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PubMed2006

Gametocytocidal activity in antimalarial drugs speeds the spread of drug resistance.

OBJECTIVE: Antimalarial drugs kill the asexual parasites responsible for causing disease and some, notably chloroquine and the artemisinins, also kill the sexual transmission stages known as gametocytes. It is invariably argued by malariologists that gametocytocidal activity is beneficial because it reduces the rate at which resistance evolves by 'reducing the transmission of resistant parasites'. This seems dubious from a population genetics perspective, where intuition would lead to the opposite conclusion. The objective was to reconcile these differing views. METHODS: The effect of gametocytocidal drug activity was quantified mathematically and calibrated using field data. RESULTS: It appears to be a robust result that gametocytocidal activity actually promotes the spread of resistance through a population; the underlying reason is that gametocytocidal activity reduces transmission of drug-sensitive forms to a greater extent than the drug resistant, thereby increasing the spread of the latter. The increased rate of spread of resistance is quantified and appears to be small providing drug coverage is moderate or low. CONCLUSIONS: Citing reduced spread of resistance as a justification for deploying gametocytocidal antimalarials is unjustified; the deliberate use of a gametocytocidal antimalarial at high coverage to reduce transmission may ultimately be counterproductive through its rapid promotion of drug resistance.

Animals↗
PubMed1988

Prolonged expression of differentiated phenotype by chondrocytes cultured at low density on a composite substrate of collagen and agarose that restricts cell spreading.

The dedifferentiation of chondrocytes in culture is frequently associated with transition from a rounded to a spread morphology. A number of culture methods which prevent cell spreading have been described; however, all have disadvantages that limit their widespread use. In this paper we describe a new technique which allows prolonged cultivation of attached chondrocytes at low density while inhibiting spreading: the cells are grown on a composite substrate of agarose and collagen. By varying the ratio of agarose to collagen in the gel, the degree of spreading can be varied. The cultures are suitable for ultrastructural and immunofluorescence analysis and for studies of the synthesis and secretion of macromolecules. In order to determine whether the differentiated phenotype was maintained on composite gels, we compared the levels of messenger RNAs for cartilage-specific proteoglycan, link protein, alpha 1 (II) and alpha 1 (I) collagens in chondrocytes grown at low density on composite gels or at high or low density on tissue culture plastic for up to 21 days. The rate of decline in the level of mRNAs encoding the cartilage-specific products and the rate of increase in the level of alpha 1 (I) collagen mRNA were slower in the composite cultures than in the cultures on plastic. This culture technique may, therefore, prolong expression of the differentiated phenotype of chondrocytes relative to cultivation on plastic and will be useful for further studies on the role of cell shape in regulating differentiated gene expression.

Animals↗
PubMed1990

Cell adhesion, spreading and neurite stimulation by laminin fragment E8 depends on maintenance of secondary and tertiary structure in its rod and globular domain.

The cell adhesion, spreading and neurite-promoting properties of mouse tumor laminin fragment E8, which contains major site(s) responsible for laminin-cell interactions, were probed by proteolytic degradation, denaturation, synthetic peptides and antibody inhibition. Removal of more than half of the N-terminal portion contributing to the rod-like domain did not effect cell attachment or spreading although neurite-promoting activity was reduced. More extensive degradation of the rod or of the globular domains of E8, or separation of the globule from the rod, also resulted in loss of cell spreading activity although weak attachment was found to an A chain subfragment comprising the globular domain and a short piece of the rod. Exposure of E8 to increasing concentrations of dissociating agents produce an apparently reversible denaturation but an irreversible loss of both attachment and neurite-promoting activities, as did reduction and alkylation of disulfide bonds in the globular domain. Although cell adhesion and spreading were blocked by antibodies to an alpha 6 integrin subunit, neurite outgrowth was unaffected, indicating two distinct receptors for these two activities. Furthermore, a synthetic peptide, the sequence of which is found in the vicinity of adhesion and neurite-promoting sites and previously implicated in neurite growth and cell attachment activities, was found to be inactive. These results indicate that the major cell attachment and neurite-promoting sites of laminin are distinct although both require the native conformation of parts of the rod and the terminal globular domain of the long arm of laminin.

Amino Acid Sequence↗
PubMed1983

Clinically unrecognised renal carcinoma: aspects of tumor morphology, lymphatic and haematogenous metastatic spread.

In a series comprising 235 clinically unrecognised renal carcinoma, metastatic spread was found in 56 cases (24%). In 82% of cases with metastases the spread involved more than one site. Lymphatic spread was diagnosed in 37 patients. Lymph node metastases were usually multiple and multifocal and were almost as common in the mediastinum as in the retroperitoneal space. In cases with involvement of these sites and/or supraclavicular nodes, concomitant metastases in the lungs were observed in 86% and in other organs in 11%. Since lymph node invasion is a strong indicator of systemic spread, the therapeutic benefit of radical lymphadenectomy seems very low, whereas a limited unilateral dissection is justified mainly for its value as a staging procedure.

Adenocarcinoma↗
PubMed1999

Spread of vasodilatation and vasoconstriction along feed arteries and arterioles of hamster skeletal muscle.

1. In arterioles of the hamster cheek pouch, vasodilatation and vasoconstriction can spread via the conduction of electrical signals through gap junctions between cells that comprise the vessel wall. However, conduction in resistance networks supplying other tissues has received relatively little attention. In anaesthetized hamsters, we have investigated the spread of dilatation and constriction along feed arteries and arterioles of the retractor muscle, which is contiguous with the cheek pouch. 2. When released from a micropipette, acetylcholine (ACh) triggered vasodilatation that spread rapidly along feed arteries external to the muscle and arterioles within the muscle. Responses were independent of changes in wall shear rate, perivascular nerve activity, or release of nitric oxide, indicating cell-to-cell conduction. 3. Vasodilatation conducted without decrement along unbranched feed arteries, yet decayed markedly in arteriolar networks. Thus, branching of the conduction pathway dissipated the vasodilatation. 4. Noradrenaline (NA) or a depolarizing KCl stimulus evoked constriction of arterioles and feed arteries of the retractor muscle that was constrained to the vicinity of the micropipette. This behaviour contrasts sharply with the conduction of vasodilatation in these microvessels and with the conduction of vasoconstriction elicited by NA and KCl in cheek pouch arterioles. 5. Focal electrical stimulation produced constriction that spread rapidly along feed arteries and arterioles. These responses were inhibited by tetrodotoxin or prazosin, confirming the release of NA along perivascular sympathetic nerves, which are absent from arterioles studied in the cheek pouch. Thus, sympathetic nerve activity co-ordinated the contraction of smooth muscle cells as effectively as the conduction of vasodilatation co-ordinated their relaxation. 6. In the light of previous findings in the cheek pouch, the properties of vasoconstriction and vasodilatation in feed arteries and arterioles of the retractor muscle indicate that substantive differences can exist in the nature of signal transmission along microvessels of tissues that differ in structure and function.

Animals↗
PubMed2005

Prediction of the ablated area by the spread of microbubbles during radiofrequency ablation of hepatocellular carcinoma.

BACKGROUND/AIM: Radiofrequency ablation (RFA) is effective for the treatment of hepatocellular carcinoma (HCC). To prevent the ablation of adjacent organs and vessels, the spread of microbubbles generated by heating during RFA was observed by ultrasonography (US) and used to predict the ablated area; however, several reports documented that discrepancies existed between the spread of microbubbles and the ablated area. PATIENTS AND METHODS: The spread of microbubbles during RFA was observed by US in 24 patients with HCC and the areas were compared with the defect of enhancement in contrast enhanced (CE)-US, using Levovist in the same plane. RESULTS: During the ablation, the posterior margin was obscure but the border could be visualized 5 min after the ablation. The size of the area of hyperechogenicity 5 min after ablation and that of the defect observed by CE-US was found to correlate (r(2)=0.91, P<0.0001). The shape of the hyperechogenicity corresponded well to the defect area, even in cases showing irregular spread of the microbubbles. CONCLUSION: The observation of microbubbles during RFA can predict the ablated area and might be useful to prevent the unfavorable ablation of adjacent organs and vessels.

Adult↗
PubMed2006

The serpin protease nexin-1 regulates vascular smooth muscle cell adhesion, spreading, migration and response to thrombin.

BACKGROUND: Protease nexin-1 (PN-1) is an important physiological regulator of thrombin in the brain. PN-1 is also present in aortic smooth muscle cells and may thus participate in vascular biology. However, little is known about its function in the vessel wall. OBJECTIVES: In this study, we investigated the effect of PN-1 overexpression in smooth muscle cells (SMCs), on their sensitivity to thrombin, and their capacity for adhesion, spreading and migration. RESULTS: Two clones exhibiting a two- to threefold increase in PN-1 expression were selected and compared with untransfected and mock-transfected cells. Overexpression of PN-1 was observed to inhibit thrombin-induced cell responses as indicated by a twofold decrease in induction of PAI-1 expression, a decreased calcium mobilization in response to low thrombin concentrations and a twofold increase in the capacity to inhibit thrombin catalytic activity. Overexpression of PN-1 did not modify adhesion, spreading, and migration of SMCs on type I collagen. In contrast, SMCs overexpressing PN-1 exhibited a 40% reduction in adhesion, a 50% reduction in spreading and a complete absence of migration on vitronectin when compared with control SMCs. CONCLUSIONS: Our studies thus reveal that PN-1 is likely to play a critical role in regulating essential cell functions such as (i) thrombin-induced responses, which are dependent on its antiprotease activity, and (ii) adhesion, spreading, and migration, which are independent of its antiprotease activity and may be related to its interaction with other partners, such as vitronectin in the present case.

Amyloid beta-Protein Precursor↗
PubMed2006

von Willebrand factor mediates platelet spreading through glycoprotein Ib and alpha(IIb)beta3 in the presence of botrocetin and ristocetin, respectively.

BACKGROUND: von Willebrand factor (VWF) plays a critical role in the process of hemostasis by mediating flow-dependent adhesion and spreading of platelets on exposed extracellular matrix proteins following vascular injury. To accomplish this, VWF binds to two distinct platelet receptors: glycoprotein (GP)Ib-IX-V and integrin alpha(IIb)beta3. OBJECTIVE: To evaluate the ability of GPIb and alpha(IIb)beta3 to mediate platelet adhesion and lamellipodia formation on immobilized VWF in the presence of the biochemical modulators, ristocetin and botrocetin. RESULTS: In the presence of botrocetin and inhibitors of adenosine diphosphate (ADP) and thromboxane A2 (TxA2), VWF is able to support formation of lamellipodia through a GPIb-dependent mechanism that is independent of alpha(IIb)beta3 and PI3-kinase. Lamellipodia formation under these conditions is incomplete. In marked contrast, in the presence of ristocetin, VWF stimulates formation of fully spread lamellipodia through a pathway that is dependent upon alpha(IIb)beta3 and PI3-kinase. Furthermore, alpha(IIb)beta3 also supports platelet spreading on VWF alone, but only in the absence of inhibitors of ADP and TxA2. The localization of filamentous actin and the Arp2/3 complex in platelets on VWF in the presence of botrocetin and ristocetin are distinct, yielding disparate lamellipodium kinetic signatures. Interestingly, botrocetin significantly enhances platelet adhesion to VWF under flow in whole blood in an alpha(IIb)beta3-independent manner, while ristocetin augments washed platelet adhesion and spreading to VWF under flow in an alpha(IIb)beta3-dependent manner. CONCLUSIONS: These observations demonstrate that VWF is able to induce lamellipodia formation through distinct receptors, and has important consequences for investigation of the role of VWF-GPIb interactions in the context of platelet regulation.

Actin Cytoskeleton↗
PubMed1988

Dentin resorption in replanted monkey incisors. Morphology of dentinoclast spreading in vivo.

Dentinoclast colonization of a dentin surface was examined with special reference to changes in plasma membrane morphology during spreading and development into actively resorbing cells. Experimental cavities on the root surfaces of freshly extracted and replanted monkey incisors with infected pulps were examined with scanning electron microscopy after predetermined time intervals. The surface morphology of the dentinoclasts during the different spreading stages, and the fact that the stages appeared in a time-related mode indicated that dentinoclasts follow the general pattern of cell attachment and spreading on solid substrata, with a few exceptions unique to mineralized tissue resorbing cells. As a result, a 3-stage spreading model was proposed. In stage 1, dentinoclasts were characterized by an abundance of filopodia projecting towards the dentin surface. The cells appeared to be exploring the surface to find an area suitable for resorption. This was followed by an increase in cell size accompanied by a progressive disappearance of the peripheral filopod fringe (stage 2). Stage 3 apparently represented the final stage of adaptation and was characterized by an active resorption of the dentin surface.

Animals↗
PubMed1998

Heat-shock protein T-cell epitopes trigger a spreading regulatory control in a diversified arthritogenic T-cell response.

Adjuvant arthritis (AA) in Lewis rats is T-cell mediated and seems to depend on T cells recognising the 180-188 epitope of mycobacterial heat-shock protein (hsp) 60. Analysis of arthritogenic T-cell clone A2b has revealed a mimicry of this particular epitope with an articular cartilage-associated target T-cell epitope. Nasal administration of synthetic peptides covering this 180-188 sequence led to epitope-specific tolerance and resistance to AA. Since this tolerisation protocol also inhibited avridine arthritis, one may conclude that this form of epitope-specific tolerance had effectuated a spreading tolerisation at the level of target antigens that included a diverse set of possible arthritis-associated antigens. In vitro anergised T cells exhibited suppressive activity in a co-culture system. As in this case--depending on the presence of the antigen of the anergic T cell--such T cells suppressed responder T cells of a different antigenic specificity, we postulated that anergic T cells may be responsible for a spreading of tolerance. It seemed that such spreading of tolerance was channelled through the antigen-presenting cells (APC) and was dependent on direct cell-cell contact. This and additional forms of spreading of tolerance could be responsible for specific nasal tolerance, causing inhibition of the development of an arthritogenic inflammatory response. This can be similarly the case for the arthritis protection that resulted from immunisation with hsps. Analysis of T-cell responses following hsp immunisations revealed that the arthritis inhibitory activity resided in T cells with specificity for a conserved part of microbial hsp 60. The same T cells cross-responded to rat self-hsp60. Low level expression of the latter molecule on non-professional APC could possibly have induced a suppressive anergic state in these autoreactive cells. Thus, immunisation with microbial hsp would have led to an expansion of such T cells, leading to raised disease-suppressive potential when selectively trapped and activated in the inflamed self-hsp-overexpressing joint. Alternatively, the cross-recognised self-hsp epitope could have the regulatory qualities of an altered peptide ligand or a partial agonist for T cells that see the microbial homologue as the full agonist.

Animals↗
PubMed1998

B-cell epitope spreading in autoimmunity.

How the immune response matures from recognizing a single or a few structures of the antigen to many is an obviously important process. Models of B-cell epitope spreading have been developed in a variety of systems. For example, immunization of animals with PPPGMRPP, one of the earliest B-cell epitopes in the anti-Sm response found in human lupus, leads to antispliceosomal autoimmunity and features of lupus. The humoral immune response spreads from PPPGMRPP to other structures of the spliceosome in an apparently reproducible sequence. B-cell epitope spreading has provided the experimental basis from which a relationship between lupus and Epstein-Barr virus was suspected. An understanding of B-cell epitope spreading is likely to lead to important principles in basic immunology and to answers to human disease problems.

Animals↗
PubMed1999

Horizontal and vertical pigment spread into surrounding piebald epidermis and hair follicles after suction blister epidermal grafting.

Following the earlier description of Carnot and Deflandre in 1896, pigment spread phenomenon in mammals was investigated using immunogenetically marked melanocytes (Billingham and Silver, Quart. Rev. Biol. 1960 35: 1-40; Billingham and Silver, Ann. N.Y. Acad. Sci. 1963 100: 348-363). In spite of a number of similar studies on vitiligo lesions, detailed evaluation of pigment spread in piebald lesions has not been reported. To gain further insight into the pigment spread phenomenon in human skin, five piebald patients were studied, on whom suction blister epidermal grafting therapy onto piebald patches was performed. In the present study, pigmentation of all epidermal grafts from normally pigmented areas spread horizontally. It was also found that pre-existing white hairs in recipient sites became pigmented within 1 year after epidermal grafting. Immunofluorescence studies using melanocyte-specific antibody NKI/beteb revealed the newly induced presence of melanocytes in the newly pigmented hair follicles. Further, to study the possible mechanisms inhibiting melanocyte migration from normal skin into piebald lesions, epidermis was grafted from border zones (containing both normal and piebald skin) into the center of hypopigmented lesions. Melanocytes clearly migrated through the border zone of grafted epidermis into surrounding recipient hypopigmented sites.

Epidermis↗
PubMed1975

Spread of tuberculosis from obstructed and non-obstructed upper urinary tract.

As part of an experimental study of the spread of urogenital tuberculosis, male guinea pigs were inoculated with tubercle bacilli (H37Rv) in the upper part of the ureter. Half of the animals were prepared by ligature of the ureter below the injection site prior to inoculation. Spread of the infection to the lower urinary tract and the genitalia occurred whether the ureter was intact or ligated. It is concluded that lymphatic spread is possible and seems to be more common than urinary (canalicular) spread.

Animals↗
PubMedDate not supplied

Could chronic pain and spread of pain sensation be induced and maintained by glial activation?

An injury often starts with acute physiological pain, which becomes inflammatory or neuropathic, and may sometimes become chronic. It has been proposed recently that activated glial cells, astrocytes and microglia within the central nervous system could maintain the pain sensation even after the original injury or inflammation has healed, and convert it into chronic by altering neuronal excitability. Glial cell activation has also been proposed to be involved in the phenomenon of spread of pain sensation ipsilaterally or to the contralateral side (i.e. mirror image pain). Substance P and calcitonin gene-related peptide, released due to an inflammatory process, interact with the endothelial cells of the blood-spinal cord and blood-brain barriers. The barriers open partially and substances may influence adjacent glial cells. Such substances are also released from neurones carrying the 'pain message' all the way from the injury to the cerebral cortex. Pro-inflammatory cytokines may be released from the microglial cells, and astroglial Ca2+-transients or oscillations may spread within the astroglial networks. One theory is that Ca2+-oscillations could facilitate the formation of new synapses. These new synapses could establish neuronal contacts for maintaining and spreading the pain sensation. If this theory holds true, it is possible that Ca2+ waves, production of cytokines and growth factors could be modified by selective anti-inflammatory drugs to achieve a balance in the activities of the different intercellular and intracellular processes. This paper reviews current knowledge about glial mechanisms underlying the phenomena of chronic pain and spread of the pain sensation.

Astrocytes↗
PubMed1995

The spread of Corynebacterium pseudotuberculosis infection to unvaccinated and vaccinated sheep.

The decrease in the prevalence of Corynebacterium pseudotuberculosis after two generations of vaccination against the disease it causes, was used to estimate the rate of control of caseous lymphadenitis (CLA). Three groups of 150 sheep, of which 50 in each group were artificially infected with C pseudotuberculosis and 100 in each group were uninfected sheep, were run separately for 40 months and shorn 5 times to promote the spread of CLA. One lot of 50 infected sheep and 2 lots of 100 uninfected sheep were vaccinated against CLA. The rate of spread of CLA was recorded. Sheep vaccinated against CLA and naturally exposed to infection had a 74% lower infection rate than unvaccinated sheep. Sheep vaccinated against CLA and exposed to only vaccinated infected sheep had a 97% lower infection rate. Unvaccinated sheep had a 76% infection rate, with 77% of the transmission occurring at the 4th and 5th shearings, without any discharging CLA abscesses being observed. This study supports the view that in Australian wool producing flocks, CLA spreads mainly from sheep with discharging lung abscesses to sheep with shearing cuts. Vaccinated sheep infected with CLA have 96% fewer lung abscesses compared with unvaccinated infected sheep and are therefore less likely to spread this disease to other sheep.

Animals↗
PubMed1995

Prevalence, spread and control of caprine arthritis-encephalitis virus in dairy goat herds in New South Wales.

A study of the prevalence, spread and control of caprine arthritis-encephalitis virus (CAEV) in dairy goat herds in New South Wales (NSW) during 1986-1988 found that 56.8% of 1484 goats in 14 dairy herds were infected with CAEV. The prevalence of CAEV infection within most herds not implementing control measures increased during the study. At the end of the study, 59.7% of 1322 goats were infected. The prevalence of CAEV increased with age. Differences between breeds were less apparent. Within seven herds with a high standard of identification of goats, 149 of 812 goats seroconverted in an ELISA. Of these newly infected goats, 142 (95.3%) were > 1 yr of age and 96 (64.4%) were > 2 yr suggesting lateral spread of the virus. Most of the goats > 2 yr of age had been in the milking herd for a minimum of 3 to 6 months. The high seroconversion rate within the milking herd suggested that factors other than the ingestion of infected colostrum and milk before weaning were important for the spread of CAEV. Observations indicated that behaviour of goats, particularly reproductive behaviour among lactating does, and milking herd management practices are important in the spread of CAEV. A high density of livestock, poor livestock control and contamination of feed, water, equipment and personnel were implicated in transmission. Poorly functioning milking machines may also be involved. CAEV was eradicated from 3 herds by the implementation of strict control measures.

Age Factors↗
PubMed2005

Longitudinal study of the spread of ovine Johne's disease in a sheep flock in southeastern New South Wales.

OBJECTIVE: The aim of this study was to apply whole flock testing over time to determine the prevalence, distribution and spread of infection in a recently infected flock, with a view to planning intervention strategies for disease control. PROCEDURE: Serology, pooled faecal culture (PFC) and histology were used to determine the distribution and persistence of infection in a sheep flock in south east New South Wales between 1997 and 2002. Partial flock testing was done up to June 2000, after which annual whole flock testing, using PFC was performed. RESULTS: Faecal shedding of M a paratuberculosis was not detected in home-bred sheep until 7 years after the introduction of infected sheep in 1993. For at least 7 years there was clustering of infection and shedding within two age groups only. The infected groups appeared to have been exposed to infection (mycobacterial contamination) at an early age (<12 months) and commenced shedding at 5 years of age or older. Groups that were exposed to contamination as adults did not shed detectable amounts of M a paratuberculosis during the study period. CONCLUSION: Clustering of detectable infection in age groups of sheep that were exposed as lambs was a feature on this farm, providing indirect evidence of finite duration of survival of M a paratuberculosis on pasture and the influence of age on the susceptibility of sheep to develop detectable M a paratuberculosis infection. Spread of infection occurred very slowly and was probably related to the long incubation period (exposure to shedding interval) of 5 years observed on this farm. The findings suggest that partial flock culling, selective grazing management and vaccination could lead to a reduction in mycobacterial contamination on farm to a level at which patent infection no longer occurs. Better understanding of disease spread within flocks over time through flock profiling using PFC will help in devising surveillance strategies (including testing protocols for market assurance testing) to detect infected flocks where there has been clustering and slow spread of infection.

Animal Husbandry↗
PubMed1974

Inward spread of activation in frog muscle fibres investigated by means of high-speed microcinematography.

1. Single fast muscle fibres of the frog were locally activated by applying current pulses to a pipette whose tip was in contact with the fibre surface, and the resulting local contractions were recorded with a high-speed ciné-camera at 1000-3000 frames/sec.2. In some but not all of the fibres examined, a moderate membrane depolarization of 20-30 mV initiated a phasic type of local contraction, which showed a definite threshold and relaxed spontaneously while the depolarization still continued.3. The phasic contraction was sometimes followed by a smaller steady contraction, which lasted as long as the depolarization went on and was regarded to be indentical with the graded type of local contraction.4. With pipettes of 20-40 mum diameter, the phasic contraction was first initiated at the depolarized fibre surface, and spread to some extent inwards with a velocity of 0.7-2 cm/sec at 18-26 degrees C. The velocity of inward spread of contraction had a Q(10) of about 2.3.5. With larger pipettes of more than 50-60 mum diameter, the phasic response was first initiated at the inner part definitely distant from the fibre surface, and the extent of contraction was greater at this part than at the superficial part during the course of the response. Furthermore, with depolarizations of nearly the threshold value, the steady contraction following the phasic one was seen only at the inner part, suggesting the reversal of the gradient of depolarization along the T tubules.6. The phasic contraction spread inwards or transversely with a considerable decrement. The response spreading across the whole diameter of the fibre could be observed only in some cases.7. The phasic response was not always sensitive to tetrodotoxin or to the removal of external sodium ions.8. These results not only give information about the nature of the regenerative mechanism within the T system, but also suggest that the organization of the T tubule network is such that the electrotonic depolarization becomes maximum at the T tubules located distant from the fibre surface when a sufficiently large area of surface membrane is depolarized.

Animals↗