857 research outputs found
Thirst
No full text J. T. Fitzsimons, “Thirst,” vol. 52, no. 2, April 1972, p. 481, line 6, the formula should read: [See PDF for Equation] </jats:p
Dearest Ellen! dearest Ellen! I'll love you no more! [first line of chorus]
No full textstrophic with choruspiano and voiceJohns Hopkins University, Levy Sheet Music Collection, Box
115, Item 181Words by E.J.B. Fitzsimons, Esqr. Music by Sir J. Stevenson, Mus. Doc.Engraved by T. Birc
Dearest Ellen! dearest Ellen! I'll love you no more! [first line of chorus]
No full textstrophic with choruspiano and voiceJohns Hopkins University, Levy Sheet Music Collection, Box
115, Item 181Words by E.J.B. Fitzsimons, Esqr. Music by Sir J. Stevenson, Mus. Doc.Engraved by T. Birc
Suppressors of cytokine signalling (SOCS) 2 and 3 diametrically control macrophage polarisation
No full textSuppressors of cytokine signalling (SOCS) 2 and 3 diametrically
control macrophage polarisation
S. Spence,* A. Fitzsimons,* C. Boyd,* J. Kessler,* D. Fitzgerald,*
J. Elliott,* J. Ni Gabhann, S. Smith, A. Sica, E. Hams,§
S. P. Saunders,§ C. Jefferies, P. Fallon,§ D. Mcauley,*
A. Kissenpfennig* & J. Johnston*
*Queen’s University Belfast, Belfast, UK, Royal College of Surgeons in
Ireland, Dubin, Ireland, Instituto Clinca Humanitas, Milan, Italy,
§Trinity College Dublin, Dublin, Ireland
M1 macrophages, induced by pro-inflammatory stimuli, and involved
in the acute response. M2 macrophages are polarised by anti-inflammatory
stimuli and mainly involved in healing. The Suppressors of
cytokine signalling (SOCS) are important regulators of both LPS and
cytokine responses but their role in macrophage polarisation is unknown.
Myeloid restricted SOCS3 deletion (SOCS3LysMcre) resulted
in profound resistance to endotoxic shock, whereas SOCS2)/) mice
were highly susceptible. This was associated with striking bias towards
M2-like macrophages in SOCS3LysMcre mice, whereas the M1-like
population was enriched in SOCS2)/) mice. Through adoptive
transfer experiments we show that these antipodal responses to endotoxic
shock and to polymicrobial sepsis (caecal ligation puncture)
were both transferable and entirely macrophage-dependent. Critically
this dichotomous response was associated with enhanced T-reg recruitment
by SOCS3)/) cells, yet in the presence of SOCS2)/)
macrophages, Foxp3+ T cells were completely absent at the inflammatory
site. The altered polarisation coincided with enhanced
IFNc- induced STAT1 in SOCS2)/) macrophages and enhanced IL-4/
IL-13 induced STAT6 phosphorylation in SOCS3)/) cells corresponding
to altered binding to traditional gene markers of M1 and M2
macrophages (iNOS, TNFa, ARG-1 and CCL-17,). In the absence of
SOCS2, macrophages seem unable to elicit an anti- inflammatory response
even when stimulated with typical M2 stimulus (IL-4/IL-13, IL-
10), whilst the absence of SOCS3 prevents a pro-inflammatory response
even in the presence of LPS/IFNc. Interestingly, the polarisation
of macrophages in the absence of SOCS2 or SOCS3 seems fixed and
irreversible. Therefore SOCS are essential controllers of macrophage
polarisation and regulate the inflammatory response
Death in the neonatal intensive care unit: changing patterns of end of life care over two decades
No full textBackground: Death remains a common event in the neonatal intensive care unit, and often involves limitation or withdrawal of life sustaining treatment. Objective: To document changes in the causes of death and its management over the last two decades. Methods: An audit of infants dying in the neonatal intensive care unit was performed during two epochs (1985–1987 and 1999–2001). The principal diagnoses of infants who died were recorded, as well as their apparent prognoses, and any decisions to limit or withdraw medical treatment. Results: In epoch 1, 132 infants died out of 1362 admissions (9.7%), and in epoch 2 there were 111 deaths out of 1776 admissions (6.2%; p<0.001). Approximately three quarters of infants died after withdrawal of life sustaining treatment in both epochs. There was a significant reduction in the proportion of deaths from chromosomal abnormalities, and from neural tube defects in epoch 2. Conclusions: There have been substantial changes in the illnesses leading to death in the neonatal intensive care unit. These may reflect the combined effects of prenatal diagnosis and changing community and medical attitudes.D J Wilkinson, J J Fitzsimons, P A Dargaville, N T Campbell, P M Loughnan, P N McDougall, J F Mill
Angiotensin, Thirst, and Sodium Appetite
No full textFitzsimons, J. T. Angiotensin, Thirst, and Sodium Appetite. Physiol. Rev. 78: 583–686, 1998. — Angiotensin (ANG) II is a powerful and phylogenetically widespread stimulus to thirst and sodium appetite. When it is injected directly into sensitive areas of the brain, it causes an immediate increase in water intake followed by a slower increase in NaCl intake. Drinking is vigorous, highly motivated, and rapidly completed. The amounts of water taken within 15 min or so of injection can exceed what the animal would spontaneously drink in the course of its normal activities over 24 h. The increase in NaCl intake is slower in onset, more persistent, and affected by experience. Increases in circulating ANG II have similar effects on drinking, although these may be partly obscured by accompanying rises in blood pressure. The circumventricular organs, median preoptic nucleus, and tissue surrounding the anteroventral third ventricle in the lamina terminalis (AV3V region) provide the neuroanatomic focus for thirst, sodium appetite, and cardiovascular control, making extensive connections with the hypothalamus, limbic system, and brain stem. The AV3V region is well provided with angiotensinergic nerve endings and angiotensin AT1receptors, the receptor type responsible for acute responses to ANG II, and it responds vigorously to the dipsogenic action of ANG II. The nucleus tractus solitarius and other structures in the brain stem form part of a negative-feedback system for blood volume control, responding to baroreceptor and volume receptor information from the circulation and sending ascending noradrenergic and other projections to the AV3V region. The subfornical organ, organum vasculosum of the lamina terminalis and area postrema contain ANG II-sensitive receptors that allow circulating ANG II to interact with central nervous structures involved in hypovolemic thirst and sodium appetite and blood pressure control. Angiotensin peptides generated inside the blood-brain barrier may act as conventional neurotransmitters or, in view of the many instances of anatomic separation between sites of production and receptors, they may act as paracrine agents at a distance from their point of release. An attractive speculation is that some are responsible for long-term changes in neuronal organization, especially of sodium appetite. Anatomic mismatches between sites of production and receptors are less evident in limbic and brain stem structures responsible for body fluid homeostasis and blood pressure control. Limbic structures are rich in other neuroactive peptides, some of which have powerful effects on drinking, and they and many of the classical nonpeptide neurotransmitters may interact with ANG II to augment or inhibit drinking behavior. Because ANG II immunoreactivity and binding are so widely distributed in the central nervous system, brain ANG II is unlikely to have a role as circumscribed as that of circulating ANG II. Angiotensin peptides generated from brain precursors may also be involved in functions that have little immediate effect on body fluid homeostasis and blood pressure control, such as cell differentiation, regeneration and remodeling, or learning and memory. Analysis of the mechanisms of increased drinking caused by drugs and experimental procedures that activate the renal renin-angiotensin system, and clinical conditions in which renal renin secretion is increased, have provided evidence that endogenously released renal renin can generate enough circulating ANG II to stimulate drinking. But it is also certain that other mechanisms of thirst and sodium appetite still operate when the effects of circulating ANG II are blocked or absent, although it is not known whether this is also true for angiotensin peptides formed in the brain. Whether ANG II should be regarded primarily as a hormone released in hypovolemia helping to defend the blood volume, a neurotransmitter or paracrine agent with a privileged role in the neural pathways for thirst and sodium appetite of all kinds, a neural organizer especially in sodium appetite, or all of these, remains uncertain. ANG II-induced drinking behavior serves as a model of how other complex behaviors involving neural and peptide inputs might be organized.</jats:p
Pretoriana, volume 1, no. 1, Sept. 1951
No full textBoodskappe / Die Burgemeester van Pretoria, Raadslid J.H. Visse; Mnr. W. Punt, M. A. --
Messages / The Mayor of Pretoria, Councillor J.H. Visse; Mr, W. Punt, M. A. -- Grondwet • Constitution -- Enige besonderhede in verband met Du Preezhoek / W. Punt. -- The origin of Palace Street / Miss J.H. Davies --
Historical Collections of the Transvaal Museum / Dr. V. FitzSimons -- "A Wanderer's Rhymes" / Dr. J. Ploeger -- Ek onthou / J.P. Kleynhans -- Die oorsprong van ons straatname / F.J. du Toit Spies -- Vondste in die Staatsmodelskool / J. Ploeger
Construction of rugged, ultrastable optical assemblies with optical component alignment at the few microradian level
No full textA method for constructing quasimonolithic, precision-aligned optical assemblies is presented. Hydroxide-catalysis bonding is used, adapted to allow optimization of component fine alignment prior to the bond setting. We demonstrate the technique by bonding a fused silica mirror substrate to a fused silica baseplate. In-plane component placement at the submicrometer level is achieved, resulting in angular control of a reflected laser beam at the sub-10-μrad level. Within the context of the LISA Pathfinder mission, the technique has been demonstrated as suitable for use in space-flight applications. It is expected that there will also be applications in a wide range of areas where accuracy, stability, and strength of optical assemblies are important
Constraints on the timing and conditions of high-grade metamorphism, charnockite formation and fluid-rock interaction in the Trivandrum Block, southern India
No full textIncipient charnockites have been widely used as evidence for the infiltration of CO₂-rich fluids driving dehydration of the lower crust. Rocks exposed at Kakkod quarry in the Trivandrum Block of southern India allow for a thorough investigation of the metamorphic evolution by preserving not only orthopyroxene-bearing charnockite patches in a host garnet–biotite felsic gneiss, but also layers of garnet–sillimanite metapelite gneiss. Thermodynamic phase equilibria modelling of all three bulk compositions indicates consistent peak-metamorphic conditions of 830–925 °C and 6–9 kbar with retrograde evolution involving suprasolidus decompression at high temperature. These models suggest that orthopyroxene was most likely stabilized close to the metamorphic peak as a result of small compositional heterogeneities in the host garnet–biotite gneiss. There is insufficient evidence to determine whether the heterogeneities were inherited from the protolith or introduced during syn-metamorphic fluid flow. U–Pb geochronology of monazite and zircon from all three rock types constrains the peak of metamorphism and orthopyroxene growth to have occurred between the onset of high-grade metamorphism at c. 590 Ma and the onset of melt crystallization at c. 540 Ma. The majority of metamorphic zircon growth occurred during protracted melt crystallization between c. 540 and 510 Ma. Melt crystallization was followed by the influx of aqueous, alkali-rich fluids likely derived from melts crystallizing at depth. This late fluid flow led to retrogression of orthopyroxene, the observed outcrop pattern and to the textural and isotopic modification of monazite grains at c. 525–490 Ma.E. Blereau, C. Clark, R. J. M. Taylor, T. E. Johnson, I. C. W. Fitzsimons, M. Santos
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