Indeed !! And for some reason after reading it, the song above started to play in my head.. (Allthough in that, the ryhming is perfect..)

Centaur Engineering Limited Registered in England and Wales with number 11569365 Registered office at Wells Point, 79 Wells Street, London W1T 3QN

Mice were sacrificed and perfused with cold PBS to minimize contamination of brain and spinal cord with blood-derived leukocytes from peripheral blood. Leukocytes from CNS were isolated by enzymatic digestion of brains followed by Percoll® density gradient centrifugation as previously described13.

Circulating eosinophils, basophils and eosinophil/basophil (Eo/B) progenitors were examined in 12 patients at the time of an exacerbation of asthma accompanied by sputum eosinophilia and after resolution of the exacerbation with inhaled corticosteroid treatment. Differential counts were performed and peripheral blood non-adherent mononuclear cells were cultured for 14 days in methyl-cellulose to determine the number of Eo/B and granulocyte-macrophage (GM) colonies without knowledge of the clinical conditions or findings. With resolution of the asthma exacerbation on beclomethasone therapy, there were significant falls in circulating eosinophils, basophils and Eo/B colonies whereas GM colonies were unchanged. To elucidate whether the observed changes could be due to systemic absorption or local action of inhaled corticosteroid, seven subjects with allergic rhinitis and no current evidence of lower airway inflammation (no symptoms of asthma and normal methacholine airway responsiveness) received 14 days’ treatment with the same dose of inhaled beclomethasone or of placebo in a double-blind randomized cross-over study. No significant changes in airway function or in circulating cell counts were observed. The results suggest reduced production of eosinophils and basophils after the resolution of an exacerbation of asthma. This effect may be due to reduced levels of airway-derived eosinophil-basophil growth and differentiation factors. Copyright © 1990, Wiley Blackwell. All rights reserved

Basu, S., Binder, R. J., Suto, R., Anderson, K. M. & Srivastava, P. K. Necrotic but not apoptotic cell death releases heat shock proteins, which deliver a partial maturation signal to dendritic cells and activate the NF-kappa B pathway. Int. Immunol. 12, 1539–1546 (2000).

Asthma is a heterogeneous inflammatory airways disorder where interleukin (IL)-1ß is thought to be a key mediator, especially in the neutrophilic subtype of asthma. The generation of active IL-1ß requires proteolytic cleavage typically mediated through the formation of a caspase-1-containing inflammasome. This study hypothesised that an IL-1ß endotype associated with the nucleotide-binding domain, leucine-rich repeat-containing family protein (NLRP)3/apoptosis-associated speck-like protein containing a caspase-recruitment domain (ASC)/caspase-1 inflammasome is characteristic of patients with the neutrophilic subtype of asthma. Participants with asthma (n=85) and healthy controls (n=27) underwent clinical assessment, spirometry and sputum induction. Sputum was processed for differential cell count, gene expression and protein mediators. NLRP3 and caspase-1 expression was also determined by immunocytochemistry. Sputum macrophages were isolated (n=8) and gene expression of NLRP3 and IL-1ß determined. There was significantly elevated gene expression of NLRP3, caspase-1, caspase-4, caspase-5 and IL-1ß in participants with neutrophilic asthma. Protein levels of IL-1ß were significantly higher in those with neutrophilic asthma and correlated with sputum IL-8 levels. Sputum macrophages, as well as sputum neutrophils in neutrophilic asthma, expressed NLRP3 and caspase-1 protein. NLRP3 inflammasome is upregulated in neutrophilic asthma and may regulate the inflammation process observed in this asthma phenotype through production of IL-1ß. Copyright © ERS 2014.

I should have also pointed out how American leaders past and present have been expressing fear that ‘Muslims’ or others would ‘destroy’ their way of life. If colonialism is so benign, then why would the US, UK or other (ex colonial and present colonial Western states) worry so much about *their way of life* changing…? Just a thought.

This is the protocol for a review and there is no abstract. The objectives are as follows: The objectives are as follows: 1). to determine the effectiveness of ciclesonide in clin… [more]

Premise1 Premise 2 Premise 3 … Therefore “if some Jews lived there in the past, all Jews have a right to live there now”.

It is well known that the PSA is not a very accurate screening test. There are other attempts to improve upon it., including using MRIs to determine whether someone has a lesion that corresponds to the elevated PSA or not.

It has been demonstrated that disease severity in C. albicans infections correlates with kidney levels of many cytokines and chemokines like IL-6, KC (CXCL1), MIP-2 (CXCL2), TNF, and MCP-1 (CCL2)30. Interestingly, these cytokines and chemokines were strongly upregulated in ONX 0914 treated mice (Figs 6D,E and 7B). In particular, MacCallum et al. demonstrated significant correlation of early kidney KC (CXCL1) concentrations with subsequent histological kidney lesion parameters30. Hence, the development of tissue pathology in C. albicans-infected mice appears to depend on relative balances of cytokine or chemokine production and of neutrophil recruitment to the kidney supporting a direct exacerbating effect of LMP7 inhibition on the pathogenesis of disseminated candidiasis. Although neutrophils represent a central arm of the anti-C. albicans immunity they may also be harmful to the host by mediating immunopathology and tissue injury31. While sepsis is the major cause of death in systemic candidiasis, the extent of kidney damage in animals showing severe symptoms contributes to the overall pathology of the disease28,30. It has been recognized for many years that the disease processes in C. albicans-infected kidneys lead to heavy host leukocyte infiltrates and microabscess formation which in turn result in tissue damage30. Hence, excessive infiltration of monocytes and neutrophils into the brain and the kidney of ONX 0914 treated mice (Fig. 5C,D) might lead to meningoencephalitis and kidney injury, respectively29,31,33,50. Indeed, at least in some experiments, we noticed that kidneys of ONX 0914 treated mice had severe swelling and pallor in gross pathology and that these mice display altered behaviour as manifested by movement disorders and neurological abnormalities (data not shown). Moreover, although the expression of KIM-1, a marker of tubular epithelial damage currently used for diagnosis of acute kidney injury in humans51, was not changed (Fig. 7C), we measured significantly elevated TNF-α and IL-6 (Fig. 7B) as well as urea and creatinine (Fig. 7A) levels in the serum of ONX 0914 treated mice. This suggests that LMP7 inhibition contributes to both death-associated pathologies, sepsis as well as renal failure, respectively.

I shouldn’t need to present to you my ‘credentials’ Jon s, but will do it anyway just for the record: I was born, raised, and educated in Israel (born in Tel Aviv and grew up in Bat-Yam, attended Yitzhak Sade primary in Bat-Yam, and Ort Yad Singalovsky high school in Yad Elilyahu). I served my two years in the Israeli army. I was trained as a מ״כית and later worked as a draftswoman in מה״ד in the army’s central HQ in Tel-Aviv. I was very close to the machinations of Israel’s first invasion of Lebanon in 1982 under Ariel Sharon. My maternal grandparents were holocaust survivors. I am a native Hebrew speaker, and my entire family is in Israel. I am not speaking from reading a book, or from being ‘brainwashed’ by evil antisemites. I am from there, it appears a little more than you are, if as Mooser says you were indeed born in the US and immigrated to Israel later.