Contributory Negligence in Product Liability

This article does not purport to be exhaustive. It does explore the extent to which classical defenses of contributory negligence, assumption of risk and their relative, misuse of product, are available in product liability actions. Caveat: By the time this printer\u27s ink is drysome of these applications may be available no longer

Appeasement of Tort Claimants

Justice does not always mean that a case should be tried. By the same token, justice does not always mean that every case should be settled without trial. One of our difficulties is that too often there is more interest in the expedient settlement of differences between litigants than in a judicial determination of rights according to principles of law

Book Reviews

El Conflicto Honduras-El Salvador y El Orden Juridico Internacional -- On July 14, 1969, the armed forces of El Salvador invaded Honduras... This book provides an almost hourly account of the events preceding the conflict, the war plans executed before the conflict started, the initiation of Inter-American System machinery for settling disputes, the heated discussions among the representatives of the different nations of the OAS, and the consequences of the war itself. Also included is the necessary background on the political and economic conditions prevailing in both countries before the war and a thorough analysis of what role law and international legal machinery played--or might have played--at different stages of the conflict. Reviewed by Jorge L. Carro ============================= United States Foreign Relations Law: Documents and Sources, Vol. 1 (Executive Agreements). Michael J. Glennon and Thomas M. Franck Dobbs Ferry, New York: Oceania Publications, Inc., 1980. Pp. ix, 474. 40.00.-- This volume on United States executive agreements is the first of a multivolume series providing important documents and other materials dealing with the foreign relations power of the federal government and its constituent parts. Reviewed by David S.Clark =========================== Towards a New International Economic Order Mohammed Bedjaoui New York and London: Holmes & Meier Publishers,1979. Pp. 287. 16.50. When tracing the ideologies that animate and condition the current North-South debate over what has come to be called the New International Economic Order, MIT economist Jagdish Bhagwati identifies two dominant schools of thought regarding the existing international economic order. Reviewed by Burns H. Westo

Connective tissue growth factor(CCN2), a pathogenic factor in diabetic nephropathy. What does it do? How does it do it?

Connective tissue growth factor (CTGF/CCN2) is a member of the CCN family of matricellular proteins. Its expression is induced by a number of factors including TGF-β. It has been associated with fibrosis in various tissues including the kidney. Diabetic nephropathy (DN) develops in about 30% of patients with diabetes and is characterized by thickening of renal basement membranes, fibrosis in the glomerulus (glomerulosclerosis), tubular atrophy and interstitial fibrosis, all of which compromise kidney function. This review examines changes in CTGF expression in the kidney in DN, the effects they have on glomerular mesangial and podocyte cells and the tubulointerstitium, and how these contribute to driving fibrotic changes in the disease. CTGF can bind to several other growth factors modifying their function. CTGF is also able to interact with receptors on cells, including integrins, tyrosine receptor kinase A (TrkA), low density lipoprotein receptor-related protein (LRP) and heparan sulphate proteoglycans. These interactions, the intracellular signalling pathways they activate, and the cellular responses evoked are reviewed. CTGF also induces the expression of chemokines which themselves have pharmacological actions on cells. CTGF may prompt some responses by acting through several different mechanisms, possibly simultaneously. For example, CTGF is often described as an effector of TGF-β. It can promote TGF-β signalling by binding directly to the growth factor, promoting its interaction with the TGF-β receptor; by triggering intracellular signalling on binding the TrkA receptor, which leads to the transcriptional repression of Smad7, an inhibitor of the TGF-β signalling pathway; and by binding to BMP-7 whose own signalling pathway opposing TGF-β is inhibited, leading to enhanced TGF-β signalling

Search for direct top squark pair production in final states with two leptons in √s=13 TeV pp collisions with the ATLAS detector

The results of a search for direct pair production of top squarks in events with two opposite-charge leptons (electrons or muons) are reported, using 36.1 fb−1 of integrated luminosity from proton–proton collisions at √s=13 TeV collected by the ATLAS detector at the Large Hadron Collider. To cover a range of mass differences between the top squark t~ and lighter supersymmetric particles, four possible decay modes of the top squark are targeted with dedicated selections: the decay t~→bχ~1± into a b-quark and the lightest chargino with χ~1±→Wχ~10 , t~→tχ~10 into an on-shell top quark and the lightest neutralino, the three-body decay t~→bWχ~10 and the four-body decay t~→bℓνχ~10. No significant excess of events is observed above the Standard Model background for any selection, and limits on top squarks are set as a function of the t~ and χ~01 masses. The results exclude at 95% confidence level t~ masses up to about 720 GeV, extending the exclusion region of supersymmetric parameter space covered by previous searches

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease