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Inflammation and oxidative stress in
vertebrate host–parasite systems
Gabriele Sorci*and Bruno Faivre
BioGe ´oSciences, CNRS UMR 5561, Universite ´ de Bourgogne, 6 Boulevard Gabriel, 21000 Dijon, France
Innate, inflammation-based immunity is the first line of vertebrate defence against micro-organisms.
Inflammation relies on a number of cellular and molecular effectors that can strike invading
pathogens very shortly after the encounter between inflammatory cells and the intruder, but in a non-
specific way. Owing to this non-specific response, inflammation can generate substantial costs for the
host if the inflammatory response, and the associated oxygen-based damage, get out of control. This
imposes strong selection pressure that acts to optimize twokey features of the inflammatory response:
the timing of activation and resolution (the process of downregulation of the response). In this paper,
we review the benefits and costs of inflammation-driven immunity. Our aim is to emphasize the
importance of resolution of inflammation as awayof maintaining homeostasis against oxidativestress
and to prevent the 'horror autotoxicus' of chronic inflammation. Nevertheless, host immune
regulation also opens the way to pathogens to subvert host defences. Therefore, quantifying
inflammatory costs requires assessing (i) short-term negative effects, (ii) delayed inflammation-
driven diseases, and (iii) parasitic strategies to subvert inflammation.
Keywords: ageing; delayed costs; immune evasion; innate immunity; nitric oxide;
reactive oxygen and nitrogen species
Immune defences may be seen as one of the most
sophisticated products of interspecific interactions.
They are the result of frequent and long 'arms races'
between hosts and parasites. As a result, hosts have
evolved complex strategies to avoid the negative effects
of parasites, and parasites have evolved many adaptive
responses to counteract and evade the hosts' defences.
Recognizing pathogenic organisms and clearing infec-
tion is the primary function of immunity (Medzhitov &
Janeway 1997). This self-defence ability exists in
unicellular organisms (that can produce microbicidal
molecules), and reaches a high complexity in
vertebrates (that possess a wide array of effectors that
operate to cope with pathogenic invaders; Armstrong &
Quikley 1999; Bulet et al. 2004).
Vertebrate immunity basically depends on two arms:
innate and acquired immunity. The protective proper-
ties of innate immunity rely on constitutively produced
receptors (pattern recognition receptors) that recognize
distinct and conserved microbial molecular structures
(pathogen-associated molecular patterns, PAMPs),
which are absent from the host: once bound, these
receptors directly activate the host's immune cells. The
outcome of this activation is the initiation of the innate
inflammatory response (Janeway & Medzhitov 2002;
Akira et al. 2006). By contrast, acquired immunity is
characterized by a vast repertoire of lymphocytes,
bearing antigen-specific surface receptors that recognize
specific antigenic configurations of pathogens and
respond by triggering cellular (cytotoxic T-cells) and
humoral (antibodies) effectors. In addition to specificity,
acquired immunity differs from innate immunity in its
ability to establish an immunological memory, which
allows a more rapid and effective response upon
re-exposure to the antigen (Cooper & Alder 2006).
The dichotomy between innate and acquired immunity,
while useful for a classification purpose, does not mean
that these two branches work independent of one
another. Acquired immunity largely depends upon the
cells of the innate immune response to drive their
functional maturation (Bayne 2003). In spite of the
intimate connection between the innate and acquired
immune responses and the major role played by the
innate effectors in the process of parasite resistance, we
still tend to focus on acquired immunity as the most
important weapon against pathogens. This is evidenced
by the biased representation of the acquired immune
effector systems that have been studied in ecological
immunity studies on vertebrates.
Inflammation is a non-specific process, elicited by
trauma or infection, characterized by the delivery of
fluids, molecules and cells from the blood into
damaged or infected tissues, whose function is to
fend off infectious agents. Although inflammation is
commonly considered a vertebrate phenomenon, an
inflammatory-like status has also been reported in
invertebrates (Libert et al. 2006) where cells releasing
toxic products and chemical signals are involved. The
systemic effects of the vertebrate inflammatory
Phil. Trans. R. Soc. B (2009) 364, 71–83
Published online 17 October 2008
One contribution of 11 to a Theme Issue 'Ecological immunology'.
*Author for correspondence (email@example.com).
This journal is q 2008 The Royal Society
Page 2
response include fever and an increased number of
leucocytes recruited for defence (Sell 2001). Several
leucocyte families, e.g. granulocytes, monocytes (the
precursors of macrophages) and lymphocytes, migrate
to the focal area of the infected tissue and secrete
metabolites, which have potent microbicidal properties
that act through phagocytosis and exocytosis (Sell
2001). Upon encounter with an intruder, inflammatory
cells produce peptides that play a key role in cellular
communication. These peptides, called cytokines, can
further activate and recruit other phagocytic cells, as
well as drive their microbicidal activity. Phagocytes can
kill engulfed pathogens mostly through the action of
endogenously produced compounds with cytotoxic
effects, such as enzymes, lytic peptides, as well as highly
reactive oxygen and nitrogen species (ROS and RNS;
Fang 2004; Swindle & Metcalfe 2007). In addition, and
besides their cytotoxicity, at a low dose, ROS and
especially nitric oxide (NO) also play a regulatory role as
modulators of cellular communication and apoptosis
(Matsuzawa et al. 2005; Swindle & Metcalfe 2007).
The effectors of inflammation endoworganismswith
efficient weapons to cope with the pervasiveness of
infectious agents. The most compelling support to this
view is the high sensitivity to infection, and the reduced
survival prospect, of organisms showing deficiencies in
the inflammatory process (Fang 2004). However,
immune systems are not infallible, and the inflam-
matory response should be viewed as a double-edged
sword that protects, but has the potential to harm, the
host. Host tissue may be damaged when immune
defences are misdirected, or overexpressed, leading to
immunopathology. Although the distinction between
immunopathologies and their origin is still debated
(McGonagle & McDermott 2006), there is little doubt
that chronic inflammation produces collateral undesir-
able effects on the host. In addition, it has been
suggested that the cost of infection is more due to an
over-reacting inflammatory response than a direct
effect of the pathogen (Ra ˚berg et al. 1998; Mackintosh
et al. 2004; Graham et al. 2005; Halliwell 2006 for
reviews). To protect their tissues from inflammatory
injury, hosts have evolved a regulatory network based
on a class of cytokines (such as interleukin-10 or
transforming growth factor-b) that control the res-
olution of inflammation once the pathogen has been
cleared (Belkaid 2007).
Although the study of the molecular and cellular
mechanisms of inflammation-based resistance is of
prime importance from a biomedical perspective,
understanding the selective forces and the constraints
shaping the evolution of the diversity of host defences
and parasite strategies to exploit the host requires an
evolutionary approach. The aim of this paper is to
provide a discussion of the evolutionary ecology of
parasite-mediated inflammation. We will first briefly
review the mechanisms, which are at the basis of the
inflammatory response, with a special focus on
the production of ROS and RNS. Then, we will
discuss the selective forces and constraints that are
likely to act on inflammation: the benefits of early and
effective protection against intruders and the inevitable
costs of non-specificity. Because parasite exposure and
host response vary with ontogeny, we will address the
question of age-related costs and benefits of inflam-
mation. Finally, we will see that the pathogens can
modify and manipulate host inflammation for their
own survival and spread. This adds considerable
complexity to the understanding of the evolutionary
ecology of parasite-mediated inflammation.
Phagocytic cells, such as macrophages and neutrophils
(heterophils in birds), are at the core of the innate
inflammatory response. Activation of phagocytic cells
induces the production of antimicrobial compounds
that, once transferred into the phagosome, play a
primordial role in killing phagocytized pathogens.
ROS and RNS are probably the most important
micromolecules that intervene during the inflam-
mation-based control of invading pathogens. The
most prominent feature of ROS and RNS is their
generic cytotoxicity. These chemically reactive
molecules cannot discriminate between the structure
of host molecules, cells and tissues and infectious
agents. This is in stark contrast to the fine-tuned
capacity of the cells and molecules of the acquired
immune system, which can recognize specific epitopes
and surgically target the defence response. In §2a, we
will first briefly describe the molecular nature of
ROS and RNS, and their production and will then see
how these reactive molecules achieve the goal of
pathogen killing.
(a) ROS and RNS
Upon stimulation by a PAMP, neutrophils and
macrophages respond by a marked increase in oxygen
(O2) uptake. This increase in O2 consumption
characterizes the so-called respiratory burst and is the
consequence of the activation of an enzymatic system
(NADPH oxidase or phox) that oxidizes NADPH into
NADPCplus superoxide anion (O$K
Superoxide, in addition to its own cytotoxic effect,
participates in the generation of other, more unstable
and damaging molecules, such as hydroxyl radicals
(OH%), hydrogen peroxide (H2O2) and hypochlorous
acid (HOCl). The half-life capacity to permeate cell
membranes and the cytotoxicity vary greatly across
different ROS. For instance, OH%has a half-life of a few
nanoseconds whereas chloramines are stable for hours
(Swindle & Metcalfe 2007).
RNS are the second class of micromolecules
secreted by phagocytic cells during the inflammatory
response. Nitric oxide (NO%) is the principal RNS
produced by neutrophils and macrophages. NO%is
generated enzymatically in a two-step reaction from
L-arginine substrate (Fang 2004). This reaction is
catalysed by a family of enzymes, the NO synthases
(NOS). The inducible NOS (iNOS) is responsible for
the burst in NO production following an inflammatory
insult. Nitric oxide has a cytotoxic effect but it can also
react with ROS to produce even more powerful
oxidants, such as peroxynitrite (ONOOK) or dinitro-
gen trioxide (N2O3) (Halliwell 2006).
2) (Fang 2004).
72 G. Sorci & B. Faivre
Review. Inflammation and oxidative stress
Phil. Trans. R. Soc. B (2009)
Page 3
(b) ROS and RNS are effective antimicrobial
The importance of ROS and RNS during the
inflammatory response, and their role as effective
antimicrobial agents, is provided by two lines of
evidence: the identification of the molecular target of
ROS and RNS in vitro and the fitness cost paid by
individuals who cannot produce these molecules.
ROS and RNS have been shown to target several
molecular structures of invading pathogens, in parti-
cular proteins, DNA and lipids. Depending on the
chemical characteristics of each radical species (for
instance, their capacity to cross lipid membranes),
different molecular patterns of the pathogen can be
targeted. For instance, Imlay & Linn (1986) showed
that hydrogen peroxide (H2O2) can kill Escherichia coli
in a dose-dependent manner, where low concentration
mostly oxidized DNA, whereas higher concentration
simultaneously oxidized several biomolecules. Nitric
oxide can inhibit bacterial respiration and DNA
replication (Fang 2004). Moreover, when in the
presence of ROS, the NO-derived oxidative damage
is greatly enhanced.
It should be noted, however, that for both ROS and
RNS, the effectiveness of their antimicrobial activity also
depends on the local redox environment. Reactive
species can be scavenged by several detoxification
systems (enzymatic and non-enzymatic). In most
cases, therefore, the microbicidal effectiveness of the
and the availability of microbial antioxidant defences.
The second line of evidence on the importance of
ROS and RNS as effective inflammatory effectors
comes from studies that have either taken advantage
of spontaneous mutations affecting the genes control-
ling the expression of phox, either using knockout
mouse strains lacking phox or iNOS.
Chronic granulomatous disease (CGD) is a human
pathology that occurs as a consequence of mutations in
subunits of NADPH oxidase. Patients affected by
CGD cannot produce superoxide anions (O$K
2) during
the respiratory burst. The disease substantially reduces
lifespan and is associated with persistent infection with
a number of pathogenic micro-organisms, such as
Staphylococcus aureus, Pseudomonas and Salmonella
(Sell 2001).
Inducible NO synthase is the major enzymatic
pathway responsible for the production of nitric
oxide. Although there is no known human deficiency
in the expression of iNOS, polymorphisms in the iNOS
promoter region have been reported in several studies
(Levesque et al. 1999; Kun et al. 2001). In most cases,
increased iNOS expression is correlated with increased
resistance to a number of different pathogens, includ-
ing Plasmodium (Anstey et al. 1996; Hobbs et al. 2002).
Similarly, human macrophages that express iNOS at
high levels in vitro are better able to kill Leishmania and
Mycobacterium parasites (Bogdan et al. 2000).
Studies on animal models have provided the best
ultimate evidence for the importance of ROS and RNS
in parasite resistance. Using knockouts lacking phox
(gp91phoxK/K), iNOS (iNOSK/K) and control wild-
type mice infected with Salmonella typhimurium,
Mastroeni et al. (2000) showed that the course of the
infection was greatly affected by the absence of
superoxide and NO (figure 1). Interestingly, inhibiting
the NADPH synthase pathway (ROS production) or
the iNOS pathway (NO production) resulted in a quite
different pattern of infection-induced mortality, with
phoxK/Kindividuals already showing massive mortality
at 3–4 days post-infection, whereas suppression of the
iNOS pathway produced substantial mortality only
approximately two weeks post-infection.
Interestingly, the functional role of NO against
invading parasites is not restricted to intracellular
micro-organisms. Brugia malayi is an extracellular
nematode that is responsible for lymphatic filariasis in
humans. Rodents can also be infected with filarial
parasites, which allow experimental tests of the
effectors of immunity against such parasites. Using
elegant experiments, Rajan et al. (1996) showed
that iNOS is an important mediator of resistance to
012345678 9 10 11 12 13 14 15 16 17 18 19 20
days post-infection
survival (%)
Figure 1. Survival of mice infected with S. typhimurium. Wild-type (C57BL/6, black circles) mice show 100% survival at
20 days post-infection. On the contrary, KO mice that do not express phox (NADPH-based respiratory burst, light
grey circles) or iNOS (NO production, dark grey circles) die during the course of the study. Interestingly, mortality was
much more rapid in the phoxK/Kgroup (100% mortality at day 5 post-infection) than in the iNOSK/Kgroup (100% mortality
at day 19 post-infection). This suggests that respiratory burst precedes the NO response during the acute inflammatory
response (adapted from Mastroeni et al. 2000).
Review. Inflammation and oxidative stress
G. Sorci & B. Faivre73
Phil. Trans. R. Soc. B (2009)
Page 4
B. malayi. Mice were infected with B. malayi larvae and
then were either injected with aminoguanidine (AG, an
inhibitor of iNOS) or left untreated. A larger number of
adult worms were yielded from AG-treated mice
compared with controls, whatever the initial number
of larvae inoculated. In a second complementary
experiment, susceptible mice (SCID mice) were
infected with Brugia larvae and then either injected
with DEA/NO (a compound that releases NO) or left
as control. In agreement with the results of the first
experiment, the number of adult worms yielded from
DEA/NO mice was much smaller compared with
control, susceptible mice (Rajan et al. 1996).
(c) How does natural selection operate on the
effectors of the inflammatory response?
This brief survey shows that early inflammatory
response is important for host resistance towards a
range of parasitic organisms, since individuals lacking
the ability to produce ROS and RNS are more
susceptible to infection and suffer from an increased
infection-induced mortality. At a first glance, one
might be tempted to believe that natural selection
operates on the effectors of inflammation to exhibit the
highest toxicity. However, we should keep in mind the
crucial feature of the innate inflammatory response:
non-specificity. ROS and RNS do not discriminate
between host and pathogen DNA, proteins or lipids. As
such, ROS and RNS can be quite costly for the host.
Therefore, one might wonder how natural selection has
shaped the effectors of the inflammatory response as to
maximize the protectiveeffect while minimizing the risk
of collateral damage. There are at least two solutions to
this problem. The first is rapidity. The effectors of
inflammation are usually activated within minutes
(another major difference from adaptive immunity
which needs days/weeks to be fully deployed).
It appears that the chronological suite of events that
are triggered by an immune insult is organized so as to
progress from the most to the less costly response. Even
within the inflammatory response, there is a chrono-
logical sequence suggesting that the more toxic ROS
produced during the respiratory burst precedes the
activation of the iNOS pathway and its milder NO
delivery (Vazquez-Torres & Fang 2001). Costly inflam-
matory response is therefore rapidly activated but it
should also be rapidly switched off to avoid the 'horror
autotoxicus' of chronic inflammation (figure 2).
Macrophages secrete a number of anti-inflammatory
molecules, such as interleukin-10 (IL-10) and trans-
forming growth factor b (TGF-b), which contribute to
the resolution (the process of downregulation) of the
inflammatory response. Once again, the dichotomy
between the innate inflammatory response (antigen
non-specific) and the acquired immune response
(antigen specific) emphasizes the intrinsically costly
nature of inflammation. This is because, at least in
principle, antigen-specific immunity can be free of cost,
in terms of autoimmunity, if T-lymphocytes with
receptors that bind to autoantigens are negatively
selected in the thymus or suppressed in peripheral
organs. The non-specific nature of inflammatory
neutrophil recruitmentrecognition
respiratory burst (ROS)
pro-inflammatory cytokines
macrophage activation
NO production
pro-inflammatory cytokines
anti-inflammatory cytokines
inflammatory response
chronic inflammation
immunological oxidative stress
persistent stimulusregulation failure
parasite manipulation
Figure 2. (a) A schematic view of the time course of acute inflammation. Once a pathogen has entered the host, pattern
recognition receptors (PRR) on cell membranes bind to some pathogen molecular signatures. This recognition phase is followed
by the recruitment of neutrophils and their respiratory burst. Sustained production of pro-inflammatory cytokines activates
macrophages. Macrophages with engulfed pathogens start the resolution process by secreting anti-inflammatory cytokines.
(b) Two of the outcomes of infection-induced inflammation: (i) clearance and resolution; and (ii) chronic inflammation and
immunological oxidative stress. Parasites, of course, can interfere with the normal outcome of the inflammatory response for
their own survival.
74 G. Sorci & B. Faivre
Review. Inflammation and oxidative stress
Phil. Trans. R. Soc. B (2009)
Page 5
effectors means, by definition, that the response
generates costs whose magnitude depends on the
intensity and duration of the response. In §3, we will
review in more detail the costs of acute and especially
chronic inflammation and how this has led to the
evolution of regulatory mechanisms.
(a) Direct and indirect costs
There is now a large body of evidence showing that
pathogen-induced inflammation is associated with an
increase in ROS and RNS production. A number of
correlative studies have reported associations between
local or systemic infections and oxidative damage. For
instance, humans infected with HIV suffer from an
increased amount of serum hydroperoxides and
malondialdehyde (the products of lipid peroxidation)
and reduced availability of antioxidants (both enzy-
matic and non-enzymatic) (Pace & Leaf 1995). Septic
shock, probably one of the most severe consequences of
the inflammatory response (Annane et al. 2005) is
accompanied by a substantial production of NO and
peroxynitrite (Titheradge 1999; Sebbane et al. 2006).
Experimental work has also shown that activation of
the inflammatory response depletes antioxidants and
exposes the host to increased risk of oxidative stress.
Zebra finches (Taeniopygia guttata), whose innate
immune response was activated by lipopolysaccharide
(LPS) injection, showed a decrease in antioxidant
status 24 hour post-injection compared with a control
group (figure 3; Bertrand et al. 2006). Although one
might wonder about the relevance of such an effect in
terms of fitness, previous work has shown that a
decrease in antioxidant status significantly predicts
short-term survival prospects (Alonso-Alvarez et al.
2006). These results, therefore, suggest that the
activation of the inflammatory response by PAMPs
can incur fitness-relevant costs.
The most compelling evidence that inflammatory
response may alter host homeostasis comes from in vivo
and in vitro experimental studies which controlled
antioxidant availability, and/or ROS and RNS pro-
duction through pharmacological treatments or using
genetically modified organisms. For instance, experi-
mental infection of mice with the retrovirus ts1
(a murine leukaemia virus) caused spongiform ence-
phalopathy, thymus atrophy and other severe neuro-
pathologies leading to death. In vitro experiments
showed that the redox-sensitive transcription factor
(Nrf2) was activated in cultured ts1-infected astrocytes.
This factor upregulates the synthesis of glutathione (an
antioxidant compound; Qiang et al. 2004). The
astrocytes surviving to the infection were those
producing the highest antioxidant defences, suggesting
that ROS and RNS scavenging are crucial for cell
survival and control of immunopathology (Qiang et al.
2006). In addition, treatment of astrocytes with
an antioxidant (a refined monosodium a-luminol)
reduced ROS accumulation and suppressed Nrf2
activation (Jiang et al. 2006). In short, this work
shows that the degree of infection-induced immuno-
pathology depends on the activation of antioxidant
compounds that scavenge ROS and RNS produced
during the inflammatory response.
Blocking ROS or RNS production by means of
specific inhibitors, or by the use of genetically modified
organisms, has provided further evidence for the link
between oxidative stress and inflammation. Humans
infected with the Sin Nombre virus, the causative agent
of cardiopulmonary syndrome, show an elevated
expression of iNOS in the lungs, especially in areas
with more severe pathology. Patients with the most
severe symptoms were those with higher plasma
NO-derived molecules NOx. A murine model of the
disease (mice infected with lymphocyte choriomenin-
gitis virus) showed, within a few days post-infection,
identical pulmonary and cardiac symptoms associated
with both elevated iNOS in the lungs and NOx in
plasma. The periodic injection of a specific iNOS
inhibitor in infected mice suppressed the cardiac
symptoms and strongly improved short-term survival
without changing virus titres (figure 4), suggesting that
oxidative damage may outweigh the direct negative
effects of viral replication (Davis et al. 2002).
(b) Immediate and delayed costs
Inflammation incurs costs. Assessing such costs is
essential if we want to appraise the outcome of selective
forces operating on the inflammatory response. Having
a complete picture, however, requires considering not
only the immediate, short-term, costs of inflammation
but also those expressed once the infection has been
cleared. Chronic inflammation may lead to delayed
negative outcomes. Probably the most important
delayed disabling consequence of chronic inflam-
mation is cancer. There is now a large body of evidence
showing that many cancers are associated with
pathogens, and epidemiologic studies attribute to
15–20% of worldwide malignancies to infection
(Coussens & Werb 2002). A wide array of pathogens
may contribute to cancer occurrence through the
inflammatory response of the host, and particularly
the release of ROS and RNS (Ames et al. 1995). Under
chronic inflammation, cells damaged by cytotoxic
products are permanently replaced, but sustained
ROS and RNS production can result in genomic
alteration (De Marzo et al. 2008). Cultured mouse
macrophages continuously exposed to interferon-g
(an effector of the inflammatory response) show a
red blood cell resistance to
a free-radical attack (min)
Figure 3. Activation of the inflammatory response by the way
of a LPS injection, which depletes antioxidant defences in
male (white bars) and female (black bars) zebra finches
(adapted from Bertrand et al. 2006).
Review. Inflammation and oxidative stress
G. Sorci & B. Faivre 75
Phil. Trans. R. Soc. B (2009)


text:
You've probably noticed all the posts here on design principles over the last year or so. Some of you have let me know you've been enjoying them and if I haven't thanked you directly let me thank you here and now.
I thought I'd take a few minutes to explain why I started writing these posts and why I think design principles are important even vital for web designers to learn and understand how to use.
Continue reading

subset: commoncrawl


text:
Product Information
I. Promenade composed by Gordon Young - Digital Sheet Music
from Triptyque for Organ and Flute
At a Glance
I. Promenade digital sheet music. Contains printable sheet music plus an interactive, downloadable digital sheet music file.
* This product is available worldwide
Arrangement Details
The Arrangement Details Tab gives you detailed information about this particular arrangement of I. Promenade - not necessarily the song.
Song Details
The Song Details Tab gives you detailed information about this song, I. Promenade.
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The Related Products shows you other products that you may also like, if you like I. Promenade.
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text:
Category:1957 singles
From Wikipedia, the free encyclopedia
This category includes articles about songs issued as singles, (45rpm phonorecords) which were released in the year 1957.
See also: 1957 in music
Pages in category "1957 singles"
The following 137 pages are in this category, out of 137 total. This list may not reflect recent changes (learn more).
- I Beg of You
- I Can't Stop Loving You
- I Like Your Kind of Love
- I'll Come Running Back to You
- I'm a King Bee
- I'm Gonna Be a Wheel Someday
- I'm Gonna Love You Too
- I'm Gonna Sit Right Down and Write Myself a Letter
- I'm Spinning
- I'm Walkin'
- In the Middle of an Island
- It Hurts Me Too
- It'll Be Me (Jerry Lee Lewis song)
- It's Not for Me to Say
- Wake Up Little Susie
- Walkin' After Midnight
- Walking Along
- White Silver Sands
- A White Sport Coat
- Who Do You Love? (Bo Diddley song)
- Who Needs You?
- Who's Sorry Now?
- Whole Lotta Shakin' Goin' On
- Wild Is the Wind (song)
- With All My Heart
- Without Love (Clyde McPhatter song)
- Wonderful! Wonderful!
- Wondering (Patti Page song)
- Words of Love


text:
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Southwest Electric Cooperative, Inc. • 1023 S Springfield Ave • PO Box 150 • Bolivar, MO 65613
Phone: 417-326-5244 • Power Outage Phone: 800-262-0326 • Email: firstname.lastname@example.com
© 2015 Southwest Electric Cooperative, Inc. This institution is an equal opportunity provider and employer.
Site Design By: Midwest Interactive
Since 1939, Southwest Electric Cooperative has empowered our member-owners with an improved quality of life through electricity.
Today, SWEC provides electric power to more than 40,000 services throughout eleven counties in southwest Missouri.
View All News
Osage strengthens wind energy portfolioSpringfield, Missouri based- Associated Electric Cooperative, Southwest Electric Cooperative's power supplier,
EPA delays carbon dioxide rule til mid-summerThe EPA had been expected to finalize its highly controversial carbon dioxide
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1023 S Springfield Ave
PO Box 150
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J7 Office
6179 N State Hwy 7
Roach MO 65787
Bluegrass Office
3905 E Farm Rd 94 Springfield MO 65803
Preston Office
RR 1 Box 144
Preston MO 65732


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I think there called "sputnik sinkers", there the ones that have the wires and the beads that 'snap' up to lock them.? I'm wondering if anyone knows of a place where I can get a mold for them? I've made a couple by drilling holes in other sinkers I have, but a mold would make it much easier. Thanks for your help!
Sputnik Sinkers?
Posted June 23 2001 - 6:14 PM
Posted June 23 2001 - 6:38 PM
Hey J,
Fuhgetabout sputniks. Never saw one work right yet. They work best to tangle everyone elses line with yours when fishing close. Pyramids are best and Hatteras style work too. You gotta pick the right weight for the right current, situation, etc.IMHO
[This message has been edited by fenderbender2001 (edited 06-23-2001).]
Posted June 23 2001 - 7:24 PM
sputnik sinkers have there time & place ;
1: NOT when fishing in crowds
2: when you need a weight greater than your rod is rated for, since a 3oz sputnik will hold better than a 3oz anything else (probally holds as well as a 5oz)
3: the wire arms need to be 'adjusted ' so they will release (sprung open a tad )
number 2 is probally the best reason I can give for these sinkers ; haven't used mine since I got the rods needed to handle any & all weights .they got me through some rough water when I didn't have the rods rated to throw ??& bait .
To answer your ? I think a Brittish site has a mold to make them ....will check & post the site .
[This message has been edited by derf (edited 06-23-2001).]
Posted June 23 2001 - 7:34 PM
Don't bother with a mold. You only loose them if you snap off. Sports Authority has them for $1.89 each. They are the ones from Breakaway USA.
Posted June 23 2001 - 7:56 PM
breakaway has'em,theyre online,i use these at times with a homeade baitclip when i feel the urge to get more distance on my casts,the torpedo design does get you a nice far cast tho and the wires are nice untill you dig in a kelp bed,on my rig i use the clip that holds the weight and the hook which slips under another hook on the clip.its a pain to tye the hook lead the right length but they do keep the bait rig from looking like a huey spinning out on a cast.the thin weight is nice too as its aerodynamic,it aint rocket science but it works for me.i dont buy the clips i make mine from 1/16" carbon steel and two pair of needlenoses.to make your own spider sinkers get some heavy copper wire,trim up 4" lengths and insert them in a 1/2" deep socket,set the socket on a flat steel plate and then pour your lead in center your loop for the line or rig while its molten with needle nose.when the tops flashed over drop it in a bucket of ice water and yank it out or tap it.usually they fall out.now ya can bend your wires the way you want.the deep sockets can be a pain but you can also use a shorty in 3/4" socket for same results if ya just want the sinker to hold bottom.like i said tho tye the hook lead so it fits nice,the weight when cast will stretch holding the baited hook ok so it wont come off till it splashes water.for me its easier ,cheaper and i dont have to wait days for a few plastic setups to do the same thing altho breakaways stuff is nice.
Posted June 23 2001 - 7:59 PM
Second Prefessa on that,have a couple also from Spts Auth. Have them in van,just in case..
eddie p
Posted June 24 2001 - 7:12 AM
I guess, from reading the above posts, that maybe I'm not using the right weights when I fish. I fish IBSP alot, and alot of times when I go the current seems to be to strong for my 6oz. pyramids. Being my bait poles are all rated for 6oz. max, I them switch to 6oz. sputniks which usually do the trick. I hear of guys using 8 - 12 ounces, but I'm retricted to the 6oz mark. Am I doing something wrong?
Posted June 24 2001 - 8:18 AM
jenty i never believe the rods info.nope i dont.i have some rods rated 1-6 oz and found that i could heave 8 and the rod still loads ok with out fear of a breakage.another rod i have is rated 1-6 oz and she whines please dont hit me im loaded to the max after a 4 oz bank sinker.experimenting is ok but dont load like gawdzilla on the rod at first,if she accepts it by the 3rd cast with a full tilt heave you should know your ok.ps i only have med. to heavy actions and i wouldnt dare do it with a soft tipped rod.
Posted June 24 2001 - 7:51 PM
So I guess trying to heave 8 oz. on the old trout rod is unacceptable?
Posted June 25 2001 - 10:26 AM
You have it 100% correct! The Sputnik sinkers in 150 gm are the biggest you will ever need. On the last front I was at seabright. Now seabright is by far the place that is the hardest to hold bottom. I was fishing two rods, and just for the info I fished Sputniks on one rod and pyramids on the other. The 130 gm Sputnik(4 1/2 ounce) held as well as an 8 oz pyramid! I expect the 150 would be like throwing a 10 oz. If the surf is not rough I use Hatteras sinkers. Once I need six ounces or more the Sputniks come out.
BTW: Your bait counts! If yor rod is rated for six ounces then you must take into account that a clam weighs~1 1/2 ounces. So when you are throwing 6 you are really throwing ~8 OZ
[This message has been edited by Prefessa (edited 06-25-2001).]
Posted June 26 2001 - 11:25 AM
Hope this helps! :-}
(they both have the molds)
Posted January 17 2008 - 11:26 PM
Heres where I got Mine 5 & 6 OZ get the Wires from them to, got my beads at Micheals Crafts
adjusti-moulds on left
Posted January 17 2008 - 11:28 PM
They're probably all set after 6 and a half years.


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My Name Is Tristaun Johnson Aka TDarius. I began rapping at the age of eleven, and progressed to other things such as writing poems, and quotes. I live In west asheville but born in Miami florida. I love music this is my dream and the love to my life i could never give it up!
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This book is at once an exploration of the chasm between and a reconciliation of mental space (the space of the philosophers and epistemologists) and real space (the physical and social spheres in which we all live). In the course of this reconciliation Lefebvre moves from metaphysical and ideological considerations of the meaning of space to its experience in cities, homes and regions.
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Ramdev, V K Singh named in riot FIR
Top Stories
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Yoga guru Ramdev and former Army chief V K Singh are among six persons named in a FIR filed by police after clashes on Sunday with a crowd which tried to march from Jantar Mantar to India Gate where people were protesting the gangrape of a 23-year-old woman on board a moving bus a week ago.
The FIR states that Ramdev went back on his word to police and tried to incite people to march to India Gate. Inspector Praveen Kumar, who lodged the FIR at Parliament Street police station, has said V K Singh was among those who addressed the crowd from a dais at Jantar Mantar.
Other speakers named in the FIR are journalist Ved Pratap Vaidik, former bureaucrat Sanjeev Sabhlok, Bawana industrialist Prakash Chand Jain and Kavi Gajender Solanki.
Based on the FIR, police have registered cases relating to rioting, attack on policemen, use of criminal force and deadly weapons.
According to Inspector Praveen Kumar, DCP (East) Prabhakar tried to stop Ramdev at the Delhi border, saying he and his supporters couldn't head to India Gate as prohibitory orders were in place. If he still wished to protest, he was free to go to Ramlila Maidan.
The FIR states that Ramdev did not agree and headed to Guru Nanak Chowk. From there, he and his supporters police estimate put the crowd strength at 5,000 scattered in different directions. Ramdev insisted on marching towards India Gate.
He reached Jantar Mantar where, the FIR states, he assured police that he and his supporters would not go to India Gate. He held a rally there and several people addressed the crowd. Inspector Kumar identified some of the speakers as Prakash Chand Jain, Sabhlok, Kavi Solanki, Ved Pratap Vaidik and V K Singh.
Ramdev then began to incite his supporters, asking them to march to India Gate. "We will all go to India Gate and join the protest there," Inspector Kumar quotes Ramdev as telling the crowd. The crowd then felled barricades and tried to head to India Gate.
... contd.


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The median home value in Santa Ynez, CA is $715,700.
This is
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The national median home value is $170,100.
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Learn more about Santa Ynez Real Estate.
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This peerless ranch, on over 200 acres in the Santa Ynez Valley, boasts rich history and an incomparable landscape. This premier Ranch has all that is needed for the operation of an ideal horse farm as well as the enjoyment of a luxurious lifestyle. A primary residence, guest house, manager's residence, 4 specialized barns, an airplane runway & hanger, and extensive staff housing provide all necessary features, while additional embellishments make this holding utterly exquisite in appearance, operation, and convenience. The main home, on a 10.45 acre parcel, enjoys 5 bedrooms, 4 baths, a swimming pool & spa, and an enchanting koi pond, while the manger's residence is a spacious retreat in its own right, offering 2 bedrooms and 2 baths. A duplex provides two dwellings, each with 2 bedrooms and 1 bath, designed as worker's quarters. The Ranch consists of 7 Parcels, 5 with Certificate Of Compliance, all in Ag Preserve.
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Casa Encantada is a magnificent estate of 123 acres in the heart of Santa Barbara's wine country. Old world craftsmanship and elegance defines the essence of this Mission style hacienda compound combining a 10,000 square-foot residence and enchanting cabana with full kitchen, fireplace, and bathrooms. The residence features massive ceilings and dramatic picture windows with views of two mountain ranges. The kitchen is outfitted with every amenity a gourmet might desire for lavish entertaining as well as intimate family gatherings. Living areas with French doors lead from all rooms to private patios, pool and gardens. Perfect for living in wine country, a large seller is located with easy access from dining and living areas. Handsome sandstone fireplaces, handcrafted iron fixtures, wide plank floors and windows enhance a timeless feel. The property includes a walnut grove and abundant water from two wells along the Santa Ynez River.
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Ballantine's calls global advertising review
By Sara Kimberley, campaignlive.co.uk, Thursday, 26 July 2012 08:00AM
Ballantine's, the Pernod Ricard Scotch whisky brand, is reviewing its global advertising business.
It has approached a number of Pernod Ricard roster and non-roster agencies about a pitch, which is expected to take place in September.
Publicis currently handles the business globally and has worked with Ballantine's intermittently for the past 20 years. Work Club looks after Ballantine's digital business.
The Pernod Ricard agency roster includes Euro RSCG, Publicis, TBWA Worldwide, M&C Saatchi and Work Club, which share creative duties on its top 14 brands, including Chivas Regal and Jameson Irish Whiskey.
Vizeum handles Ballantine's media planning and buying account.
Last year, Publicis launched a pan-regional TV ad for Ballantine's to inspire consumers to "change their plan and leave an impression".
To support the campaign, Work Club created a video featuring a tattooist. A Facebook page allowed the public to interact with him and make decisions on all aspects of his work, including what colours he used.
Pernod Ricard was unavailable for comment.Follow @SaraKimberley
This article was first published on campaignlive.co.uk
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text:
Wrinkle-Fighting Tofu Casserole
Serves six to eight.
- 2 Tbs extra virgin olive oil
- 1 large onion, finely chopped
- 1 carrot, finely chopped
- 1 stalk celery, finely chopped
- ½ cup freshly chopped flat-leaf parsley
- ½ cup freshly chopped basil
- 2 Tbs freshly chopped thyme
- 2 Tbs chopped Nicoise olives
- 1 cup whole canned plum tomatoes, seeded and chopped
- 2 Tbs chopped garlic
- 2 lbs firm tofu, pureed in a food processor
- Sea salt
- Freshly ground white pepper
Lightly grease an 8-by-10-inch baking dish with olive oil.
In a nonstick skillet, heat the olive oil over medium heat. Add the onions, carrots, and celery and sauté until tender, about 10 minutes. Add the parsley, basil, thyme, and olives and sauté two to three minutes. Stir in the tomatoes, garlic and tofu. Season with salt and pepper to taste. Remove from the heat and allow to cool.
Shape the cooled tofu mixture into a mound or loaf and transfer it to the prepared baking dish. Place the baking dish inside a larger roasting pan and fill the roasting pan with water until it comes halfway up the sides of the baking dish.
Bake 30 minutes or until golden brown.


text:
There are six movies in the "Child's Play" series, also commonly known as the "Chucky " movies. In chronological order, the films are: "Child's Play" (1988), "Child's Play 2" (1990), "Child's Play 3" (1991), "Bride of Chucky" (1998), "Seed of Chucky" (2004) and "Curse of Chucky" (2013).
Each of the films centers on serial killer Charles Lee Ray, whose soul is trapped in a child's doll as part of a voodoo ritual intended to avoid death. While the first movie is more in the vein of conventional horror films, the later entries in the series adopt a more humorous approach. The franchise is fairly successful overall, having grossed over $176 million worldwide.
Your answer is Child's Play | Child's Play 2 | Child's Play 3 | Bride of Chucky |
Childs play 1 made in 1988.
There are 5 Chucky movies: Child's Play (1988), Child's Play 2 (1990), Child's Play 3 (1991), Bride of Chucky (1998), and Seed of Chucky (2004).
I think 4. Childs Play. Childs Play 2. Bride of Chucky. Seed of chucky.


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Unravel MePaperback Shatter Me
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- Publisher: HarperCollins Publishers
- Format: Paperback | 461 pages
- Dimensions: 134mm x 198mm x 34mm | 380g
- Publication date: 31 December 2013
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The New York Times bestselling sequel to the groundbreaking dystopian novel Shatter Me! Kami Garcia, coauthor of the #1 New York Times bestselling Beautiful Creatures series, says Unravel Me is "dangerous, sexy, romantic, and intense. I dare you to stop reading."Juliette is still haunted by her deadly touch. But now that she has teamed up with other rebels with powers of their own, she'll be able to fight back against The Reestablishment to save her broken world. With the help of these new allies, she'll also finally learn the secret behind Adam's--and Warner's--immunity to her killer skin.Unravel Me is perfect for fans who crave action-packed young adult novels with tantalizing romance like Divergent by Veronica Roth, The Hunger Games by Suzanne Collins, and Legend by Marie Lu. Ransom Riggs, #1 New York Times bestselling author of Miss Peregrine's Home for Peculiar Children, raves: "A thrilling, high-stakes saga of self-discovery and forbidden love, the Shatter Me series is a must-read for fans of dystopian young-adult literature--or any literature!"
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"Juliette's experiences will keep readers on the edge of their seats, and the romantic tug-of-war will entrance them."--School Library Journal
Back cover copy
Our lips touch and I know I'm going to split at the seams. He kisses me softly then strongly like he's lost me and he's found me and I'm slipping away and he's never going to let me go.Juliette has escaped from The Reestablishment. Now she's free from their plan to use her as a weapon, and free to love Adam. But Juliette will never be free from her lethal touch. Or from Warner, who wants Juliette more than she ever thought possible. Haunted by her past and terrified of her future, Juliette knows that she will have to make some life-changing choices. Choices that may involve choosing between her heart--and Adam's life.