A COMPARISON OF THE PSYCHOLOGICAL WELL-BEING OF NEVER-MARRIED AND MARRIED AGED LIVING IN URBAN AUSTRALIA

This study, based upon analyses of the A.N.U. Ageing and The Family Project's survey, disputes the negative stereotype often applied to older people who have never-married. It shows that those who are physically and mentally able and living within the community are no more likely to suffer from depression, dissatisfaction and social relationships, loneliness, or anxiety than their married peers. The results show that never-married older people are self-sufficient individuals who enjoy spending time alone, and living without the complications associated with marriage. Social factors have little importance in the maintenance of the never-married's morale, while the opposite is true of the marrieds. In any future research on the social consequences of marital status in later life it would seem apposite to include some form of personality measure.     

Apical hypertrophic cardiomyopathy mimicking acute coronary syndrome: a case report and review of the literature

Apical hypertrophic cardiomyopathy is a form of hypertrophic cardiomyopathy localized to the left ventricular apex. It is common in Japanese and other Asian populations, where it is generally considered relatively benign. However, its presence has also been recognized, though less commonly, in non-Asian patients. In these patients, the electrocardiographic changes and symptoms associated with apical hypertrophic cardiomyopathy often mimic acute coronary syndromes. Invasive or noninvasive evaluation of the left ventricular cavity confirms the diagnosis, with the "ace-of-spades" sign on left ventriculography being pathognomonic. Its prognosis is relatively benign in terms of cardiovascular mortality; however, morbid sequelae, such as diastolic dysfunction, left atrial enlargement, apical thrombi, ventricular aneurysms, and myocardial infarction, are not uncommon. The authors present a case of apical hypertrophic cardiomyopathy in a Caucasian patient who presented with findings suggestive of acute coronary syndrome and review the literature on apical hypertrophic cardiomyopathy.     

B Cell Production of Tumor Necrosis Factor in Response to Pneumocystis murina Infection in Mice

Pneumocystis species are opportunistic fungal pathogens that induce tumor necrosis factor (TNF) production by alveolar macrophages. Here we report that B cells from the draining lymph nodes as well as lung CD4⁺ T cells are important producers of TNF upon Pneumocystis murina infection. To determine the importance of B cell-derived TNF in the primary response to P. murina, we generated bone marrow chimeras whose B cells were unable to produce TNF. The lung P. murina burden at 10 days postinfection in TNF knockout (TNFKO) chimeras was significantly higher than that in wild-type (WT) chimeras, which corresponded to reduced numbers of activated CD4⁺ T cells in the lungs at this early time point. Furthermore, CD4⁺ T cells isolated from P. murina-infected TNFKO chimeras were unable to stimulate clearance of P. murina upon adoptive transfer to recombinase-deficient (RAG1KO) hosts. Together, these data indicate that B cell-derived TNF plays an important function in promoting CD4⁺ T cell expansion and production of TNF and facilitating protection against P. murina infection.     

Identification of hepoxilin A3 in inflammatory events: a required role in neutrophil migration across intestinal epithelia

The mechanism by which neutrophils [polymorphonuclear leukocyte (PMNs)] are stimulated to move across epithelial barriers at mucosal surfaces has been basically unknown in biology. IL-8 has been shown to stimulate PMNs to leave the bloodstream at a local site of mucosal inflammation, but the chemical gradient used by PMNs to move between adjacent epithelial cells and traverse the tight junction at the apical neck of these mucosal barriers has eluded identification. Our studies not only identify this factor, previously termed pathogen-elicited epithelial chemoattractant, as the eicosanoid hepoxilin A(3) (hepA(3)) but also demonstrate that it is a key factor promoting the final step in PMN recruitment to sites of mucosal inflammation. We show that hepA(3) is synthesized by epithelial cells and secreted from their apical surface in response to conditions that stimulate inflammatory events. Our data further establish that hepA(3) acts to draw PMNs, via the establishment of a gradient across the epithelial tight junction complex. The functional significance of hepA(3) to target PMNs to the lumen of the gut at sites of inflammation was demonstrated by the finding that disruption of the 12-lipoxygenase pathway (required for hepA(3) production) could dramatically reduce PMN-mediated tissue trauma, demonstrating that hepA(3) is a key regulator of mucosal inflammation.     

Alterations of Granulopoiesis Following Chemotherapy

Clonal proliferation of marrow granulocytic progenitor cells (GPC) in vitro andthe daily urinary output of granulocyticcolony-stimulating factor (CSF) were determined in two patients with acutemyeloid leukemia (AML) in remission andone patient with malignant lymphoma receiving monthly pulses of chemotherapywith cytosine arabinoside and 6-thioguanine. During and immediately following therapy, a marked decrease of granulocytic colony-forming capacity (CFC)occurred, with an increase and return tobasal levels by 3-4 wk. In the AMLpatients, the proportion of GPC in DNAsynthesis (GPC-S), as determined by thethymidine suicide technique, declinedfrom basal levels (31%-39%) to 0%-26% after 2 days of treatment. This wasfollowed by a sharp rise in GPC-S to41%-75% 1-3 days posttherapy, with anoscillatory return of GPC-S to basal levelsby 3-4 wk. In all courses a marked increase of urinary CSF output occurredduring or 1 day posttherapy, concomitantwith the rise of the proportion of GPC-S.In the lymphoma patient, an initially highproportion of marrow GPC-S and low CFCanticipated the severe neutropenia whichfollowed therapy. These results provide abasis for determining the efficacy withwhich cytotoxic drugs destroy proliferativeactivity of GPC and for assessing thepotential for hemopoietic toxicity following chemotherapy.

Submitted on August 10, 1973 Accepted on February 27, 1974     

Design features of the Avasimibe and Progression of coronary Lesions assessed by intravascular UltraSound (A-PLUS) clinical trial

Background Although statins have been shown to be beneficial in the management of hyperlipidemia and the reduction of cardiovascular morbidity and mortality, rates of major cardiovascular events remain high despite their use. Inhibition of the acyl coenzyme A: cholesterol acyltransferase (ACAT) enzyme in the arterial wall may prevent excess accumulation of cholesteryl esters in macrophages. In addition to ACAT inhibitor monotherapy, combination of a statin with an ACAT inhibitor may be a promising approach to further prevent the progression of atherosclerosis. Methods This report describes the design and methodologic features of a double-blind, randomized, placebo-controlled trial to assess the effect of the ACAT inhibitor avasimibe at 50-, 250-, and 750-mg daily dosages on the progression of coronary atherosclerosis as assessed by intravascular ultrasound (IVUS). All patients receive background lipid-lowering therapy when necessary. The study population consists of patients with at least one 20% to 50% diameter stenosis in a coronary artery with a reference diameter of ≥2.5 mm. IVUS and coronary angiography are performed at baseline and repeated at 24 months. The primary study end point is the change from baseline in plaque volume in a 30-mm segment of the coronary artery assessed by 3-dimensional IVUS. Several other IVUS and angiographic end points are measured. Conclusions The Avasimibe and Progression of coronary Lesions assessed by intravascular UltraSound (A-PLUS) trial is among the first large imaging trials to use IVUS as a primary end point and assesses the effects of the ACAT inhibitor avasimibe on atherosclerosis progression. (Am Heart J 2002;144:589-96.)