text:
Grand Theft Auto: Vice City 10th Anniversary Edition arriving on mobiles and tablets for Christmas
Rockstar has announced a release date for the Android and iOS versions of Grand Theft Auto: Vice City.
To celebrate the tenth anniversary of the original PS2 release of Vice City, Rockstar has given the game a visual update to account for the high definition displays on cutting edge smartphones and tablets including improved character models and lighting effects as well as native support for Apple's new Retina iOS displays.
Rockstar has also enhanced the accuracy of the firing and targeting options as well as providing a fully customisable control layout.
Grand Theft Auto: Vice City 10th Anniversary Edition launches for the latest Android and iOS devices at 2.99 GBP on iTunes and 3.72 GBP on the Google Play Store.
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text:
Do Ya (album)
From Wikipedia, the free encyclopedia
|This article does not cite any references or sources. (October 2008)
|Do Ya
|Studio album by The Screaming Jets
|11 October 2008
|Rock, Pub Rock
|StockXChange Music
|The Screaming Jets and Scott Kingman with additional production by Stevie Salas and Brandon Friesen
|The Screaming Jets chronology
Do Ya is the sixth studio album by the Australian hard rock band The Screaming Jets. It was released by StockXChange Music/Sony Music. The first single "Do Ya" was taken from the album.
Track listing[edit]
- "Do Ya"
- "Supersize"
- "Change the World"
- "Mary Jane"
- "Running Blind"
- "Inside Out"
- "Falls in Place"
- "141"
- "Knock Knock"
- "Stay"
- "Heaven Help Me"
- "Forget the Rhyme"
|This 2000s hard rock album-related article is a stub. You can help Wikipedia by expanding it.

subset: commoncrawl


text:
Page 1
© 2006 Nature Publishing Group
The function of the immune system is to prevent
the takeover of the body by genomes other than that
encoded in the germline1. Central to this function is
the ability to kill. Given the fundamental conservation
of biochemistry, there are few chemical mechanisms for
killing a given target cell that lack the potential to kill
some other life form2. Therefore, it is no surprise that the
neutrophil, one of the body's main cellular components
for the destruction of microorganisms, also damages cells
and tissues of the host3,4. In fact, neutrophil-mediated
tissue damage at infected sites is so common that the
host takes stock of it when judging whether to mobilize
an immune response. Indeed, tissue injury is one of the
main sources of information that launches inflammation,
which in turn launches immunity.
To view immunology as the host's participation in
the competition between genomes helps explain what
makes the neutrophil as fascinating as it is indispen-
sable5. Surprisingly, some immunologists seem not
to share this view. Say neutrophil, and they move on,
thinking: inflammation, not immunity. They disrespect
the cell's 'nonspecificity' and consider its best-studied
behaviours — crawling, eating, and disgorging pre-
packed enzymes and partially reduced molecules of
oxygen — as rudimentary. Finally, scientists who are
interested in anti-inflammatory therapeutics are dis-
couraged from targeting neutrophils because it seems
futile to try to suppress neutrophil-dependent tissue
damage without the serious side effect of increasing the
host's risk from infection1.
The aim of this article is to dispel each of those views.
The literature on neutrophils is so vast (PubMed finds
over 76,000 papers on the subject) that few authors have
attempted to cover it comprehensively6,7. This Review
makes no such effort. On the contrary, large chunks of
neutrophil biology are neglected here, including myelo-
poiesis, chemotaxis, transendothelial migration, synthe-
sis of lipid mediators and much of signal transduction.
Instead, selected studies are marshalled to support the
following five tenets: that the neutrophil often has an
important role in launching immune responses; that
the neutrophil helps to heal tissues as well as destroy-
ing them; that the neutrophil gives instructions with
as much specificity as a lymphocyte or neuron, albeit
with specificity of a different kind; that the neutrophil
integrates information, with a circuitry of awe-inspiring
design, to tailor its responses to its spatial and temporal
context; and that the neutrophil offers potential oppor-
tunities for selective pharmacological intervention, to
both promote and restrain inflammation.
Neutrophils as decision-shapers
Neutrophils help answer one of the central questions in
immunology: what triggers an immune response? The
danger theory holds that injured host cells release alarm
signals that activate antigen-presenting cells (APCs)8. The
pattern-recognition theory posits that 'microbial non-self'
induces an innate immune response, which in turn trig-
gers an adaptive immune response9. Both views are valid,
but they leave much unexplained. For example, surgery
injures large numbers of host cells but does not promote
immune reactions to foreign compounds, such as anti-
biotics, that are present at the time. Non-pathogenic
resident microorganisms belonging to several thousand
Department of Microbiology
and Immunology, Weill Cornell
Medical College; and
Programs in Immunology and
Microbial Pathogenesis,
and Molecular Biology, Weill
Graduate School of Medical
Sciences of Cornell University,
Box 57, 1300 York Avenue,
New York 10021, USA.
Published online
17 February 2006
Danger theory
A theory that the trigger for
mounting an immune response
consists of an injury to host
cells, resulting in the release
of alarm signals that activate
antigen-presenting cells.
Pattern-recognition theory
A theory that the trigger for
mounting an immune response
consists of the recognition of
'microbial non-self' molecules
by receptors expressed by
innate immune cells.
Neutrophils and immunity: challenges
and opportunities
Carl Nathan
Abstract | Scientists who study neutrophils often have backgrounds in cell biology,
biochemistry, haematology, rheumatology or infectious disease. Paradoxically,
immunologists seem to have a harder time incorporating these host-defence cells into
the framework of their discipline. The recent literature discussed here indicates that it
is appropriate for immunologists to take as much interest in neutrophils as in their lympho-
haematopoietic cousins with smooth nuclei. Neutrophils inform and shape immune
responses, contribute to the repair of tissue as well as its breakdown, use killing mechanisms
that enrich our concepts of specificity, and offer exciting opportunities for the treatment
of neoplastic, autoinflammatory and autoimmune disorders.
Page 2
© 2006 Nature Publishing Group
of apoptotic
Extravascular tissue
Secondary lymphoid organ
Bone marrow
Cathepsin G
Cathepsin G
Prochemerin Chemerin
Immature DC or
plasmacytoid DC
B cell
αβ T cell or
γδ T cell
T cell
Neutrophil precursor
Neutrophil retention
in the bone marrow
Stromal cell
A dendritic-cell-attracting
chemokine that is generated
by neutrophil-dependent
proteolytic activation of its
precursor. Chemerin does not
yet have a 'chemokine ligand'
Plasmacytoid DCs
Immature dendritic cells (DCs)
with a morphology resembling
that of plasma cells.
Plasmacytoid DCs produce
type I interferons in response
to viral infection.
species express pathogen-like microbial patterns, but they
only elicit maturation of the neonatal immune system10
and tolerance, not an immune response.
A third view is that a normal immune response
results from the ongoing detection of signals that report
injury and signals that report infection1. Although many
different molecular signals might be involved, they can
be considered 'binary' in the sense that most of them
arise as a consequence of one of these two events, and
it generally requires at least one signal from each class
to launch a response. This binary control begins with
inflammation. Except in autoinflammatory disorders,
the triggering and continuation of an inflammatory
response generally require the simultaneous receipt of
molecular signals directly or indirectly reporting tissue
damage and the presence of a genome different from
that of the host. Signals reporting injury and infec-
tion activate epithelial cells, mast cells, macrophages,
endothelial cells, platelets and neutrophils. Binary
signalling is propagated as these cells recruit, activate
and programme APCs through further binary signals,
such as cytokines and microbial products, cytokines
and CD40 ligation, or microbial products and products
of necrotic host cells. Finally, T cells are activated and
programmed by antigen-receptor ligation together with
signals from APCs, and B cells are activated by antigen-
receptor ligation together with signals from T cells.
Therefore, inflammation imprints the immune response
with a pattern of information flow: the integration of
signals of two or more distinct classes derived directly
or indirectly from injury and infection.
As a key component of the inflammatory response,
neutrophils make important contributions to the recruit-
ment, activation and programming of APCs (FIG. 1).
Neutrophils generate chemotactic signals that attract
monocytes and dendritic cells (DCs), and influence
whether macrophages differentiate to a predominantly
pro- or anti-inflammatory state11–13. For example, neutro-
phils proteolytically activate prochemerin to generate
chemerin, one of the few chemokines that attracts both
immature DCs and plasmacytoid DCs14. Neutrophils
also produce tumour-necrosis factor (TNF) and other
cytokines that drive DC and macrophage differentia-
tion and activation12,13,15. Neutrophil activation of DCs is
fostered by cell–cell contact, in which the specific carbo-
hydrates on CD11b engage DC-specific ICAM3-grabbing
non-integrin (DC-SIGN)15. Moreover, neutrophils secrete
TNF-related ligand B-lymphocyte stimulator (BLyS)16,
which helps to drive proliferation and maturation of
B cells, and interferon-γ, which helps to drive differen-
tiation of T cells and activation of macrophages17. On
a per-cell basis, neutrophils make fewer molecules of a
given cytokine than do macrophages or lymphocytes, but
neutrophils often outnumber mononuclear leukocytes at
inflammatory sites by one to two orders of magnitude,
and they can therefore be important sources of cytokines
such as TNF at the crucial juncture at which the deci-
sion is made to mount an immune response. However,
neutrophils can also function as powerful suppressors of
T-cell activation. For example, in patients with advanced
cancer, activated neutrophils can impair T-cell receptor
(TCR) ζ-chain expression and cytokine production18.
The ability of neutrophils to augment or inhibit lym-
phocyte expansion and activation at sites of inflammation,
draining lymph nodes and in the spleen is reciprocated
by the adaptive immune system's control of the rate of
neutrophil production in the bone marrow. This can
be appreciated by looking upstream of the cytokine
granulo cyte colony-stimulating factor (G-CSF), which
is an essential regulator of neutrophil production
through several mechanisms. Stromal-cell-derived
G-CSF triggers bone-marrow neutrophils to release
matrix metallo proteinase 9 (MMP9), which solubilizes
KIT ligand, helping to mobilize progenitor cells19. G-CSF
also acts directly on the progenitors to increase their
proliferation, while suppressing stromal-cell expression
of CXC-chemokine ligand 12 (CXCL12, also known as
Figure 1 | Neutrophils interact with monocytes, dendritic cells, T cells and
B cells in a bidirectional, multi-compartmental manner. Through cell–cell
contact and secreted products, neutrophils recruit and activate monocytes, dendritic
cells (DCs) and lymphocytes, and products of monocytes, macrophages and T cells
activate neutrophils. Tissue macrophages ingesting apoptotic neutrophils produce
less interleukin-23 (IL-23). IL-23 triggers T cells in secondary lymphoid tissues to
produce IL-17. IL-17 triggers stromal cells in the bone marrow to produce granulocyte
colony-stimulating factor (G-CSF). G-CSF promotes proliferation of neutrophil
precursors and release of neutrophils into the circulation (see text for references).
BLyS, tumour-necrosis factor-related ligand B-lymphocyte stimulator; CXCL12,
CXC-chemokine ligand 12; IFNγ, interferon-γ; TNF, tumour-necrosis factor.
Page 3
© 2006 Nature Publishing Group
A collection of liquefied tissue
containing many living or dead
neutrophils and bacteria.
Latent form
A form in which activity is not
yet expressed, pending
activation by an event such as
redistribution from a particular
compartment or proteolytic
Biologically active compounds
that are primarily derived
from arachidonic acid, in part
through cyclooxygenases
and lipoxygenases, including
prostaglandins, prostacyclins,
thromboxanes, leukotrienes
and lipoxins.
Reduction of oxygen
Donation of electrons to
molecular oxygen. Donation
of up to three electrons
gives rise to reactive oxygen
intermediates (ROIs), whereas
donation of four electrons
gives rise to water. The term
'intermediate' in ROI refers to
oxygen whose reduction state
is intermediate between that of
oxygen (O2) and water (H2O).
SDF1), which helps to retain neutrophils in the bone
marrow20. In turn, G-CSF production is regulated by
interleukin-17 (IL-17), which is produced by subsets
of γδ and αβ T cells (FIG. 1). T-cell production of IL-17
is governed by IL-23, which is released from extravas-
cular macrophages. The release of IL-23 is suppressed
when macrophages ingest apoptotic neutrophils21.
The homeostatic feedback loop among macrophages,
T cells and neutrophils described earlier illustrates the
fallacy of visualizing vertebrate immunity as two separate
systems — innate and adaptive — that take turns over the
course of an encounter with antigen. Instead, elements of
more and less ancient evolutionary origin work together
from before the initiation of an immune response21, into
its first hours22, and through to its resolution. Resolution
of an immune response is marked not only by the genera-
tion of immunological memory but also, in many cases,
by the innate immune system's help in healing a wound.
Demolition and reconstruction
Wounding is a frequent initiator of immune responses
because it introduces both types of precipitants — injury
and infection — except in the unnatural instance of
surgery with aseptic technique. Although neutrophils
might delay the closure of artificial, microbiologically
sterile wounds23,24, they have three important roles in
healing natural wounds25: sterilization of microbes,
generation of signals that slow the rate of accumulation
of more neutrophils, and instigation of a macrophage-
based programme that switches the state of damaged
epithelium from pro-inflammatory and non-replicative,
to anti-inflammatory and replicative.
The principal contribution of neutrophils to wound
healing is microbial sterilization. Wounds tend to heal
poorly and lead to lethal outcomes in individuals with
insufficient neutrophils5; in individuals with neutrophils
that cannot adhere to the endothelium or extracellular
matrix and therefore fail to accumulate in infected
sites26,27; in individuals with a vasculature that is insuf-
ficient to deliver neutrophils, for example persons with
full-thickness burns; or in individuals with neutrophils
that have deficiencies in microbicidal machinery.
It is not realistic to expect neutrophils to find and eat
each bacterium in a wound before any bacteria have had
time to escape into the lymph or blood. Neutrophils that
sense tissue damage plus infection but fail to encounter a
bacterium within a short time, fire off their arsenal into
the extracellular space28. In vitro, this period of restraint
ranges from ~15 to ~45 minutes, which is thought to be
the approximate time it takes for a neutrophil to emi-
grate from the blood into the extravascular tissues. When
restraint is abandoned, what ensues is the liquefaction
of tissue — that is, the formation of pus — through neu-
trophils' release of proteases, their activation of proteases
that are expressed in a latent form by cells resident in the
tissues, and their oxidative inactivation of anti-proteases
(proteins that specifically bind and inactivate proteases)3,4.
Tissue breakdown is usually viewed as detrimental, and
therefore neutrophils are often cast in a pejorative light.
However, early, small-scale neutrophil-mediated tissue
destruction is usually a life-saving process. It serves to
disassemble the collagen fibrils that impede neutrophil–
bacterial contact and puts pressure on surrounding tissue.
This might help to collapse lymphatics and capillaries,
thereby cutting off bacterial escape routes and trapping
the microbes in a toxic soup.
At the same time, neutrophils also generate signals
with four key actions: to retard their own accumula-
tion; to suppress their own activation; to promote their
own death; and to attract and programme macrophages
to stop the damage and orchestrate repair. Among the
main endogenously derived anti-inflammatory com-
pounds are metabolites of fatty acids. These include
neutrophil-derived lipoxins, as well as macrophage-
derived resolvins and protectins that are produced in
response to the ingestion of apoptotic neutrophils29, all
of which block neutrophil recruitment. Proteinaceous
anti-inflammatory factors such as secretory leukocyte
protease inhibitor (SLPI)30 are also important (FIG. 2),
and neutrophils, as well as macrophages30 and epi-
thelial cells, produce SLPI. Despite producing SLPI,
activated neutrophils can oxidatively inactivate this
anti-inflammatory factor31. However, SLPI protects
itself from oxidative inactivation by suppressing the
neutrophil respiratory burst32. Moreover, SLPI also
puts a brake on tissue proteolysis by inhibiting neutro-
phil elastase. Macrophages and epithelial cells also
make an epithelial-cell-growth-promoting cytokine,
proepithelin (PEPI; also known as progranulin). PEPI
synergizes with SLPI in inhibiting neutrophil activa-
tion31. Although neutrophil elastase degrades PEPI to
generate pro-inflammatory epithelins, SLPI protects
PEPI in two ways: by binding and inhibiting neutrophil
elastase, and by binding and shielding PEPI from deg-
radation by neutrophil elastase. This helps to prevent
the products of degradation of PEPI from promoting
epithelial-cell production of CXCL8 (also known as
IL-8)31, which is one of the most important neutrophil
attractants. Moreover, intact PEPI signals to epithelial
cells to proliferate and close the wound31,33.
Specificity in command
Neutrophil-derived chemokines, cytokines and
eicosanoids signal with a type of specificity that is famil-
iar to immunologists: that of ligand–receptor, protein–
protein or lipid–protein interactions. But neutrophil
specificity does not stop there. One of the main func-
tions of neutrophils is to undergo the respiratory burst:
an abrupt, non-mitochondrial reduction of oxygen to
forms that are less reduced than water and far more reac-
tive, known as reactive oxygen intermediates (ROIs).
Respiratory burst products and their derivatives include
superoxide, singlet oxygen, ozone, hydrogen peroxide
(H2O2), hypohalous acids, chloramines and hydroxyl radi-
cals34 (FIG. 3). These species can interact with an unlimited
number of macromolecules. This seems to make a travesty
of specificity, as this term is most often used in immunol-
ogy, when it characterizes the crowning achievement of
the adaptive immune system, that is, the ability of TCRs,
B-cell receptors and antibodies to make distinctions so
precise that they only permit the recognition of a single
macromolecule among tens of thousands.
Page 4
© 2006 Nature Publishing Group
Epithelial cell
A lipid whose exposure on
the outer leaflet of the plasma
membrane generally correlates
with apoptosis of the cell and
promotes its uptake by other
Of necessity, however, there are different kinds of
specificity. The infectious challenges faced by the
immune system are so diverse and dire that they can only
be met by a response in which collateral damage occurs
as a matter of course35,36. No person who lives outside
a bio-containment suite reaches maturity without their
neutrophils having formed pus on multiple occasions,
which is to say, destroying some of their tissue, and often
saving their life in the process. In the familiar sense of
the term, this is an ultimate example of nonspecificity.
In fact, the specificity of ROIs is just as exquisite as that
of antibody, but it is manifest at the atomic level, rather
than the molecular level2,37. For example, ROIs lead to
oxidation of sulphurs to sulphoxides and of sulphydryls
to disulphides or to sulphenic, sulphinic or sulphonic
acids. These are specific outcomes of the interaction of
ROIs with specific atoms. That the atomic targets of ROIs
are crucial to the function of a wide array of molecules
probably accounts for the evolutionary selection of this
means of host defence.
Indeed, there are two important innovations of innate
immunity and they both involve distinctive forms of
specificity. First, molecular specificity in the recognition
of relatively invariant and widely distributed microbial
macromolecules is imparted by Toll-like receptors, lectins
and lectin receptors, scavenger receptors, C-reactive
protein, and complement and its receptors. Second,
specific, covalent chemical reactions by ROIs and reac-
tive nitrogen intermediates with a subset of atoms that
are shared by, and crucial for, the function of diverse
microbial molecules, characterizes one of innate immu-
nity's important effector functions. The first innovation
makes it difficult for a pathogen to evolve to a state that
escapes detection, and the second makes it difficult for
a pathogen to evolve to a state that escapes destruction38.
The price of these twin innovations in specificity is tissue
damage. But tissue damage is not wasted: it is used as
information and incorporated into the central decision
algorithm of the immune response. The immune system
cannot function and the host cannot live without these
two distinctive types of specificity.
Equally fundamental to an appreciation of neutrophil
biology is the following principle: the same products that
kill also signal. Homeostatic signalling depends on appro-
priately timed, brief exposures to low concentrations of
mediators. When present at the wrong time, for too long
and in high concentrations, the same mediators can kill.
In fact, across biology, killing is frequently the outcome
of excessive and inappropriate signalling, whether the
sender–receiver pairs are host-versus-microorganism,
microorganism-versus-host, host-cell-versus-host-cell,
or microbial-cell-versus-microbial-cell2. ROIs, for
example, are essential mediators of signalling by many
cytokine and hormone receptors, such as those for
insulin, platelet-derived growth factor, fibroblast growth
factor, nerve growth factor, TNF and angiotensin2. The
best-studied molecular mechanism for ROI-mediated
signalling is the temporary inactivation of tyrosine
phosphatases by reversible oxidation of their active-
site cysteine sulphydryls39. Moreover, neutrophil pro-
teases also regulate physiological processes19. In short,
a neutrophil-rich inflammatory site is buzzing with
information for every cell present; only at the epicentre
is the command for all the cells to die.
Fate decisions
Cytotoxic T cells and natural killer (NK) cells can poten-
tially kill any nucleated host cell. Neutrophils match that
capacity and top it with their additional abilities to destroy
non-nucleated cells and connective tissue. In mammals,
only neutrophils are licensed to liquefy any part of the
body. Therefore, some of the main messages sent by
neutrophils in inflammatory sites can be paraphrased as
follows. To microorganisms and host cells that stand in
the way: die. To themselves: if the site still seems infected,
summon reinforcements until the crucial concentration of
neutrophils that is required to clear a given tissue volume
of bacteria is attained40; and if infection has been brought
under control, wrap yourself in a phosphatidylserine flag
and wait for macrophages to remove your apoptotic corpse
for the safe disposal of your unexploded weapons41.
Neutrophils' decisions over their own fate are
co-ordinated through transcription factors. Hypoxia-
inducible factor 1 (HIF1) regulates both the antibacterial
activity of neutrophils42 and their apoptosis43. Forkhead
box O3A (FOXO3A) postpones neutrophil apoptosis by
Figure 2 | Neutrophils have a key role in wound healing
both by controlling microbial contamination and
by attracting monocytes and/or macrophages.
The illustration shows one pathway out of many that
are operative in wounds. Neutrophil- and macrophage-
derived secretory leukocyte protease inhibitor (SLPI)
blocks neutrophil elastase. SLPI alone, and in synergistic
combination with macrophage- and epithelial-cell-
derived proepithelin (PEPI), blocks cytokine-induced
release of proteolytic enzymes and reactive oxygen
intermediates (ROIs) by neutrophils. These actions
diminish the neutrophil-dependent proteolytic conversion
of PEPI to epithelins (EPIs), decreasing the ability of EPI
to promote epithelial-cell production of CXC-chemokine
ligand 8 (CXCL8; also known as IL-8), an important
neutrophil chemoattractant. Intact PEPI promotes
epithelial-cell proliferation, speeding closure of the
wound. Black arrows indicate processes involved in tissue
repair and regeneration. Grey arrows indicate processes
involved in host defence.
Page 5
© 2006 Nature Publishing Group
Azurophilic (also known as primary) granules:
BPI, neutrophil elastase, cathepsin G, protease 3,
azurocidin, myeloperoxidase
Specific and tertiary granules:
Lactoferrin, lipocalin, lysozyme,
LL37, MMP8, MMP9 and MMP25
Nets that trap bacteria
and neutrophil elastase
Low-molecular-weight bacterial
compounds that chelate iron
and deliver it to the bacterium
through specific receptors.
Staining with azure (blue)
components of the
Romanowski-type stains used
in standard evaluations of
haematological specimens.
In neutrophils, the earliest-
formed set of granules,
which contain many antibiotic
proteins and proteases,
are azurophilic.
suppressing transcription of CD95 ligand (CD95L; also
known as FASL)44. A protein called survivin also has an
important role in delaying the death of neutrophils at
inflammatory sites45.
Neutrophils decide the fate of microorganisms in
two general ways: by taking away and by giving. 'Taking
away' means withholding essential factors that bacteria
require, for example iron. The simplest approach is for
neutrophils to secrete the iron-binding protein lacto ferrin
into the phagosome and the extracellular environment.
However, lactoferrin faces tough competition from bac-
terial iron-binding molecules, a diverse array of com-
pounds known as siderophores. The neutrophil in turn
counters this 'counterpunch' by secreting lipocalin-2, a
protein that embraces bacterial siderophores, preventing
them from returning to the mother ship — the bacte-
rium — with their cargo46.The dedication of neutrophils
to delivering cytotoxic messages to bacteria (that is, to
'giving') is evident from two perspectives: their supply of
redundant effector molecules and their use of multiple
subcellular compartments as a source. Therefore, little of
the neutrophil is wasted. As neutrophils migrate along a
concentration gradient of a stimulus, they progressively
discharge two distinct sets of granules, activate a killing
cascade at the plasma membrane, extrude their nuclear
proteins, and finally pour out their cytosol, all with anti-
microbial effects (FIG. 3). Even the nuclei of neutro phils
contribute to host defence by extruding their chromatin,
which forms extracellular nets decorated with proteases
from the azurophil granules47. Cytosol released by
necrotic neutrophils delivers large amounts of calprotec-
tin, a bacteriostatic heterodimer of MRP8 and MRP14
(REF. 48). Neutrophils also release potently bactericidal
Payloads: prepacked or made on demand. The first
granules to be discharged are peroxidase-negative, and
these include specific granules (also known as second-
ary granules) and tertiary granules (also known as
gelatinase granules), which contain overlapping sets
of proteins50. In these two types of granules are found
the gang of 'L's' — lactoferrin, lipocalin, lysozyme and
LL37. LL37 is a chemotactic and antimicrobial peptide
released from its precursor, the cathelicidin CAP18
(cationic antimicrobial protein 18), by protease 3. Also
found in the peroxidase-negative granules are three 'M's'
— MMP8, MMP9 and MMP25. By degrading laminin,
collagen, proteoglycans and fibronectin, these MMPs
are thought to have an important role in facilitating
neutrophil recruitment and tissue breakdown50.
As the concentration of secretagogues increases, the
next granules to be emptied are peroxidase-positive
and azurophilic (also known as primary). Their bulk
contents are four α-defensins and myeloperoxidase
(MPO), the iron-containing enzyme that colours pus
green. The defensins are small, cyclic polypeptides that
trade off their relatively low molar potency against their
high abundance and broad spectrum as antimicrobial
agents51. MPO converts the relatively innocuous H2O2
into much more powerful antiseptics: hypochlorous
acid (which is the active ingredient in bleach), hypo-
bromous acid and hypoiodous acid. Hypochlorous acid
reacts with amines to give rise to longer-lived, bacteri-
cidal chloramines34. The same granules deliver a potent
protein antibiotic that is active against Gram-negative
bacteria, the lipopolysaccharide-binding bactericidal
permeability increasing protein (BPI)52, and four broad-
spectrum antibiotic proteins termed serprocidins53. The
serprocidins include three serine proteases — cathep-
sin G, neutrophil elastase and protease 3 — and a homo-
logue that lacks proteolytic activity but retains equipotent
antibacterial activity, which was independently identified
as azurocidin53 and CAP37 (REF. 54). The antimicrobial
molar potency of serprocidins is comparable to that of
formulary anti biotics, but unlike pharmaceuticals, the
enzymatically active serprocidins also degrade most of
the components of extracellular matrix. This bifunc-
tionality highlights that tissue breakdown is part of the
antimicrobial strategy of neutrophils.
Meanwhile, radical biology takes place at the plasma
membrane and its offshoot, the membrane of the nas-
cent phagosome. Studies of neutrophils have had a
crucial role in establishing the fundamental but initially
heretical principle that biochemical reactions can gener-
ate compounds with unpaired electrons (also known as
radicals) as functional products55,56. Phagocyte oxidase
(phox), which is the main ROI-producing enzyme
expressed by neutrophils, continues to lead the way in
illuminating the biochemistry of the broadly distributed
family of ROI-producing, signal-capacitating enzymes
that are termed NADPH oxidases (NOXs)57.
As a biochemical cellular component, phox is so com-
plex that its study has dominated the field of neutrophil
biology for decades. For a description of the constituents
of phox, their assembly and the diverse experimental for-
mats that investigators have used to study the activation
of phox, see Supplementary information S1 (box).
Deficiencies of phox were discovered because they
led to death from infection58. The phenotype of phox
deficiency, together with the bactericidal action of
Figure 3 | Neutrophils deliver multiple anti-microbial molecules. Microbicidal
products arise from most compartments of the neutrophil: azurophilic granules
(also known as primary granules), specific granules (also known as secondary granules)
and tertiary granules, plasma and phagosomal membranes, the nucleus and the cytosol.
BPI, bactericidal permeability increasing protein; H2O2, hydrogen peroxide; HOBr,
hypobromous acid; HOCl, hypochlorous acid; HOI, hypoiodous acid; MMP, matrix
metalloproteinase; 1O2, singlet oxygen; O2
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Arab Spring Topics
Democracy Now! is following the popular uprisings across the Middle East and North Africa.
- With estimates of well over 5,000 deaths, the uprising in Syria is believed to be the Arab Spring's bloodiest conflict to date. As the toll mounts, calls are growing for the international community to intervene by arming rebels fighting the Assad regime and even direct military intervention. We host a debate on the merits and pitfalls of foreign intervention in Syria with two guests. "I'm not opposed to helping the opposition....February 22, 2012 | Story
- Libya has just marked the first anniversary of the start of the uprising that toppled Col. Muammar Gaddafi's four-decade rule. But as Libya celebrates a new era free of the Gaddafi regime, there are growing concerns the country's lingering divisions will tear it apart. Libya remains deeply splintered by regions and factions. More than 500 militias exist throughout the country, leading to ongoing human rights abuses that resemble...February 21, 2012 | Story
U.S.-Backed Bahraini Forces Arrest and Deport Two American Peace Activists Acting as Human Rights ObserversOn Saturday, Bahrain arrested and deported two U.S. human rights lawyers, Huwaida Arraf and Radhika Sainath, for their role in recent protests. They were deported Sunday and returned to New York last night. Both Arraf and Sainath are human rights lawyers and members of the Witness Bahrain initiative, which places international observers in the country in the hopes of preventing violence by security forces. Their arrest comes just ahead of the...February 13, 2012 | Story
Ousted Maldives Pres. Mohamed Nasheed a Leading Voice for Island States Threatened by Global WarmingFor years, Mohamed Nasheed was the most vocal world leader on the threat climate change poses to residents of small island states. After becoming the first democratically elected president in Maldives, he pledged to make the nation the first carbon neutral country and once held a cabinet meeting underwater. We discuss Nasheed's ouster and his outspoken campaigning on global warming with environmental activist Bill McKibben, whose group...February 09, 2012 | Story
- Syria is seeing some of the worst violence of the 11-month uprising against Bashar al-Assad amid an ongoing international standoff over how to respond. Assad's forces have launched what appears to be one of their fiercest assaults on the flashpoint city of Homs to date. Both the United States and Britain have closed their embassies in the Syrian capital of Damascus and withdrawn diplomatic personnel, citing safety fears. As the crisis...February 07, 2012 | Story
- Street battles are raging at the gates of the Syrian capital of Damascus, and activists say at least 62 people were killed nationwide on Sunday. This comes as United Nations Secretary-General Ban Ki-moon has called on the Syrian leadership, particularly President Bashar al-Assad, to end the violence against the demonstrators immediately, and plans to take up a draft resolution this week calling on him to step down and transfer power....January 30, 2012 | Story
Egypt: Sharif Abdel Kouddous Reports from Cairo as Crowds Mark 1 Year of Revolution in Tahrir SquareAs tens of thousands of Egyptians gather in Tahrir Square to mark the first anniversary of the start of the revolution that ended Hosni Mubarak's three-decade reign, we go to Cairo to speak with Democracy Now! correspondent Sharif Abdel Kouddous, who has reported on the popular uprising since it began. "What happened on January 25th was really an uprising that was 10 years in the making, a growing resistance movement to the Mubarak...January 25, 2012 | Story
- Democracy Now! correspondent Sharif Abdel Kouddous is the central character in the new HBO documentary airing tonight, "In Tahrir Square: 18 Days of Egypt's Unfinished Revolution." The film chronicles the uprising though the reporting of Kouddous, and it looks at what the protest meant for his uncle, Mohamed Abdel Quddoos, a longtime Egyptian dissident who was arrested dozens of times by the Mubarak regime. We're joined...January 25, 2012 | Story
- On the first anniversary of the Jan. 25th protests in Tahrir Square, we'll speak to Democracy Now! correspondent Sharif Abdel Kouddous live from Cairo. We will also air an excerpt of the new HBO documentary, "In Tahrir Square," featuring Sharif. We'll talk to the filmmakers, Jon Alpert and Matt O'Neill.January 24, 2012 | Web Exclusive
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Long Lasting Mens PGF Wide Stick Deodorant-Clean Confidence 24 Hour 2.25 oz StickTough on odor
Odor fighting hops. 100% natural fragrance
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Does Not Contain: Animal testing, animal ingredients, artificial colors, flavors, fragrance and preservatives.
Warnings: Keep out of reach of children. As with all dietary supplements, consult your healthcare professional before use. See product label for more information.
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We are still working to obtain content for your car, however the video above is believed to have similar characteristics as your car.
If your convenience lights, turn signals, seat warmers, stereo, headlights or other electronic components suddenly stop working, chances are you have a fuse that has blown out. The video above shows how to check and change blown fuses in the engine bay of your 1998 Ford Escort in addition to where the fuse box diagram is located. Fuses should always be the first thing you check if your Escort is experiencing electrical difficulties because they are relatively easy and inexpensive to change yourself. The more electronics your Escort has, the more fuses it has. Some Fords have multiple fuse boxes in the engine bay, so be sure to find the fuse(s) in question. Some components may have multiple fuses, so make sure you check all of the fuses that are linked to the component that is no longer working properly.
If you need to replace a blown fuse in your Escort, make sure you replace it with one that has the same amperage as the blown fuse. If checking and replacing the fuse for the component in question doesn't work, we recommend seeking assistance from a trusted professional mechanic. They should be able to figure out if the component needs to be replaced or if there is a short or some other problem with your Escort.
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(Source: USCG Historian's Office)
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Raj Arumugam
how to make money Poem by Raj Arumugam
how to make money,
how to make money;
tell me sweet love
you tell me
how to make money
how to make an easy billion
the world's full of it
in cyberspace
and in shopping malls;
the world's full of money schemes
in our real world
and where we buy a drink
or get more fries
it's full on
about how to make money,
how to make money
make money, pal
they say
doing nothing;
I've got an auto system
and all you need is internet
and all you've got to do
is sit back and let the dollars roll
into your bank account
so tell me
how to make money,
how to make money
come in to this meeting
another group says
and we'll show you how
show you how easy it is
how easy it is to make money:
it's auto, auto, auto, fully automated
and the money keeps coming;
the money rolls
rolls in, rolls in, rolls in
tell me
how to make money,
how to make money
it's all so easy
because we want
you to enjoy the life
we've earned;
we've made our money
and we want you to share
in the happiness;
it's all so easy, dear friends –
we'll guide you each step of the way;
we'll show you how to make the money
so they'll tell us
how to make money,
how to make money:
the only thing is
what they mean is
how to make money for them, babe,
how to make money for them
with a simple transfer of money
transfer of money, transfer of money
transfer of money from the foolish
transfer of money from the foolish to the deceitful;
wealth is, dear darling,
wealth is the transfer of money
from the foolish to the cunning
how to make money,
how to make money;
tell me sweet love
you tell me
how to make money
how to make an easy billion
Raj Arumugam's Other Poems
Related Poems
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This poem has not been translated into any other language yet.
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Comments about this poem (how to make money by Raj Arumugam )
Lalitha iyer (11/17/2009 12:02:00 AM)
Oh Sir, it is really sarcastically humorous and the theme is strikingly contemparaneous. Nice, , , , , , , , , , , , (Report) Reply
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Corner building purchase kills expansion by drugstore chain
Drugstore chain still vying for prime location; local organization looking to buy space
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Backstreet Boy Nick Carter was many a girl's boy band crush back in the 90s, but now he's settling down with wife Lauren Kitt, as chronicled on his new reality show I Heart Nick Carter.
PICS: Fairytale Celeb Weddings of 2014
Nick's engagement with Lauren caused a bit of a riff with jealous fans who didn't appreciate Nick's attention being stolen away by "another woman," and cameras captured all of the madness as Nick navigated his march to the altar.
"I'm still coping with it now," said Lauren. "The death threats are a lot fewer. They're not happening quite as frequently, but I've learned that it just comes with the territory."
I Heart Nick Carter premieres Wednesday, September 10 at 10/9c on VH1. Watch the video for a sneak peek.
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Opposition attacks motion to make Commons committee debate private
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STAGE TUBE: Sneak Peek at Jonas Kaufmann and More in PARSIFAL at the Met (Video Content)
The new production of PARSIFAL opens in just 2 days! Jonas Kaufmann stars alongside Katarina Dalayman, Peter Mattei, Evgeny Nikitin, and Rene Pape. Daniele Gatti conducts. Check out a sneak peek of Francois Girard's new production below!
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36 of 38 people found the following review helpful
5.0 out of 5 stars Fast paced, suspence packed yet believable.
I am thrilled to have come across this book. It relates the story of a normal everyday American couple and their little girl who get entangled in a corrupt conspiracy. The terrific character and plot development make it utterly believable and full of suspence. It is an excellent read.
Published on 20 Sept. 2002 by reader
33 of 33 people found the following review helpful
3.0 out of 5 stars NOT THE BEST BALDACCI
David Baldacci has written several fine thrillers including "Last Man Standing" and "Absolute Power". "Total Control" has several of the same features, notably a complex plot whose contours only become clear as the reader moves further into the book. Unfortunately, the writing just isn't as sharp as in Baldacci's better works. In particular, the characters are less...
Published on 13 Sept. 2008 by 100wordreviewer
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1 of 1 people found the following review helpful
4.0 out of 5 stars Another Masterpiece From Mr Baldacci,
Nellie Kerr "thriller fan" (Aberdeen, Scotland) - See all my reviews
Initially I found this book a bit hard going, but after the first chapter the action never stops for one moment. I for one could not put it down. The story is typical of David Baldacci's style - drama, intrigue, (mild) terror with well rounded characters and a good plot. On the downside I found that there were just a few too many convenient coincidences and because the book originally came out in 1996, the explanations of computer technology are now slightly dated and redundant. Nevertheless it is a very good read.
1 of 1 people found the following review helpful
5.0 out of 5 stars Baldacci at his best,
'Total Control' starts with a multiplicity of opening scenes but as one would expect of this skilled author the treads intertwine, follow blind alleys, switch suspects but give you the 'gut feelings' of committed crime book readers to test your instincts again the evidence of the text. This is a really good read with credibility within characters and technology although sometimes futuristic for its era. I had to get up early to finish and confirm my hopes, anticipations and growing excitement of who did what in this complex commercially and financially based thriller.
8 of 10 people found the following review helpful
1.0 out of 5 stars sad,
Qubit (UK) - See all my reviews
I have read a few of Baldacchi's books, this one came as a great disappointment.
By page 80 I was sick and tired of the female lead, I mean how many times do you have to be told that the bimbo is beautiful, intelligent, upwardly mobile etc etc. By Page 250 I was starting to speed read and by 400 or so I had given up. Far far too much plodding detail, far too many characters, to the extent that time is wasted trying to figure out whether this individual is good, bad or irrelevant, usually the latter as it turns out, but by then you really don't care anyway.
I am afraid that even if 200 pages had been taken out of it this would still be a turkey. Lawyers, like used car salesman,and real estate agents,do not make good, good guys, this monotonous tome proves that at least.
Save your money.
3 of 4 people found the following review helpful
5.0 out of 5 stars This One is a Real Thriller,
J. Chippindale (England) - See all my reviews
This review is from: Total Control (Hardcover)
David Baldacci attended law school at the University of Virginia, and went on to work as a trial lawyer, and later as a corporate lawyer, in Washington, D.C. He is now a full-time writer whose best selling novels include Absolute Power, The Winner, The Simple Truth and Saving Faith. He lives in Virginia with his wife and two children.
David Baldacci is now at the forefront of the current crop of thriller writers and in my book certainly deserves to be there. His storylines are thoughtful and his characters well rounded and totally believeable. He writes consistently well, something that not all authors achieve. Many having peaks and troughs in their writing careers. Some in fact having only one good book in them. Not so with David Baldacci, whose books always sell well and never (as far as I am concerned) disappoint.
This book revolves around a young executive who is about to disappear, leaving behind a wife who has the unenviable job of sorting out the lies he has told from the truth. An air investigation squad would like to know why the plane he was in suddenly dropped from the sky. The startling truth behind his disappearance raises all sorts of issues, not least a plot to murder the country's most powerful individual . . .
13 of 17 people found the following review helpful
1.0 out of 5 stars Cliched, hackneyed, yawn inducing pot boiler.,
By A Customer
This book is just like any other John Grisham or Patricia Cornball pot boiler. It is pulp fiction of the lowest order. All the characters are cardboard cut-outs: the FBI are big, tough guys who wear sunglasses in the dark and indoors; CEOs fly around in Lear Jets killing people; lawyers also fly around in Lear Jets and act unlike any lawyer in history; and assassins kill expertly until it comes to the heroine who they just can't seem to kill (mmm, wonder why).
Baldacci is one of those authors who has clearly done a lot of research, but he feels he needs to include all this research into the novel, even if it is boring, trite and unnecessary - which it always is. As an example we are treated to pages and pages of boring guff about the Federal Bank and how it effectively controls the lifes of all Americans. It is just a longwinded section of exposition that gets us nowhere. Even worse is the long explanation about how computers give off radiation and how images on monitors are made up of pixels. Wow! And this is all introduced at a time when the heroine is desperate to download some info from a disc and does not need to have this explained, so why the pages of exposition? I can only think it's to slow down the already turgid narrative and to pad out the book further.
The ending is also one long stream of exposition as our macho FBI agent tells us the reader, via one of the baddies, the whole convoluted plot. It takes pages and pages to spell out the plot I had been trying to follow.
...I couldn't really care about any of the characters in this as they were so paper thin - the FBI hero, Lee Sawyer, is so cliched even down to the sleeping problems, divorced wife, children who hate him, dark sunglasses worn at night, etc etc etc. Yawn!
I also objected to the way the husband character disappears from the story never to be mentioned again apart from when his death is raised at the end.
Check out the review at amazon.com which comments on the inconsistencies of Baldacci's writing, like the aircrash investigator who can't recognise a friend standing 2 feet from him, it's hilarious and so true.
If this was to be made into a film it wouldn't break new ground, it would be just as bog-standard as all the other mainstream Hollywood thrillers based on books like The Firm and The Pelican Brief. Let's hope it never sees the light of day.
37 of 48 people found the following review helpful
1.0 out of 5 stars 16 Year Old Suddenly Writes Book, Makes Millions!,
By A Customer
The main female character in Total Control, Sidney, is a senior partner in a major law firm but spends most of the book acting like a 14 year old. If another partner speaks to her in a way she doesn't like, she gives them a cold look and doesn't "grace them" with a response. Sidney would have trouble holding down a job as a receptionist, much less a senior partner. If Baldacci had made her smack her gum a few more times, she could easily have gone undercover in a junior high school.
Baldacci has Inspector Clousseau's eye for detail. In one early scene on page 85, two characters meet at the site of an airplane crash, and Baldacci sets a new record for cramming the most inconsistencies into a single paragraph. Baldacci describes the daylight as "rapidly failing," but Lee Sawyer shows up wearing sunglasses, perhaps because in Baldacci's junior-high world on-duty cops are required to wear sunglasses at all times. George Kaplan "freezes" when he sees Sawyer then squints to try to make out who that person is a "bare five feet away." I can usually identify people from 5 feet away, but then again, I don't squint to see in the dark; I open my eyes wider. When Sawyer steps forward, Kaplan is able to identify him--from about two feet away by my reckoning--which is probably pretty good for someone who's squinting in the dark.
Baldacci attended the Archie Bunker school of word choice, and selects his words more for what they sound like than what they mean. He has characters "alight into" a car. (You can't alight "into" a car; you can only alight "out of" a car.) Kaplan squints in the "rapidly failing" light. "Failing?" How about "fading?" On page 378 (which is almost as dense with hilarious inconsistencies as page 85), Baldacci reports that "a twitch erupted over Sidney's left eye." A twitch can't erupt. A twitch is minor. A "spasm" could erupt. How about just writing "Her left eyelid twitched?" Later, "Sidney struggled mightily not to perceptibly wince at the remark." Aside from the split infinitive, I think it would be as easy to notice a woman "struggling mightily" as to notice her wincing "perceptibly." Still further down the page, "Sidney felt herself trembling." What's does Baldacci mean by that? Did she reach out with one hand and feel the other hand trembling, or did she "notice" rather than "feel" that she was trembling? Throughout the book, most things happen "suddenly" as in "Steve suddenly criticized Baldacci's book on amazon.com."
The book is written almost exclusively in the passive voice. The sentence construction is truly impressive in that you would never think it was possible to twist certain words into a passive formation: "Sidney's legs were put by her into the front of the car." Weird things happen with people's legs throughout the book. Lee Sawyer walks on "telephone pole size legs" (presumably Baldacci is referring to thickness, not length). In one scene, Baldacci says "Sidney's legs began walking down the street." (We never learn where the rest of her went in that particular scene.)
This book requires the reader to suspend his or her disbelief, and in that it excels. You will be able to practice suspending your disbelief in laws of physics, human nature, business practices, legal procedings, police procedure, modern computing, and virtually every other topic Baldacci addresses.
After reading the first 10 pages, I was surprised that the book had been published at all. After the first 50, I kept reading for the amusement of seeing characters that were so silly and a plot that was so contrived -- and because other people on the airplane had taken all the more literary reading material, such as Seventeen and Tiger Beat magazines.
After 250 pages, I squinted my eyes and suddenly became convinced that Baldacci was 15 or 16 years old. The author changes voice and tense frequently, but mostly writes in third person omniscient. Readers are given full access to every thought every character in the book has for the duration of the adventure, and most of those are at the junior high level. If you read the book as a description of junior high school students role playing attorneys, FBI agents, computer programmers, and so on, it actually makes a lot of sense. Reinforcing my guess, Baldacci's word choices are mostly at about the 5th grade level, but every 3 or 4 pages he throws in a word like "brook," as in "Sidney's telephone-pole sized legs would brook no thought of walking down the street." I concluded that Baldacci was studying for the SAT as he wrote this book and worked in a lot of the words from his SAT study guide.
I didn't make it all the way to the ending, but I imagine it ends something like this:
Sidney's eyelids were made to coolly squint at the Chief Justice of the Supreme Court. "Miranda Shmiranda," she extemporized. Her hand suddenly slapped the Chief Justice on the lower left side of his cheek. The Chief Justice immediately froze and winked with pain. "That will show him to deny my appeal," she thought to herself, smacking her gum as her legs walked down Wall Street and off into the sunset.
4.0 out of 5 stars Good but a little dated.,
I read this book only recently, in 2015. The slant of the plot, based as it is in the tech of the '90's, seems very old hat. It was quaint to read of what was expected of technology in the future.
However, the plot was fast paced and twisted. I twice decided I knew the bad guy only to be proved wrong. The end is a little far fetched but finishes everything neatly.
3 of 4 people found the following review helpful
3.0 out of 5 stars Too lengthy,
Robin Hood "John" (Nottingham, UK) - See all my reviews
A reasonable read but far too long. Highly improbable storyline. Not saying people with power such as this are beyond their dalliances, but mass murder!!!!?
5.0 out of 5 stars ... not read a book by David Baldacci and been disappointed. This lived up to my expections,
I have not read a book by David Baldacci and been disappointed. This lived up to my expections. He never fails to keep you guessing right to the very end. I will endeavour to read all of his books.
5.0 out of 5 stars Didn't stop for breath,
Great book, fast pace, somewhat unbelievable at times. But couldn't put it down. Would really recommend this author to friends.
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Total Control by David Baldacci (School & Library Binding - Oct. 1999)
Used & New from: �12.32


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The English lads run Chelsea, says Szczesny
Arsenal keeper mocks player power at Bridge, as Wenger is charged by Uefa for tantrum
Thursday 08 March 2012
The English players at Chelsea run the club, according to Arsenal goalkeeper Wojciech Szczesny. With yet another Chelsea manager sacked last weekend, having fallen out with senior players, Szczesny suggested the power was misplaced at Stamford Bridge.
"I think some of the English lads at Chelsea run the club, pretty much," Szczesny said. "You know, they've had 10 different managers in the last few years." The situation, Szczesny said, was "a little different" from that at Arsenal, where the players were all behind Arsène Wenger. The Arsenal manager, though, was yesterday charged by Uefa with "improper conduct" for comments he made about referee Damir Skomina after Tuesday's Champions League exit to Milan.
Szczesny believes that Chelsea will recover and hopes that they will relegate Tottenham Hotspur into the Europa League positions: "I'm sure Chelsea will pick themselves up sooner or later, but hopefully not soon enough to get in front of Arsenal. It's all in our hands now. We don't really look at any other teams. We're three points clear of Chelsea, if we don't drop any points, simply we'll keep the fourth spot, hopefully challenge Tottenham for the third spot. Ideally, we'd finish third and Chelsea would finish fourth."
Szczesny said that he was pleased to play for a club where the manager was obviously in control. "We have a fantastic manager who knows how to run the club," he said. "We have the boss, and we know who is the boss in the dressing room, and that's Arsène Wenger obviously, and the skipper Robin van Persie, who is the leader in the team."
Arsenal's recent improved form – they have won four consecutive league games – Szczesny put down to their faith in Wenger. "All the players believe in what he's doing," he said. "Sometimes things don't go our way, but we believe in the way the manager runs the club, the way we want to play football, and we know that even if things are wrong we're going to turn it around and win games, and that's what we've done in the last few weeks."
After describing the dressing-room mood as "heartbroken" after their Champions League defeat by Milan, Szczesny said that Arsenal would flourish in the league if they could replicate that performance. "I think we should look at the positives from the game," he said of the 3-0 second-leg win. "We had a great performance, kept a clean sheet, scored three goals against one of the best sides in Europe. If we can take that into the Premier League, I think teams are going to struggle against us."
Arsenal's next match is a league game at home to Newcastle United on Monday, and Szczesny was confident about their last 11 matches. "We are in a spot that gives us Champions League football next season," he said. "We shouldn't really look at the form of other teams. We should just try to win every game."
Kieran Gibbs also believes the confidence has returned to Arsenal. "We had a difficult period with lots of players out," he said. "Everyone has come together. Now we have a bigger squad, which means we can rotate more and players won't be so tired and the team looks forward."
The priority, from here, is to ensure that Arsenal are in next season's Champions League. Gibbs said that "of course" requalifying for Europe's elite tournament would help with keeping Arsenal's best players. Gibbs paid tribute to Alex Oxlade-Chamberlain, who was brilliant in midfield in the first half on Tuesday, but tired afterwards. "He didn't look out of place in midfield," Gibbs said. "He is a fantastic player. He's a great talent and is going to be an important player for us. A lot of players played their part but we just fell short."
Gibbs claimed it was only tiredness which prevented Arsenal from overturning Milan and reaching the quarter-finals.
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An adventure is only an inconvenience rightly considered. An inconvenience is an adventure wrongly considered.
Is Your Destiny Leaving You Clues?
When you experience an involuntary emotional response, whether positive or negative, it is often a clue. You have stumbled onto something that will lead you toward or away from your destiny. It's important to pay attention.
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To achieve great things, two things are needed: a plan, and not quite enough time.
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Quantity produces quality. If you only write a few things, you are doomed.


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Town Square
Oakland Airport could see direct passenger rail service in 4 years
Original post made on Dec 11, 2009
Read the full story here Web Link posted Friday, December 11, 2009, 7:13 AM
Comments (1)
a resident of Amador Estates
on Dec 11, 2009 at 1:33 pm
Do we really need this? What's the problem with taking a bus from the Bart station to the airport? Why not put the same money into K-12 education here?
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Goldies 2013: North Carolina State University, Raleigh
Promoting local companies with NC State connections fosters student engagement.
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Students dine on local products at the All Carolinas Meal.
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"Wonderful British Cosy"
One of the top 10
In this book, Hilary Carew
Superb, fantastic narrater
Persistent Justice
Please put more of the rarer Patricia Wentworth books on your list. There are many that are only collectors items in price that many reader cannot afford. />However, if you do, make them available, none other than Diana Bishop should narrate them
"Marsh and Cumberbatch. Perfect together"
The book, even though abridged, was of course superbly written. The best moments were the conversations between inspector Allyn and his mother.
Benedict Cumberbatch is beyond superb in his narration. Please, please, more of him reading Ngaio Marsh unabridged.
"Totally enjoyable"
Met my expectations in all ways but one.
It should never have been abridged., and Benedict cumberbatch should read every book of Ngiao Marsh's unabridged.
He was superb.
"Regency Reality"
A surprisingly interesting Regency novel, giving a more real picture of life in the times of the Prince Regent. No frothy filmy muslins here. Kept my interest right through. I was expecting a poor imitation of a Georgette Heyer Regency book ( I am a fan of Heyer) but was pleasantly surprised by the gutsy narrative and narrator. Good performance too.
"Enjoyable and entertaining"
These wonderful railway stories, full of nostalgia from another age were delightful and thrilling. Patrick Malahide was superb in his narration, and I will listen to this book again, just to enjoy his expert ability in the
retelling. .
"Story keeps you on your toes!"
Yes, it was very enjoyable.
Somewhat like a Sherlock Holmes mystery, with clues twisting and turning, and red herrings around the corner.
Julian Rhind-Tutt was absolutely superb in his performance. Though his depiction of Poirot was impeccable, I enjoyed his performance of Sam Kidd the most. Pure genius.
It made me quite sad, and also angry at what had been done to Patrick Ives.
A very perfect writing style for a Poirot story. Beautifully written. This story kept me interested right through, but at times seemed convoluted, so that one had to go back several times to ascertain the turn if events, and the reasons and motives behind those events. Highly recommended.
"Hugh Fraser is a Master Narrator"
Yes, as it brought the story to life.
Intriguing story. Very enjoyable.
Hugh Fraser is superb. His voice is beautiful, and he is brilliant at all the different accents and voices
Yes, indeed.
Please get Hugh Fraser to read more books.
"None such like Heyer!"
Yes. Delightful romance, good narration. Totally enjoyable.
The Nonesuch himself was as usual wonderfully elegant, but I always enjoy the minor character in all of her books, such as a sister's husband, or a slightly backward friend whose dialogue is so funny, I cannot help laughing in total enjoyment at the absurdities!
Just right.
All of them.
I never tire of reading or listening to Georgette Heyer's works.
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|Reviews for No Love Like Ours
| kaybaby1127 chapter 36 . 3/23
holy moly this is a close one maaan !
| Stacy thomas chapter 36 . 3/22
I hope there more to this story I just read it
| ffedeline chapter 36 . 3/20
Let's hope everything goes smoorhly. Update soon.
| Ricciardi78 chapter 36 . 3/19
Thank you for updating! Can't wait for the end!
| Guest chapter 36 . 3/19
I am so happy with this update, this chapter was great and I can't wait to read what happens next. Keep up the good work, I hope Jax and Tara are reunited soon. Go get your girl Jax!
| Samantha Renk chapter 36 . 3/19
I need more asap can't wait for the guys to bring Tara home thank you so much for the update
| Mrssilvers chapter 36 . 3/19
So excited for the update. Jax has to rescue Tara now, the baby has to be due ? Let him get to her in time and be there for Thomas's birth. UPDATE SOON!
| debra.joines chapter 36 . 3/19
So glad you are continuing this story. Love it
| Guest chapter 36 . 3/19
Loved it
| HGRHfan35 chapter 36 . 3/19
Welcome back. I guess the last ever episode really cut you as well. Must've been hard to get back into writing. Good luck & onto spring break
| jaceyb1 chapter 36 . 3/19
I hope Jax saves Tara! I am so glad you updated and with your crazy schedule we are happy to wait! Now don't wait too long to update after leaving us wiht a cliffhanger!
| jcampbell943 chapter 36 . 3/19
Yayyyy Jax is coming! Those men would all die before they left her there so can't wait to see what transpires. I hope Kohn ends up a gonner!
| Guest chapter 36 . 3/19
So happy ur back thought u forgot about us lol. Loved it Jax is this close too getting Tara yes. Hopfully that's the next chap
| tinera.brown1 chapter 36 . 3/19
Thank u for writing it and i can wait for the next one if i have to
| Daliah1 chapter 36 . 3/19
Being waiting for your update for a long time. Cant wait.