Tests on a 'glauert' nose-suction aerofoil in the N.P.L. 4-ft. no. 2 wind tunnel

Tests on an 8.65 per cent thick nose-suction aerofoil designed by Glauert have been made in the 4 ft No. 2 wind tunnel at the National Physical Laboratory at Reynolds numbers 0.385 and 0.577 x l0 (to the power of 6). The results show that the section stalls at a lift coefficient of 1.13 without suction. With suction quantities of 0.003, 0.0045, 0.006 and (with a wider slot) 0.012, the values of Cl(max) were respectively 1.32, 1.34, 1.36 and 1.57

CELL-TO-CELL INTERACTION IN THE IMMUNE RESPONSE : IX. REGULATION OF HAPTEN-SPECIFIC ANTIBODY CLASS BY CARRIER PRIMING

Mice primed to horse erythrocytes (HRBC) produced greatly enhanced 3,5-dinitro,4-hydroxyphenylacetic (NNP)-specific indirect plaque-forming cell (7S PFC) responses when given NNP.HRBC but no difference in hapten-specific direct (19S PFC) responses in comparison to non-carrier-primed mice. The effect was carrier specific and could not be produced by simultaneous challenge of rabbit erythrocyte (RRBC)-primed mice with RRBC and NNP.HRBC. When spleen cells from HRBC-primed mice were transferred to irradiated recipients, there was again an enhanced 7S response to NNP.HRBC. The primed spleen cells could be replaced by giving activated thymus cells to HRBC together with normal spleen as a source of B cells. It is concluded that T cells influence not only the amount but also the class of antibody formed by hapten-sensitive B cells

Tests on a 'lighthill' nose-suction aerofoil in the N.P.L. 4-ft. no. 2 wind tunnel

A series of tests on an 8.6 per cent thick nose-suction aerofoil designed by Lighthill has been made in the 4 ft No. 2 Wind Tunnel at the National Physical Laboratory at Reynolds numbers of 0.385 and 0.577 x 10(to the power of 6). The results show that the wing stalls at alpha ~= 3 deg (Cl = 1.12) without suction, the lift coefficient at the stall increasing approximately linearly with suction quantity and reaching 1.93 at Cq = 0.019 and 23 deg incidence

Consolidated Health Economic Evaluation Reporting Standards 2022 (CHEERS 2022) statement: updated reporting guidance for health economic evaluations.

Health economic evaluations are comparative analyses of alternative courses of action in terms of their costs and consequences. The Consolidated Health Economic Evaluation Reporting Standards (CHEERS) statement, published in 2013, was created to ensure health economic evaluations are identifiable, interpretable, and useful for decision making. It was intended as guidance to help authors report accurately which health interventions were being compared and in what context, how the evaluation was undertaken, what the findings were, and other details that may aid readers and reviewers in interpretation and use of the study. The new CHEERS 2022 statement replaces previous CHEERS reporting guidance. It reflects the need for guidance that can be more easily applied to all types of health economic evaluation, new methods and developments in the field, as well as the increased role of stakeholder involvement including patients and the public. It is also broadly applicable to any form of intervention intended to improve the health of individuals or the population, whether simple or complex, and without regard to context (such as health care, public health, education, social care, etc). This summary article presents the new CHEERS 2022 28-item checklist and recommendations for each item. The CHEERS 2022 statement is primarily intended for researchers reporting economic evaluations for peer reviewed journals as well as the peer reviewers and editors assessing them for publication. However, we anticipate familiarity with reporting requirements will be useful for analysts when planning studies. It may also be useful for health technology assessment bodies seeking guidance on reporting, as there is an increasing emphasis on transparency in decision making

Listeria pathogenesis and molecular virulence determinants

The gram-positive bacterium Listeria monocytogenes is the causative agent of listeriosis, a highly fatal opportunistic foodborne infection. Pregnant women, neonates, the elderly, and debilitated or immunocompromised patients in general are predominantly affected, although the disease can also develop in normal individuals. Clinical manifestations of invasive listeriosis are usually severe and include abortion, sepsis, and meningoencephalitis. Listeriosis can also manifest as a febrile gastroenteritis syndrome. In addition to humans, L. monocytogenes affects many vertebrate species, including birds. Listeria ivanovii, a second pathogenic species of the genus, is specific for ruminants. Our current view of the pathophysiology of listeriosis derives largely from studies with the mouse infection model. Pathogenic listeriae enter the host primarily through the intestine. The liver is thought to be their first target organ after intestinal translocation. In the liver, listeriae actively multiply until the infection is controlled by a cell-mediated immune response. This initial, subclinical step of listeriosis is thought to be common due to the frequent presence of pathogenic L. monocytogenes in food. In normal indivuals, the continual exposure to listerial antigens probably contributes to the maintenance of anti-Listeria memory T cells. However, in debilitated and immunocompromised patients, the unrestricted proliferation of listeriae in the liver may result in prolonged low-level bacteremia, leading to invasion of the preferred secondary target organs (the brain and the gravid uterus) and to overt clinical disease. L. monocytogenes and L. ivanovii are facultative intracellular parasites able to survive in macrophages and to invade a variety of normally nonphagocytic cells, such as epithelial cells, hepatocytes, and endothelial cells. In all these cell types, pathogenic listeriae go through an intracellular life cycle involving early escape from the phagocytic vacuole, rapid intracytoplasmic multiplication, bacterially induced actin-based motility, and direct spread to neighboring cells, in which they reinitiate the cycle. In this way, listeriae disseminate in host tissues sheltered from the humoral arm of the immune system. Over the last 15 years, a number of virulence factors involved in key steps of this intracellular life cycle have been identified. This review describes in detail the molecular determinants of Listeria virulence and their mechanism of action and summarizes the current knowledge on the pathophysiology of listeriosis and the cell biology and host cell responses to Listeria infection. This article provides an updated perspective of the development of our understanding of Listeria pathogenesis from the first molecular genetic analyses of virulence mechanisms reported in 1985 until the start of the genomic era of Listeria research

Macrophage activation during experimental murine brucellosis: a basis for chronic infection

Evidence is presented that the chronicity of infection in CBA mice after injection of Brucella abortus 19 is related to a number of factors: (i) the relative resistance of B. abortus to macrophage killing, which allowed some bacteria to survive the peak of macrophage activity occurring at 14 days; (ii) the decline in macrophage activity thereafter (this decline was related in part to the presence of fewer bacteria to stimulate the bactericidal activity and also to specific, active suppressor mechanisms not identified in this study); and (iii) the insensitivity of the persistent Brucella organisms to activated macrophages. This was not due to a selection of genetically resistant bacteria, but possibly to their inaccessibility, either within "incompetent" macrophages or outside macrophages altogether.</jats:p