Religious orientation, aging, and blood pressure reactivity to interpersonal and cognitive stressors

Background: Research on religion and health suggests general health benefits for those who are more religiously involved. Particular aspects of religiosity that may influence this finding, however, have not been sufficiently investigated.Purpose: This study was designed to explore the relationship between religious orientation (intrinsic, extrinsic) and blood pressure reactivity among older (over 60 years) and younger (18–24 years) adults exposed to two qualitatively different laboratory stressors (cognitive, interpersonal).Methods:Participants were categorized as exhibiting either a predominately intrinsic or extrinsic religious orientation based on scores on the Religious Orientation Scale. They were subsequently exposed (in counterbalanced order) to two laboratory stressors that varied in terms of whether an interpersonal confrontation was involved. Measures of blood pressure were obtained at baseline and during stressor presentation.Results: Analyses indicated that older extrinsically religious individuals demonstrated exaggerated reactivity compared to younger participants and older intrinsically religious individuals. Older intrinsically religious participants did not differ from younger persons. Similar results were found for analysis of baseline data. Extrinsic participants had greater reactivity during the interpersonal confrontation condition than did intrinsic individuals.Conclusions: These findings suggest that religious orientation may be an important variable to study regarding cardiovascular reactivity in, particularly, older adults. This research was supported in part by National Institute on Aging Grant 1 R03 AG 18554-01. A previous version of this article was presented in August 2002 as a Citation Paper at the 110th Annual Convention of the American Psychological Association, Chicago. We thank Timothy W. Smith, James A. Blumenthal, Carl E. Thoresen, and Edward M. Heath for their assistance throughout this project. We also thank Llewellyn Jones and Jodi Hildabrandt for their efforts in collecting data.     

Alimentary tract ganglioneuromatosis-lipomatosis, adrenal myelolipomas, pancreatic telangiectasias, and multinodular thyroid goiter. A possible neuroendocrine syndrome

Diffuse, alimentary tract ganglioneuromatosis-lipomatosis, bilateral adrenal myelolipomas, pancreatic telangiectasias, and a multinodular thyroid goiter were found at autopsy in a 56-year-old, white male with a history of insulin-dependent diabetes, hypertension, peptic ulcer, and remote cerebral infarction. The degree of atherosclerosis, arterionephrosclerosis, and cardiac disease found at autopsy did not correlate with the patient's history or his sudden death. The typical features of the multiple endocrine neoplasia syndrome, type II-B, were not identified. The findings in this patient may represent a variant of the multiple endocrine neoplasia complex, or a separate, previously unrecognized syndrome.     

Self-monitoring in patients with schizophrenia

BACKGROUND: The present study investigated whether a failure of self-monitoring contributes to core syndromes of schizophrenia. METHOD: Three groups of patients with a DSM-IV diagnosis of schizophrenia (n = 27), with either prominent paranoid hallucinatory or disorganization syndrome, or without these symptoms, and a matched healthy control group (n = 23) drew circles on a writing pad connected to a PC monitor. Subjects were instructed to continuously monitor the relationship between their hand movements and their visual consequences. They were asked to detect gain changes in the mapping. Self-monitoring ability and the ability to automatically correct movements were assessed. RESULTS: Patients with either paranoid-hallucinatory syndrome or formal thought disorder were selectively impaired in their ability to detect a mismatch between a self-generated movement and its consequences, but not impaired in their ability to automatically compensate for the gain change. CONCLUSIONS: These results support the claim that a failure of self-monitoring may underlie the core symptoms of schizophrenia.     

Predominance of null mutations in ataxia-telangiectasia

Ataxia-telangiectasia (A-T) is an autosomal recessive disorder involving cerebellar degeneration, immunodeficiency, chromosomal instability, radiosensitivity and cancer predisposition. The responsible gene, ATM, was recently identified by positional cloning and found to encode a putative 350 kDa protein with a Pl 3-kinase-like domain, presumably involved in mediating cell cycle arrest in response to radiation-induced DNA damage. The nature and location of A-T mutations should provide insight into the function of the ATM protein and the molecular basis of this pleiotropic disease. Of 44 A-T mutations identified by us to date, 39 (89%) are expected to inactivate the ATM protein by truncating it, by abolishing correct initiation or termination of translation, or by deleting large segments. Additional mutations are four smaller in-frame deletions and insertions, and one substitution of a highly conserved amino acid at the Pl 3-kinase domain. The emerging profile of mutations causing A-T is thus dominated by those expected to completely inactivate the ATM protein. ATM mutations with milder effects may result in phenotypes related, but not identical, to A-T.      

High throughput parallel analysis of hundreds of patient samples for more than 100 mutations in multiple disease genes

As more mutations are identified in genes of known sequence, there is a crucial need in the areas of medical genetics and genome analysis for rapid, accurate and cost-effective methods of mutation detection. We have developed a multiplex allele-specific diagnostic assay (MASDA) for analysis of large numbers of samples (> 500) simultaneously for a large number of known mutations (> 100) in a single assay. MASDA utilizes oligonucleotide hybridization to interrogate DNA sequences. Multiplex DNA samples are immobilized on a solid support and a single hybridization is performed with a pool of allele-specific oligonucleotide (ASO) probes. Any probes complementary to specific mutations present in a given sample are in effect affinity purified from the pool by the target DNA. Sequence-specific band patterns (fingerprints), generated by chemical or enzymatic sequencing of the bound ASO(s), easily identify the specific mutation(s). Using this design, in a single diagnostic assay, we tested samples for 66 cystic fibrosis (CF) mutations, 14 beta-thalassemia mutations, two sickle cell anemia (SCA) mutations, three Tay-Sachs mutations, eight Gaucher mutations, four mutations in Canavan disease, four mutations in Fanconi anemia, and five mutations in BRCA1. Each mutation was correctly identified. Finally, in a blinded study of 106 of these mutations in > 500 patients, all mutations were properly identified. There were no false positives or false negatives. The MASDA assay is capable of detecting point mutations as well as small insertion or deletion mutations. This technology is amenable to automation and is suitable for immediate utilization for high-throughput genetic diagnostics in clinical and research laboratories.