Death anxiety as a function of aging anxiety

To assess how different facets of aging anxiety contributed to the prediction of tangible and existential death anxiety, 167 Americans of various Christian denominations completed a battery of questionnaires. Multiple regression analyses, controlling for demographic variables and previously demonstrated predictors of death anxiety, revealed that the aging anxiety dimensions of physical appearance concern and fear of losses each positively predicted tangible death anxiety. In addition, the aging anxiety dimension of fear of losses predicted existential death anxiety. Results are discussed with respect to the multifaceted nature of death anxiety and how different forms of aging anxiety contribute to anxieties about death.     

Biology of depression

Research over the past three decades has led to a greater understanding of the biologic basis of depression. Observations that certain medications could improve or worsen mood led to the development of hypotheses describing the possible role of specific neurotransmitters in the brain in depression. Modifications of these original hypotheses focused on altered receptor function, failures in the regulation of neurotransmitter systems, and interactions of the monoamines with cholinergic systems. Strategies using endocrinologic measurements in the evaluation of the depressed patient have provided researchers with new clues regarding disordered neuroendocrine function in depression and clinicians with new tests to aid in diagnosis and management. Moreover, the development of standardized sleep EEG methodology has proven useful for the identification of characteristic sleep abnormalities in depression. Although there are many methodologic and clinical problems still to be resolved, the use of biological markers in the assessment of the depressed patient is increasing, and is likely to be of significant importance in the future. Finally, recent advances in molecular genetics hold promise for further advances in our understanding of the inheritance and biochemistry of depression.     

Biology of congenital obstructive nephropathy

Congenital obstructive nephropathy is a common disease affecting fetuses and young children. The kidney shows profound morphologic and functional changes. The physiologic developmental kidney program is disturbed in the most advanced cases, arguing for altered temporal/spatial expression of genes which control normal nephrogenesis. Major regulators of mesenchymal-epithelial transformation and collecting duct and tubular development such as WT1 and Sall1 are decreased with obstruction. Additional candidate genes include GDNF/cRET, LIM1 and Pax2. Excessive apoptosis is an undisputed mechanism in these processes, mediated by decreased expression of apoptosis inhibiting genes (Bcl-2, HGF, IGF, BMP7), and overexpression of pro-apoptotic genes like Bax and TGF-beta. Renin and AT2R implicated in renal vascular development are decreased. Numerous extracellular matrix genes including Matrilysin are altered. The emerging theories of the biology of congenital obstructive nephropathy suggest new targets for therapeutic interventions with profound implications for these children.     

Biology of rat cytomegalovirus infection

Cytomegalovirus infection of Brown Norway rats was studied after intraperitoneal or subcutaneous inoculation of virus. No clinical illness was apparent during the 1st month postinfection (p.i.). Low titers of virus were detected in many organs at day 4 p.i. for the intraperitoneally inoculated animals and at day 11 p.i. for those inoculated subcutaneously. Thereafter, the virus disappeared from all tested organs except the salivary glands, where it appeared on day 11 p.i. and reached high levels by 4 weeks p.i. Histologically, no abnormalities were observed. The virus had an immunosuppressive effect during the 1st week p.i., as indicated by the immune response to sheep red blood cells.