour in 7 patients (group S). RESULTS: All patients successfully completed this treatment with acceptable toxicities. The pharmacokinetic analysis showed that high platinum levels for the regional pleural exposure, which was 20- to 40-fold greater than those for the plasma in both groups. These values were equivalent between the groups, although the levels for the plasma were higher in group L than in group S. Postoperative lung damage was seen in 4 patients with no serious conditions in group L, and none in group S. The median survival for the L and S groups was 17 and 19 months, respectively. CONCLUSIONS: This less invasive modality seems to offer a safe, feasible, and pharmacokinetically advantageous procedure to have excellent local control for lung cancer with pleural spread.

Aged↗
PubMed2005

Glyceraldehyde-3-phosphate dehydrogenase in the extracellular space inhibits cell spreading.

The occurrence and the novel function of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) in the extracellular space were studied. The extracellular GAPDH with the same molecular mass as the intracellular GAPDH was detected in the conditioned medium of mammalian cultured cell lines such as COS-7, HEK293, MCF-7, HepG2, PC-12, and Neuro-2a cells. Western blot analysis represented the occurrence of GAPDH, but not alpha-tubulin (an intracellular marker protein), in the conditioned medium of COS-7 cells. Furthermore, GAPDH was found in rat serum. These results indicate that GAPDH was secreted outside of the cells. Addition of GAPDH to the cultured medium of COS-7, HEK293, and HepG2 cells allowed cells to undergo morphological changes. In COS-7 cells, the extracellular GAPDH inhibited cell spreading without influencing the cell growth. Western blot and immunofluorescent microscopy analyses revealed that the extracellular GAPDH bound to COS-7 cells in time- and dose-dependent manners. However, a mutant substituting Ser for Cys at position 151 of GAPDH resulted in no binding to the cells, no decreased cell-spreading efficiency and no cell morphological changes. These results indicate that the Cys151 was involved in the binding of GAPDH to cells and the GAPDH-inhibited cell spreading.

Animals↗