Title VII of the Civil Rights Act of 1964- Seniority Provisions of Union Collective Bargaining Agreement Held Controlling Over EEOC Affirmative Action Hiring Program. Jersey Central Power & Light Co. v. Local 327, IBEW, 508 F.2d 687 (3d Cir. 1975).

Plaintiff, Jersey Central Power & Light Company (Jersey Central), a large public utility, was economically forced to announce a series of plant wide layoffs. The collective bargaining agreement in force between Jersey Central and various unions required that layoffs be conducted in reverse order of seniority, i.e., the last person hired is the first person to be fired. A conciliation agreement among Jersey Central, the unions and the Federal Equal Employment Opportunity Commission (EEOC) called for the company to begin an affirmative action program designed to increase employment opportunities for women and minority workers. Plaintiff sought a declaratory judgment in federal district court as to its rights and obligations under the collective bargaining agreement, the conciliation agreement, Title VII of the Civil Rights Act of 1964 (Title VII) and Executive Order 11246. Plaintiff named various locals of the International Brotherhood of Electrical Workers (the Union), the EEOC, the Office of Federal Contract Compliance (OFCC), the General Services Administration (GSA), and the New Jersey Division of Civil Rights as defendants. Jersey Central took no position as to which of the two agreements must govern the proposed layoffs. The district court held that the layoffs could not alter the pre-layoff minority proportion of the work force by more than fifteen percent. On appeal, the Third Circuit reversed and held that layoffs were to be effectuated in accordance with the provisions of the collective bargaining agreement

Magnetic field effects on microwave absorbing materials

The objective of this program was to gather information to formulate a microwave absorber that can work in the presence of strong constant direct current (DC) magnetic fields. The program was conducted in four steps. The first step was to investigate the electrical and magnetic properties of magnetic and ferrite microwave absorbers in the presence of strong magnetic fields. This included both experimental measurements and a literature survey of properties that may be applicable to finding an appropriate absorbing material. The second step was to identify those material properties that will produce desirable absorptive properties in the presence of intense magnetic fields and determine the range of magnetic field in which the absorbers remain effective. The third step was to establish ferrite absorber designs that will produce low reflection and adequate absorption in the presence of intense inhomogeneous static magnetic fields. The fourth and final step was to prepare and test samples of such magnetic microwave absorbers if such designs seem practical

Endothelial cell CD36 deficiency prevents normal angiogenesis and vascular repair

Endothelial cells (ECs) maintain vascular integrity and mediate vascular repair and angiogenesis, by which new blood vessels are formed from pre-existing blood vessels. Hyperglycemia has been shown to increase EC angiogenic potential. However, few studies have investigated effects of fatty acids (FAs) on EC angiogenesis. Cluster of differentiation 36 (CD36) is a FA transporter expressed by ECs, but its role in EC proliferation, migration, and angiogenesis is unknown. We sought to determine if circulating FAs regulate angiogenic function in a CD36-dependent manner. CD36-dependent effects of FAs on EC proliferation and migration of mouse heart ECs (MHECs) and lung ECs (MLECs) were studied. We used both silencing RNA and antisense oligonucleotides to reduce CD36 expression. Oleic acid (OA) did not affect EC proliferation, but significantly increased migration of ECs in wound healing experiments. CD36 knockdown prevented OA-induced increases in wound healing potential. In EC transwell migration experiments, OA increased recruitment and migration of ECs, an effect abolished by CD36 knockdown. Phospho-AMP-activated protein kinase (AMPK) increased in MHECs exposed to OA in a CD36-dependent manner. To test whethe

Spiritual well-being may buffer psychological distress in patients with implantable cardioverter defibrillators (ICD)

Psychological distress is common in patients with implantable cardioverter defibrillators (ICDs) and has been associated with a worse prognosis. The authors examined whether spiritual well-being is associated with reduced psychological distress in patients with ICDs. The Functional Assessment of Chronic Illness Therapy-Spiritual Wellbeing (FACIT-SWB) questionnaire and the Hospital Anxiety and Depression Scale (HADS) were used to measure spiritual well-being and overall psychological distress. Multivariate linear regression was used to explore the relationship between these variables. The study sample included 46 ICD outpatients (32 M, 14 F; age range 43-83). An inverse association between HADS and FACIT-SWB scores was found, persisting after adjustment for demographics, anxiety/depression, medications, therapist support, and functional status (F = 0.001; β= -0.31, CI: -0.44, -0.19). In conclusion, spiritual well-being was independently associated with lower psychological distress in ICD outpatients. Spiritual well-being could act as a protective factor against psychological distress in these high-risk patients

Lipoprotein lipase regulates Fc receptor-mediated phagocytosis by macrophages maintained in glucose-deficient medium

During periods of intense activity such as phagocytosis, macrophages are thought to derive most of their energy from glucose metabolism under both aerobic and anaerobic conditions. To determine whether fatty acids released from lipoproteins by macrophage lipoprotein lipase (LPL) could substitute for glucose as a source of energy for phagocytosis, we cultured peritoneal macrophages from normal and LPL knockout (LPL-KO) mice that had been rescued from neonatal demise by expression of human LPL via the muscle creatine kinase promoter. Normal and LPL-KO macrophages were cultured in medium containing normal (5 mM) or low (1 mM) glucose, and were tested for their capacity to phagocytose IgG-opsonized sheep erythrocytes. LPL-KO macrophages maintained in 1 and 5 mM glucose phagocytosed 67 and 79% fewer IgG-opsonized erythrocytes, respectively, than macrophages from normal mice. Addition of VLDL to LPL-expressing macrophages maintained in 1 mM glucose enhanced the macrophages' phagocytosis of IgG-opsonized erythrocytes, but did not stimulate phagocytosis by LPL-KO macrophages. Inhibition of secreted LPL with a monoclonal anti-LPL antibody or with tetrahydrolipstatin blocked the ability of VLDL to enhance phagocytosis by LPL-expressing macrophages maintained in 1 mM glucose. Addition of oleic acid significantly enhanced phagocytosis by both LPL-expressing and LPL-KO macrophages maintained in 1 mM glucose. Moreover, oleic acid stimulated phagocytosis in cells cultured in non-glucose-containing medium, and increased the intracellular stores of creatine phosphate. Inhibition of oxidative phosphorylation, but not of glycolysis, blocked the capacity of oleic acid to stimulate phagocytosis. Receptor-mediated endocytosis of acetyl LDL by macrophages from LPL-expressing and LPL-KO mice was similar whether the cells were maintained in 5 or 1 mM glucose, and was not augmented by VLDL. We postulate that fatty acids derived from macrophage LPL-catalyzed hydrolysis of triglycerides and phospholipids provide energy for macrophages in areas that have limited amounts of ambient glucose, and during periods of intense metabolic activity

Eruptive xanthoma model reveals endothelial cells internalize and metabolize chylomicrons, leading to extravascular triglyceride accumulation

Although tissue uptake of fatty acids from chylomicrons is primarily via lipoprotein lipase (LpL) hydrolysis of triglycerides (TGs), studies of patients with genetic LpL deficiency suggest additional pathways deliver dietary lipids to tissues. Despite an intact endothelial cell (EC) barrier, hyperchylomicronemic patients accumulate chylomicron-derived lipids within skin macrophages, leading to the clinical finding eruptive xanthomas. We explored whether an LpL-independent pathway exists for transfer of circulating lipids across the EC barrier. We found that LpL-deficient mice had a marked increase in aortic EC lipid droplets before and after a fat gavage. Cultured ECs internalized chylomicrons, which were hydrolyzed within lysosomes. The products of this hydrolysis fueled lipid droplet biogenesis in ECs and triggered lipid accumulation in cocultured macrophages. EC chylomicron uptake was inhibited by competition with HDL and knockdown of the scavenger receptor-BI (SR-BI). In vivo, SR-BI knockdown reduced TG accumulation in aortic ECs and skin macrophages of LpL-deficient mice. Thus, ECs internalize chylomicrons, metabolize them in lysosomes, and either store or release their lipids. This latter process may allow accumulation of TGs within skin macrophages and illustrates a pathway that might be responsible for creation of eruptive xanthomas

Cardiac immune cell infiltration associates with abnormal lipid metabolism

CD36 mediates the uptake of long-chain fatty acids (FAs), a major energy substrate for the myocardium. Under excessive FA supply, CD36 can cause cardiac lipid accumulation and inflammation while its deletion reduces heart FA uptake and lipid content and increases glucose utilization. As a result, CD36 was proposed as a therapeutic target for obesity-associated heart disease. However, more recent reports have shown that CD36 deficiency suppresses myocardial flexibility in fuel preference between glucose and FAs, impairing tissue energy balance, while CD36 absence in tissue macrophages reduces efferocytosis and myocardial repair after injury. In line with the latter homeostatic functions, we had previously reported that CD3